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MSK > rheumatology conditions > Flashcards

rheumatology conditions Flashcards

1
Q

osteoarthritis

A
  • non-inflammatory condition
  • occurs in synovial joints

imbalance between cartilage wearing down + chondrocytes repairing it

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2
Q

osteoarthritis appearance on x-ray

A

L - loss of joint space
O - osteophytes (bone spurs)
S- subarticular sclerosis (increased density of bone along joint line)
S - subchondral cysts (fluid filled holes in bone)

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3
Q

presentation of osteoarthritis

A
  • joint pain + stiffness that’s worse with activity + @ end of day
  • bulky, bony enlargement of joint - Hebredens + bouchards nodes
  • restricted range of movements / crepitus
  • fluid around joints
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4
Q

what is the difference between heberdens nodes and bouchards nodes?

A

heberdens nodes = joints of distal finger (DIPs)

bouchards nodes = proximal finger (PIPs)

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5
Q

what is the main clinical difference between rheumatoid arthritis and osteoarthritis?

A

osteoarthritis - worse at with activity + at end of day, non-inflammatory

rheumatoid - improves with activity + worst after rest, inflammatory

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6
Q

is rheumatoid arthritis more common in men or women?

A

3 x more commo in women - usually presents middle aged + with family history

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7
Q

genes associated with rheumatoid arthritis

A

HLA DR1 - occasionally present in rheumatoid arthritis patients

HLA DR4 - often present in rheumatoid FACTOR positive patients

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8
Q

rheumatoid arthritis

A

autoimmune
inflammatory

chronic inflammation of synovial lining (synovitis) of joints, tendon sheaths + bursa - inflammation increases risk of tendon rupture

usually symmetrical + affects multiple joints = symmetrical polyarthritis

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9
Q

pathophysio of rheumatoid arthritis

A

rheumatoid factor = autoantibody in 70% of RA patients

–> it targets the Fc portion of the IgG antibody causing activation of immune system against patients own IgG causing systemic inflammation

RF is most commonly IgM but can be any

anti-CCP antibodies are distributed through circulation + form immune complexes with CCP produced in the inflamed synovium

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10
Q

signs of rheumatoid arthritis in hands

A
  • Z shaped thumb
  • swan neck = hyperextended PIP + flexed DIP
  • boutonnieres = hyperextended DIP + flexed PIP
  • ulnar deviation of fingers at the knuckle
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11
Q

extra-articular manifestations of rheumatoid arthritis

A
  • pulmonary fibrosis - caplan’s syndrome
  • broncholitis obliterans
  • Felty’s syndrome
  • lymphadenopathy
  • carpel tunnel syndrome
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12
Q

diagnosis of rheumatoid arthritis

A

clinical if - symmetrical polyarthropathy affecting small joints

check rheumatoid factor + anti-CCP
inflammatory markers - CRP + ESR

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13
Q

management of rheumatoid arthritis

A

MDT - occupational, physio, podiatry
steroids for flares
NSAIDs/COX-2 inhibitors - prescribe with PPI

1st line = monotherapy of either: methotrexate, leflunomide, sulfasalazine
2nd = 2 of above in combo
3rd = methotrexate + biological therapy (usually TNF inhibitor)
4th = methotrexate + rituximab

hydroxychloroquine = mildest rheumatic drug

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14
Q

does pregnancy improve or worsen symptoms of rheumatoid arthritis?

A

improves

medication of choice during pregnancy = sulfasalazine / hydroxychloroquine

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15
Q

management of septic arthritis

A
  • empirical IV antibiotics until sensitivities known
  • antibiotics for 3-6weeks

1st line = flucloxacillin + rifampicin

penicillin allergy, MRSA or prosthetic joint = vancomycin + rifampicin

alternative = clindamycin

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16
Q

septic arthritis investigations

A

aspirate joint prior to antibiotics, send for -

  • gram staining
  • crystal microscopy
  • culture
  • antibiotic sensitivities
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17
Q

most common causative organism of septic arthritis

A

staph aureus !

neisseria gonorrhoea (gram neg diplococcus) - sexually active
Group A Strep - strep pyogenes
haemophilus influenza
e. coli

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18
Q

diagnosis of osteoarthritis

A

no need for investigations if over 45 and has typical symptoms + NO morning stiffness or lasts under 30 mins

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19
Q

what can trigger rheumatoid arthritis?

A

infections + smoking

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20
Q

scoring used for rheumatoid arthritis

A

DAS28 score

- disease activity score - useful for monitoring + response to treatment

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21
Q

when are biologics used in the treatment of rheumatoid arthritis?

A

when 2 DMARDs tried or DAS28 >5.1

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22
Q

side effects of DMARDs

A
  • increased risk of infection
  • liver function derrangement
  • pneumonitis !
  • nausea

methotrexate

  • teratogenic - must be stopped at least 3 months prior to conception
  • needs regular blood monitoring
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23
Q

anti-TNF side effects

A
  • increased risk of infection
  • increased risk of skin cancer
  • exacerbation of heart failure
  • reactivation of latent TB
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24
Q

what gene is common in seronegative spondylarthritis’s?

A

HLA B27

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25
Q

common presentations amongst spondyloarthropathies

A
  • enthesitis = inflammation at insertion of tendons into bones
  • dactylitis = sausage digits
  • anterior uveitis, conjunctivitis
  • mucocutaneous lesions
  • aortic incompetence or heart block
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26
Q

key joints affected in ankylosing spondylitis

A

sacroiliac joints + vertebral column

inflammation causes joint pain + stiffness - can progress to fusion of joints (“bamboo spine”)

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27
Q

classic presentation of ankylosing spondylitis

A
  • young male in late teens / 20s
  • symptoms develop gradually over 3 months + can flare
  • lower back pain + stiffness + sacroiliac pain in buttock region
  • – worse with rest + improves with movement
  • – worse at night + in morning - may wake from sleep

associations = weight loss, chest pain, enthesitis, dactylitis, pulmonary fibrosis

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28
Q

what is Schobrt’s test and what is it used to diagnose?

A

used to assess mobility spine
find L5 vertebra - mark point 10cm above + 5cm below
ask patient to bend forward as far as they can + measure distance between 2 points

ankylosing spondylitis - distance <20cm

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29
Q

investigations in ankylosing spondylitis

A
  • Schober’s test
  • CRP + ESR - raised
  • x-ray of spine + sacrum
  • MRI of spine can show bone marrow oedema in early disease pre x-ray changes
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30
Q

ankylosing spondylitis x-ray appearance

A

bamboo spine
squaring of vertebral bodies
sunchondral sclerosis + erosion
syndesmophytes = areas of bone growth where lligaments insert into bone
ossification of ligaments, discs + joints (they turn into bone)
fusion of facet, sacroiliac + costovertebral joints

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31
Q

treatment of ankylosing spondylitis

A
  • NSAIDs for pain
  • steroids during flares
  • anti-TNF - etsnercept, infliximab
  • secukinumab if above inadequate
  • physio, avoid smoking
  • bisphosphonates to treat osteoporosis
  • surgery sometimes required for deformities to spine / other joints
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32
Q

psoriatic arthritis appearance on x-ray

A
  • periostitis = inflammation of periosteum causing thickened + irregular outline of bone
  • ankylosis = bones joining together causing stiffening
  • osteolysis

pencil-in-cup appearance - central erosions of bone beside joint

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33
Q

severe form of psoriatic arthritis

A

arthritis mutilans

  • occurs in phalanxes
  • osteolysis around joints + digits

-> leads to progressive shortening of digit, skin then folds as the digit shortens giving “telescopic finger”

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34
Q

reactive arthritis

A

where synovitis occurs in the joints as a reaction to a recent trigger

-> usually 1-4 weeks post infection (nothing can be cultured from synovial fluid)

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35
Q

triggers of reactive arthritis

A

gastroenteritis (enterogenic) - salmonella, shigella, yersinia

sexually transmitted infection - chlamydia

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36
Q

reactive arthritis presentation

A

“can’t see, pee or climb a tree”

  • bilateral conjunctivitis / anterior uveitis
  • circinate balantis = dermatitis of head of penis
  • warm, swollen, painful joint - acute monoarthritis affecting single joint of lower limb (knee = commonest)
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37
Q

reactive arthritis management

A
  • NSAIDs
  • steroid injections into affected joints (systemic steroids if multiple joints)
  • may resolve within 6 months + no recur
  • -> recurrent = DMARDs / anti-TNF
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38
Q

septic arthritis presentation

A

rapid onset of -

  • hot, red, swollen, painful
  • stiffness + reduced range of movement
  • systemic symptoms - fever, lethargy + sepsis
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39
Q

common causative organisms in septic arthritis

A

most common = staph aureus

  • neisseria gonorrhoea (gonococcus, gram neg diplococcus)
  • -> in sexually active, exclude in young patients
  • Group A Strep - strep pyogenes
  • haemophilus influenza
  • e. coli
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40
Q

enteropathic arthritis

A

associated with IBD - symptoms worse during flares

–> watery stool with mucus + blood

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41
Q

risk factors for gout

A
  • high purine diet (meat, seafood), diuretics
  • obesity, alcohol, psoriasis
  • renalfailure, hypothyroidism
  • fam history

rare under 20s, decreases after age 80
more common in men, very rare in premenopausal women

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42
Q

causes of gout

A

hyperuricaemia
–> hyperuricaemia results in crystallisation encouraged by lower temp (synovial fluid = 32 degrees)

  1. increased urate production
  2. reduced urate excretion
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43
Q

typical joints affected in gout

A

base of big toe (metarsophalangeal)

wrists

base of thumb (carpometacarpal)

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44
Q

gout presentation

A
  • affecting big toe, wrists, base of thumb
  • rapid onset severe pain
  • tophi - subcutaneous deposits of uric acid
  • erythema + warmth
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45
Q

gout investigations

A
  • serum uric acid raised
  • polarised microscopy of synovial fluid
  • – strongly negative birefringent needle-shaped crystals
  • – monosodium urate crystals
  • x-ray = punched out erosions with sclerotic borders
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46
Q

treatment of acute attack of gout

A

ACUTE

  • NSAIDs - not in CKD
  • colchicine
  • steroids

PREVENTATIVE treatment
-> start 2 weeks after acute attack until urate is <360

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47
Q

preventative treatment of gout

A

start 2 weeks after acute attack until urate <360

  • allopurinol (xanthine oxidase inhibitors)
  • ->DON’t give in acute, rash in elderly + renal impaired, interacts with azathioprine
  • uricosuric drugs - probenecid, sulphinpyrazone
  • interleukin-1 inhibitors

lose weight, drink less, eat less meat/seafood

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48
Q

investigations for pseudogout

A

aspirate synovial fluid

  • no bacterial growth
  • calcium pyrophosphate crystals
  • rhomboid shaped crystals
  • positive birefringent of polarised light
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49
Q

treatment of pseudogout

A
  • NSAIDs
  • colchicine
  • steroids
  • rehydration
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50
Q

what minority does SLE commonly affect?

A

more common in women + asians/afro-caribbean

usually young - middle aged

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51
Q

systemic lupus erythematosus

A

inflammatory autoimmune connective tissue disorder
effects multiple organs + systems
relapsing-remitting course - result of chronic inflammation
shortened life expectancy

52
Q

pathophysio of SLE

A

complexes of antigens + auto-antibodies form + circulate - deposition of immune complexes in basement membrane which activates complement + leucocytes

when immune system is activated by anti-nuclear antibodies it generates an inflammatory response - chronic inflammation causes necrosis + scarring and is what causes symptoms

53
Q

what part of the pathphysio of SLE drives the disease?

A

immune complexes of antigens + auto-antibodies in basement membrane which activates complement + leucocytes

54
Q

presentation of SLE

A 
photosensitive malar rash - butterfly rash
weight loss, fatigue, fever
joint + muscle pain
lymphadenopathy + splenomegaly
SOB, pleuritic chest pain
mouth ulcers, hair loss, raynauds
delirium, psychosis, seizures
55
Q

SLE investigations

A

autoantibodies

    • ANA - not very specific
    • anti-double stranded DNA - specific to SLE

FBC - normocytic anaemia
C3 + C4 levels decreased in active

56
Q

how do anti-dsDNA levels change with the activity of SLE?

A

rises with activity

57
Q

treatment of SLE

A

NSAIDS
steroids - prednisolone
hydroxychloroquine = first line for mild SLE

suncream/sun avoidance

resistant/severe SLE = methotrexate
–> biologics if unresponsive

58
Q

Sjogren’s syndrome

A

autoimmune condition affecting exocrine glands
F:M = 9:1
increased risk of lymphoma

primary or secondary (to SLE or rheumatoid arthritis)

59
Q

Sjogren’s presentation

A

dry mucous membranes

  • dry mouth
  • dry eyes
  • dry vagina
60
Q

Sjogren’s investigations

A
  • schirmer test - paper in eyelid + distance of tears measured after 5 mins
  • – normal = 15mm, bad <10mm
  • anti-Ro + anti-La
61
Q

antibodies associated with Sjogren’s syndrome?

A

Anti-Ro

Anti-La

62
Q

management of Sjogren’s

A

hydroxychloroquine to halt disease progression

artificial tears + saliva, vaginal lubricants

63
Q

complications of Sjogren’s

A
  • eye infections - conjuntivitis, corneal ulcers
  • oral problems - dental cavities, thrush
  • vaj problems - candidiasis + sexual dysfunction

lymphoma
pneumonia + bronchiectasis

64
Q

systemic sclerosis presentation

A 
limited cutaneous (face + below elbows + knees only) - CREST
C- calcinosis
R - raynaud's 
E - oEsphageal dysmotility
S - sclerodactyly
T- Telangiectasia

diffuse cutaneous (whole body) - CREST + many internal organs causing -

  • cardio probs - hypertension + CAD
  • lung probs - fibrosis
  • kidney probs - glomerulonephritis, scleroderma renal crisis
65
Q

systemic sclerosis presentation

A 
limited cutaneous (face + below elbows + knees only) - CREST
C- calcinosis
R - raynaud's 
E - oEsphageal dysmotility
S - sclerodactyly
T- Telangiectasia

diffuse cutaneous (whole body) - CREST + many internal organs causing -

  • cardio probs - hypertension + CAD
  • lung probs - fibrosis
  • kidney probs - glomerulonephritis, scleroderma renal crisis
66
Q

what is sclerodactyly?

A

skin changes in hands
-> as skin, restricts normal range of motion of joints - skin can break + ulcerate, patient can’t make fist/straighten hand properly

67
Q

autoantibodies associated with systemic sclerosis

A

antinuclear antibodies(ANA) - positive in most patients, not specific

anti-centromere - limited cutaneous
anti-Scl-70 - diffuse cutaneous (more severe)

68
Q

systemic sclerosis investigations

A

nailfold capillaroscopy

anti-centromere/anti-Scl-70 autoantibodies

69
Q

what is nail capillaroscopy and what is it used to investigate?

A

nailfold is magnified + examined to see peripheral capillaries

abnormal capillaries, avascular area, micro-haemorrhages = systemic sclerosis

patients with primary raynauds without systemic sclerosis = normal capillaries

70
Q

treatment for raynauds

A

nifedipine

71
Q

management of systemic sclerosis

A

MDT - occupational, physio
stop smoking
steroids
immunosuppressants

-> no standardised + proven treatment

72
Q

what makes polymyositis + dermatomyositis paraneoplastic syndromes?

A

they can be caused by an underlying malignancy

most common = lung, breast, ovarian, gastric

73
Q

myositis presentation

A

muscle weakness + pain
occurs bilaterally + typically proximally
mostly affects shoulders + pelvic girdle
develops over weeks

others organs = interstitial lung, dysphagia, myocarditis, weightloss, raynauds

74
Q

dermatomyositis skin features

A
  1. gottron lesions - scaly erythematous patches on knuckles, elbows + knees
  2. photosensitive erythematous rash - back, shoulders
  3. purple rash on face + eyelids (helitope rash)
  4. periorbital swelling
  5. subcutaneous calcinosis
75
Q

antibodies associated with dermatomyositis + polymyositis

A

anti-Jo-1 antibodies
anti-Mi-2
anti-nuclear

76
Q

dermatomyositis + polymyositis investigations

A

muscle biopsy = definitive diagnosis
creatine kinase
anti-Jo-1, anti-Mi-2, ANA

electromyography (EMG) - increased fibrillation, abnormal motor potentials, repetitive discharges

77
Q

management of dermatomyositis + polymyositis

A

steroids = first line, if inadequate -

    • immunosuppressants - azathioprine
    • IV immunoglobulins
    • biological therapy - infliximab

new cases should be assessed for underlying cancer

78
Q

osteoporosis

A

a reduction in bone mineral density

  • less strong bone = prone to fractures
  • can be secondary to endocrine (cushings, hyperparathyroidism) + GI (hepatic insuffieciency, vit C + D deficiency) disorders

(osteopenia = less severe reduction in density)

79
Q

osteoporosis risk factors

A 
old, reduced activity
low BMI (<18.5)
female, postmenopausal (less oestrogen which is protective against osteoporosis)
rheumatoid arthritis
alcogol + smoking
low vit D + calcium
long term corticosteroids
80
Q

osteoporosis investigations

A

DEXA scanning - provides measure of bone mineral density

normal serum calcium + phosphate

81
Q

osteoporosis treatment

A 
bisphosphonates (alendronate) - reduces osteoclastic resorption
monoclonal antibody (desunoman) - reduces osteoclast activity

diet, exercise, sun exposure
calcium + vit D supplements

82
Q

bisphosphonates side effects

A
  • reflux + oesophageal erosions
  • atypical fractures - femoral fractures
  • osteonecrosis of jaw
  • osteonecrosis of external auditory canal

examples: alendronate, risedronate, zoledronic

83
Q

MoA of bisphosphonates

A

interfere with osteoclasts + reducing their activity, preventing reabsorption of bone

84
Q

osteomalacia

A

qualitative defect
defective bone mineralisation - “soft” bones
results from insufficient vit D

when occurs in kids prior to growth plates closing = rickets

85
Q

osteomalacia risk factors

A

darker skin
low sun exposure
spends lots of time indoors
colder climates

malabsorption - IBD
chronic kidney disease - kidneys r essential in metabolising vit D to its active form

86
Q

osteomalacia treatment

A

supplementary vit D = colecalciferol

87
Q

osteomalacia investigations

A

serum 25-hydroxyvitamin D - <25 = deficiency, 25-50 = insufficiency

LOW serum calcium + phosphate
DEXA shows low mineral density

serum alkaline phosphate may be high
parathyroid hormone may be high - secondary hyperparathyroidism

88
Q

pathophysio of osteomalacia

A
  1. vit D is essential in calcium + phosphate absorption from intestines + kidneys - calcium + phosphate r required for bone construction
  2. vit D also responsible for regulating bone turnover + promoting bone reabsorption to boost serum calcium level
    * low calcium causes secondary hyperparathyroidism - parathyroid gland tries to raise calcium levels by secreting PTH which increases reabsorption from bone (causes further problems)
89
Q

Paget’s disease

A

disorder of excessive bone turnover - excessive activity of osteoblast + osteoclasts
–> not coordinated - patchy areas of high density (sclerosis) + low density (lysis)

increase risk of pathological fractures
particularly affects axial skeleton

90
Q

complications of paget’s disease

A

osteosarcoma

spinal stenosis + spinal cord compression - deformity leads to spinal cord narrowing, presses on spinal nerve causing symptoms

91
Q

polymyalgia rheumatica

A

inflammatory causing pain + STIFFNESS in shoulders, pelvic girdle + neck

occurs exclusively in those over 50
more common in women + Caucasians

strong associations with giant cell arteritis

92
Q

polymyalgia rheumatica presentation

A

bilateral shoulder/pelvic girdle pain
worse with movement + interferes with sleep
stiffness for at least 45 mins in morning
muscle strength is normal

symptoms of giant cell arteritis

93
Q

what blood abnormalities would you expect to see in a patient with fibromyalgia?

A

no abnormalities/all Ix normal - clinical diagnosis

(widespread pain, unrefreshed sleep, cognitive symptoms, fatigue) for >= 3months

94
Q

polymyalgia rheumatica investigations

A

exclude differentials
diagnosis based on clinical presentation + rapid response to steroids

raised inflammatory markers

95
Q

polymyalgia rheumatica treatment

A

15mg prednisolone daily (40-60mg if signs of giant cell arteritis)
– start reducing if good response @ 3-4weeks (reduce over 18months - 2yrs)

*if poor response after 1 week - probs not PMR, stop steroids !

96
Q

types of vasculitis affecting small vessels

A

Henoch-Schonlein purpura (HSP)

Eosinophilic granulomatosis with polyangitis (Churg-Strauss syndrome)

Microscopic polyangitis

Granulomatosis with polyangitis (Wegener’s granulomatosis)

97
Q

types of vasculitis affecting medium vessels

A

Polyarteritis nodosa

eosinophilic granulomatosis with polyangitis (Churg-Strauss syndrome)

Kawasaki disease

98
Q

types of vasculitis affecting large vessels

A

Giant cell arteritis

Takayasu’s arteritis

99
Q

Henoch-Scholein purpura (HSP)

A

IgA deposits in blood vessels of affected organs
children <10
purpuric rash on lower limbs/bum
often triggered by infection 1-3 weeks previous
management = supportive, analgesia/rest
– resolve within 8 weeks (may relapse)

100
Q

eosinophilic granulomatosis with polyangitis (Churg-Strauss)

A

small + medium vessels
lung + skin
severe asthma in late teenage years
raised eosinophils

101
Q

microscopic polyangitis

A

renal failure

SOB + haemoptysis

102
Q

causes of chest pain in SLE

A

PE
pericarditis
MI
pleurisy

103
Q

most appropriate first test in patient with SLE

A

urinalysis

-> if evidence of blood/protein, renal biopsy can be done

104
Q

what clinical features are included in the modified New York criteria for diagnosis of ankylosing spondylitis?

A

back pain > 3 months
back pain worse at rest + relieved with movement
x-ray changes of spondylitis

105
Q

x-ray finding indicative of pseudogout

A

chondrocalcinosis

106
Q

how are uric acid crystals seen under polarised light microscopy?

A

negatively birefringent, needle shaped crystals

GOUT

107
Q

which type of crystals are responsible for Milwaukee shoulder?

A

hydroxyapatite crystals

108
Q

how do calcium pyrophosphate crystals appear under polarised light microscopy?

A

positively birefringent, rhomboid/envelope shaped crystals

PSEUDOGOUT

109
Q

Z-shaped thumb + squaring of thumb base are clinical features of what diseases?

A

z-shaped thumb = rheumatoid arthritis

squaring of thumb base = osteoarthritis

110
Q

what are uricosuric agents?

A

enhance renal clearance (do not affect uric acid production but inhibit reabsorption of uric acid)

contraindicated in renal impairment

examples: probenecid, sulfinpyrazone

111
Q

what does “golder’s elbow” affect?

A

medial epicondyle

112
Q

what does “tennis elbow” affect?

A

lateral epicondyle

113
Q

Is ANCA positive in every type of vasculitis?

A

NO - large + medium vessel vasculitides are generally negative for ANCA

114
Q

granulomatosis with polyangiitis (Wegener’s granulomatosis)

A

affects respiratory tract + kidneys
presentation = saddle shaped nose, hearing loss, nose bleeds, crusty nasal secretions, cough, wheeze, haemoptysis

(small vessels)

115
Q

polyarteritis nodosa

A

associated with hep B - also hep C + HIV
medium vessels

associated with livedo reticularis rash (mottled, purplish, lace like rash)

116
Q

which types of vasculitis commonly affect kids?

A

Henoch-Schonlein purpura (HSP) - <10

Kawasaki Disease - <5

117
Q

Kawasaki disease

A

affects young (<5), medium vessels

persistent high fever >5days
erythematous rash, bilateral conjunctivitis
skin peeling of palms + soles
**“strawberry” tongue - red with prominent papillae

treatment = aspirin + IV immunoglobulins
complication = CAD
118
Q

investigations of vasculitis

A

inflam markers + urine dipstick

immunofluorescence to detect anti-neutrophil cytoplasmic antibodies (ANCA)

    • p-ANCA (MPO) = microscopic polyangiitis + Churg-Strauss syndrome
    • c-ANCA (PRS antibodies) = Wegener’s granulomatosis
119
Q

what are p-ANCA (MPO antibodies) associated with?

A 
microscopic polyangiitis (renal failure, SOB+haemoptysis)
Churg-Strauss syndrome (severe asthma in late teenager, high eosinophils)
120
Q

what are c-ANCA (PR3 antibodies) associated with?

A

Wegener’s granulomatosis (saddle shaped nose, hearing loss)

121
Q

risk factors for giant cell arteritis

A

white females over 50

associated with polymyalgia rheumatica

122
Q

giant cell arteritis presentation

A

temporal arteries prominent with reduced pulsation
unilateral headaches around temple + forehead
tender scalp
temporary visual disturbances
jaw claudication

123
Q

how is giant cell arteritis diagnosed?

A

temporal artery biopsy = “multinucleated giant cells”

presentation
raised ESR
duplex US of temporal artery = hypoechoic halo

124
Q

Takayasu’s arteritis

A

mainly aorta + it’s branches - swell + form aneurysms / become narrowed + blocked
under 40, asian, women

Px = claudication, syncope, fever, muscle aches
diagnosis = CT or MRI angiography / doppler US in carotid disease
125
Q

treatment of giant cell arteritis + Takayasu’s arteritis

A

steroids

MSK (14 decks)

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