final exam Flashcards
what is the most commonly abused legal substance?
alcohol
what is the primary cause of the problem of alcohol?
CNS effect
alcohol causes an increase in —– fluidity
membrane
alcohol’s effect on GABA receptors
enhancement of inhibitory GABA at GABA a receptors (like benzodiazepines)
alcohol’s effect on glutamate
reduction of effect of excitatory glutamate on ion channels–inhibits NMDA receptors to glutamate
effect of alcohol on endogenous opiod peptides
causes release of endogenous opiod peptides and changes (increase) levels of dopamine and serotonin
what inhibits the desire for alcohol consumption?
opioid and dopamine receptor antagonists (naltrexone)
what does chronic use of alcohol do?
alters sensitivity/structure of NMDA receptor, leading to excitatory toxic effect upon acute withdrawal
NMDA receptor antagonists
reduce incidence of seizures occuring during ethanol withdrawal and ethanol consumption
major metabolite of alcohol
acetaldehyde
effect of alchol on CNS
- early excitation due to disinhibition of inhibitory pathways (low dose)
- high dose–> depressant–sedative/hypnotic effects
- soporific effect (increases sleep time)
- behavioral changes
- disruption of motor activity
- affects sexual function
effect of alcohol on cardiovascular system
- increases catecholamines in blood
- increased activity of vascular smooth muscle at low concentration but reduced activity at high concentration
- increase in coronary blood flow
- decrease in myocardial activity
- heat loss
- acetaldehyde formed –> increase in catecholamines, tachycardia, increase CO, increase BP
acute intoxication’s effect on liver
reversible decrease in microsomal metabolic enzyme activity
chronic intoxication
induction of liver enzyme activity (P450)
cirrhosis
overall decline in liver function
nutrition depletion bc of alc
- inhibit vit A/D and decrease in pyridozine (b6)
- depletion of Zn and selenium
- marginal supply of calorie need without providing other nutritional rqments
alc’s effect on kidney
-inhibits ADH causing increased urine production and thirst
alc’s effect on sexual function
provokes desire but not performance
alc’s effect on HDL/LDL
increases it
alc’s effect on saliva and gastric
small doses increase salivation but higher reduce
alcohol retards absorption of ?
glucose, aa, thiamine, B12
alc causes – gland activation
adrenal gland
alcohol has rapid absorption where?
in stomach and intestine
> 20% alc ______ by inducing both gastric mucosal irritation and pylospasm
retards absorption
intoxication can also be achieved by?
inhalation (also exhaled)
metabolism of alc
> 95% of ingested alc is metabolized
- by non-microsomal and microsomal pathways, latter applying to chronic
- leads to production of actetaldehyde, which has multiple toxic symptoms
ethanol elimination follows —- order kinetics
zero
disulfiram
inhibits aldehyde dehydrogenase causing elevation in blood acetaldehyde levels–> hangover (flushing, headache, N/V, blurred vision, mental confusion)
how is alcohol related to heroin?
alc lowers the dose of heroin needed to overdose
short term ethanol use may cause exaggerated response to what?
oral anticoagulants and oral hypoglycemic agents
which drugs does ethanol influence absorption of?
benzo and diazepam
aspirin + nsaids +alc
cause greater gastric irritation
what can cause enhanced actaminophen toxicity?
in liver cirrhosis
reduction in drug met and depletion of glutathione
high blood alc level inhibits metabolism of?
benzo
other drugs like disulfiam
metrondazole, sulfonylurea
abrupt withdrawal of alc
anorexia, nausea, GI upset, tremors, sweating
neuromuscular hyperexcitability
gross tremors and grand mal convulsions
autonomic hyperactivity
hyperthermia and circulatory collapse
how is abstinence sydrome treated
long acting BDZ (diazepam)
-alternatives are clonidine and carbamazepine
what is used in avoidance therapy?
disulfiram
acetaldehyde
unconsciousness, hypotensive shock, sudden MI
disulfram inhibits dopamine beta hydroxyase, preserving what?
dopamine (exaggerates schiz or depression)
naltrexone
long acting
opiod antagonist
better tolerated than disulfiram
acamprosate
alcohol dependence tment programs
-working a poorly understood mech
methanol
used as industrial solvent and denaturing agent for ethanol
metabolism of methanol
same enzymes as ethanol
zero order kinetic but products different
toxicity of methanol
headache, nausea, visual disturbances, ab pain, resp disturbances –> coma/death
poisoning of methanol
due to metabolites, formaldehyde and formic acid, which cause blindness
cause of death of methanol
resp arrest
treatment of methanol od
hemodialysis, peritoneal dialysis, bicarb infusion, ethanol admin/subst
amphetamines are
cns stimulants
what are indicated for ADHD
amphetamine, methylphenidate, methamphetamine, dextroamphetamine
what are used for narcolepsy?
amphetamine, methylphenidate, dextroamphetamine
appetite suppressants (anorectics)
methamphetamine
treat obesity by activating satiety center in hypothalamus
major effect of amphetamines
CNS stimulation –> euphoria
-act at levels of cortex, subcortical areas, and spinal cord
peripheral effects of amphetamines
increase sympathetic/adrenergic effects
mech of action of amphetamines
- highly lipophilic
- rapid
- release monoamine NT from presynaptic storage sutes (indirect-acting agents)
- weak MAO inhibitors, uptake of NT’s and drugs
- euphoria (increase in dopamine)
- anxiety due to increase in NE
methamphetamine
- phenylalklyamine (parent compound)
- in cold meds
- “speed”
why is methamphetamine preferred by abusers?
- less adverse effects due to less NT
- free base –> easily smoked
ecstacy
- commonly abused (sched 1)
- molly (designer drug)
- serious effects –CV disorders and neurotoxicity
how do abusers take amph?
iv or smoking
chronic abuse of amph produces what?
tolerance
acute overdose of amph
CV and CNS stim
increase symp stim
chronic abuse of amph
anxiety, bad mood, fatigue
paranoid
toxicity of amph tx
acidification of urine with NH4Cl which increases excretion of drugs
dental issues of amph similar to?
cocaine
high dose of amph
nervousness, can’t rest
convulsion with local anesthetics
CV disorders
hypertension, vasoconstriction, hemorrhage
meth mouth
caries and heavy plaque with xerostomia
xanthine derivatives
caffeine, theophyline, theobromine
—– is the only xanthine used primarily for its CNS effect
caffeine
caffiene’s effect on CNS
- greater stim of cortex, but least on spinal cord
- clearer thougts
- excessive–> spinal cord–> convulsions
what stimulates the resp center in medulla?
caffiene
net result of caffeine on CV system?
increase in BP
increase cardiac activity
mech of action of caffiene
- inhibition of phosphodiasterase–> increase camp–> cardiac stim and SM relax
- adenosine antagonism–> bronchocnstriction, histamine release, CNS depression, methylxantines (caffiene) block effects of adenosine
- stim of caetcholaime release
- increase calcium mobilization
doxapram
not xantine or amph
- stim CNS –> greater efect on medullary resp centers (effect mediated via peripheral carotid chemorec)
- tonic clonic convulsions in large doses
- treats resp depression
