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Neuro IV > Ethanol pharmacology > Flashcards

Ethanol pharmacology Flashcards

1
Q

ETOH absorption

A

rapid, fastest in small intestine. rapid ingestion –> rapid absorption. Slowed by food

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2
Q

ETOH distribution

A

evenly distributed. Areas with high blood flow (brain, liver, kidney, lung) –> more rapid distribution

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3
Q

Time for initial CNS effect

A

5 minutes

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4
Q

Gender differences in distribution

A

women = more fat, less water per kg body weight –> higher BAC for same dose as a man

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5
Q

volume of distribution of ETOH [r] in men

A

0.68

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6
Q

volume of distribution of ETOH [r] in women

A

0.55

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7
Q

BAC calculation

A

(alcohol in body g/100ml)/[r]

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8
Q

ETOH metabolism

A

hepatic

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9
Q

location of first pass metabolism

A

gastric mucosa. Female less than male

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10
Q

Rate of metabolism

A

constant rate of 0.015-0.020% per hour

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11
Q

ETOH metabolic pathway

A

ETOH + NAD + alcohol dehydrogenase –> acetaldehyde + NADH
Acetaldehyde + NAD + aldehyde dehydrogenase –> acetate + NADH
Acetate + CoA + ATP –> Acetyl CoA + AMP + PP
Acetyl CoA –> fatty acids, cholesterol, CO2, H2O, energy

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12
Q

Effect of fructose in ETOH metabolism

A

fructose –> more rapid NADH conversion to NAD –> increased metabolic rate

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13
Q

Role of NADH in ETOH metabolism

A

must be oxidized to NAD

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14
Q

Disruptions in oxidation of NADH

A

increased blood lactate (–> acidosis, behavioral disturbances), increased Mg excretion ( –> convulsions), decreased uric acid excretion ( –> gout attacks), increased acetyl CoA ( –> increased fatty acid synthesis, decreased fat breakdown –> fatty liver), increased NADH ( –> decreased Krebs cycle activity, decreased gluconeogenesis –> hypoglycemia)

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15
Q

ETOH tolerance

A

limited compared to opioids

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16
Q

Early/minor withdrawal

A

mild agitation, anxiety, restlessness, tremor, anorexia, insomnia. Seizures possible within 6-48h after onset of withdrawal

17
Q

Late/major withdrawal

A

extreme overactivity, disorientation, confusion, disordered sensory perception. No seizures

18
Q

ETOH effects on CNS

A

sedation, analgesic, emetic, hangover,

initially anticonvulsive –> later CNS withdrawal hyperexcitability –> precipitate convulsions

19
Q

BAC = 0.05-0.08

A

impaired reaction time, impaired judgment, impaired driving ability, ataxia

20
Q

BAC = 0.08 - 0.2

A

staggering gait, inability to operate a motor vehicle

21
Q

ETOH effects on liver

A

initially reversible
later: cell death –> collagen replacement (cirrhosis) in 20% of chronic alcoholics

regeneration and enlargement –> pressure on veins –> decreased venous return, ascites, esophageal varicies, increased bleeding time

22
Q

ETOH effects on kidney

A

BAC rising –> Blocked secretion of ADH –> diuresis

Stable BAC –> antidiuresis

23
Q

ETOH GI effects

A

irritation –> gastric secretions –> gastric ulcers (especially with aspirin), pancreatitis

High doses –> blocked absorption of amino acids, glucose, folate, thiamine, B12

24
Q

Criteria for fetal alcohol syndrome

A

pre/postnatal growth retardation and altered morphogenesis (facial) and CNS involvement (mental retardation)

25
Q

Fetal alcohol syndrome incidence

A

1/1000 to 1/300

Heavy drinkers: 1/3

26
Q

ETOH effects by trimester

A

1st: morphologic abnormality
2nd: increased risk of spontaneous abortion
3rd: decreased fetal growth

27
Q

Acute ETOH DDIs

A

additive effects with CNS depressants

28
Q

DDIs in chronic ETOH use, with tolerance

A

cross-tolerance to sedative-hypnotic drugs and general anesthetics

29
Q

Alcoholic with normal liver function

A

faster metabolism, reduced concomitant drug effect, potentiated acetaminophen toxicity

30
Q

alcoholic with mild liver disease

A

normal metabolism

31
Q

alcoholic with severe liver disease

A

slower metabolism due to enzyme loss, increased effect of concimitant drugs

32
Q

management of acute ETOH intoxication

A

respiratory support, IV fluids, glucose, thiamine, K and Mg

33
Q

management of ETOH withdrawal

A

Benzos (action at GABA receptors block CNS hyperexcitability)
Clonidine (a2 agonist) for signs of autonomic hyperactivity

34
Q

Strategies for reduction of ETOH consumption

A

Disulfiram (antabuse), naltrexone,

NMDA receptor modulation (Acamprosate) –> reduced ETOH craving and relapse rates in combination with psychotherapy

Neuro IV (21 decks)

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