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3rd year_Neurology > Neuro Pharm > Flashcards

Neuro Pharm Flashcards

1
Q

Opiod receptors are this type of receptor, and have these classes

A

G-protein coupled receptors (mu, delta, kappa)

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2
Q

Receptor that binds morphine and endorphins

A

Mu opiod receptor

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3
Q

Receptor that binds enkephalins

A

Delta opiod receptor

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4
Q

Receptor that binds dynorphins

A

Kappa opiod receptor

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5
Q

Drug category; Clinical Use: cough suppression, diarrhea; SE: respiratory depression, miosis, CNS depression (coma), constipation

A

Opiod analgesics

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6
Q

Opiod drug; MOA: full mu agonist; SE: histamine release

A

Morphine

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7
Q

Opiod drug; MOA: full mu agonist; other: useful for maintenance, long duration, orally active

A

Methadone

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8
Q

Opiod drug; MOA: full mu agonist; SE: muscarinic antagonist (doesn’t cause miosis), don’t combine with SSRIs or MAOIs

A

Meperidine

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9
Q

Opiod drug; MOA: full mu agonist (the other commonly used opiod drug besides morphine)

A

Fentanyl

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10
Q

Opiod drug; MOA: partial mu agonist; given in combination with NSAIDS, antitussive

A

Codeine

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11
Q

Dextramethorphan (antitussive), diphenoxylate (antidiarrheal), loperamide (antidiarrheal)

A

OTC opiod analgesics

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12
Q

Opiod antagonist; short half-life; IV; used for acute opiod overdose

A

Naloxone

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13
Q

Opiod antagonist; PO; used to reduce ethanol craving (given to alcoholics)

A

Naltrexone

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14
Q

Anxiety, GI distress, gooseflesh, muscle spasms, rhinorrhea, sweating

A

Abstinence syndrome (withdrawal from opiods)

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15
Q

Phenytoin, carbamazepine, topiramate, lamotrigine, valproic acid

A

Epilepsy drugs that block Na channels

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16
Q

epilepsy drug; MOA: blocks Na channels; SE: gingival hyperplasia, hirsutism, hydantoin fetus, megaloblastic anemia (decreases folate absorption)

A

Phenytoin

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17
Q

epilepsy drug; MOA: blocks Na channels; SE: blood dyscrasias, teratogen

A

Carbamazepine

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18
Q

epilepsy drug; MOA: blocks Na channels; SE: Steven-Johnson syndrome

A

Lamotrigine

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19
Q

epilepsy drug; MOA: blocks Na channels, (inc GABA); SE: kidney stones

A

Topiramate

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20
Q

epilepsy drug; MOA: blocks Na channels, (inc) GABA, (-) T-type Ca++ channels; SE: rare fatal hepatotoxicity, causes fetal NTDs

A

Valproic acid

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21
Q

Ethosuximide, Valproic acid

A

Epilepsy drugs that block thalamic T-type Ca++ channels

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22
Q

Topiramate, Valproic acid, Benzodiazepines, phenobarbitol, gabapentin

A

Epilepsy drugs that increase GABA

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23
Q

epilepsy drug; MOA: (inc) GABA; SE: dependence (first line for acute seizures)

A

Benzodiazepines (diazepam, lorazepam)

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24
Q

epilepsy drug; MOA: (inc) GABA; SE: dependence (first line for pregnant women, children)

A

Phenobarbitol (barbiturate)

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25
Q

epilepsy drug; MOA:(-) T-type Ca++ channels; SE: fatigue, GI, headache, Steven-Johnson Syndrome

A

Ethosuximide

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26
Q

epilepsy drug; MOA: (inc) GABA; SE: sedation, ataxia

A

Gabapentin

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27
Q

Which acts faster, highly blood soluble anesthetics or low blood soluble anesthetics?

A

Low solubility in blood = Rapid inducation and recovery.

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28
Q

What effect does lipid solubility have on anesthetics.

A

High lipid solubility = high potency

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29
Q

What effect does minimal alveolar concentration of anesthetics have on their potency?

A

As MAC increases potency decreases.

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30
Q

List the inhaled anesthetics

A

Halothane, -flurane, NO2

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31
Q

What inhaled anesthetic has hepatotoxicity?

A

Halothane

32
Q

What inahled anesthetic has nephrotoxicity

A

Methoxyflurane

33
Q

What inhaled anesthetic is a proconvulsant?

A

Enflurane

34
Q

Increase the duration of Cl- channel opening, thereby facilitating GABAa action (decreases neuron firing)

A

Barbiturates

35
Q

Increase the frequency of Cl- channel opening, thereby facilitating GABAa action (decreases neuron firing)

A

Benzodiazepines

36
Q

zepams, zolams, and chlordiazepoxide

A

Benzodiazepines

37
Q

Drug used to treat benzodiazepine overdose, competitive antagonist at GABA receptor

A

flumazenil

38
Q

(TOM thumb) triazolam, oxazepam, midazolam

A

Short-acting benzodiazepines

39
Q

B.B. King on OPIATES PROPOses FOOLishly (Barbiturates, benzodiazepines, Ketamine, opiates, propofol)

A

Intravenous anesthetics

40
Q

High potency barbiturate used for induction of anesthesia in short procedures, decreases cerebral blood flow (IV anesthetic)

A

Thiopental

41
Q

Benzodiazepine that is the most common drug used for endoscopy, may cause severe postoperative respiratory depression (IV anesthetic)

A

Midazolam

42
Q

A PCP analog used as a dissociative anasthetic, decreases cerebral blood flow (IV anesthetic)

A

Ketamine (arylcyclohexamines)

43
Q

2 opiates used with other CNS depressants during general anesthesia (IV anesthetics)

A

Morphine, fentanyl

44
Q

Used for rapid induction of anesthesia and short procedures, less postoperative nausea than other drugs (IV anesthetic)

A

Propofol

45
Q

What are the Local anesthetics?

A

Esters - end in caine, Amide end in -caine but have a second I

46
Q

Local anesthetics MOA

A

Bloack Na channels (preferentially bind activated Na channels)

47
Q

What fibers are affected first by loacal anesthetics?

A

Small, myelinated fibers. Pain first, Pressure is last.

48
Q

What do you coadminister with local anesthetics and why?

A

Vasoconstrictors to enhance local action (except cocaine!)

49
Q

What local anesthetics causes CNS excitation and severe cardiovascular toxicity?

A

Bupivicaine

50
Q

What are neuromuscular blocking drugs used for?

A

Muscle paralysisin surgery or mechanical ventilation.

51
Q

What receptor do NMJ blocking drugs target?

A

Nm

52
Q

What is the only depolarizine NMJ blocking drug and what are it’s two phases?

A

Succinylcholine. Phase 1 = prolonged depolarization. Phase 2 = Repolarized but bloacked.

53
Q

Effect of giving cholinesterase inhibitors in each phase of succinylcholine action.

A

Phase 1: Cholinesterase inhiitors makes it worse. Phase 2: Reversed by cholinesterase inhibitors

54
Q

What are the nondepolarizing NMJ blockers?

A

Have cur in the name (end in cararine, curium or curonium)

55
Q

How do you reverse a nondepolarizing NMJ block?

A

AChE inhibitors (neostigmine, edrophonium)

56
Q

How do you treat malignant hyperthermia or neuroleptic malignant syndrome?

A

Dantrolene (prevents release of Ca2+ from SR)

57
Q

What causes malignant hyperthermia?

A

Using inhaled anesthetics (except NO2) + succinylcholine)

58
Q

What is the mneumonic for Parkinson’s treatments

A

BALSA (Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics)

59
Q

What are the 4 treatment classes for Parkinson’s?

A

Agonize dopamine receptors (bromocriptine), Inc Dopamine (Amantadine, Ldopa/carbidopa) Prevent dopamine breakdown (MAO B inh, selegiline), Curb excess cholinergics (benztropine, no effect on bradykinesia)

60
Q

What is the treatment for essential or familial tremors?

A

Beta blockers

61
Q

How does the L-dopa/carbidopa treatment work?

A

L-dopa crosses the blood brain barrier and is converted in CNS to dopamine. Carbidopa inhibits peripheral decarboxylase.

62
Q

What parkinson drug causes arrhythmais?

A

L-dopa (when it’s converted to dopamine in periphery)

63
Q

What drug is coadministered with L-dopa in parkinson’s but may enhance its side effects?

A

Selegiline (MAO-B inhibitor)

64
Q

Treatment of migraines

A

Sumatripan. 5-HT 1D agonist. Causes vasoconstriction. Short half-life. (side effect = coronary vasospasm)

65
Q

Contraindications for sumatripan

A

CAD or prinzmetals (causes coronary vasospasm)

66
Q

Memantine - mOA?

A

NMDA receptor antagonist

  • helps prevent excitotoxicity (mediated by Ca2+)
67
Q

Memantine - AEs?

A

Dizziness, confusion, hallucinations

68
Q

Donepezil - MOA?

A

Acetylcholinesterase inhibitor

69
Q

Donepezil - AEs?

A

Nausea, dizziness, insomnia

70
Q

Tetrabenazine - MOA?

A

inhibits VMAT

- limits dopamine vesicle packaging & release

71
Q

Reserpine - MOA?

A

inhibits VMAT

- limits dopamine vesicle packaging & release

72
Q

Haloperidol - MOA?

A

Dopamine receptor antagonist

73
Q

Huntington’s drugs?

A

Tetrabenazine, Reserpine, & Haloperidol

74
Q

Sumatriptan - MOA?

A

5-HT(1B/1D)-agonist

  • inhibits Trigeminal nerve activation
  • prevents vasoactive peptide release
  • induces vasoconstriction
  • ½-life < 2 hours
75
Q

Dantrolene - clinical uses?

A
  • Malignant hyperthermia (rare, life-threatening side-effect of inhalation anesthetics – except NO2 – & succinylcholine)
  • Neuroleptic malignant syndrome (toxicity of antipsychotics)

3rd year_Neurology (8 decks)

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