alcohol Flashcards

1
Q

describe how you calculate the absolute amount of alcohol (g alcohol/100ml)

A

%ABV x 0.78

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2
Q

how do you calculate units?

A

(%ABV x volume/ml)/1000

1 unit = 10mls or 8g of absolute alcohol

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3
Q

how many units should people drink? what is classified as binge drinking?

A

< 14 units/week

binge drinking = >8 units in one sitting

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4
Q

describe the 2 locations of absorption of alcohol

A

20% from stomach directly

80% from intestines

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5
Q

what is the speeds of onset of intoxication proportional to?

A
  • proportional to gastric emptying
  • post prandial, stomach does not empty as often as it needs to break down food
  • so alcohol is not absorbed very well
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6
Q

describe the metabolism of alcohol

A
  • only 90% is metabolised
  • 10% breathed off
  • 8% of metabolism occurs in liver
  • 15% occurs in GIT
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7
Q

describe the liver metabolism of alcohol

A
  • alcohol to acetaldehyde (toxic) via alcohol dehydrogenase (75%) and mixed fucntion oxidase (25%)
  • MFO most significantly up regulated in chronic alcoholics
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8
Q

what is the difference in 1 high dose bolus of alcohol compared to same absolute amount of alcohol over 4 separate doses?

A
  • one high dose bolus will saturate enzymatic system leads to higher intoxication
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9
Q

describe the GIT metabolism of alcohol

A
  • alcohol –> acetaldehyde via alcohol dehydrogenase found in stomach
  • females have less ADH than males in GIT
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10
Q

why are women more susceptible to alcohol?

A

men have more body water. more ADH = more body water

more water also allows alcohol to be more widely distributed

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11
Q

what happens next to acetaldehyde in liver and GIT metabolism?

A

acetaldehyde –> acetic acid via aldehyde dehydrogenase

polymorphisms can be found in this enzyme leads to asian flush

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12
Q

what is disulfiram?

A

inhibitor of aldehyde dehydrogenase

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

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13
Q

describe the general pharmacodynamicsof alcohol?

A
  • low potency
  • influences a lot of receptors as it has an uncompiicated shape
  • but doesn’t fit a lot of receptors very well so not a lot of efficacy
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14
Q

what are the acute effects of alcohol on the CNS?

A
  • depressant effect
  • alcohol depresses system by: inc. inhibition, reducing excitation (reducing stimulation at NMDA receptors and reducing Ca influx so less NT exocytosis)
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15
Q

how does alcohol cause CNS euphoria?

A
  • alcohol binds to mu-receptor to inhibit GABA release

- less inhibitory GABA means less inhibition on DA release by VTA DA neurones into NAcc

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16
Q

what parts of the brain does alcohol affect?

A
  • corpus callosum
  • hypothalamus (appetite, emotions, pain, temp)
  • RAS (consciousness)
  • Hippocampus (memory)
  • cerebellum (movement and coordination)
  • basal ganglia (perception of time)
17
Q

what are the acute effects of alcohol on the CVS?

A
  • cutaneous vasodilation = flushing (dec. Ca influx –> less VSM contraction, inc. prostaglandins –> vasodilators)
  • inc. HR (SNS becomes dominant and HR inc, alcohol diminishes control of brain on arterial baroreceptors so heart receives less inhibitory input)
18
Q

what is the endocrine effects of alcohol?

A
  • alcohol dehydrogenase supresses VP release

- Less VP and less water reabsorption = diuresis

19
Q

what are the chronic effects of alcohol on CNS?

A
  • dementia - cortical atrophy and dec. cerebral white matter
  • ataxia - cerebellar cortex degeneration
  • Wernicke-Korsakoff’s syndrome - due to thiamine def as less food intake as calories from alcohol
20
Q

what are the 2 parts of Wernicke-Korsakoff’s syndrome?

A
  • Wernicke’s encephalopathy (affects 3rd ventricle and aqueduct)
  • Korsakoff’s psychosis (affects dorsomedial thalamus, irreversible, impairs memory)
21
Q

what are the chronic effects on the liver, regarding NAD+?

A
  • need NAD+ for a lot of functions
  • alcohol dominates the use of NAD+
  • so NAD+ is not used for other functions
  • leads to build up of other dangerous toxic by-products
22
Q

what causes fatty liver?

A

lack of NAD+ means that the TAGs are deposited in liver

23
Q

what causes hepatitis?

A
  • mixed function oxidases unregulated in chronic alcoholics
  • generate free radicals which generate an inflammatory response
  • cytokines released e.g. IL-6, TNF-alpha
24
Q

what causes cirrhosis?

A
  • fibroblasts lay down fibrin supportive structures
  • reduce regenerative capacity of liver
  • dec. regeneration and active liver tissue
  • inc. fibroblasts
25
Q

what are the positive effects on the CVS?

A
  • dec. mortality from coronary HD
  • inc. HDLs
  • inc. tPA levels –> dec. platelet aggregation levels
  • polyphenols (red wine) may reduce free radicals
26
Q

what are the GIT chronic effects of alcohol?

A
  • damages gastric mucosa
  • can lead to stomach cancer from acetaldehyde build up
  • acetaldehyde is carcinogenic
27
Q

what are the endocrine chronic effects of alcohol?

A
  • inc. ACTH secretion –> Cushing’s ike syndrome

- dec. testosterone –> gynecomastia

28
Q

what are the symptoms of a hangover? what causes them?

A

symptoms peak as BAC approaches 0

  • nausea: irritant –> vagus –> vomiting centre of medulla
  • headache: vasodilation
  • fatigue: sleep deprivation
  • restlessness: rebound excitation as BAC –> )
  • polyuria, polydipsia (dec. VP secretion)