Rheumatology Flashcards

1
Q

Osteoarthritis risk factors

A

Obesity, excessive joint loading, overuse, age>55yo, history of joint trauma, anatomic factors causing asymmetrical joint stress, deposition diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Osteoarthritis can be classified as:

A

Idiopathic or secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Idiopathic osteoarthritis is usually due to:

A

Age-related wear and tear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Causes of secondary osteoarthritis

A

Haemochromatosis, Wilson’s disease, Ehlers-Danlos syndrome, diabetes, AVN, joint trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Early clinical features of osteoarthritis:

A

Pain on exertion that is relieved by rest, crepitus on joint movement, joint stiffness and restricted ROM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Late clinical features of osteoarthritis:

A

Constant pain (incl. night), morning joint stiffness lasting <30mins, severely restricted ROM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hand examination findings in osteoarthritis:

A

Herberden’s and Bouchard’s nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

X-ray findings associated with osteoarthritis

A

Loss of joint space, osteophytes, subchondral sclerosis and subchondral cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Non-operative/non-pharmacological management of osteoarthritis includes:

A

Weight loss, physiotherapy, regular exercise, heat therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pharmacological management of osteoarthritis includes:

A

Paracetamol/NSAIDs, intra-articular glucocorticoid injections if severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Operative management of osteoarthritis includes:

A

Joint replacement (if conservative management has failed and there is lifestyle-limiting pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Most common site of septic arthritis

A

Knee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Septic arthritis

A

Bacterial infection of joint space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Risk factors for septic arthritis

A

Prosthetic joint, joint interventions, underlying joint disease in RA, immunosuppression, DM, >age, IVDU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The two ways a joint can become septic are:

A

Haematogenous spread from a distal site (abscess, wound infection, septicaemia, gonorrhoea) or direct contamination (iatrogenic, trauma, osteomyelitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical features of septic arthritis

A

Pain in affected joint (usually monoarticular), fever, erythematous/warm/tender joint, inability to weight bear or tolerate passive ROM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

First-line investigations for septic arthritis include:

A

WCC, ESR/CRP, joint fluid aspiration, x-ray (AP/lateral)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When sending a joint fluid aspirate for analysis, the following tests should be requested:

A

WCC, Gram stain, MCS, crystal analysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What value of WCC is diagnostic for septic arthritis?

A

> 50,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In a septic arthritis, joint fluid aspirate appears:

A

Cloudy/purulent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Non-operative management of septic arthritis

A

Empiric IV Abx
Staphylococcus aureus most common pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Operative management of septic arthritis

A

Joint washout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Complications of septic arthritis

A

Arthritis, fibrous ankylosis, osteomyelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Gout definition

A

Monosodium urate crystal deposition disorder characterised by derangement in purine metabolism causing hyperuricaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Monosodium urate crystal deposits in tissues are called:

A

Tophi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Gout can be classified into:

A

Primary and secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Secondary gout is associated with diseases/medications such as:

A

Psoriasis, haemolytic anaemia, leukaemia, chemotherapy (e.g. those with high metabolic turnover)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

The most common site of first presentation of gout is:

A

The first MTP (podagra)

29
Q

Risk factors for the development of gout include:

A

Male gender, advanced age, family history, high alcohol intake, purine-rich diet, renal failure, metabolic syndrome, diuretics

30
Q

____ ____ is the end product of purine metabolism

A

Uric acid

31
Q

The rate determining enzyme of purine metabolism is:

A

Xanthine oxidase

32
Q

Disease course in gout

A

Single episode progressing to recurrent episodes of acute inflammatory arthritis, typically monoarticular

33
Q

Clinical features of gout include:

A

Severe pain/redness/joint swelling and reduced ROM, subsides spontaneously within days and may recur, abrupt onset with peak within 12hrs

34
Q

Joint fluid aspirate in gout generally appears:

A

Similar to white toothpaste

35
Q

First-line investigations in gout include:

A

Serum urate, WCC, CRP/ESR, joint aspirate, x-ray of affected joint

36
Q

The gold-standard diagnostic test for gout is:

A

Joint fluid aspirate

37
Q

Joint fluid aspirate findings in gout:

A

Needle-shaped, negatively bifringent, yellow crystals

38
Q

X-ray findings in gout

A

Punched out periarticular erosions (rat-bitten appearance), soft tissue crystal deposition

39
Q

Acute management of gout

A

First-line = NSAID or colchicine
Second-line = corticosteroids

40
Q

Chronic management of gout

A

Allopurinol (+colchicine initially as initiating allopurinol can trigger an acute flare of gout)

41
Q

Allopurinol MoA

A

Xanthine oxidase inhibitor, blocks conversion of purines to uric acid

42
Q

Second-line management options for chronic gout

A

Febuxostate, probenicid, uricase

43
Q

Complications of chronic gout

A

Uric acid nephrolithiasis, tophi

44
Q

Pseudogout definition

A

Metabolic disease leading to calcium pyrophosphate crystal deposition within the joint space leading to recurrent monoarticular arthritis

45
Q

Which affects more proximal joints - gout or pseudogout?

A

Pseudogout

46
Q

Secondary causes of pseudogout include:

A

Joint trauma/damage, metabolic disorders (hyperparathyroidism, haemochromatosis), familial chondrocalcinosis

47
Q

Most commonly affected joints in pseudogout:

A

Knee and wrist

48
Q

Differentiating features for gout vs. pseudogout

A

Longer duration of acute attacks and greater chance of systemic symptoms in pseudogout

49
Q

Joint fluid aspirate findings in pseudogout:

A

Positively-bifringent rhomboid-shaped crystals

50
Q

Acute management of pseudogout:

A

NSAIDs, splint, intra-articular steroids

51
Q

Chronic management of pseudogout:

A

Can consider prophylactic colchicine, but no therapeutic regime to treat underlying cause of CPP crystal deposition

52
Q

Seropositive conditions

A

Rheumatoid arthritis, SLE, anti-phospholipid syndrome, Sjogren’s syndrome, scleroderma, Raynaud’s syndrome, idiopathic inflammatory arthropathy

53
Q

Rheumatoid arthritis definition

A

Chronic, symmetric, erosive autoimmune disease characterised by persistent synovitis, systemic inflammation and the presence of autoantibodies.

54
Q

Rheumatoid arthritis risk factors

A

Female sex, smoking, genetic disposition

55
Q

Which genes have a strong association with the development of rheumatoid arthritis?

A

HLA-DR4 and HLA-DR1 (a DRone with 4 propellors and 1 camera)

56
Q

Pathophysiology of rheumatoid arthritis

A

Bouts of inflammation, angiogenesis and proliferation → proliferative granulation tissue with mononuclear inflammatory cells → pannus and synovial hypertrophy → invasion, progressive destruction and deterioration of cartilage and bone

57
Q

Articular manifestations of rheumatoid arthritis

A

Symmetrical polyarthralgia with associated pain and swelling.

58
Q

Which joints are commonly spared in rheumatoid arthritis?

A

DIP and first CMC joint

59
Q

In rheumatoid arthritis, morning stiffness usually:

A

lasts >30min and improves with activity

60
Q

Characteristic joint deformities in rheumatoid arthritis include:

A

Swan neck deformity, Boutonniere deformity, Z thumb deformity, ulnar deviation of the fingers

61
Q

Swan neck deformity

A

PIP hyperextension and DIP flexion

62
Q

Boutonniere deformity

A

PIP flexion and DIP hyperextension

63
Q

Z thumb deformity

A

Hyperextension of the interphalangeal joint with fixed flexion of the MCP joint

64
Q

Extra-articular manifestations of rheumatoid arthritis include:

A

Constitutional symptoms, rheumatoid nodules, pulmonary nodules, ILD, scleritis/uveitis, pericarditis

65
Q

Rheumatoid nodules

A

Non-tender, firm, subcutaneous swellings

66
Q

X-ray findings associated with rheumatoid arthritis

A

Loss of joint space, erosions (periarticular), soft tissue swelling, soft bone (periarticular osteopaenia)

67
Q

What is the earliest LESS finding in rheumatoid arthritis?

A

Peri-articular osteopaenia

68
Q
A