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Advanced Pharmacology > Test 2 > Flashcards

Test 2 Flashcards

1
Q

Alzheimer’s Med Categories

A

Cholinesterase inhibitors, NMDA receptor antagonist, Combination

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2
Q

Cholinesterase inhibitors

A

Donepezil
Rivastigmine
Galantamine

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3
Q

NMDA receptor antagonist

A

Memantine

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4
Q

Combination Alzheimer Med

A

Donepezil + Memantine

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5
Q

Cholinesterase Inhibitor MoA

A

• Selectively inhibit cholinesterase [enzyme that hydrolyzes (inactivates) Ach] in the CNS

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6
Q

Cholinesterase Inhibitor effect

A

May slow deterioration of cognitive function

– Preserves memory, learning, attention (does NOT affect the underlying degenerative process

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7
Q

Cholinesterase Inhibitors Adverse Effects - ALL

A

Diarrhea, Nausea and vomiting
Bradycardia, dizziness, syncope
Urinary incontinenced
Hypersalivation, sweating

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8
Q

Rivastigmine AE

A

Hepatotoxicity

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9
Q

Donepezil AE

A

Insomnia

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10
Q

Galantamine AE

A

Weight gain

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11
Q

Cholinesterase Inhibitors drug ineractions

A

anticholinergic drugs

drugs that induce 3A4

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12
Q

Memantine MOA

A

NMDA receptor antagonist

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13
Q

Memantine Indications

A

Indicated for moderate to severe disease

– Can be used alone or in combination with cholinesterase inhibitors

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14
Q

Memantine AE

A

– Headache, confusion, dizziness, hallucinations

– Hypertension

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15
Q

Memantine can be combined with

A

donepezil (combo drug is called Namzaric®)

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16
Q

Alzheimer’s combination agents

A

Namzaric (Donezepil & Memantime)

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17
Q

Parkinson’s drug classes

A 
Dopaminergic
COMT Inhibitors
MAO-B inhibitors
Dopamine Receptor Agonists
Acetyl Choline Receptor Agonists
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18
Q

Parinkson’s Psychosis Drg

A

Pimavanserin

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19
Q

Dopaminergic agents

A

Levodopa

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20
Q

COMT Inhibitor agents

A

Tolcapone

Entalcapone

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21
Q

MAO-B Inhibitors

A

Selegiline
Rasagaline
Safinamide

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22
Q

Dopamine Receptor Agonists

A

Pramiprexole

Ropinirole

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23
Q

Acetylcholine Receptor Agonists

A

Benztropine

Trihexyphenidyl

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24
Q

Epilepsy Drug Classes

A 
Sodium Channel Blockers
GABA Agents
Glutamate Agents
T-Type Calcium Channel Blockers
Miscellaneous
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25
Q

Sodium Channel Blockers

A

Phenytoin
Carbamazepine
Zonisamide
Lamotigrine

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26
Q

GABA Agents

A

Phenobarbital

Valproic Acid

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27
Q

Glutamate Agents

A

Topiramate
Perampanel
Levetiracetam

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28
Q

T-type Calcium Channel Inhibitors

A

Ethosuximide

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29
Q

Miscellaneous Epilepsy Drugs

A

Cannabidiol and Benzos

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30
Q

Depression Meds

A 
TCAs
MAOIs
SSRIs
SNRIs
Miscellaneous
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31
Q

TCAs

A

Amitriptyline
Doxepin
Nortriplyine

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32
Q

MAOIs

A

Selegiline

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33
Q

SSRIs

A 
Fluoxetine (Prozac)
Paroxetine (Paxil)
Sertraline (Zoloft)
Fluvoxamine (Luvox)
Citalopram (Celexa)
Escitalopram (Lexapro)
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34
Q

SNRIs

A

Venlafaxine (Effexor)
Desvenlafaxine (Pristiq)
Duloxetine (Cymbalta)
Milanacipran (Saveila)

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35
Q

Misc Depression Drugs

A

Bupropion (Wellbutrin)

Mirtazapine

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36
Q

Antipsychotic Drugs

A

D2 Receptor Agonists (Typical)
Serotonin-Dopamine Agonists (Atypical)
Newer 2nd gen antipsychotics

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37
Q

D2 Receptor Agonists (typical antipsychotics)

A

Haloperidol (Haldol)

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38
Q

Serotonin-Dopamine Agonists (atypical)

A 
Clozapine
Olnazapine
Quetiapine
Aripiprazole (Abilify) [Aristada IM]
Risperidone
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39
Q

Newer 2nd gen antipsychotics

A

Brexpiprazole

Cariprazine

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40
Q

Bipolar Meds

A

Lithium

Anti-Psychotics

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41
Q

Post Partum Meds

A

Brexanolone

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42
Q

Treatment Resistant Depression Med

A

Esketamine

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43
Q

Levodopa MoA

A

increases conc of dopamine in the brain

biosyntetic precursor of dopamine

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44
Q

Levodopa AE

A

Nausea and vomiting
Orthostatic hypotension, sedation
Depression, delirium, paranoia, delusions, hallucinations
Motor fluctuations

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45
Q

Levodopa metabolism

A

Metabolised by COMT

Less than 1% reaches brain (why we combine with meds)

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46
Q

Levodopa combined with

A

Carbidopa & COMT inhibitor

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47
Q

Levodopa + Carbidopa

A

Sinemet, Sinemet CR, & Parcopat (oral disintegrating); Rytary new control release

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48
Q

Carbidopa MoA

A

Decarboxylase inhibitor
Inhibits conversion of levodopa to dopamine in peripheral tissues
Increases amount of levodopa that enters the brain

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49
Q

Carbidopa metabolism

A

Wearing off phenomenon (2-5 years efficacy)

Titrate to minimum 75 mg daily

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50
Q

COMT Inhibitor MoA

A

Inhibits peripheral metabolism of levodopa through inhibition of COMT

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51
Q

COMT AE

A 
Hepatotoxicity (tolcapone) 
Orthostatic hypotension
Diarrhea
Hallucinations
Brown-orange urine discoloration (entacapone)
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52
Q

COMT combined with levo/carbidopa

A

Entacapone

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53
Q

Entacapone + Levodopa + Carbidopa

A

Stalevo

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54
Q

MAO-B Inhibitors MoA

A

MAO-B breaks down dopamine so these drugs irreversibly inhibit this action

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55
Q

MAO-B Inhibitor AE

A

Increase levodopa toxicity (dyskenesia, psych symptoms)

Nausea, dizziness, orth htn, hallucination, insomnia, serotonin syndrome if combined with other serotenergic agents

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56
Q

MAO-B inhibitor interactions

A

foods/drinks high in tyramine (e.g. aged cheese, smoked meat, red wines, others)

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57
Q

DA receptor agonist MoA

A

directly activates dopamine receptor in brain and elsewhere

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58
Q

DA receptor agonist advantage over levodopa

A

– Direct action on receptor – less free radicals released – Less motor fluctuations and dyskinesias
– Longer half-life = longer action

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59
Q

disadvantages of DA receptor agonists

A

– Difficult to use in elderly due to increased CNS effects – May cause or exacerbate dyskinesias

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60
Q

DA receptor agonist AE

A

– Nausea, anorexia, vomiting (reduced if taken with food)
– Postural hypotension
– Sedation and hallucinations, confusion, vivid dreams
– Impaired impulse control, sleep attacks
– Behavioral (Impulse) side effects (gambling, shopping) • Less common (<10%)

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61
Q

Ach receptor antagonist therapuetic effects

A

Helps reduce tremor more than other manifestations

Favorable effects on rigidity and bradykinesia

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62
Q

Acetylcholine Receptor Antagonists MoA

A

– Competes with Ach at muscarinic receptors

– Block dopamine reuptake–prolonging dopamine effect

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63
Q

Ach receptor antagonist AE

A

– Sedation, depression, confusion
– Dry mouth, blurred vision, constipation, urinary retention
– Patients often find them difficult to tolerate

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64
Q

PD Psychosis drug

A

Pimavanserin

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65
Q

Primavenserin MoA

A

Selectively blocks 5-HT2a and 2c receptors

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66
Q

Primavenserin AE

A

Worsening hallucinations, QTc prolongation, death

BBW: Increased mortality in elderly patients with dementia- related psychosis (all antipsychotics)

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67
Q

How do Antiepileptic Drugs Work?

A

– Limit repetitive firing of neurons
– Enhance GABA-mediated synaptic inhibition
– Attenuate Glutamate-mediated excitatory responses

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68
Q

Key Sodium Channel Blockers

A

Phenytoin
Carbamazepine
Zonisamide
Lamotrigine

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69
Q

Phenytoin use

A

• Focal and generalized seizures
• No activity against absence
seizures

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70
Q

Pheyntoin routes

A

PO and IV

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71
Q

Phenytoin max infusion rate

A

50 mg/min

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72
Q

Phenytoin pharmacokinetics

A
  • high protein binding
  • metabolized by liver
  • dose dependent: enzyme system may become saturated and small dose increase may result in large increase in levels
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73
Q

Target Phenytoin concentration

A

– Total concentration: 10 - 20 micrograms/mL

– Free concentration: 1 - 2 micrograms/mL

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74
Q

Phenytoin Concentration dependent side effects

A

– > 20 micrograms/mL = Nystagmus
– > 30 micrograms/mL = ataxia, seizures reported
– > 40 micrograms/mL = lethargy, coma

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75
Q

Adjust total phenytoin level if:

A

– Low albumin (albumin <3.2 mg/dL)

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76
Q

What causes low albumin

A

Renal disease, malnutrition, cancer, liver failure

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77
Q

Adverse Effects of Phenytoin

A
  • Nystagmus – can develop tolerance
  • Diplopia/ataxia – indication to check level (may be dosed too high)
  • Phenytoin anticonvulsant hypersensitivity syndrome (AHS): rash, increased LFTs, and fever
  • Gingival hyperplasia (A) - ~ 20% of chronic use
  • Hirsutism (B) – can be dose related
  • Gingival hyperplasia (A) - ~ 20% of chronic use
  • Hirsutism (B) – can be dose related
  • Purple glove syndrome (C) - extravasation of phenytoin (do not use)
  • Hypotension
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78
Q

Phenytoin Drug Interactions

A

Other high protein bound drugs (valproic acid)

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79
Q

Phenytoin metabolism

A

metabolized by liver, dose dependent, high protein binding; INDUCER

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80
Q

Carbamazepine indications

A

Focal and tonic clonic

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81
Q

Carbamazepine PK

A 
highly protein bound
requires TDM (goal 6-10 mcg/mL)
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82
Q

Carbamazepine metabolism

A

– Extensively hepatic metabolism to active metabolite
– Substrate and Inducer of CYP 3A4 and others
– AUTOINDUCTION: Up-regulates

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83
Q

Carbamazepine AE

A

– CNS: blurred vision, unsteadiness, headache, sedation (30%)
– Nausea/GI upset (take with food)
– Black box warnings: dermatologic reactions, blood dyscrasias (AHS)
– Hyponatremia (SIADH) –more common in elderly

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84
Q

Carbamazepine drug interactions

A

– Induces metabolism of many drugs
• Example: oral contraceptives
– Displacement interactions (high protein binding)

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85
Q

Anticonvulsant Hypersensitivity Syndrome (AHS)

A

Rare, life-threatening immunologic adverse drug reaction
Associated with several anticonvulsants
– Phenytoin, carbamazepine, lamotrigine, others
Variable onset: 2-12 weeks after exposure
Cross-reactivity between agents can occur

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86
Q

Zonisamide indications

A

Focal, generalized, and unknown seizures

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87
Q

Zonisamide metabolism

A

Oral formulation only
Requires dose increases if given with CYP 3A4 inducers
Approximately 85% excreted by kidneys unchanged

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88
Q

Zonisamide AE

A

– Somnolence, ataxia, anorexia, nervousness, fatigue
– Renal stones (rare 1%)
– Suicidal ideations
– Metabolic acidosis (rare-renal dx, severe diarrhea) – Monitor bicarbonate levels before and periodic after start

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89
Q

Zonisamide contraindications

A

– Sulfa allergy (skin reaction)

– CrCl < 50 mL/min

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90
Q

Lamotrigine indications

A

Focal, generalized, and unknown seizures

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91
Q

Lamotrigine metabolism

A

liver

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92
Q

Lamotrigine AE

A

– Dizziness, blurred vision, headaches

– Skin reactions - AHS( black box warning;d/c at firs tsign)

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93
Q

Lamotrigine drug interactions

A
  • oral contraceptives (can be reduced)
  • Fosphenytoin/phenytoin can decrease lam levels
  • Valproate can increase lam levels
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94
Q

Phenobarbital routes

A

po, IV

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95
Q

Phenobarbital indications

A

Generalized and focal seizures (not absence), status epilepticus (and refractory cases)

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96
Q

Phenobarbital MoA

A

Synaptic inhibition through increasing GABA

97
Q

Which two IV drugs cause hypotension

A

Phenobarbital & Phenytoin

98
Q

Phenobarbital metabolism

A

inducer and longer 1/2 life (2-6 days)

99
Q

Phenobarbital AE

A 
–  Hypotension/respiratory depression (IV)
–  Sedation (may develop tolerance)
–  Nystagmus and ataxia (toxicity)
–  Irritability
–  Hyperactivity (more so in children)
–  Confusion (more so in elderly)
100
Q

Seizure meds that require TDM

A

Phenobarbital, Carbamazepine, phenytoin, valproate, Keppra (w/seizures), ethosuximide

101
Q

Phenobarbital TDM

A

Goal 10-40 ug/mL)

102
Q

Valproate route

A

po, IV

103
Q

Valproate indications

A

Generalized and focal (including absence)

104
Q

Valproate MoA

A

stimulates enzyme that converts glutamate to GABA

inhibits GABA degradation

105
Q

Valproate metabolism

A

Highly protein bound
Hepatically metabolized
Inhibitor (many drug interactions)

106
Q

Valproate TDM

A

50 - 100 micrograms/ml, up to 140 for status epilepticus

107
Q

Valproate AE

A

Black box warnings: pancreatitis (rare), hepatotoxicity, teratogenicity (neural tube
defects)
CNS: headache, dizziness, somnolence, sedation, tremor

108
Q

Valproate drug interactions

A

– Displacement reactions (e.g.phenytoin)
– CYP-mediated (inhibit smetabolism of phenytoin, phenobarbital, carbamazepine) – Increases lamotrigine levels (serious skin reactions)
-slowly titrate doses

109
Q

Topiramate indications

A

Generalized and focal seizures (including absence and LGS)

110
Q

Topiramate MoA

A

Antagonizes AMPA subunit of glutamate

– Also inhibits Na channels, K efflux (hyperpolarization), enhances GABA

111
Q

Topiramate metabolism

A

Inducer/inhibitor
Excreted in urine – decrease dose for CLcr<70
does should be slowly titrated!!

112
Q

Other uses of topiramate

A

migraines and weight loss

113
Q

Topiramate AE

A

– Somnolence, dizziness, difficulty with memory and concentration, aggressive
behavior
– Weight loss, oligohydrosis (decreased ability to sweat)
– Nephrolithiasis (counsel need for fluid intake)
– Metabolic acidosis (renal disease)

114
Q

Perampanel indications

A

Generalized and focal seizures

115
Q

Perampanel MoA

A

AMPA glutamate receptor antagonist

116
Q

Perampanel AE

A

– Black Boxed Warning: neuropsychiatric disorders (aggression, anger, hostility, irritability)
– Weight gain, nausea, dizziness, headache
– CNS (dizziness, gait disturbances, sedation)

117
Q

Which seizure meds are controlled substances?

A

perampanel and phenobarbital

118
Q

Perampanel PK

A
  • Highly protein bound
  • Major 3A4 substrate
  • Use not recommended with CrCL < 30
119
Q

Levetiracetam (Keppra) indications

A

Generalized and focal seizures

120
Q

Levetiracetam (Keppra) MoA

A

Binds to a synaptic vesicle protein (SV2A) – responsible
for reducing presynaptic glutamate release

121
Q

Levetiracetam (Keppra) PK

A
  • Low protein binding (< 10%)

* Primarily excreted in urine – adjust for renal impairment

122
Q

Levetiracetam (Keppra) TDM

A

ONLY if having seizures on medication – can help verify if patient is compliant with medications

123
Q

Ethosuximide indications

A

Absence seizures

124
Q

Ethosuximide MoA

A

(T-type) Calcium Channel Inhibitor

125
Q

Ehtosuximide PK

A
  • Very low protein binding

* Metabolized by the liver

126
Q

Ehtosuximide AE

A

– Nausea and vomiting (divide dose), anorexia, weight loss, abdominal cramps
– Psychosis, mania, sleep terrors, aggressiveness – CNS depression
– Parkinsonian movements (dose related)
– Blood dyscrasias

127
Q

Ehtosuximide TDM

A

Goal 40-100 mcg/mL

128
Q

Cannabidiol MOA

A

Not entirely known, enhances cannabinoid receptors, enhances natural endocannabinoids

129
Q

Cannabidiol AE

A

diarrhea, vomiting, somnolence, LFT abnormalities

130
Q

Cannabidoil metabolism

A

Metabolized by 3a4 and 2C19 (think drug interactions)

131
Q

Benzo MoA

A

Enhances activity of GABA

132
Q

Benzo AE

A

depressed mental status, respiratory
depression, hypotension

133
Q

Benzo hosptial recommendations

A

– Lorazepam (Ativan); IV
– Diazepam (Valium); IV and rectal
– Midazolam (Versed); IM (intranasal or buccal if IM not available)
• Can also be given IV

134
Q

Avoid these epilepsy meds in pregnancy

A

phenytoin, carbamazepine, valproate, phenobarbital, topiramate

135
Q

Safest epilepsy meds in pregnancy

A

Levetiracetam and lamotrigine

136
Q

Depression meds effects 1-2 weeks

A

Improve sleep and reduced anxiety

137
Q

Depression meds effects 1-3 weeks

A

improved self care, concentration, energy level and activity level up

138
Q

Depression meds effects 2-4 weeks

A

improved mood, reduced suicidal ideation

139
Q

TCA MoA

A

Nonselective inhibition of NE and serotonin reuptake

140
Q

TCA AE

A

Orthostatic htn, sedation, dry mouth, constipation, cardiotoxicity–arrythmias, QTc prolongation, sexual dysfunction, weight gain, hepatotoxicity, seizure,

141
Q

TCA tertiary amines

A

Amitriptyline

Doxepin

142
Q

TCA secondary amines

A

Nortriplyine

143
Q

Secondary amines description

A

lack active metabolism and have linear kinetics (wider therapeutic window)

144
Q

TCA metabolism

A

Long half-lives; high concetrationsin CNS and cardiac tissue

145
Q

TCA withdrawal

A

– GI complaints, dizziness, insomnia, restlessness
– Hyper-salivation, diarrhea, headache, vivid dreams
– Gradual dose reductions of per week helps reduce symptoms

146
Q

TCA drug interactions

A

MAOI
SSRIs
Alcohol, other CNS depressants

147
Q

MAOI MoA

A

– Irreversible inhibition of monoamine oxidase (1 to 2 weeks to restore)
– Responsible for metabolism of NE, 5-HT and dopamine within the neuronal synapse
• MAO-A – non-selective (NE, 5HT)
• MAO-B – selective for dopamine

148
Q

Selegline dose for depression vs. PD

A

dosed higher for depression

149
Q

MAOIs AE

A

– Postural hypotension
– Hypertensive crisis (food interaction)
– Sleep disturbances, weight gain

150
Q

MAOIs drug interactions

A 
–  TCAs
–  SSRIs
–  Sympathomimetic agents (e.g. cocaine)
–  Linezolid (antibiotic)
–  MAO inhibition may persist for up to 10-14 days following discontinuation
151
Q

SSRI MoA

A

Blocks serotonin transporter

Reuptake of 5HT into presynaptic neuron = increased circulating 5HT
for post synaptic uptake

152
Q

Which SSRI has the longest half life and what is it?

A

Fluoxetine (prozac) – 5 days (5 week washout)

153
Q

Which SSRI has the highest percentage of weight gain?

A

Paroxetine (paxil)

154
Q

SSRI AE

A

• CNS
– Fluoxetine – activating (insomnia, anxiety, agitation) – Paroxetine – sedating
• Gastrointestinal
– Nausea, vomiting, diarrhea (highest with sertraline)
• Hematologic (monitor)
– rise risk of bleeding, esp. with aspirin, NSAIDs, anticoagulants
• Sexual dysfunction
– SSRIs have the highest percentage incidence
• Weight gain
– Paroxetine > all others
Cardio–QT prolongation
Hyponatremia

155
Q

SSRI Withdrawal Syndrome

A

– GI complaints, flu-like symptoms, anxiety, insomnia

– Most notable with paroxetine

156
Q

Which SSRIs have QT prolongation?

A

Citalopram (celexa) and escitalopram (lexapro)

157
Q

SSRI drug interaction

A

MAOIs, TCAs, Linezolid

158
Q

Waiting period after SSRI before MAOI

A

5 weeks

159
Q

Waiting period after MAOI before SSRI

A

2 weeks

160
Q

With SSRIs have fewest drug interactions?

A

citalopram (celexa) and escitalopram (lexapro), and sertraline (zoloft)

161
Q

Depression med used for smoking cessation

A

Buproprion (Wellbutrin)

162
Q

Bupropion (Wellbutrin) AE

A

– Lowers seizure threshold
• Associated with high doses and abrupt withdrawal – Activating (tremor, insomnia)
– NO sexual dysfunction/weight gain

163
Q

Mirtazapine AE

A

– Sedation–often given at bedtime (histamine blockade)
– Weight gain (higher than other options-increased appetite)
– Low incidence of sexual dysfunction

164
Q

SNRIs MoA

A

Bind to serotonin (SERT) and norepinephrine (NET) transporters
– Prevent reuptake of both 5HT and NE (selective for NE)

165
Q

SNRIs AE

A

– Hypertension (NE)
– Sexual dysfunction
– Insomnia (take in the morning) – Nausea

166
Q

First line add-ons for depression

A

Burpoprion and Mirtazapine

167
Q

Other add-ons for depression

A

– Atypical-antipsychotics
– SNRI / TCA (low doses)
– Buspirone (indicated for general anxiety disorder)

168
Q

Depression meds that target anxiety or insomnia

A

Trazodone, buspirone or mirtazipine

169
Q

Dpression rate in pregnant women

A

14-23%

170
Q

Best depression med for pregnancy

A

sertraline

171
Q

Depression meds associated w/ birth defects

A

Paroxetine (Paxil) /Fluoxetine (prozac)

172
Q

Schizophrenia positive symptoms

A 
–  Delusions
–  Hallucinations
–  Disorganized speech –  Unusual behavior
–  Hostility
–  Excitement
–  Grandiosity
173
Q

Schizophrenia negative symptoms

A 
–  Blunted affect
–  Lack of motivation and pleasure
–  Emotional withdrawal –  Uncooperativeness
–  Social withdrawal
–  Poverty of speech
174
Q

Antipsychotic Drugs MoA

A

– Dopamine (D2) receptor blockers inhibit the release of DA and thereby alleviate the positive symptoms of schizophrenia
– Serotonin (5-HT2) receptor blockers increase the release of DA and thereby alleviate the negative symptoms of schizophrenia

175
Q

Typical Antipsychotic agent

A

Haloperidol (Haldol)

176
Q

Typical Antipsychotics MoA

A

D2 receptors antagonists (Also block muscarinic, histamine and alpha-1 receptors)

177
Q

Haldol route

A

tablet, injection, solution, depot

178
Q

Typcial antipyschotics AE

A

anticholinergic side effects, orthostatic hypotension, QTc prolongation, extrapyramidal side effects, hyperprolactinemia

179
Q

Haldol AE levels

A

Very low sedating, anticholinergic and hypotensive

Very high EPS

180
Q

Advantages of atypical antipsychotics

A

Less sedation, movement disorders and tardive dyskinesia

181
Q

Disadvantages of atypical antipsychotics

A

More weight gain and metabolic disturbances

182
Q

IM version of abilify

A

aristada

183
Q

beneftis of abilify

A

less EPS and weight gain

184
Q

Abilify indications beyond schizophrenia

A

MDD and BPD

185
Q

Dosing for aristada

A

IM avail every 4-6 weeks

186
Q

Transitioning to aristada

A

must continue PO treatment of abilify for the first 3 weeks

187
Q

Abilify AE

A

Prolongation of QT
Anticholinergic effects – dry mouth, urinary retention, constipation
Weight gain
Impaired glucose tolerance
Sexual dysfunction
hematologic (clozapine–agranulocystosis)

188
Q

Which atypical antipsychotic can cause agranulocytosis

A

Clozapine

189
Q

Atypical antipsychotics that cause weight gain the most

A

clozapine and olanzapine

190
Q

Atypical antipsychotics that cause most sedation

A

clozapine and quetiapine

191
Q

Atypical antipsychotics that cause most QTc prolongation

A

Ziprasidone

192
Q

Atypical antipsychotic that doesn’t cause QTc prolongation

A

Abilify

193
Q

Atypical antipsychotic that has the highest EPS

A

Risperidone

194
Q

Antipsychotic that treats schizo and MDD

A

Brexipiprazole

195
Q

Antipsychotic that treas schizo and BD

A

Cariprazine

196
Q

Med that newer gen antipsychotic has similar AE profile

A

Abilify

197
Q

Lithium metabolism

A

Narrow range b/w therapeutic and toxic levels

Frequent need for blood levels

198
Q

Lithium warnings/contraindications

A

– Renal insufficiency
– Dehydration
– Sodium depletion
[decreased clearance – increased risk of toxicity]

199
Q

Lithium drug interactions

A

NSAIDs
– ACEI and ARBs
– Diuretics
[increased conc – increased risk of toxicity]

200
Q

Lithium AE

A

tremor, even when therapeutic
NVD
Cog impairment, fatigue
Seizures and death at v. high conc

201
Q

Brexanolone MoA

A

Modulates GABAa

202
Q

Brexanolone dosing

A

one time 60 hour infusion

203
Q

Brexanolone indications

A

post-partum depression for those with no response to SSRIs at 6-8 weeks

204
Q

Brexanolone AE

A

sedation/loss of consciousness (pulse ox needed)

205
Q

Esketamine indications

A

used in combination with oral
antidepressant for treatment-resistant depression

206
Q

Esketamine dosing

A

intranasal twice weekly in office

207
Q

Esketamine AE

A

Extreme HTN, cog impairment, unsafe in pregnancy

208
Q

Antiepileptic to avoid with sulfa allergy

A

Zonisamide

209
Q

Which cholinesterase inhibitor would you give if a patient cannot tolerate PO meds?

A

Rivastigmine – transdermal patch

210
Q

Which drug class do you have to be careful prescribing patients who are on cholinesterase inhibitors?

A

Anticholinergics

211
Q

Pharmacologic tx of Parkinson’s aims to increase _______ and decrease________ .

A

Dopamine, acetylcholine

212
Q

Dopamine from ________ normally regulates _____ in ___________

A

substantia nigra, Ach, corpus striatum

213
Q

Levodopa must be given as a combined therapy with______ which is given at____mg daily dose minimum.

A

Carbidopa, 75

214
Q

A patient with Parkinson’s disease comes in concerned about their urine that is looking brown-orange. Which medications do you suspect this patient is taking? Is this a concerning adverse effect?

A

Entancapone prescribed with levodopa/carbidopa

215
Q

A pt is prescribed Selegiline. What diet changes must you educate the patient on and why?

A

MUST avoid foods that contain Tyramine
(aged cheese, red wine, smoked meat, soy beans, etc)

Tyramine is a compound that regulates BP that can cause vasoconstriction and MAO breaks down NE
MAO inhibited with increased Tyramine → increased BP → HTN crisis → hemorrhagic stroke

216
Q

Which of the following helps reduce tremor more than other manifestations?

Pramipexole
Rasagiline
Primavanserin
Benztropine

A

Benztropine

Ach Receptor Antagonist

217
Q 
You have a 83 year old patient with dementia-related psychosis. Which medication would you be concerned about if you saw it prescribed to this patient?
Pimavanserin
Carbidopa
Tolcapone
Selegiline
A

Pimavanserin, b/c of BBW

218
Q

Name the drugs that have a risk for causing AHS?

A

Phenytoin, carbamazepine, lamotrigine

219
Q

What increases the risk for AHS?

A

HLA-B 1502 allele - southwest asian descent

220
Q

Which drug class is used for status epilepticus?

A

Benzos

221
Q

Name a drug that is highly protein bound

A

Phenytoin, perampanel, valproate, carbamazepine

222
Q

What else causes high risk for drug interactions with phenytoin?

A

– induced of 3A4, metabolized by 2C9 and 2C19 – the more pathways it impacts, the more drug interactions!

223
Q

Which oral antiepileptic is partially metabolized via autoinduction?

A

Carbamazepine

224
Q

Education points for Carbamazepine

A

Give with food, watch for rash, careful with intense exercise, birth control change? Or at least use condoms

225
Q

Antiepileptics to use during pregnancy

A

Keppra and lamictal

226
Q

A 63 year old male with PMH of controlled epilepsy on one drug, uncontrolled DMT2, and controlled HTN on one drug. Allergies: PCN and sulfa drugs.

Recently CrCl = 55 so his drug dose is decreased.

Which drug is he on?

A

Topiramate

227
Q

Antiepileptics that are excreted by the kidney

A

Zonisamide & topiramate

228
Q

What are the advantages and disadvantages of atypical antipsychotics?

A

Advantages: less sedation, fewer movement disorders and TD

Disadvantages: metabolic disturbances

229
Q

What to watch for with atypical antipsychotics

A

weight gain, glucose levels/A1C, lipids

230
Q

Which antipsychotic medication are you likely to give an elderly, overweight patient with a history of cardiac dysrhythmias?

A

Aripiprazole (Abilify)

231
Q

34 year old male with PMH depression and BMI 30 presents to clinic. Has been taking Escitalopram 20mg daily for 2 years, but recently his symptoms have increased. He reports lack of energy and inability to get out of bed in the morning or join social activities. What drug does the nurse anticipate will be added to his regimen?

A

Wellbutrin

232
Q

Why give wellbutrin to overweight patient with no energy?

A

activating! and no weight gain

233
Q

A patient taking Amitriptyline tells you after taking the medication for 2 weeks he doesn’t think it is working and just stopped taking the medication abruptly. What would you tell this patient and what effects (if any) would you expect to see?

A

Onset usually takes at least 4-6 weeks for full effect

Withdrawal syndrome
GI complaints, dizziness, insomnia, restlessness, hypersalivation, diarrhea, HA, vivid dreams

234
Q 
Pt started on Fluoxetine and comes in complaining of low energy and drive. Which drug would you consider switching the patient to?
Paroxetine
Venlafaxine
Buproprion
Mirtazipine
A

venlafaxine

235
Q 
Which of the following medication combinations would not have adverse drug interactions?
Fluoxetine, Selegiline
Fluoxetine, Bupropion
Linezolid, Sertraline
Amitriptyline, Paroxetine
A

Fluoxetine, Bupropion

SSRIs have significant interactions with MAOIs, TCAs, Linezolid (has MAO inhibition)

236
Q

Antibiotic that has MAO inhibition

A

linezolid

237
Q

_________ receptor blockers alleviate the positive symptoms of schizophrenia, and_______ receptor blockers alleviate the negative symptoms of schizophrenia.

A

D2 receptor blockers inhibit the release of DA and alleviate the positive symptoms of schizophrenia

5-HT2 receptor blockers increase the release of DA and alleviate the negative symptoms of schizophrenia

238
Q

List anticholinergic effects:

A

Dry mouth, urinary retention, constipation

239
Q

What are 3 contraindications for Lithium?

A

Renal insufficiency
Dehydration
Sodium depletion

Advanced Pharmacology (8 decks)

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