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Pharmacology > Neurology Pharmacology > Flashcards

Neurology Pharmacology Flashcards

1
Q

Neurology Pharmacology

Epinephrine (α1), brimonidine (α2)

A

MOA: ↓ aqueous humor synthesis via vasoconstriction; ↓ aqueous humor synthesis

Use: Glaucoma

Adverse Effects: Mydriasis (α1); do not use in closed-angle glaucoma. Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis

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2
Q

Neurology Pharmacology

Timolol, betaxolol, cartelol

A

MOA: ↓ aqueous humor synthesis

Use: Glaucoma

No pupillary or vision changes

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3
Q

Neurology Pharmacology

Acetazolamide

A

MOA: ↓ aqueous humor synthesis via inhibition of carbonic anhydrase

Use: Glaucoma

No pupillary or vision changes

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4
Q

Neurology Pharmacology

Cholinomimetics (Direct: pilocarpine, carbachol; Indirect: physostigmine, echothiophate)

A

MOA: ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork. Use pilocarpine in emergencies (effective at opening meshwork)

Use: Glaucoma

Adverse Effects: Miosos and cyclospasm (contraction of ciliary muscle)

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5
Q

Neurology Pharmacology

Bimatoprost, latanoprost

A

MOA: ↑ outflow of aqueous humor

Use: Glaucoma

Adverse Effects: Darkens color of iris, eyelash growth

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6
Q

Neurology Pharmacology

Morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate, pentazocine

A

MOA: Act as agonists at opioid receptors to modulate synaptic transmission - open K+ channels, close Ca2+ channels → ↓ synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.

Use: Pain, cough suppression (codeine), diarrhea (loperamide, diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone, buprenorphine + naloxone)

Adverse Effects: Addiction, respiratory depression, constipation, miosis (except meperidine → mydriasis), additive CNS depression with other drugs.

Toxicity Treatment: Naloxone or naltrexone

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7
Q

Neurology Pharmacology

Pentazocine

A

MOA: κ-opioid receptor agonist and μ opioid receptor antagonist

Use: Analgesia for moderate to severe pain

Adverse Effects: Can cause opioid withdrawal symptoms if patient is also taking full opioid antagonist

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8
Q

Neurology Pharmacology

Butorphanol

A

MOA: κ-opioid receptor agonist and μ-opioid receptor partial agonist; produces analgesia.

Use: Severe pain. Causes less respiratory depression than full opioid agonists.

Adverse Effects: Can cause opioid withdrawal symptoms if patient is also taking full opioid antagonist. Overdose not reversed easily with naloxone.

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9
Q

Neurology Pharmacology

Tramadol

A

MOA: Very weak opioid agonist; also inhibits 5-HT and norepinephrine reuptake (works on multiple neurotransmitters)

Use: Chronic pain

Adverse Effects: Similar to opioids. Decrease seizure threshold. Serotonin syndrome.

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10
Q

Neurology Pharmacology

Ethosuximide

A

MOA: Blocks thalamic T-type Ca2+ channels.

Use: 1st line for acute absence seizures

Adverse Effects: GI, fatigue, headache, urticaria, Stevens-Johnson syndrome

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11
Q

Neurology Pharmacology

Benzodiazepenes

A

MOA: ↑ GABAa action

Use: 1st line for status epilepticus

Adverse Effects: Sedation, tolerance, dependence, respiratory depression

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12
Q

Neurology Pharmacology

Phenobarbital

A

MOA: ↑ GABAa action

Use: Simple and complex partial seizures, and tonic-clonic seizures

Adverse Effects: Sedation, tolerance, dependence, induction of cytochrome P-450, cardiorespiratory depression.

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13
Q

Neurology Pharmacology

Phenytoin, fosphenytoin

A

MOA: Blocks Na+ channels; zero-order kinetics.

Use: 1st line for prophylaxis of status epilepticus; 1st line for acute tonic-clonic seizures. Simple and complex partial seizures.

Adverse Effects:
Neurologic: nystagmus, diplopia, ataxia, sedation, peripheral neuropathy.
Dermatologic: hirsutism, Stevens-Johnson syndrome, gingival hyperplasia, DRESS syndrome
Musculoskeletal: Osteopenia, SL-like syndrome
Hematologic: megaloblastic anemia.
Reproductive: Teratogenic (fetal hydantoin syndrome)
Other: Cytochrome P-450 induction

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14
Q

Neurology Pharmacology

Carbamazepine

A

MOA: Blocks Na+ channels.

Use: 1st line for simple and complex partial seizures. Tonic-clonic seizures.

Adverse Effects: Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemias), liver toxicity, teratogenesis, induction of cytochrome p-450, SIADH, Stevens-Johnson syndrome.

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15
Q

Neurology Pharmacology

Valproic acid

A

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

Use: 1st line for tonic-clonic seizures. Simple & complex partial and absence seizures.

Adverse Effects: GI distress, rare but fatal hepatotoxicity (measure LFTs), pancreatitis, neural tube defects, tremor, weight gain, contraindicated in pregnancy.

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16
Q

Neurology Pharmacology

Vigabatrin

A

MOA: ↑ GABA by irreversibly inhibiting GABA transaminase

Use: Simple and complex partial seizures

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17
Q

Neurology Pharmacology

Gabapentin

A

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

Use: Simple and complex partial seizures.

Adverse Effects: Sedation, ataxia

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18
Q

Neurology Pharmacology

Topiramate

A

MOA: Blocks Na+ channels, ↑ GABA action

Use: Simple and complex partial seizures; tonic-clonic seizures.

Adverse Effects: Sedation, mental dulling, kidney stones, weight loss

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19
Q

Neurology Pharmacology

Lamotrigine

A

MOA: Blocks voltage-gated Na+ channels

Use: Simple and complex partial seizures; tonic-clonic seizures; absence seizures.

Adverse Effects: Stevens-Johnson syndrome (must be titrated slowly)

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20
Q

Neurology Pharmacology

Levetiracetam

A

MOA: Unknown; may modulate GABA and glutamate release

Use: Simple and complex partial seizures; tonic-clonic seizures

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21
Q

Neurology Pharmacology

Tiagabine

A

MOA: ↑ GABA by inhibiting reuptake

Use: Simple and complex partial seizures

22
Q

Neurology Pharmacology

Phenobarbital, pentobarbital, thiopental, secobarbital

A

MOA: Facilitate GABAa action by ↑ duration of Cl- channel opening, thus ↓ neuron firing. Contraindicated in porphyria

Use: Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

Adverse Effects: Respiratory and CV depression; CNS depression; dependence; drug interactions (induces cytochrome P-450)

Overdose Treatment: Supportive (assist respiration and maintain BP)

23
Q

Neurology Pharmacology

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam

A

MOA: Facilitate GABAa action by ↑ frequency of Cl- channel opening, ↓ REM sleep.

Use: Anxiety, spasticity, status epilepticus, eclampsia, detoxification, night terrors, sleepwalking, general anesthetic, hypnotic.

Adverse Effects: Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.

Overdose Treatment: Flumazenil

24
Q

Neurology Pharmacology

Zolpidem, Zaleplon, eszopiclone

A

MOA: Act via the BZ1 subtype of GABA receptor.

Use: Insomnia

Adverse Effects: Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. ↓ dependence risk than benzodiazepines.

25
Q

Neurology Pharmacology

Desflurane, halothane, enflurane, isoflurane sevoflurane, methoxyflurane, N2O

A

MOA: Inhaled anesthetics. Unknown.

Effects: Myocardial depression, respiratory depression, nausea/emesis, ↑ cerebral blood flow

Adverse Effects: Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in a body cavity (N2O), malignant hyperthermia

26
Q

Neurology Pharmacology

Thiopental (IV anesthetic)

A

High potency, high lipid solubility, rapid entry into brain.

Use: Induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue and fat. ↓ cerebral blood flow.

27
Q

Neurology Pharmacology

Midazolam (IV anesthetic)

A

Use: Endoscopy. Used adjunctively with gaseous anesthetics and narcotics.

Adverse Effects: May cause severe postoperative respiratory depression, ↓ BP, anterograde amnesia

28
Q

Neurology Pharmacology

Arylcyclohexylamines (IV anesthetic)

A

MOA: PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. ↑ cerebral blood flow.

Adverse Effects: Disorientation, hallucination, bad dreams.

29
Q

Neurology Pharmacology

Propofol (IV anesthetic)

A

Use: Sedation in the ICU, rapid anesthesia induction, short procedures. Potentiates GABAa

30
Q

Neurology Pharmacology

Opioids (IV anesthetics)

A

Morphine, fentanyl used with other CNS depressants during general anesthesia.

31
Q

Neurology Pharmacology

Local anesthetics (Esters: procaine, cocaine, tetracaine, benzocaine; Amides: lidocaine, mepivacaine, bupivacaine)

A

MOA: Block Na+ channels by binding to specific receptors on inner portion of channel. Most effective in rapidly firing neurons. Can be given with vasoconstrictors to enhance local action - ↓ bleeding, ↑ anesthesia by ↓ systemic concentration.

Pharmacodynamics: In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively → need more anesthetic.

Use: Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.

Adverse Effects: CNS excitation, severe CV toxicity (bupivicaine), hypertension, hypotension, arrhythmias (cocaine), methemoglobinemia (benzocaine)

32
Q

Neurology Pharmacology

Order of nerve blockade

A

Small-diameter fibers > large-diameter

Myelinated fibers > unmyelinated fibers.

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

33
Q

Neurology Pharmacology

Order of loss of sensation

A

1) pain
2) temperature
3) touch
4) pressure

34
Q

Neurology Pharmacology

Succinylcholine

A

MOA: Depolarizing neuromuscular blocker. Strong ACh receptor agonist; produces sustained depolarization and prevents muscle relaxation.

Use: Muscle paralysis in surgery or mechanical ventilation.

Adverse Effects: hypercalcemia, hyperkalemia, malignant hyperthermia

Reversal of blockade:
Phase I (prolonged depolarization) - no antidote. Block potentiated by cholinesterase inhibitors. 
Phase II (repolarized but blocked; ACh receptors are available, but desensitized) - may be reversed with cholinesterase inhibitors.
35
Q

Neurology Pharmacology

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

A

MOA: Nondepolarizing neuromuscular blocker. Competitive antagonist, compete with ACh for receptors.

Reversal of blockade: Neostigmine (must be given with atropine to prevent muscarinic effects), edrophonium and other cholinesterase inhibitors

36
Q

Neurology Pharmacology

Dantrolene

A

MOA: Prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle by binding to the ryanodine receptor.

Use: malignant hyperthermia and neuroleptic malignant syndrome.

37
Q

Neurology Pharmacology

Baclofen

A

MOA: Activates GABAb receptors at spinal cord level, inducing skeletal muscle relaxation.

Use: Muscle spasms

38
Q

Neurology Pharmacology

Cyclobenzaprine

A

MOA: Centrally acting skeletal muscle relaxant. Structurally related to TCAs, similar to anticholinergic side effects.

Use: Muscle spasms

39
Q

Neurology Pharmacology

Bromocriptine

A

MOA: Ergot dopamine agonist

Use: Parkinson disease

40
Q

Neurology Pharmacology

Pramipexole, ropinirole

A

MOA: Non-ergot dopamine agonist

Use: Parkinson disease

41
Q

Neurology Pharmacology

Amantadine

A

MOA: ↑ dopamine release and ↓ dopamine reuptake → ↑ dopamine bioavailability

Use: Parkinson disease

Toxicity: Ataxia, livedo reticularis

42
Q

Neurology Pharmacology

Levodopa/carbidopa

A

MOA: L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine. Carbidopa blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase → ↑ L-DOPA entering CNS → ↑ central L-DOPA available for conversion to dopamine

Use: Parkinson disease

Adverse Effects: Arrhythmias from ↑ peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration, akinesia between doses.

43
Q

Neurology Pharmacology

Entacapone, tolcapone

A

MOA: Prevent peripheral L-dopa degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT → ↑ L-DOPA entering CNS → ↑ central L-DOPA available for conversion to dopamine

Use: Parkinson disease

44
Q

Neurology Pharmacology

Seligiline

A

MOA: Blocks conversion of dopamine into DOPAC by selectively inhibiting MAO-B → ↑ dopamine availability

Use: Parkinson disease (adjunctive agent to L-dopa)

Adverse Effects: May enhance adverese effects of L-dopa.

45
Q

Neurology Pharmacology

Benztropine

A

MOA: Antimuscarinic

Use: Improves tremor and rigidity but has little effect on bradykinesia in Parkinson disease

46
Q

Neurology Pharmacology

Memantine

A

MOA: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)

Use: Alzheimer disease

Adverse Effects: Dizziness, confusion, hallucinations

47
Q

Neurology Pharmacology

Donepezil, galantamine, rivastigmine, tacrine

A

MOA: AChE inhibitors

Use: Alzheimer disease

Adverse Effects: Nausea, dizziness, insomnia

48
Q

Neurology Pharmacology

Tetrabenzine, reserpine

A

MOA: Inhibit vesicular monoamine transporter (VMAT) → ↓ dopamine vesicle packaging and release

Use: Huntington disease

49
Q

Neurology Pharmacology

Haloperidol

A

MOA: D2 receptor antagonist

Use: Huntington disease

50
Q

Neurology Pharmacology

Riluzole

A

MOA: Modestly ↑ survival by ↓ glutamate excitotoxicity via an unclear mechanism

Use: ALS

51
Q

Neurology Pharmacology

Sumatriptan

A

MOA: 5-HT1b1d agonist. Inhibits trigeminal nerve activation; prevent vasoactive peptide release; induce vasoconstriction.

Use: Acute migraine, cluster headache attacks.

Adverse Effects: Coronary vasospasm, mild paresthesia.

Pharmacology (17 decks)

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