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Pharm Cardio Drugs
CV Drugs
40
Science
Graduate
06/21/2009

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Term
Bile Acid Binding Resins
Definition

Dyslipidemia

Mech: bind bile acids -> Stool -> More synth from liver -> Liver cholesterol depletion -> Stimulate LDL receptors -> More LDL taken from blood

Causes: decrease LDL, increase TG and HDL

Use: Adjuvant  w/statin b/c high LDL

SE: bloating, dyspepsia, constipation

Other: Good offset by increase in chol synth, use statin, can also interfere w/absorption of other oral drugs

Term
Statins
Definition

Dyslipidemia

Mech: Inhib hepatic HMG-CoA reductase (needed for chol synth) -> more LDL receptors expressed -> more LDL removed from blood

Response: Decrease LDL and TG, increase HDL

Use: Primary and secondary prevention of CAD, use in combo

SE: Myopathy (dose related, drugs interactions involved), hepatotoxic

Other: More than just effects on decrease cholesterol (CAD): improve endothelial cell function, enhance plaque stability, reduce inflamm

Term
Cholesterol Absorption Blockers
Definition

Dyslipidemia

Ezetimibe

Mech: Inhibit traporter in jejunum via NPC1L1 protein -> decrease cholesterol uptake -> more synth in liver -> more LDL receptors on hepatocytses -> more LDL removed from blood

Response: Decrease LDL and TGs, Increase HDL

Use: Adjuvant to statins

SE: RARE allergic rxn

Other: Bile acid binding resinds inhib absorpt of ezetimibe (use other or other w/a statin)

Term
Niacin (Nicotinic Acid)
Definition

Mech: Inhib lypolysis of TG via hormone sensitive lipase in fatty tissue -> less FFA transport to liver and hepatic TG synth -> less TG synth via inhibition of esterification of FA in liver

Increase HDL-C via decrease clearance of apoA-1

Response: Decrease LDL, TGs and VDLD, Increase HDL

Use: High triglycerides, high LDL, and low HDL-C levels

SE: Flushing, hepatotoxic, insulin-resistnace, gout, GI

Other: Using niacin + statin = increase in statin-induced myopathy. Uses sustaines-release niacin (Niaspan)

Term
Fibrates
Definition

Dyslipidimia

Mech: Binds PPARalpha (nuclear receptor that normally turns on fatty acid synth to make TGs in liver and brown adipose tissue) -> decrease TGs via stim of FA oxidation, increased liporpotein lipase synthesis and decreased apoC-III

Increase HDL-C b/c of PPARalpha stim of apoA-I and apoA-II expression

Response: Decrease LDL and TG, increase HDL

Use: Severe high TGs and low HDLs like in metabolic syndromes (Type II Diabetes)

SE: GI, urticaria (hives), hair loss

Other: Fibrates + Statin = increased statin-induced myopathy (heart disease), LDL increase in some, use is combo but has same SE for myopathy as the niacin/statin combo, good @ decreasing TGs

Term
Nitrates
Definition

Angina, Heart Failure (acute decomp)

Mech: Enter cell -> release NO -> activate gualylate cyclase -> cGMP -> vascular smooth M -> vasorelaxation (ESP VEINS RELAX TO PULL BLOOD AWAY FROM HEART)

Plates -> Inhibition of aggregation

Response: DECREASE SYSTEMIC VENOUS CONTRACTION (decrease work, decrease O2 needed, decrease filling P, decrease preload), systemic arterial contraction (decrease work, decrease O2 needed, decrease filling pressure, decrease afterload),  and pulmonary/systemic edema (decrease work), large coronary aretery contraction (increase O2 supply)

Use: under tongue or IV to terminate angina episode OR oral, patch or ointment for prophylaxis (angina)

HF: IV or sublingual for acute decomp, limited w/hydalazine or in acute decomp (because decrease preload)

SE: headache (everyone gets, will go away), flushing, hypotension

Other: Tolerance = major problem thus use intermittantly. Sildenafil and other ED drugs last longer b/c blockage of cGMP metabolism

In Stable angina = veins relax

In Varient angina = reverses spasms

Term
B-adrenergic Blockers
Definition

Stable Angina, Hypertension

Mech: competitively block B-ad receptors

Response: decrease HR and contractility, arterial blood pressure (decrease O2 demand), increase coronary flow via increase time in diastole (increase O2 supply)

HT: decrease CO, renin release and SNS to decrease BP (not sure how or why but it does)

Use: orally for chronic prophylaxis of stable, unpredictable in variant

HT: low and high dose works same, younger and middle-age HT's (non-blacks) respond best

SE: cardiac effects, bronchoconstriction, lethargy, fatigue, metnal depression, nightmares, hypoglycemia

Other: use w/caustion in people w/conduction disorders or obstructive lung disease, abrupt withdrawls can cause attacks or other ishemic symptoms (very dangerous rebound effect)

Term
Ca Channel Blockers
Definition

Chronic Stable or Variant Angina, HT

Two classes: dihydropyridine type ("pines": mainly on BV's, little effect on heart) and D,V (strong effect on heart, weak effect on BV's)

Mech: non-comp inhibit Ca++ thru V-sensitive L-type membrane Ca channels, DV also slows channel recovery time

Response: DV: decrease HR and contractility (decrease O2 demand), All: decrease systemic arterial contraction (decrease O2 demand) and coronary artery contraction (increase O2 supply)

Use: Chronic prophylaxis of stable or variant angina

SE: headache, dizzy, flushing, hypotension, leg edema, V = constipation and nausea

Other: careful in conduction issues and in combo w/B-blockers b/c can cause heart failure (VD, but can use dihydro + b-blockers), lots of drug interactions

Stable: decrease work

Variant: coronary A spasm

Term
Ranolazine
Definition

Chronic prophylaxis of Stable Angina

Mech: 1. Block "late" Na current -> stop increased intracellular Na and Ca caused by ishchemia

2. Block FA oxidation -> use glucose (more efficent) instead

Response: No affect on BP or HR, increase exercise tolerance, decrease anginal attacks

Use: Alone as oral prophylaxis of chronic stable angina OR combo w/nitrates, b-blocks, or Ca channel blocks

SE (rare): dizzy, headache, constipation, nausea

Other: efficacy and tolerability NOT change elderly and comorbid (preexisting) conditions (diabetes, heart fail)

ALMOST ALL PTS CAN TAKE SAFELY!!! (b-block have issues in diabetes and heart fail)

Term
Mech of Ischemia and how Ranolazine works
Definition

Ischemia -> Na/K ATPase + NHE + increase late Na current -> Na overload -> NCX -> Ca overload -> Mechanical dysfucntion (increase diastolic tension and decrease contractility) electrical issues (arryth) and O2 issue (increase ATP consumption and decreased ATP production)

Ranol: blocks the late Na current which stops the Na overload....YAY!

Term
Newer Drugs for Chronic Stable Angina
Definition

Ivabradine: block pacemaker current -> decrease HR

Nicorandil: open ATP-sensitive K channels -> coronary dilation

Trimetazidine: inhibit mitochondrial 3-ketoAcyl CoA thiolase -> FA use to carb use for E (more efficient)

Perhexilene: inhib mitochondrial carnitine-palmitoyl-transferase -> FA use to carb use for E

Term
Aspirin
Definition

Unstable Angina Thrombosis

Anti-platelet drug

Mech: Irreversibly acetylates COX-I -> blocks TxA2 synth -> less platelet aggregation (lasts 7-10 days b/c need to make more platelets)

Response: PHENOMENAL decrease in risk of death or MI, can see benefits in 1st day of treat!

Use: oral, use low dose to minimize bleeding potential

SE: risk of bleeding, allergy in some

Other: 5-8% show resistance to x-plate effects (have increase risk of SE's)

Term
ADP Inhibitors
Definition

Unstable Angina Thrombosis

Anti-platelet drug

Mech: inhib ADP binding to receptor -> decrease plate agg and activation

Response: decrease risk of death or MI, early is better

Use: Oral, slow onset (b/c pro-drug), long duration (4-8 days), combo w/aspirin

SE: neutropenia, thrombotic thrombocytopenic purpura, GI bleed (less than aspirin)

Other: Clopidogrel = rapidly replacing ticlopidine b/c quicker onset and less neutropenia.  Some people resistant to clopidogrel.

Term
GP IIb/IIIa Receptor Inhibitor
Definition

Unstable Angina Thrombosis (percutaenous coronary interventions)

Anti-Platelet

Mech: prevent fibrinogen mediated cross-liknage via GP IIb/IIIa receptors -> less aggregation

Response: Decrease in risk of death or MI, early is better

Use: IV, short duration of action (use in surg), oral doesn't work, combo w/aspirin and hep

SE: thrombocytopenia, bleeding

Other: best used prior to percutaneous coronary interventions than in unstable angina

Term
Heparin
Definition

Anticoag

Mech: catalyzes inhib of several coag proteases by antithrombin

X-thrombin -> inhib coag factors of intrinsic and common paths (Xa, IXa).  LMWH act on Xa mainly

Response: LMWH > Hepapin @ reducing death or MI in combo w/aspirin in unstable angina

Use: IV (hep) SC (LMWH - more reliable absportion and plasma 1/2 life)

SE: bleeding, thrombocytopenia (less is LMWH)

Other: Resistance forms b/c of differences in concentrations of heparin-binding proteins in plasma or b/c accel clearence

Anti-coags have increased risk of bleeding than x-plates, don't use in pts w/bleeding disorders

Term
Fondaparinux
Definition

X-coag

Mech: synthetic, sulfated pentasaccharide -> binds antithrombin -> selective inhib of Factor Xa

Response: reduce death or MI in ACS (acute coronary syndromes like acute myocardial ischemia) similar to heparins

Use: specific and selective, long 1/2 life, 100% bioavalable (sq) = once-daily x-coat w/out needing to monitor clotting time (unlike close monitor in heparin)

SE: bleeding (less than Heprin)

Other: overall more favorable long-term outcomes than heparin, limited data on cost effectivness (enoxaparin: heparin may still cost less)

Term
Direct Thrombin Inhib
Definition

X-Coag

Mech: bind catalytic site of thrombin -> stop substrate access

Response: stable levels of x-coag (not yet proven beneficial in unstable angina)

Use: IV, combo w/aspirin or other x-plates

SE: bleeding, unlikly to cause thrombocytopenia (low platelet #)

Other: trials underway to determine efficacy in unstable angina and other ischemic syndromes

Term
Fibrinolytics (TPA)
Definition

Fibrinolytic in MI

Mech: binds fibrin -> activate BOUND plasminogen -> plasmin -> lysis of PREFORMED clot

Response: recanalize (reallow flow) thombotic occlusion, restore coronary flow, reduce infart size, improve myocardial function and survival over short and long terms

Use: IV w/in 2 hrs of MI symptoms

SE: bleeding, stroke (esp w/heparin)

Other: less benefit in old or high BP post MI, more benefits in diabetes post MI

Life saving in acute MI, serious issues if not careful

Term
Analgesics
Definition

MI

Mech: stim mu-type opiod receptor in brain and SC

Response: decrease pain, anxiety, restlessness, ANS, venous and artial contraction (all decrease O2 demand)

Use: IV till pain relieved or toxic, some need LARGE cumulative doses but can tolerate them

SE: hypotension, resp depression, vomiting

Other: Also in Unstable angina, pain relief is a primary goal in the setting of acute chest pain due to MI

Term
Renin Angiotensin Inhib
Definition

Acute MI, HT

Ace Ininhibs, ARBs (angiotensin receptor blockers)

Mech: inhibit ACE -> block angiotensin formation  (ACEI)

OR block access of angiotensin to AT-1 type tissue receptor (ARB)

Response: decrease venous and arterial contraction, SNS, and ventricular remodeling (for 2nd prevention), TPR (HT), increase renal Na/H2O excretion

Use: post aspirin, b-blockers and reperfusion therapy (w/in 24 hrs of event)

HT: less effective in blacks and old, use w/diuretic, use ARBs (BEST SE PROFILE OR ALL HT DRUGS, but costs), excellent in protecting against nephropathy (esp diabetics), CAD and HF

SE: hypotension, cough (ACEI), angioedema (ACEI, rare)

Other: benefits clear in old, prior MI, congestive heart failure or other reduced ventricular function pts

HT: no benefic to combining ARB and ACEI in HT but happens alot

Term
Oral X-Coags
Definition

2nd prevention of MI

Warfarin and coumadin

Mech: block synth of reduced vit K (needed for synth of factors II, VII, IX and X)

Response: decrease growth of existing thrombi, prevent new thrombi formation

Use: takes days for optimal onset, monitor dose via prothrombin time

SE: bleeding, skin necrosis, MANY drug interactions

Other: lots vit K = less effective, liver diease increase effect

Heparin is too risky in the long term, and this doesn't x-coag in test tube like heparin does.

Term
Loop Diuretics
Definition

Chronic and Acute Decompensated Heart Failure, Hypertension

Lasiks

Mech: Reversibly inhibit Na/K/2Cl- cotranport on luminal membrane of epi cells of thick acending limb

Response: increase renal exrection of Na, H2O, K, Ca, Mg, CI and H, relax systemic veins (increase venous capacitance): both cause decrease preload (decreased energy needs), diuretic effect causes decrease in edema (decrease in dyspnea, like in congetive heart failure)

Use: No survival, both chronic heart failure (oral) and acute decomp (IV). Most effective diuretic

HT: pts w/renal insufficiency or resistant HT

SE: volume and K (can get lethal arythmias) depletion, metabolic alkalosis

Other: resistance to diuretic effect happens lots in HF pts, overcome w/higher dose or adding thiazide.  Combo w/K-sparing diuretic (prevent K loss), action potentiated (increased) by renin-angiotensin inhibs (ACEI or ARB), also put on low sodium, high potassium diets, ONLY diuetic used for acute decomp, less effective than thiazide in hypertenseion, use in chronic renal failure w/high BP

Term
Thiazide Diuretics
Definition

Chronic HF, Hypertension

Mech: reversibly inhib Na/Cl cotransport on luminal membraine of distal convoluted tubule

Response: increase renal excretion of Na, H2O, K+, Mg++, Cl- and H+ BUT decrease Ca excretion.  Diuretic effect causes decrease in edema (decrease in dyspnea) and proload (decrease E need).  Lower efficacy than loop diuretics, activation of renin-angiotensin-aldosterone system (limits use in hypertension)

Use: No survival, only chronic stable heart failure (oral), combo w/loop diuretics, wide use as 1st line monotherapy for hypertension (esp blacks and old), low Na diet

SE: volume depletion, K depletion, increase uric acid and glucose (make gout and diabetes worse, not cause them)

Other: combo w/K-sparing diuretic (prevent xs K loss), actions potentiated (increased) w/angiotensin inhib (ACEI or ARB), choice in hypertense w/out comorbid dx, not strong enough in hypertense w/chronic renal fail, second in heart fail to loop diuretics

Term
K+ Sparing Diuretics
Definition

Chronic Heart Failure (?), Hypertension

Block up pore

Mech: block luminal epithelial cell Na channels in late distal tubule and collecting ducts (don't act on K+ channel or transport but Na and K linked in dist tubule, block Na uptake -> block K+ secretion...Na to urine, K stays in plasma)

Response: increase Na, H2O excretion, decrease Ca, K, Mg and H excretion.  Low efficacy alone.

Use: No survival.  Combo w/loop and/or thiazide diuretics to prevent K loss.

SE: Hyperkalemia (good @ stopping loss of K), GI

Other: Aldosterone antagonists (also K sparing) block insertion of channel into membrane..the two are not the same

 Use in heart fail w/high BP

Term
Aldosterone Antagonists
Definition

Heart Failure, Hypertension

"Stop making channels"

Mech: block expression of luminal epithelial cell Na channel in late distal tubule and collecting ducts.  Competitive ant of aldosterone receptor in kidney and other tissues (heart).

Response: increase excretion of Na, H20, Cl, decrease exrection of Ca, K, Mg and H.  Low efficacy alone.  Inhibit ventricular remodeling (slows progression of disease b/c aldosterone stimulate mineralcorticoids in heart and promote fibrous laydown)

HT: monotherapy as eplerone

Use: Yes survival in combo w/standard tx for SEVERE chronic HF (independent of diuretic effects of drug)

HT: comb w/thiazide or loop diuretics to prevent hypokalemia, benefit in HF indicate potential use in HT + HF

SE: hyperkalemia, gynecomastia, impotence (spironolactone) and mestrual irregularities(spironolactone)

Other: why it's help still being worked out, use in people that don't response to other BP drugs (main use in hypertension, more SE's than other K sparing)

Term
Renin Angiotensin Inhibitors (HF) 
Definition

Chronic Heart Failure, Hypertense and Ischemia

ACEI's and ARBs (angiotensin receptor blockers)

Mech: Block angiotensin formation via ACEI OR block angiotensin binding to AT-1 type tissue receptor via ARB

Response: decrease venous and arterial contraction, VENTRICULAR REMODELING, SNS, preload and afterload, increase excretion of Na and H2O

Use: yes survival, important in current tx of systolic dysfunction, not as efficient as aldosterone inhib, decrease sx and hospitalizations

SE: hypotension, cough (ACEI) and angioedema (ACEI, rare) ARB have less SE

Other: no benefit to combo ACEI w/ARB, combo w/diuretic

Term
Direct Arterial Vasodilators
Definition

Minor for heart fail

Hydalazine

Mech: unknown (selevite arterial dilator)

Response: decrease arterolar contration -> decrease afterload -> decrease O2 demand (work)

Use: Yes survival in combo w/isosorbide dinitriate in chronic HF, most vasodilators (unless also neurohormonal inhibs) NO to survival

SE: headache, dizzy, tachy, edema 

Other: use w/inability to tolerate ACEI/AR or blacks

 

Term
Digoxin
Definition

Severe Heart Fail, Arryths

Mech: bind alpha subunit of Na/K ATP-ase -> less Na pushed out -> decrease Na/Ca exchanger -> less Ca pumped out during myocyte repol -> more contractility (unique!)

Response: decrease SNS, filling presure, edema, AV conduction, increase CO, PNS, exercise tolerance and PR (b/c slower conduction @ AV node)

Use: low theraputic index (esp in hypokalemia), restrict to serever HF or pts w/A fib, decrease sx and hospital, no survival, ventricular rate control in pts w/heart fail and A fib

SE: anorexia, nausea, vomit, blurry, arryths 

Other: lots interactions, K+ or digoxin x-ab's to tx OD (hard to use), clinical use decrease b/c cause arryth (b/c increase Ca inside myocardial cells)

Term
B agonists
Definition

Acute Decomp HF

Dopamine, Dobutamine

Mech: activatge b-receptors in heart -> increase contractility (inotropic)

ALSO: Dope activated kids -> increase renal blood flow

High dose: stimulate alpha receptors

Response: Increase CO, decrease filling P

Use: Restricted to acute decomp, decrease Sx, maintain circulatory stability, no survival

SE: tachy, aryth

Other: Dobutamin continuous IV several days in severe clinical decomp, pharm tolerance limit efficacy in long term

Term
Phosphodiesterase Inhibs
Definition

Acute Decomp HF

Mech: inhib phosphodiesterase type IIIa (SR of cardiac myocytes and vasc smooth M, not ED ones) -> increase cAMP in SR -> increase Ca in cells (similar to digoxin)

Response: increase contractility, rate of relax, CO, decrease venous and arterial contraction (DILATE ARTERIOLES), filling pressure and pulmonary arterial contraction

Use: Acute decomp HF only, decrease Sx, maintain circulatory stability, no survival

SE: hypotense, arrhyth (less so than digoxin)

Other: DRUG OF CHOICE in pts w/b-blockers that need ionotrpic support (like in decomp), chronic consistant therapy decrease survival

Term
Nesiritide
Definition

Acute Decomb HF

Mech: recomb form of human B-type natriuretic peptide (BNP)

Response: decrease venous (STRONG) and arterial contraction, and filling pressure, increase CO

Use: restricted to acute decomp HF, decrease Sx, maintain circulatory stability, NO survival

SE: hypotense, increased plasma creatine

Other: may be associated w/ risk of xs mortailty and worsening of renal insufficiency

Term
Class IA
Definition

Tachyarrhythmias (Supraventricular and Ventricular)

MEch: Block Na and K channels

Resposne: decrease conduction and automaticity (b/c Na block), increase refractoriness (b/c K block), QRS (slower conduction, b/c Na channel block) and QT (increased refractoriness b/c K channel block)

Use: wide-specturm for both supraventricular and ventricular arrythmias due to re-entry or ectopic automaticity, term A fib or flutter, comb w/stuff to tx serious ventricular arrhyth

Other: decrease ventricular contractility, musc ant, decrease clinical use b/c causes aryths

 

 

Term
Class IB
Definition

Ventricular Aryths

Mech: block Na channels (esp w/high HR or in ischemic heart damage)

Response: decrease conduction, automaticity (only in abnormal, not in normal) and QT (NOT BIG CHANGE IN EKG)

Use: Ventricualr aryth b/c re-entry or ectopic automaticity, use against digoxin-induced arryth and long Q-T syndome (mexiletine and phenytoin), good at suppring aryth caused by ischemia (MI)

Other: lidocane MUST be parenterally (not oral), little effect on EKG

Term
Class IC
Definition

Serious ventricualr arryth

Strongest Na Channel Blockers

Mech: block Na channels (slow onset and offset)

Response: decrease CONDUCTION, automaticity, increase QRS (VERY marked)

Use: SERIOUS VENTRICULAR ARRYTHS b/c re-entry, A fib and flutter, AV nodal re-entry tachy

Other: prone to cause arryth, decrease ventricular contractility

Term
Class II
Definition

Arrhythmias

Nodal Tissue

Mech: Beta blockers

Response: decrease conduction, automaticity (normal and abnormal), increase PR (delay @ AV node)

Use: Arryth w/surg, anastersia, exercise, coke or other xs SNS states, vetnricuar rate control (so vent can slow when atria going nuts) in A fib and flutter, long Q-T syndrome

 Other: decrease sudden cardiac death post MI

Term
Class III
Definition

Broad specturm anti-arryth

Mech: block K channels

Response: increase refractoriness, QT (*), decrease automaticity and PR (minor)

Use: broad supraventriculoar and ventricular aryths b/c of re-entry or ectopic automaticity, term A fib/flutter, combo w/devices for tx serious ventricualr arryth, DRUG OF CHOICE fo ventricual arryth in cardiac resuscitation, good @ tx arryth in pts w/heart fail (cause less arryths than other drugs)

Other: Amiodarone blocks alpha and beta receptors, Ca and Na channels.  Ibutilide, dofetilide and azimilide for term A fib/flut

Term
Class IV
Definition

Arrythmias

Nodal Tissue, Like Class II

Mech: block L-type Ca channel

Response: Decrease AV conduction, and automaticity, increase PR (delay @ AV node)

Use: AV nodal re-entry tachy, VENTRICULAR RATE CONTROL in A fib/flutter

Other: on EKG look liek B-blocker

Term
Adenosine
Definition

 Aryth

Mech: Open K channels -> decrease intracellular cAMP via inhib adenylate cyclase

Response: Decrease AV conduction and sinus node rate, increase PR (longer conduction @ AV node)

Use: AV nodal re-entry tachy (can mistake for anxiety attack)

Other: SHORT DURATION (acute), IV only

Term
Aliskiren
Definition

Renin Angiotensin Inhibitor for HT

Mech: block renin enzyme -> no formation of angiotensin I or II

Response: decrease angiotensin II actions, venous and arterial contraction, SNS, TPR

Increase renal Na/H2O excretion

Use: less in blacks, STRONGLY better w/diuretic, additive w/ACEI or ARB but alone has same efficacy as either of the other two alone

SE: mild, short lived, diarrhea in some, allergic rx rare but need withdrawl, Not in preggers

Other: Expensive and new/unproven

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