Pharmacology of Ethanol Flashcards

1
Q

Ethanol Absorption is rapid throughout entire GI tract; and extremely rapid in the ________.

A

small intestine

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2
Q

The more rapid the ethanol _______ , the more rapid the absorption (dependent on concentration gradient)

A

ingestion

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3
Q

Ethanol is water soluble and distributed in ________

A

total body water (will also cross the placenta)

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4
Q

Distribution / equilibration is most rapid in areas of high ________. Initial CNS effects within 5 min; peak effects within 15-60 min.

A

blood flow (brain, liver, kidney, lung)

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5
Q

Fat contains less water and thus less alcohol._______ is a factor that corrects for the volume of distribution of alcohol

A

[r]

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6
Q
r = \_\_\_\_\_\_ for men, 
r =  \_\_\_\_\_\_ for women.
A
  1. 68,

0. 55

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7
Q

Women given the same g/kg dose of ethanol as a man of equal weight will have a _______ blood alcohol concentration

A

higher

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8
Q

Metabolism is responsible for _______ of disappearance of alcohol from body.

A

90-98%

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9
Q

First pass metabolism in _________ may be important in sex differences in BAC

A

gastric mucosa

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10
Q

Metabolism occurs at a __________ of 7-10 grams of alcohol per hour

A

constant rate (zero order kinetics)

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11
Q

which enzyme is the main metabolizer of ethanol in the liver

A

Alcohol dehydrogenase

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12
Q

________ accounts for 10-25% of ethanol metabolism at higher BACs

A

CYP2E1 (previously known as Microsomal Ethanol Oxidizing System [MEOS]);

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13
Q

Aldehyde dehydrogenase is inhibited by ________

A

disulfiram

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14
Q

__________ converts acetaldehyde to acetate.

A

Aldehyde dehydrogenase

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15
Q

acetate is converted to ______. then metabolized into fatty acids and cholesterol, CO2, H2O, and energy

A

Acetyl CoA

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16
Q

what are the adverse effects of increased acetaldehyde levels

A

nausea/vomiting,
respiratory and cardiovascular collapse,
convulsions

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17
Q

Mitochondrial oxidation of NADH to NAD is insufficient with the increased levels of _______, caused by alcohol

A

NADH

18
Q

increased levels of NADH leads to disruptions in hepatic metabolic pathways:
Increased Blood lactate =________

A

acidosis -> behavioral disturbances

19
Q

Increased levels of NADH leads to disruptions in hepatic metabolic pathways:
Increased Mg++ excretion can lead to _______
Decreased Uric acid excretion may precipitate ______

A

convulsions,

gout attacks

20
Q

Increased levels of NADH leads to disruptions in hepatic metabolic pathways:
Increased Acetyl CoA leads to _________ fatty acid synthesis combined with decreased fat breakdown leads to fatty liver.
Increased NADH leads to Decreased Krebs cycle activity, -> Decreased gluconeogenesis -> ______

A

Increased,

hypoglycemia

21
Q

Alcohol produces a dose-dependent __________ effect similar to ________

A

CNS depressant

barbiturates

22
Q

Ethanol is not a stimulant at any dose, but depression of _________ neurons is seen first, resulting in a relative stimulatory phase prior to depressive actions.

A

inhibitory cortical

23
Q

The CNS effects of low-to-moderate doses of ethanol (0.05-0.250 g/dl [50-250 mg %]) are mediated via interactions with ______ and _________ receptor coupled ion channels.

A
GABA (potentiation),
glutamate NMDA (inhibition)
24
Q

alcohol may precipitate convulsions; and is ________ in epilepsy

A

contraindicated

25
Q

Effects of Alcohol on the Liver

A

Reversible damage (increased fatty acid / lipid deposition -> hepatitis).
ascites,
esophageal varicosities.
May see decreased synthesis of clotting proteins, thus increased bleeding time.

26
Q

Cirrhosis occurs in ______ of chronic alcoholics (5-25 yrs)

A

20%

27
Q

High doses of ethanol can decrease absorption of _________.

A

amino acids, glucose, folic acid, thiamine, B12

28
Q

Alcohol-induced increases in digestive secretions can produce ________.

A

pancreatitis

29
Q

Prolonged ethanol use may cause serious ulceration of the gastric mucosa, ranging from ______to actual ________.

A

gastritis,

hemorrhage

30
Q

Alcohol exerts a diuretic effect by ___________.

A

inhibiting the secretion of antidiuretic hormone

31
Q

Heavy drinkers have increased risk of cancers of the

_____________ .

A

mouth, pharynx, larynx, esophagus, liver, and lung

32
Q

can get ethanol Cross tolerance with other CNS depressants such as ______ & _____

A

anesthetics,

benzodiazepines

33
Q

what are early withdrawal Sx’s of ethanol (0-48Hr)

A

anxiety
tremor,
mild agitation

34
Q

what are some late alcohol withdrawal Sx’s (24-150 Hrs)

A

extreme overactivity,
disorientation,
confusion

35
Q

In __________. Patients display progressive external ophthalmoplegia, nystagmus, ataxia of gait, pain, loss of sensation, and weakness of the arms and legs. Results from thiamine deficiency that is secondary to alcohol intake; responds quickly to thiamine administration

A

Wernicke’s Disease

36
Q

___________. Symptoms include severe amnesia and personality alterations. Amnesic syndrome may result from interaction of thiamine deficiency with direct neurotoxic effects of alcohol.

A

Korsakoff’s psychosis

37
Q

what are the Major effects of ethanol by pregnancy trimester?

A

1st: Major morphologic abnormality
2nd: Increased risk of spontaneous abortions
3rd: Decreased fetal growth

38
Q

Ethanol can promote ______ if taken with aspirin.

A

GI bleeding

39
Q

If alcoholic with normal liver function -> faster metabolism (enzyme induction, CYP2E1); may reduce concomitant drug effect and can potentiate ______ toxicity.

A

acetaminophen

40
Q

•NMDA receptor drugs _________. Produces SOME reduction in alcohol craving and relapse rates in combination with psychotherapy.

A

Acamprosate

41
Q

Opioid antagonists _______ Shown to reduce alcohol craving, consumption, and relapse rates when used in combination with psychotherapy.

A

Naltrexone