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Pharmacology > NEURO/PSYCH > Flashcards

NEURO/PSYCH Flashcards

0
Q

Buspirone

A

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)

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1
Q

Zolpidem

A

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.

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2
Q

Secobarbital

A

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

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3
Q

Ramelteon

A

MOA: melatonin agonist of M1R and M2R–decreases sleep latency

USES: anxiolytic-sedative

EFFECTS: no abuse liability

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4
Q

Suvorexant

A

MOA: OX1R and OX2R antagonist–Orexin regulates arousal, wakefulness, and appetite

USES: insomnia

EFFECTS: hangover, no withdrawal or rebound

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5
Q

Levodopa/carbidopa

A

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.

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6
Q

Carbidopa

A

MOA: inhibits peripheral decarboxylation of L-DOPA to get more into the brain

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7
Q

Tolcapone

A

MOA: peripheral COMT inhibitors (COMT degrades catecholamines)–prevents L-DOPA degradation leading to increased dopamine availability

USES: Parkinson’s

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8
Q

Entacapone

A

MOA: peripheral COMT inhibitors (COMT degrades catecholamines)–prevents L-DOPA degradation leading to increased dopamine availability

USES: Parkinson’s

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9
Q

Trihexyphenidyl

A

MOA: anticholinergic–suppresses the excitatory drive of ach neurons on motion suppression

USES: Parkinson’s (specifically tremor)

EFFECTS: anti-SLUD (anti-ach side effects)

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10
Q

Bromocriptine

A

MOA: Dopamine agonist

USES: Parkinson’s disease.

EFFECTS: can cause dyskinesia and hallucinations

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11
Q

Pramipexole

A

MOA: Dopamine agonist

USES: Parkinson’s disease.

EFFECTS: can cause dyskinesia and hallucinations

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12
Q

Ropinirole

A

MOA: Dopamine agonist

USES: Parkinson’s disease.

EFFECTS: can cause dyskinesia and hallucinations

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13
Q

Selegiline

A

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

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14
Q

Donepezil

A

MOA: CNS specific Acetylcholinesterase inhibitor

USES: Alzheimer’s

EFFECTS: nausea, dizziness insomnia

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15
Q

Rivastigmine

A

MOA: CNS specific Acetylcholinesterase inhibitor

USES: Alzheimer’s

EFFECTS: nausea, dizziness insomnia

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16
Q

Galantamine

A

MOA: Non-specific Acetylcholinesterase inhibitor

USES: Alzheimer’s

EFFECTS: nausea, dizziness insomnia

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17
Q

Memantine

A

MOA: NDMA receptor antagonist; helps prevent excitotoxicity (mediated by calcium)

USES: Alzheimer’s

EFFECTS: dizziness confusion, hallucinations

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18
Q

Nortryptiline

A

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.

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19
Q

Phenelzine

A

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

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20
Q

Fluoxetine

A

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)

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21
Q

Duloxetine

A

SNRI

MOA: inhibits NE, 5HT re uptake

USES: depression, anxiety, fibromyalgia, pain syndromes

EFFECTS: delayed therapeutic onset, no off target effects (like TCAs)

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22
Q

Trazodone

A

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

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23
Q

Mirtazapine

A

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

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24
Q

Bupropion

A

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.

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25
Q

Lithium

A

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.

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26
Q

Sumatriptan

A

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

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27
Q

Dihydroergotamine

A

Migraine medication-ergot alkaloid

MOA: powerful non-selective vasoconstrictor

EFFECTS: contraindicated in pregnancy and patients with angina

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28
Q

Phenytoin

A

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

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29
Q

Carbamazepine

A

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

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30
Q

Oxcarbazepine

A

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

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31
Q

Lamotrogine

A

MOA: Anticonvulsant. blocks VG-Na channels

USES: GTC, complex, partial, absence

SIDE EFFECTS: titrate slowly due to possibility for Stevens-Johnson syndrome

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32
Q

Valproic acid

A

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

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33
Q

Ethosuximide

A

MOA: Anticonvulsant. blocks T-type calcium channels (underlies absence seizures)

USES: generalized absence

SIDE EFFECTS: GI, fatigue, headache, urticaria, Steven-Johnson syndrome.

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34
Q

Gabapentin

A

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

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35
Q

Phenobarbital

A

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

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36
Q

Benzodiazepines for seizures

A

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

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37
Q

Tiagabine

A

MOA: GABAergic anticonvulsant. inhibits GABA re-uptake into neurons and glia

USES: simple and complex seizures

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38
Q

Vigabatrin

A

MOA: GABAergic anticonvulsant. structured analog of GABA-irreversible inhibition of GABA transaminase

USES: simple and complex seizures

EFFECTS: retinopathy limits use of this drug

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39
Q

Topiramate

A

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

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40
Q

Leveteracitam

A

MOA: Anticonvulsant. unclear–NOT VG-Na directed (may modulate GABA and glutamate release)

USES: complex, partial and GTC seizures

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41
Q

Chlorpromazine

A

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.

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42
Q

Thioridazine

A

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.

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43
Q

Fluphenazine

A

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.

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44
Q

Haloperidol

A

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.

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45
Q

Risperidone

A

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.

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46
Q

Clozapine

A

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.

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47
Q

Olanzapine

A

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.

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48
Q

Quetiapine

A

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.

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49
Q

Ziprasidone

A

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.

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50
Q

Aripiprazole

A

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.

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51
Q

Morphine

A

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)

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52
Q

Codeine

A

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)

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53
Q

Meperidine

A

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)

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54
Q

Fentanyl

A

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)

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55
Q

Methadone

A

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)

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56
Q

Butorphanol

A

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.

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57
Q

Tramadol

A

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

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58
Q

Naloxone

A

CENTRAL ACTING Mu antagonist–use in opioid overdose

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59
Q

Naltrexone

A

CENTRAL ACTING Mu antagonist–longer duration of action than naloxone

Long acting opioid antagonist used for relapse prevention once detoxified

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60
Q

Nitrous oxide

A

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.

61
Q

Halothane

A

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)

62
Q

Enfluorane

A

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)

63
Q

Isofluorane

A

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

64
Q

Desfluorane

A

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

65
Q

Sevofluorane

A

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)

66
Q

Thiopental

A

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)

67
Q

Midazolam

A

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)

68
Q

Diazepam

A

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)

69
Q

Lorazepam

A

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)

70
Q

Flumazenil

A

Benzodiazepine antagonist–reversal agent

Half life is shorter than benzodiazepines so must administer enough

71
Q

Propofol

A

IV anesthetic. Potentiates GABAa. Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less postoperative nausea than thiopental.

72
Q

Ketamine

A

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)

73
Q

Lidocaine

A

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.

74
Q

Bupivacaine

A

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.

75
Q

Mepivacaine

A

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.

76
Q

Cocaine

A

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.

77
Q

Procaine

A

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.

78
Q

Tetracaine

A

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.

79
Q

Epinephrine

A

Vasoconstrictor used with locals

80
Q

Nortryptaline

A

Smoking cessation medication

Antidepressant–efficacy is due to effects on nerotransmitters, NOT due to any treatment of co morbid depression

81
Q

Varenicline

A

Smoking cessation medication

MOA: partial agonist of nicotinic ach receptor. Agonist activity mimics nicotine and the antagonist activity prevents nicotine from binding

82
Q

Disulfiram

A

Alcoholism drug

MOA: inhibitor of aldehyde dehydrogenase–induces accumulation of acetaldehyde whenever alcohol is consumed

83
Q

Acamprosate

A

Alcoholism drug

Reduces the craving for alcohol–presumably mediated through antagonism of the NMDA receptors

84
Q

Naltrexone

A

Alcoholism drug

Antagonizes opioid receptors, decreasing the reward sensation associated with drinking alcohol

85
Q

Methamphetamine

A

MOA: CNS stimulant. Increases catecholamines at synaptic cleft, especially NE and dopamine.

USES: ADHD, narcolepsy, appetite control

86
Q

Dextroamphetamine

A

MOA: CNS stimulant. Increases catecholamines at synaptic cleft, especially NE and dopamine.

USES: ADHD, narcolepsy, appetite control

87
Q

Methylphenidate

A

MOA: CNS stimulant. Increases catecholamines at synaptic cleft, especially NE and dopamine.

USES: first line for ADHD, narcolepsy, appetite control

88
Q

Cocaine

A

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

89
Q

Caffeine

A

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,

90
Q

Modafinil

A

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)

91
Q

Atomoxetine

A

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

92
Q

Epinephrine

A

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

93
Q

Brimonidine

A

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

94
Q

Timolol

A

MOA: beta blocker. Decreases aqueous humor synthesis

USES: glaucoma

SIDE EFFECTS: NO vision or pupillary changes

95
Q

Betaxolol

A

MOA: beta blocker. Decreases aqueous humor synthesis

USES: glaucoma

SIDE EFFECTS: NO vision or pupillary changes

96
Q

Carteolol

A

MOA: beta blocker. Decreases aqueous humor synthesis

USES: glaucoma

SIDE EFFECTS: NO vision or pupillary changes

97
Q

Acetazolamide

A

MOA: Diuretic. Decreases aqueous humor synthesis via inhibition of carbonic anhydrase.

USES: glaucoma

SIDE EFFECTS: no pupillary or vision changes

98
Q

Pilocarpine

A

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)

99
Q

Carbachol

A

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)

100
Q

Physostigmine

A

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)

101
Q

Echothiophate

A

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)

102
Q

Latanoprost

A

MOA: PGF2. Increases outflow of aqueous humor

USES: glaucoma

SIDE EFFECTS: mitosis and cycloplasm (contraction of ciliary muscle)

103
Q

Loperamide

A

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)

104
Q

Dextromethorphan

A

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)

105
Q

Diphenoxylate

A

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)

106
Q

Alprazolam

A

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)

107
Q

Chlordiazepoxide

A

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)

108
Q

Oxazepam

A

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)

109
Q

Temazepam

A

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)

110
Q

Triazolam

A

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)

111
Q

Methoxyflurane

A

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)

112
Q

Ezopiclone

A

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.

113
Q

Zaleplon

A

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.

114
Q

Secobarbital

A

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)

115
Q

Pentobarbitol

A

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)

116
Q

Phenobarbital

A

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)

117
Q

Tetrabenazine

A

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)

118
Q

Phentermine

A

MOA: CNS stimulant. Increases catecholamines at synaptic cleft, especially NE and dopamine.

USES: ADHD, narcolepsy, appetite control

119
Q

Baclofen

A

MOA: inhibits GABAa receptors at spinal cord level, including skeletal muscle relaxation

USE: muscle spasms (e.g. Acute low back pain)

120
Q

Cyclobenzaprine

A

MOA: centrally acting skeletal muscle relaxant. Structurally related to TCAs, similar to anticholinergic side effects

USE: muscle spasms

121
Q

Reserpine

A

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)

122
Q

Benztropine

A

MOA: Antimuscarinic–curbs excess cholinergic activity

USES: Parkinson’s. Improves tremor and rigidity but has little effect on bradykinesia

123
Q

Dantrolene

A

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)

124
Q

Citalopram

A

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)

125
Q

Venlafaxine

A

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

126
Q

Duloxetine

A

MOA: inhibits 5-HT and NE reuptake

USES: depression. Also indicated for diabetic peripheral neuropathy

TOXICITY: increases BP. Also stimulant effects, sedation, nausea

127
Q

Amitriptyline

A

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.

128
Q

Imipramine

A

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.

129
Q

Desipramine

A

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.

130
Q

Clomipramine

A

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.

131
Q

Doxepin

A

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.

132
Q

Amoxapine

A

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.

133
Q

Tranylcypromine

A

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)

134
Q

Phenelzine

A

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)

135
Q

Isocarboxazid

A

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)

136
Q

Selegiline

A

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)

137
Q

Varenicline

A

Partial agonist of nicotinic acetylcholine receptors in CNS. Competes with nicotine and decreases symptoms of nicotine withdrawal. Used for smoking cessation.

138
Q

Riluzole

A

Treatment for ALS. Modestly increases survival of neurons by decreasing presynaptic glutamate release.

139
Q

Primidone

A

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.

140
Q

Modafinil

A

Non-amphetamine stimulant used to treat narcolepsy

141
Q

Pentazocine

A

Opioid analgesic. Partial agonist and weak antagonist, can precipitate withdrawal symptoms in patients dependent on morphine.

142
Q

Sertraline

A

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)

143
Q

Paroxetine

A

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)

144
Q

Trifluoperazine

A

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.

145
Q

Rocuronium

A

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

146
Q

Vecuronium

A

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

147
Q

Succinylcholine

A

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

147
Q

Tubocurarine

A

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

147
Q

Atracurium

A

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

147
Q

Mivacurium

A

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

147
Q

Pancuronium

A

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

Pharmacology (13 decks)

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