PMHNP Psychopharmacology – Exam #3 Study Guide – Cannabis,
Alcohol, Anxiolytics, Depression & Schizophrenia Review
This comprehensive Q&A-style document supports preparation for the third
PMHNP Psychopharmacology exam. It covers cannabis pharmacology and
neurobiology, alcohol metabolism and effects, barbiturates and benzodiazepines,
GABAergic systems, anxiety and depression treatment, and antipsychotic drug
mechanisms. The guide integrates detailed mechanistic explanations, side effects,
historical context, and clinical applications relevant to psychiatric and substance-
related disorders.
1. What are the three main species of cannabis? Which is the most common?
What are the differnces in effect for each species?: Sativa- most common.
active properties. more stimulative
Indica- more sedative, body relaxation, has more cannabinol than THC.
Buderalis- combination, hybrid effects
2. How is cannabis classified?: as a depressant, but it also has
hallucinogenic/psychedelic effects as well
3. What are the 3 main forms of cannabis? From which part of the plant is
each derived?: marijuana- various parts of the male and female flower
sensimilla- potent form from the female flower. engineered to be seedless to
prevent male pollination. high THC content.
,hashish- sticky, thich, dark resin from the flower of the female plant (derived from
trichomes)
4. Where in the cannabis plant are the highest levels of THC found?: the flower,
higher in the female
5. How is cannabis administered? Which administration has the faster effect?
Longer duration?: inhalation or oral inhalation is faster, oral has longer duration
6. What type of compound is THC?: terpenoid, highly lipophilic.
(neither acid nor base)
7. What are the active derivatives of cannabis?: THC and cannabinol
8. How is cannabis distributed?: to tissues throughout body and brain depot binds
in fat due to highly lipophilic nature
9. How is cannabis absorbed when administered orally?: slow and irregular
absorption, some degradation by gastric enzymes, some degradation by first pass
metabolism
10. How is cannabis eliminated?: plasma levels drop rapidly, but complete
elimination is very slow due to depot binding. metabolites can be detected up to 2
weeks after administration
11. What are the main cannabis receptors? What kind of receptor are they?:
CB1- CNS
CB2- immune system
metabotropic receptors
12 Where in the brain are CB1
receptors found? What effects
do these areas mediate?: cortex-
higher cofnitive function
,hippocampus- learning, memory,
stress cerebellum- movement
brain stem- (medulla) nausea, vomiting
hypothalamus- appetite
spinal cord- pain, peripheral sensation
13. How does a CB1 antagonist affect effects of smoked marijuana in humans
compared to a placebo? Why was this study significant?: reduces effects
of feeling high/stoned, and reduces HR proved that it was the Cb1 receptor
mediating the effects
14. What are the desired effects of cannabinoids?: depressant like effect (seda-
tive like)
calm, relaxed, dream like state mild feeling of euphoria, exhilaration mild
psychedelic effect slowed sense of time, depersonalization, altered perceptions,
unusual imagery
15. What are the adverse effects of cannabinods?: weak somatic side
effects, increased HR and BP, dry mouth, dizziness impaired motor functioning
impaired cognitive functioning stimulate appetite
sympathomimetic properties
16. What effect did THC have on verbal memory recall?: people had a story
read to them while under influence of marijuana, asked to recall it after 2 hours and
6 hours. those given 7.5mg THC and those given 15mg THC performed worse than
placebo, with those given 15 being significant
17. What is state dependent learning?: learn under influence, some say you can
remember if you uuse drug again and try to recall
18. How did a Cb1 agonist affect rat performance on radial arm maze? What
happened when an agonist and antagonist were given at the same time?: a
, hippocampal infusion of CP55,940 (cb1 agonist) caused a trained rat to make more
errors on the radial arm maze (entering same arm in one session).
most of the effect of the agonist were blocked
19 What are the toxic effects of cannabinoids?: respiratory outcomes similar to
tobacco, adverse responses, neurotoxicity? (decrease grey matter in OFC) some
say marijuana deposits more tar than cigarettes
20. What adverse responses do some have to cannabis?: fear, anxiety, distrust,
paranoia, delusions, panic, loss of personal identity panic attack
21. What is the central qustion surrounding neurotoxicty of marijuana?: is the
grey matter loss due to marijuana use, or do those with loss use?
22. What is synthetic marijuana and what are its effects?: full agonist at the CB1
receptor, more potent effects. very high affinity. elevated mood, relaxation
altered perceptions anxiety, paranoia, hallucinations
tachycardia (extreme, could put into arrhythmia), nausea, vomiting
23. What are the theraputic uses of medical marijuana?: anti-emetic, analgesic,
appetite stimulant, treats glaucoma, treats muscle spasm, anti-inflammatory,
immunosuppressant
said to treat a variety of diseases, almost too many to believe
24. What are the effects of chronic marijuana use?: moderate tolerance (initially
mild reverse tolerance, then classic tolerance), moderate dependence,
antimotivational syndrome (chicken or egg)
25. How can we show that marijuana is addicting?: squirrel monkeys will bar
press for THC
26. What are the withdrawal symptoms for cannabis?: irritability, anxiety,
depression, insomnia, aggression, reduced appetite
27. How does THC affect dopamine receptors in the nucleus accumbens?: D2
D3 receptors increase, but there is no strong effect on the dopamine reward
pathway
28. What are the 2 major endocannabinoids? How are they alike and different
from cannabis?: anandaminde and 2-arachidonoylglycerol (2-AG) they are lipids
Alcohol, Anxiolytics, Depression & Schizophrenia Review
This comprehensive Q&A-style document supports preparation for the third
PMHNP Psychopharmacology exam. It covers cannabis pharmacology and
neurobiology, alcohol metabolism and effects, barbiturates and benzodiazepines,
GABAergic systems, anxiety and depression treatment, and antipsychotic drug
mechanisms. The guide integrates detailed mechanistic explanations, side effects,
historical context, and clinical applications relevant to psychiatric and substance-
related disorders.
1. What are the three main species of cannabis? Which is the most common?
What are the differnces in effect for each species?: Sativa- most common.
active properties. more stimulative
Indica- more sedative, body relaxation, has more cannabinol than THC.
Buderalis- combination, hybrid effects
2. How is cannabis classified?: as a depressant, but it also has
hallucinogenic/psychedelic effects as well
3. What are the 3 main forms of cannabis? From which part of the plant is
each derived?: marijuana- various parts of the male and female flower
sensimilla- potent form from the female flower. engineered to be seedless to
prevent male pollination. high THC content.
,hashish- sticky, thich, dark resin from the flower of the female plant (derived from
trichomes)
4. Where in the cannabis plant are the highest levels of THC found?: the flower,
higher in the female
5. How is cannabis administered? Which administration has the faster effect?
Longer duration?: inhalation or oral inhalation is faster, oral has longer duration
6. What type of compound is THC?: terpenoid, highly lipophilic.
(neither acid nor base)
7. What are the active derivatives of cannabis?: THC and cannabinol
8. How is cannabis distributed?: to tissues throughout body and brain depot binds
in fat due to highly lipophilic nature
9. How is cannabis absorbed when administered orally?: slow and irregular
absorption, some degradation by gastric enzymes, some degradation by first pass
metabolism
10. How is cannabis eliminated?: plasma levels drop rapidly, but complete
elimination is very slow due to depot binding. metabolites can be detected up to 2
weeks after administration
11. What are the main cannabis receptors? What kind of receptor are they?:
CB1- CNS
CB2- immune system
metabotropic receptors
12 Where in the brain are CB1
receptors found? What effects
do these areas mediate?: cortex-
higher cofnitive function
,hippocampus- learning, memory,
stress cerebellum- movement
brain stem- (medulla) nausea, vomiting
hypothalamus- appetite
spinal cord- pain, peripheral sensation
13. How does a CB1 antagonist affect effects of smoked marijuana in humans
compared to a placebo? Why was this study significant?: reduces effects
of feeling high/stoned, and reduces HR proved that it was the Cb1 receptor
mediating the effects
14. What are the desired effects of cannabinoids?: depressant like effect (seda-
tive like)
calm, relaxed, dream like state mild feeling of euphoria, exhilaration mild
psychedelic effect slowed sense of time, depersonalization, altered perceptions,
unusual imagery
15. What are the adverse effects of cannabinods?: weak somatic side
effects, increased HR and BP, dry mouth, dizziness impaired motor functioning
impaired cognitive functioning stimulate appetite
sympathomimetic properties
16. What effect did THC have on verbal memory recall?: people had a story
read to them while under influence of marijuana, asked to recall it after 2 hours and
6 hours. those given 7.5mg THC and those given 15mg THC performed worse than
placebo, with those given 15 being significant
17. What is state dependent learning?: learn under influence, some say you can
remember if you uuse drug again and try to recall
18. How did a Cb1 agonist affect rat performance on radial arm maze? What
happened when an agonist and antagonist were given at the same time?: a
, hippocampal infusion of CP55,940 (cb1 agonist) caused a trained rat to make more
errors on the radial arm maze (entering same arm in one session).
most of the effect of the agonist were blocked
19 What are the toxic effects of cannabinoids?: respiratory outcomes similar to
tobacco, adverse responses, neurotoxicity? (decrease grey matter in OFC) some
say marijuana deposits more tar than cigarettes
20. What adverse responses do some have to cannabis?: fear, anxiety, distrust,
paranoia, delusions, panic, loss of personal identity panic attack
21. What is the central qustion surrounding neurotoxicty of marijuana?: is the
grey matter loss due to marijuana use, or do those with loss use?
22. What is synthetic marijuana and what are its effects?: full agonist at the CB1
receptor, more potent effects. very high affinity. elevated mood, relaxation
altered perceptions anxiety, paranoia, hallucinations
tachycardia (extreme, could put into arrhythmia), nausea, vomiting
23. What are the theraputic uses of medical marijuana?: anti-emetic, analgesic,
appetite stimulant, treats glaucoma, treats muscle spasm, anti-inflammatory,
immunosuppressant
said to treat a variety of diseases, almost too many to believe
24. What are the effects of chronic marijuana use?: moderate tolerance (initially
mild reverse tolerance, then classic tolerance), moderate dependence,
antimotivational syndrome (chicken or egg)
25. How can we show that marijuana is addicting?: squirrel monkeys will bar
press for THC
26. What are the withdrawal symptoms for cannabis?: irritability, anxiety,
depression, insomnia, aggression, reduced appetite
27. How does THC affect dopamine receptors in the nucleus accumbens?: D2
D3 receptors increase, but there is no strong effect on the dopamine reward
pathway
28. What are the 2 major endocannabinoids? How are they alike and different
from cannabis?: anandaminde and 2-arachidonoylglycerol (2-AG) they are lipids
