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CMOD > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

Effector machanisms of autoimmunity

A
  1. autoantibodies

2. autoimmune T cells

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2
Q

autoimmune diseases arise via

A

the breakdown of the negative selection processes that remove self reactive t cells and b cells from the lymphocyte reservoire

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3
Q

Autoimmune responses are NEVER mediated by

A

IgE

Therefore there are no Immediate Type I autoimmunties

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4
Q

Caused by ab’s specific for components of cell surfaces pr ECM

A

Type II autoimmune disease

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5
Q

Autoimmune hemolytic anemia class

A

Type II

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6
Q

Autoimmune hemolytic anemia

A

IgG and IgM bind to RBC’s

  • ->activate classical compliment pathway
  • ->MAC destroys RBCS
  • ->C3b deposition also leads to phagocyte clearance in the SPLEEN
  • RESULT IS ANEMA
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7
Q

test for autoimmune hemolytic anemia

A

DIRECT coomb’s

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8
Q

are nucleated cells efficiently cleared through compliment activation

A

no

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9
Q

Neutropenia autoimmune class

A

Type II

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10
Q

Nutropenia MOA

A

WBC’s destroyed via most via phagocytosis

*ab responses directed at WBC surface antigens–> FC receptors recognize Ab’s

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11
Q

Common tx. for neutropenia

A

splenectomy

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12
Q

Goodpasture’s syndrome is what Autoimmune class

A

Type II

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13
Q

Goodpasture’s Syndrome MOA

A

Ab’s specific for ECM autoantigens

  • specifically alpha chain of Type Iv collagen (basement membranes)
  • ->ab’s deposit on basement membranes of renal glomeruli and tubules eliciting inflammation
  • ->kidney failure
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14
Q

tx. for Good pastures

A

removal of self-reactive ab’s and immunosuppression

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15
Q

255 of all kidney failure are related to

A

immune system

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16
Q

Acute rheumatic fever class

A

type II autoimmunity

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17
Q

Acute Rheumatic Fever MOA

A

(MOLECULAR MEMORY)
Ab’s produced in response to Strep Pyogenes (initially for protecton)–> react with self antigens on human heart (become autoantigens)–> inflammation and damage

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18
Q

Is Rheumastic fever transient or persistent

A

Transient–> t cells cannot recognize the strep surface antigens, B cells cannot be activate fully–> NO IMMUNOLOGIC MEMORY IS CREATED

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19
Q

AUTOIMMUNE CLASS FOR GRAVE’S DISEASE

A

Type II

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20
Q

Graves’ disease

A

Ab’s that bind to TSH receptors and mimic binding of TSH–> chronic overproduction of TH that is independent of regulation

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21
Q

Graves’ disease results in

A

Hyperthyroidisms–> heat intolerance, nervouseness, irritability, warm moist skin

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22
Q

Can TSH mimicking antibodies cross placenta

A

yes– baby can be born with Grave’s

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23
Q

TSH mimicking antibody in Graves is of what isoform

A

IgG–> it can cross placenta

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24
Q

tx. for adult graves

A

drugs

removal of thyroid

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25
Q

tx for grave’s infants

A

removal of anti-TSHR ab’s via total exchange of blood plasma

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26
Q

Myasthenia gravis Classification

A

Type II

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27
Q

Myasthenia gravis MOA

A

signaling from nerve to muscle is impaired

–> Ab’s bind to self-ACH recptors and cause them to be internalized–> muscle is then LESS responsive to ACH

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28
Q

Tx. of Myasthenia Gravis

A

Immunosuppressive agents, or PYROSTIGIMINE which inhibits acetylcholinesterase

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29
Q

Guillian Barre Class?

A

Type II

30
Q

Autoimmune Deficiencies that classify as MOLECULAR MIMICRY

A
  1. GBS
  2. Acute Rheumatic fever
  3. Wegener’s Granulomatosis
31
Q

GBS MOA

A

mediated by IgG specific for gangliosides–> mediate Acute Inflammatory Demyelinating Polyneuropathy (AIDP)

32
Q

GBS is most commonly caused by molecular mimickry from which organism

A

C. jejuni

33
Q

GBS morphology

A

Descending–from legs to head (happens very quickly weeks to days)

34
Q

Miller-Fischer Syndrome

A

GBS except it progresses from top to bottom

35
Q

Wegener’s is what type of Autoimmune disease

A

Type II

36
Q

Wegener’s is meadiated by which Ab’s

A

cANCA’s: anti-neutrophil cytoplasmic ab’s

37
Q

Wegener’s MOA

A

cross reactive ANCA’s(originally formed to bacterial pathogen response) bind to neutrophils–> actiavted them–> they bind to endothelial cells and cause VASCULITIS

38
Q

Autoimmune Thrombocytopenic Purpura is in what Class

A

Type II

39
Q

ITP cause

A

IgG mediated inhibition of an enezyme responsible for cleavage of VWF– (ROBBIN;s has this as ADAMSt13

Leads to thrombocytopenia, neurological symptoms and microangiopathic hemolytic anema

40
Q

Microangiopathic hemolytic anemia

A

rbc’s get cleaved (schistocytes) as they are pushed through microscopic clots

41
Q

Scleroderma (Type II) cause

A

destrcution of vascular endothelium and smooth muscle cells–. replacement with abundant collagen from fibroblasts

42
Q

Scleroderma is associated with what Ab’s

A 
Anti topo 1 (Diffuse)
anti centromere (CREST)
43
Q

Findings of CREST Systemic Scleroderma

A 
*Milder form
calcinosis
Raynaud's
esophageal dysmotility
Sclerodactyly
Telangeictasia
44
Q

Anti centromer Ab’s are specific to

A

Limited Scleroderma: CREST

45
Q

Anti Topo 1 ab’s are specific to

A

diffuse scleroderma

46
Q

Pemphigus Vulgaris (Type II autoimmunity)

A

autoimmune condition specific for 2 proteins
Desmoglein 1 and 3
*cohesion of kratinoctyes–> painful and chronic blistering of the skin

47
Q

tx for pemphisus bulgaris

A

rituximab

48
Q

SLE is what type of autoimmune

A

III

49
Q

Ab’s present in SLE

A

ANA’s (non diagnostic)
Anti-histone (non diagnostic)
Anti-SMith–> diagnostic
Anti-dsDNA–> diagnostic

50
Q

SLE pt.’s usually die from failure of what organs

A

KIDNEY

BRAIN

51
Q

Post Strep Glomerulonephritis

A

immune compex disorder that follows infections with GAS–> Ab-GAS complexes get lodged in the glomeruli resulting in inflammation that hinders kidney fxn

52
Q

Pt.s with Insulin Dependent TYPE 1 diabetes have what autoimmune process going on

A

T cell mediated autoimmune response that desstroys beta cells in islets of langerhans

53
Q

IDDM is what class of Autoimmune disease

A

TYPE IV–> T CELL MEDIATED

54
Q

CTL’s in IDDM do what

A

bind to undefined antigen on Beta cells and kill them over time–> decreased insulin production

55
Q

CD4 and Ab’s cells in IDDM do what

A

involved in producing specific for products of B cells (anti-insulin Ab’s and anti-glutamate dehydrogenase)

56
Q

RA is what type of autoimmunity

A

Type IV

57
Q

What is rehumatoid factor

A

IgM, IgA, IgG AUTOANTIBODIES that are specific to the FC recgions of human IgG molecules–> this si not required for tissue damage, but helps diagnose

58
Q

Test more specific for RA

A

anti-CCP : cyclic citrullinated proteins

59
Q

Cells found in infiltrates of all ppl with RA

A

CD4 CD8 T cells, B cells, Plasma cells, neutrophils, macrophages

60
Q

Tx for RA

A

TNF-Alpha blockers

61
Q

Multiple Sclerosis is what type

A

IV

62
Q

Cause of MS

A

immune response directed at myelin sheath

*causes sclerotic plaques of demyelinated tissue in white matter of CNS–> loss of coordination and spasticity

63
Q

Cell type responsible for demyelination in MS

A

TH1
*produce IFN gamma that activated macrophages in sclerotic plaques–> mac’s release proteases and cytokines–> demyelination

64
Q

Tpe Iv autoimmune disease that attacks exocrine glands

A

Sjogren Syndrome

65
Q

Sjogren’s is usally found

A

in conjucntion with another Autoimmune condition

66
Q

Ab’s specific for Sjogren’s

A

Anti-SS A/RO and Anti SS B/LA

67
Q

APECED is caused by a defect in…

A

AIRE gene–> impaired negative selection of t cells in the thymus (therefore b cells are affected too)

68
Q

PPL that express HLA-DR2 are

A

16 times more likely to develop goodpasture’s syndrome than those that do NOT express HLA-DR2

69
Q

Immunologically priveledges dites

A

Anterior chamber of the eye
uterus
testes

70
Q

Sympathetic ophthalmia

an alteration on what is believed to be a immune preveledged site

A

is a bilateral diffuse granulomatous uveitis (a kind of inflammation) of both eyes following trauma to one eye. It can leave the patient completely blind. Symptoms may develop from days to several years after a penetrating eye injury.

CMOD (19 decks)

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