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Step 1 Flash Cards > Neuro Drugs > Flashcards

Neuro Drugs Flashcards

1
Q

Epinephrine, Brimonidine

A

alpha 2 agonists

  • decreased aqueous humor synthesis
  • SE (epi): mydriasis, do not used in closed-angle glaumcoma
  • SE (brimonidine): blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis
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2
Q

timolol, betaxolol, carteolol

A

beta blockers

  • decreased aqueous humor synthesis
  • no pupillary or vision changes
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3
Q

acetazolamide

A

carbonic anhydrase inhibitor

  • decreased aqueous humor synthesis, no pupillary or vision changes
  • SE: somnolence, paresthesias, urinary alkalosis
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4
Q

pilocarpine, carbachol

A
  • direct cholinomimetics
  • increase outflow of aqueous humor via contraction of the ciliary muscle and opening of trabecular meshwork
  • SE: miosis and cyclospasm (contraction of ciliary muscle)
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5
Q

physostigmine, echothiophate

A

indirect cholinomimetics

  • use pilocarpine in emergencies, very effective at opening meshwork into canal of Schlemm
  • SE: miosis and cyclospasm (contraction of ciliary muscle)
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6
Q

latanoprost (PGF2a)

A

prostaglandin that increases outflow of aqueous humor

- darkens the color of the iris (browning)

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7
Q

opioid analgesics (names)

A

morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate

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8
Q

opioid mechanism

A
  • acts as agonists at opioid receptors (mu = morphine, delta = enkephaline, kappa = dynorphin) to modulate synaptic transmission - opens K channels, closes Ca channels –> decreased transmission
  • inhibit release of Ach, norepi, 5HT, glutamate, substance P
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9
Q

opioid clinical use

A
  • pain
  • cough suppression - dextrmethorphan
  • diarrhea - loperamide, diphenoxylate
  • acute pulmonary edema
  • methadone maintenance for heroin addicts
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10
Q

opioid tox

A
  • addiction, resp depression, constipation, miosis, additive CNS depression with other drugs
  • tolerance does not develop to miosis and constipation
  • uncommon: RUQ pain bc morphine causes smooth muscle contraction –> sphincter of oddi contraction
  • tox treated with naloxone or naltrexone
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11
Q

butorphanol

A

mech: mu-opioid receptor partial agonist and kappa-opioid receptor agonist, produces analgesia
- used in severe pain, causes less respiratory depression than full agonists
- can cause opioid withdrawal if the patient is also taking a full agonist
- overdose not easily reversed with naloxone

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12
Q

tramadol

A
  • very weak opioid agonist, also inhibits serotonin and norepi reuptake
  • used in chronic pain
  • tox: similar to opioids, decreases seizure threshold, serotonin syndrome
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13
Q

pentazocine

A

opioid narcotic with partial agonist activity and weak antagonist activity at mu receptors
- can cause withdrawal in a dependent person

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14
Q

ethosuximide

A
  • used in absence seizures
  • blocks thalamic T-type Ca channels
  • side effects: GI, fatigue, headache, urticaria, SJS
  • “sucks” to have silent seizures
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15
Q

phenytoin

A
  • used in all seizure types except absence, can be used in status
  • increase Na channel inactivation, zero-order kinetics
  • nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsuitism, peripheral neuropathy, megaloblastic anemia, teratogen, SLE-like syndrome, induction of cytochrome P-450, lymphadenopathy, SJS, osteopenia
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16
Q

carbamezapine

A
  • used in all types of seizures except absence
  • increases Na channel inactivation
  • SE: diplopia, ataxia, blood dyscrasias, liver tox, teratogenesis, induction of P-450, SIADH, SJS
  • 1st line treatment for trigeminal neuralgia
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17
Q

valproic acid

A
  • used in all types of seizures, 1st line in T-C seizures
  • increases Na channel inactivation, increased [GABA] by inhibiting GABA transaminase
  • SE: GI distress, rare but fatal hepatotox (measure LFTs), neural tube defects, tremor, weight gain
  • also used for myoclonic seizures and bipolar disorder
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18
Q

gabapentin

A
  • used in all types except absence seizures
  • primarily inhibits high-voltage-activated Ca channels, designed as GABA analog
  • SE: sedation, ataxia
  • also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder
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19
Q

phenobarbital

A
  • used in all types except absence seizures
  • increased GABAa action
  • SE: sedation, tolerance, dependence, induction of P450, cardiorespiratory depression
  • 1st line in neonates
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20
Q

lamotrigine

A
  • used in all types of seizures
  • blocks voltage gated Na channels
  • SE: SJS
21
Q

barbituates (phenobarb, pentobarb, thiopental, secobarbital) mech and use

A
  • mech: facilitate GABAa action by increasing duration of Cl channel opening, thus decreasing neuron firing
  • contraindicated in porphyria
  • used as sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
22
Q

whats so special about thiopental?

A

rapidly wears off due to distribution into tissues, not because of metabolism
- barbituate used for induction of anesthesia and short surgical procedures

23
Q

barbituates toxicity

A
  • resp and cardiovascular depression
  • CNS depression, dependence, drug interactions (p450 inducer)
  • overdose treatment is supportive
24
Q

long acting benzos

A

diazepam, flurazepam, chlordiazepoxide

25
Q

intermediate acting benzos

A

LET

lorazepam, estazolam, temazepam

26
Q

short acting benzos

A

TOM

- triazolam, oxazepam, midazolam

27
Q

benzo mechanism

A
  • facilitate GABAa action by increasing the frequency of Cl channel opening
  • decrease REM sleep
28
Q

benzo tox

A
  • dependence, additive CNS depression effects with alcohol
  • less risk of respiratory depression and coma than with barbituates
  • treat overdoses with flumazenil (competitive GABA antagonist)
29
Q

nonbenzo hypnotics

A
  • zolpidem, zaleplon and eszopiclone
  • act via the BZ1 subtype of the GABA receptor, effects reversed by flumazenil
  • used for insomnia
  • metabolized by p450
  • tox: ataxia, headaches, confusion, short duration and only modest day-after psychomotor depression
  • decreased risk of dependence, no muscle relaxing or anticonvulsant effects
30
Q

MAC

A

minimal alveolar concentration

  • lower MACs, higher potency
  • drugs with increased solubility in lipids –> increased potency = 1/MAC
31
Q

inhaled anesthetics names and effects

A
  • halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, NO
  • mechanism unknown
  • effects: myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow, decreased cerebral metabolic demand, decreased GFR, decreased hepatic blood flow
32
Q

inhaled anesthetics side effects

A
  • hepatotox (halothane), nephrotox (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in body cavity (NO)
  • can cause malignant hyperthermia, treat with dantrolene (usually due to ryanodine receptor mutation, this prevents further release of Ca)
33
Q

midazolam

A
  • most common drug used for endoscopy
  • used adjunctively with gaseous anesthetics and narcotics
  • may cause severe postop resp depression, decreased BP and anterograde amnesia
34
Q

ketamine

A
  • PCP analog that acts as a dissociated anesthetic
  • blocks NMDA receptors
  • CV stimulant
  • causes disorientation, hallucination and bad dreams
  • increased cerebral blood flow
35
Q

propofol

A
  • used for sedation in the ICU, rapid anesthesia induction, and short procedures
  • less post op nausea than thiopental
  • potentiates GABAa
36
Q

local anesthetics

A
  • block Na channels by binding to specific receptors on the inner portion of the channel
  • need more in infected (acidic) tissue
  • blocks small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers
  • lose pain, then temp, then touch, then pressure
  • tox: CNS excitation, cardiovascular tox, HTN, hypotension, arrhythmias
37
Q

succinylcholine

A
  • strong Ach receptor agonist
  • produced sustained depolarization and prevents muscle contraction
  • reversal of blockade not possible in phase I, cholinesterase inhibitors will overcome blockade in phase II (when the receptors are available but desensitized)
38
Q

nondepolarizing neuromuscular blocking drugs

A
  • tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
  • competitive antagonists, compete with Ach for receptors
  • reversal of blockade with neostigmine, edrophonium and other cholinesterase inhibitors
39
Q

dantrolene

A
  • prevents release of Ca from the sarcoplasmic reticulum of skeletal muscle
  • used to treat malignant hyperthermia and NMS because usually due to ryanodine receptor mutation
40
Q

bromocriptine, pramipexole, ropinirole

A

dopamine agonist used in parkinsons

41
Q

amantadine

A

increases dopamine release, also has antiviral activities

- tox: ataxia

42
Q

selegiline

A
  • selective MAOb inhibitor that prevents dopamine breakdown
  • adjunctive agent to L-dopa in treatment of parkinsons
  • may enhance adverse effects of L-dopa
43
Q

entecapone, tolcapone

A
  • COMT inhibitors that prevent L-dopa degredation

- entecapone inhibits peripheral destruction, and tolcapone inhibits peripheral and central destruction

44
Q

benztropine

A
  • antimuscarinic that improves tremor and rigidity in parkinsons but has little effect on bradykinesia
45
Q

memantine

A
  • NMDA receptor antagonist
  • helps prevent excitotoxicity (mediated by Ca)
  • tox: dizziness, confusion, hallucinations
46
Q

donepezil, galantamine, rivastigmine

A
  • AchE inhibitors used in alzheimers

- tox: nausea, dizziness, insomnia

47
Q

Huntington drugs

A
  • NT changes: dec GABA and Ach, inc dopamine
  • haloperidol - D2 receptor antagonist
  • tetrabenazine and reserpine - inhibit vesicular monoamine transporter, limit dopamine vesicle packaging and release
48
Q

sumatriptan

A
  • serotonin agonist
  • inhibits trigeminal nerve activation, prevents vasoactive peptide release, half-life < 2 hours
  • used in acute migraine and cluster headaches
  • tox: coronary vasospasm (contraindicated in pts with CAD and prinzmetal angina), mild tingling

Step 1 Flash Cards (36 decks)

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