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15021998-MSK > context week 2 > Flashcards

context week 2 Flashcards

1
Q

what does arthropathy mean

A

disease of a joint

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2
Q

what does arthritis mean

A

inflammation of joint

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3
Q

what is arthralgia

A

pain of the joint

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4
Q

there are two categories of conditions affecting joint. Name them and the common conditions .

A

non-inflammaroty - OA

inflammatroy: - seropositive = RA/CTD
- seronegative= many types

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5
Q

what are the four types of inflammatory arthritis

A

seropositive,(RA, SLE, vasculitis, scleroderma, Sjogren’s.)

seronegative (AS, psoriatic arthritis, reactive arthritits, enteropathic arthritis),

crystal (gout and pseudogout)

infectious

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6
Q

what does seropositive condition mean?

A

autimunity, many autoantibodies for many associated conditions.

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7
Q

antibody for SLE

A

anti-DNA

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8
Q

antibody for RA

A

anti-CPP

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9
Q

antibody for Strogen’s

A

anti-La

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10
Q

antibody for APS

A

anti-cardiolipin

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11
Q

antibody for small vessel vasculitis

A

ANCA

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12
Q

symptoms of inflammatory arthritis

A

morning stiffness (>30mins), helped by excursus, high CRP and PV, joint pain and associated swelling. synovitis

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13
Q

what is RA

A

immune response against synovium causing inflammatory pannus and attacking cartilage in tendon/joints.

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14
Q

where is first involved in RA

A

hands and feet

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15
Q

where must be closely monitored in RA and why?

A

C1/C2 as may compress spinal cord

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16
Q

what investigations done for RA?

A

check RF and ACPA (anti-CPP)
high ESR, CRP, PV noted.
US can detect synovial inflammation.

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17
Q

what are the extra-articular manifestations of RA

A

rheumatoid nodules, lung involvment, inc CVS risk, occular problems

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18
Q

treatment for RA

A

DMARD’s ASAP, short-term NSAID’s and steroids initially + analgesia. biological agent can be used once a few DMARD’s tried.

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19
Q

what is used to determine RA activity?

A

DAS28, >5.1 = severe and <2.6 = remission.

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20
Q

what are patients with seronegative pathologies often positive for in blood tests?

A

HLA-B27 positive

also inc ESR and CRP

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21
Q

what is Ankylosing spondylitis?

A

spine and Sacroiliac joint disease causing FUSION

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22
Q

investigations for AS

A

MRI detects early features

Schobers test determines flexibility of back

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23
Q

treatment for AS

A

physio, excersise, NSAID’s anti-TNF inhibitors (NO DMARDs’)

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24
Q

what are the common features of psoriatic arthritis?

A

psoriasis, nail pitting and onchyolitis, dactylitis

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25
Q

treatment for psoriatic arthritis

A

DMARD, then anti-TNF

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26
Q

what is enteropathic arthritis and how is it best to treat?

A

IBD related.

control IBD

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27
Q

what is reactive arthritis

A

arthritis in response to infection (GI or GU), infection triggers autoimmune arthropathies.

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28
Q

symptoms of reactive arthritis/Reiter’s syndrome

A

uveitis, urethritis, arthritis (all post-infection)

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29
Q

treatment of reactive arthritis/Reiter’s syndrome

A

self-limiting usually so NSAID’s or steroids.
treat underlying infection if necessary.

if chronic then DMARD

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30
Q

what is SLE?

A

chronic, highly variable AID. (CTD)

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31
Q

SLE commonly affects which systems?

A

skin, joint problems.
blood cells affected
nervous system commonly affected
(almost any system)

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32
Q

blood tests in SLE

A

anti-DAN, ANA, anti-Sm, antiphospolipid antibody, low complement.

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33
Q

pathogenesis of lupus

A

defective apoptosis clearnce in cell death, poor clearance allows persistence and deputisation of antigen + immune complex.

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34
Q

what is the prognosis for SLE

A

80% normal life-expectancy,
90% 10 year survival.

deaths usually due to inc CVS risk, fatal infections/side effects of medications rather than SLE itself

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35
Q

SLE symptoms and signs (20+ answers)

A

fever, weight loss, fatigue, myalgia, arthralgia, inflammatory arthritis, inc prevelence of AVN due to steroids in femoral head. discoid lupus, malaria rash, photosensitivity, raynaud’s, alopecia, lupus nephritis, leukopenia (low WCC), pneumonitis (pleuisy, pleural effusion). pericarditis, sterile endocarditis, inc ischemic heart disease, anaemia, thrombocytopenia, neurological (cerebral vassculitis, seizures, headache).

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36
Q

diagnosing SLE

A

FBC, ANA, anti-DNA, Anti-SM, low C3/C4 level (in active and renal affecting disease).
urinalyisis for glomerularnephritis
imaging of other organs (e.g: ECHO, MRI brain, CT lung)

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37
Q

why is anti-DNA good for SLE diagnosis

A

gives level of disease activity and high specificity.

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38
Q

management of SLE (general/mild)

A

HCQ (everyon), topical steroid, NSAID (skin and arthralgia). DMARD’s for arthritis/organ involvement (ASA)

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39
Q

classification and management of SLE [severe]

A

causing sever organ disease (CNA, renal…)

give IV steroid and cyclophosphamide.

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40
Q

classification and management of SLE (unresponsive)

A

not responding to other treatments

give IV immunoglobulin and ritixumab

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41
Q

monitoring SLE

A

urinalyisis for blood/protein.
check anti-DNA for disease activity
investigate symptoms as they appear
CVS risk assess (BP + cholesterol.)

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42
Q

what is Sjogren’s

A

autoimmune lymphocytes infiltrates in exocrine glands.

may be primary or secondary (SLE, RA…)

43
Q

Sjogren’s symptoms

A

causes dry mouth/eyes/vagina with arthralgia and fatigue.

parotid swelling, tooth decay, peripheral neuropathy, ILD,

44
Q

what cancer does Sjogren’s increase risk of

A

lymphoma

45
Q

treatment for Sjogren’s

A

saliva supplement, lubricate eyes, regular dental check-ups, HCQ for arthralgia and fatigue

46
Q

investigations for Sjogren’s

A

Schirmers test (occular dryness).
anti-Ro and anti-La
atypical lip biopsy.

47
Q

what is systemic sclerosis (SS)

A

CTD, vasomotor disturbance/Raynaud’s + fibrosis + subsequent atrophy of skin/cutaneous tissue.

48
Q

pathogenesis of SS

A

excessive collagen deposition causes changes.

in lung/kidney → death

49
Q

describe the skin involvement in SS

A

oedematous → indurative → atrophic.

“beaking of nose” and “tight mouth”

50
Q

what are complications of SS

A

pulmonary fibrosis/hypertension.
GI malabsorption + small bowel bacterial overgrowth
inflammatory arthritis/myositis

51
Q

describe the two types of SS

A

diffuse - rapid skin changes and to trunk, significant early organ involvement, anti-Scl-70 antibody

limited - confined to face, feet, hands, forearms,; organ involvement occurs later; Anti-Centromere antibody

52
Q

diffuse SS antibody

A

anti-Scl-70 antibody

53
Q

limited SS antibody

A

Anti-Centromere antibody

54
Q

investigations for SS

A

ANCA, anti-Scl-70 + organ screening (echo, renal, pulmonary function)

55
Q

management of SS

A

raynaud’s/digital ulcers → CCB’s, iloprost, bosentan

renal involvment = ACEi

GI = PPI for reflux

ILD = immunosuppression (cyclophosphamide)

56
Q

what is mixed Connective tissue diseases (MCTD)

A

defined condition exibiting symptoms of other CTDs

57
Q

what diseases does MCTD have symptoms of?

A

raynauds, arthraliga, myositis, sclerodactyly, ILD, pulmonary hypertension.

58
Q

diagnosing MTCD

A

anti-RNP

59
Q

managing MTCD

A

regular PFT’s and ECHO’s

manage symptoms accordingly: CCB in raynauds + significant disease = immunosupress

60
Q

what is anti-phospholipid syndrome (APS)?

A

recurrent venous/arterial thrombosis + fetal loss

61
Q

how does APS present

A

some can have no features, some continual PE/DVT or repeated pregnancy problems, some have associated RA/SLE

62
Q

when is foetus normally lost in pregnancy in APS

A

spontaneous 2nd/3rd trimersters

63
Q

what are complications of APS

A

inc CVS risk (MI/stroke), PE recurrent cauing pulmoary hypertension, migranes, fetal loss

64
Q

what is a common cutaneous finding in APS

A

livedo reticularis.

65
Q

investigations for APS

A

thrombocytopenia, prolongation of APTT,
lupus anticoagulant,
anti-cardiolipin antibodies,
anti-Beta2 glycoprotein

66
Q

management of APS

A

anticoagulation = life-long warfarin (if pregnancy then LWMH as warfarin is teratogenic)

patients with positive antibodies and no thrombotic episode require no treatment.

67
Q

what causes gout

A

urate crystals deposited in joint triggered by trauma, surgery or dehydration.

inc serum uric acid in blood (hyperuricaemia)

68
Q

where is uric acid derived from

A

purines (A and G nucleotides).

69
Q

what can hyperuricaemia occur?

A

due to renal underexcretion (exacerbated by diuretic or renal failure)

due to diet (alcohol, seafood, red meat)

[also genetic component]

70
Q

what drug exacerbates gout?

A

diuretics

71
Q

where does gout affect

A

any joint

commonly big toe (1st MTP), then ankle/knees

72
Q

symptoms of Gout

A

red, hot swollen joint, acutely and severely painful. resolves in 7-10 days

(mimic of septic arthritis)

73
Q

what can occur in chronic gout

A

gouty tophi (painless) occur because build up erupts through skin from soft tissue

erosion/destructive joint arthritis (rare)

74
Q

investigations and results in Gout

A

aspirate synovial fluid with polarised microscopy.

needle-shaped + negative birefringence= uric acid crystals

75
Q

treating gout

A

acute - NSAID, corticosteroid (once infection not possible), opiod analgesia, colchicine (if unable to tolerate NSAID).

chronic - allopurinol or febuxostat (xanthase oxidase inhibitors) prevent attacks. start on acute attack stops

76
Q

pseudogout caused by…?

A

calcium phosphonate crystals

77
Q

calcium phosphonate crystals on biopsy

A

rhomboid and positive birefringence

78
Q

what is chonedrocalcinosis?

A

deposit in cartilage + other soft tissues in absence of acute inflammation.

79
Q

pseudogout occurs where?

A

wrist, knee, ankle commonly

80
Q

pseudogout treatment

A

acute = same as gout

chronic/prophylaxis = no treatment

81
Q

what are some common muscle diseases?

A

polymyalgia rheumatica, GCA, polymyositis/ dermatomyosistis, fibromyalgia

82
Q

what is PMR

A

chronic, common, unknown atieology occurring in elderly.

83
Q

investigating PMR

A

inc ESR and CRP (no specific test)

84
Q

PMR PC

A

proximal myalgia of hip and shoulder + accompanying morning stiffness. GCA may be present

85
Q

what condition is PMR closely linked to?

A

GCA

86
Q

treatment of PMR

A

15mg prednisolone very quickly resolves (can be used as diagnostic test). reduce steroid over 18months → resolves.

87
Q

what is GCA?

A

giant cell arteritis; commonest systemic vasculitis in adults, elderly, unknown aetiology.

transmural inflammation of intimate media and adventica of arteries (patchy/skip lesions of lymphocytes, macrophages and multi-neucleated cells.)

88
Q

what occurs due to GCA in vessel wall

A

lymphocytes, macrophages and multi-neucleated cells cause inflammation and vessel wall thickens causing narrow lumen and ischemia.

89
Q

PC of GCA (signs and symptoms)

A

headache (usually occipital/temporal areas)
Visual disturbances, (blurring, vision loss, double vision, blindness)
jaw claudication (eating/talking)
scalp tenderness
focal tenderness on palpation present
thickened and non-pulsing femoral artery.
(fatigue, malaise, fever).

90
Q

what causes jaw claudication in GCA

what causes visual impairment in GCA

A

ischema of maxillary artery.

ischema of ophthalmic artery. [prolonged = permenant]

91
Q

diagnosis of GCA

A

temporal artery biopsy ASAP. not sensitive (as skip lesions) but 100% specificity.

start treatment ASAP/before biopsy

92
Q

treating GCA

A

don’t wait until biopsy - start 40mg/60mg prednisolone (later if visual disturbances) as waiting can cause problems and takes weeks for steroid to remove biopsy-able material completely.

93
Q

what is polymyositis

A

idiopathic inflammatory myopathy causing symmetrical, proximal muscle weakness (occasionally myalgia)

94
Q

who does polymyositis commonly affect

A

(F>M, 45-60years)

95
Q

pathogenesis of polymyositis

A

T-cell mediated cytotoxic process directed against muscle antigens,

CD8+ cells + macrophages surround health tissue and invade/destroy

96
Q

what antibodies are present in polymyositis

A

anti-Jo1 + anti-SRP antibiodies

also anti-RNP, ANA

97
Q

complications of polymyositis

A

dysphagia in 1/3rd of cases (poor prognostic sign)

ILD can occur (esp. in anti-Jo1 positive people)

98
Q

investigations for polymyositis

A 
inc inflmaaory markers,
inc CK
MRI for extent of muscle involvement (inflammation, oedema or scarring)
EMG abnormal
muscle biopsy crucial = gold standard
99
Q

management of polymyositis

A

prednisolone 40mg + MTX/AZA (responds well but slowly to treatment)

100
Q

dermatopolymyositis (dermatomyositis) features

A

similar to polymyositis clinically but with skin changes

investigation and treatment same as polymyositis

101
Q

skin involvement in dermatopolymyositis

A

V-shaped rash over chest.
Gottron’s papules.
heliotrope rash

102
Q

dermatopolymyositis has increase risk of what?

A

malignancy - commonly breast, ovary, colon, lung, bladder, oesophagus.

screen at time of diagnosis and 5 years afterwards (peak risk time)

[[[up to 30% of dermatomyositis arise from cancer, probably as an autoimmune response.]]]

103
Q

CREST acronym for limited systemic sclerosis

A

calcinosis, raynaud’s, esophageal dysmotility, sclerodactyly, telangiectasia.

104
Q

Antiphospholipid syndrome treatment

A

normally: Warfarin and/or aspirin

if trying to conceive - LMWH and aspirin

15021998-MSK (19 decks)

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