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Y2 - PHARM > Alcohol > Flashcards

Alcohol Flashcards

1
Q

What are the sites that alcohol can be absorbed from?

A
  • Small intestines
  • Stomach
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2
Q

What is rate of absorption related to when it comes to the stomach

A
  • Rate of alcohol absorption (if oral administration) is proportional to the rate of gastric emptying
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3
Q

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

A
  • It lowers the rate of gastric emptying
  • Thereby decreasing the rate of absorption because alcohol is held up in the stomach so it is absorbed via the stomach route more which is a slower route so slower rate of absorption
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4
Q

What are the 3 enzymes that metabolise alcohol that are produced by the liver?

A
  1. Alcohol dehydrogenase
  2. Mixed function oxidase
  3. Acetaldehyde dehydrogenase
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5
Q

How and where is alcohol metabolised, and what is it metabolised into - i.e. outline the steps in the metabolism of alcohol?

A

STEP 1

  • Alcohol dehydrogenase in the stomach metabolises alcohol into acetaldehyde first - but little effect and even less effect in women
  • Then alcohol dehydrogenase and mixed function oxidases in the liver metabolise alcohol into acetaldehyde also, greater effect here

STEP 2

  • Acetaldehyde is converted into acetic acid by acetaldehyde dehydrogenase in both the stomach and the small intestine
  • Note acetaldehyde is toxic and it is important to clear it
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6
Q

Why is the time basis for how you dose your alcohol intake important in terms of the effects you feel?

A
  • If you have a high dose very quickly then you can saturate the enzymes that metabolise the alcohol so there’ll be inefficient metabolism and thus more alcohol will enter the systemic circulation
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7
Q

Give 2 reasons why women have a lower tolerance for alcohol than men

A
  1. They have less ADH (alcohol dehydrogenase) in the stomach than men - so the arm of metabolism within the stomach is less effective
  2. They have a lower water content within their bodies so once it enters the systemic circulation, it is less diluted than in males
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8
Q

What is the basis for development of tolerance to alcohol?

A
  • Upregulation of…
  1. Mixed function oxidases
  2. ADH (alcohol dehydrogenase)
  • So alcohol is metabolised better and faster so less enters the systemic circulation where it will have its effect
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9
Q

Describe how you can be less tolerant to alcohol due to defects in one of the steps in the metabolism of alcohol and what phenomenon is this responsible for?

A
  • Common polymorphism of the aldehyde dehydrogenase enzyme
  • So less conversion of acetaldehyde into acetic acid, and remember that acetaldehyde is toxic, so you build up this toxic intermediate metabolite
  • Phenomenon: Asian flush - this polymorphism is common in Asian populations
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10
Q

What drug is used to prevent over consumption of alcohol in alcoholics and describe its physiological basis for its mechanism of action?

A
  • Disulfiram
  • Inhibits acetaldehyde dehydrogenase, thereby preventing the conversion of the toxic intermediate metabolite acetaldehyde into acetic acid
  • Acetaldehyde is off-putting so having high levels of acetaldehyde will put off the alcoholic from drinking further
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11
Q

What is the selectivity of alcohol like?

A
  • Low selectivity - it has widespread effect due to simple molecular structure
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12
Q

What is the affinity and efficacy of alcohol like?

A
  • Low for both
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13
Q

Outline the 4 physiological mechanisms behind how alcohol is a CNS depressant

A
  • Direct effect to stimulate the GABA receptors
  • Acts pre-synaptically to increase allepregnenolone which itself binds GABA receptors to increase its effect
  • Alcohol also decrease NMDA receptor activation by allosteric modulation
  • Alcohol may also impair VGCC opening, thereby preventing NT release
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14
Q

Describe the physiological mechanism behind how alcohol can stimulate euphoria, particularly when administered by inhalation

A
  • Binds opiod receptor to impair GABAergic dampening of the dopaminergic reward pathway from the ventral tegmental nucleus all the way to the nucleus accumbens within the ventral striatum
  • Thereby stimulating euphoria by potentiating the reward pathway
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15
Q

List some different brain areas that alcohol can have its depressant effects and thus cause some of the effects that it has

A
  • Corpus callosum
  • Hypothalamus - appetite, emotional, temperature regulation
  • Cerebellum - impaired balance
  • Hippocampus - impaired memory
  • Reticular activating system - impaired consciousness
  • Basal ganglia - impaired perception of time
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16
Q

Outline the effect that alcohol can have on the CVS

A
  1. CUTANEOUS VASODILATION
  • You go red due to cutaneous vasodilation
  • Due to increased acetaldehyde which…
  • Interferes with smooth muscle function in the arterioles
  • Impairs calcium entry and promotes prostaglandins, thereby causing vasodilation
  1. TACHYCARDIA
    * Due to depression of baroreceptors which normally promote PNS and inhibit SNS in order to slow HR, so by depressing their function, the reverse happens and you get tachycardia
17
Q

Outline the 3 parts of the endocrine system that alcohol can effect (3 hormones) and thus the symptoms it can cause due to these

A
  1. Acetaldehyde impairs VP synthesis and secretion - therefore causing polyuria
  2. Alcohol increases cortisol production - Cushing’s like symptoms
  3. Alcohol impairs testosterone secretion - feminisation symptoms
18
Q

Give 3 negative effects of chronic alcohol abuse in the CNS and the physiological basis for these

A
  1. Ataxia - cerebellar cortex degeneration
  2. Dementia - cortical atrophy
  3. Wernicke-Korsakoff syndrome
  • Due to THIAMINE DEFICIENCY
  • Wernicke’s encephalopathy (3rd ventricle and aqueduct) - reversible
  • Korsakoff’s psychosis (dorsomedial thalamus) - irreversible
  • Acidosis and glutamate production
19
Q

Describe the negative consequences of chronic alcohol abuse in the liver (3 stages) and the psychological basis for everything

A
  • ADH depletes NAD+ (essential component of aerobic metabolism), therefore…
  • Pyruvate starts getting converted into lactate (acidosis)
  • Acetyl CoA starts getting converted into ketones (ketosis)
  • Acidosis and ketosis impairs the liver’s ability to metaobolise lipids
  • Also the mixed function oxidase system is very active so you build up lots of damaging oxygen free-radicals
  • All this also contributes to a pro-inflammatory environment
  • There are 3 stages in the changes to the liver:
  1. Fatty liver - due to fatty TAG depostits as poor lipid metabolism - reversible
  2. Hepatitis - due to all of the above lactic acid, ketosis, oxygen free radicals, and you also see cytokine changes - IL-6 and TNF-alpha build up
    - reversible
  3. Cirrhosis - long term - eventually all the damage results in lots of inflammatory recruitment invluding fibroblasts coming alon and depositing connective tissue in place of active liver tissue - liver dysfunction - irreversible - requires transplant eventually
20
Q

What negative consequences can you get in the stomach as a result of chronic alcohol abuse and what causes this?

A
  • Due to stomach alcohol dehydrogenase, the stomach is exposed to acetaldehyde when alcohol is metabolised into acetaldehyde
  • This is toxic and irritates the gastric mucosa
  • This increases stomach ulceration
  • Also increases stomach cancer risk - carcinogenic
21
Q

What beneficial effects might moderate alcohol use have?

A
  • Protective effects against CAD
  • Improves lipid profile as…
  • Increased HDLs
  • Increased tPA levels
  • Decreased platelet aggregation
22
Q

List some signs / symptoms that occur during hangover and where possible the physiological basis behind this

A
  • Nausea - alcohol is an irritant - irritates the vagus - vomiting centre
  • Headache - vasodilation
  • Fatigue - sleep deprivation
  • Restlessness and muscle tremors
  • Polyuria and polydipsia - reduced ADH
23
Q

Define binge drinking

A
  • Drinking > 8 units in one sitting

Y2 - PHARM (27 decks)

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