Exam 2 Flashcards
How is alcohol produced?
fermentation (sugar broken down into usable forms of alcohol) of different things like grapes, grain, etc.
which disease is affected by alcohol?
Korsakoff’s disease
can you die from alcohol? how?
yes. respiratory failure
how does alcohol get to the blood?
drinken, then stomach, then small intestine, then large intestine. it can go to the blood from the stomach.
how is blood alcohol level measured?
amount of alcohol (g) per 100 milliliters (ml) of blood. 80 mg/100ml= 0.08
how is alcohol metabolized?
Ethanol is broken down by alcohol dehydrogenase into acetaldehyde is broken down by aldehyde dehydrogenase into acetate, which is then further broken down into energy, CO2, and water
What are the mechanisms of action for alcohol?
GABA (GABAa) and Glutamate (NMDA)
How does alcohol affect GABA?
it enhances the ability of GABAa to open Cl- channel. it is a positive allosteric modulator. affects the cerebellum
Positive allosteric modulator
positive: drug enhances what the NT does. allosteric: different positions
how does alcohol affect glutamate
decreases function of NMDA functioning- blocks the channel, decreasing ability for ions to flow through.affects hippocampus since NMDA is packed there
with chronic alcohol use, how is Glutamate affected?
NMDA receptors are upregulated- body makes more of them. pharmacodynamic
does alcohol affect dopamine?
yes. indirectly though. alcohol affects GABA, enhancing inhibition of the cell that inhibits the VTA, meaning more dopamine is released from the VTA
which genes affect dependence of alcohol?
alcohol dehydrogenase and aldehyde dehydrogenase
alcohol dehydrogenase
first enzyme in the pathway of alcohol. some people have a gene that causes rapid conversion of ethanol into acetaldehyde, which sucks.
aldehyde dehydrogenase
second enzyme in alcohol pathway. makes aldehyde dehydrogenase left effective, so acetaldehyde stays in the system longer, which also sucks.
difference between Anxiolytics and sedative-hypnotics?
anxiolytics are longer lasting while fast acting ones are sedative hypnotics. anxiolytics are used to make you less anxious while sedative-hypnotics are used to make you sleepy
barbiturates
-barb in name. really effective, but also risky (replaced by benzodiazepines)
anxiety meds
alprozolam (Xanax) and diazepam (Valium)
sleep meds
trozalam (Halcion) and temazepam (restoring)
Z drugs
sleep meds, pretty similar to benzodiazepines, but don’t interfere with sleep architecture, length of time, and progress
Z drug meds
zolpidem (ambiem) and eszopiclone (Lunesta)
can anxiolytics/sedative-hypnotics kill you?
yeah. barbiturates can have a high potential for overdose while benzodiazepines are rarely fatal by themselves, but can become dangerous combing them with a depressant
how does barbiturates kill you?
respiratory failure
what is the mechanism of action for anxiolytics/sedative-hypnotics?
GABAa receptors. they are positive allosteric modulators
where do different anxiolytics/sedative-hypnotics bind?
barbiturates bind at the same place as alcohol and an open the channel by themselves. benzos and Z drugs bind at different places
does anxiolytics/sedative-hypnotics have an affect on dopamine?
yes, indirectly. again, it further inhibits GABA cells that inhibit cells of the VTA, causing more dopamine to be released.
which synapses do psychomotor stimulants stimulate?
DA, NE, E, and 5-HT
catecholamines
DA, NE, and E
indoleamine
5-HT
difference between cocaine and crack cocaine?
crack can be smoked, as it has one less hydrogen and chlorine than cocaine.
difference between amphetamine and methylamphetamines?
methylamphetamines have methyl added to it, allowing it to cross into the blood-brain barrier more easier, making it more risky and more likely to lead to dependency
which ADHD meds are similar to the amphetamines?
adderall and Vyvanse
which ADHD meds are similar to cocaine?
methylphenidate (ritalin) and dexmethylphenidate (Focalin)
what cell problem is related to chronic consumption of psychomotor stimulants?
neurotoxicity (death of neurons, particularly of DA producing neurons)
is psychomotor stimulants fatal? how?
yup.through heart failure
punding
stereotyped behavior in humans
what is monoamine psychosis similar to?
schizophrenia
what are the mechanisms of action related to psychomotor stimulants?
neurotransmitter transporters (reuptake)- Dopamine Transporters (DATs) and Vascular Monoamine Transporter
what do dopamine transporters do?
reuptake of dopamine (mainly)
what do vascular monoamine transporters do?
sit on membrane of vesicles, taking the NT that came back in through reuptake and get them packaged into vesicles to maybe be released again later.
how SHOULD dopamine transporters work??
dopamine is returned to the presynaptic cell via NT transporter, gets packed into a vesicle and dopamine can’t stimulate receptors
how does cocaine affect DATs?
cocaine BLOCKS the transporter, causing more dopamine to remain in the synapse for longer and allowing cell to be stimulated by dopamine longer than normal
how do amphetamines affect DATs?
amphetamines are taken into the presynaptic cell by the transporter, enter the vesicles and pushing out dopamine via the vesicular transporter, causing the vesicles to release stored dopamine into the cytoplasm, causing the transporter to work in reverse, pushing out dopamine out of the cell
do psychomotor stimulants affect dopamine?
yes. directly. it impacts the VTA/reinforcement system directly.
what are the 3 methylxanthines?
caffeine, theophylline, and theobromine
sources of methylxanthines and what do they contain?
coffee- caffeine, tea- caffeine and theophylline, and cocoa-caffeine, theophylline, and theobromine
what is the most widely spread behaviorally active drug in the world??
caffeine
why is caffeine in some medications?
it can relieve headaches as it constricts blood vessels in the brain
is methylxanthines lethal?
technically yes, but it takes extremely high doses to lead to convulsions and death. it can be more lethal if high doses are had with someone with heart conditions.
what is the mechanism of action for methylxanthines?
Adenosine- A1 and A2a. they are antagonists for it, so methylxanthines block the receptors. metabotropic
adenosine
Neuromodulator- not a full NT but can still affect functioning of nervous system. associated with alert fulness and wakefulness. when its high, it is associated with sleepiness and fatigue
is nicotine lethal?
yes. you can die at high doses
Mainstream smoke
what a smoker breathes back out after inhaling
environmental tobacco smoke
effects of tobacco on other people, “second hand smoke”
sidestream smoke
comes from a burning cigarette between puffs. this is the more harmful one
thirdhand smoke
toxins that remain in an environment even when no one is actively smoking at the moment
risks of second hand smoke in adults
breast cancer and other cancerrs
risks of second hand smoke in children
leukemia, lymphoma, and brain tumorsr
risks of second hand smoke in babies
sudden infant death syndrome (SIDS)
mechanism of action in nicotine
acetylcholine- nicotinic. nicotine mimics acetylcholine anc binds to the receptor to open it in the absence of acetylcholine. can be found on both pre and post ionic receptors.
desensitized nicACh receptors
ACh is present, but the channel doesn’t open
nicACH presynaptic cell
enhances release of NT
nicACh postsynaptic receptor
mimics ACh and stimulates cell
nicotine and reward pathway
cells in the VTA can have ACh receptors, increasing dopamine release. very addictive.
genetic contributions of nicotine addiction
CYP2A6 breaks down nicotine into nicotine-1’-N-oxide. when it doesn’t work well, there is decreased risk of addiction. also, there are genes encoding different subunits of the receptor which are implicated in addiction
Nicotine replacement therapy
safer forms of nicotine (like patches, gums, and lozenges) are used as they’re safer than smoking. can decrease dose and may not have withdrawals.
Varenicline (Chantrix)
partially stimulates the nicotinic ACh receptor, making nicotine useless and so no need to smoke.
