Pharm final 3

kelseyfmeyer's version from 2015-05-08 19:23


Question Answer
what are the inotropic drugs?digitalis and cardiac glycosides digoxin, digitoxin..
what are the inodilators?the phosphodiesterase inhibitors (MILRINONE, IMAMRINONE, PIMOBENDAN) and also dobutamine (rin would go camping with me in the desert-- DO BUTT was great)
what kinda drug is dobutamine?B1 selective agonist (inodilator too) (BETA BUTT is a #1good guy, not an antagonist)
MOA of cardiac glycosides (INOTROPIC DRUGS)inhibits the Na/K-ATPase (inc Na in the cell, then Na exchanged for Ca with another pump, which means more Ca--> better contraction)
why would you use a cardiac glycoside?congestive heart failure and atrial arrythmias
how do cardiac glycosides affect the kidney?NO DIRECT EFFECT, just inc cardiac output which inc flow to kidney--> more diuresis
signs of cardiac tox in cardiac glycosides, why?PROTRACTED vomiting and diarrhea(stim CTZ)... also arrythmias (so tx and cause arrythmia)
how does a cardiac glycoside relate to arrythmias (how does it work)SLOW AV CONDUCTION--> tx atrial arrythmias, can tx quinidine induced ventricular arrythmias, BUT can also inc excitement--> possible arrythogenic
how do cardiac glycosides distribute?EVERYWHERE EXCEPT FAT-- CALC LEAN BODY MASS
how does the body inc the half life of cardiac glycosides?enterohepatic circulation
how could you help tx a gardiac glycoside tox?add K+ bc inhibits rate of target binding
how safe are cardiac glycosides?NARROW MARGIN OF SAFETY
how do electrolyte levels affect cardiac glycosides?HYPOKALEMIA= (inc tox/ efficacy) higher risk for arrythmias (bc k usually inhibits the CG from binding all at once). HYPERCALCEMA= also inc efficacy (or tox)(more Ca avail to trade for Na)
how does quinidine relate to cardiac glycosides?INC EFFACACY!(also inc tox) inc absorption in intestine, dec excretion in kidney, and displaces from tissue binding sites so it has another chance to reach the heart
what do phosphodiesterase inhibitors do?inc inotropy and vasodilate--> INODILATORS
how do phosphodiesterase inhibitors work?it inhibits the phosphodiesterase 3 enzyme, which leads to an accumulation of cAMP(does intracellular signal transduction)--> inc cardiac contraction and vasodilation (THREE makes hearts beat fast and vessels dilate)
what is imamrinone, and whats special about it?phosphodiesterase(3) inhibitor, Produces positive inotropic action without increasing myocardial O2 consumption (In Rin you don't need air)
PDE inhibitors are used for what?tx acute myocardial failure (ino+dilation)
Pimobendan has what unique feature?improves binding efficiency of Ca++ for cardiac myofibers to furthur improve positive inotropic action (Increases binding efficiency of cardiac myofibril to calcium ions) (bendan over so i can stick some more Ca in you) (PDE3 inodilator)
what is the Beta-1 adrenergic agonist? what is it used for? admin and period of action?Dobutamine, Congestive heart failure and cardiogenic shock, INJECT and works for 4min (fast acting and injectable for shock which is an emergency situation) (seeing a butt for the first time is shocking)
what is Aminophylline? what is it used for?phosphodiesterase inhibitor which is mainly a bronchodilator, Indicated for taking care of acute pulmonary edema associated with CHF (makes sense, congestive HF is a heart thing but this bronchodilator helps with the lungs being messed up bc of the heart)
major drawback of all vasodilatorsreflex tachycardia
PDE inhibitors for PDE3 is...the INODILATORS (three makes ppls hearts beat hard AND their vessles dilate)
*amlodipine is a what? MOA and use?VASODILATOR. Ca channel blockers Blocks ca influx leading to VD. Used for hypertension in cats (A cat is as tense as a LOD of Ca++)
Sodium nitroprusside ( is a what? used for what? given how? MOA?)VERY RAPIDLY acting dilator used for hypertension emergencies. Given by IV. works by releasing nitric oxide (dont be a prussy, just shove it in the veins and breath the nitrous because you are tense to the point of an emergency)
vasodilators cause reflex tachycardia...except for which one?Prazosin (PRAZ hilton is an asshole, but his heart is too small and slow, not too fast)
Hydralazine and Minoxidil ( what category? MOA? used for?)VASODILATORS. K+ ION INFLUX (opens K channels) hyperpolarize cell membrane. used for tx congestive heart failure associated with valvular degeneration (HYdra and MINOtaur use POTASSIUM shields to fight the pope (MITRAL=VALVES) by shoving the potassium shield down his throat till it hits his liver)
Prazosin (category? MOA? use?)VASDILATOR. Antagonist of A1 receptor, used in CHF (minimal reflex tachycardia) (PRAZ hilton is a #1A-hole antagonist)
Nitroglycerin (category? MOA? admin? use?)VASODILATOR. Releases nitric oxide, admin as sublingual, transdermal patch, or ointment (NOT ORAL). cardiogenic pulmonary edema in dogs, laminitis in horses (nitroglycerin is one hard drug, put some under your tongue and you can run free and breathe free)
isoxsuprine (Category? MOA? Does? Treats?)VASODILATOR. B2 agonist, VD of skeletal muscle blood vessels, used for navicular disease and laminitis (B2 or not B2---> shakespere pun. you see, without their hoofs, a horse would cease "2B". And there isn't smooth mm in the feet so of course itd be skele mm BVs)
Sildenafil (category? MOA? does? use?)VASODILATOR! PDE5 INHIBITOR FOR PULMONARY HYPERTENSION! (Five feels like he cant breathe bc hes so tense so he's always looking out window SILs)
which vasodilator's metabolism is affected by uremic conditions?hydralazine
WHAT ARE THE PRODRUG ACE INHIBITORS?(1) Enalapril--> enalaprilat. (2) benazepril--> benazeprilat.
what should you know about furosemide and heart stuff?IV ROUTE IS FOR TX ACUTE VENTRICUALR FAILURE--> FIRST EFFECT IS INC IN VENOUS CAPATANCE!!! in first 5 min of admin furosamide by iv route
why/when would you want to use an ACE inhibitor?heart failure and hypertension... ESP in ISCHEMIC heart condition. (bc wont cause sympathetic activation but still inc inotropy)
what is the MOA of ace inhibitors? (Three letters, 3 parts)they inhibit angiotensin converting enzyme II--> this means no angiotension, so lower BP. angiotensin also degrades bradykinin, so you wont degrade, have more bradykinin-->bradykinin prevents sympathetic activation so then safer to use in ischemic heart dz. also inhibiting angiotension means less aldosterone too--> SAVE K+ and dec Na+ (retain less water)
What are the ACE inhibitors, and which are prodrugs(*)?Captopril, Enalapril*, benazepril* (The ACE popped a CAP EN BEN)
what kinda urinating do ACE inhibitors promote?natureisis (also they are excreted in the kidney)
how do NSAIDs/anti-prostaglandin things affect ACE inhibitors?NSAIDs will DEC the effectiveness of ACE inhibitors. This is bc NSAIDs block the bradykinin induced vasodilation, bc thats controlled by prostaglandins and NSAIDs dec prostaglandins (and the ACE inhibitors are the reason there is inc bradykinin)
what would you use in Lvent failure, what wouldnt you use(would): dobutamine(inc inotropy in emergency), furosemide(IV fast vasodilation dec workload), morphine sulfate(dec dyspnea and anxiety) (DONT USE EPINEPHERINE)
CLASS 1 DOES?reduce phase 0 depol by blocking Na channels (membrane stabilize--> anesthetics) (one reduces the salt, and hence the depol, in his diet, then he is numb to the heart pain)
CLASS 2 DOES?beta blockers more effective to control arrhythmias with high level of catecholamines (beta blockers) (beta fish with a lot of catecholamine in the water would have an arrythmia for sure)
CLASS 3 DOES? (name 2)prolong action protential duration (Bretylium and amiodarone--> Ca and K channel blocker is why it's prolonged--brets potential is long and unending)
CLASS 4 DOES? (name 2)Ca channel blockers (Verapamil, Diltiazem) (four is like a calcium statue)
class 1 drug which has vagolytic action, thus inc ventricular rate?QUINIDINE
what should you know about class 1a?prolongs duration of AP and refractory period (in ones A world, everything takes a little longer)
what should you know about class 1b?shortens duration of AP and refractory period (in injured cardiac cells) (one be helping injured hearts)
what should you know about class 1c?shortens rate of depolarization in normal and injured cardiac cells (slow 1 can C all the injured and uninjured souls)
quinidine--> belongs to what class? MOA?Class I(A) vagolytic action improves AV conduction and controls atrial tachyarrhythmia(usually in cahoots with digoxin which is also anti-atrial-arrythmia so you can remember it that way) (directly prolongs refractory period and indirectly prolongs refactory period bc of the vagolytic action)
Lidocaine--> belongs to what class? used for what? note about its kineticsClass 1(b). not for maintenance therapy but tx arrhythmias- sx, emergencies, high level catecholamines- has POOR bioavail (can be replaced w/ other drugs w better oral OBB like procainimide)
Aprindine--> what class? used for what?Class 1(b) tx refractory arrhythmias, broader spec anti-arrythmic action.
what are the class 2 drugs, what are they used for?BETA BLOCKERS (they end in lol) blocking beta--> Shortens AP & prolong AV conduction, which decreases heart rate and contractility--> used in arrythmias with HIGH LEVELS OF CATECHOLAMNIES
bretylium is which class, how does it work, and what should you know about it?Class 3, Adrenergic neuronal blocking agent. Promotes release of NE followed by permanent blockage. Usually contraindicated in animals previously anesthesized with halogenated hydrocarbon anesthetics. (BRET shouldnt be using halogenated hydrocarbon anesthetics...he'd fuck it up by releasing all of it as he said "NEat!" and then the andrenergic system is permanatly blocked)
amiodarone is which class, how does it work?Block K and Ca beta channels (AMI and DARONE have my BCK(beta, Ca, K) )
What are the two drugs in class 4? what is the MOA? side effects?Ca+ channel blocker, Verapamil, Diltiazem. reduces abnormal impulse propagation in arrythmias. Side effect- hypotension and bradycardia. (VERA wang loves ZEM calcium sculptures in her wedding garden)
Verapamil which class, MOA?class 4 Ca blocker
Diltiazem which class, MOA?class 4 Ca blocker
digoxin causes what bad side effect?arrythmias! dropped beat/block because slows AV conduction, Ventricular bigeminalrhythm (And hypokalemia potentiates the arrythmias)
explain the interaction between dignoxin and quinidinequinidine displaces the digoxin from it's tissue binding site so that more of it can act with the heart, also inc intestinal absorption and dec kidney excretion (if youre gonna tx with quinidine, should wait a week or ween a week with digoxin). Digoxin treats ventricular arrythmias caused by quinidine. Quinidine treats atrial arrythmias caused by digoxin. (Kristen says: Increased Digoxin toxicity-- increased by 2- bc displaces tissue binding and PgP)
What is the effect of Digoxin and Calcium blocker?inhibits tubule secretion of Digoxin- increase digoxin con (Ca blockers are Verapamil, Diltiazem) (ok, so, the Ca blocker blocks the Ca channels in the tubules of the kidney so digoxin isnt excreted there bc its usually renal excretion)
What is the effect of Quinidine and B Blocker? inhibits B- blocker metabolism = increase neg inotropic effects (so, quinidine reduces the metabolism of beta-blockers, which means there is more beta blocker around, and beta blockers dec inotropy (since usually you're using them to stop an arrythmia where the hearts freaking out too much from too much catecholamine) but in this case its too too much)
What is the effect of a Calcium blocker and a Beta blocker together?AV block ie altenolol and Diltiazem(or verapamil)

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