Pharmacology of Ethanol Flashcards Preview

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Flashcards in Pharmacology of Ethanol Deck (24):
1

Absorption of Ethanol

Rapid throughout entire GI tract - extremely rapid in SI
More rapid the ingestion  More rapid the absorption (dependent on concentration gradient)

Presence of food slows absorption
Delays passage to small intestine
Heavy meal can decrease peak concentration by 30%

2

Distribution of Ethanol

Ethanol is water soluble and distributed in TBW

Placenta is permeable to ethanol - factor in FAS

Distribution - equilibration most rapid in areas of high blood flow -->brain, liver, kidney, lung

Initial CNS effects within 5 min

Peak effects within 15-60 min

Fat contains less water --> less alcohol distribution
Women have greater % body fat than men
Given same g/kg dose of ethanol as man of equal weight--> woman will have a higher BAC

3

Meto of etoh

liver

4

Disulfiram (sold under the trade names Antabuse and Antabus)

Disulfiram works by inhibiting the enzyme acetaldehyde dehydrogenase, which means many of the effects of a "hangover" are felt immediately after alcohol is consumed.

5

↑ NADH

↓ Krebs activity-gluconeogenesis--> hypoglycemia

6

You receive a blood chemistry workup on an individual (90 kg male) admitted to the emergency room because of a car accident. The individual seemed disoriented, and you astutely ordered a blood-ethanol level determination along with other tests. The reports indicate a blood alcohol concentration (BAC) of 0.24 gm/dl and a blood pH of 7.15 (acidotic). Which of the following is most likely responsible for the acidotic condition of your patient?

Ethanol’s actions on the GABA system of brain result in suppression of ADH release and fluid retention.
Ethanol inhibits the excretion of organic acids in the urine leading to acidosis.
Ethanol metabolism generates NADH that promotes the production of lactate from pyruvate, leading to lactic acidosis.
Ethanol metabolism generates acetaldehyde that acts to inhibit the kidney acid transport systems.

?


Ethanol metabolism generates NADH that promotes the production of lactate from pyruvate, leading to lactic acidosis.--MAYBE

7

Acute CNS Effects of Ethanol
Sedative-Hypnotic Effects

Dose-dependent CNS depressant effect – similar to barbiturates

Low-moderate dose (0.05-0.250 g/dL)--> ↑ GABA plus ↓ Glutamate neuronal function

Anxiolysis major reinforcing effect leading to abuse

8

Acute CNS Effects of Ethanol
Anticonvulsive Effects

Good anticonvulsant initially, but hyperexcitability upon withdrawal

May precipitate convulsions – contraindicated in epilepsy

9

Organ System Effects of Ethanol
Liver

Fatty liver
etoh heptis

esophageal varices

10

Organ System Effects of Ethanol
GI

Pancreatitis

11

Organ System Effects of Ethanol
CVS

Cardioprotection
=)

Moderate etoh= happy heart

s/s hypothermia, CHF

12

methamphetamine

CNS stimulants

13

heroin

Opioid analgesics

14

diazepam

Benzodiazepines

15

pentobarbital

Barbiturates

16

phencyclidine

Dissociative anesthetics

17



Alcohol’s action on the brain produces a variety of effects. Alcohol intoxication (at lethal dosages) most closely resembles intoxication with which of the following classes of abused drugs?

CNS stimulants (methamphetamine)
Opioid analgesics (heroin)- u
Benzodiazepines (diazepam)- low dose
Barbiturates (pentobarbital)- high dose
Dissociative anesthetics (phencyclidine)- nmda

Barbiturates (pentobarbital)- high dose

18

Which of the following signs is NOT characteristic of the acute alcohol (ethanol) withdrawal syndrome?
 
Tremor
Anxiety
Somnolence
Agitation
Insomnia

Somnolence

19

What is characteristic of etoh wd

Tremor
Anxiety
Agitation
Insomnia

20

Drug Interactions ETOH

Additive effects with all CNS depressants (acute)
Cross-tolerance to sedative-hypnotic drugs and general anesthetics (chronic use)
Can promote GI bleeding if taken with aspirin
Increase risk of hepatotoxicity with acetaminophen

21

Drug Interactions ETOH

Altered disposition of drugs metabolized by liver

Non-alcoholic  acute alcohol can inhibit metabolism

Alcoholic with normal liver function  faster metabolism via induction of CYP2E1

Reduce concomitant drug effect

Potentiate acetaminophen toxicity

Alcoholic with mild liver disease  normal metabolism

Alcoholic with severe liver disease (hepatitis/cirrhosis)

Slower metabolism (enzyme loss) increasing effects of concomitantly administered drugs

Disulfiram-like symptoms with metronidazole

22

Treatment of Acute Alcohol Intoxication

Support of respiration

Administration of IV fluids - glucose, thiamine, and electrolytes (K+ and Mg++)

No specific antidote available

23

Alcohol Withdrawal Syndrome

Benzodiazepines (chlordiazepoxide, lorazepam)
• Action at GABA receptors prevents emergence of CNS hyperexcitability following withdrawal of alcohol
• Hyperexcitability is due to down-regulation of GABA function and increased glutamate receptor activity
• Benzodiazepines act via principle of cross-dependence
α2 adrenergic agonists (clonidine)
• Effective for signs of autonomic hyperactivity

24

management of acute alcohol intoxication

Support of respiration
Administration of IV fluids - glucose, thiamine, and electrolytes (K+ and Mg++)
No specific antidote available