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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
type I hypersensitivity generalized reactions tx
epinephrine mainstay of treatment | -vasoconstrictor and bronchodilator
26
food allergies
are real local or systemic type I reactions 200 deaths/year eggs, nuts, shellfish
27
what causes histamine release in everyone?
chocolate, strawberries, codeine non-IgE mediated those with greater release are "allergic"
28
testing methods for allergies
skin testing *better* (prick, injection) used in diagnosis wheal and flare response radioallergosorbent test (RAST) detects IgE, less sensitive and specific
29
type II hypersensitivity definition
antibodies bind to "fixed" antigens present on cell membranes -IgM or IgG mediated cell bearing the antigen then destroyed (or function altered)
30
type II hypersensitivity mechanisms of destruction
complement activation and cell lysis/phagocytosis antibody-dependent cell cytotoxicity complement- and antibody-mediated inflammation
31
type II hypersensitivity what can also occur?
antibody-mediated cell dysfunction
32
what is type II hypersensitivity pathogenesis of?
many autoimmune diseases
33
type II hypersensitivity complement activation
Ag-Ab complex fixes complement target cell lysed by MAC Ab and/or C3b act as opsonins target cell engulfed
34
type II hypersensitivity-hemolytic transfusion reactions
ABO incompatibility ready-made IgM hemolytic disease of newborn requires sensitization and involves IgG
35
type II hypersensitivity antibody-dependent cell cytotoxicity
involves elements of innate and adaptive immunity Ab bound to target cell attracts NK cell NK cell binds Ab and induces apoptosis
36
examples of type II hypersensitivity antibody-dependent cell cytotoxicity diseases
hashimoto's thyroiditis autoimmune adrenalitis type I diabetes mellitus?
37
type II hypersensitivity complement and antibody-mediated inflammation
Ag-Ab complex fixes complement C3a/C5a attract neutrophils neutrophils bind Ab acute inflammation occurs
38
type II hypersensitivity-goodpasture's syndrome
Ab binds to lung and glomerulus basement membranes | acute inflammation destroys alveoli and nephrons
39
example of type II hypersensitivity injury
transfusion-related lung injury (TRALI), plasma transfusion
40
type II hypersensitivity-antibody-dependent cell dysfunction
Ab binds cell membrane receptor | blocks or activates receptor
41
type II hypersensitivity-myasthenia gravis
Ab binds and blocks ACh receptor at neuromuscular junction | prevents muscle stimulation
42
type II hypersensitivity-graves' disease
Ab binds and stimulates TSH receptor at thyroid gland | produces hyperthyroidism
43
type III hypersensitivity
antibodies (IgM and IgG) bind to soluble antigens in plasma when each present in the right proportions
44
what is formed during type III hypersensitivity?
Ag-Ab complexes ("immune complexes") that precipitate
45
type III hypersensitivity-where do immune complexes?
blood vessel walls (close by) glomerulus (proteins are more concentrated) skin (precipitation faster due to cooler temperature) lungs (same as skin) synovial membranes
46
type III hypersensitivity what do immune complexes do?
fix complement and induce inflammation
47
type III hypersensitivity manifestations dependent on what?
manifestations dependent on location of immune complex deposition
48
examples of type III hypersensitivity manifestations
vasculitis glomerulonephritis arthritis
49
type III hypersensitivity examples
neutrophils have nothing to attack (but attack anyway) systemic lupus erythematosus serum sickness malaise hours after immunization
50
what is involved in type IV hypersensitivity?
no antibodies, T cells
51
what happens in type IV hypersensitivity?
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
type IV hypersensitivity what could activated T cells also destroy?
activated T cells may destroy normal cells bearing similar Ag to one provoking response
53
what is type IV hypersensitivity great for?
eliminating parasite-infected cells viruses mycobacteria
54
what can type IV hypersensitivity also eliminate?
some tumor cells
55
what is type IV hypersensitivity a mechanism of?
one mechanism of acute transplant rejection
56
examples of type IV hypersensitivity
``` contact dermatitis (nickel, poison ivy, etc.) tb skin test ```
57
type IV hypersensitivity tb skin test
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
anergy
defects in Th cell number or function can inhibit type IV response
59
examples of causation of anergy
AIDS, sarcoidosis, wasting diseases
60
how to test for anergy?
``` 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
transplant rejection
donor tissues/organ seen as foreign by recipient with immune destruction matching done on basis of synergy between donor/recipient HLA antigens
62
autograft
donor and recipient are the same
63
isograft
donor and recipient are different but have same genes
64
allograft
donor and recipient are different and have different genes
65
xenograft
donor and recipient are different species
66
what is required for graft survival with allografts and xenografts?
immunosuppression
67
transplant rejection-hyperacute rejection
due to premade (or almost immediately made) antibodies antibodies directed against HLA antigens on the graft type II and III injury occurs
68
transplant rejection-acute cellular rejection
months or years after transplantation | mediated by T cells, type IV injury
69
transplant rejection-acute humoral rejection
months or years after transplantation | mediated by antibodies with both type II and III injury
70
why is it important to distinguish cellular transplant rejection from humoral?
they are treated differently
71
graft vs. host disease
can occur when immune cells are transplanted into immune-disabled recipient -bone marrow, liver
72
graft v. host disease-what cell attacks antigens of recipient?
T cells (probably NK) in graft attack HLA antigens of recipient
73
what cells are most commonly injured in graft vs. host disease?
epithelial cells skin-exfoliative dermatitis GI tract-bloody diarrhea, malabsorption liver (biliary ducts)-jaundice
74
autoimmune disease
the immune system attacks its owner | loss of tolerance
75
is autoimmune disease localized?
it can be localized or affect many organs?
76
how are self antigens attacked in autoimmune disease?
the same mechanisms as protective immunity or hypersensitivity type I rare
77
what are autoimmune diseases typically linked to?
a particular HLA I (A, B or C) or HLA II (DR) antigen but not both
78
what is the strongest autoimmune disease and HLA link?
HLA B27 and ankylosing spondylitis
79
which associations for autoimmune disease are more common in men?
HLA I
80
which associations for autoimmune disease are more common in women?
HLA II
81
what type of diseases are autoimmune diseases?
diseases of exacerbations and remissions
82
what are systemic autoimmune diseases known as
collagen vascular diseases
83
examples of autoimmune collagen vascular diseases
SLE, RA, JRA, ankylosing spondylitis, scleroderma, Sjogrens, etc. etc.
84
what are many autoimmune diseases characterized by?
the presence of antibodies
85
SLE
systemic lupus erythematosus
86
systemic lupus erythematosus
common, mostly affects young women, slightly more common in blacks unknown etiology
87
what kind of involvement in SLE?
systemic involvement, exacerbations and remissions
88
how is SLE diagnosed?
critical criteria
89
what autoantibodies are present against antigens in most cells with SLE?
``` Anti-dsDNA Anti-Ro/SSA (an RNA polymerase) Anti-Smith (nuclear proteins) Anti-blood cell, anti-neuron, anti-phospholipid many more ```
90
variable presentations in SLE
fever, skin changes, arthritis, kidney damage, inflamed serous membranes, mental changes, vasculitis, blood cytopenias
91
what is SLE often a diagnosis of?
exclusion
92
SLE smell vessel vasculitis
type III injury | accelerated atheroslerosis
93
SLE glomerular injury
type III injury | decreased renal function
94
SLE skin lesions and photosensitivity
malar rash | discoid (demarcated) rash
95
SLE arthritis
type III injury | rarely mutilating
96
SLE serositis
pleuritis, effusions and scarring | pericarditis effusions and scarring
97
SLE nonbacterial verrucous endocarditis
libman-sacks endoarditis | any valve, most often mitral
98
SLE related problems
blood cytopenias fatigue, mental changes hypercoagulability and strokes
99
SLE diagnosis
``` often delayed often diagnosis of exclusion new criteria 2019 positive ANA greater than or equal to 10 points from different domains ```
100
SLE death
death usually from kidney failure, infection heart or brain damage

Pathophysiology I (10 decks)

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