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0. Step Ia > Neuro Pharm from FA > Flashcards

Neuro Pharm from FA Flashcards

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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
Epilepsy: First line drug for Simple Partial seizure?
Carbamazepine
26
Epilepsy: First line drug for Complex Partial seizure?
Carbamazepine
27
Epilepsy: First line drugs for Generalized Tonic-Clonic seizure? (3)
Phenytoin, Carbamazepine, Valproic acid
28
Epilepsy: First line drug for Absence seizure?
Etho**sux**imide | (Sucks to have Silent Seizures)
29
Epilepsy: First line drug for Status Epilepticus (Acute)?
Benzodiazepines (diazepam, lorazepam)
30
Epilepsy: First line drug for prophylaxis of Status Epilepticus?
Phenytoin
31
Ethosuximide Use? Mech? SEs? Notes?
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
32
Benzodiadepines (diazepam, lorazepam) Use? Mech? SEs? Notes?
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)
33
Phenytoin Use? Mech? SEs? Notes?
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: **fos**phenytoin for parenteral use
34
Carbamazepine Use? Mech? SEs? Notes?
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
35
Valproic acid Use? Mech? SEs? Notes?
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
36
Gabapentin Use? Mech? SEs? Notes?
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
Phenobarbital Use? Mech? SEs? Notes?
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
Topiramate Use? Mech? SEs? Notes?
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
Lamotrigine Use? Mech? SEs?
Use: simple, complex, tonic-clonic, absence seizures Mech: Blocks voltage-gated Na channels SE: Stevens-Johnson synd. (must be titrated slowly)
40
Levetiracetam Use? Mech? SEs?
Use: Simple, Complex, Tonic-clonic seizures Mech: unknown (may modulate GABA and glutamate release) SEs: none
41
Tiagabine Use? Mech? SEs? Notes?
Use: Simple, Complex seizures Mech: Incr GABA by inhibiting uptake SEs: none
42
Vigabatrin Use? Mech? SEs? Notes?
Use: Simple, Complex seizures Mech: Incr GABA by irreversibly inhibiting GABA transaminase SEs: none
43
what is Stevens-Johnson syndrome? Which epilepsy meds cause it? (4)
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
Barbituates (Phenobarbital, pentobarbital, thiopental, secobarbital): Mechanism?
Facalitate GABA-A action by increasing duration of Cl channel opening, thus decreasing neuron firing. (BarbiDURAtes increase DURAtion) Contraindicated in porphyria.
45
Barbituates (Phenobarbital, pentobarbital, thiopental, secobarbital): Clinical Use? Toxicity?
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
Benzodiazepines (Diazepam, lorazepam, triazolam, temazepam, temazepam, oxazepam, midalozam, chlordiazepoxide, alprazolam): Mech?
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
Benzodiazepines (Diazepam, lorazepam, triazolam, temazepam, temazepam, oxazepam, midalozam, chlordiazepoxide, alprazolam): Clinical Use? Tox?
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
Nonbenzodiazepine hypnotics (Zoplidem, Zaleplon, esZopicline": Mech? How to reverse?
(All ZZZZs put you to sleep) Mech: Act via the BZ1 subtype of the GABA receptor. Reverse with flumazenil.
49
Nonbenzodiazepine hypnotics (Zoplidem, Zaleplon, esZopicline": Use? Tox?
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
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?
- 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
MAC: what is this and how does it relate to anesthetics?
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
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?
N2O: fast induction, low potency Halothane: slow induction, high potency
53
Inhaled anesthetics (halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide): Mech? Effects?
Mech is unknown (that is unsettling!) Effects: Myocardial depression, resp depression, nausea/vomiting, incr cerebral blood flow (decr cerebral metabolic demand)
54
Inhaled anesthetics (halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide): Tox?
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
Malignant hyperthermia can be caused by what class of drugs? Treatment?
Inhaled anesthetics Tx = Dantrolene
56
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?
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
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?
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
Arylcyclohexylamine: what class does it belong to? aka what? Mech? Side effects?
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
What are some opioids that are used as IV anesthetics? Used along with what other drugs?
Morphine, fentanyl Used with other CNS depressants during general anesthesia.
60
Propofol: Use? Mech? How does it compare to Thiopental?
IV anesthetic. Use: sedation in ICU rapid induction of anesthesia, short procedures. Mech: potentiates GABA-A Less post op nausea than Thiopental.
61
Local anesthetics that are Esters? (3)
- Procaine - Cocaine - Tetracaine
62
Local anesthetics that are Imides? (3)
- Ildocaine - Mepivacaine - Bupivacaine (Amides have 2 I's in the name)
63
Local anesthetics (both esters and imides): Mech?
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
Local anesthetics (both esters and imides): Principles - can be given with what? - in infected/acidic tissue, what occurs?
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
Local anesthetics (both esters and imides): Principles -what is the order of nerve blockade?
-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
Local anesthetics (both esters and imides): Principles -what is the order of sensory loss?
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
Local anesthetics (both esters and imides): Clinical Use?
minor surg procedures, spinal anesthesia. If allergic to esters, give amides
68
Local anesthetics (both esters and imides): Tox?
CNS excitation, severe CV tox (bupivacaine), HTN, hypotension, arrhythmias (cocaine)
69
Neuromuscular blocking drugs: used for what? what receptor are they selective for?
Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs autonomic) nicotinic receptor
70
Depolarizing NM blocking drugs: name one. Mech? How to reverse the effect? Complications?
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
Nondepolarizing NM blocking drugs: name 6 Mech? How to reverse the blockade?
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
Dantrolene Mech? Use?
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
Parkinsonism: due to loss of what neurons? increase of what activity? What is an acronym for the Parkinson disease drugs?
Loss of dopaminergic neurons and excess cholinergic activity BALSA: Bromocriptine, Amantidine, Levodopa/carbidopa, Selegiline, Antimuscarinics) + Benztropine
74
What Parkinson disease drugs are dopamine agonists? (3)
Bromocriptine (ergot), pramipexole, ropinirole (non-ergot) Non-ergots are preferred.
75
What Parkinson disease drugs increase dopamine? (2)
- 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
What Parkinson disease drugs prevent dopamine breakdown? (3)
- Selegiline (selective MAO type B inhibitor) - Entacapone & Tolcapone (COMT inhibitors - prevent L-dopa degradation, increases dopamine availability)
77
What Parkinson disease drugs curb excess cholinergic activity? (1)
Benztropine (antimuscarinic; improves tremor and rigidity, but has little effect on bradykinesia) "Park(insons) your Benz"
78
use what drug for essential tremor or familial tremor?
Beta-blocker (ie propranolol)
79
L-dopa/carbidopa: Mech? Use? Tox?
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
Selegiline Mech? Use? Tox?
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
Name 4 drugs for Alzheimers?
- Memantine - Donepezil - Galantamine - Rivastigmine
82
Memantine Use? Mech? Tox?
Use: Alz Mech: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+) Tox: dizziness, confusion, hallucinations
83
Donepezil, Galantamine, Rivastigmine Use? Mech? Tox?
Use: Alz Mech: AChE inhibitors Tox: nausea, dizziness, insomnia
84
Huntington's: 3 drugs?
- Tetrabenazine - Reserpine - Haloperidol
85
What are the nT changes that occur with Huntingtons?
decreased GABA decreased ACh increased dopamine
86
Tetrabenazine and Reserpine Use? Mech?
Huntington's Mech: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release
87
Haloperidol Use? Mech?
Huntingtons Mech: dopamine receptor antagonist
88
Sumatriptan Mech? Use? Tox? Half-life?
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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