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JG Year 2 > 224 RA > Flashcards

224 RA Flashcards

0
Q

What is the cause of RA?

A

Persistent synovitis leading to poly arthritis and systemic inflammation. Trigger antigen unknown

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1
Q

What is rheumatoid factor?

A

The Fc portion of IgG which is recognised by antibodies as non self

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2
Q

What is the prevalence of RA in the UK?

A

0.5-1%

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3
Q

At what age is the typical age of onset of RA?

A

30 - 50 mostly in women

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4
Q

Which cytokine is overexpressed in RA?

A

TNF-α

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5
Q

What causes the overproduction and over expression of TNF-α in RA?

A

Interaction between macrophages and T and B lymphocytes

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6
Q

What infiltrates into the synovial fluid in RA?

A

Inflammatory cells- incl polymorphs, lymphocytes and plasma cells

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7
Q

What other pyrogenic cytokine is stimulated by TNF-α?

A

IL-6

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8
Q

Which cells produce a large amount of adhesion molecule?

A

Synovial fibroblasts

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9
Q

What happens to the surface layer of lining cells in the synovium in RA?

A

Becomes hyperplastic and thickened

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10
Q

What is the cause of joint effusions in RA?

A

Vascular infiltration and increased permeability of vessels here

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11
Q

What is the mechanism of cartilage damage in RA?

A

Directly by cytokines and chondrocytes

Indirectly via blockage of normal nutrients to cartilage due to hyperplastic lining of synovium.

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12
Q

What is the mechanism of injury to the epiphyseal bone cavity in RA?

A

Fibroblasts grow along the vascular proliferation of synovium into the bone and cause damage

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13
Q

Which class of Ig is most commonly detected in investigations for RA?

A

IgM

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14
Q

What are ACPA’s in RA?

A

Anti-citrullinated peptide antibodies –> detected in Pts with RA

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15
Q

Name 2 complications of RA

A

Septic arthritis

Amyloidosis

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16
Q

Which bacteria is most common in septic arthritis?

A

Staph aureus

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17
Q

What is amyloidosis?

A

Disorder of protein metabolism with extracellular deposition of pathological insoluble proteins in organs and tissues

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18
Q

What is Boutonniere’s deformity?

A

Fixed Flexion of PIP joint

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19
Q

What can swelling and subluxation of ulnar styloid in RA lead to?

A

Rupture of extensor tendons - causing sudden onset finger drop in ring and little finger

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20
Q

What is the outcome of forward migration of the fibrofatty pad underneath the prox metacarpal joint in RA?

A

Ulcers forming under prox MT joint

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21
Q

Which bacteria is most likely to cause septic arthritis?

A

Staph A

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22
Q

Which 2 genes are thought to play a part in the genetic component of RA?

A

HLA-DR4

PTPN22

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23
Q

What are the 2 major cell types in the pannus of a rheumatic joint?

A

T-lymphocytes and macrophages

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24
Q

Name 2 complications of RA

A

Septic arthritis

Amyloidosis

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25
Q

What is amyloidosis?

A

Disorder of protein metabolism where amyloid proteins get deposited in tissues - β-pleated sheets which are resistant to proteolysis

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26
Q

What is Caplans syndrome? (occurs in RA rarely)

A

RA + pneumoconiosis

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27
Q

What type of pneumonia can occur in an RA patient?

A

BOOP (bronchiolitis obliterans organising pneumonia)

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28
Q

What are the S&S of rheumatoid vasculitis?

5 listed

A

Nail fold infarcts
Cutaneous vasculitis and necrosis of skin
Mononeuritis multiplex
Necrosing arteritis of mesenteric vessels
Leg ulcers

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29
Q

What are the possible neuro complications of RA?

4 listed

A

Carpal tunnel
Tarsal tunnel
Peripheral sensory neuropathy
Cord compression

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30
Q

Name 3 ocular manifestations of RA

A

Sicca syndrome
Scleritis/episcleritis
Scleromalacia perforans

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31
Q

What is Felty’s syndrome? (In RA)

A

Splenomegaly and neutropenia (increased risk of infection here)

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32
Q

What should be prescribed with MTX for RA?

A

Folic acid

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33
Q

What is the drug therapy for new RA diagnosis?

A

Analgesia
NSAID’s
Corticosteroids
1 DMARD

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34
Q

Name 2 DMARDs

4 listed

A

MTX
Sulphasalazine
Leflunomide
Hydroxychloroquine

35
Q

Name 2 antiTNF drugs for RA

A

Infliximab
Adalimumab
Certolimab
Rituximab

36
Q

Which cytokines does TNF-α activate in RA?

A

IL-1, IL-6, IL-8

37
Q

What do the autoantibodies target in SLE?

A

Nuclear antigens

38
Q

Which virus is associate with SLE?

A

Epstein Barr

39
Q

What causes the rashes in SLE?

A

Immune complexes causing microvascular occlusions

40
Q

What characteristic rashes are seen in SLE?

A

Malar rash (butterfly which spares nasal creases)
Discoid rash
Photosensitivity rash

41
Q

Which ABs are commonly found in serology of SLE?

4 listed

A

ANA (100%)
dsDNA (50%)
antiSM (15%)
anti-Ro/anti-La (20%)

42
Q

What is the treatment for mild SLE?

A

NSAIDs
Hydroxychloroquine
Steroids

43
Q

What DMARD is used to treat severe SLE?

A

Cyclophosphamide (alkylating agent which adds alkyl to guanine base of DNA - used as chemo)

44
Q

Which cells are involved with destruction of muscle fibres in polymyositis?

A

Cytotoxic T cells

45
Q

What’s the pathophysiology of dermatomyositis?

A

Auto antibodies causing activation of the complement system - damages muscle capillaries

46
Q

What are Gottron’s papules a sign of?

A

Dermatomyositis

47
Q

Where is the macular erythematous rash most commonly found on a pt with dermatomyositis?

A

Face and chest

48
Q

What investigation is performed to confirm a diagnosis of dermatomyositis?

A

Muscle Bx

49
Q

What are the possible serious complications which can arise in a pt with dermatomyositis?
2 listed

A

Aspiration due to swallowing difficulty

Lung fibrosis due to chest wall weakness

50
Q

Which AB is involved in limited systemic sclerosis?

A

Anti-centromere AB

51
Q

Which antibody is seen in diffuse systemic sclerosis?

A

Scl-l70 AB

52
Q

What are the clinical features of systemic sclerosis?

CREST

A 
Calcinosis
Raynauds
Esophageal and GIT dysmotility
Sclerodactyly
Telangectasia
53
Q

What are the possible complications of diffuse systemic sclerosis?
(2 listed)

A

Pulmonary HTN leading to L sided HF

Renal crisis leading to accelerated malignant HTN

54
Q

Name 2 drugs which can be used to treat systemic sclerosis and scleroderma

A

Mycophenolate mofetil

Cyclophosphamide

55
Q

What is the pathophysiology of Sjögren syndrome?

A

Lymphocytic infiltration to exocrine organs

56
Q

Which antibodies are present in Sjögren syndrome?

A

Anti-Ro and anti-La

Also RF and ANA

57
Q

What are the S&S of Sjögren syndrome?

3 listed

A

Dry eyes and mouth
Salivary gland enlargement
Purpura

58
Q

Which condition is linked to giant cell arteritis?

A

Polymyalgia rheumatica

59
Q

Name one complication of GCA

A

Blindness due to arteritis of ophthalmic artery

60
Q

Name 2 S&S of GCA

4 listed

A

Jaw claudication
Localised HA (scalp tenderness)
Temporal artery enlargement and tenderness
+ constitutional symptoms

61
Q

What is vasculitis?

A

Inflammation within the walls of vessels causing impairment to blood flow and damage to vessel integrity - leads to haemorrhage and infarction of organs

62
Q

What investigation is required in GCA?

A

Temporal artery biopsy

63
Q

Is GCA more common in men or women?

A

Women

64
Q

What is the immediate treatment of GCA?

A

High dose steroids within 24 hours

65
Q

What is Takayasu’s arteritis?

A

Granulomatous inflammation of aortic arch and branches

66
Q

Name 2 S&S of Takayasu’s arteritis

4 listed

A

Constitutional
Claudication/pulslessness of upper limbs (+/- lower limbs)
HTN due to renal artery stenosis
Neuro symptoms

67
Q

Name 2 investigations to diagnose Takayasu arteritis

A

Arteriography

Echo

68
Q

What is the treatment of Takayasu’s arteritis

A

High dose steroids

69
Q

What is the pathophysiology of granulomatous polyangiitis?

A

Ig’s against ANCAs, especially PR3 which causes increased neutrophil of activation and granuloma formation

70
Q

Which structures does granulomatous polyangiitis normally affect?

A

Midline - eyes, nose, trachea, lungs

+ kidneys

71
Q

Name 2 ENT S&S of granulomatous polyangiitis

3 listed

A

Saddle nose
Epistaxis
Sinusitis

72
Q

Name 2 pulmonary S&S of granulomatous polyangiitis

3 listed

A

Pulmonary infiltrates
Cough
Haemoptysis

73
Q

Name 2 renal S&S of granulomatous polyangiitis

3 listed

A

Microscopic haematuria
Casts
Renal failure

74
Q

What is the treatment of mild/moderate granulomatous polyangiitis?

A

MTX/azothioprine + steroids

75
Q

Which drug is used for the treatment of severe granulomatous polyangiitis?

A

Cyclophosphamide

76
Q

What is polyarteritis nodosa?

A

Necrotising inflammationof small/medium sized arteries causing lesions in bifurcation which can lead to micro aneurysms, haemorrhage and thrombosis

77
Q

Which sign is diagnostic of polyarteritis nodosa?

A

Rosary sign in arteries

78
Q

Which investigations are useful to diagnose polyarteritis nodosa?

A

Inflammatory markers in blood

Artery biopsy

79
Q

What is the treatment of polyarteritis nodosa?

A

Steroids and Immunosuppression

80
Q

Which virus is a trigger in 30% of pts with polyarteritis nodosa?

A

HepB

81
Q

What is Churg-Strauss syndrome?

A

Rare complication of asthma (moderate yo severe) leading to vascular necrosis which starts in the lungs

82
Q

How does Churg-Strauss syndrome typically present?

A

Hypergammaglobinaemia

83
Q

Which markers are present in serology in Churg-Strauss syndrome?

A

IgE
RF
ANCA

84
Q

What are the 3 stages of Churg-Strauss syndrome?

A
  1. Allergic rhinitis and asthma
  2. Eosinic infiltration - cough, pneumonia
  3. Widespread i.e. Peripheral neuropathy, renal, arthralgia, purpurin, diarrhoea, GIT bleeding, myocarditis/pericarditis
85
Q

What can be seen on CXR in a person with Churg-Strauss syndrome?

A

Bilateral, peripheral patchy parenchymal opacities

JG Year 2 (28 decks)

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