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Essentials in Dermatology
(with Multiple Choice Questions)
Second Edition
Devinder M Thappa
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Jitendar P Vij
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Acknowledgements
I would like to thank those who helped me to update chapters
1. Dr Balaji Adityan for updating
Principles of Diagnosis in Dermatology
Bacterial Infections
Viral Infections
Fungal Infections
Skin Changes in Pregnancy and Old Age
2. Dr Sakthi Kandan for
Infestations
Disorders of Hair and Nails
Metabolic and Nutritional Disorders
Skin in Systemic Diseases
3. Dr Sowmya Kaimal for
Pediatric Dermatology
Human Immunodeficiency Virus Infection (HIV) and Acquired Immunodeficiency Syndrome
(AIDS)
4. Dr Amiya Kumar Nath for
Eczema
Connective Tissue Disorders
Genetics and Genodermatoses
5. Dr Abhijit Chougule for
Differential Diagnosis for Leprosy
Treatment of Leprosy
6. Dr Kishan Kumar Agarwal for
Urticaria, Angioedema and Pruritus
Disorders of Sebaceous, Eccrine and Apocrine Glands
7. Dr Nidhi Singh for
Cutaneous Tuberculosis and Atypical Mycobacterial Infections
Vesiculobullous Disorders
Pigmentary Disorders
Following residents helped in framing MCQs for postgraduates
1. Dermatology Basics
Dr Abhijit Chougule
Dr Kishan Kumar Agarwal
2. Clinical Dermatology Part -I
Dr Rashmi Kumari
Essentials in Dermatology
Dr Balaji Adityan
Dr Ajay Kumar Singh
Dr Anuradha Priyadarshini
Dr Tukaram Sori
3. Clinical Dermatology Part -II
Dr Malathi
Dr Sathyamoorthy
4. Sexually Transmitted Diseases
Dr Sowmya Kaimal
Dr Rajalakshmi
5. Leprosy
Dr Abarna Devi
Dr Sakthi Kandan
Reviews
Most of the dermatology textbooks are too much voluminous for undergraduate students already
overburdened with other heavy weight subjects. Not only undergraduates, beginners at the
postgraduate level also face problem to acquire basic conception from such large books. So there is
always a need for a concise book which can provide clear basic conception and up-to-date knowledge
to the students.will be of immense help to the postgraduate entrance examinees.should be
collected in all undergraduate medical college libraries for the benefit of the students
Indian J Dermatol 2003; 48(4): 248.
The stated aim of the book is to have a short textbook for new entrants to postgraduate
studies in dermatology which could glimpse of the subject and understand basic dermatology before
venturing for detailed standard textbooks. The second aim stated is to fulfill the needs of students
aspiring for entering in postgraduate courses in reputed institutes.well written and fulfill the
stated aimsAn approach to attempting MCQs appears to be a very useful chapter.strongly
recommend this book to the new entrants in specialty training and those preparing for admission to
postgraduate courses
Indian J Dermatol Venereol Leprol 2004; 70(6): 393.
Contents
SECTION 1: DERMATOLOGY
1. Ten Most Influential People in Medicine and Dermatology .................................................... 3
2. History of Dermatology in the World ............................................................................................ 5
3. Microanatomy of the Skin ................................................................................................................ 8
4. Physiology, Biochemistry and Immunology of the Skin ......................................................... 13
5. Principles of Diagnosis in Dermatology ..................................................................................... 16
6. Bacterial Infections .......................................................................................................................... 31
7. Viral Infections ................................................................................................................................. 43
8. Fungal Infections ............................................................................................................................. 57
9. Infestations ........................................................................................................................................ 72
10. Papulosquamous Disorders ........................................................................................................... 82
11. Eczema ................................................................................................................................................ 99
12. Vesiculobullous Disorders ........................................................................................................... 114
13. Cutaneous Tuberculosis and Atypical Mycobacterial Infections ........................................ 127
14. Connective Tissue Disorders (Collagen Vascular Disorders) ............................................... 134
15. Pigmentary Disorders ................................................................................................................... 148
16. Keratinization Disorders .............................................................................................................. 156
17. Urticaria, Angioedema and Pruritus .......................................................................................... 166
18. Drug Eruptions, Erythema Multiforme, Stevens-Johnson Syndrome
and Toxic Epidermal Necrolysis ................................................................................................. 172
19. Disorders of Sebaceous, Eccrine and Apocrine Glands ......................................................... 180
20. Disorders of Hair and Nails ......................................................................................................... 189
21. Metabolic and Nutritional Disorders ......................................................................................... 198
22. Genetics and Genodermatoses .................................................................................................... 210
23. Skin in Systemic Diseases ............................................................................................................ 222
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Essentials in Dermatology
24. Skin Changes of Pregnancy and Old Age ................................................................................. 237
25. Pediatric Dermatology .................................................................................................................. 240
26. Benign, Pre-malignant and Malignant Tumors of the Skin .................................................. 246
27. Topical Formulary and Key Systemic Drugs ............................................................................ 257
28. Dermatosurgical Procedures ........................................................................................................ 272
SECTION 3: LEPROSY
34. Historical Milestones in Leprosy ................................................................................................ 327
35. History Taking and Examination in Leprosy ........................................................................... 330
36. Clinical Leprosy ............................................................................................................................. 333
Multiple Choice Questions .................................................................................................................... 351
Some Useful Medical Mnemonics ....................................................................................................... 441
Terminology ............................................................................................................................................. 447
Answers ..................................................................................................................................................... 465
Index ........................................................................................................................................................... 469
Essentials in Dermatology
9. Wilhelm Rontgen (1845-1923): Discoverer of
X-rays in 1895 and nobel prize winner in Physics
in 1901. The value of X-rays in the diagnosis and
treatment was recognised and accepted almost
from the outset of their discovery.
10. Sigmund Freud (1856-1939): Considered the
founder of psychoanalysis, he believed that a
complex of repressed and forgotten expressions
underlies all abnormal mental states and that
infantile mental processes are important in later
development.
History of Dermatology
in the World
Essentials in Dermatology
of DNA; inflammation-histamine, prostaglandins, cytokines, adhesion molecules;
immunology-cell mediated and humoral
immunity; tissue culture; pathogenic agentsspirochetes, viruses, prion; therapies- x-rays,
antibacterial, immunosuppressive; controlled clinical trials), and strictly
dermatological areas(books- Jadassohn,
Pillsbury, Rothman, Rook; biologykeratinocyte, melanocyte, Langerhans cell,
basement membrane; diseases- epidermolysis bullosa, pemphigus, toxic epidermal
necrolysis; people- from Unna to Katz;
therapies- local steroids, griseofulvin,
phototherapy, retinoids, Mohs surgery,
laser, cryotherapy).
EVOLUTION OF DERMATOLOGY
In India, recognition of dermatology as a
specialty distinct from internal medicine is
recent; it has still not grown to its full stature
in practice and teaching.
Therapeutics of dermatoses have been
known and practiced by our ancient
physicians for centuries. Charaka Samhita
contains one chapter on the subject.
Medical charlatans selling panaceas for
cutaneous ailments and faith healers were
commonly seen all over the country. With the
advent of scientific dermatology, their
number and importance has dwindled.
In the latter part of the 19th century, the
health authorities in then British India
became aware of the need to have data on
prevalence of dermatoses and venereal
diseases.
The first chair of dermatology was
established at Grant Medical College,
Jamshedji Jeejebhoy Hospital (JJ Hospital),
Bombay in 1895.
The second department, at the School of
Tropical Medicine in Calcutta, was started in
1923, after a gap of nearly 28 years, under
EVOLUTION OF VENEREOLOGY
Syphilis was first introduced into North India
nearly 500 years ago.
National STD Control Programme was
started in 1946. This programme continued
to operate till 1991 and with the arrival of HIV
infection in the country, the programme was
EVOLUTION OF LEPROLOGY
There is a great deal of speculation about the
early history of leprosy. The earliest records,
which give accurate descriptions of the
disease, come from India and may have been
written as early as 600 BC.
Essentials in Dermatology
DEVELOPMENT OF SKIN
Epidermis develops from ectoderm lateral to
neural crest, dermis from mesenchyme and
neural crest cell, subcutaneous fat from
mesenchyme and melanocytes from neural crest.
Foetal skin development occurs in three stagesspecification, morphogenesis and differentiation.
Its specification occurs from 0 to 60 days,
morphogenesis from 2 to 5 months, and
differentiation from 5 to 9 months.
Epidermis
It is approximately 0.4 mm to 1.6 mm in
thickness. The majority of the cells in the
epidermis are the keratinocytes. These cells are
organized into five layers-stratum corneum,
stratum lucidum (present only in palmar and
plantar skin), stratum granulosum, stratum
spinosum, and stratum basale or stratum
germinatum (Fig. 3.2).
Stratum corneum is the outermost layer
containing flattened anucleated cells without cell
organelles. The thick epidermis of palms and
soles has an additional layer underneath the
stratum corneum that is electron lucent and is
called the stratum lucidum. The stratum
granulosum is so called due to the presence of
10
Essentials in Dermatology
Fig. 3.2: Diagrammatic representation of shapes of various cells in the epidermis and changes in them as
they move up from basal cell layer to stratum corneum during the process of keratinization
Dermis
The dermis is formed by connective tissue
having fibres (collagen, elastic and reticulin) and
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Essentials in Dermatology
Functions of nails are:
1. Protect terminal phalanges
2. Cosmetic function
3. Helps in appreciation of tactile stimuli
4. Scratching of skin
5. Helps in holding minute objects with finger
tips.
Besides the above elements, dermis contains
blood vessels which form two plexuses (other
than providing nutrition to the skin, blood
vessels regulate temperature and blood
pressure), lymphatics roughly parallel the major
vascular plexuses, nerves of the skin are part of
two major systems somatic sensory and
autonomic motor, smooth muscle occurs in the
skin as arrectores pilorum, as the tunica dartos
of the scrotum and in the areolar around the
PERCUTANEOUS ABSORPTION
The skin is considered to be a composite
membrane with three anatomically distinct
layers; the stratum corneum (10 m), the viable
epidermis (100 m), and the uppermost papillary
layer of the dermis (100-200 m), each having a
different diffusion constant. Even healthy adult
human skin allows some permeation of almost
every substance, and rates of penetration of
different materials may differ by 10,000 fold.
The efficiency of the barrier differs between
body sites. The scrotum is particularly permeable
and the face, forehead, and dorsa of the hands
may be more permeable to water than the trunk,
arms, and legs. The palms are particularly
impermeable to nearly all molecules except
water.
The barrier is affected by many other factors,
such as age, environmental conditions and
physical trauma, and permeability can be
13
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Essentials in Dermatology
enhanced by various agents, permitting
increased access of topically applied drugs.
KERATINIZATION
Keratinization is a process of differentiation of
germinative cells in the basal cell layer into the
deceased cornified cells of stratum corneum.
It involves:
1. Synthesis of distinctive proteins (e.g. keratins,
filaggrins, and involucrin) and lamellar
granules, and
2. Alterations of nuclei, cytoplasmic organelles,
plasma membranes and desmosomes.
Keratin function is to provide mechanical
strength, cellular structure, and assistance in
adhesion molecule attachment. Soft keratin
desquamates as the result of enzymatic action
but the hard keratin of the hair and nails
does not, thus requiring periodic cutting.
The epidermis is the prototype of keratinizing
squamous epithelia, also present in the
oesophagus, vagina and oral mucosa.
THERMOREGULATION
The maintenance of a near constant body core
temperature of 37oC is a great advantage to
humans, allowing a constancy to biochemical
reactions which would otherwise fluctuate
widely with temperature changes.
The thermoreceptor cells of the skin are
distributed irregularly over the skin, there being
warm- and cold-sensitive thermoreceptors.
Information on changes in their stimulation in
response to changes in the temperature is sent
to the hypothalamus leading to either to
inhibition of sweating or stimulation of
shivering. Skin temperature has a greater role
in mediating the behavior, for example by
turning on the heating or putting on extra
clothing.
Thermoregulation depends on several
factors, including metabolism and exercise but
the skin plays an important part in control
through the evaporation of sweat and by direct
heat loss from the surface. Heat can be lost
through the skin surface in four ways:
1. Radiation
2. Convection
3. Conduction
4. Evaporation
SKIN FAILURE
Skin failure is defined as a loss of normal
temperature control with inability to maintain
the core temperature, failure to prevent
percutaneous loss of fluids, electrolytes and
proteins with resulting imbalance and failure of
IMMUNOLOGICAL COMPONENTS OF
SKIN
The immunological functions of the skin depend
both upon cells in the epidermis and on dermal
cellular constituents. Antimicrobial peptides
(AMPs) are a diverse group of proteins that are
involved as first line of immune defense by many
living things. In human skin, AMPs provide a
chemical barrier to potentially pathogenic microorganisms. Sebaceous lipids have been reported
to possess antibacterial properties and
glycophospholipids and free fatty acids of
stratum corneum have bacteriostatic effect
selective for pathogenic organisms.
Skin associated lymphoid tissue (SALT) is
langerhans cells, T lymphocytes, mast cells and
keratinocytes. They are involved in various
hypersensitivity reactions of the skin. Hypersensitivity is defined as inappropriate or
exaggerated immune response to a foreign or self
antigen resulting in tissue damage. Main types
of hypersensitivity responses of skin are type I
(immediate), type II (antibody-dependent
cytotoxicity), type III (immune complex disease)
and type IV(cell mediated or delayed). Urticaria
and anaphylaxis is the example for type I
hypersensitivity, transfusion reactions for type
II hypersensitivity, leukocytoclastic vasculitis for
type III hypersensitivity and allergic contact
dermatitis for type IV hypersensitivity.
15
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Essentials in Dermatology
Principles of Diagnosis in
Dermatology
Treatment history: Skin lesions are often selfmanipulated by home remedies, or over the
PHYSICAL EXAMINATION
It has been said by Goethe What is most difficult
of all? It is what appears most simple: To see with
your eyes what lies in front of your eyes .
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Essentials in Dermatology
Hand lens useful on occasions like identifying:
a. Altered skin markings in tumors.
b. Nail fold telangiectasia.
c. Burrows in scabies.
d. Wickhams striae- for this place a drop of
mineral oil on the area, which makes the
stratum corneum transparent.
Subtle genital warts- aceto-whitening,
gauze soaked with 5% acetic acid applied in
suspected area for 3 minutes, warts turn white.
Actually individual skin lesions are
analogous to the letters of the alphabet, and
groups of lesions can be analogous to words or
phrases. Basis of morphological lesions is given
in the form of table for clear understanding.
Basis of morphological lesions in dermatology
1. Impalpable change- Macule
2. Palpable change
Solid change-Papule, plaque, nodule, wheal
Primary Lesions
These are the lesions, which appear first in any
skin disease. They are the best clues to the
diagnosis. They are:
Macule: The macule is a discrete, flat,
circumscribed lesion that differs from
surrounding skin because of its color
(Fig. 5.1). It may be a small or a large macule.
Earlier used term patch is now obsolete.
Macule may be erythematous, hypo-
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Essentials in Dermatology
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Essentials in Dermatology
Special Lesions
These lesions are given below:
Comedone: It is a plug of keratin and sebum
formed in the follicular canal of
pilosebaceous unit. Comedones may be
closed or open.
Burrows: These are serpentine caves of
scabies mite at the level of stratum
granulosum. They are visible as S-shaped
brownish-black lesions, which at their distal
end have a papule housing the mite.
Alopecia means loss of hair.
Telangiectasia: It refers to individually
visible dilated vessels.
Poikiloderma: It is a combination of atrophy,
pigmentation and telangiectasia.
Purpura: It is visible extravasated blood
(Fig. 5.19). It may occur as tiny pinpoint spots
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24
Essentials in Dermatology
9. Seborrhoeic dermatitis
25
26
Essentials in Dermatology
27
Essentials in Dermatology
28
29
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Essentials in Dermatology
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
VDRL
HIV antibody detection test
Culture and sensitivity test
Patch testing
Prick testing
Intradermal testing
LE cell phenomenon
Mouse foot pad inoculation
Immunofluorescence
Hair examination and counts
Trichogram- method for analyzing hair
bulbs to identify in what stage hairs are
being lost and thus to distinguish between
different types of hair loss.
23. Electron microscopy
Bacterial Infections
Bacterial Infections
PYODERMAS
Pyoderma is a common purulent infection of the
skin caused by staphylococcal or streptococcal
organisms. They can be classified as primary
pyodermas and secondary pyodermas (Table 6.1).
Staphylococcal Pyodermas
Impetigo
Non-bullous impetigo (Impetigo contagiosa of
Tilbury Fox):
It is caused by S. aureus or group A
Streptococcus or both
Occurs in children of all ages, common
in preschool and young school children
Commonly over the face (especially
around nares) or extremities after trauma
The initial lesion is a transient vesicle or
pustule that quickly evolves into a honey
coloured crusted plaque (Fig. 6.1)
Surrounding erythema may be present
Primary pyodermas
1. Invasion of normal skin by bacteria
2. Single species of bacteria involved
3. Appearance of lesions is characteristic
e.g., impetigo, erysipelas, furuncle
4. Treatment is clear cut Drugs aimed
at the microorganism
Secondary pyodermas
1. Develop in areas of already damaged/compromised skin
2. Mixture of organisms involved
3. Not characteristic
4. Role of antibacterial treatment less defined.
Here, the aim is to treat the underlying process
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Essentials in Dermatology
Table 6.2: Non-follicular and follicular pyodermas
A. Non follicular pyodermas include
1. Impetigo
2. Ecthyma
3. Cellulitis
4. Erysipelas
5. SSSS
B. Follicular pyodermas include
1. Folliculitis
2. Furuncle
3. Carbuncle
Bullous Impetigo
Table 6.3: Cutaneous diseases caused by
staphylococci and streptococci
1. Cutaneous diseases caused by
staphylococcus include:
A. Direct infection of skin:
Impetigo, ecthyma, folliculitis, furunculosis,
carbuncle, sycosis.
B. Due to effect of bacterial toxin:SSSS, TSS.
2. Cutaneous diseases caused by streptococcus:
A. Direct infection of skin:
Impetigo, ecthyma, erysipelas, cellulitis,
vulvovaginitis, perianal infection, blistering
dactylitis, necrotizing fasciitis.
B. Due to effect of bacterial toxin:
Scarlet fever, toxic shock like syndrome
Bacterial Infections
Complications of Impetigo
Post-streptococcal acute glomerulonephritis
S. pyogenes type M-49
Scarlet fever
Urticaria
Erythema multiforme
Rheumatic fever in not a complication of
streptococcal skin infection (but of streptococcal
sore throat).
Ecthyma
Consequence of neglected impetigo
S. aureus and/ or group A Streptococcus
are causative agents
Most commonly occurs on the lower
extremities of children or neglected
elderly patients
Poor hygiene and neglect are key
elements in pathogenesis.
Dirty grayish-yellow crust surmounts a
punched out ulcer (Fig. 6.3).
Folliculitis
Pyoderma affecting the hair follicles, classified
according to depth of invasion.
Superficial folliculitis
Also known as follicular or Bockharts
impetigo
A small fragile dome shaped pustule
occurs at the infundibulum of a hair
follicle, often on scalps of children and in
the beard area, axilla, extremities and
buttocks of adults.
Differential diagnois: Miliaria pustulosa
non follicular pustules are wide spread,
which occur in hot and humid conditions
Deep folliculitis
Sycosis barbae is a deep folliculitis with
perifollicular inflammation occurring in the
bearded areas of the face (Fig. 6.4) and upper
lip.
Differential diagnosis
1. Pseudofolliculitis Papules/pustules are
irregularly scattered at the site of ingrowing
beard hairs. Neck and angle of jaw (vs.
sycosis barbae upper lip and below angles
of jaw) are preferentially involved.
2. Tinea barbae Site involved is usually
submaxillary region or the chin. Hairs are
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Essentials in Dermatology
broken or loosened (easy and painless
pluckablity) in the affected area. Loss of hair
is the norm. Suppurative or granulomatous
nodules rather than pustules characterize this
condition. Spores and hyphae can be demonstrated in the hair by KOH examination.
3. Herpetic sycosis is usually limited for a few
days and invariably shows vesicles even in
persistent lesions
4. Acne vulgaris is polymorphous condition
mainly of glabrous skin of the face where
comedones are the hallmark of that condition
Lupoid sycosis is deep, chronic form of
sycosis barbae associated with scarring usually
occurring as circinate lesion. Pustules and
papules surround a central scar (Fig. 6.5).
Differential diagnosis: Lupus vulgaris is
characterized by areas of scarring on one side
and progression on the other side. There is
absence of pustules in the lesions but it
demonstrates apple jelly nodules on diascopy.
Bacterial Infections
compromise. Typically, the patient has fever
and is irritable. The changes usually begin
periorificially or in body folds (Figs 6.7 and
6.8). Then they spread rapidly. Nikolskys
sign is positive even on apparently normal
skin. One should culture the perineum, eyes,
ears, nose and throat, looking for S. aureus as
the focus of infection is located at a distant
site. The bacteria can not be cultured from
the skin. For differential diagnosis Table 6.4.
Fig. 6.7
Fig. 6.8
Figs 6.7 and 6.8: SSSStypical periorificial and body fold involvement with peeling skin
Table 6.4: Differential diagnosis of SSSS from toxic epidermal necrolysis (TEN)
TEN
1.
2.
3.
4.
5.
6.
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Essentials in Dermatology
3. Desquamation of palms and soles 1 to 2
weeks after onset
4. Hypotension
5. Involvement of 3 or more other organ
systems
About 85 to 90 percent of cases of TSS have
occurred in women at the time of menstruation; almost all had been tampon users
(particularly of super absorbent types).
Differential diagnosis:
1. SSSS It has the presence of bullae,
Nikolskys sign is positive with skin
tenderness, but systemic organs are not
involved and patient appears wellpreserved.
2. Scarlet fever not usually associated with
hypotension and shock.
3. Kawasakis syndrome prolonged fever,
cardiac involvement, generalized
lymphadenopathy and absence of
peripheral shock.
Streptococcal Pyodermas
The major pathogen belongs to group A and is
referred to as Streptococcus pyogenes. Streptococci
colonise damaged skin, although less frequently
than staphylococci. Major complications
following streptococcal infection are rheumatic
fever (following Streptococcal pyogenes
pharyngitis), acute glomerulonephritis (both
throat and skin infection), erythema nodosum
and guttate psoriasis, and scleredema of Buschke
(following throat infection).
Impetigo and Ecthyma already discussed.
Crowding, poor hygiene, and neglected minor
skin trauma contribute to the spread of
streptococcal impetigo in families.
Bacterial Infections
Blistering Dactylitis
This is nearly always a group A streptococcal
infection in children or teenagers.
A large blister containing thin seropurulent
fluid forms on the distal phalanx, usually of
a finger, typically on a phalangeal pad.
Streptococcal Vulvovaginitis
Streptococcus pyogenes accounts for 10% of
cases of vulvovaginitis in prepubertal girls.
Diagnosis
1. Grams stained smear from the purulent
material may demonstrate streptococci or
staphylococci or both.
2. Culture and sensitivity: Swabs taken from
infected sites may be sent for culture and
sensitivity, so that appropriate antibiotic may
be instituted to treat the condition.
3. Tzanck smear in SSSS shows acantholytic
cells.
4. Histopathology: Histopathological examination is hardly required for the diagnosis.
Treatment
1. General measures such as improved
hygiene, loose light weight porous clothing,
regular bathing, use of antiseptics in bath,
antibacterial soaps, etc.
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Essentials in Dermatology
2. Wet compresses: Condys compresses for
crusted lesions of pyoderma.
3. Incision and drainage is indicated when
furuncle has become localized and shows
definite fluctuation.
4. Topical antibacterial agents such as gentian
violet, neomycin, fusidic acid or mupirocin.
5. Systemic antibacterial agents: Systemic
antibiotic therapy is indicated
i. For extensive lesions of pyoderma
ii. For erysipelas, cellulitis, carbuncle,
furunculosis, SSSS, etc.
Penicillin is preferred for streptococcal
infection whereas penicillinase resistant
penicillin such as cloxacillin and cephalosporins
are required for staphylococcal infections. Oral
antibiotics (e.g., rifampicin 600 mg orally daily
for 10 days) have been effective in eradicating S.
aureus from most nasal carriers for periods of up
to 12 weeks in cases having recurrent
furunculosis. Intranasl application of 2%
mupirocin ointment for 5 days can eliminate S.
aureus nasal carriage in 70% of healthy
individuals for up to 3 months.
NON-PYODERMAS
Erythrasma
Causative agent-Corynebacterium minutissimum, diphtheroids bacillus, gram positive,
non spore forming rod shaped organism.
Bacterial infection of the intertriginous areas
like axilla, groin, gluteal cleft, inframammary
folds, umbilicus and toe web spaces.
Usually manifest with asymptomatic red
brown macules with sharp border (Fig. 6.11).
The best way to make the diagnosis is Woods
light examination for coral red fluorescence.
Differential diagnosis: Hyperpigmented
tinea versicolor (asymptomatic in nature)
may appear like erythrasma. It predominantly affects upper trunk, individual
lesions are small, but not erythematous and
satellite lesions are more commonly seen than
Trichomycosis Axillaris
Causative agent- Corynebacterium tenuis.
Collections of this bacteria forms concretions
on hairs, usually in the axilla.
The axillary hairs are surrounded by whiteyellow (Fig. 6.12), red or black, difficult to
remove concretions that extend for several
centimetres.
Diagnosis is established by examining hair
under microscope (Fig. 6.13), if necessary to
culture the organism.
Bacterial Infections
Pitted Keratolysis
Causative agent- Corynebacterium species,
Streptomyces species, Dermatophilus congolensis and Micrococcus sedentarius.
Multiple pitted defects, 2-5 mm in size occur
in thick horny layer of soles (Fig. 6.14).
The key factor is maceration, usually arising
from hyperhidrosis, prolonged wearing of
shoes and improper hygiene.
Differential diagnosis: The lesions are easily
recognizable, but simple hyperhidrosis,
erythrasma and tinea pedis have to be
considered.
Topical erythromycin solution or benzoyl
peroxide gel can be applied once or twice
daily. Remove aggravating factors, if
possible.
Botryomycosis
Botryomycosis is a chronic suppurative,
granulomatous disorder of bacterial origin.
True non- filamentous aerobic and anaerobic
bacteria such as Staphylococcus aureus,
Pseudomonas species, Proteus vulgaris,
Escherichia coli or Micrococcus cause it.
Botryomycosis needs to be differentiated
from two other granulomatous diseases that
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form granules - mycetoma and actinomycosis, since clinically it has similar features
(Fig. 6.15).
Effective treatment of botryomycosis
depends on various factors such as the
causative agent, location of the lesion and
immune status of the host. Various drugs,
mostly as single agents given for several
weeks, have been successfully used in
botryomycosis including trimethoprimsulfamethoxazole, minocycline, erythromycin and cefazolin. In addition to
antibiotics, surgical excision and drainage of
lesions may be useful in certain patients.
Actinomycosis
Actinomycosis is a chronic suppurative
infection caused by anaerobic Actinomyces
species. Actinomycetes are bacteria producing
filamentous and branching hyphae.
Pathogenic organisms of these genera,
namely Actinomyces israelii exists as a
commensal in the oral cavity, tonsillar crypts
and genital mucosa.
This organism gains entry when there is a
disruption of mucosal barrier in the form of
trauma or surgery. The resultant disease,
actinomycosis is characterized by an early
Bacterial Infections
Cutaneous Anthrax
Causative agent- Bacillus anthracis, gram
positive bacillus,
The most common form of infection with
Bacillus anthracis is an acute cutaneous lesion
called malignant pustule.
Anthrax is primarily a disease of domestic
and wild animals, but humans become
accidentally involved through exposure to
animals and their products.
Human anthrax occurs in three clinical forms:
1) cutaneous anthrax due to direct contact
Fig. 6.17
Fig. 6.18
Figs 6.17 and 6.18: Cutaneous anthrax (Malignant pustule)typical painless lesion with central blackish
eschar surrounded by wreath of erythema, edema and vesiculation
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Ciprofloxacin, erythromycin, tetracycline
and chloramphenicol are alternative drugs
for penicillin sensitive patients.
Bacillary Angiomatosis
Causative agent: Bartonella henselae (organism
also causes Cat Scratch disease); rarely
Bartonella quintana.
Infection is most common in HIV/AIDS
patients, causes endothelial proliferation and
produces vascular tumors.
Clinically, lesions are rapidly growing
pyogenic granuloma like papules and
nodules, which often ulcerate.
Purple, papular and nodular vascular lesions
may resemble Kaposis sarcoma.
Diagnosis is based on demonstration of
organism in the skin biopsy tissue section by
Warthin Starry staining. Blood cultures are
positive in half of the cases.
Differential diagnosis: Pyogenic granuloma
and Kaposi sarcoma are close differential
diagnosis, differentiation can be made by
histopathological examination and
demonstration of the organism by Warthin
starry staining.
The mainstay of treatment is erythromycin.
Alternatively, doxycycline or ciprofloxacin
can be used.
Viral Infections
Viral Infections
MOLLUSCUM CONTAGIOSUM
Molluscum contagiosum is caused by up to
four closely related types of poxviruses,
MCV-1 to - 4 and their variants.
The incubation period for the molluscum
contagiosum (MC) has been reported to be
between 14 and 50 days.
Skin to skin transmission is presumed to be
the method of spread, including autoinoculation (the Koebner phenomenon), as
well as contact with fomites.
It mainly affects children, sexually active
adults and persons with impaired cellular
immunity including HIV infection
In small children, virtually all infections are
caused by MCV-1 whereas in patients
infected with HIV, however, MCV-2 causes
the majority of infections (60%), suggesting
that HIV infection associated molluscum
does not represent recrudescence of childhood molluscum. In all forms of infection, the
lesions are relatively similar.
Individual lesions are smooth surfaced,
firm, dome shaped pearly papules
averaging 3 to 5 mm in diameter. Some
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Diagnosis
It is made clinically when necessary,
histological examination is diagnostic.
Viral Infections
Differential Diagnosis
Solitary MC may resemble pyogenic
granuloma, keratoacanthoma or epithelioma.
Cutaneous cryptococcos is histoplasmosis,
Penicillium marneffei infection, and basal cell
carcinoma have been mistaken for
molluscum in patients with AIDS.
Treatment
In children, they may be left alone
Curettage Individual lesions can be treated
with curettage
Trichloroacetic acid (30-100%) application
10% KOH application
Podophyllin 10% to 25%
Silver nitrate
5-FU topically
Cryosurgery
Electrodesiccation
Topical cantharidin, tretinoin (0.05% - 0.1%),
cidofovir (1-3%), and imiquimod (5%) are
other options
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46
papillomas and epidermodysplasia verruciformis. HPV types 1,2,3,4,7 cause first four
forms of warts commonly. Genital warts are
usually due to HPV types 6, 11, 16 and 18.
Warts occur at any age, but are unusual in
infancy and early childhood, the incidence
of warts increases during the school years.
Incubation period has been estimated to
range between a few weeks to more than 1
year.
Warts are spread by direct or indirect
contact.
Impairment of epithelial barrier function by
moisture or trauma is predisposing factor.
Viral Infections
planus causes most difficulty. Lichen planus
favours the flexor aspects of the forearms, is
unusual on the face and is often itchy. The
mucous membranes may be involved. The flat
polygonal papules are lilac-pink and smooth and
may show Wickhams striae.
Filiform and digitate warts: Occur commonly
in the male, on the face and neck. They are
irregularly distributed, often clustered. Digitate
warts often in small groups also occur on the
scalp in both sexes where they are occasionally
confused with epidermal naevi.
Anogenital warts: It has been estimated that up
to 30 to 50% of sexually active adults are infected
with HPV, making it the most common viral STD
in some STD clinics. Most of them occur on the
penis, scrotum, urethral meatus and perianal
area in men and on the introitus, vulva,
perineum and perianal area in women. The four
morphological types are
1. Cauliflower like (condyloma acuminata)
(Fig. 7.9)
2. Papular
3. Keratotic
4. Flat topped.
Bowenoid papulosis: is a clinicopathologic
entity in which HPVs (HPV-16 is the most
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Diagnosis
Clinical diagnosis of warts is often sufficient
but atypical, subclinical or dysplastic lesions
may need laboratory confirmation of HPV
infection.
Other than histopathology of lesion
(Koilocytosis in the stratum granulosum and
stratum spinosum), detection of virus
particles by electron microscopy,
immunocytochemistry using type specific
antibodies, DNA hybridization on tissue
extracts and polymerase chain reaction may
be done.
Electrosurgery: Electrodesiccation or
electrofulguration may be done.
CO2 laser ablation.
Cryotherapy: Either using liquid nitrogen
using dipstick method or spray method, or
nitrous oxide cooled probes.
Keratolytic agents like 10 to 20% salicylic
acid topically may be used.
Formalin soaks with 2 to 3% formalin in
water every day for 15 minutes is useful for
plantar warts.
Curettage or surgical excision for warts
unresponsive to topical treatment.
Topical retinoic acid for flat warts.
Cantharidin causes blistering and focal
destruction of the epidermis.
Cidofovir and 5-FU topically.
Intralesional bleomycin.
Injection of 0.1 ml of 1:1000 candida antigen
in the base of each wart.
Topical sensitizer and systemic immunomodulators (Interferon, especially interferon
Treatment
Most common warts disappear spontaneously
within 2 year or with simple nonscarring
treatment. Commonly employed modalities of
treatment are:
Chemical cautery: Trichloroacetic acid is
used for common warts, filiform warts and
plantar warts.
Viral Infections
alpha intralesionally or intramuscularly) may
be employed depending upon the condition.
Extensive warts, even in hitherto untreatable
epidermodysplasia verruciformis, have
improved or cleared with oral isotretinoin or
etretinate.
Treatment of genital wart is discussed
separately in STD section but salient
treatment options are given below.
1. Podophyllotoxin 0.5% self administered
twice a day for 3 days in week for 4 weeks
or podophyllin 25% in tincture benzoin,
once or twice weekly.
2. Liquid nitrogen cryosurgery
3. Electrosurgery
4. Surgical excision
5. Chemical cautery
6. Topical imiquimod.
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Viral Infections
Diagnosis
Treatment
Acyclovir has modified the treatment outcome.
Primary Infection
1. Genital herpes
2. Recurrent lumbosacral herpes simplex
3. HSV infections in the newborn.
Herpetic gingivo-stomatitis
Acyclovir 5 mg/kg body weight 8 hourly for
7 to 10 days.
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Others like eczema herpeticum and
disseminated herpes need to be treated
energetically on similar lines.
Herpetic whitlow and keratoconjunctivitis
may be treated with oral acyclovir 200 mg 5
times a day for 7 to 10 days.
Recurrent Infection
Acyclovir 200 mg 5 times a day for 5 days or
Acyclovir 400 mg tds 5 days or
Acyclovir 800 mg BD 5 days
Alternative antiviral drugs are famciclovir
(125 mg, 250 mg twice daily) and valacyclovir
(500 mg, 1 gm twice daily).
For suppression of recurrences- Acyclovir
400mg twice a day for at least 1 year.
Viral Infections
usually by staphylococci or streptococci and
may be prolonged by scarring. Other notable
complications are primary varicella pneumonia, Reyes syndrome, acute cerebellar
ataxia, encephalitis, and disseminated
varicella in immunosuppressed.
Maternal varicella during the early months
of pregnancy can lead to congenital varicella
syndrome, which manifests as extensive
cutaneous scarring, muscular atrophy, limb
hypoplasia, rudimentary digits, chorioretinitis and cortical atrophy.
Fig. 7. 20: Chicken poxdew drops on rose petals
appearance
Varicella
In older children and adults, the rash is often
preceded by 2 to 3 days of fever, chills,
malaise, headache, anorexia, severe backache
and in some patients, sore throat and dry
cough.
The rash of varicella begins on the face and
scalp and spreads rapidly to the trunk (Fig.
7.19) with relative sparing of the extremities.
New lesions appear in successive crops but
their distribution remains centripetal.
The lesion starts as a 2 to 4 mm red papule,
which develops an irregular outline (rose
petal) as a thin-walled clear vesicle appears
on the surface (dew drop). This lesion, dew
drop on a rose petal is highly characteristic
(Fig. 7.20). The vesicles become umbilicated
and pustular, rupture to form crusted lesions.
A distinctive feature of varicella is the
simultaneous presence of skin lesions in all
stages of evolution in any one area of the
body.
The most common complication is the
secondary bacterial infection of skin lesions
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Viral Infections
Skin biopsy of lesions also shows histological
changes similar to those found in herpes
simplex.
Definitive diagnosis accomplished by the
isolation of virus in cell cultures and electron
microscopy.
Identification of VZV antigens in cutaneous
lesions and PCR for detection of nucleic acids
in clinical specimen are the alternative
methods of diagnosis.
Diagnosis
Tzanck smears of cutaneous lesions of
varicella and zoster show multinucleated
giant cells and epithelial cells with typical
acidophilic intra-nuclear inclusions similar
to those seen in herpes simplex.
Treatment
Symptomatic treatment is given in otherwise
healthy patients. Rest and analgesics are
advised.
Acyclovir is given in severe varicella and
zoster (ophthalmic herpes zoster, Ramsay
Hunt syndrome) and also in those patients
who are at high risk of disseminated infection
(more than 50 years of age, immunosuppressed patients). Acyclovir 800 mg 5
times a day for 7 to 10 days (in children dose
is 20 mg per kg body weight four times daily).
Alternative antiviral drugs are famciclovir
(500 mg three times daily), valacyclovir (1
gm three times daily) and foscarnet in
acyclovir resistant cases.
Valacyclovir is contraindicated in
immunosuppressed individuals. Thrombotic
thrombocytopenic purpura and hemolytic
uremic syndrome have occurred in patients
with AIDS, renal transplant and bone
marrow transplant.
For post herpetic neuralgia-topical therapy
(capsaicin, aspirin, lignocaine), nerve blocks,
and systemic therapy (systemic steroids,
carbamazepine, valproate, tricyclic
antidepressants) may be tried. Gabapentin is
the drug of choice now. Initial dose of 300
mg/day is increased over 4 weeks (up to 3600
mg/day divided into three divided doses)
until efficacy obtained or side effects
tolerable.
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Fungal Infections
Fungal Infections
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Fungal Infections
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Fungal Infections
Diagnosis
KOH mount definitive diagnosis is made by
the microscopic examination and identification of hyphae and spores in scales
(Fig. 8.13) or hair. In nails, the presence of
hyphae usually means dermatophyte
infection, rarely saprophytic fungi infection.
Cellophane tape examination and staining
with periodic acid Schiffs (PAS) reagent of
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Therapy
Topical therapy- indicated for infections of
the body and groin and superficial
involvement of the beard region, palms, and
soles
Topical agents used are
1. Whitfield ointment (contains 6% benzoic acid
and 3% salicylic acid)
Fungal Infections
Diagnosis
KOH preparation-reveals numerous short,
straight and angular hyphae and clusters of
thick walled round and budding yeasts
Spaghetti and meat ball appearance or
Banana and grapes appearance(Fig. 8.17).
Cellophane tape examination and staining
with periodic acid Schiffs (PAS) reagent and
India ink of the material taken from skin (Figs
8.18 and 8.19).
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Differential Diagnosis
1. Pityriasis alba characterized by poorly
marginated, hypopigmented, slightly scaly
patches on the cheeks of young children.
Therapy
Topical Selenium sulfide suspension (2.5%),
zinc pyrithione, ketoconazole (2%) shampoo,
sodium hyposulfite (25%), propylene glycol
and imidazole derivatives are used topically.
Systemic Ketoconazole (200 mg daily for 5 to
10 days), itraconazole (200 mg daily for 5 to 7
days) or fluconazole (single oral dose of 400
mg) are effective systemically.
Fungal Infections
CANDIDIASIS
Clinical Manifestations
Oral thrush It presents as curdy, white, easily
detachable deposits on tongue or oral mucosa
with underlying bright red and moist surface
(Figs 8.20 and 8.21). This form of candidiasis
is also known as acute pseudomembranous
candidiasis. It is the most common form of oral
candidiasis. Other forms of oral candidias is
include acute and chronic atrophic
candidiasis, chronic hyperplastic candidiasis,
and median rhomboid glossitis. Oral thrush
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diagnosis includes tinea cruris, seborrhoeic
dermatitis, flexural psoriasis and bacterial
intertrigo.
Paronychia inflammatory boggy swelling of
posterior and lateral nail folds of digits of
fingers (Fig. 8.23), commonly seen in house
wives, maidservants, due to continuous wet
job
Vulvovaginitis-frequently associated with
itching and vaginal discharge. The vaginal
mucosa shows erythema, edema and curdy
white deposits (Fig. 8.24). Candidal balanoposthitis occurs as a counter part in males
(Fig. 8.25).
Diagnosis
KOH preparation-reveal budding yeasts with
or without hyphae or pseudohyphae.
Grams stained smear-gram positive
organisms longer than bacteria.
Confirmed by culture on Sabourauds media.
Whitish mucoid colonies grow within 2 to 5
days.
Therapy
Evaluation and treatment of underlying
medical conditions
Nystatin, imidazoles and broad-spectrum
triazoles are the agents of greatest use in the
treatment of candidal infection. Gentian violet
and Castellanis paint are older effective
topical remedies.
Potassium permanganate soaks are more
effective in moist Candidal intertrigo.
Recurrent or recalcitrant infections require
oral medication with nystatin (to rid the gut
and vagina of candida organisms),
fluconazole (50 mg daily for 14 days),
ketoconazole (200 mg daily) or itraconazole
(200 mg daily).
For vaginal candidiasis, 500 mg clotrimazole
vaginal tablet once or 200 mg miconazole
tablet at bed time for 3 days or single oral dose
Fungal Infections
of 150 mg of fluconazole or twice daily dose of
itraconazole (200 mg twice a day).
CHRONIC MUCOCUTANEOUS
CANDIDIASIS
It is a rare syndrome which is characterized
by recurrent and persistent candidal infection
of skin, nail and mucous membrane. It has
autosomal dominant or recessive inheritance.
Several endocrinopathies (e.g. hypothyroidism, hypoadrenatism, etc.) may be
associated.
Treatment: Treatment of this condition
depends critically on systemic antifungal
chemotherapy. Attempts have been made to
restore T cell function, by the use of transfer
factor, or thymosin, or grafting compatible T
lymphocytes and non specific measures like
the restoration of normal iron stores.
Prolonged and repeated use of systemic
antifungals like fluconazole, itraconazole and
ketoconazole may be necessary.
TINEA NIGRA
MYCETOMA
Actinomycetoma
Madurella mycetomatis
Exophila jeanselmei
Pyrenochaeta romeroi
Fusarium species
Actinomadura madurae
Nocardia brasilensis
Actinomadura pelletieri
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Differential diagnosis
1. Chronic osteomyelitis of bacterial or
tuberculosis origin (characteristic grains
are not discharged)
2. Elephantiasis (no sinus tracts)
3. Primary cutaneous actinomycosis
(develops on the exposed sites, very rare
type of actinomycosis, caused by Actinomyces isralei, a normal inhabitant of
human mouth, thus it is an endogenous
infection).
Actinomycetomas generally respond to
antibiotics such as a combination of dapsone
with streptomycin or sulfamethoxazoletrimethoprim plus rifampin or streptomycin.
Amikacin may also be used in recalcitrant
Nocardia infections.
Of the fungal causes of mycetoma,
M. mycetomatis may respond to ketoconazole
(200 mg daily over several months). For the
others, a trial of therapy with griseofulvin or
itraconazole is worth attempting. Surgery,
usually amputation, is the definitive
procedure and may have to be used in
advanced cases.
CHROMOMYCOSIS
(CHROMOBLASTOMYCOSIS)
Fungal Infections
RHINOSPORIDIOSIS
Rhinosporidiosis is a chronic granulomatous
mycosis caused by Rhinosporidium seeberi.
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SUBCUTANEOUS ZYGOMYCOSIS
Subcutaneous zygomycosis or subcutaneous
phycomycosis (SP) has two clinically and
mycologically distinctive entities termed as
basidiobolomycosis (etiological agent:
Basidiobolus ranarum) and conidiobolomycosis (etiological agent: Conidiobolus
Fungal Infections
Differential diagnosis:
1. Lymphatic edema (no distinctive edge)
2. Subcutaneous malignant lymphoma
(grows more rapidly)
3. Subcutaneous morphea
A therapeutic trial with potassium iodide in
a clinical setting may be considered as an
important criterion for diagnosis where
facilities to culture the organism do not exist.
SPOROTRICHOSIS
It is caused by Sporothrix schenckii and is
characterized by nodulo-ulcerative and
crusted lesions arranged in a linear fashion
over the extremities with intervening
lymphatics thickened like a cord.
The best sources of diagnostic material are
smears, exudates, and biopsies (to look for
Asteroid bodies). S. schenckii is very rarely
seen in direct microscopic examination
because yeasts are usually present only in
small numbers; the organism can be readily
isolated on Sabourauds agar.
Differential diagnosis:
1. Fish tank granuloma
2. Cutaneous leishmaniasis
Potassium iodide (saturated solution) is
effective in the cutaneous types of
sporotrichosis.
Other deep fungal infections: Cryptococcosis
and aspergillosis are ubiquitous throughout the
world. In south east Asia, penicillinosis is
common whereas coccidioidomycosis and
histoplasmosis are restricted to certain
geographic regions.
CRYPTOCOCCOSIS
Cryptococcosis is an opportunistic infection
caused by the encapsulated yeast Cryptococcus
neoformans.
PENICILLIOSIS
Penicillium marneffei is the only penicillium
species that is dimorphic and can cause
systemic mycosis in human beings,
particularly those who are immunocompromised.
Features of the infection frequently include
fever, anemia, marked weight loss, cough and
diarrhea, but skin eruptions occur in the
majority.
Cutaneous manifestations usually consist of
a generalised papular eruption, in which the
papules may be umbilicated (due to central
necrosis), although necrotic papules, nodules,
folliculitis, macular rash and mouth ulcer
have also been reported.
Diagnosis depends on isolation of the
organism from blood or tissue.
Treatment includes systemic amphotericin B,
itraconazole or fluconazole.
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Infestations
Infestations
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Infestations
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CRUSTED SCABIES
(NORWEGIAN SCABIES)
Very uncommon variant of scabies.
Though the first report of crusted scabies was
in patients with leprosy, recent reports have
described an increasing incidence of this
form of scabies in patients with
immunosuppression due to immunosuppressive agents, malignancy or acquired
immunodeficiency syndrome (AIDS).
In this form of scabies, the hosts response to
the mites is modified, allowing them to
multiply. As a result of this, the mite
population becomes enormous and may
number millions.
The large adherent crusts are most often seen
over the knees and elbows as well as the
hands (Fig. 9.12) and feet. There may even
be an erythroderma.
Frequently, it can be confused with psoriasis,
chronic eczema (contact dermatitis),
Langerhans cell histiocytosis, or neurodermatitis (Fig. 9.13).
Ivermectin seems to be ideal drug for this
condition; otherwise prolonged therapy
with topical scabicidal agents is required.
Methotrexate is another option.
ANIMAL SCABIES
Contracted from pet animals-cats, dogs, or
birds.
No burrows seen, only itching and papulovesicular lesions are seen over the site of
contact-abdomen, thighs and arms.
Treatment of pet animal with scabicidal agent
and antipruritic agents for controlling itching
are required.
Human skin lesions are self limiting; resolve
spontaneously if further contact with affected
animal is stopped.
Infestations
Pediculosis Capitis
Most common in children especially girls
with long hairs.
Mode of spread- human to human contact
or sharing combs, brushes and towels.
Scalp-favorite site is area behind the ear
(Fig. 9.17) or occiput.
Nits may be found most easily on the hairs.
Adult lice often impossible to find.
In patients with scalp pruritus, secondary
pyoderma (with cervical lymphadenopathy)
and dermatitis, one should always search the
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Pediculosis Pubis
Transmission in adults occurs mostly
during sexual intercourse.
The pubic or crab louse is smaller than the
head or body louse, has resemblance to a crab
(for prominent claws in second and third
pairs of legs).
Pruritus or crawling sensation is modest in
the pubic area.
Pediculosis Corporis
Infestation associated with poor personal
hygiene, a disease of homeless.
The body louse feeds on body and lays its
eggs on seems of clothing.
Infestations
of insects such as mosquitoes, fleas, and
bedbugs.
This condition is mainly seen in childhood.
Treatment involves use of insect repellants,
topical antipruritic agents and antibacterial
with or without steroids.
PAPULAR URTICARIA
Papular urticaria occurs as episodic,
symmetrically distributed, pruritic,
urticarial papules that are caused by bites
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MYIASIS
Myiasis is the presence of fly larvae
(maggots) in the tissue.
Usually they need an entry site, such as a
chronic ulcer (trophic ulcer of leprosy) or
wound.
Most maggots only eat necrotic debris,
although some attack healthy tissue.
Clinically, myiasis is classified according to
the part of the body affected-cutaneous
myiasis (Fig. 9.22) (wound, furuncular),
nasopharyngeal myiasis, ophthalmomyiasis,
intestinal and urogenital myiasis.
Therapy-remove the maggots either after
anesthetizing the area or suffocating them
with turpentine oil or petrolatum.
LEISHMANIASIS
Leishmaniasis is a parasitic infection caused by
many species of the protozoa Leishmania,
manifested clinically as four syndromes.
Infestations
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Papulosquamous Disorders
PSORIASIS
Psoriasis is a common chronic disfiguring,
inflammatory and proliferative epidermal
skin disorder mediated by T cells that affects
approximately 1 to 3% of the world
population.
Multifactorial inheritance most likely, a
family history of psoriasis is found in 30% of
patients.
The histocompatibility antigen HLA Cw6 is
most strongly associated with psoriasis and
the coexistence of HLA B17 or B27 portends
more severe skin disease or associated
psoriatic arthritis.
The pathogenesis of psoriasis remains
unclear. The initial reaction is possibly an
intrinsic defect of keratinocytes with
increased cytokine production which leads
to expansion of CD45RO + T cells with
resultant production of type 1 cytokines.
Subsequently, it results in epidermal
proliferation, migration of neutrophils into
Classification of Psoriasis
1. Based on Morphological Types
Chronic stable plaque psoriasis (psoriasis
vulgaris) (Figs 10.1 and 10.2)
Guttate psoriasis
Pustular psoriasis
Erythrodermic psoriasis
Rupioid, elephantine and ostraceous
psoriasis.
2.
Papulosquamous Disorders
3.
Clinical Features
Most lesions of psoriasis are asymptomatic.
Its typical age of onset is in the third decade,
though it may develop at any time from birth
onward.
Erythematous papules and plaques
characterize it. The lesions are of variable
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Papulosquamous Disorders
arthritis characteristically involves the
terminal interphalangeal joints (Fig. 10.6), but
frequently the large joints are also affected,
resembling rheumatoid arthritis. However,
the rheumatoid factor is absent.
In severe cases, the disease may affect the
entire skin and presents as psoriatic
erythroderma.
Psoriasis rarely presents as generalized
pustular psoriasis (von-Zumbusch typeacute exanthematic type (Fig. 10.7) or
generalized pustular psoriasis of pregnancyImpetigo herpetiformis). Localized pustular
psoriasis occurs as acrodermatitis continua
of Hallopeau (localized to the distal portions
of the hands and feet) (Fig. 10.8) or pustulosis
palmaris et plantaris (chronic, relapsing
disorder occurring on the palms, soles, or
both).
Diagnosis
Psoriasis may be confused with seborrheic
dermatitis, secondary syphilis, dermatophyte
infections, cutaneous lupus erythematosus,
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Histopathology: The fully developed lesion
of psoriasis shows:
1. Hyperkeratosis and parakeratosis.
2. Within parakeratotic areas of the horny
layer, accumulations of neutrophils
forms, which are called as Munro microabscesses.
3. Hypo or absent granular layer.
4. Regular acanthosis.
5. Spongiform pustule of Kogoj
neutrophils accumulation in Malpighian
layer
6. There is regular elongation of the rete
ridges with thickening in their lower
portion, looking like elephant feet.
7. There is thinning of the supra papillary
portion of the epidermis.
8. The dermal papillae contain enlarged and
tortuous capillaries that are very close to
the skin surface and impart a
characteristic erythematous hue to the
lesions.
9. Sparse lymphocytic infiltrate in the upper
dermis.
Papulosquamous Disorders
Drug eruptions Always take a drug
history; many drug reactions are
psoriasiform, and in some instances lead to
true psoriasis in susceptible host.
Pityriasis lichenoides chronica It can
closely resemble guttate psoriasis but the
lesions are less evenly scattered, have
brownish red or orange brown color and are
capped by an opaque soft mica like scale.
Treatment
It is important to emphasize that psoriasis is
a treatable condition. The treatment pyramid
for psoriasis is shown in Fig. 10.9.
Despite virtual explosion in therapeutic
options, the management of psoriasis
remains a challenge to clinicians.
Topical Therapies
Emollients Such as coconut oil, vaseline,
or liquid paraffin.
Coal tar (2, 5, 10% ointment) It may be used
effectively as monotherapy or in combination
with other treatment modalities.
Goeckerman therapy consists of black crude
coal tar application all over the patients
body. This tar is left on for 24 hours per day.
UVB phototherapy is administered before the
tar is applied or after it is washed off. The
Goeckerman regimen remains an intensive
daily therapy that is usually conducted for a
period of several weeks.
Anthralin (0.1 to 10% cream or ointment)
It is moderately effective and quite safe in
plaque psoriasis. The major side effect is
staining of skin and clothing and occasional
irritation. Ingram regimen consists of a
combination of anthralin and UVB
phototherapy. Short contact treatment of 30
minutes or less is likely to reduce irritation.
Topical steroids/ intralesional steroidsTopical corticosteroids are used for treatment
over face and neck, flexures and genitalia,
where tar or anthralin would cause irritation
and cannot be used. Systemic steroids
generally not recommended due to the wellknown risk of rebound and pustular
conversion.
Vitamin D analogues are both naturally
occurring calcitriol (1, 25-dihydroxyvitamin D 3 ) and synthetic analoguescalcipotriol, tacalcitol, maxacalcitol. Vitamin
D molecule is dispensed as ointment, cream
or solution and has risk of producing
hypercalcemia in less than 1% of cases.
Tazarotene (0.1 to 0.05% gel) It is a
modified vitamin A molecule formulated as
a topical agent. It is recommended for use in
patients with total body surface involvement
of 20% or less.
Topical methotrexate gel-used for
palmoplantar psoriasis with limited efficacy.
Tacrolimus (0.03, 0.1%) effective for facial
plaques and inverse psoriasis.
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Biologic Agents
Biologics are agents that selectively block the
immunologic steps in the pathogenesis of
psoriasis. Alefacept, efalizumab, etanercept, and
infliximab are currently approved for the
treatment of adults with moderate to severe
plaque psoriasis, and phase 3 trials for
adalimumab are ongoing (Table 10.1).
All biologics approved to date for the
treatment of psoriasis are recommended for
patients who are candidates for systemic or
photo-therapy.
Table 10.1: Biologic agents and their
mechanism of action
Strategy
Biologic agents
Alefacept, denileukin
diftitox
Inhibition of T-cell
activation and migration
Efalizumab, daclizumab,
siplizumab, CTLA4Ig,
galiximab,
Ilodecakin, oprelvekin
Etanercept, infliximab,
adalimumab, ABX-IL8
Papulosquamous Disorders
Efalizumab is favorable in patients with high
risk of latent tuberculosis or evidence of
demyelinating disease.
Infliximab is advantageous where rapid
disease control is required (e.g. unstable
erythroderma).
Etanercept is the biologic of choice in stable
psoriasis where a TNF--blocking strategy is
appropriate.
Some biologics are also approved for
treatment of psoriatic arthritis; thus, patients
with psoriatic arthritis may benefit from a
biologic for both the articular and dermatologic manifestations.
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Essentials in Dermatology
Ureaplasma urealyticum, Shigella, Salmonella,
etc.
Differential diagnosis includes rheumatoid
arthritis, ankylosing spondylitis, gout,
psoriatic arthritis, gonococcal arthritis, acute
rheumatic fever, etc.
Mucocutaneous lesions are generally self
limited and clear with topical steroids.
Refractory lesions are managed like psoriasis.
Joint disease may require NSAIDS,
methotrexate or biologics (infliximab).
LICHEN PLANUS
Lichen planus (Greek leichen, tree moss;
Latin planus, flat) is a subacute or a chronic
dermatosis that may involve skin, mucous
membranes, hair follicles and nails.
The cause of lichen planus is unknown, but
several etiologies have been proposed. It is
likely that both endogenous-genetic and
exogenous-environmental components such
as drugs or infection may interact to elicit
the disease.
The prevalence of chronic liver diseases,
including primary biliary cirrhosis, alcoholic
cirrhosis, hepatitis B, and especially hepatitis
C, is increased.
HLA-B8 is more common in patients with
oral lichen planus as the sole manifestation,
Papulosquamous Disorders
The oral lesions of lichen planus are
frequently found, either as sole manifestation
of the disease or associated with cutaneous
involvement. Most often consist of a lacy,
reticular network of coalescent papules over
the buccal (Fig. 10.21) or glossal mucosa.
Besides this, it forms plaque like, atrophic,
papular, erosive and bullous lesions.
The nails are involved in about 10% of cases
and show roughening, longitudinal ridging,
thinning and dystrophy. Pterygium
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Diagnosis
The appearance of the typical papule of
lichen planus is usually sufficient to make the
correct diagnosis.
Histopathology: Microscopic features, similar
to the gross morphology, are diagnostic. The
two major pathologic findings in lichen
planus are basal epidermal keratinocyte
damage and lichenoid-interface lympho-
Papulosquamous Disorders
Differential Diagnosis
Classic lesions: Lichenoid drug eruption
(large scaly lesions in sun-exposed areas,
devoid of Wickham striae, residual
pigmentation common), lichen nitidus
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palate and gingival. On lips, target lesions
may be identified. Vesicles, erosions and
crusting are present over oral mucosa.
Associated skin lesions- target lesions may
be seen over acral extensor sun-exposed
areas).
Treatment
Topical therapy: Topical glucocorticoids are
typically used for mucosal and limited
cutaneous disease.
Intralesional therapy: Intralesional triamcinolone acetonide (5 to 10 mg/mL) is
effective in treating oral and cutaneous lichen
planus.
Systemic therapy:
1. Systemic glucocorticoids are often useful and
effective in doses greater than 20 mg/day
(e.g. 30 to 60 mg prednisolone) for 4 to 6
weeks with subsequent taper over 4 to 6
weeks.
2. PUVA photochemotherapy is usually
successful in generalized cutaneous lichen
planus.
3. The systemic retinoids demonstrate antiinflammatory activity and have been used in
the treatment of lichen planus.
4. Cyclosporine (500 mg) rinses in oral lichen
and systemic cyclosporine in recalcitrant
lichen planus has been used successfully.
5. Other agents used in lichen planus are
dapsone, griseofulvin, cyclophosphamide,
methotrexate, phenytoin and extracorporeal
photochemotherapy.
In mucosal lichen planus, topical corticosteroids, tetracycline, betamethasone mouthwashes 0.5 mg 3-4 times daily, topical tretinoin
gel, cyclosporine mouth rinses, tacrolimus, and
pimecrolimus have been used. Maintenance of
good oral hygiene and replacement of amalgam
or gold dental restorations with composite
material is frequently of considerable benefit.
Erosive oral lichen planus may respond to oral
dapsone.
Course
Lichen planus is a benign disease with
spontaneous remissions and exacerbations.
Apart from hypertrophic lichen planus, most of
LP lesions tend to involute after several months
to a year.
LICHEN NITIDUS
Lichen nitidus is a chronic dermatitis usually
asymptomatic which begins commonly in
childhood or early adulthood
It is characterized by minute, round, flat or
dome shaped, shiny, flesh colored papules
2 to 3 mm in diameter that may occur in
groups
Predominantly, the arms, trunk (Fig. 10.25)
or penis (Fig. 10.26)are involved
Koebner phenomenon may be observed (Fig.
10.27)
The histology of a typical papule is
characteristic. A circumscribed epithelioid
cell granuloma is situated immediately below
the epidermis. The rete ridges at the margin
of the infiltrate are elongated and tend to
encircle it claw clutching a ball
appearance.
Differential diagnosis:
1. Keratoses pilaris (horny follicular papules
on extensor surfaces),
Papulosquamous Disorders
2. Lichen scrofulosorum (grouped follicular
papules in small patches on trunk),
3. Lichen planus,
4. Sarcoidosis,
5. Disseminated granuloma annulare,
6. Eruptive xanthomas,
PITYRIASIS ROSEA
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Essentials in Dermatology
Round to oval salmon colored patches
following the lines of cleavage (Christmas
tree like pattern) and showing peripheral
attached thin cigarette paper like scales
(collarette of scaling) (Fig. 10.28). When
individual lesion is stretched along the long
axis, the scales tend to fold across the lines of
stretch, so called hanging curtain sign.
Variants of pityriasis rosea are vesicular,
inverse (Fig. 10.29), cervicocephalic, pityriasis
rosea gigantea (pityriasis circinata et
marginata of Vidal), pityriasis rosea urticata,
purpuric pityriasis rosea, pityriasis rosea
perstans, pustular pityriasis rosea, and
eczematous pityriasis rosea.
Treatment
Most patients require no treatment.
Topical corticosteroids or short course of oral
corticosteroid may be required in severe
cases.
Oral erythromycin may be helpful.
Itching alleviated with antipruritic lotions or
antihistamines.
PITYRIASIS RUBRA PILARIS (PRP)
Diagnosis
Usually easily diagnosed by its morphology
and distribution.
Differential Diagnosis
Pityriasis rosea must be differentiated from
tinea corporis, tinea versicolor (well defined
hypopigmented coalescing macules with branny
scales), drug eruptions (acute onset without
herald patch, pruritic protracted rash and a
tendency for lesions to become lichenoid),
psoriasis (papules and plaques with silvery
Papulosquamous Disorders
Types of PRP
Type Iadult onset classical, most common
type.
Type IIadult onset atypical.
Type IIIjuvenile onset, classical.
ERYTHRODERMA (EXFOLIATIVE
DERMATITIS)
Erythroderma is a condition which is
characterized by erythema, infiltration and
scaling involving more than 90% of the body
surface area or near universal involvement
of the body (Fig. 10.33).
Erythroderma can be caused by various
dermatological disorders: eczema, psoriasis,
drugs, lymphoma, leukaemia, pemphigus
foliaceus, ichthyosiform erythroderma,
pityriasis rubra pilaris, lichen planus,
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In erythroderma where the etiology is
unknown, called as idiopathic erythroderma
(10% of cases).
Chronic erythroderma of unknown origin
with prolonged course in the elderly is called
as red man syndrome.
Szary syndrome manifest with erythroderma, generalized lymphadenopathy and
atypical cells in peripheral smear (more than
10%).
It can be a manifestation of internal
malignancy.
Complications
Erythroderma leads to hemodynamic and
metabolic disturbances such as high out put
cardiac failure, hypothermia, dehydration
and hypoalbuminemia.
Temperature regulation is affected and
patient behaves like a poikilothermic animal.
Death may occur due to cardiac failure,
pneumonia and septicemia.
Management
It includes maintenance of the homeostasis and
treatment of the primary disease.
Eczema
11
Eczema
CLASSIFICATION OF ECZEMA
Exogenous Eczema
Irritant dermatitis
Allergic contact dermatitis
Photoallergic contact dermatitis
Eczematous polymorphic light eruption
Infective eczema
Dermatophytide
Post-traumatic eczema.
Endogenous Eczema
Atopic dermatitis
Seborrheic dermatitis
Asteatotic eczema
Discoid eczema
Pompholyx
Pityriasis alba
Stasis dermatitis
Hand eczema
Lichen simplex chronicus
Prurigo nodularis
Lichen striatus
Juvenile plantar dermatosis
Metabolic eczema or eczemas associated with
systemic disease
Eczematous drug eruptions.
It must be remembered that, endogenous and
exogenous factors may co-exist. For example,
hand eczema, which is an endogenous eczema,
is often aggravated by exogenous factors. Some
of the important endogenous (Atopic dermatitis,
seborrheic dermatitis, nummular eczema,
pompholyx, pityriasis alba, stasis dermatitis,
asteatotic eczema, lichen simplex chronicus,
prurigo nodularis, lichen striatus) and exogenous
eczema (Contact dermatitis, infective eczema/
dermatitis, polymorphous light eruption) are
discussed as follows.
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ATOPIC DERMATITIS
Atopic dermatitis (AD) or eczema is a
common chronic or relapsing dermatitis
characterized by severe pruritus, occurring
primarily in infants and children.
The age of onset is between 2 and 6 months
in the majority of cases, but it may start at
any age, even before the age of 2 months in
some cases.
The disease arises as a result of a complex
interplay between various genetic,
immunological and environmental factors.
The environmental factors include (a)
physical factors like sweating, climate, warm
surroundings, detergents and soap, synthetic
or woollen fabrics, cigarette smoke,
(b) psychological factors, (c) food items
(including tomato, orange and citrus fruits
juices, meat, fish) (d) allergens such as house
dust mite, animal hair, pollen, plants and
others such as Staphylococcus aureus and
release of exotoxins (superantigens) and
saliva in small children.
Majority of cases are associated with a
sensitization to environmental allergens
and increased serum IgE (extrinsic AD), but
about 10-30% of all cases lack any link to
the classical atopic diathesis and are
labelled as intrinsic AD.
There is no laboratory gold standard for the
diagnosis of AD. A detailed history and a
characteristic clinical picture would
establish the diagnosis. Hanifin and Rajka
have laid down certain major and minor
criteria for making a diagnosis of AD.
Eczema
Fig. 11.2
Fig. 11.3
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Essentials in Dermatology
observed on the flexural surfaces, including the
neck, antecubital or popliteal fossae, wrists and
ankles (Figs 11.2 and 11.3). There is an adult
phase, which occurs in adolescents and adults,
where lichenification of the flexures and the
hands commonly occurs.
Some important signs: Thinning of lateral
eyebrows, Hertoghes sign is sometimes present.
Hyperkeratosis and hyperpigmentation
producing a dirty neck appearance is also
frequent in atopic individuals. Atopic
individuals often exhibit perioral, perinasal and
periorbital pallor headlight sign.
Differential diagnosis: The diagnosis of atopic
dermatitis (AD) is rarely aided by investigations.
In the individual patient, one must consider a
number of other conditions. Scabies should
always be excluded, and can cause confusion
when superimposed on pre-existing AD. In the
first few months of life, the differentiation of
infantile seborrhoeic dermatitis from atopic
dermatitis can be difficult, although with time
the distinction becomes apparent. The most
useful distinguishing feature between atopic
dermatitis and seborrheic dermatitis is the
increased number of lesions on the forearms and
shins in the former and axillae in the latter. The
development of the lesions solely in the diaper
area favors a diagnosis of infantile seborrheic
dermatitis. Absent to mild pruritus is considered
a significant feature of infantile seborrheic
dermatitis. Immunodeficiency states should
also be considered in infants in whom the disease
is unusually severe, when there are recurrent
systemic or ear infections and if there is failure
to thrive, malabsorption or petechiae. Then
appropriate investigations should be performed,
for example, immunoglobulin levels and
subclasses, IgE levels, white cell count, platelets,
complement levels, and function, and T, B, and
phagocyte numbers and functions. If clinically
appropriate, one may also consider testing for
Eczema
1.
Mild AD
2.
Moderate AD
3.
Severe AD
Adult
Scalp:
Dandruff
Inflammatory
Face (may include blepharitis and
conjunctivitis)
Trunk:
Petaloid
Pityriasiform
Flexural
Eczematous plaques
Follicular.
Generalized (may be erythroderma)
In infants, the scalp (the frontal and parietal
scalp regions are covered with an oilylooking, thick, often fissured crust -crusta
lactea (milk crust, or cradle cap) (Fig. 11.4),
face and diaper areas are often involved.
Leiners disease is due to complement C5
deficiency, presents as erythroderma.
Clinically, adult patients develop erythema
and greasy scale on the scalp (with often
pruritus), paranasal areas, eyebrows,
nasolabial folds, central chest and
intertriginous folds (seborrheic areas of the
body). Rarely generalized lesions may occur.
Dandruff is usually the earliest manifestation
of seborrheic dermatitis.
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Eczema
crusts, inhibition of yeast colonization,
control of secondary infection, and reduction
of erythema and itching. For unresponsive
cases, narrow band UVB, oral ketoconazole,
itraconazole or terbinafine may be used.
Other treatment modalities include topical
metronidazole (1%) gel, topical lithium
succinate, vitamin D 3 analogues, and oral
isotretinoin.
Patients should be informed about the
chronic nature of the disease and understand
that therapy works by controlling the disease
rather than by curing it.
POMPHOLYX (DYSHIDROSIS)
Pompholyx is characterized by itchy deepseated vesiculation on the palms and sides
of the fingers. Lesions appear sago-like.
It may involve the soles of the feet.
It occurs bilaterally symmetrically, has
relapsing course.
Differential diagnosis:
1. Id eruptions: Id eruptions are pompholyxlike eruptions due to distant focus of
infections (e.g. kerion or bullous tinea
pedis)
2. Pustular psoriasis of palms and soles:
Sterile pustules, absence of clear vesicles,
and characteristic residual brown marks
as the lesions subside
3. Pemphigoid lesions occurring on the
palms
4. Bullous tinea pedis
Treatment: open wet compresses, topical
steroids and antibiotics for secondary
infection.
PITYRIASIS ALBA
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It usually disappears by adulthood.
The condition commonly affects the face.
Differential diagnosis:
1. Indeterminate leprosy: Lesion is usually
solitary to a few, hypopigmented macule
with ill-defined margins and equivocal
sensory loss.
2. Tinea versicolor: Lesions are well-defined
hypopigmented macules with branny
scales. KOH examination shows
spaghetti and meatball appearance.
3. Vitiligo-early lesions may mimic but lack
scaling.
4. Mycosis fungoides although relatively
rare may present with lesions clinically
resembling pityrasis alba.
Treatment: Emollients, mild topical steroid
or topical pimecrolimus or tacrolimus
application may suffice.
STASIS DERMATITIS
Stasis dermatitis occurs as a result of venous
stasis on the lower portions of the legs.
The dermatitis may be acute, subacute or
chronic.
It differs from other forms of dermatitis,
firstly by showing brownish black
pigmentation and secondly, by resulting in
some instances in ulceration and atrophic
scarring.
The surrounding skin may show changes due
to venous stasishyperpigmentation,
induration of skin and lipodermatosclerosis
in late stage.
Differential diagnosis:
1. Allergic contact dermatitis usually caused
by topical medications. Patch testing is
helpful.
2. Infected ulcer with infective eczematoid
dermatitis around the ulcer responds to
appropriate antibiotic therapy.
3. Discoid eczema is common on lower legs
usually on the anterior or anterolateral
aspect.
Eczema
repeated rubbing or scratching as a habit or
due to stress.
Lichenification of the skin follows chronic
scratching and/or rubbing. This may occur
without a predisposing dermatosis, or may
follow any pruriginous dermatosis. The term
lichen simplex is used when there is no
predisposing dermatosis.
It is characterized histologically by acanthosis
and hyperkeratosis and clinically by
thickened appearance of the skin, with
accentuation of skin markings so that the
affected skin surface resembles tree bark.
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LICHEN STRIATUS
It is an acquired self-limited inflammatory
linear skin disorder
Exact etiology is unknown
Children aged 5 to 15 years are commonly
affected
The most characteristic lesion is a linear band
of hypopigmented lichenoid papules that
follow Blaschkos lines (Fig. 11.11)
The lesions commonly occur on the arm or
leg
Course of the lesion may extend for 2 weeks
to 4 months.
Differential diagnosis: Epidermal naevi
(persist indefinitely), linear lichen planus or
psoriasis (easily differentiated clinically, even
in the absence of typical lesions in other sites
which should always be sought for)
Treatment: Usually none is necessary, topical
steroids, topical tacrolimus and intralesional
steroids in persistent cases.
Eczema
HAND ECZEMA
Hand eczema is not a single diagnostic entity.
It is rather a morphological presentation of
various types of eczemas largely confined to
the hands and can have a multitude of factors
responsible for causing it, singly or in
combination. Causes of hand eczema are
broadly grouped into two groups as shown
below:
Exogenous
1. Contact irritants: Chemicals (e.g. soaps,
detergents, solvents)
Physical (e.g. friction, minor trauma, cold
dry air)
2. Contact allergens: Delayed hypersensitivity (e.g. chromium, rubber) Immediate
hypersentivity (e.g. seafood)
3. Ingested allergens (e.g. drugs, nickel,
chromium)
4. Infection (e.g. bacterial infections of hand
wounds)
5. Secondary dissemination (e.g. dermatophytide reaction to tinea pedis).
Endogenous
1. Idiopathic (e.g. Discoid, hyperkeratotic
palmar eczema)
2. Immunological or metabolic defects (e.g.
atopics)
3. Psychosomatic: Stress aggravates, but
may not be causative
4. Dyshidrosis: Increased sweating aggravates, but may not be causative.
Morphological types of Hand Eczema
1. Pompholyx
2. Recurrent focal palmar peeling
3. Hyperkeratotic palmar eczema
4. Ring eczema
5. Wear and tear dermatitis
6. Fingertip eczema
7. Apron eczema
8. Discoid eczema
9. Chronic acral dermatitis
10. Gut eczema.
Differential diagnosis: The diagnosis of
hand eczema is usually self evident but
distinction from psoriasis is very difficult. In
most cases of psoriasis on hands, however,
the silvery nature of the scales, involvement
of knuckles, sharply demarcated scalloped
edges to the erythema along the borders of
the hands and fingers, and the relative
absence of pruritus are helpful pointers.
Family history of psoriasis and the presence
of nail pits in the absence of nail fold lesions
are also suggestive. Tinea can also be missed
especially when it is extensive and irritable
or secondarily infected. Unilateral scaling of
palm should always suggest tinea manuum.
Treatment of hand eczema: Avoidance of
irritants, frequent application of emollients,
and sparing use of topical steroids.
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adolescence. Patients are advised to use
emollients, 100% cotton socks and leather
shoes or sandals.
CONTACT DERMATITIS
Contact dermatitis is an eczematous dermatitis
caused by exposure to substances in the
environment. Common types of contact
dermatitis are discussed here.
Eczema
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*People at risk
*Mechanism of response
*Prior exposure required
*Nature of substance
Everyone
Nonimmunologic
No
Organic solvents, soap
Usually high
Severe, stinging or burning sensation
Large tense bullae with necrosis
No
Neutrophils
Not useful
Genetically predisposed
Delayed hypersensitivity
Yes
Low molecular weight hapten
(metal, formalin)
May be low
Pruritus
Papules or papulovesicles
Yes
Eosinophils and lymphocytes
Diagnostic
Eczema
Light sensitivity decreases with repeated sun
exposure, this phenomenon is referred to as
hardening.
Differential diagnosis: Lupus erythematosus, photosensitive drug eruption,
prurigo nodularis, and photoallergic contact
dermatitis need to be differentiated.
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Vesiculobullous Disorders
CLASSIFICATION OF
VESICULOBULLOUS DISORDERS
1. Inherited/genetic blistering disorders:
a. Epidermolysis bullosa simplex
b. Junctional epidermolysis bullosa
c. Dystrophic epidermolysis bullosa.
2. Acquired autoimmune blistering disorders:
a. Intraepidermal immunobullous diseases
1. Pemphigus vulgaris and its variant
pemphigus vegetans.
2. Pemphigus foliaceous and its variants
i. Endemic pemphigus foliaceus (Fogo
selvagem; wild fire).
ii. Pemphigus erythematosus (SenearUsher syndrome)
iii.Pemphigus herpetiformis.
3. Drug induced pemphigus.
4.. IgA pemphigus
i. Intraepidermal neutrophilic type
ii. Subcorneal pustular dermatosis type.
5. Paraneoplastic pemphigus.
6. Subcorneal pustular dermatosis (Sneddon
Wilkinson disease).
3. Subepidermal immunobullous diseases
a. Bullous pemphigoid and its variants
b. Mucous membrane pemphigoid (cicatricial pemphigoid)
Vesiculobullous Disorders
c. Pemphigoid gestationis (Herpes gestationis)
d. Linear IgA disease/Chronic bullous
dermatosis of childhood
e. Dermatitis herpetiformis
f. Epidermolysis bullosa acquisita
g. Bullous systemic lupus erythematosus.
The following discussion deals with these two
groups of disorders with special focus on the more
common entities.
EPIDERMOLYSIS BULLOSA
Epidermolysis bullosa (EB) comprises a group
of genetically determined skin disorders
characterized by blistering of the skin (Fig.
12.1) and mucosae at birth or soon afterwards,
following mild mechanical trauma (due to
increased fragility of skin). Thus an alternative
term for these disorders could be the
mechanobullous disorders.
There are three main types of EB:
EB simplex (intraepidermal split due to
disruption of basal keratinocytes)
Junctional EB (split through the basement
membrane zone)
Dystrophic EB (split in the subepidermal
level).
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Gene therapy appears as a realistic goal in
the future.
PEMPHIGUS
Pemphigus Vulgaris
Most common form of pemphigus, accounting
for up to 80% of pemphigus cases. Occurs at
any age, most commonly between fourth- sixth
decades. In India, it occurs at younger age.
It is due to IgG antibodies directed against
epidermal cell adhesion molecules
(desmoglein 3)- disruption of intercellular
cementing substanceloss of adhesion
between epidermal cells (acantholysis)
intraepidermal blistering.
Clinical Features
Almost all patients have mucosal lesions,
5070% present with painful oral erosions.
Lesions may be limited to oral cavity for
months to one year (Fig. 12.4).
Vesiculobullous Disorders
Skin flaccid bullae on normal or erythematous skin, with a predilection for scalp,
face (Fig. 12.5), trunk (Figs 12.6 and 12.7),
axillae and groins and pressure sites.
Bullae rupture producing painful erosions
that show no tendency to heal spontaneously.
Pruritus is absent or negligible.
Nikolskys sign and Bulla spread sign
(Asboe-Hansen sign) are positive. (Other
disorders with positive Nikolskys sign are
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Prognosis is poor without treatment but with
systemic steroids mortality has been reduced
to 515 %.
Pemphigus may be associated with other
autoimmune diseases such as thymoma,
myasthenia gravis and malignancies like
lymphomas and bronchogenic carcinoma.
Diagnosis
Tzanck smear from the floor of the blister
shows acantholytic cells. Acantholytic cell is
a large, rounded epidermal cell with a large
nucleus, perinuclear halo and peripheral
condensation of cytoplasm (Fig. 12.8).
Histopathological examination of a blister
shows a supra-basal cleft in the epidermis.
The basal keratinocytes remain attached to the
basement membrane but are separated from
each other and stand like a row of
tombstones.
Immunofluorescence studies are the gold
standard in diagnosis of the autoimmune
blistering disorders. In pemphigus vulgaris,
direct immunofluorescence done on the
lesional skin shows deposition of intercellular
IgG throughout the epidermis in a fish-net
pattern (Fig. 12.9). Indirect immunofluorescence done to determine levels of
pathogenic antibodies in the sera of the
Pemphigus Vegetans
It is a clinical variant of pemphigus vulgaris
characterized by vegetating lesions primarily in
the flexures (Figs 12.10 and 12.11). Initial lesions
are bullae or pustules, which rupture and
progress to form vegetating plaques.
Pemphigus Foliaceous
This disorder, characterized by blistering at a
higher level in the epidermis is less common
than pemphigus vulgaris and accounts for
only 1520 % of pemphigus cases.
It is caused by IgG antibodies directed
against intercellular adhesion molecules
(desmoglein 1) found predominantly in the
upper epidermisdisruption of intercellular
cementing substance of upper epidermal cellssubcorneal blister formation.
Clinically, pemphigus foliaceous is less severe
than pemphigus vulgaris and is characterized
by crusted, moist, scaly lesions in a
seborrheic distribution (Fig. 12.12) involving
scalp, face, chest and upper back. Blistering
may not be obvious due to the superficial level
of the split (very transient nature of blisters).
Vesiculobullous Disorders
Diagnosis
Tzanck smear from fresh erosion shows
acantholytic cells.
Histology shows a subcorneal cleft with
acantholysis.
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Pemphigus Erythematosus
It is a variant of pemphigus foliaceous characterized by immunological features of both
pemphigus and lupus erythematosus (LE), that
is, intercellular IgG and C3 in the epidermis (as
in pemphigus) and in the basement membrane
zone (as in LE) and antinuclear antibodies (as in
LE). Clinically, erythematous, scaly rash over the
nose and cheeks simulate LE while lesions on the
trunk are similar to those in pemphigus foliaceous.
Other Variants of Pemphigus
Endemic pemphigus foliaceous (Fogo
Selvagem) is a variant of pemphigus
foliaceous, endemic to certain parts of South
America and is postulated to be precipitated
by bites of the black fly (Simuliidae). The burnt
appearance and burning sensation gave the
disease its name, fogo selvagem, meaning
wild fire.
Drug induced pemphigus (penicillamine,
captopril, pyritinol, penicillin, rifampicin)
clinically commonly present as pemphigus
foliaceous.
Paraneoplastic pemphigusa polymorphous blistering eruption with mucocutaneous ulcerations having an underlying
neoplasm.
Pemphigus herpetiformissuperficial
vesicles and inflammatory papules occur in
herpetiform distribution.
IgA pemphigushas bound and circulating
IgA autoantibodies against intraepidermal
cell surface antigens and clinically may
resemble subcorneal pustular dermatosis.
Juvenile pemphigus pemphigus occurring
before 20 years of age
Neonatal pemphigus due to transplacental
transfer of maternal anti-intercellular cement
substance antibodies to the fetus. Blisters
resolve in 2 weeks.
Differential Diagnosis
When skin is involved, other autoimmune
vesiculobullous disorders need to be differentiated from pemphigus. On rare occasions, bullous
impetigo, dyskeratotic acantholytic disorders
(Dariers disease, Hailey Hailey disease, Grovers
disease) can cause a problem.
When only the oral mucosa is involved, the
following should be considered-aphthous
ulcerations, oral erosive lichen planus, herpetic
gingivostomatitis, erosive candidiasis, and
erythema multiforme.
When both skin and oral mucosa are involved,
it closely resembles erythema multiforme, Stevens
Johnson syndrome, toxic epidermal necrolysis,
bullous systemic lupus erythematosus, and
generalized bullous fixed drug eruption.
Treatment of Pemphigus
The mainstay of therapy in the pemphigus
group of disorders is with systemic steroids,
which can be given as conventional therapy
(oral prednisolone in the dose of 1 mg per kg
body weight) or as pulse therapy. An
upcoming mode of therapy is the dexamethasone cyclophosphamide pulse regimen
consisting of 100 mg of IV dexamethasone in
5% dextrose infusion on 3 consecutive days
of each month combined with IV cyclophosphamide 500 mg bolus dose on day 1 of the
pulse and oral cyclophosphamide 50 mg daily
on other days. This therapy reduces the
conventional side effects of steroids.
The other modalities of therapy include
adjuvant therapy with dapsone, azathioprine,
cyclosporine, methotrexate, gold salts,
mycophenolate mofetil, intravenous
immunoglobulin therapy and plasmapheresis
and are essentially to reduce the side effects of
steroids or to control the severe form of
pemphigus.
Vesiculobullous Disorders
Clinical Features
Preceded by pruritus with or without
urticarial wheals lasting usually for 13
weeks.
Tense bullae on normal or erythematous
skin predominantly over flexural aspects of
the limbs (Fig. 12.14), lower abdomen
(Fig. 12.15), groins and axillae. Facial skin
and scalp relatively spared.
Lesions rupture to leave erosions that heal
spontaneously with postinflammatory
hyperpigmentation.
Nikolskys sign usually negative; Bulla
spread sign +/ Mucosal lesions rare and less severe than
in pemphigus vulgaris and almost never
the presenting feature.
Bullous pemphigoid may be associated with
an underlying malignancy (gastric carcinoma
commonly) and may be associated with
diabetes mellitus, rheumatoid arthritis and
psoriasis.
Diagnosis
Tzanck smear will show numerous
eosinophils with few neutrophils but no
acantholytic cell.
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Differential Diagnosis
Bullous pemphigoid can be easily differentiated
from most other blistering disorders such as linear
IgA disease, chronic bullous disease of childhood,
dermatitis herpetiformis, erythema multiforme
and pemphigus by histology and immunofluorescence. Most difficult diseases to
differentiate from bullous pemphigoid are
epidermolysis bullosa acquisita and cicatricial
pemphigoid.
Prognosis of bullous pemphigoid is better
than pemphigus and it runs a chronic selflimiting course. It may be fatal in the active
stage in the elderly or debilitated patients.
Treatment
The mainstay of treatment is a topical or
systemic steroid depending on the severity
of the disease. Pulse dexamethasone
cyclophosphamide, methyl prednisolone or
cyclophosphamide pulse may be used. Other
modalities include cyclophosphamide,
azathioprine, dapsone, tetracycline with
nicotinamide, erythromycin, leflunomide,
sulphapyridine, methotrexate, mycophenolate mofetil, intravenous immunoglobulin
therapy and plasmapheresis.
Vesiculobullous Disorders
Characteristic
Bullous pemphigoid
Pemphigus vulgaris
Age
Pruritus
Blister
Sites
Erosion
Nikolskys sign
Oral lesions
> 60 years
++
Tense
Flexures, groins, axillae, abdomen
Spontaneously heal
Negative
40 % less severe, almost never a
presenting feature
Benign, self limiting
Middle age
Not present
Flaccid
Face, scalp, trunk, pressure points
Extend peripherally
Positive
8090 % severe commonly the
presenting symptom
Poor without treatment
Prognosis
Clinical Features
Onset at any age, usually between 2055 years
of age.
Males outnumber females.
Pruritus is the first and predominant symptom
followed by a symmetrical eruption of
erythematous papules and papulovesicles,
which are so rapidly excoriated that intact
vesicles are difficult to demonstrate
(Fig. 12.18).
Sites extensor aspects of limbs (elbows and
knees), buttocks, natal cleft, shoulders, upper
back (Fig. 12.19), face and scalp. Grouping of
lesions accounts for it being described as
herpetiformis (not associated with herpes
virus).
Oral lesions are common but asymptomatic.
Provocation of lesions occurs with iodides
orally or in iodide patch testing.
Histological examination best done on lesions
that have not blistered or ruptured and reveals
neutrophilic microabscesses at the tips of
dermal papillae.
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Direct immunofluorescence is the most
reliable diagnostic criterion and should be
performed on clinically normal skin
(preferably of the buttocks). It reveals granular
IgA deposits in dermal papillae.
Indirect immunofluorescence is negative for
anti-BMZ or dermal autoantibodies but
antithyroid and antigliadin antibodies may
be seen.
Differential Diagnosis
Dermatitis herpetiformis can be confused with
numerous conditions because of its pleomorphic
manifestations and occasional lack of diagnostic
lesions. Scabies, bullous pemphigoid before the
development of blisters, and the prurigo group of
disoders are the main issues. It also needs to be
differentiated from chronic exudative eczema,
papular urticaria, neurotic excoriations, and
transient acantholytic dermatoses. A high index
of suspicion is very helpful, even in the absence
of primary lesions. Dermatitis herpetiformis can
be diagnosed based on the typical in vivo bound
granular IgA deposits in normal appearing skin.
Treatment
Dapsone 100200 mg/day (up to 400
mg /day) is the drug of choice. It is amazingly
effective; hours to days after the first dose, the
pruritus disappears and no new lesions erupt
after 1-2 days of treatment.
Strict adherence to a gluten-free diet for
prolonged periods (e.g. 6 to 12 months) may
control the disease in some patients, obviating
or reducing the requirement for drug therapy.
LINEAR IgA DISEASE
It is a chronic acquired subepidermal blistering
disorder of children and adults, with skin and
mucous membrane involvement and characterized by linear deposition of IgA at basement
membrane zone. It consists of two main entities-
Vesiculobullous Disorders
combined with low dose steroids in refractory
cases.
Differential Diagnosis
In young infant, bullous impetigo may resemble
the initial lesions, but its response to antibiotics
differentiates it. Epidermolysis bullosa often
present at birth and family history further
differentiates it. Bullous papular urticaria rarely
affects the face or genital region and it is usually
of short duration. Childhood bullous pemphigoid
may give us similar clinical picture but the
deposition of IgG and C3 at the BMZ is diagnostic.
Treatment is the same. Dermatitis herpetiformis
only occurs in small children (usually occurs
between 20 and 55 years of age) who are
heterozygous for predisposing HLA genes.
Treatment
Dapsone is usually effective (response usually
occurs within 24-48 hours), and may be
Disorder
Site of split
Pathogenic
antibody
P. vulgaris
P. foliaceous/
erythematosus
Paraneoplastic
pemphigus
BP / HG / CP
EBA
Dermatitis
herpetiformis
CBDC
Suprabasal
Subcorneal
IgG
IgG
Suprabasal
IgG
Subepidermal
Subepidermal
Subepidermal
IgG and C3
IgG
IgA
Subepidermal
IgA
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Tense bullae are present over inflamed or
urticarial skin. Hemorrhagic bulla may be
seen. Large areas of erythema and urticaria
without blistering can be seen. Patient
complains of pruritus and does not show
prominent skin fragility, scarring or milia
formation. The clinical picture is more like a
bullous pemphigoid than a mechanobullous
disorder.
3. Cicatricial pemphigoid-like presentation is
marked by widespread mucosal involvement.
Clinical appearance is similar to cicatricial
pemphigoid. Erosions and scars over mucosal
surfaces of mouth, upper esophagus,
conjunctiva, anus or vagina are present with
or without similar lesions over glabrous skin.
4. Brunsting-Perry pemphigoid-like presentation is a chronic recurrent vesiculobullous
eruption localized to head and neck. It is
characterized by bullae healing with scarring
and has minimal to no mucosal involvement.
5. IgA bullous dermatosis-like eruption is
characterized by tense veskcles arranged in
an annular pattern and mucous membrane
involvement. It is also differentiated from
other EBA types by its DIF findings of linear
13
Tuberculosis of the skin constitutes about 10% of all extra-pulmonary tuberculosis which in turn
constitutes only a fraction of all cases of tuberculosis.
Mode of infection
Bacilli
Immunity
Tuberculin
Primary TB
* TB chancre
*Miliary TB
Inoculation
Hematogenous
+++
++
Secondary TB
*Lupus vulgaris
*TBVC
*Scrofuloderma
*TB gumma
*Orificial TB
Inoculation
Inoculation
Contiguous
Hematogenous
Autoinoculation
+/+
++
++
++
+++
+++
+++
+
+
+++
+++
++
+
-
Tuberculids
*Papulonecrotic
*Lichen scrofulosorum
*Erythema induratum
Hematogenous
+++
+++
+++
+++
+++
+++
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TUBERCULOUS CHANCRE
LUPUS VULGARIS
MILIARY TUBERCULOSIS
Miliary TB occurs due to hematogenous
dissemination of tuberculosis in infants and
children or immunosuppressed
The skin lesions are varied may manifest as
crops of bluish papules, vesicles, pustules or
hemorrhagic lesions
Diagnosis established by skin biopsy which
shows acid fast bacilli
The primary source of TB should be identified
and treated.
Differential Diagnosis
Discoid lupus erythematosus Lesions begin
as dull red macules or indurated plaques that
develop an adherent scale (carpet tack sign),
mainly over head and neck and evolve with
atrophy, scarring and pigmentary changes.
Differential Diagnosis
TBVC should be differentiated from other
warty lesions such as verruca vulgaris, lupus
vulgaris (usually not hyperkeratotic, diascopy
demonstrates apple jelly nodules), chromoblastomycosis, hypertrophic lichen planus
(has multiple itchy lesions usually over lower
legs with evidence of lichen planus
elsewhere), leishmaniasis and tertiary
syphilis.
SCROFULODERMA
Scrofuloderma results from breakdown and
involvement of skin overlying a tuberculous focus
such as lymph node, bone, joint, epididymis or
lacrimal gland.
It manifests as bluish red nodules overlying
lymph nodes or joints that break down to form
undermined ulcers with a bluish edge (Figs
13.5 and 13.6).
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Differential Diagnosis
Scrofuloderma should be differentiated from
hidradenitis suppurativa, acne conglobata,
syphilitic gumma and actinomycosis.
Cervicofacial actinomycosis is characterized
ORIFICIAL TUBERCULOSIS
Tuberculosis of mucosa or skin adjoining orifices
in a patient with advanced internal tuberculosis
is known as orificial TB (Fig. 13.8).
The affected patient is usually an adult of poor
general health
TUBERCULIDS
Tuberculids are hypersensitivity eruptions which
arise in response to an internal focus of
tuberculosis and clear with antituberculous
therapy.
Papulonecrotic Tuberculid
It is an eruption of necrotizing papules,
particularly affecting extremities and
occurring in more or less symmetric crops.
The lesions are hard, dusky papules that crust
or ulcerate to heal with atrophic scars (Fig.
13.9).
Papulopustular secondary syphilis, pityriasis
lichenoides et varioliformis acuta, ChurgStrauss granuloma, lymphomatoid papulosis,
perforating granuloma annulare, perforating
collagenosis and necrotizing or septic
vasculitis share clinical and histologic
features with papulonecrotic tuberculid.
Diagnosis
Absolute Criteria
Positive culture for M. tuberculosis
Guinea pig inoculation
PCR for M. tuberculosis.
Others
Lichen Scrofulosorum
It presents as grouped, closely set minute
perifollicular papules over the trunk (Fig.
13.10) or extremities in children with
tuberculous disease
Lichen nitidus, lichen planus, secondary
syphilis and sarcoidosis should be considered
in the differential diagnosis.
Erythema induratum
Presents as persistent or recurrent
erythematous tender nodular lesions
(Fig, 13.11) (usually ulcerate in contrast to
erythema nodosum) that occur secondary to a
tuberculous focus elsewhere.
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Treatment
Anti tubercular therapy with three or four drugs
is given for a period of 6 to 9 months based on the
type of tuberculosis. Most regimens contain
isoniazid, rifampin, ethambutol and pyrazinamide.
ATYPICAL MYCOBACTERIAL
INFECTIONS
Atypical mycobacteria can present with varied
cutaneous features in normal as well as
immunosuppressed patients. The main features
are summarized in the following table.
Disease
Clinical Features
M.marinum
M.ulcerans
Buruli ulcer
M.avium complex
M.chelonae
Injection
M.fortuitum
abscess
M. scrofulaceum Cutaneous abscesses
Treatment
Rifampin and ethambutol or
tetracycline
Surgery is the treatment of choice
followed by rifampin or
cotrimoxazole
Combined therapy of isoniazid,
rifampin and streptomycin.
Surgical debridement and amikacin
or doxycycline or ciprofloxacin
Treatment- surgical treatment
of infected lymph node.
Widespread disease- treatment
same as in M avium complex
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14
LUPUS ERYTHEMATOSUS
Lupus erythematosus (LE) is a multisystem
disease of unknown origin characterized by the
production of numerous diverse types of
autoantibodies. Lupus erythematosus have wide
spectrum of manifestations ranging from solitary
chronic skin lesions in chronic discoid lupus
erythematosus (DLE) to wide spread
polymorphous lesions in subacute lupus
erythematosus (SCLE) to multiple organ
involvement in systemic lupus erythematosus
(SLE).
Types
Localized DLE: lesions occur only on the head
or neck.
Generalized DLE: lesions are seen both above
and below the neck (Figs 14.5 and 14.6).
Prognosis
DLE has a chronic progressive course.
Patients with hematological and serological
abnormalities have 6.5% risk of developing
overt SLE.
Diagnosis
Based on clinical features and histopathology.
Direct immunofluorescence (DIF)-deposits of
IgG and C3 along the basement membrane in
affected skin in up to 80%, but normal nonsun exposed skin always negative. Negative
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brown initially, later becoming red brown in color,
have a characteristic translucence and woodgrains appearance, telangiectasia may be seen on
the surface of the lesions, no prominent follicles),
tinea faciei (KOH examination), granuloma faciale
(brown color, no scarring), psoriasis (silvery
scales), rosacea (pustules, ears spared) and
Jessners lymphocytic infiltrate. In each case,
histology is most helpful.
The hypertrophic type of DLE may be
confused with hypertrophic lichen planus,
prurigo nodularis. LE profundus should be
differentiated from other types of panniculitis.
Mucosal DLE should be differentiated from
mucosal lichen planus.
Differential Diagnosis
Lupus vulgaris (rarely symmetrical, has
progression on one side and healing with
scarring on the other side, apple-jelly nodules on
diascopy), sarcoidosis (lesions are yellowish
Histopathology
Characteristic histopathological changes are:
Hyperkeratosis with follicular plugging
Irregular atrophy of the stratum malphighi
Liquefactive degeneration of the basal cell
layer and
Patchy perivascular and periappendageal
lymphocytic infiltration.
Degenerative changes in the connective
tissueshyalinization, edema, fibrinoid
change in the upper dermis.
Valuable clues are thickened periodic acidSchiff (PAS) positive basement membrane and
deposition of mucin.
Treatment
Photoprotection and topical sunscreens
Topical high potency or intralesional steroids
Topical calicineurin inhibitors (pimecrolimus,
tacrolimus)
Systemic therapy for widespread recalcitrant
disease are antimalarials (Hydroxychloroquine 200-400 mg daily or chloroquine
250 mg daily, monitoring by an ophthalmologist required every 6-12 months), dapsone
(50-100 mg daily), thalidomide (50-200 mg
daily), corticosteroids (prednisolone 40 mg
Pathogenesis
LE is a multifactorial disease with genetic and
immunopathologic abnormalities. The release of
nuclear antigens because of enhanced apoptosis
is a key factor.
Important predisposing factors are genetic
predisposition (HLA-B8, DR2, DR3, DQwl,
DRB1), complement defects, exogenous factors
(UV radiation, and medications), and individual
factors (hormone status, altered immune status).
The 1982 Revised Criteria for
Diagnosis of SLE are:
1. Malar rash: Fixed erythema, flat or raised,
over the malar eminences, tending to spare
the nasolabial folds (Fig. 14.7).
2. Discoid rash: Erythematous raised patches
with adherent keratotic scaling and follicular
plugging; atrophic scarring may occur in
older lesions.
Treatment
Same as for discoid lupus erythematosus.
SYSTEMIC LUPUS ERYTHEMATOSUS
(SLE)
SLE a multisystem disorder, primarily affects
skin, joints and vascular system. The age of onset
is usually between 16 and 42 years occurring more
frequently in females (F: M:: 8:1).
Etiology
Exact cause is unknown but there is evidence
to suggest the role of genetic, immune and
various environmental factors.
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Essentials in Dermatology
3. Photosensitivity: Skin rash as a result of
unusual reaction to sunlight, by patient
history or physician observation.
4. Oral ulcers: Oral or nasopharyngeal
ulceration, usually painless, observed by a
physician.
5. Arthritis: Nonerosive arthritis involving two
or more peripheral joints, characterized by
tenderness, swelling, or effusion. or
6. Serositis:
a. Pleuritisconvincing history of pleuritic
pain or rub heard by a physician or
evidence of pleural effusion.
b. Pericarditisdocumented by ECG or rub
or evidence of pericardial effusion.
7. Renal disorder:
a. Persistent proteinuria > 0.5 g/day or
greater than 3+ if quantitation not
performed or
b. Cellular castsmay be red cell,
hemoglobin, granular, tubular, or mixed.
8. Neurologic disorder:
a. Seizuresin the absence of offending
drugs or known metabolic derangements,
e.g. uremia, ketoacidosis, or electrolyte
imbalance or
b. Psychosisin the absence of offending
drugs or known metabolic derangements,
e.g. uremia, ketoacidosis, or electrolyte
imbalance.
9. Hematologic disorder:
a. Hemolytic anemiawith reticulocytosis
or
b. Leukopenia < 4000/mL on two or more
occasions or
c. Lymphopenia < 1500/mL on two or more
occasions or
d. Thrombocytopenia<100,000/mL in
the absence of offending drugs.
10. Immunologic disorder:
a. Anti-DNAantibody to native DNA in
abnormal titer or
b. Anti-Smpresence of antibody to Sm
nuclear antigen or
Differential Diagnosis
SLE must be differentiated from dermatomyositis,
erythema multiforme, polyarteritis nodosa, acute
rheumatic fever, rheumatoid arthritis, pellagra,
pemphigus erythematosus, drug eruption,
hyperglobulinemic purpura, Sjogrens syndrome,
necrotizing angiitis and myasthenia gravis. In
SLE, there may be fever, arthralgia, weakness,
lassitude, diagnostic skin lesions, an increased
ESR, cytopenias, proteinuria, immunoglobulin
deposition at dermoepidermal junction and a
positive ANA test. Biopsies of skin lesions and
involved kidney may also be diagnostic.
Treatment
SLE with only cutaneous lesions and arthritis:
Photoprotection.
NSAIDs, antimalarials, prednisolone ( 1-2 mg
per kg body weight daily).
Dapsone most effective in urticarial vasculitis
and bullous SLE.
Severe Disease with
End-organ Damage
Steroid pulse therapy.
Immunosuppressants such as azathioprine
(100-150 mg daily), cyclophosphamide (50100 mg daily), methotrexate (7.5-20 mg
weekly), chlorambucil, mycophenolate mofetil
(2 gm daily) and cyclosporine (5 mg/kg body
weight daily).
Experimental Therapies
Intravenous immunoglobulins, plasmapheresis, anti CD20 (rituximab), -CD40 and
TNF alpha antibodies.
Course and Prognosis
The course of the SLE is very variable. Acute
fulminating cases are much less common than
subacute cases, which smoulder on for many
years.
SCLERODERMA
Scleroderma (Gr. Skleros hard, and derma skin)
is a connective tissue disorder characterized by
generalized or localized sclerosis of the skin. The
localized type is called morphea.
Classification
Morphea Localized (Circumscribed plaque,
morphea profundus, bullous, linear, en coup de
sabre) and generalized.
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Systemic sclerosis LM (Limited cutaneous) SSc,
DC (Diffuse cutaneous) SSc.
Occupational scleroderma Polyvinylchloride,
perchlorethylene, trichloroethylene, organic
solvents, malathion, DDT, epoxy resins, silicosis.
Iatrogenic scleroderma Bleomycin, carbidopa,
pentazocine, cocaine, appetite suppressants,
silicone or paraffin implants, GVHD.
Pseudoscleroderma Scleroedema of Buschke,
Scleromyxoedema, prophyria cutanea tarda,
phenylketonuria.
Primary systemic amyloidosis, carcinoid
syndrome, hypothyroidism.
Miscellaneous Toxic oil syndrome, eosinophilic
fascitis.
MORPHEA
Localized Morphea
Most common form of morphea.
Occurs most commonly in females than males
and primarily in young adults.
Seen commonly on the trunk.
The lesion of morphea may begin as
erythematous macule, evolve into ivory-
Fig. 14.8
Generalized Morphea
Lesions are more numerous and larger
Often coalesce to involve extensive portions
of the body.
Muscle atrophy may be associated.
Pansclerotic Morphea (Morphea
Profunda)
Sclerosis involves dermis, panniculus, fascia,
muscle and bones.
There is disabling limitation of the joints.
En Coup De Sabre
It is a variant of linear scleroderma involving
scalp parasagitally on frontal scalp and
forehead (Figs 14.8 and 14.9).
Often has the configuration of the stroke of a
saber (en coup de sabre).
Differential Diagnosis
1. Morphea-like lesions can occur in sarcoidosis
and morpheic basal cell carcinoma.
Fig. 14.9
Figs 14.8 and 14.9: En coup de sabrelinear indurated depressed lesion in the midline over the forehead
Treatment
Natural history is towards spontaneous
resolution.
Topical steroid, intralesional steroids and oral
chloroquine.
Topical calcipotriol.
Bath PUVA or UVA1.
For widespread or rapidly advancing disease
consider therapy usually reserved for systemic
sclerosis (corticosteroids, d-penicillamine,
cyclopsporine, low dose methotrexate,
etretinate, phenytoin, plasmapheresis).
Physiotherapy may be helpful in preventing
joint deformities.
Classification
Diffuse disease: Characterized by extensive
proximal and truncal skin induration.
Limited disease: Induration is confined to
hands, forearm, face, and legs. Its variant is
called CREST syndrome (ThibiergeWeissenbach syndrome) (Calcinosis,
Raynauds phenomenon, Esophageal dysfunction, Sclerodactyly and Telangiectasia).
American Rheumatism
Association Criteria
Major
Scleroderma proximal to the digits, affecting
limbs, face, neck and trunk.
Minor
Sclerodactyly (Fig. 14.10).
Digital pitted scarring (Fig. 14.11).
Bilateral basal pulmonary fibrosis.
One major criterion or two or more minor
criteria suggest the diagnosis of systemic sclerosis.
Note: These criteria have 97% sensitivity and 98%
specificity.
SYSTEMIC SCLEROSIS
It is characterized by cutaneous and internal
organ fibrosis. Raynauds phenomenon is the
earliest feature and may precede the onset of
disease by months or years. The heart, lungs,
gastrointestinal, kidney and other organs may be
involved.
Pathogenesis
Exact cause of systemic sclerosis is unknown.
Important steps in its pathogenesis include:
Excessive synthesis of collagen and matrix
macromolecules.
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Cutaneous Manifestations
Three phases of dermal involvement can be
distinguished:
1. Edematous phase (stiff, puffy, fingers)
2. Indurative phase (hard, tight, hide bound)
3. Atrophic phase (softened skin, burnt out).
Hands and Feet
Early: Raynauds phenomenon.
Swollen or tumid fingers and hands.
Round finger pad sign-fingers lose their
normal peaked contour but rather appear as
rounded hemisphere when viewed from the
side.
Painful ulcerations at fingertips (Rat bite ulcer)
with pitted scars.
Late: sclerodactyly (induration of skin over
the fingers) with tapering of fingers (Figs 14.10
and 14.11).
Skin is tightly bound down.
Leathery crepitations over joints and flexion
contractures.
Heuck-Gottron sign- loss of cuticle with
telangiectases.
Bony resorption.
Atrophy of the pulp of the fingers.
Gangrene of the fingers.
Pigmentation.
Calcinosis.
Face
Periorbital edema is the early manifestation
Late manifestations include: Mask like facies
(difficulty in eversion of lower eyelids),
thinning of lips, microstomia, radial perioral
furrowing, small sharp nose (Fig. 14.12),
telangiectasia (mat-like) and diffuse
hyperpigmentation.
Forehead is smooth and shiny, and skin is
bound down and hard.
There is reduced wrinkling on the forehead
and mandibular atrophy.
Trunk
Other Changes
Salt and pepper pigmentation (Fig. 14.13),
gangrene of fingers, mat like telangiectasia, leg
ulcers and livedo reticularis.
Differential Diagnosis
1. Generalized
morphea
(Raynauds
phenomenon is rare, systemic involvement is
unusual, no atrophic stage, no facial
telangiectasia or perioral furrowing, skin of
trunk and limbs are equally involved)
2. Pseudosclerodermas (Specific features of each
should be looked for)
3. Occupational and iatrogenic scleroderma
(History of specific exposure should arouse
the suspicion).
4. Other collagen vascular disorders- mixed
collagen vascular disorders, overlap
syndromes
5. Graft versus host disease
Prognosis and Cause of Death
Course of the disease is variable. Death occurs
from intercurrent infection, respiratory failure,
cardiac failure, renal failure, sometimes,
malignant hypertension and perforation of the
gastrointestinal tract.
Other Conditions Where Sclerodermoid
Changes are Seen
Phenylketonuria, progeria, Rothmund-Thomson
syndrome, Werners syndrome, porphyria
cutanea tarda, primary systemic amyloidosis,
Hashimotos disease, carcinoid syndrome,
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childhood diabetes mellitus and drugs
(bleomycin, pentazocine, carbidopa, and
5-hydroxytryptophan).
Treatment
There is no specific treatment and no therapy is
known to alter the course of a disease. Treatment
is primarily directed towards complications.
Pharmacological agents used for systemic
sclerosis can be grouped into various categories.
Collagen modulators: D-penicillamine (125
mg alternate days, 750-1500 mg per day),
relaxins, and interferons.
Vasoactive agents: Captopril, nifedipine and
pentoxifylline.
Immunosuppressive agents: Systemic corticosteroids (prednisolone 0.5 mg mg per kg
body weight daily), azathioprine (1-2 mg mg
per kg body weight daily), cyclophosphamide
(2 mg per kg body weight daily), cyclosporine
(3-5 mg per kg body weight daily) and
methotrexate (20-30 mg weekly).
For internal organ involvement Angiotensin
converting enzyme inhibitors are treatment of
choice for renal hypertension, proton pump
inhibitors (omeprazole 20-40 mg daily) indicated
for esophageal dysfunction and for pulmonary
hypertension intravenous prostacyclin; interstitial lung disease may respond best to
cyclophosphamide. Physical therapy can help
avoid contractures and retain function.
Cutaneous Manifestations of
Dermatomyositis
Pathognomonic
Gottrons papules: Violaceous, flat topped
papules on interphalangeal joints and
knuckles. Similar lesions may occur over other
bony prominences such as knees, elbows and
medial malleoli.
Gottrons sign: Symmetric macular violaceous
erythema with or without edema over the
above mentioned sites.
Characteristic
Periorbital violaceous erythema with
associated edema of eyelids and periorbital
tissue (heliotrope rash) (Fig. 14.14).
Periungual telangiectasia with associated
dystrophic cuticles.
Macular violaceous erythema overlying the
dorsal hands, extensor forearms and arms,
deltoids, posterior shoulders, nape of neck, V
area of neck, upper chest and forehead.
Shawl sign-erythema and scale (with or
without poikiloderma) over the shoulder
regions.
Mechanics hands: Bilaterally symmetrical
confluent hyperkeratosis distributed along the
DERMATOMYOSITIS
It is a systemic, inflammatory disease involving
primarily skin and muscles. Symmetric, proximal
muscle weakness occurs especially in the hips,
thigh, and upper arm. Patients with only
muscular symptoms and signs but no cutaneous
findings are said to have polymyositis. These can
be associated with malignancies especially in
adulthood carcinoma of lung, breast, female
genital tract, stomach, kidney and testes.
Compatible
Poikiloderma atrophicans vasculare
Calcinosis cutis.
Systemic features include arthritis (25%), oral
ulcers (20%), calcinosis (distinctive feature of
juvenile dermatomyositis), pulmonary fibrosis
(20%), gastrointestinal ulcerations and
hemorrhages, occasionally myocarditis or
myopathy.
Investigations
Skin biopsy, muscle biopsy, muscle enzymes,
electromyography, ANA, Ab-SSA, SSB, Sm,
nRNP, Jo-1and PM-1.
Diagnostic Criteria
1. Progressive symmetric proximal muscle
weakness.
2. Elevated muscle enzyme levels.
3. Abnormal electromyogram.
4. Abnormal muscle biopsy.
5. Characteristic cutaneous manifestations.
Definite: 5 plus three other criteria.
Probable: 5 plus two other criteria.
Differential Diagnosis
Includes other myopathies (inclusion body
myositis, muscular dystrophy, neuromuscular
atrophy, myasthenia gravis, thyrotoxic myopathy,
Cushings disease, sarcoidosis, alcoholism),
drugs (lipid lowering agents, hydroxyurea,
NSAIDs), overlap syndromes, vasculitis,
polymyalgia rheumatica and trichinosis.
Treatment
Skin disease: Topical steroids, hydroxychloroquine.
Muscle disease: Systemic corticosteroids are
first line therapy. Second line agents are
OVERLAP SYNDROME
The term overlap syndrome may be used
when patients exhibit symptoms of more than
one connective tissue disease.
Such patients may meet diagnostic criteria for
one disease but also have atypical
manifestations or findings suggestive of
second diagnosis.
Systemic sclerosis combined with dermatomyositis is the most frequently seen overlap
syndrome.
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Dry eyes and dry mouth occur in primary
Sjgrens syndrome or if associated with other
connective tissue disease then referred to as
secondary Sjgrens syndrome.
Most patients are aged 50 years or older and
are women.
Clinical features include xerostomia, rhinitis
sicca, vaginal dryness and dry eyes (Fig.
14.15).
Skin manifestations of SS include vasculitis,
xerosis and annular erythema.
Rheumatoid factor is usually positive.
80% of patients have anti Ro/SSA antibodies.
Increased risk of developing lymphoreticular
malignancies.
No specific treatments available, only
symptomatic management.
Fig. 14.16: Lichen sclerosus et atrophicus of the vulvatypical figure of eight or hour glass appearance
Differential Diagnosis
On trunk- morphea, annular atrophic plaque type
of DLE and vitiligo, female genitalia-vitiligo,
chronic dermatitis, erosive lichen planus,
autoimmune bullous diseases, male genitaliabalanitis in all its variants, idiopathic phimosis,
erosive lichen planus.
Treatment
MedicalTopical steroids or intralesional
steroids, topical pimecrolimus or tacrolimus,
topical testosterone, topical tretinoin, UVB and
bath PUVA therapy. Surgical correction of
adhesions may be required.
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15
Pigmentary Disorders
VITILIGO
Vitiligo is defined as a common, dermatological
disorder characterized by well-circumscribed,
milky-white cutaneous macules devoid of
Pathogenesis
The white macules of vitiligo are the result of a
loss of melanocytes. The mechanism(s) by which
the melanocytes are lost may be multiple but have
not been identified unequivocally. Seven hypotheses, not mutually exclusive, have been
proposed to explain the causation of vitiligo:
Autoimmune: Strengthened by the
demonstration of specific autoantibodies to
melanocyte cell surface antigens and the
association of vitiligo with a variety of
autoimmune disorders.
Autocytotoxic: Also called the self-destruction
theory, it proposes melanocyte destruction by
intracellular retention of various precursors
of melanin synthesis.
Neural: Especially proposed to explain the
segmental type of vitiligo.
Pigmentary Disorders
Biochemical: Accumulation of pteridines (6biopterin and 7-biopterin) in the vitiliginous
skin causes the depigmentation.
Antioxidant deficiency theory: There is an
increased level of norepinephrine and
catecholamine derivatives in vitiligo skin
which leads to tissue ischemia and increased
activity of monoamine oxidase enzyme, which
in turn causes excess production of stress
related hydrogen peroxide. Reduced catalase
activity in vitiligo skin leads to impaired
degradation of H2O2 and accumulation of
superoxide radicals causing depigmentation.
Melanocyte growth factor reduction hypothesis:
In vitiligo, there is reduced melanocyte growth
factors derived from keratinocytes, fibroblasts
and other tissues.
Intrinsic (genetic) theory: An underlying
genetic/intrinsic factor predisposes some
individuals to be more prone to develop
vitiligo.
Clinical Features
The diagnostic lesion of vitiligo is the typical
vitiligo macule, which is of variable size,
round/oval in shape, has a milky white color
and scalloped margins (Fig. 15.1).
May appear at any age, however, the peak age
at onset has been reported to be five to thirty
years.
Prevalence is the same in both sexes.
The natural course of the disease is of gradual
progression, the lesions increasing both in
number and size. In some cases there may be
a rapid downhill course of vitiligo and this
has been termed galloping vitiligo or vitiligo
fulminans.
Segmental vitiligo and vitiligo in children
have a better prognosis.
Mucous membrane involvement is also noted
in vitiligo and is commoner, or rather, easily
detectable in dark-skinned races.
Leukotrichia refers to depigmentation of the
hair and may occur in some patients.
Classification of Vitiligo
Localized
Focal vitiligo: This consists of one or more
macules in one area but not clearly in a
segmental or zosteriform distribution .
Segmental vitiligo: Number of macules
involving a unilateral segment of the body.
The lesions stop abruptly at the midline of the
affected segment (Fig. 15.1).
Mucosal vitiligo: Vitiligo affecting mucous
membranes of the lips, oral cavity or the
genitalia (Fig. 15.2).
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Generalized
Acrofacial vitiligo: Lesions on the acral areas
(hands and feet) (Fig. 15.3) and on the face,
very often the perioral areas.
Vitiligo vulgaris: Multiple macules of variable
sizes over widely scattered areas often tending
to bilateral symmetry (Fig. 15.4).
Pigmentary Disorders
Differential Diagnosis of
Localized Vitiligo Includes
Naevus depigmentosus (localized hypomelanosis present since birth), naevus anemicus
(pale area due to vasoconsconstriction), leprosy
(suspect in an endemic area, shows hypoanesthetic or anesthetic hypopigmented patch/
es), pityriasis alba (hypopigmented macular
lesions have ill defined margins with fine scaling,
self limiting course), postinflammatory hypomelanosis (such cases have preceding history of
dermatoses, and the skin lesions are ill defined),
tinea versicolor (typical localization to upper
trunk, pigmented macular lesions have fine
powdery scales, KOH +vity conclusive), ash-leaf
macules and confetti depigmentation of tuberous
sclerosis, and idiopathic guttate hypomelanosis
(tiny porcelain white macules, 2-6 mm with
distinct margins, localized to limbs in older
individuals).
Differential Diagnosis of
Generalized Vitiligo Includes
Chemical leukoderma (there is history of exposure
to phenolic germicides; confetti macules; localized
to the site of contact), leprosy (suspect in an
endemic area, has anesthetic hypopigmented
patch/es), mycosis fungoides (unpatterned
lesions, diagnosis confirmed by biopsy),
postinflammatory hypomelanosis (hypopig-
Treatment
Treatment of vitiligo can be broadly divided into
medical and surgical modalities.
Medical management
Topical therapy
1. Photoprotection: It prevents sunburn and
Koebner phenomenon, prevents tanning of
uninvolved skin and therefore lessens
contrast between normal and depigmented
skin.
2. Topical potent corticosteroids.
3. Intralesional corticosteroids: (Triamcinolone
acetonide) especially for leukotrichia on
scalp.
4. Human placental extract.
5. Topical immunomodulators: Such as
tacrolimus (0.1%, 0.03%), pimecrolimus or
tacrolimus (0.1%) combined with narrow
band UVB three times a week.
6. Calcipotriol: Can be used as monotherapy or
combined therapy (sunlight, PUVA, or
narrow band UVB, clobetasol).
7. Topical pseudocatalase + calcium + UVB
8. Vitix: Formulation containing superoxide
dismutase and catalase. It removes
hydrogen peroxide from skin, thereby helps
in repigmentation.
9. Phenytoin local application: It inhibits release
of norepinephrine and activity of monoamine
oxidase, inhibits the production of
superoxide anion and suppresses cytotoxic
T- lymphocyte activity and induces type 2
like cytokine profile.
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10. Dead sea climatotherapy in combination with
pseudocatalase: Here patients take bath in
dead sea for 15 minutes twice daily followed
by a shower to wash off salt followed by
application of pseudocatalase cream prior
to sun exposure.
11. Topical prostaglandin analogues (PGE2).
12. Cosmetic camouflage where nothing works
or when on treatment.
Systemic Therapy
Surgical Management
Indications
Stable vitiligo (i.e. no new lesions for last two
years)
Refractory to medical management.
Phototherapy
Psoralen (stimulates melanogenesis in
presence of ultra violet radiation)with
ultraviolet A therapy (PUVA)- topical and
systemic
Khellin + UVA (KUVA). Khellin is extracted
from seeds of the plant Ammi visnaga. It can
be given either topically or systemically.
Khellin is given orally 50-100 mg/day, 2.5
hours prior to sun or UVA exposure up to 15
J/cm2. But due to systemic toxicity, topical
preparation of khellin is recommended.
Modalities
Punch grafting
Split skin thickness graft
Blister grafting
Melanocyte culture and transplantation
Tattooing
Therapeutic spot and regional dermabrasion
Trypsinized autograft injection
Topical 5- fluorouracil combined with
epidermal abrasion.
ALBINISM
Autosomal recessive inherited disorder.
It is characterized by reduced melanin
synthesis in the melanocytes of the skin, hair,
and eyes, termed oculocutaneous albinism
Pigmentary Disorders
(OCA), and hypopigmentation primarily
involving the retinal pigment epithelium of
the eyes termed ocular albinism (OA).
Due to genetic abnormalities of melanin
synthesis associated with normal number
and structure of melanocytes (differentiate it
from vitiligo where melanocytes are reduced
or absent).
Tyrosinase-related OCA, the most common
type of albinism is produced by loss of
function of the melanocytic enzyme tyrosinase
resulting from mutations of the tyrosinase
gene.
Affected individuals are born with white or
blond hair and skin and blue eyes (Fig. 15.6).
PIEBALDISM
Piebaldism is an uncommon, autosomal
dominant, congenital, stable leukoderma
characterized by a white forelock and vitiligolike amelanotic macules, usually containing
a few normally pigmented or hyperpigmented macules (Fig. 15.7).
WAARDENBURGS SYNDROME
WS (Waardenburg syndromeHirschsprungs
disease or Shab-Waardenburg syndrome) is a rare
autosomal dominant disorder that is
characterized by:
Lateral displacement of the inner canthi and
of lacrimal puncta
Prominence of the nasal root and of the medial
eyebrows
Congenital deafness
Heterochromic irides
White forelock
Hypomelanotic macules.
MELASMA (CHLOASMA)
Melasma is a common acquired hypermelanosis that occurs exclusively in sunexposed areas; it is exacerbated by sun
exposure, pregnancy, oral contraceptives, and
certain anti-epilepsy drugs.
Melasma presents in one of three usually
symmetric facial patterns. The most common
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FRECKLE (EPHELIDES)
It is an area of pale brown pigmentation usually
less than 3 mm with poorly defined lateral
margins
Freckle appears as result of functionally
overactive melanocytes (though they are
normal in number )
They are seen only in fair skinned people
They are stimulated by ultra violet radiation
and fade away during winter
Histology reveals excess of melanin pigment
in the basal layer.
Pigmentary Disorders
Any child with recurrent, unexplained
abdominal pain should be examined for the
typical mucosal, and periorificial pigmented
lesions of Peutz-Jeghers syndrome.
Localized:
Melasma- like- estrogen, progesterone,
phenytoin
Knuckle pigmentation- bleomycin
Palmoplantar- cyclophosphamide, doxorubicin
Linear bleomycin (flagellate), zidovudine.
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16
Keratinization Disorders
ICHTHYOSIS
Ichthyosis (from Greek ichthys fish) denotes a
group of hereditary and acquired disorders of
keratinization characterized by the development
of dry rectangular scales.
Keratinization Disorders
Fig. 16.2
Fig. 16.3
Figs 16.2 and 16.3: X-linked recessive ichthyosislarge dirty brown scaling involving flexor and extensor
aspects of limbs and trunk but sparing rhomboidal spaces in body folds
Lamellar Ichthyosis
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Fig. 16.7
Fig. 16.8
Figs 16.7 and 16.8: Bullous congenital ichthyosiform
erythrodermano more blisters seen, body folds
show thick dark gray brown scales forming warty,
ridged pattern
Keratinization Disorders
collodion baby. As the membrane is cast off in
10 to 14 days, generalized erythema and
scaling are apparent. Scales may be large and
plate like on the legs but are apt to be fine on
the trunk, face and scalp. It has a tendency to
improve at the time of puberty. Ectropion,
deformities of the ears and sparsity of the
scalp hair are common accompaniments.
Differential diagnosis: Congenital infections
such as candidiasis, congenital psoriasis,
Nethertons syndrome, immunodeficiency
disorders, trichothiodystrophy and neutral
lipid storage disease may mimic the cutaneous
signs of non-bullous ichthyosiform
erythroderma.
A collodion baby is the usual presentation of
congenital recessive ichthyosis. Kollodes is the
Greek word for glutinous or glue like. The child is
born encased in a transparent, parchment-like
membrane, which is taut and may impair
respiration and sucking. Collodion presentation
can develop into a wide spectrum of ichthyosis
phenotypes as the child grows. Differential
diagnosis: Harlequin fetus can be easily
differentiated from collodion baby. Restrictive
dermopathy or Stiff baby syndrome produces
a generalized taut thick, tethered and unyielding
skin at birth which does not desiccate in the
neonatal period. Infective causes of
desquamation such as staphylococcal scalded
skin syndrome should be included in differential
diagnosis.
Harlequin ichthyosis (fetus) is a dramatic,
severe, and usually fatal presentation of
ichthyosis. The child is often premature and born
with massive, shiny plates of stratum corneum
separated by deep, red fissures that tend to form
geometric patterns. There are poorly developed
or absent ears and marked ectropion and
eclabium. These children are at great risk during
the neonatal period and often die shortly after
birth.
Ichthyosiform Syndromes
1. Refsums syndrome (Heredopathia atactica
polyneuritiformis)
Refsums syndrome is a rare autosomal
recessive metabolic disorder in which
there are characteristic neurological and
cutaneous clinical features:
The underlying abnormality is deficiency
of enzyme phytanic acid oxidase.
As a consequence of this deficiency,
phytanic acid (found in green vegetables)
accumulates and displaces some of the
unsaturated fatty acids, such as linolenic
acid, from the lipids through out the
tissues.
It manifests usually in the second decade.
Skin is affected by an ichthyosis very
similar to ichthyosis vulgaris.
Neurological changes include a cerebellar degenerative disorder (cerebellar
ataxia), a progressive polyneuropathy,
retinitis pigmentosa, and a sensory
deafness. Rarely, cardiac abnormalities
have been described.
DiagnosisHistopathology of the skin
shows some of the epidermal cells
containing lipid vacuoles. No or very little
phytanic acid is present in the blood.
Treatment by a phytanic acid free diet, in
which green vegetables and dairy
products are excluded, has been used.
2. Sjgrens-Larsson syndrome:
This uncommon neuroectodermal
genodermatosis appears to be inherited as
an autosomal recessive disorder.
The underlying metabolic defect is
deficiency of enzyme fatty alcohol:
nicotinamide-adenine dinucleotide
oxidoreductase.
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The skin disorder becomes evident after
the first few months of life with scaling
over the body and hyperkeratosis of palms
and soles.
The neurological component usually
starts at 2-3 years of life and remains static
after puberty, consists of a spastic diplegia
(Fig. 16.10), or occasionally a tetraplegia
with mental retardation. Other features
are seizures and degeneration of retina.
DiagnosisHistopathological changes
are similar to lamellar ichthyosis.
TreatmentDiet lacking natural fat and
containing medium chain triglycerides has
been beneficial.
3. KID syndrome:
The acronym KIDKeratitis, Ichthyosis,
and Deafness describes the salient clinical
features of this syndrome.
4. Nethertons syndrome:
It is a rare autosomal recessive disorder
characterized by concurrence of ichthyosis
linearis circumflexa, trichorrhexis
invaginata (bamboo hair) and atopic
dermatitis.
5. CHILD syndrome:
The acronym CHILD describes a very rare
disorder comprising Congenital Hemidysplasia with Ichthyosiform erythroderma
and unilateral Limb Defects mainly
skeletal hypoplasia.
6. IBIDS syndrome (Tays syndrome):
The acronym IBIDS describes Ichthyosis,
Brittle hairs, Impaired intelligence,
Decreased fertility and short Stature.
Acquired Ichthyoses
The distinction between dry skin (xerosis) from
environmental causes and acquired ichthyoses
is sometimes difficult. The sudden onset of
generalized pronounced ichthyoses in an adult
could be due to:
1. Lymphomas especially Hodgkins lymphoma
2. Internal malignancy
3. Malabsorption syndromes and malnutrition
4. Certain drugs like clofazimine
5. Hypothyroidism
6. Lepromatous leprosy
7. HIV disease.
Treatment
Emollients for scaly skin especially after bath
Salicylic acid, urea, lactic acid in ointment
form or propylene glycol-glycerine lactic acid
mixture for topical application
Oral retinoids Etretinate or Acitretin. They
are really useful in lamellar and congenital
ichthyosiform erythrodermas.
DARIERS DISEASE
Keratinization Disorders
Fig. 16.11
Fig. 16.12
Figs 16.11 and 16.12: Darier's diseasedirty, warty greasy papules in seborrheic distribution over the trunk
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Fig. 16.16:
Fig. 16.17
Figs 16.16 and 16.17: Darier's diseaseacrokeratosis verruciformis of Hopf lesions over the dorsa of hands
POROKERATOSIS
It is a chronic progressive disease which
occurs due to abnormal proliferation of a clone
of keratinocytes.
Keratinization Disorders
plantar porokeratosis, porokeratosis
palmoplantaris et disseminata and linear
porokeratosis (Fig. 16.20).
Histological hallmark is the column of
parakeratosis known as cornoid lamella.
Differential diagnosis: Multiple lesions can be
mistaken for psoriasis, lupus erythematosus,
pityriasis rubra pilaris or verrucous lichen planus.
Solitary lesions often misinterpreted as tinea,
warts, or actinic keratoses. Palmoplantar lesions
are hard to diagnose clinically; one can consider
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Type of keratoderma
Important features
Diffuse PPK with livid red border (Fig. 16.21) Marked hyperhidrosis
Diffuse PPK similar to Thost Unna type.Histology shows epidermolytic
hyperkeratosis
Honey combed palmoplantar thickening with constriction bands and mutilation, star
fish shaped keratosis on dorsa of hands and fingers (Fig. 16.22)
Palmoplantar keratoderma in a glove like distribution. Erythema is prominent with
hyperhidrosis and malodor
Diffuse PPK that is progressive. Extensor surfaces of hands, knees and elbows
shows psoriasiform plaque (Fig. 16.23)
Congenital PPK with perioral hyperkeratosis. Spontaneous amputation can occur
PPK associated with periodontosis and increased frequency of pyogenic infection
Keratinization Disorders
ACANTHOSIS NIGRICANS
Acanthosis nigricans is a nonspecific reaction
pattern involving major body folds and
mucocutaneous regions characterized by
hyperpigmented, velvety, soft, verrucous lesions
in a symmetric fashion (Fig. 16.25).
It is broadly divided into benign and
malignant form.
Benign acanthosis nigricans involves limited
body areas and is less severe than malignant
forms.
The various benign forms that are the most
common include benign familial acanthosis
nigricans, acanthosis nigricans associated
with various syndromes, endocrine disease
(especially insulin resistance diabetes
mellitus, HAIR-AN syndrome [Hyper
Androgenism, Insulin Resistance, and
Acanthosis nigricans]), obesity (pseudoacanthosis Nigricans) and drugs (Nicotinic
acidic, fusidic acid, stilbestrol, oral
contraceptives, triazinate).
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17
Urticaria,
Angioedema and Pruritus
Fig. 17.1
Fig. 17.2
Figs 17.1 and 17.2: Urticariashowing itchy erythematous wheals of various shapes and sizes
Acute Urticaria
Means urticaria of less than 6 to 8 weeks duration.
Common causes are drugs especially penicillin,
foods, especially shell fish, and rarely infections.
In India, insect bites are another important cause.
No apparent cause can be found in at least half of
acute attacks. Even if a cause can be identified
and withdrawn, it is often several days before the
urticaria subsides.
Chronic Urticaria
If urticaria lasts for more than 6 to 8 weeks
duration, it is called chronic urticaria. Culprit in
the great majority of cases remains obscure. Up to
55% of patients with chronic idiopathic urticaria
possess functional IgG antibodies directed
against the high affinity IgE receptors or less
commonly against IgE itself. These autoantibodies release histamine from human skin
mast cells and blood basophils and appear to be
the cause of the disease (autoimmune urticaria).
Immunoglobulin and complement components
may be deposited perivascularly, and can be
visualized by direct immunofluorescence
examination.
Basic pathogenic mechanisms of urticaria are
immune and nonimmune mechanisms. Immune
mechanism consists of type I hypersensitivity
mechanism (IgE mediated), through complement
activation, immune complex mechanism, or
autoimmune process. Nonimmune mechanism
works through direct release of histamine and
various mediators from mast cells, vasoactive
stimuli, aspirin, dietary pseudoallergens and due
to angiotensin converting enzyme inhibitors.
Etiological Factors(6 Is + others )
1. Ingestants
a. Foods cheese, eggs, nuts, fish, mushrooms, etc.
b. Food additives tartarzine dyes, etc.
c. Food preservatives
d. Drugs penicillin, salicylates, sulphonamides, etc.
2. Injectants
a. Insect bites
b. Injection drug, sera, blood, etc.
3. Inhalants
Pollens, animal dander, etc.
4. Infestation by parasites
Amoebiasis
Giardiasis
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168
5.
6.
7.
8.
Hookworm
Round worm.
Infection focus in teeth, tonsils, sinuses or
elsewhere.
Implantsprosthetic and hormonal
Physical causes/factors (Urticarial attacks are
brief lasting for 30 to 60 minutes):
a) Dermographism (write-on-skin) stroking
the skin with blunt metallic instrument
results in an exaggerated triple response
(Fig. 17.4).
b) Pressure urticariapressure
c) Cholinergic urticariaincrease in core
body temperature (manifest as small
intensely pruritic papules)
d) Cold urticariacold air or water (Fig. 17.5)
e) Heat urticariaheated object
f) Solar urticariasun exposure
g) Exercise inducedexercise
h) Aquagenic pruritus/urticariacontact
with water
i) Vibratory urticariahandling vibratory
instruments.
Contact urticaria Contact urticaria refers to
a wheal and flare reaction following external
contact with a substance, e.g. on coming in
Diagnosis
How to proceed in a case of urticaria?
1. Urticaria due to physical causes or drugs
excluded by history and examination (Fig.
17.6).
2. Complete food elimination followed by
gradual introduction of one dietary element
at a time helps in detection of food induced
urticaria.
3. Mask use/nasal filter use/change of place
may work for inhalants.
4. Stool examination by concentration method
on 3 consecutive days infestations are
detected and treated accordingly.
5. Look for a focus of infection. If not possible to
detect, give a course of antibiotics. Still no
response, change the antibiotic.
6. The major advance in our understanding of
chronic idiopathic urticaria (CIU) in recent
years has been the discovery that in 30-50% of
patients with so labeled chronic idiopathic
urticaria, the disease is due to an autoimmune
process, and therefore is not strictly
idiopathic.
7. The autologous serum skin test is a useful
screening test for autoimmune chronic
urticaria (AICU). In this test, 0.05 ml of the
patients serum, removed during a period of
disease activity, is injected intradermally into
the same patients uninvolved forearm skin,
along with equal volumes of saline and
histamine (10 g/ml) at adjacent sites. The
test is read 30 min later. A positive result is
recorded if the diameter of the wheal at the
serum-injected site is 1.5 mm greater than that
of the bleb at the saline-injected site. The
sensitivity and specificity of the test are
65-81% and 71-78%, respectively. Patients
with AICU are more treatment-resistant, and
their disease runs a more aggressive course,
than those with non-autoimmune CIU.
8. If still getting urticaria, then look for other
causes and treat symptomatically.
Chronic Urticaria
Antihistamines still remain the mainstay of
drug treatment.
Doxepin 25 to 50 mg at night time may be
added.
Corticosteroids-occasionally as short tapering
courses given in autoimmune chronic
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urticarias as they fail to respond to
antihistamines.
Cyclosporine-2.5 to 5 mg /kg body weight/
day is another option. Control of urticaria
usually occurs within 1 week of commencing
treatment.
Intravenous immunoglobulin.
Other drug treatments are ketotifen (1-2 mg
daily or at night), disodium cromoglycate, beta
agonist (terbutaline 2.5 mg three times daily),
calcium channel blockers (nifedipine),
leukotriene antagonists (montelukast,
zileuton), and anti IgE monoclonal antibody.
PRURITUS (ITCHING)
Pruritus may be defined simply as that
unpleasant sensation which produces the desire
to scratch. It may be localized or generalized. If
generalized, needs investigations for any systemic
cause. Certain areas of the skin, particularly
susceptible to pruritus are ear canals, perianal
and genital areas, eyelids, etc. Localized pruritus
may give clues to the etiology and is less likely to
be associated with widespread or systemic
disease. In the scalp, pruritus may be due to
psoriasis or an ongoing folliculitis, in the inguinal
or anal region due to pruritus ani, pruritus vulvae,
pruritus scroti, venereal diseases, ectoparasites
(scabies, pediculosis), in the hands and feet due
to psoriasis, pompholyx, contact dermatitis, in the
mid back due to notalgia paresthetica, macular
amyloidosis, and in the lower limbs in older
patients due to asteatosis.
Causes of pruritus can be classified as follows:
1. Dermatological disorders
2. Systemic diseases
3. Psychogenic pruritus
4. Iatrogenic pruritus.
Dermatological Disorders
Common dermatoses known to produce pruritus
are scabies, pediculosis, insect bites, eczema,
Systemic Disorders
Three important systemic disorders most likely
to play role in acquired acute pruritus are renal
disease, hepatic disease and abnormalities of the
hematopoietic system.
Renal chronic renal insufficiency
Hepatic intrahepatic and extrahepatic
biliary obstruction (cholestasis).
Abnormalities of the hematopoietic system
iron deficiency anemia, polycythemia vera
(is associated with bath pruritus), leukemia,
Hodgkins lymphoma, mycosis fungoides,
mast cell disorders.
Endocrine diabetes mellitus, myxoedema,
hyperthyroidism, hypoparathyroidism.
Intestinal parasites infestation with
hookworm, round worm, pin worm.
Collagen vascular disorders SLE, sicca
syndrome.
Neurological multiple sclerosis, brain tumor.
Pregnancy.
Psychogenic Pruritus
Psychosomatic disorders resulting in itch
commonly occur in the middle aged or older
individuals.
Iatrogenic Pruritus
Commonly induced by opium alkaloids, CNS
stimulants, antidepressants, and belladona
alkaloids.
Diagnosis
History and clinical examination is of paramount
importance. In addition, investigations outlined
Treatment
1. Eliminate causative disease if possible or treat
it appropriately.
2. Avoid provocative influences:
Friction from rough clothing.
Overheating and vasodilatation, e.g. alcohol,
hot drinks.
Keep nails short.
Soothing lotions, e.g. calamine in urticaria,
moisturisers for dry skin.
Occlusive bandaging may be done to retain
moisture in the skin.
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18
DRUG ERUPTIONS
A drug may be defined as a chemical
substance, or combination of substances,
administered for the investigation,
prevention or treatment of diseases or
symptoms, real or imagined.
Drug eruptions are some of the most
common skin disorders.
They are seen in 2 to 3% of hospitalized
patients.
These eruptions may closely mimic other skin
disorders.
General Rules
Drug allergy is most frequent in older
individuals and may be related to
development of immune response and
increased exposure to drugs.
Topical application of drugs has the greatest
propensity to induce allergy, followed by the
intravenous route and the oral route.
The drugs most often responsible for the
eruptions are antimicrobials and antipyretic/
anti-inflammatory analgesics.
The appearance of the eruption may provide
some clues to its cause (e.g. fixed drug
eruptions associated with sulphonamides).
Always keep in mind the fact that drug
eruptions are great imitators of other skin
diseases.
The most common morphologic patterns of
drug eruptions are exanthematous (40%),
along with urticaria and/or angioedema
(37%), fixed drug eruption (6%), erythema
multiforme and others.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
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Essentials in Dermatology
Urticarial eruptions: It is the second most
common type of cutaneous drug eruption.
Angiotension converting enzyme inhibitors are
the frequent causes of angioedema often without
urticaria.
Serum sickness-like reaction: Serum sicknesslike eruption consists of fever, a rash with usually
urticarial features and arthralgias occurring
within 1 to 3 weeks of initiation of the drug.
Lymphadenopathy and eosinophilia may also be
found.
Drug hypersensitivity syndrome (DHS): Also
known as drug rash with eosinophilia and
systemic symptoms (DRESS) syndrome or as
drug
induced
delayed
multiorgan
hypersensitivity syndrome (DIDMOHS). It
consists of an exanthema, hepatitis and fever.
Eighty percent of the cases have an exanthem
type eruption whereas others will develop more
serious Stevens Johnson syndrome. DHS may be
life threatening and requires prompt
discontinuation of the drug and systemic
corticosteroids.
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serum creatinine, urinanalysis and TSH may be
indicated in patients with suspected drug
induced hypersensitivity syndrome.
Third step is the invitro testing which include
Radio Allergosorbent Assays (RAST) and
Enzyme Linked Immunosorbent Assays
(ELISA). Other tests include Lymphocyte
Transformation Test (LTT), Macrophage
migration Inhibition Factor (MIF), Lymphocyte
Toxicity Assay (LTA), Basophil Degranulation
Test and Histamine Release tests.
Fig. 18.10: Toxic epidermal necrolysissheets of
necrotic tender epidermis over the back
Diagnosis
Diagnosis is basically based on suspicion and
history of drug intake. A thorough and stepwise
approach is essential to proper diagnosis of a
drug- induced skin reaction. First step in patient
evaluation should include (1) a comprehensive
drug history, (2) awareness of various clinical
manifestations of drug allergy and cutaneous
reaction, (3) awareness of factors that favor
development of allergic reactions to drugs, and
(4) awareness of the immunologic and
nonimmunologic mechanisms involved in
cutaneous reaction to drugs. A general rule of
thumb is that drugs started within one week of
the onset of the eruption are the most likely
suspects.
Second step is skin biopsy and in vivo testing.
This includes patch testing, scratch/ prick
testing and dechallenge/ rechallenge tests.
Dechallenge/ rechallenge continues to be
regarded as the most definitive method for
ascertaining drug-induced reactions. However,
it is often not an option if the patient has
experienced a life threatening condition or if
suspected agent cannot be continued. Blood
work-up may also aid in the clinical diagnosis.
A CBC with differential count may show atypical
lymphocytosis, leukopenia, leukocytosis,
eosinophilia and so on. Liver function tests,
Differential Diagnosis
Consider differential diagnoses such as
infections, collagen vascular disease, primary
skin conditions and neoplasia. Culture of skin,
blood, tissue, erythrocyte sedimentation rate,
ANA, and other tests may be ordered to help
confirm or rule out other conditions. If palpable
purpuric lesions are present, a complete physical
and laboratory examination is required with an
eye towards ruling out vasculitic involvement
of other organ systems and other causes of
vasculitis such as infections or collagen vascular
disease.
Treatment
Withdrawal of all drugs
Antihistamine (H1 antagonists)
Soothing lotion for topical application
Corticosteroids topical steroids may
provide some relief. Systemic corticosteroids
are indicated if signs and symptoms are
severe
Adrenaline in case of anaphylaxis
Other measures like fluid and electrolyte
balance maintenance, wet compresses, etc.
ERYTHEMA MULTIFORME
It is a self limited, usually mild but relapsing
exanthematic reaction of skin probably triggered
by circulating immune complexes, most often
related to recurrent herpes simplex infection,
Differential Diagnosis
Urticaria, urticarial vasculitis, figurate erythemas
(slow evolving lesions, usually asymptomatic, no
mucosal involvement), acute febrile neutrophilic
dermatosis, disseminated lesions of contact
dermatitis, bullous pemphigoid, linear IgA
dermatosis, herpes gestationis, lupus
erythematosus, exanthematous or morbilliform
drug eruption (accompanied by fever, pruritus,
eosinophilia, involving trunk and extremities,
sparing the face and pressure areas, fade with
desquamation and postinflammatory hyperpigmentation), viral exanthem (start on face and
involve the trunk, maculopapular/ urticarial/
vesicular/petechial lesions associated with fever,
conjunctivitis, and lymphadenopathy, fades
without pigmentation and scaling), fixed drug
eruption (solitary first, later new lesions appear
with repeated attacks, common on limbs, hands
and feet, genitalia and perianal area, also
STEVENS-JOHNSON SYNDROME
TOXIC EPIDERMAL NECROLYSIS
SPECTRUM
Stevens-Johnson syndrome (SJS) and Toxic
epidermal necrolysis (TEN) are closely related
severe acute mucocutaneous intolerance
reactions most often elicited by drugs and less
so by infections (Table 18.1).
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Table 18.1: Differentiating features between erythema multiforme and SJS-TEN
Features
1.
2.
3.
4.
Etiology
Course
Prodrome
Eruption
5. Typical lesions
6. Mucosal involvement
7. Body surface area
8. Constitutional symptoms
9. Pathology
Erythema multiforme
SJS-TEN
Drugs (80-95%)
Acute, self limited, episodic
Intense, skin tenderness
Disseminated, confluent, symmetric,
on face, neck, trunk
Fixed plaques, target lesions, blisters,
Macules, flat atypical target, central
Nikolskys sign ve
necrosis, Nikolskys sign +ve
Frequent, mild oral
Prominent, severe, 2-3 mucosal
involvement
<10%
<10% to >30%
Absent to moderate
Prominent to severe
Satellite cell necrosis, DEJ blister formation, Massive keratinocyte necrosis,
prominent mononuclear cell infiltrate, papillary sloughing of epidermis, dermal
dermis edematous
infiltrate slight to absent
Not involved
Not infrequent
1-3 weeks
> 2-6 weeks
None
Septicemia, pneumonia,
gastrointestinal hemorrhage, renal
and cardiac failure
0%
1-50%
Without scarring
Sequelae due to mucosal scars
Clinical Features
TEN begins with sheets of erythema covering
wide areas.
In hours, the skin lesions become painful and
extremely tender and small vesicles and
bullae appear over the involved skin (Fig.
18.10).
The epidermis can be separated from dermis
by slight tangential pressure (Nikolskys
sign).
Differential Diagnosis
As given for erythema multiforme.
Staphylococcal scalded skin syndrome (SSSS)
can be differentiated from TEN by occurrence
in children, absence of mucosal lesions and
absence of systemic features. Moreover in
SSSS, the involved skin is dry and
parchment- like while in TEN it is
erythematous, purpuric and necrotic.
Physical and chemical injury such as scalding
and burns, solar erythema and chemical
burns are other differential diagnosis,
difficult in an unconscious patient.
Treatment
Patients have to be managed in an intensive
care set up with proper maintenance of fluid
and electrolytes like Stevens Johnson
syndrome.
Role of steroids is controversial.
Intravenous immunoglobulins have been
found to be useful.
Plasmapheresis, hemodialysis, cyclophosphamide, cyclosporine, N-acetylcysteine,
thalidomide, etc are other treatment options.
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19
Disorders of Sebaceous,
Eccrine and Apocrine Glands
Ductal Hypercornification
Hypercornification of pilosebaceous ducts
presents histologically as microcomedones and
Bacteria
Acne is not infectious. However, three major
organisms isolated Propionibacteria (P. acnes,
P. granulosum, P. avidum), Staphylococcus
epidermidis and Malassezia furfur. Environment of
bacteria (i.e. low pH, reduced oxygen tension and
bacterial lipases, proteases, etc.) more important
than absolute numbers.
Inflammation
The dermal inflammation is not caused by bacteria
in the dermis but from inflammatory mediators
that diffuse from the follicle where they are
produced by P. acnes.
Natural History
Usually starts in adolescence and resolves by
mid-twenties.
At least some degree of acne affects 95% and
83% of adolescent boys and girls.
Acne develops earlier in females than in males.
At the age of 40 years, acne may persist in 1%
of males and 5% of females.
Clinical Features
Occurs predominantly on the face (99%), back
(60%) and chest (15%). Infraorbital area
spared even in severe acne.
Two types of lesions:
i. Non-inflammatory (comedones)
ii. Inflammatory
Comedones are the pathognomonic lesions of
acne (Fig. 19.1). They are conical, raised lesions
with a broad base and a plugged apex. Two
types of comedones blackheads/open
comedones (black color due to oxidation of
melanin) and whiteheads/closed comedones.
25% of the whiteheads resolve within three
days while another 75% develop into inflamed
lesions.
Inflammatory lesions include papules,
pustules and nodules or nodulocystic lesions
(Figs 19.2 and 19.3).
Nodules occur more frequently in males and
may be interconnected with sinuses.
In its most severe variant, acne can present
with cysts and abscesses.
Some amount of scarring in 90%. These could
be hypertrophic scars, keloids, atrophic scars
or ice-pick scars.
Acne severity can be graded into mild (multiple
open and closed comedones are present, with
Differential Diagnosis
Acne is rarely misdiagnosed. The commonest
mistaken diagnosis is rosacea (has facial flushing,
typically pustules occurring over erythematous
background, localization of lesions to mid-face,
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Essentials in Dermatology
absence of seborrhea, comedones, nodules, cyst
or scarring). Perioral eczema/dermatitis can be
confused with acne in females, but lesions itch,
the skin is dry and there are no comedones.
Whiteheads may be confused with milia (which
are predominantly infraorbital in distribution and
are whiter). Acneiform drug eruptions are sudden
onset, follicular monomorphous eruptions
characterized by papules and pustules
resembling acne, induced by skin exposure to
various industrial chemicals or medications.
Folliculitis due to Gram-negative organisms can
complicate acne therapy and rarely folliculitis due
to Candida may also present as multiple pustular
eruptions as may S. epidermidis folliculitis.
Demodex folliculitis can present as nonresponsive acne, which best responds to
metronidazole or topical permethrin. Rarely acne
vulgaris need to be differentiated from Pityrosporum folliculitis, acne agminata, adenoma
sebaceum lesions of tuberous sclerosis,
pseudofolliculitis barbae, plane warts,
acneiform eruption of Behcets disease.
Treatment
Treatment involves counseling, acne assessment
and appropriate and ethical prescribing based
on the history, acne severity, lesion type and the
psychological effects of the disease. The various
modalities of treatment can be classified into
topical and systemic therapies (Table 19.1).
Topical
Predominantly comedolytic:
Tretinoin (0.025%, 0.05%, 0.1% creams,
gels) (reduce number of existing
comedones and prevent formation of new
comedones by loosening ductal keratinocytes) - The best treatment for
comedones. Almost every patient benefits
from topical retinoids.
Adapalene (0.1% cream, gel, solution).
Azelaic acid (20% cream).
Predominantly antimicrobial:
Clindamycin (1% gel, solution).
Erythromycin (1.5-2% gel, solution,
ointment).
Benzoyl peroxide (2.5-10% gel, lotion,
cream).
Nadifloxacin.
Clarithromycin.
Tetracycline.
Sodium sulfacetamide- sulphur combination.
Predominantly anti-inflammatory
Adapalene.
Topical antibiotics.
Combination preparations.
Zinc and erythromycin.
Benzoyl peroxide and erythromycin.
Systemic
Oral antibiotics (oral tetracycline 250-500 mg
1-4 times a day, oral minocycline 50-100 mg
daily, doxycycline 50-100 mg daily,
erythromycin 250-500 mg 2-4 times a day,
trimethoprim 300 mg twice a day, pulse
dosing with azithromycin -250 mg daily for
three days in a week for 4-6 months or
roxithromycin).
Hormones (anti-androgens like 2 mg
cyproterone acetate with 35 microgram ethinyl
estradiol, flutamide-250 mg twice a day, oral
contraceptive pills, spironolactone 100-200
mg daily, finasteride 2.5-5 mg daily): Indicated
for women with acne located primarily on the
lower face and neck, those with PCOS and
late onset acne, late onset adrenal hyperplasia
or other identifiable endocrinologic conditions.
Isotretinoin: It is the only anti-acne agent that
affects all four of the known major etiologic
mechanisms: sebum production, comedogenesis, Propionobacterium acnes (P. acnes)
colonization of ductal and skin surface, and
monocyte chemotaxis-induced inflammation.
It is indicated for nodulocystic acne, acne
Miscellaneous
Oral zinc.
Dapsone (nodulocystic acne).
Clofazimine (acne fulminans).
NSAIDs (to reduce inflammation).
Chemical peels.
Cryotherapy.
Blue light therapy.
Surgical Procedures
Comedone extraction.
Aspiration of cysts.
Incision and drainage (large cysts).
Intralesional steroid (0.1 ml triamcinolone
injected into base of the cyst; reduces scarring).
Grade 1(Mild)
Grade II-III(Moderate)
Grade IV(Severe)
Maintenance therapy
Topical retinoids
Benzoyl peroxide
(BPO) or topical
antibiotic (A/B)
Topical retinoids
BPO or topical A/B
Isotretinoin or
Topical retinoids,
oral A/B, hormone
therapy
+
Oral A/B
Hormone Rx
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Essentials in Dermatology
polymyalgia). The disease exclusively occurs in
teenage boys. The face is often not involved.
Treated initially with high dose corticosteroids
to control inflammation and then retinoids
Differential Diagnosis
Important differential diagnoses include acne
vulgaris (typical acne lacks the redness,
telangiectasia, and flushing of rosacea), lupus
erythematosus (DLEscarring, scaling and
follicular plugging are not features of rosacea,
SLE-butterfly erythema is not pustular and is
usually associated with systemic symptoms),
perioral dermatitis (lesions itch, the skin is dry),
seborrhoeic dermatitis (scaling in typical
seborrhoeic areas) and demodex folliculitis
(clearly mimics rosacea). Nasal sarcoidosis (lupus
pernio) is the differential diagnosis for
rhinophyma.
Treatment
Papulopustular rosacea responds well to
treatment. Topical treatment with metronidazole
(1% cream, 0.75% gel, cream, lotion) is effective.
Additional topical therapies reported as effective
include tetracycline, clindamycin, erythromycin,
azelaic acid 20% cream and 15% gel, 0.025%
PERIORAL DERMATITIS
It is facial dermatosis predominantly affecting
females of childbearing years. The dermatosis is
characterized by an erythematous, micropapular,
fine scaling eruption classically affecting the
nasolabial folds, chin, and upper lip, sparing a
rim of skin at the vermilion border. In nearly every
patient, there is striking dependency on topical
steroids. A frequently heard story is that the
patient presents with the earliest signs of rash
and is given a potent topical steroid. The
condition then shows improvement but any
attempt to stop the treatment dramatically
worsens the condition after a few days.
Differential Diagnosis
The important differential diagnoses include
rosacea (usually no telangiectasia or flushing in
perioral dermatitis), lip licking cheilitis (seen
predominantly in 7-15 years old age group, the
rash is caused by repeated licking of skin around
the mouth and is marked by a scaling, pink band
around the mouth and involvement of lips),
seborrhoeic dermatitis (not usually circumoral
and the scalp, ears and eyebrows are commonly
involved), contact allergic dermatitis (does not
spare the immediate perioral area), late-onset acne
vulgaris (evidence of comedones, large papules
and cysts in wider distribution and responds
more slowly to treatment), acne agminata (difficult
to distinguish if confined to perioral area but can
be differentiated histologically) and facial AfroCaribbean childhood eruption (FACE) (do not
spare the perilabial skin, pustules do not occur,
occur often in males).
Treatment
The most important measure is usually to
discontinue the application of the topical
corticosteroids. The patient should be warned that
an initial flare may develop after the withdrawal
of a topical corticosteroid. A four week course of
oral tetracycline or its analogues such as
minocycline, doxycycline or lymecycline is
usually all that is required. Topical metronidzole,
topical erythromycin, and topical tetracycline
have also been used.
DISORDERS OF ECCRINE SWEAT
GLANDS
Disorders of eccrine sweat glands may be broadly
classified into four-chromhidrosis, hyperhidrosis,
hypo- or anhidrosis and miliaria.
Chromhidrosis
It means secretion of colored sweat. It is an
exceedingly rare functional disorder of the
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apocrine sweat glands. The colored sweat may
be yellow (most common), blue, green, or black.
Colored sweat fluoresces and is caused by
lipofuscin. Topical capsaicin satisfactorily
reduces facial and nipple chromhidrosis.
Hyperhidrosis
It means excessive sweating which could be
localized or generalized. It may occur as
consequence of a number of causes. Most
commonly excessive sweating of the palms and
soles occurs during mental stress, and may be
associated with tachycardia and vasomotor
instability.
Palmoplantar Hyperhidrosis
(Emotional Hyperhidrosis)
This type of hyperhidrosis is usually localized to
the palms, soles or/and axillae. Frequently there is
a family history and commonly begins in
childhood or around puberty. There is a tendency
of spontaneous improvement after the age of 25
years. Sweating may be intermittent (triggered by
anxiety, stress, or fear) or may be constant.
Apart from the embarrassing nature of the
disorder, complications include pompholyx,
contact dermatitis, and pitted keratolysis.
Gustatory Hyperhidrosis
Sweating on the lips, forehead and nose after
eating certain foods is known as gustatory
sweating. Gustatory sweating may be idiopathic,
post-peripheral nerve injury (parotid surgery,
auriculotemporal nerve syndrome or von Frey
syndrome, cervical sympathectomy), sensory
neuropathy (diabetes mellitus, post herpes zoster).
Treatment
Topical anticholinergics (0.5% glycopyrronium
bromide cream), formalin 1% soaks, glutaraldehyde 10% in a buffered solution, 20%
aluminium chloride have been used. Iontophoresis either using tap water or anticholinergic
Anhidrosis (Hypohidrosis)
It can result from poral occlusion, congenital or
acquired absence of sweat glands, damage to
sweat gland function or dysfunction of
sympathetic nerves in neuropathies. It may be
localized or generalized.
Miliaria
It results from the obstruction of free flow of eccrine
sweat to the skin surface and retention of the sweat
within the skin. It manifests with a variety of signs
and symptoms. Miliaria crystallina (Sudamina)
consists of non-inflammatory, superficial
subcorneal translucent vesicles that easily
rupture when rubbed with a finger. Miliaria rubra
(prickly heat) causes pruritic inflammatory
papules around the sweat pores, follows repeated
episodes of sweating in a hot humid environment.
Some of the eruptions of miliaria rubra become
pustular resulting in miliaria pustulosa. Miliaria
profunda results when sweat leaks into the
dermis and presents as multiple discrete, flesh
colored papules.
The most common complications of miliaria
are secondary infection and disturbance of heat
regulation. Periporitis staphylogenes is the name
given to multiple staphylococcal abscesses
superimposed on miliaria rubra in young infants
(Fig. 19.5). Postmiliarial hypohidrosis invariably
occurs following miliaria and sweating may be
depressed to half the normal amount for as long
Treatment
The most effective treatment is to place the patient
in a cool environment as this will avoid further
sweating. Avoidance of excessive clothing,
friction with clothing, excessive use of soap and
contact of the skin with irritants will reduce the
incidence. Calamine lotion is effective in the relief
of discomfort. Oral ascorbic acid 500 mg twice
daily has been found to diminish the severity of
miliaria.
DISORDERS OF APOCRINE GLAND
The capacity to produce an unpleasant odor is
best-known property of apocrine gland.
Physicians in the past relied heavily on detecting
special body odors in diagnosis of diseases, e.g.
fruity odour in diabetic coma, butcher shop odor
in yellow fever, freshly baked bread odor in
typhoid fever, etc.
Bromidrosis (Bromhidrosis or
Osmidrosis)
Excessive odor arising from apocrine sweat, also
known as fetid sweat or malodorous sweating. It
is chiefly encountered in axillae. Often the patient
complains of offensive axillary sweat but actually
have no offensive odor. The complaint represents
a phobia, delusion, paranoia or a lesion of the
central nervous system. True bromidrosis is
usually not recognized by the patient. Antibacterial soaps, deodoarants, frequent bathing,
changing of underclothes, shaving of the axillae
and application of aluminium chloride are all
helpful measures.
Fish Odor Syndrome
(Trimethylaminuria)
Affected individuals are unable to oxidize tertiary
trimethylamine produced by oxidation of choline
and carnitine in food. This results in formation of
excessive amounts of offensively smelling (rotting
fish) sweat. Defect in flavin containing
monooxygenase 3 (FMO3) gene causes the
disease. Diet low in carnitine and choline may
help.
Chromhidrosis
Coloured apocrine sweat.
Fox Fordyce Disease
It is a disorder of the apocrine sweat gland
comparable to prickly heat of the eccrine glands.
It is a chronic itchy papular eruption of apocrine
gland bearing areas-axillae (Fig. 19.6) and pubic
area, classically seen in women between the ages
of 15 and 35 years. Pruritus is often exacerbated
by emotional or physical stimuli of the apocrine
glands.
Differential Diagnosis
Includes lichen planus, lichen nitidus, infective
folliculitis, chronic dermatitis, and syringoma.
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Treatment
Estrogen therapy in the form of oral contraceptive
pills is universally effective. Topical tretinoin,
clindamycin solution, UV phototherapy have been
tried. Treatment response with topical steroids or
intralesional steroids is not satisfactory.
Treatment
Earliest lesions often heal quickly with
intralesional steroid therapy. Concomitant use of
antibiotics (minocycline, cephalosporins,
ciprofloxacin) is recommended. Isotretinoin (1
mg/kg/day) is effective in some patients. In severe
disease, removal of the affected area is often
required. Wide local excision and healing by
second intention is considered the surgical
treatment of choice.
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DISORDERS OF HAIR
Alopecia
Alopecia is loss of hair. It may be diffuse or patchy,
scarring or non-scarring.
Diffuse Non-scarring Alopecia
1. Androgenetic alopecia: Terminal hair is
converted into vellus hair. In men, recession of
the frontal hairline near the temples and thinning
over the vertex occurs (Fig. 20.1). In women, the
scalp hair is generally diffuse but more so in the
vertex area.
Treatment includes in males- topical
minoxidil (2 and 5% solution) or oral
finasteride competitive inhibitor of type II 5
-reductase -1 mg/day and in females
topical minoxidil 2% and antiandrogens
(spironolactone, cyproterone acetate,
flutamide) and surgical treatment such as
scalp reduction and hair transplantation.
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Underlying atopy
The presence of other autoimmune diseases
Family history of alopecia areata
Young age at onset
Nail dystrophy
Extensive hair loss
Ophiasis.
Diagnosis
The characteristic non scarring patchy loss of
hairs, the presence of exclamation point hair on
the periphery, a hair pull test indicating telogen
hair excess and in atypical cases skin biopsy
showing specific findings (a peribulbar and at
the lower one third of the follicle, a lymphocytic
infiltrate, swarm of bees, with no scarring) all
points towards the diagnosis.
Differential Diagnosis
Alopecia areata needs to be differentiated from
tinea capitis, trichotillomania and secondary
syphilis (moth-eaten appearance in beard or
scalp).
Treatment
Various modalities of treatment are available,
the simplest of which are the use of counter
irritants like phenol, benzoyl, tincture iodine,
dithranol, etc. Physical modalities like UVB
in erythema doses, grenz rays and thorium
X-ray may be used with varied success.
Considering the autoimmune etiology of the
disease various immunosuppressive drugs
have been used. Among them, corticosteroids
are important which can be used topically,
intralesionally and systemically.
Photochemotherapy, contact immunotherapy
(using dinitrochlorobenzene [DNCB], squaric
acid dibutylester [SADBE], diphencyprone),
topical minoxidil or topical cyclosporine may
be used.
Course and Prognosis
Alopecia areata, however, a serious cosmetic
problem, has unpredictable course.
Tinea capitis: Discussed earlier under
dermatophytosis.
Trichotillomania
It is the term (Greek-hair pulling
madness) first used by the French
dermatologist Hallopeau to denote a
morbid impulse to pull ones own hair.
It manifests as one or a few small oval
patches of hair loss which may occur in
any hair area of the body in children or
adults.
The patches are unusually irregular,
asymmetric, and ill defined and have
many broken hairs.
Common sites of involvement include
scalp (Fig. 20.9), eyebrows, eyelashes, and
pubic area.
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A. Shape Abnormalities
Clubbing Causes
CLUBBING
DISORDERS OF NAILS
B. Surface Abnormalities
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Fig. 20.16
Fig. 20.17
Figs 20.16 and 20.17: Pachyonychia congenitathickening of nails with subungual hyperkeratosis
C. Color Abnormalities
Color changes in nail may be due to exogenous
causes or endogenous causes.
Leukonychia: This term is used for white
discoloration of nails attributable to nail matrix
dysfunction.
Melanonychia: Means streaky hyperpigmentation of nails.
Fig. 20.19: Half and half nail proximal half white and distal half brownish
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21
Metabolic and
Nutritional Disorders
PORPHYRIA
Porphyrias are hereditary disturbances in the
synthesis of heme involving well-defined
enzymatic defects.
The term porphyria is derived from the
Greek word for purple and originally
referred to the red to purple color of the urine
of patients affected by acute intermittent
porphyria. Other forms of porphyria produce
urine that varies from pink to red to brown.
Unlike findings with hematuria and
pigmenturias (e.g., hemoglobinuria due to
hemolysis, myoglobinuria caused by
rhabdomyolysis), routine dipstick tests are
negative for the presence of heme in porphyria
patients.
Porphyrins also account for the fluorescence
of urine viewed with a Woods lamp.
Almost all are inherited in an autosomal
dominant pattern except congenital
erythropoietic porphyria which is inherited
in an autosomal recessive manner.
In addition, although the enzyme defects are
genetic and permanent, the symptoms are
often intermittent and do not appear until
puberty except in congenital erythropoietic
porphyria and hepatoerythropoietic
porphyria (both manifest in infancy or
Clinical Classification
These disorders can be classified into those
without vesicobullous lesions and those
associated with them.
The former includes delta aminolevulinic acid
dehydratase deficiency porphyria and acute
intermittent porphyria (have no cutaneous
manifestations), and erythropoietic protoporphyria (can cause photosensitivity, but
vesicobullous lesions are rare).
The latter includes congenital erythropoietic
porphyria (Gunthers disease), hepatoerythropoietic porphyria, hereditary
coproporphyria, variegate porphyria (most
prevalent in white population of South Africa)
and porphyria cutanea tarda (PCT).
Fig. 21.2
Differential Diagnosis
Other childhood photosensitivity disorders
Treatment of this disorder is aimed at the
cutaneous photosensitivity or at the anemia
and its complications. Sun protection
(clothing better than sunscreens) and
ingestion of beta carotene may ameliorate some
portion of the photodamage. Other modalities,
Fig. 21.3
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chronic transfusion regimens and splenectomy, the risks must be weighed against the
severity of the disorder in each individual
case. Bone marrow transplantation successful
in some cases.
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Differential Diagnosis
For macular amyloidosis is postinflammatory
hyperpigmentation, atopic dermatitis, lichen
simplex chronicus and fixed drug eruption.
Lichen amyloidosis needs to be differentiated from
lichen planus and lichen simplex chronicus.
Nodular amyloidosis, clinically needs
differentiation from naevus lipomatosus, lipoma,
cysts, lymphoma and histologically from all forms
of amorphous deposits, such as gout and nodular
elastosis.
Treatment is symptomatic with topical
corticosteroids (under occlusion), dimethyl
sulfoxide (DMSO) and sometimes dermabrasion.
XANTHOMATOSES
Xanthomas are composed of masses of lipid
containing histiocytes forming papular, nodular,
and plaque like lesions in the skin, tendons and
sometime in the internal organs. Xanthomas are
important clinical finding as they often evolve in
the presence of elevated blood lipids and
lipoproteins. Lipoproteins are macromolecular
complexes that carry hydrophobic plasma lipids,
particularly cholesterol and triglycerides, in the
plasma. An elevation of serum lipid levels is
called hyperlipidemia, or hyperlipoproteinemia
while the term dyslipoproteinemia signifies
Xanthelasma Palpebrarum
Soft, velvety papules and plaques arranged
around eyelids.
Common sites upper eyelid, inner canthus
(Figs 21.9 and 21.10)
Signify a systemic hyperlipidemia usually
LDL elevations
Usually occur in normolipidemic individuals
but may be seen in familial hypercholesterolemia, dysbetalipoproteinemia, mixed
hyperlipidemia. Secondary causes are
obstructive liver disease, myxedema, and
diabetes mellitus.
Treatment options includes surgical excision,
electrofulguration, trichloroacetic acid
chemical cautery , and CO2 laser.
Tuberous Xanthomas
Firm, yellow-orange, often with an erythematous halo, small papules (0.5 cm in
Tendinous Xanthomas
Slowly enlarging subcutaneous nodules
attached to tendons, ligaments, fascia and
periosteum (sub-periosteal) (Fig. 21.12).
Overlying skin appears normal.
Sites extensor tendons of hands and feet,
Achilles tendon, sub-periosteal bony
prominences such as malleoli and elbows
Occur in severe hypercholesterolemia with
raised LDL Familial hypercholesterolemia,
less frequently in secondary hypercholesterolemia (cholestasis).
Eruptive Exanthomas
Pinhead sized asymptomatic yellow papules
with a reddish base, usually fleeting in nature
and appear in crops.
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May occur in secondary hyperlipidemia of
diabetes mellitus.
Plane Xanthomas
Yellow-orange macules or slightly palpable
plaques.
May occur at any site.
Plane xanthomas over palmar creases
xanthoma palmaris et striata pathognomonic of Type III dysbetalipoproteinemia.
Plane xanthomas may occur in secondary
hyperlipidemias (biliary cirrhosis, cholestasis,
gammopathy).
Intertriginous Xanthomas
They appear as flat to slightly raised yellow
dermal plaques with corrugated surface
within or adjacent to finger webs (Fig. 21.14),
axillae, buttocks and antecubital and popliteal
fossa.
They are pathognomonic of type II hypercholestrolemia.
Lipid phenotype
Lipoprotein phenotype
(Friedrickson)
Isolated Hypercholesterolemia
Familial hypercholesterolemia
IIa
IIa
IIa
Isolated Hypertriglyceridemia
Familial hypertriglyceridemia
I, V
I, V
I, V
II b
III
Cutaneous features
Cerebrotendinous Xanthomas
Rare autosomal recessive disorder with
xanthomas in the tendons and the brain.
It is due to mutation in the sterol
27-hydroxylase (CYP27A) gene leading to
defective conversion of cholesterol to bile
acids with accumulation of cholestanol.
Severe neurologic disease and tendency to
coronary artery disease.
Tendon xanthomas.
Urinary gas chromatography is the specific
test for this disease.
Treated with oral deoxycholic acid to replace
the bile acid pool.
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Drusen of Bruchs membrane seen in fundi in
half the patients.
Sickle-shaped calcifications dorsal and lateral
to sella turcica in skull X-ray films are
pathognomonic.
The nature of hyaline material and underlying
metabolic defect is unknown. It may represent
an underlying lysosomal storage disorder
with single or multiple enzyme defects, others
have postulated it to be a disorder of collagen
metabolism or collagen synthesis.
Distinctive histologic features include extreme
dilation of blood vessels and thickening of
their walls, progressive hyalinization of sweat
glands, and infiltration of the dermis and
subcutaneous tissue with extracelluar hyaline
deposits and also demonstrable in walls of
vessels.
Differentiation from erythropoietic protoporphyria may be difficult histologically.
Xanthomatoses and amyloidosis can be
excluded histologically. In adults, differential
diagnosis is from lichen myxoedematosus and
myxedema with hoarseness have to be
considered.
There is presently no effective therapy for
lipoid proteinosis. Hoarseness may be
relieved temporarily by surgical removal of
vocal cord infiltrates. Facial lesions may be
treated by dermabrasion, chemical skin
peeling and blepharoplasty. Treatment by oral
dimethyl sulphoxide has been claimed to be
successful.
PHRYNODERMA
Phrynoderma is a type of follicular hyperkeratosis typically seen in vitamin A
deficiency.
This eruption has also been associated with
deficiencies of vitamin B complex, C, and E,
calories, and essential fatty acids.
The morphology of these lesions is variable
and may range from filiform papules to small
PELLAGRA
Pellagra is a nutritional disorder that occurs
due to deficiency of niacin or tryptophan or
both. Therapy with isoniazid, 5-fluorouracil,
6-mercaptopurine may provoke pellagra. Rare
causes are carcinoid tumors, and Hartnup
disease.
The term pellagra is derived from the Italian
words pelle agra meaning rough skin.
It is still endemic in areas of Africa and Asia
due to poor nutrition and intake of certain
cereals such as maize and jowar (Indian
millet) as staple diet.
Fig. 21.18
Fig. 21.19
Figs 21.18 and 21.19: Pellagrachest and upper limb shows Casals necklace, and glove of hyperpigmented flaking dermatosis
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ARIBOFLAVINOSIS
(ORO-OCULO-GENITAL SYNDROME)
This syndrome occurs due to vitamin B2
(Riboflavin) deficiency and is characterized
by mucocutaneous lesions of angular
stomatitis, cheilosis, glossitis, seborrhoeic
dermatitis (especially around the nose) (Fig.
21.21), scrotal (Fig. 21.22) and vulvar
dermatitis, and increased corneal vascularity.
It usually responds promptly and
dramatically to riboflavin supplementation
with 5 to 15 mg of riboflavin daily for 2 weeks
and correction of dietary errors.
ACRODERMATITIS ENTEROPATHICA
Acrodermatitis enteropathica, an autosomal
recessive disorder which appears to be due
to defective absorption of zinc from the
gastrointestinal tract.
It may be a presenting sign in cystic fibrosis or
AIDS.
Fig. 21.24
Fig. 21.25
Figs 21.24 and 21.25: Acrodermatitis
enteropathicaperianal psoriasiform dermatosis
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22
GENETICS IN DERMATOLOGY
Human genetics is the study of the range of
biological variations in human beings with each
individual showing considerable variability in
his/her expression of disease.
Human genome, the genetic material is
packaged into units called chromosomes
(Chromo-colored, somes-bodies). Each somatic
cell contains 46 including 2 sex chromosomes.
The karyotype of an individual identifies the
number and structure of chromosomes. This is
usually derived from peripheral blood cells
(T lymphocytes) that are stimulated to divide. They
are classified by the position of the centromeres
and the proportion of long and short arms.
Phenotype is the bodily manifestation of
genotype.
Genetic Principles
Gene is the sequence of bases on DNA that code
for one polypeptide.
Locus is the precise position of the gene on
chromosome.
Alleles are genes at a single locus, which may be
heterozygous or homozygous.
Dominant means full effect in heterozygous state.
Expression means effects of a gene are variable.
Penetrance is the frequency with which a gene
produces an effect. If trait is non-penetrant,
expressivity is zero.
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includes helping the patients to comprehend the
medical facts, including the diagnosis, the
probable course of the disorder and available
management, the hereditary basis of the disorder,
and the risk of recurrence in specific relatives. The
counseling also includes a discussion of the course
of action that seems appropriate in view of the
risk and the family goals.
PHAKOMATOSES (NEUROCUTANEOUS
SYNDROMES)
Phakomatoses or neurocutaneous syndromes are
a rare group of disorders including neurofibromatosis, tuberous sclerosis, von HippelLindau syndrome, and Sturge-Weber syndrome.
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Systemic features include:
1. Skeletal manifestations include bony
dysplasias especially tibia, pseudoarthrosis, cysts and scoliosis of thoracic
region.
2. CNS manifestationsApproximately 50%
of children with NF-1 exhibit a learning
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Minor features:
1. Multiple randomly distributed pits in dental
enamel
2. Hamartomatous rectal polyps
3. Bone cysts
4. Cerebral white matter migration lines
5. Gingival fibromas
6. Non-renal hamartoma
7. Retinal achromic patch
8. Confetti skin lesions
9. Multiple renal cysts.
Definite TSC: Either 2 major features, or 1 major
feature with 2 minor features.
Probable TSC: 1 major feature and 1 minor feature.
Possible TSC: Either 1 major feature, or 2 or more
minor features.
Treatment:
1. Facial angiofibromas: Dermabrasion,
electrodessication, CO2, argon or pulsed
dye laser
2. Seizures: For infantile spasms: ACTH/
steroids are useful. Seizures in children:
vigabatrin is the drug of choice.
Prognosis is related to the extent of systemic
involvement. Cardiovascular complications
occur in 1st decade, brain tumor in 2nd
decade, renal and pulmonary lymphangiomatosis in 4th decade are cause of morbidity
and mortality.
Sturge-Weber Syndrome
(Encephalofacial angiomatosis)
Sturge -Weber syndrome (SWS) is defined as
facial portwine stain in association with
ipsilateral plial (i.e. leptomeningeal) vascular
anomalies (with one or more symptoms;
epilepsy early in life, hemiparesis or
hemiplegia, gyriform intracranial calcifications and cerebral atrophy) and inconstant
ipsilateral choroidal vascular lesions with
glaucoma.
Portwine stain is usually unilateral, roughly
involving the areas supplied by ophthalmic
and maxillary divisions of trigeminal nerve,
and bilateral in 50% of cases.
Portwine stains (naevus flammeus) are
congenital vascular birthmarks that are
present at birth and persist into adulthood.
At birth, they are often pale pink macular
lesions which with time, progress to become
dark red to purple (Fig. 22.11) and even
nodular. These changes occur as a result of
progressive ectasia of cutaneous superficial
vascular plexus.
Portwine stains can either occur as isolated
cutaneous or be associated with structural
abnormalities especially of those underlying
the birth mark such as the choroidal vessels
in the eye which produce glaucoma and
leptomeningeal vessels in the brain which
causes seizures, then is known as SWS.
Xeroderma Pigmentosum
(Pigmented Dry Skin)
It is an autosomal recessive disorder characterized
by photosensitivity, pigmentary changes,
premature skin aging, neoplasia and abnormal
DNA repair.
Eight different subtypes complementation
groups A to G and XP variants.
Main defect is in the DNA excision repair
process (this is a process whereby damaged
DNA is replaced with new DNA).
XP- variants have a normal nucleotide
excision repair but the defect here is of a
reduced molecular weight of newly
synthesized DNA in UV radiated cells.
Clinical Features
Skin normal at birth.
Earliest symptoms of dryness and freckling
appear between six months and three years of
age.
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Incontinentia Pigmenti
(Bloch-Sulzberger Disease)
Incontinentia pigmenti is an uncommon
genodermatosis of the developing
neuroectoderm in which vesicular, verrucous
and pigmented lesions are associated with
developmental defects of eye, skeletal
system and central nervous system.
Incontinentia pigmenti is a complex
hereditary syndrome that principally affects
female infants. It is inherited as an X-linked
dominant disorder, caused by mutation of
NEMO gene on chromosome Xq28. The gene
is generally lethal in male fetuses.
This multisystem disorder has manifestations
of dermatological, neurological, skeletal,
ocular or dental origin.
It manifests at birth or during first weeks of
life.
In the skin, the disorder characteristically
progresses through four stages. The first stage
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Fig. 23.3: Pretibial myxoedemabilateral firm hyperpigmented plaques with orange peel texture over shins
Hypothyroidism (Myxoedema)
Deficiency of thyroid hormone may be caused
by Hashimotos thyroiditis, iodine deficiency,
iatrogenic following total thyroidectomy,
Hypoparathyroidism
Congenital absence of glands (Di Georges
syndrome), thyroid surgery, hemochromatosis,
metastatic cancer, or idiopathic in origin may be
its causes. Skin changes may be similar to that
of hypothyroidism. The skin becomes dry,
hyperkeratotic and puffy with sparse and coarse
hair. Chloasma and pellagra like pigmentary
changes can occur. Nails become opaque and
brittle with transverse ridges. Impetigo
herpetiformis, psoriatic flares and eczematous
dermatitis have been associated with
hypoparathyroidism. Normalization of serum
calcium levels with calcium and vitamin D
usually reverse skin abnormalities.
SKIN IN DIABETES MELLITUS
Diabetes mellitus (DM) is characterized by
relative or absolute deficiency of insulin, leading
to gross defects in glucose, fat and protein
metabolism.
Type I DM (Insulin dependant DM) is due to
insulin insufficiency from antibody
mediated destruction of beta cells of
pancreas.
Type II (Non-insulin dependant DM) results
from hyperglycemia mainly due to
peripheral insulin resistance.
Nearly all patients with DM have some skin
manifestations. For most manifestations the
pathogenesis remains unknown, and others
result from damage to vascular, neurologic or
immune systems. Macro and microangiopathy
contribute significantly to the cutaneous
complications of DM.
Cutaneous Manifestations of DM
1. Skin Infections
DM patients are at higher risk of contracting
bacterial and fungal infections when compared
to normal population. Staphylococcal and
streptococcal pyodermas (folliculitis, furuncle,
2. Markers of DM
Acanthosis nigricans (AN) presents as brown
to gray black papillomatous cutaneous
thickening of the flexural areas including
posterolateral neck (most common site), axillae,
groin and abdominal folds. Affected area will
have velvety appearance, and it may involve
mucous membranes also. AN can also occur in
association with obesity, internal malignancy
and with drugs such as corticosteroids and
estrogens.
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Generalized granuloma annulare presents with
numerous small annular plaques formed by 1-2
mm flesh colored papules (Fig. 23.4). These
lesions are symmetric and appear more
commonly over the abdomen, chest, thighs and
extensor of elbows, most frequently in older
adults.
Necrobiosis lipoidica (NL) is a cutaneous
disorder, often but not always associated with
diabetes mellitus. Sixty to seventy percent of
patients have DM, so patients presenting with
NL should be investigated for DM. More
commonly affects middle aged women. The skin
lesions start as skin colored or brownish red
papule which evolve slowly into well
demarcated waxy plaque of variable size. They
have sharply defined, broad violet red or pink,
elevated border and depressed yellow-orange
centre with telangiectasias. Ulcerations
commonly occur within the plaques and heal
slowly resulting in depressed scars. Almost
always affects shins, but can involve thighs,
trunk, and face, scalp (scarring alopecia). Rarely
disseminated NL can occur called as
granulomatous disciformis chronica and
progressiva.
Bullosis diabeticorum is characterized by
abrupt onset of bullae, mainly over the lower
legs, feet, toes, and occasionally over dorsa of
hands and fingers. Bullae appear over non
inflamed skin, and measured from few
millimeter to 3-5 cm in size, non-pruritic and
painless. Healing occurs within 2 to 5 weeks and
rarely leaves scar. Pathogenesis of bulla
formation is unknown. Increased skin fragility
due to glycosylation end products may be
involved.
Scleredema diabeticorum is characterized by
insidious onset of painless, symmetric induration
of skin and subcutaneous tissue mainly over
upper back, neck, and rarely face, shoulder and
anterior torso. Skin has non pitting, woody,
3. Complications of Diabetes
Macroangiopathy
Atherosclerosis induced by DM can lead to
ischemic gangrenous changes in legs and feet,
hypothermia, dry skin and nail dystrophy.
Microangiopathy
Microangiopathy causes many cutaneous
manifestations, which include:
1. Wet gangrene of footoccurs as a late
complication.
2. Erysipelas like erythemawell demarcated,
red areas occur on the legs or feet usually in
elderly diabetics.
3. Diabetic rubeosis-peculiar rosy reddening of
the face, rarely of hands and feet in long
standing diabetics.
4. Diabetic dermopathy (diabetic shin spots or
Binkley spots) Most common dermatosis
associated with diabetes. They start as crops
of asymptomatic, oval, dull red papules
0.5-1cm in diameter, which gradually evolve
into atrophic hyperpigmented lesions mainly
over shins, also over forearms, thighs and
bony prominences. If 4 or more are present,
the specificity is high for microvascular
disease in other tissues. An association seems
to exist between dermopathy and other
serious complications such as retinopathy,
nephropathy and neuropathy.
SKIN IN VASCULITIS
The term vasculitis refers to inflammation and
necrosis of blood vessels. The vasculitides are
best classified according to the size of the
involved vessels into large, medium and small
vessel vasculitis.
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C.
1.
2.
3.
4.
5.
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Microscopic Polyangiitis
Microscopic polyangiitis (MPA) involves vessels
ranging in size from capillaries and venules to
medium-sized arteries. Glomerulonephritis,
especially rapidly progressive glomerulonephritis, and alveolar hemorrhage are particularly
common in MPA and uncommon in PAN.
Antibody to myeloperoxidase, a type of PANCA, is detected in sera from 60 percent of
patients with MPA.
Benign Cutaneous PAN (BC PAN)
BC PAN is a rare vasculitic entity mostly seen in
adults. The appearance of painful, violaceous,
palpable nodules or ridges of variable size along
the course of arterioles characterize this relatively
benign condition. Mild constitutional symptoms
and arthritis of the weight bearing joints may
occur. The exact etiology of this condition is not
known.
Wegeners Granulomatosis (WG)
WG is a potentially lethal, necrotizing,
granulomatous angiitis affecting small and
medium sized vessels with a predilection for the
sinuses, nasal passages, pharynx, lungs and
kidneys. In some instances, the lesions may be
widely scattered and may involve the skin, heart,
CNS, GI tract and joints. Constitutional
symptoms such as fever and weight loss are
usually quite prominent.
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PARANEOPLASTIC DISORDERS
Paraneoplastic disorders refer to cutaneous
reaction patterns that have a statistical
association with neoplasia of various internal
organ systems.
Schnyder criteria for paraneoplastic disorders:
No other explanation for skin findings.
Skin changes improve with cancer treatment
and may reappear if cancer recurs.
Skin changes appear at about the same time
as the systemic cancer: They may precede any
clinical manifestation of the underlying
malignancy.
Statistical connection is shown.
3. Bullous Eruptions
2. Migratory Erythemas
Erythema gyratum repens is characterized by
mobile, concentric, often palpable, erythematous,
wave-like bands (migrating at the rate up to 1
cm per day), giving wood grain appearance
to skin. A peripheral scale or collarete may be
present, and frequently involves the trunk.
Tumors associated are lung cancers, myeloproliferative disorders and many other solid
cancers. Resection of the tumor may result in
resolution of lesions.
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polymorphous mucocutaneous lesions.
Pemphigus like, pemphigoid like, erythema
multiforme like, graft versus host disease like
and lichen planus like lesions occur. Associated
neoplasms are Hodgkins lymphoma, chronic
lymphocytic leukemia, Castlemans tumor, and
thymoma.
Pemphigus vulgaris has well defined
association with thymoma. Hodgkins
lymphoma and many solid tumors have also
been associated.
Bullous pemphigoid is a subepidermal autoimmune bullous disease, mainly affecting
elderly individuals characterized by large tense
blisters over normal or erythematous skin
distributed mainly over central abdomen and
flexural aspect of limbs. Significant association
with gastric carcinoma has been found.
Adult linear IgA disease is a subepidermal
bullous disease characterized by vesicles, bullae,
and urticarial plaques mainly over trunk and
extremities. An increased association with
lymphomas has been found.
Epidermolysis bullosa acquisita is a
subepidermal bullous disease characterized by
bullae, and vesicles at trauma prone sites.
Association with myeloma and leukemia has
been found.
4. Panniculitides
Erythema nodosum is characterized by crops of
painful, erythematous nodules and plaques
6. Neutrophilic Dermatoses
Pyoderma gangrenosum (PG) particularly
bullous PG is associated with myeloproliferative
disorders. Solid tumors such as carcinoma of
colon, prostate, bladder breast, bronchus and
ovary have also been reported in association with
PG (Fig. 23.12).
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9. Others
Xanthomas: Diffuse plane xanthoma can be
caused by multipl e myeloma.
24
Skin Changes of
Pregnancy and Old Age
Physiological Variations
Physiological changes are most likely caused by
hormonal changes. These include pigmentation
of nipples, areolae (Fig. 24.1), and external
genitalia. The linea alba becomes the linea nigra.
Chloasma or melasma, a mask like hyper
pigmentation of the face occurs in more than 50%
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Essentials in Dermatology
gingiva) is a pyogenic granuloma that may appear
in the second or third trimester and resolves
shortly after delivery.
Fig. 24.3
Fig. 24.4
Figs 24.3 and 24.4: Pruritic urticarial papules and plaques of pregnancy involving striae and arms
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25
Pediatric Dermatology
Pediatric Dermatology
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Table 25.1: Classification of common pediatric dermatoses
1. Infestations and infections (a) Parasitic infestationsPediculosis capitis, scabies (b) Bacterial infections
Pyodermas (c) Viral infectionsMolluscum contagiosum, warts, herpes simplex, chicken pox, herpes zoster
(d) Fungal infections-Tinea capitis, tinea corporis, pityriasis versicolor, candidiasis
2. Dermatitis and eczemaInfantile seborrheic dermatitis, diaper or napkin dermatitis, atopic dermatitis, infective
dermatitis
3. Urticaria
4. ExanthemsViral exanthems (Measles, rubella, roseola infantum, erythema infectiosum)
5. Drug eruptions
6. Pigmentary disordersPostinflammatory pigmentation, hypopigmentary disorders (Pityriasis alba, vitiligo, leprosy,
nevus achromicus, ash leaf macule, albinism), hyperpigmentary disorders (Mongolian spots, caf au lait macules)
7. Diseases of hair and nailsTinea capitis, alopecia areata, diffuse alopecia, twenty nail dystrophy
8. Genetic diseases of the skin-Ichthyoses, acrodermatitis enteropathica
9. Collagen vascular diseasesConnective tissue diseases (Lupus erythematosus, scleroderma, and dermatomyositis)
and vasculitic syndromes (Henoch-Schnlein purpura, acute hemorrhagic edema of infancy, and polyarteritis
nodosa)
10. Miscellaneous conditionsPapular urticaria, miliaria rubra, miliaria crystallina, psoriasis, hemangiomas, chilblains
Pediatric Dermatology
cervical, suboccipital and postauricular
glands and a rash of approximately 2 to 3
days duration.
An enanthem, Forschheimers sign, is present
in up to 20% of patients during the prodromal
period or on the first day of the rash. Dull-red
macules or petechiae are confined to the soft
palate.
The disease has rare sequelae apart from
devastating effect on the fetus.
Gianotti-Crosti Syndrome
Infantile papular acrodermatitis, or the
Gianotti-Crosti syndrome, presents
with symmetric erythematous lichenoid
papules on the face, extremities, and
buttocks, usually sparing the trunk.
The eruption is not pruritic and may be
accompanied by splenomegaly, hepatitis, and
lymphadenopathy.
The process often occurs in young children
after an upper respiratory tract illness.
Pathologic specimens show a perivascular
infiltration of lymphocytes and histiocytes in
the upper portion of the dermis.
While the syndrome has been associated with
hepatitis B and enterovirus infection, several
cases have been associated with acute EBV
infection.
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Fig. 25.2
Urticaria Pigmentosa
Urticaria pigmentosa is the most common type of
cutaneous mastocytosis that occurs due to the
accumulation of mast cells in the skin.
The skin lesions are itchy small, yellow tan to
reddish brown maculopapules/plaques/
nodules scattered all over the body (Figs 25.2
and 25.3).
Mild trauma such as scratching or rubbing
the lesions may cause urtication and erythema
around macules and this is known as Dariers
sign.
Urticaria pigmentosa is associated with
pruritus which may be exacerbated by
temperature, friction, spicy foods, alcohol and
drugs.
Diagnosis: Histopathology shows mast cell
infiltration in the dermis
Treatment: Avoidance of precipitating factors
and antihistaminies.
Langerhans Cell Histiocytosis (LCH)
Langerhans cell histiocytosis is a disease that
results due to the proliferation of cells like
Langerhans cells, called as LCH cell (share the
Fig. 25.3
Pediatric Dermatology
ultrastructural features with Langerhans cellscontaining Birbeck granules) in any organ. This
LCH cell is about four to five times larger than
small lymphocytes; has an irregular and
vesiculated nucleus; is often reniform (kidney
shaped); and has abundant, slightly eosinophilic
cytoplasm.
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26
Naevi
The word naevus is derived from the Latin
term meaning spot or blemish, originally
used to describe the congenital lesion or birth
mark (Mothers mark).
In modern usage, it denotes a cutaneous
hamartoma or benign proliferation of cells.
Nevi can be broadly classified into various
types according to the predominant cell type.
The various types are keratinocyte nevi (Figs
26.1 and 26.2), follicular nevi, sebaceous
nevi, apocrine nevi, eccrine nevi, connective
tissue nevi, smooth muscle nevi, elastic
nevi, fat nevi (Fig. 26.3), and vascular nevi
(Figs 26.4 to 26.7).
Melanocytic Nevi
They are benign tumors derived from
melanocytes. They are broadly classified into
acquired or congenital.
Acquired melanocytic naevi are subdivided
into junctional, compound (Figs 26.8 and
26.9) and dermal.
They begin as proliferative naevus cells along
the dermal-epidermal junction (forming a
junctional naevus)
Fig. 26.1
Fig. 26.2
Figs 26.1 and 26.2: Nevusverrucous epidermal (keratinocyte) nevus occurring on one side of the body
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Fig. 26.5
Fig. 26.6
Figs 26.5 and 26.6: NevusHemangioma of infancy over the nape of neck and face
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Fig. 26.12
Fig. 26.13
Figs 26.12 and 26.13: Dermal melanocytosisNevus of Ota in the periorbital area with scleral pigmentation
Trichoepithelioma
Trichoepithelioma is benign appendageal
tumor with follicular differentiation.
They appear at puberty as solitary or
multiple, skin colored, translucent, rounded
nodules on the face (Fig. 26.17).
The lesions are distributed predominantly in
the nasolabial folds and eyelids.
Hypertrophic Scar
Injury or surgery in a predisposed
individual can result in an abnormally large
scar called as hypertrophic scar
A hypertrophic scar represents excessive
collagen deposition at the site of wound
healing
Typically, hypertrophic scar starts as an
asymptomatic, erythematous, smooth, firm
scar seen at anatomic locations
characterized by high tensions. With time,
they flatten and become white in color.
Hypertrophic scars do not extend beyond the
limits of the original trauma and heal by
6 months.
Syringoma
Benign tumors of eccrine differentiation
More common in females
Keloids
Keloids represent exaggerated collagen
deposition at the site of wound healing.
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Glomus Tumor
This arises within the glomus body, a
neuromyoarterial receptor (the SucquetHoyer canal) that is sensitive to temperature
variations and regulates arterial blood flow.
These tumors, more common on the fingers
and toes and beneath the nail plate.
Usually seen in young adults between the
third and fourth decade of life.
They can be solitary or multiple.
Classically presents as solitary, small, blue
red nodules on the hand (nail bed) that
are characteristically associated with paroxysmal pain often elicited by changes in
temperature.
Simple excision- treatment of choice.
Dermatofibroma
Most common benign dermal fibrous tumor.
Typical dermatofibromas appear as skin
coloured to red-brown, firm, tender
nodule(s), most commonly seen on the
extremities (Fig. 26.20)
Lateral compression of the lesion with fingers
results in the depression on the topcalled
dimple sign
Histologically the fibroblasts and collagen
bundles are arranged in a storiform or
cartwheel pattern
Treatment of choicesimple excision.
PREMALIGNANT EPIDERMAL
TUMOURS
Actinic Keratosis (Senile or Solar
Keratosis)
Most common premalignant skin tumor.
These lesions occur in sun-damaged skin of
elderly people having light complexion
Clinically, these lesions are round to
irregular keratotic papules surrounded by
erythema.
Erythroplasia of Queyrat
This condition affects uncircumscised males.
Seen in the fifth and sixth decades of life.
The lesions present as sharply defined,
brightly erythematous and velvety plaque
with moist glistening or granular surface
over the glans penis (Fig. 26.22).
Differentiated from benign inflammatory
dermatoses such as psoriasis, lichen planus,
Zoons plasma cell balanitis and fixed drug
eruptions.
Bowens Disease
Refers to cutaneous plaques of
intraepidermal squamous cell carcinoma.
Chronic sunlight exposure, inorganic
arsenicals are important etiologic factors.
Clinically lesions of Bowens disease
appear as solitary, sharply defined, round
or oval to irregular erythematous
psoriasiform or eczematous plaque.
Ulceration is a sign of development of
invasive carcinoma.
Histology shows proliferating atypical
squamous cells through the full thickness of
the epidermis (wind- blown appearance)
The most effective treatment for Bowens
disease is surgical excision.
Cutaneous Horn (cornu cutaneum)
Cutaneous horn (cornu cutaneum) is the term
coined for horny skin excrescence, which in
its form and consistency resembles an
animal horn in miniature (Fig. 26.23)
The paramount consideration while making
a clinical diagnosis is the height of the
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254
Fig. 26.24
Fig. 26.25
Figs 26.24 and 26.25: Basal cell carcinomaulcerated nodule over the eyelid showing
pearly translucent border with telangiectasia
Mycosis Fungoides
Mycosis fungoides is a form of cutaneous T- Cell
lymphoma (CTCL).
It is a chronic, slowly progressive disease that
evolves from patches (patch stage) (Fig. 26.6)
Szary Syndrome
Szary syndrome is a rare special variant of
cutaneous T-cell lymphoma characterized by a
triad of featureserythroderma, peripheral
lymphadenopathy and infiltrates of atypical
cells in the skin and blood.
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Fig. 26.26: Mycosis fungoidesmultiple hypopigmented patches over the chest and abdomen
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Essentials in Dermatology
7. Bacteriostatic.
8. Pharmacologically inert.
9. Cosmetically acceptable.
For a layman, it should not Sting, stale/
stench and stain For any drug to be effective
topically, it must be formulated at the proper
concentration and in the proper vehicle.
In general, the most important vehicles for
topical use may be divided into monophasic,
biphasic, and triphasic forms.
There are three basic constituents of a
formulation, which are present singly or in
combination to form a vehicle.
They are:
1. Powders.
2. Greases.
3. Liquids.
When only one of the basic constituent is
present in a formulation vehicle, then it is called
monophasic vehicle (Powders, liquids or greases/
oils). In case two of them are present, it is called
biphasic vehicle(The combination of powder
with water gives either a drying paste or a shake
lotion. Grease or oil and powder will form either
a liniment or a protective (fatty) paste. Water and
grease, however, will mix to form emulsions in
the presence of a surfactant or emulsifier. These
then form oil in water (O/W) or water in oil
(W/O) creams) and if all the three are present, it
is called triphasic vehicle (Cooling pastes and
cream pastes are triphasic vehicles that consist of
oil-water-powder mixtures in varying proportion).
TERMINOLOGY IN TOPICAL
FORMULATION
Wet dressings are water or saline soaked cotton
gauze or cloth compresses used in the treatment
of acute inflammatory dermatoses with oozing,
weeping and crusting, bullous diseases and
ulcers.
Dosage
Sodium penicillin G (crystalline penicillin):
0.5-5 MU IM/IV 6-12 hourly.
Procaine penicillin G: 0.5-1 MU IM 12-24
hourly.
Benzathine penicillin G: 0.6-2.4 MU IM every
2-4 weeks.
Indications
Syphilis.
Streptococcal infections.
Tetanus.
Gas gangrene.
Adverse Effects/ Precautions
Hypersensitivity reactions ranging from mild
rash/fever/eosinophilia to fatal anaphylaxis.
Jarisch-Herxheimer reaction occurs within
2-12 hours of the first dose when using
penicillin for syphilis; presents as headache,
fever, chills, sweating, sore throat, myalgia/
arthralgia, tachycardia and increased blood
pressure. The condition does not recur and
does not need interruption of treatment.
Aspirin and sedation offer symptomatic relief.
Pregnancy: category B.
Drug Interactions
Probenecid inteferes with tubular secretion
of penicillin.
AMPICILLIN
Pharmacology
-lactam antibiotic, aminopenicillin group.
Interferes with bacterial cell wall synthesis.
Greater activity than natural penicillins
against enterococci and H.influenzae.
Maximal absorption when taken on empty
stomach.
Primarily excreted in urine (dose adjustment
in renal insufficiency).
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Dosage
Oral
Adults and children >20 kg 250-500 mg Q6h.
Children <20 kg 50-100 mg/kg/day in
divided doses Q6h.
Parenteral
Adults 500-1500 mg IM/ 500-3000 mg IV
Q4-6h (maximum 12 g/day).
Children 100-400 mg/kg/day IM/IV in
divided doses Q4-6h.
Indications
Skin and skin structure infections.
Adverse Effects/Precautions
Hypersensitivity reactions (eosinophilia or
rash).
Maculopapular rash (concomitant with viral
infections, e.g. infectious mononucleosis).
GIT nausea, vomiting, abdominal pain,
diarrhea.
Black hairy tongue, glossitis, stomatitis, sore
tongue.
Pregnancy: category B (FDA).
Drug Interactions
Probenecid- interferes with excretion of
ampicillin.
OCPs- Ampicillin may decrease the efficacy
of OCPs.
Allopurinol-Concomitant allopurinol
increases the risk of ampicillin rash.
CEPHALEXIN
Pharmacology
First generation cephalosporin; -lactam
antibiotic.
Same mechanism of action as penicillin but
binds to different proteins.
Well absorbed orally.
Attains high concentration in bile.
Excreted unchanged in urine.
Dosage
Adults: 250-500 mg Q6h (maximum: 4 g/day).
Children: 25-50 mg/kg/day in divided doses
Q6h.
Indications
Skin and skin structure infections (staphylococcal/streptococcal).
Genitourinary tract infections (E. coli/P.
mirabilis/K. pneumoniae).
Adverse Effects/Precautions
Generally well tolerated.
GIT- nausea, vomiting, diarrhea.
Hypersensitivity reactions (cross allergenicity
with penicillin).
Pregnancy: category B.
ERYTHROMYCIN
Pharmacology
Macrolide antibiotic; binds to the 50S ribosome
subunit and interferes with protein synthesis.
Activity against mostly gram positive, and few
gram negative organisms-Streptococcus
pyogenes, Streptococcus pneumoniae, some Staph.
aureus, N.gonorrheae, N.meningitides, B.pertussis,
Treponema pallidum, Mycoplasma, Legionella,
Chlamydia and Campylobacter.
Available as several different derivatives
estolate salt is the least susceptible to acid
degradation and the best absorbed salt,
compared to the base, stearate and ethylsuccinate formulations.
Maximum absorption when taken on empty
stomach (except estolate taken with food).
Extensively metabolized in the liver, and
excreted in bile.
Penetration of CSF is negligible.
Dosage
All derivatives except ethylsuccinate: 250-500 mg
every 6 hours (expressed in terms of base)
maximum 4g/day.
Indications
As an alternative to penicillin for
Skin and skin structure infections of mild
to moderate severity caused by Strept.
pyogenes or Staph. aureus.
Erythrasma.
Streptococcal respiratory tract infections.
Diphtheria.
Tetanus.
Syphilis and gonorrhea.
Chlamydial infections.
As a first choice drug for
Chancroid.
Adverse Effects/Precautions
GIT- nausea, vomiting, diarrhea.
Allergic reactions (more common with
estolate).
Reversible cholestatic hepatitis (with estolate).
QT prolongation.
Estolate derivative contraindicated in hepatic
dysfunction; all others used with caution.
Pregnancy: category B.
Drug Interactions
CYP3A4 inhibitor - Increased levels of
theophylline, warfarin, phenytoin, carbamazepine, disopyramide and cyclosporine.
Increased risk of myopathy when used with
HMG CoA reductase inhibitors (atorvastatin,
simvastatin, lovastatin).
Dosage
Adults: 500 mg on day 1, followed by 250 mg
once a day for 5 days.
Chlamydia and chancroid: 1g single dose.
Indications
Skin and skin structure infections (Staph.
aureus, Strep. pyogenes, Strep. agalactiae).
Nongonococcal urethritis and cervicitis
(Chlamydia).
Prevention of disseminated M. avium complex
disease in HIV infected patients.
Chancroid.
Adverse Effects/ Precautions
GIT- nausea, vomiting, diarrhea, abdominal
pain.
Rare allergic reactions.
Reversible elevation of LFT.
Pregnancy: category B.
Drug Interactions
Does not affect cytochrome P450 enzymes.
Warfarin increased PT and INR can occur;
close monitoring required.
AZITHROMYCIN
Pharmacology
Macrolide antibiotic; inhibits bacterial protein
synthesis by binding to the 50S ribosomal
subunit.
TETRACYCLINE
Pharmacology
Inhibits protein synthesis by binding to the
30S ribosomal subunit, thereby preventing
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attachment of the aminoacyl t-RNA to the A
site of the mRNA-ribosome complex; primarily
bacteriostatic.
In acne inhibits growth of propionibacterium acnes and decreases free fatty acid
concentration in sebum, resulting in
decreased inflammation and microcomedo
formation.
Maximal absorption on empty stomach (food
decreases absorption by 50% or more).
Eliminated primarily unchanged in urine
(needs dose adjustment in renal insufficiency).
Dosage
Acne vulgaris 500-1000 mg/day in 4 divided
doses for 1-2 weeks or till clinical improvement, followed by 125-500 mg/day.
Syphilis.
primary or secondary: 500 mg QID for 2
weeks
latent: 500 mg QID for 2 weeks (if duration
of infection < 1 year) 500 mg QID for 4
weeks (duration of infection unknown or
>1 year)
Indications
Acne vulgaris.
Primary, secondary or latent syphilis in nonpregnant patients with documented penicillin
allergy.
Adverse Effects/ Precautions
GIT - nausea, vomiting, diarrhea, abdominal
pain, epigastric burning, anorexia.
Maculopapular or erythematous rashes.
Hypersensitivity reactions.
Hemolytic anemia, thrombocytopenia,
neutropenia and eosinophilia.
Photosensitivity.
Precipitation of renal failure in patients with
underlying renal function.
Discoloration of teeth (in children < 8 years,
or infants of pregnant mothers who ingested
tetracycline).
Drug Interactions
Absorption of tetracycline is impaired by dairy
products, flouroquinolones, sucralfate, or any
product containing iron, zinc, calcium,
aluminium, magnesium or bismuth (separate
administration by 4 hours).
OCPs decreased efficacy of OCPs.
Warfarin elevated PT.
DOXYCYCLINE
Pharmacology
Inhibits protein synthesis by binding to the
30S ribosomal subunit, thereby preventing
attachment of the aminoacyl t-RNA to the A
site of the mRNA-ribosome complex; primarily
bacteriostatic.
In acne inhibits growth of propionibacterium acnes and decreases free fatty acid
concentration in sebum, resulting in
decreased inflammation and microcomedo
formation.
Spectrum of activity.
Cocci: all gram positive and gram negative
cocci were originally sensitive but now
many Strep. pyogenes, Strep. pneumoniae,
Staph. aureus and enterococci have become
resistant
Gram positive bacilli: Clostridia, Listeria,
Corynebacteria, Propionibacterium acnes,
Bacillus anthracis
Gram negative bacilli: H.ducreyi,
Calymmatobacterium granulomatis, Vibrio
cholerae, Yersinia pestis, Yersinia
enterocolitica, Campylobacter, H. pylori,
Brucella, Pasturella, Francisella
Dosage
100 mg twice a day.
Indications
Acne vulgaris
1st choice treatment in:
Lymphogranuloma venereum
Granuloma inguinale
Typhus, Rocky mountain spotted fever, Q
fever (Rickettsiae)
2nd choice treatment in:
Tetanus, anthrax, actinomycosis, Listeria
(to penicillin/ampicillin)
Gonorrhea (to ciprofloxacin/ceftriaxone,
especially for penicillin-resistant, nonPPNG organisms and in penicillin allergic
cases)
Chlamydial infections non-gonococcal
urethritis, endocervicitis, conjunctivitis,
pneumonia (to azithromycin)
Chancroid (to cotrimoxazole)
Adverse Effects/Precautions
GIT- nausea, vomiting, diarrhea, abdominal
pain, epigastric burning, anorexia.
Pseudotumor cerebri (increased risk when
combined with isotretinoin).
Photosensitivity.
Discoloration of teeth (in children < 8 years
and infants of pregnant women taking the
drug).
Superinfection with Candida (oral/ anogenital), pseudomembranous enterocolitis.
Pregnancy: category D.
Drug Interactions
Absorption of doxycycline is impaired by dairy
products, flouroquinolones, sucralfate, or any
product containing iron, zinc, calcium,
aluminium, magnesium or bismuth (separate
administration by 1-2 hours).
OCPs decreased efficacy of OCPs.
Warfarin elevated PT.
MINOCYCLINE
Pharmacology
Inhibits protein synthesis by binding to the
30S ribosomal subunit, thereby preventing
attachment of the aminoacyl t-RNA to the A
site of the mRNA-ribosome complex; primarily
bacteriostatic.
In acne inhibits growth of Propionibacterium
acnes and decreases free fatty acid
concentration in sebum, resulting in
decreased inflammation and microcomedo
formation.
Good activity against rickettsia, chlamydia,
mycoplasma.
Also displays activity against Staph. aureus
resistant to other tetracyclines.
Maximum absorption on empty stomach (food
may decrease absorption by up to 20%);
should be taken with adequate fluids to
reduce esophageal irritation/ulceration; can
be given with food if gastric irritation occurs.
Eliminated primarily via the hepatobiliary
system.
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Dosage
Acne vulgaris: 50 mg OD TID.
Infections due to susceptible organisms: 200
mg initial dose (orally or IV), followed by 100
mg Q12h.
Indications
Moderate to severe inflammatory acne
vulgaris.
Can be used to treat rickettsial, chlamydial,
mycoplasmal infections (although doxycycline is the preferred drug).
Adverse Effects/ Precautions
GIT nausea, vomiting, diarrhea, abdominal
pain, epigastric burning, anorexia.
Vestibular side effects dizziness, ataxia,
vertigo (dose-related, more common in
women).
SLE rare, reversible.
Pseudotumor cerebri (increased risk when
combined with isotretinoin).
Reversible skin and mucous membrane
pigmentation occurs with long-term use
Photosensitivity may be less than other
tetracyclines.
Discoloration of teeth (in children < 8 years
and infants of pregnant women taking the
drug).
Superinfection with Candida (oral and
anogenital) less frequent than tetracycline and
doxycycline.
Pregnancy: category D.
Drug Interactions
Absorption of minocycline is impaired by
sucralfate, or any product containing iron,
zinc, calcium, aluminium, magnesium or
bismuth (separate administration by 1-2
hours).
OCPs decreased efficacy of OCPs.
Warfarin elevated PT.
CIPROFLOXACIN
Pharmacology
Fluoroquinolone antibiotic; inhibits bacterial
DNA gyrase.
Most reliable for treatment of aerobic gram
negative organisms.
Enterobacteriaceae
Neisseria gonorrheae, Neisseria meningitides
H. influenzae, H. ducreyi
Campylobacter jejuni
Yersinia enterocolitica
Moderately susceptible organisms include
some streptococci, staphylococci, Pseudomonas
aeruginosa, chlamydia, and mycobacteria.
Well absorbed after oral administration.
Widely distributed throughout the body; high
tissue penetrability (except CSF).
Eliminated primarily via the kidney (dose
adjustment needed in renal insufficiency).
Dosage
250-750 mg BD, depending on the indication.
Indications
Drug Interactions
Products containing multivalent cations such
as iron, calcium, zinc, magnesium, aluminium
(e.g. antacids, multivitamins, sucralfate)
impair the absorption of ciprofloxacin
should be administered 6 hours before or 2
hours after ciprofloxacin.
Theophylline ciprofloxacin can increase
theophylline concentrations.
Warfarin increased PT.
Dosage
All preparations contain TMP and SMX in the
ratio of 1:5.
Oral one double strength TMP/SMX (160/
800 mg) tablet BD.
Intravenous 8-20 mg/kg/day of TMP in 2-4
divided doses.
TRIMETHOPRIMSULPHAMETHOXAZOLE (SEPTRAN)
Pharmacology
Trimethoprim is a diaminopyrimidine related
to the antimalarial drug pyrimethamine,
which selectively inhibits bacterial dihydrofolate reductase (DHFRase).
Sulphamethoxazole belongs to the class of
sulfonamides, which are structural analogues
of PABA, and thereby inhibit bacterial folate
synthetase.
The combination (TMP-SMX) results in a
synergistic bactericidal effect on gram positive
and gram negative organisms
Strep. pneumoniae
Strep. pyogenes
Staph. aureus
H. influenzae
Moraxella catarrhalis
Nocardia species
Stenotrophomonas maltophila
Enterobacteriaceae (most)
Pneumocystis jiroveci
Indications
Chancroid (1st choice agent).
Granuloma inguinale (2nd choice agent).
Toxoplasmosis.
Nocardia infections.
Urinary tract infections treatment and
prophylaxis.
Respiratory tract infections (acute otitis media,
acute exacerbations of chronic bronchitis,
sinusitis).
Diarrhea and dysentery.
PCP pneumonia.
Adverse Effects/ Precautions
GIT nausea, vomiting, anorexia.
Hypersensitivity rash, urticaria, StevensJohnson syndrome, TEN, erythema multiforme
and exfoliative dermatitis.
Agranulocytosis, aplastic or hemolytic
anemia (folate deficient patients at increased
risk).
Fulminant hepatic necrosis.
HIV infected patients are at much greater risk
of dermatologic and hematologic reactions,
and desensitization may be required.
Crystalluria (advised to drink plenty of water).
Pregnancy: category C.
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Drug Interactions
Warfarin antithrombotic effects can be
potentiated by TMP/SMX.
Sulfonylureas hypoglycemia as a result of
displacement from protein binding sites.
Methotrexate displacement from protein
binding sites, and competition for renal
tubular excretion, leading to bone marrow
suppression.
CORTICOSTEROIDS
The corticosteroids bind to specific cytoplasmic
receptors in the target cell and the steroid receptor
complex then undergoes modification and is
translocated to the nucleus where it causes
formation of specific mRNA which then mediates
the various biological effects. Their modes of
actions are 1) Anti-inflammatory, 2) Antiallergic
and 3) Immunosuppressive.
Dosage
The intermediate acting steroid namely
prednisolone is commonly used at a dose of 1
mg/kg body weight/day.
Indications
1. Autoimmune bullous dermatoses (pemphigus, bullous pemphigoid, epidermolysis
bullosa acquisita, etc.).
2. Drug eruptions (erythema multiforme, Stevens
Johnson syndrome, TEN).
3. Connective tissue disorders (SLE, polymyositis, dermatomyositis, progressive
systemic sclerosis).
4. Severe dermatitis (atopic dermatitis, contact
dermatitis, photodermatoses).
5. Neutrophilic dermatoses (pyoderma gangrenosum, Sweets syndrome).
6. Sarcoidosis.
7. Leprosy in severe reaction.
8. Urticaria, angioedema and capillary hemangiomas.
Contraindications
There are no absolute contraindications
The relative contraindications are: Peptic
ulcer disease, any focus of infection including
tuberculosis, hypertension, glaucoma, cataract,
hyperlipidemia, renal calculi, first trimester of
pregnancy, and children.
Side Effects
1. Metabolic disturbances: Diabetes, faciotruncal obesity, hyperlipidemia, protein
hypercatabolism, etc.
2. Bone disturbances: Osteoporosis, avascular
necrosis of the bone, growth retardation.
3. Muscular disorders: Steroid myopathy,
amyotrophy, tendon rupture.
4. Cutaneous effects: Acneiform eruptions,
atrophy, telangiectasia, easy bruising,
alopecia/hypertrichosis, cutaneous
infection, striae distense.
5. Electrolyte disturbances: Sodium retention
and potassium depletion.
6. Endocrine changes: Inhibition of the
hypothalamo-hypophyseal suprarenal axis.
7. Infections: Acute bacterial infection,
tuberculosis, viral infection, parasitic
disease.
8. Neuropsychiatric disorders: Neuropathy,
psychosis, pseudotumor cerebri.
9. Ocular effects: Posterior subcapsular
cataract, open angle glaucoma, aggravation
of an existing infection.
10. Gastric disturbances: Peptic ulcer disease.
11. Hematologic alteration: Leucocytosis,
eosinopenia and lymphopenia.
GRISEOFULVIN
Griseofulvin is the most frequently used systemic
drug in the treatment of dermatophytosis. It is a
fungistatic agent derived from Penicillium
griseofulvum with selective activity against
dermatophytes only. In addition to its antifungal
Dosage
The daily recommended dose is 10-20 mg/kg
body weight/day to a maximum of 1 gm daily,
given in a single dose or in two divided doses.
For ringworm of the trunk, hand or foot, it is given
for a period of 4 to 6 weeks. For scalp infection 8
to 12 weeks and in nail infection for 12 to 18
months.
Side Effects
Side Effects
The most commonly reported adverse effects are
headache and gastrointestinal side effects namely
dyspepsia, nausea and diarrhoea. Other side
effects are photosensitivity, urticaria, erythema
multiforme, maculopapular skin rash, serum
sickness, angioedema and vesicular eruption. The
other uncommon but serious adverse effects
include hepatic and renal insufficiency, severe
leukopenia, peripheral neuropathy, mental
confusion and blurred vision. It can also
precipitate SLE.
ACYCLOVIR
Acyclovir is a synthetic guanosine analogue
which is widely used for the treatment of herpes
simplex virus and varicella zoster virus infections.
Acyclovir, a prodrug, initially undergoes
monophosphorylation by herpes virus encoded
thymidine kinase and is activated to acyclovir
triphosphate (by cellular kinase) which is the
active antiviral moiety. Acyclovir is highly
selective because only virus infected cells are able
to phosphorylate acyclovir.
Dosage
The recommended dose for the treatment of HSV
infection is 200 mg 5 times a day or 400 mg three
times a day for 7 to 10 days. For varicella and
ANTIHISTAMINES
Classification
Class I: First generation H1 type antihistamines
These traditional antihistamines are competitive
receptor blockers (reversible) and can be displaced
by high levels of histamines and they dissociate
from the receptors easily. They are divided into 6
groups.
1. Alkylamine
Pheniramine maleate (25-50 mg 2-3 times
daily)
Chlorpheniramine maleate (4 mg thrice
daily)
2. Ethanolamine
Clemastine fumarate (1 mg twice daily)
Embramine hydrochloride (25-50 mg/
day)
Bromodiphenyl hydramine hydrochloride
Diphenhydramine hydrochloride(25-50
mg thrice daily), citrate
3. Ethylenediamine
Mepyramine maleate
Pyrilamine maleate
Tripelamine citrate, HCl
4. Phenothiazine
Promethazine HCl (25 mg twice daily)
Methdilazine HCl
5. Piperidine
Cyproheptadine HCl (4 mg thrice daily)
Azatidine maleate
6. Piperazine
Hydroxyzine hydrochloride (10 mg or 25
mg thrice daily).
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Mechanisms of action: The main effects are as
follows:
1. Anticholinergic activity
2. Anti-inflammatory effect
3. Antiallergic effect
4. Antimotion sickness effects
5. Antiemetic activity
6. Inhibit most responses of smooth muscle to
histamine.
Indications
Side Effects
1. Neurological side effects Sedation, dizziness
and tinnitus, blurred vision and diplopia,
insomnia, reduced or disturbed concentration,
irritability and tremors.
2. Gastrointestinal side effects Anorexia,
nausea, vomiting, epigastric distress, constipation (can be minimized by giving them along
with food).
3. Anticholinergic effects dry mucous
membranes, difficulty in micturition and
urinary retention, frequency and dysuria,
impotence.
4. Cutaneous side effects eczematous dermatitis, fixed drug eruption, photosensitivity,
urticaria, petechiae.
DAPSONE
Dapsone is a 4,4-Diaminodiphenyl sulphone. It
is weakly bactericidal against M.leprae. It acts by
inhibiting folate metabolism in M.leprae. In
addition to its antibacterial action, it also has antiinflammatory activityinhibits lysosomal
enzymes, interferes with myeloperoxidase system.
During daily treatment with 100 mg dapsone, it
inhibits the generation of 5-lipoxygenase product
in neutrophils.
Dosage
Dose is 6 to 10 mg/kg body weight/week. The
average adult dosage is 100 mg/day. For children
of 10 to 14 years, it is 50 mg/day and of 6 to 9
years it is 25 mg/day.
Indications
Other than its antileprosy action, it is used in
dermatology in pemphigus, bullous pemphigoid,
Side Effects
1. Hemolytic anemia especially in G6PD
deficient individuals.
2. Agranulocytosis.
3. Hepatitis.
4. Allergic rashes including FDE and exfoliative
dermatitis.
5. Dapsone syndrome (fever, jaundice, lymphadenopathy, hepatomegaly and exfoliative
dermatitis).
6. Psychosis.
CLOFAZIMINE
Clofazimine is a riminophenazine dye. Like
dapsone, it is also weakly bactericidal against
M.leprae and virtually nontoxic in the usual
dosage used. Clofazimine has both antibacterial
and anti-inflammatory activities.
Indications
Apart from its use in multidrug therapy in leprosy,
it is used in dermatology for multidrug resistant
tuberculosis, atypical mycobacterial infection,
neutrophilic dermatoses (acne, pustular
psoriasis), rhinoscleroma, leishmaniasis, etc.
Dosage
The recommended dose is 50 mg daily.
Side Effects
1. Reversible dose related reddish to brownish
black discoloration of sweat, hair, sputum,
urine and feces.
2. Ichthyosis.
3. Phototoxicity, nonspecific skin rashes and
acneiform eruptions.
4. Eosinophilic enteropathy.
5. Conjunctival pigmentation.
METHOTREXATE
Methotrexate (MTX) is a folic acid antagonist and
is widely used for the treatment of severe
psoriasis.
Dosage
1. Weekly single oral or parenteral dosage
schedule.
2. Intermittent oral schedule of three divided
doses 12th hourly over a period of 36 hours
each week.
3. Oral dose is 0.4 to 0.6 mg/kg body weight/
week (maximum 30 mg).
4. Parenteral dose is 15-25 mg/week.
Indications
1. Psoriasis psoriatic erythroderma, psoriatic
arthritis, pustular psoriasis, extensive
psoriasis vulgaris.
2. Reiters syndrome and pityriasis rubra pilaris.
3. Sarcoidosis.
4. Polymyositis and systemic lupus erythematosus.
5. Pemphigus vulgaris and other bullous
disorders.
Side Effects
1. Gastrointestinal nausea, vomiting, stomatitis, diarrhoea, ulceration, etc.
2. Hepatitic abnormal liver enzymes, hepatic,
fibrosis and cirrhosis.
3. Hematopoietic anemia, thrombocytopenia,
leucopenia, pancytopenia.
4. Pulmonary acute hypersensitivity, fibrosis,
pneumonia.
Most common side effect is nausea and
vomiting. Serious late side effect is cirrhosis of
the liver.
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PSORALENS
Of the many psoralens isolated and synthesized,
three are in routine clinical use. These include 8
methoxypsoralen (8-MOP), 5 methoxypsoralen
(5-MOP) and trimethyl psoralen (TMP). They are
active only when combined with UVA irradiation.
It interferes with DNA synthesis and blocks
epidermal cell proliferation, has immunomodulatory effects and immunosuppressive effects
along with induction of epidermal thickening and
melanogenesis.
Dosage
Oral 8-MOP is given in a dose of 0.6 to 0.8 mg/kg
body weight/day. Two hours later, the patient is
exposed to ultraviolet radiation A (UVA) at a dose
of 1 joule/square cm to begin with, which is
gradually increased to minimal erythema dose
depending on the skin type. Therapy is usually
given two to three times per week. The number of
exposures required for achieving control are
usually between 15 and 25. Maintenance therapy
involves less frequent treatments often as little as
once every two to four weeks, with eventual
discontinuation of treatment.
Indications
1. Psoriasis.
2. Vitiligo.
3. Photodermatoses.
4. Cutaneous T-cell lymphomas.
Side Effects
1. Nausea, vomiting.
2. Cutaneous Acute sunburn and erythema,
irreversible hyperpigmentation of the skin,
PUVA lentigines, actinic keratoses, premature
ageing of the skin.
3. Ocular cataract. It can be prevented by using
sunglasses on the day of treatment.
4. Carcinogenesis.
RETINOIDS
Retinoids is a generic term that includes both
naturally occurring molecules and also synthetic
compounds showing specific biological activities
resembling those of vitamin A(retinol).
Synthetic retinoids are produced by chemical
modification of vitamin A. Three generations are
known today(nonaromatic, monoaromatic, and
polyaromatic).
First generation(Nonaromatic) includes retinal and
compounds that can be derived from it
metabolically e.g. retinyl palmitate(topical),
retinyl aldehyde(topical), tretinoin(all trans
retinoic acid)(topical), 9-cis-retinoic acid, a-14hydroxyretroretinol, fenretinide(N-[4-hydroxyphenyl]-retinamide), E 5166(polyprenoic acid).
Second generation(Monoaromatic) by addition of an
aromatic ring e.g. etretinate, isotretinoin, acitretin,
isoacitretin(13-cis-acitretin), motretinide.
Third generation(Arotinoids) e.g. temarotene,
arotenoid acid, arotenoid ethyl ester, arotenoid
ethyl sulphone, arotenoid methyl sulphone,
adapalene(topical antiacne agent), tazarotene
(topical antipsoriatic agent).
Intracellularly retinoids interact with cytosolic
proteins and then enter the nucleus. By changing
the expression of growth factors, oncogenes,
keratin or transglutaminases, retinoids could
exert wide spread changes in growth and
differentiation.
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28
Dermatosurgical Procedures
SKIN BIOPSY
Skin biopsy is the commonest investigation
performed by any dermatologist. The diseased
tissue obtained is subjected to microscopic and/
or other investigations.
Indications
1. Most frequently skin biopsy is taken to
confirm a clinical diagnosis or to aid in the
establishment of a diagnosis where clinical
diagnosis is not apparent.
2. Sometimes, biopsy is excisional for the
treatment of skin lesions particularly
malignant neoplasms and other lesions for
cosmetic reasons.
3. Skin biopsy may be used for a variety of
investigative procedures such as ultrastructural examination, immunofluorescence
studies, enzyme histochemistry and
immunohistochemistry, microbiological
studies, tissue culture, etc.
Site of biopsy: Ideally, the lesion biopsied should
be an early and untreated lesion and representative of the skin disorder as a whole. If lesions
are present at all stages of evolution, it may be
appropriate to biopsy more than one lesion.
Normal skin should be included with a
diagnostic biopsy wherever possible.
ELECTROSURGICAL PROCEDURES IN
DERMATOLOGY
Electrical current of sufficiently high frequency
not to stimulate nerves or muscles can pass
through tissue with little effect other than the
Dermatosurgical Procedures
production of heat. Heat is produced from the
electrical resistance of the tissue as current travels
from one electrode to the other. When the
electrodes are both large (as in medical
diathermy), the heat is dispersed over a large
area, and no injury ensues. However, if the
emitting electrode is reduced to a small tip, the
heat produced at the point of contact is
sufficiently intense to cause localized tissue
injury.
As might be anticipated, variation in the
voltage, amperage, frequency, and method of
application gives each of the electrosurgical
modality its unique qualities. Equally important,
however, is the waveform of each current. In
practice, a spark-gap apparatus produces
damped waves, whereas a vacuum tube or
transistorized unit creates continuous waves.
Examples of the former include the Hyfrecator
(Birtcher Corp., El Monte, CA) commonly
employed in dermatology.
Electrodesiccation and
Electrofulguration
The difference between electrodesiccation and
electrofulguration lies in the placement of the
elec-trode tip. In electrodesiccation (Lat. Siccus
dry), the tip contacts the skin and causes a
radial spread of current . In electrofulguration
[Lat. fulgur lightning] the tip remains above
the skin and the charge leaps to the surface in
a diffuse, or defocused, pattern , causing
flatter and more superficial tissue destruction.
The histologic outcome of both modalities is one
of tissue desiccation.
As a result of the low heat production,
electrodesiccation and electrofulguration are best
suited for superficial and comparatively
avascular lesions such as verrucae and
seborrheic keratoses.
Electrocoagulation
Electrocoagulation [Lat. Coagulum clot or
curd] is produced by a high-frequency
alternating current of high amperage (2,5004,000 mA) and low voltage (<200 volts). This
current is generated by a spark-gap apparatus
applied biterminally through one active and one
dispersive electrode; the patient is an integral
part of the circuit.
The depth of penetration makes
electrocoagu-lation useful in the removal of thick
lesions. The greater production of heat and
conduction of cur-rent along vessels make
electrocoagulation supe-rior to electrodesiccation for hemostasis in a wet field and
for destruction of highly vascular lesions (e.g.
pyogenic granuloma).
Electrosection
Electrosection [Lat. secare to cut] may be
achieved by using either an undamped
continuous current or a mildly damped pulsed
current. The former is generated by a vacuum
tube or solid-state unit, whereas the latter is
produced by a spark-gap apparatus. Continuous
waves cause intense but sharply limited heat
production, resulting in localized tissue
destruction with little effect on the immediately
adjacent tissue. Microscopically, an incision
approximately 0. 1 mm wide results from
disintegration of cells along the cutting line.
Electrolysis
Electrolysis [Gr. Lysis dissolution] makes use
of low-voltage, low-amperage direct (galvanic)
current flowing unidirectionally between polarized electrodes. The resulting chemical
ionization causes release of acids and metallic
ions at the positive pole, with formation of
hydroxides and attraction of metallic ions at the
negative pole. The major electrosurgical
application of electrolysis has been in epilation.
Two disadvantages of electrolysis are that it is
difficult to master and is time consuming.
Although electrolysis is an inaccurate term
for the high-frequency method of hair removal,
it continues as the common expression solely by
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virtue of its frequent misusage. Thermoepilation [Gr. Therme heat + e out + pilus hair]
is a more accurate and descriptive appellation.
Electrocautery
Although not a true form of electrosurgery (no
current actually enters the patient), electrocautery [Gr. Kauterion branding iron] is, by
convention, usually included among the other
modalities. Low-voltage, high-amperage, direct
or alternating current is passed through a needle
tip that is heated to red-hot temperatures by its
resistance to the flow of current. Application of
the heated needle tip to bleeding vessels causes
coagulation. As with electrosection, too little heat
causes coagulated tissue to adhere to the needle,
whereas too much heat causes unnecessary
destruction of tissue.
Safety Considerations
Potential interference of cardiac pacemakers
from electrosurgical current has been known.
Close attention to proper grounding is important to prevent unintentional shocks or burns.
Particularly with the mono-terminal currents
used for electrodesiccation and electrofulguration, care should be taken by the operator
to maintain a firm, broad-based, skin-to-skin
contact with the patient. Alcohol is commonly
used to cleanse skin pre-operatively. If sufficient
drying time is not allowed prior to electrosurgery, the alcohol can be ignited and the
resulting flame spectacular.
CRYOSURGERY IN DERMATOLOGY
The term cryosurgery is derived from a Greek
word Kryo meaning ice. This type of surgery is
carried out by using freezing agents. The freezing
agents are called as cryogens.
The anesthetic properties of hypothermia are
known since Hippocratic times. Salt and ice
mixtures were used in the 19th century to
Dermatosurgical Procedures
depends on the lasing medium, the molecules
of which have been excited (e.g. CO2, ruby,
argon, dyes, ND-YAG, etc.).
LASERS IN DERMATOLOGY
LASER:
Light
Amplified by
Stimulated
Emission of
Radiation.
(first pioneered by Leon Goldman).
Principle
Inside a laser, one photon stimulates the
emission of another identical photon from
molecules that are in an excited state. Two
mirrors are placed on each end of the laser in
exact parallel alignment so that the photons
bounce back and forth through the excited
medium and the light is amplified by stimulating
more and more photons. The result is an
impressively bright, monochromatic, highly
collimated, coherent, and controllable beam of
light. The wavelength of the light released
Type of laser
Wavelength, nm
Typical uses
Alexandrite
755
488630
CO2
10,600
Erbium:YAG
2940
Krypton
520, 568
Nd:YAG
532, 1064
577600
510
Ruby
694
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Essentials in Dermatology
DERMABRASION
Dermabrasion means surgical abrasion in the
planes of the epidermis and dermis. It can be
achieved with the help of a manual metallic
dermabrader or a rapidly rotating wire brush or
diamond fraise.
How it works?
Lesions and defects of the epidermis, papillary
dermis, and upper reticular dermis can be
partially or completely removed by surgically
planing to the level of the reticular dermis.
During the maturation phase of wound healing,
fibroblasts replace and remodel collagen bundles
in the papillary and upper reticular dermis.
Indications Include:
Facial acne scars
Surgical and traumatic scars
Photoaging
Benign conditionssuch as rhinophyma,
adenoma sebaceum, epidermal nevi,
syringomas, small cysts, milia, and seborrheic
keratoses.
Superficial malignancies, including Bowens
disease and superficial basal cell carcinomas.
Pigmentary disorders such as melasma,
tattoos, and lentigines
Postoperative complications include scarring,
pigmentary changes, persistent erythema, and
infection. The deeper the dermabrasion, the
greater the risk of scarring.
CHEMICAL PEELS
Chemical peeling also called chemical
resurfacing or chemoexfoliation, involves the
Indications Include
Actinic keratoses
Pigmentary lesions in the form of melasma
or postinflammatory hyperpigmentation.
Acne vulgaris scars and other depressed
scars.
Photoaging
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Historical Milestones in
Sexually Transmitted Diseases
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Essentials in Dermatology
study was setup by Norwegian syphilologist,
Caesar Boeck. He collected patients between 1891
and 1910 and his successor at the Oslo
Dermatological Centre, Bruusgaard reassessed
them in 1929. The data was further reanalyzed
by Gjestland in 1955. This study is usually known
as Oslo Study.
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30
Past History
Past history of exposure if any, STD, medical or
surgical illness, hospital admission, blood
transfusion or medical illness complicating the
disease.
Treatment History
Present and recent medications, especially
antibiotics, topical and vaginal preparations.
History of drug sensitivity or any genitourinary
instrumentation e.g. cystoscopy, abortion,
dilatation, curettage etc.
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Personal History
Personal history regarding education, socioeconomic status, occupation, income, habits
(alcohol use, drug abuse, smoking), staying alone
or with family, relationship with spouse and
frequency of sexual intercourse may be essential.
Sexual History
It should be taken in detail. Exact dates of sexual
exposure, place of exposure, whether heterosexual, homosexual or bisexual, use of barrier
contraceptives during intercourse may be
enquired. Details of intercourse- genito-genital,
genito-anal, genito-oral may have relationship
to the diagnosis at hand. Further enquiry about
the sexual partner whether he/she was having
genital sore/discharge or any other related
problem, whether the concerned person has
single or multiple sexual partners need to be
known, and the frequency of sexual intercourse.
HIV Risk Assessment
Activities known to be associated with increased
risk of acquisition of HIV should be specifically
enquired about. These include involvement in
prostitution, male homosexuality or bisexuality,
having injected drugs, sexual partners from areas
of high endemicity, history of transfusions with
blood or blood products, sexual contact with
intravenous drug users, or (in the case of females)
hemophiliacs, or bisexual male partners.
Menstrual History
History regarding last date of previous
menstruation, whether menses are regular or
irregular, flow heavy or scanty, contains fresh
blood or clots, associated pain and history of post
coital bleeding or intermenstrual bleeding may
be helpful.
Obstetric History
Enquire about methods of contraception used if
any (barrier, intrauterine device, oral pills
Family History
Health status of siblings, any family history of
similar problem or death if any and cause of
death may be ascertained. This is relevant in
cases of suspected congenital syphilis as it is
more common if the mother did not receive
adequate antenatal care.
General Physical Examination
Consideration should always be given to having
another member of health care worker present
when carrying out an intimate physical
examination on the patient, who will reassure
the patient, able to assist the practitioner in
carrying out the examination and provides a
witness as protection against allegation of
indecency or misconduct. Systematic approach
to physical examination is the best means of
reassuring a patient. Since the manifestations of
STDs are not limited to the anogenital region, a
general physical examination of each patient is
ideal. Relevant systemic examination may be
undertaken after thorough genital examination.
Genital Examination
It should be done in privacy, in the presence of
natural light if possible or good light source.
Examination of the Male Patient
Patient should be fully exposed and
undergarments inspected for staining with
the discharge.
External genitalia and inguinal skin are
examined visually and by palpation with
gloved hands.
Care should be taken to inspect and palpate
penis with attention to the urethral canal and
scrotal contents for evidence of pain,
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The vagina should be examined for rugal
folds, erythema, malodour, discharge,
purulence, ulcerations and other abnormalities.
It is important to ascertain the character and
source of discharge (physiological versus
vaginal versus cervical).
Following speculum examination, bimanual
examination including both abdominal
pelvic and genitorectal assessment is
important part of the pelvic examination.
With one hand on the abdomen and the index
and middle finger of the other hand inserted
in the vaginal canal, stepwise palpation of
the abdomen, vagina, cervix, uterus and
adnexal structures is completed. Uterine size
and position should be carefully evaluated
and superior displacement of the cervix
performed to check for the presence of
tenderness.
Prior to genitorectal examination, gloves
should be changed to avoid possibility of
iatrogenic rectal inoculation of pathogens.
Genitorectal examination is done for
evaluation of the rectum and cul-de-sac.
Anoscopic and sigmoidoscopic examination
is suggested for females with proctocolitic
symptomatology and those who have
engaged in rectal intercourse.
Oropharyngeal Examination
Routine examination of oropharynx is essential
and may give useful clues to diagnosis or helps
in detection of ulcerations or pharyngitis.
Bedside Procedures
1. Two or three glass test- is done to
differentiate anterior urethritis from
posterior urethritis or infection of the
bladder. In the two glass test, patient is
asked to void the urine. If the first glass is
hazy and second glass clear, suggests
anterior urethritis. In case, haziness is seen
in second glass only, it means there is
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31
Disease or syndrome
Neisseria gonorrhoeae
Treponema pallidum
Syphilis
Haemophilus ducreyi
Chancroid
Chlamydia trachomatis
Calymmatobacterium granulomatis
Donovanosis
Hepatitis B
Herpes genitalis
AIDS
Molluscum contagiosum
Candida albicans
Vaginitis
Trichomonas vaginalis
Vaginitis
Secondary Syphilis
Lesions of secondary syphilis result from the
hematogenous dissemination of treponemes
during the evolution of the primary syphilitic
chancre and lesions appear 3-12 weeks after
the initial appearance of primary lesion.
Patients with secondary syphilis may be ill
with flu-like symptoms that include malaise,
appetite loss, fever, headache, stiff neck,
lacrimation, myalgias, arthralgias, nasal
discharge, and depression.
The skin manifestations of secondary syphilis
called syphilids are asymptomatic, polymorphous, variegate, bilateral and
symmetrical (Figs 31.2 to 31.6). The initial
finding in secondary syphilis is an evanescent
macular rash, a few days later symmetric
papular eruption appear involving the entire
trunk and the extremities, including palms
and soles. Papular lesions demonstrate
Ollendorf sign. Even nodules may appear.
They may be pustular, but never vesicular.
Because of the variety of clinical
manifestations, syphilis has been called the
the great imitator.
Lesions on mucous membranes appear as
raised gray white mucous patches.
Condylomata lata, the moist, smooth surfaced
warty intertriginous plaques are considered
to be most infectious lesion of syphilis because
of the eroded surface and large number of
spirochetes (Figs 31.7 and 31.8)
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Tertiary Syphilis
Congenital Syphilis
In congenital syphilis, the treponemes cross
the placenta and infect the fetus.
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The early clinical signs of congenital syphilis
begin to appear in the third to eighth week of
life and in all cases by 3rd month of life.
Early congenital syphilis is known for
snuffles (a persistent nasal dischargesyphilitic rhinitis), myriad of cutaneous
lesions like secondary syphilis (scaling
papules, plaques, bullae, desquamation,
condylomata lata, mucous patches) (Figs 31.10
to 31.12), furuncle of Barlow, hepatosplenomegaly (Fig. 31.13), generalized
lymphadenopathy, pseudoparalysis of Parrot
(pain from osteochondritis of the long bones,
Secondary syphilis
6 weeks to 6 months
Latent syphilis
Asymptomatic
Late syphilis
Months to years
Diagnosis
Acquired Syphilis
The most specific and sensitive method for
verifying the diagnosis of primary syphilis is
the finding of treponemes with characteristic
appearance by darkfield microscopic
examinations of fluid obtained from the
surface of the chancre. The dark field
examination is actually the only test that
specifically establishes the diagnosis of
primary syphilis.
The non-specific treponemal tests the
Venereal Disease Research Laboratory
(VDRL) and the rapid plasma reagin (RPR),
typically become reactive within 4 to 7 days of
chancre development. A titre of 1:8 or more is
said to be significant. These titre results
correspond with disease activity and should
reduce four fold within 6 to 12 months of
treatment and become undetectable several
years there after. False positive results may
occur with numerous conditions, such as
collagen vascular diseases, several chronic
infections such as HIV or tuberculosis,
advancing age, narcotic drug use, chronic
liver disease and several active infections such
as herpes.
Because of the decreased specificity of above
tests, positive results should be confirmed
with the more precise treponemal tests,
Treponema pallidum heme agglutination assay
Congenital Syphilis
A diagnosis of congenital syphilis can be
made with confidence if the mother has
reactive non-treponemal and treponemal
serologies and the infant manifests classic
signs of disease.
Congenital syphilis is also highly likely when
the infants non-treponemal antibody titre is
four fold or greater than the mothers serum,
even in the absence of physical findings.
IgM FTA ABS test is specific for congenital
syphilis, particularly if the titre rises.
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Treatment
Acquired Syphilis
Stage
Treatment
Follow up
Primary, secondary, or
early latent syphilis
2.4 million IU
intramuscular benzathine
penicillin G once
2.4 million IU
intramuscular benzathine
penicillin G weekly for 3 weeks
Neurosyphilis or
ocular syphilis
Congenital Syphilis
Diagnosis
H.ducreyi may be identified in the form of
chains (school of fish) of gram-negative
cocobacilli in the smear from the ulcer, or
preferably of pus from bubo.
Ideally it should be cultured on one of the
modern selective media at 33C in an
atmosphere of high humidity.
Ito-Reenstierna test- intradermal test with a
vaccine containing killed H.ducreyi in
suspension, producing an inflammatory
papule (0.5 to 1 cm in diameter) after 48 hours
Because of the current difficulty with
diagnosis, the CDC recommends that a
probable diagnosis can be determined by the
Treatment
WHO 2003 and Center for Disease Control and
Prevention (CDC) in 2006 recommends
Azithromycin 1 g orally in a single dose, or
Ceftriaxone 250 mg intramuscularly (IM) in a
single dose, or Ciprofloxacin 500 mg orally twice
a day for 3 days (contraindicated for pregnant
and lactating women), or Erythromycin base 500
mg orally three times (CDC) or four times (WHO)
a day for 7 days.
NACO recommends erythromycin stearate /
erythromycin base, 500 mg orally 4 times a day
for 7 days or erythromycin ethyl succinate, 800
mg orally 4 times a day for 7 days (In case of
concomitant syphilis, treatment can be given for
15 days) or ciprofloxacin, 500 mg orally twice a
day for 3-5 days or till the clearance of lesions or
ceftriaxone, 250 mg IM as a single dose or
azithromycin, 1 g orally as a single dose or
doxycycline, 100 mg orally twice daily for 7 days
or trimethoprim (80 mg) + sulphamethoxazole
(400 mg), 2 tabs orally twice a day for 2 weeks.
Treatment should be given for the period
indicated, or until such time, the lesions heal.
Fluctuant bubo should be aspirated through
the surrounding healthy skin. Aspiration should
not be done from the dependent side. Incision and
drainage or excision of bubo delays healing and
is contraindicated.
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After an incubation period of 3-30 days after
inoculation, the first stage begins with a small
painless papule or pustule that may erode to
form an asymptomatic herpetiform ulcer. This
typically heals without scarring in 1 week and
often goes unnoticed.
The second stage begins within 2-6 weeks after
the onset of primary lesion. It is referred to as
inguinal stage and consists of painful
inflammation and infection of inguinal and/
or femoral lymph nodes. Involvement is
limited to one groin in about two third of the
cases. Enlargement of tender lymph nodes
above and below the inguinal ligament may
give the bubo a grooved appearance the sign
of the groove (Fig. 31.14). Suppuration occurs
in them with the formation of multiple small
abscesses. These abscesses open on the skin
surface to form multiple sinuses, finally
healing with puckered scars. Constitutional
symptoms are very variable.
The third stage is called as genitorectal
syndrome. The interval between the early stage
and later manifestations may vary from a year
or two to many years. Patients may develop
genital elephantiasis (Esthiomene) or
anorectal syndrome. It more often develops in
women and homosexual men who engage in
receptive anal intercourse and includes
proctocolitis, peri-rectal abscess, fistula.
Diagnosis
A definitive diagnosis can be achieved with
isolation of the organism on culture and cell
typing of the isolates.
The Frei test-an intradermal test with 0.1ml of
Lygranum antigen, read at 48 to 72 hours- a
raised, red papule, at least 6 mm across.
With appropriate clinical presentation, a
complement fixation antibody titre of greater
than 1:64 is considered diagnostic of LGV.
Treatment
Center for Disease Control and Prevention (CDC)
in 2006 recommends.
Doxycycline 100 mg orally twice a day for 21
days
Alternative treatment is erythromycin base 500
mg orally four times a day for 21 days.
Some STD specialists believe that
azithromycin 1.0 g orally once weekly for 3
weeks is probably effective, although clinical
data are lacking.
WHO (2003) Recommends
Doxycycline, 100 mg orally, twice daily for 14
days.
Or
Erythromycin, 500 mg orally, 4 times daily for 14
days.
Alternative regimen
Tetracycline, 500 mg orally, 4 times daily for 14
days.
Note
Tetracyclines are contraindicated in pregnancy.
NACO recommendations are same as WHO
except for an additional therapy- trimethoprim
(80 mg) + sulphamethoxazole (400 mg) 2 tablets
twice daily for 21 days.
Fluctuant lymph nodes should be aspirated
through healthy skin. Incision and drainage or
excision of nodes may delay healing. Some
patients with advanced disease may require
Diagnosis
Treatment
Center for Disease Control and Prevention (CDC)
in 2006 recommends
Doxycycline 100 mg orally twice a day for at least
3 weeks,
Alternative regimens
Azithromycin 1 g orally once per week for at least
3 weeks and until all lesions have completely
healed
Or
Ciprofloxacin 750 mg orally twice a day for at
least 3 weeks and until all lesions have completely
healed
Or
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Erythromycin base 500 mg orally four times a
day for at least 3 weeks and until all lesions have
completely healed
Or
Trimethoprim-sulfamethoxazole one doublestrength (800mg/160mg) tablet orally twice a day
for at least 3 weeks and until all lesions have
completely healed
WHO (2003) Recommends
Azithromycin, 1 g orally on first day, then 500 mg
orally, once a day
Or
Doxycycline, 100 mg orally, twice daily
Alternative regimen
Erythromycin, 500 mg orally, 4 times daily
Or
Tetracycline, 500 mg orally, 4 times daily
Or
Trimethoprim 80 mg/sulfamethoxazole 400 mg,
2 tablets orally, twice daily for a minimum of 14
days
Treatment should be continued until all lesions
have completely epithelialized.
Note:
The addition of a parenteral aminoglycoside such
as gentamicin should be carefully considered for
treating HIV-infected patients.
NACO recommendations are same as WHO ones
except azithromycin
Other option used-Injection of streptomycin 1
gram given daily for 14 days.
Herpes Genitalis
Both HSV-1 and HSV-2 produce primary as
well as recurrent genital infections. Isolation
of HSV-2 can be successful in 80% of
instances.
HSV is the most common cause of genital
ulceration and accounts for 20% to 50% of
ulcerative lesions in patients attending
sexually transmitted disease clinics (STD
clinics).
Diagnosis
Definitive diagnosis of genital herpes is made
by viral culture of the lesions, which can
distinguish between HSV-1 and HSV-2.
Biopsy and cytologic studies may be useful in
the diagnosis, but they are unable to
differentiate between HSV-1, HSV-2 and
varicella zoster virus.
The use of specific monoclonal antibodies
directed against HSV-1 and HSV-2 proteins
have proved to be sensitive and specific.
PCR can be used to detect HSV DNA.
And a valuable bedside clinical approach in
making a rapid diagnosis of herpes infection
relies on Tzanck preparation, which can be of
great value in resource poor setting.
Fig. 31.17
Fig. 31.18
Treatment
WHO (2003) and Center for Disease Control and
Prevention (CDC) in 2006 recommends
First clinical episode of genital herpes
Acyclovir 400 mg orally three times a day for
710 days, or Acyclovir 200 mg orally five times a
day for 710 days, or Famciclovir 250 mg orally
three times a day for 710 days, or Valacyclovir
1 g orally twice a day for 710 days.
Recurrent episodes of genital herpes
Acyclovir 200 mg orally, 5 times daily for 5 days
(WHO) or 400 mg orally three times a day for 5
days, or Acyclovir 800 mg orally three times a
day for 2 days (CDC), or Acyclovir 800 mg orally
twice a day for 5 days, or Famciclovir 125 mg
orally twice a day for 5 days, or Valacyclovir 500
mg orally twice a day for 35 days, or Valacyclovir
1.0 g orally once a day for 5 days.
Suppressive therapy for recurrent genital herpes
Daily suppressive anti-viral therapy may be
employed in patients with frequent recurrences
of genital herpes (six or more recurrences per year).
Since daily antiviral suppressive therapy reduces
the recurrence rate of herpes genitalis by more
than 75%, option for daily suppressive therapy
may be discussed with all such patients suffering
from recurrent herpes genitalis.
Differential Diagnosis of
Genital Ulcer Disease
Genital ulcers are defined as breach in the
continuity of genital mucosa and /or skin. Genital
ulcer disease (GUD) may be due to sexually
transmitted diseases (STD) like syphilis, herpes
genitalis, chancroid, lymphogranuloma
venereum, donovanosis or non-STD like traumatic
ulcers, Behcets disease, lichen planus, erythema
multiforme, lichen sclerosus et atrophicus,
bullous diseases, Fourniers gangrene, squamous
cell carcinoma (Fig. 31.19), etc.
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Differentiating features of the common sexually transmitted diseases are given below
Characteristics
Syphilis
Herpes genitalis
Chancroid
LGV
Donovanosis
1. Incubation
period
9-90 days
(2-4 weeks)
mean 21 days
2-7 days
1-5 days
3 days to
6 weeks
(avg. 7 days)
1 to 4 weeks
(8 to 80 days)
2. Causative
organism
Treponema
pallidum
Herpes simplex
virus (HSV 2
and 1)
Haemophilus
ducreyi
Chlamydia
trachomatis
sero-type L1-L3.
Calymmatobacterium
granulomatis
3. Primary
lesion
Papule
Vesicle
Pustule
Papule, pustule
or vesicle
Papule
4. Number of
lesions
Usually one
Multiple, may
coalesce
Usually multiple
Usually one
Variable
5. Pain
Painless
Painful
Usually very
tender
Variable
Uncommon
6. Diameter
5 to 15 mm
1 to 2 mm
2 to 20 mm
2 to 10 mm
variable
7. Edges/
margin
Sharply
demarcated,
elevated,
round/oval
Erythematous,
sharp
Sharply
circumscribed,
ragged
undermined edges
Elevated,
round or
oval
Elevated, irregular
8. Depth
Superficial/deep Superficial
Excavated and
deep
Superficial
Elevated
9. Floor
Smooth, clean
Variable
Beefy red
granulation tissue,
bleeds readily
Erythematous,
Yellow
covered with
necrotic purulent
serous exudates exudates
Contd...
Syphilis
Herpes genitalis
Chancroid
LGV
Donovanosis
10. Base
Indurated
None
Nonindurated,
soft
Occasionally
firm
Firm
11. Inguinal
Bilateral, firm,
Bilateral firm
lymphadeno- non-tender,
and tender
pathy
discrete, shotty
30 to 60%,
unilateral, tender,
matted together,
suppuration with
formation of a
unilocular abscess
(bubo), may rupture
66% usually
None,
unilateral, less
pseudobubo
painful, Groove sign may be seen.
positive, multilocular
abcesses, rupture
to form multiple
sinuses
14 to 21 days
Self limiting
but may be
persistent.
2 to 5 days
(transient)
No tendency
to heal
13. Recurrence
Yes, in 80%
No
No
No
No.
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In females, if manifest, it leads to increased
vaginal discharge, dysuria, intermenstrual
bleeding or menorrhagia. Examination reveals
mucopurulent cervical discharge, the cervix
has erythema and oedema, swabbing the
endocervix easily induces mucosal bleeding.
Salpingitis and Bartholin gland abscesses are
possible local complications. Ascending
infection and bacteremic dissemination
(disseminated gonococcal infection) are
responsible for most of the serious morbidity.
Rectal mucosa is a frequent site of infection in
homosexual men with symptoms ranging
from minimal anal pruritus, painless
mucopurulent discharge or scant rectal
bleeding to overt proctitis.
Pharyngeal infection occurs in 3-7 percent of
heterosexual men, 10 to 20 percent of
heterosexual women, and 10 to 25 percent of
homosexually active men.
Ophthalmia neonatorum may occur due to
perinatal transmission.
Diagnosis
Isolation of N.gonorrhoeae is the diagnostic
standard for gonococcal infections.
Urethral smear is sufficiently sensitive and
specific, that the culture may be considered
optional for routine care. Grams stain has
been the most extensively studied. A diagnosis
of urethritis is made if there are more than 5
pus cells present per oil immersion field. In
addition, these pus cells have intracellular
gram-negative diplococci, confirming the
diagnosis of gonorrhea (Fig. 31.21).
Alternative Regimens
Spectinomycin 2 g in a single IM dose or Singledose cephalosporin regimens- ceftizoxime (500
mg, administered IM), cefoxitin (2 g, administered
IM with probenecid 1 g orally), and cefotaxime
(500 mg, administered IM) or Single-dose
quinolone regimens - gatifloxacin 400 mg orally,
norfloxacin 800 mg orally, and lomefloxacin 400
mg orally.
Treatment
For uncomplicated gonococcal infections of the
cervix, urethra, and rectum, Center for Disease
Control and Prevention (CDC) in 2006
recommends
Ceftriaxone 125 mg IM (intramuscular) in a single
dose, or Cefixime 400 mg orally in a single dose,
Non-gonococcal
1. Incubation
period
2-3 weeks
2-5 days
Absent
3. Discharge
Profuse, purulent
and yellowish
Scanty mucoid or
mucopurulent
4. Dysuria
Intense burning
sensation
Smarting feeling in
urethra on
passing urine
Treatment
Center for Disease Control and Prevention (CDC)
in 2006 recommends
Azithromycin 1 gm PO once or
Doxycycline 100 mg PO BD for 7 days
Alternative regimens:
Erythromycin base 500 mg PO qid for 7 days
or
Ofloxacin 300mg PO BD for 7 days or
Levofloxacin 500 mg orally for 7 days.
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Diagnostic Criteria
Minimum Criteria
Uterine/adnexal tenderness
Cervical motion tenderness
Additional Criteria
Treatment
Treatment should be initiated with minimal
criteria and needs to cover all the etiological
pathogens. Early treatment prevents
sequelae.
Parenteral therapy is given for the initial
24 48 hours and thereafter oral therapy is
continued.
Regimens include
IV Cefoxitin plus oral doxycycline (after 24 hours
IV drugs stopped and oral doxycycline
continued) or IV clindamycin and gentamicin
(24 hours) followed by oral doxycycline or IV
ofloxacin with metronidazole or IV ampicillin
plus doxycycline
Male sexual contacts (in the preceding 60 days)
should be treated.
Treatment
All women who have symptomatic BV disease require treatment.
Metronidazole 500 mg orally twice a day for 7 days, or Metronidazole gel 0.75%, one full applicator
(5 g) intravaginally, once a day for 5 days, or Clindamycin cream 2%, one full applicator (5 g)
intravaginally at bedtime for 7 days are recommended treatments.
Alternatively, patient may be treated with Metronidazole 2 g orally in a single dose, Clindamycin
300 mg orally twice a day for 7 days, or Clindamycin ovules 100 g intravaginally once at bedtime
for 3 days.
Differential diagnoses of vaginal discharge
Profile
Normal vaginal
discharge
Candidal
vulvovaginitis
Trichomonal
vaginitis
Bacterial
vaginosis
Etiology
Lactobacillus
predominant
Candida spp.
and other yeasts
Trichomonas
vaginalis
Associated with
G.vaginalis; anaerobic
bacteria, and
Mycoplasma hominis
Symptoms
None
Profuse discharge,
often malodorous;
external dysuria and
genital irritation often
present
Malodorous, increased
discharge (commonly
present at the introitus)
Amount
Profuse
Moderate to profuse
White or gray
Homogeneous, watery,
often frothy
Homogeneous,
uniformly coating
vaginal walls
Color
Consistency
pH
Usually <4.5
<4.5
Usually >5.0
Usually >4.5
Amine odor
with 10% KOH
None
None
Usually present
Present
Associated
inflammatory
signs
None
Erythema of vaginal
mucosa, introitus;
occasional cervical
petechiae; vulvar
dermatitis
None
Microscopy of
discharge
Normal epithelial
cells; lactobacilli
predominate
Leukocytes, epithelial
cells; yeast, mycelia,
pseudomycelia seen
Leukocytes; motile
trichomonads seen
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MISCELLANEOUS STDs
Anogenital Warts
The etiologic agent of anogenital warts or
condyloma acuminata is the human
papilloma virus (HPV) a non-enveloped,
double standard DNA virus.
More than 80 different genotypes of HPV have
been identified. Forty-five of these are known
to affect the genital epithelium and are considered to be sexually transmitted infections.
It is roughly estimated that up to 30% to 50%
of sexually active adults are infected with
HPV. The highest rates of infection are found
in women, 19-22 years of age and in men, 2226 years of age.
HPV 6 and 11 are most commonly associated
with genital warts, but at least 20 different
HPV genotypes have been associated with
condyloma acuminata.
The infectivity of HPV between sexual partners
is estimated to be 60%.
The most common locations of primary
infection include the fourchette in women and
Fig. 31.23
Fig. 31.24
Differential Diagnosis
Morphologically, various conditions, which need
to be differentiated from verrucous lesions of
genital warts, are condyloma lata of syphilis, nonvenereal treponematosis, hypertrophic verrucous
type of granuloma inguinale, tuberculosis
verrucosa cutis, skin tags, and malignancy. For
small genital warts, various differential diagnoses
need to be considered are pearly penile papules
(Fig. 31.25), vestibular papillomatosis, molluscum
contagiosum, seborrhoeic keratosis, Fordyces
spots, urethral caruncle, lichen planus, and
foreign body granuloma. For subclinical infection
(seldom appears reddish), candidial infection of
the vulva and repeated topical application of
antifungals need to be ruled out. Other benign
tumors like neurofibroma, lipoma, fibroepitheliomata, and normal physiological glands
like Tysons glands also need to be considered
before appropriate diagnosis is made. Around the
anus, prolapse and sentinel piles, and anal tags
Treatment
Treatment options may be categorized into
cytodestructive methods (surgical excision,
cryotherapy, laser therapy, bichloroacetic acid /
trichloroacetic acid, podophyllin and podophyllotoxin), antimetabolic therapy (5-fluorouracil), antiviral therapy (cidofovir and
interferons [IFNs]) and immunomodulation
(imiquimod)
1. Podophyllin 10-25% (applied to the warts
using cotton tipped swab once or twice a week
for up to six weeks) or podophyllotoxin 0.5%
(the solution or cream is applied with cotton
swab or finger respectively, over the
condylomas also on normal appearing skin
between the lesions twice daily for three days
followed by four days of no therapy) for local
use is first line therapy.
2. Imiquimod cream, supplied in single use
sachets, is applied to the warts with fingers
three times per week (every other night) and
the area washed with mild soap and water
the next morning. Treatment continued until
wart clearance, or for a maximum of 16 weeks
3. Cryotherapy treatment of choice for
condyloma acuminata in pregnancy.
4. CO2 laser
5. Surgery
6. Interferons (as adjuvant to surgery),
5-fluorouracil (urethral warts), cidofovir, or
retinoids are other treatment options
7. Since treatment is often unsatisfactory and is
not directed at elimination of the virus, some
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progress has been made in the development
of the HPV vaccines
8. Patient counseling- Advise female patients
about regular participation in cervical
cytology screening programmes. Use barrier
protection with new sexual contacts until
successful treatment has been completed
Molluscum Contagiosum
Molluscum contagiosum is a benign papular
condition of the skin, which is often sexually
transmitted in adults.
Molluscum contagiosum virus is the final
remaining member of poxviridae family that
specifically infects humans.
The incidence of molluscum contagiosum in
sexually active adults has been increasing
significantly throughout the past few decades.
Mechanical trauma appears to facilitate the
transmission of molluscum contagiosum
virus. There is no information about the
efficiency of sexual transmission of MCV.
Lesions begin as tiny papules, which grow
over several weeks to a diameter of 3 to 5 mm.
The flesh coloured papules are smooth, firm
and dome shaped with a highly characteristic
central umbilication. In adults lesions most
commonly occur on the thighs, inguinal
region, buttocks and lower abdominal wall
(Fig. 31.26).
Scabies
Scabies can be sexually transmitted.
When scabies spreads through sexual
transmission, the characteristic lesions are
more likely to occur on the genitalia, lower
abdomen or thigh.
The penis and bra lines are other favourite
locations for mite.
Pediculosis Pubis
Pediculosis pubis is primarily a sexually
transmitted infection occurring predo-
32
Human Immunodeficiency
Virus Infection (HIV) and Acquired
Immunodeficiency Syndrome (AIDS)
HISTORICAL BACKGROUND
AIDS was first recognized and described as a
clinical entity in mid 1981 when FriedmanKien and Gottlieb et al described groups of
gay (homosexual) men in the USA with
Kaposis sarcoma and pneumocystis carinii
pneumonia (PCP), both previously very rare
diseases and known to be linked to
immunosuppression.
In June 1983, Barr Sinoussi and Montagnier
of the Pasteur Institute in Paris reported the
discovery of a new virus isolated from a lymph
node of a gay (homosexual) man with
persistent lymphadenopathy. They called this
new virus lymphadenopathy associated
virus (LAV) and postulated that this was the
cause of AIDS.
In 1984, Gallo reported the isolation of a new
retrovirus that he called human T-cell
lymphotropic virus III (HTLV III). Serum
antibody testing for this virus was found to be
positive in almost 100% of AIDS patients.
In 1987, an international nomenclature
committee decided that the new virus should
be termed human immunodeficiency virus or
HIV rather than HTLV III or LAV.
In 1987, Clavel et al isolated a second
retrovirus from AIDS patients in West Africa,
MODE OF TRANSMISSION
HIV infection is primarily transmitted
through sexual route and less commonly
through blood transfusion, maternofetal
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Essentials in Dermatology
transmission, intravenous drug abuse, needle
stick injuries, etc.
In other words, HIV is transmitted through
semen and vaginal fluids, infected blood and
blood products, infected mother to her babybefore birth, during birth or through breast
milk.
Clinical features
CD4 count
(cells/uL)
Duration
(days)
150-800
3-14 days
2. Asymptomatic
Lymphadenopathy, headache
>300
2-10 years or
more
3. Early symptomatic
150-500
1-5 years
Late symptomatic:
50-200
Advanced: <50
Late
symptomatic:
1-4 years
Advanced:
<2 years
>500/mL (>29%)
A1
B1
C1
200 to 499/mL
(14% to 28%)
A2
B2
C2
<200/mL (<14%)
A3
B3
C3
Category A
Acute retroviral syndrome
Asymptomatic HIV infection
Persistent generalized lymphadenopathy
Category B
Symptomatic conditions occurring in a HIVinfected adolescent or adult that meet at least one
of the following criteria:
1. They are attributed to HIV infection or indicate
a defect in cell-mediated immunity
2. They are considered to have a clinical course
or management that is complicated by HIV
infection
Examples include, but are not limited to the
following:
Constitutional symptoms (fever of 38.5C
[101.3F], diarrhea >1 month)
Idiopathic thrombocytopenic purpura
Peripheral neuropathy Bartonella henselae,
B. quintana: bacillary angiomatosis
Category C
HIV encephalopathy
Progressive multifocal leukoencephalopathy
Lymphoma: Burkitts, immunoblastic or
primary CNS lymphoma
Mycobacterium avium-intracellulare complex
or M. kansasii infection: disseminated/
extrapulmonary
M. tuberculosis: pulmonary/ extrapulmonary
Mycobacterium: other species/ unidentified species - disseminated/ extrapulmonary
Pneumonia (recurrent with >2 episodes in
12 months)
Salmonella septicemia, recurrent (nontyphoid)
Candidiasis: esophageal, pulmonary
Cryptococcosis: extrapulmonary
Coccidioidomycosis: disseminated/
extrapulmonary
Histoplasmosis: disseminated/ extrapulmonary
Pneumocystis jiroveci (formerly carinii)
pneumonia
Herpes simplex virus infection:
esophageal, pulmonary, mucocutaneous
ulcers of >1 month duration
Cytomegalovirus: other than liver, spleen
or nodes
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Note
AIDS in HIV-infected adolescents and adults
aged >13 years defined by CDC includes any
one of the following criteria: (a) <200 CD4+ cells/
mL; (b) a CD4+ cell percentage of total
lymphocytes of <14 percent; or (c) any of the
following three clinical conditions: pulmonary
tuberculosis, recurrent pneumonia, or invasive
cervical cancer.
Adults
AIDS in an adult is defined by the existence of at
least two of the major signs associated with at
least one minor sign in the absence of known
Children
Pediatric AIDS is suspected in an infant or child
presenting with at least two major signs associated
with at least two minor signs in the absence of
other known causes of immunosuppression.
Major Signs
1 Weight loss or abnormally slow growth
2. Chronic diarrhea for more than 1 month
3. Prolonged fever for more than 1 month
Minor Signs
1. Generalized lymphadenopathy
2. Oropharyngeal candidiasis
3. Repeated common infections (otitis,
pharyngitis etc.)
4. Persistent cough for more than 1 month
5. Generalized dermatitis.
6. Confirmed maternal HIV infection.
Major Signs
a. Loss of weight or failure to thrive which is not
known to be due to medical causes other than
HIV infection.
b. Chronic diarrhea (intermittent or continuous)
> 1 month duration.
c. Prolonged fever (intermittent or continuous)
> 1 month duration.
Minor Signs
a. Repeat common infections (e.g. Pneumonitis,
otitis, pharyngitis etc.)
b. Generalized lymphadenopathy
c. Oropharyngeal candidiasis
d. Persistent cough for more than 1month
e. Disseminated maculo-papular dermatosis
II. Case Definition of AIDS in adults (for persons
above 12 years of age)
1. Two positive tests for HIV infection by ERS
test (ELISA/RAPID/SIMPLE) AND
2. Any one of the following criteria:
a. Significant weight loss (> 10% of body
weight) within last one month/Cachexia
(not known to be due to a condition other
than HIV infection). AND
Chronic diarrhea (intermittent or
continuous) > 1 month duration or
prolonged fever (intermittent or
continuous) > 1 month duration
b. Tuberculosis: Extensive pulmonary,
disseminated, miliary, extra-pulmonary
tuberculosis.
c. Neurological impairment preventing
independent daily activities, not known
to be due to the conditions unrelated to
HIV infection (e.g. trauma)
d. Candidiasis of the esophagus (diagnosable by oral candidiasis with odynophagia)
e. Clinically diagnosed life-threatening or
recurrent episodes of pneumonia, with or
without etiological confirmation
f. Kaposis Sarcoma
g. Other conditions: - Cryptococcal meningitis
- Neuro toxoplasmosis
- CMV retinitis
- Pencillium marneffei
- Recurrent herpes zoster or multidermatomal herpes infection
- Disseminated molluscum contagiosum
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Mucocutaneous Manifestations of
HIV Infection
Mucocutaneous diseases are amongst the first
recognized clinical manifestations of AIDS. Over
the past decade, it has become increasingly clear
that cutaneous disorders are not only associated
with terminal immunodeficiency but occur
throughout the course of HIV infection. This may
be due to impairment of the skin immune system
as evidenced by the reduced epidermal
Langerhans cell population, which explains the
development of opportunistic infections and
neoplasms of the skin and mucous membranes
in these patients.
Mucocutaneous disorders remain one of the
most important clinical markers of the stages of
HIV infection from time of seroconversion. They
range from urticarial viral exanthema to a myriad
of cutaneous opportunistic infections or
malignancies. They function as visual markers
in assessing the progression of HIV disease.
Cutaneous disorders occur more frequently as
HIV infection advances and immune function
deteriorates. They affect between 80% and 95% of
HIV infected patients. Cutaneous disorders
during HIV infection are numerous. Some have
drawn attention because of their onset, defines
some of the Center for Disease Control and
Prevention (CDC), acquired immunodeficiency
syndrome (AIDS) clinical categories, e.g. oral
candidiasis, zoster, herpes simplex, oral hairy
Treatment
There is no cure for AIDS at this time.
However, treatments are available that can
Fig. 32.4: Herpes genitalisnon-healing impetiginized ulcers over the glans penis and prepuce
Fig. 32.5: Oral hairy leukoplakiaun-removable white striations on the side and dorsa of tongue
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Fig. 32.10
Fig. 32.11
Figs 32.10 and 32.11: Extensive tinea corporis and cruris lesions in a HIV patient
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33
NRTI
NNRTI
PI
Azidothymidine(AZT)
Nevirapine (NVP)
Indinavir (IDV)
Stavudine (d4T)
Efavirenz (EFV)
Nelfinavir(NFV)
Didanosine (ddI)
Delaviridine(DLV)
Saquinavir(SQV)
Zalcitabine (ddC)
Ritonavir(RTV)
Abacavir (ABC)
Amprenavir(APV)
Tenofovir (TFV)
Lopinavir(LPV)
Emtricitabine(FTC)
Atazanavir(ATV)
Lamivudine (3TC)
Fosamprenavir(FPV)
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of HIV. Integrase inhibitors are occasionally
falsely classified as entry inhibitors.
However, unlike the latter, they do not
prevent entry of the virus into the cell.
6. Maturation inhibitors: The so-called
maturation inhibitors inhibit HIV replication
in a very late phase of the HIV reproduction
cycle, i.e., by the budding or maturation of
new virions. As is the case for integrase
inhibitors, 2005 can be counted as the
introductory year.
Stavudine (D4T) or
Azidothymidine (AZT)
+
Tenofovir (TFV)
or Abacavir (ABC)
+
Lamivudine (3TC)
Didanosine (ddI)
Nevirapine (NVP) or
Efavirenz (EFV)
Lopinavir(LPV)or
Saquinavir(SQV)
Column B
with
NVP
EFV
NFV
RTV + LPV
RTV + IDV
RTV + SQV
3-NRTI combinations
Abacavir + tenofovir + lamivudine
Didanosine + tenofovir + lamivudine
Zidovudine + lamivudine + abacavir
Pretreatment Evaluation
It is essential to confirm HIV results, complete
history and physical examination, treat OI (TB,
Toxoplasmosis, and cryptococcosis), complete
blood counts (CBC), chemistry profile, VDRL,
HBsAg. Assessment of readiness for treatment
and adherence is a must. It is desirable to get
CD4+ T-lymphocyte count and optional to get
plasma HIV RNA measurement if affordable.
For patients with pretreatment HIV RNA >1,000
copies/mL genotypic resistance testing prior to
initiation of therapy (BIII) should be considered;
if therapy is to be deferred, resistance testing may
still be considered (CIII).
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NNRTI
1. Rash-Nevirapine and delavirdine may cause
a slight rash in 15 to 20% of patients, 5 to 10%
of which discontinue treatment. The rash is
seen less frequently on efavirenz therapy,
where only 2 % of the patients discontinue
the drug. The NNRTI allergy is a reversible,
systemic reaction and typically presents as
an erythematous, maculopapular, pruritic
and confluent rash, distributed mainly over
the trunk and arms. Fever may precede the
rash. Further symptoms include myalgia
(sometimes severe), fatigue and mucosal
ulceration. The allergy usually begins in the
second or third week of treatment. Women
are more often and more severely affected. If
symptoms occur later than 8 weeks after
initiation of therapy, other drugs should be
suspected.
2. Stevens Johnsons Syndrome
3. TEN
4. Hepatitis-hypersensitive hepatitis often
occurs within the first 12 weeks. Liver toxicity
occurs more commonly in patients on
nevirapine than on other antiretroviral drugs.
5. Neuro-psychiatric-common in patients on
treatment with efavirenz. It includes
dizziness, insomnia, nightmares, mood
fluctuations, depression, depersonalization,
paranoid delusions, confusion and suicidal
ideation. These side effects are observed
mainly during the first days and weeks of
treatment. Discontinuation of therapy
becomes necessary in only 3 % of patients.
PI
1. Renal stones- occur particularly on indinavir
treatment,
Change of Therapy
Treatment Regimen Failure
Virologic failure can be defined as incomplete
or lack of HIV RNA response to antiretroviral
therapy:
Incomplete virologic response is defined as
repeated HIV RNA >400 copies/mL after 24
weeks or >50 copies/mL by 48 weeks in a
treatment-nave patient initiating therapy.
Virologic rebound is repeated detection of
HIV RNA after virologic suppression i.e.
repeated HIV RNA level >400 copies/mL
after prior suppression of viremia to <400
copies/mL.
Immunologic failure can be defined as failure
to increase the CD4 cell count by 25-50 cells/mm3
above the baseline count over the first year of
therapy, or a decrease to below the baseline CD4
cell count on therapy. Mean increases in CD4
cell counts in treatment-nave patients with
initial antiretroviral regimens are approximately
150 cells/mm3 over the first year.
Clinical progression can be defined as the
occurrence or recurrence of HIV-related events
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jerovecii pneumonia. IRIS may occur during or
shortly after the treatment of an opportunistic
infection or as a new clinical syndrome
resulting from a previously unrecognized occult
infection. Risk factors for IRIS include a low CD4
count (<50/ml), simultaneous (<30 days)
initiation of OI treatment and HAART, the
presence of latent infection(s), and a robust
virologic and immunologic response to HAART.
In addition to infectious pathogens, IRIS is
34
Leprosy has tormented humans throughout recorded history. The earliest possible account of a disease
that many scholars believe is leprosy appears in an Egyptian Papyrus document written around 1550
BC. Around 600 BC, Indian writings described a disease that resembles leprosy. In Europe, leprosy
first appeared in the records of ancient Greece after the army of Alexander the Great came back from
India and then in Rome in 62 BC coinciding with the return of Pompeiis troops from Asia Minor.
Danielssen and Boeck (1849)
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Oil of the chaulmoogra nut
Until the late 1940s, leprosy doctors all over the world
treated patients by injecting them with oil from the
chaulmoogra nut.
Shepard (1960)
Browne (1962)
Opromolla (1963)
First to use rifamycin SV (a potent antituberculosis drug) for the treatment of leprosy
Sheskin (1965)
In 2006.
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35
PRESENTING COMPLAINTS
History regarding skin patches, loss of sensation
over the patches, loss of sweating, pain in nerves,
loss of eyebrows/eyelashes, nasal stuffiness/
epistaxis, edema of legs, hoarseness of voice,
tingling and numbness in limbs, weakness of
hands and legs, eye pain/blurring of vision/
photophobia, joint pain/fever/malaise/flaring of
patches may be recorded.
PAST HISTORY
Whether, he had similar complaints in the past,
surgical correction of deformities, or lepra reaction
(type 1 or type 2).
TREATMENT HISTORY
CUTANEOUS EXAMINATION
FAMILY HISTORY
If any one in the family is suffering from leprosy,
needs to be enquired. Health status of family
members should be ascertained.
Personal History
It should focus on accommodation facility,
number of rooms available and number of
persons staying together.
GENERAL PHYSICAL EXAMINATION
One may look for pallor in longstanding
cases.
Hair loss in the form of ciliary madarosis,
superciliary madarosis and alopecia of
axillary and pubic hair may be noted in
lepromatous leprosy cases. Besides this, such
cases may show xanthelasma over the eyelids,
collapse of bridge of the nose or perforation of
the nasal septum.
Examination of mouth and pharynx may
show papules on lips, nodules on the tongue/
palate or palatal perforation.
Nails may demonstrate longitudinal ridges
and become dry, lustreless and shrunken.
Hands and feet may show disabilities and
deformities like wrist drop, foot drop, claw
hand/toes, ape thumb etc. Digits may have
autoamputation.
Testes may get involved and finally may
become atrophic.
Gynaecomastia and sparse beard may be an
indication of testicular involvement in
lepromatous leprosy cases.
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diagnosis is still in doubt take a biopsy from a
skin lesion or from an enlarged nerve that carries
only sensory fibers.
Decide
1. Does the patient have leprosy?
2. If so, where does his disease lie on the
spectrum?
3. What is the stage of activity?
Clinical Leprosy
36
Clinical Leprosy
Agent
Mycobacterium leprae was discovered by
Gerhard Henrik Armauer Hansen in 1873.
It is an acid-fast bacillus measuring 1 to 8
microns in length by 0.3 microns in diameter.
The capsule of lepra bacilli contains a
phenolic glycolipid 1 (PGL1) that renders it
chemically unique and antigenically specific.
It is an obligate intracellular parasite that
divides every 12-13 days in histiocyte and
schwann cells
The optimal temperature for growth for lepra
bacilli is 30-33 centigrade.
Incubation Period
It can show considerable variation and in most
instances between 2 and 5 years.
Mode of Spread
The various modes of spread are by inhalation,
direct contact, ingestion and insects.
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SPECTRUM OF LEPROSY
Ridley and Jopling classified leprosy taking into
account the immunological and histopathological
basis in addition to the clinical and bacteriological
findings. The classification divides leprosy into
Tuberculoid tuberculoid (TT)
Borderline tuberculoid (BT)
Borderline borderline /Mid borderline/
dimorphous leprosy (BB)
Borderline lepromatous (BL)
Lepromatous lepromatous (LL)
The two other types of leprosy, which does
not fall under Ridley and Jopling classification
but are included in Indian Leprologists
association classification are indeterminate and
polyneuritic leprosy.
Clinical Leprosy
Fig. 36.2: Borderline tuberculoid leprosy-hypopigmented hypoanesthetic macule with irregular well
defined margin
Borderline Lepromatous
Numerous but still countable lesions are seen
The copper colored macules, plaques and
nodules show a tendency towards symmetry
(Figs 36.5 and 36.6).
The lesions are shiny with minimal sensory
loss
Multiple peripheral nerves are thickened
Lepromatous Leprosy
Initially has cutaneous and mucosal lesions
Edema of lower legs and epistaxis are
considered early signs
The early skin lesions are macules which are
uncountable (Fig. 36.7)
The skin lesions are small, coppery colored,
numerous and symmetrically arranged
Over a period of time, the entire skin becomes
shiny and infiltrated, most often on the face,
especially forehead, ear lobes (Fig. 36.8),
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Clinical Leprosy
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Indeterminate Leprosy
Usually occurs as solitary, hypopigmented,
vaguely defined macules
Common in children
Sensory loss is equivocal
Most lesions heal spontaneously
Mitsuda negative patients are more likely to
develop lepromatous leprosy
Lucio Leprosy
Occurs in Mexico ( in South America), also
called as lepra bonita /beautiful leprosy
Diffuse infiltration occurs without distorting
the body contour
May mimic myxedema
Clinical Leprosy
DIAGNOSIS
Slit Skin Smear (SSS)
Consists of obtaining tissue smear from the
skin and staining with modified Ziehl-Neelsen
stain
Smear should be taken from six sites: both ear
lobes and four representative active skin
lesions
In case of single patch, smear should be taken
from two sites diagonally opposite to each
other
A SSS is positive if at least 104 bacilli are
present per gram of tissue
Grading of SSS is based on Ridleys
logarithmic scale
_ 1 to 10 bacilli in 100 fields -1 +
_ 1 to 10 bacilli in 10 fields -2 +
_ 1 to 10 bacilli in an average field -3 +
_ 10 to 100 bacilli in an average field -4+
_ 100 to 1000 bacilli in an average field -5 +
_ Clumps and globi in an average field -6+
(Fig. 36.16)
Bacteriological index gives a quantitative
measure of M. leprae from the skin
BI falls by 1 unit every year after starting the
patient on MDT
Morphological index is given as the
percentage of regularly stained bacteria
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LL Hansen- subepidermal zone is free (Grenz
zone) with diffuse infiltration of foamy
macrophages (Virchowcytes) in the dermis.
Abundant AFB, even globi may be seen.
DIFFERENTIAL DIAGNOSIS OF
LEPROSY
The first step towards diagnosing leprosy is to
think of the possibility of leprosy. The diagnosis
can easily be made if the case is classical i.e.,
having characteristic skin changes (hypopigmented patch with loss of sensation) and
nerve involvement, but this is not always the case.
Leprosy produce wide variety of clinical
situations depending upon the interaction
between M. leprae and hosts immune system such
as repeated epistaxes , paresthesias, mono or
unilateral neuralgia, muscle weakness, paralysis,
deformities, painless trauma or ulcer, chronic
asymptomatic skin lesions, madarosis, upgrading
and downgrading reactions, etc. Active leprosy
gives rise to either mono or polymorphous clinical
pictures where different skin lesions (macules,
papules, plaques, nodules, diffuse infiltration) are
variously assorted.
Before diagnosing a case of leprosy one should
be aware of following problems:
1. Bacteriological negative skin smear doesnt
rule out diagnosis.
2. AFB detection in nasal smear by itself is not
sufficient for diagnosis.
3. Lepromin test does not have any diagnostic
value.
4. Sometime, histopathological examination
may not show any evidence from suspected
leprosy lesions.
5. Leprosy presenting with only skin lesions or
nerve lesions
6. Contact with leprosy case can not be regarded
as diagnostic criteria.
Therefore to formulate a diagnosis of leprosy,
clinical, microbiological and histopathological
findings must be taken into account. The typical
Clinical Leprosy
predilection- scalp chest, back and face, presence
of pruritus helps in differentiating it from leprosy,
may have a history of cradle cap during infancy,
treatment with topical steroids and oral
antifungals like fluconazole helps in resolution),
gyrate erythemas-erythema chronicum migrans
(skin manifestation of Lymes disease, a
spirochete (Borrelia burgdorferi) infection, caused
by the bite of Ixodes ticks, starts as erythematous
macule at bite site, extends peripherally to become
annular lesion which may persist for months and
associated with fever, headache, myalgia and
arthralgia, titration of anti-Borrelia antibody helps
in diagnosis), erythema annulare centrifugum
(characterized by annular or polycyclic lesions
with raised erythematous border, cause is unclear
but in some cases hypersensitivity to tinea
infection or association with malignancy is
suspected, persists for weeks to months and tends
to recur over the years), erythema gyratum repens
(characterized by concentric raised erythematous
bands moving in waves over the body surface in
a wood-grain pattern at a speed of approximately 1 cm/day, always associated with
internal malignancy), erythema marginatum
(eruption has a serpiginous pink indurated
border, blanches on pressure and changes its
shape and is often hidden by the clothing, occurs
in association with rheumatic fever), erythema
multiforme (acute onset eruption in acral areas,
typical lesion is target lesion, recurrent form is
associated with herpes labialis)
Differential diagnoses of hypochromic macule
are nevus anemicus (a developmental anomaly,
presents as a circular patch of pale skin of normal
texture, does not flare on stroking, intradermal
injection of histamine produces a flare whereas
in leprosy the flare is delayed, feeble or entirely
absent), nevus depigmentosus (achromicus)
(birthmark, poorly demarcated hypopigmented
patches -resemble splashed paint in a dermatomal
pattern, diascopy does not show any change in
color at the edge), vitiligo (presents with
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annulare (presents typically with asymptomatic
papules arranged in a ring like fashion over the
hands and feet, disseminated lesions may
develop later on, these lesions may disappear after
a biopsy, the histology shows areas of necrosis
with collagen degeneration), granuloma
multiforme (can be confused with tuberculoid
type of leprosy, the lesions are seen on the
extremities-sun exposed areas as annular, with
well marked papular edges, evolving
simultaneously towards central healing,
coalescing of annular lesions gives rise to
circinate lesions, surroundings skin shows photo
damaging changes, the lesions persists
indefinitely or at least for several years), lichen
planus (a papulosquamous disorder characterized by itchy, violaceous flat topped, polygonal
papules especially on the flexor aspect of wrists,
shins and trunk), late secondary syphilis
(papules occur on the trunk and limbs in
secondary syphilis, associated with mucosal
erosions or snail track ulcers, Buschke
Ollendroff sign positive i.e. tenderness if lesion
is pressed with a blunt object in the center,
serological tests (VDRL) confirm the diagnosis,
histopathological examination shows endarteritis with plasma cell infiltrate, lesions
disappear in a few weeks if adequately treated
with penicillin or resolve in two months and pass
on to the early latent stage) and PKDL.
Differential diagnoses of nodular lesions are
Kaposis sarcoma (a vascular tumor characterized by the presence of bluish red or dark brown
plaques or nodules, on the distal portion of lower
extremities, may have lymph node involvement
and visceral lesions in 10 percent of patients, the
tumors may be associated with AIDS or human
herpes virus 8 (HHV8), histopathology shows
vascular formations with predominance of
endothelial cells and spindle cell formations
containing vascular slits), cutaneous
leishmaniasis (single or multiple nodules, seen
on the exposed parts i.e. at the site of insect bites.
Clinical Leprosy
granulomas with normal nerves), necrobiosis
lipoidica (observed with diabetes mellitus,
commonly over the legs and thighs as sharply
marginated, firm, depressed waxy, yellow brown
plaques with glistening surface and telangiectasia, heals with atrophy and scarring.
Histopathology shows palisading granuloma,
which is characteristic), late secondary syphilis,
mycosis fungoides (Cutaneous T cell lymphoma
(CTCL) affects the skin primarily, but ultimately,
lymph nodes and visceral organs are involved.
Skin lesions vary from erythematous patches to
plaques, tumors and erythroderma. Plaque stages
or tumor stages resemble lepromatous leprosy.
Skin biopsy shows lymphocytic infiltrate with
epidermotrophism. In the plaque stage, mycosis
cells may be seen along with a band like dermal
infiltrate), and Mycobacteria marinum infection
(Solitary erythematous nodule or plaque,
sometimes ulcerate and appear crusted, a skin
smear from the lesion may contain AFB similar in
appearance to M. leprae, but the organism can be
cultured on suitable media, a skin test using PPD
from M. marinum is positive). Other differential
diagnoses include parapsoriasis, sarcoidosis,
cutaneous leishmaniasis, erythema multiforme.
Differential diagnoses of diffuse infiltration of
the skin are lymphoma, actinic reticuloid (a
severe form of persistent photosensitivity
producing erythema, edema and thickness of the
skin on the face, neck and hands), systemic
sclerosis (patient develops a taut and thickened
skin which slowly becomes bound to
subcutaneous tissues, recurrent ulcerations
develop at the ends of fingers and terminal
phalanges become absorbed, polyarthritis of
small joints is common and finger contractures
may develop), myxedema (has many similarities
to lepromatous leprosy, thickening of the skin,
thinning of eyebrows, a hoarse voice, edematous
leg, normocytic normochromic anemia and carpal
tunnel syndrome as a complication), and
pachydermoperiostosis (a familial condition
Differential Diagnosis of
Regional Manifestations
Differential diagnosis of madarosis in
lepromatous leprosy is lymphoma, follicular
mucinosis, hypothyroidism, secondary syphilis
and alopecia areata.
Differential diagnoses of earlobe infiltration/
nodules in lepromatous leprosy is lupus vulgaris,
coccidioidomycosis, chondrodermatitis nodularis
helices, lupus erythematosus, sarcoidosis.
Differential diagnoses of deformity of nose
(cartilage destruction) in lepromatous leprosy,
leishmaniasis (cartilage destruction), tertiary
yaws, relapsing polychondritis and congenital
syphilis (bone destruction).
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and dropped foot. Late effects are loss of tendon
reflexes and trophic ulceration of feet, associated
with autonomic neuropathy leading to orthostatic
hypotension, diarrhea, loss of bladder control or
impotence. Histological examination discloses
amyloid infiltrating the affected nerves), familial
hypertrophic interstitial neuritis (Djerine
Sottas neuropathy) (Hereditary motor and
sensory neuropathy type 3, autosomal recessive,
has onset in childhood or adolescence,
characterized by slowly progressive muscular
atrophy of limbs, commencing distally with claw
hands, dropped foot, anesthesia and loss of
tendon reflexes).
Differential diagnosis of regional anaesthesia
with or without muscle wasting but with
palpable nerve thickening in some cases are
recurrent or chronic progressive (endotoxic)
polyneuritis (an acquired disorder of nerves,
cause unknown, symptoms first appear in adult
life and tendon reflexes are diminished or absent),
and peroneal muscular atrophy (Charcot
MarieTooth type) (an inherited disorder, onset
in childhood, with muscle weakness in lower
limbs, pes cavus, hammers toes and callosities of
feet, tendon reflexes of lower limbs are diminished
or absent).
Differential diagnosis of regional anaesthesia
with or without muscle wasting but without
palpable nerve thickening are syringomyelia
(anesthesia and muscle wasting develop in upper
or lower limbs depending on the localization of
the cord lesion, there is dissociated anesthesia loss of pain and temperature sensation with
preservation of touch, tendon reflexes are
diminished or lost, and the histamine test is
positive), tabes dorsalis (characterized by
dysfunction of posterior nerve roots has triad of
symptoms-lightning pain, dysuria and ataxia and
triad of signs-ArgyllRobertson pupils, areflexia
and loss of proprioception), peripheral
neuropathy (a mononeuropathy can result from
Clinical Leprosy
introduction of multidrug therapy (MDT) instead
of dapsone monotherapy in the year 1982,
following the recommendations of the WHO
study group. There has been a dramatic
downward revision of estimated number of
leprosy patients in the world from 10 to 12 million
in the mid 1980s to 0.62 million (point prevalence)
in 2001. Although these figures are highly
encouraging, the number of new cases detected
annually has remained quite stable during the
last 15 years. India harbours 65% of the world
population of leprosy patients. The total number
of registered cases in India has shown a steep
decline over the years, from 3.4 million cases in
1986 to 0.266 million cases in 2004.
The standard schedule of MDT for leprosy has
not undergone any change after its introduction
in 1982, except for the temporary introduction of
ROM therapy for single skin lesionpaucibacillary (PB) leprosy. However there have
been significant changes in the duration of
therapy and in the criteria for allocating patients
into PB and multibacillary (MB) groups for
therapy. At the time of introduction of MDT, in
1982, this allocation was based on the grading of
smear positivity, with patients with a
bacteriological index (BI) < 2 classified as PB
leprosy. In 1988 the WHO expert committee on
leprosy recommended that only initially smearnegative patients should be classified as PB. With
time, a division based on skin smear examination
was not considered suitable in field conditions
and a division based on the number of skin lesions
gained favour. In the last 22 years, an increasing
number of patients who were previously
classified as PB for treatment purposes, were
allocated to the MB group for treatment purposes,
with skin smear examination no longer
considered necessary for gouping. Patients with
more than 5 skin lesions are now being classified
as MB patients, and wherever facilities are
available for a slit skin smear examination, all
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Laboratory monitoring for drugs used to treat leprosy
Drug
Laboratory studies
Frequency
Clinical Leprosy
therapy is given with fixed duration of 6
months for PB and 12 months for MB cases.
4. U-MDT with fixed duration therapy of 6
months.
5. Monthly administered ROM for MB and PB
leprosy: Once a month ROM for 12 months in
MB and 6 months in PB leprosy cases.
6. Fully supervised regimes such as RMM
monthly regimes: Rifapentine + minocycline
+ moxifloxacin (monthly), RCM regimes:
Rifampicin + clarithromycin ( 1000mg) +
minocycline (200mg) monthly fully
supervised dose, Ampicilin/ sulbactum, or
Quadruple regime: Rifampicin (600mg) +
ofloxacin (400mg) + clofazamine (100mg) +
minocyclines (100mg) once weekly for 6
weeks. This regime is gaining importance.
REACTIONS IN LEPROSY
Reactions are acute episodes of hypersensitivity
reactions due to fluctuations in the immune
status of a leprosy patient. There are three types
of reactions; type 1 reaction, type 2 reaction and
Lucio phenomenon.
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Most important aspect of type 1 lepra reaction
is not the skin lesions but the condition of
peripheral nerves
Mild reaction can be managed with analgesics
Severe reaction and neuritis needs oral
steroids, commonly prednisolone is used in
the dose of 30 to 40 mg per day.
Other drugs used are cyclosporin,
azathioprine, clofazamine, intraneural
injections of lignocaine
Management of nerve abscess by aspiration
or neurolysis.
Lucio Phenomenon
Occurs in Lucio leprosy due to bacterial
endotoxins, precipitated by stress and strain
Characterized by painful, large, bizarre
ulceration of skin and is not accompanied by
systemic features (Fig. 36.21).
Clinical Leprosy
The lesions occur over legs, thighs and buttock
Starting of antileprosy treatment
Steroids and anti-inflammatory agents are
main stay of therapy.
COMPLICATIONS
Leprosy has been regarded as a dreaded and
stigmatizing disease, which can lead to gross
disabilities, deformities and mutilations.
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Fig. 36.25
Fig. 36.26
Figs. 36.25 and 36.26: Complications- shortening of digits of hands and feet in lepromatous leprosy
OCULAR LEPROSY
It is an important cause of preventable blindness
Due to direct leprous involvement: madarosis,
conjunctivitis, superficial punctate keratitis,
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All questions will be of objective type. Each
answer with correct response shall be
awarded one mark. There is negative marking.
More than one answer indicated against a
question will be deemed as incorrect response
Disadvantage of MCQs
It is important to note, however, what MCQs
cannot do. They cannot measure clinical performance or competence. They can occasionally be
used to test components of diagnostic reasoning
and problem solving. MCQs have also been
criticized for providing candidates with visual
clues that suggest a correct answer, one that
the candidate might not otherwise have recalled.
For some courses in JIPMER, Pondicherry,
they are combined with other test formats that
test different aspects of candidates performance
- for example, objective structured clinical
examinations, short answer questions, etc.
Marking Schemes for MCQs
There are two types of marking commonly
encountered in MCQs. These are negative
marking where marks are deducted for incorrect
answers and neutral marking where all
questions should be attempted - marks are given
for correct answers only and guessing is
encouraged. Negative marking was introduced
to reduce the amount of guessing by candidates
by punishing incorrect responses with a
negative mark.
STRATEGIES IN ATTEMPTING
MULTIPLE-CHOICE QUESTIONS
Strategy before the test
1. Try to gather as many examples as you can
of old papers and previous examples of
MCQs used by the department or school in
question in the past.
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6. Identify subject area: Identifying what
lecture, reading, or laboratory exercise the
question is from which might help you
narrow the choice of possible responses.
7. Identify what is being asked: Answer each
question as teacher intended, that is, within
the context of the course material that was
taught.
8. The cover up strategy: Some students find
it helpful to read the question and try to recall
the answer from memory before looking at
each of the four responses.
9. The true/false strategy: Identify if the
question is looking for a true or false
statement. Then label each of the four
responses as true or false and eliminate
those that do not correctly complete the
question.
10. Read each of the four responses: And do
not just stop when you come upon the one
that seems likely.
11. Do not select a response just because you
remember learning the information in the
course; it may be a true statement in its
own right, but not the best answer to the
question.
12. Do not dismiss a response because it
seems too obvious and simple an answer;
if you are well prepared for the test, some
of the questions may appear very straightforward.
13. Do not be persuaded by fancy terms in the
question; do not say to you, That sounds
impressive, so it must be the right answer.
As you read through the possible responses,
mark off the ones you know are wrong. This
will save time if you have to come back to the
question later.
Set I (1-400)
1. A patient is said to have AIDS when the
CD-4 count is
A. 200 to 499
B. <200
C. <100
D. <50
2. About autosomal dominant inheritance all
are true except
A. It is expressed in homozygotes
B. Always one parent is affected
C. 50% of children affected
D. Offspring of a non-diseased child of a
diseased parent will not have the mutant
gene.
3. Harlequin skin changes are associated
with
A. It is a normal phenomenon
B. Seen in ichthyosis
C. Septicemia
D. Atopic dermatitis
B. Systemic griseofulvin
C. Griseofulvin topically
D. Amphotericin
7. Grayish white vaginal discharge with
formation of bubbles is a feature of
A. Trichomoniasis
B. Bacterial vaginosis
C. Candida albicans
D. Gonorrhea
8. The most effective means of transfer of
HIV is
A. Sexual route
B. Perinatal route
C. Blood transfusion
D. Needle prick
9. Myiasis means
A. Infestation with Maggots
B. Infestation with fungi
C. Infestation with Bacillus anthracis
D. Infection with Bartonella hensalae
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13. All of the following are used in urticaria
except
A. Antihistamines
B. Topical glucocorticoids
C. Cyproheptadine
D. Hydroxyzine
14. Epstein Barr virus causes all of the
following diseases except
A. Burkitts lymphoma
B. Nasopharyngeal carcinoma
C. Hodgkins lymphoma
D. Kaposis sarcoma
33. A girl aged 19 with arthritis, alopecia, photosensitive rash on the cheek; diagnosis
A. SLE
B. DLE
C. Dermatomyositis
D. Systemic sclerosis
34. A child with itchy lesions of scabies over
the groin and the genitalia. What will not
to be advised?
A. Bathe and apply scabicidal
B. Treat family
C. Burn clothes
D. Antibiotics
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40. Genital elephantiasis is seen in
A. Donovanosis
B. Lymphogranuloma venereum
C. Herpes simplex
D. Syphilis
41. A patient, Gopi, had lepromatous leprosy.
Which of the following is true regarding
globi in leprosy?
A. Consists of lipid laden macrophages
B. Consists of macrophages filled with
bacteria
C. Consists of neutrophils filled with
bacteria
D. Degenerated neural tissue
42. All the following are sexually transmitted
infections except
A. Candida
B. Group B streptococcus
C. Hepatitis B
D. Echinococcus
43. Exfoliative dermatitis is seen in all the
following except
A. Pityriasis rosea
B. Pityriasis rubra pilaris
C. Psoriasis
D. Drug reaction
44. In a patient, annular erythematous lesions
on the trunk were seen circumscribed by
collarettes scales. The diagnosis is most
likely to be
A. Pityriasis versicolor
B. Pityriasis rosea
C. Pityriasis rubra pilaris
D. Lichen planus
45. Wickhams striae are seen in
A. Lichen sclerosis et atrophicus
B. Lichen planus
C. Lichen aureus
D. Lichen nitidus
46. A patient with psoriasis was started on
systemic steroids. After stopping treatment,
59. A child presents with a solitary white welldefined patch of his right thigh. What is
the diagnosis
A. Piebaldism
B. Nevus achromicus
C. Acral vitiligo D. Albinism
60. A patient gets recurrent urticaria while
doing exercising and on exposure to
sunlight. Which of the following is the most
likely cause
A. Chronic idiopathic urticaria
B. Universal dermographism
C. Cholinergic urticaria
D. Solar urticaria
61. Vasanti, a 28-year-old female, presents
with complaints of tightness of fingers.
There is also history of dysphagia. Which
of the following is the probable diagnosis?
A. Dermatomyositis
B. Scleroderma
C. Rheumatoid arthritis
D. Systemic lupus erythematosus
62. A lady approaches a physician for
contraceptive advice. On examination
there were two symmetrical painless ulcers
on vulva, which were well defined with a
firm base. Which of the following is the
most likely cause
A. Primary syphilis
B. Chancroid
C. Herpes genitalis
D. Malignancy
63. A girl presents with complaints of melena.
On examination there are pigmented
lesions involving her mouth and lips. Two
of her sisters also had similar complaints.
Which of the following is the most
probable diagnosis?
A. Cronkhite-Canada syndrome
B. Peutz Jeghers syndrome
C. Gardners syndrome
D. Behets syndrome
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64. A 30-year-old Basanti presents with light
brown lesions involving both her cheeks.
The lesions had never been erythematous.
Which of the following is the most
probable diagnosis
A. SLE
B. Chloasma
C. Air borne Contact Dermatitis
D. Photodermatitis
65. Babloo, 5 years old male, presents with
small hypopigmented scaly macules on his
cheek. Some of his classmates also have
similar lesions. Which of the following is
the most probable diagnosis
A. Pityriasis alba
B. Pityriasis rosea
C. Pityriasis versicolor
D. Indeterminate leprosy
66. Kallu, a 30-year-old man, presented with
subcutaneous itchy nodules over the left
iliac crest. On examination, they are firm,
non-tender and mobile. Skin snips contain
microfilaria and adult worms of
A. Loa Loa
B. Onchocerca volvulus
C. Brugia malayi
D. Mansonella perstans
67. All are true about Neisseria gonorrhea
except
A. Gram positive cocci
B. Causes stricture urethra
C. Involves seminal vesicles and spreads
to epididymis
D. Drug of choice is Ceftriaxone
68. A 30-year-old male, Kallu, with a history
of sexual exposure comes with a painless
granulomatous ulcer over the penis with
everted margins. The diagnosis is
A. Primary chancre
B. Chancroid
C. Lymphogranuloma venereum
D. Donovanosis
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85. Tinea capitis (Endothrix) is most
commonly caused by
A. T.mentagrophytes
B. E.floccosum
C. T.tonsurans
D. T.violaceum
86. Viable but not cultivable state is seen in
which of the following organisms
A. M leprae
B. M. tuberculosis
C. V. cholera
D. Staph. aureus
87. Regarding Henoch Schonlein purpura, all
are true except
A. Associated with glomerulonephritis
B. Palpable purpura
C. Decreased complement
D. Thrombocytopenia
88. Dyskeratosis is a feature of
A. Dariers disease
B. Pemphigus vulgaris
C. Psoriasis
D. Lichen planus
89. Regarding AIDS all are true except
A. Male to female transmission is more
common than vice versa
B. Condom provides 100% protection
C. Kissing is considered to be safe
D. Risk of transmission is more in the
presence of associated STDs
90. Staphylococcus aureus classically
causes
A. Impetigo contagiosa
B. Furuncle
C. Ecthyma
D. Blistering dactylitis
91. Which of the following is/are associated
with Swimming pool granuloma?
A. M. marinum
B. M. avium complex
C. M. ulcerans
D. M. Chelonae
C. Trichomonas vaginalis
D. Leishmania brasiliensis
107. A smear from a genital lesion shows
Donovan bodies. The diagnosis is
A. Lymphogranuloma venereum
B. Chancroid
C. Granuloma inguinale
D. Primary chancre
108. The minimum period of treatment for
multi-bacillary leprosy is
A. 1 year
B. 2 years
C. 6 months
D. 9 months
109. Refsums disease is due to defect in
enzyme
A. Phytanic acid oxidase
B. Nicotinamide-adenine dinucleotide
oxidoreductase.
C. Homogentisic acid oxidase
D. Tyrosinase
110. Vesicular lesion is seen in
A. Primary syphilis
B. Secondary syphilis
C. Tertiary syphilis
D. Congenital syphilis
111. A patient comes with recurrent abdominal
pain, and urinary examination reveals
Ehrlich aldehyde test (+) for urobilinogen.
The diagnosis is
A. Porphyria
B. Renal calculi
C. Cholelithiasis
D. Angina pectoris
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C. Asteatotic eczema
D. Seborrheic dermatitis
C. Staphylococci
D. Pneumococci
134. Endotoxins are implicated in all except
A. Psoriasis
B. Kawasaki disease
C. Atopic dermatitis
D. Seborrheic dermatitis
135. Skin lesions caused by Staphylococcus
aureus include all except:
A. Bullous impetigo
B. Staphylococcal scalded skin syndrome
C. Scarlet fever
D. Furuncle
136. Ecthyma gangrenosum is caused by
A. Staphylococcus aureus
B. Pseudomonas aeruginosa
C. Streptococcal infection
D. All of the above
137. The most common site of carbuncle
A. Nape of neck
B. Thigh
C. Face
D. Legs
138. Botryomycosis is due to
A. Bacteria
B. Fungi
C. Protozoa
D. Algae
139. Toxic shock syndrome; all are true except
A. Exotoxins producing strain of S.aureus
B. Seen in menstruating women
C. Fever, hypotension and rash are seen
D. Pastias lines are present
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C. DIC occurs in this condition
D. All are true
142. Pitted keratolysis is caused by
A. Micrococcus sedentarius
B. Dermatophilus congolensis
C. Corynebacterium
D. All the above
143. Erythrasma, all are true except
A. Caused by corynebacterium minutissimum
B. It is a gram negative rod
C. Coralred fluorescence is seen with
woods lamp
D. It is treated using clotrimazole cream
144. All are true of trichomycosis axillaris
except
A. It is caused by fungus
B. Nodular thickening of hair shaft present
C. It involves axilla commonly
D. Treatment is shaving
145. Russell bodies are seen in
A. Rhinoscleroma
B. Leishmania
C. Syphilis
D. Leprosy
146. All are true about bacillary angiomatosis
except
A. Caused by B. henselae and B. quintana
B. Seen in AIDS patients
C. Diagnosed by Warthin Starry stain
D. Treatment is by ciprofloxacin
147. All are seen in anthrax except
A. Malignant pustule is seen
B. It is usually painful
C. Parenteral crystalline penicillin is the
drug of choice
D. Incision and debridement should be
avoided
148. Apple jelly nodules are seen in
A. Sarcoidosis
B. Lupus vulgaris
C. Leprosy
D. Cat-scratch disease
149. Scrofuloderma involves all except
A. Lymph nodes B. Bone and joints
C. Epididymis
D. Penis
150. Buruli ulcer is caused by
A. M. ulcerans
B. M. marinum
C. M. bovis
D. M. leprae
151. About staphylococcal scalded skin
syndrome all are true except
A. It is caused by phage II S. aureus
B. It is a exotoxin mediated condition
C. Can be seen in infants and adults
D. Diagnosis is by demonstration of
staphylococcus by gram stain
152. All are true about Orf except
A. Ecthyma contagiosum is a synonym
B. Caused by parapox virus
C. Treatment is acyclovir
D. Disease widespread in sheep and goats
153. All are true of molluscum contagiosum
except
A. May be seen in HIV infection
B. Umbilicated vesicles are characteristic
C. Caused by molluscipox virus
D. Treatment is by curettage
154. Papular purpuric gloves and sock
syndrome is caused by
A. EBV
B. Parvovirus B19
C. HSV
D. HPV
155. Gianotti Crosti syndrome is due to
A. Hepatitis B
B. Coxsackie virus
C. EBV
D. All of the above
156. Forscheimers sign is seen in
A. Polio
B. Rubella
C. Toxoplasma
D. Roseola infantum
C. Pemphigoid
D. PLE
164. Drug induced pemphigus is seen in all
except
A. Penicillamine
B. Rifampicin
C. Chloroquine
D. Captopril
165. Acantholysis is seen in
A. Epidermis
B. Dermis
C. Dermal-epidermal junction
D. Subcutaneous tissue
166. Subepidermal bulla is seen in
A. Pemphigus vulgaris
B. Pemphigoid
C. Hailey Hailey disease
D. Transient acantholytic dermatoses
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B. Dermatitis herpetiformis
C. Pemphigus vulgaris
D. Friction blister
172. Acantholysis is due to dissolution of
intercellular cement substance in the
A. Epidermis
B. Sub-epidermis
C. Dermis
D. Basement membrane
173. A 60 years old man presented with itchy
tense hemorrhagic blisters over thigh and
lower abdomen without any oral lesions
diagnosis
A. Bullous pemphigoid
B. Pemphigus
C. Both A and B
D. Dermatitis herpetiformis
174. Koebner phenomenon seen in
A. Lupus erythematosus
B. Syphilis
C. Lupus vulgaris
D. Psoriasis
175. Not transmitted sexually
A. Syphilis
B. Yaws
C. Gonorrhea
D. Chancroid
176. Diagnostic method of choice in contact
dermatitis
A. Tzanck test
B. Intradermal test
C. Skin biopsy
D. Patch test
177. Patch test read after
A. 12 hours
B. 24 hours
C. 48 hours
D. 72 hours
178. Tzanck cell is a
A. Keratinocyte
C. Neurtrophil
B. Lymphocyte
D. All of the above
Psoriasis of nails
Lichen planus nails
Clubbing
Dermatophyte infection of nails
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207. CREST syndrome contains all except
A. Calcinosis
B. Raynauds phenomenon
C. ECG changes
D. Sclerodactyly
208. Scl-70 is characteristic of
A. CREST syndrome
B. Diffuse systemic sclerosis
C. Diabetes mellitus
D. SLE
209. All are seen in mixed connective tissue
disease except
A. Sausage digits
B. Anti U1-RNP positive
C. Pulmonary involvement in common
D. Usually of infective origin
210. Bywaters lesion, a nail fold infarct, is seen
in
A. Rheumatoid arthritis
B. Psoriatic arthritis
C. Gonococcal arthritis
D. Osteoarthritis
211. Components of antiphospholipid
syndrome except
A. Recurrent abortions
B. Arterial and venous thrombosis
C. High VDRL
D. A-partial prothrombin time decrease
212. What is vagabonds disease
A. Pediculosis corporis
B. Pediculosis pubis
C. Scabies
D. Tinea cruris
213. Treatment of pediculosis includes
A. Permethrin
B. Cotrimoxazole
C. Physostigmine ointment
D. All of the above
214. Treatment of scabies includes all except
A. 5% Permethrin
B. 1% Lindane
C. 0.5% Malathion
D. 10% Sulphur
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C. T. tonsurans
D. T. schoenleinii
235. Bullous impetigo is caused by
A. Staphylococcus aureus
B. Streptococcus pyogenes
C. Streptococcus epidermidis
D. Streptococcus haemolyticus
236. The mean incubation period of varicella is
A. 7 days
B. 14 days
C. 21 days
D. 28 days
237. A subcutaneous tuberculosis leading to
cold abscess formation and secondary
break down of the overlying skin is referred
to as
A. Lupus vulgaris
B. Scrofuloderma
C. Tuberculosis verrucosa cutis
D. Orificial tuberculosis
C. Seborrhoeic keratosis
D. Bowenoid keratosis
242. Vitiligo involving distal digits and
periorificial areas is named as
A. Vitiligo vulgaris
B. Acrofacial vitiligo
C. Focal vitiligo
D. Universal vitiligo
243. Acute vesicular eczema of hands and feet
is known as
A. House wife dermatitis
B. Nummular eczema
C. Atopic eczema
D. Pompholyx
244. Most common photodermatosis is
A. Polymorphic light eruption
B. Actinic prurigo
C. Hydroa vacciniformis
D. Chronic actinic dermatitis
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265. The commonest type of basal cell
carcinoma is
A. Ulcerative
B. Pigmented
C. Morphoeic
D. Nodulo cystic/ Nodulo-ulcerative
266. Urticaria pigmentosa is characterized by
excessive accumulation in many tissues
A. Macrophages B. Fibroblasts
C. Mast cells
D. Langerhans cells
267. Increased sebum secretion and formation
of horny plugs in follicular lumens are the
earliest abnormalities in
A. Seborrheic dermatitis
B. Sebopsoriasis
C. Acne rosacea
D. Acne vulgaris
268. Wickhams striae on the flat topped
polygonal purple colored papule are
typical of
A. Lichen planus
B. Psoriasis
C. Pityriasis rubra pilaris
D. Pityriasis rosea
269. The nails are often affected and may show
the so called thimble pitting in
A. Lichen planus
B. Psoriasis
C. Pityriasis rubra pilaris
D. Pityriasis rosea
270. The definitive technique for diagnosing
allergic contact hypersensitivity is
A. Intradermal test
B. Patch test
C. RAST test
D. Lymphocyte transformation test
271. Raised level of serum IgE and its
relationship with severity of eczema is a
feature of
A. Nummular eczema
B. Asteatotic eczema
C. Atopic dermatitis
D. Seborrheic dermatitis
272. White dermographism is typically seen in
A. Angioedema
B. Urticaria
C. Contact dermatitis
D. Atopic dermatitis
273. Gluten enteropathy is a feature of the
following blistering disorder
A. Bullous pemphigoid
B. Epidermolysis bullosa
C. Pemphigus vulgaris
D. Dermatitis herpetiformis
274. Target like lesions are commonly
encountered in
A. Erythema annulare centrifugum
B. Erythema marginatum
C. Erythema nodosum
D. Erythema multiforme
275. Pediculosis capitis is recognized by louse
eggs stuck to hair called as
A. Hair casts
B. Hair beading
C. Piedra
D. Nits
276. The best sites on which to find scabies
burrows are
A. Interdigital areas of the fingers
B. Soles
C. Abdomen
D. Back
277. Herpes zoster caused by varicella zoster
virus is primarily due to
A. Primary infection of virus
B. Autoinoculation of virus
C. Reactivation of virus
D. Re-infection of virus
278. Common warts of hands and fingers are
also known as
A. Myrmecia warts
B. Plane warts
C. Mosaic warts
D. Verruca vulgaris
C. Miliaria pustulosa
D. Miliaria profunda
286. Tinea capitis caused by Microsporum
species, under Woods lamp demonstrates
A. Bluish green fluorescence
B. Yellow fluorescence
C. Coral red fluorescence
D. Pink fluorescence
287. Dendritic cells among keratinocytes of the
stratum spinosum of the epidermis,
having distinct folded nucleus and Birbeck
granules are
A. Langerhans cells
B. Melanocytes
C. Merkel cells
D. Fibroblasts
288. Deep seated vesicles resembling tapioca
on the sides of the fingers, palms and soles
characterize
A. Pompholyx
B. Nummular eczema
C. Atopic dermatitis
D. Xerotic eczema
289. Erythema nodosum leprosum occurs in
half of patients with
A. Indeterminate leprosy
B. Tuberculoid leprosy
C. Borderline tuberculoid leprosy
D. Borderline lepromatous or lepromatous
leprosy
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292. Slit skin smear examination is used to
demonstrate organisms from the skin in
A. Pyoderma
B. Leishmaniasis
C. Donovanosis
D. Leprosy
293. A drug eruption which recurs at the same
site/s and heals with slate gray pigmentation is
A. Erythema multiforme
B. Stevens Johnson syndrome
C. Toxic epidermal necrolysis
D. Fixed drug eruption
294. A small solid elevated lesion smaller than
0.5 cm in diameter is called as
A. Macule
B. Papule
C. Vesicle
D. Nodule
295. If touching of the papule of secondary
syphilis with the head of a pin is exquisitely
tender, then sign said to be positive is
A. Ollendorfs sign
B. Auspitzs sign
C. Nikolskys sign
D. Button holing sign
296. Sharply localized oedema or wheal with a
surrounding erythematous flare occurring
within seconds to minutes after the skin
has been stroked, characterize
A. Dermatographism
B. Cholinergic urticaria
C. Pressure urticaria
D. Adrenergic urticaria
297. A collarettes of dermatitis in the V area
of neck called Casals necklace is seen in
A. Vitiligo
B. Ichthyosis
C. Contact dermatitis
D. Pellagra
298. Henderson-Paterson
bodies
are
intracytoplasmic, ovoid inclusion bodies
which are demonstrated in lesions of
A. Herpes simplex
B. Herpes zoster
C. Molluscum contagiosum
D. Warts
299. Thalidomide is the drug of choice in the
treatment of
A. Type 1 upgrading lepra reaction
B. Type 1 downgrading lepra reaction
C. Type 2 lepra reaction
D. Lucio phenomenon
300. Drug of choice for erythrasma is
A. Dapsone
B. Griseofulvin
C. Ketoconazole
D. Erythromycin
301. In secondary syphilis, chancre is still
present and active in
A. 3% cases
B. 33% cases
C. 63% cases
D. 93% cases
302. This type of eruption is not a feature of
secondary syphilis
A. Macules
B. Papules
C. Vesicles
D. Pustules
303. The Woods light examination of
erythrasma shows fluorescence which is
A. Coral red
B. Yellow
C. Blue
D. Green
304. A new effective topical agent available for
the treatment of scabies is
A. Calcipotriol
B. Mupirocin
C. Permethrin
D. Azelaic acid
305. Circle of Hebra is related to
A. Impetigo
B. Syphilis
C. Scabies
D. Leprosy
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320. The manifestations of leprosy depends on
the degree of
A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
321. The main cell of the epidermis is the
A. Keratinocyte
B. Dendrocyte
C. Melanocyte
D. Langerhans cell
322. Collagen is the major structural protein of
the dermis forming
A. 30-40% of its dry weight
B. 40-50% of its dry weight
C. 60-70% of its dry weight
D. 70-80% of its dry weight
323. A localized area of colour change in the
skin without elevation or infiltration is
called as
A. Papule
B. Nodule
C. Macule
D. Plaque
324. KOH mount of skin scraping demonstrates
spaghetti and meat balls in
A. Tinea versicolor
B. Tinea corporis
C. Tinea nigra
D. Tinea capitis
325. The generalized eruption is preceded in
most patients by the appearance of a
herald patch in
A. Psoriasis vulgaris
B. Lichen planus
C. Pityriasis rosea
D. Secondary syphilis
326. The commonest Mycobacterium tuberculosis skin infection is
A. Lupus vulgaris
B. Scrofuloderma
C. Warty tuberculosis
D. Tuberculosis cutis orificialis
327. Human papilloma virus subtypes 6, 11, 16,
and 18 are associated with
A. Plantar warts
B. Plane warts
C. Common warts
D. Genital warts
328. The drug that given systemically is not
effective in the treatment of tinea
versicolor is
A. Griseofulvin
B. Ketoconazole
C. Fluconazole
D. Itraconazole
329. The most common opportunistic fungal
infection in all stages of HIV disease is
A. Candidiasis
B. Cryptococcosis
C. Histoplasmosis
D. Coccidioidomycosis
330. Malar rash is a characteristic feature of
A. Dermatomyositis
B. Systemic lupus erythematosus
C. Systemic sclerosis
D. Rheumatoid arthritis
331. Incubation period of gonococcal urethritis
is usually
A. 2-5 days
B. 5-15 days
C. 15-20 days
D. 20-25 days
332. Commonest pathogen involved in nongonococcal urethritis in males is
A. Chlamydia trachomatis
B. Ureaplasma urealyticum
C. Trichomonas vaginalis
D. Herpes simplex virus
333. Postherpetic neuralgia is a complication of
A. Herpes simplex virus infection
B. Varicella
C. Herpes zoster
D. Cytomegalovirus infection
C. Pityriasis rosea
D. Eczema
341. Clue cells in vaginal discharge is the
diagnostic feature of
A. Bacterial vaginosis
B. Vaginal trichomoniasis
C. Candida vulvovaginitis
D. Gonococcal cervicitis
342. The causative agent of donovanosis is
A. Leishmania donovania
B. Leishmania ethiopica
C. Calymmatobacterium granulomatis
D. Borrelia burgdorferi
343. Actinomycosis is caused by
A. Actinomyces israelii
B. Madurella grisea
C. Madurella mycetomatis
D. Histoplasma capsulatum
344. The commonly employed test in the
diagnosis and monitoring of disease
activity of syphilis is
A. VDRL
B. TPHA
C. FTA-ABS test
D. ELISA test
345. Which one of the following is not true in
lepromatous leprosy
A. Lepromatous leprosy initially has
cutaneous and mucosal lesions
B. Neural changes in lepromatous leprosy
occur later
C. The skin lesions are numerous and
symmetrically arranged
D. Lepromin test is positive
346. Conclusive proof of leprosy is the
demonstration of a granuloma or the
presence of acid fast bacilli in
A. Nerves
B. Arrector pilorum muscle
C. Sweat glands
D. Sebaceous glands
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347. Erythema nodosum leprosum occurs most
commonly in lepromatous leprosy and less
frequently in
A. Borderline lepromatous leprosy
B. Borderline tuberculoid leprosy
C. Tuberculoid leprosy
D. Indeterminate leprosy
348. Which one of the following is not true in
histoid leprosy
A. Histoid leprosy is a distinctive variant
of borderline lepromatous leprosy
B. It frequently follows incomplete
chemotherapy or acquired drug
resistance
C. It is characterized by the occurrence of
well demarcated cutaneous and
subcutaneous nodules
D. Histoid leprosy lesions show the highest
loads of bacilli and the majority are solid
staining
349. Impetigo contagiosa is primarily an
endemic disease of
A. Adults
B. Adolescents
C. School children
D. Preschool children
350. A way to screen for therapeutic agents and
to identify drug resistance in leprosy was
provided by the limited growth of
Mycobacterium leprae in the
A. Mouse foot pad
B. Armadillo
C. Monkey
D. Nude mice
351. The classical staining method for
demonstrating leprosy bacilli in lesions
is
A. Giemsa Staining
B. Leishman staining
C. Modified Ziehl Neelsen staining
D. Grams staining
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370. Diascopy is most useful in detection of
nonblanchable raised purpura, the clinical
hallmark of
A. Cutaneous vasculitis
B. Hallo nevus
C. Nevus achromicus
D. Nevus flammeus
371. An infant was brought by his mother with
complaints of asymptomatic recurrent
blistering over occiput, buttocks, legs and
back of 2 months duration. Some of the
blisters spontaneously healed on their
own. Mucosa, nails and hair were normal.
Your diagnosis.
A. Pemphigus vulgaris
B. Epidermolysis bullosa
C. Miria
D. Neonatal lupus erythematosus
372. Papillary tip microabscesses are seen in
A. Pemphigus vulgaris
B. Bullous pemphigoid
C. Dermatitis herpetiformis
D. Dermatitis repens
373. A 60-year-old male was admitted to the
dialysis unit for chronic renal failure. Few
days later he developed blisters over the
dorsa of hands. On examination his blood
sugar was 342 mg%, serum creatinine 5
mg%, serum potassium 5mg/dL, Hb: 6.0
mg%, and urine porphyrin level was
normal. Your diagnosis.
A. Diabetic bullae
B. Pseudoporphyria
C. Pemphigus vulgaris
D. Bullous SLE
374. All are techniques in the investigation of
blistering disorder
A. Immunofluorescence
B. Immunoblotting
C. Electron microscopy
D. All of the above
C. Trichotillomania
D. Traction alopecia
389. An eight-year-old child has multiple
yellow crusts over the scalp of 2 months
duration. KOH examination of the crusts
yielded multiple air spaces with hyphae.
Woods lamp shows grayish fluorescence.
What is your diagnosis?
A. Favus
B. Kerion
C. Black dot tinea capitis
D. Gray patch tinea capitis
390. An ideal treatment of kerion to avoid
scarring is
A. Griseofulvin
B. Oral steroids
C. Shaving
D. A and B
391. What is calabar swelling?
A. Loiasis
B. Onchocerciasis
C. Trypanosomiasis
D. Insect bite
392. A 25-year-old HIV seropositive male
presented with fever, abdominal
distension, cough, dyspnea and mental
changes. On examination a petechial rash
around the umbilicus is seen. Few linear
tracks are seen around the trunk. How do
you establish your diagnosis?
A. Stool examination
B. Chest X-ray
C. Urine examination
D. Ultrasound abdomen
393. Larva currens is due to
A. Strongyloidiasis
B. Ancylostomiasis
C. Uncinaria
D. Bubostomum
394. Leopard skin is seen in
A. Onchocerciasis
B. Loiasis
C. Mycosis fungoides
D. Psoriasis
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395. All are true of Refsums disease except
A. Autosomal dominant
B. Phytanic acid oxidase deficiency
C. Sensorineural deafness is present
D. Chlorophyll should be avoided in diet
396. About acanthosis nigricans all are true
except
A. Seen in obese individuals
B. Individual diabetes is insulin sensitive
C. Seen in with use of nicotinic acid
D. Associated with adenocarcinoma
397. Opera glass deformity is seen in
A. Rheumatoid arthritis
B. Osteoarthritis
C. Psoriatic arthritis
D. Ankylosing spondylitis
398. Bowens disease is associated with
poisoning
A. Mercury
B. Selenium
C. Arsenic
D. Chromium
399. Koebner phenomenon is seen in all
except
A. Psoriasis
B. Xanthoma
C. Lichen planus D. Pityriasis rosea
400. In Munros microabscess, the inflammatory cell involved is
A. Neutrophil
B. Lymphocyte
C. Monocyte
D. Eosinophil
Set II (1-245)
1. Nodules are morphologically similar to
papules, but they are more than____in
diameter
A. 0.5 cm
B. 1 cm
C. 1.5 cm
D. 2 cm
2. Distinct intracytoplasmic organelles called
Birbeck granules characterize
A. Keratinocytes B. Langerhans cells
C. Melanocytes
D. Mast cells
3. Functionally, Langerhans cells are of the
monocyte macrophage lineage and
originate in
A. Thymus
B. Neuroectoderm
C. Bone marrow D. Lymph nodes
4. The sebaceous glands in the buccal
mucosa and vermilion border of the lip are
termed as
A. Meibomian glands
B. Montgomerys tubercles
C. Tysons glands
D. Fordyce spots
5. Finger nails grow on an average of 0.1 mm
per day, require about_____ to replace a
complete nail plate
A. 1-2 months
B. 2-3 months
C. 3-4 months
D. 4-5 months
6. By far, the most common cutaneous
symptom of skin disorders is
A. Pruritus
B. Pain
C. Burning sensation
D. Allodynia
7. Pruritus induced by temperature changes
in polycythemia vera is immediately
relieved by
A. H1 antagonists B. H2 antagonists
C. Aspirin
D. Ketotifen
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14. Reiters syndrome is a characteristic clinical
triad consisting of urethritis, conjunctivitis
and _____
A. Arthritis
B. Carditis
C. Neuritis
D. Uveitis
15. Impetigo of the scalp is a frequent
complication of
A. Pityriasis capitis
B. Scalp psoriasis
C. Pediculosis capitis
D. Seborrheic dermatitis
16. Treatment of choice for erythrasma is
A. Systemic erythromycin
B. Topical erythromycin
C. Topical clindamycin
D. Topical tolnaftate solution
17. Ecthyma gangrenosum which occurs in
debilitated persons, usually occurs as a
manifestation of sepsis by
A. Escherichia coli
B. Streptococcus faecalis
C. Clostridium septicum
D. Pseudomonas aeruginosa
18. Granuloma inguinale is caused by the
gram negative bacterium
A. Calymmatobacterium granulomatis
B. Haemophilus ducreyi
C. Bartonella henselae
D. Yersinia pestis
19. A rare form of secondary syphilis
presenting with severe ulcerations,
pustular or rupioid lesions accompanied
by severe constitutional symptoms is
known as
A. Condylomata lata
B. Pustular syphilid
C. Lues maligna
D. Rupial syphilid
C. Phosphorylase
D. Tyrosinase
33. Satellite macules are characteristic
of_________
A. Tuberculoid leprosy
B. Borderline tuberculoid leprosy
C. Borderline borderline leprosy
D. Borderline lepromatous leprosy
34. Larva currens is caused by__________
A. Ascariasis
B. Toxocara
C. Strongyloides
D. Ancylostoma
35. Circle of Hebra is associated with
A. Scabies
B. Pediculosis
C. Myiasis
D. Psoriasis
36. The intraepidermal split in pemphigus
vulgaris due to acantholysis is ______
A. Subcorneal
B. Stratum spinosum
C. Suprabasal
D. Subepidermal
37. Munro microabscess, a histopathological
feature of psoriasis is seen in
A. Stratum corneum
B. Stratum spinosum
C. Stratum granulosum
D. Stratum basale
38. Dennie Morgan fold is a clinical feature
of_________
A. Seborrheic dermatitis
B. Prurigo simplex
C. Atopic dermatitis
D. Allergic contact dermatitis
39. Heliotrope rash is a characteristic
periorbital rash of ____________
A. Dermatomyositis
B. Scleroderma
C. Sjogrens syndrome
D. Systemic lupus erythematosus
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40. Red grains of mycetoma are produced
by_____________
A. Actinomadura madurai
B. Actinomadura pelletieri
C. Nocardia
D. Streptomyces somaliensis
41. Ultra structurally, Langerhans cells are
characterized by a folded nucleus a n d
distinct intracytoplasmic organelles called
A. Keratohyaline granules
B. Birbeck granules
C. Melanosomes
D. Odland bodies
42. Mast cell granules stain metachromatically
because of their high content of
A. Heparin
B. Histamine
C. Tryptase
D. Prostaglandin D2
43. Variously sized, circumscribed changes in
skin colour without elevation or depression
are named as
A. Nodules
B. Papules
C. Wheals
D. Macules
44. Chancroid is an infectious contagious,
ulcerative sexually transmitted disease
caused by
A. Treponema pallidum
B. Chlamydia trachomatis
C. Herpes simplex virus
D. Haemophilus ducreyi
45. A neurosis characterized by an abnormal
urge to pull out the hair is known as
A. Dermatothlasia
B. Dysmorphophobia
C. Trichotillomania
D. Neurotic excoriation
46. Sixty percent of cases of atopic dermatitis
present in the
A. First year of life
B. Neisseria gonorrheae
C. Trichomonas vaginalis
D. Hemophilus ducreyi
59. Presence of clue cells in vaginal
discharge Gram stained smear is highly
diagnostic of
A. Candidiasis
B. Bacterial vaginosis
C. Trichomoniasis D. Donovanosis
60. Wet mount is mainly used for the diagnosis
of
A. Bacterial vaginosis
B. Candidiasis
C. Trichomoniasis
D. Donovanosis
61. Which test is indicated for the smear
diagnosis of genital herpes
A. Gram stained smear
B. Wet mount
C. Tzanck smear
D. KOH wet mount
62. Whiff test or Sniff test is diagnostic of
A. Candidiasis
B. Bacterial vaginosis
C. Trichomoniasis D. Gonorrhea
63. Acetic acid test is used to detect the
subclinical genital infection
A. Human papilloma virus infection
B. Herpes simplex virus infection
C. Donovanosis
D. Molluscum contagiosum
64. Dory flap sign due to hard chancre on
the inner surface of prepuce is a feature
of
A. Donovanosis
B. Chancroid
C. Herpes genitalis
D. Primary chancre
65. Wide spread eruptions of secondary
syphilis are characteristically
A. Non vesicular and non pruritic
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Essentials in Dermatology
B. Vesicular
C. Pruritic
D. Vesicular and pruritic
66. The commonest sites of condyloma lata are
perianal, vulva and
A. Perineal region
B. Angles of mouth
C. Axillae
D. Between toes
67. Lues maligna, an explosive form of
syphilis is also known as
A. Pustular syphilide
B. Malignant syphilis
C. Papular syphilide
D. Macular syphilide
68. The fetus may be born apparently normal,
but develops signs of early congenital
syphilis during the first few weeks or
months, called as
A. Didays law
B. Kassowitz law
C. Colles law
D. Profetas law
69. Syphilitic infant may not infect its own
mother but is capable of infecting others.
This observation is known as
A. Colles law
B. Profetas law
C. Didays law
D. Kassowitz law
70. Hutchinsons triad of late congenital
syphilis consists of interstitial keratitis,
Hutchinsons teeth and
A. Cluttons joints
B. Wimbergers sign
C. Eighth nerve deafness
D. Saber tibia
71. Parenteral is the treatment of
choice for the treatment of all stages of
syphilis
A. Sulphonamide
B. Penicillin
C. Cephalosporins
D. Macrolides
C. Macrophages
D. Monocytes
84. Tzanck smear from the base of a vesicle or
erosion of herpes genitalis may show
A. Foreign body giant cells
B. Langhans giant cells
C. Touton giant cells
D. Multinucleate giant cells
85. The definitive means for diagnosis of
herpes genitalis is
A. Tzanck smear
B. Histopathology
C. Serological study
D. Viral culture
86. Anogenital warts are frequently caused by
human papilloma virus types
A. 6, 11
B. 16, 18
C. 72, 73
D. 33, 35
87. Trichomonas vaginalis in females,
commonly infects
A. Urethra
B. Vaginal epithelium
C. Bartholins glands
D. Skenes glands
88. is the gold standard for the
diagnosis of trichomoniasis
A. Wet mount
B. Culture
C. PCR Test
D. Urine sedimentation exam
89. The incubation period of gonrrhea ranges
from
A. 1 to 14 days
B. 14 to 28 days
C. 28 to 42 days
D. 42 to 56 days
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Essentials in Dermatology
90. The incubation period of donovanosis
ranges from
A. 3 days to 3 months
B. 3 months to 6 months
C. 6 months to 9 months
D. 9 months to 1 year
91. Donovanosis, a chronic destructive and
slowly progressive disease is caused by
A. Haemophilus ducreyi
B. Gardnerella vaginalis
C. Calymmatobacterium granulomatis
D. Chlamydia trachomatis
92. Locomotor ataxia, a late manifestation of
syphilis due to parenchymatous involvement of the spinal cord is called
A. General paralysis of insane
B. Tabes dorsalis
C. Meningovascular syphilis
D. Syphilitic amyotrophy
93. The incubation period of syphilis is
A. 1-9 days
B. 9-90 days
C. 90-100 days
D. > 100 days
94. Calymmatobacterium granulomatis is a
intracellular bacterium
A. Gram negative B. Gram positive
C. Gram variable D. Acid fast
95. The primary site of infection of gonorrhea
in females is
A. Urethra
B. Vagina
C. Vulva
D. Endocervical canal
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118. are so named because they recur at
the same site with each exposure to the
medication
A. Erythema multiforme
B. Fixed drug reactions
C. Toxic epidermal necrolysis
D. Lichenoid reactions
119. Typical target lesions of erythema
multiforme are best observed on the
A. Palms and soles
B. Face
C. Trunk
D. Extremities
120. Target lesions typically appear
symmetrically and acrally, initially most
frequently on the dorsal hands in
A. Fixed drug reactions
B. Erythema multiforme
C. Toxic epidermal necrolysis
D. Lichenoid reactions
121. Typical erythema multiforme minor is
usually associated with
A. Varicella zoster virus infection
B. Mycoplasma pneumoniae
C. Radiation therapy
D. Herpes simplex infection
B. Pityriasis capitis
C. Seborrhea
D. Acne vulgaris
137. is a perifollicular, chronic, pustular
staphylococcal infection of the bearded
region
A. Sycosis barbae B. Folliculitis
C. Furunculosis D. Carbuncle
138. is an ulcerative staphylococcal or
streptococcal pyoderma, nearly always of
the shins or dorsal feet
A. Cellulitis
B. Impetigo bullosa
C. Impetigo contagiosa
D. Ecthyma
139. Sharply delineated, dry, brown, slightly
scaling patches in the intertriginous areas
of erythrasma are caused by
A. Corynebacterium diphtheriae
B. Micrococcus sedantarius
C. Clostridium perfringens
D. Corynebacterium minutissimum
140. test give quantitative as well as
qualitative results and can be used to
monitor response to therapy of syphilis
A. VDRL
B. FTA-ABS
C. TPHA
D. TPI
141. Which of the vascular anomaly disappears
by first birthday
A. Salmon patch
B. Portwine stain
C. Capillary haemangioma
D. All of the above
142. Casals collar, a hyperpigmented dermatosis in the V area of neck is seen in
A. Ariboflavinosis
B. Pellagra
C. Scurvy
D. Rickets disease
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143. Dariers sign is demonstrated in the skin
lesions of
A. Urticaria pigmentosa
B. Lichen planus
C. Psoriasis vulgaris
D. All of the above
C. Exophiala phaeoanellomyces
D. Exophiala jaenselmi
163. Wavelength of Woods light is
A. 365 nm
B. 368 nm
C. 370 nm
D. 380 nm
164. Wickhams striae is seen in
A. Psoriasis
B. Lichen simplex chronicus
C. Lichen scrofulosorum
D. Lichen planus
165. Mother patch is the initial lesion of
A. Pityriasis rosea
B. Pityriasis lichenoides chronica
C. Pityriasis alba
D. Psoriasis
166. Deep seated vesicles resembling tapioca
over the palms and soles characterize
A. Bullous pemphigoid
B. Acropustulosis
C. Pompholyx
D. Keratolysis exfoliativa
167. Keratoderma blennorrhagicum is a feature
of
A. Ritters disease
B. Psoriasis
C. Reiters disease
D. Pityriasis rubra pilaris
168. Goeckermans technique consisting of
topical coal tar use and UV radiation is used
for the management of
A. Pemphigus
B. Psoriasis
C. Lymphoma
D. Parapsoriasis
169. Auspitzs sign is pathognomonic of
A. Lichen planus
B. Reiters disease
C. Psoriasis
D. Secondary syphilis
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170. Munro micro abscesses in psoriasis are
seen in
A. Stratum corneum
B. Stratum basale
C. Stratum spinosum
D. Stratum granulosum
171. Koebners response is seen in all except
A. Psoriasis
B. Lichen planus
C. Lichen nitidus D. Lichen striatus
172. Neck sign is typically observed in
A. Scleroderma
B. Eosinophilic fascitis
C. Porphyria cutanea tarda
D. Graft versus host disease
173. Which antibody is significantly associated
with neonatal lupus erythematosus
A. Anti Ro
B. Anti Sm
C. Anti ds DNA D. Anti U1 RNP
174. Carpet tack sign is characteristic of
A. Discoid lupus erythematosus
B. Systemic lupus erythematosus
C. Dermatomyositis
D. Psoriasis
175. Gottrons sign is pathognomonic of
A. Polymyositis
B. Dermatomyositis
C. Sjogrens syndrome
D. Systemic lupus erythematosus
176. The target or iris lesion with three
zones is classic of
A. Erythema palmare
B. Erythema marginatum
C. Erythema multiforme
D. Erythema repens
177. All are components of lichenification
except
A. Thickening
B. Pigmentation
C. Excoriation
D. Increased skin markings
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198. A 60-year old man presents with itchy tense
blisters mainly on abdomen and upper
limbs, the Tzanck smear shows a
predominance of eosinophils and
Nikolskys sign is negative, so what is your
diagnosis
A. Bullous pemphigoid
B. Dermatitis herpetiformis
C. Pemphigus foliaceus
D. Pemphigus vulgaris
199. A 20-year-old male presents with well
defined hypopigmented, slightly itchy
macules on the trunk, with very fine
branny scales of tinea versicolor. Woods
lamp examination fluorescence will be
A. Yellowish brown
B. Brilliant green
C. Pale green
D. Blue
200. On diascopy, apple jelly nodules are seen
in
A. Lichen planus
B. Lupus vulgaris
C. Neurofibromatosis
D. Sarcoidosis
201. Moth-eaten alopecia is irregularly
distributed alopecia of the scalp, seen in
5% of patients with
A. Tinea capitis
B. Secondary syphilis
C. Alopecia areata
D. Androgenetic alopecia
202. Gottrons papules (flat topped violaceous
papules over the knuckles) are pathognomonic of
A. Dermatomyositis
B. Scleroderma
C. SLE
D. Sjogrens syndrome
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222. False about acne
A. Disease of adolescents
B. Comedones are the early lesions in acne
C. Fatty food increases the risk of acne
D. Propionibacterium acne plays role
223. Which of the following drug is not used in
the treatment of single lesion paucibacillary leprosy?
A. Rifampicin
B. Ofloxacin
C. Metronidazole D. Minocycline
224. Which of the following is not true of
Norwegian scabies?
A. Seen in immunocompromised person
B. Itching is severe
C. Patient will harbour million of mites
D. Methotrexate is one of the treatment
225. Which of the following is highly specific
for systemic lupus erythematosus
A. LE cell phenomenon
B. Anti ds antibody
C. Anti Ro antibody
D. Anti sm antibody
226. Following is not true about larva migrans
A. Larval migration begins 4 days after
inoculation
B. Topical ivermectin is preferred over
systemic therapy
C. Majority of cases are caused by
Ancylostoma braziliense
D. Occurs in people who go barefoot on the
beach
227. All of the following drugs are used in the
treatment of type 2 lepra reaction except
A. Clofazimine
B. Corticosteroids
C. Rifampicin
D. Thalidomide
228. Which of the following is not a topical
antifungal agent?
A. Terbinafine
B. Tioconazole
C. Tolnaftate
D. Tazarotene
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B. ILVEN
C. Syringomas
D. Papilloma
23. Mieschers granuloma is seen in histopathology of
A. Erythema nodosum
B. Erythema induratum
C. Nodular vasculitis
D. Erythema marginatum
24. Naked granulomas are seen in
A. Sarcoidosis
B. Tuberculosis
C. Histoplasmosis
D. Cat-scratch disease
25. All are type- I hypersensitivity reactions
except
A. Anaphylaxis
B. Urticaria
C. Contact hypersensitivity
D. Allergic rhinoconjunctivitis
26. All are type-II immunological reactions
except
A. Serum sickness
B. SLE
C. Complement deficiency
D. Eczema
27. Following about skin prick test is true
except
A. Result available in 15 minutes
B. Can be done in patient receiving antihistaminics
C. Cheap
D. Cannot be done in patient with extensive
eczema
28. Type-1 and type-2 cryoglobulins seen in
all except
A. Myeloma
B. Waldenstroms macroglobulinaemia
C. Lymphoma
D. Chronic infection
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29. Chronic mucocutaneous candidiasis has all
except
A. Endocrinopathy
B. Norwegian scabies
C. Candidiasis of nail
D. Malignancy
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B. Pheochromocytoma
C. Vitamin B12 deficiency
D. Stills disease
7. All are features of FranceschettiJadassohn syndrome except
A. Yellowing of teeth
B. Hypohidrosis
C. Hyperkeratosis of palms and soles.
D. Begins by 2 years of age.
8. All are true about tropical acne except
A. Occurs in persons working in hot humid
climates
B. Comedones are the common lesions
C. Face is not much involved
D. Isotretinoin may be useful
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Essentials in Dermatology
C. Bed bug
D. Pediculosis humanus
27. Muehrckes nail (narrow white bands
occurring in pairs) seen in
A. Chronic hypoalbuminemiae
B. Cirrhosis
C. Congestive heart failure
D. Diabetes mellitus
28. Term atopy was coined by
A. Russel
B. Milan
C. Coca
D. Fieldman
29. Crowes sign is seen in
A. Neurofibromatosis
B. Ataxia telangiectasia
C. Sturge-Weber syndrome
D. Tuberous sclerosis.
30. Other name for diabetic dermopathy is
A. Rose spots
B. Binkleys spots
C. Liver spots
D. Forschcimers spots
31. Most commonly used (commercial)
serotype of botulinum toxin in dermatology is
A. A
B. B
C. C1
D. E
32. Organism implicated in blastomycosis
like pyoderma all except
A. E.coli
B. Proteus
C. Pseudomonas
D. Corynebacterium
33. Good candidate for hormone therapy for
acne vulgaris are all except
A. Acne primarily located in lower face or
neck
B. Acne not responding to other oral/
topical therapies
C. Women with polycystic ovarian disease
D. Women with early onset acne
34. Cork screw hairs are seen in
A. Vitamin B12 deficiency
B. Trichotillomania
C. Scurvy
D. Woolly hair syndrome
35. Selenium deficiency manifests as
A. Woody edema
B. Perifollicular petechiae
C. Pseudoalbinism
D. Seborrheic dermatitis like eruption.
36. Button hole sign is seen inA. Anetoderma
B. Cutis laxa
C. Linear focal elastosis
D. Striae distensae
37. Louis Bar syndrome is the other name of
A. Proteus syndrome
B. Ataxia-telangiectasia
C. von-Hippel-Lindau syndrome
D. Pachyonychia congenita
38. Hutchinsons sign is seen in
A. Melanoma in nail matrix
B. Blue nevus
C. Zosteriform herpes simplex
D. Herpetic whitlow
39. Most common color in chromhidrosis is
A. Yellow
B. Green
C. Blue
D. Black
40. Pseudo-Hutchinsons sign is seen in
A. Nicotine stain of nail plate
B. Bowens disease
C. Blue nevus
D. Melanoma
41. All are true about epidermodysplesia
verriciformis except
A. Inherited susceptibility to HPV
B. Malignant changes do not occur
C. Lesions resembling pityriasis versicolor
may occur.
D. Onset may occur at any age
42. Black piedra also known as:
A. Trichosporiasis nodosa
B. Trichomycosis nodularis
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Essentials in Dermatology
C. Non epidermolytic palmoplantar
keratoderma
D. Woolly hair
55. Fish odour syndrome is because of
A. Triethylamine B. Trimethylamine
C. Carnitine
D. Choline
56. Necrosis of sweat glands seen in
histopathology of
A. Eccrine poroma
B. Eccrine nevus
C. Neutrophilic eccrine hidradenitis
D. Melanocytic nevus
57. Reversal of perception of hot and cold is
characteristic of
A. Ciguatera fish poisoning
B. Ray fish poisoning
C. Frost bite
D. Snake bite
58. Pigmented hairy epidermal nevus consists
of all except
A. Beckers nevus
B. Ipsilateral hypoplasia of breast
C. Scoliosis
D. Cataract
59. Urbach-Wiethe disease is also known as
A. Gauchers disease
B. Lipoid proteinosis
C. Fabrys disease
D. Fucosidosis
60. Knuckle pigmentation is seen in
deficiency of
A. Vitamin B1
B. Vitamin B12
C. Vitamin B3
D. Vitamin B6
61. Mauserung phenomenon is seen in
A. Icthyosis bullosa of Siemens
B. BCIE
C. Icthyosis hysterix
D. Refsums syndrome
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82. Spongiosis is a histopathological feature
of
A. Lichen planus
B. Lichen striatus
C. Psoriasis
D. Keratosis lichenoides chronicus.
83. Follicular hyperkeratosis is seen in
deficiency of all except
A. Essential fatty acid
B. Vitamin K
C. Vitamin A
D. Vitamin E
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Essentials in Dermatology
C. Candida species
D. Rhizopus species
8. Primary manifestation of Parvo virus B19
in adults is
A. Acute arthropathy
B. Rashes with slapped cheek appearance
C. Anaemia
D. Flu like syndrome
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29. Which of the following is false about mastocytosis syndrome?
A. Respiratory tract and endocrine systems
are rarely affected
B. Patients suffer from recurrent bacterial/
viral/fungal infection
C. Urticaria pigmentosa is the most
common skin manifestation
D. Dariers sign is positive
30. Reynolds syndrome is
A. CREST syndrome + Primary biliary
cirrhosis
B. CREST syndrome + Lichen planus
C. CREST syndrome + Sjogrens syndrome
D. CREST syndrome + Ulcerative colitis
31. Azure lunulae is seen in all except
A. Wilsons disease
B. Argyria
C. Following treatment with busulfan
D. Lichen planus
32. Lupus pernio is a type of
A. Sarcoidosis
B. Tuberculosis
C. Syphilis
D. Amyloidosis
33. Necrolytic migratory erythema is seen in
A. Glucagonoma syndrome
B. Diabetes mellitus
C. Internal malignancy
D. Lymes disease
34. Which of the following is false about
Erythema toxicum neonatorum
A. Idiopathic condition
B. Smear of vesicle shows eosinophils
C. Lesions spare the palms and soles
D. Lesions heal with residual pigmentation
35. Which of the following is false about
Transient neonatal pustular melanosis?
A. Idiopathic pustular eruption of newborn
B. Smear of vesicle shows neutrophils
C. Palms and soles are involved
D. Lesions heal without residual pigmentation
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Essentials in Dermatology
57. Which type of Ehlers-Danlos syndrome
has autosomal recessive inheritance
A. Hypermobility type
B. Kyphoscoliosis type
C. Vascular type
D. Arthrochalasia type
58. Prayer sign which is inability to
approximate palmar surfaces of PIP and
DIP with palms pressed together is seen
in
A. Cheiroarthropathy/Diabetic limited
joint mobility
B. Scleredema diabeticorum
C. Psoriatic arthritis
D. None of the above
59. Cigarette paper scars are characteristic of
A. Ehlers Danlos syndrome
B. Marfans syndrome
C. Pseudoxanthoma elasticum
D. Cutis laxa
60. Which of the following is pathognomonic
of dermatomyositis?
A. Gottrons papules
B. Heliotrope erythema
C. Shawl sign
D. Mechanics hand lesion
61. Hot tub folliculitis is caused by
A. Pseudomonas aeruginosa
B. Staphyloccocus aureus
C. Clostridium perfringens
D. Streptococcus pyogenes
B. Anti-U1 RNP
C. Anti-La/SSB
D. Anti-ds DNA
79. Drug induced SLE is associated with auto
antibody to
A. ds DNA
B. Sm Ag
C. Histones
D. UI RNP
80. Most frequent follicular tumour arising in
Nevus sebaceous is
A. Malignant melanoma
B. Trichoblastoma
C. Basal cell carcinoma
D. Squamous cell carcinoma
81. Hutchinsons nail sign is seen in
A. Subungual melanoma
B. Pyogenic granuloma
C. Myxoid cyst
D. Keratoacanthoma
82. Stevens-Johnson syndrome is associated
with autoantibody against
A. Desmogleins
B. Desmoplakins
C. Desmocollins D. None of the above
83. Epidermolysis bullosa acquisita is
characterised by autoantibody against
A. Collagen type VII
B. Desmoglein
C. Basement membrane zone
D. None of the above
84. Which of the following does not belong to
central centrifugal scarring alopecia?
A. Follicular degeneration syndrome
B. Folliculitis decalvans
C. Lichen planopilaris
D. Pseudopelade
85. Sweat that stains is seen in
A. Phenylketonuria
B. Alkaptonuria
C. Arginosuccinic aciduria
D. Tyrosinemia
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Essentials in Dermatology
86. Comma shaped bodies in histiocytes are
seen in electron microscopy in all except
A. Juvenile xanthogranuloma
B. Papular xanthoma
C. Benign cephalic histiocytosis
D. Sinus histiocytosis
87. Pseudo-cushing syndrome is seen in
A. Chronic alcoholism
B. Hypothyroidism
C. Diabetes
D. Porphyria
88. Gold standard in the diagnosis of Sjgren
syndrome is
A. Lip biopsy
B. Sialometry
C. Sialography
D. Buccal mucosal biopsy
89. False about Paraneoplastic acrokeratosis
of Bazex is all except
A. Nail changes occur late in the course of
the disease
B. More common in females
C. Responds to etretinate even if primary
is not treated
D. Usually associated with neoplasia of
genito urinary tract
90. Angels kiss is
A. Nevus flammeus
B. Port-wine stain
C. Hemangioma
D. Mongolian spots
91. Steinbergs sign (protrusion of thumb on
the ulnar side of the hand after making a
fist enclosing the thumb is seen in
A. Ehler Danlos syndrome
B. Marfans syndrome
C. Cutis laxa
D. Pseudoxanthoma elasticum
92. Nasal pruritus indicates an underlying
A. Brain tumour
B. CA nasopharynx
C. Hodgkins lymphoma
D. Polycythemia vera
93. Bath itch is characteristic of
A. Polycythemia rubra vera
B. Iron deficiency
C. Senile pruritus
D. Hodgkin lymphoma
94. Addicted scrotal syndrome refers to
A. Use of high potency steroid to scrotum
B. Use of antifungal creams to scrotum
C. Use of anesthetic cream to scrotum
D. Use of antibacterial cream to scrotum
95. In nostalgia parasthetica, itch is localized
to
A. Interscapular region
B. Medial aspect of thigh
C. Lateral aspect of thigh
D. Inner aspect of arm
96. In brachioradial pruritus, itch is localized
to
A. Interscapular region
B. Medial ascpect of thigh
C. Lateral aspect of thigh
D. Inner aspect of arm
97. In cholestatic pruritus, pruritogenic
substance is
A. Bile salt
B. Bile acid
C. Bile salt intermediates
D. Bilirubin
98. Aspirin is effective in pruritus due to
A. Hodgkin lymphoma
B. Polycythemia rubra vera
C. Mastocytosis
D. Internal malignancy
99. Mediator of pruritus in Hodgkins
lymphoma
A. Histamine
B. Opioid peptides
C. Seratonin
D. Leukopeptidase
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Essentials in Dermatology
13. Henderson Paterson bodies are pathognomonic of
A. Molluscum contagiosum
B. Measles
C. Chlamydial infections
D. Mycoplasma
14. The following are true about chancre
redux or monorecidive chancre except
A. Recurrence of a primary sore at the site
of the original lesion
B. A form of relapse
C. Infectious lesion
D. Treponemes cannot be obtained
15. School of fish or railroad track
appearance is seen in
A. Yersinia pestis
B. Hemophilus ducreyi
C. Neisseria gonorrhoeae
D. Calymmatobacterium granulomatis
16. True about Donovan bodies are all except
A. Gold standard for the diagnosis of
donovanosis
B. Coccobacilli
C. Located within polymorphonuclear
leukocytes
D. Resemble safety pins
17. False about Treponema pallidum
A. 6-20 microns in length
B. regular tight spirals
C. capsulated
D. flagellated
18. All are true about primary chancre except
A. Seen in more than 90% cases of syphilis
B. Painless, indurated, less than 2 cm
C. Usually single
D. Highly infectious
19. Commonly involved tissues in secondary
syphilis are all except
A. Skin
B. Bone
C. Mucous membranes
D. Lymph nodes
20. Eruptions of acquired secondary syphilis
can be all except
A. Papulosquamous
B. Macular
C. Follicular
D. Bullous
21. Monorecidive or chancre redux occurs due
to
A. Re-infection with Treponema pallidum
B. Relapsing lesion at the site of primary
chancre
C. Lesion of secondary syphilis
D. Gumma of tertiary syphilis
22. Highly infectious lesions of syphilis are all
except
A. Primary chancre
B. Gumma
C. Condylomata lata
D. Mucous patches
23. Gummatous osteoperiosteitis of skull
bones in syphilis is called
A. Worm-eaten skull
B. Moth-eaten skull
C. Hole in bone appearance
D. Pepper-pot skull
24. Syphilitic gumma commonly involves
A. Left ventricle and septum
B. Right ventricle
C. Left atrium and septum
D. Right and left ventricles
25. Bruit de Tabourka (loud and tambour-like
second sound) is heard on auscultation in
A. Hypertension
B. Syphilitic aortitis
C. Dissecting aortic aneurysm
D. Atherosclerosis
B. Pneumonia
C. Serous otitis media
D. Meningitis
33. Bacterial vaginosis can be diagnosed
clinically by the presence of ALL
EXCEPT
A. Vaginal pH > 4.5
B. Thin homogeneous milky discharge
C. Scanty or absent lactobacilli
D. Clue cells at least 30% of total vaginal
epithelial cells
34. The following condition is associated with
acute biological false positive VDRL
A. Lepromatous leprosy
B. Old age
C. SLE
D. Pregnancy
35. An infant should be evaluated for possible
congenital syphilis in all the following
conditions except
A. The mother is inadequately treated for
syphilis during pregnancy
B. If mother has received treatment more
than 4 weeks before delivery
C. Treatment of syphilis during pregnancy
with non-penicillin regimens
D. Treatment of syphilis which has not
been documented
36. Painless genital ulcer is caused by all
except
A. Amoebiasis
B. LGV
C. Histoplasmosis
D. Ulcerative penile carcinoma
37. Human papilloma virus is responsible for
all except
A. White patches on the cervix
B. Koilocytosis on cervical smear
C. Condyloma acuminata
D. Polyps on the cervix
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Essentials in Dermatology
38. In patients with perianal warts, all are true
except
A. Have higher incidence of other STDs
than general population
B. Inevitably have had receptive anal
intercourse
C. May present with pruritus ani
D. Should have proctoscopic examination
to exclude anal canal warts
39. True about gonococcal proctitis in
homosexual men
A. Is acquired by orogenital intercourse
B. Usually causes malaise
C. Is easily diagnosed on gram stain of
rectal exudates
D. Should be treated with ceftriaxone 250
mg in a single dose plus doxycycline 100
mg twice daily for 7 days
40. The following is/are appropriate methods
for diagnosis of chlamydial infection in
patients with cervicitis
A. High vaginal swab
B. Wet film
C. Direct immunofluorescence with
Chlamydia trachomatis specific
monoclonal antibody
D. Gram stain
41. All are true about clue cells except
A. Show slight enlargement of nuclei with
dense cytoplasm covered by bacterial
vaginosis organisms
B. Cell border is obscured and has serrated
appearance
C. Has clear cytoplasm covered by bacterial
vaginosis organisms
D. First described by Gardner and Duke
42. Diagnosis of atypical syphilis in advanced
HIV positive patients should be confirmed
by
A. VDRL
B. TPHA
C. FTA-Abs
D. Biopsy with special stains for T.
pallidum
43. Widespread vaginal warts can be safely
and effectively treated with all except
A. TCA cautery
B. Laser therapy
C. Topical podophyllin 5%
D. Cryosurgery
44. The following statements are true in the
etiology of cervical cancer except
A. Over 90% of invasive cervical cancer
contain HPV 16 and 18
B. Cigarette smoking is probably important
in development of cervical cancer
C. All CIN III lesions will progress to
cervical cancer if untreated
D. Immunosuppression promotes progression of CIN III to cancer
45. Plasma cell balanitis all are true except
A. It is also called Zoons balanitis
B. Results in painful penile ulcers
C. Appears as red patches on the glans/
inner prepuce
D. May be treated with topical steroids
46. CSF examination is indicated in all except
A. Serological relapse in syphilis patients
B. Syphilis with HIV infection
C. Positive syphilis serology with neurological signs
D. Latent syphilis in pregnant women
47. The recommended treatment of neurosyphilitic patients who have penicillin
allergy is
A. Tetracycline
B. Erythromycin
C. Ceftriaxone
D. Penicillin test, desensitization, penicillin
treatment
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Essentials in Dermatology
62. Most HIV-1 isolytes belong to the following
group-which is the main cause of AIDS
pandemic
A. groupM
B. group O
C. group N
D. group A
63. The main receptor for HIV-1 on T cells is
A. CD4
B. Fusin CXCR-4
C. CCR-5
D. CCR-2
64. The most important co-receptor for CD4
mediated entry of HIV-1 into T-cells is
A. CCR-2
B. CCR-4
C. CCR-5
D. Fusin CXCR-4
65. There are _______ identified subtypes of
HIV-1 under Group M in Los Alamos HIV
sequence database
A. 10
B. 11
C. 12
D. 13
66. The gene in HIV-1 that is replaced by VPX
gene in HIV-2 is
A. vpu
B. vpr
C. vif
D. env
67. HIV-1 and HIV-2 viruses belong to which
subfamily of retroviruses
A. Oncovirinae
B. Lentivirine
C. Spumavirinae D. Retrovirinae
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Essentials in Dermatology
92. Acute gonococcal infection in females
usually presents as
A. Urethritis
B. Vaginitis
C. Endocervicitis
D. Pelvic inflammatory disease
93. In the three glass test haze in the second
glass indicates
A. Anterior urethritis
B. Posterior urethritis
C. Cystitis
D. Either posterior urethritis or cystitis
94. True about gonorrhea are all except
A. The average incubation period is 2-5
days
B. Usually presents as posterior urethritis
in men
C. Usually presents as endocervicitis in
women
D. Rectal and pharyngeal infection is
common in homosexuals
95. True statements about disseminated
gonococcal infection are all except
A. The primary mucosal infection is
usually asymptomatic
B. Characteristic clinical findings include
arthritis and skin lesions
C. The organism is detected in blood
culture in 90% cases
D. Endocarditis is a fatal complication
96. Specimens in suspected gonococcal
infection are preferably collected with
A. Metallic swab sticks
B. Wooden swab sticks
C. Polyethylene terephthalate swabs
D. Calcium alginate swabs
97. The drug of first choice for the treatment
of uncomplicated lower genital tract
infection due to Chlamydia trachomatis is
A. Azithromycin B. Doxycycline
C. Erythromycin D. Tetracycline
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Essentials in Dermatology
115. Parrots nodes in congenital syphilis refer
to
A. Frontoparietal swellings secondary to
osteochondritis
B. Epitrochlear lymphadenopathy
C. Generalized lymphadenopathy
D. Syphilitic furuncle
116. Focal defects with cortical destruction seen
on the medial aspect of proximal tibial
metaphysis is known as
A. Wimbergers sign
B. Celery stick appearance
C. Bucket handle sign
D. Sarcophagus sign
117. Longitudinal lines of rarefaction extending
into the diaphysis is known as
A. Cat bite sign
B. Higoumenakis sign
C. Celery stick appearance
D. Bucket handle sign
118. Fractures through the degenerating
metaphysis, followed by exuberant callus
formation resulting in a cap over the
metaphysis is called
A. Wimbergers sign
B. Sarcophagus sign
C. Parrots node
D. Bucket handle sign
119. Periosteal new bone formation resulting
in layers of marrow trapped between
layers of subperiosteal bone is known as
A. Celery stick appearance
B. Sarcophagus sign
C. Bucket handle sign
D. Wimberger sign
120. Haematological manifestations of early
congenital syphilis include all the
following except
A. Autoimmne hemolytic anaemia
B. Leukemoid reaction
C. Basophilia
D. Thrombocytopenia
121. Neurological manifestations of early
congenital syphilis include all except
A. Acute leptomeingitis
B. Cerebrovascular accidents
C. Tabes dorsalis
D. Hydrocephalus
122. Late congenital syphilis in the child/
adolescent corresponds to ________ in the
adult
A. Secondary syphilis
B. Early latent syphilis
C. Late latent syphilis
D. Tertiary syphilis
123. Syphilitic pneumonitis- all are true except
A. Occurs due to gumma formation in the
lung
B. Intense obliterative fibrosis occurs in the
interalveolar space
C. Can be confused with ARDS
D. Also called pneumonia alba
124. The fundamental histological lesion of
congenital syphilis is
A. Interstitial fibrosis
B. Obliterative endarteritis
C. Microscopic gumma
D. Necrotizing funisitis
125. Chancre galeuse is
A. Syphilitic chancre occurring in a
cutaneous lesion of scabies
B. Oral chancre of syphilis
C. Monorecidive chancre of syphilis
D. Condylomata lata
126. Supraorbital thickening in syphilis is
called
A. Olympian brow
B. Hertoghes sign
C. Henneberts sign
D. Higoumenakis sign
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MCQs in Leprosy
1. The minimum inhibitory concentration for
dapsone is _____ g/ml
A. 0.0003
B. 0.003
C. 0.03
D. 0.03
2. All are true regarding dapsone syndrome,
except
A. Hepatitis
B. Usually develops within 6 weeks of
therapy
C. Exfoliative dermatitis
D. Arthritis
3. Monospot test is used for
A. Monitoring compliance of dapsone
B. Detecting compliance of clofazimine
C. Detecting dapsone resistance
D. Testing integrity of dermal nerve.
26. The colour of blister pack used in MBMDT regime for adult is
A. Green
B. Red
C. Orange
D. Yellow
27. In patients on regular dapsone, monsopot
test will show
A. Orange color in center, yellow color in
periphery
B. Yellow color in center, orange color in
periphery
C. Orange color in center, green color in
periphery
D. Green color in center, orange color in
periphery
28. Most common teeth to be affected in
leprosy is
A. Molar
B. Premolars
C. Upper incisors
D. Lower incisors
29. Nasal deformity in lepromatous leprosy is
due to
A. Destruction of nerves
B. Atrophy of mucosal glands
C. Vascular pathology
D. Unknown
30. Laryngeal involvement in lepromatous
leprosy includes all of the following except
A. Chronic laryngeal obstruction
B. Acute laryngeal obstruction
C. Involvement above the vocal cords
D. Involvement below the vocal cords
31. True statement among the following is
A. Lymph nodes in leprosy are matted and
rubbery
B. Mesenteric lymph nodes are never
affected
C. Bronchial lymph nodes are affected
during reaction
D. Histopathology shows focal collection
of macrophages in cortex only
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Essentials in Dermatology
32. Renal lesions in leprosy includes all except
A. Membranous glomerulonephritis
B. Acute pyelonephritis
C. Acute tubular necrosis
D. Amyloidosis
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Essentials in Dermatology
61. The M. leprae looses its acid fastness if
stained with
A. Povidone
B. Pyridine
C. Carbol fuschin D. H2SO4
62. In which year NLEP was formed?
A. 1982
B. 1898
C. 1900
D. 1850
63. In which year Indian lepers act came into
existence?
A. 1982
B. 1898
C. 1900
D. 1850
64. True about glycolipid in M.leprae are all
except
A. Forms foaming material inside the
macrophages
B. Species specific
C. Antiglycolipid antibodies are used in ELISA
D. Not species specific
65. True about lepromin reaction
A. Early reaction is due to delayed type
hypersensitivity
B. Mitsuda reaction occurs at 48 hrs
C. Mitsuda is strongly positive in LL
D. Fernandez reaction is read after 48
hours.
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Essentials in Dermatology
90. Thalidomide was found to be used in the
treatment of erythema nodosum leprosum
by
A. Mouat
B. Danielssen
C. Peterson
D. Sheskin
91. WHO recommended the use of multi drug
therapy for leprosy in the year
A. 1981
B. 1976
C. 1957
D. 1990
92. The first person to use dapsone orally were
A. Faget and Muir
B. Lowe and Smith
C. Wade and Rodriguez
D. Motta and Zuniga.
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Essentials in Dermatology
protein depletion,
pills,
propranolol,
pyrexia,
parturition and
psychic stress
Seven Ps in lichen planus
purple,
polygonal,
planar or flat,
papules,
pruritic,
persistent and
penile
Cockaynes syndrome lies in COCKAYNES
C for CNS defects,
O for lipOdystrophy,
C for color which is hyperpigmentation,
A for auditory symptom of deafness,
Y for microencephalY,
N for normal pressure hydrocephalus,
E for eye lesion of salt and pepper retina and
S for short
Describing skin lesions LES. T CABS
Location and distribution (e.g. bilateral/symmetrical)
Erythema (e.g. yes or no)
Surface features (e.g. scale, verrucous)
Type (e.g. papule, nodule, vesicle)
Color (e.g. violaceous, blue)
Arrangement (e.g. grouped)
Border/shape (e.g. linear, serpiginous)
Special sites/systemic (e.g. oral, nails, scalp)
Generalized skin hyperpigmentation With
generalized, none of the skin is SPARED
Sunlight
Pregnancy
Addisons disease
Renal failure
Excess iron (hemochromatosis)
Drugs (e.g. amiodarone, minocycline)
Type I Anaphylaxis
Type II Cytotoxic - mediated
Type III Immune - complex
Type IV Delayed hypersensitivity
Multiple Endocrine Neoplasia: Each of the MENs
is a disease of three or two letters plus a feature.
MEN I is a disease of 3 Ps (pituitary,
parathyroid, and pancreas) plus adrenal cortex
MEN II is a disease of 2 Cs (carcinoma of
thyroid and catacholamines [pheochromocytoma]) plus parathyroid for MEN IIa or mucocutaneous neuromas for MEN IIB (aka MEN III)
WBC Count: Never Let Mom Eat Beans and
60, 30, 6, 3, 1
Neutrophils 60%
Lymphocytes 30%
Monocytes 6%
Eosinophils 3%
Basophils 1%
LR6 SO4 3. Which cranial nerve controls which
eye muscle? Lateral rectus sixth nerve, superior
oblique fourth, rest third.
Bones, stones, groans and psychic moanssymptoms of an elevated serum calcium level.
C 3, 4 and 5, keeps your diaphragm alive.
S 2, 3 and 4, makes a mess on the floor.
Psoriasis: Pathophysiology
PSORIASIS : Pink Papules/ Plaques/ Pinpoint
bleeding (Auspitz sign)/ Physical injury (Koebner
phenomenon)/ Pain
Silver Scale/ Sharp margins
Onycholysis/Oil spots
Rete Ridges with Regular elongation
Itching
Arthritis/ Abscess (Munro)
Stratum corneum with nuclei, neutrophils
Immunologic
Stratum granulosum absent/ Stratum Spinosum
thickening
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Essentials in Dermatology
Delay in wound healing
DID NOT HEAL:
Drugs
Infection/ Icterus/ Ischemia
Diabetes
Nutrition
Oxygen (hypoxia)
Toxins
Hypothermia/Hyperthermia
Edema
Acidosis
Local anesthetics
Cutaneous inflammation patterns
Pus of Pig Valve
Remove the vowels: PSFPGVLV:
Psoriasiform
Spongiotic (eczematous)
Folliculitis
Panniculitis
Granulomatous
Vasculopathic
Lichenoid
Vesiculobullous
Clubbing causes
CLUBBING:
Cyanotic heart disease
Lung disease (hypoxia, lung cancer, bronchiectasis, cystic fibrosis)
UC/Crohns disease
Biliary cirrhosis
Birth defect (harmless)
Infective endocarditis
Neoplasm (esp. Hodgkins)
GI malabsorption
Albinisim type I vs. type II
One has None. Two Accumulates: Type I: have
no pigment.
Type II: No pigment at birth but accumulates as
person ages.
Malignant melanoma: 3 sites with poor
prognosis
BANS:
Back of Arm
Neck
Scalp
Symptoms of hyperthyroidism
Remember the following mnemonic when
evaluating patients for hyperthyroidism:
S: Sweating
T: Tremor or Tachycardia
I: Intolerance to heat, Irregular menstruation, and
Irritability
N: Nervousness
G: Goiter and Gastrointestinal (loose stools/
diarrhea).
5 Ts of early cyanosis:
Tetralogy, Transposition, Truncus, Total anomalous, Tricuspid atresia
Causes of hematuria
Use the mnemonic SITTT as an aid in evaluating
the cause of hematuria:
S: Stone
I: Infection
T: Trauma
T: Tumor
T: Tuberculosis
Causes of postoperative fever
Remember the following mnemonic when
determining the possible cause (s) of fever in a
patient who has recently undergone a surgical
procedure: the 5 Ws (or 6 Ws)
Wind: The pulmonary system is the primary
source of fever in the first 48 hours.
Wound: There might be an infection at the
surgical site.
Water: Check intravenous access site for signs of
phlebitis.
Walk: Deep venous thrombosis can develop due
to pelvic pooling or restricted mobility related to
pain and fatigue.
Whiz: A urinary tract infection is possible if
urinary catheterization was required. Also
Wonder drugs - drug fevers.
C - conjunctival redness
R - rash
E - extremity involvement
A - adenopathy
M - mucosal erythema
FEVER fever
Eosinophilia:
NAACP
N - Neoplasm
A - Allergy
A - Addisons
C - Cirrhosis, CVD
P - Parasite (visceral larva migrans), Periarteritis
nodosa
Endocarditis:
FAME
F - FEVER
A - ANEMIA
M - MURMUR
E - ENDOCARDITIS
Tumors that go to bone:
Kinds of tumors leaping primarily to bone
K - Kidney
O - Ovarian
T - Testicular
L - Lung
P - Prostate
T - Thyroid
B Breast
Hypercalcemia:
SHAMPOO DIRT
S - Sarcoidosis
H - Hyperparathyroidism, hyperthyroidism
A - Alkali-milk syndrome
M - Metastases, myeloma
P - Paget disease
O - Osteogenesis imperfecta
O - Osteoporosis
D - Vitamin D intoxication
I - Immobility
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Essentials in Dermatology
R - RTA
T Thiazides
Henoch-Schonlein Purpura:
JARS
J - Joints
A - Abdominal pain
R - Renal
S Skin
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Essentials in Dermatology
Anthrax: Acute infective zoonosis of herbivorous animals, sometimes transmitted to man, caused by
Bacillus anthracis and produces Malignant pustule in the skin (Greek anthrax charcoal).
Anthropophilic: Preferring humans as host.
Aphthae: Painful ulcers of the mucosae (usually oral cavity), often multiple and recurrent.
Aplasia: Failure or lack of growth or development.
Apocrine sweat glands: These tubular glands consists of two main parts the coiled secretary gland
and the straight excretory duct which opens into follicular canal just above the openings of sebaceous
glands. They are distributed along the mammary line, i.e. axillae, areolae, periumbilical area, mons
pubis, genital and perianal areas.
Appendages: The epidermis gives rise to derivative structures (pilosebaceous unit, nails and sweat
glands) called as appendages.
Aquagenic: Caused by contact with water.
Arachnodactyly: Increased length of fingers and toes, from resemblance to spiders legs.
Argyria: Ashen-grey discoloration of the skin and conjunctivae, resulting from chronic exposure to
silver or its salts.
Arthus phenomenon: Immunological reaction at site of injection of a substance (antigen) to which the
recipient has previously formed precipitating-type antibodies, resulting in formation of antigen
antibody complexes causing tissue damage, especially of a vasculitic nature.
Atopic disorders: The anaphylactic-type of disorder that results from IgE mediated reactions.
Atopy: State of excessive formation of lgE antibody following exposure to common environmental
allergens.
Atrophy: A wasting, shrinkage, diminution or lack of tissue.
Balanitis: Inflammation of glans penis (or glans clitoris).
Balanoposthitis: Inflammation of glans penis and prepuce.
Ballooning degeneration of epidermis: A type of degeneration of epidermal cells causing marked
swelling of the cells with loss of intercellular bridges, occurs in viral vesicles.
Basement membrane zone: Located beneath the basal layer, consists of the basement membrane and
of the lamina lucida, anchoring fibrils, and reticulum fibres.
Basidiobolomycosis: Disease caused by a genus of fungus causing subcutaneous phycomycosis.
Bazins disease (tuberculous): Erythema induratum affecting legs of young women.
Beaus lines: Transverse depressions on the nails following acute illnesses or debilitating medical
events.
Behets syndrome: Triad of orogenital ulceration and iritis. Pyoderma may occur and central nervous
system and other organs may be involved.
Bence-Jones protein: A low-molecular-weight protein found in urine of patients with myeloma.
Berloque dermatitis: A streaky form of pigmented contact photodermatitis, usually seen in the neck
but occasionally elsewhere, due to psoralen, as in bergamot oil in perfume.
Besniers prurigo: Flexural form of atopic dermatitis.
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Essentials in Dermatology
Colloid bodies: Another name for Civatte bodies, are round or oval, 10 micrometer eosinophilic
homogeneous bodies formed due to degeneration of epidermal cells and are extruded into the dermis.
Comedo: A greasy plug in a sebaceous follicle.
Condyloma: A wart-like growth due to hypertrophy of prickle-cell layer, commonly used for genital
and perianal lesions of viral (acuminata) or syphilitic (lata) origin.
CREST (CRST) syndrome: Calcinosis, Raynauds phenomenon, (Esophageal involvement),
Sclerodactyly, Telangiectasia.
Cryo: Meaning cold.
CTCL: Cutaneous T-Cell Lymphoma.
Cullens sign: Bluish staining around umbilicus usually denoting acute pancreatitis or ruptured
ectopic pregnancy.
Cushings syndrome: Due to adrenocortical hypertrophy. The term Cushingoid is applied to the
appearance caused by high-dose corticosteroid therapy.
Cutis laxa: Laxity or fold-like formation of skin.
Cyst: Any closed cavity or sac (normal or abnormal) with an epithelial, endothelial or membranous
lining and containing fluid or semisolid material.
Dactylitis: Inflammation or infection of a finger.
Dandruff: Popular term for pityriasis capitis, a mild form of seborrheic dermatitis.
Dariers disease: Keratosis follicularis.
Decalvans: Causing loss of hair, e.g. folliculitis decalvans.
Decubitus ulcer: Bedsore; pressure sore due to prolonged recumbency without movement
de Morgans spots (Campbell de Morgans spots): Cherry angiomas.
Dermabrasion: Surgical technique of removal of superficial lesions of the skin by abrasive methods
such as with high-speed rotary drills, or hand used dermabrader.
Dermal-epidermal junction: The dermal-epidermal junction (DEJ) is a basement membrane zone
(BMZ) that welds the epidermis to underlying dermis. It is undulated, forming dermal papillae (upward
projections of the dermis into the epidermis) and rete ridges (downward projections of epidermis into
the dermis). This DEJ is weakest at lamina lucida.
Dermatoglyphics: It is the study of the highly characteristic epidermal ridge patterns of the volar skin
of palms, soles, fingers and toes.
Dermis: The dermis is formed by connective tissue having fibres (collagen, elastic and reticulin) and
ground substance. It varies in thickness from about 1 mm on the face to 4 mm on the back and thigh.
Dhobi (dhobie, dhoby): Indian washerman, dhobie itch a colloquial term used by servicemen for
tinea cruris.
Diascopy: Examination of skin with exclusion of blood by firm pressure of glass, etc.; vitropression.
DIC: Disseminated Intravascular Coagulation
Ducreys Bacillus: Haemophilus ducreyi, the cause of chancroid.
Duhring-Brocq disease: Dermatitis herpetiformis.
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Essentials in Dermatology
Favus: A fungal infection of the scalp, usually caused by Trichophyton schoenleinii. It forms a
characteristic cup-shaped crust (scutula), which, on removal, exposes an oozing red surface.
Fernandez reaction: A delayed-type of hypersensitivity reaction to Dharmendra antigen in leprosy.
Fibroblasts: Fibroblasts are the most numerous of the cells found in loose connective tissue of dermis.
They are the source of the ground substance, collagen and elastic fibers.
Follicular plug: Hyperkeratosis distending a hair follicle opening.
Fordyce angiomata: Scrotal angiomata.
Fordyce spots: Ectopic sebaceous glands of inner surface and vermilion of lip and oral mucosa,
appearing as creamy-coloured symptomless lesions.
Fourniers gangrene: Fulminating gangrene of the external genitalia.
Fourniers sign: Bowing of the tibia seen in osteitis deformans, syphilis and yaws.
Fox-Fordyce disease: (Synonyms lichen axillaris, apocrine miliaria) intensely pruritic papular eruption
involving apocrine ducts in axillae, breasts or genital area.
Freckle: (Synonym ephelis) light-brown macules occurring in sun-exposed skin, especially in fairskinned persons.
Freis disease: Lymphogranuloma venereum.
Freis test: A diagnostic intradermal test of limited value for lymphogranuloma venereum.
Functions of the skin: Main functions of the skin are protection, thermoregulation, sensory, storage
organ, vitamin-D formation, absorption, excretion, immune surveillance, mechanical and cosmetic
function.
Furuncle: A localized painful nodular pyogenic infection originating around a hair follicle.
Gangrene: Commonly used to describe necrotizing and sloughing lesions but more properly referring
to death of tissue resulting from ischaemia.
Ghons focus: Primary tuberculous complex of the lung.
Giant cell: A cell with more than one nucleus. Langhans giant cell has peripheral ring of nuclei
whereas foreign body giant cell has haphazard arrangement of nuclei.
Giberts disease: Pityriasis rosea.
Glabrous: Smooth; commonly used to designate smooth, hairless skin; properly skin without any hair
follicles.
Gottrons sign: Erythematous papules over metacarpal and proximal interphalangeal joints in
dermatomyositis.
Granuloma: A chronic inflammatory lesion showing accumulations of macrophages which have
undergone epithelioid transformation, with or without lymphocytes and multi-nuclear giant cells;
more loosely, a nodular chronic inflammatory lesion arising in response to a variety of stimuli.
Graves disease: Hyperthyroidism due to diffuse toxic goitre.
Grenz zone: A zone of normal dermis overlying deeper pathological changes.
Ground substance: Ground substance is an amorphous material that consists mainly of water,
electrolytes, plasma proteins and mucopolysaccharides. A mucopolysaccharide consists of a longchain aminated polysaccharide (glycosaminoglycan) linked covalently to a polypeptide.
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Essentials in Dermatology
Hutchinson J Sir: British surgeon (18281913 AD). Outstanding figure in late 19th-century British
medicine. Possessed an extraordinary visual memory, he made wide-ranging contributions to many
aspects of medicine and surgery. His output was prodigious. A most careful observer and fascinating
teacher.
Hutchinsons teeth: Barrel-shaped incisors with a deep concentric notch seen in congenital syphilis.
Pegged, screwdriver teeth.
Hutchinsons triad: Interstitial keratitis, nerve deafness and tooth deformities in congenital syphilis.
Hydropic degeneration of basal cells: A type of degeneration causing vacuolization of the basal cells,
also called as liquefaction degeneration. It occurs in lupus erythematosus, dermatomyositis, lichen
sclerosus et atrophicus, lichen planus, etc.
Hypergranulosis: Increase in thickness of the granular layer of the epidermis.
Hyperkeratosis: Increase in the thickness of stratum corneum of the epidermis.
Ichthyol: A natural tar-like substance derived from bituminous deposits rich in fossilized fish.
Ichthyosis: A group of disorders of keratinization characterized by fine scaling and a feeling of dryness
of the skin (Greek ichthya rough fish skin from ichthys fish, osis).
-id, -ide: In dermatology the term ide, id, denotes a reaction occurring in a part remote from the
primary lesion, usually but not invariably due to an immunological reaction to the agent concerned or
to its component parts e.g. tuberculide, syphilide, trichophytide.
Idiopathic: Having no known cause.
Impetigo: A contagious eruption of the skin caused by the Streptococcus/Staphylococcus.
Incontinence of pigment: Loss of melanin from the cells of basal layer due to damage to these cells. It
is taken up by macrophages in the dermis.
Intertrigo: Inflammation of apposed skin surfaces such as groins, axillae and inframammary areas.
Ischaemia: State of lack of blood supply to a part or organ; arterial insufficiency.
Jarisch- Herxheimer reaction: A focal exacerbation of lesions when a disease of infective origin is
treated with potent antimicrobial agents. Seen in treatment of early syphilis with penicillin.
Kala-azar: Visceral form of leishmaniasis (Hindi kala black, Persian azar disease, poison). Also
known as Dum-Dum fever after a town near Calcutta, India.
Kaposis sarcoma: Multiple idiopathic haemorrhagic sarcoma.
Kaposis varicelliform eruption: Disseminated primary infection with viruses of herpes simplex,
vaccinia and perhaps Coxsackie A16, seen especially in atopic subjects. Now termed eczema
vaccinatum and eczema herpeticum.
Kawasakis disease: Mucocutaneous lymph node syndrome. SCREAM FEVER S - sausage fingers,
C - conjunctival redness, R-rash, E - extremity involvement, A-adenopathy, M - mucosal erythema,
FEVER-fever
Keloid: Alternative term for CHELOID and preferred by some in common usage.
Kerion: An inflammatory granuloma of hair-bearing areas due to superficial fungal infection,
particularly of zoophilic species.
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Essentials in Dermatology
Leucoplakia: Persistent white patches on mucous membranes not attributable to a known disease
process.
Libman-Sacks endocarditis: A verrucous endocarditis that may be associated with systemic lupus
erythematosus.
Lichen: An old term now restricted to a relatively small number of papular eruptions, of which lichen
planus is the most com-mon (Greek leichen a tree-moss, lichen or liverwort).
Lisch nodules: Pigmented iris hamartomas occurring in neurofibromatosis.
Livedo: A cyanotic discolouration of the skin of reticulate, patchy or mottled pattern due to venous
congestion or arterial disease.
Louse: An ectoparasitic insect belonging to the order Anoplura or Mallophaga; dermatologically,
head or body louse (Pediculus) or pubic louse (Phthirus).
Lucios phenomenon: A distinctive reactional state in the course of diffuse lepromatous leprosy
Lucio leprosy, Lepra bonita, a beautiful leprosy.
Lues: A disguised designation for syphilis but originally a term for plague.
Lupus: A term applied to lesions having an eroded or gnawed quality. Now confined to form of
cutaneous tuberculosis, especially lupus vulgaris, and lupus erythematosus where it is better fitted to
describe the discoid form.
Lyells syndrome: Another term for toxic epidermal necrolysis. Originally also included staphylococcal
scalded skin syndrome.
-lysis meaning loosening, separation or rupture.
Macrocheilia: Abnormal enlargement of lips.
Madura foot: Name for mycetoma, a tumid granulomatous fungal infection of the foot. Named after
Madura now Madurai, a town in South India.
Majocchis granuloma: A trichophytic granuloma of the dermis.
Malassezia: Name previously given to the dimorphic form of the lipophilic yeast Pityrosporum
orbiculare.
Malpighian layer: The basal and prickle-cell layers of the epidermis, also called as stratum malpighi.
Mantoux test: Intracutaneous tuberculin test for tuberculosis.
Marfans syndrome: A heritable disorder of connective tissue characterized by abnormally long
extremities, arachnodactyly and ocular and cardiovascular anomalies
Marjolins ulcer : Squamous cell epithelioma arising in an irritated scar tissue.
Martorells ulcer : Hypertensive ulcer of the leg.
Mast cell: Mastocyte widely dispersed mesenchymal cells found in the bone marrow, dermis and
other tissues, the cytoplasm of which contains numerous metachromatically staining granules. Mast
cells liberate histamines and various mediators during IgE mediated hypersensitivity responses.
Mees lines: Horizontal whitish striations observed on nails in acute arsenical poisoning but also
seen with other systemic disease.
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Essentials in Dermatology
Nigricans: Blackish; properly, becoming dark.
Nikolskys sign: Intra-epidermal cell separation or blister formation evoked by firm sliding pressure
on unaffected skin of patients with pemphigus (especially pemphigus foliaceus) and, sometimes,
epidermal necrolysis.
Nit: The egg of the louse; or the encased embryo.
Norwegian scabies: A form of extensive crusted scabies described by Boeck and seen in elderly,
immunocompromised or mentally defective patients.
Nummular: Assuming shape of coin, discoid.
Obliterans: Destroying, obliterating.
Ochre: A pigment of clay and iron oxide, of great antiquity; hence, yellow-red in color.
Ochronosis: Grayish or bluish discolouration of connective tissue and cartilage due to deposition of
a pigment derived from oxidized homogentisic acid, occurs in ALKAPTONURIA and in chronic
exposure to phenol and phenolic compounds.
Ointment: Semi-solid preparation in suitable base for application to the skin. Commonly used term
for greasy preparations as opposed to creams.
Onychia: Inflammation of nail matrix.
Onychogryphosis: Thickening and over curvature of the nail resembling a rams horn.
Onychoschizia splitting of nail plate into layers
Onychotillomania: Habit of fiddling with or pulling pieces off the nail, an obsessional or psychopathic
trait.
Ophiasis: Snake-like, curling; applied to a form of alopecia areata.
Orf: Ecthyma infectiosum. Highly contagious disease of sheep and goats caused by a parapoxvirus.
May infect man by contact.
Oslers nodes: Tender erythematous lesions occurring on pads of fingers and toes, or palms and soles
of patients with subacute bacterial endocarditis.
Oxyuriasis: Infestation by worm of genus enterobius; enterobiasis.
Pachydermoperiostosis: Hypertrophic osteoarthropathy with thickened skin.
Pachyonychia: Abnormally thick nails.
Pagets disease, extramammary: A malignant plaque occurring in anogenital area or axillae and
containing Paget cells.
Pagets disease of the nipple; mammary Pagets disease: A marginated scaly or crusted lesion of the
nipple containing intra-epidermal paget cells and associated with intraductal carcinoma of the breast.
Panniculus: A layer of fat, covering sheet or garment.
Papilloma: A nipple-like mass projecting from the surface of the skin.
Papillomatosis: Upward proliferation of subepidermal papillae.
Parakeratosis: Means retention of nuclei in the horny layer associated with a marked underdevelopment
or absence of the granular layer, seen in psoriasis and other disorders
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Essentials in Dermatology
Pruritus: A sensation of itching.
Pseudopelade: A morphological term for a pattern of follicular response to a variety of insults, often
unknown, resulting in patches of complete loss of scalp hair.
Psoriasis: A chronic, inflammatory skin disease consisting essentially of well-demarcated dull-red
plaques, though with many variants.
Mnemonic to remember features of PSORIASIS: Pink Papules/ Plaques/ Pinpoint bleeding
(Auspitzs sign)/ Physical injury (Koebner phenomenon)/ Pain Silver Scale/ Sharp margins
Onycholysis/ Oil spots Rete Ridges with Regular elongation Itching Arthritis/ Abscess (Munro)
Stratum corneum with nuclei, neutrophils Immunologic Stratum granulosum absent/ Stratum
Spinosum thickening.
Pterygium: Vascular lesions encroaching on the cornea; fusion of eponychium with proximal portion
of nail (pterygium unguis); web of skin extending from mastoid to achromial process as in Turners
syndrome (pterygium colli).
Purpura: Focal haemorrhage into the skin.
Pustule: A vesicle or bulla containing numerous neutrophils.
Pyoderma: Any purulent skin condition.
Queyrat, erythroplasia: An intra-epidermal carcinoma of male genital mucosa (glans and prepuce).
Quinkes oedema: Means angioedema.
Rash: Term for any inflammatory skin eruption
Raynauds disease: Primary idiopathic form of Raynauds phenomenon.
Raynauds phenomenon: Paroxysmal pallor, numbness and coldness of the extremities, often followed
by cyanosis, due to digital vasospasm. It occurs in a number of diseases, notably the collagen vascular
diseases.
Reiters syndrome: Non-specific urethritis, arthritis and iridocyclitis (uveitis). Patients may develop
a rupioid psoriasiform skin lesions in soles (keratoderma blennorrhagica).
Reticulate: Means lacy, webbed, net-like.
Rhagades: Cracks; fissures, a term used in congenital syphilis sequelae.
Rhinosporidiosis: A granulomatous nasal mycosis common in Sri Lanka and South India.
Ringwom: Very old term for any ring-shaped eruption; more recently used for superficial fungal
infections, dermatophytosis or tinea.
Ritters disease: Another name for staphylococcal scalded skin syndrome.
Rosacea: A condition characterized by erythema, telangiectasia and acneiform pustules commonly
affecting the central part of the face, occasionally scalp or elsewhere. Also termed acne rosacea.
Rowells syndrome: Lupus erythematosus with erythema multiforme-like lesions.
Sabourauds medium (agar): A culture medium for fungi, containing peptone and dextrose.
Sammans syndrome (synonym yellow nail syndrome): Thick, curved, slow growing yellowish
nails associated with lymphoedema.
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Essentials in Dermatology
Subcutaneous fat act as shock absorber, facilitate mobility of skin over structures that underlie and
acts as an insulator for heat.
Syndrome: A set of symptoms occurring together or the sum of signs in a morbid process.
Syphilis: Infection with Treponema pallidum.
Tabes (dorsalis): A form of neurosyphilis; locomotor ataxia.
TEN- Toxic Epidermal Necrolysis.
Thrush: Term for infection of the oral, pharyngeal and vaginal mucosae with Candida albicans.
Tinea: A fungal infection of skin, hair or nails caused by one of the dermatophytes Microsporum,
Trichophyton or Epidermophyton, except for its use in terms tinea amiantacea and tinea versicolor
(Latin tinea gnawing worm, moth).
Trachoma: Infection of conjunctiva and cornea by Chlamydia trachomatis. Trichotillomania- a
compulsion to pluck or twist out hair (Greek thrix, trichos hair, tillein to pluck, mania compulsion).
Ulcer: A well-defined area of loss of skin and subcutaneous tissue involving the whole thickness of
the skin and the underlying tissues, caused by infection, trauma or necrosis.
Urticaria: An eruption of itching wheals, of physical, systemic or (less commonly) contact origin;
nettle-rash, hives.
Vagabonds disease: A term for infestation with pediculosis corporis (French vagabond, from Latin
vagabundus one who strolls around, from vagare to wander).
Varicella: Disease caused by varicella-zoster virus; chicken-pox.
Vegetans: Exuberant; vigorous skin lesions.
Vellus: The short downy hair that replaces lanugo before or soon after birth on all hair-bearing areas
except the scalp (Latin vellus wool, down, fleece).
Venereal: Relating to or associated with sexual intercourse (Latin venereus from Venus, Veneris
goddess of love).
Verruca: Wart, excrescence; now used to denote viral wart, particularly of foot.
Vesicle: A small blister less than 5 mm in diameter.
Vitiligo: A primary loss of pigmentation from skin and hair, of unknown cause (Latin vitiligo a skin
disease possibly from vitium flaw, blemish).
Vulgaris: Common, ordinary.
Wart (synonym verruca): This term used for any horny excrescence on the skin but properly so for
lesions induced by the papovavirus.
Weal (wheal): A transient circumscribed oedematous swelling as seen in urticaria or dermographism.
Whitfields ointment: 6% benzoic acid compounded with 3% salicylic acid as ointment.
Whitlow: Acute paronychia or purulent infection (abscess) of distal finger pulp; felon. Also, specifically,
herpetic or melanotic whitlow.
Wickhams striae: A characteristic pattern of white streaking seen on papules of lichen planus.
463
Answers
Answers
Set I (1-400)
1.B
11.B
21.A
31.A
41.B
51.A
61.B
71.A
81.B
91.A
101.C
111.A
121.C
131.A
141.D
151.D
161.D
171.C
181.B
191.B
201.C
211.D
221.C
231.B
241.C
251.A
261.D
271.C
281.D
291.A
301.B
2.A
12.C
22.D
32.A
42.D
52.B
62.A
72.C
82.C
92.D
102.A
112.A
122.C
132.C
142.D
152.C
162.C
172.A
182.B
192.C
202.C
212.A
222.A
232.D
242.B
252.C
262.D
272.D
282.B
292.D
302.C
3.A
13.B
23.B
33.A
43.A
53.A
63.B
73.B
83.D
93.D
103.B
113.C
123.D
133.A
143.B
153.B
163.A
173.A
183.C
193.A
203.D
213.D
223.A
233.B
243.D
253.B
263.C
273.D
283.A
293.D
303.A
4.C
14.D
24.A
34.C
44.B
54.A
64.B
74.C
84.A
94.A
104.A
114.A
124.C
134.D
144.A
154.B
164.C
174.D
184.C
194.C
204.D
214.C
224.A
234.D
244.A
254.B
264.A
274.D
284.D
294.B
304.C
5.A
15.C
25.A
35.C
45.B
55.B
65.A
75.B
85.D
95.D
105.C
115.D
125.A
135.C
145.A
155.D
165.A
175.B
185.A
195.A
205.B
215.B
225.D
235.A
245.B
255.B
265.D
275.D
285.B
295.A
305.C
6.B
16.A
26.A
36.C
46.B
56.A
66.B
76.C
86.A
96.D
106.D
116.C
126.D
136.B
146.D
156.B
166.B
176.D
186.D
196.C
206.D
216.A
226.D
236.B
246.A
256.A
266.C
276.A
286.A
296.A
306.A
7.A
17.B
27.C
37.A
47.B
57.B
67.A
77.B
87.D
97.C
107.C
117.A
127.A
137.A
147.B
157.D
167.A
177.C
187.B
197.A
207.C
217.C
227.C
237.B
247.B
257.D
267.D
277.C
287.A
297.D
307.A
8.C
18.D
28.B
38.C
48.A
58.B
68.D
78.A
88.A
98.A
108.A
118.D
128.A
138.A
148.B
158.D
168.D
178.A
188.A
198.D
208.B
218.C
228.B
238.C
248.B
258.D
268.A
278.C
288.A
298.C
308.D
9.A
19.D
29.C
39.A
49.A
59.B
69.B
79.C
89.B
99.C
109.A
119.A
129.B
139.D
149.D
159.C
169.A
179.C
189.C
199.B
209.D
219.D
229.B
239.B
249.C
259.B
269.B
279.D
289.D
299.C
309.C
10.B
20.A
30.D
40.B
50.A
60.C
70.A
80.A
90.B
100.A
110.D
120.D
130.C
140.A
150.A
160.C
170.D
180.B
190.D
200.A
210.A
220.A
230.D
240.A
250.D
260.B
270.B
280.C
290.A
300.D
310.D
Contd...
465
466
Essentials in Dermatology
Contd...
311.A
321.A
331.A
341.A
351.C
361.D
371.B
381.A
391.A
312.B
322.D
332.A
342.C
352.A
362.A
372.C
382.B
392.A
313.A
323.C
333.C
343.A
353.D
363.C
373.B
383.A
393.A
314.A
324.A
334.D
344.A
354.D
364.A
374.D
384.A
394.A
315.B
325.C
335.D
345.D
355.A
365.C
375.D
385.A
395.A
316.D
326.A
336.A
346.A
356.A
366.B
376.A
386.A
396.B
317.A
327.D
337.D
347.A
357.A
367.B
377.B
387.B
397.C
318.B
328.A
338.C
348.A
358.C
368.A
378.B
388.A
398.C
319.A
329.A
339.C
349.D
359.B
369.D
379.A
389.A
399.D
320.D
330.B
340.C
350.A
360.C
370.A
380.A
390.D
400.A
7. C
15. C
23. B
31. B
39. A
47. D
55. C
63. A
71. B
79. D
87. B
95. D
103. C
111. B
119. A
127. A
135. B
143. A
151. D
159. C
167. C
175. B
183. B
191. B
199. A
207. D
215. A
223. C
231. C
239. D
8. D
16. A
24. A
32. A
40. B
48. B
56. B
64. D
72. B
80. B
88. B
96. A
104. A
112. C
120. B
128. A
136. D
144. C
152. C
160. B
168. B
176. C
184. B
192. C
200. B
208. B
216. D
224. B
232. B
240. D
2. B
10. C
18. A
26. D
34. C
42. A
50.C
58. A
66. A
74. A
82. A
90. A
98. D
106. D
114. A
122. A
130. A
138. D
146. B
154. C
162. C
170. A
178. A
186. A
194. A
202. A
210. C
218. B
226. B
234. B
242. D
3. C
11. A
19. C
27. B
35. A
43. D
51. B
59. B
67. B
75. C
83. B
91. C
99. B
107. C
115. C
123. B
131. B
139. D
147. A
155. A
163. A
171. D
179. B
187. A
195. A
203. A
211. A
219. C
227. C
235. C
243. A
4. D
12. D
20. A
28. D
36. C
44. D
52. D
60. C
68. D
76. C
84. D
92. B
100. A
108. B
116. B
124. D
132. D
140. A
148. D
156. D
164. D
172. A
180. D
188. C
196. C
204. D
212. D
220. A
228. D
236. C
244. B
5. D
13. B
21. B
29. D
37. A
45. C
53. A
61. C
69. A
77. A
85. D
93. B
101. C
109. A
117. C
125. D
133. B
141. A
149. A
157. B
165. A
173. A
181. D
189. B
197. A
205. B
213. B
221. B
229. D
237. B
245. B
6. A
14. A
22. B
30. A
38. C
46. A
54. D
62. B
70. C
78. D
86. A
94. A
102. B
110. D
118. B
126. B
134. A
142. B
150. D
158. C
166. C
174. A
182. A
190. D
198. A
206. A
214. C
222. C
230. A
238. A
Answers
Key to MCQs in Dermatology- Basic Sciences (1-55)
1.B
5.A
9.B
13.A
17.D
21.A
25.C
29.D
33.D
37.C
41.D
45.D
49.A
53.C
2.C
6.A
10.B
14.B
18.D
22.C
26.D
30.D
34.D
38.D
42.B
46.B
50.A
54.A
3.B
7.C
11.D
15.B
19.C
23.A
27B
31.D
35.D
39.D
43.C
47.C
51.A
55.C
4.A
8.D
12.B
16.C
20.C
24.A
28.D
32.D
36.D
40.A
44.C
48.A
52.A
2. C
10. C
18. C
26. C
34. C
42. B
50. A
58. D
66. D
74. C
82. B
90. A
98. A
106. B
3. A
11. C
19. C
27. A
35. C
43. D
51. C
59. B
67. A
75. D
83. B
91. C
99. C
107. B
4. C
12. D
20. C
28. C
36. A
44. C
52. B
60. B
68. A
76. D
84. B
92. B
100. D
108. A
5. C
13. C
21. D
29. A
37. B
45. A
53. C
61. A
69. B
77. D
85. B
93. B
101. D
109. C
6. C
14. A
22. B
30. B
38. A
46. A
54. B
62. D
70. D
78. B
86. A
94. D
102. D
110. C
7. B
15. A
23. A
31. A
39. A
47. C
55. B
63. D
71. C
79. B
87. B
95. C
103. B
8. B
16. A
24. C
32. D
40. B
48. C
56. C
64. D
72. A
80. B
88. D
96. D
104. B
7. A
15. B
23. A
31. D
39. D
47. A
55. A
63. A
71. A
79. C
87. A
95. A
8. A
16. B
24. A
32. A
40. C
48. D
56. A
64. A
72. A
80. B
88. A
96. C
2. C
10. B
18. B
26. A
34. D
42. A
50. C
58. A
66. D
74. A
82. B
90. A
98. B
3. A
11. A
19. A
27. D
35. D
43. C
51. B
59. A
67. A
75. A
83. A
91. B
99. D
4. A
12. D
20. A
28. A
36. A
44. A
52. A
60. A
68. A
76. A
84. C
92. A
5. D
13. A
21. A
29. B
37. A
45. A
53. C
61. A
69. C
77. A
85. B
93. A
6. D
14. A
22. A
30. A
38. B
46. A
54. B
62. A
70. D
78. A
86. B
94. A
467
468
Essentials in Dermatology
Key to MCQs in Sexually Transmitted Diseases (1-130)
1. B
9. A
17. C
25. B
33. D
41. C
49. A
57. A
65. B
73. C
81. C
89. A
97. A
105. D
113. C
121. C
129. C
2. D
10. A
18. A
26. B
34. D
42. D
50. D
58. C
66. A
74. A
82. A
90. C
98. A
106. B
114. A
122. D
130. D
3. D
11. D
19. B
27. C
35. B
43. C
51. A
59. D
67. B
75. B
83. D
91. A
99. B
107. D
115. A
123. A
4. D
12. B
20. D
28. A
36. A
44. C
52. D
60. B
68. A
76. A
84. B
92. C
100. C
108. C
116. A
124. B
5. C
13. A
21. B
29. A
37. D
45. B
53. C
61. C
69. B
77. D
85. C
93. B
101. D
109. D
117. C
125. A
6. D
14. D
22. B
30. C
38. B
46. D
54. A
62. A
70. B
78. D
86. D
94. B
102. A
110. B
118. D
126. A
7. D
15. B
23. A
31. B
39. D
47. D
55. D
63. A
71. A
79. D
87. C
95. C
103. D
111. B
119. B
127. B
8. C
16. C
24. C
32. D
40. C
48. D
56. C
64. D
72. D
80. D
88. B
96. C
104. C
112. D
120. C
128. A
6. A
14. C
22. A
30. D
38. A
46. A
54. A
62. A
70. B
78. C
86. B
94. D
7. D
15. C
23. B
31. B
39. D
47. A
55. D
63. B
71. C
79. B
87. B
95. A
8. C
16. D
24. B
32. B
40. C
48. D
56. A
64. D
72. C
80. C
88. B
2. D
10. B
18. C
26. B
34. A
42. A
50. D
58. B
66. B
74. A
82. B
90. D
3. A
11. B
19. C
27. A
35. A
43. C
51. C
59. D
67. C
75. B
83. A
91. A
4. A
12. B
20. D
28. C
36. D
44. A
52. D
60. A
68. A
76. C
84. A
92. A
5. D
13. A
21. B
29. D
37. A
45. D
53. A
61. B
69. A
77. C
85. A
93. C