hypersensitivity & immune deficiency Flashcards

1
Q

hypersensitivity

A

excessive/inappropriate activation of immune system leading to production of antibodies/T cell responses that cause tissue injury and disease

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2
Q

hypersensitivity reactions

A

disorders caused by immune responses

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3
Q

allergy

A

hypersensitivity to exogenous antigens such as medicines, pollen, bee stings

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4
Q

types of hypersensitivity

A

allergy, autoimmunity, alloimmunity

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5
Q

autoimmunity

A

disturbance in immunologic tolerance of self-antigens – immune system develops auto-antibodies that damage its own tissue

breakdown of tolerance either due to alteration of antigen or idiopathic (more common)

no known tx – treat symptoms & suppress immune system

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6
Q

alloimmunity

A

immune reaction to tissues of another individual, i.e. blood transfusion, organ transplant

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7
Q

type I hypersensitivity

A

IgE mediated, causes mast cell degranulation (histamine release) – anaphylactic

IgE binds to Fc receptors on mast cells (cytotropic antibody)

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8
Q

type II hypersensitivity

A

tissue-specific reactions (cells lyse) – cytotoxic

tissue cells destroyed by IgG/IgM & complement – antibody attaches to cell & causes antibody-dependent cell-mediated toxicity by NKs

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9
Q

type III hypersensitivity

A

immune complex mediated – antigen-antibody complexes form in body fluid & are deposited in vessel walls/extravascular tissues

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10
Q

type IV hypersensitivity

A

cell mediated – T cells attacking (does not involve antibodies) – delayed hypersensitivity

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11
Q

hypersensitivity process

A

sensitization (first exposure), immune response, second exposure causes symptoms

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12
Q

anaphylaxis

A

symptoms: respiratory difficulty due to vasoconstriction of pulmonary vessels, hives, vomiting, diarrhea, swelling of bronchial tract, low BP, shock

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13
Q

histamine release mechanisms

A

H1 receptors cause bronchial constriction & increase vascular permeability (tx diphenhydramine)

H2 receptors cause increased gastric secretion (tx pepsin)

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14
Q

symptoms of type I hypersensitivity

A

itching, urticaria, conjunctivitis, rhinitis, hypotension, bronchospasm, dysrhythmias, GI cramps/malabsorption

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15
Q

type I hypersensitivity management

A

tests: food challenge, skin/lab tests

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16
Q

desensitization

A

IgG blocking antibodies – small quantities of allergen injected to build resistance to reaction

17
Q

tx type I hypersensitivity

A

antihistamines, desensitization, steroids, bronchodilators, anti-leukotrienes, anti-IgE antibody, epinephrine (acute reactions only)

18
Q

examples of type IV hypersensitivity

A

acute graft rejection, TB skin test, contact allergic reactions, collagen destruction in RA, destruction of thyroid in Hashimoto disease, contact dermatitis from poison ivy

19
Q

examples of type III hypersensitivity

A

SLE, RA, some acute glomerulosclerosis, Raynauds phenomenon

20
Q

examples of type II hypersensitivity

A

blood transfusion reactions, hemolytic disease of the newborn, Goodpasture disease

21
Q

sequestered antigen

A

self-antigens not normally seen by immune system, can cause autoimmune reaction

22
Q

systemic lupus erythematosus (SLE)

A

chronic multisystem inflammatory disease – autoantibodies created against nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, etc.

most common in African-Americans & females

23
Q

symptoms of SLE

A

arthralgias/arthritis, vasculitis, rash, renal disease, hematologic changes, cardiovascular disease

presence of antinuclear antibodies (ANA) – diagnostic

24
Q

transient neonatal alloiummunity

A

fetus expresses parental antigens not found in mother

25
Q

ABO blood antigens

A

antibodies formed at birth from IgM

26
Q

transplant rejection

A

caused by MHC/HLA – HLA typing done to prevent antibody formation (matches patient/donor antigens)

27
Q

types of rejection

A

hyperacute, acute, chronic

28
Q

hyperacute rejection

A

immediate, rare – preexisting antibody to antigens in graft/transplant

29
Q

acute rejection

A

cell-mediated response against unmatched HLA antigens, occurs w/in days-months – type IV

30
Q

chronic rejection

A

occurs after several months/years – slow organ failure – weak cell-mediated type IV reaction

inflammatory damage to endothelial cells of vessels

31
Q

AIDS

A

blood-borne pathogen, currently increasing faster in women than men – effective therapies have made it a chronic disease

disables CD4 receptors on helper T cells & reverses CD4/CD8 ratio

32
Q

clinical manifestations of HIV

A

serologically negative, serologically positive but asymptomatic, early stage, AIDS

helper T cells < 200 cells/cubic mm

33
Q

transmission of HIV

A

blood, breast milk, sperm

34
Q

highly active antiretroviral therapy (HAART)

A

reverses transcriptase inhibitors, protease inhibitors – tx HIV

35
Q

tx HIV

A

HAART, entrance inhibitors, integrase inhibitors, vaccine is in development

36
Q

graft-vs-host disease (GVHD)

A

T cells in graft are mature & capable of cell-mediated destruction of tissues w/in recipient – not a problem if patient is immunocompetent

37
Q

evaluation of immunity

A

CBC with differential, quantitative determination of immunoglobulins, assay for total complement, skin tests

38
Q

tx immunodeficiencies

A

gamma globulin therapy, transplantation/transfusion, soluble immune mediators, gene therapy