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PHAR 230 > M5 L1: ethanol (alcohol) > Flashcards

M5 L1: ethanol (alcohol) Flashcards

1
Q

what is alcohol

A
  • widely consumed and socially accepted
  • most commonly abused drug in the world
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2
Q

what is the chemical structure of alcohol

A

OH- (functional group) and C atom (saturated)
valence of 4

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3
Q

make sure to look at chemical structures of methanol, ethanol, propan-2-ol, ethan-1,2-diol on the slideshow

A
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4
Q

chemical structure of ethanol (rubbing alcohol)

A

C2H5OH
used as disinfectant

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5
Q

what is ethylene glycol chem structure

A

C2H4(OH)2

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6
Q

what is ethanol

A
  • small molecule
  • produced by sugar fermentation
  • water soluble
  • organic solvent
  • volatile and flammable
    (can pass blood-brain barrier which is why it has CNS symptoms)
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7
Q

what is ethanol

A

used as: recreational drug, antiseptic/disinfectant, chemical solvent, fuel

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8
Q

how is ethanol absorbed

A

rapidly through the GIT(stomach)

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8
Q

what is peak blood level for ethanol

A

within 30 minutes (F>M)

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9
Q

what is the distribution of ethanol

A

rapid - increased Volume distribution close to total body water

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9
Q

how is ethanol metabolized

A

liver (90%) - oxidation - 2 pathways…

1st step stim or catalyzed by alcohol dehydrogenase (MEOS)
2nd step by aldehyde dehydrogenase

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9
Q

can ethanol cross membranes

A

yes!
ex: BBB and placenta

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10
Q

how is ethanol excreted

A
  • kidney thru urine
  • lungs thru breath (DUI)
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11
Q

what can fomepizole inhibit

A

alcohol dehydrogenase

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12
Q

what can disulfiram inhibit

A

alc dehydrogenase
(disulfiram works to treat alc use disorder [results in unpleasent sypt to deter person from drinking], fomeprizole does ethylene glycol treatment and methanol poisoning)

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13
Q

what is MEOS

A

microsomal ethanol-oxidizing system

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14
Q

what is fomepizole

A

treatment of methanol or ethylene glycol poisoning

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15
Q

what is disulfiram

A

treatment of alcohol dependence

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16
Q

what is the rate of metabolism for ethanol

A

zero order kinetics (= independent of time and concentration)
depends on enzymes

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17
Q

what are the 2 pathways for metabolism that ethanol uses

A
  • alcohol dehydrogenase (primary pathway) …
  • MEOS (chronic alcoholism) … Acetaldehyde -> Acetate -> CO2 or acetyl CoA
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18
Q

what does acetaldehyde accumulation cause

A

facial flushing, nausea, vomiting, dizziness, headache

19
Q

how does alcohol do what it does to the CNS

A
  • affects several neurotransmitter systems involved in the brain’s reward pathways mainly GABA and glutamate
  • increased GABA-mediated inhibition thru GABAa receptor
  • decreased glutamate-mediated excitation thru NMDA receptor

GABA has a sedative effect, glutamate has an excitatory effect

20
Q

what does ethanol do to dopamine, opioid, and cannabinoid pathways

A

increase/stim

increase in dopamine - makes you feel good/high/satisfied this can lead to addiction
stim of opioid channel - eases pain, makes you feel relieved

21
Q

what is the mech of action for a high dose of ethanol

A

Na channel blockade, electrical stabilization and decreased conduction of nerve action potential (direct effect)
overall inhibiting depolarization

22
Q

what are the effects of alcohol on the body? (ethanol pharmacodynamics)

A
  • CNS depression
    slower reaction times, sedation, impaired motor function, slurred speech, emesis, coma, respiratory death
23
Q

effect of alcohol on the heart (pharmacodynamics)

A
  • decreased myocardial contractility
  • high dose: dysrhythmia
24
Q

why does alcohol cause smooth muscle relaxation

A
  • due to decreased vasomotor center + acetaldehyde
  • vasodilation -> hypothermia (heat loss) + hypotension
  • uterine relaxation
25
Q

alcohol drug interactions

A
  • additive CNS depression with other CNS depressants
  • hepatic microsomal enzyme induction -> increased metabolism of drugs and generation of toxins, free radicles, H2O2
  • drugs w disulfiram-like reaction (ex: metronidazole, trimethoprim)
26
Q

what are long-term effects of alcohol consumption on the CNS

A
  • tolerance, addiction, dependence
  • neurotoxicity
27
Q

alcohol tolerance

A
  • may result from: ethanol-induced up-regulation of a pathway
  • results in: decreased intensity, and shortened duration of action
  • cross tolerance: sedative-hypnotics, general anesthetics
28
Q

alcohol dependence

A
  1. psychological dependence:
    - compulsion to: experience the rewarding effect, avoid the withdrawal sympt
  2. physical dependence:
    - withdrawal syndrome
    mild: hyperexcitability
    severe: seizures, psychosis, delirium tremens, coma, death
29
Q

alcohol neurotoxicity

A
  • peripheral neuropathy
30
Q

what is wernicke-korsakoff syndrome

A
  • caused by thiamine (vitamin B1) deficiency
  • manifestations: extrinsic eye muscles paralysis, ataxia, confusion-encephalopathy-coma-death
  • sequelae after treatment: korsakoff’s psychosis, memory loss, impaired vision
31
Q

what are long term effects of alc consumption in the liver

A

alcoholic fatty liver, hepatitis, cirrhosis, liver failure

32
Q

what are long term effects of alc consumption in the GI

A
  • gastritis -> peptic ulcer and GI bleeding
  • chronic pancreatitis
  • malabsorption
  • abnormal immune response
33
Q

what are long term effects of alc consumption in the CVS

A
  • cardiomyopathy and HF
  • dysrhythmias - atrial and ventricular
  • hypertension
  • fetal alcohol spectrum disorders
34
Q

what are hematologic long term effects of alc consumption

A

folic acid deficiency and decreased Fe anemia

35
Q

what are long term effects of alc consumption in the endocrine and metabolic

A
  • gynecomastia and testicular atrophy
  • hypoglycemia
  • lactic acidosis
36
Q

what are cancerous long term effects of alc consumption

A
  • mouth, pharynx, larynx, esophagus, liver
    causes: acetaldehyde, folate metabolism changes, chronic inflammation
37
Q

what is fetal alcohol spectrum disorder (FAS)

A
  • conditions in children caused from chronic maternal alcohol abuse during preg
  • mech of teratogenic effect: unknown!
  • wide spectrum: most severe is fetal alc syndrome
  • main manifestations: growth retardation, microcephaly, facial features, congenital heart defects, CNS defects
38
Q

what are CNS defects in FAS

A
  • cognitive deficits
  • impaired motor function
  • attention and hyperactivity problems (ADHD)
  • social skills problems
  • epilepsy
39
Q

what are some treatments of acute intoxication

A
  • prevent severe resp depression***
  • aspiration of vomitus
  • correct electrolyte imbalances
  • treatment of hypoglycemia and ketoacidosis
  • vitamin B1 (thiamine)
  • no antidote
40
Q

how to manage alcohol withdrawal syndrome

A
  • mild sympt don’t need treatment
  • prevention of seizures, delirium and dangerous dysrhythmias (vitamin B1, correct electrolytes, benzodiazepines)
41
Q

best ways (4) to treat alcoholism

A
  1. rehab and psychological therapy
  2. naltrexone
  3. acamprosate
  4. disulfiram
42
Q

what does naltrexone do

A

long acting opioid antagonist - blocks mu receptors
orally
help reduce craving

43
Q

what does acamprosate do

A

decreases NMDA receptor and increases GABAa receptor
orally
help reduce craving
poorly absorbed from GIT

44
Q

disulfiram

A

make pt hate drinking due to accumulation of acetaldehyde and all the effect of it
orally

45
Q

precautions while using naltrexone

A
  • pt should not be opioid dependent (opioid withdrawal)
  • do not combine w disulfiram (both are hepatotoxic)
46
Q

what is methanol (wood alc)

A
  • uses: solvent, fuel, antifreeze
  • absorption: GIT, skin, resp sys
  • toxicity: due to formaldehyde & formate, causes visual disturbances, blindness, etc. use fomepizole or ethanol (antidotes) - IV
47
Q

what is ethylene glycol

A
  • polyhydric alcohol
  • has a sweet taste
  • uses: solvent, heat exchangers, antifreeze
47
Q

what is ethylene toxicity

A
  • due to: glycolaldehyde and oxalic acid
  • effect: CNS excitation -> CNS depression -> anion gap metabolic acidosis -> renal and hepatic failure -> death
  • treatment: fomepizole or ethanol (antidotes) - IV

PHAR 230 (31 decks)

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