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Rheumatology SB > Immunology > Flashcards

Immunology Flashcards

1
Q

definition of monogenic disorders

A

single gene defects causing autoimmune diseases

rare

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2
Q

features of IPEX syndrome

A

very early onset insulin dependent diabetes
severe malabsorption syndrome
eczema
autoimmune thyroid disease

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3
Q

mutation in what gene causes IPEX syndrome

A

FOXP3

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4
Q

what is HLA

A

Human leukocyte Antigen complex
what is used to control T cells
Class 1 - controls CD8 cells
Class 2 - controls CD4 cells

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5
Q

what diseases in HLA DR3 associated with

A

Graves disease
SLE
Type 1 diabetes (also DR4)

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6
Q

what HLA is associated with RA

A

HLA DR4

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7
Q

what is HLA B27 associated with

A

Ankylosing Spondylitis

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8
Q

what class of HLA do all nucleated cells express

A

Class I

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9
Q

what cells express Class II HLA

A

antigen presenting cells

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10
Q

why do we need polymorphism in HLA molecules

A

to maximise the net ability to bind peptides

only a few peptides will bind to a specific HLA

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11
Q

what are factors contributing to autoimmune disease

A

Genes
Environment
Immune regulation

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12
Q

what are the 4 types of hypersensitivity reactions in the Gel and Coomb’s classification

A

Type I: Immediate hypersensitivity
Type II: Direct cell killing
Type III: Immune complex mediated
Type IV: Delayed type hypersensitivity

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13
Q

what are the two clinical classifications of autoimmune diseases

A

Organ specific diseases

Non-organ specific or multi-system autoimmune disease

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14
Q

example of autoimmune diseases of Type III hypersensitivity

A

SLE

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15
Q

pathogenesis of type III hypersensitive reactions

A

1 - circulating antigen binds to immune complexes
2 - immune complex deposition in small vessels
3 - causes complement activation
4 - infiltration of macrophages and neutrophils

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16
Q

what is the abnormality in SLE

A

disturbed regulation of B cells activity

characterised by ANA proteins

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17
Q

what are antibodies are seen in SLA

A

Anti-DNA antibodies
Anti-nuclear antibodies
Antibodies to extractable nuclear antigens etc

18
Q

in SLE, what could soft heart sounds be a sign of

A

pericardial effusions

19
Q

anti-nuclear antibodies are very uncommon and specific for autoimmune diseases - true or false

A

false
very common and often found in normal individuals
associated with female sex and older age

20
Q

what diseases are anti-nuclear antibodies an intrinsic part of diagnostic criteria

A

Mixed connective tissue disease

Autoimmune hepatic disease

21
Q

what are speckled antibodies associated with

A

ENA e.g. Ro and La

SLE and Sjogrens

22
Q

what is anti-centromere associated with

A

Limited scleroderma (CREST)

23
Q

what is an antibody highly specific for SLE

A

anti-dna binding antibodies

24
Q

what are the 3 pathways of complement activation

A

1 - classical pathway C1 C4 C2
2 - lectin
3 - alternative pathway

25
Q

what complement gets switched on in complement activation

A

C3

26
Q

what does activation of C3 lead to

A

Membrane attack complex

27
Q

what does the formation of antibody-antigen immune complexes cause

A

activate complement cascade via classical pathway

causes inflammation of tissues

28
Q

what can be measured to act as a marker of disease activity

A

unactivated C3 and C4

29
Q

what is the American criteria for SLE

A

SOAP BRAIN MD

Serositis – pleurisy or pericarditis
Oral ulcers
Arthritis - nonerosive, 2 or more peripheral joints with tenderness or swelling
Photosensitivity

Blood disorders - Leukopenia, lymphopenia, thrombocytopenia, hemolytic anemia
Renal involvement- proteinuria, cellular casts
Antinuclear antibodies
Immunologic phenomena - dsDNA; anti-Smith (Sm) antibodies; antiphospholipid antibodies
Neurologic disorder - Seizures or psychosis in the absence of other causes

Malar rash - Fixed erythema over the cheeks and nasal bridge
Discoid rash - Erythematous raised-rimmed lesions with keratotic scaling and follicular plugging, often scarring

30
Q

how many of the criteria do you need to be diagnosed with SLE

A

4 out of 11

31
Q

management of SLE

A

decrease inflammation
- corticosteroids

decrease production of antibody
- immunosuppressive agents

32
Q

example of Type IV autoimmune condition

A

RA

33
Q

what is RA characterised by

A

destruction of joint cartilage

inflammation of the synovium

34
Q

what is Type IV pathogenesis

A

1 - infiltration of synovium by activated CD4+ cells
2 - production of cytokines
3 - recruitment of phagocytes and activated B cells
4 - B cells produce immunoglobulin
5 - activation of synovial fibroblasts
6 - produce additional synovium

35
Q

synovial histology of RA

A
  • intense infiltration of inflammatory cells
  • intimal lining layer hyperplastic
  • accumulation of CD4+ T cells, macrophages, B cells
36
Q

signs of a RA joint

A
  • Infiltration of synovium primarily with activated CD4+ cells
  • Directly stimulate breakdown of bone and increased vascular formation
  • Chronic production of inflammatory cytokines in synovium
  • Destruction of cartillage and bone by matrix metalloproteases (MMPs)
37
Q

what cytokines have a critical role in the pathogenesis of RA

A

TNF

IL1

38
Q

what do TNF and IL1 do in RA

A

Potent stimulators of fibroblasts, osteoclasts and chondrocytes
Stimulate release of matrix metalloproteinases
Mediators of joint damage

39
Q

new revolutionary treatment in RA and how does it work

A

Anti-TNF antibodies
e.g. Infliximab, adalimumab
blocks attachment of cytokine to receptor

40
Q

what are serological test for RA

A

Rheumatoid factor

  • antibody directed against the common region of human IgG
  • IgM anti-IgG antibody most commonly tested
41
Q

all patients with RA have Rf - true or false

A

false

only 50% of patients will

42
Q

what is a more specific test for RA then Rf

A

Anti-CCP antibody

Rheumatology SB (7 decks)

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