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Finals > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

How does ankylosing spondylitis present?

A

it present in late teens, symptoms develop over 3 months. There is lower back and sacroiliac pain, stiffness, worse and night and in the morning and wakes the pt up from sleep. It improves with movement and there are flares and potential vertebral fractures

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2
Q

What are the signs of ankylosing spondylitis?

A

weight loss, fatigue, chest pain, plantar fasciitis, enthesitis, achilles tendonitis, dactylitis, anaemia, anterior uveitis, heart block, aortitis, restrictive lung disease, pulmonary fibrosis and IBD

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3
Q

how is ankylosing spondylitis investigated?

A

Schoeber’s test
inflammatory markers
HLA B27
XR spine
MRI

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4
Q

what are the findings on XR and MRI for AS?

A

XR - squaring of vertebral bodies, subchondral sclerosis and erosions, syndesmophytes, ossification, fusion of facet
MRI - bone marrow oedema

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5
Q

how is AS managed?

A

NSAIDs, steroids, anti TNF, monoclonal ABs, physio, exercise, avoid smoking, bisphosphonates, complication treatment, surgery for deformities

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6
Q

what are the risk factors for osteoarthritis?

A

female, FHx, trauma, age, obesity, occupation

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7
Q

what is the pathophysiology for OA?

A

imbalance between cartilage wear and repair from chondrocytes

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8
Q

how is OA diagnosed?

A

> 45 with pain related to activity, no or little morning stiffness and XR (loss of joint space, osteophytes, subchondral sclerosis, subchondral cysts)

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9
Q

how does OA present?

A

joint pain and stiffness that is worse with activity - deformity, instability, decreased function, Herberden’s and Bouchard’s nodes, weak grip, reduced ROM, squarring of base of thumb

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10
Q

how is OA managed?

A

patient education, weight loss, physio, occupational therapy, orthotics, analgesia, PPI, opiates, IA steroids, joint replacement

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11
Q

what is psoriatic arthritis?

A

it is an inflammatory arthritis that is associated with psoriasis, and is a seronegative spondyloarthropathy

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12
Q

how does psoriatic arthritis present?

A

psoriatic plaques, sacroiliitis, back stiffness, nail pitting and oncholysis, dactylitis, enthesitis, eye disease, aortitis, amyloidosis

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13
Q

how is psoriatic arthritis investigated?

A

PEST tool to screen, XR - periostitis, ankylosis, osteolysis, dactylitis, pencil in cup appearance

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14
Q

what is a complication of psoriatic arthritis?

A

arthritis mutilans - severe - progressive digit shortening and telescopic fingers

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15
Q

how is psoriatic arthritis managed?

A

NSAIDs, DMARDs, antiTNF, usekinumab

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16
Q

what is reactive arthritis?

A

synovitis due to infection - warm, swollen, painful joint
bilateral conjunctivits, anterior uveitis, circinate balanitis

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17
Q

how is reactive arthritis investigated?

A

r/o septic
genetic - HLAB27

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18
Q

how is reactive arthritis managed?

A

aspirate, gram stain, culture and sensitivities, crystal exam, NSAIDS, steroids, DMARDs, antiTNF

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19
Q

how does rheumatoid arthritis present?

A

symmetrical distal polyarthropathy, pain, swelling, stiffness, fatigue, weight loss, flu like, weakness, Z shaped thumb, swan neck and Boutonierres, ulnar deviation, PF, Felty’s, secondary sjorgen’s, bronchiolitis obliterans, anaemia, CV disease, Rheumatoid nodules, CTS, amyloidosis, lymphadenopathy

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20
Q

how is rheumatoid arthritis investigated?

A

clinical, RF, antiCCP, CRP, ESR, XR (joint destruction and deformity, soft tissue swelling, periarticular osteopenia, boney erosions)

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21
Q

how is rheumatoid arthritis managed?

A

steroids, NSAIDs, COX-2i, PPIs, methotrexate, biologics, surgery

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22
Q

what is SLE?

A

it is an inflammatory autoimmune connective tissue disease due to chronic inflammation - relapsing and remitting

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23
Q

how does SLE present?

A

fatigue, weight loss, arthralgia, myalgia, fever, photosensitive malar rash, lymphadenopathy, splenomegaly, SOB, pleuritic chest pain, mouth ulcers, hair loss, Raynaud’s

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24
Q

how is SLE investigated?

A

autoantibodies, FBC, C3 and 4, CRP, ESR, Igs, urinalysis and urine protein creatinine ratio, renal biopsy

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25
Q

what are some complications of SLE?

A

CV disease, infection, anaemia, decreased WCC and platelets, lupus nephritis, neuropsychatric, recurrent miscarriage, preterm birth etc

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26
Q

how is SLE managed?

A

NSAIDs and steroids, hydroxychloroquine, immunosuppressants, biologics

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27
Q

what is systemic sclerosis?

A

it is an autoimmune inflammatory and fibrotic connective tissue disease with limited or diffuse pattern

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28
Q

how does systemic sclerosis present?

A

hard, shiny, tight skin, decreased ROM, ulceration, telangiectasia, calcinosis, Raynauds, swallowing difficulty, acid reflux, oesophagitis, SOB, renal failure, dry cough, HTN

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29
Q

how is systemic sclerosis investigated?

A

nailfold capillaroscopy, autoantibodies (ANA, anticentromere, antiSCl70)

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30
Q

how is systemic sclerosis managed?

A

avoid smoking, cold, occupation and physiotherapy, gently skin stretching and emollients
immunosuppressants and steroids, PPIs, promotilities, analgesia, ABx, anti HTN, supportive

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31
Q

how does polymyalgia rheumatica present?

A

bilateral shoulder pain radiating to the elbows, pelvic girdle pain, worse with movement and interferes with sleep, stiffness in morning, low mood, loss of weight, fatigue, fever, pitting oedema, upper arm tenderness, CTS

32
Q

how is PR investigated?

A

clinical and response to steroids, inflammatory markers, bloods, serum protein electrophoresis, urine

33
Q

how is PR managed?

A

prednisolone, and wean off slowly
bisphosponates, vit D, Ca, PPI

34
Q

how does giant cell arteritis present?

A

severe unilateral headache, scalp tenderness, jaw claudication, visual changes, painless sight loss, fever, muscle aches, weight loss, fatigue, peripheral oedema, loss of appetite

35
Q

how is GCA diagnosed?

A

clinical, ESR >50, TA biopsy, FBC, LFTs, increased CRP, USS

36
Q

how is GCA managed?

A

steroids, aspirin, PPI, vascular surgery

37
Q

what is poly and dermatomyositis?

A

inflammation in the muscles (and skin)

38
Q

how do poly/dermatomyositis present?

A

muscle pain, fatigue, weakness, shoulder and pelvic girdle, gottron lesions, photosensitive erythematous rash, purple rash, periorbital oedema, subcutaneous calcinosis

39
Q

how is poly/dermaomyositis investigated?

A

clinical, increased CK, autoantibodies, EMG, muscle biopsy

40
Q

how are poly/dermatomyositis managed?

A

r/o cancer, corticosteroids, immunosuppressants, azathioprine, IVIg, biologics

41
Q

how does vasculitis present?

A

purpura, joint and muscle pain, peripheral neuropathy, renal impairment, HTN, anterior uveitis and scleritis, fatigue, fever, weight loss, anorexia, anaemia

42
Q

how is vasculitis investigated?

A

CRP, ESR, ANCA (p and c)

43
Q

how is vasculitis managed?

A

steroids, immunosuppressants

44
Q

give some examples of vasculitis?

A

small - HSP, eosinophilic granulomatosis with polyangitis
medium - polyarteritis nodosa, Kawasaki
large - GCA

45
Q

how does antiphospholipid present?

A

livedo reticularis, Libmann Sacks endocarditis, thrombocytopenia

46
Q

how is antiphospholipid investigated?

A

lupus anticoagulants and antibodies, Hx of thrombus and pregnancy complication

47
Q

how is antiphospholipid managed?

A

warfarin, LMWH and aspirin in pregnancy

48
Q

what are complications of antiphospholipid?

A

thrombosis, recurrent miscarriage, MI, CVA, still birth, preeclampsia

49
Q

what is bechets and how does it present?

A

it is an inflammatory condition associated with HLA B51 and presents with mouth ulcers, genital ulcers, skin lesions, eye changes such as uveitis, MSK issues such as stiffness, GI, CNA and venous issues

50
Q

how is bechets investigated?

A

pathergy test - look for weal > 5mm

51
Q

how is bechets managed?

A

steroids, colchicine, anaesthetic topically, immunosuppressants, biologics

52
Q

what is gout?

A

it is a crystal arthropathy - high uric acid - negative birefringent crystals in needle shape and monosodium urate

53
Q

how does gout present?

A

gouty tophi, hot, swollen, tender joint

54
Q

what are the risk factors for gout?

A

male, obesity, high purine intake, alcohol, diuretics, CVD, CKD, FHx

55
Q

how is gout diagnosed?

A

aspiration, XR (maintained joint space, lytic lesions, punches out erosions, sclerotic border with overhanging edges)

56
Q

how is gout managed?

A

flare - NSAIDs, colchicine, steroids
prophylaxis - allopurinol and lifestyle

57
Q

what is pseudogout?

A

it is a crystal arthropathy - calcium pyrophosphate - positive birefringent and rhombus shaped crystals

58
Q

how is pseudogout managed?

A

NSAIDs, colchicine, joint aspiration, steroids, washout/arthrocentesis if severe

59
Q

what is osteoporosis?

A

it is a reduction in BMD with decreased strength and increased risk of fractures

60
Q

what are the risk factors for osteoporosis?

A

female, post menopause, steroids, obesity, increasing age, decreased mobility, SSRIs, PPIs, antiepileptics, antioestrogens, alcohol, smoking

61
Q

how is osteoporosis investigated?

A

FRAX tool, BMD from DEXA

62
Q

how is osteoporosis managed?

A

activity, weight loss, Ca and vit D intake, avoid falls, stop smoking and reduce alcohol, calcichew D3, bisphosphonates, HRT, denosumab, strontium ranelate, raloxifene

63
Q

what is sjorgen’s syndrome?

A

autoimmune affecting the exocrine glands resulting in dry mucous membranes, eyes, and vagina

64
Q

what is sjorgen’s associated with?

A

anti Ro and anti La ABs

65
Q

what are some complications of sjorgen’s?

A

eye disease, oral problems, vaginal problems, pneumonia, bronchiectasis, peripheral neuropathy, renal impairment, NHL, vasculitis

66
Q

how is sjorgen’s investigated and managed?

A

ix - Schilmer test
mx - artificial tears, saliva, vagina lubricants, hydroxychloroquine

67
Q

what is osteomalacia?

A

it is soft bones due to defective mineralisation due to insufficient vitamin D

68
Q

how does osteomalacia present?

A

fatigue, bone pain, muscle weakness, muscle aches, fractures

69
Q

how is osteomalacia investigated?

A

serum 25-hydroxy-vitamin D, ca, P, ALP, PTH, XR, DEXA

70
Q

how is osteomalacia managed?

A

vitamin D (cholecalciferol) - treatment and maintenance

71
Q

what is pagets disease of the bone?

A

it is a disorder of bone turnover - not coordinated - lysis and sclerosis - mishapen and prone to fracture

72
Q

how does pagets present?

A

bone pain and deformity, fractures, hearing loss

73
Q

how is pagets investigaed?

A

XR (bone enlargement and deformity, osteoporosis circumscripta, cotton wool skull, V shaped defects), biochemistry (increased ALP, normal Ca and P)

74
Q

how is pagets managed?

A

bisphosphonate, NSAIDs, Ca, Vit D when on bisphosphonates, surgery, ALP monitoring

75
Q

what are some complications of pagets?

A

osteosarcoma, spinal stenosis, SCC

Finals (16 decks)

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