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Cardio Drugs Mech
Mechanisms of Action
| Question | Answer |
|---|---|
| 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
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