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Year 5 Path > Immuno - autoimmune and autoinflamm disease > Flashcards

Immuno - autoimmune and autoinflamm disease Flashcards

1
Q

Graves disease - pathophysiology?

A

anti-TSH receptor antibodies –> activation of TSH receptor that is not responsive to -ve feedback

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2
Q

What type of hypersensitivity disorder is Graves disease

A

Type II

  • antibodies against self –> receptor activation
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3
Q

Which thyroiditis is associated with high T4? and which one with low T4?

A

High T4 = De Quervains (painful)

Low T4 = Hashimoto’s (anti-TPO)

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4
Q

Hashimoto’s thyroiditis - clinical Fx

A

Features of hypothyroidism (constipation, lethargy, cold intolerance)

GOITRE - irregular!

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5
Q

Why is there goitre in hashimoto’s thyroiditis?

A

Lymphocyte infiltration of the thyroid due to binding of autoantibodies

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6
Q

Which autoantibody is associated with Hashimoto’s

A

Anti-THRYOGLOBULIN

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7
Q

WHY is measuring anti-thyroid antibodies a bit shit

A

LOADS of women>65yo with antithyroid antibodies without any thyroid disease..only a small proportion actually have hypothyroidism

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8
Q

Low TSH. Normal T3/T4. What is the Dx and what is the significancd

A

Subclinical hyperthyroidism - may progress to primary hyperthyroidism, esp if they have anti-TPO +ve

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9
Q

Pathophysiology of T1DM? Therefore what type of hypersensitivity is it?

A

CD8+ T cells recognise auto antigens on beta cells

Type IV - t cell mediated

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10
Q

What auto antigens are recognised by T-cells in T1DM?

A

GAD65

IA2 (islet antigen 2)

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11
Q

Antibodies seen in T1DM

A

anti-islet cell
anti-GAD
anti-insulin
anti-IA2

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12
Q

Clinical Fx of B12 deficiency

A
  • Degeneration of cord
  • Optic neuropathy
  • Peripheral neuropathy
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13
Q

Pernicious anemia - what is it?

A
  • Autoantibodies to gastric parietal cells + intrinsic factor
    B12 malabsorption –> deficiency –> neurological Fx
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14
Q

Case: drooping eyelids + weakness on repetitive activity + Sx worse at end of day

Dx?

A

Myasthenia gravis

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15
Q

Myasthenia gravis = pathophysiology

A

Anti-AChR antibodies

Therefore ACh can’t bind and muscle cell is not depolarised –> no contraction

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16
Q

Special test for Dx of Myaesthenia gravis

A

Tension test

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17
Q

Myasthenia gravis - what type of hypersensitivity disorder is it?

A

Type II - antibody against a self antigen

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18
Q

Good pasture’s syndrome - what is the offending antibody?

A

Antibody vs alpha3 subunit of Type IV collagen

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19
Q

Immunohistochemistry for anti-GBM: what is a +Ve result?

A

linear IgG deposition along GBM

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20
Q

Best antibody for detecting rheumatoid arthritis

A

Anti-CCP

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21
Q

Name 2 genetic predispositions to rheumatoid arthritis?

A

1) HLA DR4 + 1 subtypes

2) PAD2 and 4 PMs

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22
Q

How does HLA affect susceptibility of RA?

A

Certain alleles of HLA DR4 and HLA DR1 bind to ARTHRITOGENIC PEPTIDES + CITRULLINATED PEPTIDES w high affinity

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23
Q

What infection is associated with rheumatoid arthritis? why?

A

P gingivalis - gum infection

It expresses PAD enzyme?! thus promotes citrullination

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24
Q

How does PAD polymorphism –> RA development?

A

PAD2 and 4 = involved in citrullination of arginine

Certain polymorphisms are associated with increased activity –> high load of citrullinated proteins

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25
Q

What is rheumatoid factor

A

Antibody directed against Fc region of IgG.

This antibody is an IgM

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26
Q

B cell involvement in Rheumatoid arthritis - give 2 ways

A

1) Type 2 response = anti-CCP activity –> complement, NK and macrophage activation
2) Type 3 response = immune complexes formed (by Anti-CCP and RF) + deposited –> complement activation

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27
Q

How is the point affected (macroscopically) in RA

A

Increased synovial fluid volume

Inflamed synovial tissue -> panes formation which invades cartilage + adj tissue

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28
Q

4 diseases assoc with ANA +ve

A

SLE
Sjogren’s
Scleroderma
Dermatomyositis

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29
Q

ANA +ve - is this result specific to autoimmune disease?

A

NO it is often found in normal individuals

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30
Q

Which cells are used to test for ANAs?

A

Hep2 cells

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31
Q

Pathogenesis of SLE

A

Antibodies against intracellular proteins

IMMUNE COMPLEXES formed + deposited in tissues

Complement activation + activation of cells expressing Fc receptors

32
Q

How does staining pattern for IgG differs in good pasture’s disease vs lupus nephritis?

A

Goodpastures = linear

Lupus nephritis = lumpy bumpy, because there is immune complex deposition

33
Q

What type of hypersensitivity reaction is SLE?

A

Type III = immune complex

34
Q

You request an anti nuclear antibody test on two patients with joint pain
Patient A’s result is 1:640
Patient B’s result is 1:80
Based on this information, which has the “strongest” (i.e most positive) antibody?

A

Patient A

35
Q

Which autoantibody test is highly specific for SLE?

A

anti-dsDNA

36
Q

anti-ENA vs anti-dsDNA antibodies

Which one is useful in monitoring disease activity, and in which disease?

A

anti-dsDNA, in SLE

37
Q

homogenous staining of the nucleus is associated with..?

A

anti-dsDNA

38
Q

Speckled staining is associated with antibodies to…?

A

ENA? and Ro/La/Sm/U1RNP

39
Q

Anti-Ro and Anti-La

A

Sjogren’s syndrome

40
Q

How does measuring complement levels help in monitoring disease in SLE?

A

can measure levels of UNACTIVATED C3 + C4

  • LOW levels is associated with more active disease (they’re being consumed because pathway is activated)
41
Q

2 major antibody tests in anti-phospholipid syndrome?

A

1) Anti-cardiolipin

2) lupus anti-coagulant

42
Q
  • Inflammation with Th17 and Th2 cells dominating
  • Cytokines –> activation of fibroblasts and fibrosis
  • Polymorphisms within type I collagen alpha 2 chains and fibrillin 1 may be important
  • Polymorphisms in TGF-b have also been described
  • Cytokines lead to activation of endothelial cells and contribute to microvascular disease
  • Loss of B cell tolerance to nuclear antigens
A

Systemic sclerosis

43
Q

Systemic sclerosis - which cells predominate?

Why is there telangiectasia + raynaud’s?
Why sclerodactyly?

A

Inflammation predom Th17 and Th2 cells

Cytokine activation of endo- cells –> microvasc damage

Cytokine activation of fibroblasts –> fibrosis

44
Q

autoantibody in diffuse systemic sclerosis?

A

Anti-topoisomerase

45
Q

autoantibody in limited systemic sclerosis?

A

Anti-centromere

46
Q

Dermatomyositis + polymyositis - type of hypersensitivity ?

A

Dermatomyositis - Type III immune complex mediated vasculitis

Polymyositis = Type Iv CD8 cells kill myofibres

47
Q

Anti-Jo1

A

dermatomyositis

48
Q

anti-snRP

A

polymyositis

49
Q

3 types of small vessel vasculitis assoc with ANCA?

A

1) Granulomatosis with polyangiitis/Wegener’s granulomatosis

2) Eosinophilic granulomatosis with polyangiitis/Churg-Strauss
3) microscopic polyangiitis

50
Q

How do ANCAs lead to vasculitis?

A

In inflammation, antigens of primary granules in neutrophil cytoplasm get expressed on neutrophil CSM

ANCAs recognise these leading to neutrophil activation –> endothelial damage

51
Q

cANCA is associated with antibodies to what?

A

Proteinase 3

52
Q

pANCA is associated with antibodies to what?

A

myeloperoxidase

53
Q

cANCA and pANCA are associated with which diseases?

A

cANCA = wegener’s/granulomatous polyangiitis

pANCA = Churg strauss and MPA

54
Q

Difference btw auto inflammatory and autoimmune diseases?

A 
Autoinflamm = defect in innate immune response
Autoimmune = defect in adaptive immune response
55
Q

Name 2 diseases which are mixed auto inflammatory + autoimmune processes?

A

Ank spon

Psoriatic arthritis

56
Q

Name 2 monogenic auto inflammatory diseases

A

Familial Mediterranean Fever

TRAPS - TNF Receptor Associated Periodic Syndrome

57
Q

Clinical features of familial mediterranean fever?

A

Periodic fevers

+ Peritonitis/Pleuritis/pericarditis/arthritis

58
Q

MEFV gene encodes…?

A

Pyrin Marenostrin

59
Q

2 step management of familial mediterranean fever?

A

Colchicine + Etanercept

60
Q

2 cytokines which are often affected in monogenic auto inflammatory conditions?

A

IFNalpha + IL1

61
Q

Mutation in AIRE protein - which disease si this?

A

APS aka APECED

Autoimmune polyendocrine syndrome

62
Q

in APS (autoimmune polyendocrine syndrome), which 2 glands are affected? How does this manifest?

A

Parathyroids + adrenal

–> hypoPTH + addison’s

63
Q

Foxp3 mutation - which disease is this?

A

IPEX = immune dysregulation, polyendocrine, enteropathy, X-linked

Foxp3 = T reg cells

64
Q

what does IPEX stand for?

A

immune dysregulation, polyendocrinopathy, enteropathy, X-linked

65
Q

any mutation in the FAS pathway - which disease is this?

A

ALPS = autoimmune lymphoproliferative syndrome

66
Q 
In ALPS (autoimmune lymphoproliferative syndrome), which cell type is at high levels? 
Findings on examination?
A

Lymphocytes are v v high
Splenomegaly
Large LNs

assoc with lymphoma

67
Q

Major mutation often seen in Crohn’s disease

A

NOD2 mutation

68
Q

NOD2 mutation - how does this lead to Crohns’?

A

Affects recognition of bacteria –> inappropriate response to bacteria –> crypt inflamm + granuloma formation + ulceration

69
Q

Drugs used to treat Crohns’ - name 4

A

Steroids
Azathioprine
MEsalazine
Infliximab

70
Q

Normal function of HLA B27?

A

Ag presentation to CD8+ t cells

71
Q

Normal function of IL23 receptor?

A

differentiation of Th17 cells

72
Q

In Ank Spon, which areas are vulnerable to enhanced inflammation?

A

insertion points of ligaments + tendons

73
Q

HLA DR15 - which disease?

A

Anti-GBM

74
Q

Name a polygenic auto inflammatory disease

A

Crohns’

75
Q

3 aspects of peripheral tolerance

A

1) T-reg cells (CD24+Foxp3+)
2) Costimulation - T cells require recognition of antigen AND costimulatory molecule. If costimulatory molecule is absent –> T cell anergy
3) Immune privilege

76
Q

3 parts of the body with immune privilege?

A

CNS
Eyes
Testes

Year 5 Path (63 decks)

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