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Step 1 Pharmacology > Neurology Pharm > Flashcards

Neurology Pharm Flashcards

1
Q

How do glaucoma drugs work

A

Dec. IOP via dec. amount of aqueous humor (inhibits synthesis/secretion or inc. drainage)

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2
Q

alpha-agonists

A

Epinephrine, Brimonidine (alpha2)

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3
Q

beta-blockers for glaucoma side effects

A

No pupillary or vision changes

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4
Q

acetazolamide glaucoma side effects

A

no pupillary or vision changes

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5
Q

What beta blockers are used in glaucoma

A

Timolol, betaxolol, carteolol

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6
Q

What duretics used for glaucoma

A

Acetazolamide

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7
Q

What alpha agonists used in glaucoma

A

epinephrine, brimonidine

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8
Q

What cholinomimetics used in glaucoma

A

Direct: pilocarpine, carbachol
Indirect: Physostigmine, echothiophate

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9
Q

What is latanoprost

A

Prostaglandin PGF2alpha, darkens color of iris

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10
Q

How do the glaucoma drugs work

A

The alpha agonists, beta blockers, diuretics all decrease aqueous humor synthesis.
Cholinomimetics and prostaglandin increase aqueous humor outflow.

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11
Q

Delta opioid receptor ligand

A

enkephalin

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12
Q

Kappa opioid receptor ligand

A

dynorphin

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13
Q

Opiates MOA on ion channels

A

open K+ channels, close Ca2+ channels, decerase synaptic transmission. inhibit ACh, NE, 5-HT, glutamate, substance P.

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14
Q

Diarrhea opiates

A

loperamide and diphenoxyllate

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15
Q

Opiate tolerance that doesn’t go away

A

No tolerance to miosis or constipation

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16
Q

Butorphanol

A

Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia. Less resp. depression than full agonists. Can’t reverse with naloxone very easily.

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17
Q

Tramadol

A

Very weak opioid agonist; also a SNRI, [Tram It All]

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18
Q

Tramadol use

A

Chronic pain, but decreases seizure threshold and can cause serotonin syndrome.

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19
Q

What drugs can be used for absence seizures

A

Ethosuximide, valproate, and lamotrigine

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20
Q

What drugs are used in status epilepticus?

A

Benzos and Phenytoin(PPx)

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21
Q

What are the first line agents for tonic clonic seizures

A

Phenytoin, Carbamazepine, and Valproate.

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22
Q

What is the first line agents for Simple and complex seizures

A

Carbamazepine only, Carbamazepine is best for all partial seizures and tonic clonic.

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23
Q

What drugs can’t be used for partial seizures

A

Ethosuximide (Thalamic channels) and Benzos

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24
Q

Ethosuximide side effects

A

EFGHIJ: Ethosuximide causes, Fatigue, GI distress, Headache, Itching, and Stevens-Johnson syndrome.

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25
Q

Tx eclampsia seizures

A

1st line is MgSO4, benzos are second line.

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26
Q

ethosuximide MOA

A

Thalamic T-type Ca2+ channels

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27
Q

Topiramate non-seizure use

A

Migraine PPx

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28
Q

1st line for trigeminal neuralgia

A

Carbamazepine

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29
Q

Carbamazepine MOA

A

Inc. Na+ channel inactivation

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30
Q

Phenytoin MOA

A

Inc. Na channel inactiation; zero order kinetics

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31
Q

Valproate MOA

A

Inc. Na channel inactivation, inc. GABA conc. by inhibiting GABA transaminase

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32
Q

Gabapentin MOA

A

Blocks high voltage-activated Ca channels, GABA analog

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33
Q

Topiramate MOA

A

Blocks Na channels, inc. GABA action

34
Q

Lamotrigine MOA

A

Blocks voltage-gated Na channels

35
Q

Levetiracetam MOA

A

Unknown; may modulate GABA and glutamate release

36
Q

Tiagabine

A

Inc. GABA by inhibiting re uptake

37
Q

Vigabatrin MOA

A

Inc. GABA by irreversibly inhibiting GABA transaminase

38
Q

Barbiturates MOA

A

Prolong GABAa opening duration.

39
Q

Barbiturates contraindication

A

Porphyria

40
Q

Barbiturates overdose tx

A

Assist respiration and maintain BP

41
Q

Benzos MOA

A

Increase GABAa frequency of opening. Decrease REM.

42
Q

Flumazenil MOA

A

competitive antagonist at GABA benzo receptor

43
Q

Nonbenzodiazepine hypnotics

A

Zolpidem, Zaleplon, esZopiclone “All ZZZs put you to sleep.”

44
Q

Nonbenzo hypnotics MOA

A

Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil.

45
Q

Anesthetic dec. solubility in blood leads to

A

rapid induction and recovery times

46
Q

Anesthetic inc. solubility in blood leads to

A

inc. potency

47
Q

Potency formula

A

1/MAC

48
Q

Inhaled anesthetics Effects

A

Myocardial depression, resp. depr. N/V, INCREASED Cerebral blood flow (dec. cerebral metabolic demand)

49
Q

Halothane tox

A

hepatotoxicity

50
Q

Methoxyflurane tox

A

nephrotoxicity

51
Q

Enflurane tox

A

proconvulsant

52
Q

Nitrous oxide tox

A

Expansion of trapped gas in a body cavity

53
Q

What drugs cause malignant hyperthermia

A

All inhaled anesthetics except nitrous oxide and succinyl choline. HEREDITARY CONDITION. Tx is dantrolene.

54
Q

Thiopental drug class

A

Barbiturates

55
Q

Thiopental pharmacokinetics

A

high potency, high lipid solubility, rapid entry into brain, rapidly redistributed. DECREASES CEREBRAL BLOOD FLOW.

56
Q

Midazolam use

A

Most common drug for endoscopy

57
Q

Midazolam toxicity

A

Severe postop resp. depressino, dec. BP, anterograde amnesia.

58
Q

Arylcyclohexylamines

A

Ketamine, blocks NMDA receptors

59
Q

Ketamine effects

A

CV stimulant, disorientation, hallucinations, bad dreams. Inc. cerebral blood flow.

60
Q

Propofol

A

Potentiates GABAa

61
Q

Amide local anesthetics

A

Have 2 I’s in the name, bupivicaine, lidocaine, mepivacaine.

62
Q

Local anesthetics MOA

A

binds Na+, especially when activated, so best in rapidly firing neurons.

63
Q

Fact: tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.

A

.

64
Q

Fact: in infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively, need more anesthetic.

A

.

65
Q

What are the alkaline anesthetics?

A

Local anesthetics are all weak bases!!! So acidic tissue is bad for all local anesthetics. So sick tissue needs more anesthetic than happy tissue.

66
Q

Order of nerve blockade for local anesthetics

A

Small diameter > large diameter. myelinated > unmyelinated

67
Q

Order of loss with local anesthetics

A
  1. Pain
  2. Temp
  3. Touch
  4. Pressure
68
Q

Which local anesthetic is toxic to the heart

A

Bupivicaine

69
Q

Which local anesthetic causes arrhythmias:

A

Cocaine

70
Q

Depolarizing neuromuscular blockers toxicity

A

HyperCa, hyperK, malignant hyperthermia

71
Q

Nondepolarizing blockers

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

72
Q

Nondepolarizing MOA

A

Competitive antagonists at NMJs, all are like curare

73
Q

Nondepolarizing antidote

A

Neostigmine (msut be given with atropine to pervent muscarinic effects like bradycardia), edrophonium, and other AChEIs.

74
Q

Phase I of succinylcholine

A

Prolonged depolarization, no antidote, AChEIs potentiate the effect.

75
Q

Phase II of succinylcholine

A

Repolarized but blocked; ACh receptors available but desensitized: antidote of AChEIs

76
Q

Non-ergot DA agonists

A

Pramipexole and ropinirole

77
Q

parkinson drugs

A

BALSA

Bromocriptine, Amantadine, Levodopa (w/ carbidopa), Selegiline (and COMT inhibitors), Antimuscarinics

78
Q

Amantadine MOA

A

May inc. DA release, antiviral for flu A and rubella; toxicity=ataxia

79
Q

Selegiline MOA

A

selective MAO type B inhibitor

80
Q

COMT inhibitors

A

Entacapone, tolcapone: prevent L-dopa degradation

81
Q

Benztropine MOA

A

Antimuscarinic; improves tremor and rigidity but little effect on bradykinesia

Step 1 Pharmacology (17 decks)

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