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First Aid STEP 1 - Neurology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

How do epinephrine and brimonidine treat glaucoma?

A

ALPHA-AGONISTS

decrease aqueous humor synthesis

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2
Q

What are side effects of epinephrine and brimonidine?

A 
mydraisis
BLURRY VISION
ocular hyperemia
foreign body sensation
ocular allergic reactions
ocular pruritis
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3
Q

How do beta-blockers (Timolol, Betaxolol, and Carteolol) treat glaucoma?

A

decrease aqueous humor synthesis

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4
Q

How does acetazomalide treat glaucoma?

A

decrease aqueous humor synthesis

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5
Q

How do pilocarpine and carbachol treat glaucoma?

A

DIRECT CHOLINOMIMETICS

increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

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6
Q

How do physostigmine and echothiophate treat glaucoma?

A

INDIRECT CHOLINOMIMETICS

use of pilocarpine in emergencies - very effective at opening meshwork in canal of Schlemm

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7
Q

How does Latanoprost (PGF) treat glaucoma?

A

increase outflow of aqueous humor

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8
Q

What is a side effect of Latanoprost?

A

darkens color of iris (browning)

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9
Q

What is the MOA of opioid analgesics?

A

Act as agonists at opioid receptors (mu= morphine) to modulate synaptic transmission

Opens K+ channels, closes Ca2+ channels –> decrease synaptic transmission

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

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10
Q

What are side effects of opioid analgesics?

A 
addiction
respiratory depression
constipation
miosis 
additive CNS depression with other drugs

**Tolerance does NOT develop to miosis and constipation

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11
Q

What is the antidote for opioid OD?

A

naloxone and naltrexone (opioid receptor antagonist)

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12
Q

What is the MOA of butorphanol?

A

mu-opioid receptor PARTIAL agonist and kappa-opioid receptor agonist –> produces analgesia

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13
Q

What is the MOA, TU, and TOX of tramadol?

A

MOA: very weak opioid agonist; also inhibits serotonin and NE repute (works on multiple neurotransmitters)

TU: chronic pain

TOX: similar to opioids, decreases seizure threshold, 5HT syndrome

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14
Q

What is the MOA, TU, and TOX of ethosuximide?

A

MOA: blocks thalamic T-type Ca2+ channels

TU: absence seizures

TOX: fatigue, GI distress, HA, itching, and Stevens-Johnson Syndrome

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15
Q

What is the MOA, TU, and TOX of benzodiazepines (when talking about seizures)?

A

MOA: increase GABA-A action

TU: status epilepticus

TOX: sedation, tolerance, dependence, respiratory depression

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16
Q

What is the MOA, TU, and TOX of phenytoin?

A

MOA: increase Na+ channel inactivation, zero-order kinetics

TU: simple, complex, tonic-clonic (1st line), and status epilepticus seizures

TOX: nystagmus, megaloblastic anemia, Stevens-Johnson syndrome, osteopenia, gingival hyperplasia, ataxia, hirsutism

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17
Q

What is the MOA, TU, and TOX of carbamazepine?

A

MOA: increase Na+ channel inactivation

TU: simple, complex, and tonic-clonic (all 1st line)

TOX: agranulocytosis, aplastic anemia, live toxicity, SIADH< Stevens-Johnson Syndrome, diplopia

**Also, 1st line treatment for trigeminal neuralgia

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18
Q

What is the MOA, TU, and TOX of valproic acid?

A

MOA: increase Na+ channel inactivation, increase GABA concentration by inhibiting GABA transaminase

TU: simple, complex, tonic-clonic (1st line), absence seizures

TOX: GI, fatal hepatotoxicity (measure LFTs), NEURAL TUBE DEFECTS (spina bifida), tremor, wt gain

**Also used for myoclonic seizures, bipolar disorder

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19
Q

What is the MOA, TU, and TOX of gabapentin?

A

MOA: primarily inhibits high-voltage-activated Ca2+ channels; designed as GABA analog

TU: simple, complex, tonic-clonic seizures

TOX: sedation, ataxia

**Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder

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20
Q

What is the MOA, TU, and TOX of phenobarbital?

A

MOA: increase GABA-A action

TU: simple, complex, tonic-clonic seizures

TOX: sedation, tolerance, dependence induction of cyt P-450, cardiorespiratory depression

**1st line in neonates

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21
Q

What is the MOA, TU, and TOX of topiramate?

A

MOA: blocks Na+ channels, increase GABA action

TU: simple, complex, tonic-clonic seizures

TOX: sedation, mental dulling, kidney stones, wt loss

**Also used for migraine prevention

22
Q

What is the MOA, TU, and TOX of lamotrigine?

A

MOA: blocks VG-Na+ channels

TU: simple, complex, tonic-clonic, and absence seizures

TOX: Stevens-Johnson Syndrome (MUST BE TITRATED SLOWLY)

23
Q

What is the MOA, TU, and TOX of levetiracetam?

A

MOA: unknown

TU: simple, complex, tonic-clonic seizures

24
Q

What is the MOA, TU, and TOX of tiagabine?

A

MOA: increase GABA by inhibiting repute

TU: simple and complex seizures

25
Q

What is the MOA, TU, and TOX of vigabatrin?

A

MOA: increase GABA by irreversibly inhibiting GABA transaminase

TU: simple and complex seizures

26
Q

What is the MOA, TU, and TOX of barbiturates?

A

phenobarbital, pentobarbital, thiopental, secobarbital

MOA: facilitate GABA-A action by increasing DURATION of Cl- channel opening –> decreases neuronal firing

TU: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

TOX: respiratory and CV depression, dependence, drug interactions (induces P-450)

OD Tx: supportive (assist respiration and maintain BP)

*Contraindicated in porphyria

27
Q

What is the MOA, TU, and TOX of benzodiazepines?

A

MOA: facilitated GABA-A action by increasing FREQUENCY of Cl- channel opening

TU: anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (esp. EtOH withdrawal - DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)

TOX: dependence, additive CNS depression effects with EtOH (less risk than barbiturates)

OD Tx: flumazenil (competitive antagonist of GABA benzodiazepine receptor)

28
Q

What is the MOA, TU, and TOX of nonbenzodiazepine hypnotics?

A

zolpidem (ambien), zaleplon, eszopiclone

MOA: act via the BZ1 subtype of the GABA receptor

TU: insomnia

TOX: ataxia, HAs, confusion

OD Tx: flumazenil

29
Q

How does lipid solubility affect the potency and induction time of anesthetics?

A

LOW blood and lipid solubility –> fast induction and low potency

HIGH lipid and blood solubility –> high potency and slow induction

30
Q

What is the MOA, TU, and TOX of inhaled anesthetics?

A

halothane, enflurance, isoflurance, sevoflurane, methoxyflurane, nitrous oxide

MOA: unknown

Effects: myocardial depression, respiratory depression, N/V, increase cerebral blood flow (decreases cerebral metabolic demand)

TOX: halothane - hepatotoxicity, malignant hyperthermia
desflurane - airway irritability
methoxyflurane - nephrotoxicity
enflurane - pro-convulsant

OD Tx: dantrolene

31
Q

Which IV anesthetic has high potency, high lipid solubility, rapid entry into the brain and whose effect is terminated by rapid redistribution into tissue?

A

thiopental (barbiturate)

32
Q

Which IV anesthetic is MC used for endoscopy?

A

midazolam (benzodiazepine)

33
Q

Which PCP analog can be used as an IV anesthetic?

A

ketamine

34
Q

What is the MOA of ketamine?

A

blocks NMDA receptors –> CV stimulant –> disorientation, hallucination, bad dreams, and increase cerebral blood flow

35
Q

What are the uses of propofol as an IV anesthetic?

A

sedation in ICU
rapid anesthesia induction
short procedures

36
Q

What is the MOA, TU, and TOX of local anesthetics?

A

Esters - procaine, cocaine, tetracaine
Amides - lidocaine, mepivacaine, bupivacaine, (amides have 2 I’s in name)

MOA: block Na+ channels by binding to specific receptors on inner portion of channel

37
Q

What drug can be given with local anesthetics to enhance local action?

A

vasoconstrictors

38
Q

What is the order of nerve blockade of local anesthetics?

A

small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers

39
Q

What is the order of loss of sensation?

A
  1. pain
  2. temperature
  3. touch
  4. pressure
40
Q

What should you remember about allergies and local anesthetics?

A

If allergic to esthers, give amides!

41
Q

What is the mechanism of succinylcholine in neuromuscular blockade?

A

DEPOLARIZING

strong ACh receptor agonist –> produces sustained depolarization and prevents muscle contraction

42
Q

What is the mechanism of non depolarizing neuromuscular blocking drugs?

A

tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

MOA: competitive antagonists

43
Q

What is the reversal treatment for non depolarizing neuromuscular blocking drugs?

A

neostigmine and edrophonium

44
Q

What is the MOA, TU, and TOX of dantrolene?

A

MOA: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

TU: used to treat malignant hyperthermia and neuroleptic malignant syndrome

45
Q

What are the drugs used to treat Parkinson disease?

A 
Bromocriptine - DA agonist
Amantadine - increase DA
L-dopa/carbidopa - increase DA
Selegiline - MOA -B inhibitor
Benztropine - antimuscarinic
46
Q

What is the MOA, TU, and TOX of L-dopa (levodopa)/carbidopa?

A

MOA: increase level of DA in brain b/c L-dopa can cross BBB and is converted by dopa decarboxylase in the CNS to DA

*Carbidopa inhibits peripheral decarboxylase to increase the bioavailability of L-dopa and to limit peripheral SEs

TOX: dyskinesia (“on-off” phenomenon)

47
Q

What is the MOA, TU, and TOX of selegiline?

A

MOA: selectively inhibits MOA-B

48
Q

What are the MOA, TU, and TOX of the following Alzheimer drugs?

Memantine
Donepezil, galantamine, rivastigmine

A

Memantine
MOA: NMDA receptor antagonist; helps prevent excitotoxicity

TOX: dizziness, confusion, hallucinations

Donepezil, galantamine, rivastigmine
MOA: AChE inhibitors
TOX: nausea, dizziness, insomnia

49
Q

What is the MOA of treatment of Huntington Disease?

A

Tetrabenzine and reserpine - inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release

Haloperidol - DA receptor antagonist

50
Q

What is the MOA, TU, and TOX of sumatriptan?

A

MOA: 5-HT agonist; inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction

TU: acute migraine, cluster HA

TOX: coronary vasospasm

*contraindicated in CAD or Prinzmetal angina

First Aid STEP 1 - Neurology (6 decks)

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