MSK Flashcards

1
Q

Red flag back pain sx

A

<20/>55y, acute onset in elderly, b/l leg pain, trauma, weakness, WL/fever/night sweats, steroids/HIV, progressive non-mechanical continuous pain, nocturnal pain, worse supine, h/o malignancy, thoracic back pain, morning stiffness (AS), neurological disturbance, local bony tenderness, infection, leg claudication (spinal stenosis)

Acute pain need to r/o:

  • cauda equina
  • acute cord compression
  • trauma
  • retroperitoneal referral from duodenal ulcer, AAA, pancreatitis
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2
Q

Simple lower back pain

A

muscular strain or disc degeneration, spasm of vertebral muscles can cause intense pain. May lead to sciatica/other nerve root signs.

Can’t find specific cause but often related to trauma/musculo-ligamentous strain

Only image with CT/MRI + bloods if >4w/suspect sinister cause

Majority get better in 3-6w, focus on analgesia (para/ibu/naprox/opioids), warmth, swimming, physio. Avoid bed rest after the first 48h

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3
Q

Degenerative disc disease

A

compresses dorsal nerve roots causing radicular pain in dermatomal distribution, may lead to herniation

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4
Q

Disc prolapse

A

severe pain after back strain is usual presentation, forward flexion + extension limited.

  • L4/L5 (L5 root compression) - weak toe extension, reduced sensation outer dorsum of foot
  • L5/S1 - compresses S1 root - calf pain, weak plantar flexion, reduced sensation over sole of foot/posterior calf, reduced ankle jerk

M: brief rest, early mobilisation, analgesia, PT, discectomy in continuing pain

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5
Q

Spondylolithiasis

A

displacement of one lumbar vertebra upon the one below, usually L5 on S1. Age-related spondylosis or congenital malformation. Pain +/- sciatica +/- hamstring tightness causing waddling gait

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6
Q

Spinal stenosis

A

narrowed lumbar SC often due to osteophytes with OA, can cause nerve ischaemia so get spinal claudication (pain worse when walk, aching heavy legs, better on leaning forwards). MRI.

  • Spinal stenosis: pain after variable distance, relieved on leaning forward as less compression (standing still can make it worse)
  • Vascular intermittent claudication: pain on reproducible distance, often relieved quickly by standing still

M: NSAIDs, epidural injections, decompressive laminectomy

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7
Q

Inflammatory spondyloarthropathies e.g. ankylosing spondylitis

A

insidious onset, early morning stiffness >45min, diffuse non-specific buttock, pain improves with activity, may have other joint/bowel/eye involvement. E.g. ankylosing spondylitis

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8
Q

Neoplastic causes of back pain

A

o Metastatic spinal cord compression – emergency. Pain, weakness, UMN signs, absent reflex at level of lesion. Cauda equina syndrome – LMN signs
o Bone mets – progressive constant pain. E.g. myeloma, lymphoma, breast/bronchus/kidney/thyroid/prostate
o Pain from pancreas tumours

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9
Q

Paget’s disease

A

Increased but not uncontrolled bone turnover, commoner with age

The skull, spine/pelvis, and long bones of the lower extremities are most commonly affected.

CF: bone pain, isolated rise in ALP, normal calcium/phosphate usually, bowing of tibia, bossing of skull. Skull XR-thickened vault.

M: if pain/#/deformities with bisphosphonate (oral or IV)

Comps: deafness (cranial nerve entrapment)
bone sarcoma (1% if affected for > 10 years)
fractures
skull thickening
high-output cardiac failure

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10
Q

Infections of the spine

A
  • Pyogenic infections – may have normal WCC and no fever. Pain, restricted movement. Usually discitis with Staph commonest, RF in DM/immunosuppression/urinary surgery
  • Pott’s disease (TB of spine) – systemic sx, gradual onset, stiffness + pain, most common T10-L1, can get abscess, Pott’s paraplegia when cord compressed
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11
Q

What is sciatica?

A

Aka lumbar radiculopathy

  • Pain, tingling, numbness due to impingement of lumbosacral nerve roots as they emerge from SC, felt in dermatome. May also have myotomal weakness
  • Sx extend to BELOW KNEE from buttocks, across back of thigh to outer calf and often to foot
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12
Q

What may cause sciatica?

A

herniated IV disc (90%, esp L4/5 and L5/S1), spondylolisthesis (proximal vertebra moves forward relative to a distal vertebra), spinal stenosis (narrowing of SC, usually pain relieved leaning forward and worse with extension, may be congenital or due to spondylolisthesis, if central often causes spinal claudication [b/l calf pain paraesthesia on walking], if lateral often causes sciatica), infection and cancer

Can lead to permanent nerve damage (esp if sig muscle wasting), psychosocial impact

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13
Q

How do you assess a pt who p/w back pain?

A
  • History including for red flags
  • Exam: gait, posture, skin changes, rashes (shingles), deformity, back swelling, neuro (sensation, reflexes), ROM including SLR, loss of anal tone if suspecting CES
  • Suspect non-specific LBP if pain varies with posture + time, and worse with movement
  • Suspect sciatica if u/l leg pain radiating below knee to foot/toes, LBP (less severe than leg pain), numbness/tingling/muscle weakness dermatomal distribution, positive SLR test (raising leg whilst straight more painful, below knee and/or more nerve compression sx)
  • SLR is only positive if goes below the knee
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14
Q

Management of back pain

A
  • Urgent neurosurgical r/v for neuro deficit, refer if other red flags
  • Non-specific LBP: treat modifiable RF, encourage activity, analgesia,
  • Angalesia - NSAID (+ gastroprotection) if not CI (don’t offer paracetamol alone), can try codeine/co-codamol
  • Sciatica - consider low dose amitriptyline, duloxetine, gabapentin, pregabalin
  • Return in 3-4w if worse/not improving
  • If considered high risk consider physio, group exercise programmes, CBT
  • Assess psychosocial issues predisposing to chronic pain
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15
Q

What is the difference between sprains and strains?

A
  • Sprain: ligament injury. Joint suddenly forced outside usual ROM, may look/feel like a # with inflammation, bleeding, painful to move. Grade I mild no joint instability, grade II intermediate, grade III severe with joint instability
  • Strain: overstretching + tearing of muscles/tendon (non-medical term). Hamstring injury most common, cos muscle stretched beyond limits/forced to contract too strongly. First, second and third degree
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16
Q

How do you manage sprains + strains?

A
  • PRICE: Protect, Rest 2-3d, Ice 15mins every 2-3h initially (not directly on skin), Compression with bandage to limit swelling + help rest, Elevation to reduce swelling
  • Avoid HARM: Heat (more inflame), Alcohol (more swell less healing), Running, Massage
  • Gently move to stop stiffness, joint support may help
  • Physio if not settling
  • Analgesia – paracetamol, +/- NSAID, +/- topical anti-inflammatory
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17
Q

Plantar fasciitis

A

traction + overuse injury of the plantar fascia (CT running from calcaneum to base of each toe, forms longitudinal arch). Often near heel (1-2cm distal from calcaneal tuberosity) as this is wear fascia is thinnest

RF: running/jumping, suddenly increasing exercise, running on hard ground, bad shoes, obesity, flat feet, high arch, pregnancy

Often have tight Achilles, may have limited ankle DF, palpate back of heel to r/o Achilles tendonitis, reproduce pain when palpate the plantar fascia

M: natural course up to 1y. Adv WL, good shoes, arch support, run on softer surface, NSAIDs + ice when bad, stretching exercises

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18
Q

Psoriatic arthritis

A

• Seronegative inflammatory arthritis affecting up to 30% with psoriasis, usually skin before joint involvement, lag time 5-10y
o But ~20% of people with PA don’t get cutaneous psoriasis
• Often initially asymmetrical then similar to RA, usually DIPJ involvement + nail dystrophy. Pain/peripheral joint swelling (esp knees, ankles, hands, feet) or dactylitis (swelling of an entire digit), night pain in axial skeleton + tendon insertions (enthesitis, esp Achilles tendon and/or planta fascia), nail changes in up to 90%
• M – intra-articular steroids, anti-TNF alpha agents e.g. etanercept. Better joint prognosis than RA

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19
Q

Reactive arthritis

A
  • Sterile synovitis occurring after an infection, often dysenteric (e.g. Salmonella, Shigella) or from Chlamydia
  • CF: acute, asymmetrical pain + swelling days-weeks after infection, may get some skin lesions similar to psoriasis
  • M: Abx, cultures, screen partners, NSAIDs, oral/injected steroids. May need DMARD if relapses
20
Q

Ankylosing spondylitis - what is it?

A

• Chronic inflammatory axial spondyloarthritis affecting sacroiliac joints + spine. F>M, usually presents in 20-30s, insidious onset
o Is axial spondyloarthritis with sacroiliitis on XR
o

21
Q

Pathophysiology of ankylosing spondylitis

A

Likely triggered by environmental factor in people with genetic predisposition
• In Europe >90% are HLA-B27 positive
• Inflammatory cells + cytokines cause CI, fibrosis, ossification of outer fibres of IV discs which eventually form syndesmophytes (progresses to the bamboo spine appearance)

22
Q

CF of Ankylosing spondylitis

A

low back pain + early morning stiffness, radiation to buttocks/thigh, inflammation of sacroiliac joints, worse with inactivity (better with exercise), tends to ascend spine as progresses

40% have peripheral arthritis – usually large joint + asymmetrical

Fatigue due to inflammation + night pain

Extra-articular features e.g. acute anterior uveitis (most common), prostatitis, aortic/mitral incompetence, psoriasis, IBD

23
Q

Investigation findings for ank spond

A

o XR sacroiliac joints – depends on progress, may have bridging syndesmophytes (areas of calcification), bamboo spine (ossification of the ALL + facet joint fusion), erosion in other areas .MRI better for detecting early disease
o CRP + ESR usually raised, autoantibodies negative

24
Q

When to refer a pt with suspected AS?

A

Refer to rheum if suspect – if LBP starting before 45y and lasting longer than 3m, plus 4+ of other criteria (see CKS). NSAIDs whilst they wait

Refer same day to ophth if suspect anterior uveitis)

25
Q

How is AS managed?

A

 Advice: explanation of condition, prognosis, likely sx, flare management plan, self care e.g. stretching
 Treatment options + adrs
 Self help, charities, support groups
 Flares – NSAID, try another if not helping, or refer

26
Q

Complications of AS

A

spinal fusion, spinal # from osteoporosis, hip involvement 1/3, anterior uveitis, cardiac comps (systemic inflammation, worse with long use of NSAIDs), lung (e.g. apical fibrosis, dyspnoea from costovertebral involvement), neuro from vertebral # e.g. cauda equina, drug ADRs, decreased QOL + work productivity

27
Q

Causes of gout

A

o Reduced urate excretion – elderly, male, post-menopausal women, impaired renal function, HTN, diuretics, aspirin
o Excess urate production – alcohol/sweeteners/red meat/seafood, genetics, lympho/myeloproliferative disorders, psoriasis, tumour lysis syndrome, HTN, DM, CKD

28
Q

CF of gout

A

acute monoarthropathy with severe inflammation, >50% at 1st MTP joint, also common at ankle/foot/small joints of hand/wrist/elbow/knee. Can be polyarticular

Tophi – urate deposits in pinna/tendons/joints

Renal disease – stones, interstitial nephritis

29
Q

Investigations in gout

A

XR shows periarticular erosions, normal joint space + soft tissue swelling

polarised light microscopy of synovial fluid shows negatively birefringent urate crystals that are needle-shaped

serum urate often high

30
Q

Management of gout

A

o Acutely – high dose NSAID, or colchicine if CI, or if both CI start steroids. Can continue allopurinol if already on it
o Prophylaxis – if >1 attack in a year, or tophi/renal stones. Allopurinol – titrate until plasma urate is low, s/e are rash, fever, reduced WCC. Wait 3w after acute episode as can trigger a flare
o Lifestyle – weight loss, avoid starvation/alcohol excess/purine rich meats/aspirin
o Screen for HTN + DM + lipids + CKD – gout is an independent RF for CVD

31
Q

Pseudogout

A
  • CPPD arthropathy – crystals in joint cause acute synovitis v similar to gout but more common in elderly women + usually in the knee/wrist
  • Fluid – rhomboidal, weakly-positive birefringent crystals, looks purulent so send for culture to r/o septic arthritis
  • Symptom control only, may aspirate fluid to reduce pain
32
Q

What is RA?

A

Autoantibodies to a part of IgG (rheumatoid factor) and CCP, causing chronic inflammation systemically with persistent synovitis of joints/tendon sheaths/bursae. Peak onset in 40s-50s, F>M.

33
Q

Pathophysiology of RA

A
  • Too much pro-inflammatory (IL-1, IL-6, TNF-alpha) + not enough anti-inflammatory (IL-4, TGF-beta) – leads to synovitis, bone + cartilage destruction by osteoclasts, immune complex formation, ectopic lymphoid tissue in synovium
  • Swelling + inflammatory cells – thickened synovium
  • Vascular proliferation
  • Cartilage thins + bone exposed because normal nutrition routes blocked
  • Fibroblasts cause bony erosions
34
Q

CF of RA

A
  • Typical: symmetrical swollen, painful, stiff small joints of hands + feet (peripheral polyarthritis), worse in morning, can fluctuate, can involve larger joints. Onset weeks-months. Initially inflammation without joint damage (e.g. swollen tender MCP/PIP etc), stiffness + pain worse in morning, may disturb sleep. Fatigue.
  • -Soft tissue problems: frozen shoulder, carpal tunnel, de Quervain’s tenosynovitis
  • Extra-articular features in 40%
35
Q

What are the extra-articular features a/w RA?

A

o Nodules – elbows, lungs, vasculitis…
o Normochromic normocytic anaemia – almost universal
o Muscle wasting around joints
o Eye – episcleritis, scleritis, keratoconjunctivitis sicca
o Systemic sx – fatigue, fever, WL
o Neuro – peripheral sensory neuropathies, compression neuropathies e.g. CTS, cord compression
o Amyloidosis of kidneys – proteinuria, nephrotic syndrome, CKD (rare)
o Felty’s syndrome – RA + splenomegaly + neutropenia
o Cardioresp – IHD, pericarditis, pericardial effusion, pleural disease, ILD

36
Q

Osteoarthritis pathophysiology

A
  • Breakdown of articular surface so becomes rough, friction creates cartilage shedding, inflammatory response in synovium (stiffness/aching after exercise)
  • Synovial irritation
  • Remodelling – limited cartilage repair, osteophytes (new bone covered in fibrocartilage) which restrict joint movement
  • Eburnation (looks polished) + subchondrol cyst formation
  • Disorganisation – joint progressively stiffer + more deformed due to osteophytes enlarging + bone wearing away
37
Q

Radiological features of OA

A

LOSS:

Loss of joint space, Osteophytes, Sclerosis of weight-bearing surface + Subchondral bone cysts

38
Q

CF of OA

A

pain (worse in weight bearing, synovitis after exercise), loss of movement (osteophytes + change of joint space, occurs over time), altered function (often subconsciously restrict activities)

39
Q

Management of OA

A

Info for advice

Self-care

Analgesia: Initially: paracetamol, topical NSAIDs (regular not as needed). If not working try oral NSAIDs (stop the topical one), opioids e.g. codeine, topical capsaicin. Consider pain clinic if not working

Consider physiotherapy/MSK clinic – for things like muscle strengthening, additional stretching esp good for hips, joint supports, intra-articular steroid injections

Consider OT for assistive devices like walking aids, raised toilet seats, grab rails

Consider podiatry cos pain in one joint may cause increased stress at other sides

Consider ortho surgery referral before they have severe functional limitation – if PC management not helping, sig impact on QOL, atypical sx, sudden worsening

40
Q

Rotator cuff disorders (SITS muscles)

A

o Cause subacromial shoulder pain at top + lateral side of shoulder, worse when lifting arm/overhead activities, can have night pain. Active movements restricted, passive movements tend to be more full, both painful. May have painful arc between 70-120 deg abduction (though not S+S sign) or pain on abduction with thumb down esp against resistance
o May have h/o repetitive movements around shoulder height or heavy lifting, typically 35-75y
o Rotator cuff tendinopathy (shoulder impingement) – between acromion + rotator cuff tendons. Essentially the same as supraspinatous tendinopathy, tendinitis and subacromial bursitis
o Partial rotator cuff tears
o Consider traumatic tear (tends to be younger active people) from dislocation/traction injury, may have positive drop arm test (can’t support weight when abducted to 90 deg) – needs surgical repair
o M: rest acutely, then exercise +/- physio, offer analgesia, consider subacromial corticosteroid injection (normally only do this once, and can only do up to twice if person previously benefited, cos of risk of tendon damage). If not helping after 6w refer to secondary

41
Q

Frozen shoulder

A
o	Pain (gradual onset, deltoid region), stiffness, progressive restriction of A+P movements (esp external rotation). No obvious crepitus
o	Typically 40-60y. Primary (idiopathic) or secondary to trauma/RC disease/CV disease/hemiparesis/DM/thyroid dysfunction
o	Often more severe sx in diabetics
o	Pain-predominant and stiffness-predominant phases, then resolution over 12-42m
o	Don’t routinely XR, GH joint appears normal
o	M: explain what to expect (pain first then improves but stiffness worsens then gradually resolves over m/y), adv on activitiy modification (avoid things worsening pain but continue to use it to ease spasm), adv analgesia/hot packs/support arm with pillows in bed, consider PT, may need intra-articular steroid injection. If nothing working in 3m refer
42
Q

Shoulder instability

A

o Abnormal movement of head of humerus, can cause pain, subluxation or dislocation. May also have joint laxity (asymptomatic movement over normal ROM) or just this alone
o Usually people <35y
o May be traumatic (shoulder doesn’t heal in correct position), atraumatic (common in adolescent females with hypermobile joints) or due to unbalanced muscle patterning (a/w poor posture)
o CF: feeling that it moves partly/completely out of joint, non specific like aches/intermittent clicking, may get hand/arm weakness, tingling/numbness. Often no abnormality O/E
o Look for abnormal shoulder contour – may be a sign of posterior dislocation
o May lead to OA
o Refer immediately to ED if suspect acute dislocation
o M: encourage early mobilisation, refer to PT, refer urgently to ortho if suspect RC tear, may need to refer to shoulder surgeon for various reasons

43
Q

ACJ disorders

A

o ACJ OA: often no sx, usually >60, may have h/o injury or weightlifting. CF – tender ACJ, worse when raise arm up, may have other RC disorders
o ACJ injuries: stretching/tearing of acromioclavicular or coracoclavicular ligaments or subluxation/dislocation of ACJ, often after falling onto shoulder
o O/E – tender ACJ, limiting ROM, high arc pain, positive cross arm test

44
Q

Glenohumeral OA

A

o Less common but can cause sig pain. As shoulder is non-weightbearing primary OA is rare so usually secondary e.g. after trauma, chronic rotator cuff tear + systemic arthritis
o Causes deep joint pain + restricted activities, global restriction in A+P movement, severe loss of passive ER
o Need XR
o Self care with WL, consider need for OT if ADL restricted, analgesia (regular paracetamol, oral NSAID or codeine dep on CI), consider steroid injection for short term management, consider physiotherapy

45
Q

Causes of shoulder pain

A
  • Rotator cuff disease
  • Frozen shoulder
  • OA
  • Instability
  • Trauma
  • Inflammatory arthritis
  • PMR
  • AVN of humeral head
  • Referred from neck (e.g. degenerative disc disease) or diaphragm/lungs e.g. apical lung Ca
  • Bone mets
  • Early herpes zoster in C5-T1 dermatomes
46
Q

How do you examine a shoulder?

A

o Inspect for muscle wasting swelling deformity
o Palpate clavicle, proximal humerus, scapula, SC joint, AC joint, GH joint – tenderness, warmth, swelling, crepitus
o A+P+resisted movement of shoulder – flexion, extension, abduction, adduction, IR, ER
o Painful arc of abduction if possible
o Cross-arm test – pain over ACJ when raise affected arm to 90 deg then adducts it – positive test
o Examine for referred pain e.g. ROM in C spine

47
Q

Polymyalgia rheumatica

A

Pathology unknown. Typically sudden onset severe pain + stiffness in shoulders/neck/hips/lumbar spine (i.e. proximal/girdle pain), worse in mornign, patients usually >50y, some get peripheral joint inflammation, some get systemic sx like fever/tired/WL/depression/night sweats.

DDx – polymyositis (proximal muscle ache + weakness), myopathy (weak but not pain or stiff); but in these CK levels would be raised. Also new onset TA, hypothyroidism, malignancy, infection, OA

Ix – ESR/CRP (PMR usually has raised inflammatory markers), ALP/GGT may also be raised as acute phase, mild normochromic normocytic anaemia, CK to rule out the other things.
- 10-30% also have GCA!

M – usually dramatic reduction in sx after 2d of prednisolone, then mostly need a maintenance dose for 2y to reduce flares + reduce risk of GCA