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Medicine > Neuro Pharm > Flashcards

Neuro Pharm Flashcards

1
Q

NSAIDs

A

Abortive therapy for headaches.

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2
Q

Triptans

A

Terminate pain by activating serotonin 5-HT1B/1D receptors
Analogs of serotonin– 1st line for acute migraine
Equally effective for moderate to severe migraine and cluster headaches.
Not recommended in pregnancy.
Frequent use –> medication-overuse headache

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3
Q

Sumatriptan

A

Poor oral bioavailability and metabolized in liver by MOA-A.
AE: Chest tightness, weakness, somnolence, dizziness, skin paresthesias, CORONARY VASOSPASM
CI: IHD, history of MI/angina, uncontrolled HTN, PAD
DI: MAOIs or SSRIs (increased risk of serotonin syndrome)

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4
Q

Triptans CI in severe renal/hepatic impairment

A

Naratriptan and frovatriptan
These two are not metabolized by MAO and do not have DI with MAO

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5
Q

Ergot Alkaloisd

A

Ergotamine and Dihydroergotamine

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6
Q

Ergotamine

A

Oral, SL, rectal
Oral absorption poor, often combined with caffeine to increase absorption

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7
Q

Dihydroergotamine (DHE)

A

Intranasal and parenteral
Injectable often used for intractable migraine along with antiemetic
Fewer side effects than ergotamine

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8
Q

Ergot alkaloids AE

A

N/V, limb paresthesias or pain
Nasal spray - stinging/rhinitis, unpleasant taste
Give antiemetic for N/V

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9
Q

Ergot alkaloids CI

A

IHD, PAD, HTN, pregnancy
Has sig effect in coronary arteries

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10
Q

Ergot Alkaloids DI

A

Avoid concurrent triptans; beta blockers, strong CYP3A4 inhibitors as they reduce hepatic hepatic metabolism of ergot alkaloids

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11
Q

Ergotism

A

Severe peripehral ischemia - cold, numb, painful ext, and claudication
Overdose- vascular occlusion and gangrene

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12
Q

NSAIDs

A

MOA: COX inhibitors, block PG synthesis
Good evidence for aspirin, ibuprofen, and naproxen
Indicated in mild to moderate migraine, can be used in severe migraine if past response was good

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13
Q

NSAIDs AE

A

GI upset

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14
Q

NSAIDs CI

A

PUD, renal insufficiency, heart failure

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15
Q

Acetaminophen/ASA/Caffeine

A

Acetaminophen MOA: inhibits PG synthesis in the CNS by blocking the COX
Aspirin MOA: inhibits COX 1 and 2 irreversibly
Caffeine MOA: vasoconstrictor

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16
Q

Acetaminophen/ASA/Caffeine AE and CI

A

AE: GI upset, insomnia
CI: PUD, renal disease

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17
Q

Opioids

A

Not preferred due to AE (nausea, drowsiness, constipation) and abuse potential.
Overuse of opioids can lead to rebound, medication overuse, dependence, and abuse potential
Indicated for severe migraine attacks when all other abortive treatments have failed

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18
Q

Butorphanol nasal spray

A

Opioid agonist/antagonist at mu opioid rec

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19
Q

Tramadol

A

Dual action analgesic
Agonist at mu opioid rec
Inhibits reuptake of NE and serotonin
Indicated for moderate to severe migraine pain
Toxicity associated with seizures, relative CI in seizure disorder
Potential for serotonin syndrome with other serotonergic drugs or enzyme inhibiting drugs

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20
Q

Calcitonin Gene-related peptide receptor antagonist

A

Gepants
Rimegepant
Ubrogepant
Atogepant

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21
Q

CGRP/gepants

A

Route: oral
MOA: inhibit the actions of CGRP which is a potent vasodilator and pain-signaling neurotransmitter
Indication: only considered for patients who can’t use triptans or have failed two triptans

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22
Q

Selective Serotonin G-HT1F agonist
“ditans”

A

Lasmiditan
Route: oral
MOA: binds selectively to 5-HT1F rec which is distinct from triptans which bind to 5HT 1B/1D

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23
Q

Lasmiditan

A

Treat migraine by decreasing trigeminal system stimulation without causing vasoconstriction.
5-HT 1F expressed in trigeminal system but not found in cerebral vessels. 5-HT1F are found in the neocortex and hippocampus

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24
Q

Lasmiditan AE

A

Dizziness, sedation, paresthesia, hallucinations, euphoria, risk of serotonin syndrome

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25
Q

Lasmiditan Indication

A

Should only be considered for patients who can’t use triptans or who have failed two triptans

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26
Q

Antiemetics

A

Metoclopramide - dopamine rec antagonist
Prochlorperazine - antihistamine
Used as adjunct for ergot alkaloid and triptans
May be given for intractable migraine headache - via IV
AE: sedation, dystonic reactions (metoclopramide)

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27
Q

Dexamethasone

A

Rescue therapy for status migrainosus (severe, continuous headache for >72 hours and up to 1 week
May be used as adjunct to abortive therapy

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28
Q

Mild to moderate acute migraine attack

A

NSAID or acetaminophen

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29
Q

Moderate to severe acute migraine attack

A

Triptan
If fail triptan, can try ergot alkaloids
Patients who failed two triptans can be considered for therapy with CGRP antagonist or lasmiditan

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30
Q

Prophylaxis of migraine headaches Indications

A

Two or more attacks per month with >3 days’ disability
CI to serious AE with or failure of acute treatments
Use of abortive medications >2x/week
Presence of uncommon migraine conditions (hemiplegic, prolonged aura, migranous infarction)

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31
Q

Antiepileptics

A

Valproate
Topiramate
MOA: unclear for migrane (Increased GABA and decreased glutamine, Na/Ca ion channel activity)
AE: Valproate - nausea, fatigue, tremor, WEIGHT GAIN, hair loss
Topiramate - paresthesias, fatigue, taste perversion, weight loss, DIFFICULTY WITH MEMORY, language
Both are teratogenic and CI in pregnancy

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32
Q

Beta blockers

A

Metoprolol, propranolol (most common), timolol
MOA: May attenuate the second phase of migraine by blocking vasodilation mediated by ebta 2 rec
AE: fatigue, exercise intolerance, bradycardia, hypotension
Caution in severe obstructive pulmonary disease
May aggravate comorbid depression
Not recommended in 2nd and 3rd trimesters

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33
Q

Antidepressants

A

MOA: May down regulate 5-HT2 rec
Amitriptyline (TCA)
AE: Sedation, dry mouth, weight gain, orthostatic hypotension
Venlafaxine (SNRI)
AE: Nausea, vomiting

Increased risk of serotonin syndrome if given with a truptan

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34
Q

Menstrual migraine

A

NSAIDs or triptans

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35
Q

Monoclonal Ab against CGRP rec

A

Eptinezymab, erenumab, fremanezumab, galcanezumab
Route: SQ once/month or every 3 months
MOA: inhibit the actions of CGRP which is a potent vasodilator and pain-signaling NT
Indication: migraine prevention in patients with adherence issues or unable to take other oral agents for prevention
Used for PREVENTION of migraines

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36
Q

Monoclonal Ab agaisnt CGRP rec for cluster headaches

A

Galcanezumab

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37
Q

Atogepant

A

FDA approved for prophylaxis and acute management

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38
Q

Onabotulinumtoxin A

A

FDA approved for prophylaxis in adults with chronic migraine
>15 headache days/months for >4 hours/day

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39
Q

Prophylaxis for HA in healthy or comorbid HTN or angina

A

Beta blocker therapy
Verapamil if beta blocker CI or ineffective

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40
Q

Prophylaxis for HA in comorbid depression or insomnia

A

Tricyclic antidepressant
Amitriptyline

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41
Q

Prophylaxis for HA in comorbid seizure disorder or bipolar illness

A

Anticonvulsant - valproate and topiramate
If ineffective, beta blockers

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42
Q

Prophylaxis for HA in headaches that recur in predictable pattern (menstrual migraine)

A

NSAID or triptan

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43
Q

Abortive therapy in pregnancy

A

Acetaminophen for short term use
Avoid NSAIDs in 3rd trimester (premature closure of ductus arteriosus)
Ergots CI

Prophylaxis not recommended

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44
Q

Abortive therapy cluster headache

A

Inhaled oxygen - DOC
Triptans

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45
Q

Prophylaxis of cluster headache

A

verapamil, lithium, glucocorticoids (prednisone), valproic acid, topiramate, ergotamine, melatonin, capsaicin, galcanezumab

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46
Q

Tension Headache

A

Non-pharm: biofeedback, acupuncture, relaxation training, physiotherapy
Medications: NSAIDs, acetaminophen

Prophylaxis with amitriptyline with or without regular OMT

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47
Q

What converts levodopa to dopamine in peripheral tissues?

A

L-aromatic amino acid decarboxylase (LAAD)

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48
Q

Does L-dopa cross BBB?

A

Yes, dopamine does not.

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49
Q

What drug is given with L-dopa?

A

Carbidopa which is an LAAD inhibitor that increases amount of L-dopa that goes to brain tissue to be converted to dopamine in the brain

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50
Q

L-dopa considerations

A

Absorbed from proximal duodenum
Dietary amino acids compete for transport into the circulation and may also decrease movement in the brain so protein restricted diets/separation of high protein meals may be advised
Large first pass effect; 95% metabolized in gut wall and liver which is why it’s given with carbidopa

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51
Q

L-dopa AE

A

N/V, orthostatic hypotension, sedation, agitation/delirium/psychosis, nightmares/vivid dreams, cardiac arrhythmia (action of dopamine on alpha and beta adrenergic rec, arrhythmias can be enhanced in patients with cardiac disease

Most concerining AE is neuroleptic malignant syndrome which can occur if there is abrupt withdrawal of L dopa

52
Q

L-dopa DI

A

Anticholinergic drugs which could delay gastric emptying and decrease absorption
MAO-A inhibitors (phenelzine) - inhibit breakdown of dopamine and may lead to hypertensive crisis
Antipsychotic drugs block dopamine and may reduce effectiveness

53
Q

Common motor complications of carbidopa/levodopa combination with long-term treatment

A

End of dose “wearing off” - motor fluctuations

On-off phenomenon - random severe motor fluctuations

Peak-dose dyskinesia - oral and facial musculature; writhing/flinging movements of limbs

Start hesitation “freezing” - usually occurs when patient wakes in morning and drug has worn off

54
Q

Catechol-O-methyltransferase (COMT) inhibitors

A

Metabolizes levodopa to 3-O-methyldopa in the gut/liver
Increases bioavailability and half-life of levodopa, stabilizes levels in the brain
No anti-parkinsonian effects on their, extends the effects of levodopa
Indicated for “wearing off”

55
Q

3 COMT inhibitors

A

Tolcapone - only one that crosses BBB
Opicapone and entacapone - Do not cross BBB

56
Q

COMT inhibitors AE

A

General: diarrhea, nausea, brown/orange urine (tolcapone and entacapone only)

Tolcapone: fetal hepatotoxicity; monitor LFTs

Entacapone: safer due to lack of hepatotoxicity, taken with each dose of levodopa, available in combination with carbidopa/levodopa

Opicapone: scheduled once daily, avoid food within 1 hour

57
Q

Monoamine Oxidase (MAO)

A

Type A and Type B
Both present in the CNS and periphery
Both inactivate monoamines of intestinal origin

MAO-A - metabolizes NE, serotonin, and dopamine
MAO-B - metabolizes dopamine selectively, responsible for oxidative metabolism of dopamine in the brain

Non-selective MAO inhibitors can cause hypertensive crisis because they inhibit both MAO A and B
As long as MAO-A is not block, blocking MAO-B has little effect on tyramine metabolism

58
Q

MAO-B inhibitors

A

Selective irreversible inhibition that interferes with degradation of dopamine resulting in prolonged dopaminergic activity

May spare neurons from oxidative stress by decreasing the formation of hydrogen peroxide from DOPAC

59
Q

Selegiline

A

MOA-B inhibitor

Indicated in early PD or later with L-dopa to improve wearing off. Can be used as monotherapy to delay use of L-dopa

Metabolized to demethylselegiline, amphetamine and methamphetamine

60
Q

Rasagiline

A

Indicated in early PD and advanced
Monotherapy in early PD = less funcitonal decline, better long term outcomes

High fat meal decreases absorption

Metabolized to inactive metabolite by CYP 1A2 (ciprofloxacin levels increase)

61
Q

3 MAO-B inhibitors

A

Selegiline
Rasagiline
Safinimide

62
Q

MAO-B inhibitors AE

A

Confusion, hallucinations, hypotension, insomnia, dyskinesias

63
Q

MAO-B inhibitors DI

A

Serotonin syndrome with SSRIs, meperidine, other serotonergic drugs

64
Q

Dopamine REceptor Agonists

A

Activate dopamine receptors (D2) in the striatum
Longer duration of action and less fluctuations (no “on/off”)
Can be used as first line in younger patients to delay time to L-dopa by about 3 years
Can be used as adjunct to levodopa in advanced PD

65
Q

Pramipexole

A

Dopamine rec agonist
MOA: Selective for D2 and D3 rec
Renally excreted, dose adjustment in renal insufficiency

66
Q

Ropinirole

A

Dopamine rec agonist
MOA: selective for D2 receptors
Metabolized by CYP1A2, fluoroquinolone antibiotics increase serum levels; omeprazole decreases levels

67
Q

Rotigotine

A

Dopamine rec agonist
MOA: selective for D3>D2>D1
Transdermal patch only, no dosage adjustment needed for hepatic or renal insufficiency

68
Q

Dopamine rec agonists (pramipexole, ropinirole, and rotigotine)

A

Delay need for levodopa if started early
Reduce the “off” periods in advanced PD
May decrease the levodopa dose needed
Indicated for restless leg syndrome

69
Q

Apomorphine

A

Dopamine rec agonist
Binds D4>D2=D3=D5>D1
Extensive 1st pass metabolism
Rapid onset about 10 min

Indicated for acute intermittent freezing or akinesia in advanced PD
Rescue therapy

Most common AE: N/V
Patient should be premedicated with trimethobenzamide 3 days prior to using apomorphine and during therapy

CI with 5HT3 rec blockers (dolasetron, granisetron, ondansetron) due to severe hypotension and syncope

70
Q

Bromocriptine

A

Non-selective D2 rec agonist
Ergot alkaloid
Used in advanced PD for wearing off and on-off motor fluctuations

71
Q

Most common AE of dopamine rec agonist

A

Nausea

Others include: confusion, dyskinesias, sedation, vivid dreams, hallucinations, orthostatic hypotension, dry mouth and sleep attacks

72
Q

Dopamine receptors agonists (pramipexole and ropinirole)

A

Intense urges have been reported with pramipexole and ropinirole such as gambling, shopping and sexual activity

73
Q

Dopamine rec agonists CI

A

History of psychotic illness, recent MI, and active PUD (bromocriptine)

74
Q

Istradefylline MOA

A

Adenosine rec antagonist
MOA: selective antagonist at the adenosine A2a rec (A2AR)

A2AR colocalize with D2 rec in the indirect pathway of the basal ganglia
Adenosine activation of A2AR decreases dopamine affinity for the D2 rec (inhibiting D2 function)

A2AR antagonist block this effect of adenosine, increasing D2 function. Blocking this A2A rec can increase the activity of dopamine or dopamine agonists at the D2 rec

Indications: adjunct to levodopa/carbidopa for “off” episodes

75
Q

Istradeylline AE and DI

A

Dyskinesia, dizziness, insomnia

DI: strong CYP3A4 inhibitors

76
Q

Amantadine MOA

A

Dopaminergic agent and anticholinergic effects, also block NMDA rec

Potentiate dopamine activity; may increase release of dopamine from neurons or may inhibit reuptake of dopamine by these neurons

May act by blocking NMDA rec, decreasing the excitatory effects of glutamate or by blocking muscarinic rec

Adjunct to treat motor fluctuations and dyskinesias

77
Q

Cholinesterase Inhibitors (3 of them) for treatment of Alzheimer’s

A

Donepezil, rivastigmine, galantamine

All cross BBB
Donepezil and galantamine are metabolized by CYP2D6 and 3A4
Rivastigmine is hydrolyzed in plasma
All renally eliminated

Firstline for mild to moderate AD

78
Q

AE of Cholinesterase inhibitors

A

Nausea, anorexia, vomiting, diarrhea, bradycardia and syncope
Start low and go slow

79
Q

DI of cholinesterase inhibitors

A

Anticholinergic agents may decrease benefit Diphenhydramine, tolterodine and oxybutynin (urinary incontinence), and TCAs (imipramine, amitriptyline)

80
Q

NMDA Rec blocker for Alzheimer Disease

A

Memantine
MOA: N-methyl-D-aspartate antagonist; blocks excitotoxic effects of glutamate

Considered for moderate to severe AD

81
Q

AE of Memantine

A

Dizziness, confusion, hallucinations, delusions, headache, constipation
Reduce dose with creatinine clearance of < 30mL/min

82
Q

Vitamin E complications in AD treatment

A

Vitamin E doses >400 IU/day for a year or two may increase the risk of death in healthy people and those with chronic diseases
Vitamin E may also increase the risk of bleeding and hemorrhagic stroke

82
Q

Beta-amyloid Monoclonal Ab

A

Aducanumab and lecanemab-irmb
MOA: Monoclonal Ab against soluble and insoluble amyloid; reduces amyloid beta plaques

82
Q

AE of Aducanuman and lecanemab-irmb

A

Hemosiderosis, microhemorrhage, brain edema, headache, and falling

82
Q

Firstline treatment for Noncognitive symptoms of AD

A

Non-pharm interventions

83
Q

Brexpiprazole

A

MOA: serotonin 5-HT1A and dopamine D2 and D3 rec partial agonist
Indications: Schizophrenia, Adjunct for major depression, Agitation in patients with Alzheimer’s dementia

AE: Weight gain, akathisia (inability to sit still), sedation
Increased mortality in older patients with dementia

84
Q

Treatment of Huntington Disease

A

Movement disorder: tetrabenazine, deutetrabenazine, and reserpine (dopamine depleting agents); post-synaptic dopamine rec blockers such as haloperidol or olanzapine

Depression, irritability, OCD: SSRIs (avoid anticholinergic drugs like TCAs)

Psychosis, paranoia: antipsychotics

85
Q

Tetrabenazine

A

MOA: depletes cerebral dopamine by preventing intraneuronal storage; inhibits vesicular monoamine transporter type 2 (VMAT2), decreases monoamine uptake into synaptic vesicles and depleting monoamine stores

Hepatic metabolism by CYP2D6, renal excretion

86
Q

Tetrabenazine AE

A

Sedation/somnolence, fatigue, insomnia, depression, akathisia, anxiety, nausea

87
Q

Tetrabenazine DI

A

Strong CYP2D6 inhibitors like fluoxetine, CI with MAO inhibitors

88
Q

Deutetrabenazine

A

MOA: An isotopic isomer of tetrabenazine in which six hydrogen atoms have been replaced by deuterium atoms. Incorporation of deuterium slows the rate of drug metabolism, allowing less frequent dosing

Indications and AE same as tetrabenazine

89
Q

Atypical Antipsychotics for HD

A

Risperidone, olanzapine, aripiprazole

MOA: non-selective antagonist 5HT2 and D2 rec

Indication: 2nd line for Huntington’s chorea, for when people fail tetrabenazine and have chorea and psychiatric symptoms

AE: Hyperprolactinemia, weight gain, akathisia, extrapyramidal reaction, parkinsonism

90
Q

Riluzole for treatment of ALS

A

MOA: Has not been fully elucidated; V-gated Na channel blocker; Inhibits glutamatergic transmission by increasing glutamate uptake

High fat meal decreases absorption; metabolized by CYP1A2; excreted in urine

AE: Increased LFTs, nausea, abdominal pain, diarrhea

DO: CYP1A2 inhibitors/inducers: quinolones can increase levels; omeprazole, rifampin, smoking can decrease levels; Take at least 1-2hr before meals

Increases tracheostomy free survival by 2-3 months but no effect on symptoms

91
Q

Edaravone for tx of ALS

A

MOA: Unknown, may be due to free radical scavending and antioxidant properties

Undergoes sulfation and glucuronidation; excreted via urine

AE: hypersensitivity reactions, confusion, gait disturbance, headache

92
Q

Sodium Phenylbutyrate/ Taurursodiol PB-TURSO for ALS treatment

A

MOA: used in combination to reduce neuronal cell death
Sodium phenylbutyrate: histone deacetylase inhibitor that reduce the adaptive stress response
Taurursodiol: hydrophilic bile acid that maintains mitochondrial integrity by reducing membrane permeability. possibly increases threshold for cellular apoptosis

Time to tracheostomy/permanent assisted ventilation by 7.3 months

93
Q

Tofersen for Treatment of ALS

A

MOA: antisense oligonucleotide that downregulates SOD1
SOD1 variant leads to toxic protein misfolding
SOD1 variant accounts for 15% of familial ALS

Indication: familial ALS due to SOD1 variant

Efficacy: associated with reduced progression in several measures including slower declines in ALSFRS-R, vital capacity, and grip strenght

94
Q

Treatment for sialorrhea in ALS

A

Glycopyrrolate - muscarinic rec antagonist (DOC)
Amitriptyline - antidepressant with anticholinergic properties

95
Q

Treatment for Pain and Agitation in ALS

A

Opioids and/or BZDs

96
Q

Treatment for Spasticity in ALS

A

Baclofen - GABAb agonist
Tizanidine - agonist of alpha2 adrenergic rec in CNS, increases presynaptic inhibition
Clonazepam - BZD

97
Q

Other Treatments for ALS

A

Physical therapy to enhance independence and safety
Speech therapy to help patients speak louder and more clearly, and with non-verbal communication
Nutritional support - numerous small meals, easy to swallow

98
Q

BZD sedative-hypnotic

A

MOA: facilitate the activity of gamma-aminobutyric acid (GABA); bind to alpha1 (BZ1) and alpha 2(BZ2) subunits of the GABA ionophore (GABAa rec)
BZDs bind to allosteric site formed by cleft between alpha and gamma subunits; facilitates GABA binding and increases the frequency of chloride channel opening
Increase likelihood of GABA binding, making it more potent

Decreases sleep latency, increase stage 1 and 2, decrease stage 3 slow wave sleep and REM

99
Q

Clhordiazepoxide and diazepam

A

BZDs that are converted to long-acting active metabolites

100
Q

Alprazolam, midazolam, and triazolam

A

BZDs that are converted to a short-acting active metabolite

101
Q

Benzodiazepines that have no active metabolites

A

Oxazepam, Temazepam, Lorazepam

Out The Liver

102
Q

BZDs effects and indications

A

Dose-dependent depression of the CNS: sedative (short-term), anxiolytic –> hyponosis and anesthesia
Given orally, have low incidence of resp depression, coma or death unless administered with another CNS depressant
Antergrade Amnesia - interfere with the formation of new memory
Anticonvulsant effects
Decrease muscle spasm
Alcohol withdrawal

103
Q

BZD AE

A

Motor incoordination
Dizziness
Drowsiness
Impairment of concentration, judgment and planning
Driving/psychomotor skills
Disinhibition
Physical dependence leading to withdrawal symptoms

104
Q

BZD withdrawal syndrome

A

Rebound anxiety
Rebound sleep disorder
Headache
Insomnia
Irritability
Muscle twitches
Seizures
Taper gradually to avoid withdrawal symptoms

105
Q

BZD DI

A

Alcohol and other CNS depressants potentiate effects
CYP450 inducers may decrease serum levels like rifampin
CYP450 inhibitors may increase serum levels like ketoconazole

CI in pregnancy

106
Q

Treatment of BZD overdose

A

Flumazenil

MOA: competitive BZD rec antagonist
Given IV
AE: seizures, arrhythmias, blurred vision, emotional lability and dizziness

107
Q

Barbiturates and Sleep

A

Sedation
Suppress slow wave and REM sleep
Effective for up to 2 weeks; lose ability to induce and maintain sleep after this period

108
Q

Barbiturates binding site

A

Bind to multiple pockets at the interface between the subunits within the transmembrane domain and increase the duration of Cl channel opening both in the presence and in the absence of GABA
Increases maximal effect which is why get resp depression, coma and death

109
Q

Barbiturates AE

A

Respiratory depression, physical and psychological dependence; agitation, confusion, nightmares, hallucinations, hangover

110
Q

Barbiturates DI

A

CI with CYP450 3A4 inhibitors: azole antifungals, protease inhibitors, other antiretrovirals
Additive effects with other CNS depressants

Pregnancy: teratogenic

111
Q

Treatment of Barbiturate overdose

A

Supportive care
Na bicarbonate to alkalinize the urine to enhance elimination for long-acting barbiturates only (phenobarbital butalbital)

112
Q

Non-BZD sedative-hypnotics

A

Zolpidem, Zaleplon, eszopiclone
MOA: Act selectively at the BZ1 rec in the CNS; selective for alpha 1 rec
Distributed to CNS and metabolized in liver via CYP3A4, excreted in urine

Reduce sleep patency
Increase total sleep time
Little effect on sleep stages

Indication: Insomnia

113
Q

Non-BZD sedative-hypnotics AE

A

Drowsiness, dizziness
Impaired memory
Psychomotor slowing
Bitter aftertaste (eszopliclone)
Complex sleep-related behavior: driving, talking on the phone, eating, with no memory of the vent
Anaphylaxis and facial swelling as early as first dose

Less potential for tolerance and dependence than BZDs but still C4

114
Q

Non-BZD sedative hypnotics DI

A

Avoid other CNS depressants including alcohol
CYP3A4 inhibitors such as -azole antifungals and erythromycins inhibit eszopiclone metabolism

115
Q

Remelteon

A

Melatonin Rec Agonist
MOA: high affinity for the MT1 and MT2 receptors, thought to be involved in the circadian rhythm and normal sleep-wake cycle
No affinity for GABA or other NTs
Active metabolite: M-II

Decreases sleep latency- indicated to treat sleep onset insomnia

Not a controlled substance

116
Q

Ramelteon Pharmacokinetics

A

Rapidly absorbed,; extensive first pass mtabolism; high fat food decreases the C max
Eliminated in urine

117
Q

Ramelteon AE

A

Somnolence, dizziness, nausea, fatigue, headache, insomnia
Increased serum prolactin levels

118
Q

Ramelteon DI

A

Strong CYP1A2, 2C9 and 3A4 inhibitors (fluconazole and ketoconazole) increase conc significantly
Strong CYP enzyme inducers (rifampin) decrease conc

119
Q

Orexin rec antagonist

A

Suvorexant, Lemborexant, Daridorexant

120
Q

Orexin Rec Antagonist

A

MOA: orexin rec antagonist
Alters the signaling of orexins, NTs responsible for regulating the sleep-wake cycle
Blocks the binding of wake-promoting neuropeptides orexin A and orexin B to rec (dual orexin rec antagonist, DORA)

121
Q

Orexin Rec Antagonist AE

A

Sleep paralysis
Cataplexy like symptoms - leg weakness lasing from seconds to a few mintues

122
Q
A

Medicine (5 decks)

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