Pharmacology Flashcards Preview

First Aid STEP 1 - Neurology > Pharmacology > Flashcards

Flashcards in Pharmacology Deck (50)
Loading flashcards...
1

How do epinephrine and brimonidine treat glaucoma?

ALPHA-AGONISTS

decrease aqueous humor synthesis

2

What are side effects of epinephrine and brimonidine?

mydraisis
BLURRY VISION
ocular hyperemia
foreign body sensation
ocular allergic reactions
ocular pruritis

3

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

decrease aqueous humor synthesis

4

How does acetazomalide treat glaucoma?

decrease aqueous humor synthesis

5

How do pilocarpine and carbachol treat glaucoma?

DIRECT CHOLINOMIMETICS

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

6

How do physostigmine and echothiophate treat glaucoma?

INDIRECT CHOLINOMIMETICS

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

7

How does Latanoprost (PGF) treat glaucoma?

increase outflow of aqueous humor

8

What is a side effect of Latanoprost?

darkens color of iris (browning)

9

What is the MOA of opioid analgesics?

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

10

What are side effects of opioid analgesics?

addiction
respiratory depression
constipation
miosis
additive CNS depression with other drugs

**Tolerance does NOT develop to miosis and constipation

11

What is the antidote for opioid OD?

naloxone and naltrexone (opioid receptor antagonist)

12

What is the MOA of butorphanol?

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

13

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

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

14

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

MOA: blocks thalamic T-type Ca2+ channels

TU: absence seizures

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

15

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

MOA: increase GABA-A action

TU: status epilepticus

TOX: sedation, tolerance, dependence, respiratory depression

16

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

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

17

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

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

18

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

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

19

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

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

20

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

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

21

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

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

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

MOA: blocks VG-Na+ channels

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

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

23

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

MOA: unknown

TU: simple, complex, tonic-clonic seizures

24

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

MOA: increase GABA by inhibiting repute

TU: simple and complex seizures

25

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

MOA: increase GABA by irreversibly inhibiting GABA transaminase

TU: simple and complex seizures

26

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

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

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

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

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

zolpidem (ambien), zaleplon, eszopiclone

MOA: act via the BZ1 subtype of the GABA receptor

TU: insomnia

TOX: ataxia, HAs, confusion

OD Tx: flumazenil

29

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

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

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

30

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

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