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Pathophysiology I > Immune Injury > Flashcards

Immune Injury Flashcards

1
Q

what does immune response protect against?

A

invaders and toxins

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2
Q

hypersensitivity reactions

A

excessive/inappropriate immune response

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3
Q

types of hypersensitivity reactions

A

types I, II, III, IV

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4
Q

autoimmune disorders

A

misdirected immune response

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5
Q

immunodeficiency disorders

A

deficient immune respone

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6
Q

type I hypersensitivity aka

A

anaphylaxis, immediate hypersensitivity

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7
Q

type I hypersensitivity results from what

A

antigen binding to IgE on mast cell/basophil surfaces

“allergen”

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8
Q

type I hypersensitivity-what happens after antigen binds to IgE?

A

degranulation with histamine (and other mediator) release into tissues

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9
Q

type I hypersensitivity reaction time

A

reaction immediate and over within hours

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10
Q

type I hypersensitivity-what must happen before allergy manifests?

A

mast cells/basophils must be “primed”

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11
Q

type I hypersensitivity-what does first exposure result in?

A

1st exposure results in IgE production and binding to mast cells/basophils

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12
Q

type I hypersensitivity-what does subsequent exposure result in?

A

mast cell/basophil degranulation

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13
Q

type I hypersensitivity-what is the most prominent mediator?

A

histamine

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14
Q

type I hypersensitivity-what does histamine produce?

A

vasodilation
increased capillary permeability
bronchial smooth muscle contraction

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15
Q

type I hypersensitivity-what does IgE normally protect against?

A

parasitic worm infections

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16
Q

type I hypersensitivity-what manifestations are designed to expel a worm?

A 
itching
sneezing
coughing
vomiting 
diarrhea
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17
Q

type I hypersensitivity-what do mast cells also release (besides histamine)?

A

eosinophil and neutrophil chemotactic factors

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18
Q

type I hypersensitivity-acute phase

A

seconds to minutes after exposure

-histamine release with immediate/transient effects

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19
Q

type I hypersensitivity-late phase timeline

A

hours after acute phase

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20
Q

type I hypersensitivity-late phase steps

A

infiltration of tissues by lymphocytes and eosinophils
release of leukotrienes (C4, D4, E4) and prostaglandins (D2)
similar effects to histamine but prolonged

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21
Q

type I hypersensitivity local reactions examples

A

generally not dangerous
urticaria (hives)-wheal and flare effect of histamine (e.g. mosquito bite)
allergic rhinitis (hay fever)-sneezing, itchy eyes from airborne allergies
allergic (extrinsic) asthma-bronchoconstriction from inhaled allergens

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22
Q

type I hypersensitivity local reactions-how to treat

A

treated with antihistamines or steroids

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23
Q

type I hypersensitivity generalized reactions importance and examples

A

are life threatening

anaphylaxis, penicillin injections, certain foods

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24
Q

type I hypersensitivity generalized reactions sx

A

whole-body vasodilation/capillary leak
anaphylactic shock
edema of tongue/larynx can obstruct airway
intense bronchoconstriction

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25
Q

type I hypersensitivity generalized reactions tx

A

epinephrine mainstay of treatment

-vasoconstrictor and bronchodilator

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26
Q

food allergies

A

are real
local or systemic type I reactions
200 deaths/year
eggs, nuts, shellfish

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27
Q

what causes histamine release in everyone?

A

chocolate, strawberries, codeine
non-IgE mediated
those with greater release are “allergic”

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28
Q

testing methods for allergies

A

skin testing better (prick, injection) used in diagnosis
wheal and flare response
radioallergosorbent test (RAST)
detects IgE, less sensitive and specific

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29
Q

type II hypersensitivity definition

A

antibodies bind to “fixed” antigens present on cell membranes
-IgM or IgG mediated
cell bearing the antigen then destroyed (or function altered)

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30
Q

type II hypersensitivity mechanisms of destruction

A

complement activation and cell lysis/phagocytosis
antibody-dependent cell cytotoxicity
complement- and antibody-mediated inflammation

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31
Q

type II hypersensitivity what can also occur?

A

antibody-mediated cell dysfunction

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32
Q

what is type II hypersensitivity pathogenesis of?

A

many autoimmune diseases

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33
Q

type II hypersensitivity complement activation

A

Ag-Ab complex fixes complement
target cell lysed by MAC
Ab and/or C3b act as opsonins
target cell engulfed

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34
Q

type II hypersensitivity-hemolytic transfusion reactions

A

ABO incompatibility
ready-made IgM
hemolytic disease of newborn
requires sensitization and involves IgG

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35
Q

type II hypersensitivity antibody-dependent cell cytotoxicity

A

involves elements of innate and adaptive immunity
Ab bound to target cell attracts NK cell
NK cell binds Ab and induces apoptosis

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36
Q

examples of type II hypersensitivity antibody-dependent cell cytotoxicity diseases

A

hashimoto’s thyroiditis
autoimmune adrenalitis
type I diabetes mellitus?

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37
Q

type II hypersensitivity complement and antibody-mediated inflammation

A

Ag-Ab complex fixes complement
C3a/C5a attract neutrophils
neutrophils bind Ab
acute inflammation occurs

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38
Q

type II hypersensitivity-goodpasture’s syndrome

A

Ab binds to lung and glomerulus basement membranes

acute inflammation destroys alveoli and nephrons

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39
Q

example of type II hypersensitivity injury

A

transfusion-related lung injury (TRALI), plasma transfusion

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40
Q

type II hypersensitivity-antibody-dependent cell dysfunction

A

Ab binds cell membrane receptor

blocks or activates receptor

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41
Q

type II hypersensitivity-myasthenia gravis

A

Ab binds and blocks ACh receptor at neuromuscular junction

prevents muscle stimulation

42
Q

type II hypersensitivity-graves’ disease

A

Ab binds and stimulates TSH receptor at thyroid gland

produces hyperthyroidism

43
Q

type III hypersensitivity

A

antibodies (IgM and IgG) bind to soluble antigens in plasma when each present in the right proportions

44
Q

what is formed during type III hypersensitivity?

A

Ag-Ab complexes (“immune complexes”) that precipitate

45
Q

type III hypersensitivity-where do immune complexes?

A

blood vessel walls (close by)
glomerulus (proteins are more concentrated)
skin (precipitation faster due to cooler temperature)
lungs (same as skin)
synovial membranes

46
Q

type III hypersensitivity what do immune complexes do?

A

fix complement and induce inflammation

47
Q

type III hypersensitivity manifestations dependent on what?

A

manifestations dependent on location of immune complex deposition

48
Q

examples of type III hypersensitivity manifestations

A

vasculitis
glomerulonephritis
arthritis

49
Q

type III hypersensitivity examples

A

neutrophils have nothing to attack (but attack anyway)
systemic lupus erythematosus
serum sickness
malaise hours after immunization

50
Q

what is involved in type IV hypersensitivity?

A

no antibodies, T cells

51
Q

what happens in type IV hypersensitivity?

A

Th cells are presented Ag by APC (with MHC II)
Th then activate Tc cells and macrophages
Th cells selectively destroy cells bearing same Ag with MHC I
angry macrophages destroy normal tissues as well
no complement involved

52
Q

type IV hypersensitivity what could activated T cells also destroy?

A

activated T cells may destroy normal cells bearing similar Ag to one provoking response

53
Q

what is type IV hypersensitivity great for?

A

eliminating parasite-infected cells
viruses
mycobacteria

54
Q

what can type IV hypersensitivity also eliminate?

A

some tumor cells

55
Q

what is type IV hypersensitivity a mechanism of?

A

one mechanism of acute transplant rejection

56
Q

examples of type IV hypersensitivity

A 
contact dermatitis (nickel, poison ivy, etc.)
tb skin test
57
Q

type IV hypersensitivity tb skin test

A

extract of M. tuberculosis injected into dermis
if sensitized (previously exposed), type IV reaction occurs
-memory Th and Tc cells spring to life
-macrophages recruited
angry macrophages destroy some normal tissue at site
“lump” of fibrin macrophages at 48-72 hours
don’t test someone with known exposure

58
Q

anergy

A

defects in Th cell number or function can inhibit type IV response

59
Q

examples of causation of anergy

A

AIDS, sarcoidosis, wasting diseases

60
Q

how to test for anergy?

A 
skin tests with common antigens
candida, mumps, tetanus
often done in conjunction with TB test
people with normal T cell function should have a bump
no bump=anergic
61
Q

transplant rejection

A

donor tissues/organ seen as foreign by recipient with immune destruction
matching done on basis of synergy between donor/recipient HLA antigens

62
Q

autograft

A

donor and recipient are the same

63
Q

isograft

A

donor and recipient are different but have same genes

64
Q

allograft

A

donor and recipient are different and have different genes

65
Q

xenograft

A

donor and recipient are different species

66
Q

what is required for graft survival with allografts and xenografts?

A

immunosuppression

67
Q

transplant rejection-hyperacute rejection

A

due to premade (or almost immediately made) antibodies
antibodies directed against HLA antigens on the graft
type II and III injury occurs

68
Q

transplant rejection-acute cellular rejection

A

months or years after transplantation

mediated by T cells, type IV injury

69
Q

transplant rejection-acute humoral rejection

A

months or years after transplantation

mediated by antibodies with both type II and III injury

70
Q

why is it important to distinguish cellular transplant rejection from humoral?

A

they are treated differently

71
Q

graft vs. host disease

A

can occur when immune cells are transplanted into immune-disabled recipient
-bone marrow, liver

72
Q

graft v. host disease-what cell attacks antigens of recipient?

A

T cells (probably NK) in graft attack HLA antigens of recipient

73
Q

what cells are most commonly injured in graft vs. host disease?

A

epithelial cells
skin-exfoliative dermatitis
GI tract-bloody diarrhea, malabsorption
liver (biliary ducts)-jaundice

74
Q

autoimmune disease

A

the immune system attacks its owner

loss of tolerance

75
Q

is autoimmune disease localized?

A

it can be localized or affect many organs?

76
Q

how are self antigens attacked in autoimmune disease?

A

the same mechanisms as protective immunity or hypersensitivity
type I rare

77
Q

what are autoimmune diseases typically linked to?

A

a particular HLA I (A, B or C) or HLA II (DR) antigen but not both

78
Q

what is the strongest autoimmune disease and HLA link?

A

HLA B27 and ankylosing spondylitis

79
Q

which associations for autoimmune disease are more common in men?

A

HLA I

80
Q

which associations for autoimmune disease are more common in women?

A

HLA II

81
Q

what type of diseases are autoimmune diseases?

A

diseases of exacerbations and remissions

82
Q

what are systemic autoimmune diseases known as

A

collagen vascular diseases

83
Q

examples of autoimmune collagen vascular diseases

A

SLE, RA, JRA, ankylosing spondylitis, scleroderma, Sjogrens, etc. etc.

84
Q

what are many autoimmune diseases characterized by?

A

the presence of antibodies

85
Q

SLE

A

systemic lupus erythematosus

86
Q

systemic lupus erythematosus

A

common, mostly affects young women, slightly more common in blacks
unknown etiology

87
Q

what kind of involvement in SLE?

A

systemic involvement, exacerbations and remissions

88
Q

how is SLE diagnosed?

A

critical criteria

89
Q

what autoantibodies are present against antigens in most cells with SLE?

A 
Anti-dsDNA
Anti-Ro/SSA (an RNA polymerase)
Anti-Smith (nuclear proteins)
Anti-blood cell, anti-neuron, anti-phospholipid
many more
90
Q

variable presentations in SLE

A

fever, skin changes, arthritis, kidney damage, inflamed serous membranes, mental changes, vasculitis, blood cytopenias

91
Q

what is SLE often a diagnosis of?

A

exclusion

92
Q

SLE smell vessel vasculitis

A

type III injury

accelerated atheroslerosis

93
Q

SLE glomerular injury

A

type III injury

decreased renal function

94
Q

SLE skin lesions and photosensitivity

A

malar rash

discoid (demarcated) rash

95
Q

SLE arthritis

A

type III injury

rarely mutilating

96
Q

SLE serositis

A

pleuritis, effusions and scarring

pericarditis effusions and scarring

97
Q

SLE nonbacterial verrucous endocarditis

A

libman-sacks endoarditis

any valve, most often mitral

98
Q

SLE related problems

A

blood cytopenias
fatigue, mental changes
hypercoagulability and strokes

99
Q

SLE diagnosis

A 
often delayed
often diagnosis of exclusion
new criteria 2019
positive ANA
greater than or equal to 10 points from different domains
100
Q

SLE death

A

death usually from kidney failure, infection heart or brain damage

Pathophysiology I (10 decks)

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