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Step 1 Pharmacology > Neurology > Flashcards

Neurology Flashcards

1
Q

What do glaucoma drugs do?

A

↓ IOP via ↓ amount of aqueous humor (inhibit synthesis/secretion or ↑ drainage).

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2
Q

Glaucoma drugs (α-agonists) - What is the mechanism of Ephedrine?

A

↓ aqueous humor synthesis via vasoconstriction

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3
Q

Glaucoma drugs (α-agonists) - What are the side effects of Ephedrine?

A

Mydriasis; do not use in closed-angle glaucoma

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4
Q

Glaucoma drugs (α-agonists) - What is the mechanism of Brimonidine (α2)?

A

↓ aqueous humor synthesis

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5
Q

Glaucoma drugs (α-agonists) - What are the side effects of Brimonidine (α2)?

A

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

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6
Q 
Glaucoma drugs (β-blockers) - What is the mechanism of timolol, betaxolol, and
carteolol?
A

↓ aqueous humor synthesis

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7
Q 
Glaucoma drugs (β-blockers) - What are the side effects of timolol, betaxolol, and
carteolol?
A

No pupillary or vision changes

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8
Q

Glaucoma drugs (diuretics) - What is the mechanism of Acetazolamide?

A

↓ aqueous humor synthesis via inhibition of

carbonic anhydrase

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9
Q

Glaucoma drugs (diuretics) - What are the side effects of Acetazolamide?

A

No pupillary or vision changes

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10
Q 
Glaucoma drugs (Cholinomimetics) - What is the mechanism of Direct Cholinomimetics (pilocarpine,
carbachol)?
A

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

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11
Q 
Glaucoma drugs (Cholinomimetics) - What are the side effects of Direct Cholinomimetics (pilocarpine,
carbachol)?
A

Miosis and cyclospasm (contraction of ciliary muscle)

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12
Q

Glaucoma drugs (Cholinomimetics) - What is the mechanism of Indirect Cholinomimetics (physostigmine, echothiophate)?

A

Use pilocarpine in emergencies—very effective at opening meshwork into canal of Schlemm

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13
Q

Glaucoma drugs (Prostaglandin) - What is the mechanism of Latanoprost (PGF2α)?

A

↑ outflow of aqueous humor

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14
Q

Glaucoma drugs (Prostaglandin) - What are the side effects of Latanoprost (PGF2α)?

A

Darkens color of iris (browning)

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15
Q

What are the Opioid Analgesics?

A

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

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16
Q

What is the mechanism of Opioid Anelgesics?

A

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

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17
Q

What is the clinical use of Opioid Anelgesics?

A

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

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18
Q

What is the toxicity of Opioid Anelgesics?

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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19
Q

What is the mechanism of Butorphanol?

A

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

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20
Q

What is the clinical use of Butorphanol?

A

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

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21
Q

What is the toxicity of Butorphanol?

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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22
Q

What is the mechanism of Tramadol?

A

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

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23
Q

What is the clinical use of Tramadol?

A

Chronic pain.

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24
Q

What is the toxicity of Tramadol?

A

Similar to opioids. Decreases seizure threshold. Serotonin syndrome.

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25
Q

What is Ethosuximide used for?

A 
Simple: 
Complex: 
Tonic-Clonic: 
Absence: Yes (First line)
Status Epilepticus:
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26
Q

What are Benzodiazepines (diazepam, lorazepam) used for?

A 
Simple: 
Complex: 
Tonic-Clonic: 
Absence: 
Status Epilepticus: Yes (First line for acute)
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27
Q

What is Phenytoin used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: Yes (First line)
Absence: 
Status Epilepticus: Yes (First line for prophylaxis)
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28
Q

What is Carbamazepine used for?

A 
Simple: Yes (First line)
Complex: Yes (First line)
Tonic-Clonic: Yes (First line)
Absence: 
Status Epilepticus:
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29
Q

What is Valproic acid used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: Yes (First line)
Absence: Yes 
Status Epilepticus:
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30
Q

What is Gabapentin used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: Yes 
Absence: 
Status Epilepticus:
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31
Q

What is Phenobarbital used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: Yes 
Absence: 
Status Epilepticus:
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32
Q

What is Topiramate used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: Yes 
Absence: 
Status Epilepticus:
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33
Q

What is Lamotrigine used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: Yes 
Absence: Yes 
Status Epilepticus:
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34
Q

What is Levetiracetam used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: Yes 
Absence: 
Status Epilepticus:
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35
Q

What is Tiagabine used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: 
Absence: 
Status Epilepticus:
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36
Q

What is Vigabatrin used for?

A 
Simple: Yes 
Complex: Yes 
Tonic-Clonic: 
Absence: 
Status Epilepticus:
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37
Q

What is the mechanism of Ethosuximide?

A

Blocks thalamic T-type Ca2+ channels

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38
Q

What are the Side Effects of Ethosuximide?

A

GI, fatigue, headache, urticaria, Steven-Johnson syndrome

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39
Q

What is the mechanism of Benzodiazepines

(diazepam, lorazepam)?

A

↑ GABAA action

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40
Q

What are the Side Effects of Benzodiazepines

(diazepam, lorazepam)?

A

Sedation, tolerance, dependence, respiratory depression

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41
Q

What else are Benzodiazepines used for?

A

Eclampsia seizures (1st line is MgSO4)

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42
Q

What is the mechanism of Phenytoin?

A

↑ Na+ channel inactivation; zero-order kinetics

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43
Q

What are the Side Effects of Phenytoin?

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

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44
Q

What is an additoinal fact about Phenytoin?

A

Fosphenytoin for parenteral use

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45
Q

What is the mechanism of Carbamazepine?

A

↑ Na+ channel inactivation

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46
Q

What are the Side Effects of Carbamazepine?

A

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

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47
Q

What other condition is Carbamazepine a first line drug for?

A

Trigeminal neuralgia

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48
Q

What is the mechanism of Valproic acid?

A

↑ Na+ channel inactivation, ↑ GABA concentration

by inhibiting GABA transaminase

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49
Q

What are the Side Effects of Valproic acid?

A

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

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50
Q

What else is Valproic acid used for?

A

Myoclonic seizures, bipolar disorder

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51
Q

What is the mechanism of Gabapentin?

A

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

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52
Q

What are the Side Effects of Gabapentin?

A

Sedation, ataxia

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53
Q

What else is Gabapentin used for?

A

Peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder

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54
Q

What is the mechanism of Phenobarbital?

A

↑ GABAA action

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55
Q

What are the Side Effects of Phenobarbital?

A

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

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56
Q

When is Phenobarbital 1st line therapy?

A

For neonates

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57
Q

What is the mechanism of Topiramate?

A

Blocks Na+ channels, ↑ GABA action

58
Q

What are the Side Effects of Topiramate?

A

Sedation, mental dulling, kidney stones, weight loss

59
Q

What else is Topiramate used for?

A

Migraine prevention

60
Q

What is the mechanism of Lamotrigine?

A

Blocks voltage-gated Na+ channels

61
Q

What are the Side Effects of Lamotrigine?

A

Stevens-Johnson syndrome (must be titrated slowly)

62
Q

What is the mechanism of Levetiracetam?

A

Unknown; may modulate GABA and glutamate release

63
Q

What is the mechanism of Tiagabine?

A

↑ GABA by inhibiting re-uptake

64
Q

What is the mechanism of Vigabatrin?

A

↑ GABA by irreversibly inhibiting GABA transaminase

65
Q

What is Steven-Johnson Syndrome?

A

Prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital). Skin lesions progress to epidermal necrosis and sloughing.

66
Q

What are the barbiturates?

A

Phenobarbital, pentobarbital, thiopental, secobarbital

67
Q

What is the mechanism of barbiturates?

A

Facilitate GABAA action by ↑ duration of Cl− channel opening, thus ↓ neuron firing (barbidurates ↑ duration). Contraindicated in porphyria.

68
Q

What is the clinical use of barbiturates?

A

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

69
Q

What is the toxicity of barbiturates?

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).

70
Q

What are the Benzodiazepines?

A

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

71
Q

What is the mechanism of Benzodiazepines?

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).

Benzos, barbs, and EtOH all bind the GABAA receptor, which is a ligand-gated Cl− channel.

72
Q

What is the clinical use of Benzodiazepines?

A

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

73
Q

What is the toxicity of Benzodiazepines?

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).

74
Q

What are the Nonbenzodiazepine hypnotics?

A

Zolpidem (Ambien), Zaleplon, esZopiclone. “All ZZZs put you to sleep.”

75
Q

What is the mechanism of Nonbenzodiazepine hypnotics?

A

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

76
Q

What is the clinical use of Nonbenzodiazepine hypnotics?

A

Insomnia

77
Q

What is the toxicity of Nonbenzodiazepine hypnotics?

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.

78
Q

Anesthetics (General Principles) - What property must CNS drugs have to work?

A

CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.

79
Q

Anesthetics (General Principles) - What property do drugs that have ↓ solubility in blood have?

A

Drugs with ↓ solubility in blood = rapid induction and recovery times.

80
Q

Anesthetics (General Principles) - What property do drugs that have ↑ solubility in lipids have?

A

Drugs with ↑ solubility in lipids = ↑ potency = 1/MAC

81
Q

Anesthetics (General Principles) - What is MAC?

A

Minimal Alveolar Concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g., skin incision).

82
Q

Anesthetics (General Principles) - Give examples of drugs that have ↑ and ↓ blood and lipid solubility.

A

N2O has ↓ blood and lipid solubility, and thus fast induction and low potency.
Halothane, in contrast, has ↑ lipid and blood solubility, and thus high potency and slow induction.

83
Q

What are the inhaled anesthetics?

A

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

84
Q

What is the mechanism of inhaled anesthetics?

A

Mechanism unknown.

85
Q

What are the effects of inhaled anesthetics?

A

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

86
Q

What is the toxicity of inhaled anesthetics?

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.

87
Q

Intravenous anesthetics - What are the key features of Barbiturates?

A

Thiopental—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.

88
Q

Intravenous anesthetics - What are the key features of Benzodiazepines?

A

Midazolam 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.

89
Q

Intravenous anesthetics - What are the key features of Arylcyclohexylamines (Ketamine)?

A

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

90
Q

Intravenous anesthetics - What are the key features of Opioids?

A

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

91
Q

Intravenous anesthetics - What are the key features of Propofol?

A

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

92
Q

What are the Local Anesthetic esters?

A

Procaine, cocaine, tetracaine

93
Q

What are the Local Anesthetic amides?

A

Lidocaine, mepivacaine, bupivacaine (amides have 2 I’s in name)

94
Q

What is the mechanism of Local Anesthetics?

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.

95
Q

Why are Local Anesthetics given with vasoconstrictors (usually epinephrine)?

A

Enhance local action— ↓ bleeding, ↑ anesthesia by ↓ systemic concentration.

96
Q

What happens to Local Anesthetics in acidic tissue?

A

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

97
Q

What is the order of the nerve blockade?

A

Order of nerve blockade: small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers.
Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure.

98
Q

What is the clinical use of Local Anesthetics?

A

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

99
Q

What is the toxicity of Local Anesthetics?

A

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

100
Q

What are Neuromuscular blocking drugs used for?

A

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

101
Q

Neuromuscular blocking drugs (Depolarizing) - What are the features of Succinylcholine?

A

Strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction.

102
Q

Describe the reversal of blockade of depolarzing neuromuscular blocking drugs?

A

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)—antidote
consists of cholinesterase inhibitors.

103
Q

What are the complications of Depolarizing Neuromuscular blocking drugs?

A

Complications include hypercalcemia, hyperkalemia, and malignant hyperthermia.

104
Q

What are the nondepolarizing Neuromuscular blocking drugs and what are there features?

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium—competitive antagonists—compete with ACh for receptors.

105
Q

Describe the reversal of blockade of nondepolarizing Neuromuscular blocking drugs.

A

Reversal of blockade—neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.

106
Q

What is the mechanism of Dantrolene?

A

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

107
Q

What is the clinical use of Dantrolene?

A

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

108
Q

What is Parkinsonism due to?

A

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity.

109
Q

Parkinson disease - What are the dopamine agonists?

A

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

110
Q

Parkinson disease - What drugs ↑ dopamine?

A

Amantadine (may ↑ dopamine release); also used as an antiviral against influenza A and rubella; toxicity = ataxia
L-dopa/carbidopa (converted to dopamine in CNS)

111
Q

Parkinson disease - What drugs prevent dopamine breakdown?

A

Selegiline (selective MAO type B inhibitor); entacapone, tolcapone (COMT inhibitors — prevent L-dopa degradation → ↑ dopamine availability)

112
Q

Parkinson disease - What drugs curb excess cholinergic activity?

A

Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia)

113
Q

Parkinson disease - What do you use for essential of familial tremors?

A

β-blocker (e.g., propranolol)

114
Q

What is the mechanism of L-dopa (levodopa)/carbidopa?

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.

115
Q

What is the clinical use of L-dopa (levodopa)/carbidopa?

A

Parkinson’s disease

116
Q

What is the toxicity of L-dopa (levodopa)/carbidopa?

A

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

117
Q

What is the mechanism of Selegiline?

A

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

118
Q

What is the clinical use of Selegiline?

A

Adjunctive agent to L-dopa in treatment of Parkinson disease.

119
Q

What is the toxicity of Selegiline?

A

May enhance adverse effects of L-dopa.

120
Q

Alzheimer drugs - What is the mechanism of Memantine?

A

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

121
Q

What is the clinical use of Memantine?

A

Dizziness, confusion, hallucinations.

122
Q

Alzheimer drugs - What is the mechanism of donepezil, galantamine, and rivastigmine?

A

AChE inhibitors.

123
Q

What is the clinical use of Memantine?

A

Nausea, dizziness, insomnia.

124
Q

What are the neurotransmitter changes in Huntington’s disease?

A

↓ GABA, ↓ ACh, ↑ dopamine

125
Q

Huntington’s disease - What is the mechanism of tetrabenazine and reserpine?

A

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

126
Q

Huntington’s disease - What is the mechanism of Haloperidol?

A

Dopamine receptor antagonist

127
Q

What is the mechanism of Sumatriptan?

A

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

128
Q

What is the clinical use of Sumatriptan?

A

Acute migraine, cluster headache attacks

129
Q

What is the toxicity of Sumatriptan?

A

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

130
Q

What drug is used to treat bedwetting (sleep enuresis)?

A

Oral desmopressin acetate (DDAVP), which mimics ADH; Benzodiazepines are useful for night terrors and sleepwalking.

131
Q

What drug is useful for night terrors and sleepwalking?

A

Benzodiazepines

132
Q

What do you treat Essential termor (postural tremor) with?

A

β-blockers, primidone

133
Q

What do you treat Ischemic stroke with?

A

tPA (if within 3-4.5 hours of onset and no hemorrhage/risk of hemorrhage). Reduce risk with medical therapy (e.g., aspirin, clopidogrel); optimum control of blood pressure, blood surgars and lipids; and treat conditions that ↑ risk (e.g., atrial fibrillation).

134
Q

What drug helps treat Amyotrophic lateral scleorsis (ALS)?

A

Riluzole treatment modestly ↑ survival by ↓ presynaptic glutamate release.

135
Q

What drug is used to treat Facial nerve palsy?

A

Corticosteroids

136
Q

What is used to treat Diabetic retinopathy?

A

Peripheral retinal photocoagulation, anti-VEGF injections

137
Q

What is used to treat Age-related macular degeneration?

A

Anti-vascular endothelial growth facto injections (anti-VEGF) or laser

138
Q

What is used to treat Multiple sclerosis?

A

β-interferon, immunosuppression, natalizumab. Symptomatic treatment for neurogenic bladder (catherization, muscarinic antagonists), spasticity (baclofen, GABA receptor agonist), and pain (opioids)

139
Q

What drug is associated with a ↑ risk of Progressive multifocal leukoencephalopathy?

A

Natalizumab

140
Q

What is the treatment for Cluster headaches?

A

Inhaled O2, sumatriptan

141
Q

What is the treatment for Tension headaches?

A

Analgesics, NSAIDs, acetaminophen; amitriptyline for chronic pain

142
Q

What is the treatment for Migraine headaches?

A

Abortive therapies (e.g., triptans, NSAIDs) and prophylactic (propranolol, topiramate, calcium channel blockers, amitriptyline)

Step 1 Pharmacology (18 decks)

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