IMMUNOLOGY ● is how your body recognizes and
defends itself against bacteria,
Why there are new strain of viruses?
● Pathogens can rapidly evolve and
adapt to avoid detection and
neutralization by the immune
system. As a result, multiple defense
mechanisms have also evolved to
recognize and neutralize pathogens
Immune function is affected by  (is closely associated with the
● age and by a variety of other
factors,
● central nervous system function,
● emotional status, “LOVENAT”
● Medications,
● the stress of illness,
● Trauma
●  and surgery.
Dysfunctions involving the immune
system occur across the life span. Many
are genetically based; others are
acquired.
Immune System
● comprises CELLS & MOLECULES
● functions as the body’s defense
mechanism against invasion
● The immune system comprises
cells and molecules with
specialized roles in defending
against infection and invasion by
other organisms.
Immunity  The primary function of the lymph
● refers to the body’s specific
protective response to an
invading foreign agent or
organism
Immunology  recycled blood plasma.
● is the study of protection from
foreign macromolecules or
invading organisms and the
body’s responses to them.
Immunopathology
● refers to the study of diseases
resulting from dysfunctions within
the immune system.
Immune response 
viruses, and substances that
appear foreign and harmful.
LYMPHATIC SYSTEM
● Major part of immune system
● is a part of the circulatory system,
cardiovascular system)
comprising a network of conduits
( tube/channel/duct)
● [a natural or artificial channel
through which something (as a
fluid) is conveyed] called
lymphatic vessels that carry a
clear fluid called lymph (from
Latin lympha "water goddess")
unidirectionally towards the
heart. 
● ***The circulatory system
processes an average of 20 liters
of blood per day through capillary
filtration which removes plasma
while leaving the blood cells.
Roughly 17 liters of the filtered
plasma actually get reabsorbed
directly into the blood vessels,
while the remaining 3 liters are
left behind in the interstitial fluid.
system is to provide an
accessory route for these excess
3 liters per day to get returned to
the blood.Lymph is essentially
PRIMARY FUNCTION OF LYMPHATIC
SYSTEM & IMMUNE SYSTEM
● Draining excess interstitial fluids
● Transporting dietary lipids
● Carrying out immune responses
Organs of Immune System
  Based on the Functions:
1.Primary Lymphatic Organs ●  they monitor intestinal bacteria
populations and preventing
•Bone Marrow growth of pathogenic bacteria in
the intestine
•Thymus
Primary Lymphatic Organs
2.Secondary Lymphatic Organs ● the sites where pluripotent
(substances having the capacity
•Lymph Nodes
to produce several distinct
biological responses) stem cells
•Lymph Nodules
divide and become
●  Tonsils
immunocompetent
● - Peyer’s Patches A. BONE MARROW
●  the bone marrow is the
•Spleen production site of the WBCs
involved in immunity.
MAJOR COMPONENT OF IMMUNE ● is the flexible tissue found in the
SYSTEM interior of bones.
● bone marrow, ● a key component of the lymphatic
● white blood cells (WBCs) system, producing the
produced by the bone marrow, lymphocytes that support the
● lymphoid tissues. body's immune system.
- Lymphoid tissues includes (they are 2 types:
made of same tissue, the lymphoid ● Red Marrow - Red blood cells,
tissue) platelets and most white blood
● thymus gland, cells arise in red marrow.
● Spleen, ● Yellow Marrow – fat
● lymph nodes, cells/adipocyte cell- it gives rise
● Tonsils to our adipose tissue, a loose
● adenoids, (mass of soft tissue fibrous connective tissue that are
behind the nasal cavity, WBC specialized for storage of
circulate through the adenoids & triglycerides are commonly
other lymphoid tissue, reacting to referred to as fats.
invaders. Triglycerides/fats– store energy, insulate
*** adenoids is present at birth and in us and protect our vital organ. They also
childhood but in adolescent years it act as messenger, helping protein to do
starts to shrink and at adulthood most their jobs
people’s adenoids disappear) B lymphocytes - mature in the bone
● and similar tissues in the marrow and then enter the circulation.
gastrointestinal, respiratory, and T lymphocytes - move from the bone
reproductive systems marrow to the thymus, where they
Peyer’s patches/ a.k.a. aggregated mature into several kinds of cells
lymphoid nodules capable of different functions.
● are small masses of lymphatic
B.  Thymus
tissue found through the ileum
region of the small intestine.
 – bilobed organ (mediastinum -  between
sternum & aorta)
Bilobed - Having or consisting of two
lobes.
●  Located at anterior superior
mediastinum, in front of the heart
and behind the sternum.
● decreases in size after puberty.
(thymic involution)
● Reservoir of mature T
lymphocytes
Lobule – Outer cortex
●  Large number of T cells
         -  Central medulla
●   widely scattered, more mature T
cells
Cells in the THYMUS are:
•Thymic stromal cell
● Thymic cortical epithelial cells
● Thymic medullary epithelial cells
● Dendritic cells
•Cells of hematopoietic origin
● Developing T-cells = thymocytes
● (derived from bone marrow
resident hematopoietic stem
cells).  length and do not have capsules.
Developing T-cells are referred to as
thymocytes and are of hematopoietic
origin. > Stromal cells include
● thymic cortical epithelial cells,
● thymic medullary epithelial cells,
and 
● dendritic cell
FUNCTIONS of THYMUS
● Immature T cells migrate from the
bone marrow to the thymus (via)
the blood.
● The epithelial cells secrete a
hormone called thymosin, which
stimulates the maturation of T
cells after they leave the thymus
and migrate to other lymphatic
tissues.
● The thymus is the site of
maturation of T cells (which will
leave the thymus and provide
immunity)
II. Secondary Lymphatic Organs
A. Lymph Nodes
  - containing large numbers of leukocyte
 -  mammary glands, axillae & groin
- The lymph nodes also serve as centers
for immune cell proliferation.
- are masses of lymphatic tissue.
  Functions:  
● to filter lymph
● serve as a center for the production
of PHAGOCYTES
nodes - are usually larger, 10 to 20 mm
in length, and are encapsulated; 
Nodules- range from a fraction of a
millimeter to several millimeters in
B. Lymph Nodules  (tonsil,peyer patches)
● The remaining lymphoid tissues,
such as the tonsils and adenoids
and other mucoid lymphatic
tissues, contain immune cells that
defend the body’s mucosal
surfaces against microorganisms.
● small, localized collection of
lymphoid tissue, usually located
in the loose connective tissue
beneath wet epithelial (covering
or lining) membranes, as in the
digestive system, respiratory
system, and urinary bladder.
 ● The nodule differs from a lymph They live for about three to four
●
node in that it is much smaller days in the average human
and does not have a well-defined body. 
connective-tissue capsule as a ● Leukocytes are found throughout
boundary. It also does not the body, including the blood and
function as a filter, because it is lymphatic system.
not located along a lymphatic ● The number of leukocytes in the
vessel.  blood is often an indicator of
disease. 
C.  Spleen ● There are normally approximately
● is located in the upper left portion of 7000 white blood cells per
the abdominal cavity (behind microliter of blood. 
stomach). ● They make up approximately 1%
of the total blood volume in a
contains 2 types of tissue:
healthy adult
● white pulp = contains lymphocytes  BASIC TYPES OF LEUKOCYTES
& macrophages
● red pulp = site for old and injured A. Phagocytes
RBC’s to be   destroyed. ● cells that “chew up”  invading
FUNCTIONS: organism
B. Lymphocytes
● Removal and destruction of
● cells that allow the body to
foreign particles and worn blood remember and recognize previous
cells from blood. invaders and help the body destroy
 - Macrophages remove and them.
destroy bacteria and damaged or PHAGOCYTIC CELLS TYPES
worn red blood cells and 1. Neutrophil
platelets    through phagocytosis. 2. Eosinophil
3. Mast Cells 
● stores and releases blood during
4. Macrophages 
hemorrhage.
● Monocyte becomes
● in immunity as a site of B cell
macrophages
proliferation into plasma cells.
5. Dendritic Cells
● Storage of platelets, 1/3 of body
supply
● Production of cells during fetal Leukocytosis - An increase in the
life. number of leukocytes over the upper
White blood cells/Leukocytes  limits 
(also spelled "leucocytes") Leukopenia - a decrease below the
● are cells of the immune system lower limit 
involved in defending the body
against both infectious disease TYPES OF PHAGOCYTES
and foreign materials
● All leukocytes are produced and I. GRANULOCYTES
derived from a multipotent cell in ● Granular leukocytes, or
the bone marrow known as a granulocytes(so called because
hematopoietic stem cell.  of granules in their cytoplasm),
 ● fight invasion by foreign bodies or
toxins by releasing cell
mediators, such as histamine,
bradykinin, and
prostaglandins,
● and engulfing the foreign bodies
or toxins.
● Granulocytes include neutrophils,
eosinophils,and basophils
Neutrophils
● 60 – 70% of WBC (62%)
● Polymorphonuclear (PMN) [because
their nuclei have multiple lobes]
● Primary  phagocyte; 1 to arrive;
st
(bacteria and fungi)
● 6 – 12 hours after initial injury
● Contain enzymes & other
antibacterial substances
● Life span of 6-10 hours to few days
(5.4 days)
● Their activity and death in large
numbers forms pus.
● multilobed
Eosinophils
● 1 – 3% of WBC (2.3%)
● Bilobed
● Contain a protein that is highly toxic
to large parasitic worms
● Controls the release of serotonin &
histamine
● Modulates allergic inflammatory
responses
● LS: 8-12 days (circulate 4-5 hours)
Basophils
● .3 - .5% of WBC (.4%)
● Bi-lobed or tri-lobed
● Releases histamine, bradykinin,
serotonin, leukotrines in acute
hypersensitivity reaction
Bradykinin - is a peptide that causes
blood vessels to dilate (enlarge), and
therefore causes blood pressure to
lower.
Histamine -  is an organic nitrogen
compound involved in local immune
responses as well as regulating
physiological function in the gut and
acting as a neurotransmitter.
● Histamine triggers the
inflammatory response.
Histamine increases the
permeability of the capillaries
to white blood cells and some
proteins, to allow them to engage
pathogens in the infected tissues
Serotonin - is a monoamine
neurotransmitter,  thought to be a
contributor to feelings of well-being and
happiness.
Leukotrienes- are fatty signaling
molecules. They were first found in
leukocytes (hence their name). One of
their roles (specifically, leukotriene D4) is
to trigger contractions in the smooth
muscles lining the trachea; their
overproduction is a major cause of
inflammation in asthma and allergic
rhinitis
II. AGRANULOCYTES
Monocytes/Macrophages
● 5.3% (2-3%)
● Kidney shaped
●  also function as phagocytic
cells, engulfing, ingesting, and
destroying greater numbers and
quantities of foreign bodies or
toxins than granulocytes
● Monocytes share the "vacuum
cleaner" (phagocytosis) function
of neutrophils, but are much
longer lived as they have an extra
role: they present pieces of
pathogens to T cells so that
the pathogens may be
recognized again and killed.
This causes an antibody
response to be mounted.
● Monocytes eventually leave the
bloodstream and become tissue
macrophages, which remove
 dead cell debris as well as GIANT CELLS Connective
attacking microorganisms. tissue
● Once monocytes move from the
bloodstream out into the body
tissues, they undergo changes Lymphocytes
(mature) allowing phagocytosis ● primary cell of the immune
and are then known as system
● represents 25 – 35% of blood
macrophages.
MACROPHAGES leukocytes
● About 60% to 70% of
● mature forms of blood monocytes lymphocytes in the blood are T
● general scavenger cells of the body cells, and about 10% to 20% are
● Process & present antigen to B cells
specific lymphocytes ● B cells & T cells are the small
● One important role of the granular lymphocytes
macrophage is the removal of ● NK(natural killer) cell are the
necrotic cellular debris in the large granular lymphocytes
lungs. Removing dead cell ● Involved in cellular and humoral
material is important in chronic immunity
inflammation, as the early stages 3 KINDS OF LYMPHOCYTES
of inflammation are dominated by 1.B (bursa derived) lymphocytes / B
neutrophil granulocytes, which cells(small granular lymphocytes)
are ingested by macrophages if ● mature in the bone marrow
they come of age ● essential for humoral immunity
● B cells make antibodies that can
bind to pathogens, block pathogen
Name of Cell Location invasion, activate the complement
system, and enhance pathogen
ALVEOLAR Pulmonary
destruction.
MACROPHAGES alveolus of the
2. T (thymus cells) Lymphocytes / T cells
lungs
(small granular lymphocytes)
HISTIOCYTES Connective ● mature in the thymus
tissue ● responsible for cell-mediated
immunity
KUPFFER CELLS LIVER 3. Natural Killer Cells
● Large granular lymphocytes 
MICROGLIA Neural ● Not identifiable as either T or B
tissue/Brain cells
● Non specific effector cells that
EPITHELOID CELLS Granulomas 
can kills tumor and virus infected
OSTEOCLASTS Bone  cells
● Do not need to recognize a
SINUSOIDAL LINING spleen specific antigen before being
CELLS activated
● NK cells are a part of the innate
INTRAGLOMERULAR kidney
immune system and play a major
MESANGIAL CELLS
role in defending the host from
 both tumors and virally infected
cells.  glycoproteins; the term "cytokine"
● NK cells distinguish infected cells
and tumors from normal and
uninfected cells by recognizing
changes of a surface molecule
called MHC (major
histocompatibility complex) class
I agents, such as interleukins and
● NK cells are activated in
response to a family of cytokines
called interferons.  during all phases of an immune response
● Activated NK cells release
cytotoxic (cell-killing) granules
which then destroy the altered
cells
● They were named "natural killer
cells" because of the initial notion
that they do not require prior
activation in order to kill cells
which are missing MHC class I.
MAJOR HISTOCOMPATIBILITY
COMPLEX (MHC)
● group of genes responsible for
the recognition of self from non-
self
2 major types:
1.MHC 1 or HLA- (human leukocyte
antigen)
● first identified in leukocytes;
found on the surface of almost all
hosts
2.MHC 2
● found mainly on immune system
cells
MHC 1&2= PRESENT ANTIGEN TO T
CELLS
CYTOKINES
-(Greek cyto-, cell; and -kinos,
movement) are small cell-signaling
protein molecules that are secreted
by numerous cells and are a category
of signaling molecules used
extensively in intercellular
communication. Cytokines can be
classified as proteins,peptides, or
encompasses a large and diverse family
of regulators produced throughout the
body by cells of diverse embryological
origin.
- The term "cytokine" has been used to
refer to the immunomodulating
interferons.
- regulatory proteins that are produced
•Molecules that form a communication link
between immune cells & other tissues &
organs of the body
  a. Interleukin 1 / IL-1
  - mediator of the inflammatory
response
 b. Interleukin 2 / IL – 2
  - necessary for the proliferation and
function of helper T, cytotoxic T, B cells,
& NK cells
 c. Interferons / IFNs
  - protect neighboring cells from
invasion by intracellular parasites,
including viruses, rickettsiae, malarial
parasites and other organisms
MAST CELLS
● contains many granules rich in
histamine and heparin
● has a role in allergy & anaphylaxis
● involved in wound healing and
defense against pathogens.
● Although best known for their role
in allergy and anaphylaxis, mast
cells play an important protective
role as well, being intimately
involved in wound healing and
defense againstpathogens
● The mast cell is very similar in
both appearance and function to
the basophil, a type ofwhite blood
 cell. However, they are not the ASSESSMENT
same, as they both arise from
different cell lines Health History - age, nutrition, infection
● can be stimulated to degranulate and immunization, allergies, disorders and
by direct injury, cross-linking of diseases (autoimmune diseases,
neoplastic), chronic illness and surgery,
Immunoglobulin E (IgE)
special problems like burns, medications
receptors, or by activated and blood transfusions, lifestyle and other
complement proteins. factors.
DENDRITIC CELLS Physical Assessment
1. Respiratory System
● together with macrophages, present ● Changes in respiratory rate
antigen to T cells ● Cough (dry or productive)
● found in lymphoid tissues and other ● Abnormal lung sounds (wheezing,
body areas where antigen enters the crackles, ronchi)
body ● Rhinitis
● “Messenger” ● Hyperventilation
● Dendritic cells (DCs) are antigen- ● Bronchospasm
presenting cells, (also known as 1. Cardiovascular System
● Hypotension
accessory cells) of the
● Tachycardia
mammalian immune system. ● Dysrhythmia
Their main function is to process ● Vasculitis (inflammation of the blood
antigen material and present it vessels)
on the cell surface to the T ● Anemia
cells of the immune system. 1. Gastrointestinal System
They act as messengers between ● Hepatosplenomegaly
the innate and the adaptive ● Colitis
immune systems. ● Vomiting
● Dendritic cells are present in ● Diarrhea
those tissues that are in contact 1. Genitourinary System
● Frequency and burning sensation
with the external environment,
during urination
such as the skin (where there is a ● Hematuria
specialized dendritic cell type ● Discharges
called the Langerhans cell) and 1. Skin
the inner lining of the nose, lungs, ● Rashes
stomach and intestines. They can ● Lesions
also be found in an immature ● Dermatitis
state in the blood. Once ● Hematomas or purpura
activated, they migrate to the ● Edema or urticaria
lymph nodes where they interact ● Types of edema
with T cells and B cells to initiate 1. Weeping edema -
seeping/leeking out of
and shape the adaptive immune
fluid when pressed.
response. At certain development 2. Brawny edema
stages they grow branched ● Inflammation
projections, the dendrites that 1. Neurosensory System
give the cell its name (δένδρον or ● Cognitive dysfunction
déndron being Greek for "tree"). ● Hearing loss
● Visual changes
 ● Headaches and migraines
● Ataxia (loss of muscle movement)
● Tetany (excessive muscle
movement)
Common Laboratory Tests/Diagnostic
Tests
1. White blood cell count and
Differential
- assesses the ability of the body to
respond and eliminate infection.
- leukocyte and lymphocyte test
1. Bone marrow biopsy  of allergens in a laboratory.
- bone marrow biopsy or aspiration
- sites:  tests
a. back of the
hipbone/posterior iliac crest
b. sternum
● Procedural interventions
1. Obtain informed
consent.
2. Position client to
prone position or
his/her side.
3. Cleanse the skin.
4. Assist in application
of a local anesthetic
over the site.
● After the procedure
1. Lie flat for 5-10 mins.
to provide pressure
over the procedure
site.
2. Paracetamol
(acetaminophen) for
pain and to relieve
soreness of the site.
3. Monitor for signs of
bleeding and
infection.
3. Hypersensitivity Test
1. Scratch test/prick test (little
discomfort) - checks for a
skin reaction to common
allergy - provoking
substances, such as foods,
molds, dust, plants, or animal
proteins.
2. Patch test (painless) - test
involves the application of
various test substances to
the skinnunder adhesive tape
that are then left in place for
48 hours.
3. Intradermal test (skin testing)
4. Radioallergosorbent test
(RAST) - it test for the
amount of specific IgE
antibodies in the blood. The
blood test measures the
levels of allergy antibody, or
IgE, produced when your
blood is mixed with a series
4. Specific antigen - antibody
1. Radioimmunoassay - used to
measure concentrations of
antigen.
2. Immunofluorescence -
technique uses the specificity
of antibodies to their antigen
to target fluorescent dyes to
specific biomolecule target
within a cell.
3. Agglutination - used to
determine infection and to
identify pathogens and blood
types.
4. Complement fixation test -
widely used to diagnose
infections, particularly with
microbes that are not easily
detected by culture methods
and in rheumatic diseases. 
Other tests:
1. Enzyme-linked
immunosorbent assay
(ELISA)
2. Western Blot (Protein
immuno blot) - test for the
validity of ELISA.
3. CD4 and CD8 cell count
4. P24 antigen test
5. Polymerase chain reaction
(pcr)
6. Phagocytic cell function test -
how well could the cell engulf
foreign body materials.
Alterations in the Immune Response
Immunologic Disorder
1. Immune Deficiency
 2. Autoimmune Disorder 7. Pessistent thrush in mouth/skin in a
3. Allergy Hypersensitivity  year
4. Gammopathy 8. Need for intravenous antibiotics to
4 Primary Immune Aberrations: clear infection
I. Immunodeficiencies 9. 2x more deep-seated infections
-Abnormality in one or more branches of the (meningitis, cellulitis or sepsis)
immune system that renders a person 10.  A history of primary immune
susceptible to diseases normally prevented deficiency
by an intact immune system PRIMARY IMMUNODEFICIENCY
II. Autoimmunity Other symptoms:
-Formation of antibodies against self-cells ● Frequent or unusual infections
-Factors: Genetics, environment, sex ● Prolonged diarrhea
Autoantibodies -  AB produced against ● Poor childhood growth
one’s own cells PRIMARY IMMUNODEFICIENCY
III. Hypersensitivities DISORDERS
-An exaggerated or inappropriate immune Characteristic:
response ● Rare disorders with genetic origins
-Divided into 4 categories based on the ● Seen primarily in infants and young
immunologic mechanisms involved in the children
reaction ● Symptoms usually develop early in
IV. Gammopathies life
-AKA “Hypergammaglobulinemias” ● Seldom survive to adulthood
-Disturbance in synthesis of ● May involve one or more
immunoglobulins; proteins having antibody components of the immune system
activity increase greatly in the blood TYPES OF INHERITED B-CELL
Classified into 2: DEFICIENCIES
● Monoclonal gammopathy 1st type:
-Presence of a homogenous serum ● Lack of differentiation of B-cell
immunoglobulin protein. (precursors into mature B cells)
● Polyclonal gammopathy ● Plasma cell are lacking - leads to
-Heteregeneous increase in Complete lack of antibody
immunoglobulins involving more than one production
cell line 2nd type:
- Depress synthesis of normal ● Results from a lack of differentiation
immunoglobulins of B cells into plasma cells
● Diminished antibody production
IMMUNODEFICIENCY I. Antibody/B Cells
2 Classifications: Immunodeficiency
● Primary Immune Deficiency A. X-agamma globulinemia (Bruton’s
● Congenital or inherited disease)
● Secondary Immune Deficiency ● Hypogammaglobulinemia
● Acquired later in life B. Selective: IgA, IgM, IgG deficiency -
10 warning signs of PID lack of both serum and secretory IgA
1. 8x more ear infections within 1 yr B-Cell Deficiencies
2. 2x more sinus infections within 1 yr A. X-linked Agammaglobulinemia
3. 2x more antibiotics with little effects -First immunodeficiency to be identified
4. 2x more pneumonias in a year - AKA Bruton Type Agammaglobulinemia, 
5. Poor growth X-Linked infantile Agammaglobulinemia or
6. Recurrent deep skin/organ Congenital Agammaglobulinema
abscesses Clinical Features:
 ● Spleen, lymph nodes, tonsils,
adenoids, peyer’s patches decrease
in size or absent in individuals
● Ig G depleted
● Serious enteroviral infections
● Chronic pulmonary disease
● Skin disease
● Inflammatory bowel disease (UC &
chron’s disease)
● CNS complications
NOTE: T-lymphocytes elevated
B. Hypogammaglobulinemia
-AKA Common Variable Immunodeficiency
(CVID)
- term that defects (ranging from IgA def. To
panhypoglobulinemia)
Clinical Features:
● Growth retardation
●  abnormalities in lymphoid tissues
and organs  Treatment: NO CURE
● Skin and mucus membrane
abnormalities
● Ear, nose, throat abnormalities
● pulmonary/CV/neurologic
abnormalities
Other Manifestations:
Common Sites are:
● Inner ear: Otitis media
● Sinuses: Sinusitis, rhinitis
● Lower respiratory tract: pneumonia,
bronchitis
● Meninges: Meningitis
● Blood stream: Sepsis
**DX & TREATMENT SIMILAR TO XLA**
Iga - 80-350 mg/dl
IgG - 620-1400 mg/dl
IgM - 45-250 mg/dl
IgD - .3-3 mg/dl
IgE - .002-2 mg/dl
Diagnostic Tests
● low , IgG: 200 mg/dl
● IgA, IgM, IgD and IgE: Low or
absent
● WBC counts: are normal
● B-lymphocytes: absent
● T-cell responses: Normal
TREATMENT
GOAL: Maintain IgG at 500 mg/dl
● There is no cure for X-linked
Agammaglobulinemia
● Gammaglobulin Replacement
therapy: IV Ig dose of 300 mg/kg
every 3 weeks or more monthly
PROGNOSIS:
● Without gammaglobulin treatment,
these patients may die from
infections at an early age.
C. Selective IgA Deficiency
● It is the total absence or severe
deficiency of IgA
● Blood serum levels for IgA deficient
persons are usually found to be
7mg/dl
● Usually asymptomatic
Diagnostic:
● IgA: 7 mg/dl or less
● IgA replacement
● Palliative: immunosuppressive
therapy, antibiotics
PROGNOSIS:
● Many persons with selective IgA
deficiency live their full life span
without any problems
II. T Cell Immunodeficiency
A. Di George’s Syndrome - congenital
failure of the thymus gland
- lack of T cell in chromosome 22
B. Hodgkins disease - neoplasm of the
lymphoid tissue, impaired T cell function
- an autosomal recessive inheritance
affecting the thymus and endocrine glands.
MANIFESTATIONS: DiGeorge syndrome
C - Cardiac Abnormality
A - Abnormal Facies
T - Thymic Aplasia
C - Cleft palate
H - Hypoparathyroidism/Hypocalcemia
Manifestations:
Chronic mucutaneous candidiasis
● Candidal infection
● Nails may be markedly thickened,
fragmented, and discolored
● Skin are hyperkeratotic
(hypertrophy)
Diagnostic Findings
1. Lymphocyte count - NV = 16-45%
less than 16%
Medical/Surgical Management
● P. carinii prophylaxis
● Management of hypocalcemia and
improve cardiac contractility
● Treatment for CHF to patients with
congenital disease
● Administration of human leukocyte
antigen
III. Combined B & T Cell
Immunodeficiency
A.  Wiskott-Aldrich syndrome (WAS)
● X-linked recessive disease
accompanied by thrombocytopenia
and eczema
B. Ataxia - telangiectasia
● Loss of muscle coordination and
blood vessel dilation
ATAXIA-TELANGIECTASIA
● AKA “LOUIS-BAR SYNDROME”
● Autosomal recessive disorder
● With accompanying IgA, IgG, IgE
deficiencies
● With Cerebral ataxia, telangiectasis,
recurrent infections of the lungs and
sinuses and increased incidence of
cancer
HALLMARK SIGNS:
● ATAXIA - uncoordinated mucle
movement
● TELANGIECTASIA - vascular
lesions caused by dilated blood
vessels
● Usually appears in the first 4
years of life
● On 2nd decade of life - mental
retardation, lung disease and
physical disability becomes severe
Medical management:
● Antimicrobial therapy
● Postural drainage and physical
therapy for lung conditions
● Transplantation of fetal thymus
tissue and IVIG administration
C. Severe combined
immunodeficiency
● Bubble boy disease
● Equates to an almost absent
immune system
Characteristics:
● Lymphoid aplasia
● Thymic dysplasia
Manifestations:
● Onset of symptoms occurs within the
first 3 months
● Pneumonia and other respiratory
infections
● Diarrhea
● Poor growth and development
● Vomiting 
● Fever
●  Skin rash
Medical Management
● No definite medical mgt
● IV Ig administration
Surgical Management
● Stem cell transplant
● Bone marrow transplant
● Thymus gland transplantation
SWISS TYPE AGAMMAGLOBULINEMIA
● Severe combined immunodeficiency
● Inherited x-linked
● Affected children have lymphopenia
● Thymus is always hypoplastic or
absent
● Lymph nodes are not visible
● Lymph nodes in tonsils, gut and
appendix are hypoplastic
● Most die on the first year of life
IV. Phagocytic Cell Disorder
Characteristics:
● Increase incidence of bacterial and
fungal infections
● Recurrent furunculosis (boils)
● Cutaneous abscesses
● Bronchitis, pneumonia
● Chronic otitis media and sinusitis
1. HYPERIMMUNOGLOBULINEMIA
(formerly known as Job
Syndrome)
● White blood cells cannot produce an
inflammatory response to the skin
infections
Clinical feature:
● May be asymptomatic
● Severe neutrophenia
● Accompanied by deep and painful
mouth ulcers, gingivitis, stomatitis
and cellulitis
1. Chronic granulomatous disease
 ● Produces recurrent or persistent
infections of the soft tissues, lungs
and other organs
● These are resistant to aggressive
treatment with antibiotics
Characteristics:
● Excessive inflammation even when
there is not an infection
● Diarrhea
● Bladder and kidney problems
Management
P - prophylactic antibiotic
R - raw foods should be AVOIDED
O- pv/live virus vaccine should AVOIDED
T - teach frequent handwashing
E- exercise
C - contagious dse should be avoided
T- therapy: BM transplantation; IVIG
SECONDARY IMMUNODEFICIENCY
Common Causes:
● Malnutrition
● Chronic stress
● Burns
● Certain autoimmune disorders
● Certain viruses
● Exposure to immunotoxic
medications and chemicals
● Self-administration of recreational
drugs and alcohol
ACQUIRED IMMUNODEFICIENCY
SYNDROME
HIV
● A retrovirus that causes AIDS
● Major types: HIV 1 & HIV 2
● IP: 10 years
TRANSMISSION:
● Unprotected sex/penetrative sex
● Injection drug use/blood products
● Vertical transmission
AIDS
● Is an infectious disease of the
immune system caused by the
retrovirus HIV 1
● Is a secondary immunodeficiency
disorder that results from HIV
infection which is transmitted by
blood, semen or vaginal fluids
COURSE OF INFECTION
I. Primary infection phase
● Initial response to HIV invasion:
Destruction of HELPER T CELL/
CD4 cells and increase in viral load
● Appears 2-4 weeks after infection
and lasts for 2 weeks
II. Latency Phase
● Over the next 2 to 10 years, virus
slowly destroys T helper cells in
lymphatic tissues throughout the
body
III. Overt Phase
● As immune response weakens,
patient develop “indicator diseases”
with s/s of OPPORTUNISTIC
INFECTION CD4 drops to 200mg/dl
IV. Seroconversion
● The point at which an infected
person converts to from being
negative for the presence of HIV
antibodies in the blood to being
positive
V. Window Period
● Time after infection and before
seroconversion
● Last 3-4 weeks
CD4 CELLS
● 650-1200 cells/mm3: competent
immune system
● 500-200 cells/mm3: suppressed
immune system
● <200 cells/mm3: AIDS (according to
CDC)
VIRAL LOAD
● <10,000 (Low risk)
● 10,000 - 100,000 (moderate risk)
● 100,000> (high risk)
DIAGNOSTIC: 3 conditions
● Presence of HIV
● T4 cell count is below 200 (CD4)
● Presence of 1 or more of AIDS
specified conditions
CDC CLASSIFICATION SYSTEM FOR HIV
INFECTION
● Cat A = >500 cells/ul
● Cat B = 200-499 cell/ul
● Cat C = <200 cells/ul
Clinical Categories: According to Clinical
Manifestions
1. CATEGORY A
 ● Includes person who are ● The alveoli becomes filled with
asymptomatic or have persistent foamy protein rich fluid that impairs
generalized lymphadenopathies gas exchange
PRIMARY HIV INFECTION ● S/sx: Mild cough, fever, SOB, weight
● Fever, myalgias, night sweats, loss
fatigue, sore throat, GI problems, 2. Mycobacterium tuberculosis
lymphadenopathies, rashes,
headache 3. AIDS dementia complex (HIV related
S/Sx of ACUTE HIV INFECTION encelopathy)
● Fever ● A syndrome of cognitive and motor
● Fatigue dysfunction
● Rash ● Sx: impairment in attention,
● Headache concentration and swallowing of
● Lymphadenopathy mental speed, agility, pathetic
● Pharyngitis behavior
● Arthralgia 4. Kaposi’s sarcoma
● Myalgias ● Is a malignancy of the endothelial
● Night sweats cells that line small blood vessel
● GI problems: diarrhea ● Lesions are nodules or blotches that
● Aseptic meningitis may be red, purple, brown or black
● Oral and genital ulcers and are usually papular
● Sometimes invade cervix causes
cervical cancer
HIV WASTING SYNDROME
● Caused by anorexia metabolic
1. CATEGORY B abnormalities, endocrine
●Persons with symptoms of immune dysfunction, malabsorption and
deficiency not serious enough to be cytokine dysregulation.
AIDS defining Gynecologic
● Median time is 10 years ● Recurrent vaginal candidiasis
● CD4 count falls gradually from the ● Genital ulcer disease
normal range ● Venereal warts
2. CATEGORY C Diagnosis
● Includes AIDS defining illness ● ELISA - Enzyme Linked
● Patients have Opportunistic Immunosorbent Assay
infections ● Western Blot Assay - confirmatory
AIDS DEFINING CONDITIONS: ● Orasure- Saliva
● Opportunistic infections: ● CD4 cell count
● Pneumocystasi carinii ● Polymerase chain reaction (PCR)
pneumonia (PCP) ELISA & WESTERN BLOT
● Candidiasis ● With positive result
● Cytomegalovirus ● Antibodies to HIV are present in
● Herpes simplex blood 
● Mycobacterium avium ● HIV is PROBABLY active
complex (MAC) ● Despite HIV infection, client does not
● Mycobacterium tuberculosis necessary have AIDS
● REcurrent pneumonia ● Client is NOT IMMUNE to AIDS
● Histoplasmosis 5 means of HIV PREVENTION
1. Pneumocystis Carinii Pneumonia A = abstain from sex
(PCP) B = be faithful
C = correct & consistent use of condom
D = do not use illegal drugs/share needles
E = educate yourself
HEALTH TEACHINGS
● Promote Good nutrition
● Promote self care
● Provide counseling
Other Management with AIDS
● Identification of persons at risk
● Obtaining a complete, accurate
sexual history is important
● Identify if IV drug user
● Check for other risk factors
● With high risk for HIV/AIDS - counsel
about significant of testing and
necessity for follow up
● Educational and counseling
strategies with AIDS
GUIDELINES FOR CARE OF THE
PERSON WITH HIV
● Prevent infection
● Wash hands frequently
● Use gentle soap; avoid bar soap that
may irritate skin
● Provide for daily showering/basin
bath’ avoid tub bath if rashes are
present
● Use separate washcloth for lesions
● Use soft toothbrush, nonbrasive
toothpaste.
● Prevent skin breakdown
● Elevate and support areas of edema
● Observe surgical site and IV
insertion sites daily for signs of
infection
● Change dressings (if any) daily
● Avoid eating fresh fruits/vegetables;
uncooked/rare foods
● Carry out infection control measures
according to institution’s policy
● Administer prescribed antibiotics, IV
fluids/Antipyretics
● Encourage Increase OFI
● Monitor daily  I/O records
● Weigh patient daily
● Instruct patient in deep breathing
coughing exercise to PX: atelectasis
and fever
● Modify alterations with body
temperature: TSB, DBE, and
Coughing
PREGNANCY & AIDS
● Zidovudine (AZT) - recommended
for prevention of maternal fetal HIV
transmission and administer AFTER
14 WEEKS OF AOG with PO
medicine; IVTT DURING LABOR;
and to the NEONATE post birth for 6
weeks
● Nevirapine - reverse transcriptase
inhibitor
Post partum period
● Monitor for signs of infection
● Place mother in isolation if mother is
immunosuppressed
● RESTRICT BREASTFEEDING
● infant/neonate is seen by physician
at birth, 1 week, 2 weeks, 1 month, 2
month and 4 months of life
CHILD WITH AIDS
● PCP prophylaxis 1-12 months
● Need for additional prophyplaxis is
determined by CD4 counts
● IMMUNIZATIONS
● Ensure administration of
pneumococcal and influenza
vaccine: prevents
streptococcal infection
● AVOID VARICELLA
VACCINE
HEALTH TEACHINGS
● Discard unused refrigerated
formula and food for 24 degree
● Change diapers frequently, clean
up spills with BLEACH solution
(10:1) ratio
● Provide high CHON, high calorie
diet, monitor weight daily
● Avoid exposing the child to other
illnesses
Medications (ANTIRETOVIRAL)
GOAL:
● To suppress infection, prolonging
life
● To treat opportunistic infection
● Effectiveness: monitored by viral
load count, CD4 cell counts
(higher than 500)
Nucleoside reverse transcriptase inhibitors
(NRTI)/ nucleoside analogs
● Blocking the elongation of the DNA
 ● Ex. Zidovudine (AZT, Retrovir), 1. Monoarticular – affects a single joint
Didanosine (DDI, Videx), Zalcitabine
(DDC, HIVID) 2. Polyarticular – affects multiple joints
Protease inhibitors (protease - a viral
enzyme) Further classification
● Bind to the protease enzyme and
inhibit its action 1. Inflammatory
● Ex. Ritonavir (norvir), Indinavir
(Crixivan) 2. Noninflammatory
Non nucleoside reverse transcriptase
inhibitors (NNRTI) Rheumatoid arthritis
● Ex. Nevirapine (Viramune),
Delavirdine (rescriptor) - RA is a systemic inflammatory disease
Others: Interferons: Alpha interferons, that affects 0.3% to 1.5% of the
gamma-interferons
population, with women affected two to
Receive pneumococcal, influenza hepatitis
B, vaccines three times more frequently than men.
To prevent PCP/the CD4 lower than 200 =
trimethoprime - sulfamethoxazole o   Peak: 40-60 y.o.
(Pentamidine)
o   Onset: 30-50 y.o.

Rheumatic Disease - Primary process is inflammation as a

result of immune response
-  Condition causing a chronic often
intermittent pain in the bone? - Regeneration occurs as a secondary
process
-  Inflammation of the joint
- Pannus – proliferation of newly formed
Remission – period that a symptom is synovial tissue infiltrated with
reduce inflammatory cells

Exacerbation – recurrent of disease? Pathogenesis

Common site Predisposing factors:

-  Skeletal muscle ·         Hereditary

-  Bones ·         An aberrant type of immune

response leading to destruction of joint
-  Cartilage architecture

-  Ligaments ·         Rheumatoid factor

-  Tendons ·         Location of inflammation: blood,

synovial joint, synovial membrane
-  Joints
Manifestations
Classification:
-  Fatigue
-  Anorexia 4. Symmetric joint swelling for 6 or more
weeks
-  Weight loss
5. Rheumatoid nodules
-  Generalized aching and stiffness
(30mins-several hours) 6. Serum rheumatoid factor identified by
a method that is positive in less than 5%
-  Subluxation of joints – of normal subjects
dislocation/disformation
7. Radiographic changes typical of
-  Swan neck deformity rheumatoid arthritis on hand or wrist
(Hyperextension of PIP  joint and partial radiographs
flexion of DIP)

-  Boutonniere deformity
Stages of RA
-  Bulge sign
Stage 1 – this is the early stage of RA,
-  Genu valgus there is inflammation of the joint but
there is no damage to the bones
-  Joint contractures
Stage 2 – moderate stage of RA, the
-  Baker’s cyst synovium’s inflammation causes
damage to the joint cartilage. ROM in
-  Increase ESR the joints may become limited
-  Rheumatoid nodules: ulna Stage 3 – severe RA, damage extends
no only to the cartilage but to the bones
-  Ulcerations of lower extremities
o   disfiguration

Classification of rheumatoid arthritis
Four or more of the following condition
must be present to establish a dx of
rheumatoid arthritis:
Stage 4 – the end stage of RA, the joints
may become destroyed and the bones
fused together (ankylosis)
Diagnostics

1. Morning stiffness for at least 1 hour -  Physical exam

and present for at least 6 weeks
-  Rf (Rheumatoid Factor) test bind
2. Simultaneous swelling of three or
-  Presence of 4 major criteria
more joints for at least 6 weeks
-  Anti-cyclic citrullinated peptide
3. Swelling of wrist,
(CCP) antibodies (IgG)
metacarpophalangeal, or proximal
interphalangeal joints for 6 or more -  Synovial fluid analysis
weeks
Treatment
Symptom Control:
·         Regulating activity by pacing,
establishing priorities, and setting
realistic goals
·         Long-term adherence to the
prescribed treatment modalities
·         Proper posture, positioning, body
mechanics, and the use of supportive
shoes
·         ROM
·         Goals of pharmacologic therapy:
o   Reduce pain, decrease
inflammation, maintain or
restore joint function and
prevent bone and cartilage
destruction
·         NSAIDS and ASA
o   Celecoxib, rofecoxib and
valdecoxib
·         Disease modifying antirheumatic
drugs (DMARDs) include:
-  Gold salts, hydroxychloroquine,
sulfasalazine, methotrexate and
azathioprine
Chrysotherapy/aorotherapy – therapy
which uses the application of gold salts
compound
-  Reduce the inflammation and
progression of the disease that’s why it
is used.
·         Methotrexate
o   Most potent: effect can
be seen in 1 month
o   Interfere with purine
metabolism, leading to the
release of adenosine, a
potent anti-inflammatory
compound
·         Corticosteroids – used because of
anti-inflammatory effect
·         Anti-rheumatic drugs – inhibits the
expansion of T cells during inflammatory
response
o   Leflunomide,
etanercept, infliximab and
adalimumab
Surgical treatment
-  Synovectomy - remove partial or
all of the synovial membrane of the joint
-  Tenosynovectomy – excision of
tendon sheet
-  Arthroplasty – a surgical
reconstruction/replacement of the joint
-  Arthrodesis – surgical
immobilization of a joint by fusing
together by adjacent bones
Nursing management
-  Administer prescribed medication
-  Provide pain relief
-  Promote self-care
-  Promote adequate rest and sleep
-  Encourage body alignment by the
client to prevent contractures
-  Collaborate with physical
therapist
-  Recommend weight reduction if -  Strawberry tongue
appropriate
-  Red lips
-  Discuss maintaining optimal
nutritional status -  Pallor or proximal fingernails

KAWASAKI DISEASE -  Conjunctival redness

-  Founder is a Japanese doctor in -  Lethargy

1969
-  Irritability
-  Also known as Kawasaki
syndrome or mucocutaneous lymph -  Cardiac complications in 5-20%
node syndrome
-  Rash over trunk
-  A rare childhood illness that
affects the blood vessels and it causes -  Occasional intermittent colicky
inflammation in the walls of medium-size abdominal pain
arteries throughout the body
-  Superficial skin layers
-  A form of systemic vasculitis desquamate easily

-  The most common cause of -  Red soles & palms

acquired heart disease in children
·         Conjunctivitis
Risk factor
·         Rashes
-  Age – children 5 years old or
·         Adenopathy
younger
·         Strawberry tongue and red lips
-  Sex – boys are 1.5x more likely
to get it than girls ·         Hand and swollen feet
-  Ethnicity – Asian descent Vasculitis – definitive sign
Stages of Kawasaki Diagnostic Test
Stage 1 – Acute febrile phase (first 10 -  CBC
days)
-  Platelet count
Stage 2 – subacute phase (day 11 to
25) -  IgM, IgG
Stage 3 – Convalescent phase (day 40 -  ESR, CRP, alpha1 antitrypsin
to 70)
-  Liver enzymes
S/Sx
-  HDL and Triglycerides
-  High fever
-  Urinalysis Multiple myeloma

-  ECG, cardiac Catheterization and -  A malignant disease of the most

Angiocardiography mature form of B lymphocyte, the
plasma cell
-  Serum CK-MB
-  Proliferation of plasma cell from
Medical management BM into the hard bone tissue causing
erosion of the bone
- The principal goal of treatment for
Kawasaki disease is to prevent coronary -  Unknown cause
artery disease and to relieve symptoms
Effects of proliferation of plasma
- Full dose of intravenous cells:
immunoglobulin
1. Interfere with normal production of
- Aspirin therapy blood cells

- Analgesics/antipyretics -  Leukopenia

- Thrombolytic therapy -  Anemia

- Anti-Inflammatory Drugs – ibrupofen, -  Thrombocytopenia

Naproxen, Plasma exchange
2. May cause soft tissue masses/lytic
Gammopathy lesions

-  Disturbance of synthesis -  Plasmacytomas – malignant

Macroglobulinemia – presence of
increased levels of macroglobulins in
the circulating blood
-  There is diffuse infiltration of
bone marrow and also, in many cases,
of the spleen, liver or lymph nodes
plasma tumor going within axial
skeleton/tissue
Risk Factors
-  Chronic immune stimulation
-  Autoimmune disorders

Hodgkin’s disease -  Exposure to ionizing radiation

-  A type of lymphoma which is a -  Occupation exposure to

cancer originating from WBC called pesticides or herbicides
lymphocytes
Classic triad
-  Characterized by the orderly
spread of disease from one lymph node -  Plasmacytosis
group to another and by the
development of systemic symptoms with -  Lytic bone lesion (plasmacytoma)
advanced disease
-  M. protein or bence jones protein
S/Sx -  X-ray of bone

-  Characterized by widespread -  (+) bence jones protein in the

bone destruction urine: urine electrophoresis

-  Bone pain (back ribs) -  (+) M protein: serum protein

electrophoresis
-  Anemia
MANAGEMENT
-  Hypercalcemia (constipation,
thirst, altered mental status, 1. Prevent infection
dehydration, confusion and coma)
2. Chemotherapy:
-  Increase uric acid
a. Vincristine
-  Splenomegaly (Oncovin)

-  Frequent recurring of infections b. Cyclophosphamide

(Cytoxan)
-  Spontaneous pathologic fractures
c. Dexamethasone
-  Blood viscosity (due to  increase (decadron)
IgA)
3. Thalidomide – progression of the
Complications cancer cell

-  Bone pain 4. BM transplant

-  Hypercalcemia 5. Ambulation & adequate hydration

-  Renal failure 6. Meds shown to strengthen the

bone, controlling bone pain and bone
-  Spinal cord compression fracture: by diminishing osteoclast
activating factor (bisphosphonates)
-  Immunosuppression bc of
chemotherapy a. Pamidronate
(Aredia)
C – calcium (elevated)
b. Zoledronic Acid
R- renal failure (Zometa)
A – anemia 7. Thalidomide (Thalomid): a
sedative having antimyeloma effect.
B- bone lesions
a. Inhibits cytokines
Diagnostic tests
(Vascular endothelial
-  Bone marrow biopsy growth factor), IL-6 and
tumor necrosis factor
 2. Drug-induced Lupus
Autoimmune Disease erythematosus

Autoimmunity – production of antibodies -  Drugs that can trigger lupus

against the tissues of your own body --hydralazine, fronistil, isoniazid,
thoracin, penicillin
Effects/causes:
- highly reconversible.
-   Failure to display self-
antigens - disappear once the medication has
stop
-   Presence of genetic
abnormalities 3. Neonatal Lupus erythematosus

-   Self-reactive clones of - infant born with an SLE mother

Tcells and B cells
- develop during 1 week of life
st

Lupus erythematosus
- benign and self-limited
-   Collection of autoimmune
diseases, in which the human 4. Systemic Lupus Erythematosus
immune system becomes
hyperactive and attacks - An autoimmune disorder, non-
normal, healthy tissues contagious, chronic, progressive
inflammatory disease of the connective
Lupus- wolf tissue

Erythematosus – reddened - period of exacerbation of the disorder

Classification -common in women 15-40 years old

1. Discoid lupus erythematosus  

3 division Risk factors

-   Localized – above the -   Genetic Abnormality –

neck runs in the family

-   Generalized – less -   Viral Infection

common
-   Medications
-   Childhood discoid lupus
erythematosus–low frequency S/sx
of photosensitivity and high
portion of SLE - Butterfly Rash over cheeks

o   THE SAME CLINICAL - Erythematous Rash to exposed

Sunlight
MANIFESTION OF SLE
- Tachypnea -   Anemia

- Cough Clinical Symptoms of SLE

- Pleural Inflammation/Effusion
Organ Symptoms
-Weight loss system
-Fatigue
Musculoskeletal Arthritis, arthralgia
- Fever increase infection

- Arthritis Constitutional Fever (absence of

infection), fatigue,
- Raynaud’s Phenomenon weight loss

- Pericarditis
Skin Malar (butterfly)rash,
- Vascular Inflammation alopecia,
photosensitivity
Characteristic of skin lesions: ,purpura, Raynaud’s
phenomenon, urticaria,
- Margins are bright red vasculitis

- may extend beyond the hairline

Gastrointestinal Nausea, vomiting,
- May occur in the exposed part of the abdominal pain
neck
Renal Proteinuria, hematuria,
- May spread to the mucous membrane
nephrotic syndrome
and other tissues of the body

- Do not ulcerate, but cause Hematologic Anemia,

degeneration and atrophy of tissues thrombocytopenia,
involved leukopenia

Systemic involvement of other

organs Cardiac Pericarditis,
endocarditis,
-   Lupus nephritis myocarditis

-   Pleuritis
neurologic Seizures, psychosis,
-   Pericarditis peripheral and cranial
neuropathies
-   Peritonitis

-   Neuritis – inflammation of
the nerve
 o   U/A
pulmonary Pulmonary
hypertension, pleurisy, o   Blood chemistries
parenchymal disease
o   Complement Levels

  o   ANA – the ana test

measures the pattern and
Raynaud’s phenomenon – patient is amount of autoantibody
exposed in a cold setting can cause which can attack the
blood vessel spasm body’s tissues as if they
were foreign material
Diagnostic criteria for SLE
o   Anti-extractable nuclear
o   Serositis – Pleuritis or pericarditis or
antigen (anti-ENA) –
peritonitis
confirmatory test of SLE
o   Oral Ulcers
o   Extractable nuclear
o   Arthritis antigens

o   Photosensitivity o   Anti-Smith and anti-

double stranded DNA
o   Blood
o   Anti cardiolipin
o   Renal Disorder antibodies

o   Antinuclear antibody o   Skin biopsy

o   Immunologic Disorder o   Kidney biopsy

o   Neurologic disorder TREATMENT

o   Malar Rash -   NSAIDS

-   Antimicrobials
o   Discoid Rash
-   Corticosteroids
Diagnostic exams for SLE:
-   Immunosuppressive
-   Medical History
-   Alternative Therapies
-   Complete Physical exam
o   Special diet
-   Laboratory tests:
o   Nutritional supplement
o   CBC
o   Fish oils –
o   ESR
cardioprotective effect
 o   Ointments and creams
o   Chiropractics
o   Sunscreens
o   Exercise and rest
o   Stress reduction
o   Family planning
o   Yearly influenza and
pneumococcal vaccination
What to avoid
-   Aromatic amines present
in cleaning agents and hair
dyes
-   Silicone and silica dust
-   Alfalfa sprouts due to their
high L-canavanine content
-   Hydrazines found in some
mushrooms and in tobacco
smoke
-   Tartrazines found as
preservatives in food dyes
-   Ultraviolet light
-   Excess alcohol’
Medications
-Anti-inflammatory analgesics-NSAIDS
-Antimalarial drug: Hydroxychloroquine
(Planequil)
-Corticosteroids (Prednisone) in high
doses
-Topical Corticosteroids
- Cytotoxic Agents or antineoplastic
Other management
-   Kidney dialysis
-   Total Hip replacement also
known as total hip
arthroplasty
-   Plasmapheresis –removal
of treatment and return of
blood circulation
Goal: improve mobility
Corona Virus
Strains: Mers Cov, SARS, Covid 19
1.)  Middle east Respiratory Syndrome
-   Is a viral respiratory illness
and was reported in Saudi
arabia in 2012 and has
spread to several other
countries including the United
States. Most people infected
with MER-CovC developed
severe acute respiratory
illness
Etiologic Agent: MERS-Coronavirus,
Camel
Mode of Transmission: Close contact
with infected person
Incubation Period: 5 to 6 days but can
range from 2 to 14 days
S/Sx
-   Fever
-   Cough
 -   SOB -   SOB

-   Diarrhea -   Low white cell count

-   Nausea and Vomiting -   Flu-like symptoms such as

joint pain and malaise
Diagnostic Test
-   Symptoms appear 3-7
-   Polymerase Chain days after exposure
reaction (PCR) – confirmatory
test used to detect viral RNA -   2 stages

-   ELISA – screening test o   Stage 1 – flu like

used to detect the presence prodrome begin 2-7days
and concentration of specific after incubation
antibodies that bind to a viral
protein o   Stage 2 – lower
respiratory tract phase
-   NO VACCINE AVAILABLE
Diagnostic Tests
Treatment – supportive management
-   Pulse oximetry
-   Based on the
manifestation of the client -   Blood cultures

SEVERE ACUTE RESPIRATORY -   Sputum grain stain and

SYNDRME (SARS) culture

-A serious, potentially life-threatening -   Viral respiratory pathogen

viral infection caused by the test – influenza A and B
Coronaviridae family, the SARS- viruses and respiratory
associated coronavirus. Initially began in syncytial virus
the Guangdong province of Southern
China. SARS is characterized by a -   Legionella and
phase of cytokine storms with various pneumococcal urinary antigen
chemokines and cytokines being test
elevated
-   WBC-decreased
-Start sa cat then transferred to humans
-   Mild hyponatremia and
S/Sx hypokalemia

-   Coughing -   Elevated lactate

dehydrogenase alanine
-   Headache aminotransferase and hepatic
transaminase
-   Sorethroat

-   Fever
 -   Elevated creatine kinase  Etiologic agent: Influenza A virus
level subtype H1N1

-   Serum antibodies to Mode of transmission: close and direct

SARS-CoV in single serum contact with infected person
specimen
Incubation period: Ranges from
-   RT-PCR (reverse 1to4days with an average of 2 days up
transcriptase polymerase to 7 days
chain reaction)
Clinical Features Pandemic Influenza
-   Chest radiograph – (H1N1 Influenza)
interstitial infiltrates

-   NO VACCINE to ready Uncomplicated Complicated

combat the virus influenza Influenza
 
fever SOB and
  dyspnea
Prevention
Cough, runny nose LRT
-Wash hands often with soap and water (pneumonia)
for 20s or use alcohol based sanitizers

-Cover nose and mouth with tissue Sore throat CNS

when coughing or sneezing, then throw involvement
tissue in the trash

-Avoid touching the eyes, nose and Muscle Pain Severe

mouth with unwashed hands dehydration

-Avoid personal contact such as kissing

Malaise Secondary
or sharing cups or eating utensils with
complication
sick people

-Clean and disinfect frequently touched No dyspnea, SOB COPD, asthma

surfaces such as doorknobs and toys

INFLUENZA GIT symptom Renal Failure

H1N1 influenza – referred to as swine
flu, a highly contagious respiratory
disease in pigs that can be transmitted
Diagnostic Test
to humans
-   PCR
 -   Rapid antigen or antibody Within a few days after symptoms begin:
immunoassays
-   Antigen-capture enzyme-
-   Viral Culture linked immunosorbent assay
testing
Medical and treatment management
-   IgM ELISA
-   Antipyretic
-   PCR
-   Analgesics
-   Virus Isolation
-   Increase fluid consumption
Later in disease course or after recovery
-   Bedrest
- IgM and IgG antibodies
-   Antiviral Agents -Retrospectively in deceased patients
(Oseltamivir/Zanamivir)
- Immuohistochemistry testing
-   Isolation
- PCR
-   Vaccination – influenza
virus vaccine trivalent - Virus Isolation
(Fluzone, Flucelvax)

-   Influenza viral quadrivalent

(Afluria Quadrivalent, Fluarix)

EBOLA VIRUS Benign Prostatic Hypertrophy

Ebola Hemorrhagic Fever is a rare and
deadly disease caused by infection with
one of the ebola virus strain. Ebola can
cause disease in humans and
nonhuman primates
-AKA benign prostatic hyperplasia and
characterized by proliferation of the
cellular elements of the prostate
Risk factors:

Etiologic agents: ebola virus -   Aging Process

Mode of transmission: Direct contact -   Hormonal Imbalance

with blood or bloody fluids, objects of a (Estrogen, Androgen)
person infected with ebola and infected
animals S/Sx

Incubation Period: 2 to 21 days after - Weak urine stream

exposure to Ebola, but the average is 8
- Frequent urination
to 10 days
- Dribbling after urination
Diagnostic Tests
- Urge to urinate Complications

- Leakage of urine (Overflow -   Urinary tract infections

incontinence)
-   Urinary stones
 
-   Kidney damage
Diagnostic Tests
-   Bleeding in the urinary
-Digital Rectal Examination tract

-Urinalysis -   A sudden inability to void

- Urine culture -   Hydroureter

- Prostate-specific Antigen (PSA) -   Hydronephrosis

- Serum electrolytes -   Bladder neck strictures

post TUR
- Blood Urea Nitrogen (BUN)
-   Retrogade ejaculation
- Ultrasonography
-   Epididymitis
- Endoscopy of the Lower Urinary Tract
Surgical Management
- Cystoscopy
-   TURP
- Renal Biopsy (TRANSURETHRAL
RESECTION OF THE
Medical Management PROSTATE)
-Pharmacologic Management: -   Open prostatectomy
o   Terazosin (Hytrin) –A1- Adrenergic -   Transurethral incision of
receptor blocker relaxes bladder the Prostate (TUIP)
sphincter
-   Transurethral microwave
o   Finastride(PROSCAR) – inhibits 5- therapy (TUMT)
alpha red. Reduction of glandular
hyperplasia -   Transurethral needle
ablation of the prostate
-Balloon dilation – to relax smooth (TUNA)
muscle of the bladder neck and prostate
-   Prostatic stents
- Immediate catheterization
*Maintain urine irrigation
-Watchful waiting – to monitor disease
progression  
Pelvic Inflammatory Disease -   Irregular menstrual cycles

An infection of the female reproductive -   Having a pain during

organs. Several different types of intercourse
bacteria can cause PID, including the
same bacteria that cause the sexually -   Pain in the low back
transmitted disease. PID can become
extremely dangerous even life -   Fever
threatening if the infection spreads to
the blood -   Fatigue

Etiologic Agent: -   Diarrhea or vomiting

Most cases of PID are polymicrobial, but -   Difficulty when urinating or

these are the common pathogens: painful urination

-   N. Gonorrhea Diagnostic Tests

-   Chlamydia -   Pelvic examination

Risk Factor: -   Cervical Culture

-   Having sex under the age -   Urine Test

of 25 years old
-   Pelvic Ultrasound
-   Having multiple partners
-   Endometrial Biopsy
-   Having sex without any
-   Laparoscopy
protection such as condoms
Long term complication Of PID
-   Recently having an
intrauterine Device (IUD) -   Infertility
inserted
-   Ectopic pregnancy
-   Douching
-   Chronic pelvic pain
-   Having history of Pelvic
inflammatory disease -   Tubo-ovarian abscess
  Prevention: teach client to practice safe
sex
S/Sx
-   Screening for other
-   Lower abdominal pain and sexually transmitted disease
pelvic pain
 
-   Heavy vaginal discharge
with foul odor