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10 Cards in this Set

  • Front
  • Back
ETOH Absorption
-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
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
ETOH: Alcohol Dehydrogenase
-Gender difference
-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
-CYP levels

-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
ETOH: Acetaldehyde Dehydrogenase
-acetaldehyde --> acetate --> CO + H2O

-inhibited by disulfuram
-Asians are ALDH deficient
-->both lead to flushing, vomiting and dizziness
ETOH: Max. BAL factors
-Rate of absorption
-Rate of metabolism
ETOH: Chronic effects on CNS
-Loss of white and grey matter in the frontal lobe

-Reduced brain metabolism


-Neuropathy (saturday night palsy)
ETOH: Acute and Chronic effects on CVS
-Reduced myocardial contractility

- increased BP
- dilated cardiomyopathy
- increased triglycerides
ETOH: Acute effects on kidney
-Decreases ADH secretion--> diuresis and kaluresis

- vasodilation leads to diuresis

- decreased uric acid excretion
ETOH: Acute and chronic effects on GI tract
- secretion of gastrin, pepsin, histamine, and acid --> all lead to peptic ulcer disease

-gastritis and esophageal cancers