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Finals > Rheum > Flashcards

Rheum Flashcards

1
Q

What is monoarthritis

A

1 joint involved

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2
Q

What is oligoarthritis

A

<= 5 joints affected

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3
Q

What is polyarthritis

A

> 5 joints affected

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4
Q

Give examples of monoarthritis

A

gout
septic
osteo

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5
Q

Give examples of oligoarthritis

A 
reactive
psoriatic
gout
osteo
ankylosing spondylitis
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6
Q

Give examples of polyarthritis

A

symmetrical:
RA
osteo

asymmetrical
reactive
psoriatic

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7
Q

What conditions is Raynaud’s present in

A

SLE
polumyositis
dermatomyositis

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8
Q

State some signs in the hands that are typical of RA

A 
Z deformity of thumb
ulnar deviation
swan neck deformity
boutonniere deformity
nail pitting
nail fold vasculitis
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9
Q

What is Z deformity of the thumb

A

MCP flexion

IP hyperextension

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10
Q

What is swan neck deformity

A

PIP hyperextension

DIP flexion

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11
Q

What is Boutonniere deformity

A

PIP flexion

DIP extension

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12
Q

What are the key investigations in suspected RA?

A

Bloods: FBC, CRP, ESR, U+E, LFT, RF, ANA, anti-cyclic citrullinated peptide antibodies
Imaging: XR hands and feet, CXR, US/MRI joints

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13
Q

What can happen to CRP and ESR in RA?

A

inflammatory markers, so raised

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14
Q

Does a raised RF diagnose RA?

A

no!

can be raised in other infam diseases and in healthy!

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15
Q

What can a raised ANA (antinuclear antibodies) suggest?

A

SLE
RA
healthy!

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16
Q

What are the systemc problems causes in RA

A

lympadenopathy
pulmonary fibrosis
peripheral nerve entrapment

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17
Q

What vaccines need to be given to those taking DMARDs?

A

influenza - annual
pneumococcal - 10y
live vaccines contraindicated

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18
Q

Does RF or anti-CCP antibodies have a greater specificity for RA?

A

anti-CCP antibodies

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19
Q

What factors indicate a poor prognosis for RA?

A 
rheumatoid factor positive
poor functional status at presentation
HLA DR4
X-ray: early erosions (e.g. after < 2 years)
extra articular features e.g. nodules
insidious onset
anti-CCP antibodies
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20
Q

What complications can methotrexate cause?

A

liver cirrhosis
pneumonitis
myelosupression

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21
Q

What complications can prednisolone cause?

A 
Cushingoid features
Osteoporosis
Impaired glucose tolerance
Hypertension
Cataracts
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22
Q

What monitoring needs to happen in methotrexate treatment

A

Monitoring of FBC & LFTs is essential due to the risk of myelosuppression and liver cirrhosis

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23
Q

How long does is take for DMARDs to produce a full response

A

2-6m

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24
Q

Why are DMARDs the best treatment for inflammatory arthritis

A

suppress disease progress
control the signs and symptoms
limit joint damage.

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25
Q

What treatment should be initiated in newly diagnosed active rheumatoid arthritis,

A

combination of DMARDs (including methotrexate and at least one other DMARD)
a short-term corticosteroid,
within 3 months of the onset of persistent symptoms.

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26
Q

When should you consider changing DMARD for a patient?

A

If a disease-modifying anti-rheumatic drug does not lead to an objective benefit within 6 months, it should be replaced by a different one.

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27
Q

When can a TNF inhibitor be prescribed in RA

A

an inadequate response to at least two DMARDs including methotrexate

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28
Q

What type of hypersensitivity reaction is SLE?

A

type III

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29
Q

What are someof the risk factors for SLE?

A

afro-caribbean
exposure to sunlight
drugs:
EBV

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30
Q

What are the key initial features of SLE?

A 
fever
rash
mouth ulcers
joint pain
lympadenopathy
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31
Q

What are key immunological findings in SLE?

A 
antinuclear antibody (ANA)
ds-DNA antibody
RF
anti-Smith:
 anti-U1 RNP, 
SS-A (anti-Ro) and 
SS-B (anti-La)
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32
Q

Which immunological finding is most sensitive for SLE?

A

ANA (95%)
ds-DNA (70%)
anti-Smith 30%

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33
Q

Which immunological finding is most specific for SLE?

A

ds-DNA (90%)
anti-Smith (90%)
ANA

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34
Q

What systems are affected with symptoms of SLE?

A 
skin
serosa
mucosa
joints
kidneys
brain
blood
immune!
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35
Q

How does SLE affect the skin

A

malar rash - butterfly, does not affect nasolabial folds
discoid rash
photosensitivity

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36
Q

How does SLE affect the mucosa

A

ulcers in mouth, nose, vagina

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37
Q

Describe the discoid rash in SLE

A

in sun exposed areas
scaly, erythematous, well demarcated rash
Lesions may progress to become pigmented and hyperkeratotic before becoming atrophic

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38
Q

How does SLE affect the serosa

A

serositis!
eg. pleuritis
pericarditis

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39
Q

How does SLE affect the joints

A

arthralgia

non-erosive arthritis - >=2 peripheral joints

40
Q

How does SLE affect the kidneys

A

proteinuria

glomeulonephritis

41
Q

How does SLE affect the blood

A

anaemia (haemolytic)
thrombocytopenia
leukopaenia

42
Q

How does SLE affect the brain

A

seizures
psychosis
anxiety and depression

43
Q

How does SLE affect the immune system

A

ANA
anti ds-DNA
anti-Smith
anti-phospholipid

44
Q

What are the diagnostic criteria of SLE?

A

4 of the following present:

malar rash
dicoid rash
photosensitivity
oral ulcers
serositis
proteinuria/glomerulonephritis
joint problems
CNS problems
haematological problems
immuniological probs (anti ds-DNA, anti-Smith)
ANA
45
Q

What tests can be used in monitoring SLE?

A

anti ds-DNA -
complement levels - low C3/C4 in active disease due to formation of immune complexes
ESR raised in flare up

46
Q

Which drugs can cause SLE?

A

chlorpromazine, methyldopa, hydralazine, isoniazid, d-penicillamine

47
Q

Describe the treatment of SLE if there is no major organ involvement

A

anitmalarials - hydroxychloroquine
low dose steroids
azathioprine/methotrexate

48
Q

Describe the treatment of SLE if there is major organ involvement

A

cyclophosphamide
mycophenylate mofetil
calcineurin inhibitors eg. ciclosporin/tacrolimus

49
Q

What diseases is there an increased risk of in SLE?

A

cardiovascular disease

osteoporosis

50
Q

What is antiphospholipid syndrome?

A

antibodies affect coagulation leading to pro-thrombotic state

51
Q

What problems are caused by antiphospholipid syndrome

A

CLOTS

Coagulation defect
Livedo reticularis
Obstetric - miscarriage
Thrombocytopenia

52
Q

What is livedo reticularis

A

mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by swelling of the venules owing to obstruction of capillaries by small blood clots.

53
Q

What joints does ankylosing spondylitis most commonly affect?

A

sacroiliac

spine

54
Q

Which HLA is most commonly associated with ank spond?

A

HLA B27

55
Q

Is ankylpsing spondylitis sero negative or positive?

A

sero negative

56
Q

What is the typical presentation of ankylosing spondylitis

A

20/30y male
gradual onset back pain and stiffness
worse at night, improves with movement
pain radiates to thighs and buttocks

57
Q

Why is there a progressive loss of spinal movement in ank spond?

A

spinal fusion!

58
Q

What are some features of ank spond on spinal examination?

A 
reduced lateral flexion of lumbar spine
reduced forward flexion
Schober's test <5cm
decreased thoracic expansion
sacroilitis

neck hyperextension
thoracic kyphosis
question mark posture

59
Q

What are some systemic symptoms of ank spond?

A 
apical lung fibrosis, 
Acute iritis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
and cauda equina syndrome
onycholysis, 
 fatigue,
60
Q

What is Schober’s test? What disease is it used to test in?

A

line is drawn 10 cm above and 5 cm below L5/the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible

Ankylosing spondylitis

61
Q

What is the first feature of ankylosing spondylitis on xray?

A

sacroilitis - subchondral erosions, sclerosis

62
Q

What are the later features of ank spond on xray?

A

squaring of lumbar vertebrae
‘bamboo spine’ (late & uncommon)
syndesmophytes:
apical fibrosis on CXR

63
Q

What is the management of ank spond?

A

Exercise!
physio - maintain posture and mobility
NSAIDs for pain
TNF alpha inhibitors in severe cases which failed to respond to NSAIDs

64
Q

What can spirometry show in ankylosing spondylitis?

A

a restrictive defect due to a combination of pulmonary fibrosis, kyphosis and ankylosis of the costovertebral joints.

65
Q

What are syndesmophytes?

A

calcification between corners of vertebrae due to ossification of outer fibers of annulus fibrosus

66
Q

What are the signs of systemic sclerosis in the hands?

A

Swelling (non-pitting oedema) of fingers and toes

Skin becomes hard and thickened - this may limit joint movement or cause joint contractures

Swelling and sclerosis reduce hand movements, so patients may be unable to make a fist, or to place the palmar surfaces together - the ‘prayer sign’.

Fingertips may have pitting, ulcers or loss of bulk from finger pads.

Raynaud’s phenomenon.

67
Q

What are the key pathophysiological features of systemic sclerosis?

A

excessive collagen deposition by fibroblasts

damages blood vessels

68
Q

What are the first features of systemic sclerosis

A

skin thickening and hardening in hands or face
Raynaud’s
oesophageal symptoms

69
Q

What are the three kinds of systemic sclerosis?

A

limited
diffuse
scleroderma

70
Q

Describe the features of limited systemic sclerosis

A 
affects face, hands and feet
CREST
slow onset, slow progression
affects internal organs
anti-centromere antibodies
71
Q

What does CREST stand for? What does this mean?

A

Calcinosis - calcium deposits in skin
Raynaud’s
Esophageal dysmotility
Sclerodactyly - tightening of skin in fingers
Telangiectasia - dilation of capillaries in skin

72
Q

Describe the features of diffuse systemic sclerosis

A

affects upper arm, trunk and thighs
more rapid onset and progression
scl-70 antibodies

73
Q

Describe scleroderma

A

no multi organ involvement

localised thickening of areas of skin - plaques or linear

74
Q

What are the facial features of systemic sclerosis

A 
Tightening of facial skin.
Tight lips (microstomia)
75
Q

If systemic sclerosis is suspected, which antibodies should be tested for?

A

scl-70
anti-centromere
Anti-RNA polymerase III

76
Q

How is systemic sclerosis managed?

A

exercise/physio
DMARDs: methotrexate, mycophenolate mofetil or cyclophosphamide
monitor BP and renal function
ACEi if renal failure

77
Q

Which joints does psoriatic arthritis commonly affect

A

DIP
symmetrical polyarthritis
sacroilitis

78
Q

What percentage of people with psoriasis develop arthropathy?

A

10%

79
Q

What changes occur in the hands in psoriatic arthritis>

A

pitting
onycholysis
dactylitis - sausage fingers

80
Q

How is psoriatic arthritis managed?

A

NSAIDs
methotrexate or ciclosporin if skin disease alsoproblemaic
resistant = anti-TNF

local steroid injections to reduce joint inflammation

81
Q

What is Sjogren’s syndrome

A

autoimmune disorder affecting exocrine glands resulting in dry mucosal surfaces.

82
Q

What are the symptoms of sjogren’s

A

dry eyes: keratoconjunctivitis sicca
dry mouth
vaginal dryness

83
Q

What immunological findings are associated with sjogren’s?

A

RF - 100%
ANA - 70%
anti-Ro - 70%
Anti-La - 30%

84
Q

What is Schirmer’s test?

A

holding filter paper near conjunctival sac to measure tear production

85
Q

What is the pathophysiology of Gout

A

deposition of monosodium urate crystals in the synovium due to hyperuricaemia

86
Q

What are some factors that increase the risk of gout

A

increased production

  • cytotoxic drugs,
  • psoriasis
  • eating liver, kidneys, oily fish, yeast

decreased exretion

  • diuretics (thiazide and loop)
  • CKD
87
Q

what is the differential diagnosis for gout

A 
septic arthritis
reactive arthritis
pseudogout
trauma
cellulitis
88
Q

what are the symptoms of gout

A

acute severely painful swollen joint (peak at 12hrs, lasts for 6-10d)

89
Q

What can trigger an attack of gout

A

alcohol
stress
trauma
exercise

90
Q

what are some signs of chronic gout

A

urate tophi

uric acid renal stones

91
Q

what investigations should be carried out in suspected gout

A

FBC
joint aspiration - MC+S
xray joint

92
Q

What are the signs of gout on xray

A

subcutaenous tissue swelling
punched out juxta articular erosions with sclerotic margins
preserved joint space
no periarticular osteopaenia

93
Q

why do you need to do an FBC in gout?

A

a myeloproliferative disorder could be the cause - increased cell turnover

94
Q

What is the treatment for an acute episode of gout?

A

NSAIDs, steroid injection

colchicine

95
Q

What is the treatment for the prophylaxis of gout?

A

not started until 2 weeks since resolution of flare up

allopurinol

96
Q

What are the indications for prophylaxis of gout

A 
two episodes within a year
tophi
renal disease
renal stones
prophylaxis if taking cytotoxins or diuretics

Finals (32 decks)

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