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Neuro Pharm Flashcards

1
Q

Glaucoma drugs: classes and specific drugs

A
  1. alpha agonists: epinephrine, brimonidine
  2. beta blockers: timolol, betaxolol, careolol
  3. diuretics: acetazolamide
  4. cholinomimetics:
    direct: carbachol, pilocarpine
    indirect: physostigmine, echothiophate
  5. prostaglandin: latanoprost
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2
Q

Glaucoma - Epinephrine

  1. mechanism
  2. side effects
  3. c/i
A
  1. alpha agonist: decrease aq humour synthesis through vasoconstriction
  2. mydriasis, stinging
  3. DO NOT USE in closed angle glaucoma
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3
Q

Glaucoma - Brimonidine

  1. mechanism
  2. side effects
A
  1. alpha 2-agonist, decreases aq humor synthesis

2. none

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4
Q

Glaucoma - Beta blockers

  1. mechanism
  2. side effects
A
  1. decrease aq humour secretion
  2. none

timilol, betaxolol, carteolol

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5
Q

Glaucoma - Acetazolamide

  1. mechanism
  2. side effects
A
  1. decrease aq humour secretion by decreasing HCO3- via inhibition of carbonic anhydrase
  2. none
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6
Q

Glaucoma - Cholinomimetics

  1. mechanism
  2. side effects
A
  1. Increase outflow of aq humour, contract ciliary muscle (which produces aq humour) and opens trabecular network into canal of Schlemm
  2. miosis, cyclospasm (accomodate)
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7
Q

Which glaucoma drug do you use in an emergency?

A

Pilocarpine

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8
Q

Glaucoma - Latanoprost

  1. mechanism
  2. side effects
A
  1. Prostaglandin (PGFa2), increase outflow of aq humour

2. Darkens iris (browning)

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9
Q

Opioid analgesics - drugs

A 
Morphine
Fentanyl
Codeine
Heroin
Methadone
Meperidine
Dextromethorphan
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10
Q

Opioid analgesics - mechanism

A

Agonist at opioid receptors, mu (morphine), delta (enkephalin), kappa (dynorphin)

Open K close Ca channels –> decrease synaptic transmission

Inhibit release of ACh, NE, 5HT, glutamate, substance P

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11
Q

Opioid analgesics - use

A 
Pain
Cough suppression (dextromethorphan)
Diarrhea (loperamide and diphenoxylate)
Acute pulmonary edema
Maintenance program for addicts (methadone)
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12
Q

Which opioid is used for cough suppression?

A

Dextromethorphan

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13
Q

Which opioids are used for diarrhea?

A

Loperamide and diphenoxylate

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14
Q

Which opioids are used for maintenance in drug addicts?

A

Methadone

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15
Q

Toxicity of opioid analgesics

A 
Tolerance
Respiratory depression
Constipation
Miosis
CNS depression with other drugs
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16
Q

What do you treat opioid toxicity with?

A

Opioid receptor antagonists:
naltrexone
naloxone

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17
Q

What do you NOT develop tolerance to when using opioids?

A

Miosis

Constipation

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18
Q

Butorphanol

Mechanism
Use
Toxicity

A
  1. Partial agonist at opioid mu receptors, agonist at kappa
  2. Pain, causes less respiratory depression than full agonists
  3. Causes withdrawal if on full agonists
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19
Q

Which opioid causes less respiratory depression in comparison to other opioids?

A

Butorphanol

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20
Q

Tramadol

  1. Mechanism
  2. Use
  3. Toxicity
A
  1. Weak opioid agonist, inhibits Serotonin and NE reuptake (works on multiple neurotransmitters)
  2. chronic pain
  3. decreases seizure threshold
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21
Q

Phenytoin

  1. Tx’s which seizures
  2. Mechanism
  3. Which drug can be used parenterally?
A
  1. Simple Partial
    Simple Complex
    1st line for Generalized Tonic-Clonic
    1st line for Status
  2. Use dependent blockade of Na+ channels, decrease refractory period, inhibit glutamate release form excitatory presynaptic neurons
  3. Fosphenytoin
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22
Q

Phenytoin toxicity

A 
Gingival hyperplasia in kids
Hirsutism
Megaloblastic anemia (decreases folate absorption)
Teratogenesis (fetal hydantoin syndrome)
SLE-like syndrome
Cyt-P450 inducer
SJS
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23
Q

Carbamezapine

  1. Tx’s which seizures
  2. Mechanism
  3. SE
A

1st line for all Simple Partial, Simple Complex, Generalized Tonic-Clonic

  1. Increases Na channel inactivation
  2. diplopia, ataxia, blood dyscrasias, liver tox, teratogenesis, cP450 inducer, SIADH, SJS
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24
Q

Which drug is 1st line for trigeminal neuralgia?

A

Carbamezapine

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25
Q

Lamotrigine

  1. Tx’s which seizures
  2. Mechanism
  3. SE
A
  1. PS, PC, GTC
  2. Blocks voltage-gated Na channels
  3. SJS
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26
Q

Gabapentin

  1. Tx’s which seizures
  2. Mechanism
  3. SE
  4. other uses
A
  1. PS, PC, GTC
  2. GABA analogue, blocks high voltage activated Ca channels
  3. Sedation, ataxia
  4. peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder
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27
Q

Topiramate

  1. Tx’s which seizures
  2. Mechanism
  3. SE
  4. other uses
A
  1. PS, PC, GTC
  2. Blocks Na channels, increases GABA action
  3. sedation, metal dulling, kidney stones, weight loss
  4. migraine preention
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28
Q

Phenobarbital

  1. Tx’s which seizures
  2. Mechanism
  3. SE
A
  1. PS, PC, GTC
  2. Increases duration of Cl- channel opening, increases GABA action
  3. sedation, tolerance, dependence, cP450 inducer
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29
Q

Which AED is the first line for kids and pregnant women?

A

Phenobarbital

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30
Q

Which drugs are first line for GTC seizures?

A

Phenytoin
Carbamezapine
Valproic acid

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31
Q

Valproic acid

  1. Tx’s which seizures
  2. Mechanism
  3. SE
  4. other uses
A
  1. PS, PC, 1st line for GTC
  2. Increase Na inactivation, increase GABA action via GABA transaminase inhibition
  3. GI distress, hepatotoxicity, neural tube defects, tremor, weight gain
  4. myoclonic seizures, bipolar disorder
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32
Q

Which AED is also used for myoclonic seizures?

A

Valproic acid

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33
Q

Ethosuximide

  1. Tx’s which seizures
  2. Mechanism
  3. SE
A
  1. 1st line for absence seizures
  2. Block Ca channels in thalamus
  3. fatigue, GI distress, headact, itching, SJS, urticaria
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34
Q

Benzo’s

  1. Tx’s which seizures
  2. Mechanism
A
  1. first line for acute status epilepticus

2. increase frequency of Cl- channel opening

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35
Q

Tiagabine

  1. Tx’s which seizures
  2. Mechanism
A
  1. PS, PC

2. inhibit GABA reuptake

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36
Q

Vigabatrin

  1. Tx’s which seizures
  2. Mechanism
A
  1. PS, PC

2. inhibits GABA transaminase, increasing GABA

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37
Q

Levetiracetam

  1. Tx’s which seizures
  2. Mechanism
A
  1. PS, PC, GTC

2. Unknown

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38
Q

Which AEDs are first line for status epilepticus?

A

Prophylaxis: Phenytoin

Acute: Benzo

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39
Q

Which AED is used for seizures in eclampsia?

A

Benzo

MgSO4 is first line

40
Q

What are the only drugs for absence seizures?

A

ethosuximide is first line for absence and is only used for that
valproic acid can be used

41
Q

Most of the seizure drugs are associated with what classes?

A

simple, complex, tonic-clonic

42
Q

Benzodiazepine toxicities

A

Sedation
Tolerance
Dependance

43
Q

Stevens-Johnsons syndrome

Sx’s
AEDs that have this SE

A
  1. Prodrome of malaise and fever

Rapid onset erythematous/purpuric macules (oral, ocular, genital)

Epidermal necrosis and sloughing

  1. Ethosuximide
    Carbamezapine
    Lamotrigine
    Phenytoin
44
Q

Phenytoin is also what type of drug in addition to being an AED?

A

Class I antiarrhythmic

45
Q

Barbiturates:

  1. Examples of drugs
  2. Use
  3. Toxicites
  4. Tx overdose?
A
  1. Phenobarbital, pentobarbital, Thiopental
    , secobarbital
  2. Anxiety, seizures, insomnia, induction for anesthesia
  3. additive CNS depression
    respiratory/CV depression
    induction of Cyt-P450
  4. symptom management – assist respiration and increase BP
46
Q

Which AED is contraindicated in porphyria?

A

Barbiturates

47
Q

Benzodiazepines

  1. use
  2. list short-acting drugs
  3. toxicity
A
  1. anxiety, spasticity, epilepticus, detox from EtOH, night terrors, sleep walking, general anesthetic, hypnotic
  2. Triazolam
    Oxazepam
    Midazolam
  3. dependance
    additive CNS depression with EtOH
    less risk of respiratory depression and coma
48
Q

How do you Tx benzo overdose?

A

Flumazenil

GABA receptor antagonist

49
Q

Which benzo’s have the highest addictive potential?

A

Short acting

Triazolam
Oxazepam
Midazolam

50
Q

Which 2 AEDs are used for acute status epileptices?

A

Diazepam
Lorazepam

(Benzo’s)

51
Q

How do CNS drugs cross BBB?

A
  1. soluble in lipid

OR

  1. transporter
52
Q

Drugs with decreased solubility in the blood have:

A

rapid induction and recovery times

53
Q

Drugs with increased solubility in lipids have:

A

Increased potency

54
Q

Potency of anesthetic drug =

A

1/MAC

MAC = minimal alveolar concentration

55
Q

What does a large MAC mean in terms of potency?

A

low potency

56
Q

MAC

A

minimal alveolar concentration at which 50% of population is anesthetized

57
Q

how do barbiturates and benzos effect the GABA receptor?

A

barbiturates increase the duration of the Cl- channel opening while benzos increase the frequency

58
Q
  1. What are the nonbenzodiazepine hypnotics?
  2. MOA
  3. clinical use
  4. toxicity
A
  1. zolpidem, zaleplon, eszopliclone
  2. BZ1 subtype of GABAR, reversed with flumazenil
  3. insomnia
  4. ataxia, heaches, confusion
59
Q

Halothane has increased blood and lipid solubility, what does this mean in terms of potency and induction?

A

increased blood solubility: slow induction

increased lipid solubility: high potency

60
Q

Mechanism of anesthetic action in lungs

A

increases rate and depth of ventilation

61
Q

Mechanism of anesthetic action in blood

A

increased blood solubility: increase gas required to saturate blood –> slow induction time

62
Q

Mechanism of anesthetic action in tissue (i.e. brain)

A

increased solubility: increased gas required to saturate tissue –> slower onset of action

63
Q

Inhaled anesthetics

  1. Drug examples
  2. Mechanism
  3. Effects
  4. Toxicity
A
  1. Halothane, isoflurane, nitrous oxide
  2. unknown
  3. myocardial and respiratory depression
    nausea/emesis
    increased cerebral blood flow (decreased cerebral metabolic demand)
  4. Hepatotoxicity - halothane
    Nephrotoxicity - methoxyflurane
    Proconvulsant - enflurane
    Malignant hyperthermia
64
Q

How do you treat malignant hyperthermia?

A

dantrolene

65
Q

IV anesthetics (5)

A 
Barbiturates
Benzodiazepine
Ketamine
Opiates
Propofol
66
Q

Thiopental

  1. Potency, lipid solubility, entry time into brain
  2. use
  3. effect terminated by
  4. effect on cerebral blood flow
A

IV anesthetic, barbiturate

  1. high potency, high lipid solubility, rapid entry
  2. induction anesthesia, short surgical procedures
  3. redistribution into fat and tissues
  4. decreases cerebral blood flow
67
Q

Benzo’s

  1. use in anesthesia
  2. used in conjuction with
  3. toxicity
A
  1. IV anesthetic, midazolam most commonly used for endoscopy
  2. gas anesthetics and narcotics
  3. severe post-op respiratory depression, amnesia
68
Q

Ketamine
(arylcyclohexamine)

  1. analog of
  2. blocks which receptors
  3. simulates
  4. side effects
A
  1. PCP, dissociative anesthesia
  2. NMDA
  3. CV system
  4. disorientation, hallucination, bad dreams, increases cerebral blood flow
69
Q

Opiates used as IV anesthetics

A

Morphine, fentanyl

70
Q

Propofol

  1. use
  2. mechanism
A
  1. IV rapid induction of anesthesia, short procedures
  2. potentiates GABA
    -A

Less post-op nausea than thiopental

71
Q

Ester local anesthetics

A

Procaine, cocaine, tetracaine

72
Q

Amide local anesthetics

A

lidocaine, mepivacaine, bupivacaine

amides have 2 i’s each

73
Q

Local anesthetics: mechanism

A

block Na channels

binds better to activated Na channels, so most effective in rapidly firing neurons

74
Q

Tertiary local amides penetrate membrane in what form and bind to ion channels in what form?

A

penetrate in uncharged

bind in charged form

75
Q

In infected (acidic) tissue, how must local anesthetics be administered differently?

A

Alkaline anesthetics are charged and can’t penetrate acidic membrane effectively, so must administer more

76
Q

Order of nerve blockade in local anesthetics

A

small fibers > large fibers

myelinated fibers > unmyelinated

Size factor predominates over myelination.

77
Q

Order of sensory loss in local anesthetics

A

Pain>temperature>touch>pressure

78
Q

Local anesthetics are usually given with what drug and why?

A

Vasoconstrictors (epi), they enhance local action

*except cocaine

79
Q

Local anesthesia toxicity

A 
CNS excitation
Severe CV toxicity (bupivacaine)
HTN
Hypotension
Arrhythmias (cocaine)
80
Q

NMJ blockers

  1. use
  2. selective for which receptor
  3. types
A
  1. muscle paralysis in surgery or mechanical ventilation
  2. Motor nicotinic
  3. Depol and Non-depol
81
Q

Succinylcholine

  1. class
  2. reversal of blockade
  3. complications
A
  1. cholinomimetic, NMJ depolarizing blocker
  2. Phase 1: prolonged depol, no antidote
    , potentiated by cholinesterase inhibitors
    Phase 2: repolarized but blocked, can reverse with AChE inhibitors (neostigmine)
  3. Hypercalemia, Hyperkalemia, malignant hyperthermia
82
Q

Non-depolarizing NMJ blockers

  1. examples
  2. mechanism
  3. reversal of blockade
A
  1. tubocurarine, atracurium, pancuronium, etc.
  2. competitive antagonists for ACh
  3. AChE inhibitors (neostigime, edrophonium, etc.)
83
Q

Dantrolene: use and mechanism

A

tx for malignant hyperthermia and neuroleptic malignant syndrome

prevents release of Ca from sarcoplasmic reticulum of skeletal muscle

84
Q

Malignant hyperthermia is caused by

A

concomitant use of inhalational anesthetics (except N2O) and succinylcholine

85
Q

Parkinson’s has excess____ activity

A

cholinergic due to loss of dopaminergic neurons

86
Q

PD drug classes

A
  1. dopamine agonists - Bromocriptine
  2. drugs that increase dopamine - Amantadine, L-dopa/carbidopa
  3. prevent dopamine breakdown - Selegiline
  4. decrease cholinergic activity - Benztropine
87
Q

Dopamine agonists in PD:

examples
side effects

A
  1. Bromocriptine (ergot), pramipexole, ropinorole (non-ergot, preferred)
  2. gambling
88
Q

Amantadine in PD

A

Increases dopamine release

also used as antiviral against influenza A

toxicity: ataxia

89
Q

Selegiline

  1. MOA
  2. examples
  3. adjunctive to what PD drug
  4. toxicity
A
  1. selective MAO-B inhibitor, which prefers metabolism of dopamine instead of NE or 5-HT
  2. Entacapone, tocapone (COMT inhibitors)
  3. L-dopa
  4. enhance adverse effects of L-dopa
90
Q

Benztropine in PD: MOA

A

anti-muscarinic (decreased cholinergic activity), improves tremor and rigidity, but little effect on bradykinesia

Park your Benz””

91
Q

L-Dopa/carbidopa toxicity

A

arrhythmias from peripheral conversion of L-dopa

Long-term: dyskinesia after administration
Short-term: akinesia b/w doeses

92
Q

Why is carbidopa given in PD?

A

peripheral decarboxylase inhibitor

decreases peripheral side effects of L-dopa and increases bioavailability in brain

93
Q

AD Drugs (2)

  1. MOA
  2. toxicity
A

Memantine

  1. NMDA receptor antagonist, helps prevent excitotoxicity mediated by Ca
  2. dizziness, confusion, hallucinations

Donezapil, galantamine, rivastigmine

  1. AChE inihibitor
  2. Nausea, dizziness insomnia
94
Q

Huntington’s Drugs

  1. alterations in NTs
  2. drug classes and examples
A
  1. Increased dopamine, decreased GABA and ACh
  2. Reserpine + tetrabenzine - amine depleting
    Haloperidol - dopamine receptor antagonist
95
Q

Sumatriptan

  1. MOA
  2. Half-life
  3. Use
  4. Toxicity
  5. c/i in
A
  1. 5-HT agonist. Causes vasoconstriction, inhibits trigeminal activation and vasoactive peptide release.
  2. s angina

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