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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
Gout is caused by deposition of
Momosodium urate (MSU) crystals around/in joints leading to inflammation
26
A risk factor if gout is
High Uric acid levels
27
3 causes of hyperuricaemia
Genetic tendency Increased intake of purine rich foods Reduced excretion (kidney failure)
28
What is pseudogout caused by deposition of
Calcium pyrophosohate dihydrate (CPPD) crystals
29
Risk factors of pseudogout
Background osteoarthritis Elderly patients Intercurrent infection
30
In Crystal arthritis, tissue deposition of monosodium urate (MSU) crystals leads to:
Gouty arthritis Top hi (depositions of MSU in tissue, often around hands, feet, elbows and ears)
31
4 Clinical features of Crystal arthritis
Abrupt onset Usually monoarthritis Big toe 1st MTPJ most commonly affected Can also affect other joints- feet,ankle,knee,wrist,finger,elbow
32
What would a blood test in a patient with gout show
Increased C-reactive protein - inflammatory marker Increased serum urate
33
What would an X-ray of a patient presenting with gout show
Normal X-ray If recurrent attacks - juxta-articular erosions develop
34
Gout Crystal shape and birefringence
Urate crystals have a needle shape Negative for light microscopy
35
What is the key investigation for any acute monoarthritis
Joint aspiration Synovial fluid analysis Send to lab for : microbiology Polarising light microscopy to detect crystals
36
Pseudogout Crystal shape and birefringence
CPPD crystals are rhomboid shaped Positive for birefringence
37
Gout treatment for an acute attack
Main aim to reduce inflammation - non-steroidal anti-inflammatory drugs NSAIDs Glucocorticoids
38
Chronic Gifu treatment
Aim - reduce uric acid levels Lifestyle : avoids purine rich food e.g. beer Pharmacological - allopurinol, febuxostat (xanthine oxidase inhibitors)
39
3main categories of immune-mediated inflammatory joint diseases
Rheumatoid arthritis Seronegative inflammatory arthritis Systemic lupus erythematosus
40
What kind of condition is rheumatoid arthritis
Chronic autoimmune disease
41
What is the primary site of pathology of RA
Synovium
42
Synovitis is
Inflammation of the synovial membrane
43
What 3 locations is synovium found at
Synovial joints Tenosynovium surrounding tendons Bursa
44
5 key features of chronic arthritis
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
Pattern of joint involvement in RA
Symmetrical Polyarthritis Affects both small and large joints- most commonly hands, wrists and feet
46
Describe a healthy synovial membrane
1-3 cell layer that lines synovial joints - maintains synovial fluid
47
Synovial membrane in RA
Synovium becomes proliferated mass of tissue due to : Neovascularisation Lymphangiogenesis Inflammatory cells : activated B and T cells, plasma cells, mast cells, activated macrophages
48
Why does inflammation of Synovium occur in RA
Cytokine network controls recruitment, activation and effector functions Cytokine imbalance - excess of pro-inflammatory and anti-inflammatory cytokines
49
Pathogenesis of RA
Cytokine tumour necrosis factor-alpha (TNFa) is the dominant pro-inflammatory cytokine in the rheumatoid Synovium
50
Compare blood test Haemoglobin levels in RA, Osteoarthritis and septic arthritis
RA - low (anaemia) OA- normal SA- usually normal
51
Compare white cell count in RA, Osteoarthritis and septic arthritis
RA - normal OA-normal SA- increased (leucocytosis)
52
Compare levels of C-reactive protein in RA, Osteoarthritis and septic arthritis
RA- high OA- normal SA- high
53
Two types of antibodies found in blood of RA patients
Rheumatoid factor Antibodies to citrullinated protein antigens (ACPA)
54
Rheumatoid factor is an antibody that
Recognises the Fc portion of IgG as their target antigen Typically IgM antibodies Positive in 80% of RA patients
55
Clinical test to detect ACPA
Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’
56
Which antibodies are more specific for RA, Anti-CCP or RF
Anti-CCP antibodies Ab positivity is associated with more aggressive/erosive disease
57
What 3 identifiable features would be present on an X-ray of a patient with RA
Soft tissue swelling Peri-articular osteopenia Bony erosions - only in established disease
58
What 3 identifiable features would be present in an Ultrasound of a patient with RA
Better test for detecting synovitis -synovial hypertrophy -increased blood flow May detect early erosions (not visible on X-ray)
59
What 3 imaging investigations can be carried out to diagnose RA and which one is the best at diagnosing
X-ray MRI - can be expensive and time-consuming Ultrasound - nest as can be used in assessment in early arthritis
60
Principles or management of RA
Early recognition of symptoms, referral and diagnosis Prompt initiation of treatment : joint destruction = inflammation x time Aggressive pharmacological treatment to surprises inflammation
61
Two pharmacological treatments of RA and their function
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
Seronegative inflammatory arthritis includes (4)
Psoriatic arthritis Reactive arthritis Ankylosing spondylitis IBD-associated arthritis
63
What is Seronegative inflammatory arthritis
Family of conditions with overlapping clinical features and oathogenesis RF and CCP antibodies not present in blood but immune mediated conditions
64
Main clinical presentation of psoriatic arthritis
Classically asymmetrical arthritis affecting IPJs
65
What 3 things can psoriatic arthritis also manifest as
Symmetrical involvement of small joints Oligoarthritis of large joints Spinal and sacroiliac joint inflammation
66
What is Reactive arthritis and what does it present following
Sterile inflammation following Infection elsewhere in the body
67
Two common infections of reactive arthritis
Urogenital (chlamydia trachomatis) Gastrointestinal (samonella, shingella)
68
3 Important extra-articular manifestations of Reactive arthritis
Enthesitis Skin inflammation Eye inflammation
69
What can reactive arthritis be a first manifestation of
HIV Hep C
70
What age group is most at risk of developing reactive arthritis
Young adults with genetic predisposition and environmental trigger
71
When do symptoms of reactive arthritis onset
1-4weeks after infection (may be mild)
72
How is synovial fluid culture different in septic arthritis compared to reactive arthritis
SA - positive RA- sterile
73
Use of antibiotic therapy for septic arthritis compared to reactive arthritis
SA- yes RA- no (not for joint disease but in cases of STIs treatment may be required)
74
Joint lavage in septic arthritis compared to reactive arthritis
SA- yes for large joints RA - no

BRS 5: Musculoskeletal & Rheumatology (6 decks)

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