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Year 2 LCRS Pharmacology > 15: Drugs of Abuse: Alcohol > Flashcards

15: Drugs of Abuse: Alcohol Flashcards

1
Q

What is one unit of Alcohol?

A

1 unit = 10ml or 8g of absolute alcohol

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2
Q

How would you calculate one unit of alcohol?

A

(%Alcohol x V(ml))1000

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3
Q

What is currently considered the “safe level” of alcohol consumption per week?

What is binge drinking?

A

Men & Women; = 14 units/week LOW RISK

Binge drinking i.e. > 8 units in one sitting)

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4
Q

What is the ROA of Alcohol?

A

Oral

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5
Q

Explain the effects of a full/ empty stomach on the pharmacokinetics of Alcohol

A
  • 20% of alcohol is absorbed in the stomach
  • 80% in the small intestine

With full stomach: gastric emptiing is slow –> slower absorbtion on the stomach and small intestine

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6
Q

How much of the total alcohol in the body gets metabolised?

What happens to the rest?

A

90% gets metabolised in body, 10% gets directly excreted

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7
Q

Where does phase 1 of Metabolism of Alcohol happen?

A

85% in the liver

15% directly in GI tract

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8
Q

Explain Step 1 in Alcohol metabolism

A

In the liver (85%)

  • Alcohol dehydrogenase (75%)
  • Mixed function oxidases (25%)

In the GI tract (15%)

  • Alcoholdehydrogenase

Into: Acetaldehyde

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9
Q

Why do women have a lower alcohol tolerance than men?

A

Mainly 2 reasons

  1. less Alcoholdehydrogenase (in GI tract)
  2. Less total body water –> same amount is more concentrated in women
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10
Q

Explaint Step 2 in the Metabolism of Alcohol

A

Acetaldehyde – Aldehydedehydrogenase –> Acetic Acid

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11
Q

Name a drug that can be used in alcohol conversion therapy

Explain why it might work

A

Disulfiram can be used –> inhibits Aldehydedehydrogenase and therefore causes a buid up of Acetaldehyde

  • Acetaldehyde is the toxic component that makes you feel bad from drinking –> feel effects from drinking
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12
Q

What is the concept behind the “Asian Flush”?

A

There are genetic polymophisms in the enzxme Aldehydedehydrogenase that cause an build up of Acetaldehyde in some popoulation groups

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13
Q

Explain the potency of alcohol

A

It is a small, simple molecule –>

  • low potency
  • but binds weakly to many targets

High dose required to see effects!

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14
Q

What is the pharmacological use of alcohol?

Why?

A

Ther is no use for it–> because it is very very unspecific

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15
Q

What are the primary effects of Alcohol on the body?

A

Overally: it has a depressant effect (but CNS agitation might occur at low doses –> increased CNS exitability)

  • +ve on GABA
  • -ve on NMDA receptors
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16
Q

Why do people get talkative with alcohol, though its overall effects are depressant?

Which factors influence this?

A
  • It can cause CNS agitation + increased exitability at low doses, dependant on
    • personaltiy
    • environment
      • social/ non-social setting
17
Q

What are the effects of Alcohol on GABA ?

A

It has a pre+post synaptic increasing effects on GABA

  • Pre-synaptic: Increase Neuro-active steroids that enhance GABA function (Allopregnelone)
  • Post-synatpit: interacts with GABA receptors (Cl-influx when binding to it)
18
Q

What are the effects of Alcohol on NMDA receptors?

A

It binds to NMDA receptors and inhibits them

–> Decrease

19
Q

What are the effects of Alcohol on Calcium channels?

A

Decreasing effect on Calcium influx –> decreased neurotransmitter efflux

–> inhibitory

20
Q

Explain how Alcohol can induce Euphoria

A
  • It binds to opioid receptors
  • Endogenous opioids switch off GABA–>
    • causing disinhibiton of the reward system
      • Euphoria
21
Q

Summaris the effects Alcohol has on the CNS

A

Slowing down of:

  • Corpus Collosum - decreased rules and logic+ impulse retardation
  • Hypothalamus - Controls appetite, emotions, temperature, and pain sensation.
  • Reticular Activating System –Consciousness
  • Hippocampus - Memory
  • Cerebellum - Movement and coordination
  • Basal Ganglia – Perception of time
22
Q

What are the effects of Alcohol on the vasculature

A
  • Causes Vasodilation
    • decreased Ca2+ influx –> SM relaxation –> cutaneous vasodilation
    • increase in prostaglandins (possibly due to Acetaldehyde)
23
Q

Explain the effects of Alcohol on HR

A

It increases HR due to an decrease in Baroreceptor fiering

24
Q

Explain the endocrine effects of Alcohol

A

It Supresses the secretion of ADH – >polyuria

25
Q

Explain the effects of chronic alcohol abuse on the CNS

A

Main issue: Thiamine reduce (due to lack of thiamine in diet, because many calories got from Alcohol)

Mainly damaging things build up in regions with high metabolic demand in brain

  • Dementia – Cortical atrophy/¯ volume cerebral white matter
  • confusion (encephalopathy), oculomotor symptoms
  • Ataxia – Cerebellar cortex degeneration - gait
26
Q

What is Wernicke-Korsakoff syndrome?

Explain its backround

A

Associated with Thiamine defficiency due to chroinic alcohol abuse –>

  1. Wernicke’s encephalopathy – (hypothalamus/thalamus) (acute+ reversible)
    • agitation, ataxia and ophtalmoplegia
  2. Korsakoff’s psychosis – (deep brain e.g. hippocampus (irreversible)
    • Anterograde+ Retrograde amnesia
    • might lead to confabulation (filling memory gaps with stories)

Via

Neurological injury due to cellular energy deficienty

  • oxidative damage,
  • mitochondrial injury leading to apoptosis,
  • and directly stimulating a pro-apoptotic pathway
27
Q

Explain the effects of chronic alcohol abuse on the liver

A
  1. Alcohol metabilism required NAD+ for metabolism –> used up and not there for other processes like
    • Triglyceride metabolism (increased NADH leads to production of fatty acids, low NAD+ leads to reduced fatty acid acitvation)
      • Fatty liver (reversible)
    • Other liver metabolism (e.g. lack of pyruvate in Krebs cycle)
      • Acidosis
      • Ketocis
    • Induces: Oxidative stress
  2. Hepatitis
    1. ​due to accumulation of free radicals and cytokine changes
    2. Acetaldehyde –> Forms acetaldehyde adducts –> immunogenic and can upregulate transcription of collagen I directly + transforming growth factor-beta 1 (TGF-beta1).
  3. Cirrhosis (due to fibroblast repari of damaged hepatocytes)
28
Q

What is Liver Cirrhosis?

How is it connected to chronic alchol abuse?

A

In cirrhosis: fibroblasts replace hepatocyted and causes a

  • decrease in active liver tissue
  • decrease in heüatpcyte regeneration
29
Q

What are the beneficial effects of alcohol on the CVS?

A

Only in low doses : 2-4 units/day –>

  • increase in HDL
  • decreased risk of mortality from coronary artery disease
  • tPA levels/¯ platelet aggregation

Thought to be mediated via Polyphenols

30
Q

What are the effects of Alcohol on the GI tract?

A

Carciogenic:

  • Damage to the Mucusa via metabolism in GI tract–> Acetaldehyde in mucosal wall of GI tract
31
Q

What are the damaging effects of Alcohol on the Endocrine system?

A

It

  • increases ACTH
  • Decreases Testosterone
32
Q

Explain the Symptoms of a Hangover

A
  1. Nausea
    1. Acetaldehyde –> Irritant –> Vagus –> Vomiting center
  2. Headache
    1. Acetaldehyde –> Vasodilation
  3. Fatigue
      1. Sleep deprivation,
      1. ‘Rebound’
  4. Restlessness and muscle tremors ‘Rebound’
  5. Polyuria and polydipsia ↓ ADH secretion

Year 2 LCRS Pharmacology (38 decks)

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