NUR 228 Exam 1 Flashcards

1
Q

Hypersensitivity

A

a NORMAL immune response that is inappropriately triggered OR excessive OR produces undesirable effects on the body.

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2
Q

What are two basic triggers?

A

antigen-antibody reaction
antigen-lymphocyte interaction

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3
Q

What is in common between types I, II, III hypersensitivity reactions?

A

they are all mediated by antibodies produced by B cells
-specifically PLASMA cells

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4
Q

What causes type IV hypersensitivity

A

mediated by T cells

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5
Q

What kind of hypersensitivity reactions does meds typically cause?

A

type I and IV

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6
Q

What type of hypersensitivity reaction does PCN cause

A

all four types

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7
Q

What kind of mediated reaction is type I

A

IgE mediated reaction

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8
Q

Type I hypersensitivity reaction

A

caused by B cells
Immediate reaction
occurs after being sensitized to an antigen

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9
Q

what antigens cause type I hypersensitivity?

A

environmental(pet dander, bee stings)
Foods (nuts, seafood, eggs)
Medications (penicillin, contrast dye)

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10
Q

What are key immune cells involved in Type 1 reaction?

A

B lymphocytes
IgE (antibody)
Mast cells (granulocyte)

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11
Q

Etiology of Type 1

A

Genetic link
1 parent allergic=30%
2 parents allergic= 50%

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12
Q

What is the pathogenesis of type 1?

A

-person exposed
-IgE antibody made
-IgE antibody attaches to mast cell
-person exposed again
-allergen binds to the IgE antibodies that are attached to the mast cells
-triggers the release of chemical mediators from the mast cell

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13
Q

Potent vasodilation causes

A

stuffy nose
lower blood pressure
wheals on skin

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14
Q

Increased vascular permeability causes

A

edema
runny nose

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15
Q

Bronchial smooth muscle constriction causes

A

breathing difficulties
wheezing

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16
Q

Stimulates irritant receptors causes

A

itching

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17
Q

Atopic reactions

A

local
inherited tendency to become sensitive to allergens
Ex: allergic rhinitis, asthma, urticaria(hives)

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18
Q

Anaphylactic reaction

A

systemic
life threatening because of bronchial constriction, airway obstruction, vascular collapse.
treat quickly

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19
Q

Most common triggers of atopic and anaphylactic reactions?

A

Atopic: pollen, dust, mold, animal dander
Anaphylactic: meds, bee stings, foods

20
Q

What causes the symptoms from a type 1 hypersensitivity reaction?

A

release of chemical mediators

21
Q

What is type II caused by?

22
Q

Etiology of Type II reactions

A

exposure to antigen or foreign tissue/cells
antigens are located on cell surface

23
Q

What are the key characteristics of a type II reaction

A

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

24
Q

what immune cells are involved with a type II reaction?

A

antibodies (IgG and IgM)
complement
WBCs (phagocytes)

25
what are the examples of antigens of type II
blood some of your body's own cells (autoimmune) erythroblastosis fetalis
26
What are some example disorders from type II
blood transfusion reaction newborn/mother Rh incompatibility autoimmune disorders certain drug reactions
27
What are some examples of type II manifestations of a transfusion rx?
Fever Chills angina N/V restlessness and anxiety headache
28
What kind of reaction is type III?
Immune complex reaction
29
Key characteristics of type III hypersensitivity
antigen-antibody COMPLEXES (attach to each other) form deposit into tissues inflammatory response causes tissue damage
30
Etiology of Type III HSRx?
autoimmune low grade infection inhaled antigens from molds or contaminated plants
31
What are possible offending antigens for type III?
bodys own tissues/dna Inhaled antigens from mold or contaminated plants bacteria or viruses
32
What are key immune cells involved in type III sensitivity?
IgG and IgM antibodies that clump with antigens complement neutrophils and mast cells
33
Type III Pathogenesis?
antigen-antibody complex formed in blood deposits in tissue activation of complement + chemoattraction of neutrophils Fc Receptor Release of enzymes and free radicals Tissue distruction
34
What are clinical manifestations of Type III?
depends on where the complexes are deposited in the tissue Rheumatoid arthritis: joints Glomerulonephritis: kidney failure Systemic lupus erythematosus: skin and organs
35
What are the primary differences between type II and type III?
type II- reactions occur on the cell surface and result in direct cell death or malfunction type III- immune complexes are deposited into tissues and the resulting INFLAMMATION destroys the tissue
36
What is type IV hypersensitivity?
Delayed hypersensitivity
37
What are key characteristics of Type IV hypersensitivity
delayed hypersensitivity response NO antibody involvement
38
What are key immune cells for type IV
T cells Cytokines Mast cells and macrophages
39
Etiology of type IV
delayed cellular reaction to an antigen
40
What are some antigens for type IV
plant oils cosmetics nickel tuberculin organ transplant skin graft
41
Type IV pathogenesis
small incomplete antigen (hapten) penetrates the skin Hapten combines with human protein to form the complete antigen T cells become aware of antigen T cells attack the antigen via: -direct attack of t cell -release of cytokines -macrophages
42
what are clinical manifestations of type IV
generally peak 48-72 hours contact dermatitis tuberculin hypersensitivity
43
Autoimmunity
the immune system recognizes "self" cells as foreign an immune responses is initiated your bodies own tissues are injured
44
Etiology of autoimmunity
genetic factors environmental triggers
45
antigenic mimicry
some viruses/bacteria look like "self" self cells similar to these foreign cells are attacked
46
Risk factors of autoimmunity
over age 50 genetics female African american, hispanic, asian, native american viral bacterial infections
47