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USMLE1 - Neurology > Neuro Pharm > Flashcards

Neuro Pharm Flashcards

32
Q

Epinephrine for eye. Class of drug? Mechanism? SE’s?

A

alpha-agonist. Decreases aqueous humor synthesis due to vasoconstriction. SE: mydriasis, stinging; do not use in closed-angle glaucoma.

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32
Q

Brimonidine. Class of drug? Mechanism? SE’s?

A

alpha-agonist. Decreased aqueous humor synthesis. SE: no pupillary or vision changes.

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33
Q

Timolol, betaxolol, carteolol Class of drug? Mechanism? SE’s?

A

beta-blockers. Decrease aqueous humor secretion SE: no pupillary or vision changes.

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33
Q

Acetazolamide Class of drug? Mechanism? SE’s?

A

Diuretic. Decrease aqueous humor secretion due to decreased HCO3- (via inhibition of carbonic anhydrase) SE: no pupillary or vision changes.

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34
Q

Pilocarpine, carbachol, physostigmine, echothiophate Class of drug? Mechanism? SE’s?

A

Cholinomimetics. Direct (pilocarpine, carbachol) and Indirect (physostigmine, echotiophate). Increase outflow of aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies; very effective at opening canal of Schlemm. SE: Miosis, cyclospasm.

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34
Q

Latanoprost (PGF-2alpha) Class of drug? Mechanism? SE’s?

A

Prostaglandin. Increases outflow of aqueous humor. SE: darkens color of iris (browning).

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35
Q

Opioid analgesics (7)

A

Morphine Fentanyl Codeine Heroin Methadone Meperidine Dextromethorphan

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35
Q

Mechanism of opioid analgesics (morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan, diphenoxylate)

A

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

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36
Q

Clinical toxicity of opioid analgesics

A

Pain, acute pulmonary edema
dextromethorphan: cough suppression
loperamide and diphenoxylate: diarrhea
methadone: addicts maintenance program

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36
Q

Toxicity of opioid analgesics

A

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

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37
Q

Mechanism of butorphanol

A

Partial agonist at opioid mu receptors, agonst at kappa receptors.

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37
Q

Clinical use of butorphanol

A

Pain; causes less respiratory depression than full agonists.

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38
Q

Toxicity of butorphanol

A

Causes withdrawal if on full agonist.

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38
Q

Mechanism of tramadol

A

Very weak opioid agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters – “tram it all “ in).

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39
Q

Clinical use of tramadol

A

Chronic pain.

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39
Q

Toxicity of tramadol

A

Similar to opioids. Decreases seizure threshold.

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40
Q

Phenytoin. Mechanism and Uses.

A 
Used in partial seizures (simple and complex). 1st line drug for Tonic-clonic seizures. 1st line drug for prophylaxis of status seizures. Mechanism: use-dependent blockade of Na+ channel; increase refractory period; inhibition of glutamate release from excitatory presynpatic neuron.
 Also class IB antiarrhythmic (shorten AP)

Fosphenytoin for parenteral use.

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40
Q

Used in partial seizures (simple and complex). 1st line drug for Tonic-clonic seizures. 1st line drug for prophylaxis of status seizures. Mechanism: increased Na+ channel inactivation. What epilepsy drug does this describe?

A

Phenytoin

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41
Q

Carbamazepine. Mechanism and Uses.

A

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. Mechanism: increases Na+ channel inactivation. *Also 1st line drug for trigemnial neuralgia.

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41
Q

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. Mechanism: increases Na+ channel inactivation. *Also 1st line drug for trigemnial neuralgia. What epilepsy drug does this describe?

A

Carbamezepine

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42
Q

Lamotrigine. Mechanisms and Uses.

A

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks VG-Na+ channels.

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42
Q

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks VG-Na+ channels. What epilepsy drug does this describe?

A

Lamotrigine

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43
Q

Gabapentin. Mechanisms and Uses.

A

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA release. *Also used for peripheral neuropathy.

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43
Q

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA release. *Also used for peripheral neuropathy. What epilepsy drug does this describe?

A

Gabapentin

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44
Q

Topiramate. Mechanisms and Uses.

A

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks Na+ channels, increases GABA action;

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44
Q

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks Na+ channels, increases GABA action What epilepsy drug does this describe?

A

Topiramate

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45
Q

Phenobarbital. Mechanisms and Uses.

A

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA-A action. *1st line in pregnant women, children.

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45
Q

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA-A action. *1st line in pregnant women, children. What epilepsy drug does this describe?

A

Phenobarbital

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46
Q

Valproic Acid. Mechanisms and Uses

A

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. May also be used in absence seizures. Mechanism: increases Na+ channel inactivation, increases GABA concentration. *Also used for myoclonic seizures.

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46
Q

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. May also be used in absence seizures. Mechanism: increases Na+ channel inactivation, increases GABA concentration. *Also used for myoclonic seizures. What epilepsy drug does this describe?

A

Valproic acid

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47
Q

Ethosuximide. Mechanisms and Uses

A

1st line drug for absence seizures. Mechanism: blocks thalamic T-type Ca2+ channels.

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47
Q

1st line drug for absence seizures. Mechanism: blocks thalamic T-type Ca2+ channels. What epilepsy drug does this describe?

A

Ethosuximide

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48
Q

Benzodiazepines (specifically diazepam or lorazepam). Mechanism and Uses.

A

1st line for acute status seizures. Mechanism: increase GABA-A action. *Also used for seizures of eclampsia (1st line to prevent seizures of eclampsia is MgSO4)

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48
Q

1st line for acute status seizures. Mechanism: increase GABA-A action. *Also used for seizures of eclampsia (1st line to prevent seizures of eclampsi is MgSO4) What epilepsy drug does this describe?

A

Benzodiazepines (diazepam or lorazepam)

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49
Q

Benzodiazepines (diazepam or lorazepam). Toxicity

A

Sedation Tolerance Dependence

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49
Q

Carbamazepine. Toxicity

A

Diplopia Ataxia Blood dyscrasias (agranulocytosis, aplastic anemia) Liver toxicity Teratogenesis Induction of cytochrome P-450, SIADH, Stevens-Johnson syndrome

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50
Q

Ethosuximide. Toxicity

A

GI distress Fatigue Headache Urticaria Stevens-Johnson syndrome (“EFGH = E thosuximide, F atigue, G I, H eadache”)

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50
Q

Stevens-Johnsons syndrome. What is it and which epileptic drugs?

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.
Carbamazepine, Ethosuximide, Lamotrigine

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51
Q

Phenobarbital. Toxicity

A

Sedation Tolerance Dependence Induction of cytochrome P-450

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51
Q

Phenytoin. Toxicity

A

Nystagmus Diplopia Ataxia Sedation Teratogenesis (fetal hydantoin syndrome) SLE-like syndrome Induction of cytochrome P-450.
Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decreased folate absorption).

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52
Q

Valproic Acid. Toxicity

A

GI distress, rare but fatal hepatotoxicity (measure LFTs) Neural tube defects in fetus (spina bifida) Tremor Weight gain. Contraindicated in pregnancy.

52
Q

Lamotrigine. Toxicity

A

Stevens-Johnson syndrome

53
Q

Gabapentin. Toxicity

A

Sedation Ataxia

53
Q

Topiramate. Toxicity

A

Sedation Mental dulling Kidney stones Weight loss

54
Q

Clinical use of phenytoin

A

Tonic-clonic seizures. Also a class IB antiarrhythmic.

54
Q

Toxicity of phenytoin

A

Nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of cytochrome P-450. Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decreased folate absorption). Teratogenic (fetal hydantoin syndrome).

54
Q

Phenobarbital, Pentobarbital, Thiopental, Secobarbital. Mechanisms.

A

Facilitate GABA-A action by increasing duration of Cl- channel opening, thus decreasing neuron firing. (“BarbiDURAT e [increased DURAT ion]”)

55
Q

Phenobarbital, Pentobarbital, Thiopental, Secobarbital. Clinical use.

A

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

55
Q

Phenobarbital, Pentobarbital, Thiopental, Secobarbital. Mechanisms. Toxicity

A

Dependence, additive CNS depression effects w/ EtOH, respiratory or CV depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytochrome P-450).
Tx overdose w/ Sx managment (assist respiration, increase BP) Contraindicated in pregnancy.

56
Q

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

A

Benzodiazepines. Facilitate GABA-A action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half-lives and active metabolites. (“FRE enzodiazepines [increased FRE quency]”)

56
Q

Short acting benzodiazepines

A

TOM thumb T riazolam O xazepam M idazolam. Highest addictive potential.

57
Q

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

A

Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially EtOH withdrawal - DTs), night terrors, sleep walking, general anesthetics (amnesia, muscle relaxation), hypnotic (insomnia)

57
Q

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

A

Dependence, additive CNS depression effects w/ EtOH. Less risk of respiratory depression and coma than w/ barbiturates.
Tx overdose w/ flumazenil (competitive antagonist at GABA receptor)

58
Q

General principles of anesthetics: CNS drugs must be…?

A

CNS drugs must be lipid soluble (cross the BBB) or be actively transported.

58
Q

General principles of anesthetics: Solubility and drug effect?

A

Drugs with low solubility in blood = rapid induction and recovery times. Drugs with high solubility in lipids = high potency = 1 / MAC (where MAC = Minimum Alveolar Concentration at which 50% of the population is anesthetized. Decreases w/ age). e.g., N2O has low blood and lipid solubility, and thus fast induction and low potency. Halothane, in contrast, has high lipid and blood solubility, and thus high potency and slow induction.

59
Q

Inhaled anesthetics (6)

A

all “ane” except NO
Halothane Enflurane Isoflurane Sevoflurane Methoxyflurane Nitrous oxide

59
Q

Inhaled anesthetics (haloethane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide). Mechanisms.

A

Unknown!

60
Q

Effects of inhaled anesthetics (haloethane, enflurance, isoflurane, sevoflurane, methoxyflurane, NO)

A

Myocardial depression Respiratory depression Nausea/emesis Increased cerebral blood flow (decreased cerebral metabolic demand)

60
Q

Toxicity of inhaled anesthetics

A

Hepatoxicity (halothane) Nephrotoxicity (methoxyflurane) Proconvulsant (enflurane) Malignant hyperthermia (rare) Expansion of trapped gas (nitrous oxide)

61
Q

IV anesthetics (list)

A

B arbiturates B enzodiazepines Arylcyclohexylamins (K etamine) Opiates Propofol (“BB K ing on OPIATES POPO ses FOOL ishly”)

61
Q

Barbiturates (as IV anesthetics). Which one, characteristics, cerebral blood flow.

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 to tissue (i.e. skeletal muscle) and fat. Decreased cerebral blood flow.

62
Q

Benzodiazepines (as IV anesthetics). Which one, adjunctive with, side effects. treatment of overdose?

A

Midazolam most common drug used for endoscopy; used adjuctively w/ gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decrease BP (Tx overdose w/ flumazenil), and amnesia.

63
Q

Arylcyclohexamines (Ketamine) – as IV anesthetics. Mechanism. Side effects. Cerebral blood flow.

A

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

64
Q

Opiates (as IV anesthetics). Which one.

A

Morphine, fentanyl used w/ other CNS depressants during general anesthesia.

65
Q

Propofol (as an IV anesthetic). Used for. Mechanism

A

Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental. Potentiates GABA-A.

66
Q

Local anesthetics (list, 2 types (3, 3))

A

Esters: Procaine, cocaine, tetracain; Amides: lIdocaIne, mepIvacaIne, bupIvacaIne (“amI des have 2 I ‘s in their names)

67
Q

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 effecctive in rapidly firing neurons. Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels in charged form.

68
Q

3 principles of local anesthetics

A
  1. ) In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively. More anesthetic is needed in these cases.
  2. ) 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: pain (lose first) > temperature > touch > pressure (lost last).
  3. ) Except for cocaine, given w/ vasoconstrictors (usually epinephrine) to enhance local action: decreased bleeding, increased anesthesia by decreasing systemic concentration.
69
Q

Clinical use of local anesthetics

A

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

70
Q

Toxicity of local anesthetics

A

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

71
Q

Neuromuscular blocking drugs (generally). Uses and Mechanism.

A

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

72
Q

Depolarizing neuromuscular blocking drugs

A

Succinylcholine (complications include hypercalcemia and hyperkalemia) Reversal of blockade: Phase I (prolonged depolarization) – no antidote. Block potentiated by cholinesterase inhibitors. Phase II (repolarized but blocked) – antidote consists of cholinesterase inhibitors (e.g., neostigmine)

73
Q

Nondepolarizing neuromuscular blocking drugs

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium. Competitive: compete w/ ACh for receptors. Reversal of blockade: neostigmine, edrophonium, and other cholinesterase inhibitors.

74
Q

Dantrolene. Uses.

A

Used in Tx of malignant hyperthermia, which is caused by use of inhalation anesthetics (except N2O) and succinylcholine. Also used to Tx neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)

75
Q

Mechanism of dantrolene

A

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

76
Q

What is Parkinson’s dz due to (that is addressed by anti-PD drugs)? What agents are used?

A

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity. “BALSA” B romocriptine A mantadine L evodopa (with carbidopa) S elegiline (and COMT inhibitors) A ntimuscarinics

77
Q

Parkinson’s dz drugs, strategy: Agonize dopamine receptors Agents?

A

Bromocriptine (ergot alkaloid and partial dopamine agonist) Pramipexole Ropinirole

78
Q

Parkinson’s dz drugs, strategy: Increase dopamine Agents?

A

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

79
Q

Parkinson’s dz drugs, strategy: Prevent dopamine breakdown Agents?

A

Selegiline (selective MAO type B inhibitor); Entacapone, Tolcapone (COMT inhibitors - prevent L-dopa degeneration, thereby increasing dopamine availabiltiy)

80
Q

Parkinson’s dz drugs, strategy: Curb excess cholinergic activity Agents?

A

Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia). (“Tx your tremor before you drive your Mercedes-BENZ “)

81
Q

For Tx of essential familly tremors?

A

Use beta-blocker.

82
Q

Mechanism of L-dopa (levodopa)/carbidopa

A

Increase level of dopamine in brain. Unlinke dopamine, L-dopa can cross BBB and is converted by dop decarboxylase in the CNS to dopamine.

83
Q

Clinical use of L-dopa (levodopa)/carbidopa

A

Parkinsonism

84
Q

Toxicity of L-dopa (levodopa)/carbidopa

A

Arrhythmias from peripheral conversion to dopamine. Long-term use can –> dyskinesia following administration, akinesia btw doses. Carbidopa, a peripheral decarboxylase inhibitor, is given w/ L-dopa in order to increase the bioavailability of L-dopa in the brain and to limit peripheral SE’s.

85
Q

Mechanism of selegiline

A

Selectively inhibits MAO-B (preferentially metabolizes dopamine over NE and 5-HT), thereby increasing the availability of dopamine.

86
Q

Clinical use of selegiline

A

Adjunctive agent to L-dopa in Tx of Parkinson’s dz.

87
Q

Toxicity of selegiline

A

May enhance adverse effects of L-dopa.

88
Q

Mechanism of Sumatriptan

A

5-HT[1B/1D] agonist. Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release. Half-life is < 2 hours.

89
Q

Clinical use of sumatriptan

A

Acute migraine, cluster HA attacks.

90
Q

Toxicity of Sumatriptan

A

Coronary vasospasm (contraindicated in pts w/ CAD or Prinzmetal’s angina) Mild tingling.

91
Q

Alzheimer’s drugs: Memantine mechanism?

A

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

92
Q

Alzheimer’s drugs: Memantine Toxicity?

A

Dizziness, confusion, hallucinations.

93
Q

Alzheimer’s drugs: Donepezil mechanism?

A

Acetylcholinesterrase inhibitor

94
Q

Alzheimer’s drugs: Donepezil Toxicity?

A

Nausea, dizziness, insomnia.

95
Q

Tiagabine. Mechanism and Uses.

A

Partial (simple/complex) epilepsy; inhibits GABA reuptake

96
Q

Vigabatrin. Mechanism and Uses.

A

Partial (simple/complex). Irreversibly inhibits GABA transaminase -> increases GABA

97
Q

Levetiracetam. Mechanisms and Uses.

A

Unknown mechanism; may modulate GABA and glutamate release. Used for partial (simple/complex) and tonic-clonic epilepsy.

98
Q

What is the mechanism of action of anesthetics in the lungs?

A

Increased rate + depth of ventilation = increased gas tension

99
Q

What is the mechanism of action of anesthetics in blood?

A

Increased blood solubility = increased blood/gas partition coefficient = increased solubility = increased gas required to saturate blood = slower onset of action

100
Q

What is the mechanism of action of anesthetics in tissue (e.g. brain)?

A

AV concentration gradient increased = increased solubility = increased gas required to saturate tissue = slower onset of action

101
Q

What are the drugs used for Huntington’s?

A

Huntington’s: decrease dopmaine, decrease GABA +ACh.
Reserpine + tetrabenazine - amine depleting
Haloperidol - DA receptor antagonist

USMLE1 - Neurology (4 decks)

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