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388 Cards in this Set
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Types of GABA receptors?
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GABA A: Cl influx
GABA B: K efflux BelKin AC |
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Benzodiazepines: MOA?
Effect observed on graph |
1. Act through BZ-1 + BZ-1 receptors(part of GABA complex)
2. Potentiate GABA 3. Increase frequency of opening of GABA channels "FRENZODIAZEPINES" 4. Work on Gamma-subunit of GABA thru BZ-1 and BZ-2 5. Cl efflux thru GABA produces hyperpolarization-->depression BZ-1: Sedation BZ-2: Anti-anxiety + impaired cognition "LEFT SHIFT OBSERVED ON GRAPH": potentiation |
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Benzodiazepines have/do not have GABA mimetic activity?
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No GABA mimetic activity
"BENZOs have NO gaba mimetic activity" |
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Barbiturates have/do not have GABA mimetic activity?
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Barbiturates have GABA mimetic activity
BarBs have MiMetic activity. "BBM" |
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Benzodiazepines:
Uses? |
1. Sedative
2. Anxiety 3. Insomnia 4. Night terrors 5. Sleep walking 6. Anesthesia 7. Anti-epileptic 8. Panic phobias |
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Benzodiazepines: Effect on REM sleep?
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Sedative effect but reduce duration of REM sleep.
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Benzodiazepines: Drugs and respective uses?
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1. Alprazolam: Anxiety
2. Diazepam: i. Anxiety ii. Alcohol withdrawal iii. Antiseizure iv. Pre-op sedation 3. Lorazepam: i. Anxiety ii. Anti-seizure iii. Pre-op sedation 4. Oxazepam: i. Sleep disorders ii. Anxiety 5. Midazolam: i. IV- anesthesia ii. Pre-op sedation 6. Temazepam: Sleep disorders |
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Benzodiazepines: Short T1/2?
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1. Triazepam
2. Oxazepam 3. Midazolam TOM thumb- short (T1/2) |
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Benzodiazepines: Drugs that do not undergo liver metabolism?
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Oxazepam
Temazepam Lorazepam Out The Liver |
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Barbiturates uses?
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Phenobarbital: seizures
Thiopental: IV pre-anesthetic medication |
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Barbiturates: Pharmacokinetics?
C/I: condition? |
1. General inducers of cytp450
2. C/I in porphyrias: D-ALA induction ** See induction graph ** |
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Sedatives: cross tolerance with?
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Alcohol (ethanol)
Barbs BZDs (higher dose required for BZDs in chronic alcoholics) |
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Withdrawal signs for BZDs?
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1. Rebound Insomnia
2. Seizures 3. Anxiety |
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Withdrawal signs for alcohol/barbs?
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1. Anxiety
2. Agitation 3. Life-threatening seizures. |
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Alcohol: Withdrawal Management?
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Supportive
Long acting BZDs |
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Drug interactions with alcohol/BZs?
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Additive effects with:
Additive depression with: 1. Anesthetics 2. A/histaminics 3. Opiates 4. B-blockers Metabolism induction: 1. OC pills 2. Carbamazepine 3. Phenytoin 4. Warfarin |
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BZs overdose: Rx?
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Flumazenil
Flumazenil MOA? |
Competitive BZ receptor a/agonist
(No effect on alcohol or barb overdose) |
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Non BZ drugs that act on BZ receptors?
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1. Zaleplon
2. Zolpidem |
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Zolpidem/Zaleplon: MOA?
Use? Advantage for use? |
MOA: BZ-1 receptor agonist
(No effect on cognition) Use: Sleep disorder Advantage: No addiction Less abuse liability Less tolerance |
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Buspirone:
MOA? Use? Advantage of use? How long does it take for effect? |
1. 5HT-1A partial agonist
(No effect on GABA) Use: Generalized anxiety disorder Advantage: Non sedative 1-2 weeks for effects. |
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Alcohol: MOA for sedation?
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GABA mimetic activity
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All alcohols cause ____?
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Metabolic acidosis
Acidosis due to? |
1. Glycolic acid/Oxalic acid
2. Formic acid 3. Acetic acid 4. Lactic acid |
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Ethyene glycol toxicity?
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1. CNS depression
2. Acidosis 3. Nephrotoxicity |
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Methanol toxicity?
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1. CNS depression
2. Acidosis 3. Ocular damage` |
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Ethanol toxicity?
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1. CNS depression
2. Acidosis 3. Acetaldehyde toxicity Acetaldehyde toxicity? |
1. NV
2. Headache 3. Hypotension 4. Folate deficiency(inactivation) 5. Thaimine deficiency(absorption) |
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Drugs that cause disulfiram like effect?
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1. Metronidazole
2. Cefoperazone 3. Cefotetan 4. Chlorpropamide 5. Griseofulvin 6. Omeprazole 7. Aripiprazole 8. Ketoconazole |
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Component in alcohol metabolism responsible for hangover?
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Acetaldehyde
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Fetal alcohol syndrome?
Mechanism of effects? |
1. Growth restriction
2. Midfacial hypoplasia 3. Microcephaly 4. Mental retardation Mechanism: Inhibition of cell migration |
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Fomepizole: MOA?
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1. Inhibitor of alcohol dehydrogenase
(high alcohol levels require hemodialysis) |
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MCC of Mental retardation?
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Fetal alcohol syndrome
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Anticonvulsants:
Drugs and MOA? |
1. Block Na channels in inactive state:
a. Phenytoin b. Carbamazepine 2. Facilitation of GABA: a. Barbiturates b. benzodiazepines 3. Block glutamate receptors: a. Lamotrigine (AMPA) b. Topiramate (AMPA) c. Felbamate (NMDA) 4. Block T-type Ca channels: a. Ethosuxamide b. Valproic acid |
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DOC for partial seizures?
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1. Phenytoin
2. Carbamazepine 3. Valproic acid |
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DOC for General- tonic clonic seizures?
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1. Phenytoin
2. Carbamazepine 3. Valproic acid |
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DOC for absence seizures?
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1. Ethosuxamide
2. Valproic acid |
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DOC for status epilepticus?
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1. Lorazepam
2. Diazepam 3. Phenytoin 4. Fosphenytoin |
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Advantages of using fosphenytoin over phenytoin for antiseizure medication?
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Fosphenytoin- more water soluble
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Barbiturates not used for Rx of status epilepticus?
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Prolonged opening of Cl- channels --> hydrops/swelling --> Irreversible neurological damage
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T-type ca channel blockers?
L-type ca channel blockers? |
T-type:
1. Ethosuxamide 2. Valproic acid 3. "Dipines" L-type: 1. Verapamil 2. Ethosuxamide |
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Phenytoin:
MOA? Uses? |
MOA:
1. Blocks axonal sodium channels (in blocked/inactivated state) "DOSE DEPENDENT BLOCKING of Na channels" 2. Inhibits glutamate release 3. Prevents seizure PROPAGATION Uses: Seizures: Partial/GTCS |
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Phenytoin: Pharmacokinetics?
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1. Variable absorption
2. Non linear kinetics for absorption 3. Cytochrome P450 induction 4. Zero order kinetics for elimination ** 1. Increased absorption followed by plateau 2. Constant elimination independent of concentration of drug in blood Therefore requires therapeutic drug monitoring. Tendency to accumulate enough to cause toxicity. |
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Phenytoin: side effects?
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1. CNS depression
2. Hirsutism 3. Gingival hyperplasia 4. Megaloblastic anemia 5. Aplastic anemia 6. Osteomalacia 7. Teratogenic effects: a. Cleft lip and palate b. Microcephaly c. Hypoplastic nails/fingers d. IUGR e. Development delay f. Craniofacial feature defects |
Gingival hyperplasia-
1. CCBs 2. Phenytoin 3. Cyclosporine |
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Fetal hydantoin syndrome?
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Fetal hydantoin syndrome:
Phenytoin teratogenicity a. Cleft lip and palate b. Microcephaly c. Hypoplastic nails/fingers d. IUGR e. Development delay f. Craniofacial feature defects |
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Carbamazepine:
MOA? Uses? |
Blocks inactivated Na channels
Uses: 1. Seizures 2. Bipolar disorders 3. Trigeminal neuralgia |
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Carbamazepine:
Pharmacokinetics? |
Induction of cytochrome P450
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Carbamazepine:
Side effects? |
1. CNS depression
2. Megaloblastic anemia 3. Aplastic anemia (agranulocytosis) 4. Osteomalacia 5. SJS/ Exfoliative dermatitis 6. Dilutional hyponatremia (increased ADH secretion) 7. Teratogenic: i. Cleft lip and palate ii. Spina bifida 8. Diplopia 9. Ataxia |
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Valproic acid: MOA?
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1. Block inactivated Na channels
2. Inhibition of GABA transaminase 3. Blockade of T-type Ca channel "Wall off like a pro" : block everything |
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Valproic acid: Uses?
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1. Seizure states(all)
2. Bipolar mania 3. Migraines Seizure states inclusive of: 1. Absence seizures 2. Myoclonic seizures |
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Valproic acid: pharmacokinetics?
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Inhibits cytochrome P450
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Antiseizure drugs and effect on P450?
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Induced by:
Carbamazepine Phenytoin Inhibited by: Valproic acid |
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Valproic acid: side effects?
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1. Hepatotoxicity
2. Thombocytopenia 3. Pancreatitis 4. Alopecia |
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Drugs used in trigeminal neuralgia?
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1. Amitryptiline
2. B-blockers 3. Carbamazepine 4. Gabapentin Drugs used in trigeminal neuralgia: "ABC" and gabapentin |
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Drug used in bipolar disorder and seizures?
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1. Carbamazepine
2. Valproic acid |
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Drug used as IB a/arrhythmic and Seizures?
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Phenytoin
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A/seizure drugs causing:
1. Thromocytopenia 2. Agranulocytosis 3. SJS 4. Pancreatitis 5. Osteomalacia 6. Dilutional hyponatremia 7. Alopecia 8. Hepatotoxicity 9. Dilantin embropathy 10. Ataxia? |
1. Thrombocytopenia:
Valproic acid 2. Agranulocytosis: Phenytoin Carbamazepine 3. SJS: i. Lamotrigine ii. Felbamate iii. Carbamazepine iv. Ethosuximide 4. Pancreatitis: Valproic acid 5. Osteomalacia: i. Phenytoin ii. Carbamazepine 6. Dilutional hyponatremia: Carbamazepine 7. Alopecia: Valproic acid 8. Hepatotoxicity: i. Valproic acid ii. Lamotrigine iii. Felbamate 9. Dilantin embryopathy: Phenytoin 10. Ataxia: i. Gabapentin ii. Carbamazepine iii. Phenytoin |
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A/seizure drug causing"
"Fizzy Kinky hair"? |
Valproic acid (alopecia)
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Antiseizure drug associated with:
i. Spina bifida ii. Cleft lip/palate iii. Cleft lip/palate + Spina bifida? |
Cleft lip/palate: Phenytoin
Spina bifida: Valproic acid Cleft lip/palate + Spina bifida: Carbamazepine |
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Pharmac Drugs inducing pancreatitis?
(Step 1 relevant) |
1. Alcohol
2. Valproic acid 3. Didanosine 4. Zalcitabine 5. Asparagine |
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Drugs that increase ADH secretion?
(Step-1 relevant) |
1. Antipsychotics
2. Antidepressants 3. Anti convulsant: Carbamazepine Drug that decreases ADH? |
Lithium
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Drugs associated with lupus-like syndrome
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1. Phenytoin
2. Isoniazid 3. Hydralazine 4. Procainamide |
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Antiseizure drug also used for migraines?
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Valproic acid
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Ethosuximide:
MOA? Use? |
MOA: T Ca channel blockade in THALAMUS
Use: Absence seizures |
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Phenytoin/carbamazepine: effect on OC pill effect?
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Effect mitigated due to P450 induction
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OC pill effect enhanced by ____(a/seizure drug)
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Valproate- inhibition of P450
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Safest antiseizure drug for pregnancy?
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Phenobarbital
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Felbamate and lamotrigine: MOA?
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1. Block Na channels
2. Block glutamate receptors (felbamate blocks glutamate) |
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Gabapentin: MOA? uses?
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MOA:
1. Enhances GABA effects 2. Blocks Ca channels Uses: 1. Seizures GTCS and Partial 2. Neuropathic pain |
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DOC for seizure(status epilepticus) prophylaxis?
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Phenytoin
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DOC for GTCS?
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Phenytoin
Carbamazepine Valproic acid |
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DOC for Absence seizures?
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Ethosuximide
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DOC for Status epilepticus?
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BZDs-
Diazepam Lorazepam |
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Felbamate: side effects?
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1. SJS
2. Hepatoxicity 3. Aplastic anemia |
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Lamotrigine: side effects?
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1. SJS
2. Hepatoxicity 3. Aplastic anemia |
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Anticonvulsants have additive side effects with ______?
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CNS depressants
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Antiseizure drug that may predispose to infective endocarditis?
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Phenytoin
(gingival hyperplasia-->gingivitis--> septicemia--> infective endocarditis) |
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Antiseizure drug associated with cerebral herniation?
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Carbamazepine
(increased ADH--> dilutional hyponatremia--> neuronal hydrops + raised ICT---> herniation) |
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A/seizure drug associated with generalized lymphadenopathy?
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Phenytoin
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Vigabatrin: MOA?
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Irreversibly inhibits GABA transaminase---> increases GABA concentration
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Which antiepileptic drug may cause sedation, tolerance, and dependence in addition to inducing cytochrome P450 enzymes?
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Phenobarbital
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Which types of seizures are treated with benzodiazepines? What is the mechanism of action?
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Status epilepticus; increase the action of GABA
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Status epilepticus; increase the action of GABA
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Agranulocytosis and aplastic anemia
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Which types of seizures are treated with tiagabine? What is its mechanism of action?
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Simple and complex partial seizures; inhibits GABA reuptake
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What is the first-line agent used to prevent seizures in patients with eclampsia?
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Magnesium sulfate
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Dose dependent blocking of Na channels in antiseizure theraypy: associated drug?
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Phenytoin
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Drug that blocks Na channels and glutamate release?
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Phenytoin
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A/seizure drug associated with kidney stones and weight loss?
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Topiramate
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Topiramate: MOA?
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1. Inactivates sodium channels 2. Increases GABA action
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If magnesium sulfate fails to prevent seizures in a patient with eclampsia, what class of drugs could also be used?
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BZDs
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Drug that inactivates Na channels and gutamate receptors?
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1. Felbamate
2. Lamotrigine |
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Gabapentin: adverse effects?
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1. Sedation
2. Ataxia |
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Ethosuximide side effects?
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1. Fatigue
2. GI distress 3. Headache "EFGH" |
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Levetiracetam: MOA?
Use? |
MOA: unknown
GABA/Glutamate modulator(in theory) Use: GTCS and partial Levetiracetam provides "leverage" (modulation) |
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Which types of seizures are treated with gabapentin
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GTCS and partial
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Vigabatrin: use?
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Partial seizures only
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Modulator drug used in a/seizure medication?
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Levetiracetam
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Modulator drug used in a/seizure medication?
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Levetiracetam
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Modulator drug used in a/seizure medication?
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Levetiracetam
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MAC?
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Minimum alveolar concentration
Measure of potency |
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Relationship between MAC and potency?
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Inverse: More the potency less the MAC
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Relationship between MAC and lipid solubility?
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Inverse: More the MAC less the solubility
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Nitrous oxide:
MAC? Blood-gas ratio? |
MAC: 104%
Blood-gas ratio: 0.5 |
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Halothane:
MAC? Blood-gas ratio? |
MAC: 0.8%
Blood-gas ratio: 2.3 |
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Nitrous oxide: CV effect?
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None
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Halothane: CV effect?
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Sensitizes the heart to catecholamines
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Nitrous oxide: Metabolism?
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No metabolism--> therefore quick induction and quick recovery
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Nitrous oxide: adverse effects?
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1. Diffusional hypoxia(NO displaces O2 reduces pO2)
2. Spontaneous abortion (NO stimulates contraction) |
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Halothane: Adverse effects?
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1. Malignant hyperthermia
2. Hepatitis 3. Cardiac arrhythmias |
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Relationship between blood gas ratios and recovery?
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Inverse relationship
(High blood gas ratio implies slower onset and recovery Low blood gas ratio implies faster onset and recovery) |
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IV anesthetics?
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1. Thiopental
2. Midazolam 3. Propofol 4. Fentanyl 5. Ketamine |
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Thiopental: MOA?
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Barbiturate used for induction.
(Barbiturate: GABA-A channel activator) |
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Thiopental: pharmacokinetics?
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1. High lipid solubility
2. Rapid onset 3. Short acting(re-distribution) |
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Thiopental: short T1/2: reason?
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Redistribution
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Midazolam: MOA?
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BZD
(GABA-A channel activator: frequency) Uses: 1. Anesthesia induction 2. Pre-operative sedation 3. Anterograde amnesia 4. (Outpatient surgery) |
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Midazolam: adverse effect?
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1. Respiratory depression
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Propofol: Use?
Adverse effects? |
Use:
1. Inuduction and maintenance of anesthesia 2. Antiemetic Adverse effects: 1. CNS depression 2. Cardiac depression Propofol: Props up and maintains anesthesia. (Propofol appears like milk) |
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Fentanyl:
MOA? |
MOA: Opiate
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Ketamine: MOA?
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NMDA receptor antagonist
"Ketamine kills off NMDA receptors" ---> DISSOCIATIVE ANESTHESIA |
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Ketamine:
Adverse effects? |
Adverse effects:
1. "Emergent" Delirium 2. Hallucinations 3. Cardiovascular stimulation 4. Raised ICT |
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Ketamine effect: patient description?
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Dissociation
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IV anesthetics used for anesthesia induction only?
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1. Thiopental
2. Midazolam 3. Ketamine |
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IV anesthetics used for anesthesia induction and maintenance?
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1. Propofol
2. Fentanyl |
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Ketamine is an analogue of _____(drug of abuse)
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Phencyclidine ("Angel dust")
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Ketamine primarily used in ______population?
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1. Pediatric population
(burns/manipulating fx) 2. Geriatric population (For CVS stimulation) KEtamine is for Kids and Elderly |
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Local anesthetics: classification?
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Esters:
1. Procaine 2. Cocaine 3. Benzocaine Amides: 1. Lidocaine 2. Bupivicaine 3. Mepivicaine Am I before kane? Yes: Am I dead? |
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Local anesthetics metabolism?
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Esters metabolized by esterase
Amides metabolied by amidase |
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Local anesthetics: MOA?
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1. Non ionized form crosses the membrane--> Within cell (acidic environment)--> dissociates into ions--> Blocks Inactivated Na channels
2. Slow recovery 3. Prevents PROPAGATION of action potentials |
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Nerve fibers sensitivity: order?
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#1. Types B and C
#2. Type A-d #3. Type A-b and A-g #4. Type A-a Recovery: order? |
#1. Type A-a
#2. Type A-b and A-g #3. Type A-d #4. Types B and C |
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Fibers most sensitive to local anesthetic blockade? function?
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B and C: Dull pain
"B and C: most sensitive, dull and painful: they're bull crap" |
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Fibers least sensitive to local anesthetic blockade? function?
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A-a and A-b:
Muscle stretch |
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Local anesthetic administration?
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Co-administered with alpha-1 agonist
Why are alpha-1 agonists co-administered with local anesthetics? |
1. Reduce systemic absorption by inducing vasoconstriction
(reduce toxicity) 2. Prolong effect |
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Local anesthetics: adverse effects?
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Neurotoxicity
Cardiotoxicity Allergies: Allergies in local anesthetics due to? |
PABA formation(all esters)
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Local anesthetic that does not require co-ad
ministration with alpha-1 blocker? |
Cocaine
Why not? |
Cocaine is NE re-uptake blocker
--> Increases NE --> Alpha-1 stimulation --> Vasoconstriction |
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Disadvantages of using cocaine as a local anesthetic?
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1. Increased risk of MI
2. Nasal septum infarction |
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Na channel blockers/"toxins"?
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Tetrodotoxin: puffer fish
Saxitoxin: algae Batrachotoxin: Frogs(golden) Ciguatoxin: fish MOA? |
Class Ia: block activated Na channels--> prolong Na influx
Can lead to fatal arrhythmias |
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No of subunits in nicotinic receptors?
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Five subunits:
2 alpha 1 beta 1 delta 1 gamma |
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MOA of Ach on muscle contraction?
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ACh binds to two alpha subunits--> opens Na channel--> depolarization--> contraction
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Skeletal muscle relaxants:
MOA? use? |
MOA:
Blocks nicotinic ACh receptors at NM junction 1. Anesthesia protocols 2. Immobility |
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Muscle relaxants: Classification?
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1. Non depolarizing/competitive:
a. Atracurium b. Mivacurium 2. Depolarizing/ non competitive: a. Succinyl choline |
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Atracurium/Mivacurium: MOA?
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Nicotinic antagonist
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Atracurium/Mivacurium: pattern of paralysis induced?
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"Progressive paralysis"
Face--> limbs--> Respiratory muscles |
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Atracurium/Mivacurium: Effect on CNS?
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None
Effect on smooth muscles/cardiac effects? |
None
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Atracurium effects: Reversible/irreversible with AChE inhibitors?
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Reversible
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Atracurium: Advantage over other relaxants?
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Safe in renal/hepatic impairment
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Atracurium: pharmacokinetics?
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1. Rapid recovery
2. Spontaneous inactivation to laudanosine ATRACURIUM Kha ke nau do athara ho jaa |
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Atracurium: adverse effects?
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Inactivated compound of atracurium (laudanosine)--> seizures
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Mivacurium: Pharmacokinetics?
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1. Very short acting
2. Metabolized by plasma cholinesterase |
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Succinyl choline: MOA?
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1. Nicotinic agonist
2. Non-competitive 3. Works in two phases- Phase 1: Prolonged depolarization--> flaccid paralysis Phase 2: Desensitization |
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Succinyl choline: Pharmacokinetics?
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1. Short duration
2. Rapidly hydrolyzed by "Pseudocholinesterase" |
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AchE inhibitors MOA?
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Inhibit AChE-->
Increased ACh--> Repeated depolarization--> Paralysis |
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Succinyl choline: adverse effects?
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1. Hyperkalemia*
2. Malignant hyperthermia 3. Hypecalcemia *hyperkalemia: Enhances effects of succinyl choline MALIGNANT HYPERTHERMIA? |
AD disorder
>50% pts have ryanodine receptor mutation(control Ca level release from SER)--> Succinyl choline---> Increased Ca levels--> Contraction--> Malignant hyperthermia Succinyl choline enhanes affinity of A-site of Ca channels--> Increased Ca influx |
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Malignant hyperthermia: Rx?
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Dantrolene
Dantrolene: MOA? Other uses? |
Blocks Ca release from SER
Uses: 1. Malignant hyperthermia 2. Malignant neuroleptic syndrome |
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Central skeletal muscle relaxants?
MOAs? |
1. BZDs: GABA-A
2. Baclofenac: GABA-B Use? |
Spasticity
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Which intravenous lipid-based anesthetic, used for rapid anesthesia induction, results in less postoperative nausea than thiopental?
|
Propofol
|
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|
A nerve blockade has the greatest effect on nerves that are _____ (myelinated/unmyelinated) and _____ (large/small). _____ (Myelination/Size) predominates over _____ (myelination/size)
|
1. Myelinated;
2. Small; 3. Size; 4. Myelination Therefore, small myelinated nerves are anesthetized first, followed by small unmyelinated fibers and then large fibers |
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|
Which drug is commonly mixed with local anesthesia (except for cocaine) to enhance the local anesthesia action, to decrease bleeding, and to decrease systemic concentration?
|
Epinephrine;
(vasoconstriction, which leads to less dilution of the anesthetic agent) |
|
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|
Phase I depolarization in neuromuscular blockade is potentiated by _____
|
Cholinesterase inhibitors
|
|
|
|
Name four inhaled anesthetics
|
1. Halothane,
2. Enflurane, 3. Isoflurane, and 4. Sevoflurane |
|
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|
Toxicities caused by:
1. Halothane 2. Methoxyflurane 3. Enflurane? |
1. Halothane: Hepatotoxicity
2. Methoxyflurane: Nephrotoxicity 3. Enflurane: Proconvulsant |
|
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|
Antidote for a nondepolarizing neuromuscular blocking drug?
|
1. Neostigmine or
2. Edrophonium |
|
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|
What is the antidote to phase I (prolonged depolarization) action of succinylcholine?
|
There is no antidote
|
|
|
|
What is the only commonly used anesthesia induction agent that does not lower blood pressure?
|
Ketamine
|
|
|
|
What are four common adverse effects of inhaled anesthetics?
|
1. Myocardial depression
2. Despiratory depression 3. Emesis 4. Increased cerebral blood flow |
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|
Local anesthetics penetrate infected tissue _____ (less/more) efficiently because of the ______ (decreased/increased) acidity in the tissue.
|
Less; increased
|
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|
The use of which two drugs concomitantly may result in malignant hyperthermia in a patient who is genetically susceptible?
|
Inhalation anesthetics with succinylcholine
|
|
|
|
What is the mechanism of action of propofol?
|
Propofol potentiates GABAA
|
|
|
|
Name six nondepolarizing neuromuscular blocking drugs.
|
1. Tubocurarine,
2. Atracurium, 3. Mivacurium, 4. Pancuronium, 5. Vecuronium, 6. Rocuronium |
|
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|
What are two common adverse effects of midazolam?
|
1. Amnesia
2. Respiratory depression |
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|
List the order in which the following sensation is lost during nerve blockade from first to last: pressure, pain, touch, and temperature.
|
Pain, temperature, touch, and pressure
|
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|
What is the antidote for phase II (repolarized but blocked) action of succinylcholine?
|
Neostigmine or other cholinesterase inhibitors
|
|
|
|
What are the effects of ketamine and thiopental on cerebral blood flow?
|
Ketamine increases cerebral blood flow whereas thiopental decreases it
|
|
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|
Inhaled anesthetics may cause a(n) _____ (decrease/increase) in cerebral blood flow.
|
Increase
(Inhaled anesthetics Increase cerebral blood flow) |
|
|
|
What amide, which is used in local anesthesia, may cause severe cardiovascular toxicity?
|
Bupivacaine
|
|
|
|
What is the most common drug used for anesthesia during endoscopy?
|
Midazolam
|
|
|
|
Which barbiturate is commonly used for the induction of anesthesia and short surgical procedures?
|
Thiopental
|
|
|
|
Local anesthetics preferentially bind to ______ (activated/inactivated) sodium channels, so they are most effective in ______ (rapidly/slowly) firing neurons.
|
Activated; rapidly
|
|
|
|
Use of succinylcholine may cause what two electrolyte abnormalities?
|
1. Hyperkalemia and
2. Hypercalcemia |
|
|
|
Endogenous opiate peptides: types?
|
1. Endorphins (Mu)
2. Enkephalins (Delta) 3. Dynorphins (Kappa) |
|
|
|
Opiate receptors: types?
|
Mu
Kappa Delta |
|
|
|
Prototype Mu agonist?
|
Morphine
|
|
|
|
Morphine: MOA?
|
Stimulates opiate interneurons to act on Gi coupled u receptors on 'regular' neurons--> decreased cAMP--> Decreased release of NE/substance P
|
|
|
|
Morphine: effects?
|
1. Analgesia- more pain tolerance/ dissociation
2. Sedation 3. Constipation and cramping (Longitudanal muscle relaxation and Constrictor contraction) 4. Urinary retention and urgency 5. Biliary pressure increases 6. Miosis 7. Cerebral vasodilation(histamine) 8. Cough suppression 9. Nausea/vomiting (CTZ) 10. Respiratory depression |
|
|
|
Morphine: contra-indications?
|
1. Head trauma
2. Biliary stones/colics 3. Pulmonary dysfunction 4. Hepatic/renal dysfunction 5. Adrenal/thyroid deficiency 6. Pregnancy (Head trauma: C/I d/t vasodilation) (Hepatic/renal dysfunction: accumulation) (Adrenal/thyroid defects: exaggerated response) Pregnancy- neonatal depression) |
|
|
|
Opiate safe in pregnancy?
|
Meperidine
|
|
|
|
Morphine: Pharmacokinetics ?
|
Glucoronidation--->
Morphine-6-glucoronide (More potent than morphine) |
|
|
|
Morphine levels: how would you detect them?
|
Order morphine and morphine-6-glucoronide for testing/screening
|
|
|
|
Classic triad for Opiate toxicity?
|
1. Pinpoint pupil
2. Respiratory depression 3. Coma |
|
|
|
Opiate that does not produce pinpoint pupils?
|
Meperidine
|
|
|
|
Opiates that are full agonists?
|
1. Meperidine
2. Methadone 3. Codeine(weak) |
|
|
|
Opiates that are partial agonists?
|
Buprenorphine
|
|
|
|
Opiates that are Mixed agonist/antagonists?
|
Nalbuphine
Pentazocine |
|
|
|
Opiates that act on Kappa and gamma receptors?
|
1. Nalbuphine
2. Pentazocine ****STIMULATE KAPPA**** ****ANTAGONIZE MU***** |
|
|
|
Opiate antagonists?
|
Naloxone
Naltrexone Methyl-naltrexone |
|
|
|
Opiate antagonist that decreases alcohol craving?
|
Naltrexone
|
|
|
|
Opiate antagonist that helps in opiate poisoning producing respiratory depression?
|
Naloxone
|
|
|
|
Opiate antagonist that helps in opiate induced constipation?
|
Methyl-naltrexone
|
|
|
|
Opiate chiefly used in cough supression?
|
Codeine
Dextromethorphan |
|
|
|
Opiate with antimuscarinic effects?
|
Meperidine
|
|
|
|
Meperidine: the 2 adverse effects?
|
1. Serotonin syndrome
2. Seizures These effects caused due to? |
Normeperidine--(serotonin reuptake inhibitor)
Meperidine---(metabolized by P450)--->Normeperidine |
|
|
Opiate used for opiate de-addiction?
|
Methadone
How does it act? |
Long t1/2 ("Tapering") therefore prevents withdrawal symptoms after stopping
|
|
|
Buprenorphine: MOA?
|
Partial Mu agonist
(Precipitates withdrawal if used with an agonist) |
|
|
|
Advantage of using partial/mixed opiate agonists?
|
Stimulate Kappa--> dysphoria as a side effect--> decreased abuse liability
|
|
|
|
Opiates: Tolerance?
|
Pharmacodynamic at level of cAMP: cells ramp up cAMP level production for unknown reasons
|
|
|
|
Opiate tolerance observed to all effects except which two?
|
1. Miosis
2. Constipation |
|
|
|
Opiates: withdrawal signs?
|
1. Yawning
2. Lacrimation/salivation/rhinorrhea 3. Anxiety/sweating/goosebumps 4. Muscle cramps 5. CNS pain(Thalamic) |
|
|
|
Opiate withdrawal symptoms: management?
|
1. Clonodine: alpha-2 agonist---> decreases NE release thereby mitigating effects
2. Methadone 3. Supportive |
|
|
|
Opiate used for diarrhea?
|
Loperamide
|
|
|
|
Dopamine: functions?
|
1. Nigrostriatal pathway: initiation of movement
2. Mesolimbic/mesocortical pathway Reinforcement Psychosis Addiction 3. Tuberoinfundibular pathway Inhibits prolactin release 4. CTZ Induces vomiting 5. Thermal regulation: dopamine--> hyperthermia 6. Appetite reduces appetite--> anorexia |
|
|
|
Dopamine receptors: receptors?
|
D1: Gs coupled
D2: Gi coupled (D2A: Nigrostriatal D2C: Mesolimbic) |
|
|
|
Classic triad of parkinsonism?
|
1. Bradykinesia: d/t dopamine
2. Tremors: d/t Ach 3. Rigidity: d/t Ach |
|
|
|
Drugs used in Parkinsonism?
|
1. Dopamine precursor:
Levodopa 2. Dopamine analogues/receptor agonists: 1. Bromocriptine 2. Pergolide 3. Antimuscarinics: i. Benztropine ii. Diphenhydramine iii.Trihexiphenidyl DIed TRying to PARK my BENZ 4. MAO-b inhibitor: Selegeline "MAO SELong" (Mao Zedong) |
|
|
|
Antiparkinson drugs also used in prolactinoma?
|
Bromocriptine
Pergolide |
|
|
|
Levodopa: MOA?
|
Prodrug of dopamine
|
|
|
|
Levodopa converts to dopamine with?
|
Aromatic amino acid decarboxylase
(AAAD) |
|
|
|
Levodopa always co-administered with?
|
1. Carbidopa
2. Tolcapone/entacapone Why are these drugs co-administered? |
1. Carbidopa inhibits peripheral AAAD. therefore
i. increases levodopa availability to brain ii. Prevents peripheral side effects of dopamine (hypotension) 2. Tolcapone/entacapone: i. Inhibits COMT therefore prevents Levodopa---COMT---> 3-O-methyldopa 3-o-methyl dopa is a partial agonist therefore in presence of dopamine acts as an antagonist |
|
|
Levodopa: side/adverse effects?
|
1. Dyskinesia
2. On-Off effects: due to fluctuating levels of dopamine 3. Psychosis 4. Hypotension 5. Vomiting |
|
|
|
Tolcapone toxicity?
|
Hepatotoxic
|
|
|
|
Dopamine: functions?
|
1. Nigrostriatal pathway: initiation of movement
2. Mesolimbic/mesocortical pathway Reinforcement Psychosis Addiction 3. Tuberoinfundibular pathway Inhibits prolactin release 4. CTZ Induces vomiting 5. Thermal regulation: dopamine--> hyperthermia 6. Appetite reduces appetite--> anorexia |
|
|
|
Dopamine receptors: receptors?
|
D1: Gs coupled
D2: Gi coupled (D2A: Nigrostriatal D2C: Mesolimbic) |
|
|
|
Classic triad of parkinsonism?
|
1. Bradykinesia: d/t dopamine
2. Tremors: d/t Ach 3. Rigidity: d/t Ach |
|
|
|
Drugs used in Parkinsonism?
|
1. Dopamine precursor:
Levodopa 2. Dopamine analogues/receptor agonists: 1. Bromocriptine 2. Pergolide 3. Antimuscarinics: i. Benztropine ii. Diphenhydramine iii.Trihexiphenidyl DIed TRying to PARK my BENZ 4. MAO-b inhibitor: Selegeline "MAO SELong" (Mao Zedong) |
|
|
|
Antiparkinson drugs also used in prolactinoma?
|
Bromocriptine
Pergolide |
|
|
|
Levodopa: MOA?
|
Prodrug of dopamine
|
|
|
|
Levodopa converts to dopamine with?
|
Aromatic amino acid decarboxylase
(AAAD) |
|
|
|
Levodopa always co-administered with?
|
1. Carbidopa
2. Tolcapone/entacapone Why are these drugs co-administered? |
1. Carbidopa inhibits peripheral AAAD. therefore
i. increases levodopa availability to brain ii. Prevents peripheral side effects of dopamine (hypotension) 2. Tolcapone/entacapone: i. Inhibits COMT therefore prevents Levodopa---COMT---> 3-O-methyldopa 3-o-methyl dopa is a partial agonist therefore in presence of dopamine acts as an antagonist |
|
|
Levodopa: side/adverse effects?
|
1. Dyskinesia
2. On-Off effects: due to fluctuating levels of dopamine 3. Psychosis 4. Hypotension 5. Vomiting |
|
|
|
Tolcapone toxicity?
|
Hepatotoxic
|
|
|
|
Selegiline: MOA? Use?
|
Seligiline is MAO-B inhibitor therefore prevents conversion of Levodopa--> 3-O-methyldopa:
Partial agonist acts as antagonist in presence of dopamine |
|
|
|
Selegiline: Side effects?
|
1. Dyskinesia
2. Psychosis 3. Insomnia. |
|
|
|
Insomnia as a side effect observed in seligeline: Reason?
|
Seligeline---> Amphetamines
(Amphetamines cause agitation/insomnia) |
|
|
|
Dopamine receptor agonists?
|
1. Bromocriptine
2. Pergolide 3. Pramipexole |
|
|
|
Bromocriptine/pergolide: uses besides a/parkinsonism?
|
1. Prolactinoma
2. Acromegaly Extrapyramidal effects? |
1. Psychosis
2. Decreased prolactin sectretion 3. Decreased growth hormone |
|
|
Added advantage of using pergolide/ pramipexole for Parkinsonism?
|
A/oxidant effects: protective for dopaminergic neurons
|
|
|
|
Drugs reducing ACh functions?
|
1. Benztropine
2. Diphenhydramine 3. Trihexiphenidyl |
|
|
|
Effects of Antimuscarinics on parkinsonism?
|
1. Reduces resting tremors
2. Reduces rigidity |
|
|
|
Antimuscarinics have no effect on _____ symptom in Parkinsonism?
|
Bradykinesia
|
|
|
|
Antimuscarinics: side effect?
|
1. Blurred vision
2. Mydriasis: ppt angle closure glaucoma 3. Constipation 4. Urinary retention 5. Coma 6. Convulsions 7. Cardiotoxicity |
|
|
|
Amantadine: the 2 MOA?
|
1. Antimuscarinic
2. Dopamine releaser |
|
|
|
Amantadine side effects?
|
1. Blurred vision
2. Mydriasis: ppt angle closure glaucoma 3. Constipation 4. Urinary retention 5. Coma 6. Convulsions 7. Cardiotoxicity 8. LIVEDO RETICULARIS: "PATHOGNOMIC" bluish discoloration due to vasodilation |
|
|
|
Drug used in A/parkinsonism converted to amphetamine?
|
Selegiline
|
|
|
|
Schizophrenia: Positive symptoms?
|
1. Delusions
2. Hallucinations 3. Paranoia |
|
|
|
Schizophrenia: Negative symptoms?
|
1. Amotivation
2. Social withdrawal 3. Flat affect |
|
|
|
Schizophrenia: dopamine hypothesis?
|
1. Symptoms arise due exess dopamine levels in mesolimbic pathway.
2. Dopamine agonism has psychotic effects 3. Serotonin agonism has a psychotic effects |
|
|
|
Dopamine blockade: uses/ how does it help?
|
1. Schizophrenia
2. Schizoaffective disorder 3. Bipolar disorders 4. Tourette syndrome 5. Drug/radiation emesis |
|
|
|
Dopamine blockade: side effects?
|
1. Acute EPS: Dystonia(painful muscle spasm: torticollis), akathisia
2. Chronic EPS: Tardive dyskinesia (d/t upregulation and increased sensitization of receptors) 3. Weight gain- obesity related problems 4. Malignant hyperthermia 5. Dysphoria 6. Increased prolactin: i. Galactorrhea ii. Amenorrhea iii. Gynecomastia |
|
|
|
Antipsychotic that has a very similar side effect profile as quinidine?
|
Thioridazine
(No cinchonism) |
|
|
|
Typical antipsychotics: effects?
|
1. EPS symptoms
2. M block 3. Alpha block 4. Sedation |
|
|
|
Typical antipsychotics: Name the drug?
|
1. Thioridazine
2. Haloperidol 3. Chlorpromazine 4. Fluphenzine "Sulphur and (typical) halogens: fluorine and chlorine" |
|
|
|
Typical Antipsychotic with minimum EPS side effects?
|
Thioridazine
"ThioRIDazine" is RID off EPS side effects. Also RIDS you off- i. M effects ii. Alpha effects iii. alertness (sedation) |
|
|
|
Thioridazine: side effects?
|
Side effects due to
1. M block, 2. alpha block 3. Sedation 4. RETINAL DEPOSITS |
|
|
|
Typical antipsychotic associated with:
1. Corneal deposits 2. Retinal deposits |
1. Corneal deposits: Chlorpromazine
2. reTinal deposits: Thioridazine |
|
|
|
Antipsychotic associated with Neuroleptic Malignant syndrome?
|
HALOperidol
Recollect that HALOthane also causes malignant hyperthermia |
|
|
|
Antipsychotic that is most likely to produce Tardive Dyskinesia?
|
HALOperidol
(Halo: all spartans are moving/fighting all the time- tardive dyskinesia) |
|
|
|
Antipsychotics with maximum EPS side effects?
|
HALOperidol
Fluphenazine |
|
|
|
Antipsyhotics with maximum sedation?
|
Thioridazine and Chlorpromazine
|
|
|
|
Antipsychotics with maximum alpha block?
|
1. Thioridazine
2. Chlorpromazine 3. Clozapine (Thio=Sulphur=Sedation) |
|
|
|
Antipsychotics with minimum sedation?
|
1. Haloperidol and
2. Fluphenazine (When you are playing HALO and having FUN you ain't sedated) |
|
|
|
Atypicals antipsychotics: Name em?
|
1. Quetapine
2. Risperodone 3. Aripiprazole 4. Olanzepan 5. Clozapine "Queen Rania Aids Orphans and Children" |
|
|
|
The only antipsychotic with no EPS block?
|
Clozapine
(EPS are CLOZed and shut down) |
|
|
|
Features of atypical antipsychotics?
|
1. D receptor block AND
2. 5 HT-2 receptor block. |
|
|
|
Why are EPS never observed with clozapine?
|
Because it blocks just D2C receptors and not D2A
|
|
|
|
Clozapine: Adverse effects?
|
1. Agranulocytosis
2. Weight gain 3. "Wet pillow syndrome" 4. Seizures (WWW and seizures) WBC-agranulocytosis Weight gain Wet pillow |
|
|
|
2nd line drug used after clozapine in a patient with agranulocytosis?
|
Olanzapine
|
|
|
|
Partial agonist antipsychotic?
|
Aripiprazole
(AriPiprazole: Agonist Partial) |
|
|
|
Ariprazole: MOA?
|
Partial agonist at D2 receptors
|
|
|
|
Antipsychotics with available parenteral forms?
|
Haloperidol and
Fluphenazine |
|
|
|
Atypical antipsychotic with maximum alpha block?
|
Clozapine
|
|
|
|
Atypical antipsychotic with maximum muscarinic block?
|
Olanzapine
|
|
|
|
Typical antipsychotics chiefly block ____receptors.
|
D2A
|
|
|
|
Antipsychotic that specifically acts only on D2C receptor?
|
Clozapine
|
|
|
|
MAO-A inhibitors: use?
effect? |
Atypical depression: Depression that does not respond to reuptake inhibitors
Effect: Increases NE and serotonin levels |
|
|
|
MAO-A inhibitors: drug interactions
|
I. Increased NE: Hypertensive crysis
1. Tyramine 2. TCAs 3. Alpha-1-agonists 4. Levodopa II. Serotonin syndrome: 1. SSRIs 2. TCAs 3. Meperidine |
|
|
|
Serotonin syndrome: symptoms?
|
1. Sweating
2. Rigidity 3. Myoclonus 4. Hyperthermia 5. Seizures |
|
|
|
Serotonin syndrome: rx?
|
Cyproheptadine
|
|
|
|
TCAs: Name em?
|
1.Amitryptyline
2. Imipramine 3. Clomipramine |
|
|
|
TCA used for neuropathic pain?
|
Amitryptyline
ABC for neuropathic pain Amitryptyline |
|
|
|
TCA used for enuresis?
|
Imipramine
|
|
|
|
TCA used for Obsessive Compulsive disorder?
|
Clomipramine
Clomipramine for Compulsive disorder |
|
|
|
TCA MOA?
|
1. 5HT and NE reuptake inhibitor
2. A/muscarinic block 3. Alpha-1 block |
|
|
|
TCA uses?
|
1. Major depression
2. Anxiety states (phobia/panic) 3. Obsessive-compulsive disorder 4. Neuropathic pain 5. Enuresis 6. Fibromyalgia |
|
|
|
TCAs: Side effects?
|
Alpha-1
Muscarinic blockade 3Cs: 1. Cardiotoxicity 2. Coma 3. Convulsions HYPERPYREXIA RESPIRATORY DEPRESSION |
|
|
|
TCAs: drug interactions?
|
1. Hypertensive crysis with MAO-A
2. Serotonin syndrome: SSRIs, meperidine, MAO-A inhibitors 3. Interferes with guanethidine and alpha-2 agonists |
|
|
|
SSRIs: drugs?
|
1. Fluoxetine
2. Paroxetine 3. Sertraline |
|
|
|
SSRI: MOA?
|
Selective block of 5-HT reuptake
|
|
|
|
SSRI: uses?
|
Major depression
OCD Bulimia Anxiety disorder Premenstrual dysphoric disorder |
|
|
|
SSRIs: side effects?
|
1. Anxiety/Agitation
2. Bruxism 3. Anorgasmia 4. Weight loss |
|
|
|
SSRI always co-administered with?
|
Alprazolam
Why are SSRIs co-administered with Alprazolam? |
Initial administration of SSRIs has no antidepressant effects but instead produces agitation/anxiety---> suicide
Alprazolam controls agitation and anxiety |
|
|
SSRIs: drug interactions?
|
1. Serotonin syndrome with:
i. TCAs ii. MAO-A inhibitors iii. Meperidine |
|
|
|
Drugs used in smoking cessation?
|
1. Bupropion
2. Varenicline MOA of both? |
Bupropion: Dopamine reuptake blocker
Varenicline: Partial nicotinic agonist |
|
|
Antidepressant associated with priapism and cardiac arrhythmias?
|
Trazadone
("TrazaBONEr") MOA of trazadone? |
Serotonin re-uptake inhibition
Strong alpha-1 blocker |
|
|
Venlafaxine: MOA?
|
Non selective reuptake blocker
NO AUTONOMIC EFFECTS SNRI |
|
|
|
Antidepressant used in anorexia nervosa?
|
Mirtazapine
MOA? Side effects? |
MOA:
Alpha-2 antagonist--->NE release 5HT-2and 5HT-3 antagonist Side effects: 1. Sedation 2. Weight gain 3. Dry mouth |
|
|
DOC for bipolar disorders?
|
Lithium
|
|
|
|
Lithium: MOA?
|
1. Prevents recycling of inositol
--> Reduces DAG and IP3 levels 2. ***Decreases cAMP*** |
|
|
|
Lithium: Side effects?
|
1. Seizures
2. Hypothyroidism 3. Nephrogenic diabetes insipidus 4. Ebstein's anomay (Teratogenic) OR LMNOP to recall Lithium adverse effects, Movement [tremor], Nephrogenic diabetes insipidus, HypOthyroidism, Pregnancy problems) |
|
|
|
Lithium may be succesfully removed from the system/body with ______
|
1. Ameloride
2. Triampterene |
|
|
|
Drugs used in bipolar disorder?
|
1. Valproic acid
2. Carbamazepine 3. Gabapentin 4. Lithium |
|
|
|
DOC for bipolar disorder in pregnancy?
|
Gabapentin
|
|
|
|
Teratogenic effect of lithium?
|
Ebstein's anomaly
|
|
|
|
Hypothyroidism in lithium toxicity: why?
|
1. Lithium inhibits peripheral de-iodinase (T4-->T3)
2. Lithium antagonizes effect of TSH |
|
|
|
Diabetes insipidus in lithium toxicity: why?
|
Lithium reduces cAMP
ADH increases cAMP therefore ADH effect neutralized by Li |
|
|
|
Drugs used in ADHD and MOA?
|
1. Methylphenidate: Amphetamine like
2. Atomoxetine: NE re-uptake blocker Side effect profile of: Methylphenidate: Insomnia Restlesness CVS toxicity Atomoxetine: Side effect: TCA side effects |
|
|
|
Cocaine: MOA?
|
1. Na channel blocker
2. NE reuptake inhibition 3. 5HT reuptake inhibition 4. Dopamine reuptake inhibition |
|
|
|
Amphetamines: MOA?
|
1. Dopamine reuptake inhibitor
2. NE reuptake inhibitor 3. NE releaser 4. Dopamine releaser 5. MAO inhibitor |
|
|
|
Increased NE effects?
|
1. Central excitation
2. CVS stimulation (BP and HR) 3. Mydriasis |
|
|
|
Increased 5HT effects?
|
1. Aggressive behavior
2. Weight loss (appetite loss) 3. Dyskinesia (?) |
|
|
|
Increased dopamine effects?
|
1. Psychosis (hallucinations etc)
2. Dyskinesia 3. Endocrine problems (prolactin etc) 4. Temperature - hypothermia(?) |
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Cocaine toxicity?
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Due to NE release:
1. MI 2. Strokes 3. Nasal septum infarct 4. Cardiac arrhythmias Excess Dopamine: 1. Psychosis 2. Cocaine 'delirium' Excess 5HT: 1. Serotonin syndrome |
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Amphetamine toxicity?
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Due to NE release:
1. MI 2. Strokes 3. Cardiac arrhythmias Excess 5HT: 1. Serotonin syndrome |
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Opioids: associated neurotransmitters involved?
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1. NE
2. DA 3. 5HT 4. GABA |
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Opioids effects?
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1. Sedation
2. Euphoria 3. Cough suppression 4. Constipation 5. Miosis 6. Respiratory depression |
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Opioid toxicity?
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Severe respiratory depression
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Centre of the brain associated with addiction?
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Nucleus accumbens.
(You get addicted: you get "accustomed" : nucleus accumbens) |
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Opioid withdrawal: effects?
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1. Yawning
2. Lacrimation 3. Rhinorrhea 4. ANS stimulation 5. Tremendous pain (centrally originating) 6. Muscle cramping **Not Fatal** |
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Marijuana:
MOA? Effects? |
MOA:
CB1 and CB2 receptor stimulation Effects: 1. Hallucinations/delusions 2. Euphoria 3. Sedation 4. Tachycardia(vasodilation) 5. Red conjunctive (vasodilation) |
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Cocaine withdrawal?
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1. Depression- Severe
2. Anhedonia 3. Anxiety |
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Marijuana toxicity?
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Associated with smoking
Flashbacks |
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Marijuana withdrawal?
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Irritability
Anxiety |
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PCP(phencyclidine) MOA? effects(adverse)?
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NMDA receptor antagonist
(glutamate) Effects: 1. Dissociation 2. Paranoia 3. Rhabdomyolysis 4. Convulsions/death 5. Nystagmus NYSTAGMUS ATAXIA (Muscle inco-ordination) HYPERTENSION TACHYCARDIA DETACHMENT |
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Ketamine: MOA? effects?
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NMDA/glutamate receptor antagonist
effects: 1. Hallucinations 2. Paranoia 3. Rhabdomyolysis 4. Convulsions |
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MDMA: "Ecstasy": MOA?
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Similar to amphetamines
Hallucinogenic Neurotoxic dehydration |
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Inhalant: effects?
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Multiple organ damage
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Drugs of abuse with intense abuse liablity?
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Opioids
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Milder version of PCP?
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Ketamine
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Butarphanol: MOA?
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Partial agonist at Mu receptor
Agonist at kappa receptor |
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What effect may L-dopa have on the heart?
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Arrhythmias
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What is the benefit of butorphanol over other opioid analgesics?
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Butorphanol causes less respiratory depression than full agonists
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What changes in neurotransmitter release result from opioid receptor agonists?
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They inhibit release of acetylcholine, norepinephrine, serotonin, glutamate, and substance P
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What is the toxic effect of tramadol?
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Decreases seizure threshold
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Amantadine is effective against which viral infections?
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Influenza A
Rubella |
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Which analgesic drug is a weak opioid agonist and inhibitor of serotonin and norepinephrine uptake?
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Tramadol
(Decreases release Decreases reuptake of neurotransmitters) |
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What is the toxicity of butorphanol?
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Withdrawal if a patient is on a full opioid agonist, due to its partial agonist activity
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Which two opioid agonists are used to alleviate diarrhea?
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Loperamide and diphenoxylate
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Amantadine toxicity is characterized by what symptom?
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Ataxia
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For which parkinsonian symptoms is benztropine effective?
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Tremor and rigidity, but not bradykinesia (remember: decrease your tremor before you drive your Mercedes-BENZ)
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What is the drug class of choice for treating anorexia and bulimia?
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SSRIs
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What are the three first-line drug classes for the treatment of depression?
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Serotonin-norepinephrine reuptake inhibitors, selective serotonin reuptake inhibitors, and tricyclic antidepressants
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Name the tricyclic antidepressants.
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Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin, and amoxapine
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A patient presents with depressed mood, decreased interest, decreased appetite, and poor sleep. He reports sleeping only approximately 3 hours a night. What are two treatment options for this patient?
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Trazodone and mirtazapine; both are sedating antidepressants
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What two drug classes are used in the treatment of atypical depression?
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Monoamine oxidase inhibitors and selective serotonin reuptake inhibitors
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It normally takes how many weeks for an antidepressant to show some clinical benefit?
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2-3 weeks
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What neurotransmitter receptors are blocked by mirtazapine?
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An a2 - and serotonin antagonist
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Typical antipsychotics block which receptors?
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D2
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What is the mechanism of action of buspirone (a psychiatric medication)?
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It stimulates serotonin receptors (class 1A receptors)
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Neuroleptic malignant syndrome?
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FEVER:
Fever(hyperthermia) Encephalopathy Vitals- unstable Elevated enzymes Rigidity |
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A patient presents with priapism after starting an antidepressant medication for insomnia and depression. What medication is this patient taking?
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Trazodone, which is a heterocyclic antidepressant
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What are the three first-line drug classes for the treatment of anxiety?
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1. SSRIs
2. BZDs 3. Buspirone 4. Venlafaxine |
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What is the treatment for Tourette"s syndrome?
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Antipsychotics; often haloperidol
Pimozide(?) |
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PTSD: first line of drug for treatment?
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SSRIs
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Do monoamine oxidase inhibitors work on noradrenergic neurons, serotonergic neurons or both?
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Both
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Maprotiline: MOA?
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NE reuptake inhibitor
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What is the least sedating tricyclic antidepressant?
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Desipramine
("Desi banda jab prem mein padta hai to use neend nahi aati") |
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A patient with a history of bipolar disorder, controlled with lithium, presents with massively increased urination and thirst. Can this patient be treated with exogenous antidiuretic hormone?
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No, this patient is suffering from nephrogenic diabetes insipidus secondary to lithium use, which will not respond to antidiuretic hormone
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Why might a patient complaining of sedation with a prior antidepressant be prescribed bupropion?
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Bupropion may cause insomnia
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Sedation in neuroleptics observed due to _______ effects
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Antihistaminic
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What is the treatment for neuroleptic malignant syndrome?
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Dopamine agonists and dantrolene
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What might be seen on an electrocardiogram of a patient taking lithium?
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Electrocardiogram consistent with heart block
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Atypical antipsychotic medications block what type of receptors in addition to dopamine receptors?
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5-hydroxytryptamine2, α, H1
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Which neuroleptics are low-potency drugs with a low incidence of neurologic adverse effects?
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Thioridazine and chlorpromazine
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Bupropion is ______antidepressant
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Heterocyclic
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Which neuroleptics are high-potency drugs with neurologic adverse effects?
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Haloperidol, fluphenazine, and trifluoperazine
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What are the three first-line drugs (all mood stabilizers) for the treatment of bipolar disorder?
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Lithium, valproic acid, and carbamazepine; atypical antipsychotics can also be used
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What extrapyramidal adverse effect of neuroleptics is irreversible?
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Tardive dyskinesia
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Bupropion is contraindicated in what patients?
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Patients with bulimia or history of seizure disorders
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What adverse effects are avoided with use of buspirone?
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Sedation, addiction, and tolerance, which are seen with benzodiazepines and barbiturates
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What are the major toxicities of tricyclic antidepressant overdose?
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3Cs
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What two drugs or drug types are used in the treatment of obsessive-compulsive disorder?
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Selective serotonin reuptake inhibitors and clomipramine
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Maprotiline, a heterocyclic antidepressant, blocks the reuptake of what substance?
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Norepinephrine
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A patient on haloperidol experiences torticollis and tremor. What is an alternative treatment option?
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Atypical antipsychotics, because these drugs have a lower risk of extrapyramidal symptoms
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What tricyclic antidepressant should be used in the elderly to treat depression, to lessen the chances of anticholinergic adverse effects?
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Nortriptyline
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What are the indications for venlafaxine?
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Depression and generalized anxiety disorder
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Atypical antidepressants useful in treating _____ (positive/negative/both) types of schizophrenia symptoms.
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Both
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How is tricyclic antidepressant toxicity treated?
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Intravenous NaHCO3 to prevent cardiac arrhythmias(cardiotoxicity)
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Antidepressant drug class used to treat fibromyalgia?
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TCAs
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TCA drug with minimum seizure related complication?
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Desipramine
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What are the indications for atypical antidepressant use?
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Schizophrenia, mania, Tourette"s syndrome, and obsessive-compulsive disorder
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Which antidepressant is commonly used for insomnia?
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Trazodone
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True or False? Sexual adverse effects are major adverse effects of bupropion.
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False; bupropion is the one heterocyclic antidepressant that does not cause sexual adverse effects
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A patient on treatment for depression presents with a temperature of 105° F and rigidity. What is the treatment for this condition?
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Cyproheptadine, a serotonin receptor antagonist
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Name the monoamine oxidase inhibitors.
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Phenelzine and tranylcypromine
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What is the most common adverse effect of long-term atypical antipsychotic use?
|
Severe weight gain, which can lead to type II diabetes
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What are the adverse effects of mirtazapine?
|
Sedation, increased appetite, weight gain, dry mouth
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An elderly patient presents to the emergency room with delirium associated with hallucinations of her deceased husband. She recently started a new drug for depression. What could cause her presentation?
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The anticholinergic effects of her depression treatment (tricyclic antidepressant)
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Place the following extrapyramidal adverse effects of neuroleptics in the order in which they occur: akathisia, akinesia, dystonia, tardive dyskinesia.
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Dystonia (within 4 hours), akinesia (within 4 days), akathisia (within 4 weeks), and tardive dyskinesia (after 4 months)
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A patient presents with rigidity, myoglobinuria, autonomic instability, and hyperpyrexia after recently starting a medication for schizophrenia. What adverse effect is this patient experiencing?
|
Neuroleptic malignant syndrome; he should be treated with dantrolene and bromocriptine
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Duloxetine:
MOA? Uses? |
MOA: SNRI
Uses: General anxiety Depression Peripheral neuropathy |
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What are the symptoms of acute dystonia? When does dystonia develop after use of neuroleptics?
|
Abnormal muscle contractions and involuntary twisting movements; it usually develops 4 hours after drug administration
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Name two serotonin-norepinephrine reuptake inhibitors.
|
Venlafaxine, duloxetine
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What is the reason for the long half-life of neuroleptics?
|
They are highly lipid soluble, so there is a large volume of distribution; therefore, it takes a long time for them to be removed from the body
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How do antipsychotics cause galactorrhea?
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Dopamine receptor antagonism releases inhibition on the prolactin-secreting cells of the pituitary
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