Rheum Flashcards

(95 cards)

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
what are the extra-articular manifestations seen in ankylosing spondylitis?
the 5 As. achilles tendonitis, apical lung fibrosis, anterior uveitis, aortic regurgitation, amyloidosis in the kidneys.
26
Name 3 seronegative arthritides
ankylosing spondylitis, enteropathic arthritis, psoriatic arthritis.
27
what is Schober's test?
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.
28
what is the classic posture seen in advanced ankylosing spondylosis?
kyphosis and neck hyperextension.
29
what is seen on the XR of ankylosing spondylitis patients?
1 sacroilitis 2 vertebral syndesmosiytes 3 bamboo spine
30
what is gout?
gout is crystal monoarthropathy caused by the deposition of monosodium rate crystals
31
what are the risk factors for gout?
increased cell destruction - cytotoxic medications, leukaemia, intake - purine rich foods, alcohol excess reduced excretion - diuretics, renal impairment genetics being male
32
What is the most commonly affected joint in gout?
1st MTP
33
what is management of acute gout?
NSAIDs Colchicine glucocorticoids if renal impairment
34
when should allopurinol be used in gout?
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).
35
what do the crystals in gout look like under polarised light?
negatively birefringent needle shaped crystals
36
what are the crystals made out of in pseudogout?
calcium pyrophosphate
37
what do the crystals in pseudo gout look like under polarised light?
positively birefringent rhomboid shaped crystals
38
what is Libman-Sack's endocarditis?
endocarditic vegetations due to Ig deposition. seen in SLE.
39
what is Jacob's arthropathy?
non-erosive joint deformity due to soft-tissue abnormalities.
40
what is the best marker for disease activity in SLE?
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
What is the ACR diagnostic criteria?
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
what is the medical treatment for SLE?
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
what vessels are affected in GCA?
large vessels
44
what condition is closely linked to GCA?
PMR
45
how does GCA present?
unilateral headache of acute onset, scalp tenderness, jaw / tongue claudication, amaurosis fugax (painless transient monocular blindness - due to anterior ischaemic optic neuropathy)
46
what is the most important investigations to do in GCA?
temporal artery biopsy - repeat if negative due to skip lesions
47
what is the treatment for GCA?
high dose steroids (60mg pred/day), can use steroid sparing agents once in remission. typically, treater two years.
48
what kind of vessels does Takayasu's arteritis affect?
large vessels - typically aorta and major branches of aortic arch.
49
how does Takayasu's arteritis present
initially systemic with fatigue, fever, arthralgia. Then, ischaemic phenomena - arm claudication, visual disturbance, TIA, stroke, seizure, haemoptysis, haematyria, abdominal pain.
50
how does PAN present?
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
what viral disease is PAN associated with?
Hep B
52
what is microscopic polyangiitis?
it is a small-vessel vasculitis without evidence of necrotising granulomatous inflammation
53
what are the symptoms of MPA?
constitutional symptoms, haematuria, haemoptysis. no upper resp tract infections.
54
what is ANCA association of PAN?
none
55
what is the ANCA associated of MPA?
pANCA
56
what is the ANCA association with GwPA?
cANCA
57
what is the ANCA association with EGPA?
pANCA
58
what's the new name for Wegner's?
Granulomatosis with polyangiitis
59
how does GPA present?
URT - nasal obstruction / ulceration, epistaxis, saddles nose, septal perforation lungs - cough, haemoptysis, pleuritic chest pain, cavitation renal - rapidly progressive crescentic GN, proteinuria, haematuria.
60
what is the classic triad seen in EGPA?
allergic rhinitis and late onset asthma eosinophilia vasculitis
61
what is the genotype associated with Behcets disease?
HLA-B5
62
how does Behcets disease usually present?
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
why should you worry about polymyositis?
because it is often attribute to an underlying malignancy (lung, pancreatic, ovarian, bowel)
64
how does polymyositis present?
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
what is a common non-muscle system involvement seen in polymyositis?
interstitial lung disease (present in 30%)
66
what auto-antibody is seen in polymyositis?
anti-Jo1
67
what is the treatment in polymyositis?
high-dose prednisolone, then azathioprine / methotrexate long-term
68
which malignancies are associated with adult dermatomyositis?
breast and lung
69
what skin manifestations are seen in dermatomyositis?
``` 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
what enzyme is raised in polymyositis and dermatomyositis?
creatine kinase
71
how does polymyalgia rheumatica present?
``` abrupt onset (<2w) symmetrical shoulder and hip morning stiffness, tenderness and aching. no weakness. systemic symptoms. ```
72
what is the treatment for PMR?
prednisolone - NSAIDs are ineffective. | don't forget to safety net re: GCA.
73
what is fibromyalgia?
it is a poorly-understood long-term medical condition characterised by chronic widespread pain and a heightened pain response to pressure.
74
what are the risk factors for fibromyalgia?
low SES, middle-aged, women, divorce, low education low mood, etc
75
what is the treatment for fibromyalgia?
low-dose amitriptyline pregabalin + tramadol high-dose venlafaxine
76
what is sjorens syndrome?
an autoimune disorder characterised by lymphocytic infiltrates into exocrine organs.
77
what are the symptoms of sjorens syndrome?
xerostomia (dry mouth, food sticking, hoarseness, dysphagia) xerophthalmia (dry eyes, grittiness) parotid swelling systemic symptoms.
78
what is Schemer's test?
suspend strip of filter paper from lower eye-lid to test rate of wetting.
79
what is treatment for sjoren's syndrome?
PO muscarinics such as pilocarpine, cevimeline hypermellose eye drops chewing gum and citric acid for saliva NSAIDs and hydroxycloroquin if MSK involvement
80
what is amyloidosis?
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
what causes amyloidosis?
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
how can amyloidosis present?
renal failure, hepatomegaly, restrictive cardiomyopathy, macroglossia
83
what is the key investigation to do in amyloidosis?
biopsy with congo-red stain. there will be apple-green birefringence under polarised light.
84
what is the treatment for amyloidosis?
treat cause | if primary, PO melphalan and prednisolone
85
what is the prognosis for amyloidosis?
poor. 1-2y.
86
what is dequervain's tenosynovitis?
it is inflammation of the abductor policies tendon usually caused by repetitive movement
87
what is systemic sclerosis?
it is an autoimmune disorder characterised by increased fibroblast activity which causes abnormal growth of connective tissue.
88
what would be seen on skin biopsy in systemic sclerosis?
onion skinning - intimal thickening around small arteries.
89
what is the difference in cutaneous symptoms between diffuse and limited systemic sclerosis?
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
what are the features of CREST syndrome?
``` 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
what are the systemic symptoms seen in diffuse systemic scleroderma that are not seen in CREST?
fibrosis of lungs, heart, GI tract. renal crises and malignant hypertension.
92
what autoantibody is positive in limited systemic sclerosis?
anti-centromere
93
what autoantibody is positive in diffuse systemic sclerosis?
anti-topoisomerase (scl70)
94
what are the 3 antibodies associated with anti-phospholipid syndrome?
anti-phospholipid, anti-cardiolipid, lupus anti-coagulant
95
how does anti-phospholipid syndrome present?
arterial and venous thromboses, unprovoked and in unusual sites. pregnancy complication (miscarriage or early / severe preeclampsia).