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Step 1 AB > Neuro Drugs > Flashcards

Neuro Drugs Flashcards

1
Q

Alpha agonists used to treat Glaucoma

A

Epinephrine (alpha 1) - decreased aqueous humor synthesis via vasoconstriction
Brimonidine (alpha 2) - decreased aqueous humor synthesis

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2
Q

S/E of Epinephrine

A

Mydriasis (alpha 1) –> don’t use in acute closed angle glaucoma

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3
Q

Mechanism of beta blockers in Glaucoma

A

Decrease aqueous humor synthesis

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4
Q

Acetazolamide mechanism in Glaucoma

A

Decrease aqueous humor synthesis via inhibition of carbonic anhydrase

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5
Q

Direct cholinomimetics used for glaucoma

A

Pilocarpine, Carbachol

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6
Q

Latanoprost (mechanism, use and S/E)

A

Mech - increases outflow of aqueous humor (a prostaglandin PGF2alpha)
Use - Glaucoma
S/E - Darkens color of iris (browning)

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7
Q

Uses of opioids

A 
Pain
Cough suppression
Diarrhea (loperamide, diphenoxylate)
Acute pulmonary edema
Maintenance programs for heroin addicts
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8
Q

Butorphanol

a. Mechanism
b. Use
c. Toxicity

A

a. K opioid agonist and mu opioid partial agonist –> produces anesthesia
b. Severe pain (less resp depression that full agonists)
c. Can cause opioid withdrawal symptoms if patient is also taking full agonist

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9
Q

Tramadol

a. Mechanism
b. Use
c. Toxicity

A

a. Very weak opioid agonist; also inhibits 5-HT and NE reuptake (tram it all = multiple receptors)
b. Chronic pain
c. Decreases seizure threshold, serotonin syndrome

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10
Q

Ethosuximide

a. Mechanism
b. Use
c. Toxicity (EFGHIJ)

A

a. Blocks thalamic T type Ca channels
b. Absence seizures
c. Fatigue, GI distress, Headache, Itching, stevens Johnson syndrome

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11
Q

1st line for acute status epilepticus

A

Benzodiazepines

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12
Q

Phenytoin

a. Mechanism
b. Use
c. Toxicity

A

a. Increases Na channel inactivation; zero order kinetics
b. Prophylaxis of status epilepticus, treatment of simple, complex, tonic-clonic seizures
c. Gingival hyperplasia, hirsutism, megaloblastic anemia, fetal hydantoin syndrome, SLE like syndrome, p-450 induction, Stevens johnson, osteopenia, nystagmus, diplopia, ataxia, sedation

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13
Q

Carbamazepine

a. Mechanism
b. Use
c. Toxicity

A

a. Increases Na channel inactivation
b. Trigeminal neuralgia, simple/complex/tonic-clonic seizures
c. Liver toxicity, Stevens johnson, p-450 inducer, teratogen, SIADH, aplastic anemia, agranulocytosis

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14
Q

Valproic acid

a. Mechanism
b. Use
c. Toxicity

A

a. Increased Na channel inactivation by increasing GABA concentration
b. All seizures, bipolar disorder
c. Hepatotoxic, teratogen

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15
Q

Gabapentin

a. Mechanism
b. Use
c. Toxicity

A

a. Inhibits high voltage activated Ca channels (GABA analog)
b. Simple or complex seizures, peripheral neuropathy or postherpetic neuralgia
c. Sedation, ataxia

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16
Q

Phenobarbital

a. Mechanism
b. Use
c. Toxicity

A

a. Increases GABAa action
b. First line in neonates; simple/complex/tonic-clonic seizures
c. P450 inducer, tolerance, sedation, cardiorespiratory depression

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17
Q

Treatment for absence seizure

A

Ethosuximide, Valproic acid, Lamotrigine

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18
Q

Mechanism of barbiturates

A

Facilitate GABAa action by increasing DURATION of Cl channel opening –> decreased neuronal firing

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19
Q

Mechanism of benzodiazepines

A

Facilitate GABAa action by increased frequency of Cl channel opening

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20
Q

Which BDZs have short half life? (ATOM)

A

Alprazolam
Triazolam
Oxazepam
Midazolam

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21
Q

NonBDZ hypnotics

A

Zolpidem
Zaleplon
EsZopiclone

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22
Q

Difference between BDZs and Zolpidem/Zaleplon/Eszopiclone

A

Less potential for tolerance and addiction
No anticonvulsant properties
No muscle relaxing effects
Not used for anesthesia

23
Q

What affects speed of induction and recovery times?

A

Decreased solubility in blood = rapid induction and recovery time

24
Q

What determines anesthetic potency?

A

Inversely proportional to minimal alveolar concentration

Drugs with increased solubility in lipids

25
Q

NO vs. Halothane as anesthetics

A

NO has low blood and lipid solubility –> fast induction and fast recovery, low potency
Halothane has high blood and lipid solubility –> slow induction/recovery and high potency

26
Q

Which drugs cause malignant hyperthermia (fever and severe muscle contractions)?

A 
Inhaled anesthetics (halothane, enflurane, isoflurane, sevoflurane, methoxyflurance, N2O)
Succinylcholine (neuromusclar blocking drug)
27
Q

Which anesthetics can be used for brain surgery?

A

Barbiturates are good because they cause decreased cerebral blood flow

28
Q

Ketamine mechanism

A

Blocks NMDA receptors –> act as dissociative anesthetics

Cardiovascular stimulants, cause disorientation, bad dreams, hallucination

29
Q

Mechanism of local anesthetics

A

Block Na channels by binding receptors on INNER portion of channel (preferentially bind activated Na channels; tertiary amines penetrate membrane in uncharged form and then bind to ion channels as charged form)

30
Q

Why do you need more local anesthetic in infected tissues?

A

Infected tissues are acidic and alkaline anesthetics are charged/cannot penetrate membrane effectively

31
Q

What can you give with local anesthetics to enhance action?

A

Epinephrine (vasoconstrictor)

32
Q

Order of nerve blockade

A

Small myelinated > small unmyelinated > large myelinated > large unmyelinated

33
Q

Order of loss of sensations with local anesthetic

A

Pain > temp > touch > pressure

34
Q

What are the local anesthetics?

A

Esters - Procaine, Cocaine, Tetracaine

Amides - Lidocaine, Mepivicaine, Bupivacaine (two Is in name)

35
Q

What is succinylcholine?

A

Depolarization neuromuscular blocking drug –> Ach receptor agonist that produces sustained depolarization and inhibits muscle contraction

36
Q

What are the non depolarizing neuromuscular blockers?

A

Tubocurarine, Atracurium, Mivacurium, Pancuronium, Vecuronium, Rocuronium –> competitive antagonists of Ach nicotinic muscular receptors

37
Q

Baclofen mechanism and use

A

Inhibits GABAb receptors at spinal cord level –> skeletal muscle relaxation (used for muscle spasms)

38
Q

Cyclobenzaprine mechansim and use

A

Centrally acting skeletal muscle relaxant used for muscle spasms (Has similar anticholinergic side effects)

39
Q

Dopamine agonists used for Parkinsons

A

Ergot - Bromocriptine

Non-ergot (preferred) - Pramipexole, Ropinirole

40
Q

Mechanism of Amantadine

A

Causes increased dopamine release and decreased dopamine reuptake

41
Q

Mechanism of Carbidopa

A

Prevents peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase (reduces peripheral S/E)

42
Q

Mechanism of Entacapone, Tolcapone

A

Prevent peripheral L-DOPA degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT (Tolcapone also inhibits central COMT but causes hepatotoxicity)

43
Q

Drugs that prevent dopamine breakdown

A

Selegiline - inhibits MAOb (dopamine not converted to 3-MT)

Tolcapone - blocks conversion of dopamine to DOPAC by inhibiting central COMT

44
Q

Benztropine mechanism

A

Antimuscarinic that improves tremor in Parkinson patients

45
Q

S/E of L-dopa

A

Arrhythmias from increased conversion to catecholamines

46
Q

Donepezil

A

AchE inhibitor used for Alzheimers

47
Q

Galantamine

A

AchE inhibitor used for Alzheimers

48
Q

Rivastigmine

A

AchE inhibitor used for Alzheimers

49
Q

Tacrine

A

AchE inhibitor used for Alzheimers

50
Q

Neurotranmistter changes in Huntingtons

A

Increased dopamine

Decreased GABA, Ach

51
Q

Treatment for Huntingtons

A

Tetrabenazine and Reserpine - inhibit VMAT to limit dopamine vesicle packaging and release
Haloperidol - D2 receptor antagonist

52
Q

Triptans

a. Mechanism
b. Use
c. Toxicity

A

a. 5-HT1b/1d agonists –> induce vasoconstriction, prevent vasoactive peptide release, inhibit trigeminal nerve activation
b. migraine, cluster headache attacks
c. Coronary vasospasm (C/I in patients with Prinzmetal angina and CAD), Mild paresthesia

53
Q

When are triptans C/I?

A

In patients with prinzmetal angina and CAD, pregnancy

Step 1 AB (29 decks)

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