Pathophysiology of inflammatory and degenerative joint disease Flashcards
week 2
5 word description of rheumatoid arthritis:
Chronic, symmetrical, inflammatory, deforming, polyarthritis
Which joints does RA usually not effect?
distal interphalangeal joints
EMS =
Early morning stiffness
2 antibodies tested for in RA:
- Rheumatoid factor
- Anti-citrullinated protein antibody (Anti-CCP)
Which cytokines can play a bid role in RA?
Tumour necrosis factor alpha (TNF-a)
Functions of TNF-a in RA (6):
- Increases pro-inglammatiory cytokines and chemokine (IL-1, IL-6, IL-8)
- Increase adhesion molecules
- Increase vascular endothelial growth factor
- Increase acute phase response
- Increase Keratinocyte hyper proliferation
- Increase metalloproteinase synthesis
Function of vascular endothelial growth factor (VEGF)
Increased angiogenesis
CRP:
C-reactive protein, part of the acute phase response. Broad inflammatory marker.
What does increased keratinocyte hyper proliferation cause?
Skin plaques
In RA, what is the bone eroded by?
Osteoclasts (RANK-L expression increased in other cells activated them).
List some systemic problems in RA:
- Skeletal muscle breakdown
- Rheumatoid nodules
- Fever
- Pleural effusion
- Increased hepcidin, decreased iron
- Atheromatous plaques in blood vessels
Which type of arthritis is often asymmetrical?
Osteoarthritis
Risk factors for OA:
Female, age, family history, obesity, oestrogen deficiency, occupation, past trauma
Treatment aims in OA:
Patient education and information access
Pain relief
Optimisation of function
Modification of disease process
What is the most common inflammatory arthritis in men?
Gout
Name 3 common comorbidities in gout:
- Renal impairment
- Coronary heart disease
- Metabolic syndrome (obesity, dyslipidaemia, hypertension, T2 diabetes)
Non-modifiable risk factors for gout:
Age, male, race, genetic factors, impaired renal function
Modifiable risk factors for gout:
Hyperuricaemia, high-purine diet, alcohol consumption, obesity, certain meds (e.g. diuretics)
Hyperuricaemia =
Abnormally high levels of uric acid in the blood.
where does urate in the body come from?
- Cell turn over
- Diet
Ways to modify risk of gout:
- Modify purine-rich foods
- Reduce alcohol intake
- Obesity
- Modify medications
What are purines broken down into?
Uric acid - excretes in the urine
What can cause too much rate in blood?
- over productions (increased synthesis, high cell turn-over)
- increased consumption of purines
- under excretion of purines
Podagra =
a classic symptom of gout. gout affecting the big toe.