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neuro drugs Flashcards

1
Q

Glaucoma:
a-agonists:
Epi and Brimonidine (a2)

A

Epi: decrease Aq H synthesis via vasoconstriction

side effects: mydriasis, do not use in closed angle glaucoma

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2
Q

Glaucoma:

Brimonidine (a2 agonist)

A

decreases Aq H synthesis

side effects: blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions and ocular pruitius

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3
Q

Glaucoma:

B-blockers: timolol, betexolol, carteolol

A
  • decrease Aq H synthesis

- side effects no pupillary or vision changes

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4
Q

Glaucoma:

acetozolamide

A

decreases Aq H synthesis via inhibition of CA

-no pupillary or vision change side effects

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5
Q

Glaucoma:

Pilocarpine and carbachol

A
  • direct cholinomimetics
  • incease outflow of aqueous humor via contraction of ciliary muscle and opening of the trabecular meshwork

side effects: mitosis, cyclospasm (contraction of ciliary muscle)

Use pilocarpine in emergencies

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6
Q

Glaucome:

physostigmine and echothiphate

A 
inderect cholinomimetics (AchEI)
-incease outflow of aqueous humor via contraction of ciliary muscle and opening of the trabecular meshwork

side effects: mitosis, cyclospasm (contraction of ciliary muscle)

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7
Q

Glaucoma:

Latonoprost PGF2alpha

A

prostaglandin
-increase outflow of aqeous humor
side effects:
darked color of the iris –> browning

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8
Q

opiods: which one do we use for pain, cough suppression?

A

dextropmethorphan…. although you were prescibed codeine once

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9
Q

opiods: which one do we use for diarrhea?

A

loperamide and diphenoxylate

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10
Q

opiods: which one do we use for maintenance program for heroid addicts?

A

methadone

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11
Q

How do we treat toxicity of opiods?

A

naloxone or naltrexone (opiod receptor antagonists)

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12
Q

name some opiods

A

morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan and diphenoxylate

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13
Q

opiods basics

A

-act an opiod receipts, mu = morphine, delta (enkephalin), kappa = dynophin to modulate synaptic transmission
OPEN K+ channels CLOSE Ca2+ channels –> decrease synaptic transmission
-inhibit the release of ACh, NE, 5-Ht, glutamate, substance P

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14
Q

what are toxicities of opiods?

A
  • addiction
  • respirator depression
  • constipation
  • miosis (pinpoint pupils)
  • additive CNS depression with other drugs
  • tolerance does not develop to miosis and constipiation!
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15
Q

Butophanol

A
  • mu-opiod receptor PARTIAL agonist and kappa-opiod recept agonist
  • produces analgesis

use: severe pain migraine/labor, causes less respiratory depression

tox:
opiod withdrawal symptoms if patient is also taking full opiod agonist (competition opiod receptors). the overdose is not easily reversed with naloxone =(

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16
Q

Tramadol

A

Tram it all!

-very weak opiod agonist, also inhibits sertoning and NE reuptake.

use:
chronic pain
tox: similiar to opiods, decreases seizure threshold, SERETONIN SYNDROME

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17
Q

Which epilepsy drugs work by inactivation Na channels or blocking them?

A 
Phenytoin
Carbamazepine
Valproic acid (has some gaba)
Topiramate (block)
Lamotrigine (voltage gated Na channels)
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18
Q

Which epilepsy drugs work via GABA

A 
Benzodiazepines
Valproic acid (some Na)
Phenobarbitol
Topiramate (some Na)
Levetiracetam
Tiagabine
Vigbatrin
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19
Q

Steven johnson syndrome

A

prodrom of malaise and fever followed by rapid onset of erythematous.purpuric macules (oral, occular, genital). Skin lesions progress to epidermal necrosis and sloughing

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20
Q

Ethosuximide

A

Sux to have silent seizures

  • 1st line abscence seizures
  • blocks thalamic T-type Ca2+ chanels

side effects:
GI, fatigue, headache, urticaria, Steven johnson

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21
Q

Benzodiazepines for seizures

diazepam and lorazapam

A

1st line in acute status elipticus
-increased GABAa action increasing frequency of Cl channel opening
side effects: sedation, tolerance, depedance, respiratory depression

also use for eclampsia seizures (note first line is mgso4)

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22
Q

First line for eclampsia seizures?

A

MgSo4

second: benzooos

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23
Q

Phenytoin

A

work on all seizures but abscence
1st line for tonic clonic
1st line prophylaxis for status elipticus
fosphentoid for parenteral use

increases na channel inactivation, note that it has zero order kinetics~~~

Side effects: nystagmus, diplopia, ataxia, sedation, gingical hyperplasia, hirsutisim, peripheral neuropathy, megloblastic anemia, teratogenesis , SLE like syndrome, lymphadenopathy, steven Johnson syndrome and osteopenia

INDUCES P-450!!

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24
Q

Carbamazepine

A

use for all focal seizures and tonic clonic, it is 1st line for these

-increases Na channel inactivation
side effects: diplopia, ataxia, blood dyscrasias (AGRANULOCYTOSIS APLASTIC ANEMIA), liver toxicity, teratogenesis, SIADH, Steven Johnson syndrome

INDUCES c P-450!!

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25
Q

Valproic acid

A

Treat all seizures except status ellipticus
1st line in tonic clonic (so is carbamazapine)
-can be used for myoclonic seizures (drop)

-increases Na channel inactivation, increases GABA concentraion by inhibiting GABA transaminase

side effecs: GI distrsss, rare but fatal HEPATOTOXICITY (measure lfts), neural tube defects in fetus (spin bifid a), temor, wt gain,

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26
Q

Gabapentin

A

Can use for simple, complex and tonic clonic

  • inhibits high voltage activated Ca channels
  • side effects: sedation, ataxia

used for: peripjeral neuropathy, posttherpetic neuralgia, migraine prophylaxis and bipolar disorder

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27
Q

Phenobarbital

A

can use for simple, complex and tonic clonic
1st line for neonates

-increases GABA action

side effects:
sedation, tolerance, dependance, cardiorespiratory depression

INDUCES P450!

28
Q

which epilepsy drugs indue P450?

A

phenytoin, carbamazepine, phenobarbitol

29
Q

Topiramate

A

simple, complex and tonic clonic
-used for migraine prevention

blocks the Na channels and increased GABAa action

side effects: sedation, mental dulling, Kidney stones, wt loss

30
Q

Lamotrigrine

A

simple, complex, tonic clonic and abscence seizures

blocks volatege-gated Na channels

side effects: must be titrated slowly or…..
STEVEN JOHNSON SYNDROME

31
Q

Levetiracetam

A

simple, complex, tonic clonic

-may modulate GABA and glutamate release

32
Q

Tiagabine and vigabatine

A

simple and complex focal seizures
increase GABA
tiagabine - inhbits GABA reuptake
Vigabatrin - inhbits GABA transaminase

33
Q

Barbituates: phenobarbitol pentobarbitol, thipental, secobarbital

A
  • facilitate GABA action by inscreasing DURATION of Cl channel opening , thus decreasing neuron firing
  • contraindicated in porphyria

clinical: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
tox: resp and cardiovascular depression, CNS depression can be exacerbated with EtOH, dependence, drug interactions due to INDUCTION OF P450
overdose: supportive

34
Q

Benzodiazepines:

diazepam, lorazepam, triazolam, temazepam, oxazepam, midaolam, chlorodiazepoxide, alprazolam

A
  • facilitate GABA action by increasing FREQUENCY of Cl channel opening.
  • decrease REM sleep
  • most have long half lives

triazolam, oxazepam and midazolam are short acting –> higher addictive potential

clinical use: anxiety, spasticity, status elepticus (lorazepam and diazepam), detoxification (especially alcohol withdrwal and delerium tremens), night terros, sleep walking, general anesthetic (amnesia, muscl relaxation), hypnotic (insomnia)

tx: dependence, additive CNS depression effects with eton, less risk of resp depression and coma than barbs

treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)

35
Q

Which benzos are short acting?

A

triazolam, oxazepam and midazolam are short acting –> higher addictive potential

36
Q

What do we use to treat oversode of benzos?

A

Flumazenil a competitive antagoinist at the GABA benzodiazepine receptor

37
Q

Zolpidem (ambien)
Zaleplon, esZoicoline
zzzzzzzz sleepppyyy hypnotics

A

-act via BZ1 subtype of the GABA receptor.
reversed with flumazenil

treat: insomnia

tox: ataxia, headaches, confusion, short duration as they are rapidly metab at liver
- cause only modest day after psychomotor depression and few amnestic effects
- less dependance than benzodiazepines

38
Q

anesthesia general principles

A

CNS drugs must be lipid soluble
increased solubility in lipids = increased potency
Drugs with decreased solubility in the blood= rapid induction and recovery times

example) halothane has high lipid solubility and blood solubility, so it will be more potent and have slow induction
example) N2O decreased blood solubility and lipid solubility so its less potent but a faster induction and recovery time

39
Q

MAC minimal alveolar concentration of inhaled anesthetic

A

MAC required to prevent 50% of subjects from moving in respinse to noxious stimulus (like a skin incision)
potency = 1/MAC

40
Q

malignant hyperthermia caused?

A

rare life threatning hereditary condition caused by inhaled anesthetics (not N2O) and succinylcholine

  • fever
  • muscle contractions

treat: dantrolene (prevents the release of Ca from the SR)

41
Q

Inhaled anesthetics: halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide

A

mechanism: unknown ahahah
Effects:myocardial depression, resp depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)

tox:
halothane - hepatoxicity
Methoxyflurane - nephrotoxicity
enflurane - proconvulsant
N2O - expansion of trapped gas in body cavity

can cause malignant hyperthermia (not N2O)

42
Q

name some intravenous anesthetics?

A

barbituates (thiopental), benzodiazepines (midazolam), arylcyclohexylamines (ketamine), opiods (morphine and fentanyl), propofol

43
Q

Thiopental

A

-barbituate
-high potency, high lipid solubility, rapid entry into brain
-used for induction of anesthesia and short surgical procedures
-effect is terminated by rapid redistribution into tissue and fat.
decreased cerebral blood flow

44
Q

Midazolam

A

-benzo
-most common drug used for endoscopy
-used adjectively with gases anesthetics and narcotics
0may cause severe postoperative resp depression
-decreased BP
-antergrade amnesia
treat overdose as per usual with friendly flumazenil

45
Q

Arylcyclohexylamines (ketamine)

A

PCP analogue that acts as dissociative anesthetic

  • block NMDA receptors
  • cadiovascular stimulant
  • cause disorientation, hallucination and bad dreams
  • increases cerebral blood flow
46
Q

morphine and fentanyl

A

are used with other CNS depressants during general anesthesia

47
Q

propofol

A

used for sedation in ICU
rapid anethesia induction, short procedures
less postoperative nausea than thiopental
potentiates GABA

48
Q

Name some local anesthetics

A

Esters: procaine, cocaine, tetracaine
amides: lidocaine, mepivacaine, bupivacaine (note the two I’s)

49
Q

Local anesthetics:Esters: procaine, cocaine, tetracaine

amides: lidocaine, mepivacaine, bupivacaine (note the two I’s)

A
  • block Na channels by binding to specific receptors on inner potion of channel. preferentially bind to ACTIVATED na channels, so most effective in RAPIDLY firing neurons.
  • tertiary amine anesthetics penetrate membrane in UNCHARGED form then bind to ion channels in CHARGED form.
  • can be given with epi to enhance local acton via vasoconstriction (decrease bleeding and increased anesthesia by decreasing systemic concentration
  • in infected tissues (acidid) the alkaline anesthetics are charged and cannot penetrate membrane effectively –> need more anesthetic (Nh3 to NH4+)

treat: minor surgical procedures, spinal anesthesia, if allergic to esters give the amides
tox: CNS excitation, severe cardiovascular tox (bupivacaine_, HTN, hypotension and arryhthmias (cocaine)

50
Q

what is the order of nerve block by local anesthetics?

A

small diameter fibers > large diameter

myelinated fibers> unmyelinated fibers

but size factor predominates

so small myelinated fibers> small unmyelinated fibers> large myelinated fibers? large unmyelinated fibers

51
Q

What is the order of sensation loss by local anesthetics?

A
  1. pain
    2, temp
  2. touch
  3. pressure
52
Q

Neuromuscular blocking drugs:

Depolarizing Succinylcholine

A

-strong Ach receptor agonist such that it produces sustained depolarization and prevents muscle contraction so it cause the depolarization as it is an agonist but is so strong it gets stuck

Phase 1: prolongue depolarization, the block potentiated by cholinesterase inhibitors no antidote
phase 2: eventually some receptors become desensitized, some Ach receptors become available. So repolarized but still blocked. Antidote - cholinesterase inhibitors –> increase Ach

Complications:

  • hypercalcemia
  • hyperkalemia (recall not only Na is release on binding to nicotinic receptor but also K)
  • malignant hyperthermia (fever and severe muscle contractions)
53
Q

Neuromuscular blocking drugs:
Nondepolarizing:
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

A

-competitive antagonists of Ach receptors, prevent depolarization but prevents Ach from binding

reverse the blockade:
ACEI neostygmine but give atropine too to prevent muscarinic effects such as bradycardia you could also use edrophonium

54
Q

atropine

A

competitive antagonist of muscarinc Ach receptors

55
Q

Dantrolene

A

treat malignant hyperthermia and neuroleptic malignant syndrome (toxicity of antipsychotic drugs)
- prevents Ca release from the SR in skeletal muscle

56
Q

Parkinson disease drugs

BALSA

A 
BALSA
Bromocriptine
Amantadine
Levodopa with cabidopa
Selegiline with compt inhibitors
Antimuscarinics
57
Q

For essential of familiar tremors use:

A

b-blocker propranolol

58
Q

Bromocriptine

A

DA agonist

59
Q

Amantidine

A

may increase DA release

-also used as an antiviral against Influenza A and rubella; toxicity = ataxia

60
Q

Levodopa and carbidopa

A

converted to DA in CNS by dopa decarboxylase
cabidopa is a peripheral decarboxylase inhibitor, so that increased bioavailbiltiy of L-dopa to the brain and limit the peripheral effects

tox: arrhythmias from peripheral formation of catecholamines. Long term use can lead to dyskinesia following administration “on off phenomena”, akinesia between doses.

61
Q

Selegiline

A

selective MAO type B inhibitor (MAO B is DA over 5HT and NE) thus increases its availability

may enhance adverse effects of Ldopa

62
Q

entacapone, tolcapone

A

COMT inhibitors, they prevent L-dopa degradation

63
Q

Benzotropine

A

antimuscarinic, improves the tremor and rigidity in Parkinson disease but has little effect on bradykinesia

64
Q

Memantine

A

Alzheimers drugs
NMDA receptor antagonist, helps prevent excitotxicity (mediated by Ca)
dizzy, confusion side effects

65
Q

AChE inhibitors: donepezilm galantamine and rivastigmine

A

alzheimers

side effects nausea dizzyness insomnia

66
Q

Huntington drugs:

A

Recall in huntington decreased GABA, ACh but increased dopamine

treat:
tetrabenazine and reserpine - inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.

Haloperidol: DA receptor antagonist

67
Q

Sumitriptan

A

5-HT1b/1d agonist
-inhibits trigeminal nerve activation, prevents vasoactive peptide release VIP, induces vasoconstriction, half life is < 2hours

clinical: acute migraine, cluster headache attacks
tox: coronary vasospasm contraindicated in patients with CAD anor prinzmetal angian, mild tingling

organ systems (25 decks)

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