alcohol Flashcards
calculating units and safe levels for week, and units for binge drinking
%alcohol*volume (ml) to find absolute alcohol- 1 unit= 10 ml alcohol
men and women< 14 units/week= low risk
binge drinking> 8 units at one time
drinking on full stomach vs empty stomach
full- less gastric emptying as stomach breaking down food, and only a bit of alcohol is absorbed directly from stomach, so little gets to intestine
empty- fast gastric emptying= faster speed of onset as alcohol absorbed much better in intestine than stomach
thus speed of onset depends on gastric emptying
metabolism of alcohol
90% broken down, 10% excreted
most of breaking down done by liver- alcohol broken down mostly by alcohol dehydrogenase, some by mixed function oxidase into ACETALALDEHYDE
some broken down by alcohol dehydrogenase in STOMACH
acetaladehyde toxic, so broken down into ACETIC ACID by aldehyde dehydrogenase
why do we become tolerant to alcohol
mixed function oxidase upregulated, so liver more efficient at breaking it down
what happens when you drink too fast
alcohol spills into systemic circulation, as enzymes are saturated
why women more affected by alcohol than men
women have less alcohol dehydrogenase in stomach
also less BODY water than men, so more concentrated
why is disulfiram effective for alcoholics
inhibits enzyme in 2nd step= more acetalaldehyde
this is toxic, so makes you feel worse, so if alcoholics have more of this, less likely to drin
disulfiram genetic polymorphism
common genetic thing in asians, which have less of aldehyde dehydrogenase= more acetaladehyde= Asian flush+ more nauseous
important feature of alcohol
LOW potency as simple molecule, so doesn’t bind to a particular target very well compared to other drugs- thus need a lot more of it t have a similar effect
thus doesn’t have a specific pharmalogical target, and had low affinity/efficacy
overall effect of alcohol and what dependent on
DEPRESSANT (slows thing down)
does however depend on degree of CNS excitability, which depends on personality, but also environment ie non social or social
if your CNS not very excitable eg due to non-social setting, has more of depressant effect
generally low dose excites CNS ie more confident/excited, high dose leads to alcohols main depressant effect
targets of alcohol+ mechanism
GABA receptors- alcohol directly acts on receptor, as well as releasing more allopregnanolone from presynaptic membrane= more GABA
inhibits NMDA receptors (less glutamate) and Ca2+ channels
alcohol and euphoria- mechanism
like cannabis, GABA is surpressed, so less inhibition of reward pathway
alcohol acts on opioid receptor like opiates, which supresses GABA
effects of alcohol in the brain
corpus callosum- needed for logic/rules
hypothalamus- eating/temp
RAS- consciousness
hippocampus- memory
cerebellum- movement
all impaired as it’s depressant
mechanism of cutaneous vasodilation/Asian flush
acetalaldehyde causes less Ca2+ entry and more prostaglandins= less contraction of precapillary sphincters
CVS effects of alcohol
depresses baroreceptor activity- baroreceptor switch on when stretched to inhibit SNS/ increase PNS, so leads to TACHYCARDIA