Neuro Pharm from FA Flashcards
where are the M receptors on the eye? what is their function?
pupillary sphincter (M3) - causes miosis
ciliary muscles (M3) - accomodation
where are the a1 receptors on the eye? what is their function?
pupillary dilator (a1)
causes mydriasis
where are the ß receptors on the eye? what is their function?
ciliary epithelium
produces aqueous humor
Glaucoma Drugs: overall mechanism?
Decr IOP via decr amount of aqueous humor. (inhibit synthesis/secretion, or increase drainage)
Epinephrine.
Class? Mech? SE?
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
Brimonidine
Class? Mech? SE?
Class: Glaucoma drug, Alpha-2 agonist
Mech: decr aqueous humor synthesis
SEs: Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis
Timolol, Betaxolol, Carteolol
Class? Mech? SE?
Class: Glaucoma drugs, beta-blockers
Mech: decr aqueous humor synthesis
SE: None given
Acetazolamide
Class? Mech? SE?
Class: Glaucoma drug, diuretic
Mech: decr aqueous humor synthesis via inhibition of carbonic anhydrase.
SE: None given
Pilocarpine, Carbachol
Class? Mech? SE?
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
Physostigimine, Echothiophate
Class? Mech? SE?
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)
Latanoprost (PGF-2alpha)
Class? Mech? SE?
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!!)
Big picture for glaucoma:
which drugs decr IOP by decreasing synthesis of aqueous humor? (6)
Alpha-agonists: Epinephrine, Brimonidine
Beta-blockers: Timolol, Betaxolol, Cartelol
Diuretics: Acetazolamide
Big picture for glaucoma:
which drugs decr IOP by increasing drainage/outflow of aqueous humor? (5)
Cholinomimetics: Pilocarpine, Carbachol, Physostigmine, Echothiophate
Prostaglandin: Latanoprost
List the opioid analgesics? (8)
Generally, clinical uses?
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
Morphine
Class? Mech? Use? Toxicity?
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)
Fentanyl
Class? Mech? Use? Tox?
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)
Codeine
Class? Mech? Use? Tox?
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)
Loperamide
Class? Mech? Use? Tox?
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)
Methadone
Class? Mech? Use? Tox?
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)
Meperidine
Class? Mech? Use? Tox?
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)
Dextromethorphan
Class? Mech? Use? Tox?
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)
Diphenoxylate
Class? Mech? Use? Tox?
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)
Butorphanol
Class? Mech? Use? Tox?
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
Tramadol
Class? Mech? Use? Tox?
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.
Epilepsy: First line drug for Simple Partial seizure?
Carbamazepine
Epilepsy: First line drug for Complex Partial seizure?
Carbamazepine
Epilepsy: First line drugs for Generalized Tonic-Clonic seizure? (3)
Phenytoin, Carbamazepine, Valproic acid
Epilepsy: First line drug for Absence seizure?
Ethosuximide
(Sucks to have Silent Seizures)
Epilepsy: First line drug for Status Epilepticus (Acute)?
Benzodiazepines (diazepam, lorazepam)
Epilepsy: First line drug for prophylaxis of Status Epilepticus?
Phenytoin
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
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)
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: fosphenytoin for parenteral use
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
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
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
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
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
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)
Levetiracetam
Use? Mech? SEs?
Use: Simple, Complex, Tonic-clonic seizures
Mech: unknown (may modulate GABA and glutamate release)
SEs: none
Tiagabine
Use? Mech? SEs? Notes?
Use: Simple, Complex seizures
Mech: Incr GABA by inhibiting uptake
SEs: none
Vigabatrin
Use? Mech? SEs? Notes?
Use: Simple, Complex seizures
Mech: Incr GABA by irreversibly inhibiting GABA transaminase
SEs: none
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
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.
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)
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”
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)
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.
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.
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)
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)
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
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)
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.
Malignant hyperthermia can be caused by what class of drugs?
Treatment?
Inhaled anesthetics
Tx = Dantrolene
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.
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.
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.
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.
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.
Local anesthetics that are Esters? (3)
- Procaine
- Cocaine
- Tetracaine
Local anesthetics that are Imides? (3)
- Ildocaine
- Mepivacaine
- Bupivacaine
(Amides have 2 I’s in the name)
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
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.
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.
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)
Local anesthetics (both esters and imides): Clinical Use?
minor surg procedures, spinal anesthesia.
If allergic to esters, give amides
Local anesthetics (both esters and imides): Tox?
CNS excitation, severe CV tox (bupivacaine), HTN, hypotension, arrhythmias (cocaine)
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
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
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
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)
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
What Parkinson disease drugs are dopamine agonists? (3)
Bromocriptine (ergot), pramipexole, ropinirole (non-ergot)
Non-ergots are preferred.
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)
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)
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”
use what drug for essential tremor or familial tremor?
Beta-blocker (ie propranolol)
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.
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
Name 4 drugs for Alzheimers?
- Memantine
- Donepezil
- Galantamine
- Rivastigmine
Memantine
Use? Mech? Tox?
Use: Alz
Mech: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)
Tox: dizziness, confusion, hallucinations
Donepezil, Galantamine, Rivastigmine
Use? Mech? Tox?
Use: Alz
Mech: AChE inhibitors
Tox: nausea, dizziness, insomnia
Huntington’s: 3 drugs?
- Tetrabenazine
- Reserpine
- Haloperidol
What are the nT changes that occur with Huntingtons?
decreased GABA
decreased ACh
increased dopamine
Tetrabenazine and Reserpine
Use? Mech?
Huntington’s
Mech: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release
Haloperidol
Use? Mech?
Huntingtons
Mech: dopamine receptor antagonist
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?)
