Class 3 Flashcards
Adaptive Immunity
3rd line of defence (1st = skin, 2nd = inflammatory response) Involves specificity (memory B cells), Memory (MHC), Inducibility (Immunization) & self-tolerance
T cells
mediate cellular immunity
B cells
produce antibodies (immunoglobulins A, D, E, G, M) that are dumped into plasma & mediate humoral immunity
Immunosuppression
Weakened response
Hypersensitivity
exaggerated response (inappropriate response to antigen)
Alloimmunity
Rejection of other person’s tissues
Ex: transplant, transfusion.
Hyperacute rejection: pt already has antibodies to antigens of organ (quick response)
Acute Rejection: marcophages & phagocytes attack antigen (not as fast)
Chronic Rejection: gradual loss of function of organs due to attack accumulation over the years
Stress directly influences immunity through…
Hypothalamic & endocrine hormones and neurotransmitters from ANS (epinephrine & norepinhephrine)
Receptors for all these compounds are found on immune cells in spleen & lymphoid tissue.
Autoimmunity
Attacking of one’s own tissues
Immune System Response to Stress
- Increase of glucocorticoids & catecholamines (epi/norepinephrine) secretion during stress.
- This increase results in decreased cellular immunity (T-cells, NK & macrophages)by suppressing T-helper cells
- Increase humoral immunity (B-cells) by stimulating T-helper 2 cells
- Increase acute inflammation locally
- Atrophy of thymus & lymphnodes
Immune Deficiencies
Failure of immune mechanisms of self-defense
- Primary (congenital): genetic anomaly, single gene mutation that is not inherited
- Secondary (acquired): caused by aftermath of a previous illness
Causes of Secondary Deficiencies
Aging
Psychologic stress
Malnutrition
Malignancies
Trauma
Medical treatments
Infections
AIDS***Most common example
-Complications of other conditions.AIDS Secondary Deficiencies
Bone cancers (b/c bone marrow provides WBC)
Chemotherapy & radiation reactions
(kills cancer & stem cells in bone marrow)
Cause = HIV
Immune Deficiencies Manifestations
Recurrent, unusual severe infections (Phagocytic & Complement deficiencies –> can’t fight pus-forming bacteria)
B cell deficiencies (Humoral) then recurrent bacterial infections
T cell deficiencies (Cellular) then causes viral, fungal & atypical infections
Immunodeficiencies Treatments
Gamma Globulin Therapy (inject antibodies for a specific infection from plasma of 1 person to another)
Transplantation/Transfusion (Blood)
Primary Immunodeficiency
Rare
B-Lymphocyte deficiency: low levels of immunoglobulins (hypgammaglobulinemia) or no immunoglobulins
(agammaglobulinemia)
- Selective IgA deficiency (decreases levels of IgA)
- Bruton agammaglobulinemia (blocked development of mature B cells, resulting in repeated infections, inability to synthesize antibodies) –>X-linked disorder, frequent ear & resp infections
T-Lymphocyte Deficiency:antibody production is diminished due to no T- cells to develop B cells
- Chronic mucocutaneous candidiasis (T cells can't respond to specific infection agent (C. albicans) --> C.albicans
- DiGeorge Syndrome (thymic aplasia/hypoplasia, parathyroid gland development diminished, thymus can't produce T cells which activate B cells & low Ca2+ levels & results in tetany & rigidness
Complement Deficiencies
Congenital deficiency
Risk for recurrent life-threatening infections at early age
Associated with Neisseria genus (meningitis/gonorrhea)
Phagocytic Deficiencies
Chronic granulomatous disease (defect in mechanism of killing bacteria)
AIDS
Caused by HIV (retrovirus) which depletes CD4 T-helper cells
Transmitted via sex, blood, placenta, breastfeeding (more cases in women than men)
HIV Retrovirus Pathogenesis Mechanism
Viral genetic info is in form of RNA
Reverse transcriptase converts RNA into DNA
Integrase (from virus) inserts new DNA into affected cell’s genetic material
HIV Clinical Manifestations
Early symptoms: serologically negative (no antibodies) OR serologically positive (antibodies for HIV) but asymptomatic OR early stages of HIV (Flu symptoms)OR AIDS
Decrease of CD4+ T cell numbers
Diagnosis is made in association with other clinical conditions such as opportunisitic infections or cancer
AIDS Risk Factors
Unprotected sex
AIDS Treatment
HIghly active antiretroviral therapy (makes it a chronic condition)
Includes protease inhibitors & reverse transcriptase inhibitors
Vaccine?
Hypersensitivity
Altered immunologic response to an antigen that results in disease or damage to host
Allergy (effects of hypersensitivity to environmental antigens)
Autoimmunity (disturbance in immunologic tolerance of self-antigens)
Type I
Type II
Type III
Type IV
Type I Hypersensitivity
IgE mediated (body is sensitive to this antigen, after second exposure to antigen, mast cells rupture releasing histamine)
Histamine causes increased permeability in vessels, vasodilation, constriction of lungs & increased GI tract peristalsis (nausea)
Involves allergies
Treat with antihistamines
Manifestations: itching, rash, conjunctivites, rhinitis, edema, cramps
Anaphylactic Reaction
Type I Hypersensitivity
Genetic predisposition (more mast cells than average)
Extreme allergic reaction (Hives, itchy, wheezing, difficulty breathing, hypotension, tachycardia, GI effects
Treated with Adrenaline, corticosteroids (decrease inflammation in airways) & antihistamines
Type II Hypersensitivity
Tissue specific (certain tissue is target for immune response) IgG & IgM (Cell may be destroyed via antibody & complement causing lysis of cell) Cell destruction can be caused through phagocytosis by macrophages from antibodies Hemolytic Disease (Newborn): baby develops jaundice, Mom = Rh- Baby = Rh +, worst during the second baby because antibodies to blood are developed
Type III Hypersensitivity
Immune Complex Mediated Antibody binds to soluble antigen in the blood and this complex is deposited into tissue (usually kidneys) Serum sickness (complexes deposited in bvessels, joints, kidneys) Ex: Raynaud phenomen temperature dependentdeposition --> Cryoglobulins Arthus reaction (antigen is under skin and forms inflammation response, lesions_
Type IV Hypersensitivity
Cytotoxic T lymphocytes (directly kill antigen) or Lymphokine producing T-helper1 cell mediated (produce cytokines that activate phagocytic cells for destruction)
Ex: acute graft rejection, TB skin test, contact allergic reactions
Autoimmunity
Breakdown of tolerance, body recognizes self-antigens as foreign
Cause not understood
Ex: Hasimoto’s Thryoiditis (destruction of thyroid gland) & Systemic Lupus erythematosus
Systemic Lupus Erythematosus (SLE)
Chronic multisystem inflammatory disease
Auto-antibodies form against nucleic acids*, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets…
Deposition of circulating immune complexes containing antibody & host DNA
10X more common in females
Clinical manifestations: Arthralgias/arthritis, rash (Malar/Butterfly rash on face), renal disease, hematologic changes, cardiovascular disease
Immunosuppressive Techniques
Corticosteroids (suppress immune response)
Cytotoxic drugs (destroys lymphoid tissue to suppress immune response)
Anti-lymphocyte Serum (destroys only sensitized T-cells that are about to destroy transplanted organ)
Prevent Transplant Rejection by tissue typing (HLA- A, B, C, D)
