Gout Pathophys Flashcards
Define Gout. Why is is called “disease of kings”
Inflammatory arthritis caused by an accumulation of EXCESS urate crystals (monosodium urate crystals) in joint fluid
disease of kings due to its association of rich foods & alcohol consumption
What are the 2 types of presentation of gout?
Hyperuricemia
1. Increase production of serum uric acid OR Decrease elimination of serum uric acid
2. Tophaceous gout: more severe and chronic + tophi presence
Can be a combination of both
What does an increase in serum uric acid result in?
Deposition of monosodium crystals in synovial fluid of joints
What is uric acid a by-product of?
By-product of purine metabolism (biggest risk factor)
Is hyperuricemia a prerequisite for gout?
No, some patients can have gout and normal SUA levels
What are normal SUA levels? What about if associated with tophi or severe gout?
Normal: <360 umol/L
With tophi or sever gout: <300 umol/L
What are some causes of OVER production of Uric acid? what abut UNDER-excretion?
Over production <10%
- too much alcohol
- too much rich foods
Under-excretion 90%+
- renal impairment
- hypertension
- Meds
How to diagnose gout?
Using polarized light microscopy
- Yellow, needle-like crystals are daignostic for gout
Explain why renal impairment is a risk factor for gout?
Main cause of under excretion of uric acid
Renal impairment (= decreased GFR) causes secretion/reabsorption of urate to fail resulting high serum concentration of uric acid
- gout can indicate early kidney disease
Why is hypertension a risk factor for gout?
serum urate levels may be a partial intermediate on the pathway between HTN and gout
- meds used to treat HTN (diuretics) can also precipitate a gout attack
Explain the relation of DM and gout
They are both linked together
- insulin resistance may play a role in development of gout/hyperucricemia
Why is obesity a risk factor of gout?
Extra weight slows down the kidneys ability to remove uric acid
Explain the effect of beta blocks and Alpha 1 blockers on gout
Decrease GFR –> increase SUA levels
Explain the effect of diuretics on gout
increase urination = risk of dehydration
- remaining serum more concentrated with uric acid
- decrease in GFR and decrease in excretion rate
- increase uric acid reabsorption in proximal tubules
Explain the effect cyclosporine on gout
decreases GFR, increases uric acid reabsorption in proximal tubules
Explain the effect aspirin on gout
increase uric acid reabsorption + decrease uric acid secretion
Explain gout at a cellular level after the deposition of MSU crystals
- Activate leukocytes and induce inflammatory response (gout attack)
- Inflammatory cells produce chemokines –> DESTROY cartilage and bone
- Deposits can extend out from a joint and destroy ligaments –> lead to subcutaneous MSU deposits –> erode through skin (TOPHI)
Why does the severe pain of gout occur overnight?
Lower body temperature at night –> increase urate crystal formation
Where is the first place to get gout? Why?
In big toe (PODAGRA)
- uric acid at cooler temperatures turns into crystals
- big toe is the farthest from the heart so it is the coolest part of the body
What is the gold standard for diagnosis of gout
Joint fluid aspirations
Explain asymptomatic hyperuricemia
High uric acid levels, no symptoms of gout
- no therapy required if there is no symptoms
- recommend some non-pharms
360+ umol/L in females
420+ umol/L in males
Explain acute gout attack (gouty arthritis)? how long does it take to subside
Urate crystals have been deposited cause gout flare
- subsides in 3-10 days
- triggered by: stress, alcohol, drugs
Explain intercritical gout
Asymptomatic period in between attacks of gout
- more urate crystals being deposited
- recurrent attack 6-24 months
Explain pseudogout
Mainly in the knee
- Irritated by calcium pyrophosphate dehydrate crystals (CPPD)
