rheumatology and bone disease I and II Flashcards

1
Q

rheumatoid arthritis

A

disease of synovial joints
autoimmune systemic infalmamtory illness
symmetrical joint inflammation and demfromity

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2
Q

pain history of rheumatoid arthritis

A

inflammatory pain

  • early morning stiffness (more than 30 mins), less stiff after lunch but then stiffen in the evening
  • better after movement
  • stiffness after rest
  • ease with use/exercise
  • swelling
  • may have flue like symptoms, feverish, hot etc
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3
Q

clinical features of rheumatoid arthritis

A
boggy swelling (more soft tissue than expected around the joints)
knuckesl MCP joints, fingers sit lower than the level of the palm due to sub luxation
Z thumb deformity 
ulner deviation of fingers
swan neck deformity
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4
Q

what causes swam neck deformity

A

tendons move anchor points due to arthritis
flexion of distal point
extension of PIP point

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5
Q

extra articular features of joints

A
lungs
- nodules
lung firbosis
pleural effusions
cardio
- pericardial infalmamtion
- myocarditis
- valve inflmamtion
kidneys
- amyloidosis
skin
- rheumatoid nodules
secondary sjogrens syndrome
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6
Q

blood tests show what in rheumatoid arthrtis

A

anaemia
high/low platelts
high inflammatory markers (CRP and ESR)

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7
Q

CRP/ESR

A

measure of inflammation or infection in blood stream
- CRP produced in response to pro inflmamtory cytokines
ESR - found on RBCs

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8
Q

X ray rheumatic arthriris

A

osteopenia around joints
soft tissue swelling

late
- erosions
joint space narrow
subluxation/dislocation
fusion (ankylosis)
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9
Q

treatment of rheumatoid arthrosi

A

immediate relief
NSAIDS
steroids

Control of disease

  • DMARDS eg methotrexate
  • biological drugs eg anti TNF
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10
Q

DMARDS

A

disease modifying anti rheumatic drugs

e.g. methorexate

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11
Q

biologic drugs

A

anti TNF

B cell depletion

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12
Q

side effects of treatments for rheumatic fever

A

1) infection
- all increase risk
- for biologic drugs: reactivation of TB
2) bone marrow toxicity
- low WBC count/low platlets/pancytopenia
- pts often have lots of blood test
3) hepatotoxic
- abnormal liver tests
4) gastric upset
- nausea, diarrhoea, flatulence
5) skin rashes

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13
Q

methotrexate

A
never prescribe with trimethoprim
really excreted
nauseas
mouth ulcers
lung complications
1x weekly dose
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14
Q

rheumatoid neck

A

erosive change at C1/2
subluxation at atlanto axial level or at sunaxial levels

ligament damaged by inflammation
dens starts to move into the same leading to spinal compression
numbness/tingle of hands etc. ataxic gate

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15
Q

juvenila idiopathic arthritis

A

inflammatory arthritis occurring before 16
jaw underdevelopment, TMJ inflammation leads to alter Md growth
malocclusion
micrognathia

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16
Q

spondylarthropathy conditions

A

ankylosing spondylitis
psoriatic arthritis
enteropathic athritis
reactive arthritis

all closely related condiions

17
Q

ankylosing spondylitis

A

inflammatory arthritis of spine and sarcophagus iliac joitns
back pain
stooped posture
neck ridge fused

18
Q

common features of spondyloarthropathy

A

enteritis
dactylitis
skin/nail psoriasis
inflammatory bowl disease

19
Q

osteoarthritis

A

degenerative process
exaggerated repair responce
cartilage damaged puts
pressure on bones

20
Q

osteophytes

A

spikes of calcium

21
Q

OA treatment

A
  • physiotherapy/exercises
  • weight loss (lower limb joints)
  • paracetamol, co codamol
  • NSAIDS
  • surgery as final result (for uncontrolled pain, joint failure eg knee giving away)
22
Q

what leads the response to gout

A

neutrophil lead inflammatory responce

23
Q

why does gout occur

A

patient has high serum urate

c

24
Q

causes of gout

A
  • genetic predisposition (enzyme defects)
  • renal impairment (kidneys)
  • diuretics
  • dehydration
  • intercurrent illness
  • high alcohol/fructose/red meat/shellfish
  • part of metabolic syndrome – central obesity, diabetes, high BP, high cholesterol
25
Q

treatment for gout

A

Acute
- colchicine (reduces neutrophil activity)
- steroids
- NSAIDS
Prevention of future attacks
- urate lowering drugs eg allopyrinol and febuxostat (both xanthine oxidase inhibitor

26
Q

common connective tissue diseases

A

1) systemic lupus erythematosus (SLE)
2) scleroderma
3) primary sjogrens
4) polymyositis/dermatomyositis

27
Q

scleroderma/systemic scelroros

A

progressive skin tightening and thickening

severe raynauds - (can lead to gangrene)

28
Q

types of sclerosis

A

limited systemic sclerosis LcSSc

diffuse systemic sclerosis DcSSc (widespread)

29
Q

LcSSc

A

associated with pulmonary hypertension

severe acid efflux

30
Q

DcSSc

A

associated with pulmonary fibrosis

scleroderma renal crisis

31
Q

telangiectasica

A

small spots around the mouth

32
Q

sjogrens syndrome

A

1) primary
- occurring on its own without associated rheumatic illness but with its own systemic manifestations
2) secondary
- occurring with rheumatic illness eg RA
- associated with other auto immune disorders including interstitial lung disease, autoimmune liver disease

33
Q

polymyositis

A

inflammation of muscles

painless wasting o he muscles

34
Q

dermatomyositis

A

inflammation of muscles and skin
photosensitivity rash around the eyes
ulceration of muscosa

35
Q

treatment for connective tissue diseases (pyrimid going up in severity)

A
  • NSAIDS/steroids
  • DMARDs
  • cytotoxic drugs
  • biologic drugs