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BRS 5: Musculoskeletal & Rheumatology > 5.7: Introduction to rheumatology (part 1 of 2) > Flashcards

5.7: Introduction to rheumatology (part 1 of 2) Flashcards

1
Q

Arthritis is a

A

Disease of the joints

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2
Q

2 major divisions of arthritis

A

Degenerative joint disease (osteoarthritis)
Inflammatory joint disease

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3
Q

Pathological changes during osteoarthritis

A

Cartilage loss, bony remodelling

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4
Q

Epidemiology of osteoarthritis

A

More prevalent with increasing age
Previous joint trauma
Jobs involving heavy manual labour

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5
Q

What kind of onset and progression does osteoarthritis present with

A

Gradual onset
Slow progressive disorder

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6
Q

4 symptoms and signs of osteoarthritis

A

Joint pain - worse with activity better with rest
Joint crepitus - creaking, cracking, grinding sound on moving joint
Joint enlargement
Limitation of range of motion

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7
Q

3 types of joints affected by degenerative joint disease

A

Joints of the hand (: Distal interphalangeal joints, proximal interphalangeal joints, first carpometacarpal joint )
Spine
Weight bearing joints of lower limbs (: knees, hips, first metatarsophalangeal joint)

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8
Q

4 radio graphic features of osteoarthritis

A

Joint space narrowing
Subchondral bony sclerosis
Osteophytes
Subchondral cysts

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9
Q

Define inflammation

A

A physiological response to deal with injury or infection

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10
Q

What can excess or inappropriate inflammatory reactions lead to

A

Damage to host tissues

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11
Q

What 5 things does inflammation manifest clinically as

A

Red (rubor)
Pain (dolor)
Hot (calor)
Swelling (tumor)
Loss of function

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12
Q

4 Physiological, cellular and molecular changes during inflammation

A

Increased blood flow
Migration of white blood cells (leucocytes)
Activation p/differentiation of leucocytes
Cytokine production

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13
Q

3 main causes of joint inflammation

A

Infection (secondary inflammation)
Crystal arthritis (secondary inflammation)
Immune- mediated (autoimmune) primary inflammation

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14
Q

Secondary inflammation occurs in response to

A

A noxious insult

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15
Q

Example of Non-sterile inflammation

A

Infection

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16
Q

2 examples of sterile inflammation

A

Crystal arthritis
Immune-mediated inflammation

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17
Q

Cause of septic arthritis

A

Bacterial infection of a joint (spread of blood)

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18
Q

3 risk factors of septic arthritis

A

Immunosuppressed (e.g. diabetes)
Pre-existing joint damage
Intravenous drug use (IVDU)

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19
Q

Why is septic arthritis a medical emergency

A

If untreated can rapidly destroy a joint

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20
Q

Clinical presentations of septic arthritis

A

Acute, red, hot, painful swollen joint
Usually only one joint affected
Typically fever - systemically unwell

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21
Q

Diagnosis of septic arthritis

A

Joint aspiration
Sample sent for urgent gram stain and culture

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22
Q

Common organisms causing septic arthritis

A

Staphylococcus aureus, strepococci
Gonococcus (affects multiple joints - polyarthritis, less likely to cause joint destruction)

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23
Q

Treatment of septic arthritis

A

Surgical wash out and intravenous antibiotics

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24
Q

2 types of Crystal arthritis

A

Gout
Pseudogout

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25
Q

Gout is caused by deposition of

A

Momosodium urate (MSU) crystals around/in joints leading to inflammation

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26
Q

A risk factor if gout is

A

High Uric acid levels

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27
Q

3 causes of hyperuricaemia

A

Genetic tendency
Increased intake of purine rich foods
Reduced excretion (kidney failure)

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28
Q

What is pseudogout caused by deposition of

A

Calcium pyrophosohate dihydrate (CPPD) crystals

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29
Q

Risk factors of pseudogout

A

Background osteoarthritis
Elderly patients
Intercurrent infection

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30
Q

In Crystal arthritis, tissue deposition of monosodium urate (MSU) crystals leads to:

A

Gouty arthritis
Top hi (depositions of MSU in tissue, often around hands, feet, elbows and ears)

31
Q

4 Clinical features of Crystal arthritis

A

Abrupt onset
Usually monoarthritis
Big toe 1st MTPJ most commonly affected
Can also affect other joints- feet,ankle,knee,wrist,finger,elbow

32
Q

What would a blood test in a patient with gout show

A

Increased C-reactive protein - inflammatory marker
Increased serum urate

33
Q

What would an X-ray of a patient presenting with gout show

A

Normal X-ray
If recurrent attacks - juxta-articular erosions develop

34
Q

Gout Crystal shape and birefringence

A

Urate crystals have a needle shape
Negative for light microscopy

35
Q

What is the key investigation for any acute monoarthritis

A

Joint aspiration
Synovial fluid analysis
Send to lab for : microbiology
Polarising light microscopy to detect crystals

36
Q

Pseudogout Crystal shape and birefringence

A

CPPD crystals are rhomboid shaped
Positive for birefringence

37
Q

Gout treatment for an acute attack

A

Main aim to reduce inflammation
- non-steroidal anti-inflammatory drugs NSAIDs
Glucocorticoids

38
Q

Chronic Gifu treatment

A

Aim - reduce uric acid levels
Lifestyle : avoids purine rich food e.g. beer
Pharmacological - allopurinol, febuxostat (xanthine oxidase inhibitors)

39
Q

3main categories of immune-mediated inflammatory joint diseases

A

Rheumatoid arthritis
Seronegative inflammatory arthritis
Systemic lupus erythematosus

40
Q

What kind of condition is rheumatoid arthritis

A

Chronic autoimmune disease

41
Q

What is the primary site of pathology of RA

A

Synovium

42
Q

Synovitis is

A

Inflammation of the synovial membrane

43
Q

What 3 locations is synovium found at

A

Synovial joints
Tenosynovium surrounding tendons
Bursa

44
Q

5 key features of chronic arthritis

A

Polyarthritis
Early morning stiffness around joints
MY lead to joint damage and destruction
Auto-antibodies usually detected in blood
Extra-articular disease can occur

45
Q

Pattern of joint involvement in RA

A

Symmetrical
Polyarthritis
Affects both small and large joints- most commonly hands, wrists and feet

46
Q

Describe a healthy synovial membrane

A

1-3 cell layer that lines synovial joints - maintains synovial fluid

47
Q

Synovial membrane in RA

A

Synovium becomes proliferated mass of tissue due to :
Neovascularisation
Lymphangiogenesis
Inflammatory cells : activated B and T cells, plasma cells, mast cells, activated macrophages

48
Q

Why does inflammation of Synovium occur in RA

A

Cytokine network controls recruitment, activation and effector functions
Cytokine imbalance - excess of pro-inflammatory and anti-inflammatory cytokines

49
Q

Pathogenesis of RA

A

Cytokine tumour necrosis factor-alpha (TNFa) is the dominant pro-inflammatory cytokine in the rheumatoid Synovium

50
Q

Compare blood test Haemoglobin levels in RA, Osteoarthritis and septic arthritis

A

RA - low (anaemia)
OA- normal
SA- usually normal

51
Q

Compare white cell count in RA, Osteoarthritis and septic arthritis

A

RA - normal
OA-normal
SA- increased (leucocytosis)

52
Q

Compare levels of C-reactive protein in RA, Osteoarthritis and septic arthritis

A

RA- high
OA- normal
SA- high

53
Q

Two types of antibodies found in blood of RA patients

A

Rheumatoid factor
Antibodies to citrullinated protein antigens (ACPA)

54
Q

Rheumatoid factor is an antibody that

A

Recognises the Fc portion of IgG as their target antigen
Typically IgM antibodies
Positive in 80% of RA patients

55
Q

Clinical test to detect ACPA

A

Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’

56
Q

Which antibodies are more specific for RA, Anti-CCP or RF

A

Anti-CCP antibodies
Ab positivity is associated with more aggressive/erosive disease

57
Q

What 3 identifiable features would be present on an X-ray of a patient with RA

A

Soft tissue swelling
Peri-articular osteopenia
Bony erosions - only in established disease

58
Q

What 3 identifiable features would be present in an Ultrasound of a patient with RA

A

Better test for detecting synovitis
-synovial hypertrophy
-increased blood flow
May detect early erosions (not visible on X-ray)

59
Q

What 3 imaging investigations can be carried out to diagnose RA and which one is the best at diagnosing

A

X-ray
MRI - can be expensive and time-consuming
Ultrasound - nest as can be used in assessment in early arthritis

60
Q

Principles or management of RA

A

Early recognition of symptoms, referral and diagnosis
Prompt initiation of treatment : joint destruction = inflammation x time
Aggressive pharmacological treatment to surprises inflammation

61
Q

Two pharmacological treatments of RA and their function

A

Glucocorticoid therapy (steroids) : useful acutely but avoid long term use due to side effects
DMARDs - disease modifying anti-rheumatic drugs , immunomodulatory drugs that half or slow disease process

62
Q

Seronegative inflammatory arthritis includes (4)

A

Psoriatic arthritis
Reactive arthritis
Ankylosing spondylitis
IBD-associated arthritis

63
Q

What is Seronegative inflammatory arthritis

A

Family of conditions with overlapping clinical features and oathogenesis
RF and CCP antibodies not present in blood but immune mediated conditions

64
Q

Main clinical presentation of psoriatic arthritis

A

Classically asymmetrical arthritis affecting IPJs

65
Q

What 3 things can psoriatic arthritis also manifest as

A

Symmetrical involvement of small joints
Oligoarthritis of large joints
Spinal and sacroiliac joint inflammation

66
Q

What is Reactive arthritis and what does it present following

A

Sterile inflammation following Infection elsewhere in the body

67
Q

Two common infections of reactive arthritis

A

Urogenital (chlamydia trachomatis)
Gastrointestinal (samonella, shingella)

68
Q

3 Important extra-articular manifestations of Reactive arthritis

A

Enthesitis
Skin inflammation
Eye inflammation

69
Q

What can reactive arthritis be a first manifestation of

A

HIV
Hep C

70
Q

What age group is most at risk of developing reactive arthritis

A

Young adults with genetic predisposition and environmental trigger

71
Q

When do symptoms of reactive arthritis onset

A

1-4weeks after infection (may be mild)

72
Q

How is synovial fluid culture different in septic arthritis compared to reactive arthritis

A

SA - positive
RA- sterile

73
Q

Use of antibiotic therapy for septic arthritis compared to reactive arthritis

A

SA- yes
RA- no (not for joint disease but in cases of STIs treatment may be required)

74
Q

Joint lavage in septic arthritis compared to reactive arthritis

A

SA- yes for large joints
RA - no

BRS 5: Musculoskeletal & Rheumatology (6 decks)

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