CNS Drugs Flashcards
Train-of Four Pattern (TOF)
TOF = 1 (phase 1 of depolarizing block or no drug present)
TOF < 1 (phase 2 of depolarizing block or nondepolarizing block)
*Dantrolene, curare-like drugs, and succinylcholine phase 1 will have TOF < 1
Levodopa
MOA: prodrug L-dopa converted to dopamine by dopa decarboxylase (aka aromatic L-amino acid decarboxylase or AAAD), given w/ Carbidopa
Metabolism: food delays absorption
Use: tx sx’s of Parkinson dz
SE: on-off effects (dyskinesia d/t dopamine level fluctuations), psychosis, hypotension
*efficacy decreases as pathology progresses
CI: angle-closure glaucoma
Drugs used as supportive management of Barbiturate withdrawal sx’s?
IV Diazepam or Lorazepam for the seizures
Nitrous Oxide
MAC is high (so low potency), Blood/Gas is small (fast onset/recovery)
SE: diffusional hypoxia d/t NO displacing O2
steeper arterial tension curve bc decreased solubility so fast onset of action
Fluphenazine (typical)
Class: Phenothiazines (sulfa drug)
Exists in depot IM form
Ramelteon
MOA: agonist at melatonin receptors MT1 and MT2 in suprachiasmatic nucleus of hypothalamus (Gi coupled receptors)
Use: insomnia (induction only) - has NO dependence issues
SE: drowsiness and dizziness
CI: use w/ Fluvoxamine d/t the CYP-1A2 inhibition
Mesocortical D2 antagonism SE
Worsens -ve sx’s (= dysphoria), which decreases compliance
Duloxetine and Milnacipran
SNRIs
MOA: decrease reuptake of 5-HT and NE (no ANS SEs)
Use: tx Fibromyalgia (Pregabalin is a voltage-dependent Ca2+ blocker also approved for this condition)
Ketamine
MOA: noncompetative antagonist of NMDA glutamate receptor (analog of phencyclidine)
Use: dissociative anesthetic (causes analgesia and amnesia), used in emergent trauma BUT avoid in head trauma bc it increases ICP
SE: vivid dreams, hallucinations, elevated ICP
Thioridazine (typical)
Class: Phenothiazines (sulfa drugs)
Strongest antimuscarinic, so most likely to cause torsades - BUT “autotreats” acute EPS
SE: torsade (leading to arrhythmias and sudden death), retinal pigments/deposits
Apomorphine
Use: rescue therapy for tx of “off” episodes of akinesia in pt’s on dopaminergic therapy
SE: QT prolongation, dyskinesia, drowsiness, sweating, hypotension
Pramipexole / Ropinirole / Rotigotine
MOA: D2 agonists (Pramipexole is also D3 agonist)
Effect: antioxidant properties Katy decrease progression of dz
Use: Parkinson dz, tx restless leg syndrome (RLS), antidepressant effects
Thiopental
(Barbiturate)
Anesthetic induction
Lithium
MOA: blocks inside 5’-monophosphate, stabilizes inactive forms of Gs and Gi, decreases PKC activity
Metabolism: Vd close to total body water (~60%), really cleared, reabsorbed in PCT like Na+ (Na+ depletion like with increased sweating can cause Li+ toxicity)
Drug interaction: diuretics decrease Li+ clearance and increase toxicity, NSAIDs and ACEIs facilitate PCT reabsorption and cause Li+ toxicity (Triamterene and Amiloride increase clearance of Li+ to decrease toxicity potential)
Carbidopa
MOA: irreversible inhibitor of peripheral AAAD
Effect: allows L-dopa to cross BBB before being converted to dopamine
Use: conjunction with Levodopa to tx Parkinson dz
Ziprasidone (atypical)
MOA: strong 5-HT blockade at 1, 2, 6, 7 receptors, blocks all subtypes of DA receptors and blocks 5-HT and NE reuptake
😳
Desipramine
TCA
Use: cocaine craving and withdrawal
(Safe in pregnancy)
Rasagiline
MOA: irreversible inhibitor of MAO type B
Effect: prevents breakdown of dopamine to dihydrosyphenylacetic acid (DOPAC)
SE: (none) no amphetamine metabolites
Bath salts
Substituted cathinones w/ cocaine or amphtamine-like pharmacology, produced as “legal substitutes” of Cocaine, Methamphetamine or MDMA
SE: agitation, HTN, tachycardia, hallucinations, sz, rhabdomyolysis, acute renal failure
Lithium Teratogenicity
Epstein anomaly (septal tricuspid leaflet displaced downward toward apex of RV), large RA and small RV, assoc. w/ Wolff-Parkinson-White Syndrome
MAOIs
MOA: inhibit MAO(A) or MAO(B) in outer membrane of mitochondria
Effect: increase levels of NE, 5-HT, and DA
Interactions: tyramine-rich foods/beverages, α1 agonists cause HTN crisis d/t increased NE, Serotonin Syndrome d/t interaction w/ SSRIs, TCAs, Meperidine, Dextromethorphan and St. John’s wort
Selegiline (Deprenyl)
MOA: selective inhibitor of MAO type B (so NO tyramine interactions)
Effect: prevents breakdown of dopamine to dihydrosyphenylacetic acid (DOPAC), enhances effects of Levodopa
Use: adjunct to Levodopa to tx Parkinson Dz
SE: metabolized to amphetamine (sympathomimetic) and can produce +ve amphetamine screen on drug test
Thiopental / Methohexital
Barbiturate
MOA: GABA(A) enhancers, prolong the duration of Cl- channel opening
PK: ultra-short acting
Use: induction and maintenance of anesthesia, lowers ICP
SE: severe respiratory depression potential
Benzodiazepines SEs
Drowsiness, sedation, rebound insomnia (worse w/ short-acting agents), anterograde amnesia, anxiolytics are class D for pregnancy and sedatives are class X for pregnancy (except for Quazepam) Tx: Flumazenil is non-selective benzodiazepines site antagonist used in OD (also used in OD of “Z drug”)
Amoxapine
TCA
Use: psychotic depression
Phenytoin
MOA: blocks voltage gated Na+ channels, keeping them in an inactivated state (Class 1B antiarrhythmic)
Effect: decreases conduction of APs (enhances refractoriness)
PK: zero-order elimination, inducer of CYP450s, narrow therapeutic range
Use: tx any sz type EXCEPT absence
SE: gingival hyperplasia, hirsurism, folate and Vit D deficiency, SLE-like rxn (acts as hapten), teratogenic
Fluoxetine
SSRI
PK: inhibition of CYP 3A4 (and 2D6)
Interactions: increases levels of Alprozolam and Carbamazepine (bc 3A4 metabolizes Benzos)
(Safe in pregnancy)
Olanzapine (atypical)
MOA: strong 5-HT2A blockade
Effect: improves -ve sx’s
SE: weight gain, sz
Antidepressants in Pregnancy
Safe SSRIs (Fluoxetine, Ser
Temazepam
Intermediate-acting sedative benzo w/ few active metabolites
*sudden withdrawal causes rebound insomnia
Alprazolam
Use: panic disorder
*only benzo used for anxiety assoc w/ depression
Haloperidol (typical)
Class: Butyrophenones
MOA: potent D2 blockade
Use: IV in acute management of psychosis and mania
SE: severe EPS
THC
MOA: CB1 > CB2 agonist
Effect: decreased 5-HT release from CTZ = antiemetic, decreased Leptin release in hypothalamus = appetite stimulant
Dronabinol / Nabilone
Cannabinoid
Use: tx nausea, and cancer/aids anorexia
Felbamate
MOA: NMDA receptor blocker
Use: antiepileptic
SE: aplastic anemia
Sertraline
2nd most potent SSRI, 2nd most selective SSRI (👇🏽 likelihood to cause bleeding abnormalities)
(Safe in pregnancy)
Citalopram
Most selective SSRI w/ 👇🏽 likelihood to cause bleeding abnormalities (indicated if pt has bleeding disorder, or if pt is taking Warfarin or Aspirin)
PK: NO inhibition of CYP 450
(Safe in pregnancy)
Esters (local Anesthetics)
“x-caine”
Procaine (short-acting) / Cocaine / Tatracaine (long-acting)
SE: HS rxn d/t PABA (allergen)
Malignant Hypethermia
SE of Succinylcholine and Chlorofluorocarbons
ROS: contractions d/t prolonged Ca2+ release, 👆🏽ETC activity leads to 👆🏽heat produced from ETC, stress of the heat 👆🏽SANS activity; lactic acidosis as anaerobic processes attempt to make ATP too
Fetal Hydantoin Syndrome
Cause: Phenytoin taken by mother during pregnancy
ROS: cleft lip/palate, microcephaly, epicalthal folds, broad nasal bridge, absent nails, hypoplasia of distal phalanges, congenital heart defects (VSD, pulmonary stenosis, transposition)
SNRIs
Venlafaxine / Desvenlafaxine / Duloxetine / Milnacipran
Cannabinoid Receptors
CB1 (neuronal) and CB2 (peripheral) are Gi coupled = CNS depressants
Sevoflurane
Chlorofluorocarbon, least likely to cause respiratory irritation (ok to use for induction)
Local Anesthetics MOA
Inhibit voltage-gated Na+ channels
- Cross cell membrane: drugs are weak bases so require alkaline pH to be unionized to cross the membrane
- Bind w/ in the Na+ channel: the cationic form is active drug
- Stabilize the inactivated state of the Na+ channel once bound
Cocaine
MOA: blocks DA, NE and 5-HT reuptake; also blocks voltage-dependent Na+ channels (NO effect on mobile pool, unlike amphetamines)
Use: local anesthetic (does not require epinephrine bc it has intrinsic sympathomimetic activity d/t the NE reuptake inhibition)
SE: vasoconstriction, hypertension, ischemia
*#1 cause of ED visits involving elicit drugs
Toparamate
MOA: blocks AMPA/kainate receptors, CA inhibitor
Use: migraine prophylaxis, tx obesity when used in combination w/ Phentermine
Desflurane
Chlorofluorocarbons w/ small Blood/Gas, most likely to cause respiratory irritation so avoid in induction
”Z drugs”
Zolpidem / Zaleplon / esZopiclone
MOA: strong affinity for GABA(A) receptors w/ α1 subunits
PK: Zapelon t1/2 is 1h, esZopiclone t1/2 is 6h
SE: Class C in pregnancy, drowsiness and motor impairment, parasomnia (somnambolism)
OD tx: Flumazenil
Midazolam
Use: pre-operative sedation (bc it’s so short-acting)
SE: respiratory depression/arrest (usually nbd tho bc you’re in a pre-op hospital sorta setting)
Selegiline
MOA: selective MAO(B) inhibitor
Effect: increases DA primarily
Use: available as skin patch, tx for Parkinson Dz
Benzodiazepines approved for EtOH withdrawal
Chlordiazepoxide, Clorazepate, Diazepam, Oxazepam
Tolcapone and Entacapone
MOA: COMT inhibitors —> prevent conversion of dopamine to 3-O-methyldopa (3OMD)
Effect: increases t1/2 of L-dopa, increased fraction of L-dopa reaching CNS
Use: add to Levodopa-Carbidopa as pathology of Parkinson dz progresses
SE: hepatotoxic (Tolcapone only)
Perioral Tremor (EPS)
Timeline: weeks-months
ROS: “rabbit syndrome” (muscle movement of mouth)
Antidote: antimuscarinics
Tardive Dyskinesia (EPS)
Timeline: months-years
Mechanism: upregulation and sensitization of D2 receptors after long-term tx
ROS: oral and facial dyskinesia w/ chorea and athetosis
NO TX (Diazepam may help)
*less likely to occur w/ Atypical Antipsychotics
Suvorexant
MOA: orexin receptor antagonist
Use: tx insomnia (induction and maintenance of sleep)
CI: narcolepsy
Blood-Gas Partition Coefficient
Measures solubility of anesthetic in the blood, so smaller blood-gas ratio indicates faster onset as more of the drug is reaching the CNS (bc it’s not as soluble in blood)
*the more soluble an anesthetic is in the blood, the longer it takes to get to the CNS
Lamotrigine
MOA: blocks voltage-gated Na+ channels
Effect: inhibits glutamate release
Use: adjuvant for sz, tx BP disorder
SE: rash, Class C in pregnancy
Fluvoxamine
SSRI
PK: inhibition of CYP 1A2 (which metabolizes TCAs)
Interaction: increased levels of TCAs (so dont combine)
Lamotrigine
MOA: inhibits voltage-sensitive Na+ channels and inhibits release of glutamate
Use: Bipolar disorder
SE: skin rashes, sz w/ abrupt withdrawal, teratogenic (cleft lip/palate)
Pentobarbital
(Barbiturate)
Drug-induced coma for severe brain trauma
Lithium SEs
GI sx’s (take w/ food), tremors (add Propranolol to tx if needed), polyuria (d/t decreased response to ADH Gs-coupled receptor in collecting duct), thyroid dysfunction (d/t decreased TSH response), teratogenicity**
Benztropine and Trihexyphenidyl
MOA: muscarinic antagonist that cross BBB
Effect: potentiate dopamine effect in basal ganglia
SE: Atropine-like (dry mouth, eyes, mydriasis, cycoplegia, tachycardia, constipation, urine retention, BPH)
Ethosuximide
MOA: blocks T-type Ca2+ channels (T = transient) in the thalamus
Effect: burst of thalamic neuron activity
Use: only tx absence sz
Akathisia (EPS)
Timeline: days/weeks/months
ROS: restlessness
Antidote: dose-reduction of antipsychotic, benzodiazepines, non-selective β-blockers, antimuscarinics (Clonazepam or Propranolol)
Chlorofluorocarbons (Halothane fam)
MAC is low (so high potency), Blood/Gas is higher (slower onset)
SE: malignant hyperthermia risk (tx w/ Dantrolene), respiratory irritation (coughing), hepatotoxic
more flat arterial tension curve bc increased solubility so slow onset of action
General Anesthetics MOA
Ehnance GABA(A) activity
Amides (local Anesthetics)
“x-i-x-caine”
Prilocaine (short-acting) / Lidocaine / Buvicaine (long-acting)
Benzodiazepines approved for status epilepticus
Diazepam and Lorazepam (bc they are long-acting and are available IV)
Pregabalin
Use: chronic pain
Acute Dystonic Reaction (EPS)
Timeline: within days
ROS: muscle spasms of upper body (tongue, face, neck, back) = spasmodic torticollis
Antidote: antimuscarinics (Benztropine, Trihexyphenidyl,Diphenhydramine)
Local anesthetic effect on fiber type over time (fast to slow)
C-fibers (pain), Aδ (temp), Aγ and Aβ (touch), Aα (motor)
fast to slow - and small diameter to larger diameter
SSRIs
MOA: block 5-HT reuptake (less anticholinergic activity)
use: first-line agents for chronic depression, panic, generalized anxiety disorders, bulimia, OCD, PTSD
SE: GI upset (diarrhea), sexual dysfunction (anorgasmia, 👇🏽libido, 👇🏽arousal), stimulant effect (anxiety, agitation), bleeding abnormalities (caution w/ Aspirin or Warfarin)
Minimal Alveolar Concentration (MAC)
Measure of anesthetic potency defined as concentration of gas in lungs that is able to prevent movement in 50% of pt’s (analogous to ED50)
*higher MAC = lower potency (so they are inversely related)
Succinylcholine
MOA: nicotenic agonist; phase 1 - depolarization, phase 2 - desensitization and channel blockade (can be antagonized by AChE inhibitors)
Effect: depolarizes the NMJ, stimulates ANS ganglia and muscarinic receptors (could reduce HR)
Metabolism: rapidly metabolized by liver and plasma cholinesterases
CI: pt w/ poor cholinesterase metabolism
Chlorpromazine (typical)
Class: Phenothiazines (sulfa drug)
Prominent ANS SEs, and deposits in cornea/lens
Trazodone (and Nefazodone)
SARIs
MOA: 5-HT(2A) antagonist and reuptake inhibitors, also block α1 receptors
SE: hypotension, arrhythmias and priapism (d/t α1 blockade)
*Trazodone blocks H1 receptors and acts as sedative
Buspirone
MOA: partial agonist at 5-HT(1A) receptors
Use: anxiolytic (takes several wks to work)
SE: drowsiness and dizziness
CI: use w/ MAOIs (can cause HTN crisis)
TCAs
MOA: block NE and 5-HT reuptake, also block α1, M and H1 receptors
Metabolism: metabolized by CYP450
Interactions: additive anticholinergic effects, additive sympathomimetic effects, antagonism w/ α2 agonists*
Antiepileptic rx in Pregnancy
PK: inducers of CYP enzymes can decrease efficacy of oral contraceptives
*Supplement folate @ 4mg/day, check maternal AFP (α-fetoprotein) levels during pregnancy to monitor for neural tube defects
DOC in Bipolar Disorder?
Lithium
*Lamotrigine (anticonvulsant) indicated for maintenance during pregnancy
Nondepolarizing NM Blockers MOA
Competitive antagonist at skeletal muscle Nm (nicotenic) ACh receptor
*reversed using AChI - Neostigmine
Pimozide (typical)
Class: Diphenylpiperidines
Use: Tourette syndrome and tic disorders
Bromocriptine
MOA: D2 receptor agonist
Effect: inhibition of indirect pathway (👇🏽cAMP)
Use: adjunct or alt therapy to Levodopa for Parkinson,m hyperprolactinemia and acromegaly
SE: dyskinesia, hallucination, psychosis
Valproate
MOA: anticonvulsant that enhances GABA activity, decreases degradation of GABA in CNS
Use: Bipolar Disorder
SE: sedation, GI upset, hepatotoxicity, agranulocytosis, neural tube defects
Neuroleptic Malignant Syndrome (EPS)
Timeline: weeks-months
ROS: Catalonia, high fever, rhabdomyolysis (myoblobinemia), stupor, CV instability
Antidote: Dantrolene + Bromocriptine (and STOP antipsychotic immediately)
Phencyclidine
MOA: antagonist of NMDA glutamate receptor and binds nicotenic receptors
SE: violence, agitation, rhabdomyolysis
Aripiprazole (atypical)
MOA: 5-HT2A antagonist, 5-HT1A partial agonist, partial D2 agonist
Use: mania, Autism spectrum
Propofol
PK: poorly water soluble
Use: induction and maintenance of anesthesia
SE: propofol infusion syndrome (metabolic acidosis, hyperkalemia, rhabdomyolysis, retail failure, CV collapse)
Benzodiazepines
MOA: binds GABA(A) receptor at allosteric site distinct from GABA (cannot open Cl- channels w/o GABA = potentiation)
Effect: increases frequency of Cl- ion channels opening —> hyperpolarization of cell which inhibits APs
Use: α1 mediates sedation and α2 mediates anxiolysis
PK: most have active metabolites through CYP3A4 metabolism (except Lorazepam and Oxazepam)
Paroxetine
Most potent SSRI and strong anticholinergic (more likelihood for cardiotoxic SEs)
PK: NO active metabolite, inhibitor of CYP 2D6
SE: weight gain
Batrachotoxin
MOA: prevents inactivation, prolongs Na+ entry
SE: hallucinations
*frog toxin
Phenelzine and Tranylcypromine
Nonselective MAOIs
What drugs have life-threatening withdrawal sx’s?
Barbiturates and EtOH d/t the life-threatening seizures caused by withdrawal
Valproic Acid
MOA: inhibits GABA-transferase (👆🏽GABA), inhibits T-type Ca2+ channels, inhibits voltage-gated Na+ channels, inhibits histone deacetylases
PK: inhibits CYP2C9 (no induction of CYP450s)
Use: tx all type of sz including absence, prophylaxis of migraine, tx mania in BP disorder
SE: alopecia, pancreatitis (fatal), thrombodytopenia (w/ 👆🏽BT), teratogenic (neural tube defects)
Bupropion
MOA: increase DA and NE (blocks reuptake and enhances release
Use: smoking cessation (Varenicline is alternative tx)
SE: potent inhibitor of CYP 2D6
(Safe in pregnancy)
Pancuronium
MOA: competitive antagonist at Nm receptor and antimuscarinic
Longer-acting
Carbamazepine
MOA: blocks inactivated Na+ channel
Effect: prevents propagation of APs
PK: inducer of CYP (induces its own metabolism so tolerance develops)
Use: DOC for trgeminal neuralgia, tx mania in BP disorder
SE: SIADS (at high doses), rashes (including SJS👺), aplastic anemia of WBCs mainly, teratogenicity (neural tube defects and urinary tract defects)
Clomipramine
TCA
Use: tx OCD
Serotonin Syndrome
SSRI SE
ROS: rigidity, hyperthermia, ANS instability, myoclonus (pathognomonic)
Tx: Benzos for sedation, consider Cyproheptadine or Chlorpromazine
Baclofen
MOA: GABA(B) agonist, activates the Gi receptor
Effect:👇🏽 cAMP, activates PKA,👆🏽 K+ conductance
Use: tx spasticity (UMN lesions, MS)
Atomoxetine
MOA: selective NE reuptake inhibitor (NRI)
SE: SI (no abuse potential and no withdrawal)
Dantrolene
MOA: binds to ryanodyne receptor channel RyR1 inhibiting Ca2+ release from SR inside skeletal muscle cell
Use: antidote to malignant hyperthermia (caused by Succinylcholine, or chlorofluorocarbons), and used tp tx neuroleptic malignant syndrome
Amantadine
MOA: antiviral that increases synthesis and release of DA, blocks reuptake of DA, and blocks muscarinic receptors
SE: livedo retidularis (mottling pattern of skin)
Tetrodotoxin
MOA: blocks activated Na+ channel (similar to class 1A) Use: identifies fast Na+ channels in physio *puffer fish toxin
Clozapine (atypical)
MOA: strong D4 and 5-HT2A blockade
SE: agranulocytosis, weight gain, sz (antimuscarinic), hypersalivation (5-HT blockade in mouth)
Nigrostriatal D2 antagonism SE
Causes EPS (= dyskinesias), which decreases compliance
Mivacurium
Shortest duration of action w/ slow onset of action
PK: metabolized by plasma cholinesterase
SE: histamine release (red-man like sx’s)
Local Anesthetics SEs
CNS toxicity: can induce life-threatening sz, to avoid when giving high doses you co-administer IV benzo (Diazepam / Lorazepam)
CV toxicity: vasodilation, bradycardia, CV collapse
Imipramine
TCA
Use: enuresis (but Desmopressin is DOC)
Treatment of Bipolar Disorder during pregnancy
Lamotrigine alternative to Lithium for maintenance, Babapentin and Clonazepam (benzos) safe as anti-panic or acute mania tx during pregnancy (Class D), or Atypical antipsychotics can be used (Class C)
Amitriptyline
TCA
Use: neuropathic pain, migraine
(Safe in pregnancy)
Gabapentin
Use: management of chronic pain
Mirtazapine
NaSSA
MOA: α2 antagonist, blocker of 5-HT(2A), 5-HT(2C), 5-HT(3) and H1
Effect: increased NE synthesis and release, and increased 5-HT release (d/t the α2 antagonism via α1 receptors at raphe nucleus)
Use: anorexia nervous (weight gain via 5-HT(2C) and H1 blockade), anxiolytic
SE: sedation (d/t H1 blockade)
Atypical Antipsychotics
MOA: strong 5-HT2A blockers, and weak D2 antagonists
Effect: improve -ve sx’s, decrease +ve sx’s
Use: first-line therapy for Schizophrenia
SE: few EPS and few hyperprolactinemia sx’s
Opioids used as Anesthetics
Fentanyl / Meperidine / Tapentadol
Tuberoinfundibular D2 antagonism SE
Increased prolactin leads to gynecomastia and menstrual irregularities, increased eating = obesity (long-term use has increased death rates d/t obesity related complications)
Atracurium
Not metabolized, can be spontaneously inactivated via Hofmann degradation resulting in byproduct Laudanosine which causes seizures
Cannabinoid SEs
Hypotension (d/t vasodilation) causing dizziness and then palpitations from reflex tachycardia, conjunctival injection (d/t vasodilation), additive CNS depression (opioids and EtOH), additive CV toxicity (Amphetamines, antimuscarinics, TCAs, antipsychotics), opposes effects of β-blockers (increased risk of ischemic CV dz)
Typical Antipsychotics
MOA: D2 (and D1) antagonists in mesolimbic pathway (antimuscarinic, α1 antagonism, H1 antagonism)
Effect: improve/decrease +ve sx’s, worsen -ve sx’s by causing dysphoria
SE: extrapyrimidal sx’s (EPS), hyperprolactinemia, lower sz threshold (antimuscarinic), orthostatic hypotension (α1 antagonism), weight gain (H1 antagonism)
Quazepam
Long acting sedative benzo that is only Class D (not X)
Etomidate
Use: induction of anesthesia, off-label use in Cushing Syndrome (bc it blocks steroidogenesis)
*not analgesic
Fosphenytoin
Water-soluble prodrug of Phenytoin
Use: can be rapidly infused w/o SEs assoc w/ the highly alkaline IV soln of Phenytoin
Drug-induced Parkinsonism (EPS)
Timeline: weeks
ROS: bradykinesia, rigidity, resting remor
Antidote: antimuscarinics (Benztropine, Diphenhydramine, Amantadine)
Phenobarbital and Primidone
(Barbiturate)
Anticonvulsants
Amphetamine / Methylphenidate / Dexmethylphenidate
MAO: increase fleas of DA, NE and 5-HT from MOBILE POOL and block reuptake of these amines
Use: ADHD, Narcolepsy, obesity, sleep apnea
SE: assoc w/ increased NE (anxiety, palpitations, HTN, hydriasis, loss of appetite), high abuse potential
Risperidone (atypical)
MOA: strong 5-HT2A blockade, some α1 blockade
SE: hypotension (reflex tachycardia)
IV Anesthetics
Midazolam or Dexmedetomidine (α2 agonist) to sedate the pt and Atropine-like drugs to dry up secretions
Vigabagrin
MOA: inhibitor of GABA transaminase
*assoc w/ weight gain
Quetiapine (atypical)
MOA: strong H1 and α1 antagonism (NO antimuscarinic activity)
SE: hypotension (reflex tachycardia), weight gain, sexual dysfunction
Barbiturates
MOA: bind allosteric site on GABA(A) receptor than benzos; GABA-mimetic @ high doses annnd block Complex I of ETC
Effect: increase duration of Cl- ion channel opening —> prolonged hyperpolarization which decreases the # of APs
PK: CYP450 inducers (except Secobarbital)
SE: powerful CNS and respiratory depression, OD can lead to coma and death
