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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
Valproic acid
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,
26
Gabapentin
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
27
Phenobarbital
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
which epilepsy drugs indue P450?
phenytoin, carbamazepine, phenobarbitol
29
Topiramate
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
Lamotrigrine
simple, complex, tonic clonic and abscence seizures blocks volatege-gated Na channels side effects: must be titrated slowly or..... STEVEN JOHNSON SYNDROME
31
Levetiracetam
simple, complex, tonic clonic | -may modulate GABA and glutamate release
32
Tiagabine and vigabatine
simple and complex focal seizures increase GABA tiagabine - inhbits GABA reuptake Vigabatrin - inhbits GABA transaminase
33
Barbituates: phenobarbitol pentobarbitol, thipental, secobarbital
- 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
Benzodiazepines: | diazepam, lorazepam, triazolam, temazepam, oxazepam, midaolam, chlorodiazepoxide, alprazolam
- 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
Which benzos are short acting?
triazolam, oxazepam and midazolam are short acting --> higher addictive potential
36
What do we use to treat oversode of benzos?
Flumazenil a competitive antagoinist at the GABA benzodiazepine receptor
37
Zolpidem (ambien) Zaleplon, esZoicoline zzzzzzzz sleepppyyy hypnotics
-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
anesthesia general principles
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
MAC minimal alveolar concentration of inhaled anesthetic
MAC required to prevent 50% of subjects from moving in respinse to noxious stimulus (like a skin incision) potency = 1/MAC
40
malignant hyperthermia caused?
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
Inhaled anesthetics: halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
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
name some intravenous anesthetics?
barbituates (thiopental), benzodiazepines (midazolam), arylcyclohexylamines (ketamine), opiods (morphine and fentanyl), propofol
43
Thiopental
-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
Midazolam
-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
Arylcyclohexylamines (ketamine)
PCP analogue that acts as dissociative anesthetic - block NMDA receptors - cadiovascular stimulant - cause disorientation, hallucination and bad dreams - increases cerebral blood flow
46
morphine and fentanyl
are used with other CNS depressants during general anesthesia
47
propofol
used for sedation in ICU rapid anethesia induction, short procedures less postoperative nausea than thiopental potentiates GABA
48
Name some local anesthetics
Esters: procaine, cocaine, tetracaine amides: lidocaine, mepivacaine, bupivacaine (note the two I's)
49
Local anesthetics:Esters: procaine, cocaine, tetracaine | amides: lidocaine, mepivacaine, bupivacaine (note the two I's)
- 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
what is the order of nerve block by local anesthetics?
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
What is the order of sensation loss by local anesthetics?
1. pain 2, temp 3. touch 4. pressure
52
Neuromuscular blocking drugs: | Depolarizing Succinylcholine
-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
Neuromuscular blocking drugs: Nondepolarizing: Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
-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
atropine
competitive antagonist of muscarinc Ach receptors
55
Dantrolene
treat malignant hyperthermia and neuroleptic malignant syndrome (toxicity of antipsychotic drugs) - prevents Ca release from the SR in skeletal muscle
56
Parkinson disease drugs | BALSA
``` BALSA Bromocriptine Amantadine Levodopa with cabidopa Selegiline with compt inhibitors Antimuscarinics ```
57
For essential of familiar tremors use:
b-blocker propranolol
58
Bromocriptine
DA agonist
59
Amantidine
may increase DA release | -also used as an antiviral against Influenza A and rubella; toxicity = ataxia
60
Levodopa and carbidopa
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
Selegiline
selective MAO type B inhibitor (MAO B is DA over 5HT and NE) thus increases its availability may enhance adverse effects of Ldopa
62
entacapone, tolcapone
COMT inhibitors, they prevent L-dopa degradation
63
Benzotropine
antimuscarinic, improves the tremor and rigidity in Parkinson disease but has little effect on bradykinesia
64
Memantine
Alzheimers drugs NMDA receptor antagonist, helps prevent excitotxicity (mediated by Ca) dizzy, confusion side effects
65
AChE inhibitors: donepezilm galantamine and rivastigmine
alzheimers | side effects nausea dizzyness insomnia
66
Huntington drugs:
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
Sumitriptan
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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