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eLCRS - 팜 > Pharm 15: Drugs of Abuse 3 (Alcohol) > Flashcards

Pharm 15: Drugs of Abuse 3 (Alcohol) Flashcards

1
Q

what is the guidance level of alcohol consumption for male + females?

A

< 14 units/week

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2
Q

note:

BLOOD LEVELS – 0.01% = 10mg/100ml blood

A

-

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3
Q

____ of alcohol = absorbed in stomach

___ absorbed in GIT

A

20% of alcohol absorbed in stomach

o 80% absorbed in GIT –> more effective absorption

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4
Q

why do you get drunk more easily on empty stomach?

A

Speed of onset directly proportional to gastric emptying

so you get drunk on empty stomach because fluid in stomach promotes increased emptying –> so alcohol enters GIT faster –> better absorption in s.int

–> higher bioavailability of alcohol

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5
Q

Describe the metabolism of alcohol

in the liver + GIT

A

metabolism of alcohol

  • 85% occurs in liver
  • 15% occurs in stomach/GIT:
    note: 10% is unmetabolised (e.g breath)

in the liver:

  • there are 2 enzymes
    a) alcohol dehydrogenase (75%)
    b) mixed function oxidase (25%)
  • -> alcohol is converted to acetaldehyde (toxic effects)

in GIT:
- alcohol = very water soluble + small molecule
- -> well absorbed in stomach lining
- alcohol dehydrogenase in stomach breaks down alcohol to acetaldehyde
(lower in females)

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6
Q

A man and a woman of similar height and weight share a bottle of wine. Explain why the blood alcohol levels in the woman are likely to be higher.

A

when M + F of similar height/weight have same amount of wine equally –>

a) capacity to metabolism alcohol in stomach = lower in females
- 50% less alcohol dehydrogenase in stomach

b) also men tend to have higher body water
- -> alcohol = very water soluble
- -> more diluted in men
- -> more concentrated in women

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7
Q

mote: alcohol = LOW pharmacological potency

A

-

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8
Q

What is the effect of alcohol on the CNS? (acute)

A

alcohol = depressant

  • increases GABA receptor activation
  • binds to NMDA receptor –> decrease activity –> decrease allosteric modulation
  • decrease Ca2+ channel opening –> less neurotransmitter release

others:
- RAS affected –> unconscious
- Hippocampus –> memory loss
- cerebellum –> movement lost

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9
Q

What is the effect of alcohol on the CVS (acute) ?

A

o Cutaneous vasodilation (flush)

  • there is decreased Ca2+ entry –> less constriction of capillary sphincters
  • and an Increase in prostaglandins
  • -> causing raised acetaldehyde (asian flush)

o Centrally-mediated decrease in baroreceptor sensitivity –> causes increase in HR

o Chronic alcohol = associated with increased BP

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10
Q

What is the effect of alcohol on the endocrine system? (acute)

A
  • causes Diuresis (polyuria)
  • -> due to excess acetaldehyde
  • -> can inhibit ADH secretion
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11
Q

what are the effects of alcohol on the CNS? (chronic)

why do they occur?
hint: link to thiamine

A
  • largely due to thiamine deficiency
  • thiamine = important cofactor for enzymes involved in energy metabolism
  • less thiamine –> impairs cerebral energy utilization –> impairs brain function (esp regions w high metabolic demand)

–> impaired metabolism –> causes NMDA driven excitotoxicity –> mitochondrial impairment –> reactive oxygen species leak into system –> causes cell death

  • Wernicke-Korsakoff syndrome
    (due to thiamine deficiency)
  • Wernicke’s encephalopathy (reversible)
    –> confusion / oculomotor symptoms/ gait problems
  • Korsakoff’s psychosis
    (irreversible)
  • -> memory problems

–> eventually dementia + ataxia

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12
Q

what are the effects of alcohol on the liver? (chronic)

A
  • liver need NADP but alcohol –> uses up NADP
  • low NADP+ :
    a) impaired beta-oxidation of fat
    –> fat builds up in liver as TAG (reversible at early stage)
    –> constant depletion causes deranged metabolic processes to leak free radicals
    (which are pro inflammatory / tissue damage )

= free radicals + acetaldehyde –> can cause hepatitis

constant inflammatory profile –> causes fibroblast infiltration –> fibroblast replace hepatocyte –> cirrhosis

b) impairs TCA cycle
- -> ketones / lactic acid forms

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13
Q

What is the effect of alcohol on the CVS (chronic) ?

A

BENEFICIAL effects when low levels of alcohol:

  • Decreased mortality from coronary artery disease
  • Increases HDLs
  • Increased tPA levels –> decreases platelet aggregation
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14
Q

What is the effect of alcohol on the GIT (chronic) ?

A

GIT: 15% alcohol metabolised here via alcohol dehydrogenase

exposure to Acetaldehyde –> damage to gastric mucosa –> linked to stomach cancer

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15
Q

What is the effect of alcohol on the endocrine system (chronic) ?

A
  • Increased ACTH secretion –> Cushing’s-like syndrome

- Decreased testosterone secretion –> feminine features e.g. breast growth

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16
Q

explain Hangover symptoms:

a) Nausea
b) Headache
c) Fatigue
d) Restlessness and muscle tremors
e) Polyuria and polydipsia

A

(symptom peak as BAC nears 0)

rebound excitation
a) Nausea
acetaldehyde build up = irritant –> activates vomiting centre via vagus nerve

b) Headache
- -> vasodilation / acetaldehyde build up

c) Fatigue
- -> rebound effect

d) Restlessness and muscle tremors
- -> rebound effect / sleep deprivation

e) Polyuria and polydipsia
- -> decreased ADH secretion

17
Q

Alcohol dosing
Absolute amount =

Units =

A

Alcohol dosing
Absolute amount = %ABV x 0.78 = g alcohol / 100ml

Units = %ABV x volume (ml) / 1000

i.e 1 unit = 10ml or 8g of absolute alcohol

18
Q

When you become tolerant to alcohol, what enzyme is affected?

A

mixed function oxides will be upregulated

19
Q

what happens to the acetaldehyde produced from the metabolism of alcohol in the liver + GIT?

A
  • acetaldehyde = converted to acetic acid (inert)

via aldehyde dehydrogenase

20
Q

why do you get asian flush wowzerz

A
  • genetic polymorphism –> in asians
  • aldehyde dehydrogenase is less effective
  • -> causes build up of acetaldehyde
  • -> more severe effects of alcohol
21
Q

why is disulfiram effective as a alcohol aversion therapy?

A
  • disulfiram = aldehyde dehydrogenase inhibitor
  • -> you get build up of acetaldehyde

acetaldehyde –> aversive effects

22
Q

how does alcohol cause euphoria?

A
  • binds to opiate receptor
  • switches off GABA
  • increase in Dopamine release in NAcc
  • increase in euphoric effect / reward pathway
23
Q

disinhibition/ CNS agitation of alcohol depends on what 2 factors?

A

(disinhibition/ CNS agitation)

  • depends on
    a) personality
    b) non social setting / social setting

eLCRS - 팜 (36 decks)

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