Neuro Drugs 2 Flashcards

1
Q

Acetazolamide

A
  • Inhibits CA used to treat open angle and closed angle glaucoma
  • Decreaes HCO3 and decreases humor production
  • Causes metabolic acidosis and alkalinization of urine
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2
Q

Epinephrine

A
  • Constriction via alpha 2 leading to decreased humor production
  • S/E is myadriasis, blurry vision, optic pruritis, can precipitate closed angle glaucoma
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3
Q

Brimonidine

A
  • Alpha 2 agonist leads to decrease B2 activation and decreased humor production
  • Causes
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4
Q

Litanaprosct

A

-PGF2a agonist causes opening of canals and increased flow

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5
Q

Pilocarpine, carbachol, physostigmine, ecothiophate

A
  • Cholinergic agonists cause contriction of pupillary and opening of angle
  • DOC in closed angle glaucoma
  • Cholinergic S/E, miosis, cyclospasm (Ciliary muscle paralysis)
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6
Q

Timlol

A
  • Beta antagonist leads to decreased humor production

- No effect on vision

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7
Q

Opiod

A
  • Mu is morphine, kappa is enkephalin, dela is dynoprhin
  • All work to open Cl and decrease Ca and NT release in pain neurons (inhibiitory interneurons)
  • Leads to decreasd Pain
  • Can also be used to treat diahrrea (Loperamide, diphenoxylate) Cought (Dextromethophan), acute pulmonary edema
  • Methadone has a longer half life and can be used to decrease addiction, Naloxone combined with buprenoprhine can do the same thing
  • S/E: respn depression, constipation, miosis
  • Overdose treat with naloxone (competetive antagonist of mu R)
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8
Q

Butorphanol

A
  • Partial mu agonist and kappa agonist used to treat chornic pain with fewer S/E
  • Partial agonist activities can precipitate withdrawl
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9
Q

Tramadol

A
  • Partial mu agnost and also seretonoin and other effects
  • Used in chronic pain to cause fewer S/E
  • Lower siexure threshold is major S/E
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10
Q

Partial Siezures

A
  • First line is carbemezapine

- Also phenytoin, valproate, new drugs, all but bezos and ethosuximide

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11
Q

Complex

A
  • First line is phenytoin, carbemezapine, valproate

- Other new drugs can be used (lamotragine, topiramate, gabapentin, etc)

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12
Q

Absence

A

Ethosuximide first and Valproate second (T type Ca)

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13
Q

Status Epilepticus

A

Benzos are given for aute phase also IV phenytoin

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14
Q

Phenytoin

A
  • Use dependent Na channel block, also inhibits glutamate release
  • Use in simple and complex siezures and also for status
  • S/E: Gingival Hyperplasia, Fetal hydantoin (neural tube defects, heart defects, cleft lip, microcephaly), Hirsuitism, Megaloblastic Anemia (folate), SLE like syndrome, ataxia, diplopia
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15
Q

Carbemezapine

A
  • Similiar to phenytoin, Except add agranulocytosis and aplastic anemia to list
  • DOC for partial siezures, SIADH
  • All epileptic drugs could cause stevens johsnons (Fatigue and fever followed by mucosal desquamating rash and epidermal necrolysis at Epi/dermal junction)
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16
Q

Valproate

A
  • Multiple, Na, increase GABA, T type Ca
  • Second line for absence, second line for partial, first line for diffuse
  • Causes neural tube defects, fatal hepatotoxicity, weight gain
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17
Q

Ethosuximide

A
  • DOC for absence siezures, blocks T type Ca channels

- Stevens Johsnons and GI, uticaria

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18
Q

Phenobarbtol

A
  • DOC for pregnancy and children, protein binding limits transplacental transfer
  • Causes GABA duration increase leading to potentiation
  • S/E: Resp depression, P450 inducer
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19
Q

Lamotrigne

A

Na channel blocker

-Second line for complex and partial, minimal S/E

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20
Q

Gabapentin

A

V gated Ca channels

Can be used in siezures, but often used in peripheral neural pain syndromes

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21
Q

Topirimate

A
  • Increase GABA and decrease Na
  • Second line siezure and prophylaxis for migranes
  • S/E: kidney stones and weight loss
22
Q

Tiagabine, Vigaartin

A
  • Tiagabine blocks GABA uptake, second line for partial

- Vigabatrin blocks GABA deamination, second line for partial

23
Q

Levitracetam

A

-Unkown mechanism , scond line for parital and diffuse

24
Q

Barbs

A

-Bind to GABAa receptor and increase duration of opening leading to increased Cl Flux
-Leads to depression of neural signals
-Siezures (phenobarbitol), anesthesiaamnesia (Thiopental, decreased T1/2)
S/E: Respiratory depresion, inducers of P450s
-Contraindicated in porphyria

25
Q

Benzos

A
  • GABAa inreased frequency of opening, decreased S/E, reversed by flumezanil
  • Used as amnestic, anxiolytic. Anterograde amnesia
  • Used in status, DT, secondary to MgSO4 for ecplamptic siezures
  • S/E: Resp depression in the context of alcohol
  • Long is Diazepam (Metabolized to active)
  • Med (Lorazepam)
  • Short (Triazolam)
  • US (Midazolam)
  • Often used in anesthesia protocol
26
Q

Z Drugs

A
  • Milder side effects because of shorter half life and not metabolized to active products when compared to benzos.
  • Used as sleep aid
27
Q

Inhaled Anesthetics

A
  • Speed of induction is inversely proportional to blood solubility. N2O is minimally bloo soluble leads to rapid iduction while halothane is highly lipid soluble and leads to slow induction.
  • MAC minimum Concentration to anesthetize 50% of population. Inversely correlated to potency. High potency halothane has low MAC while low potency N2O has high MAC
  • Increase Cerebral Blood flow but decrease demand
28
Q

N2O

A

Rapid induction, not blood soluble. Need high MAC

-Can cause gas expansion and spontaneous abortions

29
Q

Halothane

A
  • Potent, low MAC but slow indcution

- Can cause hepatic necrosis days after surgery

30
Q

Other S/e

A

Methoxyflurane is nephrotoxic

  • Enflurane is proconvulsant
  • All can cause malignant hyperthermia excpet N20 due to genetic mutation in RyR
31
Q

Barbituates

A
  • Thiopental, IV
  • Highly lipid soluble, rapid induction, but also rapidly redistributes to fat leading to rapid stop of function
  • Decrease Cerebral Blood Flow
32
Q

Benzos

A
  • Most common is midazolam which is ultra short acting, combined with oiods and inhaled
  • Anterograde amnesia
  • Post surgical decrease in Resp/BP, tx with flumezanil
33
Q

ketamine (Arylcyclohylamines)

A
  • NMDA receptor antagoinst
  • Leads to dissociative amnesia, hallucinations, bad dreams
  • Commonly used for short procedures in kids like bone setting
  • Increase Cerebral Blood flow, don’t use in trauma
34
Q

Propofol

A
  • GABAa potentiator

- Rapid induction and rapid recvery with minimal post surgical N/V

35
Q

Local Anestetics

A
  • Esthers: CocaIne, (Slow acetylators, increase hypersensitivity, PABA cross react)
  • Amides: LIdoaIne
  • Present in uncharged amine form that enters cell, then protonated and blocks Na channels from inner membrane in a use dependent fashion
  • Blockage occurs from small to large diameter neurons. Pain, Temp, Touch, Pressure, and rarely motor
  • Often administered with epinephrine or alpha agonist to constrict vessels and maintain high local concentration
  • If infected and acid tissues will stay in charged amide form and can’t enter cell, more is needed
  • S/E is Arryhtmias, BP Changes, and cardiotox
36
Q

Succinylchline

A
  • Depolarizing neuromuscular blocker leads to depolarization of membrane and stuck in that state. Binds tighly to AchR
  • Phase I is complete depolarization and no antidote is possible, treatment with AchEI will potentiate block
  • Phase 2 is repolarization, but desensitization. Tx with AchEI can lead to recovery
  • S/E: Hyper Ca, and K. Also malignant hyperthermia, treat with dantolene
37
Q

Tubocurarine (Curium)

A
  • Used in intubaion, non depolarizing
  • AchR antagonist leads to blockage of receptors
  • Antidote is AchEI (Neostigmine and edrophonium)
38
Q

Dantrolene

A

-Prevents Ca release from SR used in malignant Hyperthermia caused by succinylcholine or typical antispychotics

39
Q

Parkinsons Basics

A
  • Decreasd DA leads to bradykinesia

- Increased Ach leads to tremor and rigidity

40
Q

DA agonists

A
  • Bromocriptine

- Repriridne, paramexole (preferred)

41
Q

Increase DA centrally

A
  • Carbidopa/L-Dopa: L Dopa can cross BBB and be converted into DA by L-Dopa decarboylase
  • Carbidopa prevents peripheral conversion via AAAD (Leads to increase Central effects and decreasd peripheral effects)
  • Dosing problems leads to akinesia and dyskinesia
  • Also arrytjmias from peripheral effects
42
Q

Increase DA release

A

-Amantadine: Causes DA release, also antiviral against rubella and influenza

43
Q

Prevent DA breakdown

A

-MAO-B inhibitor prevents DA breakdown with minimal effect on MAO-A (Decrease risk of tyramine induced hypertensive crisis or seretonin syndrome)

44
Q

Entacapone, Tolcapone

A

-Prevent the conversion of L-Dopa to 3-O-mehtyldopa (inactive) by COMT

45
Q

Benztropine

A
  • Muscarinic antagonist
  • Curbs elevated Ach leads to improvment in tremor and rigidity
  • Causes anticholinergic S/E (Angle closure glaucoma)
46
Q

Memantine

A

-NMDA receptor antagonist, used to inhbit ecititoxicity in Alzhiemers

47
Q

Donepazil, galantamine, rivastigmine

A

-Central AchEI

48
Q

Huntingtons

A
  • Increased DA and decreased GABA/Ach
  • Haloperidol blocks D2 Receptors
  • Reserpine, blocks VMAT mediated loading of DA into vesiceles
49
Q

Sumitriptan

A
  • Seretonin analog used in abortive treatment of cluster and migrane headaches
  • Causes vasoconstriction and decreasd trigeminal activation
  • Contraindicated in patienst with prinmetal angina, may also precipitate hypertensive crisis (sereTONIN)
  • Short T1/2
50
Q

Propsognosia

A

-Inability to recognize the meanings and associations of objects. Propsognosia. Associaed with infarction in Occipitotemporal association corticies (MCA)