CNS part 2 Flashcards
Drugs to Manage Schizophrenia
a. First generation antipsychotics (FGA) – the class are the ________
phenothiazines
How First generation antipsychotics (AKA conventional antipsychotics) (class = phenothiazines) work-
what’s their MOA^ and what do they cause?
– Block receptors for dopamine in CNS: In particular, they block dopamine2 (D2) receptors in the mesolimbic area in the brain
–
* Cause serious movement disorders - extrapyramidal symptoms [EPS]
Do First-generation antipsychotics (phenothiazines) work better than other classes, such as 2nd gens?
Both groups/gens have equal efficacy; Drugs in all groups equivalent with respect to antipsychotic actions
(1st and 2nd gen antipsychotics are equally effective)
a. First generation antipsychotics (FGA) – the class are the phenothiazines.
Side effects- 1st just list the 4 types of extrapyramidal symptoms (EPS) and what some of them mean
Acute dystonia- muscle spasm of face (eyes), neck or back (opisthotonus)
Parkinsonism
Akathisia- pacing and squirming
Tardive dyskinesia-facial grimacing, slow involuntary tongue rolling, lip smacking, and pill-rolling
List the onset of the 4 types of extrapyramidal symptoms- after being treated with phenothiazines, when would you see each of them appear?
– Acute dystonia - first few hours/days of treatment
– Parkinsonism – within 1st month
– Akathisia – within first 2 months
-– Tardive dyskinesia- late onset
(– 1st three have an earlier onset (spasms, twitches and tremors)
Is Tardive dyskinesia reversible?
NO- it can be irreversible
How would acute dystonia be treated?
tx with diphenhydramine (Benadryl) & benztropine (anti-ChE eft/drugs)
How would parkinsonism be treated?
(tx w/ no levodopa or DA agonists)
How would Akathisia be treated?
tx with anti-ChE drugs
How would Tardive dyskinesia be treated?
by switching to SGA
no actual treatment?
What are some other adverse effects of 1st gen antipsychotics/phenothiazines
(focus on bold)
- Anticholinergic effects from cholinergic blockade
- Orthostatic hypotension
- Sedation – at beginning of tx
- Neuroendocrine effects – gynecomastia, galactorrhea
- Seizures from conventional reducing seizure threshold
- Sexual dysfunction – 25-60%
- Dermatologic effects – UV sensitivity & pigment deposits (phenothiazines)
- Agranulocytosis – chlorpromazine…reg check WBCs
- Severe dysrhythmias – prolonged QT interval..risk for ventricular arrythmias (chlorpromazine, haloperidol, thioridazine, pimozide)
1st gen/conventional antipsychotics will end with what?
also what’s a high potency agent drug?
-azine
Haloperidol
Drugs to manage schizophrenia b. Must know neuroleptic malignant syndrome including how to recognize and manage
- Neuroleptic malignant syndrome (NMS)
– Rare but serious reaction
– Risk of death without treatment
– Sweating, rigidity, sudden high fever*, autonomic instability (HR/BP could be up/down), seizures - tx w/ dantrolene to reduce muscle rigidity which helps reduce fever and bromocriptine (Dompaine agonist)
Cardinal signs of NMS (neuroleptic malignant syndrome)
Cardinal features are as follows:
- Severe muscular rigidity
- Hyperthermia (temperature >38°C)
- Autonomic instability
- Changes in the level of consciousness
c. Second generation antipsychotics (SGA) also known as the
atypical antipsychotics
Why has the use of Second generation antipsychotics (SGA) /atypical antipsychotics superseded the use of the FGAs (1st gens)
- Less risk of EPS (the 4types) than conventionals
Side effects of Second generation antipsychotics (SGA) /atypical antipsychotics
Metabolic effects:
weight gain, new-onset DM, and dyslipidemia
Drugs to manage schizophrenia:
d. Be familiar with the drug Clozapine which is unique
MOA plus one thing to note
- First atypical – now 2nd line for schizophrenia
- MOA
– Blocks dopamine (low affinity – lower EPS)
– Blocks serotonin
Clozapine therapeutic use
– Schizophrenia
– Levodopa-induced psychosis
Clozapine AEs (important)
– Fatal agranulocytosis – monitor WBCs before & post
– Seizures in ~3%
– Metabolic efx
– EPS
– Myocarditis
– Older adult patients with dementia
* About double the mortality rate – not used for dementia
II. Antidepressants
a. Know the different classes of antidepressants including the following:
i. ______ inhibitors
ii. _______ antidepressants
iii. __________
iv. _____________
v. Atypical antidepressant – _______
II. Antidepressants
a. Know the different classes of antidepressants including the following:
i. MAOI inhibitors
ii. Tricyclic antidepressants
iii. Selective Serotonin Reuptake Inhibitors (SSRIs)
iv. Selective Serotonin Norepinephrine Reuptake Inhibitors (SSNRI)
v. Atypical antidepressant – Bupropion
MAO inhibitors (MAOI) are the DOC for
atypical depression
MAO inhibitors:
* As effective as TCAs or SSRIs, but more _______
What’s the risk?
more dangerous
Risk of triggering hypertensive crisis if the patient eats foods rich in tyramine
Mech of action of MAO inhibitors
– Inactivate monoamine neurotransmitters (NE, serotonin, and dopamine)
All current MAOIs cause ______________ inhibition- – when changing/starting other antideps, keep at least __ ______ b/t MAOIs and other deps (5 wks w/ fluoxetine [VERY long ½ life….2-4d, metabolite 7-15d]. MAOIs are also _____
All current MAOIs cause irreversible inhibition- – when changing/starting other antideps, keep at least 2 weeks b/t MAOIs and other deps (5 wks w/ fluoxetine [VERY long ½ life….2-4d, metabolite 7-15d]. MAOIs are also nonselective
Adverse effects of MAOIs
- direct CNS stimulation – anxiety, insomnia, agitation, hypomania & mania
- Orthostatic hypotension – from NE binding to what receptors in vasomotor center? Alpha 2 receptors
- Hypertensive crisis from dietary tyramine
– tyramine stims release of accumulated NE (& epi) – NE activates which adrenergic receptors?
MOA of MAOIs
– MAOI prevents breakdown (-ase) of NE in neurons
FYI-
– NE regulates cardiac fx and vascular tone …what receptors & eft?
– Inhibiting hepatic & intestinal MAO allows dietary tyramine to enter systemic circ intact
Pt teaching for MAOIs
Avoid tyramine-containing foods like
yeast extracts, most cheeses, fermented sausages, and aged fish or meat – to name some…. salami, pepperoni, bologna.
Why does tyramine need to be avoided with MAOI’s?
causes hypertensive crisis
Drug interactions for MAOI inhibitors and what it will cause (there’s two)
Taking it with antidepressants: TCAs and SSRIs
* TCAs: hypertensive episode; SSRIs: serotonin syndrome/crisis
Tricyclic Antidepressants MOA
Mechanism of Action
* Block neuronal reuptake of:
– Norepinephrine (NE)
– Serotonin (5HT)
Tricyclic antidepressants are best used for
patients with major depression and neuropathic pain
Most common adverse effects of Tricyclic antidepressants
- sedation
- orthostatic hypotension - for hosp pts, need to monitor regularly
- anticholinergic effects
Most dangerous adverse effects of Tricyclic antidepressants
cardiac toxicity
- lethal w/ OD
Tricyclic antidepressants may increase risk of what? and when
- May increase risk of suicide early in treatment
A/E of Tricyclic Antidepressants- know all
- Orthostatic hypotension
- Anticholinergic effects (TCAs block Cho receptors)
- Diaphoresis
- Sedation
- Cardiac toxicity –
- increase risk of dysrhythmias – **must have EKG b/f tx and then monitor periodically after
- Seizures – lowers seizure threshold**
- Hypomania
- “Yawngasm”
TCA Toxicity:
* Clinical manifestations – (antiCHo efx:
hyperthermia, flushing, dry mouth & dilation of pupils)
Treatment for TCA Toxicity
Physostigmine
TCA drugs end with
-tyline
TCA- when should it be given
initial doses should be low; give at bedtime
SSRIS are most commonly prescribed antidepressants- why?
As effective as TCAS but causes fewer SEs (hypotension, sedation, or anticholinergic efx)
Death by overdose is extremely rare- OD doesn’t cause cardiac toxicity
SSRI MOA
– Selective inhibition of serotonin reuptake
– Produce CNS excitation (insomnia & agitation)
- SSRIs have fewer side effects than ____
(fewer anticholinergic effects & lower risk of ____toxicity)
- SSRIs have fewer side effects than TCAs
(fewer anticholinergic effects & lower risk of cardiotoxicity)
SSRI side effects
– Gastrointestinal disturbances: nausea, vomiting, diarrhea
– Headaches, insomnia
– Anxiety, agitation
– Sexual dysfunction (loss of libido, impotence)
* 50% to 70% of patients experience
– Allergic skin reactions
– Weight loss short term; but weight gain if taken longer than 6 months can experience a 20 lb + gain
– Tremors, seizures
– Life threatening – Serotonin Syndrome
* Neonatal abstinence syndrome (NAS) and persistent pulmonary hypertension of the newborn (PPHN ) when used late in pregnancy
* Bleeding disorders – need 5HT for plt activation (so antiplatlet meds are a drug interaction)
SSRIs life-threatening AE, when it occurs, and what to look for
Serotonin syndrome – deaths have occurred
2–72 hours after treatment
AMS (agit, confusion, hallucinations, disorientation…)
myoclonus
hyperreflexia
excessive sweating
tremor
fever
How does serotonin syndrome resolve? Risk is increased with..?
after discontinuation of drug
risk increased with concurrent use of MAOIs
SSRI _________ syndrome – dizziness, nausea, tremor, dysphoria – starts days to wks past last dose & persist for 1-3 wks. SO _____ ______
withdrawal
TAPER DOSE
SSRI drug interaction- risk for? how long to separate for?
Monoamine oxidase inhibitors (MAOIs)
– Risk of serotonin syndrome
* separate SSRIs and MAOIs by at least 2 weeks (5 wks w/ fluoxetine [long ½ life]
b. Can any antidepressant be stopped immediately or do they need to be tapered?
c. 20% to 56% of patients can experience withdrawl syndrome from discontinuation
a. Occurs with __________________________________________
d. Risk of discontinuation syndrome increases if someone takes a medication for > __ months
e. Another problem – over time, follow up of patients on these medications declines
f. Time to taper down an antidepressant varies from individual to another
c. 20% to 56% of patients can experience withdrawl syndrome from discontinuation
a. Occurs with MAO inhibitors, TCA, SSRIs, SNRIs
d. Risk of discontinuation syndrome increases if someone takes a medication for > 6 months
e. Another problem – over time, follow up of patients on these medications declines
f. Time to taper down an antidepressant varies from individual to another
MOA of Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs)
How it works: Blocks NE and serotonin uptake
SNRIs have serious reactions if combined with
MAOIs
also fyi dont take w alcohol
Side effects of Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs)
prob not that important
– Nausea/vomiting
– Dizziness
– Headache
– Anorexia
– Nervousness/Anxiety
– Sweating
– Insomnia/somnolence
– Weight loss/anorexia
– Diastolic hypertension
– Sexual dysfunction
– Hyponatremia (in older adult patients)
– Neonatal withdrawal syndrome
Atypical Antidepressants: what drug?
Bupropion (Wllbutrin)
Atypical Antidepressants: Bupropion (Wllbutrin)
Actions and uses
* Acts as _______ and _______ ______
* Antidepressant effects begin in __-___weeks
* Does not affect serotonergic, cholinergic, or histaminergic transmission; works w/ dopamine
* Does not cause ____ ____
* Increases _____ _____ and pleasure
* ______ – approved for _____ cessation
Actions and uses
* Acts as stimulant and suppresses appetite
* Antidepressant effects begin in 1–3 weeks
* Does not affect serotonergic, cholinergic, or histaminergic transmission; works w/ dopamine
* Does not cause weight gain
* Increases sexual desire and pleasure
* Zyban – approved for smoking cessation
Most notable A/E of Atypical Antidepressants: Bupropion (Wllbutrin)
It can cause seizures
- MAOIs can increase the risk of
bupropion toxicity
III. Sedatives/hypnotics- what class?
Benzodiazepines
Uses of Benzodiazepines- focus on bold
Uses
* DOC to treat anxiety and some insomnia
* Used to induce general anesthesia
* Used to manage seizure disorders
* muscle spasm & spasiticity (DOC)
* panic disorder
* withdrawal from alcohol
Side effects of the benzodiazepines;
IV from can cause ______ and _______
- CNS depression – drowsy, lightheadedness, incoordination
- Anterograde amnesia
- [not sure what this mean, watch panopto] Sleep- driving, cooking/eating, phone calls, sex
– WORSE WHEN TAKEN WITH OTHER CNS deps (ETOH, etc.)
– IV form – hypotension & cardiac arrest - Paradoxical effects – insomnia, excitation, euphoria, anxiety & rage
- Respiratory depression – less w/ oral dose unless combo with other CNS depressants; IV DANGER
- Use cautiously in pt. with obstructive sleep apnea, COPD
Abuse potential for benzodiazepines
lower than with barbiturates & other CNS depressants (Sched IV)
Category for pregnancy and lactation (benzodiapzepines)
Cat D & X (is cat D for preg and X for lactation? check panopto)
Benzodiapzepines toxicities
IV - life threatening in 2%
and overdose
Benzodiapzepines toxicities
IV - life threatening in 2%
and overdose
what will each be treated with?
– Intravenous toxicity – life-threatening in 2%
– Tx: gastric lavage & dialysis
– OD Treatment: flumazenil [Romazicon]
* may not reverse resp depression
* IV over 30 secs
* lasts about 1 hr, so plan for repeated doses
c. Zolpidem (Ambien), Zaleplon (Sonata), and eszopiclone (Lunesta) are used to treat..
insomnia, not anxiety
- Zolpidem (Ambien)
– Sedative-hypnotic
– Helps with falling asleep & staying asleep
- Zaleplon (Sonata)
– New class of hypnotics, pyrazolopyrimidines
– Helps with falling asleep only
– Prolonged use does not appear to cause tolerance
- Eszopiclone (Lunesta)
– For treating insomnia
– No limitation on how long it can be used
d. Review patient teaching for melatonin
- Take right before bedtime & turn off stimulation (i.e., TV, computer, lights)
Can the drugs that treat insomia be used longterm
yes
a. Review the different classes of drugs that can be used to manage anxiety disorders
- Benzodiazepines, MOI inhibitors, SNRIs (for generalized and social anxiety disorders), sedatives like Barbiturates, Benzodiazepines (double check these- Nadine)
b. Buspirone (Buspar) is an
antianxiety medication
b. Buspirone (Buspar) – know advantages and disadvantages of buspar as an antianxiety medication
– Non-CNS depressant –
– 3 benefits
* does not cause sedation
* Has no abuse potential
* Does not intensify the effects of CNS depressants
- Adverse effects:
- Dizziness
- Nausea
- Headache
- Nervousness
- Lightheadedness
- Excitement
- Stimulants/ADHD: Trade names:
Ritalin and Concerta
a. Know how methylphenidate works to manage ____
ADHD
increase the levels of norepinephrine & dopamine
Methylphenidate treats
ADHD
Methylphenidate is a highly
- Highly abused substance; close monitoring is required
Methylphenidate potential side effects
Dizziness
Insomnia, weight loss
Seizures
Palpitations
Arrhythmias
Abdominal pain
Rash
Thrombocytopenia
High blood pressure
Make tic’s worse
Increase in blood sugar (glucose)
Instructions on how to take Methylphenidate:
- Give the drug at least __ hours before ______ to avoid ____ interference
- After prolonged use, ____ the dosage gradually to prevent acute rebound depression
- Advise the patient to avoid ______ ____ until the drug’s CNS effects are known
- Tell patient to avoid drinks containing _______ -> inc. the effect of amphetamines
- Give the drug at least 6 hours before bedtime to avoid sleep interference
- After prolonged use, reduce the dosage gradually to prevent acute rebound depression
- Advise the patient to avoid hazardous activities until the drug’s CNS effects are known
- Tell patient to avoid drinks containing caffeine -> inc. the effect of amphetamines
a. What are the goals of anesthesia?
Goals of general anesthesia:
* Analgesia (loss of pain perception)
* Unconsciousness (loss of awareness of one’s own surroundings)
* Amnesia (Inability to recall what took place)
* Skeletal muscle relaxation
* Reflex reduction
b. What does the nurse monitor in the PACU?
- Periodic assessment of _____ _____, _____ ____, and ____ ____ should be done during emergence and recovery.
◦ Particular attention should be given to monitoring oxygenation and ventilation. - Routine monitoring of _____ and____ ______ should be done during emergence and recovery, and electrocardiographic monitors should be immediately available.
- Assessment of ________ ______ should be performed during emergence and recovery for patients who have received nondepolarizing neuromuscular blocking agents or who have medical conditions associated with neuromuscular dysfunction.
- ______ _____ should be periodically assessed during emergence and recovery.
- Periodic assessment of airway patency, respiratory rate, and oxygen saturation should be done during emergence and recovery.
◦ Particular attention should be given to monitoring oxygenation and ventilation. - Routine monitoring of pulse and blood pressure should be done during emergence and recovery, and electrocardiographic monitors should be immediately available.
- Assessment of neuromuscular function should be performed during emergence and recovery for patients who have received nondepolarizing neuromuscular blocking agents or who have medical conditions associated with neuromuscular dysfunction.
- Mental status should be periodically assessed during emergence and recovery.
What else will the nurse monitor in the PACU
- Temp
- Pain
- N/V
- Post-op hydration status
- Urine output and urinary voiding
- Drainage and bleeding
c. What are the signs and symptoms of malignant hyperthermia? How is it managed?
? I think this is on other lecture but double check
d. Neuromuscular blocking agents – what happens to the patient when they receive? What remains intact?
Patient will not be able to breath on their own!
– ** Does not affect consciousness or perception of pain
- Two classes of drugs to manage Alzheimer’s dementia;
Cholinergic & anti-cholinergice drugs
Peripheral nervous system- There is only one cholinergic drug meaning it enhances the cholinergic activity by binding to _________ receptors. That drug is the ___
binding to acetylcholine receptors
Urecholine
Then we have the anti-cholinergic drugs that ____ the receptor for acetylcholine. That would be _______ for example.
block; atropine
Then we have a class of drugs that ______ the amount of acetylcholine neurotransmitter ______ to bind with receptors. These are the __________ ______
They don’t work on the receptors but prevent the ______ of the neurotransmitter thus make more of it ______. This would include the______ drugs.
Then we have a class of drugs that enhance the amount of acetylcholine neurotransmitter available to bind with receptors. These are the cholinesterase inhibitors.
They don’t work on the receptors but prevent the breakdown of the neurotransmitter thus make more of it available. This would include the stigmine drugs.
Atropine is the same thing as
anticholinergic drugs
Atropine/anticholiergic MOA:
competitively antagonizes the actions of acetylcholine & other cholinergic agonists at the muscarinic receptors
- Cholinesterase Inhibitors MOA:
prevent breakdown of ACh by acetylcholinesterase & thus inc. availability of ACh at the cholinergic synapses
We have another class of cholinesterase inhibitor drugs working the same way as above (prevent breakdown of Ach) BUT the big difference is instead of targeting the peripheral nervous system (muscle, glands, etc), they target the _____ _____ ____ - the ____. This class is the drugs used for _____ Because this class causes _______, they are given at ____.
We have another class of cholinesterase inhibitor drugs working the same way as above (prevent breakdown of Ach) BUT the big difference is instead of targeting the peripheral nervous system (muscle, glands, etc), they target the central nervous system - the brain. This class are the drugs used for dementia. Because this class causes bradycardia, they are given at night.
Adverse effects of atropine/anticholinergic drugs
notice which is dose-dependent
- CNS: Blurred vision, mydriasis, cycloplegia, photophobia, increased IOP, headache, flushing, nervousness, weakness, dizziness, insomnia, mental confusion or excitement (after even small doses in the elderly), nasal congestion
- CV: Palpitations, tachycardia (higher doses)
- GI: Dry mouth, altered taste perception, nausea, vomiting, dysphagia, heartburn, constipation, bloated feeling, paralytic ileus, gastroesophageal reflux
- GU: Urinary hesitancy and retention; impotence
- Other: Decreased sweating and predisposition to heat prostration, suppression of lactation
Adverse effects of Cholinesterase Inhibitors:
– GI: N/V, dyspepsia, diarrhea
– CNS: dizziness, HA
– CV: bradycardia (dose dependent)
- MOA (alr above): competitively antagonizes the actions of acetylcholine & other cholinergic agonists at the muscarinic receptors
Atropine
Indications/uses of atropine
- Symptomatic bradycardia
- Preoperative reduction of secretions & blockage of cardiac vagal reflexes
- Adjunct tx. Of peptic ulcer disease
- Functional GI disorders
- Muscarinic agonist poisoning (mushrooms)
- Organophosphate poisoning
- Ophthalmic preparations
Diagnostically to produce mydriasis and cycloplegia-pupillary dilation in acute inflammatory conditions of the iris and uveal tract
Contraindications of atropine
- Glaucoma (inc. IOP)
- Use w/ caution w/ Asthma (inc. thick secretions in airway)
- Intestinal atony
- Urinary obstruction
- Tachycardia
Any time you see a neurotransmitter with “ase” at the end - it is an ____ that impacts the ________
Any time you see a neurotransmitter with “ase” at the end - it is an enzyme that impacts the neurotransmitter.
______ is the antidote to _____ drugs and ______drugs are the antidote to______
Atropine is the antidote to stigma drugs and stigmine drugs are the antidote to atropine
Anticholinergic side effect picture summary
hot as a hare
dry as a bone
blind as a bat
red as a beet
mad as a hatter
“Stigmine” drugs – indication
Neostigmine:
- Uses:
– Myasthenia gravis
– Reversal of competitive neuromuscular blockade
“Stigmine” drugs –side effects
Neostigmine:
– Excessive salivation
– Inc. gastric secretions
– Inc. tone & motility of GI tract (diarrhea)
– Urinary urgency
– Bradycardia
– sweating
– Miosis
– Spasm of accommodation
“Stigmine” drugs –antidote
Neostigmine:
– Overdose can lead to excessive muscarinic stimulation & respiratory depression
– Called a
“cholinergic crisis”
– Treatment – atropine except for breathing issues-
* Respiratory depression managed w/ mechanical ventilation
Other uses of stigmine drugs:
* Physostigmine – drug of choice for treating _______ w/ atropine, antihistamines
* Pyridostigmine (Mestinon)- also used for treatment of _______ ______
Other uses of stigmine drugs:
* Physostigmine – drug of choice for treating poisoning w/ atropine, antihistamines
* Pyridostigmine (Mestinon)- also used for treatment of myasthenia gravis
SUMMARY:
I was asked about cholinergic and anti-cholinergic drugs. I agree - it can be confusing. I hope this information helps clarify.
Peripheral nervous system There is only one cholinergic drug meaning it _______ the _______ activity by binding to _______ receptors. That drug is the ________
Then we have the anti-cholinergic drugs that_____ the receptor for ____________. That would be _____ for example.
Then we have a class of drugs that enhance the _______ of acetylcholine neurotransmitter _______ to bind with receptors. These are the cholinesterase inhibitors.
They don’t work on the ______ but _______ the breakdown of the neurotransmitter thus make ______ of it available. This would include the ______ drugs.
Atropine is the antidote to stigma drugs and stigmine drugs are the antidote to atropine Central nervous system
We have another class of cholinesterase inhibitor drugs working the same way as above BUT the big difference is instead of targeting the peripheral nervous system (_____, glands, etc), they target the central nervous system - the brain. This class are the drugs used for ______Because this class causes bradycardia, they are given at ____
Any time you see a neurotransmitter with “ase” at the end - it is an enzyme that impacts the neurotransmitter.
I was asked about cholinergic and anti-cholinergic drugs. I agree - it can be confusing. I hope this information helps clarify.
Peripheral nervous system There is only one cholinergic drug meaning it enhances the cholinergic activity by binding to acetylcholine receptors. That drug is the Urecholine.
Then we have the anti-cholinergic drugs that block the receptor for acetylcholine. That would be Atropine for example.
Then we have a class of drugs that enhance the amount of acetylcholine neurotransmitter available to bind with receptors. These are the cholinesterase inhibitors.
They don’t work on the receptors but prevent the breakdown of the neurotransmitter thus make more of it available. This would include the stigmine drugs.
Atropine is the antidote to stigma drugs and stigmine drugs are the antidote to atropine Central nervous system
We have another class of cholinesterase inhibitor drugs working the same way as above BUT the big difference is instead of targeting the peripheral nervous system (muscle, glands, etc), they target the central nervous system - the brain. This class are the drugs used for dementia. Because this class causes bradycardia, they are given at night.
Any time you see a neurotransmitter with “ase” at the end - it is an enzyme that impacts the neurotransmitter.
