Neurology - Pharmacology

avicinid's version from 2015-08-02 16:29

Glaucoma drugs

Question Answer
epinephrine and brimonidine arealpha agonists (brimonidine is alpha-2)
MoA of epinephrine and brimonidinedecrease aqueous humor synthesis (epinephrine via vasoconstriction. Do not use in closed-angle)
side effect of epinephrinemydriasis -- closed angle glaucoma in CHF pt tx in hospital: sudden painful vision loss
epinephrine contraindicated inclosed-angle glaucoma. other side efx blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus
side efx of brimonidineblurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus
timolol, betaxolol and carteolol arebeta blockers. they decrease humor synthesis
MoA in glaucomadecrease aqueous humor synthesis
MoA action in glaucomadecrease aqueous humor synthesis via inhibition of carbonic anhydrase
direct cholinomimeticspilocarpine, carbachol
indirect cholinomimeticsphysostigmine, echothiophate
clinical use of pilocarpinepilocarpine (very effective at opening meshwork into canal of Schlemm)
side efx of cholinomimeticsmiosis and cyclospasm (contraction of ciliary muscle)
latanoprost is aprostaglandin (PGF2alpha)
latanoprost mechanism in glaucomaincrease outflow of aqueous humor
side effects of latanoprostdarkens color of iris (browning)
acute angle closure glaucomaacetazolamide

Opiod analgesics

Question Answer
opioid analgesicsmorphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan, diphenoxylate
mu =morphine
delta =enkephalin
kappa =dynorphin
MOA of opioid analgesicsopen K channels, close Ca channels, decreasing synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate and substance P. Potassium efflux increases hyperpolarization of post-synaptic neurons blocking pain transmission
opioids inhibit release ofACh, NE, 5-HT, glutamate, substance P
dextromethorphancough suppression
loperamide and diphenoxylatediarrhea
use of methadone and buprenorphine + naloxonemaintenance programs for heroin addicts
tox of opioidsaddiction, respiratory depression, constipation, miosis, additive CNS depression with other drugs
opioid withdrawal symptomsrestlessness, agitation, pupillary dilation, tachycardia, diarrhea
acute detoxmethadone, clonidine
long term detoxmethadone, buprenorphine w/ naloxone, natrexone
no tolerance tomiosis and constipation
opioid tox treated withnaloxone or naltrexone (opioid receptor antagonists)
butorphanol mechanismmu-opioid partial agonist and kappa-opioid agonist
butorphanol advantage over full opioid agonistsless respiratory depression
use of butorphanolsevere pain (migraine, labor)
problem with butorphanol overdosenot easily reversed by naloxone
tox of butorphanolcan cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for receptor)
tramadol moavery weak opioid agonist; also inhibits serotonin and NE reuptake
use of tramadolchronic pain
tox of tramadolsimilar to opioids, decreases seizure threshold. serotonin syndrome
serotonin syndromeoccurs when SSRI given in conjunction w/other serotonergic agents
sympt of serotonin syndrome1) NM excitation 2) autonomic stimulation 3) altered mental status
Opoids cause biliary colic howcontraction of smooth muscle in pshincter of Oddi
medications decrease tolerance to morphineNMDA receptor blockers, like ketamine, block actions of glutamate (excitatory neurotransmitter)


Question Answer
myoclonicquick repetitive jerks
tonic-clinicgrand mal
atonicdrop seizures
status epilepticuscontinuous or recurring seizu
generalized seizuresconsciousness is lost
simple partialconsciousness not impaired
complex partialconsciousness impaired

Epilepsy Drugs

Question Answer
phenytoin is first line fortonic-clonic seizures and status epilepticus prophylaxis
phenytoin also works forsimple and complex seizures
phenytoin mechanismincreases sodium channel inactivation
Important SE of PhenytoinGingival hyperplasia, hirsutism, P-450 inducer, fetal hydantoin syndrome and SJS
carbamazepine is 1st line fortrigeminal neuralgia
carbamazepine MOAincrease sodium channel inactivation
carbamazepine is also 1st line fortrigeminal neuralgia
carbamazepine A/Eaplastic anemia, SIADH, SJS, inducer CYP450
lamotrigine works onsimple, complex and tonic clonic seizures
lamotrigine mechanismblocks voltage-gated sodium channels
gabapentin works onsimple, complex and tonic-clonic seizures
gabapentin mechdesigned as GABA analog, but inhibits high-voltage-activated Ca channels
gabapentin is also used forperipheral neuropathy, post-herpetic neuralgia, migraine prophylaxis, bipolar disorder
topiramate works onsimple, complex and tonic-clonic seizures
topiramate mechblocks Na channels, increases GABA action
topiramate is also used formigraine prevention
phenobarbital works onsimple, complex and tonic-clonic seizures
phenobarbital mechincreases GABAa action
phenobarbital is 1st line in these patientsneonates
valproic acid is 1st line intonic-clonic
valproic acid also works insimple, complex, myoclonic and absence seizures
valproic acid mechincreases Na channel inactivation, increases GABA concentration
valproic acid a/eNT defects, alopecia, pancreatitis
ethosuximide is 1st line forabsence seizures
ethosuximide mechblocks thalamic T-type Ca channels
benzodiazepines are first line foracute status epilepticus
benzodiazepine mechincrease GABAa action
benzodiazepines also used forseizures of eclampsia (1st line is MgSO4)
tiagabine works forsimple, complex
tiagabine mechinhibits GABA reuptake
vigabatrin mechirreversibly inhibits GABA transaminase, increasing GABA
Fever, generalized lymphadenopathy, facial edema, diffuse skin rash, eosinophilla and internal organ dysfunctionDress syndrome happens 2-8 weeks after exposure to high risk drugs such as anticonvulsants
Drug given if patient has both absence seizures and tonic clonic seizuresvalproate
status epilepticus1) IV lorazepam 2)phenytoin 3)pheno 4) intubate and give general anesthesia

Barbs and Benzos

Mnemonic for MOA of BARBS and BENZOS: Barb likes it longer, Ben likes it more often.
Question Answer
barbiturate used for induction of anesthesiathiopental
supportive treatment of barbiturate overdoseassist respiration and maintain BP
barbiturates have drug interactions fromP-450 induction
potentially fatal toxicity of barbituratesrespiratory and cardiovascular depression
barbiturate CNS depression can be exacerbated byalcohol use
treatment for Barb toxicitysupportive
benzodiazepine mechfacilitate GABAa opening by increasing frequency of Cl-channel opening.
benzodiazepine metabolites areactive
short acting benzodiazepines (with higher addictive potential)triazolam, oxazepam, midazolam
benzodiazepams used for status epilepticuslorazepam and diazepam
benzodiazepam function as general anestheticamnesia, muscle relaxation
clinical uses of benzosanxiety, spasticity, alcohol withdrawal, night terrors, sleepwalking, anxiety
treat benzo overdose withflumazenil (competitive antagonist at GABA benzodiazepine receptor)
less risk of this with benzos than barbituratesrespiratory depression and coma
some non-benzo hypnoticsZolpidem (Ambien), saleplon, eszopiclone
non-benzo hypnotics act byBZ1 subtype of GABA receptor
effects of non-benzo hypnotics reversed byflumazenil
clinical use of non-benzo hypnotics (Z drugs)insomnia and short half life

Inhaled Anesthetics

Question Answer
in anesthetics, drugs with low solubility in blood haverapid induction and recovery times
in anesthetics, drugs with high lipid solubility haveincreased potency = 1/MAC. These drugs are easier to get into the CNS
MAC varies withage and is additive
increased MACdecreased potency
a small blood/gas ratiorapid onset of anesthesia and more rapid recovery
anesthetic with fast induction and low potencyN2O. Fast induction because it has low solubility in blood (small blood/gas ratio). Less potent because decreased solubility in fat (high MAC)
anesthetic with slow induction and high potencyhalothane. Slow induction because it has an increased solubility in blood. High potency because it has a increased solubility in lipids (low MAC).
some inhaled anestheticshalothane, enflurane, isoflurane, sevoflurane, methoxyflurane, Nitrous Oxide
mechanism of inhaled anestheticsunknown
effects of inhaled anestheticsmyocardial depression, respiratory depression, nausea/emisis, increased cerebral blood flow and decreased cerebral metabolic demand
toxicity of halothanehepatotoxicity. can lead to fulminant hepatitis
toxicity of methoxyfluranenephrotoxicity
toxicity of enfluraneproconvulsant
rare toxicity of all but NO, with inherited susceptibilitymalignant hyperthermia
toxicity of nitrous oxideexpansion of trapped gas in body cavity
Affect of inhalational anesthetics on cardiovascularmyocardial depression leading to a decrease in CO
Affect of inhalational anesthetics on respiratory systemall except NO cause respiratory depression
Which two inhalational anesthetics are preferred in asthma patientshalothane and sevoflurane have bronchodilation properties
Affect of inhalation anesthetics on the kidneysdecreased GFR, decreased RPF, increased vascular resistance
Affect of inhalational anesthetics on the brainincreased ICP and cerebral blood flow
Affect of inhalational anesthetics on the liverdecreased hepatic blood flow

IV anesthetics

Question Answer
thiopental (barbituate) used forinduction of anesthesia and short surgical procedures
midazolam commonly used forendoscopy with gaseous anesthetics and narcotics
midazolam may causes severe postoperativerespiratory depression, decreased BP, amnesia
ketamine actiondissociative anesthetics block NMDA receptors
thiopental action on cerebral blood flowdecrease
ketamine action on cerebral blood flowincrease
ketamine toxicitiesdisorientation, hallucination, bad dreams
opioids used during general anesthesiamorphine, fentanyl
mechanism of propofolPotentiates GABAa
propofolless postoperative nausea
propofol clinical usesedation in ICU, rapid anesthesia induction, short procedures

Local anesthetics

Question Answer
ester local anestheticsprocaine, cocaine, tetracaine
naming trick of amide local anesthetics2 Is in the name (lidocaine, mepivacaine)
mechanism of local anestheticsblock Na channels by binding to receptors on inner portion of channel
local anesthetics preferentially bind toactivated Na channels, so most effective on rapidly firing neurons
3° amine local anesthetics penetrate membrane inuncharged form, then bind channels as charged form
usual vasoconstrictor given with local anestheticsepinephrine, enhances local action
need more anesthetic in infected tissue becausetissue is acidic, and anesthetics are alkaline; charged, cannot penetrate membrane
order of loss in local anestheticspain, temp, touch, pressure
toxicity of local anestheticsCNS excitation, hypertenson, hypotension
toxicity of cocainearrhythmias
toxicity of bupivacainesevere cardiovascular toxicity
order of nerve blockade by local anestheticssmall myelinated, small unmyelinated, large myelinated, large unmyelinated

NMJ blocking drugs

Question Answer
succinylcholine (depolarizing actionstrong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction
reversal of succinylcholine phase I (prolonged depolarization)no antidote; cholinesterase inhibitors potentiate block
reversal of succinylcholine phase IIcholinesterase inhibitors (neostigmine)
complications of succinylcholine usehypercalcemia, hyperkalemia, malignant hyperthermia
some nondepolarizing NMJ blockerstubocurarine, atracurium, etc
MOA nondepolarizing NMJ blockerscompete with ACh for receptors
reversal of nondepolarizing NMJ blockerscholinesterase inhibitors such as neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia)
moa dantroleneprevents CA release from sarcoplasmic reticulum of skeletal muscle. Inhibits opening of the ryanodine receptor.
dantrolene treatsmalignant hyperthermia, neuroleptic malignant syndrome (toxicity of antipsychotics)
MOA baclofeninhibits GABAb receptors at spinal cord inducing skeletal muscle relaxation.
Clinical use of baclofenmuscle spasms
MOA cyclobenzaprinecentrally acting skeletal muscle relaxant.
clinical use cyclobenzaprinemuscle spasms

Parkinson's Drugs

Question Answer
preferred dopamine agonists in parkinson'snon-ergots (pramipexole, ropinirole)
bromocriptineergot dopamine agonist
amantadineincreases dopamine (decreasing reuptake)
amantadine aeataxia
non-parkinson use amantadineantiviral against influenza A
L-dopa/carbidopa converted todopamine in CNS
entacapone, tolcapone COMT inhibitors; prevent L-dopa degradation. enta inhibits peripheral methylation of l-dopa. Tolca inhibits peripheral & central
benztropine actionantimuscarinic. atropine effects
benztropine benefitsimproves tremor and rigidity, but little effect on bradykinesia
reason L-dopa is givencan cross BBB, converted to dopamine in CNS by dopa decarboxylase
reason carbidopa is given with L-dopainhibits peripheral decarboxylase
tox L-dopaarrhythmias from increased peripheral formation of catecholamines
long-term use of L-dopadyskinesia following administration, akinesia between doses
Selegiline mechanismselectively inhibits MAO-B (CNS), which preferentially metabolizes dopamine over NE and 5-HT, increasing availability of dopamine. prevents formation MPP
clinical use selegilineadjunctive agents to L-dopa in treatment of parkinson's
tox selegilinemay enhance adverse effects of L-dopa
restless legropinirol
benign essential tremorbeta blocker

Alzheimer's Drugs goal to inhibit breakdown of acetylcholine

Question Answer
memantine mechanismNMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca)
memantine toxicitydizziness, confusion, hallucinations
donepezil, galantamine, rivastigmine mechacetylcholinesterase inhibitors
donepezil, galantamine, rivastigmne toxicitynausea, dizziness, insomnia

Huntington's disease drugs

Question Answer
huntington's neurotransmitter changesdecreased GABA, decreased ACh, increased dopamine
tetrabenazine and reserpine mechinhibit VMAT; limit dopamine vesicle packaging and release
haloperidol mechdopamine receptor antagonist


Question Answer
sumatriptan mechanism5-HT1b/1d agonist
sumatriptan inhibitstrigeminal nerve actiation, prevents vasoactive peptide release, induces vasoconstriction
half life sumatriptan< 2 hours
clinical use of sumatriptanacute migraine, cluster headache attacks
toxicities of sumatriptancoronary vasospasm, mild tingling
sumatriptan contraindicated inCAD and prinzmetal's
treatment ALSriluzole