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quiz 3 immunopathology Flashcards

1
Q

pathogenesis of type I reaction

A

antigen, APC, Th2, B cell, plasma cell makes IgE, IgE to mast cell FcRe for degranulation

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2
Q

type I initial response timing and characteristics

A
  • 5 mins to one hour

- glandular secretion, vasodilation, smooth muscle contraction, vascular leakage

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3
Q

type I secondary response timing and characteristics

A
  • 2 hours to days

- eosinophils, basophils, neutrophils, T-cells, tissue damage, mucosal damage, remodeling

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4
Q

what do eosinophils secrete?

A
  • major basic protein
  • 15 HETE
  • peroxidase
  • arylsulphatase
  • PAF
  • LTC4
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5
Q

what secretes major basic protein and what does it do?

A
  • eosinophils
  • mast cell degranulation
  • epithelial desquamation
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6
Q

what secretes 15 HETE and what does it do?

A
  • eosinophils
  • mucus secretion
  • epithelial desquamation
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7
Q

two examples of localized type 1 reactions

A
  • urticaria - skin

- atopic keratoconjunctivitis

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8
Q

structural changes of airways in chronic asthma

A
  • basement membrane thickening
  • gland hyperplasia
  • epithelial shedding
  • muscle hyperplasia
  • matrix remodeling
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9
Q

what is the main principle of type II reactions?

A

antibodies participate directly in damaging tissue

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10
Q

cytotoxic/anti-tissue antibody reactions (type II)

A
  • antibodies fix complement

- antibodies bind to antigens on cell surfaces and damage occurs at those locations

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11
Q

two processes of hemolysis in type II reactions

A
  • antibodies bind RBC and either fix complement (lysis by MAC) or opsonization leads to phagocytosis by PMN in spleen or liver
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12
Q

acute vs delayed hemolysis occurs when…..

A
  • acute - antibodies already exist in bloodstream (immediate)
  • delayed - 1-2 weeks, antibody titer slowly rises
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13
Q

what is the infant disease related to type II hemolysis?

A

erythroblastosis fetalis

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14
Q

what is good pasture’s disease? what type of hypersensitivity reaction?

A
  • type II
  • anti-collagen type IV
  • basement membrane of glomeruli and alveoli of lung
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15
Q

what is rheumatic fever? what type of hypersensitivity reaction?

A
  • type II
  • follows group A strep infection
  • ## vegetations on mitral valve leaflets
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16
Q

molecules in group A strep that cross react with tissues (4)

A

hyaluronidase - cartilage - arthritis
group A carbohydrate - heart valves - endocarditis
cell walls - basal ganglia - chorea
M protein - heart muscle - myocarditis

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17
Q

what is an aschoff body?

A
  • nodule in heart caused by rheumatic fever

- focal inflammation including T-cells, abnormal macrophages, giant cells, necrotic center,

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18
Q

what is an anitschkow monocyte?

A
  • associated with rheumatic fever

- enlarged macrophages inside aschoff bodies

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19
Q

what is grave’s disease? what type of hypersensitivity reaction?

A
  • type II

- overproduction of thyroid hormone because antibody stimulates TSH receptor constitutively

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20
Q

myasthenia gravis? what type of hypersensitivity?

A
  • type II
  • blocks acetylcholine at post synaptic neuromuscular junction
  • muscle weakness
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21
Q

what is the strict definition of tolerance?

A

absence of detectable antigen-specific immunity

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22
Q

clinical definition of tolerance?

A

absence of pathogenic autoimmunity (or acceptance of allograft) ideally without continued immunosuppression

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23
Q

why might something be tolerated?

A
  • antigen inaccessible to immune system
  • T-cells are destroyed before they reach the periphery (negative selection
  • T-cells destroyed in periphery before, after, or during interaction with antigen
  • antigen leaves T-cells ineffective (anergy)
  • T cells suppress other lymphocytes (Tregs)
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24
Q

explain T-cell positive selection

A

thymocyte must recognize MHC/peptide above a certain threshold

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25
explain T-cell negative selection
recognition of MHC above a certain threshold leads to deletion
26
explain the significance of PTPN-22
- gene most often implicated in autoimmune disease | - lymphocytes hyper reactive because of a failure to down regulate tyrosine kinase
27
explain the significance of NOD-2
- Crohn Disease - encodes cytoplasmic sensor of microbes - mutant fails to sense microbes and allows tissue invasion, inflammatory responses against normal flora
28
explain the significance of IL-2Ra and IL-7Ra
- receptors associated with MS | - may control maintenance or development of Tregs
29
explain molecular mimicry, example
- antigen looks like human antigen | - rheumatic fever
30
explain the adjuvant effect
- an up-regulation of co-stimulators | - may break tolerance for self-antigen
31
Tregs are also known as....
CD4+CD25+
32
what does CD25+ mean?
presence of IL-2Ra, expressed on Tregs and active T-cells
33
what is IPEX?
- x-linked autoimmune diseased cause by depletion of T-regs | - defect in FOXP3
34
general features of immune disease
- progressive - epitope spreading as tissue is destroyed - pathogenesis based on underlying immune response - overlap
35
what are the three general types of autoimmunity?
- generally type II and III - generally type IV - mixed T and B cell
36
3 systemic type III hypersensitivity reactions
- SLE - lupus - serum sickness - drug reactions
37
five most common manifestations of SLE
- hematologic (thrombocytopenia, lymphopenia, leukopenia, anemia) - arthritis - skin (malar rash, discoid rash, photosensitivity) - fever - fatigue
38
3 major sources of SLE
- genetic - immunological - environmental
39
genetic aspect of SLE
- both MHC and non-MHC sources of gene influence | - family members and twins higher risk
40
immunologic aspect of SLE
- can't get rid of self reactive B cells
41
environmental aspect of SLE
- photosensitivity - sex hormones - drugs
42
signs and symptoms of rheumatoid arthritis
- fatigue - weight loss - myalgias - sweating - fever - morning stiffness - lymphadenopathy
43
morphologic alterations in joints due to rheumatoid arthritis
- invasion of synovia by lymphocytes, DCs, macrophages - increased vascularity - fibrin aggregation - osteoclastic activity - Pannus - erodes cartilage - fibrous ankylosis - pannus bridge across bones in place of cartilage
44
immunologic aspect of rheumatoid arthritis
- 80% have rheumatoid factor which are autoantibodies to Fc portion of IgG - Th1 and Th17 cells are in synovial fluid very early
45
most important immunological mediator in RA?
TNF - antagonists have proven effective
46
common diseases associated with type IV hypersensitivity
- rheumatoid arthritis | - type I diabetes melitus
47
localized type III reactions
- arthritis - vasculitis - glomerulonephritis - arthus reaction - pneumonitis
48
4 directions for antigen-antibody complexes
- Fc interactions - complement activation - platelet aggregation - activation of Hageman factor
49
which two types of cells lead to necrosis in type III hypersensitivity reactions?
neutrophils and monocytes
50
Hageman factor leads to....
microthrombi activation if kinins ultimately vasodilation and edema
51
C3b leads to
phagocytosis
52
C3a and C5a lead to
vascular permeability via cell lysis
53
which cells do most of the damage in type III HS reactions?
neutrophils
54
post-strep glomerulonephritis is what type of HS reaction?
type III - localized
55
what do you find in the glomerular tufts of glomeruli in post-strep glomerulonephritis?
neutrophils
56
what makes the lumpy-bumpy look of the staining in glomerulonephritis?
IgG-antigen complexes
57
what type of HS reaction is vasculitis?
type III - localized
58
very small vessel vasculitis is often associated with....
drug reactions
59
what type of HS reaction is serum sickness?
type III - systemic
60
main cell types involved in type IV HS reactions
- sensitized T-cells | - macrophages
61
three categories of type IV HS reactions
- delayed type (DTH) - T-cell mediated cytotoxicity - rejection of a transplanted organ
62
delayed type hypersensitivity cells involved
- CD4+, macrophages, APCs
63
T-cell mediated cytotoxicity cells involved
- mostly CD8+ cells
64
organ rejection cells involved
- CD4, CD8 | - possibly B cells and antibodies as well
65
bad things that come from macrophages, monocytes, microglial cells in type IV reactions
- TNF a/b - IL-1 - superoxides - nitric oxide - hydroxyl radicals - neuron toxins
66
transplantation rejection reactions - 3 types, timing
hyperacute - moments to 48 hours acute - weeks to months chronic - months to years
67
hyperacute rejection actors
- preformed antibodies - ag-ab reaction at endothelium - rapid thrombosis of vessels
68
two categories of acute rejection and actors
cellular - sensitized CD4 and CD8 cells, lymphocytes, macrophages humoral - anti-graft antibodies, vasculitis, thrombosis
69
direct vs indirect rejection pathways
direct - APC is in the graft | indirect - APC is in the recipient
70
Bruton's
- x-linked, mostly in males - tyrosine kinase - precursors can't differentiate to B cells - bacterial infections, encephalitis, intestinal giardia
71
common variable immune deficiency
- looks like Bruton's - B cells can't turn to plasma cells - both genders equally
72
isolated IgA deficiency
- leading cause of transfusion anaphylaxis | - anti-IgA antibodies are naturally occurring, so recipient reacts to IgA in donor blood
73
hyper IgM syndrome
- X-linked | - too much IgM, not enough E, A, G
74
treatment for B cell humoral immunodeficiency syndromes
- immunoglobulin replacement therapy | - 100-400 mg/kg body weight every 3-4 weeks
75
DiGeorge syndrome
- pharyngeal pouches - no thymus - T- cell deficiency
76
SCID
- low T and low B cells - death in first year of life without bone marrow replacement - can be either x-linked recessive or autosomal recessive
77
wiskott aldrich
- x-linked recessive | - low IgM, normal IgG, high E and A
78
hereditary angiodema
- C1 inhibitor deficiency | - lots of hageman factor, C1, mast cell degranulation

pathology (15 decks)

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