Neuro Pharm Flashcards
1
Q
NSAIDs
A
Abortive therapy for headaches.
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
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)
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
5
Q
Ergot Alkaloisd
A
Ergotamine and Dihydroergotamine
6
Q
Ergotamine
A
Oral, SL, rectal
Oral absorption poor, often combined with caffeine to increase absorption
7
Q
Dihydroergotamine (DHE)
A
Intranasal and parenteral
Injectable often used for intractable migraine along with antiemetic
Fewer side effects than ergotamine
8
Q
Ergot alkaloids AE
A
N/V, limb paresthesias or pain
Nasal spray - stinging/rhinitis, unpleasant taste
Give antiemetic for N/V
9
Q
Ergot alkaloids CI
A
IHD, PAD, HTN, pregnancy
Has sig effect in coronary arteries
10
Q
Ergot Alkaloids DI
A
Avoid concurrent triptans; beta blockers, strong CYP3A4 inhibitors as they reduce hepatic hepatic metabolism of ergot alkaloids
11
Q
Ergotism
A
Severe peripehral ischemia - cold, numb, painful ext, and claudication
Overdose- vascular occlusion and gangrene
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
13
Q
NSAIDs AE
A
GI upset
14
Q
NSAIDs CI
A
PUD, renal insufficiency, heart failure
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
16
Q
Acetaminophen/ASA/Caffeine AE and CI
A
AE: GI upset, insomnia
CI: PUD, renal disease
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
18
Q
Butorphanol nasal spray
A
Opioid agonist/antagonist at mu opioid rec
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
20
Q
Calcitonin Gene-related peptide receptor antagonist
A
Gepants
Rimegepant
Ubrogepant
Atogepant
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
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
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
24
Q
Lasmiditan AE
A
Dizziness, sedation, paresthesia, hallucinations, euphoria, risk of serotonin syndrome
25
Lasmiditan Indication
Should only be considered for patients who can't use triptans or who have failed two triptans
26
Antiemetics
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)
27
Dexamethasone
Rescue therapy for status migrainosus (severe, continuous headache for >72 hours and up to 1 week
May be used as adjunct to abortive therapy
28
Mild to moderate acute migraine attack
NSAID or acetaminophen
29
Moderate to severe acute migraine attack
Triptan
If fail triptan, can try ergot alkaloids
Patients who failed two triptans can be considered for therapy with CGRP antagonist or lasmiditan
30
Prophylaxis of migraine headaches Indications
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)
31
Antiepileptics
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
32
Beta blockers
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
33
Antidepressants
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
34
Menstrual migraine
NSAIDs or triptans
35
Monoclonal Ab against CGRP rec
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
36
Monoclonal Ab agaisnt CGRP rec for cluster headaches
Galcanezumab
37
Atogepant
FDA approved for prophylaxis and acute management
38
Onabotulinumtoxin A
FDA approved for prophylaxis in adults with chronic migraine
>15 headache days/months for >4 hours/day
39
Prophylaxis for HA in healthy or comorbid HTN or angina
Beta blocker therapy
Verapamil if beta blocker CI or ineffective
40
Prophylaxis for HA in comorbid depression or insomnia
Tricyclic antidepressant
Amitriptyline
41
Prophylaxis for HA in comorbid seizure disorder or bipolar illness
Anticonvulsant - valproate and topiramate
If ineffective, beta blockers
42
Prophylaxis for HA in headaches that recur in predictable pattern (menstrual migraine)
NSAID or triptan
43
Abortive therapy in pregnancy
Acetaminophen for short term use
Avoid NSAIDs in 3rd trimester (premature closure of ductus arteriosus)
Ergots CI
Prophylaxis not recommended
44
Abortive therapy cluster headache
Inhaled oxygen - DOC
Triptans
45
Prophylaxis of cluster headache
verapamil, lithium, glucocorticoids (prednisone), valproic acid, topiramate, ergotamine, melatonin, capsaicin, galcanezumab
46
Tension Headache
Non-pharm: biofeedback, acupuncture, relaxation training, physiotherapy
Medications: NSAIDs, acetaminophen
Prophylaxis with amitriptyline with or without regular OMT
47
What converts levodopa to dopamine in peripheral tissues?
L-aromatic amino acid decarboxylase (LAAD)
48
Does L-dopa cross BBB?
Yes, dopamine does not.
49
What drug is given with L-dopa?
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
50
L-dopa considerations
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
51
L-dopa AE
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
L-dopa DI
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
Common motor complications of carbidopa/levodopa combination with long-term treatment
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
Catechol-O-methyltransferase (COMT) inhibitors
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
3 COMT inhibitors
Tolcapone - only one that crosses BBB
Opicapone and entacapone - Do not cross BBB
56
COMT inhibitors AE
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
Monoamine Oxidase (MAO)
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
MAO-B inhibitors
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
Selegiline
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
Rasagiline
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
3 MAO-B inhibitors
Selegiline
Rasagiline
Safinimide
62
MAO-B inhibitors AE
Confusion, hallucinations, hypotension, insomnia, dyskinesias
63
MAO-B inhibitors DI
Serotonin syndrome with SSRIs, meperidine, other serotonergic drugs
64
Dopamine REceptor Agonists
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
Pramipexole
Dopamine rec agonist
MOA: Selective for D2 and D3 rec
Renally excreted, dose adjustment in renal insufficiency
66
Ropinirole
Dopamine rec agonist
MOA: selective for D2 receptors
Metabolized by CYP1A2, fluoroquinolone antibiotics increase serum levels; omeprazole decreases levels
67
Rotigotine
Dopamine rec agonist
MOA: selective for D3>D2>D1
Transdermal patch only, no dosage adjustment needed for hepatic or renal insufficiency
68
Dopamine rec agonists (pramipexole, ropinirole, and rotigotine)
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
Apomorphine
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
Bromocriptine
Non-selective D2 rec agonist
Ergot alkaloid
Used in advanced PD for wearing off and on-off motor fluctuations
71
Most common AE of dopamine rec agonist
Nausea
Others include: confusion, dyskinesias, sedation, vivid dreams, hallucinations, orthostatic hypotension, dry mouth and sleep attacks
72
Dopamine receptors agonists (pramipexole and ropinirole)
Intense urges have been reported with pramipexole and ropinirole such as gambling, shopping and sexual activity
73
Dopamine rec agonists CI
History of psychotic illness, recent MI, and active PUD (bromocriptine)
74
Istradefylline MOA
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
Istradeylline AE and DI
Dyskinesia, dizziness, insomnia
DI: strong CYP3A4 inhibitors
76
Amantadine MOA
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
Cholinesterase Inhibitors (3 of them) for treatment of Alzheimer's
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
AE of Cholinesterase inhibitors
Nausea, anorexia, vomiting, diarrhea, bradycardia and syncope
Start low and go slow
79
DI of cholinesterase inhibitors
Anticholinergic agents may decrease benefit Diphenhydramine, tolterodine and oxybutynin (urinary incontinence), and TCAs (imipramine, amitriptyline)
80
NMDA Rec blocker for Alzheimer Disease
Memantine
MOA: N-methyl-D-aspartate antagonist; blocks excitotoxic effects of glutamate
Considered for moderate to severe AD
81
AE of Memantine
Dizziness, confusion, hallucinations, delusions, headache, constipation
Reduce dose with creatinine clearance of < 30mL/min
82
Vitamin E complications in AD treatment
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
Beta-amyloid Monoclonal Ab
Aducanumab and lecanemab-irmb
MOA: Monoclonal Ab against soluble and insoluble amyloid; reduces amyloid beta plaques
82
AE of Aducanuman and lecanemab-irmb
Hemosiderosis, microhemorrhage, brain edema, headache, and falling
82
Firstline treatment for Noncognitive symptoms of AD
Non-pharm interventions
83
Brexpiprazole
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
Treatment of Huntington Disease
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
Tetrabenazine
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
Tetrabenazine AE
Sedation/somnolence, fatigue, insomnia, depression, akathisia, anxiety, nausea
87
Tetrabenazine DI
Strong CYP2D6 inhibitors like fluoxetine, CI with MAO inhibitors
88
Deutetrabenazine
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
Atypical Antipsychotics for HD
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
Riluzole for treatment of ALS
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
Edaravone for tx of ALS
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
Sodium Phenylbutyrate/ Taurursodiol PB-TURSO for ALS treatment
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
Tofersen for Treatment of ALS
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
Treatment for sialorrhea in ALS
Glycopyrrolate - muscarinic rec antagonist (DOC)
Amitriptyline - antidepressant with anticholinergic properties
95
Treatment for Pain and Agitation in ALS
Opioids and/or BZDs
96
Treatment for Spasticity in ALS
Baclofen - GABAb agonist
Tizanidine - agonist of alpha2 adrenergic rec in CNS, increases presynaptic inhibition
Clonazepam - BZD
97
Other Treatments for ALS
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
BZD sedative-hypnotic
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
Clhordiazepoxide and diazepam
BZDs that are converted to long-acting active metabolites
100
Alprazolam, midazolam, and triazolam
BZDs that are converted to a short-acting active metabolite
101
Benzodiazepines that have no active metabolites
Oxazepam, Temazepam, Lorazepam
Out The Liver
102
BZDs effects and indications
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
BZD AE
Motor incoordination
Dizziness
Drowsiness
Impairment of concentration, judgment and planning
Driving/psychomotor skills
Disinhibition
Physical dependence leading to withdrawal symptoms
104
BZD withdrawal syndrome
Rebound anxiety
Rebound sleep disorder
Headache
Insomnia
Irritability
Muscle twitches
Seizures
Taper gradually to avoid withdrawal symptoms
105
BZD DI
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
Treatment of BZD overdose
Flumazenil
MOA: competitive BZD rec antagonist
Given IV
AE: seizures, arrhythmias, blurred vision, emotional lability and dizziness
107
Barbiturates and Sleep
Sedation
Suppress slow wave and REM sleep
Effective for up to 2 weeks; lose ability to induce and maintain sleep after this period
108
Barbiturates binding site
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
Barbiturates AE
Respiratory depression, physical and psychological dependence; agitation, confusion, nightmares, hallucinations, hangover
110
Barbiturates DI
CI with CYP450 3A4 inhibitors: azole antifungals, protease inhibitors, other antiretrovirals
Additive effects with other CNS depressants
Pregnancy: teratogenic
111
Treatment of Barbiturate overdose
Supportive care
Na bicarbonate to alkalinize the urine to enhance elimination for long-acting barbiturates only (phenobarbital butalbital)
112
Non-BZD sedative-hypnotics
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
Non-BZD sedative-hypnotics AE
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
Non-BZD sedative hypnotics DI
Avoid other CNS depressants including alcohol
CYP3A4 inhibitors such as -azole antifungals and erythromycins inhibit eszopiclone metabolism
115
Remelteon
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
Ramelteon Pharmacokinetics
Rapidly absorbed,; extensive first pass mtabolism; high fat food decreases the C max
Eliminated in urine
117
Ramelteon AE
Somnolence, dizziness, nausea, fatigue, headache, insomnia
Increased serum prolactin levels
118
Ramelteon DI
Strong CYP1A2, 2C9 and 3A4 inhibitors (fluconazole and ketoconazole) increase conc significantly
Strong CYP enzyme inducers (rifampin) decrease conc
119
Orexin rec antagonist
Suvorexant, Lemborexant, Daridorexant
120
Orexin Rec Antagonist
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
Orexin Rec Antagonist AE
Sleep paralysis
Cataplexy like symptoms - leg weakness lasing from seconds to a few mintues
122
