Pharm 2 - Final 3

drraythe's version from 2015-11-10 19:52


Question Answer
What are the inotropic drugs?Digitalis & Cardiac Glycosides Digoxin, Digitoxin..
What are the Inodilators?The Phosphodiesterase Inhibitors (MILRINONE, IMAMRINONE, PIMOBENDAN) & also Dobutamine (rin would go camping w/ 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 (↑ Na in the cell, then Na exchanged for Ca w/ another pump, which means more Ca → better contraction)
Why would you use a Cardiac Glycoside?Congestive heart failure & atrial arrhythmias
How do Cardiac Glycosides affect the kidney?NO DIRECT EFFECT, just ↑ cardiac output which ↑ flow to kidney → more diuresis
Signs of cardiac tox in Cardiac Glycosides, why?PROTRACTED (prolonged) vomiting & diarrhea (stim CTZ)... also arrhythmias (so Tx & cz arrhythmia)
How does a Cardiac Glycoside relate to arrhythmias (how does it work)SLOW AV CONDUCTION → Tx atrial arrhythmias, can Tx Quinidine induced ventricular arrhythmias, BUT can also ↑ excitement → possible arrhythmogenic
How do Cardiac Glycosides distribute?EVERYWHERE EXCEPT FAT - CALC LEAN BODY MASS
How does the body ↑ the half-life of Cardiac Glycosides?Enterohepatic circulation
How could you help Tx a Cardiac 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 = (↑ tox/ efficacy) higher risk for arrhythmias (bc k usually inhibits the CG from binding all at once). HYPERCALCEMA = also ↑ efficacy (or tox) (more Ca avail to trade for Na)
How does Quinidine relate to Cardiac Glycosides?↑ EFFACACY! (Also ↑ tox) ↑ Absorption in intestine, ↓ excretion in kidney, & displaces from tissue binding sites so it has another chance to reach the heart
What do Phosphodiesterase Inhibitors do?↑ inotropy & vasodilate → INODILATORS
How do Phosphodiesterase Inhibitors work?It inhibits the Phosphodiesterase 3 enzyme, which leads to an accumulation of cAMP (does intracellular signal transduction) → ↑ cardiac contraction & vasodilation (3 makes hearts beat fast & vessels dilate)
What is Imarinone & whats special about it?Phosphodiesterase (3) Inhibitor, Produces positive inotropic action w/o ↑ 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 further improve positive inotropic action (↑ binding efficiency of cardiac myofibril to calcium ions) (bendan over so i can stick some more Ca in you) (PDE3 Inodilator)
What is the Β-1 adrenergic agonist? What is it used for? Admin & period of action?Dobutamine, congestive heart failure & cardiogenic shock, INJECT & works for 4min (fast acting & injectable for shock which is an emergency situation) (seeing a butt for the 1st 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 w/ CHF (makes sense, congestive HF is a heart thing but this bronchodilator helps w/ the lungs being messed up bc of the heart)
Major drawback of all VasodilatorsReflex tachycardia
PDE inhibitors for PDE3 is...The INODILATORS (3 makes ppls hearts beat hard & their vessels dilate)
*Amlodipine is a what? MOA & 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 & breath the nitrous bc you are tense to the point of an emergency)
Vasodilators cz reflex tachycardia...except for which 1?Prazosin (PRAZ Hilton is an asshole, but his heart is too small & slow, not too fast)
Hydralazine & Minoxidil (What category? MOA? Used for?)VASODILATORS. K+ ION INFLUX (opens K channels) hyperpolarize cell membrane. Used for Tx congestive heart failure associated w/ valvular degeneration (HYdra & 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 1 hard drug, put some under your tongue & you can run free & breathe free)
Isoxsuprine (Category? MOA? Does? Txs?)VASODILATOR. B2 agonist, VD of skeletal muscle blood vessels, used for navicular Dz & laminitis (B2 or not B2 → Shakespeare pun. you see, w/o their hoofs, a horse would cease "2B". & 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! (5 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
(2) Benazepril → Benazeprilat
What should you know about Furosemide & heart stuff?IV ROUTE IS FOR TX ACUTE VENTRICUALR FAILURE → 1st EFFECT IS ↑ IN VENOUS CAPATANCE!!! In 1st 5 min of admin Furosemide by IV route
Why/when would you want to use an ACE inhibitor?Heart failure & hypertension... ESP in ISCHEMIC heart condition. (bc wont cz sympathetic activation but still ↑ inotropy)
What is the MOA of ace inhibitors? (3 letters, 3 parts)They inhibit Angiotensin Converting enzyme II → this means no Angiotensin, 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 Angiotensin means less Aldosterone too → SAVE K+ & ↓ Na+ (retain less water)
What are the ACE inhibitors, & 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 ↓ the effectiveness of ACE inhibitors. This is bc NSAIDs block the Bradykinin induced vasodilation, bc thats controlled by prostaglandins & NSAIDs ↓ prostaglandins (& the ACE inhibitors are the reason there is ↑ Bradykinin)
What would you use in Lft-vent failure, what would & wouldnt you useWould: Dobutamine (↑ inotropy in emergency)
Furosemide (IV fast vasodilation ↓ workload)
Morphine Sulfate (↓ dyspnea & anxiety)
CLASS 1 DOES?Reduce phase 0 depol by blocking Na channels (membrane stabilize → anesthetics) (1 reduces the salt & hence the depol, in his diet, then he is numb to the heart pain)
CLASS 2 DOES?β-blockers more effective to control arrhythmias w/ high level of Catecholamines (β-blockers) (beta fish w/ a lot of Catecholamine in the water would have an arrhythmia for sure)
CLASS 3 DOES? (Name 2)Prolong action potential duration (Bretylium & Amiodarone → Ca & K channel blocker is why it's prolonged - brets potential is long & unending)
CLASS 4 DOES? (Name 2)Ca channel blockers (Verapamil, Diltiazem) (4 is like a calcium statue)
Class 1 drug which has vagolytic action, thus ↑ ventricular rate?QUINIDINE
What should you know about Class 1a?Prolongs duration of AP & refractory period (in ones A world, everything takes a little longer)
What should you know about Class 1b?Shortens duration of AP & refractory period (in injured cardiac cells) (1 be helping injured hearts)
What should you know about Class 1c?Shortens rate of depolarization in normal & injured cardiac cells (slow 1 can C all the injured & uninjured souls)
Quinidine → belongs to what class? MOA?Class 1a vagolytic action improves AV conduction & controls atrial tachyarrhythmia (usually in cahoots w/ Digoxin which is also anti-atrial-arrhythmia so you can remember it that way) (directly prolongs refractory period & indirectly prolongs refectory period bc of the vagolytic action)
Lidocaine → belongs to what class? Used for what? Note about its kineticsClass 1b. 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 Procainamide)
Aprindine → what class? Used for what?Class 1b Tx refractory arrhythmias, broader spec anti-arrhythmic action.
What are the Class 2 drugs, what are they used for? β-BLOCKERS (they end in lol) blocking β → Shortens AP & prolong AV conduction, which ↓ heart rate & contractility → used in arrhythmias w/ HIGH LEVELS OF CATECHOLAMNIES
Bretylium is which class, how does it work, & 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 anesthetized w/ halogenated hydrocarbon anesthetics. (BRET shouldnt be using halogenated hydrocarbon anesthetics...he'd fuck it up by releasing all of it as he said "NEat!" & then the adrenergic system is permanently blocked)
Amiodarone is which class, how does it work?Block K & Ca β-channels (AMI & DARONE have my BCK(β, Ca, K) )
What are the 2 drugs in Class 4? What is the MOA? SFx?Ca+ channel blocker, Verapamil, Diltiazem. Reduces abnormal impulse propagation in arrhythmias. SFx- hypotension & 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 cz what bad SFx?Arrhythmias! Dropped beat/block bc slows AV conduction, Ventricular bigeminal rhythm (& hypokalemia potentiates the arrhythmias)
Explain the interaction btwn Digoxin & QuinidineQuinidine displaces the Digoxin from it's tissue binding site so that more of it can act w/ the heart, also ↑ intestinal absorption & ↓ kidney excretion (if youre gonna Tx w/ Quinidine, should wait a week or ween a week w/ Digoxin). Digoxin Txs ventricular arrhythmias czd by Quinidine. Quinidine Txs atrial arrhythmias czd by Digoxin. (Kristen says: ↑ Digoxin toxicity - ↑ by 2- bc displaces tissue binding & PgP)
What is the effect of Digoxin & Calcium blocker?Inhibits tubule secretion of Digoxin - ↑ 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 & β-Blocker?Inhibits β-blocker metabolism = ↑ neg inotropic effects (so, Quinidine reduces the metabolism of β-blockers, which means there is more β-blocker around, & β-blockers ↓ inotropy (since usually you're using them to stop an arrhythmia where the hearts freaking out too much from too much Catecholamine) but in this case its too much)
What is the effect of a Calcium blocker & a β-blocker together?AV block ie Atenolol & Diltiazem (or Verapamil)

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