Pathophysiology of inflammatory and degenerative joint disease Flashcards

week 2

1
Q

5 word description of rheumatoid arthritis:

A

Chronic, symmetrical, inflammatory, deforming, polyarthritis

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2
Q

Which joints does RA usually not effect?

A

distal interphalangeal joints

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3
Q

EMS =

A

Early morning stiffness

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4
Q

2 antibodies tested for in RA:

A
  • Rheumatoid factor

- Anti-citrullinated protein antibody (Anti-CCP)

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5
Q

Which cytokines can play a bid role in RA?

A

Tumour necrosis factor alpha (TNF-a)

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6
Q

Functions of TNF-a in RA (6):

A
  1. Increases pro-inglammatiory cytokines and chemokine (IL-1, IL-6, IL-8)
  2. Increase adhesion molecules
  3. Increase vascular endothelial growth factor
  4. Increase acute phase response
  5. Increase Keratinocyte hyper proliferation
  6. Increase metalloproteinase synthesis
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7
Q

Function of vascular endothelial growth factor (VEGF)

A

Increased angiogenesis

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8
Q

CRP:

A

C-reactive protein, part of the acute phase response. Broad inflammatory marker.

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9
Q

What does increased keratinocyte hyper proliferation cause?

A

Skin plaques

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10
Q

In RA, what is the bone eroded by?

A

Osteoclasts (RANK-L expression increased in other cells activated them).

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11
Q

List some systemic problems in RA:

A
  • Skeletal muscle breakdown
  • Rheumatoid nodules
  • Fever
  • Pleural effusion
  • Increased hepcidin, decreased iron
  • Atheromatous plaques in blood vessels
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12
Q

Which type of arthritis is often asymmetrical?

A

Osteoarthritis

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13
Q

Risk factors for OA:

A

Female, age, family history, obesity, oestrogen deficiency, occupation, past trauma

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14
Q

Treatment aims in OA:

A

Patient education and information access
Pain relief
Optimisation of function
Modification of disease process

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15
Q

What is the most common inflammatory arthritis in men?

A

Gout

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16
Q

Name 3 common comorbidities in gout:

A
  • Renal impairment
  • Coronary heart disease
  • Metabolic syndrome (obesity, dyslipidaemia, hypertension, T2 diabetes)
17
Q

Non-modifiable risk factors for gout:

A

Age, male, race, genetic factors, impaired renal function

18
Q

Modifiable risk factors for gout:

A

Hyperuricaemia, high-purine diet, alcohol consumption, obesity, certain meds (e.g. diuretics)

19
Q

Hyperuricaemia =

A

Abnormally high levels of uric acid in the blood.

20
Q

where does urate in the body come from?

A
  • Cell turn over

- Diet

21
Q

Ways to modify risk of gout:

A
  • Modify purine-rich foods
  • Reduce alcohol intake
  • Obesity
  • Modify medications
22
Q

What are purines broken down into?

A

Uric acid - excretes in the urine

23
Q

What can cause too much rate in blood?

A
  • over productions (increased synthesis, high cell turn-over)
  • increased consumption of purines
  • under excretion of purines
24
Q

Podagra =

A

a classic symptom of gout. gout affecting the big toe.