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128 Cards in this Set

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Atorvastatin, Lovastatin
*increase hepatic LDL receptor expression via the sterolstat (inhibits HMG CoA Reductase)
Ezetimibe
*increased hepatic LDL receptor production via the sterolstat
Colesevelan
*ion exchange resins
Niacin
*AKA Vit B3
Gemfibrozil
*activation of lipoprotein lipase especially in skeletal muscle
Fenofibrate
*activation of lipoprotein lipase especially in skeletal muscle
Isosorbide mononitrate
*NO donor that preferentially dilates veins
Sublingual NTG
*sublingual admin allows all of absorbed NTG to reach heart via the SVC & thus be distributed to both arteries & veins via CO
Diltiazem
*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract
Verapamil
*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract
(a dyhydropyridine)
*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract
Aspirin
*acetylsalicylic acid (aspirin) is converted to salicyclate by hepatic first pass metabolism acetylsalicylic acid IRREVERSIBLY inhibits COX-1 in platelets in the portal blood salicyclate REVERSIBLY inhibits COX 1 & 2 this leads to inhibition of TXA2 inhibition of platelet aggregation large doses can escape first pass metabolism & inhibit PGI2 & PGE2 in vascular endothelial cells but they have nuclei so they can resume COX 1 production w/in 6-10h
Tirofiban
*blocks the IIb/IIIa receptors which allow fibrinogen to bind platelets together blocks platelet aggregation caused by any factor
Clopidogrel
*block the P2Y(12) purinergic receptor on platelets keeps ADP from binding this inhibits the inhibition of adenyl cyclase adenyl cyclase inc cAMP dec Calcium conc in cell platelets won’t aggregate
Heparin
*blocks adhesion of platelets by maintaining the electronegativity of the damaged vascular wall prevents platelet adhesion, aggregation & the “release” rxn
Heparin
*antithrombin III is a circulating factor in blood it binds to activated clotting factors to keep them from doing their job heparin enhances this process 1000X by binding to antithrombin III making it more accessible to the protease site of the activated clotting factor
Enoxaparin
*LMW heparins that primarily inhibit activated factor 10
Danaproid
*non-heparin glycosaminoglycan heparan
Lepirudin
*direct inhibitor of thrombin (IIa)
Protamine sulfate
*see comparison chart
Warfarin
*clotting factors 2,7,9 & 10 require post translational γ-carboxylation of 9-12 glut residues which is coupled to the oxidative metabolism of reduced vit K to its epoxide vit K is regenerated from vit K epoxide via vit K epoxide reductase warfarin inhibits vit K epoxide reductase no reduced vit K= no modification & clotting factors won’t work
Phytonadione
*see comparison chart
Alteplase
*recombinant tPAenzymatic activation of plasminogen to plasmin endogenous inhibitors of plasmin & tPA are overwhelmed & the specificity of plasmin for the thrombin in thrombi is lost systemic fibrinolytic state ensues due to degredation of clotting factors 5 & 8, & fibrinogen
Streptokinase
*binding of S near carboxy terminus of plasminogen induces a conformational change that exposes protease activity near the amino terminus of plasminogen this cleaves plasmin from another plasminogen molecule plasmin attacks thrombi or circulating factors 5 & 8 or fibrinogen
Aminocaproic acid
*see comparison chart
Quinidine
Class IA
Procainamide
Class IA
Lidocaine
Class IB
Esmolol
Class II
Amiodarone
Class III
Dofetilide
Class III
Sotalol
Combined Class II & III
Diltiazem
Class IV
Digoxin
*acts centrally to inc efferent vagal activity
Adenosine
*inc K conductance to hyperpolarize the AV node
Hydrochlorothiazide
*not known, but fall in BP is dependent on maintaining a neg Na balance b/c high salt intake reverses the anti-HTN effect
Lisinopril
*ACE inhibitors prevent conversion of Ang I Ang II
Valsartan
*Angiotensin II receptor antagonists (ARB)
Felodipine
*calcium channel blockers block L type Ca channels in VSM & cardiac muscle
Timolol
*beta-blockers
Labetolol
*blocks beta 1 in heart
α-methyldopa
Clonidine
*highly lipid soluble alpha 2 agonist which enters the brain & dec symp outflow by stim postsynaptic alpha 2 receptors in rostral ventrolateral medulla symp reflexes are attenuated but not blocked
Hydralazine
*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established
Minoxidil
*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established
Diazoxide
*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established
Sodium nitroprusside
*when nitroprusside comes into contact w/ RBCs, NO is released causing vasodilation & inhibition of platelet aggregation via stim of guanyl cyclase inc cGMP relaxes VSM
Thiosulfate
*combines w/ CN to form thiocyanate which is excreted renally
methylene blue
*hemoglobin combines w/ nitrite to form methemoglobin (high affinity for CN) then reacts w/ cytochrome oxidase-Fe-CN to form cyanohemoglobin which combines w/ thiosulfate to make thiocyanate which is excreted renally
Furosemide
*act on Loop of Henle to inhibit Na/K/2 Cl cotransporter causes a saluresis
Isosorbide dinitrate
*donate NO to dilate venules dec preload
Lisinopril
*ACE inhibitors block Ang I from being converted to Ang II
Valsartan
*ARB block binding of Ang II to its receptor AT1
Isosorbide dinitrate + hydralazine
Eplerenone
*aldosterone receptor antagonists
Carvedilol
*blocks beta 1, beta 2 & alpha 1 adrenoceptors
Digoxin
*direct positive inotropic effect
Morphine
*dec SNS activity by analgesic effects & inhibition of carotid baroreflex
Dopamine
*low dose= stimulates D1 receptors in renal arterioles causing venodilation
Dobutamine
*stim beta 1 & beta 2 receptors
Milrinone
*inhibits type III PDEase inc cAMP in cardiac myocytes
Nitroglycerin
*given iv infusion
Sodium nitroprusside
*rapidly converted to NO which causes balanced vasodilation
Rosuvastatin, Pravastatin, Atorvastatin, Lovastatin
*increase hepatic LDL receptor expression via the sterolstat (inhibits HMG CoA Reductase); ; *atorvastatin, simvastatin, lovastatin & rosuvastatin are the most potent of the statins
Ezetimibe
*increased hepatic LDL receptor production via the sterolstat; (blocks the protein mediated transporter which absorbs dietary chol from the GI tract)
Cholestyramine; Colestipol; Colesevelan
*ion exchange resins; *increased hepatic LDL receptor production via the sterolstat; (swap Cl- for neg charged bile acids: bound bile acids are lost in the feces)
Niacin
*AKA Vit B3; *MOA is unknown
Gemfibrozil
*activation of lipoprotein lipase especially in skeletal muscle
Fenofibrate
*activation of lipoprotein lipase especially in skeletal muscle
Topical Nitroglycerin (glyceryl trinitrate); Isosorbide dinitrate; Isosorbide mononitrate
*NO donor that preferentially dilates veins
Sublingual NTG
*sublingual admin allows all of absorbed NTG to reach heart via the SVC & thus be distributed to both arteries & veins via CO
Diltiazem
*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract
Verapamil
*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract
Amlodipine; (a dyhydropyridine)
*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract
Aspirin
*acetylsalicylic acid (aspirin) is converted to salicyclate by hepatic first pass metabolism acetylsalicylic acid IRREVERSIBLY inhibits COX-1 in platelets in the portal blood salicyclate REVERSIBLY inhibits COX 1 & 2 this leads to inhibition of TXA2 inhibition of platelet aggregation large doses can escape first pass metabolism & inhibit PGI2 & PGE2 in vascular endothelial cells but they have nuclei so they can resume COX 1 production w/in 6-10h
Abciximab; Tirofiban
*blocks the IIb/IIIa receptors which allow fibrinogen to bind platelets together blocks platelet aggregation caused by any factor
Ticlopidine; Clopidogrel
*block the P2Y(12) purinergic receptor on platelets keeps ADP from binding this inhibits the inhibition of adenyl cyclase adenyl cyclase inc cAMP dec Calcium conc in cell platelets won’t aggregate
Heparin
*blocks adhesion of platelets by maintaining the electronegativity of the damaged vascular wall prevents platelet adhesion, aggregation & the “release” rxn
Heparin
*antithrombin III is a circulating factor in blood it binds to activated clotting factors to keep them from doing their job heparin enhances this process 1000X by binding to antithrombin III making it more accessible to the protease site of the activated clotting factor
Dalteparin; Enoxaparin
*LMW heparins that primarily inhibit activated factor 10
Danaproid
*non-heparin glycosaminoglycan heparan ; *promtes binding of ATIII to factor Xa
Lepirudin
*direct inhibitor of thrombin (IIa)
Protamine sulfate
*see comparison chart
Warfarin
*clotting factors 2,7,9 & 10 require post translational γ-carboxylation of 9-12 glut residues which is coupled to the oxidative metabolism of reduced vit K to its epoxide vit K is regenerated from vit K epoxide via vit K epoxide reductase warfarin inhibits vit K epoxide reductase no reduced vit K= no modification & clotting factors won’t work
Phytonadione
*see comparison chart
Alteplase
*recombinant tPAenzymatic activation of plasminogen to plasmin endogenous inhibitors of plasmin & tPA are overwhelmed & the specificity of plasmin for the thrombin in thrombi is lost systemic fibrinolytic state ensues due to degredation of clotting factors 5 & 8, & fibrinogen
Streptokinase
*binding of S near carboxy terminus of plasminogen induces a conformational change that exposes protease activity near the amino terminus of plasminogen this cleaves plasmin from another plasminogen molecule plasmin attacks thrombi or circulating factors 5 & 8 or fibrinogen
Aminocaproic acid
*see comparison chart
Quinidine
Class IA; *blocks Na & K channels, blocks alpha receptors & muscarinic receptors
Procainamide
Class IA; *blocks Na & K channels w/ less anticholinergic effect than quinidine; *no effect to block alpha receptors but may block ganglionic nicotinic receptors to cause hypotension
Lidocaine
Class IB; *only affects the ventricles!; *blocks Na channels; *dec ERP & APD of fast fibers
Atenolol; Propanolol; Esmolol
Class II; *blockade of cardiac beta receptors
Amiodarone
Class III; *blocks inward Na & outward K channels; *non-competitive alpha & beta blockade
Dofetilide
Class III; *delays repolarization; -blocks outward repol K current; -delayed repol inc APD & ERP in fast fibers
Sotalol
Combined Class II & III; *I isomer causes non-selective, competitive blockade of beta receptors; *d&I isomers inhibit the rapid component of the outward K repol current (only beta blocker where d isomer is active)
Verapamil; Diltiazem
Class IV; *blockade of calcium channels in slow fibers, esp AV node
Digoxin
*acts centrally to inc efferent vagal activity; *dec symp outflow at therapeutic window; *inc dp/dt via partial inhibition of the Na/K ATPase
Adenosine
*inc K conductance to hyperpolarize the AV node; *inhibits ability of symp stim to inc Ca conductance in AV node; *half-life = only 10 seconds
Hydrochlorothiazide
*not known, but fall in BP is dependent on maintaining a neg Na balance b/c high salt intake reverses the anti-HTN effect
Captopril; Enalapril; Lisinopril
*ACE inhibitors prevent conversion of Ang I Ang II; *initial fall in BP is related to pretreatment value of PRA; *plasma aldo is maintained by ACTH & plasma K conc; **blockade of ACE also prevents the breakdown of bradykinin which is a vasodilator & activate prostaglandin synthesis**
Losartan; Valsartan
*Angiotensin II receptor antagonists (ARB); *competitively block the AT1 receptor ; **no effect on bradykinin metabolism
Nifedipine; Amlodipine; Felodipine
*calcium channel blockers block L type Ca channels in VSM & cardiac muscle
Atenolol; Metoprolol; Propanolol; Timolol
*beta-blockers; *dec TPR by unknown mechanism
Labetolol
*blocks beta 1 in heart; *blocks alpha 1 in arterioles & venules; *partial agonist at beta 2
α-methyldopa
Clonidine
*highly lipid soluble alpha 2 agonist which enters the brain & dec symp outflow by stim postsynaptic alpha 2 receptors in rostral ventrolateral medulla symp reflexes are attenuated but not blocked
Hydralazine
*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established
Minoxidil
*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established
Diazoxide
*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established
Sodium nitroprusside
*when nitroprusside comes into contact w/ RBCs, NO is released causing vasodilation & inhibition of platelet aggregation via stim of guanyl cyclase inc cGMP relaxes VSM
Thiosulfate
*combines w/ CN to form thiocyanate which is excreted renally
Nitrite+thiosulfate+; methylene blue
*hemoglobin combines w/ nitrite to form methemoglobin (high affinity for CN) then reacts w/ cytochrome oxidase-Fe-CN to form cyanohemoglobin which combines w/ thiosulfate to make thiocyanate which is excreted renally;
Furosemide
*act on Loop of Henle to inhibit Na/K/2 Cl cotransporter causes a saluresis
Isosorbide mononitrate; Isosorbide dinitrate
*donate NO to dilate venules dec preload
Captopril; Enalapril; Lisinopril
*ACE inhibitors block Ang I from being converted to Ang II; *”balanced vasodilators”
Losartan; Valsartan
*ARB block binding of Ang II to its receptor AT1; *”balanced vasodilators”
Isosorbide dinitrate + hydralazine
Spironolactone; Eplerenone
*aldosterone receptor antagonists
Carvedilol
*blocks beta 1, beta 2 & alpha 1 adrenoceptors
Digoxin
*direct positive inotropic effect; *acts w/in CNS to enhance efferent vagal activity & dec efferent SNS activity; *inhibit Na/K ATPase activity at doses above therapeutic window
Morphine
*dec SNS activity by analgesic effects & inhibition of carotid baroreflex
Dopamine
*low dose= stimulates D1 receptors in renal arterioles causing venodilation; *intermediate dose= stim D1 & Beta 1 receptors; *large dose= begin to stim vascular alpha 1 receptors
Dobutamine
*stim beta 1 & beta 2 receptors
Milrinone
*inhibits type III PDEase inc cAMP in cardiac myocytes
Nitroglycerin
*given iv infusion; *converted to NO vasodilation
Sodium nitroprusside
*rapidly converted to NO which causes balanced vasodilation