Exam 3 Flashcards
what are the two sources of cannabis?
cannabis indica and cannabis sativa
what’re the cannabinoids?
THC and CBD. newly discovered are THCP and CBDP
bodily effects of cannabis
bloodshot eyes, sensation of dry mouth, hunger, increased heart rate (which can be dangerous for those with cardiovascular problems) and drowsiness
mood and behavioral effects of cannnabis?
subjective pleasant, feelings of anxiety, increased sensory sensitivity reported, impairs driving, creativity (?)
medical usefulness of cannabis?
glaucoma-buildup pressure of the eyeball (releases pressure), stops nausea and vomitting, pain relief, appetite stimulation, reduces muscle spasms
harmful effects of cannabis
acute psychotic reaction is possible, while under the influence symptoms of psychotic episodes, smoking-related health problems, driving while impaired, brain differences in hippocampus and nucleus accumbens, cannabinoid hypermedia syndrome
is cannabis lethal?
no known cases of overdose deaths of THC/overdose
mechanism of action for Cannabis?
binds to heteroreceptors CB1 and CB2, mimicking the endogenous receptors, decreeing the release of the NT that would’ve been released
where is CB1 located?
nervous system (like the brain)
where is CB2 located?
immune system
endogenous cannabinoids
Anandamide and 2-AG. they are neuromodulators that are released by the postsynaptic cell to suppress the NT from releasing the NT in the presynaptic cell.
DSI and DSE
depolarization-induced suppression of inhibition and depolarization induced suppression of excitation. basically suppressing glutamate (DSE) or GABA (DSI)
is cannabis a drug of abuse?
yep
tolerance for cannabis
down regulation of cannabinoid receptors in animals, and tolerance for some effects in humans. also, potential sensitization
what is the classification of opioids?
drugs with similar properties to opium or morphine
which opioids are analgesics
opium, morphine, codeine, oxycontin, fentanyl, and methadone
which opioids are non analgesics/do other things
opium also stops constipating, codeine is also a antitussive (cough suppressant), heroin has no medical use, and methadone treats addiction
bodily effects of opioids
analgesia, cough inhibition, small pupils, consipation, respiratory center is depressed
mood and behavioral effects of opioids
positive feelings and euphoria (but in a calm sense of well being way)
harmful effects of opioids
convulsions (with repeated use), spread of hepatitis or HIV when needles are shared, decreased fertility in males and females
is opioids lethal?
yup!! depression of respiratory center (especially when taken with alcohol and anxiolytics and sedative hypnotics)
mechanism of action for opioids
opioid receptors in presynaptic heteroreceptors and postsynaptic metabotropic receptors. inhibits release of NT. mimics endogenous opioids. binds to receptor, decreasing NT (like GABA) release, leading to increase of DA release
where does opioids act and how?
brain, spinal cord, and digestive system. rewards in the VTA, nucleus accumbens and cortex. pain in PAG (brainstem) and spinal cord
is opioids a drug of abuse?
yup!
tolerance for opioids?
to most effects, tolerance develops so doses increase. to constriction of pupils and consipation, it doesn’t increase.
is there cross tolerance for opioids?
yes!
treating opioid addiction types?
maintenance therapy and overdose rescue kits
maintenance therapy
methadone binds to receptors and remains bound. taking heroin would not affect the individual. its cheap, safe, reliable, oral, once a day, etc.
overdose rescue kits
naloxone blocks opioid receptor. can reverse and overdose.
what does antipsychotics treat?
bipolar disorders, depression sometimes, but mainly schizophrenia
symptoms of schizophrenia?
hallucinations (auditory, visual, etc), paranoia (type of delusions. though process), restlessness, agitation
positive symptoms of schizophrenia
symptoms in excess/distortion of what is “normal”- hallucinations and delusions
negative symptoms of schizophrenia
less of what a “normal” person experiences- flat affect and emotionless
typical antipsychotic medications
first medications. chlorpromazine (thorazine) and haloperidol (haldol)
atypical antipsychotic medications
clozapine (clozaril) and risperidone (risparedol)
how effective are antipsychotics?
quite effective at treating positive symptoms not not for negative ones. typical medication can make negative symptoms worse
side effects pf antipsychotics
extrapyramidal symptoms (slow movements and tremors like Parkinsons. linked more to typical meds) and weight gain, increased risk of cardiovascular diseases
harmful effects of antipsychotics
low risk of death/no real concern. high therapeutic index. is tardive dyskensia- excess movement of head and mouth)
mechanism of action of typical antipsychotics
Block D2 dopamine receptors (metabotropic)
mechanism of action of atypical antipsychotics
block D3 and D4 dopamine receptors along with blocking 5-HT2a receptors. all metabotropic. blocking serotonin increases dopamine in movement parts of brain.
dopamine theory of schizophrenia
symptoms of schizophrenia are a result of excess dopamine. psychomotor stimulants enhance dopamine, producing symptoms that look like schizophrenia. blocking dopamine treats symptoms. doesn’t fully address schizophrenia as some drugs that produce psychosis affect glutamate, not dopamine
are antipsychotics a drug of abuse?
no. not really pleasant and doesn’t have recreational value. the drugs aren’t abused or anything because they block dopamine and most drugs that are abused increase dopamine. they are used to treat medical diagnoses
does dependence develop for antipsychotics?
not really. higher doses aren’t necessary, but they can change, but not steady incremental doses. withdrawal symptoms are mild if any.
does addiction develop for antipsychotics?
nope.
what does antidepressants treat
depression typically.
how does efficacy and safety change with the generations of antidepressants?
efficacy doesn’t change. safety and tolerability improves.
first generation antidepressants
Monoamine oxidase inhibitors and tricyclic antidepressants
examples of MAOIs
isocarboxazid (marplan) and moclobemide (aurorix)
examples of tricyclic antidepressants
amitriptyline (elavil) and nortriptyline (pamelor)
second generation antidepressants
Selective serotonin reuptake inhibitors (SSRIs)
examples of SSRIs
fluoxetine (prozac) and citalopram (celexa)
examples of third generation antidepresssants
venlafaxine (Effexor) and bupropion (Wellbutrin)
what is the efficacy of antidepressants
60-70% of some symptoms and 28-50% of all symptom relief, it takes several weeks to show clinical benefits
side effects of antidepressants
weight gain, dry mouth, dizziness, constipation, insomnia, and sexual dysfunction
harmful effects of MAOIs
increased blood pressure if tyramine-rich foods are eaten (can be life threatening)
harmful effects of TCAs
can lower seizure threshold (risky at high doses) and cardiovascular problems
harmful effects of SSRIs
“serotonin syndrome” including disorientation, agitation, fever, diarrhea, impaired coordination (only if taken more than prescribed or with another SSRI)
harmful effects of third genneration antidepressants
no specific ones as it’s not as a cohesive group as the others
lethal effects of antidepressants
most risk is low, but TCAs have the highest risk as they lower seizure thresholds and have cardiovascular risk
other medical uses of antidepressannts
anxiety disorders, OCD (certain Serotonin ones), PTSD (only certain types), depression in bipolar disorder (debated though), ADHD (Wellbutrin)
mechanism of action for MAOIs
Monoamine oxidase breaks down monoamine NTs in cytoplasm, so MAOIs inhibit the enzyme leading to more NT available
mechanism of action TCA
block reuptake of NNE and 5-HT, block NT transporter so NT is more available
mechanism of action for 2 Gen SSRI
block reuptake of 5-HT
mechanism of action for 3rd gen antidepressants
variable mechanism of action but typically blocks reuptake
are antidepressants drugs of abuse?
nope.
dependence of antidepressants
tolerance is unclear. there are bad withdrawal symptoms and they SHOULD NOT be stopped abruptly.
symptomss of withdrawal of antidepressants
restlessness, anxiety, chills, delusion, discontinuation syndrome
what do hallucinogens do?
causes hallucinations- visual imagery, altered perception of one’s body, increased emotionality, feeling of well-being
what do psychedelics do?
gain personal insight or empathy
how are club drugs classified?
recreational
examples of hallucinogens, psychedelics, and club drugss
LSD, psilocybin, ecstacy, mescaline, peyote, PCP, ketamine, salvia, dextromethorphan, GHB, mephedrone
LSD
resembles serotonin structurally. sythetic. lysergic acid diethyl amide
effects of LSD
hallucinations or visual imagery, provides insight, appreciation of art and music
harmful effects of LSD
acute psychosis, “psychedelic crisis”-unpleasant experience, flashbacks (hallucinogen persisting perception disorders- rare. hallucinations after taking drug)
is LSD lethal?
pretty safe for lethality and overdose. you will get worse effects ,but you won’t die
mechanism of action for LSD
stimulates some 5-HT receptors, but blocks others. more common in peripheral nervous system
is LSD a drug of abuse?
yup
tolerance of LSD
develops quickly, but dissipates quickly
psilocybin
resembles serotonin structurally. derived from mushrrooms
effects of psilocybin
spiritual experiences, pleasurable changes in mood or perception
harmful effects of psilocybin
dysphoria, anxiety ,and headaches
mechanism of action of psilocybin
stimulates 5-HT2a receptors
MDMA
ecstasy and Molly. methylendioxymethamphetamine. resembles methamphetamine structurally. stimulant
effects of MDMA
euphoria, increased sociability, endurance, sharpened sensory perception
harmful effects of MDMA
hyponatraemia (imbalance of salts in blood. lack thereof) and hyperthermia (too hot).
longterm effects of MDMA
sleep disorders, depression, anxiety, impulsiveness, hostility, and memory impairment
is MDMA a drug of abuse?
yup. acute tolerance develops rapidly though.
Ketamine usage
dissociative anesthetic (patients are “awake but appear disconnected from their environment). you’re not gonna be unconscious, but you won’t remember or feel uncomfortable. used for children!
effects of ketamine
anesthesia, amnesia for events that occurred while under the influence of the drug. high therapeutic index
mechanism of action of ketamine
antagonist to the NDMA glutamate receptor
drugs that impact NT transporter (6-7)
SSRIs (5-HT transporter), 3rd Gen Antidepressants (variable), cocaine (DA transporter), (meth)amphetamines (DA), TCAs (NE and 5-HT), MDMA (5-HT)
drugs that impact vesicular transporter (1)
(meth)amphetamines
drugs that impact heteroreceptor (2)
cannabis (CB1 and CB2) and opioids (opioid receptors)
drugs that impact presynaptic inotropic receptor (1)
nicotine (nicotinic receptor)
drugs that impact postsynaptic ionotropic receptors (4)
alcohol (GABAa and NMDA glutamate), anxiolytics and sedative hypnotics (GABAa), nicotine (nicACH receptor)
drugs that impact postsynaptic ionotropic receptors (4)
alcohol (GABAa and NMDA glutamate), anxiolytics and sedative hypnotics (GABAa), nicotine (nicACH receptor) and ketamine (NDMA glutamate)
drugs that impact postsynaptic metabotropic receptors (6)
methylxanthines (Adenosine A1 and A2a receptors), opioids (opioid receptor), typical antipsychotic (D2), atypical antipsychotic (D3, D4, 5-HT2a), LSD (5-HT), and psilocybin (5-HT2a)
