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Phase 2a Conditions > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is the definition of osteoarthritis?

A

Mechanical and biologic events that destabilise the normal process of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix, and subchondral bone and lead to new bone formation

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2
Q

What is the clinical presentation of osteoarthritis?

A

Joint pain exacerbated by exercise, joint stiffness after rest (gelling), reduced joint functionality, bony deformities (proximal interphalangeal joints (Bouchard nodes) and distal interphalangeal joints (Heberden nodes)), joint malalignment, asymmetrical, crepitus

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3
Q

What are the investigations of osteoarthritis?

A 
o	CRP: slightly elevated
o	Rheumatoid factor and antinuclear antibodies: negative
o	X-ray:
	oLoss of joint space
	oOsteophytes
	oSubchondral sclerosis
	oSubchondral cysts
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4
Q

What is the treatment of osteoarthritis?

A

Exercise, paracetamol, weak opioid, intra-articular corticosteroid injection, arthroplasty, osteotomy, joint fusion

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5
Q

What is the definition of rheumatoid arthritis?

A

Chronic systemic autoimmune disorder which causes symmetrical inflammation of the synovial joints, leading to joint and periarticular tissue destruction

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6
Q

What is the aetiology of rheumatoid arthritis?

A

HLA-DR4

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7
Q

What is the pathophysiology of rheumatoid arthritis?

A

Abnormal, autoimmune response, which targets synovial joints resulting in chronic inflammation and joint damage.

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8
Q

What is the clinical presentation of rheumatoid arthritis?

A

Symmetrical, polyarthritis of the small joints of the hands and feet, joint pain exacerbated by rest or inactivity, joint stiffness in the early morning which lasts longer than an hour

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9
Q

What are the investigations of rheumatoid arthritis?

A

o FBC: normocytic anaemia (anaemia of chronic disease)
o CRP and ESR: elevated
o Rheumatoid factor: positive in 70% (non-specific but high values are more specific)
o Anti-cyclic citrullinated peptide antibody: positive in 80% (highly specific)
o X-rays of the hands and feet:
oLoss of joint space
oErosions
oSoftening of bones (osteopenia)
oSoft tissue swelling

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10
Q

What is the treatment of rheumatoid arthritis?

A

Lifestyle modifications, NSAIDs, DMARDS (methotrexate), TNF-alpha blockers (etanercept), B-cell inhibitors (rituximab), IL-6 blockers (tocilizumab), T cell activation blockers (abatacept), steroids (reduce symptoms and inflammation, and in cases of exacerbation)

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11
Q

What is the definition of gout?

A

Inflammatory arthritis associated with hyperuricaemia and intra-articular monosodium urate crystals

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12
Q

What is the aetiology of gout?

A

Hyperuricaemia (overproduction, increase purine intake, decreased uric acid secretion)

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13
Q

What is the pathophysiology of gout?

A

High urate levels result in supersaturation and crystal formation which deposit in the joints, leading to gout

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14
Q

What is the clinical presentation of gout?

A

Acute onset of severe joint pain, with swelling, effusion, warmth, erythema, and/or tenderness of the involved joint, Tophi (nodular deposits of uric acid crystals in soft tissues of the body)

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15
Q

What are the investigations of gout?

A

o Serum uric acid: elevated
o Arthrocentesis with synovial fluid analysis: elevated WCC and strongly negative birefringent needle-shaped monosodium urate crystals under polarised light

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16
Q

What is the treatment of gout?

A

o Acute attacks: NSAIDS, colchicine, corticosteroids

o Long-term: lifestyle modifications, allopurinol (xanthine oxidate inhibitor)

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17
Q

What is the definition of calcium pyrophosphate deposition disease?

A

Inflammatory arthritis associated with intra-articular calcium pyrophosphate crystals

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18
Q

What is the pathophysiology of calcium pyrophosphate deposition disease?

A

Excess pyrophosphate production by chondrocytes causes local CCP supersaturation and crystal formation

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19
Q

What is the clinical presentation of calcium pyrophosphate deposition disease?

A

o Acute: Acute onset of severe joint pain, with swelling, effusion, warmth, erythema, and/or tenderness of the involved joint, fever, malaise
o Chronic: Severe pain, stiffness, crepitus, and loss of function

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20
Q

What are the investigations of calcium pyrophosphate deposition disease?

A

o Arthrocentesis with synovial fluid analysis: intracellular or extracellular positively birefringent rhomboid-shaped crystals under polarized light
o X-ray: cartilage calcification

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21
Q

What is the treatment of calcium pyrophosphate deposition disease?

A

Symptomatic (high dose NSAIDs, colchicine, corticosteroids)

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22
Q

What is the definition of osteoporosis?

A

Metabolic bone disease characterised by a generalise reduction in bone mass, increased bone fragility and predisposition to a fracture

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23
Q

What is the aetiology of osteoporosis?

A

Steroid use, hyperthyroidism and hyperparathyroidism, alcohol and tobacco, testosterone decrease, early menopause, renal or liver failure, erosive/inflammatory bone disease, dietary calcium decrease, diabetes mellitus
(SHATTERED)

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24
Q

What is the clinical presentation of osteoporosis?

A

Asymptomatic until a fracture occurs

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25
Q

What are the investigations of osteoporosis?

A

o X-ray: fracture

o Bone densitometry DEXA scan: < -2.5

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26
Q

What is the treatment of osteoporosis?

A

Lifestyle modifications, bisphosphonates (alendronate), hormone replacement therapy, teriparatide

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27
Q

What is the definition of ankylosing spondylitis ?

A

Seronegative, chronic, multisystem inflammatory disorder involving primarily the sacroiliac joints and axial skeleton

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28
Q

What is the aetiology of ankylosing spondylitis ?

A

HLA-B27

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29
Q

What is the clinical presentation of ankylosing spondylitis?

A

Inflammatory back pain (worse at night) and stiffness (morning stiffness relieved by exercise), sacroiliac inflammation, enthesitis (especially Achilles’ tendonitis and plantar fasciitis), iritis/uveitis

30
Q

What are the investigations of ankylosing spondylitis ?

A

o FBC: normocytic anaemia
o CRP and ESR: elevated
o X-ray: erosions, syndesmophytes, progressive calcification of syndesmophytes can lead to bamboo spine (fusion of spinous processes), fusion of the sacroiliac joints
o HLA-B27 genetic test: positive
o Shober’s Test: assesses mobility of the spine

31
Q

What is the treatment of ankylosing spondylitis ?

A

Physiotherapy, NSAIDs, DMARDs (methotrexate), TNF-alpha blockers (etanercept), local steroid injections

32
Q

What is the clinical presentation of psoriatic arthritis?

A

Symmetrical polyarthritis of the DIP joints

33
Q

What are the investigations of psoriatic arthritis?

A

X-ray: erosive changes, pencil-in-cup deformity

34
Q

What is the treatment of psoriatic arthritis?

A

NSAIDs, DMARDs (methotrexate), TNF-alpha blockers (etanercept)

35
Q

What is the definition of reactive arthritis?

A

Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually GI or genital

36
Q

What is the aetiology of reactive arthritis?

A

Salmonella, shigella, chlamydia

37
Q

What is the clinical presentation of reactive arthritis?

A

Pain and stiffness, enthesitis, keratoderma blennorrhagia (brown, raised plaques on soles and palms)

38
Q

What are the investigations of reactive arthritis?

A

o CRP and ESR: elevated
o Infectious serology
o X-ray: enthesitis with periosteal reactions

39
Q

What is the treatment of reactive arthritis?

A

NSAIDs, local steroid injections, DMARDs (methotrexate (if symptoms last > 6 months)

40
Q

What is the definition of septic arthritis?

A

Infection within a joint (knee > hip > shoulder)

41
Q

What is the aetiology of septic arthritis?

A

S.aureus, N.gonorrhoeae, S.epidermis

42
Q

What is the clinical presentation of septic arthritis?

A

Hot, red, swollen joint, fever

43
Q

What are the investigations of septic arthritis?

A

o Joint aspiration for fluid microscopy: neutrophils

o Joint fluid culture

44
Q

What is the treatment of septic arthritis?

A

Joint drainage, broad spectrum antibiotics, specific antibiotics (usually flucloxacillin, vancomycin or ceftriaxone)

45
Q

What is the definition of osteomyelitis?

A

Infection of the bone and/or bone marrow

46
Q

What is the aetiology of osteomyelitis?

A

S.aureus, pseudomonas, E.coli, S.epidermidis, salmonella (sickle cell disease)

47
Q

What is the clinical presentation of osteomyelitis?

A

Pain, swelling, tenderness, warmth, erythema, fever, sinus tracts (chronic osteomyelitis)

48
Q

What are the investigations of osteomyelitis?

A

o FBC: elevated WCC
o CRP and ECR: elevated
o Bone biopsy: inflammatory cell, oedema, vascular congestion, necrotic bone (sequetra), new bone formation, neutrophil exudates

49
Q

What is the treatment of osteomyelitis ?

A

IV antibiotics (usually flucloxacillin), surgical debridement

50
Q

What is the definition of Systemic Lupus Erythematosus?

A

Multisystem autoimmune disease characterised by autoantibody production against nuclear and cytoplasmic autoantigens

51
Q

What is the aetiology of Systemic Lupus Erythematosus?

A

Defective phagocytosis

52
Q

What is the clinical presentation of Systemic Lupus Erythematosus?

A

Butterfly rash, mouth ulcer, Reynard’s phenomenon, fatigue, depression, weight loss

53
Q

What are the investigations of Systemic Lupus Erythematosus?

A

Auto-antibodies (ANA or Anti-dsDNA): positive

54
Q

What is the treatment of Systemic Lupus Erythematosus?

A

UV protection, screening for organ involvement, prednisolone (flares), DMARDs (hydroxychloroquine), NSAIDs

55
Q

What is the definition of osteomalacia?

A

Inadequate mineralisation of bone

56
Q

What is the aetiology of osteomalacia?

A

Calcium deficiency (vitamin D deficiency)

57
Q

What is the clinical presentation of osteomalacia?

A

Bone pain and tenderness, fractures, proximal myopathy

58
Q

What are the investigations of osteomalacia?

A 
o	Bone biopsy: incomplete mineralisation
o	Serum calcium: low
o	Serum phosphate: low
o	Serum alkaline phosphatase: raised
o	X-ray: loss of cortical bone
59
Q

What is the treatment of osteomalacia?

A

Vitamin D supplementation

60
Q

What is the definition of giant cell arteritis?

A

Vasculitis of head and neck arteries

61
Q

What is the clinical presentation of giant cell arteritis?

A

Headache, scalp tenderness, jaw claudication, acute blindness, malaise

62
Q

What are the investigations of giant cell arteritis?

A

Temporal artery biopsy: lymphohistiocytic infiltrate

63
Q

What is the treatment of giant cell arteritis?

A

Immediate prednisolone, methotrexate, osteoporosis prophylaxis

64
Q

What is the definition of Wegener’s Granulomatosis?

A

Systemic ANCA-associated vasculitis

65
Q

What is the clinical presentation of Wegener’s Granulomatosis?

A

o Upper respiratory tract: sinusitis, otitis, nasal crusting
o Lungs: pulmonary haemorrhage/nodules, inflammatory infiltrates
o Kidney: glomerulonephritis
o Skin: ulcers, purpura, nodules
o Eyes: uveitis, scleritis, episcleritis

66
Q

What are the investigations of Wegener’s Granulomatosis?

A

o c-ANCA: positive
o Urinalysis: haematuria, proteinuria
o Renal biopsy: necrotising glomerulonephritis
o Lung biopsy: necrotising granulomatous inflammation and necrotising vasculitis

67
Q

What is the treatment of Wegener’s Granulomatosis?

A

Aggressive immunosuppression

68
Q

What is the definition of Paget’s Disease?

A

Metabolic bone disease characterised by excessive chaotic bone turnover in localised parts of the skeleton

69
Q

What is the pathophysiology of Paget’s Disease?

A

Exaggerated osteoblast activity which leads to grossly thickened, poorly organised, weak bone, which is prone to deformity and pathological fracture

70
Q

What is the clinical presentation of Paget’s Disease?

A

Asymptomatic, bone pain, deafness, fractures, bowing of the femur and tibia

71
Q

What are the investigations of Paget’s Disease?

A

o Serum alkaline phosphatase: elevated

o X-ray: localised enlargement of bone

72
Q

What is the treatment of Paget’s Disease?

A

Bisphosphonates, analgesia

Phase 2a Conditions (9 decks)

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