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1 - Finals > 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

1) physio, psych, podiatry
2) DMARDs - MTX or sulfasalazine (other options = chloroquine, leflunomide, sulfasalazine, gold)
adjunct - corticosteroid (low dose pred) + NSAID (lowest effective dose) short term

3) biologics e.g. rituximab, tocilizumab, abatacept - expensive, only use if failure to respond to 2 DMARDs after 2 trials of 6/12

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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 some risk factors for secondary osteoporosis

A

SHATTERED + FRAX (parental #) + SEDENTARY (decreased loading):
S - steroids + Cushing’s
H = hyperthyroid, hypercalciuria
A - alcohol and tobacco
T - thin (BMI<19) or anorexia
T - testosterone decreased (primary hypogonadism or anti-androgens e.g. in prostate Ca Rx)
E - early menopause (<45y)
R - renal/liver function - renal osteodystrophy in CKD, chronic liver disease
E - erosive/inflammatory disease - RA, MM, metastasis
D - dietary calcium/T1DM - malabsorption, malnutrition

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25
Q

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

A

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

usually asymptomatic until #, may notice loss of height, kyphosis

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26
Q

what is the gold standard investigation for osteoporosis? what is the T score?

A

DEXA bone scan for bone mineral density (BMD)
T score and Z score:
osteoporosis = -2.5
osteopaenia = -1 to -2.5
T score compares to normal adult, Z score compares to patient of same age group (more useful in kids, not that helpful in elderly).
standard deviations.

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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, balance work (tai chi, physio), falls prevention - medication review!

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28
Q

how would you medically treat osteoporosis?

A

bisphophonates e.g. alendronate, zolendronate
calcium + vit D (AdCal D3, Accrete D3)
if low testosterone - add.

strontium ranelate or denosumab (monoclonal ab to RANKL) - if intolerant to bisphosphonates.

HRT is preventative, but not used to treat.

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29
Q

explain the pathophysiology of SLE

A

inflammatory, multisystem autoimmune disease with antinuclear antibodies, usually affecting skin and joints.

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

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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.

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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

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60
Q

give 3 extra-muscular signs of polymyositis/dermatomyositis

A

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

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61
Q

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

A

muscle biopsy

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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.
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63
Q

how would you manage polymyositis/dermatomyositis?

A

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

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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

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65
Q

explain the pathophysiology of Raynaud’s

A

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

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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.

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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.

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68
Q

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

A

beta blockers

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69
Q

what gene is associated with ankylosing spondylitis?

A

HLA-B27

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70
Q

what is ankylosing spondylitis?

A

seronegative spondylarthopathy of axial skelent - spine and sacroiliac joints.

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71
Q

does ankylosing spondylitis more commonly affect men or women?

A

men

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72
Q

describe the clinical features of ankylosing spondylitis

A

inflammatory back pain + enthesitis

progressive loss of spinal movement.
stiffness and pain waking in early morning. gradual onset. improves with moving but not with rest.

tenderness at sacroiliac region (felt in buttocks) or limited spinal motion.
usually a 20-30yo M.

severe disease - kyphosis and neck hyperextension - question mark posture.
may also get fever and wt loss.

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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.

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74
Q

name 2 diseases associated with ankylosing spondylitis

A

osteoporosis
aortic valve incompetence
pulmonary fibrosis

overlaps with psoriatic arthritis, enteropathic arthritis (IBD), reactive arthritis.

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75
Q

what antibody is NEVER seen with ankylosing spondylitis?

A

rheumatoid factor

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76
Q

how would you treat ankylosing spondylitis?

A

no cure.
NSAIDs, physio, exercises.
2nd line = TNF alpha blocker (etanercept) if NSAIDs fail.

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77
Q

give 4 clinical features of psoriatic arthritis

A

symmetrical polyarthritis OR asymmetrical oligoarthritis (up to 5), affects DIP joints most commonly, nail dystrophy, dactylitis, asymmetrical oligoarthritis, spinal arthritis, acneiform rashes, palmo-plantar pustulosis

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78
Q

what is reactive arthritis?

A

a sterile arthritis that tends to follow dysentery or UTIs

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79
Q

give some possible causative organisms of reactive arthritis

A

campylobacter, salmonella, shigella.

**chlamydia

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80
Q

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

A

urethritis, arthritis (typically lower limb) and conjunctivitis

can’t see can’t pee can’t climb a tree

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81
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.

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82
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.

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83
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.

affects any organ but spares pulmonary and glomerular arteries. nerve and skin most commonly affected.

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84
Q

list some features of polyarteritis nodosa

A

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

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85
Q

what investigation would you carry out in polyarteritis nodosa?

A

angiography - microaneurysms and focal narrowing (rosary sign).

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

no ANCA - as no small vessel involvement, differentiates it from other vasculitic disease.

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86
Q

how would you treat polyarteritis nodosa?

A

prednisolone ± cyclophosphamide (DMARD).

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87
Q

what hepatic disease is associated with PAN?

A

hepatitis B.

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88
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.

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89
Q

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

A

giant cell temporal arteritis

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90
Q

how would you treat polymyalgia rheumatica?

A

prednisolone will improve within 24-48hrs.

  • start high - 15mg for 3 weeks
  • titrate down (10mg for 4-6 weeks, etc)

PPI and Ca/VitD/bisphosphonate for gut and bone protection.

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91
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.

other Ix - ESR/CRP acute phase protein response. FBC, U&E, LFT, bone profile, protein electrophoresis, TFT, CK, RF, urinalysis

92
Q

give 3 precipitating factors of an acute gout attack

A

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

93
Q

give 3 risk factors for gout

A

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

94
Q

what is gout?

A

deposition of monosodium urate crystals in and near joints.

95
Q

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

A

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

96
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

97
Q

how would you manage an acute gout attack?

A

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

98
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

99
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.

100
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

101
Q

how does pseudo-gout present differently from gout?

A

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

102
Q

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

A

septic arthritis

103
Q

how would you treat pseudo-gout?

A

NSAIDs or colchicines, aspiration of joint.

corticosteroid injection, if no infection.

104
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.

105
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.

106
Q

list 2 other problems that fibromyalgia is associated with

A

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

107
Q

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

A

over 3 months

108
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

109
Q

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

A

nothing - all would be normal.

diagnosis of exclusion.

110
Q

how would you manage fibromyalgia?

A

1st line = amitriptyline + CBT
2nd line = gabapentin or pregabalin.
education, structured exercise programmes.
NOT steroids or NSAIDs.

111
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.

112
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.

113
Q

back pain red flags?

A

TUNA FISH
Trauma
Unexplained wt loss, loss of appetite - cancer/myeloma
Neurological symps incl. bowel/bladder dysfunction - cauda equina
Age >50 or <20
Fever and night sweats - osteomyelitis/cancer
IVDU/immunosuppression - osteomyelitis
Steroid use - immunocompromised + osteoporotic #

114
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.

115
Q

what is myeloma?

A

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

116
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

117
Q

describe the clinical features caused by osteolytic bone lesions in myeloma

A

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

118
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.

119
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

120
Q

what would blood tests show in a myeloma patient?

A

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

121
Q

how would myeloma be treated?

A

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

122
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

123
Q

give 3 clinical features of septic arthritis

A

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

suspect in any patient with acutely inflamed joint, as can destroy a joint in <24hrs.

124
Q

give 3 risk factors for septic arthritis

A

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

125
Q

what investigations would you perform in septic arthritis?

A

urgent joint fluid aspiration for MC&S, gram stain and WCC ± blood cultures and skin swab.
acute phase markers - ESR, CRP, WCC raised.

XR not that useful, CT/MRI more sensitive for periarticular abscess, osteomyelitis etc.

126
Q

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

A

main - staph aureus.

H influenzae, Salmonella

127
Q

what are the clinical features of osteomyelitis?

A

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

128
Q

how would you investigate osteomyelitis?

A

plain radiograph is best screening - areas appear dark, soft tissue swelling, periosteal thickening, patchy osteopenia.

also FBC, blood cultures, ESR/CRP etc.

129
Q

name 2 bisphosphonates. what are they used to treat? what must you tell patient?

A

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

risk of upper GI SEs - take sitting upright w/plenty of water first thing before food - leave 1hr before eating.

130
Q

how do bisphosphonates work?

A

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

131
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.

132
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.

133
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.

134
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.

135
Q

what is strontium ranelate used to treat?

A

severe osteoporosis

136
Q

what points should you cover when describing a fracture?

A

complexity, type, comminution (‘shortening’ the bone), location, displacement

simple = closed, compound = open

FIG-TACOS:
fissure, impaction, greenstick, transverse, avulsion, comminuted, oblique, spiral

137
Q

what are the components of the FRAX score?

A

estimates 10yr risk of # using BMD
- age, sex, BMI = 3 person
- prev #, parent hip #, low femoral neck BMD = 3 #
- alcohol, smoking, glucocorticoids = 3 things put in
- RA, secondary osteoporosis = 2 conditions
(also - T1DM, osteogenesis imperfecta, hyperthyroidism (untreated), hypogonadism, prem. menopause, malnutrition, malabsorption, chronic liver disease)

138
Q

what are the 5 most common #? what are the particularly important ones and why?

A
  • clavicle, arm, wrist (Colles’), hip, ankle
    important:
  • scaphoid, femoral head - both can lead to avascular necrosis, progressing to joint destruction and osteoarthritis
139
Q

what 3 things should you cover when assessing a #?

A

mechanism of injury
sound/feeling of break
loss of function
- also skin status?

140
Q

what are the bones of the wrist?

A

“scared lovers try positions that they can’t handle”
(1st layer) - scaphoid, lunate, triquetrum, pisiform
(2nd) - trapezium, trapezoid, capitate, hamate

141
Q

what are the different types of wrist fracture?

A

Colles = distal radius with dorsal displacement fragments
Smith’s = distal radius with volar displacement
Scaphoid - risk of AVN!. usually due to FOOSH in 20-30yo.

142
Q

what is the typical sign of a scaphoid #?

A

tenderness in anatomical snuffbox (between extensor pollicis longus and extensor pollicis bravus)

anatomical snuffbox also contains sensory branch of radial nerve.

needs 4 scaphoid views on XR as difficult to see.

143
Q

how do you generally treat a wrist #? what about specifically for scaphoid #?

A

reduction via manipulation (give anaesthesia!!). immobilisation initially, but avoid full cast as swelling can impede circulation

Scaphoid - presumptive cast immobilisation (6-8 weeks) + repeat exam and XR at 10-14 days - beware AVN!

144
Q

info on Colles’ # - who gets it and how? complications? rx?

A

distal # of radius ± ulnar w/dorsal displacement of fragments.
usually osteoporotic old lady, FOOSH, with forced dorsiglexion of wrist.

lateral XR = “dinner fork” appearance
complication - risk of median (or ulnar) nerve damage

Rx = reduction and immobilisation (6W)

145
Q

how do people get a Smiths’ #? appearance on XR, possible complications?

A

= reverse Colles’ i.e. distal # of radius with volar displacement

fall backwards

appearance = garden spade deformity

comp. = median nerve damage

146
Q

define #NOF? what are the different types?

A

from proximal to 5cm below lesser trochanter - most common admission to ortho trauma ward.

intracapsular # - femoral neck, between edge of femoral head and insertion to capsule. can lead to AVN.
extracapsular trochanteric # - distal to insertion, involving or between trochanters.
extracapsular subtrochanteric # below lesser trochanter to 5cm distal.

147
Q

how does a #NOF present?

A

old, unstable, osteoporotic patient usually.
pain in outer upper thigh or groin, radiate to knee, no weight bearing.
affected leg shortened, adducted and externally rotated.

148
Q

how should you investigate a #NOF patient?

A

XR - AP and lateral (follow shenton’s line to see the #)
MRI can help if suspect # but can’t see on XR

FBC, cross match, renal function, glucose, ECG

give analgesia but not NSAIDs

149
Q

what are the different #NOF management options?

A

needs surgery within 1 day!
Intracapsular:
- undisplaced = internal fixation with screws (dynamic hip screw, DHS)
- displaced - hemiarthroplasty - replace femoral head. some cases might do THR.
Extracapsular:
- internal fixation with screws (DHS)

150
Q

what complications are we worried about in a #NOF?

A

infection, haemorrhage, AVN, DVT, HAP
all should get VTE prophylaxis.

mortality is v high! 33% in 3 months!

151
Q

what are the different joints in the ankle?

A

the actual ankle joint where tibia and fibula meet talus = tibiotalar, does plantar and dorsiflexion

syndesmosis join = tibia to fibular
the subtalar joint = talus and calcaenous - inversion and eversion.

ankle # is a break in one or more of tibia, fibula or talus.

152
Q

outline the Ottawa ankle rules

A

tell you when to XR a ?ankle#

  • age >55
  • inability to wt bear (4 steps) now and at time of injury
  • bone tenderness at posterior edge/tip of lateral malleolus (from 6cm above it)
  • bone tenderness at posterior edge or inferior tip of medial malleolus

XR midfoot as well if bone tenderness at base of 5th metatarsal, cuboid or navicular.

views = AP, lateral, oblique (15 degrees)

153
Q

how does an ankle # present?

A

similar to severe sprain - immediate severe pain, swelling (localised or up leg), bruising, tenderness.
consider break if obvious deformity, inability to weight bear, bony tenderness.

154
Q

what is a Potts #?

A

fracture of distal tibia and fibular (bimalleolar) - unstable and requires urgent treatment

155
Q

what is a snowboarders #?

A

lateral process of talus, due to dorsiflexion and inversion

156
Q

how are ankle #s treated?

A

immediate reduction (before XR, but sedate/analgesia!) if neurovascular compromise or dislocation (obvious deformity)

generally:

  • reduce, stabilise in moulded cast for 4-6wks
  • analgesia, elevation
  • re-assess neurovascular status.

monitor - XR at reduction, 48h, 7 days, then 2 weekly (managed by # clinic)

157
Q

what is compartment syndrome?

A

main worrying complication of fractures!!
6 Ps = pain, parasthesia, pallor, paralysis, perishingly cold - PAIN OUT OF PROPORTION

requires urgent fasciotomy.
occurs post # or reperfusion.

post fasciotomy risk is of myoglobinuria –> renal failure (manage with aggress IV fluids)

158
Q

what are the different stages of fracture healing?

A

1) Haematoma formation *hours - MP and inflamm leukocytes move to area and begin secreting pro-inflammatory agents
2) Fibrocartilaginous callus formation (soft callus) *days - Inflammation leads to angiogenesis and increased number of chondrocytes. Secrete collagen and proteoglycans - fibrocartilage
3) Bony callus formation *weeks- Endochondral ossification and direct bone formation. Soft callus replaced by woven bone
4) Bone remodelling *months - Woven bone replaced by organised cortical bone. Continually remodelled therefore no scarring.

159
Q

what is the average length of time taken for healing for different types of #?

A

3-12 weeks (phalanges 3 weeks, radius 4-6, humerus 6-8, NOF or femur 12)

160
Q

what is frozen shoulder?

A

one of the most common causes of intrinsic shoulder pain, affects glenohumeral joint.
due to thickening and contraction of glenohumeral joint capsule ± formation of adhesions.
get pain and loss of function either spontaneously or post rotator cuff injury.

161
Q

how does frozen shoulder present? management?

A

loss of external rotation = classic.
usually age 40-65, associate with diabetes and thyroid disease.
may be spontaneous or post rotator cuff injury.

Rx = analgesia/tens machine, activity, physio

162
Q

briefly outline the bone remodelling process

A
  • Osteocytes send signal to osteoclasts and osteoblasts
  • Osteoclasts resorb bone matrix: resorption pit - increases serum Ca
  • Osteoclasts undergo apoptosis and send signals to osteoblasts
  • Osteoblasts synthesise bone matrix
  • Bone matrix undergoes mineralisation

there’s lots of weird cytokines etc (IL1, IL6, RANK, etc) but I don’t care to learn them

163
Q

pathophysiology of osteoporosis?

A
  • increased breakdown of osteoclasts
  • decreased bone formation by osteoblasts
  • BMD then decreases with age (primary) or secondary to other factors (e.g. steroids)
164
Q

what Ix would you do in osteoporosis, apart from DEXA scan of proximal femur?

A

XR - often normal, won’t see anything till lose 30% BMD - radiolucency, cortical thinning, biconcave vertebrae

other Ix - to ID treatable causes, rule out Dx of MM
FBC, ESR, CRP
U&E, LFT, TFT, serum Ca
testosterone/gonadotrophins

165
Q

what are the key side effects to know about for bisphosphonates?

A

ostenecrosis of the jaw

upper GI - difficulty swallowing, oesophagitis, gastric ulcers

166
Q

what is osteomalacia? what about Ricket’s?

A 
osteomalacia = disorder of mineralisation of bone matrix after fusion of epiphyses
Ricket's = this, before fusion (so in kids)

bones are normal size but SOFT.

due to vitamin D deficiency leading to low calcium and phosphate
low calcium and phosphate leads to secondary hyperPTH.

167
Q

what are the important sources of vitamin D?

A

90% is sunlight.

dietary = oily fish, liver, egg yolks, fortified cereals (not dairy)

168
Q

give some risk factors for osteomalacia/rickets

A 
dark skin
extremities of age
pregnancy
obesity
alcohol
vegetarianism
poverty
family Hx
169
Q

give some different possible aetiologies of osteomalacia/rickets

A
  • lack of sunlight or adequate diet
  • GI malabsorption e.g. surgery, short bowel, pancreatic disease, CF, coeliac
  • renal disease - get defective 1,25 form of vit D (this is the active hormone) = renal osteodystrophy
  • liver disease = cirrhosis
  • drugs = anticonvulsants, rifampicin (acts on liver)
  • genetic - hypophosphataemic rickets, vit-D dependent rickets type I and II
170
Q

how does rickets present?

A 
leg bowing = genu varum
knock knees = genu valgum
- in first few months = craniotabes (softening of skull), frontal bossing, rachitic rosary (enlarged end segment ribs)
- dental abnormalities
- delayed walk/waddling gait

hypocalcaemia symps = convulsions, irritable, tetany etc

171
Q

how does osteomalacia present?

A
  • widespread bone pain + tenderness (low back pain and hips)
  • proximal muscle weakness - waddling gait if severe
  • fatigue
  • symptoms of underlying disease
  • costochondral swelling, spinal curvature, hypocalcaemia
172
Q

how might you investigate vit D deficiency/rickets?

A
  • Serum 25-hydroxyvitamin D - low
  • Renal function, electrolytes, LFT, PTH
  • Ca: low, PO4: low (generally at renal phosphate wasting), PTH: high, ALP: very high
  • FBC: anaemia if malabsorption
  • Urinary calcium - low, urinary phosphate - high
  • XR - *Looser pseudofractures with sclerotic borders (parallel) - bilateral at femoral neck
  • DEXA - low BMD
  • Iliac crest biopsy - failed mineralisation
173
Q

management of rickets/osteomalacia?

A

if vit D deficient - calcium + vit D supplements
if inherited/acquired disorder - calcitriol + sodium phsophate

when starting vit D supplements always monitor Ca regularly for a few weeks

174
Q

what is Paget’s disease of bone?

A

increased turnover of bone in axial skeleton (lumbosacral spine, pelvis, skull, femur, tibia)

  • lytic phase = increased bone resorption by osteoclasts
  • scleroitc phase = rapid bone formation by osteoblasts - disorganised and mechanically weaker and deformity (/larger)

genetics - usually have family Hx - AD SQSTM1 mutation.

175
Q

how does Paget’s disease of bone present? what are the worrying complications?

A

often asymptomatic, might have raised alk phos.
- bone pain and deformity, with increased skin temperature, pain at night.

complications:

  • deformity - sabre tibia, kyphosis, skull bossing, enlarged maxilla/jaw
  • pathological #s w/heavy bleeding as bone is very vascular
  • deafness/tinnitus due to CN 8 compression by ear ossicles
  • increased vascularity can lead to high output cardiac failure
176
Q

what would investigations show in Paget’s disease of bone?

A
  • ALP high, Ca/PO4/PTH normal
    XR:
  • osteolysis and osteosclerosis (lytic and sclerotic long bone)
  • blade of grass lesion between health and sclerotic long bone
  • cotton wool pattern of multifocal sclerosis in skull
  • isotope bone scans
177
Q

how can you treat Pagets disease of bone?

A
  • pain: NSAIDs, paracetamol
  • antiresorptive = bisphosponates (IV Zolendronate single dose popular option)
  • monitor ALP
178
Q

which joints of the hand are typically affected by OA vs RA?

A 
OA = DIP
RA = MCP, MTP (foot), PIP
179
Q

what is Felty’s syndrome?

A

triad of RA, neutropenia and splenomegaly - increased susceptibility to infection, lung and skin infections; LUQ pain and anaemia of chronic disease.

also get - leg ulcers and brown pigmentation of legs, lymphadenopathy.

180
Q

what disease score is used in monitoring RA?

A

DAS28 (disease activity score)

<3.2 = well controlled, >5.1 = active

181
Q

XR features of gout?

A

early - soft-tissue swelling

late/chronic - punched out lesions, tophi, sclerosis

182
Q

what is Ehler Danos?

A

defect in structure, production or processing of collagen (genes = COL5A or COL3A)

suspect if joint + skin + *hypermobility

women > men x8

183
Q

how can Ehler Danos present? management?

A
  • skin - increased elasticity + fragility
  • joints - laxity, hypermobility, pes planus, prone to dislocation
  • CV - dizziness, palpitations, heart valve abnormalities, mitral valve prolapse, aortic root dilatation
  • ocular - abnormal globe, cornea
  • hearing - tinnitus due to ossicle laxity

management = physio, regular gentle exercise, genetic counselling
- periodic echo for floppy mitral valve or aortic root dilatation

184
Q

what is Marfan’s disease? mechanism?

A

inherited connective tissue disorder with characteristic skeletal, dermatological, cardiac, aortic and ocular malformations.

  • decreased extracellular microfibril formation
  • AD fibrillin gene FBN1

leading cause or aortic root dilatation and aortic dissection.

185
Q

list different features of Marfan’s disease?

A
  • Skin: striae
  • CV: aortic dilatation, dissection, mitral regurgitation
  • Lungs: pleural rupture - pneumothorax
  • Eyes: lens dislocation, closed angle glaucoma
  • Skeleton: arachnodactyly, hypermobility, pectus excavatum
  • Facial: retrognathia, high arched palate, enopthalmos
  • Walker’s sign - encircles wrist with overlapping finger and thumb
186
Q

investigation and management for Marfans?

A

need annual ECHO monitoring aortic root width.
CV MRI every 5yrs.

management - MDT (geneticist, ophthalmologist, cardiologist, orthopaedics)
avoid maximal exertion (scuba diving, wt lifting)

*prophylactic beta blockers = propranolol (reduce MAP and pulse rate)

187
Q

what are the seronegative arthropathies?

A

group of rheumatic diseases with involvement of 1) axial skeleton 2) peripheral joints 3) enthesitis (tendons/ligaments) and dactylitis.

they are Rheumatoid Factor NEGATIVE (hence seronegative)
usually a HLA thing (chromosome 6).
conditions - ank spond, Reiter’s synd, enteropathic arthritis, psoriatic arthritis, Behcet’s disease, JIA

188
Q

what are the criteria for diagnosing a seronegative arthropathy?

A

inflammatory spinal pain or synovitis (in lower extremities) PLUS one of:

  • fam hx - ank spond, psoriasis, reactive arthritis, IBD
  • past/present psoriasis
  • past/present IBD
  • past/present pain alternative between buttocks
  • past/present spontaneous pain in achilles or plantar fascia
  • diarrhoea one month before arthritis
189
Q

list some extra-articular features of ankylosing spondylitis

A
  • Eyes: acute anterior uveitis - 40% (painful red eye and photophobia)
  • *CV: aortitits and *dissection of the aorta and aortic regurgitation
  • Lung: restrictive lung disease: costovertebral/sternal involvement limits chest expansion, apical fibrosis
190
Q

what would you find on examination of a patient with ankylosing spondylitis?

A

reduced chest expansion <5cm
Schober’s test = reduced forward flexion <5cm + loss of lumbar lordosis
reduced lateral flexion

191
Q

what would you find on investigation of a patient with ankylosing spondylitis?

A
  • pelvic XR - sacroilitis (blurring, loss of definition) uni/bilateral
  • HLA B27 +ve
  • XR whole spine (BESS) - Bamboo spine, (late) Erosion, Squaring, Syndesmophytes
192
Q

what would you find on investigation of a patient with psoriatic arthritis?

A
  • plain film XR feet and hands - erosion in DIP, periarticular new bone formation, osteolysis, *pencil in cup deformity
  • ESR/CRP normal or elevate
  • RF only +ve in 2-10%
  • anti-CCP -ve
193
Q

how would you treat psoriatic arthritis?

A

NSAID + physio ± joint injection.

if progressive peripheral disease and high ESR/CRP can consider DMARD (MTX)

194
Q

investigations and treatment of reactive arthritis?

A

Ix - very high ESR/CRP.
joint aspiration - rule out septic/crystal arthropathies.
culture - stool, throat, UG tract (STI screen) for causative organism
serology for chlamydia (PCR or NAAT) and contact tracing

Rx - NSAID + rest ± intra-articular steroids ± abx for chlamydia

195
Q

what is enteropathic arthritis?

A

arthritis associated with IBD, coeliac etc.
axial arthritis + lower limb arthritis + enthesitis + bowel symptoms + anterior uveitis

Rx - similar to how you treat the bowels - sulfasalazine.

196
Q

what is Behcet’s disease?

A

recurrent oral ulcers - usually presentation.
HLA B51.
multisystem feature - genital ulcers, anterior uveitis, erythema nodosum, non-erosive arthritis in lower limb.
Rx - topical corticosteroids, systemic steroids for a year or 2.
gets better with time.

197
Q

list the different large, medium and small vessel vasculitises?

A

large vessel - PMR, GCA, Takyasu’s arteritis
medium - PAN, Kawasaki’s
small - Wegener’s/GPA, Churg-Strauss

198
Q

what is giant cell arteritis?

A

large vessel vasculitis - inflammatory granulomatous arteritis of aorta and large cerebral arteries.
main risk is that 20% get anterior ischaemic optic neuritis (AION) –> sudden visual loss = medical emergency.

tends to occur in W>M (x2) over age 50yrs.
50% have associated PMR.

199
Q

how does GCA present?

A

recent onset temporal headache + scalp tenderness + transient visual symps (e.g. diplopia) + jaw claudication (on chewing)
± malaise/myalgia/fever.

O/E - abnormality on palpation of temporal artery (absent pulse, beaded, tender).

200
Q

how do you investigate GCA?

A

**ESR >50
must also do temporal artery biopsy!!
shows granulomatous inflammation, multinucleated giant cells, intimal hypertrophy and inflammation.

201
Q

how do you manage GCA?

A

high dose oral pred (1mg/kg/day) for 4 weeks then taper, + aspirin (lowers risk of visual problems).
consider need for Ca/vitD/bisphosphonates - osteoporosis with steroids.

202
Q

how can you split up the small vessel vasculitic diseases?

A

ANCA associated = microscopic polyangitis, GPA (Wegener’s), EGPA (Churg-Strauss)

Immune complex mediated = cryoglobulinemic vasculitis, IgA vasculitis (Henoch-Schonlein), anti-GBM disease

203
Q

what is the classic triad in Wegener’s granulomatosis (GPA - granulomatosis with polyangitis)?

A

ELK disease = ENT, Lungs, Kidneys
upper resp tract involvement (saddle nose deformity)
lower resp tract involvement
glomerulonephritis

204
Q

what are the possible features of Wegener’s granulomatosis?

A
  • Upper resp: otorrhoea, sinus pain, nasal discharge, hoarseness, stridor, *Saddle nose deformity, nasal septal perforation, subglottic stenosis
  • Lower resp: SOB, cough, haemoptysis, chest pain, dyspnoea, rhonchi, reduced air entry
  • Renal: oedema, HTN, haematuria (later)
  • Ocular: redness, pain, tearing, proptosis, visual blurring marked bilateral periorbital oedema from kidney…
  • Cutaneous: palpable purpura or petechia
  • MSK: myalgia and arthralgia
  • Neurological: numbness, weakness, etc….
205
Q

what investigations might you do in Wegener’s granulomatosis?

A

Kidney - urinalysis and microscopy + RENAL BIOPSY
Lung - CT chest (cavitating lung nodules)

ANCA - by immunofluroescence (c-ANCA)
FBC - anaemia, ESR - raised.

206
Q

outline management options for Wegener’s

A

life-threatening/organ involvement = remission with IV methylpred (3d) + oral pred + cyclophosphamide

non-lifethreatening = as above but MTX instead of cyclophosphamide

207
Q

what is the typical triad for Churg Strauss (EGPA)?

A

tissue eosinophilia, granulomatous inflammation, vasculitis

consider in adult onset asthma

208
Q

what are the diagnostic criteria for Churg-Strauss?

A

Asthma (wheeze), eosinophilia in peripheral blood, paranasal sinusitis, pulmonary infiltrates, histological confirmation vasculitis, *mononeuritis multiplex

209
Q

what other features are possible in Churg Strauss?

A
  • ENT - allergic rhinitis, paranasal sinusitis, nasal polyposis
  • Lower RT - pneumonitis, haemoptysis
  • Renal - glomerulonephritis - HTN
  • *Peripheral neuropathy - mononeuritis multiplex
  • Skin - purpura, skin nodules
210
Q

investigations in Churg-Strauss?

A

p-ANCA (antimyeloperoxidase Ab) - 40%
FBC - eosinophilia + anaemia, elevated ESR/CRP
CXR - pulmonary infiltrates
Pulmonary CT - peripheral consolidation - ground-glass attenuation
Biopsy small necrotising granulomas and necrotising vasculitis

211
Q

what scoring system is used in both Churg-Strauss and PAN?

A

five factor score:

  • proteinuria
  • serum creatinine
  • GI tract involvement
  • cardiomyopathy
  • CNS involvement –> higher mortality
212
Q

management for Churg-Strauss?

A

corticosteroids + asthma control.

  • for remission = IV methylpred 3d then oral pred
  • if scoring on the five factor score incl. cyclophosphamide
213
Q

what is microscopic polyagnitis?

A

p-ANCA mediated small vessel vasculitis.
rapidly progressive glomerulonephritis and pulmonary haemorrhage

affects lungs and kidneys
Rx - pred and cyclophosphamide

214
Q

what is cryoglobulinaemic vasculitis?

A

inflammation due to cryoglobulins
presents - Arthralgia, purpura, hepatic involvement, Raynaud’s, glomerular disease
assoc. w/hep C

ANCA -ve.

215
Q

what is IgA vasculitis?

A

same as HSP.

presents as Young man with previous URTI - GpA strep (pyogenes)
IgA immune complexes are deposited in small vessels.

triad = arthralgia, abdo pain, purpuric rash (on buttocks and extensor).
also get - low grade fever, vomiting, joint pain. 40% get nephrotic syndrome.

Rx = steroids if kidney function affected, simple analgesia if just pain.

216
Q

what is anti-GBM disease/Goodpastures?

A

condition affecting alpha 3 chain of type 4 collagen, anti-GBM Ab attacks basement membrane in glomerulus and alveoli.

glomerulonephritis + pulmonary haemorrhage –> haemoptysis and renal failure.

217
Q

how does Goodpasture’s present? Ix and Rx?

A

male age 20-30 or 60-70 w/ reduced UO, haemoptysis, oedema, SOB, cough etc.
Ix - abnormal renal function.
*renal biopsy = crescentic glomerulonephritis - needs doing urgently!!
anti-GBM positive.

Rx - if reversible renal or any pulmonary involvement = oral pre + cyclophosphamide + plasmapheresis.
if pulmonary haemorrhage - supportive + smoking cessation.

218
Q

give some contraindications for renal biopsy

A
  • Sole native kidney
  • ESRD
  • Neoplasm
  • Bleeding disease
  • Uncontrolled severe HTN
  • Acute pyelonephritis
219
Q

what tests are in a vasculitis screen?

A

haematology: FBC, ESR, clotting screen
biochem:
- U+E + Cr - renal function
- LFT: PAN and cryo assoc HBV and HCV
- CRP
- Immunoglobulins and protein electrophoresis
Immunology: ANCA, RF, complement (C3/C4), anti-cardiolipin, cryoglobulins
Microbiology: HBV and HCV serology, urine microscopy and culture
Radiology: CXR

220
Q

how do you treat septic arthritis?

A

usually requires surgical drainage and lavage + high dose IV abx for 2/3weeks, then oral for 3/4 (6 weeks total)
if suspect gram+ use vancomycin, if suspect gram- use 3rd gen cephalosporin.
fluclox for staph.

if prosthetic join - remove joint and fill with abx impregnated spacer.

221
Q

what is osteomyelitis? staging?

A

infection of bone marrow, may spread to cortex and periosteum via Haversian canals –> inflammatory destruction of bone.

Stage 1 = medullary cavity only
Stage 2 = superficial involving cortical bone only
Stage 3 = localised involving medullary and cortical bone
Stage 4 = diffuse entire bone thickness

222
Q

risk factors for osteomyelitis?

A

trauma, prosthetics, diabetes, chronic joint disease, IVDU, alcoholism, immunosuppresion.

223
Q

how does osteomyelitis present?

A

acutely febrile + bacteraemic + painful immobile limb (if long bone infection) - swelling, tenderness, erythema.

if vertebral body infected (tends to be where in adults) - post acute septicaemic episode, localised oedema, erythema, tenderness or chronic back pain. Pott’s disease = from haematogenous spread of TB.

224
Q

management of osteomyelitis?

A

1) bone and soft tissue debridement (send for cultures)
2) stabilise bone and immobilise
3) local abx
4) reconstruction

analgesia + limb splinting if long bone.
initial broad spec abx = vancomycin + cefepime (IV). then culture directed, usually IV 2 weeks, oral 4 weeks.

225
Q

what types of cancer commonly metastasise to the spine?

A

prostate
breast
lung
renal

226
Q

what usually causes cervical back pain? presentation?

A

cervical spondylosis
chronic disc degeneration - cervical osteoarthritis.

simple neck pain + radiculopathy (pain, numbness, tingling, weakness in upper limbs) + myelopath
worse on movement
cervical stiffness across all movements

227
Q

how might you manage/investigate cervical back pain?

A

3-4 weeks = reassure + encourage normal movements
4-12 weeks = physio, try yoga/pilates.

plain XR shows osteophytes, narrowing of disc space, encroachment of intervertebral foramen.
if neuropathy –> requires MRI.

1 - Finals (15 decks)

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