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”)