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LCRS Pharma > Alcohol > Flashcards

Alcohol Flashcards

1
Q

how is a unit calculated?

A

%ABV x volume consumed divide by 1000

1 unit is 8g/10ml absolute alcohol

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2
Q

what is the low risk drinks limit in men and women?

A

<14 units a week

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3
Q

what is the definition of binge drinking?

A

> 8 units in one sitting

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4
Q

which two places is alcohol absorbed?

A

o 20% from the stomach directly.

o 80% from the intestine.

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5
Q

what is alcohol absorption like post-prandial?

A

stomach does not empty into small intestine during digestion so alcohol is not absorbed well therefore a decreased onset of its effects

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6
Q

what is speed of onset of intoxication proportional to?

A

gastric emptying

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7
Q

how much alcohol is metabolised?

A

90% metabolised,

10% breathed off

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8
Q

where is alcohol metabolised?

A

85% in the liver

15% in the GIT

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9
Q

what is alcohol broken down into?

A

acetaldehyde (toxic)

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10
Q

what is involved in the breakdown of alcohol in the liver?

A

75% - Alcohol dehydrogenase.

25% - Mixed function oxidase.

CYP2E1
catalase
aldehyde dehydrogenase

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11
Q

what happens to mixed function oxidase in chronic alcoholics?

A

upregulated so the alcohol is broken down faster

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12
Q

how does dosage of alcohol affect intoxication?

A

one high dose will saturate the enzymatic system and lead to higher intoxication than 4 separate lower doses

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13
Q

what is involved in the breakdown of alcohol in the GIT?

A

100% alcohol dehydrogenase found in the stomach lining

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14
Q

what is the different in alcohol dehydrogenase in men and women?

A

women have 50% less alcohol dehydrogenase in the GIT

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15
Q

why are women more susceptible to alcohol?

A

1) women have a lower body water content (50%) compared to men (59%) therefore the alcohol is diluted less in women.
2) Women have greater adipose tissue aswell so alcohol is less well distributed like in men.
3) Men have more alcohol dehydrogenase so metabolise alcohol better

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16
Q

what is acetaldehyde converted to in the liver and GIT?

A

acetic acid (Acetate) via aldehyde dehydrogenase

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17
Q

what leads to the asian flush?

A

polymorphism in aldehyde dehydrogenase

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18
Q

what is an inhibitor of aldehyde dehydrogenase?

A

disulfiram- blocks the enzyme to cause a build up of acetaldehyde

used to put people off alcohol

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19
Q

what is the use of disulfiram?

A

alcohol aversion therapy as the build up of the toxic acetaldehyde makes you feel sick and not want to drink

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20
Q

why is alcohol considered to have low pharmacological potency?

A

it is a small, uncomplicated molecule that can bind to many targets generally and not very well therefore a lot of it is required. It has a low efficacy

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21
Q

what is the acute effect of alcohol on the CNS?

A

depressant effect dependent on environment (social or non-social setting) and the personality of the individual

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22
Q

how does alcohol have a depressant effect on the CNS?

A

 Increasing inhibition – pre- and post-synaptic (via GABA)
 Reducing excitation – reducing stimulation at NMDA receptors and reducing Ca2+ influx so less NT exocytosis

but this is difficult to assess in a functionally complex system like the CNS

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23
Q

how does alcohol induce euphoria?

A

binds to “mu”-receptors to inhibit GABA release. Less GABA means less inhibition on DA release by VTA neurones to the NAcc.

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24
Q

what parts of the brain does alcohol affect?

A

o Corpus callosum – information from left to right.
o Hypothalamus – controls appetite, emotions, pain, temperature.
o RAS – consciousness.
o Hippocampus – memory.
o Cerebellum – movement & coordination.
o Basal ganglia – perception of time.

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25
Q

how does alcohol cause flushing?

A

cutaneous vasodilation due to decreased Ca2+ influx so VSM contract less
also increased prostaglandins (vasodilators)

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26
Q

how does alcohol increase heart rate?

A

diminished control of the brain on arterial baroreceptors so the heart receives reduced inhibitory input
SNS becomes dominant and HR increases

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27
Q

how does alcohol cause diuresis?

A

Alcohol dehydrogenase suppresses the release of antidiuretic hormone/vasopressin
less vasopressin means less water reabsorption

28
Q

what are the chronic effect on the CNS of alcohol?

A

 Dementia – cortical atrophy and decreased cerebral white matter.
 Ataxia – cerebellar cortex degeneration.
 Wernicke-Korsakoff’s Syndrome – due to thiamine deficiency

29
Q

what comes under Wernicke-Korsakoff’s syndrome?

A

thiamine deficiency is due to calories into the body being replaced by alcohol calories. The brain requires thiamine in its metabolic function. The deficiency
this leads to:
o Wernicke’s encephalopathy (reversible) – affects the 3rd ventricle and aqueduct.
o Korsakoff’s psychosis (irreversible) – affects the dorsomedial thalamus (impairs memory (they make memories up)

30
Q

how can chronic alcohol use lead to acidosis, ketosis and lipid build up etc?

A

alcohol consumes a lot of NAD+ required for other functions so they can not be used in metabolism, leading to the build up of toxic by products

31
Q

what is the effect of a lack of NAD+ on the liver?

A

fat deposition leading to a fatty liver

  • NADH is required for the beta oxidation of lipids
  • this is prevented due to low numbers
32
Q

how does chronic alcohol use lead to hepatitis?

A

mixed function oxidases are upregulated in chronic alcoholics and these generate free radicals which then generate an inflammatory response. Cytokines are also released (increased IL-6 and TNF-a)

33
Q

what is cirrhosis?

A

fibroblasts lay down fibrin supportive structures that reducen the regenerative capacity of liver.
There is a decrease in functional, active liver and increased fibroblasts.

  • chronic hepatitis can recruit fibroblasts that lay down connective tissue to replace active liver
34
Q

what are the positive effect on the CVS of alcohol?

A

 Decreased mortality from coronary heart disease (men with 2-4 units/day).
 Increased HDLs.
 Increased tPA levels–> decreased platelet aggregation levels.
 Polyphenols (red wine) may reduce free radicals.

35
Q

what are the GIT effects of alcohol?

A

Damages gastric mucosa in proportion to the dose

- can lead to stomach cancer due to acetaldehyde (carcinogen) build up

36
Q

what are the endocrine effects of alcohol?

A

o Increased ACTH secretion –> Cushing’s-like syndrome.

o Decreased testosterone–> gynecomastia.

37
Q

when do symptoms peak in a hangover?

A

at 0 blood alcohol

38
Q

what are the symptoms of hangover?

A

o Nausea [Irritant–>vagus–>vomiting centre of medulla.
o Headache [Vasodilation]
o Fatigue [Sleep deprivation, ‘rebound’]
o Restlessness and muscle tremors [‘rebound’ – rebound excitation as BAC=0]
o Polyuria, polydipsia [Decreased VP secretion]

39
Q

what can cause tolerance to alcohol?

A

increased and quicker metabolism

40
Q

which receptors does alcohol exert its effects?

A
  • GABA (enhanced)
  • NMDA receptors (depressed)

this leads to CNS depression

41
Q

what is the effect of enhancing GABAergic activity and depressing NMDA receptor activity on the brain?

A

depressive effect

42
Q

how is the depressive effect on the CNS achieved? what ions are involved

A

GABA enhancement and NMDA depression means:
- increase chloride influx
- decreased calcium influx
in the brain neurones so depresses CNS activity

43
Q

what are the primary structural targets of alcohol in the brain?

A
  • hypothalamus
  • RAS
  • hippocampus
  • cerebellum,
  • basal ganglia
44
Q

hypothalamus function

A

influence on appetite, emotion, temperature and pain sensation

45
Q

RAS function

A

consciousness

46
Q

hippocampus function

A

memory

47
Q

cerebellum function

A

movement and coordination

48
Q

basal ganglia function

A

time perception

49
Q

why does drinking faster get you drunk quicker?

A

liver enzymes for 1st pass metabolism are saturated

50
Q

what are the 4 enzymes involved in alcohol metabolism?

A

Alcohol dehydrogenase
CYP2E1
Catalase
aldehyde dehydrogenase 2

51
Q

what are the stages of alcohol metabolism?

A

alcohol to acetaldehyde to acetate/ethanoic acid

52
Q

what catalyses the acetaldehyde to ethanoic acid/acetate?

A

aldehyde dehydrogenase 2

53
Q

how is alcohol excreted? what happens to unmetabolised alcohol?

A

mostly through bile

unmetabolised alcohol via sweat, breath, urine

54
Q

what are the acute side effects of alcohol?

A
  • nausea
  • headache
  • fatigue
  • polyuria
  • increased heart rate
55
Q

why does alcohol cause nausea?

A

irritant to stomach

56
Q

why does alcohol cause headache?

A

vasodilation by acetaldehyde

57
Q

why does alcohol cause fatigue?

A

brain activity increase

restlessness

58
Q

why does alcohol cause polyuria?

A

decreased vasopressin

59
Q

why does alcohol cause increased heart rate?

A

decreased sensitivity of baroreceptors

decreased PNS and increased SNS output therefore

60
Q

what are the chronic side effects of alcohol?

A
  • dementia
  • stomach ulceration
  • Cushings-like symptoms
  • Wernicke-Korsakoff Syndrome
  • fatty liver
  • hepatitis
  • cirrhosis
61
Q

why does chronic alcohol consumption cause Cushings-like symptoms?

A

alcohol increases ACTH secretion

62
Q

why does chronic alcohol consumption cause Wernicke-Korsakoff syndrome?

A

there is a thiamine deficiency leading to mitochondrial damage

eventually there’s Korsakoff’s psychosis due to hippocampal apoptosis

63
Q

what causes mitochondrial damage?

A

thiamine deficiency in chronic alcoholics

64
Q

what causes Korsakoff’s psychosis?

A

hippocampal apoptosis

65
Q

why does chronic alcohol consumption cause a fatty liver?

A
  • alcohol metabolised into acetaldehyde required NAD+
  • this produces the NADH product
  • NADH prevents beta oxidation of lipids
  • this builds up fat
66
Q

why does chronic alcohol consumption cause hepatitis?

A
  • up regulation of CYP450 enzymes occurs with chronic drinking
  • these generate free radicals that damage hepatocytes
  • there will be recruitment of IL-6 and TNFalpha causing inflammation
67
Q

why does chronic alcohol consumption cause cirrhosis?

A
  • hepatitis leads to the recruitment of fibroblasts
  • fibroblasts lay down new connective tissue
  • this connective tissue replacing active liver so reducing liver function

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