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Pharm > 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 angle glaucoma

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2
Q

Brimonidine (in neurology)

A

1) Use: Glaucoma
2) Class/MOA: Alpha 2 agonist, decreases aqueous humor synthesis
3) blurry vision, ocular redness, pruritus, foreign body sensation, allergic rxn. A2 agonist so you don’t BRIM ON

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3
Q

Timolol, betaxolol, carteolol (in neurology)

A

1) Use: Glaucoma

2) Beta blockers, decreases aqueous humor secretion

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4
Q

Acetazolamide (in Neurology)

A

1) Use: Glaucoma
2) Class/MOA: Diuretic, decreases aqueous humor secretion by inhibiting carbonic anhydrase (NaHCO3 diuresis) Same drug used for altitude sickness! when you climb a mtn you get glaucoma from pressure!!

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5
Q

Direct Cholinomimetics (Pilocarpine*, Carbachol) or Indirect Cholinomimetics (Physostigmine, Echhothiophate)

A

1) Use: Glaucoma
2) Class/MOA: Cholinomimetics, increases the outflow of the aqueous humor; contract ciliary muscle and open trabecular meshwork
3) Miosis, cyclospasm (from contraction of ciliary muscle)
4) use Pilocarpine** in emergencies, very effective at opening meshwork into canal of Schlemm

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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)”Latanoprost makes your eyes look more Latan.”

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7
Q

Opioid Analgesics (morphine)

A

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 (hyperpolarization). Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with naloxone or naltrexone (opiod receptor antagonist).

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8
Q

Butorphanol

A

1) Pain; causes less respiratory depression than Full agonists 2) Partial agonist at opioid mu receptors, agonist at kappa receptors.

3) Causes withdrawal if on full opioid agonist (competition for opioid receptors)
4) OD not easily reversed w NaloxoneBu/you TOR your PHANnie, and now you’re in a lot of pain. Use Butorphanol to partially block your mu (~”Bu”) and Kappa

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9
Q

Tramadol

A

1) Use: Chronic pain
2) Class/MOA: Very weak opioid agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters - “tram it all” in)
3) Similar to opioids. Decreases seizure threshold. Implicated in Serotonin Syndrome*** when used concomitantly with Serotoninergic drugs

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10
Q

Phenytoin

A

1) 1st line Tonic-clonic. 1st line prophylax Status Epilepticus. Simple, Complex
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) Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogen (“fetal hydantoin syndrome”), SLE-like sxs, induction of P450, LYMPHADENOPATHY (“pseudolymphoma”), SJS syndrome, osteopenia
4) Fosphentoin for parenteral use. Phenytoin metabolized by P450-gingival hyperplasia bc Phenytoin incr expression of PDGF. Macrophages exposed to PDGF stimulate proliferation of gingival cells and alveolar bone

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11
Q

Carbamazepine

A

1) 1st line in: Tonic-clonic, Simple, and Complex
2) Class/MOA: Increases Na+ channel inactivation –>reduce ability of Na+ channels to recover from inactivation
3) Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytrochrome P-450, SIADH, SJS syndrome
4) 1st line for trigeminal neuralgia, also used as a Mood Stabilizer

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12
Q

Gabapentin

A

1) the big three (tonic-clonic, simple, complex)
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 makes you feel gabaSPENTIN –> sedation, ataxia (walking crooked cause you’re so tired)

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13
Q

Topiramate

A

1) big three seizures
2) Class/MOA: Blocks Na+ channels, increases GABA action
3) Sedation, mental dulling, kidney stones, weight loss.
4) Migraine prevention. Forgot to put your TOP on again bc your in pain (kidney stones) and crash dieting (weight loss) so you can look sexy for your MATE who turns out to be your teacher but you didn’t notice bc too much GABA was making you dull.

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14
Q

Phenobarbital

A

1) big three seizures
2) Class/MOA: increased GABAA action
3) Sedation, tolerance, dependence, induction of cytrochrome P-4504) Fun Facts: 1st line in pregnant women, children BARBIe is a toy for kids, EH?/”incr gabaA action. kids get tolerant and dependent on barbie for falling asleep (sedated) at night. Oh yeah, and induce P450

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15
Q

Valproic acid

A

1) 1st line in tonic-clonic. Absence, simple, complex, MYOCLONIC too.
2) Class/MOA: Increases Na+ channel inactivation, increases GABA concentration
3) GI distress, rare but fatal hepatotoxicity (measure LFT), neural tube defects in fetus (spinal bifida), tremor, weight gain. Contraindicated in pregnancy. Val was a drinker and a fornicator! Gotta check her LFTs and make sure she doesn’t get pregnant bc dead baby.

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16
Q

Ethosuximide

A

1) 1st line in Absence seizures
2) Class/MOA: Blocks thalamic T-type Ca2+ channels –> Hyperpolarization
3) GI distress, fatigue, headache, urticaria, Steven’s-Johnson syndrome (Every Friday Go Home to Steven’s house- Ethosuximide, Fatigue, GI, Headache, SJS) Ethics SUX, I’m gonna be ABSENT next time we have that class.

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17
Q

Benzodiazepines (diazepam or lorazepam)

A

1) 1st line for acute Status Eplipepticus
2) Class/MOA: Increases GABAA action (incr affinity for receptor) INCREASED FREQUENCY of CL channel opening
3) Side effects/ADEs: sedation, tolerance, dependence

4) also used for seizures of eclampsia (1st line is MgSO4) and alcohol withdrawa

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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. Decr 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)

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19
Q

Tiagabine

A

1) Simple, Complex

2) Class/MOA: inhibits GABA reuptake”Tia for Gabine!” i.e. inhibits GABA reuptake so it can be invited for tea for two

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20
Q

Vigabatrin

A

1) Simple, Complex

2) Class/MOA: Irreversibly inhibits GABA transaminase - increases GABA VItalize GABA by inhibiting TRINsaminase

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21
Q

Levetiracetam

A

1) the big three

2) Class/MOA: Unknown, may modulate GABA and glutamate release

22
Q

Barbiturates (Phenobarbital, Pentobartibal, 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 BZ1 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.

24
Q

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

A

1) Use & Effects: Anesthetic –> myocardial depression, respiratory distress, nausea/emesis, decr renal fxn*, incr cerebral blood flow by decr cerebral vasc. resistance (decr cerebral metabolic demand) but –> incr ICP
2) Class/MOA: mechanism unknown
3) Side effects/ADEs: Hepatotoxicity (Halothane), Nephrotoxicity (Methoxyflurane), Proconvulsant/~Epilepticy (Enflurane), malignant hyperthermia (rare), expansion of trapped gas (NO)

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 skeletal muscle* and adipose tissue. Decrease in cerebral blood flow.
2) Class/MOA: high potency, high lipid solubility, rapid entry into the brain

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.

27
Q

Intravenous Anesthetic: Arylcyclohexylamines (Ketamine)

A

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

28
Q

Intravenous Anesthetic: Opiates (morphine, fentanyl)

A

used with other CNS depressants during general anesthesia

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 anesthesia. 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 firing neurons. tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channel as charged form.
3) Side effects/ADEs: CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension and arryhthmias (cocaine).
4) Principle: 1) in infected (acidic) tissue, alkaline anesthetics are charged and can’t penetrate membranes effectively. More anestetic is needed in these cases. 2) order of nerve blockage- small diamaeter 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 (lose last).Give w vasoconstrictor/EPI to enhance local action

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) strong Ach receptor agonist –> sustained depolarization/prevent m contraction.
3) hypercalcemia, hyperkalemia, Hyperthermia*
4) 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, verocuronium, rocuronium).

A

1) Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
2) Competitive antagonist for Ach Nicotinic receptors
4) reversal of blockage (incr Ach): neostigmine, edrophonium and other cholinesterase inhibitors.

33
Q

Dantrolene

A

1) Use: used in the treatment of malignant hyperthermia, which is caused by inhalation anesthetics (except N2O) 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

34
Q

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

A

1) Use: Parkinson’s

2) Class/MOA: agonize dopamine receptors BROs do DOPe (agonizes receptors)

35
Q

Amantadine

A

1) Use: Parkinson’s, also used as a antiviral against influenza A and rubella; toxicity = ataxia
2) Class/MOA: Increase dopamine release

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.

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

38
Q

Entacapone, tolcapone

A

1) Use: Parkinson’s
2) Class/MOA: prevent dopamine breakdown, COMT inhibitor - prevent peripheral L-dopa degradation, thereby increasing dopamine availability/incr quantity of dopamine entry into brain
3) Tolcapone: hepatotoxicity. al -CAPONE had L-Dopa’s back, prevented its degradation by blocking COMT

39
Q

Benztropine

A

1) Use: Parkinsons
2) antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia
4) Fun Facts: Park your Mercedes-Benz

40
Q

Memantine

A

1) Use: Alzheimer’s drug
2) NMDA receptor antagonist, helps prevent excitotocity (mediated by Ca2+)
3) Side effects/ADEs: Dizziness, confusion, hallucinations. Memantine is a meme of Ketamine –> blocks NMDA receptors, causes hallucinations

41
Q

Donepezil, falantamine, rivastigmine

A

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

42
Q

Reserpine + tetrabenazine

A

1) Use: Huntington’s drug

2) Inhibit VMAT; limit dopamine vesicle packaging and release

43
Q

Haloperidol

A

1) Use: Huntington’s drug

2) Class/MOA: dopamine receptor antagonist

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 life <2 hrs
3) Coronary vasospasm, mild tingling. 4) Fun Facts: A SUMo wrestler TRIPs ANd falls on your head! Sumo wrestlers are fat and have coronary vasospasm

45
Q

Fentanyl

A

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 (hyperpolarization). Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

46
Q

Codeine

A

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 (hyperpolarization). Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

47
Q

Heroin

A

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 (hyperpolarization). Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

48
Q

Methadone

A

1) Maintenance programs for addicts
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 (hyperpolarization). Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

49
Q

Meperidine

A

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 (hyperpolarization). Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

50
Q

Dextromethorphan

A

1) Pain, cough suppression
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 (hyperpolarization). Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

51
Q

Diphenoxylate

A

1) Diarrhea (+ loperamide =immodium)
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 (hyperpolarization). Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

52
Q

Lamotrigine

A

1) the big three seizures
2) blocks voltage-gated Na+ channels
3) SJS

Pharm (15 decks)

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