Lecture 6 - Gout 1 Flashcards
Hyperuricemia
Elevated Serum Uric Acid
Tophus
Calculus contains sodium rate that develops around fibrous tissues around joins, typically in patients with gout
Podagra
Painful condition of big toe caused by gout
Uricase
enzyme that oxidatively degrade uric acid, thereby catalyzing conversion to soluble allantoin, which is more soluble than uric acid
found in most animals, not in humans
Uricosuric meds
Meds given to increase elim of uric acid
Uric Acid Pathway
Hypoxanthine (Via Xanthine Oxidase ) -> Xanthine (via Xanthine Oxidase) - > Uric Acid (excreted by kindey, metabolized via rate oxidase in animals)
Gets converted to Allantoin in animals
Uric acid comes from?
Metabolism of purines
How is Uric acid eliminated in humans?
Gut and Kidney
Hyperuricemia SUA
> 7mg at 37C for men
> 6mg at 37C for women
Do all patients with hyperuricemia develop acute gout flares?
No
in absence of gout, asymptomatic hyperuricemia does not require treatment
Best description of gout?
Patients with gout will have recurrent acute attacks separated by intercritical periods
Risk Factors for Gout
- Inc age
- Male > female
- injury
- Hyperuricemia** most important
- Fasting
- Recent srugery
- Food/drinks
- Meds
- Medical conditions
- Genetics
Food/Drink risk factors for Gout
Food high in purine = red meat
Foods/drinks w/ high fructose corn syrup = soda
Alcohol
Meds that can cause overproduction
Cytotoxic chemotherapy
Meds that can cause under excretion
Cyclosporine + Tacrolimus
Diuretics (loop/thiazide)
Niacin
Low dose salicylates (< 2g/day)
Medical Condition Risk factors pointed out
Overproduction:
Myeloproliferative disorders
Lymphoproliferative disorders
Underexcretion:
Renal insufficiency
Volume depletion
CVD, common Risk factors
Risk Factors: Genetics
HGPRT deficiency: Leads to more Guanylic acid, leading to more uric acid
PRPP over activity: can increase Hypoxanthien leading to uric acid
Acute Goute Pathophysiology
Uric acid crystals deposit into joint, bringing immune cells that cause them to rupture and perpetuates an inflammatory response
Acute Gout Presentation
12-24hrs after exposure to risk factor
lower extremities
redness, swelling, warmth, extreme pain of the joints
Mot common areas for gout attack
big toe joint = paragraph
can get in knee, finger, wrists elbows
Difference with pseudo gout?
caused by calcium pyrophosphate crystals
can only tell by “tapping joint” looking at fluid after microscope
How to get diagnosis of gout?
Tapping joint and looking at fluid under microscope = gold standard
if cant do that, often do clinical diagnosis
Acute Gout management Treatment
want to rapidly relive symptoms
prevent recurrent attacks
prevent complications associated with chronic deposition of urate crystals
self limiting, can go away on its own but don’t want to do that
** Dont dx ULT in acute attack **
Nonpharm treatment options of Gout
Ice
Rest affected point
Patient education
Pharm treatment options of Gout
Colchicine
NSAIDs
Steroids (systemic/intra-articular)
IL-1 antagonists
FDA approved NSAIDs for gout
Indomethacin (Indocin)
Naproxen (Naprosyn)
Sulidac (Clinoril)
NSAIDs ADR
Inc BP, NA/Water retention, gastritis, GI bleeding
NSAIDs CI
Hx of allergy
HF
Renal Insufficiency
Hx of previous GI
NSAIDs DI
ACE/ARBs Cyclosporine Tacrolimus Tenofovir Lithium Anti-platelet/anticoag Corticosteroids
NSAIDs monitoring efficacy
efficacy, lower pain, reduced number of flairs
NSAIDs monitoring safety
CBC LFTs SCr Fecal occult blood test Black tarry stools BP Edema