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31 Cards in this Set

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Alcohol major metabolism
via ADH (NAD+ dependant) in the liver via oxidation where acetalaldehyde is generated, which is then further oxidized by Ald. dehydrogenase into acetate.
Minor Alchol Metabolism pathway?
via CYP2E1, which is NADPH dependant. Also metabolizes acetaminophin, methanol, and ethylene glycol.
Why is Alcohol metab. zero-order kinetics of elimination?
because NAD+ is in limited supply so ADH is saturated.//

saturation reached once in excess of 0.1 mg/ml.
Avg metabolic rate in adults?
7 gm/hr
ADH inhibitor
Fomepizole: Used in delaying metabolism of toxic alcohols such as methanol, and ethylene glycol which also use ADH.
Alcohol Effects: Liver
NAD+ depletion > fatty acid synthesis increased, FA oxidation decreased, free FA in plasma increased, TG accumulation in liver. All due to altered redox potential from increased NADH:NAD+ ratio.
Alcohol Effects: GI Tract
stim. gastric acid secretion > ulcers. Intestines > reduces absorption causing diarrhea and pancreatitis.
Alchol Effects: CVS
peripheral vasodilatin, flushing, feeling of warmth, body heat loss, hypothermia. //

To compensate, sympathetic tone increased > tachycardia and arrhythmais.// Also, cardiomyopathies and increase risk of strokes.
Alcohol effects; Brain
CNS depression causing the sx of intoxication. Done via release of dopamine by disinhibition causing euphoria
Where does the release of DA occur via inhibition by Eth?
in Nucleus Accumbens which leads to activation of the reward pathways. CNS effects are related to [Eth] in blood.
Eth action in Brain: Mechanism?
Eth disrupts or alters function of neuronal receptors and enzymes >> causing reduction in firing of neurons.
What receptors are altered by Eth in CNS?
Glu (NMDA-R): reducing synaptic transmission.//

GABA mediated increase in Cl- conductance through action at an allosteric site.
Eth effects on ADH?
inhibits ADH, leads to diuresis, dehydration. Done by inhibition of SON and PVN neurons in HT.
Eth effect on LHRH?
depress reproductive function by inhibition of LHRH secretion in HT. Done via CB1-R indirectly via release of endogenous endocannabinoids.
Mgmt of acute Eth toxicity?
Remove Eth from stomach, supportive, antacid or H2 blockers to decrease gastric secretions, Thiamine. //

AVOID CNS stimulants OR depressnts. //
Methanol Toxicity?
less potent CNS depressant than CNS, metabolic acidosis, blindnes and death. Acidosis is due to formatin of formic acid
Cause of blindness due to Methanol tox?
It's the formaldehyde toxicity at the retina because of high local acitivity of retinol dehydrogenase, a homolog of ADH.
Treatment of Methanol Tox?
use alchol of Fomepizole to occupy or inhibit respectively the ADH and retard formation of formaldehyde.
Higher Alcohols upto decanol
more potent as CNS depressants than Ethanol. Very toxic. Ethylene glycol results in renal failure and uremia. Fomepizole can also be used to inhibit ADH.
Benefits of Alcohol at moderate 3-7 drinks per week?
yes beneficial at reducing risks of cardiac infarcts and cognitive decline in elderly probably due to reduced incidence of small strokes.
How is alchol benifical at small quantities?
Resveratrol: in red wine, antioxidant.//

Procyanidins: enhance vascular health in red wines esp from SW France.//

Also, Alcohol induced elevation of HDL cholesterol. //
Metabolic tolerance in alcohol
CYP2E1 increased resulting in increase rate of metabolism. Affects metabolism of other drugs metabolized by P450 enzymes.
Pharmacodynamic tolerance of alcohol?
Dose-Response curve shifts to the right, requiring higher doses. Also, cross tolerance with other CNS depressants incl. barbiturates and general anesthetics. Less tolerant to acute lethal effects.
Physical dependance on alcohol.
True withdrawal aka abstinence syndrome; sx slow in onset 12-24 hrs. Sx include tremors, hyperreflexia, vomiting, visual hallucinations, DELIRIUM TREMENS (DT) about day 3-4; hyperthermia, VC collapse, grand mal seizures.
Other effects of chrnonic alcohol:
Peripheral neuropathy, pellagra due to thiamine deficiency.// Wernicke's encephalopathy (thiamine def.)// Korsakoff's psychosis, cerebellar degeneration.//
Chronic alcohol: GI
gastritis, ulcers, pancreatitis
Chronic Alcohol: Liver
accumulation of acetaldehyde, CYP2E1 induction resluting in toxicity of precursors of hepatotoxicins and carinogens. Results in necrosis, fibrosis, and cirrhosis. Eventually causing liver failure.
Alcohol drug interraction
Acute: inhibition of drug metabolism by P450 enzymes.

Chronic: induction of CYP2E1, increasing metabolism rates of acetaminophen, halothane and other anesthetics.
Teratogenesis due to alcohol?
most frequent cause of mental deficiency in the west. Cause of Fetal Alcohol Syndrom: facial abnormalities, small head, low IQ, low weight, prenatal and postnatal stunting of growth.
Tx of Alcohol: withdrawal syndrome
reduce sx with benzodiazepine to supress seizures, fluid, electrolyte and vitamin esp. Thiamine supplementations.
Alcohol Tx: maintaining alcohol-free state
Disulfiram (antabuse): Ald. dehydrogenase inhibitor > acetalaldehyde accumulation >> unpleasant sxs. //

Naltrexone: opiate antagonist, reduces reinforcing effects of alcohol.//

Acamprosate: GABA analog, reduce hyperexcitability, reduce cravings.//