IMMUNE SYSTEM

I. DEFINITIONS:
 Immunity – ability of the body to resist the invasion of pathogens &
their toxins
 Antigen – foreign proteins that are considered invaders; could be
autoantigen when proteins originate from own body
 Antibodies – aka Immunoglobulins (Ig) are part of the body’s plasma;
fights against antigens

II. FUNCTIONS OF IMMUNE SYSTEM:

1. Defense – protects body from external antigens
2. Homeostasis – maintains balance of systems
3. Surveillance – perceives & responds to mutated cells (bad cells)

III. COMPONENTS OF IMMUNE SYSTEM:

1. Bone Marrow – produces WBC; Lymphoid cells differentiates into
B & T Lymphocytes; releases mature B lymphocytes into the blood
circulation
2. Lymphoid Tissues:
 Spleen – (rbc graveyard) acts like a filter that purifies blood &
removes worn-out erythrocytes from the blood; red pulp – where old
& injured cells are destroyed; white pulp – where concentration of
lymphocytes are found
 Lymph Nodes – distributed throughout the body; connected by lymph
channels & capillaries which remove foreign materials from lymph
before they enter the bloodstream; filters & kills antigen; generates
lymphocytes & monocytes
 Tonsils & Adenoids – protect surfaces of mucous membranes

IV. NON-SPECIFIC IMMUNOLOGIC DEFENSE:

 A type of immunity that is effective against any harmful agent
entering the body
 Aka PHAGOCYTIC IMMUNE RESPONSE
 First line of defense
 Involves WBCs (granulocytes, macrophages) which have the
ability to ingest foreign particles; engulf & destroy invading agents
 Apoptosis – programmed cell death; body’s way of destroying
unwanted cells such as cancer cells or cells that die a natural death
 It is the body’s natural immunity that can discriminate friend from foe
but cannot distinguish between agents & pathogens.

 *A. Natural mechanism includes:

 Physical barriers – intact skin, cilia of the respiratory tract

 Chemical barriers – acidic juices, enzymes in tears & saliva,

sebaceous & sweat secretions to destroy invading bacteria & fungi
  Biologic response modifiers – INTERFERONS (proteins formed
when cells are exposed to viral or foreign agents that are capable of
activating other components of the immune system)

 *B. Actions of the WBC:

 Neutrophils – first to arrive at the site injury
 Eosinophils & basophils – activated in response to allergic
reactions & stress; eosinophils (hypersensitivity reactions);
basophils (plays a role in inflammatory response)
 Granulocytes – release cell mediators (histamine, bradykinin,
prostaglandin) to engulf the foreign toxins; fights infections
 Monocytes – circulates in the blood but also settles in tissue where
they are transformed into macrophages; can engulf larger particles
than neutrophils; five times as many in one ingestion

 *C. Inflammatory response – mast cells release chemical mediators

which produces the typical signs of infection (redness, swelling, pain,
heat)- always activated when injury is present

 *D. Natural Killer (NK) cells – these lymphocytes are responsible

for immune surveillance & host resistance to infection

COMPLEMENT SYSTEM
group of at least 20 circulating plasma proteins, made in the liver & are
sequentially activated in the presence of an antigen
 Complement – circulating plasma proteins which are made in the
liver and activated when an antibody couples with an antigen
 Complement Cascade – the sequential interaction of circulating
plasma proteins (like a falling domino effect) which alters the cell
membranes where antigen-antibody complex forms
 Activated complement molecules attract macrophages &
granulocytes to area of antibody-antigen reactions

COMPLEMENT-MEDIATED IMMUNE RESPONSE

RESPONSE EFFECTS
Cytolysis Lysis & destruction of cell membranes of
body cells & pathogens
Opsonization Targetting of the antigen so that it can be
easily engulfed & digested by macrophages &
other phagocytic cells ( pinpointing)
Chemotaxis Chemical attraction of neutrophils &
phagocytic cells to the antigen
Anaphylaxis Activation of mast cells and basophils with
release of inflammatory mediators that produce
smooth muscle contraction & increased
vascular permeability
Agglutination Clumping of antigens (kumpol-kumpol)
Neutralization Deactivates viruses
V. SPECIFIC IMMUNOLOGIC DEFENSE
 A type of immunity effective against specific harmful agents entering
the body (patayin nya lang ang kaaway na kilala nya)

VI. TYPES OF SPECIFIC IMMUNITY:

1. NATURAL (Innate): immune responses that exist without prior
exposure to an immunologically active substance; genetically
acquired immunity

2. ACQUIRED: immune responses that develop during course of

person’s lifetime (eg. Baby gets immunity from mother)

CLASSIFICATIONS OF ACQUIRED IMMUNITY

TYPE ANTIGEN/ANTIBODY SOURCE DURATION

1. Active Antibodies are produced by the body in long
response to infection (sickness)
a. Antibodies are formed in response of active lifelong
Natural infection of body;
Results from a disease & recovering
successfully
b. Antigens (vaccines/toxoids) are Many years; the
Artificial administered to the person to stimulate immunity must
antibody production; conferred by be reinforced by
immunization boosters
2. Passive Antibodies are produced from other source short
(animal/human)
a. Antibodies are transferred normally from an 6mos to 1 year
Natural immune mother to her baby thru the
placenta or colostrum
b. Immune serum (antibody) is injected (ex. 6mos to 1 year
Artificial Anti-Tetanus; immune serum globulin)

VII. MECHANISM OF SPECIFIC IMMUNE RESPONSES:

A. HUMORAL IMMUNE RESPONSE

 Antibody-mediated defense
 Involves the formation of antibodies by plasma cells in response to
foreign proteins
 Production of circulating antibodies (gamma globulin) that survives
only for days
 B lymphocytes are involved in antibody production
 Functions: bacterial phagocytosis, bacterial lysis, virus & toxin
neutralization, anaphylaxis, allergic hay fever & asthma
  ANTIBODIES & THEIR FUNCTIONS: (“GAMED”)

ANTIBODY DESCRIPTION FUNCTION

IgM Principally an antibody of  Provides an early immune
the blood; 1st antibody response
produced in response to an  Activates the complement
antigen system
 Stimulates ingestion by
macrophages
IgG The most prevalent  Triggers complement
antibody in the blood; fixation
major antibody in tissue  Activates macrophages
spaces; produced in the ingestion
immune response later than  Only antibody to cross
IgM placental barrier **BQ**
 Neutralizes microbial toxins
& has anti-viral & some
antibacterial actions
IgA Resides under the epithelial  Acts as protective barrier
mucosal cells esp. in GIT; against micro-
also found in tears, saliva, organisms at several point
sweat, colostrum & breast or entrance (blocking force
milk; produced later in the since it’s in the mucosa of
immune response organs)
 Easily crosses cellular
barriers
 Protects mucous
membranes of GIT & RT
 May function to protect
GIT of nursing infants
IgD Normally present only in  Exact function is unknown
minute concentration in  May have role in activating
blood; found in the B cells
lymphocyte surfaces
IgE Normally present only in  Responds primarily to
minute concentration in allergic & parasitic
blood infections

B. CELLULAR IMMUNE RESPONSE

 Mediated by T cells: persist in tissues for months or years
 Occurs thru T cell system: on exposure to antigen, the lymphocyte
tissue releases large number of activated T cells into the lymph
system ( T cells mature in the lymph system )
 Involves attack of microbes by special Killer T cells formed from
the lymphocytes
  Functions of T cells:
 transplant rejection,
 delayed hypersensitivity,
 tuberculin reaction,
 tumor surveillance/destruction,
 intracellular infections

 On exposure to antigen, proliferate & differentiate into one of the

several types of T cells

 Main Groups of T cell:

1. Helper T cell – attacks foreign invaders directly; initiates &
augments inflammatory response

2. Cytotoxic T cell – aka killer cells; lyse cells infected with virus;
plays a role in graft rejection

3. Suppressor T cell – suppresses the function of Helper T cells &

Cytotoxic T cells (to stop them from bugbog kung patay na bacteria)

4. Memory T cell – remembers contact with an antigen & on

subsequent exposure mounts an immune response

VIII. STAGES OF SPECIFIC IMMUNE RESPONSE:

A. RECOGNITION STAGE
 Recognition of antigens as foreign or non-self
 Accomplishes recognition lymph nodes & lymphocytes for surveillance
 Lymphocytes come in contact with antigen surface & with help of
macrophages, either removes the antigen or picks up an imprint of the
structure

B. PROLIFERATION STAGE
 Lymphocyte containing the antigenic message returns to nearest lymph
node
 Once in the node, lymphocyte stimulates dormant T & B cells to
enlarge, divide & proliferate
 T Lymphocytes differentiates into Cytotoxic (killer) T cells
 B Lymphocytes produces & releases antibodies

C. RESPONSE STAGE
 Stage when humoral & cellular immune response takes place
 Cytotoxic T cells & antibodies are released in the bloodstream

D. EFFECTOR STAGE
  Antibodies or Cytotoxic T cells reaches & couples with the antigen on
the surface of foreign invader
 The coupling results in destruction of invading microbes or the
complete neutralization of the toxin

IMMUNOLOGIC DISORDERS

I. ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)

A. DEFINITION
 The most severe form of a continuum of illnesses associated with
Human Immunodeficiency Virus (HIV) infection.
 It causes a slow degeneration of the immune system with the
development of opportunistic infections, malignancies & frequently,
impairment of the central nervous system.

B. ETIOLOGY
 The causative agent is a retrovirus ( gP20 surrounds the virus,a protein
which the body naturally has, thus the immune system cannot recognize
it) that damages the immune system by infecting & depleting the T4
helper lymphocytes
 Transmitted by sexual contact through exposure to blood & blood
components & perinatally from an infected mother to the child

C. RISK FACTORS FOR HIV TRANSMISSION

 Homosexual or bisexual men
 Intravenous drug users
 Transfusion of blood products
 Heterosexual contacts of HIV+ individuals
 Newborn babies of mothers who are seropositive

D. CLINICAL MANIFESTATIONS
 1. Following Exposure to HIV Infection:
 Shortly following exposure (6days to 7weeks), there is an acute flu-
like illness lasting 2-4 weeks

 Manifested by fever, sweats, myalgia (muscle pain), arthalgia (joint

pain), malaise, sore throat, lymphadenopathy, maculopapular rash,
fungal & viral infections of the mouth.

 2. Development of AIDS-Related Diseases:

 Pulmonary: persistent cough, SOB, chest pain, fever, Pneumocystis

carinii pneumonia (most common pulmonary infection in AIDS
pxs), even though pneumocytis carinii is the weakest form of bacteria.
  GI: diarrhea, wt loss, anorexia, abdominal cramping, rectal urgency
(tenesmus-opening of sphincter) caused by enteric pathogens such as
Salmonella, Shigella, Campylobacter, Cytomegalovirus, Entamoeba
Histolytica

 Oral: appearance of oral lesions, white plaques on oral mucosa and

angular cheilitis from Candida albicans from mouth &
esophagus; vesicles with ulceration from viruses; white lesions on
margins of tongue from hairy leukoplakia; oral warts & associated
with gingivitis

 CNS: cognitive, motor & behavioral symptoms (AIDS dementia

complex); demonstrated by mental slowing, impaired memory &
concentration, loss of balance, lower extremity weakness, ataxia, &
social withdrawal

 Malignancies: (cancers) Kaposi’s Sarcoma (rare & aggressive tumor

involving the skin, lymph nodes, GI tract & lungs; Non-Hodgkin’s
Lymphoma (malignancies of lymphoid tissue); Burkitt’s Lymphoma

E. DIAGNOSTIC EVALUATION
 1. History of risk factors/high-risk behaviors
 2. Positive blood test for HIV

 ELISA (Enzyme-Linked Immunosorbent Assay) – serologic test

for detecting antibody to HIV

 Western Blot Test – used to confirm a positive result of ELISA

 HOW TO TELL IF PX HAS FULL BLOWN AIDS:

 Decreased circulatory T4 lymphocyte cells/ or CD4 count – LESS
THAN 200 = FULL BLOWN AIDS)
 Presence of indicator diseases: Kaposi’s sarcoma, Pneumocytis carinii

INFANTS:
- Are tested for ELISA to test for HIV antibodies.
- If positive elisa, this indicates that the mother has been infected with
HIV, thus elisa is only to confirm maternal infection not infant infection.
- The test to confirm HIV infection in infants is called P24 antigen
assay, it is a protein component of HIV.

F. MANAGEMENT
 1. Monitor for respiratory status; provide care as appropriate for
respiratory problems; ex. Pneumonia – eg. Position px high fowlers, or
give O2 as ordered for SOB

 2. Assess neurological status; (aids-related dementia) reorient pt as

needed; provide safety measures for the confused/disoriented pt
 3. Monitor pt’s nutritional intake (anorexic); provide supplements, total
parenteral nutrition as ordered (TPN)

 4. Assess skin daily (esp perianal area) for signs of breakdown; keep
skin clean & dry; turn q4hours while in bed

 5. Inspect oral cavity daily for ulcerations, signs of infections; instruct

pt to rinse mouth with normal saline & hydrogen peroxide or normal
saline & sodium bicarbonate rinses

 6. If severe leukopenia develops (prone to infections), institute

neutropenic precautions:
 a. Prevent trauma to skin & mucous membranes; ex. avoid enemas,
rectal temp; minimize all parenteral injections (mucous membranes
may be destroyed and can be an entry point for microbes)

 b. Don’t place pt in a room with pts having infections (isolation)

 c. Screen visitors for colds, infections, etc.

 d. Don’t allow fresh fruits, vegetables, flowers or plants in pt’s room

– same with low WBC- infection prone

 e. Mask pt when leaving room for walks, Xrays, etc.

 f. Provide emotional support for pt/significant others; help decrease

sense of isolation

 Patient Teaching:
 1. Clean kitchen & bathroom surfaces regularly with disinfectants

 2. Avoid direct contact with pet’s litter boxes or stool (toxoplasmosis),

bird cage droppings (histoplasmosis-affecting lungs), & water in fish
tanks

 3. Avoid contact with people with infections

 4. Need to eat a well-balanced diet with plenty of fluids

 5. Use safer sex practice (use of condoms)

 6. Do not donate blood, semen, organs

 7. Do not share razors, toothbrushes or other items that may draw

blood

 8. Inform doctor, dentist, sexual partner of the diagnosis

 Institute Universal Precautions: (any mucous membranes and body
fluids are contaminated based on the universal precautions)

 1. Use of appropriate barrier precautions to prevent skin & mucous

membrane exposure when contact with blood or body fluid is
anticipated

 2. Wear gloves when touching blood & body fluids, mucous

membranes, or non-intact skin of all patients when handling items or
surfaces soiled with blood or body fluids, and when performing
venipuncture & other vascular access procedures

 3. Change gloves after contact with each pt; wash hands immediately
after glove removal

 4. Wear masks and protective eyewear/face shields during procedures

that are likely to generate droplets of blood or other body fluids to
prevent exposure of mucous membranes of mouth, nose, eyes

 5. Wear gloves during procedure likely to generate splashes of blood

or other body fluids

 6. Take precautions to prevent injuries caused by needles, scalpels, &

other sharp instruments or devices; do not reach, bend or break
needles by hand; place used disposable syringes, needles, or other
sharp items in puncture-resistant containers for disposal.

F. MEDICATIONS:

 a. ZIDOVUDINE (AZT) (Anti-viral Therapy) – appears to halt viral

replication; may prolong survival time
 Taken every 4 hours round the clock (rtc)
 Taken either with food or an empty stomach
 Check with doctor before taking other OTC drugs

 B. Treatment of opportunistic infections of organ-specific

symptoms:
 1. Use of antifungal drugs (clotrimazole, amphotericin,
ketoconazole);
 Ganciclovir for Cytomegalovirus disease; Acyclovir for viral
infections;
 Metronidazole for amebiasis/giardiasis

 Radiation & Chemotherapy for management of malignancies
  Trimethoprim-sulfamethoxazole or pentamidine for P. Carinii
pneumonia

II. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

A. DEFINITIONS: - INFLAMMATION OF ORGANS

 Systemic Lupus Erythematosus (SLE) is a chronic, inflammatory,
autoimmune disease involving multi-organ systems & producing
widespread damage to connective tissues, blood vessels, serosal
surfaces & mucous membranes.

 Discoid Lupus Erythematosus (DLE) is a chronic eruption of the skin

which although often disfiguring does not pose a threat to life; DLE
may later become SLE

B. CLINICAL FEATURES:
 Etiology is not understood – genetic, hormonal & environmental
factors thought to play a role

 A lupus-like syndrome can be brought on by certain drugs

(procainamide)

 Most frequently found in young women with signs & symptoms

referable to the joints & skin

 Is characterized by spontaneous remission & exacerbations (signs

and symptoms may suddenly appear, then disappear, then appear again)

 Multiple organ involvement is explained by the deposit of antigen-

antibody complexes throughout the body – kidneys, skin, brain, heart,
& joints

C. CLINICAL MANIFESTATIONS:
 1. Joints – pain on motion, tenderness, effusion or peri-articular soft-
tissue swelling; fatigue, fever, wt loss

 2. Skin:
 Erythematous flat or raised rash over malar eminences (butterfly
rash) aka MALAR RASH **BQ**

 Brittleness or loss of scalp hair

 Photosensitivity **BQ** with rashes developing after sun exposure

 Oral ulcers
 3. Hematologic – hemolytic anemia, leukopenia, thrombocytopenia
  4. Cardiopulmonary – pleural effusion, pericarditis, cardiac
tamponade (accumulation of fluid in the pericardial
space) –

 Nsg int: Monitor V/S

 5. Renal – proteinuria, hematuria, renal insufficiency, renal failure

 Nsg. Int. – Monitor V/s and daily weight

 6. CNS – psychosis, seizures, cognitive impairment, movement

disorders
 Mgt: Institute seizure precautions and safety measures with CNS
involvement

D. DIAGNOSTIC EVALUATION:
 Abnormal titer of Antinuclear Antibodies (ANA) a count of number
of antibodies.
 ANA elevated - inflammation
 Positive Lupus Erythematosus (LE) cell preparation
 ↑ESR
 Renal Function Studies (BUN, CREATININE INCREASES)

E. MANAGEMENT:
 1. Assess symptoms to determine systems involved

 2. Monitor VS, I&O, daily wts.

 3. Institute seizure precautions & safety measures with CNS

involvement
(siderails up, dim lights, lower voices, limit visitors)

 4. Adequate rest

 5. Use of daily heat & exercises as prescribed for arthritis

 6. Avoid physical & emotional stress – can stimulate exacerbation

 7. Avoid direct exposure to sunlight (wear hats, sunglasses, umbrellas,

sunscreen)- coz of photosensitivity

 8. Avoid exposure to persons with infections

9.Plasmapheresis (wash plasma portion of blood) to provide temporary

reduction in amount of circulating antibodies

F. MEDICATIONS:
  1. Aspirin & NSAIDS to relieve mild symptoms such as fever &
arthritis

 2. Corticosteroids (lowest dose) to suppress inflammatory response in

acute exacerbations or severe disease

 3. Immunosuppressive agents such as Azathioprine (Imuran),

Cyclophosphamide (Cytoxan) to suppress immune response when pt
is unresponsive to more conservative therapy

III. SYSTEMIC SCLEROSIS/SCLERODERMA

A. DEFINITION: sclero - hardening

 A generalized disorder of connective tissue characterized by hardening
&/or thickening of the skin & fibrotic degenerative & inflammatory
changes with vascular insufficiency resulting in joint changes &
dysfunction of certain internal organs (GI, heart, lungs, kidneys)

B. CLINICAL FEATURES:
 Thought to be an autoimmune disease
 Affects women more often than men, usually bet ages 30-50
 Prognosis not as good as for lupus

C. CLINICAL MANIFESTATIONS:
 1. Hands & Face:
 Usually starts insidiously on hands & face
 Painless pitting edema of fingers, hands, feet, legs, face; edema
gradually replaced by thickening & tightening of skin which acquires
a tense, wrinkle-free appearance
 Wrinkles & lines are obliterated
 Skin is dry – sweat secretion over involved areas are suppressed
 Face appears mask-like – immobile, expressionless, mouth becomes
rigid (“bird mouth”)
 Conditions spreads slowly; extremities become stiff & immobile;
fingers are semi-flexed, immobile & useless; the hands are claw-like
 Cutaneous manifestations may be accompanied or preceded by
Raynaud’s phenomenon- caused by no blood circulation in the
fingers (manifesting FLAG SIGN – red, yellow, blue per finger)

 2. Internal Effects:
 a. Heart becomes fibrotic – causing congestive heart failure (heart
cannot pump properly), dysrhythmias, angina

 b. Esophagus is hardened with disruption of normal esophageal

peristalsis, gastroesophageal reflux with heartburn & dysphagia

 c. Pulmonary fibrosis – hardened lungs - dyspnea

  d. Intestines become hardened – digestive disturbances

 e. Progressive renal failure – leading cause of death

 CREST SYNDROME – seen in scleroderma

 Calcinosis, -calcium goes out of your fingers
 Raynaud’s Phenomenon, - triggered by cold temp.
 Esophagitis,
 Sclerodactyly, the hard, shiny appearance of fingers caused by excess
connective tissue buildup. This is a common feature of scleroderma, but it
may also occur in other ...

 Telangiectasias – spider veins coming out from the skin

D. DIAGNOSTIC EVALUATION:
 Physical examination to detect fibrotic changes in skin, lungs, heart,
esophagus
 Circulating antibodies against antinuclear antibodies are found

E. MANAGEMENT:
 1. Improving nutritional intake:
 Encourage mouth stretching exercises to maintain oral opening;
maintain adequate oral hygiene
 Maintain upright posture during & after eating; ↑HOB on blocks at
night – to minimize reflux & esophagitis
 Eat foods that are soft, yet forms bolus (ex. mashed potatoes,
puddings)
 Encourage intake of a well-balanced diet with supplementary protein
& Vit C

 2. Maintaining skin integrity:

 Lubricate skin with topical cream & prescribed lubricants to prevent
fissuring & ulcerations
 Avoid detergents & other drying agents
 Monitor body temp carefully as sweat secretion is ↓

 3. Optimize Tissue Perfusion to Skin & Body Organs:

 Keep environment warm
  Use warm baths & massage to maintain joint mobility & ↓ edema
 Avoid exposure to cold, trauma to hands, smoking which aggravates
Raynaud’s phenomenon

 4. Others: Surgical treatment of esophageal stricture;

 management of renal failure- dialysis,
 pulmonary fibrosis,
 pericarditis- thoracentesis

F. MEDICATIONS:
 1. Treated symptomatically; (supportive treatment only)
 NSAIDs to treat joint & muscle pain;
 vasodilating drugs for Raynaud’s phenomenon;
 topical preparations to replace natural oils in skin