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

M5 L1: ethanol (alcohol) Flashcards

(51 cards)

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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

Study These Flashcards
A

facial flushing, nausea, vomiting, dizziness, headache

19
Q

how does alcohol do what it does to the CNS

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

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

22
what are the effects of alcohol on the body? (ethanol pharmacodynamics)
- CNS depression slower reaction times, sedation, impaired motor function, slurred speech, emesis, coma, respiratory death
23
effect of alcohol on the heart (pharmacodynamics)
- decreased myocardial contractility - high dose: dysrhythmia
24
why does alcohol cause smooth muscle relaxation
- due to decreased vasomotor center + acetaldehyde - vasodilation -> hypothermia (heat loss) + hypotension - uterine relaxation
25
alcohol drug interactions
- 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
what are long-term effects of alcohol consumption on the CNS
- tolerance, addiction, dependence - neurotoxicity
27
alcohol tolerance
- 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
alcohol dependence
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
alcohol neurotoxicity
- peripheral neuropathy
30
what is wernicke-korsakoff syndrome
- 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
what are long term effects of alc consumption in the liver
alcoholic fatty liver, hepatitis, cirrhosis, liver failure
32
what are long term effects of alc consumption in the GI
- gastritis -> peptic ulcer and GI bleeding - chronic pancreatitis - malabsorption - abnormal immune response
33
what are long term effects of alc consumption in the CVS
- cardiomyopathy and HF - dysrhythmias - atrial and ventricular - hypertension - fetal alcohol spectrum disorders
34
what are hematologic long term effects of alc consumption
folic acid deficiency and decreased Fe anemia
35
what are long term effects of alc consumption in the endocrine and metabolic
- gynecomastia and testicular atrophy - hypoglycemia - lactic acidosis
36
what are cancerous long term effects of alc consumption
- mouth, pharynx, larynx, esophagus, liver causes: acetaldehyde, folate metabolism changes, chronic inflammation
37
what is fetal alcohol spectrum disorder (FAS)
- 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
what are CNS defects in FAS
- cognitive deficits - impaired motor function - attention and hyperactivity problems (ADHD) - social skills problems - epilepsy
39
what are some treatments of acute intoxication
- prevent severe resp depression*** - aspiration of vomitus - correct electrolyte imbalances - treatment of hypoglycemia and ketoacidosis - vitamin B1 (thiamine) - no antidote
40
how to manage alcohol withdrawal syndrome
- mild sympt don't need treatment - prevention of seizures, delirium and dangerous dysrhythmias (vitamin B1, correct electrolytes, benzodiazepines)
41
best ways (4) to treat alcoholism
1. rehab and psychological therapy 2. naltrexone 3. acamprosate 4. disulfiram
42
what does naltrexone do
long acting opioid antagonist - blocks mu receptors orally help reduce craving
43
what does acamprosate do
decreases NMDA receptor and increases GABAa receptor orally help reduce craving poorly absorbed from GIT
44
disulfiram
make pt hate drinking due to accumulation of acetaldehyde and all the effect of it orally
45
precautions while using naltrexone
- pt should not be opioid dependent (opioid withdrawal) - do not combine w disulfiram (both are hepatotoxic)
46
what is methanol (wood alc)
- 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
what is ethylene glycol
- polyhydric alcohol - has a sweet taste - uses: solvent, heat exchangers, antifreeze
47
what is ethylene toxicity
- 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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