question: what determines the impact alcohol has on CNS?
- time period of drinking
- mixed w/ food or drugs
- how often you normally drink (tolerance)
- where (environment where alc. is consumed)
- size, weigh, genetic makeup of person
question: where does majority of alc. get absorbed? broken down?
- absorbed = small intestine
⤷ enters blood stream + goes to liver - break down = liver
⤷ happens w/ enzymes
explain: genetic diff. in absorption of alc.
- alcohol dehydrogenase (ADH)
⤷ responsible for initial metabolism of alc. in body - diff. forms of ADH change lvls of activity
- ADH1B = higher in XY than XX
explain: ADH1B
- form of alcohol dehydrogenase
- higher in XY than XX
⤷ results in higher metabolism and lower BAC after drinking same amount
explain: agonist vs antagonist
- agonist = agonist binds to recep. + activates it
- antagonist = binds to recep. + blocks/reduces ability of other mol. from binding
explain: up vs down regulation
- UP = increase in # of recep/ or increase sensitivity of recep. to ligand
- DOWN = vv
explain: hyperpol. vs depol.
- hyperpol = increase electric potential
⤷ less likely for AP - depol = decrease in electric potential
⤷ more likely for AP
explain: glutamate (acute vs chronic effects?, beha. effects?)
ACUTE
- recep. antagonism + reduced glutamate release
⤷ memory loss
CHRONIC
- upregulate recep. + rebound increase in glutamate release
⤷ rebound hyperexcitability of abstinence syndrome
- hyperexcitability + Ca+ influx
⤷ brain damage
**glutamate = excitatory NT
define: tolerance + withdrawal
- tolerance = adaption of a substance over time ⤷ needs more of a substance to exp. same lvl of intoxication they once had w/ lower doses
- withdrawal = set of symptoms when a person stops/reduces use of a substance they are dependent on
explain: GABA (acute vs chronic effects?, beha. effects?)
ACUTE
- increase in GABA induced Cl= influx
⤷ sedative effects
CHRONIC
- decrease in GABA function w/out change in recep. #
⤷ tolerance + signs of excitability during w/drawal
**GABA = inhibitory NT
explain: dopamine (acute vs chronic?, beha. effects?)
ACUTE
- increase in dopamine transmission in mesolimbic tract
⤷ reinforcement
CHRONIC
- reduced firing rate, release, and metabolism
⤷ -ive affect as sign of w/drawal
explain: mesolimbic tract
- involved in regulation of reward, motivation, and emotional processing
explain: opioids (acute vs chronic?, beha. effects?)
ACUTE
- increase in endogenouse opioids synth and release
⤷ reinforcement
CHRONIC
- decrease in endorphins
⤷ dysphoria
explain: mechanism of. alc breakdow
alcohol -> acetaldehyde
⤷ via alcohol dehydrogenase
acetaldehyde -> acetic A
⤷ via acetaldehyde dehydrogenase
acetic A -> CO2 + H2O + energy
⤷ dia oxidation
name: types of enz. that can break down alc
- mainly liver enz.
- ex. cytoghrom P450 famioly
⤷ converts alc -> acetaldehyde
question: what happens in flushing?
- acetaldehyde accumulation -> flushing of the skin
⤷ also nausea, head ache, increase HR - happens when increase lvls of aldehyde dehydrogenase is less active
explain: alcohol induced vomiting
- protective mech. of body against toxins
- found that area postrema has been implicated as chemoreceptor trigger zone for vomiting
⤷ on dorsal surface of medulla oblongata of brainstem)
explain: brain damage due to chronic alcohol consumption
- MRI found tissue shrinkage
- DTI found abnormalities in white matter
⤷ loss of myelin, enlargement of microtubules - diff. sized ventricles shows tissue loss/death
name + explain: layers of meninges
OUTER
- dura mater = tough double layer
- arachnoid membrane = very thing
- pia mater - moderately tough tissue
**subarachnoid space between arachnoid and pia mater
question: what is the purpose of CSF?
- cushion from shock + sudden psi changes
- in ventricles, brain, spinal column
⤷ subarachnoid space
question: what is cerebral aqueduct?
- connects vents 1-3 w/ vent 4
explain: cerebral security
- brain and spinal cord are protected
- by CSF
- by blood vessels
⤷ packed densely (blocks large molecules from entering + more bbb) - spinal cord
⤷ interlocking bones
