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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
type II pathogenesis
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
type II response example disorders
- blood transfusion rxn - newborn/mother Rh incompatibility - autoimmune disorders (hemolytic anemia, myasthenia gravis, graves disease) - certain drug rxn
27
transfusion rxn
- fevers, chills, rushing - inc HR, dec BP - chest pain, back pain - N/V - restlessness - anxiety - headache
28
type III key characteristics
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
type III antibodies
IgG IgM
30
type III possible offending antigens
body's own tissue and/or DNA inhaled antigens from mold or contaminated plants bacteria or viruses
31
key immune cells involved in type III immunity
antibodies (IgG and IgM) that clumps w antigens complement neutrophils (release toxins and chemical mediators)
32
type III pathogenesis
- 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
clinical manifestations of type III
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
type II vs type III
- 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
type IV key characteristics
- delayed hypersensitivity response - no antibody involvement
36
type IV key immune cells
- T cells (no B cells) - cytokines - mast cells and macrophages
37
etiology of type IV
delayed cellular reaction to an antigen
38
possible source antigens for type IV
- plant oils - cosmetics, clothing, dyes, adhesives - nickel alloys - TB antigen - organ transplant or skin graft - gluten
39
pathogenesis of type IV
- 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
type IV pathogenesis image
- 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
clinical manifestations of type IV
- peaks at 48-72 hrs - contact dermatitis (redness, edema, itching, blisters) - tuberculin hypersensitivity (redness, induration, inflammation)
42
4 different types summary: type I
- allergens - IgE on mast cells - mediator release
43
4 different types summary: type II
- IgG and IgM - antibodies attach to cells - cell lysis
44
4 different types summary: type III
- IgG and IgM - antibodies complexes - accumulate in tissues - inflammation
45
4 different types summary: type IV
- delayed T cell activation - cytokines

NUE 325: Pathopharm I (23 decks)

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