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MSII Pharmacology > Unit 3 - Non-Medicinal Drug Use > Flashcards

Unit 3 - Non-Medicinal Drug Use Flashcards

1
Q

what are the CNS depressants and how do they work?

A

augment activity at GABA-A receptor complex, increasing Cl- influx, hyperpolarizing cell (inhibitory)
-include alcohol, barbiturates, benzodiazepines, and inhalants

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2
Q

alcohol absorption?

A

very rapidly absorbed by diffusion through membranes

  • very small molecule that easily crosses membranes
  • -mouth mucus membrane, stomach, small intestine (most here)
  • -lungs absorb alcohol vapor
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3
Q

what does the rate of alcohol absorption depend on?

A
  1. concentration of alcoholic beverage

2. stomach (empty has higher and faster peak, slower drop; full has lower and slower peak)

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4
Q

what does food in the stomach do to alcohol?

A
  1. dilutes alcohol
  2. delays stomach emptying
  3. increases effective rate of alcohol metabolism
    - some enzyme oxidation in stomach
    - slower delivery to liver through portal circulation > liver oxidation
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5
Q

what are blood alcohol units?

A

BAC (blood alcohol concentration)

  • based on plasma or serum in hospital, or whole blood legally
  • 100 mg% = 100 mg/dL = 1 mg/mL = 0.10% (wt/vol) = 22 nM
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6
Q

explain alcohol distribution?

A

total body water, as small molecule can easily cross all membranes

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7
Q

how is alcohol eliminated?

A

90-98% metabolized (oxidized)

-routes are urine, breath, and sweat

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8
Q

how is alcohol metabolized?

A

mostly in liver, some stomach

  • small intestines > portal circulation > liver
  • alcohol dehydrogenase, acetaldehyde dehydrogenase, and microsomal ethanol oxidizing system
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9
Q

what is alcohol dehydrogenase?

A

ADH - dimeric Zn-containing metallo-enzyme in liver cytoplasm, and a bit in gastric mucosa
-ethyl alcohol + NAD+ –> acetaldehyde + NADH + H+

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10
Q

what is acetaldehyde dehydrogenase?

A

ALDH - 1 in liver cytoplasm, 2 in liver mitochondria

-acetaldehyde + NAD+ + H2O –> acetate + NADH + H+

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11
Q

what is the “Asian flush” due to?

A
  1. “atypical” B2 allele with enhanced rate of hepatic ADH (increases metabolism to acetaldehyde)
  2. lack of functional ALDH2 causes build-up
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12
Q

what happens if there is a high magnitude of alcohol consumed?

A

tremendous load for liver, causing dramatic change in redox state

  • all NAD-dependent reactions in liver are affected by alcohol
  • -impaired gluconeogenesis leads to hypoglycemia
  • -increased lactic acid and ketone body production
  • -inhibits uric acid excretion (hyperuricemia)
  • -decreases fatty acid oxidation and increases TG and FA synthesis
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13
Q

what is the rate-limiting factor in alcohol oxidation?

A

supply of NAD+; causes saturation (zero-order) kinetics results

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14
Q

what is microsomal ethanol oxidizing system?

A

MEOS P450 (esp. CYP2E1)

  • smooth ER mixed function oxidase
  • more important factor at high levels of alcohol, and with chronic alcohol consumption
  • induced by chronic exposure to alcohol and barbiturates
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15
Q

what three drugs have cross-tolerance and what is it for?

A

alcohol, barbiturates, and benzodiazepines have X-tolerance for inhibitory neurotransmitter GABA-A and intrinsic Cl- channel
-opens Cl- channel –> hyperpolarizatin –> inhibition

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16
Q

effects of alcohol on CNS

A
  1. potency as a drug is very weak
  2. CNS depressant - dose-related graded effects
    - mild mood alteration –> intoxication –> coma –> death
  3. acute intoxication (mild or moderate)
17
Q

what is “mild intoxication” from alcohol?

A

“impairment”; 25-100 mg% BAC

  • loss of inhibitions, altered mood, impaired cognition, incoordination, sedation
  • due to preferential involvement of polysynaptic neuronal pathways in reticular formation (cerebral cortex, brain stem, cerebellum)
18
Q

what is “intoxication” from alcohol?

A

> 100 mg%

  • diplopia, nystagmus, dysarthria, ataxia
  • vestibular and cerebellar dysfunction –> stupor –> death
  • blackouts are dangerous outcome
  • temporal correlation between peak BAC and peak bheavioral effects, thus behavioral effects correlate with BAC
19
Q

between males and females, which have higher BAC?

A

women have higher BAC due to gastric metabolism and less body H2O

20
Q

what happens to the liver if chronic heavy drinking?

A

fatty liver, although uncertain pathology
-progression: lipid metabolism alteration –> fatty liver –> hepatitis –> necrosis –> fibrosis –> cirrhosis –> hepatic failure –> death

21
Q

what happens if there is constant exposure to acetaldehyde?

A

increase lipid peroxidation and damage to membranes and mitochondria

  • depletion of glutathione and some vitamins
  • alteration in protein transport
22
Q

wwhat are cardiovascular effects of alcohol?

A

most studies show moderate alcohol consumption is protective

  • increases HDL to decrease CDH
  • but all-cause mortality has U-shaped relationship (as other causes of mortality, caused by actions while intoxicated)
23
Q

effect of alcohol on dementia?

A

decreased dementia with 1-6 drinks/week compaired to abstaining

24
Q

what are GI and endocrine effects of alcohol?

A
  1. GI irritation –> inflammation –> chronic gastritis
  2. well-known diuretic effect from decreased secretion of antidiuretic hormone
  3. stressor to stimulate adrenal cortex
  4. decreased testosterone synthesis
    - male alcoholics –> hypogonadism and feminization, gynecomastia
  5. suppresses uterine motlity and milk ejection
25
Q

explain what fetal alcohol syndrome causes

A
  1. growth deficiency (pre- and postnatal body length and weight below mean)
  2. dysmorphic characteristics (facial features, limb abnormalities)
  3. CNS manifestations (neurobehavioral effects)
    - microcephaly, tremor, seizures, slow development, hyperactivity, learning problems, memory problems
26
Q

what are drug interactions with alcohol

A
  1. pharmacokinetic interactions with many drugs
    - acute (while alcohol is on board): metabolism of other drugs will be inhibited if they undergo oxidative metabolism
    - chronic (induces P450, thuus metabolism of some other drugs may be enhanced, which also contributes to tolerance of alcohol)
  2. pharmacodynamic interactions
    - additive CNS depression with other CNS depressants
27
Q

what is methyl alcohol and treatment?

A

windshield washer antifreeze

  • formaldehyde and formic acid are highly toxic metabolites –> severe acidosis
  • visual disturbances –> blindness
  • treatment = ethyl alcohol (to tie up alcohol dehydrogenase) + bicarbonate (to decrease acidosis state)
28
Q

what is ethylene glycol and treatment?

A

autommotive antifreeze

  • oxidized to oxalic acid, which is very toxic to kidney
  • -renal insufficiency
  • -acidosis
  • -CNS excitement –> depression
29
Q

what does disulfiram do?

A

inhibit acetaldehyde dehydrogenase, so that acetaldehyde cannot be converted into acetic acid
-worsens their toxic effects, so used as alcoholism treatment

30
Q

what is treatment for both methanol and ethylene glycol poisoning?

A
  1. ethyl alcohol (vodka; maintain 100 mg/dL)

2. alcohol dehydrogenase inhibitor (4-methylpyrazole)

31
Q

what is isopropyl alcohol and treatment?

A

rubbing alcohol

  • causes gastritis, acidosis, and CNS symptoms
  • no antidote, so must use symptomatic and supportive treatment
32
Q

what are barbiturates?

A

multi-use, generally replaced by benzodiazepines

  • augment activity at GABA-A receptor complex to produce CNS inhibition
  • cause drowsiness, confusion, impaired judgement, slurred speech
33
Q

what are phenobarbital and thiopental?

A

barbiturates still in use today

  • phenobarbital: anti-seizure
  • thiopental: induce anesthesia
34
Q

what are benzodiazepines?

A

augment activity at GABA-A receptor complex to produce CNS inhibition

  • many benzos, and widely used to induce anesthesia, treat anxiety, sleep aids, and for recreation
  • cause alcohol-like drunkenness with relaxation, loss of inhibition, impaired judgement, and loss of short-term memory
35
Q

what are CNS stimulants?

A

amphetamine and cocaine

-increase CNS catecholamine, especially dopamine, directly or indirectly by several mechanism

MSII Pharmacology (43 decks)

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