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10 Cards in this Set
- Front
- Back
ETOH Absorption
-Location -Active or passive -Rate in fasting state -Factors on rate |
-Small intestine>>stomach
-passive--> not saturable -30 mins to peak BAL fasting -[ETOH] of drink; food fat>CHO>protein; pattern of consumption |
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ETOH Distribution
-Volume of distribution -Women vs Men |
- 0.5-0.7L/kg ~total body water
- ETOH enters fat more slowly; women have more fat, thus less TBW, thus achieve higher BAL for the same dose |
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ETOH: Alcohol Dehydrogenase
-Product -Kinetics -Location -Gender difference -Polymorphism |
-ETOH --> acetaldehyde
-1st order kinetics; saturated after BAL of 10-100 mg/dL -Mainly in the liver; also in brain and stomach -Men have higher stomach ADH activity -Mutant lower ADH levels in Asians associated with higher risk of alcoholism |
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ETOH: MEOS
-Product -Kinetics -CYP levels -Byproducts |
MEOS: CYP 2E1
-ETOH --> acetaldehyde -Zero order kinetics: MEOS kicks in when ADH is saturated -CYP E21 upregulated in response to increased consumption --> basis for tolerance -toxic byproducts |
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ETOH: Acetaldehyde Dehydrogenase
-Product -Inhibitor -Polymorphism |
-acetaldehyde --> acetate --> CO + H2O
-inhibited by disulfuram -Asians are ALDH deficient -->both lead to flushing, vomiting and dizziness |
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ETOH: Max. BAL factors
-Vd -Rate of absorption -Rate of metabolism |
?
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ETOH: Chronic effects on CNS
|
-Loss of white and grey matter in the frontal lobe
-Reduced brain metabolism -Wernicke's/Korsakoff -Neuropathy (saturday night palsy) |
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ETOH: Acute and Chronic effects on CVS
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Acute
-Vasodilation -Reduced myocardial contractility -Arrhythmias Chronic - increased BP - dilated cardiomyopathy - increased triglycerides |
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ETOH: Acute effects on kidney
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-Decreases ADH secretion--> diuresis and kaluresis
- vasodilation leads to diuresis - decreased uric acid excretion |
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ETOH: Acute and chronic effects on GI tract
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Acute
- secretion of gastrin, pepsin, histamine, and acid --> all lead to peptic ulcer disease -emesis Chronic -pancreatitis -gastritis and esophageal cancers |