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Finals > Rheum > Flashcards

Rheum Flashcards

1
Q

what does the ACR / EULAR diagnostic criteria look at in RA?

A

joint involvement, acute phase markers, serology and duration of symptoms. Need 6 or above for definite diagnosis.

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2
Q

what is Felty’s syndrome?

A

neutropenia, spenomegaly, RA

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3
Q

what is Caplan’s syndrome?

A

pneumoconiosis and RA

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4
Q

what is the classic pattern of joint involvement in RA?

A

symmetrical synovitis involving MCP, PIP, MTP, wrists and knees.

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5
Q

what genes are associated with RA?

A

HLA DR4 / DB1

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6
Q

what are the hand deformities seen in RA?

A

dorsal wrist subluxation, fingers subluxation, ulnar deviation of the fingers, z thumb, boutonniere’s deformity (flexed PIP, extended DIP), swan neck deformity (hyperextended PIP, flexed DIP)

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7
Q

what are rheumatoid nodules?

A

Subcutaneous central areas of fibroid necrosis

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8
Q

what are rheumatoid nodules associated with?

A

extensive disease, RhF positivity and extra-articular manifestations. they can be exacerbated by methotrexate therapy.

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9
Q

what extra-articular manifestations are there in RA?

A

lungs -pulmonary fibrosis, obliterative bronchitis, pleural effusion
heart - pericarditis, coronary artery disease
skin - vasculitis, raynauds
renal -amyloiosis

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10
Q

how are anti-CCP antibodies better than anti-RF?

A

they are more specific (98%) - just as sensitive though (~70%)

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11
Q

what are the XR signs seen in RA?

A
  1. junta-articular osteopenia
  2. joint erosion
  3. joint destruction and damage
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12
Q

what does the DAS28 mean?

A

this looks at # swollen joints, # tender joints, ESR / CRP and patients global assessment of health.
>5.1 = high disease activity
<3.2 = low disease activity
<2.6 = low disease activity

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13
Q

where are Heberden’s and Bouchard’s nodes?

A

In osteoarthritic hands. Heberdens is at the DIP and Bouchards are at the PIP.

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14
Q

what kind of XR would you want in osteoarthritis knees?

A

weight-bearing

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15
Q

what would you see on an XR of an osteoarthritic joint?

A

Loss of joint space
osteophyres (bony spurs at joint margins)
sub-chondral sclerosis and cysts

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16
Q

what is reactive arthritis?

A

a sterile arthritis which occurs in response to an infection

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17
Q

what organisms are associated with reactive arthritis?

A

urogenital - chlamydia

enterobacteria - Yerisnia, Shigella, salmonella, campylobacter

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18
Q

what are possible extra-articular manifestations in reactive arthritis?

A

sterile conjunctivitus, sterile urethritis, keratoderma blenorrhagica (papulaosquamous rash on soles of feet)

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19
Q

which genotype of people are likely to develop reactive arthritis?

A

HLAB27

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20
Q

what is seen in the joint fluid aspirate in reactive arthritis?

A

gains macrophages (reiter’s cells)

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21
Q

what is the treatment for septic arthritis?

A

arthocentesis, washout and debridement
IV antibiotics for 6w OPAT
early PT

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22
Q

what are the most common causative organisms in septic arthritis?

A

S. Aureus, S. Pneumoniae, N Gonococcus

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23
Q

how many psoriasis patients will suffer from arthritis?

A

10%

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24
Q

how does psoriatic arthritis present?

A

asymmetrical joint involvement, DIPs > PIPs, sacroilitis.
nail changes - onycholysis (pitted nails which appear to be lifted off the skin at the distal edges), hyperkeratosis
dactylitis
extra-articular manifestations are more common
XR - pencil in cup deformity, arthritis multilans (destruction of bones of feet and hands)

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25
Q

what are the extra-articular manifestations seen in ankylosing spondylitis?

A

the 5 As. achilles tendonitis, apical lung fibrosis, anterior uveitis, aortic regurgitation, amyloidosis in the kidneys.

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26
Q

Name 3 seronegative arthritides

A

ankylosing spondylitis, enteropathic arthritis, psoriatic arthritis.

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27
Q

what is Schober’s test?

A

5cm below and 10cm lumbosacral junctions (where back dimples are) and ask patients to bend over. <5cm extension is pathological. This is used to support a diagnosis of ankylosing spondylitis.

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28
Q

what is the classic posture seen in advanced ankylosing spondylosis?

A

kyphosis and neck hyperextension.

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29
Q

what is seen on the XR of ankylosing spondylitis patients?

A

1 sacroilitis
2 vertebral syndesmosiytes
3 bamboo spine

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30
Q

what is gout?

A

gout is crystal monoarthropathy caused by the deposition of monosodium rate crystals

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31
Q

what are the risk factors for gout?

A

increased cell destruction - cytotoxic medications, leukaemia,
intake - purine rich foods, alcohol excess
reduced excretion - diuretics, renal impairment
genetics
being male

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32
Q

What is the most commonly affected joint in gout?

A

1st MTP

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33
Q

what is management of acute gout?

A

NSAIDs
Colchicine
glucocorticoids if renal impairment

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34
Q

when should allopurinol be used in gout?

A

it is used in patients who have >2 attacks / yr. It should be started 3w after an acute attack has resolved (can make acute attack worse).

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35
Q

what do the crystals in gout look like under polarised light?

A

negatively birefringent needle shaped crystals

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36
Q

what are the crystals made out of in pseudogout?

A

calcium pyrophosphate

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37
Q

what do the crystals in pseudo gout look like under polarised light?

A

positively birefringent rhomboid shaped crystals

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38
Q

what is Libman-Sack’s endocarditis?

A

endocarditic vegetations due to Ig deposition. seen in SLE.

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39
Q

what is Jacob’s arthropathy?

A

non-erosive joint deformity due to soft-tissue abnormalities.

40
Q

what is the best marker for disease activity in SLE?

A

complement - C3 and C4 both fall in severe active disease. C3 is normal and C4 falls in active disease. they are both normal in inactive disease.

41
Q

What is the ACR diagnostic criteria?

A

need 4 out of 11:

  • skin (malar rash, photosensitive rash, discoid rash, oral ulcers)
  • systemic (serositis, renal involvement, neuro insolemment, non-erosive arthritis in >2 joints)
  • haematological abnormalities
  • immunological abnormalities
  • ANA positive
42
Q

what is the medical treatment for SLE?

A

hydroxychlorquine, low dose steroids, azathioprine / MTX.

If major organ involvement, use a more aggressive approach - IV cyclophosphamide, tacrolimus, biologics, mycophenalate.

for an acute flare: IV cyclophosphamide and high-dose prednisolone

43
Q

what vessels are affected in GCA?

A

large vessels

44
Q

what condition is closely linked to GCA?

A

PMR

45
Q

how does GCA present?

A

unilateral headache of acute onset, scalp tenderness, jaw / tongue claudication, amaurosis fugax (painless transient monocular blindness - due to anterior ischaemic optic neuropathy)

46
Q

what is the most important investigations to do in GCA?

A

temporal artery biopsy - repeat if negative due to skip lesions

47
Q

what is the treatment for GCA?

A

high dose steroids (60mg pred/day), can use steroid sparing agents once in remission. typically, treater two years.

48
Q

what kind of vessels does Takayasu’s arteritis affect?

A

large vessels - typically aorta and major branches of aortic arch.

49
Q

how does Takayasu’s arteritis present

A

initially systemic with fatigue, fever, arthralgia.
Then, ischaemic phenomena - arm claudication, visual disturbance, TIA, stroke, seizure, haemoptysis, haematyria, abdominal pain.

50
Q

how does PAN present?

A

initially myalgia, arthralgia, malaise.
Then palpable purpura, lived reticularis and punched out ulcers on skin.
then organ affects:
- renal - infra-renal arterial aneurysm,haemturia, hypertension
- GI - malena, abdo pain
- heart failure

51
Q

what viral disease is PAN associated with?

A

Hep B

52
Q

what is microscopic polyangiitis?

A

it is a small-vessel vasculitis without evidence of necrotising granulomatous inflammation

53
Q

what are the symptoms of MPA?

A

constitutional symptoms, haematuria, haemoptysis.

no upper resp tract infections.

54
Q

what is ANCA association of PAN?

A

none

55
Q

what is the ANCA associated of MPA?

A

pANCA

56
Q

what is the ANCA association with GwPA?

A

cANCA

57
Q

what is the ANCA association with EGPA?

A

pANCA

58
Q

what’s the new name for Wegner’s?

A

Granulomatosis with polyangiitis

59
Q

how does GPA present?

A

URT - nasal obstruction / ulceration, epistaxis, saddles nose, septal perforation
lungs - cough, haemoptysis, pleuritic chest pain, cavitation
renal - rapidly progressive crescentic GN, proteinuria, haematuria.

60
Q

what is the classic triad seen in EGPA?

A

allergic rhinitis and late onset asthma
eosinophilia
vasculitis

61
Q

what is the genotype associated with Behcets disease?

A

HLA-B5

62
Q

how does Behcets disease usually present?

A

oral / genital ulceration, ocular involvement (anterior / posterior uveitis, iritis, retinal vasculitis), erythema nodosum, papulopustular rash (resembles acne)
Pathergy in the skin (exaggerated skin injury after minor trauma)

63
Q

why should you worry about polymyositis?

A

because it is often attribute to an underlying malignancy (lung, pancreatic, ovarian, bowel)

64
Q

how does polymyositis present?

A

symmetrical proximal straital muscle weakness which affects legs > arms (difficult rising from chair, climbing stairs etc).
can progress to laryngeal, laryngeal and rest muscle involvement.
systemic features are present too (malaise, fever)

65
Q

what is a common non-muscle system involvement seen in polymyositis?

A

interstitial lung disease (present in 30%)

66
Q

what auto-antibody is seen in polymyositis?

A

anti-Jo1

67
Q

what is the treatment in polymyositis?

A

high-dose prednisolone, then azathioprine / methotrexate long-term

68
Q

which malignancies are associated with adult dermatomyositis?

A

breast and lung

69
Q

what skin manifestations are seen in dermatomyositis?

A 
heliotrope rash (lilac rash on eyelids and periorbital oedema)
Gottron's papules - scaly, erythematous lesions affecting the dorsum of the hands, knuckles, and extensor surfaces of other small joints. They are characteristic of dermatomyositis.
Shawl sign - photosensitive rash over back and shoulders
70
Q

what enzyme is raised in polymyositis and dermatomyositis?

A

creatine kinase

71
Q

how does polymyalgia rheumatica present?

A 
abrupt onset (<2w) symmetrical shoulder and hip morning stiffness, tenderness and aching. no weakness.
systemic symptoms.
72
Q

what is the treatment for PMR?

A

prednisolone - NSAIDs are ineffective.

don’t forget to safety net re: GCA.

73
Q

what is fibromyalgia?

A

it is a poorly-understood long-term medical condition characterised by chronic widespread pain and a heightened pain response to pressure.

74
Q

what are the risk factors for fibromyalgia?

A

low SES, middle-aged, women, divorce, low education low mood, etc

75
Q

what is the treatment for fibromyalgia?

A

low-dose amitriptyline
pregabalin + tramadol
high-dose venlafaxine

76
Q

what is sjorens syndrome?

A

an autoimune disorder characterised by lymphocytic infiltrates into exocrine organs.

77
Q

what are the symptoms of sjorens syndrome?

A

xerostomia (dry mouth, food sticking, hoarseness, dysphagia)
xerophthalmia (dry eyes, grittiness)
parotid swelling
systemic symptoms.

78
Q

what is Schemer’s test?

A

suspend strip of filter paper from lower eye-lid to test rate of wetting.

79
Q

what is treatment for sjoren’s syndrome?

A

PO muscarinics such as pilocarpine, cevimeline
hypermellose eye drops
chewing gum and citric acid for saliva
NSAIDs and hydroxycloroquin if MSK involvement

80
Q

what is amyloidosis?

A

it is the accumulation of proteins in abnormal, insoluble fibres called amyloid fibrils and deposit in the extracellular space of one or more organs.

81
Q

what causes amyloidosis?

A

primary: AL amyloid. Caused by waldenstrom’s macroglobulinaemia, myeloma, lymphoma

Secondary: AA amyloid. Caused by serum amyloid associated protein which is acute phase protein produced in chronic inflammation. Can be seen in RA, IBD, TB, bronchiectasis.

82
Q

how can amyloidosis present?

A

renal failure, hepatomegaly, restrictive cardiomyopathy, macroglossia

83
Q

what is the key investigation to do in amyloidosis?

A

biopsy with congo-red stain. there will be apple-green birefringence under polarised light.

84
Q

what is the treatment for amyloidosis?

A

treat cause

if primary, PO melphalan and prednisolone

85
Q

what is the prognosis for amyloidosis?

A

poor. 1-2y.

86
Q

what is dequervain’s tenosynovitis?

A

it is inflammation of the abductor policies tendon usually caused by repetitive movement

87
Q

what is systemic sclerosis?

A

it is an autoimmune disorder characterised by increased fibroblast activity which causes abnormal growth of connective tissue.

88
Q

what would be seen on skin biopsy in systemic sclerosis?

A

onion skinning - intimal thickening around small arteries.

89
Q

what is the difference in cutaneous symptoms between diffuse and limited systemic sclerosis?

A

diffuse cutaneous can display scleroderma anywhere, whereas in limited systemic sclerosis it is listed to the forearm, calves and face.
They can both have microstomia.

90
Q

what are the features of CREST syndrome?

A 
calcinosis (calcium deposits in skin)
Raynaud's
Esophogeal dysmotility
Sclerodactyly
Telangiectasia

NB: pulmonary hypertension is 6x more common in limited than diffuse systemic sclerosis.

91
Q

what are the systemic symptoms seen in diffuse systemic scleroderma that are not seen in CREST?

A

fibrosis of lungs, heart, GI tract. renal crises and malignant hypertension.

92
Q

what autoantibody is positive in limited systemic sclerosis?

A

anti-centromere

93
Q

what autoantibody is positive in diffuse systemic sclerosis?

A

anti-topoisomerase (scl70)

94
Q

what are the 3 antibodies associated with anti-phospholipid syndrome?

A

anti-phospholipid, anti-cardiolipid, lupus anti-coagulant

95
Q

how does anti-phospholipid syndrome present?

A

arterial and venous thromboses, unprovoked and in unusual sites. pregnancy complication (miscarriage or early / severe preeclampsia).

Finals (12 decks)

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