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KG - pharmacology 3 > KG - Pharm 3, Exam 1, Alcohol > Flashcards

KG - Pharm 3, Exam 1, Alcohol Flashcards

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1
Q

DSM-IV criteria for alcohol abuse?

A

social life of individual impaired for at least 1 month as a result of alcohol

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2
Q

DSM-IV criteria for alcoholism?

A
  • occurrence of tolerance and dependence as a result of prolonged alcohol abuse
  • continuous or periodic lack of control over drinking, preoccupation with alcohol, use of alcohol despite adverse consequence, and distortions in thinking (esp denial)
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3
Q

describe: genetic component to being prone to alcoholism

A
  • marked increase in release of B-endorphins in dopamine reward pathway (activate meso-limbic pathway)
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4
Q

ALCOHOL: pharmokinetics?

A
  • absorption from stomach, small intestine
  • peak BAC w/in 30-90 min after last drink
  • evenly distributed, crosses BLOOD-BRAIN BARRIER
  • crosses placenta (fetal BAC same as mom)
  • may compete for metabolism/inhibit breakdown of some drugs (Benzos, barbiturates, TCAs)
  • metabolized by multiple enzyme systems (ADH, MEOS, CYP2E1)
  • induces CYP450s
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5
Q

ALCOHOL: metabolism

A
  1. metabolized by alcohol dehydrogenase to acetaldehyde
  2. acetaldehyde oxidized by dehydrogenase to acetate
    - oxidation reqs cofactor (NAD+)
  3. NAD+ saturated at low concentration
    - less NAD+ for other enzymes
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6
Q

ALCOHOL: what order kinetics?

A

zero order kinetics

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7
Q

ALCOHOL: relationship between rate and concentration

A

rate is INDEPENDENT of concentration

- 10 g/hr

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8
Q

ALCOHOL: what accumulates and happens due to this accumulation?

A
  • lactate & acetyl-CoA accumulate

- Fatty acid synthesis & lactic acidosis occur due to the accumulation

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9
Q

why do women (typically) have greater side effects to alcohol?

A

LEVELS ADH IN GI TRACT LOWER IN WOMEN

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10
Q

ALCOHOL: describe - aldehyde dehydrogenase deficiency

A

w/ this deficiency, acetaldehyde accumulates (TOXIC)

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11
Q

ALCOHOL: describe - Microsomal-ethanol oxidizing system (MEOS)

A
  • chronic consumption induces MEOS

- more alcohol needed for same effect

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12
Q

ALCOHOL: describe - CYP2E1 pathway

A
  • MINOR METABOLIC PATHWAY
  • chronic consumption induces 2E1
  • increases acetaminophen toxicity
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13
Q

Which drug inhibits aldehyde dehydrogenase?

A

DISULFIRAM

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14
Q

Which drug inhibits alcohol dehydrogenase?

A

FOMEPIZOLE

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15
Q

Alcohol tolerance: Pharmocokinetic

A
  • ETHANOL INDUCES CYP2E1 & MEOS

- chronic users have increased ethanol metabolism

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16
Q

Alcohol tolerance: Pharmacodynamic

A
  • DOWN REG OF GABA RECEPTORS
  • UP REG OF NMDA RECEPTORS (black outs)
  • withdrawal due to pharmacodynamic tolerance
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17
Q

Alcohol tolerance: cross tolerance?

A
  • cross tolerance to Benzos & barbiturates (bc also act on GABA receptors)
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18
Q

ALCOHOL: Mechanism of action

A
  • CNS DEPRESSANT
  • BINDS TO GABAa RECEPTOR TO INCREASE Cl- INFLUX AND ENHANCE INHIBITORY GABA TRANSMISSION
  • increase dopamine in mesolimbic pathway
  • inhibits effect of glutamate on NMDA receptor
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19
Q

Effects of alcohol: CNS, low concentrations

A
  • DISINHIBITION

- decreased anxiety, mild euphoria, confidence increases, memory/concentration affected, mood swings

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20
Q

Effects of alcohol: CNS, increased dose

A
  • motor function & judgment impaired, speech slurred, ataxia

- CNS DEPRESSANT & SEDATIVE properties become apparent

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21
Q

Effects of alcohol: what causes ANTEROGRADE AMNESIA (blackouts)?

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A
  • blockage of NMDA receptors
22
Q

Effects of alcohol: smooth muscle

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A
  • ethanol = VASODILATOR (due to acetaldehyde metabolite)
  • HYPOTHERMIA
  • relaxes uterus (used for prevention premature labor)
23
Q

Effects of alcohol: heart

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A
  • depression myocardial contractility
24
Q

Effects of alcohol: kidney

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A
  • decreases ADH

- DIURETIC EFFECT

25
Describe: acute alcohol toxicity
- emesis, stupor, coma, resp depression, death - metabolic & electrolyte disturbances - hypothermia (cutaneous vasodilation) - decr BP, CO
26
Treatment for acute alcohol toxicity?
- manage resp depression | - prevent emesis
27
why do we get hangovers?
- buildup of acetaldehyde - dehydration - beg of withdrawal
28
TREATMENT: seizures due to acute alcohol toxicity
treat w/ benzos or anticonvulsants - LORAZEPAM (Ativan) = benzo - PHENYTOIN (Dilantin) = anticonvulsant
29
Effects chronic abuse: Liver/GI tract
- GASTRITIS, PANCREATITIS - LIVER DISEASE (most common) - FATTY LIVER --> FIBROSIS --> CIRRHOSIS - metal of alcohol lowers concentration of glutathione, results in oxidative stress/tissue damage - ALCOHOLIC HEPATITIS - LIVER CANCER (usu 10 yrs post-consumption)
30
Effects chronic abuse: malnutrition
- deficiencies in FOLATE, THIAMINE
31
Effects chronic abuse: CNS
- WERNICKE-KORSAKOFF SYNDROME = paralysis eye muscles, ataxia, confusion, coma, death (THIAMINE DEF) - KORSAKOFF'S PSYCHOSIS = chronic memory loss - PERIPHERAL NEUROPATHY
32
Effects chronic abuse: cardiovascular
- CARDIOMYOPATHY = due to direct effects acetaldehyde - ARRHYTHMIAS = binges can cause incr in bp - HTN - incr risk stroke, heart dz
33
Effects chronic abuse: carcinogenicity
- incr car. of tobacco
34
Effects chronic abuse: blood
- mild anemia
35
Effects chronic abuse: sexual dysfunction
- testicular atrophy - impotence - gynecomastia
36
Effects chronic abuse: immune
- resp infections
37
Effects chronic abuse: teratogenicity
fetal alcohol syndrome - microcephaly, mental retardation, poor coordination, flattened face, joint abnormalities, heart defects, impaired immune system
38
Effects chronic abuse: muscles
- skeletal muscle atrophy
39
Effects chronic abuse: temp
- hypothermia
40
Alcoholism: best way to treat?
- combo pharmacologic + psychosocial (AA) treatments
41
NALTREXONE: moa
- OPIOID RECEPTOR ANTAGONIST - BLOCKS ABILITY OF ALCOHOL TO STIMULATE REWARD PATHWAY - reduces craving (decreases rate of relapse
42
NALTREXONE: adverse effects/contraindications
- large doses may cause liver damage | - do not use in pts w/ liver failure
43
ACAMPROSATE: moa
- STRUCTURAL ANALOGUE OF GABA - balance between GABA and glutamate disturbed - RESTORES NORMAL BALANCE OF GABA & GLUTAMATE - increases abstinence & decreases likelihood of relapse - EXCRETED BY KIDNEY - NO LIVER TOXICITY
44
DISULFIRAM: moa
- INHIBITS ALDEHYDE DEHYDROGENASE - ACETYLDEHYDE BUILDS UP - causes flushing, nausea, confusion - long duration of action - EFFECTS CAN BE SEVERE - vomiting, sweating, chest pain, vertigo, blurred vision, shock - dangerous, NOT recommended
45
ANTIDEPRESSANTS: when to use?
many alcoholics have level of depression - help depression, may reduce craving to drink
46
describe: mild alcohol withdrawal
- anxiety, irritability, insomnia, nausea, tachycardia
47
describe: severe alcohol withdrawal
- hallucinations, DTs, seizures, arrhythmias, hypotension
48
treatment: alcohol withdrawal?
- restore electrolyte imbalances - hydration - DIAZEPAM (Valium) = to PREVENT seizures & DTs, tapers symptoms - LORAZEPAM (Ativan) = to treat seizures - PHENYTOIN (Dilantin) = secondary drug to treat seizures
49
describe: methanol poisoning
- VISUAL DISTURBANCES (like being in a snowstorm) - smell formaldehyde on breath - METABOLIZED BY ALCOHOL DEHYDROGENASE TO TOXIC ALDEHYDES AND OXALATES - transient CNS excitation, then depression, then severe METABOLIC ACIDOSIS - bradycardia, coma, seizures, cessation of respiration
50
Treatment: methanol poisoning
- support respiration - lavage - alkalization for acidosis - dialysis - FOMEPIZOLE = ALCOHOL DEHYDROGENASE INHIBITOR - -> CAN ALSO USE ETHANOL

KG - pharmacology 3 (11 decks)

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