G-protein coupled receptors (mu, delta, kappa)
Opiod receptors are this type of receptor, and have these classes
Mu opiod receptor
Receptor that binds morphine and endorphins
Delta opiod receptor
Receptor that binds enkephalins
Kappa opiod receptor
Receptor that binds dynorphins
Drug category; Clinical Use: cough suppression, diarrhea; SE: respiratory depression, miosis, CNS depression (coma), constipation
Opiod drug; MOA: full mu agonist; SE: histamine release
Opiod drug; MOA: full mu agonist; other: useful for maintenance, long duration, orally active
Opiod drug; MOA: full mu agonist; SE: muscarinic antagonist (doesn't cause miosis), don't combine with SSRIs or MAOIs
Opiod drug; MOA: full mu agonist (the other commonly used opiod drug besides morphine)
Opiod drug; MOA: partial mu agonist; given in combination with NSAIDS, antitussive
OTC opiod analgesics
Dextramethorphan (antitussive), diphenoxylate (antidiarrheal), loperamide (antidiarrheal)
Opiod antagonist; short half-life; IV; used for acute opiod overdose
Opiod antagonist; PO; used to reduce ethanol craving (given to alcoholics)
Abstinence syndrome (withdrawal from opiods)
Anxiety, GI distress, gooseflesh, muscle spasms, rhinorrhea, sweating
Epilepsy drugs that block Na channels
Phenytoin, carbamazepine, topiramate, lamotrigine, valproic acid
epilepsy drug; MOA: blocks Na channels; SE: gingival hyperplasia, hirsutism, hydantoin fetus, megaloblastic anemia (decreases folate absorption)
epilepsy drug; MOA: blocks Na channels; SE: blood dyscrasias, teratogen
epilepsy drug; MOA: blocks Na channels; SE: Steven-Johnson syndrome
epilepsy drug; MOA: blocks Na channels, (inc GABA); SE: kidney stones
epilepsy drug; MOA: blocks Na channels, (inc) GABA, (-) T-type Ca++ channels; SE: rare fatal hepatotoxicity, causes fetal NTDs
Epilepsy drugs that block thalamic T-type Ca++ channels
Ethosuximide, Valproic acid
Epilepsy drugs that increase GABA
Topiramate, Valproic acid, Benzodiazepines, phenobarbitol, gabapentin
Benzodiazepines (diazepam, lorazepam)
epilepsy drug; MOA: (inc) GABA; SE: dependence (first line for acute seizures)
epilepsy drug; MOA: (inc) GABA; SE: dependence (first line for pregnant women, children)
epilepsy drug; MOA:(-) T-type Ca++ channels; SE: fatigue, GI, headache, Steven-Johnson Syndrome
epilepsy drug; MOA: (inc) GABA; SE: sedation, ataxia
Low solubility in blood = Rapid inducation and recovery.
Which acts faster, highly blood soluble anesthetics or low blood soluble anesthetics?
High lipid solubility = high potency
What effect does lipid solubility have on anesthetics.
As MAC increases potency decreases.
What effect does minimal alveolar concentration of anesthetics have on their potency?
Halothane, -flurane, NO2
List the inhaled anesthetics
What inhaled anesthetic has hepatotoxicity?
What inahled anesthetic has nephrotoxicity
What inhaled anesthetic is a proconvulsant?
Increase the duration of Cl- channel opening, thereby facilitating GABAa action (decreases neuron firing)
Increase the frequency of Cl- channel opening, thereby facilitating GABAa action (decreases neuron firing)
-zepams, zolams, and chlordiazepoxide
Drug used to treat benzodiazepine overdose, competitive antagonist at GABA receptor
(TOM thumb) triazolam, oxazepam, midazolam
B.B. King on OPIATES PROPOses FOOLishly (Barbiturates, benzodiazepines, Ketamine, opiates, propofol)
High potency barbiturate used for induction of anesthesia in short procedures, decreases cerebral blood flow (IV anesthetic)
Benzodiazepine that is the most common drug used for endoscopy, may cause severe postoperative respiratory depression (IV anesthetic)
A PCP analog used as a dissociative anasthetic, decreases cerebral blood flow (IV anesthetic)
2 opiates used with other CNS depressants during general anesthesia (IV anesthetics)
Used for rapid induction of anesthesia and short procedures, less postoperative nausea than other drugs (IV anesthetic)
Esters - end in caine, Amide end in -caine but have a second I
What are the Local anesthetics?
Bloack Na channels (preferentially bind activated Na channels)
Local anesthetics MOA
Small, myelinated fibers. Pain first, Pressure is last.
What fibers are affected first by loacal anesthetics?
Vasoconstrictors to enhance local action (except cocaine!)
What do you coadminister with local anesthetics and why?
What local anesthetics causes CNS excitation and severe cardiovascular toxicity?
Muscle paralysisin surgery or mechanical ventilation.
What are neuromuscular blocking drugs used for?
What receptor do NMJ blocking drugs target?
Succinylcholine. Phase 1 = prolonged depolarization. Phase 2 = Repolarized but bloacked.
What is the only depolarizine NMJ blocking drug and what are it's two phases?
Phase 1: Cholinesterase inhiitors makes it worse. Phase 2: Reversed by cholinesterase inhibitors
Effect of giving cholinesterase inhibitors in each phase of succinylcholine action.
Have cur in the name (end in cararine, curium or curonium)
What are the nondepolarizing NMJ blockers?
AChE inhibitors (neostigmine, edrophonium)
How do you reverse a nondepolarizing NMJ block?
Dantrolene (prevents release of Ca2+ from SR)
How do you treat malignant hyperthermia or neuroleptic malignant syndrome?
Using inhaled anesthetics (except NO2) + succinylcholine)
What causes malignant hyperthermia?
BALSA (Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics)
What is the mneumonic for Parkinson's treatments
Agonize dopamine receptors (bromocriptine), Inc Dopamine (Amantadine, Ldopa/carbidopa) Prevent dopamine breakdown (MAO B inh, selegiline), Curb excess cholinergics (benztropine, no effect on bradykinesia)
What are the 4 treatment classes for Parkinson's?
What is the treatment for essential or familial tremors?
L-dopa crosses the blood brain barrier and is converted in CNS to dopamine. Carbidopa inhibits peripheral decarboxylase.
How does the L-dopa/carbidopa treatment work?
L-dopa (when it's converted to dopamine in periphery)
What parkinson drug causes arrhythmais?
Selegiline (MAO-B inhibitor)
What drug is coadministered with L-dopa in parkinson's but may enhance its side effects?
Sumatripan. 5-HT 1D agonist. Causes vasoconstriction. Short half-life. (side effect = coronary vasospasm)
Treatment of migraines
CAD or prinzmetals (causes coronary vasospasm)
Contraindications for sumatripan