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Phase 2A > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What groups of people does septic arthritis affect?

A

Patients with prosthetic joints

Risk factors: DM, immunosuppressed

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2
Q

What are the common causes of septic arthritis?

A

S. epidermidis
Gonococcal (young, sexually active)
Strep. pyogenes
Pseudomonas aeruginosa

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3
Q

How is septic arthritis treated?

A 
Aspirate for pain
IV antibiotics
Joint washout
RICE
Physio
Temporarily stop immunosuppressive drugs but double prednisolone to prevent adrenal crisis
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4
Q

What are the risk factors for rheumatoid arthritis?

A

High birth weight, DM, obesity, smoking, silica exposure, genetic susceptibility

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5
Q

What is the pathophysiology involved in rheumatoid arthritis?

A

It is an autoimmune disease associated with autoantibodies to IgG and citrullinated cyclic peptide leading to persistent synovitis and systemic inflammation

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6
Q

What is the epidemiology of rheumatoid arthritis?

A

Age of onset: 30-50

Female > male

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7
Q

What are the symptoms of rheumatoid arthritis?

A

Symmetrical swollen, painful and stiff small joints of hands and feet, worse in the morning; larger joints can be involved

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8
Q

What are the signs of rheumatoid arthritis?

A 
Swollen MCP, PIP, wrist or MTP joints
Ulnar deviation of fingers
Dorsal wrist subluxation
Boutonniere and swan neck deformity of fingers
Z deformity of the thumbs
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9
Q

What tests are used to diagnose rheumatoid arthritis?

A

Bloods: FBC (normochromic and normocytic anaemia), ESR, CRP & plasma viscosity (high), LFTs, antinuclear antibodies, rheumatoid factor, anti-cyclic citrullinated peptide, joint aspirate - rule out gout, pseudogout and septic arthritis
X-ray of the joint

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10
Q

What are the X-ray findings of rheumatoid arthritis?

A

Soft tissue swelling, juxta-articular osteopenia, decreased joint space, bony erosions

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11
Q

What is the treatment for rheumatoid arthritis?

A

NSAIDs - pain relief
DMARDs - azathioprine, ciclosporin, penicillamine, leflunomide, methotrexate and sulfasalazine. Can be used with steroids, reduce damage to the joints
Biologics - rituximab, etanercept (TNF inhibitor), abatacept (T cell stimulator modulator)
Surgery - synovectomy and excision arthroplasties

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12
Q

What are the risk factors for osteoarthritis?

A

Genetic factors, obesity, ageing, abnormal bone density joint injury, decreased muscle strength, joint laxity or malalignment, occupation

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13
Q

What is the pathophysiology involved in osteoarthritis?

A

There is localised loss of cartilage, remodelling of adjacent bone and associated inflammation

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14
Q

What is the epidemiology of osteoarthritis?

A

Increasing age

Female > male

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15
Q

What are the symptoms of osteoarthritis?

A

Joint pain exacerbated by exercise and relieved by rest, joint stiffness in the morning or after rest, decreased function and participation restriction

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16
Q

What are the signs of osteoarthritis?

A

Joint swelling/synovitis, periarticular tenderness, crepitus, bony swelling and deformity due to osteophyte formation
Heberden’s nodes (DIP)
Bouchard’s nodes (PIP)

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17
Q

What tests are used to diagnose osteoarthritis?

A

MRI - rule out other diagnoses
Bloods: FBC U&Es, LFTs, CRP - should be normal
Joint aspiration - rule out septic arthritis and gout

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18
Q

What are the x-ray findings of osteoarthritis?

A

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

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19
Q

What is the treatment of osteoarthritis?

A

Education and lifestyle advice e.g. lose weight
Analgesia - topical, oral or transdermal
Steroid injections
Surgery - for uncontrolled pain and significant limitation of function; replace joints e.g. knee and hip

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20
Q

What are the risk factors for SLE?

A

Genetics (C4A null allele), UV light, EBV, drugs e.g. chlorpromazine, methyldopa, hydralazine, isoniozid

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21
Q

What is the pathophysiology of SLE?

A

It it a multisystemic autoimmune disease where autoantibodies are made against a variety of autoantigens leading to tissue damage via immune complex formation, deposition and complement activation

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22
Q

What is the epidemiology of SLE?

A

Women > men

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23
Q

What are the symptoms of SLE?

A

Fatigue, weight loss, malaise, arthralgia, oral ulcers, photosensitive skin rashes, pleuritic chest pain, headache, paraesthesiae

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24
Q

What are the signs of SLE?

A

Malar (butterfly) rash, discoid rash, non-erosive arthritis, pleuritis or pericarditis, proteinuria, seizures, haemolytic anaemia, leukopenia, thrombocytopenia

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25
Q

What tests are used to diagnose SLE?

A

Bloods: FBC, ESR, plasma viscosity, complement (low C3 and C4, high C3d and C4d), autoantibodies: ANA, anti-dsDNA, antiphospholipid antibodies

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26
Q

What is the treatment for SLE?

A

Avoid sunlight exposure and decrease CV risk factors
NSAIDs - for arthritis and fever
Antimalarials - Chloroquine (if NSAIDs ineffective for joint/skin problems)
Rash - topical steroids
Flares - steroids, cyclophosphamide, mycophenolate, azathioprine, methotrexate
Biologics - rituximab

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27
Q

What is the aetiology of ankylosing spondylitis?

A

Genetics

HLA B27

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28
Q

What is the pathophysiology involved in ankylosing spondylitis?

A

It is a seronegative, chronic inflammatory disease causing sacroiliitis, inflammatory back pain, enthesitis and anterior uveitis

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29
Q

What is the epidemiology of ankylosing spondylitis?

A

Male > female

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30
Q

What are the symptoms of ankylosing spondylitis?

A

Back pain in the morning, morning stiffness >30 mins, pain improves with movement, pain in one or both buttocks

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31
Q

What are the signs of ankylosing spondylitis?

A

Retention of lumbar lordosis during spinal flexion, progressive loss of spinal movement, enthesitis e.g. Achilles tendonitis, dactylitis

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32
Q

What tests are used to diagnose ankylosing spondylitis?

A

Bloods: FBC (normocytic anaemia), ESR (increased), CRP (increased), HLA B27 (positive), RF (negative),
XR spine - sacroiliac changes, ascending spread of disease, syndesmophyte, ossification
MRI - joint erosions and fluid

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33
Q

What is the treatment for ankylosing spondylitis?

A

Exercise and physio, NSAIDs for pain relief
DMARDs - azathioprine, ciclosporin, penicillamine, methotrexate, leflunomide and sulfasalazine
Biologics - rituximab, etanercept, abatacept
Local steroid injections

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34
Q

What is the aetiology of psoriatic arthritis?

A

It occurs in people with psoriasis or a family history of psoriasis; the risk factors are the same

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35
Q

What is the pathophysiology of psoriatic arthritis?

A

It is an inflammatory arthritis affecting the joints and connective tissue, it can present before skin disease. Inflammation is T-lymphocyte driven.

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36
Q

What is the epidemiology involved in psoriatic arthritis?

A

60-70% are HLA B27 positive

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37
Q

What are the symptoms of psoriatic arthritis?

A

Stiffness and joint pain, psoriasis (in some cases), nail lesions - pitting, onycholysis, conjunctivitis and uveitis

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38
Q

What are the signs of psoriatic arthritis?

A

Joint involvement - symmetrical, polyarthritis, asymmetrical oligoarthritis, DIPJ, spine, arthritis mutilans, enthesitis, dactylitis, synovitis, nail changes

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39
Q

What tests are used to diagnose psoriatic arthritis?

A

Bloods: FBC (anaemia), ESR (increased)
Xray - erosive changes with “pencil in cup” deformity in severe cases, synovitis
Joint aspirate (high WCC)
Rheumatoid factor - usually negative

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40
Q

What is the treatment for psoriatic arthritis?

A

Exercise
NSAIDs for pain relief
DMARDs - azathioprine, ciclosporin, penicillamine, sulfasalazine, leflunomide, methotrexate
Biologics - rituximab, etanercept, abatacept
Intra-articular injections of corticosteroids for local synovitis

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41
Q

What organisms commonly cause reactive arthritis?

A

Shigella, Salmonella, Chlamydia trachomitis, HIV, enterococci, Ureaplasma urealyticum

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42
Q

What is the pathophysiology involved in reactive arthritis?

A

It is a sterile synovitis following an infection, can be chronic or relapsing. The infection is usually dysentery or an STI

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43
Q

What is the epidemiology involved in reactive arthritis?

A

60-85% are HLA B27 positive

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44
Q

What are the symptoms of reactive arthritis?

A

Conjunctivitis, urethritis, swelling in knee, heel or ball of foot, flaky skin patches on the sole, scaly skin patches on genitalia, lower back pain, diarrhoea

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45
Q

What are the signs of reactive arthritis?

A

Mouth ulcers, enthesitis, circinate balanitis (painless penile ulceration secondary to chlamydia), nail dystrophy

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46
Q

What tests are used to diagnose reactive arthritis?

A

Bloods: ESR (increased), CRP (increased), infectious serology e.g. HIV, stool culture if the patient has had diarrhoea
Xray - enthesitis with periosteal reaction
ECG

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47
Q

What is the treatment for reactive arthritis?

A

NSAIDs for pain relief
Steroids for flare ups
Antibiotics - treat the underlying cause
DMARDs for relapsing cases

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48
Q

What is the aetiology of enteropathic arthritis?

A

It occurs in 10-15% of IBD cases - both Crohn’s disease and ulcerative colitis. The risk factors for these diseases are the same

49
Q

What is the pathophysiology of enteropathic arthritis?

A

It is unclear, there is selective mucosal leakiness may expose the individual to antigens that trigger synovitis

50
Q

What is the epidemiology of enteropathic arthritis?

A

50-60% are HLA B27 positive

51
Q

What are the symptoms of enteropathic arthritis?

A

Asymmetrical arthritis, mainly affects the lower limb joints, sacroiliitis or spondylitis can also occur

52
Q

What are the signs of enteropathic arthritis?

A

Oral ulcers, pyoderma gangrenosum (painful ulcers), symptomatic uveitis, erythema nodosum

53
Q

What tests are used to diagnose enteropathic arthritis?

A

Bloods: FBC (possibly iron deficiency anaemia, leukocytosis or thrombocytosis), ESR (increased), CRP (increased)
Stool: MC&S
Fluid aspiration - mononuclear inflammatory cells

54
Q

What is the treatment of enteropathic arthritis?

A

Treat the underlying IBD - remission of IBD leads to improvement of symptoms
Monoarthritis - intra-articular corticosteroids

55
Q

What are the risk factors for osteoporosis?

A

Family history, increasing age, steroid use, alcohol excess, smoking, early menopause

56
Q

What is the pathophysiology involved in osteoporosis?

A

There is increased bone breakdown by osteoclasts and decreased bone formation by osteoblasts leading to a loss of bone mass

57
Q

What are the symptoms of osteoporosis?

A

Pain, reduced mobility, height loss, fracture e.g. vertebral crush fracture, Colles’ fracture, fracture of proximal femur

58
Q

What are the signs of osteoporosis?

A

Signs of fracture

59
Q

What tests are used to diagnose osteoporosis?

A

Plain radiographs - evidence of a fracture
DEXA scans to measure bone mineral density - gives a T score (standard deviation) >-1 = no evidence of osteoporosis; -1 to -2.5 = osteopenia;

60
Q

What is the treatment for osteoporosis?

A

Conservative: weight-bearing exercise, alcohol and smoking cessation
Pharmacological: bisphosphonates (e.g. alendronic acid), calcium and vitamin D (e.g. AdCal D3), denosumab (anti-RANKL mAb), HRT in post-menopausal women

61
Q

What is the aetiology of polymyalgia rheumatica?

A

Unknown - genetic and environmental factors may be important in disease pathogenesis

62
Q

What is the pathophysiology involved in polymyalgia rheumatica?

A

It is a systemic inflammatory condition of the elderly; it is not a true vasculitis

63
Q

What are the symptoms of polymyalgia rheumatica?

A

Sudden onset of severe pain and stiffness in the shoulders and neck, the hips and lumbar spine - lasts 30m - several hours
Tiredness, weight loss

64
Q

What are the signs of polymyalgia rheumatica?

A

Fever, depression

65
Q

What tests are used to diagnose polymyalgia rheumatica?

A

Bloods: FBC, U&Es, LFTs, ESR (increased), CRP (increased), plasma viscosity (increased), bone profile, creatinine kinase, TFTs, protein electrophoresis, rheumatoid factor
MSU - urinalysis (+/- Bence Jones protein to rule out myeloma)
CXR
USS of the shoulders if diagnosis is unknown

66
Q

What is the treatment of polymyalgia rheumatica?

A

Corticosteroids

Calcium and vitamin D +/- bisphosphonates for osteoporosis prophylaxis

67
Q

What is the aetiology of polyarteritis nodosa?

A

Unknown; there is an occasional association with hepatitis B antigenaemia

68
Q

What is the pathophysiology involved in polyarteritis nodosa?

A

It is a necrotising vasculitis that causes aneurysms and thrombosis in medium-sized arteries resulting in infarction in affected organs and severe systemic symptoms

69
Q

What are the symptoms of polyarteritis nodosa?

A

Malaise, weight loss, myalgia, skin lesions e.g. purpura, livedoid, subcutaneous nodules, necrotic ulcers, post-prandial abdominal pain

70
Q

What are the signs of polyarteritis nodosa?

A

Fever, haematuria, proteinuria, hypertension, mononeuritis multiplex, AKI

71
Q

What tests are used to diagnose polyarteritis nodosa?

A

FBC (anaemia, leukocytosis), ESR (increased), CRP (increased), AMCA (negative)
Biopsy - fibrinoid necrosis of vessel walls with microaneurysm formation, thrombosis and infarction
ECG
USS of the abdomen
Angiography - microaneurysm

72
Q

What is the treatment of polyarteritis nodosa?

A

Control BP meticulously
Corticosteroids and immunosuppressive drugs e.g. azathioprine
Hepatitis B should be treated with antivirals

73
Q

What is the aetiology of gout?

A

It can be hereditary, increased dietary purines (red meat, seafood), alcohol excess, diuretics, leukaemia, cytotoxics e.g. tumour lysis, hyperuricaemia

74
Q

What is the pathophysiology of gout?

A

It is caused by deposition of monosodium urate crystals i or near joints; it is associated with raised plasma urate

75
Q

What are the symptoms of gout?

A

Red, tender, hot, swollen joint; most often the MTPJ (big toe), possibly fatigue

76
Q

What are the signs of gout?

A

Possibly a fever, monoarthropathy

77
Q

What tests are used to diagnose gout?

A

Aspiration of joint fluid - polarised light microscopy of fluid shows Needle-shaped Negatively birefringent crystals
Bloods: U&Es, creatinine and eGFR, serum uric acid (usually >600 micromol/L)
X-ray: peri-articular erosions, normal joint space, soft tissue swelling

78
Q

What is the treatment for gout?

A

Dietary advice - reduce alcohol, reduce weight, avoid low dose aspirin
Acute gout: NSAIDs or coxib (e.g. etoricoxib) if contraindicated then colchicine (it’s slower to work), in renal impairment use steroids (PO, IM or intra-articular)
RICE affected joint
Prophylaxis: allopurinol (blocks xanthine oxidase), given if >1 attack in 12 months, there’s tophi or renal stones

79
Q

What is the aetiology of pseudogout?

A

It may be precipitated by dehydration, hyperparathyroidism, hypothyroidism, long term steroid use, haemochromatosis, Wilson’s disease, acromegaly and dialysis

80
Q

What is the pathophysiology of pseudogout?

A

There is inflammation of joints caused by the deposition of calcium pyrophosphate in articular and periarticular tissues

81
Q

What are the symptoms of pseudogout?

A

Acute hot swollen wrist or knee or it presents as an OA type joint

82
Q

What are the signs of pseudogout?

A

No obvious physical signs

83
Q

What tests are used to diagnose pseudogout?

A

Aspirate joint and polarised light microscopy of synovial fluid - rhomboid-shaped Positively birefringent crystal and culture fluid as sepsis can co-exist
Xray - chondrocalcinosis, investigate for underlying causes

84
Q

What is the treatment for pseudogout?

A

Intra-articular steroids, oral steroids, colchicine or NSAIDs
Long term control: correct metabolic abnormalities or underlying cause

85
Q

What is the aetiology of Paget’s disease?

A

Both genetic and environmental factors are thought to play a role; autosomal dominance inheritance has been described.

86
Q

What is the pathophysiology involved in Paget’s disease?

A

There is an increased rate of bone turnover leading to disordered architecture of bone resulting in a loss of strength and elasticity.
There are 3 disease stages: osteolysis, mixed phase and osteosclerosis

87
Q

What are the symptoms of Paget’s disease?

A 
70% of patients are asymptomatic. 
Bone pain (deep, boring pain), fracture
88
Q

What are the signs of Paget’s disease?

A

Bony deformity and enlargement, typically of the pelvis lumbar spine, skull, femur and tibia

89
Q

What tests are used to diagnose Paget’s disease?

A

X-ray - patchy cortical thickening with sclerosis, osteolysis and deformity
Bloods: U&Es, Ca2+ and PO4- are normal; Alk Phos is markedly raised

90
Q

What is the treatment for Paget’s disease?

A

Analgesia and physical aids
Bisphosphonates e.g. alendronic acid
Surgery - joint replacement and osteotomy

91
Q

What are the complications of Paget’s disease?

A

Fracture, spinal cord compression, secondary osteoarthritis

92
Q

What is the aetiology of osteomalacia?

A

Vitamin D deficiency (malabsorption, poor diet, lack of sunlight)

93
Q

What is the pathophysiology involved in osteomalacia?

A

There is impaired bone mineralisation leading to the accumulation of unmineralised osteoid and softening of the bone

94
Q

What are the symptoms of osteomalacia?

A 
Bone pain and tenderness, fractures
In children (rickets): growth retardation, valgus and varus deformities
95
Q

What are the signs of osteomalacia?

A

In adults: proximal myopathy

In children: hypotonia, frontal bossing of the skull

96
Q

What tests are used to diagnose osteomalacia?

A

Bloods: FBC, U&Es, bone profile, PTH, vitamin D
(low Ca, low PO4, low vit D; high alk phos, high PTH)
Bone biopsy - incomplete mineralisation
Xray - pseudofractures, widened, cupped and frayed growth plates in rickets

97
Q

What is the treatment for osteomalacia?

A

Vitamin D replacement
Treatment of pain and any underlying condition
Orthopaedic intervention may be required

98
Q

What is the cause of fibromyalgia?

A

Unknown

99
Q

What is the pathophysiology of fibromyalgia?

A

A theory is that it’s due to central sensitisation where there is increased reactivity of pain sensitive neurones in the brain or spinal cord

100
Q

What are the symptoms of fibromyalgia?

A

Pain - predominantly of the neck and back (can be all over), aggravated by stress, cold and activity, associated with generalised morning stiffness, subjective swelling of extremities, paresthesiae of the hands and feet
Extreme fatigue, non-restorative sleep, headache, diffuse abdominal pain

101
Q

What are the signs of fibromyalgia?

A

There are no obvious physical signs

102
Q

What tests are used to diagnose fibromyalgia?

A

All investigations are normal
Bloods: FBC, TFTs, Vit D, U&Es, ANA, dsDNA, ESR, CRP, CK, Ca
Examination: Anxious, flat affect, obvious discordance between symptoms and signs, multiple tender sites at predictable anatomical sites, skinfold tenderness

103
Q

What is the treatment for fibromyalgia?

A 
Therapy to reduce pain and improve ROM
Acupuncture, chiropractic, trigger point injections, epidural 
Low dose amitriptyline 10-25 mg
Graded aerobic exercise program 
CBT
104
Q

What are the risk factors for septic arthritis?

A

Increasing age, DM, prior joint damage e.g. RA, joint surgery, hip or knee prosthesis +/- skin infection, immunodeficiency e.g. HIV

105
Q

What is the pathophysiology involved in septic arthritis?

A

There is infection in a native or prosthetic joint (or more than one joint) producing inflammation. Can be acute or chronic

106
Q

What organisms cause septic arthritis?

A

S. aureus (most common in adults

Streptococci, Neisseria gonorrhoeae, E. coli (elderly patients, IVDU and ill patients)

107
Q

What are the symptoms of septic arthritis?

A

A single swollen joint with pain on active or passive movement - classic
Can be polyarticular, vomiting (systemic symptom)

108
Q

What are the signs of septic arthritis?

A

A swollen, warm, tender joint

Fever, hypotension, rigors, drainage sinus, abscess around the joint or loosening of the implant

109
Q

What tests are used to diagnose septic arthritis?

A

Bloods: FBC, CRP and ESR, cultures, immunology
Joint aspirate - MC&S of synovial fluid
Imaging - XR, USS, CT, MRI, radionuclide scans

110
Q

What is the treatment of septic arthritis?

A

Surgical drainage and lavage of the joint, debridement and exchange arthroplasty
High dose IV antibiotics (for 2-3 weeks) then oral antibiotics (for 2-4 weeks)

111
Q

What is the aetiology of osteomyelitis?

A

Haematogenous: infection resulting from haematological bacterial seeding from a remote site
Direct: direct contact of infected tissue with bone

112
Q

What are the risk factors for osteomyelitis?

A

Trauma, prosthetic orthopaedic device, DM, peripheral arterial disease, IVDU, HIV/AIDS, sickle cell anaemia, TB, immunosuppression, alcoholism

113
Q

What is the pathophysiology of osteomyelitis?

A

There is infection of the bone marrow, it may spread to the bone cortex and periosteum via the Haversian Canals leading to inflammatory destruction of the bone.

114
Q

What is the epidemiology of osteomyelitis?

A

Haematogenous - children

Direct - adolescents and adults

115
Q

What organisms cause osteomyelitis?

A

S. aureus, H. influenzae, Streptococcus, E. coli, Proteus, Pseudomonas, Coagulase-negative Staphylococcus

116
Q

What are the symptoms of osteomyelitis?

A

Dull pain at the site, may be aggravated by movement

117
Q

What are the signs of osteomyelitis?

A

Fever, rigors, sweats, malaise, tenderness, warmth, erythema, swelling, draining sinus tract, non-healing fracture, deep/large ulcer

118
Q

What tests are used to diagnose osteomyelitis?

A

Bloods: FBC, CRP & ESR, cultures
Imaging: XR (>1-2 weeks before bone changes), MRI (marrow oedema from 3-5 days), CT, nuclear bone scan if metal work makes CT/MRI impossible
Bone biopsy - Micro, PCR and histology

119
Q

What is the treatment for osteomyelitis?

A

Surgical: debridement, hardware placement or removal
Medical: antibiotics tailored to MC&S findings, pending culture - broad spectrum empiric findings
Prolonged duration - 12 months for TB osteomyelitis

Phase 2A (11 decks)

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