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Pharmacology and Therapeutics > 14. Alcohol > Flashcards

14. Alcohol Flashcards

1
Q

What is the worst country in the world in terms of the amount of alcohol consumed per capita?

A

Ireland

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2
Q

What is ABV?

A

Alcohol by volume

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3
Q

How do you calculate absolute amount?

A

%ABV x 0.78 = grams of alcohol/100ml

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4
Q

How do you calculate units of alcohol?

A

[%ABV x actual volume (ml)] / 1000

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5
Q

How much alcohol is there in 1 unit?

A

10ml or 8mg of absolute alcohol

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6
Q

What considered the low risk level of alcohol for men and women?

A

14 units or less per week

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7
Q

What does ‘low risk’ refer to when talking about alcohol?

A

Risk of alcohol-related problems in life

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8
Q

What is binge drinking defined as?

A

Drinking >8 units in one sitting

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9
Q

Which part of the population does the binge drinking category mainly relate to?

A

18% of 16-24 year olds on a weekly basis

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10
Q

What does 0.01% blood alcohol mean?

A

10mg alcohol / 100ml blood

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11
Q

What is the UK drink driving limit?

A
  • 0.08%
  • 80mg alcohol / 100ml blood
  • Usually 1-2 drinks depending on weight
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12
Q

Where is alcohol absorbed in the body?

A
  • Stomach (20%)

* Intestines (80%)

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13
Q

What is the speed of onset of alcohol proportional to in the stomach?

A

Gastric emptying

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14
Q

How does drinking on a full stomach influence blood alcohol levels?

A
  • Delayed gastric emptying
  • Alcohol housed in the stomach
  • Absorption is less effective here than in the intestines
  • Therefore, longer onset and lower bioavailability
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15
Q

How much alcohol is metabolised and where?

A
  • 90% is metabolised, 10% doesn’t change
  • Some excreted through lungs unchanged
  • 85% of the 90% is metabolised in the liver (many ways)
  • 15% of the 90% is mainly metabolised in the stomach to a certain degree (alcohol dehydrogenase)
  • Females have 50% less stomach alcohol dehydrogenase
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16
Q

Describe how the liver enzymes metabolise alcohol

A
  • Alcohol => acetaldehyde [alcohol dehydrogenase (75%) and mixed function oxidase - CYP450 (25%)]
  • This is a very toxic product - don’t want it building up
  • Acetaldehyde => acetic acid [aldehyde dehydrogenase]
  • Happens in the liver and stomach to produce an inert product
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17
Q

How relevant is the solubility of alcohol in absorption?

A
  • Alcohol is very water soluble so you would expect poor absorption
  • However, it is really small and can easily diffuse across the lipid membrane through gaps
  • Water/lipid solubility becomes irrelevan
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18
Q

Outline the distribution of alcohol in men and women?

A
  • Men generally have more body water than women
  • Therefore, alcohol is more concentrated and has a more powerful effect in women
  • Women also metabolise alcohol less effectively, so blood alcohol levels are higher
19
Q

What causes asian flush?

A
  • Very common genetic polymorphism in the aldehyde dehydrogenase enzyme
  • Ineffective metabolism of acetaldehyde
  • Build up
  • Toxicity (nausea)
20
Q

What is disulfiram and how does it work?

A
  • Drug that blocks aldehyde dehydrogenase
  • Used in alcohol aversion therapy
  • Acetaldehyde builds up whenever they drink
  • Puts them off drinking
21
Q

How potent is alcohol?

A
  • Low pharmacological potency
  • Very simple molecule
  • Therefore, fits many targets but has a weak effect in them
  • Consequence: have to drink a lot to have an effect - 200μg/ml (nicotine/cocaine are 20/200ng/ml)
22
Q

Can you identify a pharmacological target for alcohol?

A

Not really, it has many targets

23
Q

Describe the affinity and efficacy for the targets of alcohol

A

Not very good, weak for both

24
Q

What is the primary acute effect of alcohol on the CNS

A
  • High dose - depressant
  • Low dose - CNS excitation
  • Also depends on personality and environment (higher excitation in social environment caused by disinhibition)
25
Q

What are the 3 main CNS receptor targets of alcohol and how does it effect them?

A 
GABA receptors (inhibitory NT)
• Direct - increases function of the receptors
• Indirect - acts pre-synaptically, increasing allopregnenolone, which can bind to a GABA receptor

NMDA receptors (memory and excitement)
• Decrease of receptor activation
• Binds to receptor - allosteric modulation

Calcium channels
• Interference with opening
• General NT release from neurones impacted

26
Q

How can alcohol cause a euphoric effect?

A
  • Alcohol binds to the opioid receptors in the CNS
  • This switches off the GABA receptors
  • Firing rate of dopaminergic neurones is increased
27
Q

Which tissues are interfered with and impaired by alcohol?

A
  • Corpus callosum - passes info from left brain (rule, logic) to right brain (impulse, feelings) and vice versa
  • Hypothalamus - controls appetite, emotions, temp, pain
  • Reticular activating system - consciousness
  • Hippocampus - memory
  • Cerebellum - movement and coordination
  • Basal ganglia - perception of time
28
Q

Why does alcohol cause redness?

A

• Increased acetaldehyde
• Interference with smooth muscle function in arterioles
- calcium entry impaired and prostaglandins promoted
• Cutaneous vasodilaiton

29
Q

What acute effect can alcohol have on the heart?

A
  • Alcohol depresses baroreceptors
  • No stimulation of PNS, loss of inhibition of SNS
  • Tachycardia caused
30
Q

What acute effects does alcohol have in the endocrine system?

A
  • Acetaldehyde inhibits vasopressin production
  • Less aquaporins in collecting ducts
  • Increased diuresis (polyuria)
  • Increased ACTH
  • Increased cortisol production
  • Can produce ‘Cushing’s like’ syndrome
  • Negative effect on testosterone secretion
  • Can have feminisation symptoms
31
Q

How does alcohol have an effect on dementia?

A
  • Chronic use
  • Cortical atrophy
  • Decreased volume of cerebral white matter
  • Confusion (encephalopathy)
  • Oculomotor symptoms
32
Q

How does chronic use of alcohol affect gait?

A
  • Ataxia

* Cerebellar cortex degeneration

33
Q

What is Wernicke-Korsakoff syndrome and it’s relation to alcohol?

A
  • Vision changes, ataxia, impaired memory
  • Chronic alcohols get a lot of their calories from alcohol - bad diet
  • Thiamine (B1) deficiency
  • Important co-factor in ATP formation
  • Impaired Kreb’s cycle - oxidative stress in brain
  • Mitochondrial injury and eventual apoptosis
34
Q

What is affected in Wernicke’s encephalopathy?

A
  • Affects 3rd ventricle and aqueduct
  • Some mitochondrial injury
  • Apoptosis
35
Q

What is affected in Korsakoff’s psychosis?

A
  • Progression from mitochondrial injury to cell apoptosis in the brain
  • Irreversible
  • Patient will probably die
  • Particularly associated with the hippocampus - problems with memory
36
Q

How does the chronic consumption of alcohol affect aerobic metabolism?

A

• Alcohol dehydrogenase causes the depletion of NAD+
• As a result:
- pyruvate starts getting converted to lactate
- acetyl CoA start getting converted to ketones
• Liver now exposed to acidosis and ketosis
• Ability of liver to metabolise fats and lipids is impaired - build up of fat in the liver
• If the mixed function oxidase system is used a lot, free oxygen radicals begin to be released into the blood

37
Q

How does an acute alcohol binge cause a fatty liver?

A

• Inability to sufficiently
metabolise fats and lipids
• Stored in the liver
• Glycerol and fatty acids are directed to the liver to produce triacylglycerols instead of the mitochondria and hepatocytes

38
Q

How does chronic alcohol consumption cause hepatitis?

A
  • Kreb’s cycle permanently disrupted
  • Generation of acidosis, ketosis and oxygen free radicals in the liver
  • Creates a pro-inflammatory environment
  • All promote WBC influx
  • Increase in IL-6 and TNF alpha
  • Reversible
39
Q

How does chronic alcohol consumption cause cirrhosis?

A
  • If an inflammatory profile remains, fibroblasts may begin to infiltrate the liver
  • Increased connective tissue laid down in place of active liver tissue
  • Reduce metabolic capacity
  • At some point, there is so little active tissue that a transplant is required
40
Q

What GIT problems can arise from chronic alcohol consumption?

A

• Exposure of stomach tissue to acetaldehyde
• Damage of gastric mucosa
- ulceration is common
- stomach cancer risk (carcinogenic effect)

41
Q

What positive effect is there on the CVS of men who drink 2-4 units of alcohol a day?

A

Decrease in mortality from coronary artery disease

42
Q

What positive effect can polyphenols in alcohol have on the CVS profile?

A

Positive
• Increased HDLs
• Increased tPA
• Decreased platelet aggregation

43
Q

When do hangover symptoms tend to peak?

A
  • As blood alcohol concentration reaches 0

* Rebound excitation - depressant effect is lost and CNS becomes very active

44
Q 
What causes the following symptoms of a hangover:
• nausea
• headache
• fatigue
• restlessness and muscle tremors
• polyuria and polydipsia
A
  • Nausea - alcohol is an irritant => vagus => vomiting centre
  • Headache - vasodilation (pressure) and acetaldehyde
  • Fatigue - sleep deprivation, rebound causing poor quality sleep
  • Restlessness and muscle tremors - rebound
  • Polyuria and polydipsia - lower ADH secretion

Pharmacology and Therapeutics (33 decks)

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