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Phase 2a - Systems > MSK/Rheumatology > Flashcards

MSK/Rheumatology Flashcards

1
Q

describe the disease process behind osteoarthritis

A

general wear and tear, a chronic degenerative disease.
loss of articular cartilage - exposed bone becomes sclerotic.
attempts at repair produces osteophytes (nodules).

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2
Q

describe the usual onset of osteoarthritis

A

> 50yrs, slow and gradual

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3
Q

describe the pattern of joint involvement of osteoarthritis

A

asymmetrical.

finger joints, thumbs + weight bearing joints (hip/knee)

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4
Q

what hand changes are common to osteoarthritis?

A

Heberden’s (DIP) + Bouchard’s (PIP) nodes.

NO swelling.

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5
Q

what systemic features are present in osteoarthritis?

A

NONE

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6
Q

describe the character of the pain from osteoarthritis

A

increases with movement, worse at the end of the day.

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7
Q

what would the lab findings be in osteoarthrits?

A

RhF -ve, ANA -ve, raised CRP, normal ESR

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8
Q

what would be the radiological findings in osteoarthritis?

A

LOSS.

Loss of joint space, Osteophytes, Subchondral cysts, Sclerosis.

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9
Q

what main features would you use to differentiate between rheumatoid and osteoarthritis?

A

pattern of joint involvement.
absence of systemic features of OA.
RA has marked early morning stiffness lasting >60mins.

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10
Q

how would you treat osteoarthritis?

A

exercise for local muscle strength/aerobic fitness.
analgesia - paracetamol ± topical NSAIDs.
codeine/short-term oral NSAID (+PPI).
intra-articular steroid injections.
joint replacement surgery.

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11
Q

describe the disease process behind rheumatoid arthritis

A

chronic systemic inflammatory, autoimmune disease.
production of cytokines (IL-1,2,4,6,8 + TNFalpha) by T cells = inflammation.
local rheumatoid factor production.
synovitis => pannus formation => pannus destroys articular cartilage and subchondral bone.

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12
Q

describe the usual onset of rheumatoid arthritis

A

aged 30-50. rapid, within a year.

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13
Q

describe the pattern of joints affected by rheumatoid arthritis

A

symmetrical.
small and large joints on both sides.
>3 affected, hands usually involved.

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14
Q

what hand changes are common to rheumatoid arthritis?

A

swan neck deformity, Boutonniere’s deformity, Z thumb, ulnar deviation, hot swollen joints.

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15
Q

what systemic features are present in rheumatoid arthritis?

A

elbow and lung nodules, vasculitis, pericarditis, carpal tunnel, Sjorgen’s, Raynaud’s, lymphadenopathy, fever, fatigue

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16
Q

describe the character of the pain from rheumatoid arthritis

A

morning stiffness >60 mins.

pain is accompanied by stiffness.

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17
Q

what would the lab findings be in rheumatoid arthritis?

A

RhF +ve, anti-CCP +ve (highly specific for RA), raised CRP, raised ESR

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18
Q

what would be the radiological findings in rheumatoid arthritis?

A

LESS.

Loss of joint space, Erosions, Soft bone, Swelling of soft tissue.

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19
Q

how would you treat rheumatoid arthritis?

A

DMARDs - sulfasalazine, methotrexate.
Biological agents - infliximab, rituximab, tocilizumab etc.
NSAIDs - diclofenac, ibuprofen.
Steroids for flare ups (IM methylprednisolone).

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20
Q

what is the diagnostic criteria for rheumatoid arthritis?

A 
need 4 out of 7:
morning stiffness >1h.
3+ joints affected.
arthritis in hand joints.
symmetrical.
rheumatoid nodules.
RhF+ve.
radiological changes.
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21
Q

what rheumatoid arthritis treatment requires regular pregnancy tests in women of child-bearing age and why?

A

methotrexate - it’s a folic acid antagonist, risk of neural tube defects is high.

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22
Q

what disease lowers your risk of developing osteoarthritis?

A

osteoporosis

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23
Q

define osteoporosis, in general terms

A

low bone mass and micro-architectural deterioration leading to bone fragility and increased fracture risk

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24
Q

give 5 risk factors for osteoporosis

A

age, parental history, alcohol (>4units/day), RA, BMI less than 19, steroids (5mg/d prednisolone).
Hyperthyroidism, hyperparathyroidism, hypercalciuria.
Alcohol and tobacco use.
Thin (BMI less than 19)

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25
Q

what fractures might alert you that a patient could have osteoporosis?

A

thoracic and lumbar vertebrae.
proximal femur.
distal radius (Colles’ fracture).

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26
Q

what is the gold standard investigation for osteoporosis?

A

DEXA bone scan.

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27
Q

what lifestyle measures should an osteoporosis patient take?

A

smoking cessation, low alcohol intake, weight bearing exercises, calcium and vit D rich diet, home help.

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28
Q

how would you medically treat osteoporosis?

A

bisphophonates e.g. alendronate, zolendronate
calcium + vit D.
strontium ranelate - if intolerant to bisphosphonates.

HRT is preventative, but not used to treat.

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29
Q

explain the pathophysiology of SLE

A

apoptotic cells and cell fragments aren’t cleared efficiently by phagocytes - taken to lymph nodes, taken up by APCs.
APCs present self-antigens from these fragments to T cells, activating B cell proliferation and production of autoantibodies.

Leads to antibody formation, immune complex deposition, complement activation and influx of neutrophils = clinical manifestations.

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30
Q

what 3 genes is SLE associated with?

A

HLA-B8, DR2, DR3

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31
Q

what are the WHO diagnostic criteria for SLE?

A

need 4 out of 11 - SOAP BRAIN MD

Serositis
Oral ulcers
ANA +ve
Photosensitivity

Blood disorders 
Renal disorder
Arthritis
Immunological disorder
Neurological disorder

Malar rash
Discoid rash

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32
Q

what autoantibodies might you find in a patient with SLE?

A

ANA, anti-Ro, anti-dsDNA, anti-La

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33
Q

what histological features might you see on investigation of a patient with SLE?

A

deposition of IgG and complement in kidneys and skin

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34
Q

give 6 symptoms of SLE

A

Raynaud’s, chest pain, dyspnoea, depression, fatigue, dry eyes/mouth, abdominal pain, joint pain, muscle pain, polyneuropathy/sensory loss

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35
Q

give 6 signs of SLE

A

malar rash, discoid rash, photosensitivity rash, purpura, weight loss, lymphadenopathy, oral/nasal ulcers, bruising, proteinuria, fever, pallor due to anaemia

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36
Q

how might you monitor SLE activity?

A

anti-dsDNA antibody titres.
complement - low C3/C4.
ESR.

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37
Q

what ESR/CRP results would make you think of SLE?

A

multisystem disorder with raised ESR but normal CRP

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38
Q

how would you manage a severe flare of SLE?

A

IV cyclophosphamide and high-dose prednisolone.

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39
Q

how would you manage the cutaneous symptoms of SLE?

A

topical steroids, strong sunblock/avoid sun exposure

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40
Q

describe maintenance treatment for SLE

A

NSAIDs, hydroxychloroquine, low-dose steroids, azathioprine/methotrexate or mycophenolate

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41
Q

how would lupus nephritis be managed?

A

needs more intense immunosuppression than SLE:

cyclophosphamide/mycophenolate

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42
Q

what are the 4 characteristic clinical features of anti-phospholipid syndrome?

A

coagulation defect, livedo reticularis (blue/pink mottling), obstetric problems (miscarriages), thrombocytopenia (bleeding)

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43
Q

what is antiphospholipid syndrome?

A

associated with SLE, or a primary disease.

there are antiphospholipid antibodies causing CLOTS - leads to the features of miscarriages, livedo reticularis etc

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44
Q

what are the 3 diagnostic investigations to be carried out in antiphospholipid syndrome?

A

lupus anticoagulation test, anti-beta2 glycoprotein test, anticardiolipin test.

indicate +ve blood test for antiphospholipid antibodies.

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45
Q

how would you manage a patient with antiphospholipid syndrome?

A

warfarin, if there’s recurrent thrombosis.

if high IgG but asymptomatic, then give aspirin/clopidogrel as prophylaxis.

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46
Q

what 2 genes are associated with Sjogren’s syndrome?

A

HLA-B8/DR3

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47
Q

give 2 secondary causes of Sjogren’s

A

SLE, RA, scleroderma

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48
Q

what is the characteristic feature of Sjogren’s and where is it seen?

A

dryness - eyes, mouth (vagina) - and parotid enlargement.

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49
Q

what tests would you do to diagnose Sjogren’s?

A

Schirmer’s test - filter paper on inside of eyelid for 5 mins, if less than 5mm moistened - positive for Sjogrens

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50
Q

how would you treat Sjogrens?

A

artificial tears and saliva replacement.

NSAIDs and hydroxycholoroquine for arthralgia.

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51
Q

explain the pathophysiology behind systemic sclerosis

A

autoimmune dysfunction causes overproduction of collagen.
T cells accumulate in skin and secrete cytokines which stimulate collagen deposition and stimulate fibroblasts.

scleroderma (skin fibrosis) + vascular disease.

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52
Q

what are the features of CREST syndrome?

A 
Calcinosis of subcutaneous tissue.
Raynaud's.
oEsophageal and gut dysmotility.
Sclerodactyly - swollen, tight digits.
Telangiectasia (spider veins).
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53
Q

what parts of the body is skin involvement limited to in CREST syndrome?

A

hands, feet and face

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54
Q

what parts of the body are affected by diffuse systemic sclerosis?

A

diffuse skin involvement.

heart, lungs, GI tract and kidneys all involved.

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55
Q

what antibodies might you find on investigation of a patient with systemic sclerosis?

A

ANA, RhF, ACA, anti-topoisomerase, anti-RNA polymerase

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56
Q

how would you treat systemic sclerosis?

A

IV cyclophosphamide.

ACEi/ARBs reduce risk of renal problems.

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57
Q

what is myositis?

A

inflammation of striated muscle

58
Q

what are the features of polymyositis?

A

progressive symmetrical proximal muscle weakness with myalgia ± arthralgia.
muscle weakness causes dysphagia, dysphonia (e.g. hoarseness), respiratory weakness.

59
Q

give 3 features of dermatomyositis

A

macular rash, lilac-purple rash on eyelids with oedema, nailfold erythema, roughened red papules over knuckles/elbows/knees, subcutaneous calcification

60
Q

give 3 extra-muscular signs of polymyositis/dermatomyositis

A

fever, arthralgia, Raynaud’s, interstitial lung fibrosis, myocardial involvement

61
Q

what investigation is needed to confirm a diagnosis of polymyositis/dermatomyositis?

A

muscle biopsy

62
Q

what would blood tests show in a patient with polymyositis/dermatomyositis?

A 
muscle enzymes (ALT, AST, LDH, CK, aldolase) are raised in plasma.
autoantibodies - anti-Mi2, antiJo1.
63
Q

how would you manage polymyositis/dermatomyositis?

A

oral prednisolone.
resistant disease - azathioprine/methotrexate.
screen for malignancy

64
Q

give 4 causes of Raynaud’s phenomenon

A

SLE, systemic sclerosis, RA, polycythaemia rubra vera, hypothyroidism, Buerger’s disease.

primary = Raynaud’s disease

65
Q

explain the pathophysiology of Raynaud’s

A

peripheral digital ischaemia due to vasospasm precipitated by cold and relieved by heat

66
Q

what are the clinical features of Raynaud’s?

A

skin pallor, then cyanosis, then hot and red.

numbness then burning sensation and severe pain due to hyperaemia.

67
Q

how would you manage a patient with Raynaud’s?

A

keep hands and feet warm - gloves, heating pads.
smoking cessation.
nifedipine - CCB, vasodilates.

68
Q

what class of drugs should be stopped in patients with Raynaud’s?

A

beta blockers

69
Q

what gene is associated with ankylosing spondylitis?

A

HLA-B27

70
Q

what is ankylosing spondylitis?

A

chronic inflammatory disease of spine and sacroiliac joints, with unknown aetiology

71
Q

does ankylosing spondylitis more commonly affect men or women?

A

men

72
Q

describe the clinical features of ankylosing spondylitis

A

back pain.

progressive loss of spinal movement.
severe disease - kyphosis and neck hyperextension - question mark posture.

also - enthesitis, costochondritis, fatigue, acute iritis.

73
Q

describe the back pain experienced in ankylosing spondylitis

A

radiating from sacroiliac joints to hips/buttocks.

worse at night, improves towards end of day.

74
Q

name 2 diseases associated with ankylosing spondylitis

A

osteoporosis
aortic valve incompetence
pulmonary fibrosis

75
Q

what antibody is NEVER seen with ankylosing spondylitis?

A

rheumatoid factor

76
Q

how would you treat ankylosing spondylitis?

A

no cure.
NSAIDs, exercises.
TNF alpha blocker (etanercept) if NSAIDs fail.

77
Q

give 4 clinical features of psoriatic arthritis

A

symmetrical polyarthritis, affects DIP joints, nail dystrophy, dactylitis, asymmetrical oligoarthritis, spinal arthritis, acneiform rashes, palmo-plantar pustulosis

78
Q

how would you treat psoriatic arthritis?

A

NSAIDs - but can worsen skin lesions.

sulfasalazine or methotrexate.

79
Q

what is reactive arthritis?

A

a sterile arthritis that tends to follow dysentery or UTIs

80
Q

give some possible causative organisms of reactive arthritis

A

campylobacter, salmonella, shigella.

chlamydia, ureaplasma

81
Q

what are the 3 cardinal symptoms of reactive arthritis? aka Reiter’s syndrome

A

urethritis, arthritis and conjunctivitis

82
Q

list some clinical features of reactive arthritis

A

asymmetrical joint involvement, generally of lower limbs.
skin lesions may resemble psoriasis.
iritis.
keratoderma blenorrhagica (bown plaques on soles and palms).
mouth ulcers.
enthesitis.

83
Q

how would you treat reactive arthritis?

A

methotrexate and sulfasalazine

84
Q

what is vasculitis?

A

inflammatory disorder of blood vessel walls, causing destruction (aneurysm/rupture) or stenosis.
affect different vessels/organs - all feature overwhelming fatigue and raised ESR/CRP.

85
Q

what is the underlying pathology of polyarteritis nodosa?

A

a vasculitis - fibrinoid necrosis of vessel walls with microaneurysm formation, thrombosis and infarction in medium sized arteries.

86
Q

list some features of polyarteritis nodosa

A

general - fever, malaise, weight loss, myalgia.
skin - purpura, livedo reticularis, ulcers, gangrene.
cardiac - angina, HF, pericarditis.
renal - hypertension, haematuria, renal failure.
GI - pain or perforation, malabsorption.
GU - orchitis.

87
Q

what investigation would you carry out in polyarteritis nodosa?

A

angiography for liver, kidney and intestine microaneurysm.

bloods - high WCC, anaemia, raised ESR and CRP.

88
Q

how would you treat polyarteritis nodosa?

A

prednisolone + cyclophosphamide.

89
Q

what hepatic disease is associated with PAN?

A

hepatitis B.

90
Q

describe the clinical features of polymyalgia rheumatica

A

age >50yrs.
subacute (less than 2wks) of bilateral aching, tenderness and morning stiffness in shoulder and proximal limb muscles.

± mild polyarthritis, tenosynovitis and carpal tunnel syndrome.
± weight loss, fatigue, fever, anorexia

NO weakness.

91
Q

what is a common presenting problem in patients with polymyalgia rheumatica?

A

giant cell temporal arteritis

92
Q

how would you treat polymyalgia rheumatica?

A

prednisolone.

PPI and alendronate for gut and bone protection.

93
Q

how would you differentiate polymyalgia rheumatica from a myositis/myopathy?

A

creatinine kinase levels are NORMAL in PMR - would be raised in myositis/myopathy.

94
Q

give 3 precipitating factors of an acute gout attack

A

excess alcohol, shellfish, sudden cessation/starting of gout therapy, trauma, surgery, infection, dehydration

95
Q

give 3 risk factors for gout

A

high alcohol intake, obesity, >50yo, red meat intake, FHx, thiazide diuretics

96
Q

what is gout?

A

deposition of monosodium urate crystals in and near joints.

97
Q

describe how a patient might present with an acute attack of gout

A

hot, swollen, very very painful joint, usually the big toe

98
Q

what investigation might you carry out in gout, and what might you see?

A

polarised light microscopy of synovial fluid - negatively birefringent needle crystals

99
Q

how would you manage an acute gout attack?

A

high-dose NSAID or coxib (diclofenac, etoricoxib) and colchicine

100
Q

how would you prevent recurrent gout attacks?

A

start allopurinol, but wait until 3 wks after the attack (can precipitate an attack intially!) - xanthine oxidase inhibitor.

lose weight, avoid long fasts, cut down alcohol excess and red meat consumption

101
Q

give some chronic features of gout

A

tophi (smooth white deposits on skin) on the ears, fingers or achilles tendon.
chronic joint pain, tophi may ulcerate.

102
Q

what crystal is deposited in pseudo-gout? how does this appear on polarised light microscopy of synovial fluid?

A

calcium pyrophosphate

positively birefringent rhomboid crystals

103
Q

how does pseudo-gout present differently from gout?

A

usually occurs in larger joints (e.g. knee) - but pain is similar

104
Q

what disease must you assume a patient presenting with acute pseudo-gout has until proven otherwise?

A

septic arthritis

105
Q

how would you treat pseudo-gout?

A

NSAIDs or colchicines, aspiration of joint.

corticosteroid injection, if no infection.

106
Q

list 3 of the ‘yellow flag’ psychosocial risk factors for developing persisting chronic pain

A

belief that pain and activity are harmful.
sickness behaviours e.g. extended rest.
social withdrawal.
emotional problems e.g. low mood, anxiety or stress.
problems at work.
problems claiming compensation/time off from work.
overprotective family or lack of support.
inappropriate expectations of treatment.

107
Q

list 3 risk factors for chronic pain.

A

‘yellow flag’ psychosocial factors.
also:
female sex, middle age, low household income, divorced, low educational status.

108
Q

list 2 other problems that fibromyalgia is associated with

A

chronic fatigue syndrome, irritable bowel syndrome, chronic headaches syndrome.

109
Q

how long must symptoms have lasted for to diagnose a patient with fibromyalgia?

A

over 3 months

110
Q

give 3 clinical features of fibromyalgia

A

presence of pain on palpation of 11/18 tender points, morning stiffness, poor concentration, low mood and sleep disturbance

111
Q

what would you expect to see on investigation of a patient with fibromyalgia?

A

nothing - all would be normal.

diagnosis of exclusion.

112
Q

how would you manage fibromyalgia?

A

CBT, education, structured exercise programmes.
amitriptyline - tricyclic antidepressant.
tramadol may help pain.
NOT steroids or NSAIDs.

113
Q

describe the disease course of mechanical lower back pain

A

starts suddenly, often precipitated by injury (e.g. lifting heavy boxes at work), usually self-limiting, may be recurrent.

114
Q

give 3 signs you may see on examination of a patient with mechanical lower back pain

A

scoliosis, stiff back, visible and palpable muscular spasm causing local pain and tenderness.

115
Q

list 5 red flag features of mechanical lower back pain that would prompt you to investigate it

A

aged 20-55.
if pain is constant, progressive.
worse when supine.
morning stiffness.
bilateral/alternating leg pain (cauda equina!)
unrelieved by rest, night pain, thoracic pain.
PMHx of TB, HIV, immunosuppression, infection, malignancy.
fever, night sweats, weight loss, abdominal mass, neurological disturbance, leg claudication/weakness/numbness, major trauma.

116
Q

how would you manage a patient with mechanical lower back pain if there was no sinister cause?

A

adequate analgesia - paracetamol, codeine.

avoid bed rest - encourage exercise and physiotherapy.

117
Q

what is myeloma?

A

abnormal proliferation of a single clone of plasma cells, leading to production of monoclonal immunoglobulins (IgG or IgA).

118
Q

what would be found in the urine of someone with myeloma?

A

Bence Jones proteins - paraproteinaemia leads to excretion of kappa/lambda light chains in urine

119
Q

describe the clinical features caused by osteolytic bone lesions in myeloma

A

backache, pathological fractures (e.g. long bone, ribs), vertebral collapse.
hypercalcaemia.

120
Q

what other clinical features, apart from those associated with osteolytic bone lesions, may be present in a myeloma patient?

A

anaemia, neutropenia or thrombocytopenia (due to marrow infiltration) - anaemia symptoms, infections and bleeding.
renal impairment due to light chain deposition in tubules.

121
Q

what are the diagnostic criteria for myeloma?

A

2 out of 3:
paraproteinaemia on serum protein immunofixation or Bence Jones proteins in urine.
radiological (MRI/CT) evidence of lytic bone lesions.
increase in bone marrow plasma cells - bone marrow aspiration/biopsy

122
Q

what would blood tests show in a myeloma patient?

A

normocytic, normochromic anaemia, thrombocytopaenia, leucopenia.
ESR high.
hypercalcaemia.

123
Q

how would myeloma be treated?

A

chemo - melphalan + prednisolone, or VAD (vancristin, adriamycin + dexamethasone) if fit.
supportive -
analgesia, bisphosphonates, local radiotherapy etc

124
Q

what is the most likely causative organism in a case of septic arthritis? where does it come from?

A

staph aureus - from pneumonia or skin infection

125
Q

give 3 clinical features of septic arthritis

A

hot, swollen, painful and immobile joint, can affect more than one joint

126
Q

give 3 risk factors for septic arthritis

A

underlying joint disease, diabetes mellitus, immunosuppression, renal failure, prosthetic joints, recent surgery, IVDU, >80yo.

127
Q

what investigations would you perform in septic arthritis?

A

urgent joint fluid aspiration for MC&S ± blood cultures and skin swab

128
Q

before your cultures come back, what antibiotic would you prescribe to treat septic arthritis? if it came back as MRSA +ve, what would you give?

A

flucloxacillin.

vancomycin for MRSA.

129
Q

what is the main causative organism for osteomyelitis? name 2 others

A

main - staph aureus.

H influenzae, Salmonella

130
Q

what are the clinical features of osteomyelitis?

A

fever, local pain, erythema. sinus formation if chronic.

131
Q

how would you investigate osteomyelitis?

A

CT/MRI or bone scan

132
Q

if a patient with sickle cell anaemia presented with osteomyelitis, what organism would you suspect?

A

salmonella

133
Q

how would you treat osteomyelitis?

A

flucloxacillin + immobilisation of joint + fusidic acid

134
Q

name 2 bisphosphonates. what are they used to treat?

A

alenronate, zoledronate, disodium pamidronate.
used for osteoporosis, severe hypercalcaemia of malignancy, myeloma and breast cancer bone metastases to reduce pathological fractures.

135
Q

how do bisphosphonates work?

A

reduce bone turnover by inhibiting osteoclasts and promoting apoptosis.
reduce bone loss and improve bone mass.

136
Q

what class of drug is allopurinol? how does it work?

A

xanthine oxidase inhibitor.
blocks metabolism of xanthine (produced from purines) to uric acid.
results in lower plasma uric acid concentrations and reduces precipitation of uric acid in the joints or kidneys.
useful in gout and to prevent kidney stones.

137
Q

how does cholchicine work?

A

GOUT.
inhibits microtubule polymerisation by binding to tubulin, which is essential for mitosis.
also inhibits neutrophil motility and activity, which leads to a net anti-inflammatory effect which is useful for acute attacks.

138
Q

how does methotrexate work as a treatment for rheumatoid arthritis?

A

inhibits dihydrofolate reductase, which converts dietary folic acid to tetrahydrofolate (FH4), which is required for DNA and protein synthesis.
lack of FH4 prevents cellular replication.
also has anti-inflammatory and immunosuppressive effects, mediated by IL-6 and -8 and TNF-alpha.

139
Q

what aminosalicylate is a treatment option for rheumatoid arthritis and how does it work?

A

sulfasalazine - DMARD.

releases 5-ASA, which has anti-inflammatory and immunosuppressive effects.

140
Q

what is strontium ranelate used to treat?

A

severe osteoporosis

Phase 2a - Systems (18 decks)

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