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Mercy CLS 1: Immunology > 13) Hypersensitivity > Flashcards

13) Hypersensitivity Flashcards

1
Q

define hypersensitivity rxn

A

exaggerated/inappropriate immune response with damage to host

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2
Q

basic mechanism of TI HS rxn

A

IgE mediated
binds to masts and basos
histamine release

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3
Q

general sx of TI HS rxn

A

rhinitis
asthma
anaphylaxis

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4
Q

basic mechanism of TII HS rxn

A

IgG/IgM binds to cell and activates complement

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5
Q

immediate HS rxn (within minutes)

A

type I

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6
Q

cytotoxic HS rxn

A

type II

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7
Q

immune complex HS rxn

A

type III

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8
Q

TIII HS rxn timeframe

A

within hours

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9
Q

TIV HS rxn timeframe

A

1-2 days

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10
Q

cell mediated/delayed type HS rxn

A

type IV

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11
Q

basic mechanism of TIII HS rxn

A

IgG or IgM - Ag complexes accumulate in blood/tissues
granulocytes release damaging enzymes

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12
Q

basic mechanism of TIV HS rxn

A

T-cell cytokines activate macros, causing damage

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13
Q

3 phases of TI HS rxn

A
  • sensitization
  • activation
  • effector response
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14
Q

first exposure to Ag, IgE attaches to masts/basos

A

sensitization stage (type I)

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15
Q

reaginic Ab

A

IgE

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16
Q

stimultes/suppresses IgE production

A

stimulates: IL-4
suppresses: IFN-𝛾

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17
Q

begins activation phase of TI HS rxn

2 forms

A

challenge/2nd exposure to Ag

cutaneous injection
IV/parenteral injection

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18
Q

wheal & flare rxn part of type —- HS rxn

A

I

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19
Q

wheal & flare peaks in —— mins

sx

A

10-15

erythema
edema
“hives”

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20
Q

required for Ig to cause degranulation

A

2 Fc receptors crosslinked by Ag

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21
Q

triggers of mast cell degran

A
  • IgE
  • C3a, C5a
  • drugs
  • lectins
  • extreme heat & cold
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22
Q

control mechanism for mast cell degran (TI HS rxn activation phase)

A
  • adenylate cyclase converts ATP to cAMP during degranulation
  • sustained increase in intracellular cAMP slows or stops degranulation
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23
Q

2 types of mediators involved in TI HS rxn effector phase

A
  • preformed mediators - stores in granules
  • newly-synthesized mediators
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24
Q

main preformed mediator

A

histamine

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25
Q

storage of histamine

A

electrostatic interaction with heparin

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26
Q

histamine binding sites

A

H1 (smooth muscle, endothelials)
H2 (mucosal membranes)

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27
Q

effects of histamine

A
  • smooth muscle constriction
  • vascular permeability
  • release of stomach acid
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28
Q

antihistamines block —–

A

H1

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29
Q

chemotactic factors involved in effector phase of TI HS rxn

A
  • GM-CSF
  • IL-5
  • TNF-a
  • ECF
  • PAF
  • IL-8
30
Q

late indicator of IgE mediated rxn

31
Q

newly-synthesized mediators and source

A
  • leukotrienes (arachidonic acid + lipoxygenase)
  • prostaglandins/thromboxanes (arachidonic acid + cyclooxygenase)
  • PAF (platelets)
32
Q

cause prolonged constriction of smooth muscle even in presence of histamine

A

leukotrienes

33
Q

cause bronchoconstriction and chemotactic for grans

A

prostaglandins
thromboxanes

34
Q

induces plt aggregation and release of histamine from them

potent bronchoconstrictor and vasodilator

35
Q

mediator that can cause shock-like sx

36
Q

arachidonic acid released from…

A

membrane lipids

37
Q

phase of TI HS rxn occurring after mast cell degranulation and activation

A

late phase rxn

38
Q

mechanism of late phase rxn

A
  • ECF and IL-5 recruits eos and neuts to site
  • they are activated
  • eos release PAF, MPB, ECP
  • neuts phagocytize Ag-AB complexes and release PAF, leukotrienes
39
Q

neurotoxin and helminthotoxin

A

eosinophil cationic protein

40
Q

examples of TI HS rxn

A
  • allergic rhinitis/hay fever
  • food allergies
  • atopic dermatitis
  • asthma
  • insect bite allergies
41
Q

airborne allergen reacts with IgE-sensitized mast cells in nasal passages/conjunctiva

A

allergic rhinitis (TI)

42
Q

food allergen reacts with IgE-sensitized mast cells in GI tract

A

food allergy (TI)

43
Q

allergen contacts skin, activating masts and attracting eos

A

atopic dermatitis

44
Q

red and pus-filled skin rash

A

atopic dermatitis

45
Q

chronic obstruction of lower airways related to chemicals, pollen, dust, viral Ag

46
Q

2 methods of TI HS rxn detection

A
  • skin allergy test
  • RAST (quantitative)
47
Q

RAST

A

radioallergosorbent test

48
Q

explain RAST principle

A
  • allergen on bead/disc placed in pt serum
  • IgE binds
  • wash
  • add anti-IgE conjgate radioactively labelled
  • measure radioactivity
49
Q

pharm interventions for TI HS rxn

A
  • cromolyn sodium: prevents influx of Ca, degranulation
  • corticosteroids: block arachidonic pathway
  • antihistamine: block H1
  • epinephrine: reverses effects of histamine (life-threatening rxn)
50
Q

method of inducing tolerance to Ag by injecting pt with increasing doses over time

A

immunotherapy/hyposensitization

51
Q

2 ways hyposensitization works

A
  • induction of tolerance
  • production of IgG that binds Ag before IgE can
52
Q

allergy shots are better for Ags ———-

A

in circulation
(less IgG on mucosa)

53
Q

complement fixation in TII HS rxn leads to —- or —–

A

lysis or opsonization

54
Q

examples of Ab-mediated cellular dysfunction

A

autoAb bind to cell receptors
- myasthenia gravis (ACh receptor)
- Graves (TSH receptor)

55
Q

examples of TII HS rxn

A
  • trxn
  • cold agglutinin
  • HDFN
  • goodpastures
  • pemphigus vulgaris
  • myasthenia gravis
  • Graves
  • drug-induced (chloramphenicol)
56
Q

Arthus rxn

A

TIII HS rxn
increasingly severe sx at site of inoculation
first mild redness and swelling
after several exposures - hemorrhagic, necrosis

57
Q

complement fixes to Ab-Ag complexes and releases anaphylatoxins

A

TIII HS rxn

58
Q

examples of TIII HS rxn

A
  • serum sickness
  • infection-associated immune complex disease (Goodpasture, rheumatic fever)
  • hypersensitivity pneumonitis (Farmer’s lung)
59
Q

serum sickness

A

TIII HS rxn
injection of serum from another species
make Ab to foreign Ig

60
Q

———- size complexes most harmful

A

small/medium

large complexes removed by phagocytes

61
Q

rheumatic fever

A

TIII HS rxn

follows type A strep infection

62
Q

cause of Farmer’s lung

A

inhaling actinomycetes spores in moldy hay

can cause Arthus type rxn in lungs

63
Q

examples of TIV HS rxn

A
  • contact sensitivity (metals, poison ivy)
  • allograft rejection
  • cutaneous basophil hypersensitivity
64
Q

TIV HS reaction description

A
  • takes days
  • erythema, induration
  • does not cause necrosis
  • resolves slowly
  • mainly macros, few neuts
65
Q

—– suppresses TH2 and expands TH1, contributing to macrophage activation in TIV HS rxn

66
Q

giant cells made of clusters of epitheloids formed by macros accumulating in tissue

A

granuloma
TIV HS rxn

67
Q

rejected graft tissue is invaded by…

A

Ag-specific lymphs and monos

68
Q

skin injection of Ag
takes 24 hours
redness, no induration
may have link to parasites

A

cutaneous basophil hypersensitivity

69
Q

example of cause of cutaneous basophil hypersensitivity

A

tick bites

70
Q

activates macros to release inflammatory mediators

71
Q

↑ expression of adhesion molecules on blood vessels

Mercy CLS 1: Immunology (19 decks)

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