Lecture 1 - Definitions etc Flashcards
what is an alcohol?
organic liquid with a hydroxyl group on the end
name 4 alcohols
which type is commonly in drinks?
methanol
ethanol - in drinks
propanol
butanol
how does methanol poisoning come about and what does it cause?
in anti-freeze, dodgy home brewing etc
metabolised to formaldehyde then formic acid causing blindness and renal failure
how is methanol poisoning treated? how does this work?
alcohol +/- dialysis
ethanol and methanol both metabolised by alcohol dehydrogenase so ethanol causes competitive inhibtion of the enzyme and formic acid cant be formed
weekly unit limit?
14
spaced over few days
symptoms of alcohol withdrawal?
“seeing spiders”
suddenly unwell during hospital stay or coming round from anaesthetic
how is alcohol absorbed and what can affect the rate?
limited amount in stomach, most absorbed in small bowel
eating slows gastric emptying so slower absorption
antihistamines and metoclopramide increase emptying so faster absorption
why is drinking on an empty stomach bad?
faster gastric emptying so faster absorption without being metabolised in the stomach first
do men handle alcohol better than women?
generally yes
men have higher lean body mass % than women of same weight so more fluid to dilute the alcohol
women often have lower alcohol dehydrogenase levels
which is absorbed quicker, spirits or aerated drinks (prosecco)?
aerated
spirits irritate gastric mucosa so slow emptying causing delayed effect (can hit you suddenly)
do some ethnic groups handle alcohol better?
yes
some have little/no/ineffective alcohol dehydrogenase (Asians, aborigines, eskimos)
causes flushing, nausea, headaches etc
how is alcohol metabolised?
alcohol > acetaldehyde (causes hangover)(alcohol dehydrogenase)
acetaldehyde > acetate (aldehyde dehydrogenase)
acetate > CO2 and H2O
90% in liver, some in brain/pancreas
at what rate is alcohol removed from blood?
15mg/100ml/hr (1 unit per hr)
when does alcohol conc peak?
60 mins after consumption
how is alcohol tolerance achieved?
alcohol dehydrogenase upregulated via activation of alternative pathways in heavy drinking, e.g:
- MEOS
- catalase
- induction of CP450
what are some consequences of alternative pathways?
inhibition of krebs cycle = anaerobic pathway = lactic acid (sore legs)
inhibits gluconeogenesis/glucogenolysis = use fats/proteins as substrates so get the munchies
impairs fatty acid oxidation = excess keogenesis and lipid synthesis (makes you fat)
how does alcoholic ketoacidosis occur?
consequence of other pathways so you make ketones
what is alcoholic ketoacidosis associated with?
malnourished chronic alcoholics
what is the difference between alcoholic and diabetic ketoacidosis?
alcoholic = low/normal glucose, high ketones diabetic = high glucose, high ketones
how does alcohol supress the CNS?
increases GABBA levels which inhibits neurotransmitters
where does alcohol effect and what does this affect?
cortex - disinhibition
limbic system - memory, confusion etc
cerebellum - coordination, balance, speech
reticular formation - consciousness (less stimulated = sleepy)
lower brain stem (breathing, BP, gag reflex)
what do different levels of alcohol do?
<100 = cortex
100-200 = limbic system, cerebellum
>200 (stupor) = reticular formation, lower brain stem
why does alcohol make you pee more?
drink more volume
directly inhibits ADH so reduced water reabsorption
what causes a heavy heartbeat after drinking?
alcohol is a negative inotrope (reduces force of contraction > SV decreases > HR increases)
