NEURO/PSYCH Flashcards
Buspirone
MOA: stimulates 5-HT1a receptors
USES: generalized anxiety disorder. Does not cause sedation, addiction, or tolerance. Takes 1-2 weeks to take effect. Does not interact with alcohol (vs. barbiturates, benzodiazepines)
Zolpidem
MOA: Nonbenzodiazepine hypnotic (z drug). act via the BZ1 subtype of the GABA receptor; effects reversed by flumazenil.
CLINICAL USES: insomnia
TOXICITY: ataxia, headaches, confusion. Short duration because of liver metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Decreased dependence risk than benzodiazepines.
Secobarbital
MOA: facilitates GABA-A action by increasing duration of Cl- channel opening
USES: sedative for anxiety, seizures, insomnia, induction of anesthesia
EFFECTS: respiratory and cv depression can be fatal, CNS depression can be exacerbated by alcohol, DDIs (induces cytochrome p450), tolerance, withdrawal
Ramelteon
MOA: melatonin agonist of M1R and M2R–decreases sleep latency
USES: anxiolytic-sedative
EFFECTS: no abuse liability
Suvorexant
MOA: OX1R and OX2R antagonist–Orexin regulates arousal, wakefulness, and appetite
USES: insomnia
EFFECTS: hangover, no withdrawal or rebound
Levodopa/carbidopa
MOA: increases level of dopamine in brain. Unlike dopamine, L-DOPA can cross the BBB and is converted by dopa decarboxylase in the CNS to dopamine. Carbidopa is a peripheral decarboxylase inhibitor, and is given with L-DOPA to increase bioavailability of L-DOPA in the brain and to limit peripheral side effects
USES: Parkinson’s
EFECTS: only 5% of L-DOPA gets to brain before peripheral conversion to DA and later NE–>peripheral toxicity including vomiting, orthostatic hypotension, and arrhythmias. NEVER prescribe L-DOPA alone–always with carbidopa. Long term use can lead to dyskinesia following administration (“on-off” phenomenon), a kinesics between doses.
Carbidopa
MOA: inhibits peripheral decarboxylation of L-DOPA to get more into the brain
Tolcapone
MOA: peripheral COMT inhibitors (COMT degrades catecholamines)–prevents L-DOPA degradation leading to increased dopamine availability
USES: Parkinson’s
Entacapone
MOA: peripheral COMT inhibitors (COMT degrades catecholamines)–prevents L-DOPA degradation leading to increased dopamine availability
USES: Parkinson’s
Trihexyphenidyl
MOA: anticholinergic–suppresses the excitatory drive of ach neurons on motion suppression
USES: Parkinson’s (specifically tremor)
EFFECTS: anti-SLUD (anti-ach side effects)
Bromocriptine
MOA: Dopamine agonist
USES: Parkinson’s disease.
EFFECTS: can cause dyskinesia and hallucinations
Pramipexole
MOA: Dopamine agonist
USES: Parkinson’s disease.
EFFECTS: can cause dyskinesia and hallucinations
Ropinirole
MOA: Dopamine agonist
USES: Parkinson’s disease.
EFFECTS: can cause dyskinesia and hallucinations
Selegiline
MOA: selectively inhibits MOA-B, which preferentially metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine.
USES: adjunctive agent to L-DOPA in treatment of Parkinson’s disease
EFFECTS: may enhance adverse effects of L-DOPA
Donepezil
MOA: CNS specific Acetylcholinesterase inhibitor
USES: Alzheimer’s
EFFECTS: nausea, dizziness insomnia
Rivastigmine
MOA: CNS specific Acetylcholinesterase inhibitor
USES: Alzheimer’s
EFFECTS: nausea, dizziness insomnia
Galantamine
MOA: Non-specific Acetylcholinesterase inhibitor
USES: Alzheimer’s
EFFECTS: nausea, dizziness insomnia
Memantine
MOA: NDMA receptor antagonist; helps prevent excitotoxicity (mediated by calcium)
USES: Alzheimer’s
EFFECTS: dizziness confusion, hallucinations
Nortryptiline
MOA: blocks reuptake of NE and 5-HT
USES: major depression, peripheral neuropathy, chronic pain, migraine prophylaxis.
TOXICITY: sedation, alpha1 blocking effects including postural hypotension, atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). Can cause prolonged QT interval. Tertiary YCAs (amitriptyline) have more anticholinergic effects than secondary TCAs (nortriptyline). TRI-Cs: Convulsion, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects. Treatment: NaHCO3 to prevent arrhythmia.
Phenelzine
MOAi
MOA: blocks oxidative deamination of monoamines (NE, DA, 5-HT)
USES: atypical depression, anxiety, hypochondriasis
Effects: 2-3 w before therapeutic effects, low therapeutic index, food/drug interactions–potentiate sympathomimetic amines–avoid wine and cheese
Fluoxetine
MOA: SSRI. 5-HT specific reuptake inhibitor.
USES: depression, generalized anxiety, panic disorder, OCD, bulimia, social phobias, PTSD
EFFECTS: takes 4-8 weeks to have an effect
TOXICITY: fewer than TCAs. GI distress, SIADH, sexual dysfunction. Serotonin syndrome: with any drug that increases 5-HT–hyperthermia, confusion, myoclonus, cardiovascular instability, flushing, diarrhea, seizures. Treat with cyproheptadine (5-HT2 receptor antagonist)
Duloxetine
SNRI
MOA: inhibits NE, 5HT re uptake
USES: depression, anxiety, fibromyalgia, pain syndromes
EFFECTS: delayed therapeutic onset, no off target effects (like TCAs)
Trazodone
Multimodal serotonergic agent
MOA: primarily blocks 5-HT2 (anti-depressant)and alpha1 receptors
USES: primarily used for insomnia, as high doses are needed for antidepressant effects.
TOXICITY: sedation, nausea, priapism, postural hypotension
Mirtazapine
Atypical anti-depressant
MOA: alpha2 antagonist (increases release of NE and 5-HT) and potent 5-HT2 and 3 receptor antagonist
TOXICITY: sedation (which may be desirable in depressed patients with insomnia), increased appetite, weight gain (which may be desirable in elderly or anorexic patients), dry mouth
Bupropion
Atypical antidepressant. Also used for smoking cessation. Increases NE and dopamine via unknown mechanism.
TOXICITY: stimulant effects (tachycardia, insomnia), headache, seizures in anorexic/bulimic patients. No sexual side effects.
Lithium
MOA: not known. Possible related to inhibition of phosphoinositol cascade.
USES: mood stabilizer for bipolar disorder; blocks relapse and acute manic events. Also SIADH.
SIDE EFFECTS: low therapeutic index;
LMNOP: Lithium side effects:
Movement (tremor)
Nephrogenic diabetes insipidus (ADH antagonist)
hypOthyroidism
Pregnancy problems (teratogenic-fetal heart defects)
TOXICITY: tremor, hypothyroidism, polyuria (causes nephrogenic DI), teratogenesis. Causes Ebstein anomaly in newborn if taken by pregnant mother. Narrow therapeutic window requires close monitoring of serum levels. Almost exclusively excreted by kidneys; most is reabsorbed at PCT with sodium. Thiazide use is implicated in lithium toxicity in bipolar patients.
Sumatriptan
MOA: 5-HT1B and 1D receptor agonist. 1B-vasoconstriction; 1D-prevents peripheral nerve release of CGRP. Inhibits trigeminal nerve activation and prevents vasoactive peptide release. Half life is
Dihydroergotamine
Migraine medication-ergot alkaloid
MOA: powerful non-selective vasoconstrictor
EFFECTS: contraindicated in pregnancy and patients with angina
Phenytoin
MOA: Anticonvulsant. blockade of VG-Na channels–prolongs refractory period. Zero order kinetics.
USES: first line for prophylaxis of status epilepticus. first line for GTC seizures. Also used for simple and complex seizures.
SIDE EFFECTS: nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogen (fetal hydantoin syndrome), SLE-like syndrome, induction of CYP450, lymphadenopathy, Stevens-Johnson syndrome, osteopenia
Carbamazepine
MOA: Anticonvulsant. increases VG-Na inactivation–prolongs refractory period
USES: first line for trigeminal neuralgia. First line for simple, complex, and GTC seizures.
SIDE EFFECTS: diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cyp450, SIADH (can present with hyponatremia), SJS
Oxcarbazepine
Anticonvulsant–keto derivative of carbamazepine; prodrug that he plus reduce toxicity of liver and also prevents aplastic anemia
USES: partial seizures with or without secondary generalization
Lamotrogine
MOA: Anticonvulsant. blocks VG-Na channels
USES: GTC, complex, partial, absence
SIDE EFFECTS: titrate slowly due to possibility for Stevens-Johnson syndrome
Valproic acid
MOA: Anticonvulsant. inactivates VG-Na channels; also increases GABA by inhibiting its metabolism
USES: first line for GTC. Simple, complex, absence seizures. Also used for myoclonic seizures, bipolar disorder.
SIDE EFFECTS: GI distress rare but fatal hepatotoxicity, neural tube defects in fetus, tremor, weight gain, contraindicated in pregnancy
Ethosuximide
MOA: Anticonvulsant. blocks T-type calcium channels (underlies absence seizures)
USES: generalized absence
SIDE EFFECTS: GI, fatigue, headache, urticaria, Steven-Johnson syndrome.
Gabapentin
MOA: primarily inhibits VG-Ca channels; GABA analog but not an agonist
USES: neuropathic pain (peripheral neuropathy, postoperative neuralgia, migraine prophylaxis, bipolar disorder). Also for simple, complex, GTC seizures.
SIDE EFFECTS: sedation, ataxia
Phenobarbital
Barbiturate used as anticonvulsant
MOA: non-selective CNS depression via GABA-mimetic activity at GABA-A receptor –limits spread of seizures and elevates threshold
USES: simple, complex, and GTC. First line in neonates
SIDE EFFECTS: sedation, tolerance, dependence, induction of cyp450, cardiorespiratory depression
Benzodiazepines for seizures
Diazepam and lorazepam
MOA: increases GABAa action
USES: first line for acute status epilepticus. Also used for eclampsia seizures (1st line is magnesium)
TOXICITY: sedation, tolerance, dependence, respiratory depression
Tiagabine
MOA: GABAergic anticonvulsant. inhibits GABA re-uptake into neurons and glia
USES: simple and complex seizures
Vigabatrin
MOA: GABAergic anticonvulsant. structured analog of GABA-irreversible inhibition of GABA transaminase
USES: simple and complex seizures
EFFECTS: retinopathy limits use of this drug
Topiramate
MOA: anticonvulsant. Blocks Na+ channels. enhances efficacy of GABA at GABA-A receptors
USES: simple, complex, GTC seizures. Also used for migraine prevention.
SIDE EFFECTS: sedation, mental dulling, kidney stones, weight loss
Leveteracitam
MOA: Anticonvulsant. unclear–NOT VG-Na directed (may modulate GABA and glutamate release)
USES: complex, partial and GTC seizures
Chlorpromazine
MOA: low potency typical antipsychotic. Block dopamine D2 receptors (increase cAMP).
USES: schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome
TOXICITY: highly lipid soluble and stored in body fat, thus very slow to be removed from body. Non-neurological side effects: arising from blocking muscarinic (dry mouth, constipation), alpha1 (hypotension), and histamine (sedation) receptors. Can cause QT prolongation.
OTHER EFFECTS: Neuroleptic Malignant Syndrome: rigidity, myoglobinuria, autonomic instability, hyperreflexia. Treat with dantrolene, D2 agonist (bromocriptine). Tardive Dyskinesia: stereotypic oral-facial movements as a result of long-term antipsychotic use.
Thioridazine
MOA: low potency typical antipsychotic. Block dopamine D2 receptors (increase cAMP).
USES: schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome
TOXICITY: highly lipid soluble and stored in body fat, thus very slow to be removed from body. Non-neurological side effects: arising from blocking muscarinic (dry mouth, constipation), alpha1 (hypotension), and histamine (sedation) receptors. Can cause QT prolongation.
OTHER EFFECTS: Neuroleptic Malignant Syndrome: rigidity, myoglobinuria, autonomic instability, hyperreflexia. Treat with dantrolene, D2 agonist (bromocriptine). Tardive Dyskinesia: stereotypic oral-facial movements as a result of long-term antipsychotic use.
Fluphenazine
MOA: high potency typical antipsychotic. Block dopamine D2 receptors (increase cAMP).
USES: schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome
TOXICITY: highly lipid soluble and stored in body fat, thus very slow to be removed from body. Extrapyramidal system side effects (e.g. Dopamine receptor antagonism leads to hyperprolactinemia and galactorrhea). Side effects arising from blocking muscarinic (dry mouth, constipation), alpha1 (hypotension), and histamine (sedation) receptors. Can cause QT prolongation.
OTHER EFFECTS: Neuroleptic Malignant Syndrome: rigidity, myoglobinuria, autonomic instability, hyperreflexia. Treat with dantrolene, D2 agonist (bromocriptine). Tardive Dyskinesia: stereotypic oral-facial movements as a result of long-term antipsychotic use.
Haloperidol
MOA: high potency typical antipsychotic. Block dopamine D2 receptors (increase cAMP).
USES: schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome
TOXICITY: highly lipid soluble and stored in body fat, thus very slow to be removed from body. Extrapyramidal system side effects (e.g. Dopamine receptor antagonism leads to hyperprolactinemia and galactorrhea). Side effects arising from blocking muscarinic (dry mouth, constipation), alpha1 (hypotension), and histamine (sedation) receptors. Can cause QT prolongation.
OTHER EFFECTS: Neuroleptic Malignant Syndrome: rigidity, myoglobinuria, autonomic instability, hyperreflexia. Treat with dantrolene, D2 agonist (bromocriptine). Tardive Dyskinesia: stereotypic oral-facial movements as a result of long-term antipsychotic use.
Risperidone
MOA: atypical antipsychotic. Mechanism not completely understood. Varied effects on 5-HT2, dopamine, and alpha and histamine receptors.
USES: schizophrenia–both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, anxiety, mania, Tourette syndrome.
TOXICITY: fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. May increase prolactin (causing lactation and gynecomastia) leading to deceased GnRH, LH, FSH (causing irregular menstruation and fertility issues). prolong QT interval.
Clozapine
MOA: atypical antipsychotic. Mechanism not completely understood. Varied effects on 5-HT2, dopamine, and alpha and histamine receptors.
USES: schizophrenia–both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, anxiety, mania, Tourette syndrome.
TOXICITY: fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. Olanzapine/clozapine may cause significant weight gain. May also cause agranulocytosis (requires weekly WBC monitoring) and seizures. May prolong QT interval.
Olanzapine
MOA: atypical antipsychotic. Mechanism not completely understood. Varied effects on 5-HT2, dopamine, and alpha and histamine receptors.
USES: schizophrenia–both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, anxiety, mania, Tourette syndrome.
TOXICITY: fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. Olanzapine/clozapine may cause significant weight gain. May prolong QT interval.
Quetiapine
MOA: atypical antipsychotic. Mechanism not completely understood. Varied effects on 5-HT2, dopamine, and alpha and histamine receptors.
USES: schizophrenia–both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, anxiety, mania, Tourette syndrome.
TOXICITY: fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. May prolong QT interval.
Ziprasidone
MOA: atypical antipsychotic. Mechanism not completely understood. Varied effects on 5-HT2, dopamine, and alpha and histamine receptors.
USES: schizophrenia–both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, anxiety, mania, Tourette syndrome.
TOXICITY: fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. May prolong QT interval.
Aripiprazole
MOA: atypical antipsychotic. Mechanism not completely understood. Varied effects on 5-HT2, dopamine, and alpha and histamine receptors.
USES: schizophrenia–both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, anxiety, mania, Tourette syndrome.
TOXICITY: fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. May prolong QT interval.
Morphine
MOA: analgesic. Mu opioid receptor agonist–modulates synaptic transmission by opening k+ channels, closing ca++ channels and thus decreasing synaptic transmission. Inhibits release of ACh, NE, 5-HT, glutamate, substance P.
USES: pain, acute pulmonary edema
TOXICITY: addiction (increases DA in nucleus accumbens upon activation receptors within GABA interneurons), respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
Codeine
MOA: analgesic. Mu opioid receptor agonist–modulates synaptic transmission by opening k+ channels, closing ca++ channels and thus decreasing synaptic transmission. Inhibits release of ACh, NE, 5-HT, glutamate, substance P. Oral prodrug that is demethylated to morphine.
USES: pain, acute pulmonary edema
TOXICITY: addiction (increases DA in nucleus accumbens upon activation receptors within GABA interneurons), respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
Meperidine
MOA: analgesic. Mu opioid receptor agonist–modulates synaptic transmission by opening k+ channels, closing ca++ channels and thus decreasing synaptic transmission. Inhibits release of ACh, NE, 5-HT, glutamate, substance P. Oral prodrug that is demethylated to morphine.
USES: pain, acute pulmonary edema. Metabolized via methylation–can be used during pregnancy because fetus has the enzyme for its metabolism
TOXICITY: addiction (increases DA in nucleus accumbens upon activation receptors within GABA interneurons), respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
Fentanyl
MOA: analgesic. Mu opioid receptor agonist–modulates synaptic transmission by opening k+ channels, closing ca++ channels and thus decreasing synaptic transmission. Inhibits release of ACh, NE, 5-HT, glutamate, substance P. Most potent opioid agonist due to high affinity for receptor–can cause rigidity
USES: pain, acute pulmonary edema
TOXICITY: addiction (increases DA in nucleus accumbens upon activation receptors within GABA interneurons), respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
Methadone
MOA: analgesic. Mu opioid receptor agonist–modulates synaptic transmission by opening k+ channels, closing ca++ channels and thus decreasing synaptic transmission. Inhibits release of ACh, NE, 5-HT, glutamate, substance P. Oral prodrug that is demethylated to morphine.
USES: long acting oral opiate used for heroin detoxification or long term maintenance
TOXICITY: addiction (increases DA in nucleus accumbens upon activation receptors within GABA interneurons), respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
Butorphanol
MOA: Mu opioid receptor partial agonist and kappa opioid receptor agonist. Produces analgesia
USES: severe pain (migraine, labor, etc). Causes less respiratory depression then full opioid agonists.
TOXICITY: can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors). Overdose not easily reversed with naloxone.
Tramadol
MOA: Weak Mu opioid partial agonist. Also inhibits serotonin and NE reuptake (works on multiple pain pathways)
USES: chronic pain
TOXICITY: similar to opioids. Decreases seizure threshold. Serotonin syndrome. It’s actions cannot be completely blocked by opioid antagonist
Naloxone
CENTRAL ACTING Mu antagonist–use in opioid overdose
Naltrexone
CENTRAL ACTING Mu antagonist–longer duration of action than naloxone
Long acting opioid antagonist used for relapse prevention once detoxified
Nitrous oxide
MOA: Inhalational anesthetic. Unknown mechanism.
EFFECTS: preoperative anxiolytic, anesthetic adjunct (CANNOT be used alone because MAC=105%), myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)
TOXICITY: DOES NOT cause malignant hyperthermia.
Halothane
MOA: Inhalational anesthetic. Unknown mechanism.
EFFECTS: myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)
TOXICITY: **hepatotoxicity, can cause malignant hyperthermia–rare, life-threatening hereditary condition in which inhaled Anesthetics (except NO) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene (muscle relaxant)
Enfluorane
MOA: Inhalational anesthetic. Unknown mechanism.
EFFECTS: myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)
TOXICITY: **preconvulsant, can cause malignant hyperthermia–rare, life-threatening hereditary condition in which inhaled Anesthetics (except NO) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene (muscle relaxant)
Isofluorane
MOA: Inhalational anesthetic. Unknown mechanism.
EFFECTS: very pungent (used for Maitenance and NOT induction), myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)
TOXICITY: can cause malignant hyperthermia–rare, life-threatening hereditary condition in which inhaled Anesthetics (except NO) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene (muscle relaxant)
EFFECTS: ), hypotension (systemic vasodilation), malignant hyperthermia
Desfluorane
Inhalational anesthetic
MOA: inhibition of Na channels
PK: no metabolism–simply exhaled; low boiling point–volatile at room temp
EFFECTS: very pungent–used for Maitenance and NOT induction, malignant hyperthermia, initial bronchial irritation
Sevofluorane
MOA: Inhalational anesthetic. Unknown mechanism.
EFFECTS: NO pungency–most popular induction agent, myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)
TOXICITY: can cause malignant hyperthermia–rare, life-threatening hereditary condition in which inhaled Anesthetics (except NO) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene (muscle relaxant)
Thiopental
MOA: Barbiturate. Facilitates GABAa action by increasing duration of Cl- channel openin. Thus decreases neuron firing. Contraindicated in porphyria.
USE: rapid induction of anesthesia–high potency, high lipid solubility, rapid entry into brain. Effect terminated by rapid redistribution into tissues (I.e. Skeletal muscle and fat). Sedative for anxiety, seizures, insomnia.
EFFECTS: decreases cerebral blood flow
TOXICITY: respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence, drug interactions (induces cyp450). Overdose treatment is supportive (assist respiration and maintain BP)
Midazolam
MOA: Benzodiazepine. Facilitate GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep. Excellent amnesia properties.
USES: most common drug for endoscopy–used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decreased BP. Also used for anxiety, spasticity, detoxification (especially alcohol withdrawal), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
SIDE EFFECTS: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Diazepam
MOA: Benzodiazepine. Facilitate GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting and have higher addictive potential)
USES: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
SIDE EFFECTS: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Lorazepam
MOA: Benzodiazepine. Facilitate GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting and have higher addictive potential)
USES: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
SIDE EFFECTS: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Flumazenil
Benzodiazepine antagonist–reversal agent
Half life is shorter than benzodiazepines so must administer enough
Propofol
IV anesthetic. Potentiates GABAa. Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less postoperative nausea than thiopental.
Ketamine
MOA: IV anesthetic. PCO analog that acts as dissociative anesthetic. Blocks NMDA receptor.
USE: analgesia with cardiac stimulation
EFFECTS: disorientation, hallucination, and bad dreams. Increases cerebral blood flow (contraindicated with increased ICP)
Lidocaine
MOA: Amide local anesthetic. Blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective on rapidly firing neurons. Metabolized by liver–more stable.
PRINCIPLE: can be given with vasoconstrictors (usually epinephrine) to enhance local action–decrease bleeding, increase anesthesia and decrease systemic concentration (vasoconstriction decreases rate of absorption into blood). In infected (acidic) tissue, alkaline Anesthetics are charged and cannot penetrate membrane effectively–need more anesthetic (more acidic the pKa of the drug, faster the onset). Order of nerve blockade: small diameter fibers>large diameters. Myelinated fibers>unmyelinated fibers.
USES: minor surgical procedures, spinal anesthesia.
Bupivacaine
MOA: Amide local anesthetic. Blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective on rapidly firing neurons. Metabolized by liver–more stable.
PRINCIPLE: can be given with vasoconstrictors (usually epinephrine) to enhance local action–decrease bleeding, increase anesthesia and decrease systemic concentration (vasoconstriction decreases rate of absorption into blood). In infected (acidic) tissue, alkaline Anesthetics are charged and cannot penetrate membrane effectively–need more anesthetic (more acidic the pKa of the drug, faster the onset). Order of nerve blockade: small diameter fibers>large diameters. Myelinated fibers>unmyelinated fibers.
USES: minor surgical procedures, spinal anesthesia.
Mepivacaine
MOA: Amide local anesthetic. Blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective on rapidly firing neurons. Metabolized by liver–more stable.
PRINCIPLE: can be given with vasoconstrictors (usually epinephrine) to enhance local action–decrease bleeding, increase anesthesia and decrease systemic concentration (vasoconstriction decreases rate of absorption into blood). In infected (acidic) tissue, alkaline Anesthetics are charged and cannot penetrate membrane effectively–need more anesthetic (more acidic the pKa of the drug, faster the onset). Order of nerve blockade: small diameter fibers>large diameters. Myelinated fibers>unmyelinated fibers.
USES: minor surgical procedures, spinal anesthesia.
Cocaine
MOA: Ester local anesthetic. Blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective on rapidly firing neurons. Metabolized by plasma cholinesterases–less stable than amides
PRINCIPLE: can be given with vasoconstrictors (usually epinephrine) to enhance local action–decrease bleeding, increase anesthesia and decrease systemic concentration (vasoconstriction decreases rate of absorption into blood). In infected (acidic) tissue, alkaline Anesthetics are charged and cannot penetrate membrane effectively–need more anesthetic (more acidic the pKa of the drug, faster the onset). Order of nerve blockade: small diameter fibers>large diameters. Myelinated fibers>unmyelinated fibers.
USES: minor surgical procedures, spinal anesthesia. If allergic to esters (metabolized to PABA), give amides.
Procaine
MOA: Ester local anesthetic. Blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective on rapidly firing neurons. Metabolized by plasma cholinesterases–less stable than amides
PRINCIPLE: can be given with vasoconstrictors (usually epinephrine) to enhance local action–decrease bleeding, increase anesthesia and decrease systemic concentration (vasoconstriction decreases rate of absorption into blood). In infected (acidic) tissue, alkaline Anesthetics are charged and cannot penetrate membrane effectively–need more anesthetic (more acidic the pKa of the drug, faster the onset). Order of nerve blockade: small diameter fibers>large diameters. Myelinated fibers>unmyelinated fibers.
USES: minor surgical procedures, spinal anesthesia. If allergic to esters (metabolized to PABA), give amides.
Tetracaine
MOA: Ester local anesthetic. Blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective on rapidly firing neurons. Metabolized by plasma cholinesterases–less stable than amides
PRINCIPLE: can be given with vasoconstrictors (usually epinephrine) to enhance local action–decrease bleeding, increase anesthesia and decrease systemic concentration (vasoconstriction decreases rate of absorption into blood). In infected (acidic) tissue, alkaline Anesthetics are charged and cannot penetrate membrane effectively–need more anesthetic (more acidic the pKa of the drug, faster the onset). Order of nerve blockade: small diameter fibers>large diameters. Myelinated fibers>unmyelinated fibers.
USES: minor surgical procedures, spinal anesthesia. If allergic to esters (metabolized to PABA), give amides.
Epinephrine
Vasoconstrictor used with locals
Nortryptaline
Smoking cessation medication
Antidepressant–efficacy is due to effects on nerotransmitters, NOT due to any treatment of co morbid depression
Varenicline
Smoking cessation medication
MOA: partial agonist of nicotinic ach receptor. Agonist activity mimics nicotine and the antagonist activity prevents nicotine from binding
Disulfiram
Alcoholism drug
MOA: inhibitor of aldehyde dehydrogenase–induces accumulation of acetaldehyde whenever alcohol is consumed
Acamprosate
Alcoholism drug
Reduces the craving for alcohol–presumably mediated through antagonism of the NMDA receptors
Naltrexone
Alcoholism drug
Antagonizes opioid receptors, decreasing the reward sensation associated with drinking alcohol
Methamphetamine
MOA: CNS stimulant. Increases catecholamines at synaptic cleft, especially NE and dopamine.
USES: ADHD, narcolepsy, appetite control
Dextroamphetamine
MOA: CNS stimulant. Increases catecholamines at synaptic cleft, especially NE and dopamine.
USES: ADHD, narcolepsy, appetite control
Methylphenidate
MOA: CNS stimulant. Increases catecholamines at synaptic cleft, especially NE and dopamine.
USES: first line for ADHD, narcolepsy, appetite control
Cocaine
CNS stimulant
MOA: blocks reuptake of biogenic amines–>potentiates dopamine, NE, and serotonin synapses (primary effects on dopamine); blocks sodium channels, leading to local vasoconstriction and anesthesia
USES: nose procedures for its vasoconstrictive properties
EFFECTS: therapeutic-insomnia, motor tics, weight loss; Above therapeutic-euphoria, dizziness tremor, chills, vomiting, convulsions, coma, arrhythmia; Chronic abuse-drug induced psychosis, social withdrawal, addiction, depression and fatigue
Caffeine
CNS stimulant
MOA: adenosine receptor antagonist at lower doses–>blocking adenosine mitigates it’s fatigue-related reactions; PDE inhibitor at higher doses–>increased cAMP–>bronchodilation–>rrspiratory stimulation
EFFECTS: stimulation, diuresis, stimulation of cardiac muscle, relaxation of smooth muscle; side effects-nervousness, insomnia, tachycardia, tachypnea,
Modafinil
Mild CNS stimulant
MOA: inhibits dopamine and NE transporters, increases histamine release (promotes wakefulness), stimulates hypocretin and Orexin neurons (increases wakefulness)
USES: narcolepsy, shift-work sleep disorder, CONTRAINDICATED IN KIDS (dermatological toxicity)
Atomoxetine
MOA: selective NE reuptake inhibitor (SNRI); NON STIMULANT
USE: ADHD IN ADULTS ONLY; not a first line medication–used as alternative to stimulants with bad reactions
EFFECTS: GI symptoms, decreased appetite, mood swings, insomnia, sexual side effects
Epinephrine
MOA: decreases aqueous humor synthesis via vasoconstriction
USES: glaucoma
SIDE EFFECTS: mydriasis (do not used in closed angle glaucoma), blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis
Brimonidine
MOA: Alpha 2 agonist. decreases aqueous humor synthesis.
USES: glaucoma
SIDE EFFECTS: mydriasis (do not used in closed angle glaucoma), blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis
Timolol
MOA: beta blocker. Decreases aqueous humor synthesis
USES: glaucoma
SIDE EFFECTS: NO vision or pupillary changes
Betaxolol
MOA: beta blocker. Decreases aqueous humor synthesis
USES: glaucoma
SIDE EFFECTS: NO vision or pupillary changes
Carteolol
MOA: beta blocker. Decreases aqueous humor synthesis
USES: glaucoma
SIDE EFFECTS: NO vision or pupillary changes
Acetazolamide
MOA: Diuretic. Decreases aqueous humor synthesis via inhibition of carbonic anhydrase.
USES: glaucoma
SIDE EFFECTS: no pupillary or vision changes
Pilocarpine
MOA: direct cholinomimetic. Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork.
USES: emergency glaucoma situation
SIDE EFFECTS: mitosis. And cyclospasm (contraction of ciliary muscle)
Carbachol
MOA: direct cholinomimetic. Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork.
USES: glaucoma
SIDE EFFECTS: mitosis. And cyclospasm (contraction of ciliary muscle)
Physostigmine
MOA: indirect cholinomimetic. Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork.
USES: glaucoma
SIDE EFFECTS: mitosis and cyclospasm (contracture of ciliary muscle)
Echothiophate
MOA: indirect cholinomimetic. Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork.
USES: glaucoma
SIDE EFFECTS: mitosis and cyclospasm (contracture of ciliary muscle)
Latanoprost
MOA: PGF2. Increases outflow of aqueous humor
USES: glaucoma
SIDE EFFECTS: mitosis and cycloplasm (contraction of ciliary muscle)
Loperamide
MOA: analgesic. Mu opioid receptor agonist–modulates synaptic transmission by opening k+ channels, closing ca++ channels and thus decreasing synaptic transmission. Inhibits release of ACh, NE, 5-HT, glutamate, substance P. Oral prodrug that is demethylated to morphine.
USES: diarrhea
TOXICITY: addiction (increases DA in nucleus accumbens upon activation receptors within GABA interneurons), respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
Dextromethorphan
MOA: analgesic. Mu opioid receptor agonist–modulates synaptic transmission by opening k+ channels, closing ca++ channels and thus decreasing synaptic transmission. Inhibits release of ACh, NE, 5-HT, glutamate, substance P. Oral prodrug that is demethylated to morphine.
USES: cough suppression
TOXICITY: addiction (increases DA in nucleus accumbens upon activation receptors within GABA interneurons), respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
Diphenoxylate
MOA: analgesic. Mu opioid receptor agonist–modulates synaptic transmission by opening k+ channels, closing ca++ channels and thus decreasing synaptic transmission. Inhibits release of ACh, NE, 5-HT, glutamate, substance P. Oral prodrug that is demethylated to morphine.
USES: diarrhea
TOXICITY: addiction (increases DA in nucleus accumbens upon activation receptors within GABA interneurons), respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist)
Alprazolam
MOA: Benzodiazepine. Facilitate GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting and have higher addictive potential)
USES: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
SIDE EFFECTS: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Chlordiazepoxide
MOA: Benzodiazepine. Facilitate GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting and have higher addictive potential)
USES: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
SIDE EFFECTS: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Oxazepam
MOA: Benzodiazepine. Facilitate GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting and have higher addictive potential)
USES: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
SIDE EFFECTS: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Temazepam
MOA: Benzodiazepine. Facilitate GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting and have higher addictive potential)
USES: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
SIDE EFFECTS: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Triazolam
MOA: Benzodiazepine. Facilitate GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting and have higher addictive potential)
USES: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
SIDE EFFECTS: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)
Methoxyflurane
MOA: Inhalational anesthetic. Unknown mechanism.
EFFECTS: myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)
TOXICITY: **nephrotoxicity, can cause malignant hyperthermia–rare, life-threatening hereditary condition in which inhaled Anesthetics (except NO) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene (muscle relaxant)
Ezopiclone
MOA: Nonbenzodiazepine hypnotic (z drug). act via the BZ1 subtype of the GABA receptor; effects reversed by flumazenil.
CLINICAL USES: insomnia
TOXICITY: ataxia, headaches, confusion. Short duration because of liver metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Decreased dependence risk than benzodiazepines.
Zaleplon
MOA: Nonbenzodiazepine hypnotic (z drug). act via the BZ1 subtype of the GABA receptor; effects reversed by flumazenil.
CLINICAL USES: insomnia
TOXICITY: ataxia, headaches, confusion. Short duration because of liver metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Decreased dependence risk than benzodiazepines.
Secobarbital
MOA: Barbiturate. Facilitates GABAa action by increasing duration of Cl- channel openin. Thus decreases neuron firing. Contraindicated in porphyria.
USE: Sedative for anxiety, seizures, insomnia.
TOXICITY: respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence, drug interactions (induces cyp450). Overdose treatment is supportive (assist respiration and maintain BP)
Pentobarbitol
MOA: Barbiturate. Facilitates GABAa action by increasing duration of Cl- channel openin. Thus decreases neuron firing. Contraindicated in porphyria.
USE: Sedative for anxiety, seizures, insomnia.
TOXICITY: respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence, drug interactions (induces cyp450). Overdose treatment is supportive (assist respiration and maintain BP)
Phenobarbital
MOA: Barbiturate. Facilitates GABAa action by increasing duration of Cl- channel openin. Thus decreases neuron firing. Contraindicated in porphyria.
USE: Sedative for anxiety, seizures, insomnia.
TOXICITY: respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence, drug interactions (induces cyp450). Overdose treatment is supportive (assist respiration and maintain BP)
Tetrabenazine
MOA: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicles packaging and release
USES: Huntington’s disease (neurotransmitter changes in Huntington’s: decreased GABA and ACh, increased dopamine)
Phentermine
MOA: CNS stimulant. Increases catecholamines at synaptic cleft, especially NE and dopamine.
USES: ADHD, narcolepsy, appetite control
Baclofen
MOA: inhibits GABAa receptors at spinal cord level, including skeletal muscle relaxation
USE: muscle spasms (e.g. Acute low back pain)
Cyclobenzaprine
MOA: centrally acting skeletal muscle relaxant. Structurally related to TCAs, similar to anticholinergic side effects
USE: muscle spasms
Reserpine
MOA: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicles packaging and release
USES: Huntington’s disease (neurotransmitter changes in Huntington’s: decreased GABA and ACh, increased dopamine)
Benztropine
MOA: Antimuscarinic–curbs excess cholinergic activity
USES: Parkinson’s. Improves tremor and rigidity but has little effect on bradykinesia
Dantrolene
MOA: prevents the release of calcium from the sarcomas in reticulum of skeletal muscle
USE: used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)
Citalopram
MOA: SSRI. 5-HT specific reuptake inhibitor.
USES: depression, generalized anxiety, panic disorder, OCD, bulimia, social phobias, PTSD
EFFECTS: takes 4-8 weeks to have an effect
TOXICITY: fewer than TCAs. GI distress, SIADH, sexual dysfunction. Serotonin syndrome: with any drug that increases 5-HT–hyperthermia, confusion, myoclonus, cardiovascular instability, flushing, diarrhea, seizures. Treat with cyproheptadine (5-HT2 receptor antagonist)
Venlafaxine
MOA: inhibits 5-HT and NE reuptake
USES: depression. Venlafaxine is also used in generalized anxiety disorder, panic disorder,PTSD.
TOXICITY: increases BP. Also stimulant effects, sedation, nausea
Duloxetine
MOA: inhibits 5-HT and NE reuptake
USES: depression. Also indicated for diabetic peripheral neuropathy
TOXICITY: increases BP. Also stimulant effects, sedation, nausea
Amitriptyline
MOA: blocks reuptake of NE and 5-HT
USES: major depression, peripheral neuropathy, chronic pain, migraine prophylaxis.
TOXICITY: sedation, alpha1 blocking effects including postural hypotension, atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). Can cause prolonged QT interval. Tertiary YCAs (amitriptyline) have more anticholinergic effects than secondary TCAs (nortriptyline). TRI-Cs: Convulsion, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects. Treatment: NaHCO3 to prevent arrhythmia.
Imipramine
MOA: blocks reuptake of NE and 5-HT
USES: major depression, peripheral neuropathy, chronic pain, migraine prophylaxis.
TOXICITY: sedation, alpha1 blocking effects including postural hypotension, atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). Can cause prolonged QT interval. Tertiary YCAs (amitriptyline) have more anticholinergic effects than secondary TCAs (nortriptyline). TRI-Cs: Convulsion, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects. Treatment: NaHCO3 to prevent arrhythmia.
Desipramine
MOA: blocks reuptake of NE and 5-HT
USES: major depression, peripheral neuropathy, chronic pain, migraine prophylaxis.
TOXICITY: sedation, alpha1 blocking effects including postural hypotension, atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). Can cause prolonged QT interval. Tertiary YCAs (amitriptyline) have more anticholinergic effects than secondary TCAs (nortriptyline). TRI-Cs: Convulsion, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects. Treatment: NaHCO3 to prevent arrhythmia.
Clomipramine
MOA: blocks reuptake of NE and 5-HT
USES: major depression, peripheral neuropathy, chronic pain, migraine prophylaxis.
TOXICITY: sedation, alpha1 blocking effects including postural hypotension, atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). Can cause prolonged QT interval. Tertiary YCAs (amitriptyline) have more anticholinergic effects than secondary TCAs (nortriptyline). TRI-Cs: Convulsion, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects. Treatment: NaHCO3 to prevent arrhythmia.
Doxepin
MOA: blocks reuptake of NE and 5-HT
USES: major depression, peripheral neuropathy, chronic pain, migraine prophylaxis.
TOXICITY: sedation, alpha1 blocking effects including postural hypotension, atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). Can cause prolonged QT interval. Tertiary YCAs (amitriptyline) have more anticholinergic effects than secondary TCAs (nortriptyline). TRI-Cs: Convulsion, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects. Treatment: NaHCO3 to prevent arrhythmia.
Amoxapine
MOA: blocks reuptake of NE and 5-HT
USES: major depression, peripheral neuropathy, chronic pain, migraine prophylaxis.
TOXICITY: sedation, alpha1 blocking effects including postural hypotension, atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). Can cause prolonged QT interval. Tertiary YCAs (amitriptyline) have more anticholinergic effects than secondary TCAs (nortriptyline). TRI-Cs: Convulsion, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects. Treatment: NaHCO3 to prevent arrhythmia.
Tranylcypromine
MOA: Nonselective MAO inhibition increases levels of amine neurotransmitters (NE, 5-HT, dopamine)
USES: atypical depression, anxiety
TOXICITY: hypertensive crisis (most notably with ingestion of tyramine, which is found in many foods such as wine and cheese); CNS stimulation. Contraindicated with SSRIs, TCAs, St. John’s Wort, meperidine, dextromethorphan(to prevent serotonin syndrome)
Phenelzine
MOA: Nonselective MAO inhibition increases levels of amine neurotransmitters (NE, 5-HT, dopamine)
USES: atypical depression, anxiety
TOXICITY: hypertensive crisis (most notably with ingestion of tyramine, which is found in many foods such as wine and cheese); CNS stimulation. Contraindicated with SSRIs, TCAs, St. John’s Wort, meperidine, dextromethorphan(to prevent serotonin syndrome)
Isocarboxazid
MOA: Nonselective MAO inhibition increases levels of amine neurotransmitters (NE, 5-HT, dopamine)
USES: atypical depression, anxiety
TOXICITY: hypertensive crisis (most notably with ingestion of tyramine, which is found in many foods such as wine and cheese); CNS stimulation. Contraindicated with SSRIs, TCAs, St. John’s Wort, meperidine, dextromethorphan(to prevent serotonin syndrome)
Selegiline
MOA: Nonselective MAO inhibition increases levels of amine neurotransmitters (NE, 5-HT, dopamine)
USES: atypical depression, anxiety
TOXICITY: hypertensive crisis (most notably with ingestion of tyramine, which is found in many foods such as wine and cheese); CNS stimulation. Contraindicated with SSRIs, TCAs, St. John’s Wort, meperidine, dextromethorphan(to prevent serotonin syndrome)
Varenicline
Partial agonist of nicotinic acetylcholine receptors in CNS. Competes with nicotine and decreases symptoms of nicotine withdrawal. Used for smoking cessation.
Riluzole
Treatment for ALS. Modestly increases survival of neurons by decreasing presynaptic glutamate release.
Primidone
First line medication for treatment of essential tremor. It is also a narrow spectrum anticonvulsant that can be used to treat partial seizures. Metabolites are phenobarbital and phenylethylmalonamide–serum levels are monitored. Can cause CNS depression during initiation.
Modafinil
Non-amphetamine stimulant used to treat narcolepsy
Pentazocine
Opioid analgesic. Partial agonist and weak antagonist, can precipitate withdrawal symptoms in patients dependent on morphine.
Sertraline
MOA: SSRI. 5-HT specific reuptake inhibitor.
USES: depression, generalized anxiety, panic disorder, OCD, bulimia, social phobias, PTSD
EFFECTS: takes 4-8 weeks to have an effect
TOXICITY: fewer than TCAs. GI distress, SIADH, sexual dysfunction. Serotonin syndrome: with any drug that increases 5-HT–hyperthermia, confusion, myoclonus, cardiovascular instability, flushing, diarrhea, seizures. Treat with cyproheptadine (5-HT2 receptor antagonist)
Paroxetine
MOA: SSRI. 5-HT specific reuptake inhibitor.
USES: depression, generalized anxiety, panic disorder, OCD, bulimia, social phobias, PTSD
EFFECTS: takes 4-8 weeks to have an effect
TOXICITY: fewer than TCAs. GI distress, SIADH, sexual dysfunction. Serotonin syndrome: with any drug that increases 5-HT–hyperthermia, confusion, myoclonus, cardiovascular instability, flushing, diarrhea, seizures. Treat with cyproheptadine (5-HT2 receptor antagonist)
Trifluoperazine
MOA: high potency typical antipsychotic. Block dopamine D2 receptors (increase cAMP).
USES: schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome
TOXICITY: highly lipid soluble and stored in body fat, thus very slow to be removed from body. Extrapyramidal system side effects (e.g. Dopamine receptor antagonism leads to hyperprolactinemia and galactorrhea). Side effects arising from blocking muscarinic (dry mouth, constipation), alpha1 (hypotension), and histamine (sedation) receptors. Can cause QT prolongation.
OTHER EFFECTS: Neuroleptic Malignant Syndrome: rigidity, myoglobinuria, autonomic instability, hyperreflexia. Treat with dantrolene, D2 agonist (bromocriptine). Tardive Dyskinesia: stereotypic oral-facial movements as a result of long-term antipsychotic use.
Rocuronium
MOA: NON-DEPOLARIZING neuromuscular blocker. Selective for motor (vs. autonomic) nicotinic receptor. Competitive antagonist that competes with ach for receptor.
REVERSAL OF BLOCKADE: neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
USES: muscle paralysis in surgery or mechanical ventilation
SIDE EFFECTS: hypercalcemia, hyperkalemia, malignant hyperthermia
Vecuronium
MOA: NON-DEPOLARIZING neuromuscular blocker. Selective for motor (vs. autonomic) nicotinic receptor. Competitive antagonist that competes with ach for receptor.
REVERSAL OF BLOCKADE: neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
USES: muscle paralysis in surgery or mechanical ventilation
SIDE EFFECTS: hypercalcemia, hyperkalemia, malignant hyperthermia
Succinylcholine
MOA: DEPOLARIZING neuromuscular blocking agent. Selective for motor (vs. autonomic) nicotinic receptor. Strong ach receptor AGONIST–produces sustained depolarization and prevents muscle contraction.
REVERSAL OF EFFECTS: Phase I-prolonged depolarization–no antidote. Block potentiated by cholinesterase inhibitors. Phase II-repolarized but blocked–ach receptors are available, but desensitized. Antidote consists of cholinesterase inhibitors (e.g. Neostigmine)
USES: muscle paralysis in surgery or mechanical ventilation
SIDE EFFECTS: hypercalcemia, hyperkalemia, and malignant hyperthermia
Tubocurarine
MOA: NON-DEPOLARIZING neuromuscular blocker. Selective for motor (vs. autonomic) nicotinic receptor. Competitive antagonist that competes with ach for receptor.
REVERSAL OF BLOCKADE: neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
USES: muscle paralysis in surgery or mechanical ventilation
SIDE EFFECTS: hypercalcemia, hyperkalemia, malignant hyperthermia
Atracurium
MOA: NON-DEPOLARIZING neuromuscular blocker. Selective for motor (vs. autonomic) nicotinic receptor. Competitive antagonist that competes with ach for receptor.
REVERSAL OF BLOCKADE: neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
USES: muscle paralysis in surgery or mechanical ventilation
SIDE EFFECTS: hypercalcemia, hyperkalemia, malignant hyperthermia
Mivacurium
MOA: NON-DEPOLARIZING neuromuscular blocker. Selective for motor (vs. autonomic) nicotinic receptor. Competitive antagonist that competes with ach for receptor.
REVERSAL OF BLOCKADE: neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
USES: muscle paralysis in surgery or mechanical ventilation
SIDE EFFECTS: hypercalcemia, hyperkalemia, malignant hyperthermia
Pancuronium
MOA: NON-DEPOLARIZING neuromuscular blocker. Selective for motor (vs. autonomic) nicotinic receptor. Competitive antagonist that competes with ach for receptor.
REVERSAL OF BLOCKADE: neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors
USES: muscle paralysis in surgery or mechanical ventilation
SIDE EFFECTS: hypercalcemia, hyperkalemia, malignant hyperthermia
