L7:pathophysiology of joint disease Flashcards

(42 cards)

1
Q

RF=

A

rheumatoid factor

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2
Q

CCP=

A

cyclic citrullinated peptide

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3
Q

joints affected by RA

A

MCPs
MTPs
wrists

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4
Q

5 key features of RA

A
  • Chronic
  • symmetrical
  • inflammatory
  • deformity
  • polyarthritis
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5
Q

primary site of pathology in RA

A

synovium

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6
Q

synovitis=

A

inflammation of the synovial cells

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7
Q

first cell to be triggered in RA

A

T-cells

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8
Q

what do triggered T cells in RA do

A

stimulate macrophage, fibroblast and B-cell activity

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9
Q

most important cytokines in RA

A

TNF-alpha

IL-1

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10
Q

what do fibroblasts produce

A

some inhibitory cytokines

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11
Q

after being activated by T-cells what do B-cells do

A

produce antibodies RF and Anti-CCP

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12
Q

what do RF and anti-CCP cause

A

synovial cell proliferation, synovitis and potential tissue damage

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13
Q

what do -mab drugs block

A

cytokines (especially TNF-alpha)

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14
Q

what effect does TNF-alpha have on hepatocytes

A

stimulates C-reative protein (CRP)

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15
Q

what does prolonged inflammation lead to

A

bone damage

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16
Q

5 consequences of chronic systemic inflammation

A
  1. early IHD
  2. hypercholesterolaemia
  3. osteoporosis
  4. insulin resistance
  5. sacropenia
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17
Q

why is there increased CV mortality with RA

A

accelerated atherosclerosis

18
Q

what inflammatory markers can predict erosion

19
Q

HAQ=

A

health questionnaire used to assess function

20
Q

most common joint disorder=

A

osteoarthritis

21
Q

joints affected in osteoarthritis (4)

A

DIP
PIP
CMC
MTPI

22
Q

when do you get symptoms with osteoarthritis

A

with activity

23
Q

6 risk factors for Osteoarthritis

A
age
female sex
genetics 
obesity 
oestrogen deficiency 
BMD
24
Q

central core treatments for osteoarthritis (3)

A
  • education and information
  • exercise and strengthening
  • weight loss
25
what builds up over time with recurrent gout
soft tissue deposits of uric acid called tofi
26
why aren't women as susceptible to gout
oestrogen stimulates the kidneys to excrete more uric acid
27
3 common comorbidities in gout
renal impairment coronary heart disease metabolic syndrome
28
what diet is bad for gout
high-purine diet
29
uric acid formation uses which pathway
purine metabolic pathway
30
key enzymes in purine metabolic pathway
xanthine oxidase
31
2 medications targeting xanthine oxidase
allopurinol, febuxostat
32
2 ways uric acid can accumulate
over production of urate | underexcretion of urate
33
4 triggers for gout attacks
- direct trauma - medications - rapid weight loss - dehydration/ acidosis
34
podagra=
gout affecting big toe
35
how do gout attacks often start
rapidly over night or in the early morning
36
what joint are 50% of gout attacks in
metatarsophalangeal joint of first toe
37
what is present in joints in gout
monosodium urate crystals
38
what do men with gout have a large increase risk of
kidney stones
39
attacks of gout caused by
deposition of urate crystals in joints resulting in inflammation
40
what allows gout diagnosis (2)
crystals in joints or tophus aspirate
41
most common bacteria causes septic arthritis
Staphylococcus aureus
42
antibiotic regime for septic arthritis
IV antibiotics for 2 weeks then 4 weeks oral antibiotics on return home