Term
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Definition
| Mech: bind bile acids -> Stool -> More synth from liver -> Liver cholesterol depletion -> Stimulate LDL receptors -> More LDL taken from blood |
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Term
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Definition
| Mech: Inhib hepatic HMG-CoA reductase (needed for chol synth) -> more LDL receptors expressed -> more LDL removed from blood |
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Term
| Cholesterol Absorption Blockers |
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Definition
| 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 |
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Term
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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 |
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Term
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Definition
| 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 |
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Term
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Definition
| Mech: Enter cell -> release NO -> activate gualylate cyclase -> cGMP -> vascular smooth M -> vasorelaxation (ESP VEINS RELAX TO PULL BLOOD AWAY FROM HEART) |
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Term
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Definition
| Mech: competitively block B-ad receptors |
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Term
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Definition
| Mech: non-comp inhibit Ca++ thru V-sensitive L-type membrane Ca channels, DV also slows channel recovery time |
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Term
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Definition
Mech: 1. Block "late" Na current -> stop increased intracellular Na and Ca caused by ishchemia
2. Block FA oxidation -> use glucose (more efficent) instead
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!
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Term
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Definition
| Mech: Irreversibly acetylates COX-I -> blocks TxA2 synth -> less platelet aggregation (lasts 7-10 days b/c need to make more platelets) |
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Term
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Definition
| Mech: inhib ADP binding to receptor -> decrease plate agg and activation |
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Term
| GP IIb/IIIa Receptor Inhibitor |
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Definition
| Mech: prevent fibrinogen mediated cross-liknage via GP IIb/IIIa receptors -> less aggregation |
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Term
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Definition
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 |
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Term
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Definition
| Mech: synthetic, sulfated pentasaccharide -> binds antithrombin -> selective inhib of Factor Xa |
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Term
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Definition
| Mech: bind catalytic site of thrombin -> stop substrate access |
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Term
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Definition
| Mech: binds fibrin -> activate BOUND plasminogen -> plasmin -> lysis of PREFORMED clot |
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Term
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Definition
| Mech: stim mu-type opiod receptor in brain and SC |
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Term
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Definition
Mech: inhibit ACE -> block angiotensin formation (ACEI)
OR block access of angiotensin to AT-1 type tissue receptor (ARB) |
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Term
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Definition
| Mech: block synth of reduced vit K (needed for synth of factors II, VII, IX and X) |
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Term
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Definition
| Mech: Reversibly inhibit Na/K/2Cl- cotranport on luminal membrane of epi cells of thick acending limb |
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Term
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Definition
| Mech: reversibly inhib Na/Cl cotransport on luminal membraine of distal convoluted tubule |
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Term
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Definition
| 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) |
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Term
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Definition
| 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). |
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Term
| Renin Angiotensin Inhibitors (HF) |
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Definition
| Mech: Block angiotensin formation via ACEI OR block angiotensin binding to AT-1 type tissue receptor via ARB |
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Term
| Direct Arterial Vasodilators |
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Definition
| Mech: unknown (selective arterial dilator) |
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Term
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Definition
| 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!) |
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Term
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Definition
Mech: activate b-receptors in heart -> increase contractility (inotropic)
ALSO: Dope activated kids -> increase renal blood flow
High dose: stimulate alpha receptors
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Term
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Definition
| 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) |
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Term
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Definition
| Mech: recomb form of human B-type natriuretic peptide (BNP) |
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Term
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Definition
| Mech: Block Na and K channels |
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Term
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Definition
| Mech: block Na channels (esp w/high HR or in ischemic heart damage) |
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Term
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Definition
| Mech: block Na channels (slow onset and offset) |
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Term
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Definition
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Term
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Definition
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Term
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Definition
| Mech: block L-type Ca channel |
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Term
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Definition
| Mech: Open K channels -> decrease intracellular cAMP via inhib adenylate cyclase |
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Term
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Definition
| Mech: block renin enzyme -> no formation of angiotensin I or II |
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Term
| Newer Drugs for Chronic Stable Angina |
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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 |
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