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Skin tutorial

Alopecia areata:
Alopecia areata (AA) is a recurrent non-scarring type of hair loss that can affect any hair-bearing area
The most widely accepted hypothesis is that AA is a T-cell mediated autoimmune condition that is most likely to occur in genetically predisposed individuals.

Alopecia totalis refers to the total absence of scalp and hair.


Alopecia universalis refers to total loss of body and scalp hair.

The scalp appears normal in alopecia areata. The near pathognomic exclamation point hairs may be present, particularly at the periphery of areas of hair loss.

AA most often is asymptomatic, but some patients (14%) experience a burning sensation or pruritus in the affected area. A scalp biopsy is generally unnecessary to establish the diagnosis of alopecia areata, except in the uncommon presentations.

Associated conditions;
Atopic dermatitis is seen in 9-26% of patients with AA.
Vitiligo is seen with an incidence varying from 1.83% compared to 0.3% in control subjects. Thyroid disease: Clinically evident thyroid disease was found in 0.85% of 1700 patients with AA.

Diabetes mellitus: The incidence of type I diabetes mellitus was significantly higher Others associations: Pernicious anemia, MG, ulcerative colitis, lichen planus, and Candida endocrinopathy syndrome

Precipitating factors;
Major life events Febrile illnesses Drugs Pregnancy Trauma

Despite these findings, most patients with AA fail to report a triggering factor preceding episodes of hair loss.

Physical findings:
Presence of smooth slightly erythematous (peach color) or normal-colored alopecic patches is characteristic.

Presence of exclamation point hairs is pathognomonic sign. Positive pull test at the periphery of a plaque usually indicates that the disease is active, and further hair loss can be expected.

DDx; Non-scarring alopecia


Trichotillomania:
Alopecic patches have unusual shapes and sizes and show broken hairs, no inflammation or epidermal change occurs. A scalp biopsy can be helpful if the diagnosis is difficult clinically.

Tinea capitis:
The diagnosis is suggested by erythema, scaling, and crusting locally on the scalp.

Telogen effluvium (TE)


Exclude these when hair loss is diffuse. Differentiating TE from diffuse AA is difficult in absence of an obvious precipitating factor that can result in TE.

Secondary Sy : moth eaten alopecia

Drug :
Thallium, heparin, chemotherapy Chronic vitamin A intoxication

Endocrine
Hypo/hyperthyroid, hypopituitarism Hypo/hyperparathyroidism

Systemic disease
Dermatomyositis SLE Cachexia malignancy

Intralesional steroids:
Intralesional steroids are the first-line treatment in localized conditions. Triamcinolone acetonide (Kenalog) is used most commonly. Adverse effects mostly include pain during injection and minimal transient atrophy (10%). Injections are administered every 4-6 weeks.

Topical steroids

Prednisone:
Systemic prednisone is not an agent of choice for AA because of the adverse effects associated with both short-term and long-term treatment.
Alopecia totalis, alopecia universalis

Dinitrochlorobenzene (DNCB)

Key points
Check palms and soles..10 Check oral cavity5 Check lymph node status..10 Describe lesions.40
Hyperkeratotic papules of palms and soles 20 Hyperpigmentation and mottling depigmented macules20

Key points
Dx Chronic arsenic poisoning..20 Associated diseases.15 Bowens disease5 Squamous cell CA.5 Internal malignancy5

Chronic arsenic poisoning:


Arsenic has been used as a medicinal agent, a pigment, a pesticide, and an agent of criminal intent. Arsenic is primarily used in the production of glass and semiconductors. It is also found in certain water supplies and seafood.

Arsenic is listed as a presumed carcinogenic substance based on the increased prevalence of lung and skin cancer observed in human populations with multiple exposures (primarily through industrial inhalation).

Physical findings;
Acute exposures
Generally manifest with the choleralike GI symptoms of vomiting and severe diarrhea. These patients will experience acute distress, dehydration (often), and hypovolemic shock.

Chronic toxicity
is more insidious and may manifest as a classical dermatitis hyperkeratosis papules of palms and soles Hyperpigmentation and mottling depigmented macules ("dew drops on a dusty road" appearance).

Affect the nipples, axillae, groin and other pressure points, spare the oral mucosa Transverse whitish narrow fingernail bands, Mees line Peripheral neuropathy (usually a painful paresthesia that is symmetrical and stockingglove in distribution).

Diffuse alopecia of scalp hair and acrodermatitis and thromboangiitis-like changes of the legs or gangrene Their inhalation may result of nasal septum perforation
Other systemic intoxication such as neuropathy, anemia, leukopenia, thrombocytopenia Diagnosis of the arsenic exposure may be difficult,high arsenic in hair and nail

Arsenical keratoses develop at sites of friction and trauma, especially on the palms and soles (heels and toes), as multiple, punctate, hard, yellowish, often symmetric, cornlike papules usually 2 to 10 mm in diameter. Most arsenical keratoses persist for years without evolving into invasive SCC.

Chronic hepatic and renal damage is common with chronic exposure. Associated conditions;
Bowens disease.
Bowen disease is a squamous cell carcinoma (SCC) in situ with the potential for significant lateral spread.

Squamous cell carcinoma. Internal malignancy.

Arsenic can be chelated with dimercaprol, but by the time cutaneous and other neoplasms have developed, there are likely to be no traces of arsenic left to remove.

Excision, cryosurgery Retinoids

Key points;
Check nail and surrounding tissues10 Check interdigital web.10 Check oral cavity...10 Check axilla, groin, inframammary..1

Periungual swelling..10 Nail dystrophy, onycholysis.............................10 Other site of candida infection...10 Dx : candida paronychia10

Associated conditions;(2/4)20
Too many hand washing. DM. Steroid usage and immunosuppressive agents. Chronic cutaneous candidiasis.

Candida paronychia:
Candida organisms occasionally cause infection in the periungual area and underneath the nailbed.

The yeast is believed to play an etiologic role in this condition, but bacteria also may act as copathogens.

Progression to total nail dystrophy has been associated specifically with C albicans and usually has been limited to women with 2 important predisposing conditions, ie, Cushing syndrome and Raynaud disease.
Disease is more common in people who frequently submerge their hands in water.

Physical findings;
The nailfold becomes erythematous, swollen, and tender, with an occasional discharge. Loss of the cuticle occurs, along with nail dystrophy and onycholysis with discoloration around the lateral nailfold. A greenish color with hyponychial fluid accumulation may occur that results entirely from Candida, and not Pseudomonas, infection.

A potassium hydroxide (KOH) preparation is helpful and is likely to show yeast organisms.

Host factors that predispose patients to infections are numerous. Endocrine diseases such as DM, Cushing syndrome, hypoparathyroidism, hypothyroidism, and polyendocrinopathy are associated with increased susceptibility to infection.

A. Pseudomembranous candidiasis or thrush. Note the characteristic white patches on the palate. B. Atrophic candidiasis under dentures. C. Candida perlche with erythema and fissuring at the corners of the mouth. D. Hyperplastic candidiasis of the tongue. E. Black hairy tongue is characterized by pigmented hypertrophied filiform papillae of the dorsum of the tongue and is usually associated with oral antibiotic therapy

FIGURE 206-3 Candidal intertrigo.

A. Erythematous, eroded plaques involving the scrotum and inguinal area with satellite lesions. B. Confluent and discrete erythematous, eroded areas with pustular and erosive satellite lesions

C. The infant shows red macular plaques on the vulva surrounded by a delicate collar. Outside the main lesions are a few satellite lesions D. Erosio interdigitalis blastomycetica. Erythematous eroded areas between the fingers occurring in a waitress.

Treatment with topical agents usually is not effective but should be tried for chronic candidal paronychia.
Keep hands as dry as possible Use glove for all wet works Nystatin or imidazoles cream Topical steroid

kenacomb

Skin and oral mucosa treatement


Nystatin oral tablets 100,000 unit qid Oral suspension 1-2 teaspoon held in mouth for 5 min and then swallowed Fluconazole 200 mg po once followed by 100mg/ day 2-3 wks Itraconazole 100 mg od or bid 2 wks

Nail treatment
Griseofulvin 1-2 gm/day 6 mo for fingernail 12 mo for toe nail Itraconazole 400 mg / day [200 mg bid ] * 7 day every 1 mo 2 mo [ finger nail] 3 mo [ toe nail ] Terbinafine 250 mg/d 6 wk for fingernail 12 wk for toe nail