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Drugs > Neurology > Flashcards

Neurology Flashcards

1
Q

Epinephrine (in Neurology)

A

1) Use: Glaucoma
2) Class/MOA: alpha agonist, decreases aqueous humor synthesis due to vasoconstriction
3) Side effects/ADEs: Mydriasis, stinging: do not use in closed glaucoma
4) Fun Facts

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2
Q

Brimonide (in neurology)

A

1) Use: Glaucoma
2) Class/MOA: Alpha agonist, decreases aqueous humor synthesis
3) Side effects/ADEs: no pupillary of vision changes
4) Fun Facts

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3
Q

Timolol, betazolol, carteolol (in neurology)

A

1) Use: Glaucoma
2) Class/MOA: Beta blocker, decreases aqueous humor secretion
3) Side effects/ADEs: no pupillary or vision changes
4) Fun Facts

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4
Q

Acetazolamide (in Neurology)

A

1) Use: Glaucoma
2) Class/MOA: Diuretic, decreases aqueous humor secretion due to decreased HCO3- (via inhibition of carbonic anhydrase)
3) Side effects/ADEs: No pupillary or vision changes
4) Fun Facts

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5
Q

Direct Cholinomimetics (pilocarpine, carbachol) or Indirect Cholinomimetics (physostigmine, ecchothiophate)

A

1) Use: Glaucoma
2) Class/MOA: Cholinomimetics, increases the outflow of the aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies, very effective at opening meshwork into canal of Schlemm
3) Side effects/ADEs: Miosis, cyclospasm
4) Fun Facts

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6
Q

Latanoprost (PGF 2 alpha)

A

1) Use: Glaucoma
2) Class/MOA: Prostaglandin, increase the outflow of aqueous humor
3) Side effects/ADEs: darkens color of iris (browning)
4) Fun Facts

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7
Q

Opiod Analgesics (morphine, fentanyl, codeine, heroine, methandone, meperidine, dexomethophan diphenoxylate)

A

1) Use: Pain, cough suppression (dextromethophran), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance program for addicts (methadone).
2) Class/MOA: Acts as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappy = dynorphin) to modulate synaptic transmission - open K+ channels, close Ca2+ channels = decrease in synaptic transmission. Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Side effects/ADEs: Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with nalazone or naltrexone (opiod receptor antagonist).
4) Fun Facts

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8
Q

Butorphanol

A

1) Use: Pain; causes less respiratory depression than dull agonists
2) Class/MOA: Partial agonist at opiod mu receptors, agonist at kappa receptors.
3) Side effects/ADEs: Causes withdrawal if on full opiod agonist.
4) Fun Facts

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9
Q

Tramadol

A

1) Use: Chronic pain
2) Class/MOA: Very weak opiod agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters - “tram it all” in)
3) Side effects/ADEs: Similar to opiods. Decreases seizure threshold.
4) Fun Facts

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10
Q

Phenytoin

A

1) Use: Epilepsy drug, used in: partial simple, partial complex, 1st line for generalized tonic clonic, 1st line for prophylaxis of generalized status seizures. Also a class IB antiarrhytimic.
2) Class/MOA: Increases Na+ channel inactivation, I.E. use-dependent blockade of Na+ channels: increase refractory period, inhibition of glutamate release from excitatory presynaptic neuron
3) Side effects/ADEs: Nystagmus, diplopia, ataxias, sedation, teratogenesis (fetal hydantion syndrome), SLE-like syndrome, induction of cytrocrome P-450. Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirtuim, meglobastic anemia (decrease in folate absorption).
4) Fun Facts: fosphentoin for parenteral use

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11
Q

Carbamazepine

A

1) Use: Epilepsy drug, used in: first line in partial simple, partial complex & generalized tonic clonic seizures
2) Class/MOA: Increases Na+ channel inactivation
3) Side effects/ADEs: Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytrochrome P-450, SIADH, Steven’s-Johnson syndrome
4) Fun Facts: fist line for trigeminal neuralgia

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12
Q

Gabapentin

A

1) Use: Epilepsy drug, used in: partial simple, partial complex & generalized tonic clonic seizures
2) Class/MOA: Designed as a GABA analog, but primarily inhibits HVA Ca2+ channels
3) Side effects/ADEs: sedation, ataxia
4) Fun Facts: also used for peripheral neuropathy and bipolar disorder

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13
Q

Topiramate

A

1) Use: Epilepsy drug, used in: partial simple, partial complex & generalized tonic clonic seizures
2) Class/MOA: Blocks Na+ channels, increases GABA action
3) Side effects/ADEs: Sedation, mental dulling, kidney stones, weight loss.
4) Fun Facts

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14
Q

Phenobarbital

A

1) Use: Epilepsy drug, used in: partial simple, partial complex & generalized tonic clonic seizures
2) Class/MOA: increased GABAA
3) Side effects/ADEs: Sedation, tolerance, dependence, induction of cytrochrome P-450
4) Fun Facts: 1st line in pregnant women, children

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15
Q

Valproid acid

A

1) Use: Epilepsy drug, used in: partial simple, partial complex, 1st line in tonic clonic generalized seizures and in absence generalized seizures.
2) Class/MOA: Increases Na+ channel inactivation, increases GABA concentration
3) Side effects/ADEs: GI distress, rare but fatal hepatotoxicity (measure LFT), neural tube defects in fetus (spinal bifida), tremor, weight gain. Contraindicated in pregnancy.
4) Fun Facts: Also used for myoclonic seizures

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16
Q

Ethosuximide

A

1) Use: Epilepsy drug, used in: 1st line in generalized absence seizure
2) Class/MOA: Blocks thalamic T-type Ca2+ channels
3) Side effects/ADEs: GI distress, fatigue, headache, urticaria, Steven’s-Johnson syndrome (EFGH- Ethosuximide, Fatigue, GI, Headache)
4) Fun Facts

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17
Q

Benzodiazepines for epilepsy (diazepam or lorazepam)

A

1) Use: Epilepsy drug, used in: 1st line for acute generalized status seizures
2) Class/MOA: Increases GABAA action
3) Side effects/ADEs: sedation, tolerance, dependence
4) Fun Facts: also used for seizures of eclampsia (1st line is MgSO4)

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18
Q

Benzodiazepines for neurological problems (diazepam, lorazepam, triazolam, temazepam, oxzepam, midazolam, chlodiazepoxide, alprazolam))

A

1) Use: anxiety, spacticity, status epileptics (lorazepam and diazepam), detoxification (especially in alcohol DTs-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
2) Class/MOA: Facilitate GABAA action by increasing frequency of Cl- channel opening, decreasing REM sleep. Most have long half-lives and active metabolites. FREnzodiazepines (Increase FREquency), short acting = TOM thumb (Triazolam, Oxzepam, Midazolam … also has the highest addictive potential). Benzos, barbs, and EtOH all bind GABA(A)-R which is a ligand-gated chloride channel.
3) Side effects/ADEs: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
4) Fun Facts: treat overdose with flumazenil (competitive antagonist at GABA benxodiazepine receptor)

19
Q

Tiagabine

A

1) Use: epilepsy drug, used in: partial simple and partial complex seizures
2) Class/MOA: inhibits GABA reuptake
3) Side effects/ADEs:
4) Fun Facts

20
Q

Vigabatrin

A

1) Use: epilepsy drug, used in: partial simple and partial complex seizures
2) Class/MOA: Irreversibly inhibits GABA transaminase - increases GABA
3) Side effects/ADEs:
4) Fun Facts

21
Q

Levetiracetam

A

1) Use: epilepsy drug, used in: partial simple and partial complex seizures and in generalized tonic-clonic seizures
2) Class/MOA: Unknown, may modulate GABA and glutamate release
3) Side effects/ADEs:
4) Fun Facts

22
Q

Barbiturates (Phenobarbital, Phenobarbital, thiopental, secobarbital)

A

1) Use: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
2) Class/MOA: facilitate GABAA action by increasing duration of Cl- channel opening, thus decreasing neuron firing (barbiDURATe - increase DURATion).
3) Side effects/ADEs: dependence, additive CNS depression effects with alcohol, respiratory or cardiovascular depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytrochrome P-450)
4) Fun Facts: treat overdose with symptom management (assist respiration, increase blood pressure). Contraindicated in porphyria.

23
Q

Nonbenzodiazepine hypnotics (zolpidem aka ambien, zaleplon, eszopiclone)

A

1) Use: Insomnia
2) Class/MOA: act via the BZI receptor subtype and are reversed by flumazenil
3) Side effects/ADEs: Atazia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnesic effects. Lower dependence risk than benzodiazepines.
4) Fun Facts

24
Q

Inhaled anesthetics (halothane, enflurane, isoflurane, sevodlurane, methoxyflurane, NO)

A

1) Use & Effects: Anesthetic - myocardial depression, respiratory distress, nausea/emesis, increase cerebral blood flow (decrease cerebral metabolic demand
2) Class/MOA: mechanism unknown
3) Side effects/ADEs: Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (endlurane), malignant hyperthermia (rare), expansion of trapped gas (NO)
4) Fun Facts

25
Q

Intravenous anesthetic: Barbiturate (thiopental)

A

1) Use & Effects: intravenous anesthetic, used for induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (I.e. skeletal muscle) and fat. Decrease in cerebral blood flow.
2) Class/MOA: high potency, high lipid solubility, rapid entry into the brain
3) Side effects/ADEs:
4) Fun Facts:

26
Q

Intravenous anesthetic: Benzodiazepines (Midazolam)

A

1) Use: intravenous anesthetic, used for endoscopy; used adjunctively with gaseous anesthetics and narcotics
2) Class/MOA:
3) Side effects/ADEs: may cause severe postoperative respiratory distress, decrease in blood pressure (treat overdose with flumazenil) and amnesia.
4) Fun Facts

27
Q

Intravenous Anesthetic: Arylcyclohexylamines (Ketamine)

A

1) Use: intravenous anesthetic
2) Class/MOA: PCP analogs that act as dissociate anesthetics, blocks MNDA receptors.
3) Side effects/ADEs: cardiovascular stimulant, causes disorientation, hallucination and bad dreams, increases cerebral blood flow.
4) Fun Facts

28
Q

Intravenous Anesthetic: Opiates (morphine, fentanyl)

A

1) Use: used with other CNS depressants during general anesthesia
2) Class/MOA:
3) Side effects/ADEs:
4) Fun Facts

29
Q

Intravenous Anesthetics: Propofol

A

1) Use: rapid anesthesia induction and short procedures.
2) Class/MOA: Potentates GABAA receptors.
3) Side effects/ADEs: Less postoperative nausea than thiopental.
4) Fun Facts: Not recommended for home use by pop stars

30
Q

Local Anesthetics (esters: procaine, cocaine, tetracain; amides-lidocaine, mepivaciane, bupicacaine - amides have 2 I’s in each name)

A

1) Use: Minor surgical prodeedures, spinal anestheia. If allergic to esters, give amides.
2) Class/MOA: block Na+ channels by binding to specific receptors on inner portion of channel. Perferentially bind to activated Na+ channels, so most effective in rapidly firig neurons. 3 degree amine local anesthetics penetrate membrnae in uncharged form, then bind to ion channel as charged form.
3) Side effects/ADEs:CNS excitation, severe cadiovascular toxifity (bupivacaine), hypertension, hypotension and arrhthmias (cocaine).
4) Fun Facts/Principle: 1) in infected (acidic) tissue, alkaline anesthetics are charged and can’t penetrate membranes effectivly. More anestetic is needed in these cases. 2) order of nerve blockage- small diamaeter fibers > large diameter. Mylinated fibers > unmylinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers >small unmylinated fibers > large mylinated fibers > large unmylinated fibers. Order of loss - pain (lose first) > temperature > touch > pressure (lose last). 3) Except for cocain, given with vasoconstrictors (usually epinephrine) to enhance local action - decreases bleeding, increases anesthesia by decreasing systemic contraction.

31
Q

Neuromuscular Blocking Drugs, Depolarizing (Succynlcholine)

A

1) Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
2) Class/MOA:
3) Side effects/ADEs: hypercalcemia and hyperkalemia
4) Fun Facts: for reversal of blockage: Phase I) prolonged depolarization: no antidote. Block potential by cholinesterase inhibitors. Phase II) repolarized by blocked: antidote consists of cholinesterase inhibitors (e.g. neostigmine).

32
Q

Neuromuscular blocking drugs, Nondepolarizing (tubocuraine, atracurium, mivacurium, pancuronium, vecronium, rocuronium).

A

1) Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
2) Class/MOA: Competitive, compete with Ach for receptors
3) Side effects/ADEs:
4) Fun Facts: reversal of blockage: neostigmine, edrophonium and other cholinesterase inhibitors.

33
Q

Dantrolene

A

1) Use: used in the treatment of malignant hypertension, which is caused by inhalation anesthetics (except N2)) and succinylcholine. Also used to treat neuropleptic malignant syndrome (a toxicity of antipsychotic drugs)
2) Class/MOA: Prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle
3) Side effects/ADEs:
4) Fun Facts

34
Q

Bromocriptine (ergot), pramipexole, ropinirole (non ergot, preferred)

A

1) Use: Parkinson’s
2) Class/MOA: agonize dopamine receptors
3) Side effects/ADEs:
4) Fun Facts

35
Q

Amatadine

A

1) Use: Parkinson’s, also used as a antiviral against influenza A and rubella; toxicity = ataxia
2) Class/MOA: Increase dopamine
3) Side effects/ADEs:
4) Fun Facts

36
Q

L-dopa/carbidopa

A

1) Use: Parkinson’s
2) Class/MOA: increase dopamine, converted to dopamine in the CNS. Unlike dopamine, L-dopa can cross the blood brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.
3) Side effects/ADEs: Arrhythmias from peripheral conversion to dopamine. Long term use can cause dysskinesia following administration, akinesia between doses. Carbidopa, a peripheral decarboxylase inhibitor is given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects.
4) Fun Facts

37
Q

Selegiline

A

1) Use: Adjunctive agent to L-dopa in treatment of Parkinson’s disease.
2) Class/MOA: prevent dopamine breakdown, selective MAO type B inhibitor, which preferentially metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine.
3) Side effects/ADEs: may enhance adverse effects of L-dopa
4) Fun Facts

38
Q

Entacapone, tolcaptone

A

1) Use: Parkinson’s
2) Class/MOA: prevent dopamine breakdown, COMT inhibitor - prevent L-dopa degradation, thereby increasing dopamine availability
3) Side effects/ADEs:
4) Fun Facts

39
Q

Benztropine

A

1) Use:
2) Class/MOA: Curb excess cholinergic activity, antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia
3) Side effects/ADEs:
4) Fun Facts: Park your Mercedes-Benz

40
Q

Memantine

A

1) Use: Alzheimer’s drug
2) Class/MOA: NMDA receptor antagonist, helps prevent excitotocity (mediated by Ca2+)
3) Side effects/ADEs: Dizziness, confusion, hallucinations
4) Fun Facts

41
Q

Donepezil, falantamine, rivastigmine

A

1) Use: Alzheimer’s drug
2) Class/MOA: acetylcholinesterase inhibitor
3) Side effects/ADEs: Nausea, dizziness, insomnia
4) Fun Facts

42
Q

Reserpine + tetrabenazine

A

1) Use: Huntington’s drug
2) Class/MOA: amine depleting
3) Side effects/ADEs:
4) Fun Facts

43
Q

Haloperidol

A

1) Use: Huntington’s drug
2) Class/MOA: dopamine receptor agonist
3) Side effects/ADEs:
4) Fun Facts

44
Q

Sumatriptan

A

1) Use: Acute migraine, cluster headache attacks.
2) Class/MOA: 5-HT 1B/1D agonist. Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release. Half-lifes angina), mild tingling.
4) Fun Facts: A SUMo wrestler TRIPs ANd falls on your head!

Drugs (16 decks)

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