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NUE 325: Pathopharm I > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

hypersensitivity

A

a normal immune response that is
- inappropriately triggered
- excessive response
- produces undesirable effects on the body

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2
Q

triggers of hypersensitivity

A
  • specific antigen-antibody rxn
  • specific antigen-lymphocyte interaction
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3
Q

four types of sensitivity

A
  • type I, II, III: mediated by antibodies produced by B cells (specifically plasma cell)
  • type IV: mediated by T cells
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4
Q

type I rxn

A

IgE

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5
Q

type I characteristics

A

immediate rxn (15-20 mins)
reaction occurs after being sensitized to an antigen
occurs at second exposure

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6
Q

antigens of type I

A
  • env like pet dander, bee stings
  • foods like nuts, seafood, eggs
  • medications like penicillin, contrast dye
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7
Q

type I etiology

A
  • 1 parent allergic = 30%
  • 2 parent allergic = 50%
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8
Q

key cells involved in type I rxn

A
  • B lymphocytes
  • IgE antibodies
  • mast cells (granulocytes)
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9
Q

type I pathogenesis

A
  • antigen will bind to B cell (first exposure)
  • plasma cells will produce antibodies, specifically IgE
  • IgE will attach to mast cells
  • when exposed again, the antigen will bind to the IgE antibody on mast cell which will trigger the release of chemical mediators from mast cell
  • chemical mediators can result in numerous affects
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10
Q

chemical mediators of type I result in

A

intravascular compartment
- anaphylactic shock
skin
- urticaria, atopic dermatitis, wheal flare rxn, angioedema
respiratory system
- rhinitis, asthma
GI system
- N, V, D, cramping

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11
Q

reasons for type I clinical manifestations mediator activities
- potent vasodilation

A

stuffy nose
lower bp
wheals on skin

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12
Q

reasons for type I clinical manifestations mediator activities
- inc vascular permeability

A

edema
runny nose

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13
Q

reasons for type I clinical manifestations mediator activities
- bronchial smooth muscle constrictions

A

breathing difficulties
wheezing

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14
Q

reasons for type I clinical manifestations mediator activities
- stimulates irritant receptors

A

itching (pruritus)

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15
Q

type I atopic rxns (local rxn)

A

inherited tendency to become sensitive to allergens
- ex: allergic rhinitis, asthma, urticaria

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16
Q

most common triggers of atopic rxn

A

pollen
dust
molds
animal dander

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17
Q

type I systemic rxn

A

results in anaphylaxis, a systemic release of chemical mediators

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18
Q

why is anaphylaxis life threatening

A

bronchial constriction
airway obstruction
vascular collapse (shock)

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19
Q

most common triggers of anaphylaxis type 1

A

medications
bee stings
foods

20
Q

type II rxn

A

cytotoxic rxn

21
Q

etiology of type II

A

exposure of antigen or foreign tissue/cell (not your own cells)
antigens are located on the cell surface

22
Q

key characteristics of type II

A

antigen stimulate antibody production
antibodies recognize and attach to cell surface antigens
direct destruction of targeted cells that contain antigen
- cell lysis
- phagocytosis

23
Q

immune cells involved type II

A

antibodies IgG an IgM
complement
WBCs (phagocytosis)

24
Q

examples of type II antigens

A

blood
some of your body’s own cells (auto immune conditions)
erythroblastosis fetalis (Rh factor btw baby and mom)

25
Q

type II pathogenesis

A

type a will have b antibodies, type b will have a antibodies
- when one blood type is put into the other the antibodies will bind with the blood type and cause clumping
clumping results in
- donor cells burst –> kidney damage
- small vessels blocked –> reduced blood supply

26
Q

type II response example disorders

A
  • blood transfusion rxn
  • newborn/mother Rh incompatibility
  • autoimmune disorders (hemolytic anemia, myasthenia gravis, graves disease)
  • certain drug rxn
27
Q

transfusion rxn

A
  • fevers, chills, rushing
  • inc HR, dec BP
  • chest pain, back pain
  • N/V
  • restlessness
  • anxiety
  • headache
28
Q

type III key characteristics

A

antigen antibody complex complexes that circulate around the body which will be deposited into tissues causing inflammatory response from tissue damage (often at the joints)

29
Q

type III antibodies

A

IgG
IgM

30
Q

type III possible offending antigens

A

body’s own tissue and/or DNA
inhaled antigens from mold or contaminated plants
bacteria or viruses

31
Q

key immune cells involved in type III immunity

A

antibodies (IgG and IgM) that clumps w antigens
complement
neutrophils (release toxins and chemical mediators)

32
Q

type III pathogenesis

A
  • antigen-antibody complex forms in the blood which will deposit in the tissue
  • the deposition causes activation of complement and chemoattraction of neutrophils which will release enzymes and free radicals
33
Q

clinical manifestations of type III

A

depends on where the complexes are deposited in the tissue
- rheumatoid arthritis: whatever joints its deposited in
- glomerulonephritis: kidney failure
- systemic lupus erythematosus: skin and many organs

34
Q

type II vs type III

A
  • type II: rxn occurs on the cell surface and result in direct cell death or manifestation
  • type III: immune complexes are deposited into tissues and the resulting inflammation destroys the tissue
35
Q

type IV key characteristics

A
  • delayed hypersensitivity response
  • no antibody involvement
36
Q

type IV key immune cells

A
  • T cells (no B cells)
  • cytokines
  • mast cells and macrophages
37
Q

etiology of type IV

A

delayed cellular reaction to an antigen

38
Q

possible source antigens for type IV

A
  • plant oils
  • cosmetics, clothing, dyes, adhesives
  • nickel alloys
  • TB antigen
  • organ transplant or skin graft
  • gluten
39
Q

pathogenesis of type IV

A
  • small, incomplete antigen, called a hapten penetrates the skin
  • hapten binds with human protein to form complete antigen
  • T cells become aware of antigen
  • T cells attack the antigen via direct attack of T cells, release of cytokines (inflammation), macrophages (cell destruction)
40
Q

type IV pathogenesis image

A
  • exposure to hapten with formation of complete antigen
  • recognition and processing of antigen by antigen processing cell
  • migration of APC to lymph node where antigens are presented to T cells
  • release of cytokines that stimulate proliferation of T cells and activates macrophages
  • activated T cells and macrophages migrate to epidermis, release inflammatory mediators ,cause cell destruction
41
Q

clinical manifestations of type IV

A
  • peaks at 48-72 hrs
  • contact dermatitis (redness, edema, itching, blisters)
  • tuberculin hypersensitivity (redness, induration, inflammation)
42
Q

4 different types summary: type I

A
  • allergens
  • IgE on mast cells
  • mediator release
43
Q

4 different types summary: type II

A
  • IgG and IgM
  • antibodies attach to cells
  • cell lysis
44
Q

4 different types summary: type III

A
  • IgG and IgM
  • antibodies complexes
  • accumulate in tissues
  • inflammation
45
Q

4 different types summary: type IV

A
  • delayed T cell activation
  • cytokines

NUE 325: Pathopharm I (23 decks)

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