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Pathopharmacology Fundamentals > Module 7 Hypersensitivity > Flashcards

Module 7 Hypersensitivity Flashcards

1
Q

Hypersensitivity is a normal immune response that is… (3)

A

Inappropriately triggered, excessive, or produces undesirable effects on the body

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2
Q

2 basic mechanisms that trigger hypersensitivity

A

antigen-antibody reaction or antigen-lymphocyte interaction

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3
Q

Four types of hypersensitivity: 1-3

A

mediated by antibodies produced by B cells, specifically plasma cells

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4
Q

Hypersensitivity type 4 is mediated by

A

T cells

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5
Q

B lymphocytes are immature until

A

they come across antigen and become a mature plasma cell

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6
Q

Types 1-3 is an

A

immediate reaction

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7
Q

type 4 will take longer because

A

T cells don’t have the immediate reaction like B cells do

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8
Q

Type 1 hypersensitivity

A

IgE mediated reaction

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9
Q

IgE is in response to someone developing an

A

allergy (ex: pet dander, pollen)

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10
Q

antibodies aka

A

immunoglobulins

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11
Q

Type 1 hyper sensitivity can become

A

anaphylactic

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12
Q

Type 1 hypersensitivity is

A

immediate

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13
Q

Type 1 hypersensitivity requires a

A

previous exposure to the antigen

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14
Q

Most allergens are

A

proteins

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15
Q

Type1 : If 1 parent is allergic

A

30% chance offspring will be allergic

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16
Q

Type 1: If both parents allergic

A

50% chance offspring will be allergic

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17
Q

Key cells involved in type 1 sensitivity

A

B lymphocytes, IgE antibodies, mast cells

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18
Q

allergy medications block chemical mediator release by blocking

A

histamine

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19
Q

allergic rhinitis

A

runny nose

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20
Q

uticaria

A

hives

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21
Q

asthma have

A

overactive mast cells

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22
Q

systemic release of chemical mediators

A

anaphylaxis

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23
Q

During anaphylaxis

A

bronchial constriction, airway obstruction, vascular collapse from widespread vasodilation (low BP)

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24
Q

type 2 hypersensitivity

A

cytotoxic reaction

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25
Q

type 2 hypersensitivity exposure to a

A

foreign tissue or cell type, antigens are located on cell surface

26
Q

example of a type 2 hypersensitivity

A

organ transplant

27
Q

in type 2 hypersensitivity

A

antigen-antibody complex attacks foreign cells, lyses them, and then phagocytes clean up

28
Q

cells involved in type 2 hypersensitivity

A

IgG and IgM, phagocytes, complement cells (kill the foreign cells)

29
Q

Examples of type 2 hypersensitivity

A

blood, diabetes, erythroblastosis fetalis

30
Q

erythroblastosis fetalis

A

hemolytic anemia in the fetus, rh factor

31
Q

type 2 hypersensitivity leads to

A

kidney damage because the small blood vessels are clogged AND less RBCs so no oxygen supply

32
Q

Autoimmune disorders than can cause type 2 hypersensitivity

A

hemolytic anemia, myasthenia gravis, graves disease

33
Q

medication used to treat rh factor

A

rhogam

34
Q

signs and symptoms of a blood transfusion reaction

A

fever, chills, flushing, tachycardia, hypotension, chest or back pain, nausea, vomiting, restlessness, anxiety, headache

35
Q

we take patient’s

A

temperature before and after a blood transfusion because this is one of the first signs

36
Q

type 3 hypersensitivity

A

immune complex reaction

37
Q

example of type 3 reaction

A

RA

38
Q

type 3 hypersensitivity reaction step 1

A

antigen-antibody complex circulate in body and deposit into various tissues

39
Q

type 3 hypersensitivity reaction step 2

A

the antigen-antibody complex causes inflammation in the tissue that it is lodged in and this is the type 3 reaction we see

40
Q

etiology of hypersensitivity type 3

A

autoimmune attack, low grade infection, inhaled antigens from molds or contaminated plants, bacteria or viruses

41
Q

key cells involved in type 3 hypersensitivity

A

IgG, IgM, complement, neutrophils, mast cells

42
Q

neutrophils release toxins and chemical mediators that

A

cause tissue destruction

43
Q

mast cells dump chemical mediators that cause the

A

inflammatory response

44
Q

Type 3 clinical manifestations (3)

A

rheumatoid arthritis (joints), glomerulonephritis (kidney failure), systemic lupus erythematous (skin)

45
Q

in type 2 hypersensitivity, the complexes attack the foreign cell

A

directly

46
Q

in type 3 hypersensitivity, the complexes do NOT destroy the foreign cells, they

A

cause inflammation in tissues where the complexes are stuck and the inflammation is what causes the tissue to be destroyed

47
Q

type 4 hypersensitivity

A

delayed hypersensitivity

48
Q

examples of type 4 hypersensitivity

A

poison ivy, TB skin test, jelly fish sting, jewelry reaction, crohn’s disease

49
Q

in type 4 hypersensitivity

A

there are no antibodies involved

50
Q

key cells in type 4

A

T cells, cytokines, mast cells, macrophages

51
Q

steps of type 4 hypersensitivity

A

hapten comes through skin and created complete antigen, t cells recognize and attack to release cytokines (inflammation), macrophages clean up

52
Q

type 4 generally peak in

A

48-72 hours

53
Q

two most common type 4 reactions

A

contact dermatitis, and tuberculin hypersensitivity

54
Q

3 pharmacology options

A

immunosuppressants, antihistamines, epinephrine

55
Q

suppress histamine mediator activity

A

antihistamines

56
Q

suppress cell mediated immunity and inflammatory response

A

immunosuppressants and corticosteroids

57
Q

halts mediator activity

A

epinephrine

58
Q

epinephrine works on

A

alpha and beta receptors

59
Q

where are alpha receptors

A

arteries

60
Q

where are beta receptors

A

in the heart, lungs, arteries, skeletal muscles

61
Q

for epi subcut use a

A

TB syringe

62
Q

teach patients when taking epinephrine to

A

take exactly as directed and to contact HCP immediately after taking it

Pathopharmacology Fundamentals (13 decks)

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