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0. Step Ia > Neuro Pharm from FA > Flashcards

Neuro Pharm from FA Flashcards

1
Q

where are the M receptors on the eye? what is their function?

A

pupillary sphincter (M3) - causes miosis

ciliary muscles (M3) - accomodation

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2
Q

where are the a1 receptors on the eye? what is their function?

A

pupillary dilator (a1)

causes mydriasis

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3
Q

where are the ß receptors on the eye? what is their function?

A

ciliary epithelium

produces aqueous humor

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4
Q

Glaucoma Drugs: overall mechanism?

A

Decr IOP via decr amount of aqueous humor. (inhibit synthesis/secretion, or increase drainage)

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5
Q

Epinephrine.

Class? Mech? SE?

A

Class: Glaucoma drug, a1, ß1, ß2 agonist

Mech: decr aqueous humor synthesis via vasoconstriction via a1 receptors

SE: Mydriasis (pupil dilation); do not use in closed-angle glaucoma

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6
Q

Brimonidine

Class? Mech? SE?

A

Class: Glaucoma drug, Alpha-2 agonist

Mech: decr aqueous humor synthesis

SEs: Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis

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7
Q

Timolol, Betaxolol, Carteolol

Class? Mech? SE?

A

Class: Glaucoma drugs, beta-blockers

Mech: decr aqueous humor synthesis

SE: None given

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8
Q

Acetazolamide

Class? Mech? SE?

A

Class: Glaucoma drug, diuretic

Mech: decr aqueous humor synthesis via inhibition of carbonic anhydrase.

SE: None given

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9
Q

Pilocarpine, Carbachol

Class? Mech? SE?

A

Class: Glaucoma drugs, Direct cholinomimetics

Mech: incr outflow of aq humor via contraction of ciliary muscle and opening of trabecular meshwork

SE: Miosis and cyclospasm (contracton of ciliary muscle)

Note: use pilocarpine in emergencies - very effective at opening meshwork into canal of Schlemm

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10
Q

Physostigimine, Echothiophate

Class? Mech? SE?

A

Class: Glaucoma drugs, Indirect Cholinomimetic

Mech: incr outflow of aq humor via contraction of ciliary muscle and opening of trabecular meshwork

SE: Miosis and cyclospasm (contracton of ciliary muscle)

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11
Q

Latanoprost (PGF-2alpha)

Class? Mech? SE?

A

Class: Glaucoma drug, Prostaglandin

Mech: increased outflow of aqueous humor

SE: darkens color of iris (browning), and lengthens eyelashes (this was actually on the boards!!)

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12
Q

Big picture for glaucoma:

which drugs decr IOP by decreasing synthesis of aqueous humor? (6)

A

Alpha-agonists: Epinephrine, Brimonidine

Beta-blockers: Timolol, Betaxolol, Cartelol

Diuretics: Acetazolamide

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13
Q

Big picture for glaucoma:

which drugs decr IOP by increasing drainage/outflow of aqueous humor? (5)

A

Cholinomimetics: Pilocarpine, Carbachol, Physostigmine, Echothiophate

Prostaglandin: Latanoprost

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14
Q

List the opioid analgesics? (8)

Generally, clinical uses?

A

Morphine

Fentanyl

Codeine

Loperamide

Methadone

Meperidine

Dextromethorphan

Diphenoxylate

Clinical use of this class (every drug not used for every item): Pain control, cough suppression, diarrhea, acute pulm edema, maintenance programs for heroin addicts

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15
Q

Morphine

Class? Mech? Use? Toxicity?

A

Class: Opioid receptor agonist (**mu receptor = morphine, **delta = enkephalin, kappa = dynorphin). Modulates synaptic transmission – opens K channels, closes Ca2+ channels -> decr synaptic transmission via hyperpolarization. Inhibits release of ACh, Norepi, 5-HT, glutamate, Substance P

Clinical use: Pain, Acute pulm edema

Tox: Addiction, resp depression, constipation, miosis, addictive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Tox treated with naloxone or naltrexone (opioid receptor antagonists)

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16
Q

Fentanyl

Class? Mech? Use? Tox?

A

Class: Opioid receptor agonist (mu receptor = morphine, ​delta = enkephalin, kappa = dynorphin). Modulates synaptic transmission – opens K channels, closes Ca2+ channels -> decr synaptic transmission via hyperpolarization. Inhibits release of ACh, Norepi, 5-HT, glutamate, Substance P

Clinical use: Pain, Acute pulm edema

Tox: Addiction, resp depression, constipation, miosis, addictive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Tox treated with naloxone or naltrexone (opioid receptor antagonists)

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17
Q

Codeine

Class? Mech? Use? Tox?

A

Class: Opioid receptor agonist (mu receptor = morphine, ​delta = enkephalin, kappa = dynorphin). Modulates synaptic transmission – opens K channels, closes Ca2+ channels -> decr synaptic transmission via hyperpolarization. Inhibits release of ACh, Norepi, 5-HT, glutamate, Substance P

Clinical use: Pain, Acute pulm edema

Tox: Addiction, resp depression, constipation, miosis, addictive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Tox treated with naloxone or naltrexone (opioid receptor antagonists)

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18
Q

Loperamide

Class? Mech? Use? Tox?

A

Class: Opioid receptor agonist (mu receptor = morphine, ​delta = enkephalin, kappa = dynorphin). Modulates synaptic transmission – opens K channels, closes Ca2+ channels -> decr synaptic transmission via hyperpolarization. Inhibits release of ACh, Norepi, 5-HT, glutamate, Substance P

Clinical use: Pain, Acute pulm edema, Diarrhea

Tox: Addiction, resp depression, constipation, miosis, addictive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Tox treated with naloxone or naltrexone (opioid receptor antagonists)

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19
Q

Methadone

Class? Mech? Use? Tox?

A

Class: Opioid receptor agonist (mu receptor = morphine, ​delta = enkephalin, kappa = dynorphin). Modulates synaptic transmission – opens K channels, closes Ca2+ channels -> decr synaptic transmission via hyperpolarization. Inhibits release of ACh, Norepi, 5-HT, glutamate, Substance P

Clinical use: Pain, Acute pulm edema, Maintenance programs for heroin addicts

Tox: Addiction, resp depression, constipation, miosis, addictive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Tox treated with naloxone or naltrexone (opioid receptor antagonists)

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20
Q

Meperidine

Class? Mech? Use? Tox?

A

Class: Opioid receptor agonist (mu receptor = morphine, ​delta = enkephalin, kappa = dynorphin). Modulates synaptic transmission – opens K channels, closes Ca2+ channels -> decr synaptic transmission via hyperpolarization. Inhibits release of ACh, Norepi, 5-HT, glutamate, Substance P

Clinical use: Pain, Acute pulm edema

Tox: Addiction, resp depression, constipation, miosis, addictive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Tox treated with naloxone or naltrexone (opioid receptor antagonists)

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21
Q

Dextromethorphan

Class? Mech? Use? Tox?

A

Class: Opioid receptor agonist (mu receptor = morphine, ​delta = enkephalin, kappa = dynorphin). Modulates synaptic transmission – opens K channels, closes Ca2+ channels -> decr synaptic transmission via hyperpolarization. Inhibits release of ACh, Norepi, 5-HT, glutamate, Substance P

Clinical use: Pain, Acute pulm edema, Cough suppression

Tox: Addiction, resp depression, constipation, miosis, addictive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Tox treated with naloxone or naltrexone (opioid receptor antagonists)

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22
Q

Diphenoxylate

Class? Mech? Use? Tox?

A

Class: Opioid receptor agonist (mu receptor = morphine, ​delta = enkephalin, kappa = dynorphin). Modulates synaptic transmission – opens K channels, closes Ca2+ channels -> decr synaptic transmission via hyperpolarization. Inhibits release of ACh, Norepi, 5-HT, glutamate, Substance P

Clinical use: Pain, Acute pulm edema, Diarrhea

Tox: Addiction, resp depression, constipation, miosis, addictive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Tox treated with naloxone or naltrexone (opioid receptor antagonists)

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23
Q

Butorphanol

Class? Mech? Use? Tox?

A

Class: Opioid agonist

Mech: Mu-opioid receptor partial agonist and kappa opioid receptor agonist. Causes analgesia

Use: Severe pain (labor, migraine). Causes less resp depression than full opioid agonists

Tox: If pt is also taking full opioid agonist, can cause opioid withdrawal symptoms (due to competition for opioid receptors). Overdose not easily reversed with naloxone

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24
Q

Tramadol

Class? Mech? Use? Tox?

A

Class: Opioid agonist (weak)

Mech: Very weak opioid agonist. Also inhibits serotonin and norepi reuptake - works on multiple neurotransmitters (“tram it all” in with tramadol)

Use: Chronic pain

Tox: similar to opioids. Decreases seizure threshold. Serotonin syndrome.

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25
Q

Epilepsy: First line drug for Simple Partial seizure?

A

Carbamazepine

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26
Q

Epilepsy: First line drug for Complex Partial seizure?

A

Carbamazepine

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27
Q

Epilepsy: First line drugs for Generalized Tonic-Clonic seizure? (3)

A

Phenytoin, Carbamazepine, Valproic acid

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28
Q

Epilepsy: First line drug for Absence seizure?

A

Ethosuximide

(Sucks to have Silent Seizures)

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29
Q

Epilepsy: First line drug for Status Epilepticus (Acute)?

A

Benzodiazepines (diazepam, lorazepam)

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30
Q

Epilepsy: First line drug for prophylaxis of Status Epilepticus?

A

Phenytoin

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31
Q

Ethosuximide

Use? Mech? SEs? Notes?

A

Use: Absence seizures

Mech: blocks thalamic T type Ca2+ channels

SEs: fatigue, GI, urticaria, Steven-Johnson synd.

EFGHIJ: Ethosuximide causes Fatigue, GI distress, Headache, Itching, and Stevens-Johnson synd.

Notes: Sucks to have silent seizures

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32
Q

Benzodiadepines (diazepam, lorazepam)

Use? Mech? SEs? Notes?

A

Use: first line for acute status epilepticus

Mech: increases GABA-a action

SEs: sedation, tolerance, dependence, resp depression

Notes: also for eclampsia seizures (first line is MgSO4)

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33
Q

Phenytoin

Use? Mech? SEs? Notes?

A

Use: simple, complex, tonic-clonic (first line), prophy for status epilepticus

Mech: increases Na channel inactivation; zero-order kinetics

Ses: nystagmus, doplopia, ataxia, sedation, gingical hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, tertatogenesis (fetal hydantoin syndrome), SLE like synd, induction of cytochrome P-450, Stevens-Johnson synd, osteopenia

Notes: fosphenytoin for parenteral use

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34
Q

Carbamazepine

Use? Mech? SEs? Notes?

A

Use: Simple, Complex, Tonic-Clonic seizures (first line for each)

Mech: incr Na channel inactivation

SEs: diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450, SIADH, Steven-Johnson synd.

Notes: first line for trigeminal neuralgia

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35
Q

Valproic acid

Use? Mech? SEs? Notes?

A

Use: tonic clonic seizures (first line), simple, complex, absence seizures

Mech: incr Na channel inactivation, Incr GABA concentration by inhibiting GABA transaminase

SEs: GI distress, rare but fatal hepatotixicity (measure LFTs), neural tube defects -> spina bifida, tremor, weight gain, contraindicated in preg.

Notes: also used for myoclonic seizures, bipolar d/o

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36
Q

Gabapentin

Use? Mech? SEs? Notes?

A

Use: simple, complex, tonic-clonic seizures

Mech: Inhibits high-voltage-activated Ca channels. Designed as GABA analog

SEs: sedation, ataxia

Notes: also used for peripheral neuropathy, postherpetic neuralgia, migraine prophy, bipolar d/o

37
Q

Phenobarbital

Use? Mech? SEs? Notes?

A

Use: simple, complex, tonic-clonic seizures

Mech: incr GABAa action

SEs: sedation, tolerance, dependence, induction of cytochrome P-450, cardioresp depression

Note: first line in neonates

38
Q

Topiramate

Use? Mech? SEs? Notes?

A

Use: simple, complex, tonic-clonic seizures

Mech: Blocks Na channels, incr GABA action

SEs: sedation, mental dulling, kidney stones, weight loss

Note: also used in migraine prevention

39
Q

Lamotrigine

Use? Mech? SEs?

A

Use: simple, complex, tonic-clonic, absence seizures

Mech: Blocks voltage-gated Na channels

SE: Stevens-Johnson synd. (must be titrated slowly)

40
Q

Levetiracetam

Use? Mech? SEs?

A

Use: Simple, Complex, Tonic-clonic seizures

Mech: unknown (may modulate GABA and glutamate release)

SEs: none

41
Q

Tiagabine

Use? Mech? SEs? Notes?

A

Use: Simple, Complex seizures

Mech: Incr GABA by inhibiting uptake

SEs: none

42
Q

Vigabatrin

Use? Mech? SEs? Notes?

A

Use: Simple, Complex seizures

Mech: Incr GABA by irreversibly inhibiting GABA transaminase

SEs: none

43
Q

what is Stevens-Johnson syndrome?

Which epilepsy meds cause it? (4)

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.

Caused by:

Carbamazepine

Ethosuximide

Lamotrigine

Phenytoin

44
Q

Barbituates (Phenobarbital, pentobarbital, thiopental, secobarbital): Mechanism?

A

Facalitate GABA-A action by increasing duration of Cl channel opening, thus decreasing neuron firing. (BarbiDURAtes increase DURAtion)

Contraindicated in porphyria.

45
Q

Barbituates (Phenobarbital, pentobarbital, thiopental, secobarbital): Clinical Use? Toxicity?

A

Use: Sedative for anxiety, seizures, insomnia, induction of anesthesia (Thiopental)

Tox: Resp and CV depression can be fatal. CNS depression (can be exacerbated by EtOH use). Dependence. Drug interactions: induces cytochrome p-450.

Overdose treatment is supportive (assist resp, maintain BP)

46
Q

Benzodiazepines (Diazepam, lorazepam, triazolam, temazepam, temazepam, oxazepam, midalozam, chlordiazepoxide, alprazolam): Mech?

A

Facilitate GABA-A action by increasing frequency of Cl- channel opening. Decr REM sleep. Most have long half-lives and active metabolites.

(Exception: Triazolam, oxazepam, midazolam are short acting –> higher addictive potential. But short-acting best for minimizing side effects)

“FREnzodiazepines increase FREquency”

47
Q

Benzodiazepines (Diazepam, lorazepam, triazolam, temazepam, temazepam, oxazepam, midalozam, chlordiazepoxide, alprazolam):

Clinical Use? Tox?

A

Use: Anxiety, spasticity, status epilepticus (lorazepam, diazepam), detox (esp alcohol withdrawal w/ DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)

Tox: Dependence, addictive CNS depression effects with alcohol. Less risk of resp depression and coma than with barbituates.

Treat OD with Flumazenil (competitive antagonist at GABA benzodiazepine receptor)

48
Q

Nonbenzodiazepine hypnotics (Zoplidem, Zaleplon, esZopicline”: Mech? How to reverse?

A

(All ZZZZs put you to sleep)

Mech: Act via the BZ1 subtype of the GABA receptor.

Reverse with flumazenil.

49
Q

Nonbenzodiazepine hypnotics (Zoplidem, Zaleplon, esZopicline”: Use? Tox?

A

Use: Insomnia

Tox: 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.

Lower risk of dependence than Benzodiapezines.

50
Q

What is a requirement for anesthetic drugs?

If drug has low solubility in blood, how does that affect its function?

If drug has high solubility in lipids, how does that affect its function?

A
  • Must be lipid soluble in order to cross the blood-brain barrier, or actively transported
  • Low solubility in blood –> rapid induction and recovery times
  • High solubility in lipids –> high potency (1/MAC)
51
Q

MAC: what is this and how does it relate to anesthetics?

A

MAC = Mean Alveolar Concentration (of inhaled anesthetic) that is required to prevent 50% of patients from moving in response to noxious stimulus (ie skin incision)

52
Q

N2O has low solubility in blood and lipid –> what is its speed of induction and potency?

Halothane has high solubility in blood and lipid –> what is its speed of induction and potency?

A

N2O: fast induction, low potency

Halothane: slow induction, high potency

53
Q

Inhaled anesthetics (halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide): Mech? Effects?

A

Mech is unknown (that is unsettling!)

Effects: Myocardial depression, resp depression, nausea/vomiting, incr cerebral blood flow (decr cerebral metabolic demand)

54
Q

Inhaled anesthetics (halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide): Tox?

A

Hepatotoxicity (halothane)

Nephrotoxiticy (methozyflurane)

Proconvulsant (enflurane)

Expension of trapped gas in a body cavity (NO).

Can cause malignant hyperthermia: rare, life threatening hereditary condition in which inhaled anesthetics (except NO) and succinylcholine induce fever and severe muscle contractions.

55
Q

Malignant hyperthermia can be caused by what class of drugs?

Treatment?

A

Inhaled anesthetics

Tx = Dantrolene

56
Q

which barbiturate is used as an IV anesthetic?

what are the qualities that allow it rapid entry to CNS? what types/duration of procedures is it used for?

What terminates its anesthetic effect?

A

Thiopental

High potency, high lipid solubility –> rapid entry into brain.

Used for induction of anesthesia and short surg procedures.

Effect terminated by rapid redistribution into tissue (ie skel muscle) and fat. Decreases cerebral blood flow.

57
Q

what is the most common IV anesthetic used for endoscopy?

what class does it belong to?

what can it cause in post-op?

Tx for overdose?

A

Midazolam (Benzodiazepine)

Used along with gaseous anesthetics and narcotics.

May cause severe post-op resp depression, decreased BP and anterograde amnesia.

OD treated with flumazenil.

58
Q

Arylcyclohexylamine: what class does it belong to? aka what?

Mech?

Side effects?

A

IV Anesthetic. (aka Ketamine)

PCP analog, acts as dissociative anesthetic. Blocks NMDA receptors.

CV stimulant, can cause disorientation, hallucination, bad dreams.

Increases cerebral blood flow.

59
Q

What are some opioids that are used as IV anesthetics?

Used along with what other drugs?

A

Morphine, fentanyl

Used with other CNS depressants during general anesthesia.

60
Q

Propofol: Use? Mech?

How does it compare to Thiopental?

A

IV anesthetic.

Use: sedation in ICU rapid induction of anesthesia, short procedures.

Mech: potentiates GABA-A

Less post op nausea than Thiopental.

61
Q

Local anesthetics that are Esters? (3)

A
  • Procaine
  • Cocaine
  • Tetracaine
62
Q

Local anesthetics that are Imides? (3)

A
  • Ildocaine
  • Mepivacaine
  • Bupivacaine

(Amides have 2 I’s in the name)

63
Q

Local anesthetics (both esters and imides): Mech?

A

Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels - therefore most effective in rapidly firing neurons.

Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind ions as charged form

64
Q

Local anesthetics (both esters and imides): Principles

  • can be given with what?
  • in infected/acidic tissue, what occurs?
A

Can be given with vasoconstrictors (usually epi) to enhance local action. decreases bleeding, increases anesthesia by decreasing systemic concentration.

-In infected/acidic tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively –> need more anesthetic.

65
Q

Local anesthetics (both esters and imides): Principles

-what is the order of nerve blockade?

A

-Order of nerve blockade:

small-diameter fibers > large diameter.

myelinated > unmyelinated.

Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers.

66
Q

Local anesthetics (both esters and imides): Principles

-what is the order of sensory loss?

A

Order of sensory loss:

(1) pain (2) temp (3) touch (4) pressure

(pain/temp are carried by ALS/STT neurons; unmyelinated. touch/pressure carried by DC-ML neurons; myelinated)

67
Q

Local anesthetics (both esters and imides): Clinical Use?

A

minor surg procedures, spinal anesthesia.

If allergic to esters, give amides

68
Q

Local anesthetics (both esters and imides): Tox?

A

CNS excitation, severe CV tox (bupivacaine), HTN, hypotension, arrhythmias (cocaine)

69
Q

Neuromuscular blocking drugs: used for what? what receptor are they selective for?

A

Used for muscle paralysis in surgery or mechanical ventilation.

Selective for motor (vs autonomic) nicotinic receptor

70
Q

Depolarizing NM blocking drugs: name one.

Mech?

How to reverse the effect?

Complications?

A

Succinylcholine

Mech: strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction.

Reversal of Phase I (prolonged depolarization): no antidote. Block potentiated by cholinesterase inhibitors

Reversal of Phase II (repolarized but blocked, ACh receptors are available but desensitized): antidote = cholinesterase inhibitors

Complications: hypercalcemia, hyperkalemia, malignant hyperthermia

71
Q

Nondepolarizing NM blocking drugs: name 6

Mech?

How to reverse the blockade?

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 like bradycardia), edrophonium, other cholinesterase inhibitors

72
Q

Dantrolene

Mech? Use?

A

Mech: prevents the release of Ca2+ from the SR of skeletal muscle

Use: treatment of malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)

73
Q

Parkinsonism: due to loss of what neurons? increase of what activity?

What is an acronym for the Parkinson disease drugs?

A

Loss of dopaminergic neurons and excess cholinergic activity

BALSA: Bromocriptine, Amantidine, Levodopa/carbidopa, Selegiline, Antimuscarinics)

+ Benztropine

74
Q

What Parkinson disease drugs are dopamine agonists? (3)

A

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

Non-ergots are preferred.

75
Q

What Parkinson disease drugs increase dopamine? (2)

A
  • Amantadine (may increase dopamine release). also used as an antiviral against Inf A and rubella. Toxicity = ataxia
  • L-dopa/carbidopa (converted to dopamine in CNS)
76
Q

What Parkinson disease drugs prevent dopamine breakdown? (3)

A
  • Selegiline (selective MAO type B inhibitor)
  • Entacapone & Tolcapone (COMT inhibitors - prevent L-dopa degradation, increases dopamine availability)
77
Q

What Parkinson disease drugs curb excess cholinergic activity? (1)

A

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

“Park(insons) your Benz”

78
Q

use what drug for essential tremor or familial tremor?

A

Beta-blocker (ie propranolol)

79
Q

L-dopa/carbidopa: Mech?

Use?

Tox?

A

Mech: incr level of dopamine in brain. Unlike dopamine, L-dopa can cross the BBB and is converted by dopa decarboxylase in the CNS to dopamine. 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

Use: Parkinson’s

Tox: Arrythmias from increased peripheral formation of catecholamines. Long term use can lead to dyskinesia following administration (on-off phenomenon), akinesia between doses.

80
Q

Selegiline

Mech? Use? Tox?

A

Mech: selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepi and 5-HT, thereby increasing the availability of dopamine.

Use: Adjunctive agent to L-dopa for treating Parkinson’s

Tox: May enhance adverse effects of L-dopa

81
Q

Name 4 drugs for Alzheimers?

A
  • Memantine
  • Donepezil
  • Galantamine
  • Rivastigmine
82
Q

Memantine

Use? Mech? Tox?

A

Use: Alz

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

Tox: dizziness, confusion, hallucinations

83
Q

Donepezil, Galantamine, Rivastigmine

Use? Mech? Tox?

A

Use: Alz

Mech: AChE inhibitors

Tox: nausea, dizziness, insomnia

84
Q

Huntington’s: 3 drugs?

A
  • Tetrabenazine
  • Reserpine
  • Haloperidol
85
Q

What are the nT changes that occur with Huntingtons?

A

decreased GABA

decreased ACh

increased dopamine

86
Q

Tetrabenazine and Reserpine

Use? Mech?

A

Huntington’s

Mech: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release

87
Q

Haloperidol

Use? Mech?

A

Huntingtons

Mech: dopamine receptor antagonist

88
Q

Sumatriptan

Mech? Use? Tox?

Half-life?

A

Use: Acute migraine, cluster headaches

Mech: 5-HT (1B/1D) agonist. Inhibits trigeminal nerve activation. Prevents vasoactive peptide release; induces vasoconstriction.

Halflife < 2hrs

Tox: Coronary vasospasm (contraindicated in pts with CAD or Prinzmetal angina); mild tingling

“SUMO wrestler TRIPs ANd falls on your HEAD” (seriously?)

0. Step Ia (28 decks)

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