Gout의 원인, 증상, 합병증, 진단, 치료, 치료약물 등 gout의 전반적인 내용에 대해
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The Clinical Problem
The Gout Attack
Clinical phases of gout
Biochemical Basis of Gout
Classification of gout
Hyperuricemia : cause and classification
purine nucleotide synthesis
Uric acid crystals
ADDITIONAL RISK FACTORS
Diet and Lifestyle
Approaches to Lowering Uric Acid Levels
Pharmacologic Antihyperuricemic Therapy
Uricosuric Therapy:Creatinine Clearence: <80 mL
Areas of uncertainity
<The Clinical Problem>
- A definitive diagnosis
the direct identification of urate crystals in the joint
the exclusion of infection
- Serum urate levels are frequently normal during attacks of acute gout
- among postmenopausal women in association with diuretic-treated hypertension and renal insufficiency
- organ-transplant recipients who are treated with cyclosporine have an increased risk of gout
* Gout 사진
* 사진 설명
▪ Have hyperuricemia for years before developing symptoms
▪ 75% of initial gout attacks begin in the lower extremities
▪ Podagra most cases begin in big toe (50%)
▪ Sudden, intense pain
▪ Little pain otherwise
▪ Also affected:
▫ Insteps, heels, ankles, knees, fingers, wrists, and elbows
< Clinical phases of gout>
-Acute gouty arthritis
▪ Gout attack
▪ Most significant presentation
-Intercritical asymptomatic gout
▪ Between attacks
-Chronic tophaceous gout
▪ Long term problem
-12 yrs from onset to chronic
-Impair quality of life, not shorten life
-Most chronic gout patients die of renal failure
▪ Acidic urine saturated with uric acid crystals
▪ As a nidus for calcium oxalate or phosphate stone
-Acute gouty nephropathy
▪ Massive malignant cell turnover
▫ With treatment of myeloproliferative or lyphoproliferative disorders
▪ Blockage of urine flow secondary to the precipitation of uric acid in the
CD and ureter
-Chronic urate nephropathy
▪ H & P for hyperuricemia
▫ Drugs like diuretics?
▫ Lead exposure?
▫ Renal disease?
▫ Acute arthritis?
▫ Hypertension or CVD?
▫ Family history?
■ Lab tests
- Creatinine clearance
- Liver function
- Uric acid levels (serum and urine)
■ Synovial fluid aspiration
- Usually of 1st MTP joint (big toe)
- Increased white cell count (neutrophils)
* 사진 : Monosodium Urate Crystals
▪ Plain film X-ray
▫ S.T. swelling and edema in joints
▫ Punched out lesions and fractures
▫ Interosseous tophi and joint space narrowing
▪ CT scan
x ray 사진 3장 : Plain film X-rays of foot and hand of gout affected individuals
<Diet and Lifestyle>
▪ weight reduction
▪ decreased alcohol consumption
▪ control of hyperlipidemia
▪ control of hypertension
▪ decrease consumption of foods
with high purine content
Used alone, these measures will not reduce uric acid levels
(Medicine is also needed)
■ Avoid excessive alcohol
▪ Ethanol increases uric acid production
▪ Beer has a high guanosine content which promotes production
■ Avoid high purine foods
▪brain, kidney, liver and heart
▪Peas and beans
■ Moderate protein intake
■ Low-fat diet
■ Treat ...
■ Treat ...
■ Acute Gout
▪ Within the first few hours
▪ hours: 0.6 mg once every hour for up to 3 hr (maximum, 3 pills)
▪ low-dose oral colchicine can
be used as follows for prophylaxis against acute gout
particularly before the initiation of antihyperuricemic therapy
■ Side Effects:
▪BM suppression for IV.
► 0.6 mg orally twice daily in patients with
creatinine clearance ≥50 ml/min
► 0.6 mg orally per day in patients with
creatinine clearance of 35 - 49 ml/min
► 0.6 mg every 2 - 3 days in patients with
creatinine clearance of 10 - 34 ml/min
< The Choice?>
- between a medication that reduces urate production and one that increases urate excretion
- 24-hour urinary urate excretion to identify patients who overproduce urate
- a daily urinary urate excretion in excess of 800 to 1000
<Areas of uncertainity>
Asymptomatic hyperuricemia alone
direct, deleterious effects on arterial smooth-muscle cells, glomeruli,and systemic blood pressure...