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Rheum-Chelsey > Neuro/Pysch Drugs > Flashcards

Neuro/Pysch Drugs Flashcards

1
Q

MOA for Epinephrine in Tx Glaucoma?

A

Alpha agonist: decrease aqueous humor synthesis via vasoconstriction

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2
Q

MOA of Brimonidine in Tx glaucoma?

A

Decrease aqueous humor synthesis (a2 agonist)

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3
Q

Ade’s of epi?

A

Mydriasis; do not use in closed-angle glaucoma

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4
Q

Ade’s of brimonidine?

A

Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus

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5
Q

MOA of timolol, betaxolol, and carteolol in Tx of glaucoma?

A

aqueous humor synthesis

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6
Q

Ade of timolol, betaxolol, and carteolol?

A

No pupillary or vision changes

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7
Q

MOA of Acetazolamide in Tx of glaucoma?

A

Decrease aqueous humor synthesis via inhibition of carbonic anhydrase

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8
Q

Ade’s of acetazolamide?

A

No pupillary or vision changes

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9
Q

MOA of the direct and indirect cholinomimetics?

A

Increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

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10
Q

Which drugs are direct cholinomimetics? Which are indirect?

A

Direct=(pilocarpine, carbachol)

Indirect=(physostigmine, echothiophate)

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11
Q

What can pilocarpine be specifically used for?

A

Use pilocarpine in emergencie; very effective at opening meshwork into canal of Schlemm

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12
Q

Ade’s of the cholinomimetics?

A

Miosis and cyclospasm (contraction of ciliary muscle)

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13
Q

MOA of Latanoprost (PGF2α) in Tx glaucoma?

A

Increase outflow of aqueous humor

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14
Q

Ade of latanoprost?

A

Darkens color of iris (browning)

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15
Q

What are the opioid analgesics?

A

Morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate.

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16
Q

MOA of opioids?

A

Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission—open K+ channels, close Ca2+ channelsŽ-> decrease synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.

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17
Q

Clinical use for opioids?

A

Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone).

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18
Q

Opioids ades?

A

Addiction, 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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19
Q

Moa of butophanol?

A

Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia.

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20
Q

What’s butophanol used for?

A

Severe pain (migraine, labor, etc.). Causes less respiratory depression than full opioid agonists.

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21
Q

Butorphanol ades?

A

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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22
Q

Moa of tramadol?

A

Very weak opioid agonist; also inhibits serotonin and norepinephrine reuptake (works on multiple neurotransmitters—“tram it all” in with tramadol).

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23
Q

What’s tramadol used for?

A

Chronic pain

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24
Q

Ade’s of tramadol?

A

Similar to opioids. Decreases seizure threshold. Serotonin syndrome.

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25
Q

Drugs used to Tx absence seizures?

A

Ethosuximide (1st line), valproic acid, lamotrigine

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26
Q

Moa of ethosuximide?

A

Blocks thalamic T-type Ca2+ channels

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27
Q

Ade’s of ethosuximide?

A

“EFGHIJ”—Ethosuximide causes Fatigue, GI distress, Headache, Itching, and Stevens-Johnson syndrome

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28
Q

Moa of benzo’s (diazepam, lorazepam)?

A

Increase GABAa action

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29
Q

Ade’s with benzo’s

A

Sedation, tolerance, dependence, respiratory depression

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30
Q

For what kind of seizures would you use benzo’s?

A

Status epilepticus (1st line for acute). Also for eclampsia seizures (1st line is MgSO4)

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31
Q

Moa of phenytoin?

A

Increase Na+ channel inactivation; zero-order kinetics

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32
Q

Ade’s of phenytoin?

A

Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome) SLE-like syndrome, induction of cytochrome P-450, lymphadenopathy, Stevens- Johnson syndrome, osteopenia

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33
Q

When would you use phenytoin?

A

1st line for tonic clonic; 1st line prophylaxis for status epilepticus, also used for simple and complex. Note: Fosphenytoin for parenteral use

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34
Q

Moa of carbamazepine?

A

Increase Na+ channel inactivation

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35
Q

Ade’s of carbamazepine?

A

Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450, SIADH, Stevens-Johnson syndrome

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36
Q

Uses of carbamazepine?

A

1st line for simple, complex, and tonic clonic. Also 1st line for trigeminal neuralgia

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37
Q

Valproic acid moa?

A

Increase Na+ channel inactivation, increase GABA concentration
by inhibiting GABA transaminase

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38
Q

Ade’s of valproic acid?

A

GI, distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated in pregnancy

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39
Q

Uses for valproic acid?

A

1st line for tonic clonic, also used for simple, complex and absence. Also used for myoclonic seizures and bipolar disorder

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40
Q

Moa Gabapentin?

A

Primarily inhibits high voltage activated Ca2+ channels; designed as GABA analog

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41
Q

Ade’s of gabapentin?

A

Sedation, ataxia

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42
Q

Uses of gabapentin?

A

Simple, complex, and tonic clonic. Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder

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43
Q

Phenobarbital moa?

A

Increase GABAa action

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44
Q

Phenobarbital ade’s?

A

Sedation, tolerance, dependence, induction of cytochrome P-450, cardiorespiratory depression

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45
Q

Uses of phenobarbital?

A

Simple, complex, and tonic clonic. 1st line in neonates

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46
Q

Topiramate moa?

A

Blocks Na+ channels, and increases GABA action

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47
Q

Ades of topiamate?

A

Sedation, mental dulling, kidney stones, weight loss

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48
Q

What’s topiramate used for?

A

Simple, complex, and tonic clonic. Also used for migraine prevention

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49
Q

Lamotrigine moa?

A

Blocks voltage-gated Na+ channels

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50
Q

Uses for Lamotrigine?

A

Simple, complex, tonic clonic and absence

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51
Q

Lamotrigine ade’s?

A

SJS (must titrate slowly)

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52
Q

Levetiracetam moa?

A

Unknown; may modulate GABA and glutamate release

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53
Q

Uses for Levetiracetam?

A

Simple, complex, and tonic clonic

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54
Q

Tiagabine moa?

A

Increase GABA by inhibiting re-uptake

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55
Q

Uses for tiagabine?

A

Simple and complex

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56
Q

Vigabatrin moa?

A

Increase GABA by irreversibly inhibiting GABA transaminase

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57
Q

Uses for Vigabatrin?

A

Simple and complex

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58
Q

Primidone moa?

A

Metabolized to phenobarbital and phenylethylmalonamide

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59
Q

MOA of barbiturates (Phenobarbital, pentobarbital, thiopental, secobarbital)?

A

Facilitate GABAa action by increasing duration of Cl- channel opening, thus decreasing neuron firing (barbidurates increase duration). Contraindicated in porphyria.

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60
Q

Clinical use of barbiturates?

A

Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).

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61
Q

Barbiturates ades?

A

Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence; drug interactions (induces cytochrome P-450).
Overdose treatment is supportive (assist respiration and maintain BP).

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62
Q

Moa of benzo’s (Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)?

A

Facilitate GABAa action by increasing frequency of
Cl- channel opening. Decrease REM sleep. Most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short actingŽ and have higher addictive potential).

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63
Q

Uses for benzo’s?

A

Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).

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64
Q

Ades with benzo’s?

A

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 recep

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65
Q

What are the nonbenzo hypnotics?

A

Zolpidem (Ambien), Zaleplon, esZopiclone. “All ZZZs put you to sleep.”

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66
Q

MOA for nonbenzo hypnotics?

A

Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil

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67
Q

What are the nonbenzo hypnotics used for?

A

Insomnia

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68
Q

Ade’s of the nonbenzo hypnotics?

A

Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Lower dependence risk than benzodiazepines.

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69
Q

What properties must anesthetics have to get into the CNS?

A

lipid soluble (cross the blood-brain barrier) or be actively transported.

70
Q

What kind of anesthetics have rapid induction and recovery times?

A

Drugs with low solubility in blood

71
Q

Which anesthetics have high potency?

A

Drugs with high solubility in lipids. Increased potency = 1 /MAC

72
Q

What’s MAC?

A

Minimal Alveolar Concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g., skin incision).
Examples: N2O has low blood and lipid solubility, and thus fast induction and low potency. Halothane, in contrast, has high lipid and blood solubility, and thus high potency and slow induction.

73
Q

What are the inhaled anesthetics?

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, and nitrous oxide. MOA is unknown

74
Q

Effects of inhaled anesthetics?

A

Myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow (decrease cerebral metabolic demand).

75
Q

Ades halothane?

A

Hepatotoxicity

76
Q

Ades of methoxyflurane?

A

Nephrotoxicity

77
Q

Ades of enflurane?

A

Proconvulsant

78
Q

Ades of nitrous oxide?

A

Expansion of trapped gas in a body cavity

79
Q

What severe side effect is assoc with the inhaled anesthetics?

A

Can cause malignant hyperthermia—rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene.

80
Q

What are the IV anesthetics?

A

barbiturates, benzo’s, arylcyclohexylamines (Ketamine), opioids, and propofol.
“B. B. King on OPIOIDS PROPOses FOOLishly”

81
Q

Barbiturates: Use/properties for IV anesthesia?

A

Thiopental—high potency, high lipid solubility, rapid entry into brain. Used for induction
of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (i.e., skeletal muscle) and fat. Decreases cerebral blood flow.

82
Q

Benzo’s: Use/properties for IV anesthesia?

A

Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decreases BP (treat overdose with flumazenil), and anterograde amnesia.

83
Q

Arylcyclohexylamines (Ketamine): Use/properties for IV anesthesia?

A

PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. Increases cerebral blood flow.

84
Q

Opioids: Use/properties for IV anesthesia?

A

Morphine, fentanyl used with other CNS depressants during general anesthesia.

85
Q

Propofol: Use/properties for IV anesthesia?

A

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

86
Q

What are the local anesthetics?

A

Esters—procaine, cocaine, tetracaine.

Amides—LidocaIne, mepivacaIne, bupivacaIne (amides have 2 I’s in name).

87
Q

MOA of local anesthetics?

A

Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.

88
Q

Principles for local anesthetics?

A 
Can be given with vasoconstrictors (usually epinephrine) to enhance local action— decrease bleeding, increase anesthesia by decreasing systemic concentration.
In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively so Žneed more anesthetic.
89
Q

Order of nerve blockade when using local anesthetics?

A

Small-diameter fibers > large diameter.
Myelinated fibers > unmyelinated fibers.
Overall, size factor predominates over myelination such that small myelinated fibers
> small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers.
Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure.

90
Q

Uses for local anesthetics?

A

Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.

91
Q

Ades of the local anesthetics?

A

CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).

92
Q

What are neuromuscular blocking drugs used for?

A

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

93
Q

What’s a Depolarizing NM blocking drug?

A

Succinylcholine—strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction

94
Q

Reversal of blockade for the depolarizing NM blockers?

A 
Phase I (prolonged depolarization): no antidote. Block potentiated by cholinesterase inhibitors. ƒ 
Phase II (repolarized but blocked; ACh receptors are available, but desensitized): antidote
consists of cholinesterase inhibitors.
95
Q

Complications of succinylcholine?

A

Hypercalcemia, hyperkalemia, and malignant hyperthermia.

96
Q

What are the non-depolarizing NM blockers?

A

(Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium): competitive antagonists that compete with ACh for receptors.

97
Q

Reversal of blockage for non-depolarizing NM blockers?

A

Neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.

98
Q

Dantrolene moa?

A

Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.

99
Q

What’s dantrolene used for?

A

Used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).

100
Q

Parkinson’s: neuroTx probs?

A

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity.

101
Q

Strategy for Tx parkinsons?

A

Dopamine agonists, increase dopamine, prevent dopamine breakdown, and curb excess cholinergic activity

102
Q

Dopamine agonists?

A

Bromocriptine (ergot), pramipexole, ropinirole (non-ergot); non-ergots are preferred

103
Q

What drug can you use to increase dopamine?

A

Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; toxicity = ataxia
L-dopa/carbidopa (converted to dopamine in CNS)

104
Q

What drug can you use to prevent dopamine breakdown?

A

Selegiline (selective MAO type B inhibitor); entacapone, tolcapone (COMT inhibitors— prevent l-dopa degradationŽ and increase dopamine availability)

105
Q

What drugs can you use to curb excess cholinergic activity?

A

Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia)
Park your Benz

106
Q

MOA of L-dopa/carbidopa?

A

Increase level of dopamine in brain. Unlike dopamine, l-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine. Carbidopa, a peripheral decarboxylase inhibitor, is given with l-dopa to increase the bioavailability of l-dopa in the brain and to limit peripheral side effects.

107
Q

Ades with L-dopa/carbidopa?

A

Arrhythmias from increased peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (“on-off” phenomenon), akinesia between doses.

108
Q

Moa of selegiline?

A

Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby increasing the availability of dopamine.

109
Q

When’s selegiline used?

A

Adjunctive agent to l-dopa in treatment of Parkinson disease

110
Q

Ades with selegiline?

A

May enhance adverse effects of l-dopa

111
Q

Memantine- use and moa?

A

Used for alzheimers. NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).

112
Q

Ades of memantine?

A

Dizziness, confusion, hallucinations.

113
Q

Moa and use of donepezil, galantamine, rivastigmine?

A

Alzheimers. AChE inhibitors.

114
Q

Ades of donepezil, galantamine, rivastigmine?

A

Nausea, dizziness, insomnia.

115
Q

NeuroTx changes in huntingtons?

A

Decreased GABA and Ach

Increased dopamine

116
Q

Tx for huntingtons?

A

Tetrabenazine and reserpine—inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.
ƒ Haloperidol—dopamine receptor antagonist.

117
Q

Moa of sumitriptan?

A

5-HT1B/1D AGONIST. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half-life < 2 hours.

118
Q

Uses for triptans?

A

Acute migraine, cluster headache attacks

119
Q

Ades with triptans?

A

Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling.

120
Q

Tx for ADHD?

A

Methylphenidate

121
Q

Tx anxiety?

A

SSRIs, SNRIs and buspirone

122
Q

Tx bipolar?

A

Li, carbamazepine, and valproic acid

123
Q

Tx bulimia?

A

SSRIs

124
Q

Tx depression?

A

SRIs, SNRIs, TCAs, bupropion, mirtazapine (especially with insomnia)

125
Q

Tx OCD?

A

SSRIs, clomipramine

126
Q

Tx panic disorder?

A

SSRIs, venlafaxine, benzodiazepines

127
Q

Tx PTSD?

A

SSRIs

128
Q

Tx social phobias?

A

SSRIs, β-blockers

129
Q

Tx tourette’s?

A

Antipsychotics (e.g., haloperidol, risperidone)

130
Q

What are the CNS stimulants and what are is their moa?

A

Methylphenidate, dextroamphetamine, methamphetamine, phentermine.
They increase catecholamines at the synaptic cleft, especially norepinephrine and dopamine.

131
Q

Uses for CNS stimulants?

A

ADHD, narcolepsy, appetite control.

132
Q

What are the typical Antipsychotics (neuroleptics)?

A

Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine (haloperidol + “-azines”).

133
Q

MOA of typical antipsychotics?

A

All typical antipsychotics block dopamine D2 receptors (Increase[cAMP]).

134
Q

Uses for the typical antipsychotics?

A

Schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome

135
Q

Toxicity with typical antipsychotics?

A

Highly lipid soluble and stored in body fat; thus, very slow to be removed from body.
Extrapyramidal system side effects (e.g., dyskinesias). Treatment: benztropine or diphenhydramine.
Endocrine side effects (e.g., dopamine receptor antagonismŽ: hyperprolactinemia &galactorrhea).
Side effects arising from blocking muscarinic (dry mouth, constipation), α1 (hypotension), and histamine (sedation) receptors.

136
Q

What other serious ADEs are seen with the typical antipsychotics?

A

Neuroleptic malignant syndrome (NMS)— rigidity, myoglobinuria, autonomic instability, hyperpyrexia. Treatment: dantrolene, D2 agonists (e.g., bromocriptine).
Tardive dyskinesia—stereotypic oral- facial movements as a result of long-term antipsychotic use. Potentially irreversible.

137
Q

What are the high potency typical antipsychotics?

A

Trifluoperazine, Fluphenazine, Haloperidol (Try to Fly High)—neurologic side effects (EPS symptoms).

138
Q

What are the low potency typical antipsychotics?

A

Chlorpromazine, Thioridazine (Cheating Thieves are low)—non-neurologic side effects (anticholinergic, antihistamine, and α1-blockade effects).

139
Q

Which drug can cause corneal deposits? Which can cause retinal deposits?

A

Chlorpromazine=corneal and thiordazine=retinal

140
Q

Haloperidol ade?

A

NMS, tardive dyskinesia.

141
Q

What’s the evolution of the EPS side effects?

A

4 hr-acute dystonia (muscle spasm, stiffness, oculogyric crisis)
ƒ4 day-akathisia (restlessness)
ƒ 4 wk-bradykinesia (parkinsonism) ƒ 4 mo-tardive dyskinesia

142
Q

NMS Sx?

A

For NMS, think FEVER: Fever,

Encephalopathy, Vitals unstable, Enzymes, Rigidity of muscles

143
Q

What are the atypical antipsychotics?

A

Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone.

144
Q

MOA for the atypical antipsychotics?

A

Not completely understood. Varied effects on 5-HT2, dopamine, and α- and H1-receptors.

145
Q

Clinical use for the atypical antipsychotics?

A

Schizophrenia—both positive and negative symptoms. Also used for bipolar disorder, OCD, anxiety disorder, depression, mania, Tourette syndrome.

146
Q

ADEs with the atypical antipsychotics?

A

Fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. Olanzapine/clozapine may cause significant weight gain. Clozapine may cause agranulocytosis (requires weekly WBC monitoring) and seizure. Risperidone may increase prolactin (causing lactation and gynecomastia)Ž low GnRH, LH, and FSH (causing irregular menstruation and fertility issues). Ziprasidone may prolong the QT interval.

147
Q

Li moa?

A

Not established; possibly related to inhibition of phosphoinositol cascade.

148
Q

What’s Li used for?

A

Mood stabilizer for bipolar disorder; blocks relapse and acute manic events. Also SIADH.

149
Q

Ades with Li?

A

Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist causing nephrogenic diabetes insipidus), teratogenesis. Fetal cardiac defects include Ebstein anomaly and malformation of the great vessels. Narrow therapeutic window requires close monitoring of serum levels. Almost exclusively excreted by the kidneys; most is reabsorbed at the proximal convoluted tubules following Na+ reabsorption.

150
Q

What’s buspirone’s moa?

A

Stimulates 5-HT1A receptors.

151
Q

What’s buspirone used for?

A

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).

152
Q

What are the SSRI’s and what’s their moa?

A

Fluoxetine, paroxetine, sertraline, citalopram. 5-HT–specific reuptake inhibitors.

153
Q

Uses for SSRI’s

A

Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD. It normally takes 4–8 weeks for antidepressants to have an effect.

154
Q

Ades with SSRI’s?

A

Fewer than TCAs. GI distress, sexual dysfunction (anorgasmia andlibido). Serotonin syndrome with any drug that increases 5-HT (e.g., MAO inhibitors, SNRIs, TCAs)—hyperthermia, confusion, myoclonus, cardiovascular collapse, flushing, diarrhea, seizures. Treatment: cyproheptadine (5-HT2 receptor antagonist).

155
Q

What are the SNRI’s and what’s their moa?

A

Venlafaxine, duloxetine. Inhibit 5-HT and norepinephrine reuptake.

156
Q

Clinical uses for the SNRI’s?

A

Depression. Venlafaxine is also used in generalized anxiety and panic disorders; duloxetine is also indicated for diabetic peripheral neuropathy.

157
Q

ADEs with SNRIs?

A

Increase BP most common; also stimulant effects, sedation, nausea.

158
Q

What are the TCAs and their moa?

A

Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine (all TCAs end in -iptyline or -ipramine except doxepin and amoxapine).
Block reuptake of norepinephrine and 5-HT.

159
Q

Indications for TCAs?

A

Major depression, OCD (clomipramine), fibromyalgia.

160
Q

TCAs ADEs?

A

Sedation, α1-blocking effects including postural hypotension, and atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth). 3° TCAs (amitriptyline) have more anticholinergic effects than 2° TCAs (nortriptyline) have. Desipramine is less sedating, but has a higher seizure incidence.
Tri-C’s: Convulsions, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects (use nortriptyline). Treatment: NaHCO3 for cardiovascular toxicity.

161
Q

What are the MAOIs and what’s their moa?

A

Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline (selective MAO-B inhibitor).
Nonselective MAO inhibition will increase levels of amine neurotransmitters (norepinephrine, 5-HT, dopamine).

162
Q

Uses for MAOIs?

A

Atypical depression, anxiety, hypochondriasis.

163
Q

ADEs with the MAOIs?

A

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, and dextromethorphan (to prevent serotonin syndrome).

164
Q

What are the atypical antidepressants?

A

Bupropion, Mirtazapine and Trazodone

165
Q

MOA of bupropion?

A

Also used for smoking cessation. Increase norepinephrine and dopamine via unknown
mechanism.

166
Q

ADEs with bupropion?

A

Stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients. No sexual side effects.

167
Q

MOA of mirtazapine?

A

α2-antagonist (Increases release of norepinephrine and 5-HT) and potent 5-HT2 and 5-HT3
receptor antagonist.

168
Q

Ades of mirtazapine?

A

Sedation (which may be desirable in depressed patients with insomnia),appetite, weight gain (which may be desirable in elderly or anorexic patients), dry mouth.

169
Q

MOA of trazadone?

A

Primarily blocks 5-HT2 and α1-adrenergic receptors. Used primarily for insomnia, as high
doses are needed for antidepressant effects.

170
Q

ADEs with trazadone?

A

Sedation, nausea, priapism, postural hypotension.

Rheum-Chelsey (6 decks)

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