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CNS and Psych

Pharmacology: CNS & Psych

What amino acid are the following neurotransmitters derived from: 1. dopamine 2. 5HT 3. norepinephrine 1. tyrosine 2. tryptophan 3. tyrosine
Major inhibitory neurotransmitter of the: 1. brain 2. spinal cord 1. GABA 2. glycine
1. ___ increase the frequency of GABA receptor channel is open 2. ___ increase the duration of the GABA receptor being open. 1. benzodiazepines 2. Barbiturates, alcohol
Identify the class of drug based on the suffix: 1. -barbital 2. -azepam 3. -azolam 4. -pental 1. barbiturate 2. benzodiazepine 3. benzodiazepine 4. barbiturate
1. Which of the following can lead to coma: barbiturates, benzodiazepines, ethanol? 2. Why? 1. barbiturates, ethanol 2. have a dose-dependent response; effect of benzodiazepines peak at medullary depression
What are the withdrawal signs of barbiturates and ethanol? opposite of effect of drug 1. anxiety 2. agitation 3. delirium tremens (with alcohol)
What are the withdrawal signs of benzodiazepines? opposite of effect of drug 1. rebound insomnia 2. anxiety 3. seizures if BZs were used as an antiepileptic
1. Zolpidem mechanism of action 2. Use? 3. Other drugs in this class 1. BZ1 receptor agonist; trade name ambien 2. sleep disorders 3. Zaleplon (sonata), Eszopiclone (lunesta)
Mechanism of action: 1. buspirone 2. felbamate 3. lamotrigine 1. 5-HT 1A partial agonist (increases serotonin release) 2. block Na+ channels and glutamate receptors 3. block Na+ channels and glutamate receptors
Two subtypes of benzodiazepine receptors within the GABA-A receptor 1. BZ1 mediates 2. BZ2 mediates 1. sedation 2. antianxiety, impaired cognitive functions
1. nonspecific benzodiazepine receptor antagonist used in overdose 2. Neuromuscular blocker that can raise extracellular K+ concentration 3. MOA of sertraline 1. flumazenil 2. succinylcholine 3. SSRI (Zoloft)
1. How do barbiturates effect the P450 system? 2. Why are barbiturates contraindicated in porphyrias? 1. general inducer of P450 2. barbiturates stimulate heme synthesis and exacerbate symptoms of porphyria
1. inhibitor of alcohol dehydrogenase 2. inhibitor of aldehyde dehydrogenase 1. fomepizole 2. disulfiram
What are the effects of increased acetaldehyde? 1. nausea and vomiting 2. headache 3. hypotension 4. combines with folate and thiamine to decrease available supply
Drugs that cause disulfiram-like effects: 1. ketoconazole 2. metronidazole 3. griseofulvin 4. cefoperazone
Mechanism of action: 1. Phenytoin 2. Valproic acid 3. Ethosuximide 1. (class 1B drug) blocks inactivated axonal Na+ channels 2. blocks inactivated Na+ channel, GABA transaminase (↑ GABA), T-type calcium channels 3. blocks T-type Ca2+ channels in thalamic neurons
1. Drug of choice for petit mal seizures 2. Safest anticonvulsant during pregancy? Why? 1. petit mal = absence seizure; DOC is ethosuximide 2. phenobarbital; b/c of high plasma protein binding
Mechanism of action 1. carbamazepine 2. Gabapentin 1. (class 1B drug) blocks inactivated axonal Na+ channels 2. binds presynaptic N-type Calcium channels to prevent neurotransmitter release
Side effects shared by phenytoin and carbamazeoine 1. osteomalacia (↓ vitamin D) 2. megaloblastic anemia (↓ folate) 3. aplastic anemia
1. Drug of choice for trigeminal neuralgia 2. Why does the sedative effect of benzodiazepines peak before the patient reaches a coma while that of barbiturates and alcohol does not? 1. carbamazepine 2. BZs require GABA to cause an effect and the CNS runs out of GABA before coma. Barbiturates and alcohol do not depend on GABA
1. Which drug is more soluble in the blood: nitrous oxide or halothane? 2. Which drug has a faster onset and recovery? 1. halothane is more soluble in blood and therefor 2. nitrous oxide more readily enters CNS to exert its effects
1. barbiturate used for induction of anesthesia 2. benzodiazepine used for preoperative sedation 3. opiate used for induction and maintenance of anesthesia 1. thiopental (very short acting) 2. midazolam 3. fentanyl
1. Mechanism of action of propofol 2. Dissociative anesthetic associated with hallucination 1. inhibits NMDA receptors; GABA-A receptor agonist 2. Ketamine
How do you tell if a local anesthetic is an ester or an amide? 1. esters have one "i" in their name 2. amides have two "i's"
1. What is the mechanism of action of local anesthetics 2. Where on their receptor do local anesthetics bind? 3. First line treatment for Wilson's disease 1. block activated Na+ channels 2. inner portion of the Na+ channel 3. Penicillamine - a chelator of copper
1. First line drug for status epilepticus 2. Used for status epilepticus prophylaxis 1. lorazepam 2. phenytoin
Mechanism of action of: 1. nondepolarizing skeletal muscle relaxant 2. depolarizing skeletal muscle relaxant 1. nicotinic antagonist 2. nicotinic agonist
How do AChE inhibitors affect: 1. nondepolarizing skeletal muscle relaxants 2. depolarizing skeletal muscle relaxants 1. reverse action 2. do not reverse action; may enhance muscle depolarization and prolong effects
1. Treatment for malignant hyperthermia 2. Mechanism of this drug? 1. dantrolene 2. decreases skeletal muscle contractility by blocking Ca2+ release from the sarcoplasmic reticulum
Succinylcholine 1. mechanism of action 2. metabolism 1. depolarizing skeletal muscle relaxant 2. hydrolyzed by pseudocholinesterase
1. Antidote for respiratory depression induced by opioids. 2. Why can O2 not be given? 1. naloxone or naltrexone 2. opioids ↓ the respiratory center response to pCO2; body relies on peripheral O2 receptors for respiratory drive and giving O2 will ↓ the respiratory drive
1. Mechanism of action of meperidine 2. How may meperidine cause serotonin syndrome? 1. (Demerol)kappa opiate receptor agonist 2. it is metabolized to normeperidine, an SSRI
1. Mechanism of action of amitriptyline 2. Atomoxetine mechanism of action 1. TCA; blocks 5HT and NE reuptake 2. (straterra) SNRI
Treatment for 1. neuroleptic malignant syndrome 2. tardive dyskinesia 1. dantrolene 2. use newer antipsychotic medications
What are the 5 classes of glaucoma drugs 1. α-agonist 2. β-blocker 3. diuretics 4. cholinomimetics 5. prostaglandin
Five agents used to treat Parkinson's disease BALSA 1. Bromocriptine 2. Amantadine 3. Levodopa 4. Selegiline 5. Antimuscarinics
1. Which two enzymes metabolize dopamine? 2. Which enzyme converts levodopa into dopamine? 1. COMT and MAO type B 2. dopa decarboxylase
1. Selective MAO-B inhibitor 2. Which neurotransmitter does this increase? 1. Selegiline 2. increases dopamine (used in parkinson's)
Mechanism of all typical antipsychotics Block dopamine D2 receptors
Mechanism of action 1. Tizanidine 2. Botulinum toxin 1. presynaptic α2 receptor agonist → ↓ excitatory neurotransmitter release 2. cleaving SNAP-25 in presynaptic nerve ending to prevent docking and release of ACh vesicles
Mechanism of action 1. clonidine 2. clozapine 3. clonazepam 1. (blood pressure drug) presynaptic α2 receptor agonist 2. (antipsychotic) 5HT2, dopamine antagonist 3. (benzodiazepine) GABA type A agonist
Baclofen MOA GABA type B agonist
Four important mechanisms of action of anticonvulsants: 1. ↓ Na+ influx 2. ↑ GABA-mediated hyperpolarization 3. block NMDA receptors 4. ↓ presynaptic Ca2+ influx through type-T channels in thalamic neurons
What are the two phases of depolarizing skeletal muscle relaxants 1. phase I: prolonged depolarization, flaccid paralysis 2. phase II: repolarization and receptor desensitization
1. Cause of malignant hyperthermia 2. Cause of neuroleptic malignant syndrome 1. ↑ muscle depolarization from skeletal muscle relaxants (succinylcholine) 2. ↓ DA in the CNS or blockade of D2 receptors in the nigrostriatal pathway
How do opioids effect: 1. respiration 2. vascular system 3. smooth muscle 1. ↓ response to ↑pCO2 2. vasodilation through histamine release 3. longitudinal muscles relax, circular muscles constrict (↓ peristalsis, urinary retention, miosis)
1. Why does the opioid agonist meperidine not cause miosis and GI/GU spasm? 2. MOA of tolcapone 1. it also acts as an antimuscarinic 2. inhibits peripheral and central COMT to prevent L-dopa breakdown 3. inhibits peripheral COMT to prevent L-dopa breakdown
1. prodrug that is converted to dopamine 2. Which drug is given in conjunction with it and why? 1. levodopa 2. carbidopa inhibits aromatic amino acid decarboxylase so levodopa is not converted to dopamine until it crosses the BBB
Mechanism of action: 1. selegiline 2. bromocriptine 3. amantadine 1. inhibits MAO type B 2. dopamine receptor agonist 3. antiviral; blocks muscarinic receptors and ↑ dopamine release
1. Which class of drugs is used to manage acute extrapyramidal symptoms of dopamine blockade? 2. Why do atypical antipsychotics not have as severe of extrapyramidal side effects as seen in typical antipsychotics? 1. antimuscarinic drugs 2. they block the D4 and 5HT2 receptors in addition to the D2. Typical block only D2.
1. All atypical antipsychotics block __ receptors 2. Why do some typical antipsychotics have less extrapyramidal symptoms than others? 1. 5HT2 2. less EPS is associated with ↑ antimuscarinic action
1. opioids bind to which GPCRs 2. Which ion channels are affected by opioid binding? 1. bind Mu opioid receptors coupled to Gi (inhibit adenylate cyclase) 2. K+ channels open and Ca2+ channels close
1. Mechanism of action of Tramadol 2. Antimuscarinic used to treat parkinson's disease 3. Memantine mechanism of action 1. weak μ agonist and inhibits NE and 5-HT reuptake 2. Benztropine 3. NMDA receptor antagonist
1. What is the mechanism of tolerance to opiates? 2. Mechanism of action of pergolide 1. ↓ adenylate cyclase →↓nociceptive neurotransmitter release (e.g. substance P) 2. D2 agonist used on parkinsonism
1. How do ester and amide local anesthetics compare in their duration of action? 2. How does inflammatory tissue effect local anesthetic action? 1. esters have short duration while amides are longer 2. inflammation makes tissue more acidic. anesthetics are weak bases and need a basic pH to be unionized and cross membranes
1. IV anesthetic that is an NMDA receptor antagonist 2. What are bromocriptine and pergolide used for? 1. ketamine 2. hyperprolactinemia (DA agonist)
Mechanism of action 1. Tricyclic Antidepressants 2. Topiramate 3. Tiagabine 1. blocks reuptake of 5HT and NE reuptake 2. Blocks Na+ channels, ↑ GABA action 3. inhibits GABA reuptake
What are the intravenous anesthetics? BB King on OPIATES PROPOses FOOLishly 1. Barbiturates - Thiopental 2. Benzo - Midazolam 3. Ketamine 4. Opiates - morphine, fentanyl 5. Propofol
Mechanism of action of Natalizumab as used in the treatment of multiple sclerosis binds α4 integrin on leukocytes and reduces migration into the CNS
How is the risk of systemic toxicity reduced when using local anesthetics? epinephrine used to cause vasoconstriction
What is the difference between MAC and AP50? 1. MAC is the partial pressure that makes 50% of subjects not move to noxious stimuli 2. AP50 is partial pressure that blocks painful stimuli in 50% of patients
How do local anesthetics differ from anticonvulsants in their mechanism of action on the Na+ channel? 1. local anesthetics block the open channel 2. Anticonvulsants block the inactivated channel
Which antiepileptics are associated with: 1. agranulocytosis/aplastic anemia 2. Stevens-Johnson syndrome 3. hepatotoxicity 1. carbemazepine 2. lamotrigine, ethosuximide, carbamazepine 3. Valproic acid, carbamazepine
What do the following coefficients describe in regard to inhalation anesthetics: 1. λ1 2. λ2 1. blood/gas barrier; defines rate of induction/recovery from anesthesia 2. brain/blood barrier; defines ability to pass through the blood-brain barrier
Treatment for organophosphate toxicity Organophoshates are irreversible cholinesterase inhibitors 1. Atropine 2. Pralidoxime (2PAM)
1. IV anesthetic that accumulates in fat 2. α2 agonist used in spasticity 1. Thiopental 2. Tizanidine
1. Best abortive agent(s) for a cluster headache 2. Best abortive agent(s) for migraine 1. Oxygen 2. tripans, dihydroergotamine
1. Mechanism of action of naloxone 2. Ziconitide MOA 1. antagonist at mu and kappa opioid receptors 2. N-type Ca2+ antagonist (spinal infusion for pain management)
Migraine prophylaxis options 1. Beta-blockers 2. Calcium channel blockers 3. TCAs 4. Anticonvulsives
Treatment : 1. alcohol withdrawal/delerium tremens 2. bulimia 3. anxiety 4. atypical depression 5. typical depression 1. benzodiazepines 2. SSRIs 3. Benzo, Buspirone, SSRIs 4. MAOIs, SSRIs 5. SSRIs, SNRIs, TCAs
Alzheimer's drugs: 1. non-competitive, NMDA receptor antagonist 2. AChE inhibitors 1. Mementine 2. donepezile, galantamine, rivastigmine
Prevents MPTP-induced cell death in the substantia nigra Selegiline
Treatment for: 1. Tourette's syndrome 2. Social phobias 3. Bipolar disorder 4. Obsessive-Compulsive Disorder 5. ADHD 1. antipsychotics 2. SSRIs 3. Lithium, Valproic acid, Cabamazepine, atypical antipsychotics 4. SSRIs 5. Atomoxetine (SNRI), methylphenidate, amphetamines
1. Antipsychotic associated with weight gain and glucose intolerance? 2. Which antipsychotics better control negative symptoms? 3. Which antipsychotics work only on positive symptoms? 1. Olanzapine and clozapine 2. Atypical antipsychotics 3. Typical antipsychotics
Mechanism of action: 1. LSD 2. Flunitrazepam 3. Primidone 1. 5HT2a partial agonist 2. (rohypnol, "roofies"), benzodiazepine/GABA-A agonist 3. ↑GABA-A; metabolized to phenobarbital
1. Mechanism of action of methylphenidate 2. Which antipsychotic is a 5HT2 antagonist and D2 partial agonist? 1. increases DA and NE release and inhibits reuptake 2. aripiprazole
Psychiatric patient with excessive thirst and high urine output. What drug might be the cause? 1. Lithium causes nephrogenic diabetes insipidus 2. Clozapine/Olanzapine cause diabetes mellitus must check for glucose in urine
1. Symptoms of TCA toxicity? 2. Treatment for TCA toxicity? 1. Convulsions, coma, cardiotoxicity (prolongs QT interval) 2. Sodium bicarbonate - NaHCO3 (alkalinates plasma)
1. Mechanism of action of Trazadone 2. Medical use 3. Side effect 1. inhibits serotonin reuptake 2. insomnia 3. priapism
Mechanism of action 1. phenelzine 2. Vigabatrin 3. Ropinirole and pramipexole 1. nonselective MAO Inhibitor 2. inhibits GABA transaminase (used for partial epilepsy) 3. D2 agonist for parkinsons
1. Meningitis prophylaxis for close contacts of sick individual 2. Treatment for serotonin syndrome 1. rifampin 2. cyproheptadine
Antipsychotic associated with the following side effects: 1. agranulocytosis 2. retinal deposits 3. corneal deposits 1. clozapine 2. thioridazine 3. chloropromazine
What are the two low potency antipsychotics? 1. chlorpromazine 2. thioridizine (↓ EPS, ↑ anticholinergic side effects)
Presentation of Akathisia vs Tardive Dyskinesia 1. Akathisia - restlessness 2. Tardive Dyskinesia - oral-facial movements followed by involuntary choreoathetosis
Which anesthetic can cause hepatotoxicity all inhaled anesthetics (halothane is most common cause)
Lithium side effects LMNOP Lithium side effects Movement (tremor) Nephrogenic diabetes insipidus hypOthyroidism Pregnancy problems (epstein's anomaly)
Drug used for bipolar disorder and seizures. Valproic acid
Why is rifampin useful for meningitis prophylaxis? Rifampin is secreted into mucus membranes, the site needed to prevent colonization of meningitis causing bacteria
What is the progression of extra-pyramidal side effects from antipsychotic drugs and time frame? 4 hours - dystonia (muscle spasms) 4 days - bradykinesia (parkinsonism: slowed movement, ↑ muscle tone, resting tremor 4 weeks - akathisia (restlessness) 4 months - tardive dyskinesia
Clinical use: 1. loperamide 2. dextromethorphan 3. Buprenorphine 1. opioid used for diarrhea 2. opioid used as an antitussive 3. heroine abstinence (partial μ agonist)
Drug prescribed for anorexia with depression. Mirtazapine - causes weight gain and treats depression
Why does it take 2-4 weeks for SSRIs to take effect? 5HT receptors in the raphe nuclei need to be selective desensitized
Mechanism of action of Mirtazapine α2 antagonist (↑ release of NE and serotonin)
Major side effects of SSRIs 1. GI distress 2. sexual dysfunction
Drug used to treat depression. No sexual side effects. Bupropion
Antipsychotic that causes agranulocytosis clozapine
High potency atypical antipsychotics 1. haloperidol 2. trifluoperazine 3. fluphenazine
What is the different side effect profile of high potency vs low potency typical antipsychotics 1. high potency has more extra pyramidal side effects and less anticholinergic 2. low potency has less EPS effects and more anticholinergic
Main side effect of monoamine oxidase inhibitors when taken alone. orthostatic hypotension
Antidepressant medication also used for: 1. insomnia 2. weight gain 1. Trazodone 2. Mirtazapine
Used to treat narcolepsy. modafinil
When would electroconvulsive therapy be warranted? major depressive episode that is 1. not responding to antidepressant meds 2. antidepressant meds are contraindicated 3. high risk for immediate suicide
What is the cause of tardive dyskinesia? super sensitivity of the DA receptors after chronic blockade
Good antipsychotic in the elderly. Risperidone; minimal antihistamine and alpha blocking activity so little sedation and less hypotension lead to less falls
Which opiate can lead to serotonin syndrome when taken in combination with MAOIs? meperidine (Demerol)
Which opiate dilates pupils? meperidine (Demerol)
Mechanism of action of: 1. Bupropion 2. Trazodone 3. Mirtaapine 1. NDRI (Norepinephrine/dopamine reuptake inhibitor) 2. SARI (serotonin antagonist and reuptake inhibitor) 3. NASA (norepinephrine and serotonin antagonist)
SSRI with the longest half-life. Fluoxetine (Prozac)
Created by: amichael87



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