Year 5 MSK questions Flashcards

1
Q

Is septic arthritis more common in native or prosthetic joints

A

more common in prosthetic joints

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2
Q

what is the most common causative agents for spetic arthritis

1) streptococci
2) Staphylocccus aureus
3) Neisseria gonorrhoea
4) HIB in children
5) TB

A

S. Aureus is the most common causative agent

but all other options here are also common causative agents –> streptococci 2nd most common

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3
Q

What is the most important diagnostic investigation for septic arthritis

1) FBC
2) CRP/ESR
3) urgent joint aspiration
4) X-ray of affected joint
5) Skin swabs/sputum/throat swab/urine culture

A

most important investigation =urgent joint aspiration –> for synovial fluids gram stain and culture & synovial fluids WBC

all options here are required investigations

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4
Q

Which of the following is the most appropriate & common management for septic arthritis

1) immobilise joint to prevent muscle stiffness and wasting
2) flucloxacillin & sodium fusidate for 1-2 weeks
3) flucloxacillin & gentamicin for 1-2 weeks
4) Oral penicllin, ciprofloxacin for 2 weeks

A

flocloxacillin and sodium fusidate for 1-2 weeks = most common initial treatment for S.aureus infection

immobilise joint to prevent muscle stiffness and wasting - should do in all scenarios

flucloxacillin & gentamicin for 1-2 weeks = if immunosuppressed

Oral penicllin, ciprofloxacin for 2 weeks = if gonococcus/meningocccus

Ticoplanin = if MRSA

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5
Q

what is another name for temporal arteritis

A

giant cell arteritis

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6
Q

which artery does temporal arteritis most commonly affect

1) abdominal aorta
2) internal carotid artery
3) external carotid artery

A

external carotid artery whcih supplies the temporal side of the face, jaw and back of haed

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7
Q

which of the following symptom is most resemblant for late stage temporal artertitis?

1) temproal headahce
2) scalp tenderness
3) Dipolar/blurred vision/amaurosis fugax
4) facial pain
5) jaw/tongue claudication

A

3) Dipolar/blurred vision/amaurosis fugax - can also lead to perminant vision loss

all other options are symptoms of temproal arteririts but much earlier stage

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8
Q

which of the following conditon is associated with temproal arteritis?

1) polymyalgia rheumatica
2) aortic aneruysm/dissection
3) intermittent or persistent brain ischaemia/brain stem stroke
4) subclavian steal syndrome
5) all of the above

A

5) all of the above

polymyalgia rheumatica - same spectrum of disease

subclavian steal syndriome = intermittent or persistent brain ischaemia/brain stem stroke

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9
Q

what is the most important investigation for temporal arteritis

A

temporal artery biopsy

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10
Q

what does temporal artery biopsy show

A

vasculitis characterised bt predominance of mononuclear cell infiltration or ganulomatous inflammation, giant cell

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11
Q

which of the following is the most appropriate initial treatment for tmproal arteritis without visual symptoms

1) prednisolone 60mg + aspirin 75 mg
2) prednisolone 40mg + aspirin 75 mg
3) prednisolone 20mg + aspirin 75 mg
4) prednisolone 60mg + aspirin 150 mg
5) prednisolone 40mg + aspirin 150 mg

A

2) prednisolone 40mg + aspirin 75 mg - for TA without visual symptoms

prednisolone 60mg + aspirin 75 mg - for TA with visual symptoms + urgent same day opatham referral

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12
Q

what are some of the symptoms of cauda equina syndrome

A

pain

radicular sensory changes

loss of sensation in perianal area

leg weakness

loss of bowel and bladder function

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13
Q

what are some of the clinical features of spinal cord compression

A

backpain

numbness/paraesthesia

weakness or paralysis

bladder and bowel dysfunction

hyper-reflexia

sensory loss

muscle weakness or wasting

loss of tone below the level of suspected injury

hypotension and bradycardia (neurogenic shock)

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14
Q

which of the following is the most important investigation for spinal cord compression in the event of a trauma

1) MRI spine
2) CT head
3) CT Spine

A

CT spine

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15
Q

Management of spinal cord compression caused by acute trauma

A

Immobilisation + decompression/stabilisation surgery

IV corticosteroid –> dexamethasone

VTE prophylaxis

maintenance of volume and BP

prevention of gastric ulcers

nutritional support

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16
Q

Management of non-traumatic intervertebral disc compression

A

decompressive laminectomy

VTE prophylaxis

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17
Q

Management of SCC caused by malignant spinal compression

A

16 mg dexamethasone +/- surgery +/- radiotherapy

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18
Q

Is male or female more susceptive for osteoarthritis

A

Female is 3 x male

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19
Q

what is the pathophysiology of osteoarthritis

A

damage to cartilage –> repair attempt but is disordered –> cartilage ulceration exposes underlying bone to inc stress –> bone attempts to repair but produces abnor sclerotic subchondral bone and overgrowth at join margins (osteophytes)

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20
Q

which of the following secondary causes of osteoarthitis

1) RA
2) Gout
3) Seronegative spndyloarthropathy
4) Paget’s disease of bone
5) all of the above

A
RA 
gout 
seronegative spondyloarthropathy 
Paget's disease of bone 
vascular necrosis eg corticosteriod therapy 
haemarthrosis
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21
Q

which of the following symptom is not commonly associated with osteoarthritis

1) relieved by rest
2) worse on exercise
3) worse on rest
4) involvement of PIP joint

A

worse on rest - it is more common associated with RA

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22
Q

what are the acronym “LOSS” stands for when it is related to radiological changes caused by osteoarthritis

A

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

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23
Q

which of the following is an appropriate management for osteoarthritis

1) azathioprine
2) vit D - calcium supplement
3) Bisophopnates
4) topical capsaicin
4) None of the above

A

topical capsaicin

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24
Q

which T score describes osteoporosis

1) -1.4
2) -1.9
3) -2.4
4) -2.9
5) -3.4

A

4) T score of -2.5 or less (ie 2.5 SD lower to the median number) = osteoporosis
- 1 to -2.5 = osteopenia
- 1 = normal

T score of -2.5 or less & 1 fracture = severe osteoporosis

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25
Q

what is the single most important clinical feature of osteoporosis

A

low-trauma fragility fracture

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26
Q

what is the most used risk assessment of osteoporosis fracture risk

A

FRAX risk assessment (10 - year risk of fracture)

27
Q

what is the most important investigation conducted for osteoporosis

A

DEXA scan - bone density scan conducted in either the hip, wrist and spine

28
Q

what is the general regime of managing osteoporosis

A

Vit D + calcium = colecalciferol

Bisphosphonates (alendronate) reduced activity of osteocast

29
Q

What is the main pathology/aetiology of ankylosing Spondylitis

A

a from of chronic inflammation of bones which results in fusion of the bones, especially common in the spine and iliosacro joint

aetiology unknown

30
Q

what is the gene affected in ankylosing spondylitis

A

HLA B27

31
Q

what are some of the most common intra-articular symptoms of ankylosing spondylitis

A

back/buttock pain which is worsen by rest and improved by exercise.

morning pain is common

Chest pain can be present due to involvment of costosternal / costovertebral joints

reduced range of movment

Question Mark Posture –> loss of lumbar lordosis, exaggravated thoracis kyphosis with neck sticking forward like a question mark

Peripheral enthesitis –> where tendon and ligament insert into bone –> causing plantar fascilitis & Achilles tedonitis

Peripheral athritis –> hip, shoulder and chest wall

32
Q

what are some of the most common extra-articular symptoms of ankylosing spondylitis

A

fever, weight loss, fatigue

acute anterior uveitis

aortitis & aortic regurgitation & heart block

IgA nephropathy & amyloidosis

cauda equina syndrome, atlanto-axial subluxation

osteopenia nad osteoporosis

33
Q

investigation for ankylosing spondylitis

A

FBC - normochromic normocytic anaemia of chronic disease

U&E - kidney damage

ALP - elevated due to chronic disease

CRP - often elevated

X-ray of the joint involved - most helpful

MRI - for early AS

DEXA - osteoporosis

Schober’s test

34
Q

which creteria is used to diagnose AS

A

modiefed New York Criteria

Clinical criteria

1) low back pain for > 3 months - worsened by rest and improve by exercise
2) limitation of lumbar spine motion
3) limit to chest wal expanision

Radiological criteria
1) sacroiliitis in X-ray

Definite AS = radiological + at least 1 of clinical criteria

Possible AS = all 3 clinical criteria or just radiological criteria

35
Q

Management for anklosing spondylitis ?

A

symptoms control

1st line - NSAIDs + PPI +/- pain ladder
2nd line - TNF-alpha inhibitos (etanercept) / mnoclonal antibody against TNF eg (adelimumab)
oral corticosteriods for short term measurement

36
Q

Is male more common to get RA or OA

A

Neither - female more common to get both

37
Q

what is the pathophysiology of RA

A

production of rheumatoid factor in synovium by plasma cells

rheumatoid factor interact with macrophages, T and B cells –> overproduction of TNF & macrophages also releases chemoattrants to de-activate osteoblast but activate osteoclast –> bone erosion & further bone damages

38
Q

which genes are more susceptible to RA

A

HLA-DR4 and HLA-DRB

39
Q

what are the most prominent associating symptoms of RA

A

joint pain most commonly affecting the MCP, PIP (DIP is usually OA and never affected)

worse with rest and better with exercise

progressive, symmetricla, peripheral polyarthritis

ulnar deviation, Z thrumb, swan neck & Boutonniere deformity

40
Q

what are some of the common extra-artiuclar problem of RA

A

fatigue and weakness

vasculitis

fibrosing alveolitis

pleural and pericardial effusions

Raynaud’s

carpel tunnel syndrome

splenomegaly

osteoporosis

amyloidosis

41
Q

which criteria is used to diagnose RA

A

the ACR/EULAR 2010 criteria for RA

if more than 6/10 = diagnostic

42
Q

what are some of the investigations for RA

A

FBC - anaemia

U&E

CRP/ESR - acute phase proteins

Serology - rheumatoid factors & anti citrullinated peptide antibodies

X-ray of affected joints

aspiration of joint to exclude septic arthritis

43
Q

what is the mainstay management of RA

A

simple analgesia +/- NSAIDs or COX2 inhibitors

DMARDs - disease modifying antirhuematic rugs eg methotrexate, sulfaszalazine, leflunomide

corticosteroids - short term measure - oral/intra-articular injection

44
Q

what is the treatment

A

Methotrexate + 1x DMARDs + glucocorticoids (cortisone)

45
Q

which drug can you use if RA fails to response

A

if 2 x 6 month trial of traditional DMARDs therapy fails to control symptoms

46
Q

Definition of Polymyalgia Rheumatica

A

inflammatory condition of unknown cause which is characterised by severe bilateral pain and morning stiffness of the shoulder neck and pelvic girdle

47
Q

what is the earliest age which polymyalgia rheumatica has been reported?

A

50 yrs old

48
Q

what are the 4 diagnostic criteria for polymyalgia rheumatica

A

1) 50 yrs old
2) subacute/acute onset of bilateral, severe and persistent pain in the neck, shoulder and pelvic girdle
3) morning stiffness > 45 min
4) evidence of acute phase response (raised ESR/CRP) - can still be diagnosed if ESR/CRP normal if classic clinical picture & response to steroids

49
Q

what are some of the clinical features of polymyalgia rheumatica

A

pain in the neck, shoulder and pelvic girdle

morning stiffness

proximal weakness

systemic - low grade fever, malaise, fatigue, anorexia, weight loss, depression

upper arm tenderness

carpal tunnel syndrome

50
Q

investigations for polymyalgia rheumatica

A

basically a diagnosis of exclusion

ESR/CRP

FBC, U&Es, LFT, Bone profile, TFTs, CK

protein electrophoresis

Rheumatoid factors

Urinary Bence Jones’ protein (multiple myeloma)

Anti-nuclear antibody (SLE)

USS of shoulder +/- hip if uncertain  subdeltoid bursitis

51
Q

what is the treatment for polymyalgia rheumatica

A

prednisolone

weak 1-3 15mg daily prednisolone then reducing dose

52
Q

what causes gout

A

accumulation of uric acid which results in crystal in the joint space –> can be explained by increase purine intake from cheese, meat and red wine

53
Q

is male or female more likely to get gout

A

male 3.6:1

54
Q

which joint is the most commonly affected joints in Gout

A

big toe, metattatso-phalangeal joint (then ankle, wrist, base of thumb)

55
Q

what are some of the clinical features of gout

A

sudden onset severe pain associated with swelling, redness, warmth and tenderness –> reach max pain in 24 hours

Tophi maybe able to be felt

56
Q

what are the investigations for gout

A

asppiration of joints –> -ve birefringence polarised light

joint x-ray - space between joint maintined, lytic lesions, punched out erosions,

serum uriac acid - not acute phase investigation

57
Q

management of gout

A

acute flare

  • NSAIDs (diclofenac) + PPI
  • colchicine

prophylaxis
- allopurionol/ febuxostat

58
Q

which molecules cause pseudogout

A

calcium pyrophosphate

59
Q

which of the following is a risk factor for pseudogout

1) inc meat consumption.
2) hypoparathyroidism
3) infection
4) haemochromatosis
5) CKD

A

Haemochromatosis

other causes 
•	Dehydration 
•	intercurrent illness 
•	hyperparathyroidism 
•	long-term use of steroids 
•	hypothyroidism 
•	any causes of arthritis 
•	haemochromatosis 
•	Wilson’s disease 
•	Acromegaly 
•	Dialysis
60
Q

single most prominent clinical features for pseudogout

A

sudden onset, red, hot, tender joint & swelling in one joint

61
Q

which does pseudogout affects the most?

A

knee –> wrist –> shoulders –> ankles –> hands and feet

62
Q

investigation for pseudogout?

A

join spiration –> _ve bifringement in polarised light

joint x-ray –> linear opacification of articular cartilage

serum calcium - elevated

serum PTH - elevated

63
Q

management of pseudogout

A

supportive + symptomatic control - RICE, NSAIDs, colchicine