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Pharmacology > FA Neurology > Flashcards

FA Neurology Flashcards

1
Q

Glaucoma Drugs

A

α-agonists (epinephrine, brimonidine), β-blockers (timolol, betaxolol, certeolol), diuretics (acetazolamide), cholinomimetics (direct: pilocarpine, carbachol; indirect: physostigmine, echothiophate), Latanoprost (PGF2α)

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2
Q

Epinephrine Mechanism [glaucoma]

A

↓ aqueous humor synthesis via vasoconstriction

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3
Q

Epinephrine Side Effects [glaucoma]

A

Mydriasis; do not use in closed-angle glaucoma

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4
Q

Brimonidine (α2) Mechanism [glaucoma]

A

↓ aqueous humor synthesis

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5
Q

Brimonidine (α2) Side Effects [glaucoma]

A

Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus

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6
Q

Timolol Mechanism [glaucoma]

A

↓ aqueous humor synthesis

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7
Q

Betaxolol Mechanism [glaucoma]

A

↓ aqueous humor synthesis

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8
Q

Carteolol Mechanism [glaucoma]

A

↓ aqueous humor synthesis

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9
Q

Timolol Side Effects [glaucoma]

A

No pupillary or vision changes

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10
Q

Betaxolol Side Effects [glaucoma]

A

No pupillary or vision changes

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11
Q

Carteolol Side Effects [glaucoma]

A

No pupillary or vision changes

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12
Q

Acetazolamide Mechanism [glaucoma]

A

↓ aqueous humor synthesis via inhibition of carbonic anhydrase

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13
Q

Acetazolamide Side Effects [glaucoma]

A

No pupillary or vision changes

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14
Q

Pilocarpine Mechanism [glaucoma]

A

Direct cholinomimetic. ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

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15
Q

Carbachol Mechanism [glaucoma]

A

Direct cholinomimetic. ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

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16
Q

Pilocarpine Side Effects [glaucoma]

A

Miosis and cyclospasm (contraction of ciliary muscle)

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17
Q

Carbachol Side Effects [glaucoma]

A

Miosis and cyclospasm (contraction of ciliary muscle)

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18
Q

Physostigmine Mechanism [glaucoma]

A

Indirect cholinomimetic. ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

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19
Q

Physostigmine Side effects [glaucoma]

A

Miosis and cyclospasm (contraction of ciliary muscle)

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20
Q

Echothiophate Mechanism [glaucoma]

A

Indirect cholinomimetic. ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

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21
Q

Echothiophate Side Effects [glaucoma]

A

Miosis and cyclospasm (contraction of ciliary muscle)

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22
Q

Latanoprost (PGF2α) mechanism [glaucoma]

A

Prostaglandin; ↑ outflow of aqueous humor

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23
Q

Latanoprost (PGF2α) side effects [glaucoma]

A

Darkens color of iris (browning)

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24
Q

Opioid Analgesics

A

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

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25
Q

Opiod Analgesic Mechanism

A

Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission – open K+ channles, close Ca2+ channels → ↓ synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.

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26
Q

Opiod Analgesic Use

A

Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone)

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27
Q

Opioid Analgesic Toxicity

A

Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

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28
Q

Butorphanol Mechanism

A

Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia.

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29
Q

Butorphanol Use

A

Severe pain (migraine, labor, etc.). Causes less respiratory depression than full opioid agonists.

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30
Q

Butorphanol Toxicity

A

Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors). Overdose not easily reversed with naloxone.

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31
Q

Tramadol mechanism

A

Very weak opioid agonist; also inhibits serotonin and norepinephrine reuptake (works on multiple neurotransmitters – “tram it all” with tramadol).

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32
Q

Tramadol Use

A

Chronic pain.

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33
Q

Tramadol Toxicity

A

Similar to opioids. Decreases seizure threshold. Serotonin syndrome.

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34
Q

Ethosuxamide Use [Seizures]

A

1st line absence seizures

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35
Q

Benzodiazepine (diazepam, lorazepam) Use [Seizures]

A

1st line for acute status epilepticus. Also for eclampsia seizures (1st line is MgSO4)

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36
Q

Phenytoin Use [Seizures]

A

Simple and complex partial (focal) seizures. 1st line tonic-clonic seizures. 1st line prophylaxis status epilepticus. Fosphenytoin for parenteral use.

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37
Q

Carbamazepine Use [Seizures]

A

1st line simple and complex partial (focal) seizures. 1st line tonic-clonic seizures. 1st line for trigeminal neuralgia.

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38
Q

Valproic Acid Use [Seizures]

A

Simple and complex partial (focal) seizures, absence seizures. 1st line tonic-clonic seizures. Also used for myoclonic seizures, bipolar disorder.

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39
Q

Gabapentin Use [Seizures]

A

Simple and complex partial (focal) seizures, tonic-clonic seizures. Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder.

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40
Q

Phenobarbital Use [Seizures]

A

Simple and complex partial (focal) seizures, tonic-clonic seizures. 1st line in neonates.

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41
Q

Topiramate Use [Seizures]

A

Simple and complex partial (focal) seizures, tonic-clonic seizures. Also used for migraine prevention.

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42
Q

Lamotrigine Use [Seizures]

A

Simple and complex partial (focal), tonic-clonic, and absence seizures.

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43
Q

Levetiracetam Use [Seizures]

A

Simple and complex partial (focal) seizures, tonic-clonic seizures.

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44
Q

Tiagabine Use [Seizures]

A

Simple and complex partial (focal) seizures.

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45
Q

Vigabatrin Use [Seizures]

A

Simple and complex partial (focal) seizures.

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46
Q

Ethosuxamide Mechanism [Seizures]

A

Blocks thalamic T-type Ca2+ channels

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47
Q

Benzodiazepine (diazepam, lorazepam) Mechanism [Seizures]

A

↑ GABAₐ action

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48
Q

Phenytoin Mechanism [Seizures]

A

↑ Na+ channel inactivation; zero-order kinetics

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49
Q

Carbamazepine Mechanism [Seizures]

A

↑ Na+ channel inactivation

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50
Q

Valproic Acid Mechanism [Seizures]

A

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

51
Q

Gabapentin Mechanism [Seizures]

A

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

52
Q

Phenobarbital Mechanism [Seizures]

A

↑ GABAₐ action

53
Q

Topiramine Mechanism [Seizures]

A

Blocks Na+ channels, ↑ GABA action

54
Q

Lamotrigine Mechanism [Seizures]

A

Blocks voltage-gated Na+ channels

55
Q

Levetiracetam Mechanism [Seizures]

A

Unknown; may modulate GABA and glutamate release

56
Q

Tiagabine Mechanism [Seizures]

A

↑ GABA by inhibiting re-uptake

57
Q

Vigabatrin Mechanism [Seizures]

A

↑ GABA by irreversibly inhibiting GABA transaminase

58
Q

Ethosuxamide Side Effects [Seizures]

A

GI, fatigue, headache, urticaria, Stevens-Johnson syndrome. EFGHIJ - Ethosuxamide causes Fatigue, GI distress, Headache, Itching, and Stevens-Johnson syndrome

59
Q

Benzodiazepine (diazepam, lorazepam) Side Effects [Seizures]

A

Sedation, tolerance, dependence, respiratory depression

60
Q

Phenytoin Side Effects [Seizures]

A

Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome), SLE-like syndrome, induction of cytochrome P-450, lymphadenopathy, Stevens-Johnson syndrome, osteopenia

61
Q

Carbamazepine Side Effects [Seizures]

A

Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450, SIADH, Stevens-Johnson syndrome

62
Q

Valproic Acid Side Effects [Seizures]

A

GI, distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated in pregnancy

63
Q

Gabapentin Side Effects [Seizures]

A

Sedation, ataxia

64
Q

Phenobarbital Side Effects [Seizures]

A

Sedation, tolerance, dependence, induction of cytochrome P-450, cardiorespiratory depression

65
Q

Topiramate Side Effects [Seizures]

A

Sedation, mental dulling, kidney stones, weight loss

66
Q

Lamotrigine Side Effects [Seizures]

A

Stevens-Johnson syndrome (must be titrated slowly)

67
Q

Barbiturates

A

Phenobarbital, pentobarbital, thiopental, secobarbital

68
Q

Barbiturate Mechanism

A

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

69
Q

Barbiturate Use

A

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

70
Q

Barbiturate Toxicity

A

Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence; drug interactions (induces cytochrome P-450). Overdose treatment is supportive (assist respiration and maintain BP).

71
Q

Benzodiazepines

A

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

72
Q

Benzodiazepine Mechanism

A

Facilitate GABAₐ action by ↑ frequency of Cl- channel opening. ↓ REM sleep. Most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting → higher addictive potential).

73
Q

Benzodiazepine Use

A

Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxant), hypnotic (insomnia).

74
Q

Benzodiazepine Toxicity

A

Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor).

75
Q

Nonbenzodiazepine Hypnotics

A

Zolpidem (Ambien), Zaleplon, Eszopiclone

76
Q

Nonbenzodiazepine Hypnotic Mechanism

A

Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil.

77
Q

Nonbenzodiazepine Hypnotic Use

A

Insomnia

78
Q

Nonbenzodiazepine Hypnotic Toxicity

A

Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. ↓ dependence risk than benzodiazepines.

79
Q

Inhaled Anesthetics

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.

80
Q

Inhaled Anesthetic Mechanism

A

Mechanism unknown.

81
Q

Inhaled Anesthetic Effects

A

Myocardial depression, respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral metabolic demand).

82
Q

Inhaled Anesthetic Toxicity

A

Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in a body cavity (nitrous oxide). Can cause malignant hyperthermia – rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene.

83
Q

IV Anesthetics

A

Barbiturates (thiopental), Benzodiazepines (midazolam), Arylcyclohexylamines (ketamine), Opioids (morphine, fentanyl), Propofol

84
Q

Thiopental [IV Anesthetic]

A

High potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (i.e. skeletal muscle) and fat. ↓ cerebral blood flow.

85
Q

Midazolam [IV Anesthetic]

A

Most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, ↓ BP (treat overdose with flumazenil), and anterograde amnesia.

86
Q

Arylcyclohexylamines (ketamine) [IV Anesthetic]

A

PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. ↑ cerebral blood flow.

87
Q

Opioids [IV Anesthetic]

A

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

88
Q

Propofol [IV Anesthetic]

A

Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less postoperative nausea than thiopental. Potentiates GABAₐ.

89
Q

Local Anesthetics

A

Esters - procaine, cocaine, tetracaine.

Amides - lidocaine, mepivacaine, bupivacaine.

90
Q

Local Anesthetic Mechanism

A

Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.

91
Q

Local Anesthetic Principle

A

Can be given with vasoconstrictors (usually epi) to enhance local action – ↓ bleeding, ↑ anesthesia by ↓ systemic concentration. In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effective → need more anesthetic.
Order of nerve blockade: small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated > small unmyelinated > large myelinated > large unmyelinated fibers. Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure.

92
Q

Local Anesthetic Use

A

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

93
Q

Local Anesthetic Toxicity

A

CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).

94
Q

Neuromuscular Blocking Drugs

A

Depolarizing - Succinylcholine

Nondepolarizing - Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

95
Q

Neuromuscular Blocking Drug Use

A

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

96
Q

Depolarizing Neuromuscular Blocking Drug Mechanism

A

Succinylcholine - strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction.
Reversal of blockade:
Phase I (prolonged depolarization) - no antidote. Block potentiated by cholinesterase inhibitors.
Phase II (repolarized but blocked; ACh receptors available but desensitized) - antidote consists of cholinesterase inhibitors.

97
Q

Depolarizing Neuromuscular Blocking Drug Toxicity

A

Hypercalcemia, hyperkalemia, malignant hyperthermia.

98
Q

Nondepolarizing Neuromuscular Blocking Drug Mechanism

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium - competitive antagonists - compete with ACh for receptors.
Reversal of blockade:
Neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.

99
Q

Dantrolene Mechanism

A

Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.

100
Q

Clinical Use

A

Used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).

101
Q

Parkinson Disease Drugs

A

Dopamine agonists (bromocriptine, pramipexole, ropinirole), ↑ dopamine (amantadine, L-dopa/carbidopa), prevent dopamine breakdown (selegiline, entecapone, tolcapone), curb cholinergic activity (benztropine)

102
Q

Dopamine agonists

A

Bromocriptine (ergot), pramipexole, ropinirole (non-ergot); non-ergots are preferred

103
Q

Amantadine Use

A

Parkinsonism - may ↑ dopamine release; also used as an antiviral against influenza A and rubella

104
Q

Amantadine Toxicity

A

Ataxia

105
Q

L-dopa/Carbidopa Mechanism

A

↑ level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine. Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa to ↑ the bioavailability of L-dopa in the brain and to limit peripheral side effects.

106
Q

L-dopa/Carbidopa Use

A

Parkinson disease

107
Q

Selegiline Mechanism

A

Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby ↑ the availability of dopamine

108
Q

Selegiline Use

A

Adjunctive agent to L-dopa in treatment of Parkinson disease

109
Q

Entecapone, Tolcapone Mechanism

A

COMT inhibitors - prevent L-dopa degradation → ↑ dopamine availability

110
Q

Benztropine Use

A

Antimuscarinic used to improve tremor and rigidity in Parkinson disease. Has little effect on bradykinesia.

111
Q

L-dopa/Carbidopa Toxicity

A

Arrhythmias from ↑ peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (“on-off” phenomenon), akinesia between doses.

112
Q

Selegiline Toxicity

A

May enhance adverse effects of L-dopa

113
Q

Alzheimer Drugs

A

Memantine, donepezil, galantamine, rivastigmine

114
Q

Memantine Mechanism

A

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

115
Q

Memantine Toxicity

A

Dizziness, confusion, hallucinations

116
Q

Donepezil, Galantamine, Rivastigmine Mechanism

A

AChE inhibitor

117
Q

Donepezil, Galantamine, Rivastigmine Toxicity

A

Nausea, dizziness, insomnia

118
Q

Huntington Drugs

A

Tetrabenazine, reserpine, haloperidol

119
Q

Tetrabenazine, Reserpine Mechanism [Huntington Disease]

A

Inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.

120
Q

Haloperidol Mechanism [Huntington Disease]

A

Dopamine receptor agonist

121
Q

Sumatriptan Mechanism

A

5-HT1B/1D agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half-life < 2 hours.

122
Q

Sumatriptan Use

A

Acute migraines, cluster headache attacks

123
Q

Sumatriptan Toxicity

A

Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling.

Pharmacology (14 decks)

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