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drugs that change the world > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

what is alcohol?

A

are molecules containing 1 or more hydroxyl groups (OH-) attached to a carbon atom (C) that can be attached to other C atoms
- ethanol is an alchohol widley consumed by humans

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2
Q

how is ethanol made?

A
  • is a metabolite made by brewers yeast during the metabolism of sugars to extract energy for their needs
  • fermentation requires the absence of oxygen
  • cell growth is carefully monitored in fermentation vats since excessive alchohol levels are toxic to yeast
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3
Q

Alcohol and ancient egypt (3000BC-300BC)

A
  • early producers of beer from barley
  • the god Osiris taught people to make beer
  • used for currency of trade
  • strong religious element
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4
Q

Alchohol and Ancient rome

A
  • wine had large economic value
  • strong social acceptance
  • excess drinking criticised moderation is a virtue
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5
Q

types of alchohol: Beer

A
  • most popular beverage
  • made from starchy grains suh as barley and wheat
  • ancient beers: thick and fibrous
  • modern beers: clear and carbonarted, higher alcohol content
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6
Q

types of alchohol: wine

A
  • produced from fruit commonly grapes also berres

- longer fermentation time than beer, higher alcohol content than beer

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7
Q

Types of alcoholic beverages: spirits

A
  • produced through distillation
  • technically quite complex
  • boiling a fermented produts and capturing the steam in a condenser which then drips down and is collected
  • vodka, rum, gin
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8
Q

Types of Alcohlic beverages: fortified wines

A
  • wine to which spirits have been added
  • orginiated c1700s in countirs with strong maritime economis
    eg port, sherry, vermouth
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9
Q

What are the pharmcokinetics of alcohol?

A
  • ethanol displays what chemists call amphipathic or amphilphilic character
    (combination of fatloving and water loving properties
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10
Q

Pharmokinetics of alcohol - Absorption

A
  • after oral consumption alcohol is quickly absorbed into the blood
  • absorbed mostly from the upper intestine and the stomach
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11
Q

Pharmokinetics of alcohol - Distraibution

A
  • wide distrabiution via blood
  • manly distrbutes into total body water TBW
  • vol approx 40-45 in adults
  • alcohol readily crosses membranes although penetrance into body fat is poor
  • explains why increased peak BAC seen in females then males
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12
Q

Pharmokinetics of alcohol - Metabolism

A
  • in gut wall (minor) and livere (major) protects the body against EtOH
  • mainly 95% of alcohol dehydrogenase and alldehyde dehydrogenase
  • inherited polymorphisms in ADH and ALDH genes influnce rate at which EtOH and acetaldehyde are metabolised
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13
Q

Pharmokinetics of alcohol - excretion

A
  • a tiny amount og EtOH is excreted directly by kidneys (in urine)
  • EtOh s excretd in exhaled breath
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14
Q

Pharmacodynamics of Alcohol: Effects on the Brain

A
  • depress functioning of the brain to produce calming, relaxation, disinhibtion, drowsiness or coma/death
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15
Q

Mechanism of Etoh on brain functions

A
  • low potency
  • EtOH mainly produce nonspecfiic effects on neuronal membrane fluidity
  • EtOH receptors are often ion channels that regulate ion flows into nerve cells
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16
Q

What are the two key receptors on alcohol and brain function

A

1- glutamate receptors: Neuronal inhibition

2- GABA receptors: neuronal inhibition

17
Q

glutamate receptors - normal role

A
  • major excitatory amino acid involed in communication between brain cells involved in learning, memory, and other roles. It normally switches target neurons
18
Q

GABA receptors

A
  • the inhibitory neurotransmitter regulates chloride entry into neurons, causing sedation and decreased anxiety. It normally switches off target neurons.
19
Q

glutamate receptors - role in CNS effect of alcohol

A
  • Ethanol binds to NMDA-type glutamate receptors, decreasing their responsiveness to released glutamate.
20
Q

GABA receptors- role in CNS effect of alcohol

A
  • Ethanol binds to the
    same protein subunit
    on the GABA receptor as volatile anaesthetics, causing
    strong inhibition.
21
Q

The disinhibition hypothesis

A
  • EtOH produces graded, reversible depression of behaviour and cognition
  • low doeses main outcome is suppression of inhibitory neuronal networks that produce social restraint
22
Q

Alchohol use disorder

A
  • EtOH tolerance due to faster liver metabolsm
  • failed relationships and employment loss
  • psychiatric symptoms and neurotoxicity
  • severe cognitive distruption
  • need for organ transplants and long term care

drugs that change the world (21 decks)

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