Pharm 2 - Cardio 2

isabellepjk's version from 2017-10-11 15:07


Question Answer
*What is the major drawback for all vasodilators?Reflex tachycardia
Sodium Nitroprusside (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 nitro bc you are tense to the point of an emergency)
**Hydralazine & Minoxidil (MOA? used for? use? admin? metabolism?)Produces VD of arteries by opening potassium channels in arteriolar smooth muscle membranes → hyperpolarizes cell membrane.
Used for CHF associated w/ valvular degeneration (mitral & aortic)
Oral admin
metabolism affected by the liver.
Prazosin (MOA? use?)Antagonist of A1 receptor, used in CHF (minimal reflex tachycardia).
Digoxin + Prazosin gives positive inotropic & peripheral VD
(Praz Hilton is an #1 A(hole). he has minimal reflexes on how to be a decent person)
Nitroglycerin (MOA? admin? use?)MoA → Releases Nitric Oxide
admin as sub-lingual, trans-dermal patch, or ointment. (Oral not recommended bc subjected to 1st pass & bioavail is low). Ointment used for cardiogenic pulmonary edema.
Can be used for laminitis in horses.
Emergency tx of angina.
Isoxsuprine (MOA? Does? Txs?)B2 agonist,
VD of skeletal muscle blood vessels, used for navicular dz & laminitis
*Amlodipine & Diltiazem (MOA? use?)Block Ca influx leading to VD.
Hypertension in cats (amlodipine)
**Sildenafil (MOA? does? use?)Inhibits PDE 5,
involved w/ degradation of cGMP.
Mostly seen in lung tissues & erectile tissue.
Used clinically for pulmonary hypertension in dogs.

(5 windowSILs for a GMPy DOG to look out from & breathe the fresh air & relax from it's tense outlook)

Check yo'self

Question Answer
*Hypertensive emergenciesSodium Nitroprusside
*MOA of releasing Nitric OxideSodium Nitroprusside, Nitroglycerin
*Opening potassium channels in arteriolar smooth muscle membranes → hyperpolarizes cell membraneHydralazine & Minoxidil
Used for CHF associated w/ valvular degeneration (NAME THE VALVES)The MITRAL & AORTIC valves. Hydralazine & Minoxidil
*Combined w/ Digoxin for pos inotropic effects & peripheral vasodilationPrazosin (paraz hilton has many guests on his sHow, like Digoxin!)
*Used in CHF w/ minimal reflex tachycardiaPrazosin
*Sublingual, transdermal patch, or ointment as admin - NOT ORALNitroglycerin
*Cardiogenic pulmonary edema, emergency tx of anginaNitroglycerin
*LaminitisNitroglycerin, Isoxsuprine
*Navicular dzIsoxsuprine
*β-2 agonistIsoxsuprine
Vasodilates SKELE MM BVsIsoxsuprine
*Ca++ channel blockers? DONT ADMIN WITH WHAT?Amlodiprine & Diltiazem
*Used for hypertension in catsAmlodipine
*Pulmonary hypertension in dogsSildenafil
*Which drug inhibits PDE5 (Which leads to what)Inhibit PDE5 → ↑ levels of cGMP. This is SILDENAFIL (that dog cant get his fil of the sil )

ACE inhibitors

Question Answer
*What are ACE inhibitors used for?
What do they cause
Heart failure & hypertension

What does ACE (the thing the drugs are inhibiting) do? (2) Where is it usually released from in the body? (2)ACE(ANGIOTENSIN-CONVERTING-ENZYME) is essential for converting Ang-1 to Ang-2. Also degrades Bradykinin. Released from lungs & kidney
What is going on if you inhibit Angiotensin 2 from being formed? (In terms of ions)↓ AT2 means ↓ Aldosterone, so ↓ Na in body & ↑ K in body
Which ion do you lose & which ion do you save in ACE inhibitors?ACE inhibition → ↓ Angiotensin 2 → ↓ Aldosterone → lose Na+ & save K+ (ACE at saving K & ACE at a low Na diet)
*What is going on w/ Bradykinin when you use an ACE inhibitor? What is the result of this? What condition is this desirable in?Inhibit ACE → Bradykinin NOT broken down, so more Bradykinin around → so there is vasodilation but the Bradykinin prevents the SYMPATHETIC ACTIVATION that VD normally would → safer to use in ischemic heart dz (Brady pushes the vessels open & tackles away the sympathetic nerves from working, so you can breathe easy about the parts that cant breathe easy)
*What type of heart dz are ACE inhibitors good to use w/ & why?Good for use in ISCHEMIC HEART DZ, bc ACE inhibitors inhibit the breakdown of Bradykinin & more Bradykinin will prevent the sympathetic system from reacting to the vasodilation (Which would make the ischemic condition worse otherwise)
~What is are not-prodrug ACE inhibitor drug?Captopril (right to the point, pop a CAP in your head, don't have to wait bc not a prodrug) (ALL END IN PRIL. So like ACEPRIL → APRIL)
What are the prodrug ACE inhibitors? What are their active metabolites ( & where are they metabolized)Metabolized in the LIVER
(1) Enalapril → Enalaprilat
(2) Benazepril → Benazeprilat (put an ACE bandage EN BENs liver....CAP doesnt need 1 cause he bust a cap 1st like a PRIL) (ACE is such a prilly man!)
*What diuretic group would you combine w/ the ACE Inhibitors & why would you do that?Can be combined w/ THIAZIDE diuretics to take care of mild CHF leading to hypertension (they make up for the fact that Thiazides are K-losing bc ACE inhibits Aldosterone which means ACE is K-sparing & compensates for that then)
*How do NSAIDs relate to 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)
How are ACE inhibitors excreted?Kidney

Left ventricular failure

Question Answer
How would you immediately Tx a Lft Ventricular Failure? & then would be the maintenance therapy?Tx: Dobutamine, Furosemide (IV), Morphine Sulfate (opiate analgesic). Then maintenance tx w/ Digoxin
*Why would you use Dobutamine in LVF?Enhances contractility
(it is a β-1 agonist which has inotropic effects... & you can IV inject it & it works SUPER FAST, w/in 16 min. half-life of 4 min tho, which is why need constant infusion & why youd use Digoxin & not this for the maintenance)
**Why would you use Furosemide in LVF & how do you admin?Admin via IV.
It is a Loop Diuretic & it reduces the preload by ↑ venous capacity (LOOPS ARE VENODILATORS) → redistributes congested blood from lungs to peripheral vessels. ↓ WORK LOAD ON FAILING HEART
*Why would you use Morphine Sulfate in LVF?HYPERCAPNIA/DYSPNEA
It is an opiate analgesic, which ↓ response of higher medullary center to ↑ levels of CO2 → relieves the dyspnea & anxiety associated w/ LVF
***Which drug is contraindicated in LVF?Epinephrine


The Class Game!

Question Answer
*Class I does?Membrane stabilizers/local anesthetic agents (One is stable & numb when he lives out in the woods)
Membrane stabilizers/local anesthetic agents is what Class?Class I
*Class II does?β-blockers (β blockers has 2 Bs in it → Class II)
Β-blockers is what Class?Class II
*Class III does?Agents that prolong action potential duration & refractory period (i want to prolong the action 3 times, even if it means you have a longer refractory period, bc i wanna go 3 times in a night)
Agents that prolong action potential duration & refractory period are what Class?Class III
*Class IV does?Ca channel blockers (4 strong bones & teeth, Ca!)
Ca channel blockers are what Class?Class IV
*Phenytoin, Quinidine, Lidocaine, Procainamide are from what Class?Class I
*Propranolol, Atenolol, Esmolol. Metoprolol are from what Class?Class II
*Bretylium, Amiodarone are from what Class?Class III
*Verapamil, Diltiazem are from what Class?Class IV
*Class IA does what?(Class I in general are membrane stabilizers/local anesthetic agents) reduces Phase 0 of the action potential; prolong the duration of action potential & refractory period
Reduces Phase 0 of the action potential; prolong the duration of action potential & refractory period is Class I__?A
*Class IB does what?(Class I in general are membrane stabilizers/local anesthetic agents) reduces Phase 0 depolarization & conduction velocity, minimal shortening effect on action potential duration & refractory period
Reduces Phase 0 depolarization & conduction velocity, minimal shortening effect on action potential duration & refractory period is Class I__?B
*Class IC does what?Reduces the rate of depolarization in normal & injured cardiac cells
*Reduces the rate of depolarization in normal & injured cardiac cells is Class I_?C
*Quinidine, Procainamide, Disopyramide are in Class I__?A
*Phenytoin, Lidocaine, Tocainide, Aprindine, Indecainide are in Class I_?B
*Flecainide, Encainide, Lorcainide are in Class I_?C
Explain Class I A, B & CAll Class ones reduce Phase 0 of the action potential (Which is rapid depol phase of Na, means drugs are blocking Na channels) . A PROLONGS duration of action potential/refractory period. B SHORTENS action potential/refractory period. C just reduces the rate of depol. (SO. LONG, SHORT, NADA)

Class I

Question Answer
Class I in GENERAL are?Membrane stabilizers/ Local anesthetic agents
*Class IA does what?Reduces Phase 0 depol. of AP by blocking Voltage-Gated (VG) Na channels, which ↑ threshold of exitability – prolonging duration of AP & refractory period
**Quinidine does what? Used for what? Class?)vagolytic action improves AV conduction & controls atrial tachyarrhythmia– Used for atrial arrhythmia. Class IA (usually in cahoots w/ Digoxin which is also anti-atrial-arrhythmia so you can remember it that way) (directly prolongs refractory period & indirectly prolongs refractory period bc of the vagolytic action) MUSCUARINIC
*Procainamide does what? Used for what? Class?)Vagolytic action here is less prominent more preferred for ventricular arrhythmias. Class IA (PRO-V you can Tx the ventricular arrhythmia)
What are the 3 drugs in Class IA?Quinidine, Procainamide & Disopyramide ( A1 sauce made w/ quinine sounds gross. adding procaine, no matter how much of a pro it is at numbing, will not help the pyramid-sized DISgusting flavor)
*Which CLASS IA is preferred for atrial arrhythmia? Which for ventricular arrhythmia?Atrial = Quinidine
Ventricular = Procainamide
*Class IB does what?Reduces Phase 0 depolarization & conduction velocity in injured cardiac cells minimal shortening effect on AP duration & refractory period (B for butthurt, aka injured cells))
*Lidocaine admin? Speed of action? Use? Class?)Class IB. RAPID onset w/ pronounced effects in a short period of time. Given only IV (poor oral absorb). Produces more efficacious effect used for arrhythmias during surgery/anesthesia or infarctions (emergencies) → not good for maintenance (poor oral absorp & short half-life), Corrects Epi & Digitalis induced arryth. (Lidocaine...remember from pharm 1? inject to save from arrhythmia in an emergency bc fast & IV. only really good for emergencies tho)
*Phenytoin admin? Speed? Use? Class?Class IB. Poor oral absorb. Tx Ventricular Arryth. & Digitalis induced Arryth.
*You should never give Phenytion with?Chloramphenicol (Both have ph in the name)
*What are the signs of Phenytion Tox?Postural ataxia & hypermetric gait (both start w/ 'P' or makes them walk Phenny)
Tocainide admin? Metabolism? Use? Class?)Class IB. ORAL admin, less hepatic metabolism (so avoids 1st pass) & can be used as maintenance tx for arrhythmia (We B eating (oral) toc to maintain our figures)
Special thing about Tocainide?No 1st pass effect
**Aprinidine (spectrum? What does it do? What does it Tx? SFx? Class?)Class IB Broader spectrum anti-arrhythmic . Abolishes premature complexes & ventricular tachycardia.
Only down side – SFx that produces Leukopenia, Hypotension, Hepatotoxicosis & Ataxia.
It is reserved for Refractory (resistant to other drugs) arrhythmias. (This App is great as a last resort, but it B full of crappy SFx)
*Aprinidine SFx?Leukopenia, Hypotension, Hepatotoxicosis & Ataxia
Indecainide (How strong? SFx? Usually compared to? Class?)Class IB. More potent w/ less SFx compared to Aprinidine (INDECated to be even better than the AP(rinidine) before on this website, bc stronger w/ less SFx! & theyre in the same Class of prices (B) )
*Class IC does what?Reduces rate of depolarization in normal & injured cardiac cells
no effect on AP duration and Refractory period
*What are the drugs in Class IC? What do they do?Flecainide
Lorcainide – effective against ventricular tachycardia & premature beats of atrial or ventricular origin W/O AFFECTING THE AP!! (I C FLECs EN LORis cool CAIN (cane), the CAIN she uses to beat hyper, premature ventricles into submission)
*Class IC drugs are used to Tx?Effective against ventricular tachycardia & premature beats of atrial or ventricular origin (remember, FLECs EN LORis CAIN to beat the hyper ventricle & the jumping the gun ventricle & atria)
Whats so special about the Class IC drugs?They work w/o affecting the AP!