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First Aid STEP 1 - Neurology > Pharmacology > Flashcards

Pharmacology Flashcards

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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?

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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?

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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?

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A

MOA: unknown

TU: simple, complex, tonic-clonic seizures

24
Q

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

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A

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
31
Which IV anesthetic has high potency, high lipid solubility, rapid entry into the brain and whose effect is terminated by rapid redistribution into tissue?
thiopental (barbiturate)
32
Which IV anesthetic is MC used for endoscopy?
midazolam (benzodiazepine)
33
Which PCP analog can be used as an IV anesthetic?
ketamine
34
What is the MOA of ketamine?
blocks NMDA receptors --> CV stimulant --> disorientation, hallucination, bad dreams, and increase cerebral blood flow
35
What are the uses of propofol as an IV anesthetic?
sedation in ICU rapid anesthesia induction short procedures
36
What is the MOA, TU, and TOX of local anesthetics?
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
What drug can be given with local anesthetics to enhance local action?
vasoconstrictors
38
What is the order of nerve blockade of local anesthetics?
small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers
39
What is the order of loss of sensation?
1. pain 2. temperature 3. touch 4. pressure
40
What should you remember about allergies and local anesthetics?
If allergic to esthers, give amides!
41
What is the mechanism of succinylcholine in neuromuscular blockade?
DEPOLARIZING strong ACh receptor agonist --> produces sustained depolarization and prevents muscle contraction
42
What is the mechanism of non depolarizing neuromuscular blocking drugs?
tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium MOA: competitive antagonists
43
What is the reversal treatment for non depolarizing neuromuscular blocking drugs?
neostigmine and edrophonium
44
What is the MOA, TU, and TOX of dantrolene?
MOA: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle TU: used to treat malignant hyperthermia and neuroleptic malignant syndrome
45
What are the drugs used to treat Parkinson disease?
``` Bromocriptine - DA agonist Amantadine - increase DA L-dopa/carbidopa - increase DA Selegiline - MOA -B inhibitor Benztropine - antimuscarinic ```
46
What is the MOA, TU, and TOX of L-dopa (levodopa)/carbidopa?
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
What is the MOA, TU, and TOX of selegiline?
MOA: selectively inhibits MOA-B
48
What are the MOA, TU, and TOX of the following Alzheimer drugs? Memantine Donepezil, galantamine, rivastigmine
Memantine MOA: NMDA receptor antagonist; helps prevent excitotoxicity TOX: dizziness, confusion, hallucinations Donepezil, galantamine, rivastigmine MOA: AChE inhibitors TOX: nausea, dizziness, insomnia
49
What is the MOA of treatment of Huntington Disease?
Tetrabenzine and reserpine - inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release Haloperidol - DA receptor antagonist
50
What is the MOA, TU, and TOX of sumatriptan?
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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