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Pharmacology I > Module 5 > Flashcards

Module 5 Flashcards

CNS Drugs Part 2

1
Q

Parkinson’s Disease Pathophysiology

A

progressive degeneration of neurons in the substantia nigra causing loss of DA transmission and reduced thalamic stimulation of the cortex

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2
Q

Parkinson’s Disease sx

A

rest tremor, bradykinesia, rigidity, and postural defect causing a tendency to stoop

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3
Q

effect of D1 receptors on neuronal activity

A

excitatory

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4
Q

effect of D2 receptors on neuronal activity

A

inhibitory

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5
Q

Levodopa (L-DOPA) MOA

A

dopamine precursor that crosses the blood-brain barrier and is converted to dopamine by dopamine decarboxylase

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6
Q

Levodopa adverse effects

A

hallucinations/confusion, dyskinesia, peripheral effects including nausea (interaction with DA receptors in gut), hypotension, and arrhythmia

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7
Q

Carbidopa MOA

A

peripheral inhibitor of DA decarboxylase (DDC) allowing Levodopa to make it to CNS without being metabolized in the periphery (does not cross the blood-brain barrier), reduces peripheral side effects of Levodopa

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8
Q

Entacapone MOA

A

inhibits COMT (catechol-o-methyl transferase) enzyme mostly in the periphery preventing the degradation of Levodopa in the periphery

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9
Q

Entacapone adverse effects

A

dyskinesia, nausea, and diarrhea

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10
Q

Levodopa adjustment to reduce motor fluctuation

A

increase the number or frequency of Levodopa dosages

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11
Q

Selegiline MOA

A

selectively inhibits MAO B in the striatum preventing the metabolism of DA, NE, and 5-HT (serotonin), reduces the dose of Levodopa needed

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12
Q

Selegiline adverse effects

A

partly metabolized to amphetamine causing amphetamine-like side effects, serotonin syndrome can be induced by combining with tyramine-rich foods or SSRIs, can cause drug interactions due to metabolism by CYP450

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13
Q

Bromocriptine MOA

A

Ergot alkaloid with more selective D2 receptor agonist activity but with some activity at D1, D3, and 5-HT receptors, does not rely on existing DA neurons

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14
Q

Bromocriptine clinical use

A

used to delay the need for Levodopa and to treat advanced Parkinson’s disease

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15
Q

Bromocriptine adverse effects

A

similar to levodopa but with more risk of psychotic effects, poses risk of cardiac valve fibrosis with long-term use

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16
Q

Ropinirole MOA

A

less selective dopamine receptor agonist than Bromocriptine with D2, D3, and D4 receptor agonist activity

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17
Q

Ropinirole clinical uses

A

Parkinson’s and restless leg syndrome

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18
Q

Ropinirole adverse effects

A

reduced risk of cardiac valve fibrosis compared to Bromocriptine, can increase risky behavior due to D3 agonism, can cause drug interactions due to metabolism by CYP450

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19
Q

Trihexyphenidyl MOA

A

muscarinic Ach receptor antagonist that is often given in combination with DA agonists, excreted in the urine unchanged

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20
Q

Trihexyphenidyl clinical use

A

often given in combination with DA agonists effective at reducing dyskinetic movements and spastic contractions

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21
Q

Trihexyphenidyl adverse effects

A

causes anticholinergic side effects including sedation, confusion, constipation, and urinary retention

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22
Q

Amantadine MOA

A

antiviral drug that increases DA release and blocks NMDA glutamate receptors, has an anti-Parkinson’s affect

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23
Q

Amantadine clinical use

A

less effective at treating Parkinson’s compared to Levodopa and used as last resort

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24
Q

Amantadine adverse effects

A

causes confusion and psychosis

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25
Q

Huntington’s disease pathophysiology

A

Inherited autosomal dominant disease characterized by involuntary movements (chorea), personality changes, and bradykinesia due to neuronal loss in the caudate nucleus/putamen and striatum and loss of GABA function

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26
Q

Deutetrabenazine MOA

A

inhibitor of VMAT-2 (vesicular monoamine transporter) which prevents the storage of neurotransmitters in vesicles and reduces involuntary hyperkinetic movements seen with Huntington’s (longer half-life relative to tetrabenazine)

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27
Q

Deutetrabenazine adverse effects

A

similar to antipsychotics including akathisia, drowsiness, tremor, and depression, some patients are poor metabolizers due to the requirement of CYP450

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28
Q

Deutetrabenazine contraindications

A

contraindicated with MAO inhibitors and in uncontrolled depression with suicide risk

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29
Q

Deutetrabenazine clinical use

A

used to treat Huntington’s, Tourette’s, and Tardive dyskinesia (involuntary facial movements)

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30
Q

Alzheimer’s Dementia pathophysiology

A

the accumulation of beta-amyloid plaques and neurofibrillary tangles in the hippocampus and cortex causing cholinergic damage, loss of enzymes for Ach synthesis, and loss of cholinergic neurons in the basal forebrain

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31
Q

Donepezil MOA

A

acetylcholinesterase inhibitor that readily enters the CNS and raises Ach levels in damaged areas of the brain and may also increase Ach synthesis and release

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32
Q

Donepezil clinical use

A

administered once daily (relatively long half-life) in the treatment of Alzheimer’s Dementia

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33
Q

Donepezil adverse effects

A

overactive gut motility from cholinergic effects causing nausea, vomiting, and diarrhea, causes sleep disturbances - vivid dreams, no major drug interactions

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34
Q

Memantine MOA

A

NMDA receptor antagonist that blocks pathological activation of NMDA receptors and is thought to reduce excitotoxicity (noise which causes confusion)

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35
Q

Memantine clinical use

A

not as effective as monotherapy as Donepezil but useful for patients who do not respond or cannot tolerate Donepezil side effects, usually combined with Donepezil

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36
Q

Memantine adverse effects

A

dizziness, headache, constipation, and confusion

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37
Q

Epilepsy

A

An assortment of different seizure types and syndromes that have in common the sudden, excessive, and synchronous discharge of cerebral neurons causing abnormal electrical activity that can result in events including LOC, abnormal movements, atypical or odd behavior, and distorted perceptions of limited duration but that can recur if untreated.

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38
Q

Idiopathic epilepsy

A

seizures without specific anatomic cause, such as trauma or neoplasm, most cases of epilepsy are idiopathic

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39
Q

Symptomatic epilepsy

A

seizures caused by illicit drug use, tumor, head injury, hypoglycemia, meningeal infection, or alcohol withdrawal

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40
Q

Partial simple seizure

A

caused by a group of hyperactive neurons exhibiting abnormal electrical activity which are confined to a single locus in the brain, no LOC and often exhibit abnormal movement of a single limb or muscle group controlled by that area in the brain.

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41
Q

Partial complex seizure

A

exhibits complex sensory hallucinations and mental distortion, altered consciousness and memory

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42
Q

Generalized seizure

A

a complex seizure that involves both hemispheres of the brain and causes LOC and altered memory - include tonic-clonic, absence, and myoclonic seizures, infantile spasm, and status epilepticus

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43
Q

status epilepticus

A

two or more seizures that occur without full recovery of consciousness between them - life threatening

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44
Q

tonic-clonic seizure

A

LOC followed by tonic (continuous contraction) and clonic (rapid contraction and relaxation phases)

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45
Q

absence seizure

A

brief abrupt self-limiting loss of consciousness - may stare and exhibit rapid eye blinking lasting 3-5 seconds

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46
Q

myoclonic seizure

A

short episodes of muscle contractions that may recur within several minutes

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47
Q

General mechanism of antiseizure drugs (AEDs)

A

block Na+ or Ca2+ voltage-gated channels, enhance inhibitory GABA-ergic impulses, interfere with excitatory glutamate transmission

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48
Q

Benzodiazepines MOA

A

bind to GABA inhibitory receptors increasing the frequency of chloride channel opening

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49
Q

Benzo with shortest half-life but longest duration of action in the brain

A

Lorazepam

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50
Q

Diazepam admin

A

available for rectal admin to avoid or interrupt prolonged generalized tonic-clonic seizures or clusters (children and patients with AMS)

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51
Q

Benzodiazepine clinical use in seizures

A

diazepam and lorazepam are most often used as adjunctive therapy for myoclonic as well as partial and generalized tonic-clonic seizures

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52
Q

Carbamazepine MOA

A

blocks sodium channels reducing the propagation of abnormal impulses in the brain thereby inhibiting the generation of repetitive action potentials in the epileptic focus and preventing spread

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53
Q

Carbamazepine clinical use

A

used primarily prophylactically to treat partial seizures and secondarily generalized tonic-clonic seizures (DO NOT prescribe for patients with ABSENCE seizures because it could increase seizures)

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54
Q

Carbamazepine admin

A

administered orally and absorbed slowly and erratically resulting in large variations of serum concentrations, inducer of CYP and UGT enzymes

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55
Q

Carbamazepine contraindications

A

Do not prescribe to patients with ABSENCE seizures!! not well tolerated in the elderly

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56
Q

Ethosuximide MOA

A

most likely inhibits T-type calcium channels reducing the propagation of abnormal electrical activity in the brain

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57
Q

Ethosuximide clinical use

A

drug of choice for treating primary generalized absence seizures - “ET sux a mind” until all thoughts are absent!

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58
Q

Gabapentin MOA

A

analog of GABA but does not act on GABA receptors, enhance GABA actions, or become converted to GABA (unknown MOA)

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59
Q

Gabapentin clinical use

A

approved as adjunct therapy for partial seizures and for the treatment of postherpetic neuralgia

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60
Q

Gabapentin admin

A

requires dose reduction in renal disease but is well tolerated in the elderly, does not bind to plasma proteins and is excreted unchanged through the kidneys

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61
Q

Lamotrigine MOA

A

blocks sodium channels as well as high-voltage-dependent calcium channels

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62
Q

Lamotrigine clinical use

A

treatment for a wide variety of seizure types including partial, generalized, and absence seizures, Lennox-Gastaut Syndrome, and bipolar disorder, tolerated well in elderly

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63
Q

Lamotrigine pharmacokinetics

A

half-life is 24-35 hours which is shortened by CYP-inducing drugs like carbamazepine and phenytoin and increased by greater than 50% if given in combo with valproate (must reduce dose if given in combo), metabolized through the UGT pathway

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64
Q

Lamotrigine adverse effects

A

rapid titration can cause a rash which may progress to life-threatening Stevens-Johnson Syndrome

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65
Q

Levetiracetam/Keppra clinical use

A

approved for adjunct therapy of partial, myoclonic, and primary generalized tonic-clonic seizures in adults and children

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66
Q

Levetiracetam admin

A

administered orally and well absorbed, excreted in urine unchanged

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67
Q

Levetiracetam adverse effects

A

dizziness, sleep disturbances, headache, and weakness

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68
Q

Oxcarbazepine MOA

A

prodrug that is rapidly reduced to the 10-monohydroxy (MHD) metabolite which blocks sodium channels preventing the spread of abnormal discharge, thought to modulate calcium channels

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69
Q

Oxcarbazepine clinical use

A

used to treat partial onset seizures in adults and children

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70
Q

Oxcarbazepine adverse effects

A

hyponatremia

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71
Q

Phenobarbital MOA

A

a barbiturate that enhances the inhibitory effects of GABA-mediated neurons

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72
Q

Phenobarbital clinical use

A

used primarily in the abortive treatment of status epilepticus, levels must be monitored with continuous use and patients must be tapered off when stopped (being used more and more in hospital settings to sedate patients and to prevent seizures in alcohol withdrawal)

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73
Q

Phenytoin MOA

A

blocks voltage-gated sodium channels by selectively binding to the channel in the inactive state and slowing its rate of recovery, at high doses it can block voltage-depending calcium channels and interfere with release of monoaminergic neurotransmitters

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74
Q

Phenytoin clinical use

A

treatment of partial and generalized tonic-clonic seizures and for status epilepticus

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75
Q

Phenytoin pharmacokinetics

A

exhibits saturable enzyme metabolism at a low serum concentration where small increases in the daily dose can cause large increases in plasma concentration resulting in toxicity

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76
Q

Phenytoin toxicity

A

depression of the CNS in the cerebellum and vestibular system causing nystagmus and ataxia especially in the elderly

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77
Q

Phenytoin adverse effects

A

gingival hyperplasia causing the gums to grow over the teeth, peripheral neuropathies and osteoporosis can develop with long-term use, causes tissue damage and necrosis with IM use (DO NOT give IM!!)

78
Q

Fosphenytoin MOA

A

prodrug that is rapidly converted to phenytoin in the blood reaching high levels within minutes (given IV or IM)

79
Q

Pregabalin MOA

A

binds to the alpha-2-gamma site, a subunit of voltage-gated calcium channels in the CNS, inhibiting neurotransmitter release

80
Q

Pregabalin clinical use

A

used to treat partial onset seizures, neuropathic pain, postherpetic neuralgia, and fibromyalgia

81
Q

Pregabalin adverse effects

A

drowsiness, blurred vision, weight gain, and peripheral edema

82
Q

Topiramate MOA

A

has a broad spectrum of antiseizure activity which includes blocking of voltage-dependent sodium channels, increasing the frequency of chloride channel opening by binding to GABA-A receptor, reducing high voltage calcium currents (L type), and inhibiting carbonic anhydrase

83
Q

Topiramate clinical use

A

used to treat partial and primary generalized seizures and in migraine prevention

84
Q

Topiramate pharmacokinetics

A
  • inhibits CYP2C19 and is induced by phenytoin and carbamazepine
  • lamotrigine causes an increase in topiramate concentration
  • co-administration of topiramate with ethinyl estradiol reduces efficacy of the birth control
85
Q

Topiramate adverse effects

A
  • somnolence, weight loss, and paresthesia, and increased renal stones
  • glaucoma, oligohidrosis, and hyperthermia have been reported related to carbonic anhydrase activity
86
Q

Divalproex/Valproate MOA

A

combination of valproic acid and sodium valproate that is converted to valproate when it reaches the GI tract and is thought to block sodium channels, GABA transaminase, and action at the T-type calcium channels

87
Q

Divalproex/Valproate clinical use

A

has a broad spectrum of activity against partial and primary generalized epilepsies

88
Q

Valproate pharmacokinetics

A

inhibits CYP2C9, UGT, and epoxide hydrolase systems and can cause significant interactions with other highly protein-bound drugs due to it being 90% bound to albumin

89
Q

Valproate adverse effects

A

may cause rare hepatic toxicity causing a rise in hepatic enzymes in plasma which should be monitored frequently, TERATOGENICITY is of great concern

90
Q

Zonisamide MOA

A

a SULFONAMIDE derivative with a broad spectrum of action with multiple effects on neuronal systems thought to be involved in seizure generation, metabolized by CYP3A4

91
Q

Zonisamide clinical use

A

used for treatment of patients with partial seizures

92
Q

Zonisamide adverse effects

A

CNS effects, kidney stones, and oligohidrosis (patients should be monitored for increased body temp and decreased sweating)

93
Q

Drugs contraindicated in pregnancy

A

Valproate and barbiturates (phenobarbital) are contraindicated, however, no antiepileptic drug has proven safe in pregnancy (drugs should be prescribed at lowest effective dose and drug levels monitored during pregnancy)

94
Q

Migraine aura

A

spreading depression of neuronal activity accompanied by reduced blood flow in the most posterior part of the cerebral hemisphere which gradually spreads forward over the surface of the cortex to other contiguous areas of brain

95
Q

Sumatriptan MOA

A

serotonin agonist which acts at a subgroup of serotonin receptors found on small peripheral nerves that innervate the intracranial vasculature

96
Q

Sumatriptan admin

A

administered subcutaneously, intranasally, or orally with parental admin having the quickest onset (20 minutes)

97
Q

Sumatriptan clinical use

A

Rapidly and effectively abort 70% of migraine headaches and can also be used for cluster headaches, DO NOT USE in patients with CAD

98
Q

Sumatriptan adverse effects

A

elevation of blood pressure and cardiac events, pain and pressure in the chest, neck, throat, and jaw

99
Q

Ergotamine MOA

A

complex binding to several receptors acting as an agonist and structurally similar to serotonin, dopamine, and epinephrine - causes vasoconstriction

100
Q

Ergotamine admin

A

given IV with similar efficacy as sumatriptan, can cause nausea

101
Q

Ondansetron MOA

A

selectively blocks the 5-HT3 receptors in the periphery and in the CNS

102
Q

Ondansetron adverse effects

A

can cause headaches and cardiac arrhythmias (monitor for prolonged QT intervals)

103
Q

Phenylzine MOA

A

irreversible nonselective MAO inhibitor (MAO-A and B) affecting NE, 5-HT, and DA transmission used as an antidepressant

104
Q

Phenylzine adverse effects

A
  • interacts with Tyramine-rich foods causing excess release of NE from adrenergic neurons and stimulation of the sympathetic nervous system resulting in hypertensive crisis (Tyramine is usually metabolized in the small intestine by MAO-A but if inhibited it can be taken up by adrenergic neurons in the ventrolateral medulla)
  • weight gain, orthostatic hypotension, insomnia, hepatotoxicity, sexual dysfunction
  • has narrow therapeutic index
105
Q

Foods to avoid with MAOI antidepressants

A

aged cheese, draft beer, dried/aged food (smoked foods and tofu)

106
Q

Phenylzine drug interactions

A

ephedrine/pseudoephedrine and amphetamine which can cause hypertensive crisis and antidepressants such as reuptake inhibitors which can cause hypertensive crisis and serotonin syndrome

107
Q

Tricyclic antidepressants (TCAs) MOA

A

5-HT reuptake transporter (SERT) and NE transporter (NET) blockers which result in enhanced 5-HT and NE signaling

108
Q

TCA adverse effects

A
  • drowsiness, sedation, weight gain due to blockade of H1 receptors
  • blurred vision, dry mouth, constipation, urinary retention, tachycardia, and cognitive dysfunction due to blockade of mAch receptors
  • postural hypotension, dizziness, and reflex tachycardia due to alpha 1 and 2 partial block
  • cardiac conduction delays dangerous in overdose due to Na+ channel block
  • has a narrow therapeutic index
109
Q

Secondary amine TCAs

A

Desipramine and Nortriptyline

110
Q

Tertiary amine TCAs

A

Imipramine, Amitriptyline, and Clomipramine

111
Q

What subgroup of TCAs have less side effects?

A

secondary amines (desipramine and nortriptyline)

112
Q

What subgroup of TCAs have more anticholinergic effects?

A

tertiary amines (amitriptyline, imipramine, and clomipramine)

113
Q

TCA drug interactions

A

other antidepressants, Na+ channel blockers, antimuscarinic drugs, and CYP450 substrates

114
Q

SSRI adverse effects

A

serotonin syndrome, GI disturbances due to activation of 5-HT in the gut, weight gain, anxiety, agitation, insomnia, suicidal thoughts especially in children and adolescents, headache, sweating, and sexual dysfunction

115
Q

SSRI with the lowest risk for children

A

Fluoxetine

116
Q

Serotonin syndrome symptoms

A

hyperreflexia, CNS excitation, anxiety/agitation, autonomic excitation - hypertension and hyperthermia (usually only seen in SSRI overdose or SSRIs combined with other antidepressants)

117
Q

Serotonin syndrome treatment

A

benzodiazepine sedation or cyproheptadine (anti-histamine)

118
Q

SSRI with the most side effects

A

Paroxetine (Paxil)

119
Q

Advantages of SNRIs over SSRIs

A

less likely to cause weight gain and possibly have greater efficacy than single-action agents like SSRIs

120
Q

SNRI adverse effects

A

nausea is most common, can cause emergent hypertension with high doses, metabolized by CYP450 and can cause inhibition at high doses

121
Q

SNRI most commonly prescribed due to lower cost

A

Venlafaxine, duloxetine, and desvenlafaxine

122
Q

Duloxetine clinical use

A

used to treat major depression, generalized anxiety disorder, diabetic peripheral neuropathy, fibromyalgia, and osteoarthritis

123
Q

Venlafaxine clinical use

A

used to treat major depression, generalized anxiety disorder, panic disorder, and social phobia

124
Q

Bupropion MOA

A

noradrenergic-dopaminergic reuptake inhibitor (NDRI) which has no effect on serotonin transmission

125
Q

Bupropion clinical use

A

used to treat depression without sexual adverse effects (can increase libido) ADD, and nicotine dependence,

126
Q

Bupropion adverse effects

A

lowers seizure threshold and can cause SEIZURES, metabolized by CYP450 and inhibits it at high doses, may cause anxiety - DO NOT prescribe for ANXIETY

127
Q

Trazodone MOA

A

5-HT receptor antagonist

128
Q

Trazodone clinical use

A

very sedating antidepressant and is commonly used as a hypnotic at low doses

129
Q

Mirtazapine MOA

A

alpha-2 receptor antagonist which increases the release of NE and 5-HT from presynaptic neuron

130
Q

Mirtazapine clinical use

A

used to treat patients who are “failing to thrive” and for whom weight gain is desirable or experience side effects with serotonergic agents

131
Q

Mirtazapine adverse effects

A

weight gain and sedation due to anti-histamine effects

132
Q

Main drug categories used to treat depression

A

serotonergic drugs (SSRIs, SNRIs, TCAs, and MAOIs) and bupropion

133
Q

Main drugs used to treat OCD

A

SSRIs

134
Q

Main drugs used to treat panic disorder

A

SNRIs, TCAs, and MAOIs for prevention (Paxil is the only SSRI that can be used safely for panic)

135
Q

Main drugs used to treat PTSD

A

SSRIs

136
Q

Main drugs used to treat insomnia and depression

A

trazodone and mirtazapine

137
Q

Main drugs used to treat pain syndromes

A

TCAs and SNRIs

138
Q

Main drug used to treat ADD and nicotine dependence

A

Bupropion

139
Q

Main drugs used to treat eating disorders

A

SSRIs (fluoxetine) and mirtazapine

140
Q

Class A mood stabilizers

A

stabilize mood from ABOVE baseline (mania) without causing depression (most treatments for bipolar are more effective at Class A than Class B)

141
Q

Class B mood stabilizers

A

stabilize mood from BELOW baseline (depression) without accelerating mania

142
Q

Lithium MOA

A

blocks the recycling of inositol phosphates desensitizing signaling through Gq-coupled receptors effecting 5-HT synthesis and release

143
Q

Lithium pharmacokinetics

A

absorbed in GI tract and slowly passes through the blood-brain barrier, can also pass to unborn fetus and to milk, 95% eliminated in urine

144
Q

Lithium adverse effects

A

weight gain, hypothyroidism, tremor, has a narrow therapeutic index and levels should be monitored in the blood

145
Q

Lithium intoxication

A

vomiting, diarrhea, tremor, ataxia, coma (reversed by dialysis)

146
Q

Lithium drug interactions

A

antidepressants and diuretics

147
Q

Antiseizure drugs that also have antimanic properties

A

Valproate, carbamazepine, and lamotrigine (can use in Li+-refractory patients)

148
Q

Benzodiazepine clinical use

A

short-term abortive treatment of anxiety, panic attacks, phobia, insomnia, alcohol withdrawal, agitation, sedation, status epilepticus, or as an adjunct to preventative treatment only when necessary (safer than barbiturates)

149
Q

Benzo with the longest half-life

A

Clonazepam

150
Q

Benzo adverse effects

A

sedation, ataxia/falls, impaired motor performance, impaired cognition, anterograde amnesia, and disinhibition of impulses

151
Q

Treatment of benzo overdose

A

Flumazenil

152
Q

Benzodiazepine of choice for sleep induction

A

Temazepam (half-life = 5 hours), next best is lorazepam (if CYP induction/inhibition is of great concern)

153
Q

Buspirone MOA

A

partial agonist at pre and post-synaptic 5-HT A1 receptors and has some antagonist activity at D2 receptors

154
Q

Buspirone clinical use

A

non-sedating anxiolytic with some antidepressant and antipsychotic activity most effective with chronic use not acute panic attacks (no abuse potential)

155
Q

Buspirone adverse effects

A

dizziness, headaches, GI upset, and combination with MAOIs may cause tachycardia and hypertension

156
Q

Zolpidem/Eszoplicone MOA

A

an agonist that binds similar to benzodiazepines but to only a subset of GABA receptors (alpha-1 sub-receptor) that are associated with sleep and produces pure sedation

157
Q

Zolpidem/Eszoplicone adverse effects

A

high therapeutic index unless combined with other CNS depressants, can cause daytime drowsiness, complex sleep behaviors, similar abuse potential to benzos

158
Q

Zolpidem/Eszoplicone pharmacokinetics

A

readily absorbed orally with short elimination half-lives, sublingual form for waking during the night (faster onset than oral), metabolized by CYP450 oxidation

159
Q

Haloperidol MOA

A

antagonist of D2 receptors in the basal ganglia increasing inhibitory output and resulting in reduced psychotic symptoms by inhibition of corticothalamic circuits

160
Q

Haloperidol adverse effects

A

sedation, hypotension, extrapyramidal symptoms (EPS), dystonic reactions, parkinsonian symptoms (tremor and rigidity), akathisia, and hyperprolactinemia causing gynecomastia

161
Q

Neuroleptic Malignant Syndrome

A

life-threatening neurologic emergency associated with the use of antipsychotic agents with symptoms including autonomic instability, hyperpyrexia, elevated CK, and renal failure due to myoglobinuria

162
Q

Drug used to treat neuroleptic malignant syndrome

A

IV Bromocriptine often in ICU

163
Q

Risperidone MOA

A

high potency second-generation atypical antipsychotic that blocks D2 and 5-HT2 receptors with less EPS than Haloperidol

164
Q

Quetiapine MOA

A

second-generation atypical antipsychotic that blocks D1, D2, 5-HT1A and 5-HT2 receptors with similar efficacy to Risperidone and even less EPS

165
Q

Quetiapine adverse effects

A

very sedating with other D2-related side effects (useful in psychotic patients with sleep disorders)

166
Q

Aripiprazole MOA

A

second-generation atypical antipsychotic that is a partial agonist/antagonist at D2 and 5-HT1 receptors

167
Q

Aripiprazole clinical use

A

used to treat psychosis, mania, and major depression

168
Q

Aripiprazole pharmacokinetics

A

can be given orally or IM and is metabolized by CYP450 so can cause drug interactions

169
Q

Clozapine MOA

A

low potency second-generation atypical antipsychotic that blocks multiple receptors and is effective against positive and negative symptoms of schizophrenia

170
Q

Clozapine adverse effects

A

increased risk of agranulocytosis and often reserved for patients with EPS of Haloperidol

171
Q

Atypical antipsychotic adverse effects

A

metabolic side effects including diabetes, weight gain, and hyperglycemia

172
Q

Morphine MOA

A

mu opioid receptor agonist that causes CNS effects

173
Q

Effects of mu opioid receptor activation

A

analgesia, drowsiness, change in pain perception, euphoria, and cough suppression

174
Q

Opioid adverse effects

A

nausea, constipation/vomiting, itching, respiratory depression

175
Q

Codeine MOA

A

a low potency opioid agonist which is a prodrug that is converted to codeine-6-glucuronide and morphine by CYP450

176
Q

Codeine clinical use

A

administered orally and used to treat pain (mixed with NSAIDS), cough, and diarrhea

177
Q

Hydrocodone MOA

A

same as morphine but less subject to first-pass metabolism with more problems with drug interactions

178
Q

Hydrocodone clinical use

A

typically combined with non-opioid painkillers such as acetaminophen or ibuprofen, prescribed as last resort

179
Q

Oxycodone clinical use

A

administered as time-release tablets meant to extend its effectiveness and often combined with aspirin (Percodan) or acetaminophen (Percocet)

180
Q

Opioid used to treat chronic pain in inpatient setting

A

morphine (half-life = 4 hours)

181
Q

Opioid used to treat chronic pain in outpatient setting

A

methadone or time-release oxycodone (half-life = 15-40 hours)

182
Q

Opioid used to treat short-term pain

A

codeine or oxycodone (half-life = 4-6 hours)

183
Q

Morphine pharmacokinetics

A

metabolized by glucuronidation and first-pass metabolism leads to low oral bioavailability

184
Q

Fentanyl pharmacokinetics

A

potent (50-100x more active than morphine), short-acting opioid agonist that is administered IV, metabolized by CYP3A, and excreted in urine (half-life = 2-4 hours)

185
Q

Heroin MOA

A

opioid agonist that is highly lipid soluble (crosses the blood-brain barrier into CNS more readily) and is converted into morphine

186
Q

Methadone MOA

A

a long-acting, orally active synthetic derivative of morphine that causes less euphoria

187
Q

Methadone adverse effects

A

can cause prolongation of QT interval and arrhythmia

188
Q

Buprenorphine MOA

A

nonselective partial opioid receptor agonist/antagonist with slow onset of action and slow departure from receptors, reduces craving and blocks effects of heroin

189
Q

opioid overdose symptoms

A

stupor, coma, pinpoint pupils, depressed respiration, and needle marks

190
Q

Dextromethorphan MOA

A

D isomer of morphine that doesn’t cross the blood-brain barrier and is a centrally acting cough suppressant (does NOT act on known opioid receptors)

191
Q

Loperamide MOA

A

agonist of opioid receptors in the gut achieving antidiarrheal activity (methadone skeleton), cannot cross the blood-brain barrier

192
Q

Naloxone MOA

A

opioid receptor antagonist used to treat opioid overdose causing dramatic reversal

Pharmacology I (5 decks)

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