Neuro drug cards

Question 1

Phenytoin

Answer 1

MOA: Use dependent blocade of Na channel, inhibtion of glutamate release from excitatory presynpatic neuron

Clinical use: tonic clonic seizures, also class IB antiarrhythmic

Toxicity: nystagmus, ataxia, diplopia, sedation, SLE, induction of p450, chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia, (reduce folate abs) teratogenic

Question 2

Barbiturates

Answer 2

Phenobarbital, pentobarbital, thiopental, secobarbital

MOA: facilitates GABAa by increasing duration of Cl- channel opening, thus decreasing neuron firing,
contraindicated in porphyria

Clinical use: sedative for anxiety, seizure, insomina, induction of anesthesia (thiopental)

Toxicity:respiratory/cardiac depression (can be fatal), CNS depressin (worsened by EtOH), dependent, drug interaction (p450).

Overdose treatment is supportive

Question 3

Benzo

Answer 3

MOA: facilitates GABAa action by increasing frequency of Cl- channel opening. Decreases REM sleep, most have long half lives and active metabolites.
*exceptions: triazolam, exazepam, midazolam are short

Clinical use: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detox (DT), night terrors, sleepwalking, general anesthesia (amnesia, muscle relaxation), hypnotic (insomnia)

Toxicity: dependence, additive CNS depression effect, less risk of respiratory depression and coma than with barbituates.

Treat overdose with flumazenil (competitive antagonists at GABA benzo receptor)

Question 4

Nonbenzo hypnotics

Answer 4

Zolpidem (Ambien), zaleplon, eszopiclone

MOA: act via the BZ1 subtype of GABA receptor, effects reverse by flumazenil

Clinical use: insomnia

Toxicity: ataxia, HA, confusion, short duration because of rapid metabolism by liver enzymes. Unlike over sedative-hypnotics, cause only modest day after psychomotor depression and few amnestic effects

Lower dependence risk than benzo

Question 5

Anesthetic general principel

Answer 5

1) CNS drug must be lipid soluble or be actively transported
2) low solubility in blood = rapid induction and recovery time
3) high solubility in lipid = high potency =1/MAC

MAC: minimal alveolar concentration at which 50% of the population is anesthetized, varies with age

Example: N2O has alow blood and lipid solubilit, so fast induction and low potency. Halothane has high lipid and blood solubility, and thus high potency and slow induction.

Question 6

Inhaled anesthetic

Answer 6

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, NO

MOA: unknown
Effects: myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decrease cerebral metabolic demand)

Toxicity: hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), maligant hyperthermia (all but NO), expansion of trapped gas in a body cavity (NO)

Question 7

IV anesthetics:

Answer 7

Barbituate
Benzo
Arylcyclohexylamines (ketamine)
Opioid
Propofol

“BB King on opioid PROPOses FOOLishly”

Question 8

IV anesthetics: barbiturates

Answer 8

Thiopental: high potency, high lipid solubility, rapid entry into brain, used for induction of anesthesia and short surgical procedures.

Effect terminated by rapid redistribution into tissue (skeletal) and fat.

Decreases blood flow (bc CNS sedation)

Question 9

IV anesthetics: benzo

Answer 9

Midazolam most common durg used for endoscopy; used adjunctively with gaseous anesthetics and narcotics
May cause severe post op respiratory depression, reduce BP (treat overdose with flumazenil) and amnesia

Question 10

IV anesthetics: arylcyclohexylamine (ketamine)

Answer 10

PCP analog that acts as dissociative anesthetics
Blcoks NMDA receptor
CV stimulant
Causes disorientation, hallucination, and bad dreams
Increases cerebral blood flow (bc CNS stimulation. vs. barbiturate)

Question 11

IV anesthetics: opioid

Answer 11

Morphine, fetanyl used with other CNS depressants during general anesthesia.

Question 12

IV anesthetics: propofol

Answer 12

Used for sedation in ICU, rapid anesthesia and induction, and short procedures.

Less post op nausea than thiopental.
Potentiates GABAa

Question 13

Local anesthetics: mechanism

Answer 13

Amy has 2 I’s, ester has only one 1

MOA: blocks Na channel by binding to specific receptors on inner portion of channel. Preferentially binds to activated Na+ channels, so most effective in rapidly firing neurons. 3’ amine penetrate membrane in uncharged form, then bind to ion channels as charged form.

Question 14

Local anesthetics: principle

Answer 14

Given with vasoconstrictors (epi) to enhance local action; decrease bleeding, increase anesthesia by reducing systemic concentraiton.

In infected tissue (acidic), alkaline anesthetics are charged and cannot penetrate effectively, so need more

Order of nerve blocks: small-diameter > large fiber
Myelinated > unmyelinated, but size factor predominates.
small myelinated > small unmyelinated > large myelinated > large unmyelinated.

Order of loss: pain, temp, touch, pressure

Question 15

Local anesthetics: use and toxicity

Answer 15

Use: minor procedure, spinal anesthesia, if allergic to ester, give amide

Toxicity: CNS excitation, severe CV toxicity (bupivacaine), HTN, hypotension, and arrhythmias (cocaine)

Question 16

NM blocking drugs

Answer 16

Used for muscle paralysis in surgery or mechanical ventrilation
Selective for motor (vs. autonomic) nicotinic receptor

Question 17

NM blocking: depolarizing

Answer 17

Succinylcholine: ACh receptor agonist; produces sustained depolarizing and prevents muscle contraction

Reversal of blockage:
Phase 1 (prolonged depolarization): no antidote, blcok potentiated by cholinesterase inhibitor
Phase II (repolarized but blocked): ACh receptors are available but not desensitized--antidote consists of cholineserase inhibitor

Complications: hypercalcemia, hyperkalemia, malignant hyperthermia

Question 18

NM blocking: nondepolarizing

Answer 18

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium.

Competitive antagonist: competes with ACh for receptor

Reversal of blockade: neostigmine, edrophonium and other cholinesterase inhibitor

Question 19

Dantrolene

Answer 19

MOA: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

Clinical use: treatment of malignant hyperthermia
Also used to treat neuroleptic malignant syndrome (toxiticity of antipsychotic drug)