Pharm Flashcards
Bethanechol - MoA
Cholinomimetic - activates bladder and bowel smooth muscle; resistant to AChE
Carbachol - clinical use
constricts pupil and relieves intraocular pressure in glaucoma
Carbachol - MoA
Cholinomimetic - binds ACh receptor
Methacholine - Clinical use
challenge test for asthma diagnosis
Methacholine - MoA
cholinomimetic - stimulates muscarinic receptors in airway causing bronchoconstriction
Pilocarpine - clinical use
stimulator of sweat, tears, and saliva
treats open angle and closed angle glaucoma
Pilocarpine - MoA
Cholinomimetic - contracts ciliary muscle of eye (open-angle glaucoma), contracts pupillary sphincter (closed-angle glaucoma); resistant to AChE
Rivastigmine/Donepezil - clinical use
alzheimer disease
Rivistigmine/Donepezil - MoA
Anti-cholinesterase - increases ACh
Edrophonium - clinical use/MoA
diagnosis of myasthenia gravis (improves symptoms by increasing ACh in synapse)
Neostigmine - clinical use
Post-op and neurgenic ileus and urinary retention; myasthenia gravis, reversal of NMJ blockade
Neostigmine - MoA
Anti-AChE - increases ACh
No CNS penetration
Physostigmine - clinical use
anticholinergic toxicity (atropine overdose)
Physostigmine - MoA
anti-AChE - increases ACh
Crosses BBB - CNS activity
Pyridostigmine - clinical use
myasthenia gravis - long acting, increases muscle strength
Pyridostigmine - MoA
anti-AChE - increases ACh
Does NOT penetrate CNS
Cholinomimetic agents - contraindications
exacerbation of COPD, asthma, and peptic ulcers in susceptible patients
Cholinesterase inhibitor poisoning
Organophosphates - irreversibly inhibit AChE
DUMBBELSS - diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle and CNS, lacrimation, sweating, salivation
Antidote - Atropine + Pralidoxime (given early - regenerates AChE)
Atropine - clinical use
treat bradycardia and for ophthalmic applications (produces mydriasis and cycloplegia)
Atropine - MoA and effects
Muscarinic antagonist: Eye - pupil dilations and cycloplegia Airway - decreases secretions Stomach - decreases acid secretion Gut - decreases motility Bladder - decreases urgency (cystitis)
Atropine toxicity
Atropine Man - HOT as a hare (inc body temp due to dec sweating) DRY as a bone (dry mouth, dry skin) RED as a beet (flushed skin) BLIND as a bat (cycloplegia) MAD as a hatter (disorientation)
Benzotropine - clinical use
Parkinson disease, acute dystonia
Benzotropine - MoA
muscarinic antagonist (CNS)
Glycopyrrolate - clinical use
parental: preop use to reduce airway secretions
Oral: decrease drooling, peptic ulcers
Glycopyrrolate - MoA
Muscarinic antagonist - GI/Respiratory
Hyocyamine/dicyclomine - clinical use
antispasmodics for IBS
Hyoscyamine/dicyclomine - MoA
muscarinic antagonist - GI
ipratropium/tiotroprium - clinical use
COPD and asthma relief
ipratropium/tiotropium - MoA
muscarinic antagonist - Respiratory
solifenacin/tolterodine - clinical use
reduce bladder spasms and urge urinary incontinence - overactive bladder
solifenacin/tolterodine - MoA
muscarinic antagonists - genitourinary
scopolamine - clinical use
motion sickness
scopolamine - MoA
muscarinic antagonist - CNS
Albuterol/Salmeterol - clinical use
Albuterol - acute asthma
Salmeterol - long-term asthma/COPD control
Albuterol/Salmeterol - MoA
sympathomimetic - B2>B1 adrenergic agonist
Dobutamine - clinical use
heart failure (inotropic>chronotropic), cardiac stress testing
dobutamine - MoA
sympathomimetic - B1>B2,alpha adrenergic agonist
Dopamine - clinical use
unstable bradycardia, HF, shock
inotropic and chronotropic alpha effects predominate at high dose
dopamine - MoA
sympathomimetic - D1=D2> beta > alpha adrenergic agonist
Epinephrine - clinical use
anaphylaxis, asthma, open-angle glaucoma
alpha effects predominate at high dose
epinephrine - MoA
sympathomimetic - beta > alpha adrenergic agonist
much stronger effect at B2-receptor than norepinephrine
isoproterenol - clinical use
electrophysiologic eval of tachycardia; can worsen ischemia
isoproterenol - MoA
sympathomimetic - B1 = B2 adrenergic agonist
norepinephrine - clinical use
hypotension (decreases renal perfusion)
norepinephrine - MoA
sympathomimetic - alpha1 > alpha 2 > B1 adrenergic agonist
Significantly weaker at B2 than epinepherine
Phenylephrine - clinical use
Hypotension (vasoconstrictor); ocular procedures (mydriatic); rhinitis (decongestant)
Phenylephrine - MoA
sympathomimetic - alpha 1 > alpha 2 adrenergic agonist
amphetamine - clinical use
narcolepsy, obesity, ADHD
amphetamine - MoA
indirect sympathomimetic general agonist
reuptake inhibitor
releases stored catecholamines
“turns on the faucet and blocks the drain”
cocaine - clinical use
vasoconstriction and local anesthesia
cocaine - MoA
indirect sympathomimetic - general agonist reuptake inhibitor (blocks the drain)
cocaine - contraindications
do not give beta-blockers when suspected cocaine intoxications - can lead to unopposed alpha 1 activations -> extreme hypertension
ephedrine - clinical use
nasal decongestion, urinary incontinence, hypotension
ephedrine - MoA
indirect sympathomimetic - general agonist
releases stored catecholamines
Clonidine - clinical use
hypertensive urgency, does not decrease renal blood flow
Clonidine - MoA
sympatholytic - alpha 2 agonist
Clonidine - toxicity
CNS depression, bradycardia, hypotension, respiratory depression, miosis
methyldopa - clinical use
HTN in pregnancy
methyldopa - MoA
sympatholytic - alpha 2 agonist
Methyldopa - toxicity
SLE-like syndrome, direct Coombs + hemolysis
Bethanechol - clinical use
postop ileus, neurogenic ileus, urinary retention
Phenoxybenzamine - clinical use
pheochromocytoma (preoperatively) to prevent catecholamine crisis (hypertension)
phenoxybenzamine - MoA
alpha blocker (irreversible)
side effects - orthostatic hypotension and reflex tachycardia
Phentolamine - MoA
alpha blocker (reversible)
side effects - orthostatic hypotension and reflex tachycardia
Phentolamine - clinical use
give to patients on MAI inhibitors who eat tyrosine rich foods
Mirtazapine - clinical use
anti-depressant
side effects - sedation, increased serum cholesterol, increased appetite
Mirtazapine - MoA
alpha 2 selective blocker
Prazosin, terazosin, doxazosin, tamsulosin (-osin) - MoA
Selective alpha 1 blocker
Prazosin, terazosin, doxazosin, tamsulosin (-osin) - clinical use
urinary symptoms of BPH, PTSD (prazosin)
hypertension (NOT tamsulosin)
side effects - first dose orthostatic hypotension, dizziness, headache
Beta blocker effects - Angina
decrease heart rate and contractility, resulting in decreased O2 consumption
Beta blocker effects - MI
decrease mortality (metoprolol, carvedilol, bisoprolol)
beta blocker effects - SVT
decrease AV conduction velocity - class II antiarrhythmics (esmolol and metoprolol)
Beta blocker effects - hypertension
decrease CO, decrease renin secretion
Beta blocker effects - HF
decrease mortality in chronic HF
Beta blocker effects - glaucoma
Timolol - decreases secretion of aqueous humor
Beta blocker - toxicity
impotence, cardiovascular adverse effects (bradycardia, AV block, HF), CNS effects (seizures, sedation, sleep alterations), dyslipidemia (metoprolol), asthma/COPD exacerbations
B1 selective antagonists (B1>B2)
acebutolol, atenolol, esmolol, metoprolol
Non-selective Beta antagonists
pindolol (partial agonist), propranolol, timolol
Non-selective alpha and beta antagonists
carvediol and labetalol
Antihypertensive therapy - primary HTN
thiazide diuretics, ACE-I, ARBs, dihydropyridine calcium channel blockers
antihypertensive therapy - HTN w/ HF
diuretics, ACE-I/ARBs, beta-blockers, aldosterone agonists
antihypertensive therapy - diabetics
ACE-I, ARBs - protective against diabetic nephropathy
Calcium channel blockers, thiazide diuretics, beta-blockers
antihypertensive therapy - pregnancy
methyldopa (alpha-agonist), hydralazine, labetalol, nifedipine
Dihydropyridine calcium channel blockers - clinical use
(Amlodipine)
HTN, Angina (including Prinzmetal), Raynaud phenomenon
Dihydropyridine calcium channel blockers - MoA
(Amlodipine)
block voltage dependent calcium channels - decreased intracellular calcium - decreased muscle contractility (vascular smooth muscle)
Dihydropyridine calcium channel blockers - toxicity
(amlodipine)
reflex tachycardia, gingival hyperplasia
non-dihydropyridine calcium channel blockers - MoA
Diltiazem and verapamil
block voltage dependent calcium channels - decreased intracellular calcium - decreased muscle contractility (heart) - decreases CO
non-dihydropyridine calcium channel blockers - clinical use
diltiazem and verapamil
HTN, angina, atrial fibrillation/flutter
non-dihydropyridine calcium channel blockers - toxicity
verapamil - hyperprolactinemia, constipation, AV block
hydralazine - clinical use
severe HTN, HF
safe during pregnancy; administer w/ beta blocker to prevent reflex tachycardia
hydralazine - MoA
increases cGMP - smooth muscle relaxation
vasodilates arterioles > veins
decreases afterload
hydralazine - toxicity
compensatory tachycardia (contraindicated in angina, CAD), fluid retention, headache, angina
Lupus-like syndrome in slow-acetylators
Nitroprusside - clinical use
hypertensive emergency
Nitroprusside - MoA
increases cGMP via direct release of NO - dilation of arterioles and veins
Nitroprusside - toxicity
cyanide toxicity - releases cyanide
Fenoldopam - clinical use
hypertensive emergency
Fenoldopam - MoA
dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation
decreases BP, increases natriuresis
Nitrates - nitroglycerin, isosorbide dinitrate and mononitrate
MoA
vasodilate by increasing NO in vascular smooth muscle - increased cGMP and smooth muscle relaxation
dilate veins»_space; arterioles - decreases preload
Nitrates - nitroglycerin, isosorbide dinitrate and mononitrate
Clinical use
angina, acute coronary syndrome, pulmonary edema
Nitrates - nitroglycerin, isosorbide dinitrate and mononitrate
toxicity
reflex tachycardia (treat with beta blockers), hypotension, flushing, headache
HMG-CoA reductase inhibitors (statins) - MoA
inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)
HMG-CoA reductase inhibitors (statins) - lipid profile effects
decrease LDL»_space;> TG = VLDL
increase HDL
HMG-CoA reductase inhibitors (statins) - toxicity
hepatotoxic - increased LFT
myopathy when used with fibrates or niacin
Bile acid resins (cholestyramine) - MoA
prevent intestinal reabsorption of bile acids - liver uses cholesterol to produce new bile acids
Bile acid resins (cholestyramine) - lipid profile effects
decreases LDL
slightly increases HDL and TG
Bile acid resins (cholestyramine) - toxicity
GI upset, decreased absorption of other drugs and fat-soluble vitamins
Ezetimibe - MoA
prevents cholesterol absorption at the small intestine brush border
Ezetimibe - lipid profile effects
decreases LDL
Ezetimibe - toxicity
rarely increases LFT, diarrhea
Fibrates (gemfibrozil) - MoA
upregulate LPL - increase TG clearance
Active PPAR-alpha to induce HDL synthesis
Fibrates (gemfibrozil) - lipid profile effect
decrease TG»>LDL, increase HDL
Fibrates (gemfibrozil) - toxicity
myopathy (inc risk w/ statins)
cholesterol gallstones
Niacin (B3) - lipid profile effect
decreases LDL>TG
increases HDL
Niacin (B3) - MoA (lipids)
inhibits lipolysis in adipose tissue; reduces hepatice VLDL synthesis
Niacin (B3) - toxicity (lipid-lowering agent)
red, flushed face (due to inc PG) - decreased by taking NSAIDS
hyperglycemia, hyperuricemia
Cardiac glycosides (digoxin) - MoA
inotrope
directly inhibits sodium-potassium ATPase - indirectly inhibits sodium-calcium exchange - increases intracellular calcium - + inotropy
Indirect - stimulates vagus nerve - decreases HR
Cardiac glycosides (digoxin) - clinical use
HF, atrial fibrillation
Cardiac glycosides (digoxin) - toxicity
cholinergic - nausea, vomiting, diarrhea, blurry vision, arrhythmias, AV block
hyperkalemia - poor prognosis
Factors increasing toxicity - renal failure, hypokalemia, verapamil, amiodarone, quinidine
Cardiac glycosides (digoxin) - antidote
slowly normalize potassium, cardiac pacer, anti-digoxin Fab fragments, magnesium
Quinidine - MoA
Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
increases APD and ERP in ventricular AP (decreases slope of phase 0)
increases QT interval (prolongs repolarization - phase 3)
Procainamide - MoA
Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
increases APD and ERP in ventricular AP (decreases slope of phase 0)
increases QT interval (prolongs repolarization - phase 3)
Disopyramide - MoA
Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
increases APD and ERP in ventricular AP (decreases slope of phase 0)
increases QT interval (prolongs repolarization - phase 3)
Quinidine - clinical use
Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
atrial and ventricular arrythmias, re-entrant and ectopic SVT and VT
Procainamide - clinical use
Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
atrial and ventricular arrythmias, re-entrant and ectopic SVT and VT
Disopyramide - clinical use
Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
atrial and ventricular arrythmias, re-entrant and ectopic SVT and VT
Quinidine - toxicity
Cinchonism (headache and tinnitus)
thrombocytopenia
torsades de pointes due to long QT
Procainamide - toxicity
Reversible SLE - like symptoms (slow acetylators)
thrombocytopenia
torsades de pointes due to long QT
Disopryamide - toxicity
Heart failure
thrombocytopenia
torsades de pointes due to long QT
Lidocaine - MoA
Class IB antiarrhythmic - blocks inactive sodium channels (phase 0)
decrease slope of phase 0 and shorten AP duration
preferentially affect ischemic or depolarized purkinje and ventricular tissue
Mexiletine - MoA
Class IB antiarrhythmic - blocks inactive sodium channels (phase 0)
decrease slope of phase 0 and shorten AP duration
preferentially affect ischemic or depolarized purkinje and ventricular tissue
Lidocaine - clinical use
acute ventricular arrhythmias (post-MI)
digitalis induced arrythmias
Mexiletine - clinical use
acute ventricular arrhythmias (post-MI)
digitalis induced arrythmias
Lidocaine - toxicity
least cardiotoxic antiarrhythmics
CNS stimulation - seizures; CNS depression; CV depression
Mexiletine - toxicity
least cardiotoxic antiarrhythmics
CNS stimulation - seizures; CNS depression; CV depression
flecainide - MoA
Class IC antiarrhythmic - blocks fast sodium channels (phase 0)
decreases slope of phase 0, significantly prolongs ERP in AV node and accessory bypass tracks
No effect of ERP in purkinje and ventricles; minimal effect on AP duration
Propafenone - MoA
Class IC antiarrhythmic - blocks fast sodium channels (phase 0)
decreases slope of phase 0, significantly prolongs ERP in AV node and accessory bypass tracks
No effect of ERP in purkinje and ventricles; minimal effect on AP duration
Flecainide - clinical use
SVTs, including atrial fibrillation
last resort in refractory VT
Propafenone - clinical use
SVTs, including atrial fibrillation
last resort in refractory VT
Flecainide - toxicity
pro-arrhythmic (post-MI) - sudden death
Propafenone - toxicity
pro-arrhythmic (post-MI) - sudden death
Class II antiarrhythmics
Beta blockers!
Esmolol (cardioselective)
metoprolol, propranolol, atenolol, timolol, carvedilol
Class II antiarrhythmics - MoA
Beta blockers
decrease SA and AV nodal activity by decreasing cAMP and calcium currents
suppress abnormal pacemaker activity by decreasing slope of phase 4 (prolonged depolarization)
Class II antiarrhythmics - clinical use
SVT, ventricular rate control in atrial flutter and atrial fibrillation
Class II antiarrhythmics - toxicity
impotence, exacerbation of COPD/asthma, CV effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alteration)
may mask symptoms of hypoglycemia
Amiodarone - MoA
Antiarrhythmics - Class III (mimics I,II,III,IV) - potassium channel blocker - slows phase 3 - prolongs repolarization
increases AP duration, increases ERP, increases QT
Ibutilide - MoA
Antiarrhythmics - Class III - potassium channel blocker - slows phase 3 - prolongs repolarization
increases AP duration, increases ERP, increases QT
Sotalol - MoA
Antiarrhythmics - Class III - potassium channel blocker - slows phase 3 - prolongs repolarization
increases AP duration, increases ERP, increases QT
Dofetilide - MoA
Antiarrhythmics - Class III - potassium channel blocker - slows phase 3 - prolongs repolarization
increases AP duration, increases ERP, increases QT
Amiodarone - clinical use
atrial fibrilation, atrial flutter, VT
Sotalol - clinical use
atrial fibrilation, atrial flutter, VT
Ibutilide - clinical use
atrial fibrilation, atrial flutter
Dofetilide - clinical use
atrial fibrilation, atrial flutter
Amiodarone - toxicity
pulmonary fibrosis (check PFTs)
hepatotoxicity (check LFTs)
hyperthyroidism (Check TFTs)
acts as hapten - blue/grey skin deposits - photodermatitis
neurologic effects
constipation
CV effects - bradycardia, heart block, HF
Class IV antiarrhythmics
verapamil, diltiazem
calcium channel blockers - block slow calcium channels - slow rise of AP (phase 0) and prolong repolarization (phase 3)
decrease conduction velocity, increase ERP, increase PR
prevent nodal arrhythmias, rate control in atrial fibrillation
Adenosine
antiarrhythmic - increases potassium efflux - hyperpolarizes the cell and decreases intracellular calcium (Gi coupled - decreases cAMP)
diagnose/abolish SVT
Very short acting
Aspart, glulisine, lispro - MoA
rapid acting insulin - bind insulin receptor (tyrosine kinase)
Liver: increases glucose stored as glycogen
Muscle: increases glycogen, protein synthesis; increases potassium uptake
Fat: increases TG storage
Detemir, glargine - MoA
long acting insulin - bind insulin receptor (tyrosine kinase)
Liver: increases glucose stored as glycogen
Muscle: increases glycogen, protein synthesis; increases potassium uptake
Fat: increases TG storage
Metformin - MoA
biguanide - mechanism unknown
increases glycolysis, peripheral glucose uptake (insulin sensitivity)
decreases gluconeogenesis
Metformin - clinical use
oral - first line therapy for T2DM
cause modest weight loss
can be used in pts w/o islet cell function
Metformin - toxicity
GI upset, lactic acidosis (contraindicated in renal insufficiency)
Chlorpropamide, tolbutamide - MoA
first gen sulfonylureas
close potassium channel in beta-cell membrane - cell depolarizes - insulin release via calcium influx
Chlorpropamide, tolbutamide - clinical use
first gen sulfonylureas
stimulate release of endogenous insulin in T2DM.
Requires some islet cell function to work (not for T1DM).
Chlorpropamide, tolbutamide - toxicities
first gen sulfonylureas
risk of hypoglycemia (renal failure)
disulfiram-like effects
Glimepiride, glipizide, glyburide - MoA
2nd gen sulfonylureas
close potassium channel in beta-cell membrane - cell depolarizes - insulin release via calcium influx
Glimepiride, glipizide, glyburide - clinical use
2nd gen sulfonylureas
stimulate release of endogenous insulin in T2DM.
Requires some islet cell function to work (not for T1DM).
Glimepiride, glipizide, glyburide - toxicity
2nd gen sulfonylureas
risk of hypoglycemia (renal failure)
Pioglitazone, rosiglitazone - MoA
Glitazones/thiazolidinediones
increase insulin sensitivity in peripheral tissue
binds to PPAR-gamma nuclear transcription regulator
Pioglitazone, rosiglitazone - clinical use
Glitazones/thiazolidinediones
mono- or combined therapy for T2DM
Pioglitazone, rosiglitazone - toxicity
Glitazones/thiazolidinediones
weight gain, edema
hepatotoxicity, HF, increased risk of fractures
exenatide, liraglutide - clinical use/MoA
GLP-1 analogs - T2DM
increase insulin
decrease glucagon
exenatide, liraglutide - toxicity
GLP-1 analogs - T2DM
nausea, vomiting, pancreatitis
linagliptin, saxagliptin, sitagliptin - clinical use/MoA
DPP-4 inhibitors - T2DM
increase insulin
decrease glucagon
linagliptin, saxagliptin, sitagliptin - toxicity
DPP-4 inhibitors
mild urinary or respiratory infections
pramlintide - clinical use/MoA
amylin analogs - T2DM, T1DM
decrease gastric emptying
decrease glucagon
pramlintide - toxicity
hypoglycemia, nausea, diarrhea
canagliflozin - clinical use/MoA
SGLT-2 inhibitors - Type 2 DM
block reabsorption of glucose in PCT
canagliflozin - toxicity
SGLT-2 inhibitors
glucosuria, UTIs, vaginal yeast infections
acarbose, miglitol - clinical use, MoA
alpha-glucosidase inhibitors - T2DM
delayed carbohydrate hydrolysis and glucose absorption - decreased postprandial hyperglycemia
propylthiouracil - MoA/clinical use
block thyroid peroxidase, inhibiting the oxidation of iodide and then organification (coupling) or iodine - inhibition of thyroid hormone synthesis
Blocks 5-deiodinase - decreases peripheral conversion of T4 to T3
hyperthyroidism; can be used in pregnancy
methimazole - MoA/clinical use
block thyroid peroxidase, inhibiting the oxidation of iodide and then organification (coupling) or iodine - inhibition of thyroid hormone synthesis
Hyperthyroidism