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Pharmacology > Alcohol > Flashcards

Alcohol Flashcards

1
Q

Describe the epidemiology of alcohol usage

A

There is heavy alcohol use in Western Europe. The worst place in the world in terms of the amount of alcohol drunk per capita is Ireland.

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2
Q

How is the absolute amount of alcohol (g) calculated?

A

% ABV x 0.78 = grams of alcohol/100ml (ABV = alcohol by volume)

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3
Q

How are the units of alcohol calculated?

A

%ABV x actual volume (ml)/1000

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4
Q

What is one unit of alcohol?

A

10ml or 8g of absolute alcohol

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5
Q

What is the amount of alcohol that is safe to drink per week?

A

14 units or less per week for men and women

low risk means there is a low chance of having alcohol related problems in life

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6
Q

What is binge drinking defined as?

A

drinking > 8 units in one sitting

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7
Q

What is approximately the legal drinking limit?

A

1-2 drinks bu depends on weight as if you are heavier you can handle more alcohol

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8
Q

What is the risk of drinking alcohol on driving?

A

More risk of having an accident even in low amounts

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9
Q

How much alcohol is absorbed from the stomach and intestines?

A

S - 20%

I - 80%

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10
Q

How does drinking on a full stomach affect its absorption?

A
  • Alcohol is far more effectively absorbed from the small intestine
  • Therefore, in order to absorb alcohol quickly, it needs to get into the intestine as quickly as possible
  • The method for doing this is to drink on an empty stomach (fluid stimulates gastric emptying)
  • Drinking on a full stomach delays gastric emptying (this houses the alcohol in the stomach, where it is far less effectively absorbed)
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11
Q

How much alcohol is metabolised?

A

90% - the remaining 10% doesn’t change at all

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12
Q

Where is some alcohol lost?

Where is the majority of alcohol metabolised?

A
  • We excrete some of it through our lungs unchanged (e.g. breath test assesses amount of alcohol)
  • Once alcohol is absorbed, the first place it goes to is the liver (85% of the 90% is metabolised here)
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13
Q

What are the 2 main groups of enzymes that metabolise alcohol?

A

The liver metabolises alcohol in many ways, but there are 2 major groups of enzymes that predominate

  • Alcohol dehydrogenase (75%)
  • Mixed function oxidase (25%)
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14
Q

How does alcohol tolerance come about?

A
  • Tolerance to alcohol: comes about by upregulation of mixed function oxidase enzymes by the liver
  • Hence, you need to drink more alcohol to get the same effect
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15
Q

What happens when alcohol is taken in large amount in one go compared to if it is taken in smaller quantities many times?

A
  • If you add a lot of alcohol in one go, the liver enzymes can metabolise a certain amount of it
  • But if there is too much, lots of alcohol gets through the liver and into the blood
  • The liver enzymes become saturated with alcohol
  • Breaking it down into doses over several hours allows the liver to metabolise and recover
  • Less alcohol gets into the systemic circulation
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16
Q

Where does the remaining 15% of alcohol metabolism occur?

How does this differ in females?

A
  • If 85% of total amount metabolism is via the liver, the other 15% is somewhere else
  • This is predominantly the stomach (there is alcohol dehydrogenase in the stomach)
  • As the alcohol is absorbed across the stomach, it is metabolised by stomach enzymes to a certain degree
  • Females tend to have a lot less stomach alcohol dehydrogenase
  • So in females, this arm of metabolism isn’t as effective
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17
Q

Why does alcohol have a more powerful effect on women than on men?

A
  • Alcohol is very water-soluble
  • Men generally have more body water than women
  • Blood alcohol levels in the woman are higher because they metabolise it less effectively (less alcohol dehydrogenase in the stomach)
  • More alcohol gets across into the bloodstream
  • Once in the blood, alcohol is less well diluted and distributed
  • Hence more powerful effects in women
18
Q

What is the first step in alcohol metabolism and which enzymes doe this?

What is important to note about the metabolite produced?

A

Alcohol dehydrogenases and oxidases convert alcohol -> acetylaldehyde

Acetaldehyde is a very toxic, so we don’t want it building up in the blood

19
Q

What is the second step in alcohol metabolism?

Where does this occur and what does it produce?

A

An enzyme, aldehyde dehydrogenase, converts acetaldehyde -> acetic acid

  • This reaction occurs both in the liver and the stomach to produce an inactive product
20
Q

What is a common polymrophism affecting alcohol metabolism, what does it result in and which people is it common in?

A
  • In the aldehyde dehydrogenase enzyme
  • Very common in Asian populations
  • This polymorphism results in ineffective metabolism of acetaldehyde -> build up -> toxicity (nausea)
21
Q

What is the name of a drug that blocks aldehyde dehydrogenase?

What is its use?

A

Disulfiram

If this is given to alcoholics, whenever they drink alcohol, acetaldehyde builds up -> puts them off

22
Q

What is the pharmacological target of alcohol?

A

It has many targets as it is not very potent and is a simple molecule so can fit into many targets (hence you have to drink a lot to get an effect)

23
Q

What are the acute effects of alcohol on the CNS?

A
  • Alcohol is primarily a depressant
  • CNS agitation may occur (CNS excitation is only seen at a very low dose)
  • CNS excitation also depends on your personality and the environment (social/non-social setting)
24
Q

How can alcohol interact with different receptors in the CNS?

A
  • Alcohol can interact with GABA receptors (seems to have a positive effect on GABA receptors)
  • Alcohol may directly affect the GABA receptor itself -> increase function
  • There is evidence for alcohol acting pre-synaptically, to increase allopregnenolone (indirect effect)
  • Allopregnenolone can bind to a GABA receptor to increase its effect
  • Alcohol may decrease NMDA receptor activity
  • Alcohol may interfere with calcium channel opening (-> impacts general NT release)
25
Q

Does alcohol cause euphoria? If so how?

A
  • Alcohol behaves a bit like heroine when it comes to euphoria
  • Many people use versions of alcohol that are inhalable, which can cause euphoria
  • In this case, it binds to the opioid receptors in the CNS
  • Alcohol switches off the GABA receptor via the opioid receptor (as opposed to cannabinoid receptors in cannabis)
  • GABA is switched off -> increased firing rate of dopaminergic neurones
26
Q

What are the effects of alcohol in the brain?

A

Alcohol affects all these tissues hence interferes with these processes

  • Corpus Collosum: Passes info from left brain (rules, logic) to right brain (impulse, feelings) and vice versa
  • Hypothalamus: Controls appetite, emotions, temperature, and pain sensation
  • Reticular Activating System: Consciousness
  • Hippocampus: Memory
  • Cerebellum: Movement and coordination
  • Basal Ganglia: Perception of time
27
Q

What are the effects of alcohol on the blood vessels and why?

A
  • Anyone who drinks enough alcohol might see a degree of redness (cutaneous vasodilation)
  • This is thought to be due to increased acetaldehyde
  • Acetaldehyde interferes with smooth muscle function in the arterioles
  • Calcium entry is impaired and prostaglandins are promoted -> vasodilation
28
Q

Why does alcohol cause tachycardia?

A
  • Alcohol causes tachycardia (due to a depressant effect on the baroreceptors)
  • Baroreceptors, if firing well, enhance parasympathetic function and inhibit sympathetic function
  • Alcohol depresses baroreceptors -> no stimulation of PNS + loss of inhibition of SNS
29
Q

What effect does alcohol have on vaospressin, cortisol, testosterone and any other endocrine effects?

A
  • Increased diuresis (polyuria) is related to increased acetaldehyde
  • Acetaldehyde inhibits vasopressin production -> less AQPs in the collecting ducts -> loss of fluid
  • Alcohol increases cortisol production (can produce ‘Cushing’s like’ syndrome as alcohol increases ACTH)
  • Alcohol has a negative effect on testosterone secretion (can have feminisation symptoms)
30
Q

How can alcohol severely affect the CNS?

A

Dementia – Cortical atrophy/decreased volume cerebral white matter

Ataxia – Cerebellar cortex degeneration

31
Q

What is Wernicke’s Korsakoff Syndrome?

What causes it and why?

A

Due to thiamine deficiency - seen in chronic alcoholics. Two seperate conditions that can occur together

  1. Wernicke’s encephalopathy (3rd ventricle & aqueduct, reversible reversible part)
  2. Korsakoff’s psychosis (dorsomedial thalamus, irreversible part)
  • Thiamine deficiency is indirectly related to chronic alcohol use due to an alcoholic’s poor diet
  • You need carbohydrate to obtain thiamine – your neurones need thiamine to function
  • If you don’t have thiamine, you see acidosis and excessive glutamate production
32
Q

What happens to the liver due to NAD+ being used up?

A
  • A consequence of alcohol binging is the depletion of NAD+
  • If you drink too much alcohol, lots of NAD+ is used up
  • NAD+ is needed for many stages in aerobic metabolism
  • As a result, if you are chronically abusing alcohol:

Pyruvate starts getting converted to lactate

Acetyl CoA starts getting converted to ketones

Your liver is now being exposed to lactic acid (acidosis) and ketones (ketosis). The ability of the 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

33
Q

Why do alcoholics end up with fatty livers?

Is it reversible or not?

A
  • Acutely, after going on an alcohol binge, one of the things seen is fatty liver
  • This is the acute presentation of liver problems related to alcohol
  • This is related to the inability to sufficiently metabolise fats and lipids
  • They just store in the liver.- This is reversible, and not particularly dangerous in isolation
  • Instead of glycerol and fatty acids being directed towards the mitochondria, they are directed to the liver to produce triacylglycerols
34
Q

Hepatitis of the liver (noninfective): what causes it, what is it and is it reversible?

A
  • If alcohol is being abused long-term, the Krebs cycle is being permanently disrupted.
  • There is a permanent generation of acidosis, ketosis and oxygen free radicals in the liver
  • This creates a very pro-inflammatory environment
  • Hepatitis describes the changes associated with chronic alcohol use (increased ketones, lactic acid, free radicals)
  • These all promote WBC influx. In hepatitis, we see both blood and hepatic cytokine changes
  • We see an increase in IL-6 and TNF alpha
  • Hepatitis is still reversible
35
Q

Cirrhosis of the liver: what is it and is it dangerous and why?

A
  • Long term, if the inflammatory profile of the liver remains, there can be some real problems
  • Fibroblasts may begin to infiltrate the liver
  • Fibroblasts increase the amount of connective tissue being laid down, in place of active liver tissue
  • The end form of alcohol-induced liver damage is where the inflammatory environment is so bad, that active liver tissue begins to be replaced (cirrhosis)
  • Decreased hepatocyte regeneration, increased fibroblasts and decreased active liver tissue
  • At some point, there is so little left of active liver tissue, that a liver transplant is required
36
Q

What are some GIT problems caused by chronic alcohol abuse?

A
  • If you drink alcohol chronically, GIT problems may arise
  • Due to stomach alcohol dehydrogenase, chronic use of alcohol results in exposure of stomach tissue to acetaldehyde
  • Acetaldehyde can lead to damage to gastric mucosa
  • Ulceration is common in chronic alcoholics – strongly associated with acetaldehyde
  • Stomach cancer risk increases in alcoholics – carcinogenic effects
37
Q

What are some beneficial effects of alcohol use?

Why may this be?

A
  • There is evidence that low levels of alcohol semi-regularly protects against CVS
  • E.g. a glass or red wine may have a protective effect against coronary artery disease
  • It may be that there are compounds in the alcohol, as opposed to the type of alcohol being drank
  • E.g. Polyphenols in alcohol may be beneficial
  • There is a positive CVS profile (increased HDLs, increased tPA levels, decreased platelet aggregation)
  • In men who drank 2-4 units a day there was a decrease in mortality from CAD
38
Q

When do hangover symptoms peak?

A

As blood alcohol concentration reaches 0

39
Q

What are some hangover symptoms? What causes them?

A

Nausea: Alcohol is an irritant -> Vagus -> Vomiting centre

Headache: vasodilation

Fatigue: 1. Sleep deprivation, 2. ‘Rebound’

Restlessness and muscle tremors: ‘Rebound’

Polyuria and polydipsia: ↓ ADH secretion

40
Q

What is the cure for a hangover?

A

Try to counter the rebound effect by going back to sleep. Sleeping yourself through the rebound effect will make you feel better.

41
Q

What is rebound effect?

A
  • Rebound excitation occurs as blood alcohol levels decrease,
  • It means that certain physiological variables (e.g., sleep variables, such as the amount of REM sleep) change in the opposite direction to the changes induced by alcohol and even exceed normal levels once alcohol is eliminated from the body

Pharmacology (26 decks)

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