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Cardio Drugs Mech

Mechanisms of Action

QuestionAnswer
Bile Acid Binding Resins Mech: bind bile acids -> Stool -> More synth from liver -> Liver cholesterol depletion -> Stimulate LDL receptors -> More LDL taken from blood
Statins Mech: Inhib hepatic HMG-CoA reductase (needed for chol synth) -> more LDL receptors expressed -> more LDL removed from blood
Cholesterol Absorption Blockers 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
Niacin (Nicotinic Acid) 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
Fibrates 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
B-adrenergic Blockers Mech: competitively block B-ad receptors
Nitrates Mech: Enter cell -> release NO -> activate gualylate cyclase -> cGMP -> vascular smooth M -> vasorelaxation (ESP VEINS RELAX TO PULL BLOOD AWAY FROM HEART)
Ca Channel Blockers Mech: non-comp inhibit Ca++ thru V-sensitive L-type membrane Ca channels, DV also slows channel recovery time
Ranolazine Mech: 1. Block "late" Na -> stop inc intracell Na/Ca b/c ishchemia2. Block FA ox -> use glucRanol: blocks the late Na current which stops the Na overload
Aspirin Mech: Irreversibly acetylates COX-I -> blocks TxA2 synth -> less platelet aggregation (lasts 7-10 days b/c need to make more platelets)
ADP Inhibitors Mech: inhib ADP binding to receptor -> decrease plate agg and activation
GP IIb/IIIa Receptor Inhibitor Mech: prevent fibrinogen mediated cross-liknage via GP IIb/IIIa receptors -> less aggregation
Heparin Mech: catalyzes inhib of several coag proteases by antithrombinX-thrombin -> inhib coag factors of intrinsic and common paths (Xa, IXa). LMWH act on Xa mainly
Fondaparinux Mech: synthetic, sulfated pentasaccharide -> binds antithrombin -> selective inhib of Factor Xa
Direct Thrombin Inhib Mech: bind catalytic site of thrombin -> stop substrate access
Fibrinolytics (TPA) Mech: binds fibrin -> activate BOUND plasminogen -> plasmin -> lysis of PREFORMED clot
Analgesics Mech: stim mu-type opiod receptor in brain and SC
Renin Angiotensin Inhib Mech: inhibit ACE -> block angiotensin formation (ACEI)OR block access of angiotensin to AT-1 type tissue receptor (ARB)Mech HT: Block angiotensin formation via ACEI OR block angiotensin binding to AT-1 type tissue receptor via ARB
Oral X-Coags Mech: block synth of reduced vit K (needed for synth of factors II, VII, IX and X)
Loop Diuretics Mech: Reversibly inhibit Na/K/2Cl- cotranport on luminal membrane of epi cells of thick acending limb
Thiazide Diuretics Mech: reversibly inhib Na/Cl cotransport on luminal membraine of distal convoluted tubule
K+ Sparing Diuretics 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)
Aldosterone Antagonists 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).
Direct Arterial Vasodilators Mech: unknown (selective arterial dilator)
Digoxin 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!)
B agonists Mech: activate b-receptors in heart -> increase contractility (inotropic)ALSO: Dope activated kids -> increase renal blood flowHigh dose: stimulate alpha receptors
Phosphodiesterase Inhibs 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)
Nesiritide Mech: recomb form of human B-type natriuretic peptide (BNP)
Class IA Mech: Block Na and K channels
Class IB Mech: block Na channels (esp w/high HR or in ischemic heart damage)
Class IC Mech: block Na channels (slow onset and offset)
Class II Mech: Beta blockers
Class III Mech: block K channels
Class IV Mech: block L-type Ca channel
Adenosine Mech: Open K channels -> decrease intracellular cAMP via inhib adenylate cyclase
Aliskiren Mech: block renin enzyme -> no formation of angiotensin I or II
Newer Drugs for Chronic Stable Angina Ivabradine: block pacemaker -> dec HRNicorandil: open ATP-sens K chan -> heart dilTrimetazidine: inhib mito 3-ketoAcyl CoA thiolase -> FA -> Carb for EPerhexilene: inhib mitochondrial carnitine-palmitoyl-transferase -> FA use to carb use for E
Created by: chavezc3