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47 Cards in this Set
- Front
- Back
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what is the enzyme on which swainsonine exerts its inhibitory effects?
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golgi-alpha-mannosidase II
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what amino acid is the first molecule involved in the biosynthesis of swainsonine?
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L-lysine
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what ion does swainsonine displace at the substrate?
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Zn+2
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how is the toxicity of swainsonine conferred
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build up of glycogens in golgi lysosomes
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what are the target receptors of Vilazodone?
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SSRIs and 5HT1A
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what is the cause of serotonin syndrome?
a. too much activity of CYP3A4 b. not enough activity of CYP3A4 c. extremely low levels of serotonin d. extremely high levels of serotonin e. two of the above |
E. B&D
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Vilazodone is dangerously addictive (T/F)
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False
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which of the following would decrease serotonin levels
a. inhibiting CYPC19 b. inhibiting CYP2D6 c. inducing CYP3A4 d. administering Vilazodone e. administering MAOIs |
C. inducing CYP3A4
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vilazodone functions by _____ the concentration of neurotransmitter _____.
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increasing .. serotonin
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what potential problem could occur with chronic ampakine usage?
a. inverse of desired effect b. addiction c. down regulation of AMPA receptors d. all of the above e. two of the above |
E. A&C
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BDNF binds and influences downstream processes through:
a. GPCR b. trk c. ionotropic receptor d. all of the above |
b. tyrosine receptor kinase
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ampakines ameliorate deficits of sleep deprivation in non-human primates by modulating activity of the:
a. medial temporal lobe and dorsal prefrontal cortex b. cerebllum and basal ganglia c. brain stem and amygdala d. parietal cortex and hippocampus |
a. MTL and DPC
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where does CX614 bind on the AMPA receptor?
a. at active site b. at allosteric site c. in the channel d. unknown. CX614 is still a research drug |
b. at allosteric site
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when given to methamphetamine-sensitized rats, CX614:
a. activated AMPA receptors in ventral tegmental tract. increased da levels b. activated BDNF, causing regeneration of dopamine cells c. activated the parietal cortex which reduced hemisphere asymmetries d. caused an increase in spinning behavior |
c. activated the parietal cortex which reduced hemisphere asymmetries
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what is the transporter that reboxetine inhibits?
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noradrenergic reuptake transporter
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what is the enzyme that initiates the first step of metabolism of reboxetine, the dealkylation of the ethoxy aromatic ring?
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cytochrome P450
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interaction between reboxetine and which receptors are most likely the causes of dry mouth and constipation?
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M2 (constipation), M3 (dry mouth)
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in which area of the brain does the overall noradrenergic concentration decrease when reboxetine is used?
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locus coeruleus
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what receptor does buprenorphine act on? what is buprenorphine's role on this receptor?
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Mu receptor partial agonist
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describe the logic behind opioid replacement therapy
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no high but staves off withdrawal
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what are the two clinical applications of buprenorphine
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pain relief and opioid replacement therapy
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what makes buprenorphine a safer opioid than its competitors such as morphine or methadone?
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less tolerance, mild withdrawal, limit on respiratory depression, not immunosuppressive
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What are the most common side effects of famotidine use?
a.Vomiting, anorexia, and arrhythmia b.Dizziness, diarrhea, and constipation c.Prolonged QT interval, dizziness, and hallucinations d.Depression, diarrhea, and hypergastrinemia |
B
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what predecessor of famotidine was the first "blockbuster drug" drug however had multiple drug interactions unlike famotidine?
a. nizatidine b. ranitidine c. cemitidine d. pepcid |
c. cemitidine
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Which of the options most clearly describes the mechanism with which famotidine inhibits gastric secretion of acid?
a. It takes the acid level in your stomach down by neutralizing acid and coating the stomach. b. It competitively inhibits histamine H2 receptor site to prevent binding. c. It reduces the effects of a serotonin, which causes nausea and vomiting. d. It predominantly blocks the potassium channels, thereby prolonging the repolarization in parietal cells. e. None of the above |
B.
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Which of following comparisons between cimetidine and famotidine is incorrect?
a. Famotidine has minimal inhibitory effects on the metabolism of other drugs whereas cimetidine inhibits metabolisms of many other drugs. b. Famotidine, in most cases, has longer duration of action than cimetidine. c. Famotidine was proved to be about 20 times more potent than cimetidine on an equimolar basis. d. Famotidine inhibits many isozymes of the cytochrome P450 enzyme system whereas cimetidine does not. e. Famotidine and cimetidine have a rather similar molecular structure. |
D
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Which of the following is NOT a characteristic of famotidine?
a. Poor bioavailability b. Used to treat stomach ulcers, erosive esophagitis, and GERD c. Inhibits histamine release in mast cells d. Often used in combination with antacids to promote delivery |
C
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Clinically, what condition is atropine no longer used for due to the lack of evidence of therapeutic benefit?
a. Symptomatic sinus bradycardia b. Tachycardia c. Asystole d. AV block |
C
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What is the basic mechanism of action for atropine?
a. Nicotinic receptor agonist b. Muscarinic receptor agonist c. Nicotinic receptor antagonist d. Muscarinic receptor antagonist |
D
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Historically Atropine has been used for all of the following EXCEPT:
a. Poisoning b. cosmetic use c. witches brew d. Insomnia |
D
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Which of the following is true in respect to the metabolism of atropine?
a. Metabolism of atropine is not stereoselective b. As most of atropine is metabolized, none of it is excreted in the urine unchanged. c. Atropine is metabolized by enzymatic hydrolysis mainly in the liver. d. All of the above are true |
C
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__________________ is the drug that rescues the adverse effects that THC has on memory formation in the hippocampus.
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Rimonabandt
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Which endocannabinoid receptor is the most highly expressed in the central nervous system?
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CB1
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_________________ is the name used to describe the four physiological effects (catalepsy, sedation, analgesia, and hypothermia) of Cannabis.
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The Tetrad
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The Cannabis tetrad consists of all of the following EXCEPT:
a. Catalepsy b. Sedation c. Aphasia d. Analgesia e. Hypothermia |
C
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How does lamotrigine metabolism differ from metabolism of other antiepileptic drugs?
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lamotrigine is metabolism by glucuronic acid conjugation in the liver whereas other AEDs are metabolized by the cytochrome P450 system.
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Why is lamotrigine such an effective anti-epileptic drug?
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It blocks voltage gated sodium channels. This drug leaves initial action potential responses intact, but prevents the initiation of late epileptiform discharge.
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Compare and contrast comedication of lamotrigine with carbamazepine and lamotrigine with valproate.
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Carbamazepine increases lamotrigine clearance by approximately 30% to 50%, and valproate decreases lamotrigine CL by approximately 60%.
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Why do estrogen-containing oral contraceptives decrease the effectiveness of lamotrigine?
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Ethinylestradiol in these contraceptives is a UDP-glucuronosyl transferase inducer, meaning it will induce gluronidation of other glucuoronidated drugs, like lamotrigine.
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Lamotrigine is a Pregnancy Category C drug because it inhibits ___________, the enzyme that reduces dihydrofolate to tetrahydrofolate.
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dihydrofolate reductase
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Lamotrigine has been known to cause Stevens-Johnson syndrome, a severe skin reaction that occurs when the ________ separates from the _________ via _________ apoptosis.
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epidermis, dermis, keratinocyte
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List two structural similarities and one structural difference between phenytoin, carbamazepine and lamotrigine.
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have phenyl groups, are polar
Lamotrigine lacks an amide while CBZ and phenytoin have amide groups |
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How does lamotrigine affect calcium current?
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Blocks voltage gated sodium channels which leads to less excitatory neurotransmitter release (e.g. aspartate and glutamate). This leads to less NMDA activity and thus less calcium influx.
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Describe the addictive properties of lamotrigine.
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No potential for addiction
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Clonazepam is used to treat substance abuse withdrawal syndrome. Name an abused
substance whose withdrawal effects can effectively be alleviated by clonazepam. Explain your reasoning. |
Opiate users – augment euphoric effect
Methadone patients – increase euphoria and decrease anxiety Cocaine users – to ease the “crash” of rapid decline in euphoria Alcohol abusers – Depending on population 29-76% of alcohol abusers will also abuse clonazepam |
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What is the effect of clonazepam’s half life on potential overdose and addiction
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Long half-life of the drug also means there is considerable risk of overdose
Not recommended for long term use due to the high potential for dependence |
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Describe Clonazepam’s mode of action
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Like all benzodiazepine drugs, clonazepam’s binds to the benzodiazepine site of the GABAA receptor between the gamma (γ2) and alpha (α1) subunits, potentiating its activity. This in turn leads to an increased influx of Cl- into the cell, which hyperpolarizes the cell and inhibits the firing of action potentials. There is some evidence it may also block some subtypes of Ca2+ channels and enhance modulatory release of acetylcholine, further inhibiting signaling activity of neurons. Because of its primary activity to block excessive neuronal firing, clonazepam is most commonly prescribed to treat epileptic disorders and severe anxiety disorders.
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