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VW B1 CNS Pharm
IS-B1-CNS Pharm
| Question | Answer |
|---|---|
| Dose dependent decrease in firing rate of critical neurons throughout brain. GABAergic activation leads to sedation, reduced anxiety and pharmacologic hypnosis | Benzodiazepine Effect |
| Binds GABA-A channels, allosterically increases ability of GABA to bind its site. Increased FREQUENCY of opening of GABA bound GABA-A channel. Increase in GABA-mediated Cl- conductance (hyperpolarizes neuronal membranes). No profound anesthesia. | Benzodiazepine MOA |
| Additive effects with other sedative-hypnotics. Drug interactions with CYP inhibitors and inducers. Valproate and benzodiazepines may cause psychotic episodes | Benzodiazepine Drug Interactions |
| Dose-dependent: motor incoordination, amnesia. headache, diplopia, vertigo, nausea and vomiting, GI distress. Psych disturbances and dependence (withdrawal symptoms including: ortho hypotension, and T/C seizures.Less dependence than short benzos | Benzodiazepine Toxicity |
| Clinical Use: Anxiety, Ethanol Withdrawal, Preanesthetic. Long Acting. Active Metabolites | Chlordiazepoxide |
| Clinical Use: Anxiety, Status Epilepticus, Seizure Disorders, Skeletal Muscle Relaxation, Preanesthetic, Ethanol Withdrawal. Long Acting. Active Metabolites. Erratic IM bioavailability. | Diazepam |
| Clinical Use: Insomnia ONLY. Long Acting. Active Metabolites | Flurazepam |
| Clinical Use: Insomnia, Anxiety. Long Acting. Active Metabolites. | Quazepam |
| Clinical Use: Seizures, Mania, Movement Disorders. Intermediate Acting. | Clonazepam |
| Clinical Use: Anxiety, Seizures, Ethanol Withdrawal. Intermediate Acting. PRODRUG activated in stomach. Active Metabolites. | Clorazepate |
| Clinical Use: Insomnia ONLY. Intermediate Acting. NO active metabolites. | Estazolam |
| Clinical Use: Anxiety, Preanesthetic, Seizure, Insomnia. Intermediate Acting. No active metabolites. NON-LIVER metabolism. | Lorazepam |
| Clinical Use: Anxiety, Ethanol Withdrawal. Intermediate Acting. No active metabolites. NON-LIVER metabolism. | Oxazepam |
| Clinical Use: Insomnia ONLY. Intermediate Acting. Slow oral absorption. No Active Metabolites. NON-LIVER metabolism. | Temazepam |
| Clinical Use: Anxiety, Agoraphobia. Short Acting. Rapid oral absorption. No Active Metabolites. | Alprazolam |
| Clinical Use: Insomnia ONLY. Short Acting. MOST RAPID ONSET. Short DOA. | Triazolam |
| Clinical Use: Preanesthetic and Intraoperative. Short Acting. MOST RAPIDLY METABOLIZED. No active metabolites. | Midazolam |
| Reverses effects of Benzos and "Z's". Competitively inhibits binding of benzos on GABA-A receptors. Clinical Use: Benzo overdose. Short duration. Rapid 1st pass. IV only. Tox: confusion, vertigo, nausea, induce seizure in Benzo dependents. | Flumazenil |
| decrease in firing rate of critical neurons throughout the brain. GABAergic activation-sedation, reduced anxiety and hypnosis. at high doses can activate GABA channels directly (without GABA) and inhibit Na+ currents-general anesthesia | Barbiturate - Effects |
| Low doses--binds allosterically to GABA-A channels and prolongs DURATION of opening of GABA bound GABA-A channels resulting in and increase in GABA-mediated Cl- conductance High doses activate GABA channels directly, inhibit Na+ | Barbiturates MOA |
| Severe depression in combination with other CNS depressants (like alcohol), Isoniazid, methylphenidate and MAOI. Induction of hepatic microsomal enzymes effecting metabolism of other drugs, steroid hormones (BCPs). Metabolism of vit. D and K accelerated | Barbiturates Drug Interactions |
| therapeutic doses: similar to benzo; drowsiness, residual effects including vertigo, GI. Paradoxical excitement. Enhancement of porphyrin synthesis. Barbiturate Poisoning: respiratory depression, comatose, hypotension (inhibits autonomic ganglia). | Barbiturates Toxicity |
| Contraindications: Patients with Porphyria (enhanced porphyrin synthesis). Patients with respiratory depression. | Barbiturates Contraindications |
| Clinical Use: 2nd line for simple partial, and grand mal Seizures, adjunct for Status Epilepticus, Daytime Sedation. Oral, IM and IV | Phenobarbital |
| Clinical Use: Insomnia, Preanesthetic, Emergency Mgmt of Seizures. Oral, IM and IV. Na+ salts only for parenteral admin. | Amobarbital and Pentobarbital |
| Clinical Use: Insomnia ONLY. Oral only. Excreted Unchanged. | Aprobarbital |
| Clinical Use: Insomnia, Preanesthetic. Oral only. Redistribution reduces duration. | Butabarbital Sodium |
| Clinical Use: Seizures (2nd line), Daytime Sedation. Oral only. | Mephobarbital |
| Clinical Use: Insomnia, Preanesthetic, Emergency Mgmt of Seizures. Oral, IM, IV and RECTAL. Na+ salts only for parenteral admin. | Secobarbital |
| Clinical Use: Preanesthetic, Induction of Anesthesia, Emergency Mgmt of Seizures. IV, Rectal only. Sodium Salt. | Thiopental |
| MOA: partial agonist of 5-HT (1A, D2) receptor. Clinical Use: GAD. Weeks to establish, extensive 1st pass. Active Metabolites. Interactions: Rifampin, ^ and v CYP3A4. Tox: Tach, GI. Pupil Constrict. ^ BP w/ MAOI. | Buspirone |
| Similar to Barbs. Clinical Use: Sedation in Children. Oral and Rectal. Converted to Trichloroethane (active metabolite). Tox: acute: GI distress. Chronic: Hepatic Damage, withdrawal. | Chloral Hydrate |
| Similar to Barbs. Clinical Use: Sedation. Oral. Redistribution shortens duration. Interactions: enhances hepatic metab of oral anticoagulants. Tox: GI, hypotension, facial numbness. Excitement with pain. Contrain: Porphyria | Ethchlorvynol |
| Similar to Barbs. Antihistamine. Clinical Use: Anxiety and Insomnia. Oral. Tox: GI. Idiosyncratic excitement, fever, thrombocytopenia | Hydroxyzine |
| Similar to Barbs. Clinical Use: Anxiety, Muscle Relaxant. Oral. Tox: overdose can cause severe hypotension, resp depression and death. | Meprobamate |
| Similar to Barbs. Clinical Use: Delirium in Hospitalized patients. Oral or rectal damages tissues. IV. 75% metab in liver, 25% exhaled. | Paraldehyde |
| Decrease in firing rate of specific neurons that contain BZ1 subtype of GABA-A channels. | BDZ1 Subclass drug effects |
| Selectively binds allosterically to the BZ1 (omega1)-GABA-A channel increases FREQUENCY of opening of GABA bound GABA-A channels resulting in and increase in GABA-mediated Cl- conductance (hyperpolarizes neuronal membranes) | BDZ1 Subclass drug MOA |
| CYP P450 inducers decrease T1/2 and inhibitors increase T1/2 | BDZ1 Subclass drug interactions |
| similar to diazepam but with minimal muscle relaxing and anticonvulsant effects as well as less development of tolerance and dependence. Reduced alteration in normal sleep architecture as compared to other sedative hypnotics | BDZ1 Subclass drug toxicities |
| Clinical Use: Insomnia. Short Acting. Metabolized by CYP3A4. T1/2 1.5 - 3.5 hours | Zolpidem |
| Clinical Use: Insomnia. Short Acting. Metabolized by CYP3A4. T1/2 1 hours | Zaleplon |
| Clinical Use: Insomnia. Short Acting. T1/2 6 Hours. Metabolized by CYP3A4 | Eszopiclone |
| Melatonin recep agonist (MT1 and 2suprachismatic nuclei). Clin Use: Insomnia. No interact with GABA receptors. Liver CYP1A2 and CYP2C9 inhibitors. *^ conc.of Cipro, fluvoxamine, tacrine, and fluconazole. Tox: endocrine (v testosterone, ^ prolactin). | Ramelteon |
| state dependent Na+ channel blockade, prolongs inactivated state, Ca++ mediated neurotransmitter release | Hydantoin Class MOA |
| Induces CYP 3A4 enzymes (many drug interactions, .eg. increases metabolism of BCP). Isoniazid, fluoxetine, sulfonamides increase levels. Altered folate metabolism. Serum protein binding effected by other drugs. Binds thyroid-binding globulin. | Hydantoin Class Drug Interactions |
| Clinical Use: 1st choice partial seizures. Used for T/C Seizures. In combo for Status Epilepticus. Neuropathic pain. Trigeminal Neuralgia. Pk - Oral dose dependent metabolism. Prep contains propylene glycol (cardiotoxic). | Phenytoin |
| Toxicities: Neurologic - nystagmus, ataxia, diplopia, incoordination, confusion, sedation neuropathy. Systemic: gingival hyperplasia, osteomalacia, skin rash, idiosyncratic reactions. | Phenytoin and Fosphenytoin Toxicities |
| Clinical Use: 1st choice partial seizures. Used for T/C Seizures. In combo for Status Epilepticus. Neuropathic pain. Trigeminal Neuralgia. IV and IM. No PEG (safe for cardio). Converted to phenytoin in body. | Fosphenytoin |
| Clinical Use: similar to phenytoin but less efficacious. Nivanol is active metabolite. Tox: increased dermatitis, agranulocytosis or hepatitis. | Mephenytoin |
| This drug is similar to phenytoin but has less severe toxicities. | Ethotoin |
| similar to phenytoin, also inhibition of catecholamine uptake | Tricyclic Class MOA |
| good oral absorption, plasma protein bound (not displaced by other drugs), induces microsomal enzymes, active metabolites | Tricyclic Class P-kinetics |
| CYP inducers (e.g. phenobarbital and phenytoin) may increase and inhibitors (erythromycin, isoniazid, cimetidine, fluoxetine) may inhibit metabolism. Is a CYP inducer itself so metabolism of phenytoin, barbiturate, and contraceptives may be increased. | Tricyclic Class Drug Interactions |
| Acute: stupor or coma, hyperirritability, convulsions, and respiratory depression. Chronic: drowsiness, vertigo, diplopia, and blurred vision. Hematologic (aplastic anemia, leukopenia), hepatotoxicity, hyponatremia, SJS (skin rash) in Asians - HLA allele | Tricyclic Class Toxicities |
| Clinical Use: 1st choice partial seizures. Used for T/C Seizures. Neuropathic pain. Trigeminal Neuralgia. Mania, Mood Stabilization. Dementia. | Carbamazepine |
| Similar to Carbamazepine but less potent and less toxic | Oxcarbazepine |
| Similar to phenytoin with active metabolite = phenobarbital. Metabolized to PEMA and phenobarbital - steady state after 20 days. | Primidone |
| Similar to phenytoin, inhib Ca++ channels and glutaminergic receptors. Clin Use: 1st line T/C seizures, monotherapy for partial seizures in adults. Myoclonic. Atypical Absence. Lennox Gastaut. Alt. therapy for absence seizures. Bipolar Depression. | Lamotrigine - Clinical Use |
| Rapid absorption, 55% protein bound. Valproate doubles T1/2, decreased by CYP inducing drugs and BCPs. Tox: Neuro, diplopia, somnolence, ataxia. Skin rash. SJS in children | Lamotrigine - Kinetics, interactions and Tox |
| NMDA block. Clinical Use: 3rd line refractory partial seairues, Lennox Gastaut. Interact: increased plasma phenytoin and valproic acid, decreased carbamazepine. Tox: aplastic anemia and hepatitis (why 3rd line) | Felbamate |
| Kainate and AMPA receptor inhib. Like GABA inhib effects. Clin Use: 1st line T/C seizures, atyp absense, myoclonic, atonic, Lennox-Gastaut and West's syndrome. Migraines! Slow admin! BCP less effective. Tox: 1st month. Urolithiasis. Teratogenic | Topiramate |
| Inhibits GABA transaminase (more GABA release). Clin Use: Partial seizures, West's, infantile spasm. RENAL elimination. Tox: Drowsiness, vertigo, weight gain, psychosis, visual field, intramyelinic edema. | Vigabatrin |
| Alters GABA metab. Decreased Ca++ entry. Clin Use: Adjunct for partial seizures, neuropathic pain, Migraines. RENAL elimination. Short T 1/2. No hepatic enzymes = no drug interactins. Tox: vertigo, headache, tremor, somnolence. | Gabapentin and Pregabalin |
| Inhibits GABA upatek (GAT-1 transporter). Clin Use: Adjunct partial seizures. Oral, good bioavail. No effect on other seizure durgs. Tox: nervous, vertigo, tremor, concentration, depression. Psychosis, confusion, Rash. | Tiagabine |
| Inhibits Na+, ^ GABA levels. Clin Use: 1st line T/C, partial and absence, atyp absence and myoclonic. Bipolar, Migraine. P-k: protein bound.Inter: displaces phenytoin. Inhibits pbarb,carba and pheny). Tox: GI, hepatotox (kids <2), thromcypenia, defects. | Valproic Acid |
| Increased CO2 decreasing depolarizing action of bicarb ions. Diuretic. Inhibits Ca. Clinical Use: Epileptic women during menses. | Acetazolamide |
| Raises threshold of thalamic firing. Inhibits gCA++, Na+/K+atpase and GABA aminotransferase. Clin Use: 3rd line Absence Seizures. Liver metabolized. Tox: Hemeralopia, metabolic acidosis, derm and reversible nephrotic syndrome. | Trimethadione |
| Reduce thalamic firing. Inhibits gCA++, Na+/K+atpase and GABA aminotransferase. Clin Use: 1st line Absence Seizures. Oral, partitions in water compartments, metab in liver. Inter: Valproic acid v clearance. Tox: GI, lethargy, rash, marrow suppression. | Ethosuximide |
| Interferes with synaptic vesicle SV2A. Clin Use: Adjunct partial seizures. Excreted in urine. Tox: somnolence, asthenia, anemia, leukopenia. | Levetiracetam |
| Na and Ca channel conductance. Clin Use: Adjunct partial and T/C seizures, myoclonic and infantile spasms. Tox: drowsiness, cognitive impairment. | Zonisamide |
| Clinical Use: Epilepsy Patients with Porphyria. Tox: skin rash, sedation, behavioral changes. | Bromide |
| Inhances activation of Na+ channels, blocks CRMP-2. Clinical Use: Adjunct Partial seizures. Tox: vertigo, headache, nausea, diplopia. | Locosamide |
| Depresses spontaneous and evoked activity of neurons either by the Meyer-Overton hypothesis on ion conductance or by direct activation of the GABA-A chloride channel, activation of ligand gated K+ channels or inhibition of nicotinic Ach receptors or all | Fluranes / Gas MOA |
| Decrease tidal volume, increase rate, decrease in minute ventilation, respiratory depressant (reduce responses to CO2 and hypoxia), pooling of mucus, loss of gag reflex (regurgitation and subsequent aspiration of stomach contents) | Fluranes Respiratory Effects |
| Decrease metabolic rate, increased cerebral blood floor (decrease in vascular resistance) = not good choice for neurosurgery | Fluranes Neuro Effects |
| Use: Induction or Maintenance. Decrease in mean arterial pressure. Bradycardia, increase in right atrial pressure. Medium onset, recovery and solubility. Tox: hepatotox, fluoride ion production (nephrotox), malig hyperthermia. | Halothane |
| Similar to Halothane with fewer HR effects, decrease in CO. Less Hepatotox. | Enflurane |
| Use: Maintenance only. Transient tach due to symp discharge, decrease vascular resistance. Poor induction agent, rapid recovery. | Desflurane |
| Use: Induction or Maintenance. Similar to Halothane. Slow onset and recovery. Less hepatotox, more renal tox. | Methoxyflurane |
| Use: Induction or Maintenance. Transient tach due to symp discharge, decrease vascular resistance. Medium onset, recover and solubility. Less hepatotox, more renal tox. | Isoflurane |
| Similar to Halothane, rapid onset and recovery. Less hepatotox. | Sevoflurane |
| Use: Induction, in combinate to reduce dose of others. Produces symp discharge, balance negative effects of other inhalants. Rapid onset and recovery. Tox: Amnesia, hypoxia. | Nitrous Oxide |
| Similar to Thiopental - used as general anesthetic. | Methohexital and Thiamylal |
| Use: Induction or Maintenance. Antiemetic properties for day surgery. Rapid onset and recovery. Decrease in systemic BP, negative inotropic effects. Tox: hypotension, apnea, pain. Expensive. Acidosis in children. | Propofol |
| Use: CV Stability, decrease steroidogenesis. Rapid onset and Moderately fast recovery. Good choice for CV Surgeries. Tox: involuntary muscle movements, GI, pain, adrenocortical suppression, hypotension, electrolyte imbalance and oliguria. | Etomidate |
| Use: Dissociative anest, induction children, geriatric (poor risk) and CV shock. Moderately rapid onset and recovery. NMDA inhib. CV stimulation. Increases cerebral blood flow, O2 consumption. Tox: vivid dreams, illusions. Contra: ^ intracranial pressure. | Ketamine |
| Use: Balance with anesthesia. Neuroleptanesthesia, CV stability, marked analgesia. Slow onset and recovery. Naloxone reversal avail. | Opioids: Fentanyl, Remifentanil, Alfentanil |
| state dependent blockade of voltage-dependent sodium channels, prevent depolarization and conduction of action potentials in excitable cells especially neurons when localized next to neurons | Local Anesthetic MOA |
| Most sensitive: rapid firing, small diameter "C" fibers and medium firing, medium diameter, myelinated B sympathetic preganglionic fibers. Least sensitive: Large diameter, slow firing, myelinated "A" type motor neuron fibers. | Local Anesthetic Nerve Selectivity |
| widely distributed if not locally injected. Weak base must be lipophilic to pass membrane and block channels, hydrophilic to bind to channel. pH dependent ionization important Hydrolyzed rapidly via butyrylcholinesterase. Except benzocaine - topical only | Ester Pharmacokinetics |
| Long Acting. Tox: CNS, respiratory and cardio collapse. Permanent nerve damage. Vasodilator, heart block, arrhythmias, hypotension. Metabolites -> hypersensitivity reactions. | Tetracaine |
| Medium Acting. Tox: CNS, respiratory and cardio collapse. Permanent nerve damage. Blocks Norepi reuptake - VASOCONSTRICTION, hypertension, cerebral hemorrhage, arrhythmias and MI's. | Cocaine |
| Short acting version of Tetracaine | Procaine |
| Surface active version of Ester | Benzocaine |
| similar in absorption and distribution and ionization to esters. Metabolism via CYP in liver (longer duration), liver function important in metabolism. Most bound by plasma protein, which effects clinical effect and toxicity | Amides Pharmacokinetics |
| Similar to Tetracaine with more cardiotoxic effects | Bupivacaine |
| Long Acting and Similar to Tetracaine | Ropivacaine and Etidocaine |
| Medium Acting and Similar to Tetracaine | Lidocaine and Mepivacaine |
| Medium Acting, Similar to Tetracaine. Metabolized to products which can cause methemoglobinemia (treat with methylene blue) | Prilocaine |
| Alters membrane-bound neuronal ion conductance and GPCR receptors: Acute decrease NMDA channel conductance and increase GABA-A cl- channel conductance. Chronic exposure: adaptive changes in channel number. | Ethanol - MOA |
| Clinical Use: Methanol and Ethylene Glycol poisoning. IV to saturate alcohol dehydrogenase. | Ethanol - Clinical Use |
| Acute Mgmt: prevent respiratory depression and aspiration, glucose to manage hypoglycemia and thiamine to protect against Wernicke-Korsakoff syndrome | Ethanol - Acute Management |
| Withdrawal Mgmt: Withdrawal symptoms (motor agitation, anxiety, insomnia, seizures, visual hallucinations, delirium tremens): Mild-thiamine, restore electrolytes. Moderate to severe--thiamine, electrolytes, benzodiazepine - seizures | Ethanol - Withdrawal Management |
| Drugs used to decrease chronic ethanol use: | Naltrexone, Acamprosate, Disulfiram |
| zero order kinetics (saturatable). Ethanol converted to acetaldehyde by alcohol dehydrogenase (NAD+ required). Acetaldehyde converted to acetate by aldehyde dehydrogenase (NAD+ required). Metabolized by MEOS at high doses | Ethanol - P-kinetics |
| Acute: CNS and CV depressant, SM relaxant. Chronic: liver disease, chronic pancreatitis, gastritis, malabsorption of vitamins. Neurotox (Wernicke-Korsakoff syndrome), cardiomyopathy, arrhythmias, hypertension, anemia (folic acid), endocrine, FAS. | Ethanol - Toxicities |
| MOA and tox: Formaldehyde formed by conversion of methanol via alcohol dehydrogenase results in in toxicity | Methanol - MOA |
| Management: Ethanol IV with dextrose in water or Fomepizole to inhibit conversion by alcohol dehydrogenase. Hemodialysis. Bicarbonate for acidosis. Folic acid to speed breakdown of formaldehyde | Methanol - Management |
| metabolized by alcohol dehydrogenase to formaldehyde. Formaldehyde is metabolized to CO2 by folate-dependent systems | Methanol - P-kinetics |
| Visual disturbances ("snow storm"), blurred vision, formaldehyde on breath or urine, bradycardia, prolonged coma, seizures, metabolic acidosis with elevated anion gap and osmolar gap, decrease in serum bicarbonate | Methanol - Toxicities |
| MoA and tox: metabolized by alcohol dehydrogenase to oxalic acid. Similar to methanol poisoning. alcohol dehydrogenase converts ethylene glycol into oxalic acid (renal toxic crystals) | Ethylene Glycol - MOA and P-kinetics |
| 1) Acute Stage: excitation followed by CNS depression. 2) 4-12 hrs = severe metabolic acidosis (acid metabolites accumulate), anion gap and osmolar gap acidosis. 3) condensation of oxalate crystals in renal tubules (renal failure) | Ethylene Glycol - Toxicity |
| Required for syntesis of thiamine pyrophosphate. Clin Use: to prevent Wernicke - Korsakoff syndrome in chronic alcoholics. IV administration. No Toxicities. | Thiamine |
| MU Opioid antagonist, decreases binding in reward pathways. Clin Use: reduce cravings for alcohol and relapse in short term. IM or oral. Tox: hepatotox, avoid with disulfiram. Withdrawl worsens in patients with other opioid addictions. | Naltrexone |
| NMDA receptor antagonist. Clin Use: reduce cravings for alcohol and relapse in short term. Oral delayed release. Tox: GI and rash. | Acamprosate |
| inhibits aldehyde dehydrogenase (build up of acetaldehyde = HELL hangover. Clin Use: Deterrent of alcohol use. Oral. Tox: Hepatotox. Inhibits metabolism of other drugs. | Disulfiram |
| Inhibits alcohol dehydrogenase. Clin Use: prevents conversion of Ethylene Glycol or Methanol into toxic compounds. IV only. Tox: headache, vertigo, allergic rx rare. | Fomepizole |
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