Carrrr

Front 1

Atorvastatin, Lovastatin

Back 1

*increase hepatic LDL receptor expression via the sterolstat (inhibits HMG CoA Reductase)

Front 2

Ezetimibe

Back 2

*increased hepatic LDL receptor production via the sterolstat

Front 3

Colesevelan

Back 3

*ion exchange resins

Front 4

Niacin

Back 4

*AKA Vit B3

Front 5

Gemfibrozil

Back 5

*activation of lipoprotein lipase especially in skeletal muscle

Front 6

Fenofibrate

Back 6

*activation of lipoprotein lipase especially in skeletal muscle

Front 7

Isosorbide mononitrate

Back 7

*NO donor that preferentially dilates veins

Front 8

Sublingual NTG

Back 8

*sublingual admin allows all of absorbed NTG to reach heart via the SVC & thus be distributed to both arteries & veins via CO

Front 9

Diltiazem

Back 9

*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract

Front 10

Verapamil

Back 10

*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract

Front 11

(a dyhydropyridine)

Back 11

*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract

Front 12

Aspirin

Back 12

*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

Front 13

Tirofiban

Back 13

*blocks the IIb/IIIa receptors which allow fibrinogen to bind platelets together blocks platelet aggregation caused by any factor

Front 14

Clopidogrel

Back 14

*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

Front 16

Heparin

Back 16

*blocks adhesion of platelets by maintaining the electronegativity of the damaged vascular wall prevents platelet adhesion, aggregation & the “release” rxn

Front 17

Heparin

Back 17

*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

Front 18

Enoxaparin

Back 18

*LMW heparins that primarily inhibit activated factor 10

Front 19

Danaproid

Back 19

*non-heparin glycosaminoglycan heparan

Front 20

Lepirudin

Back 20

*direct inhibitor of thrombin (IIa)

Front 21

Protamine sulfate

Back 21

*see comparison chart

Front 22

Warfarin

Back 22

*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

Front 23

Phytonadione

Back 23

*see comparison chart

Front 24

Alteplase

Back 24

*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

Front 25

Streptokinase

Back 25

*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

Front 26

Aminocaproic acid

Back 26

*see comparison chart

Front 27

Quinidine

Back 27

Class IA

Front 28

Procainamide

Back 28

Class IA

Front 29

Lidocaine

Back 29

Class IB

Front 30

Esmolol

Back 30

Class II

Front 31

Amiodarone

Back 31

Class III

Front 32

Dofetilide

Back 32

Class III

Front 33

Sotalol

Back 33

Combined Class II & III

Front 34

Diltiazem

Back 34

Class IV

Front 35

Digoxin

Back 35

*acts centrally to inc efferent vagal activity

Front 36

Adenosine

Back 36

*inc K conductance to hyperpolarize the AV node

Front 37

Hydrochlorothiazide

Back 37

*not known, but fall in BP is dependent on maintaining a neg Na balance b/c high salt intake reverses the anti-HTN effect

Front 38

Lisinopril

Back 38

*ACE inhibitors prevent conversion of Ang I Ang II

Front 39

Valsartan

Back 39

*Angiotensin II receptor antagonists (ARB)

Front 40

Felodipine

Back 40

*calcium channel blockers block L type Ca channels in VSM & cardiac muscle

Front 41

Timolol

Back 41

*beta-blockers

Front 42

Labetolol

Back 42

*blocks beta 1 in heart

Front 43

α-methyldopa

Front 44

Clonidine

Back 44

*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

Front 45

Hydralazine

Back 45

*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established

Front 46

Minoxidil

Back 46

*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established

Front 47

Diazoxide

Back 47

*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established

Front 48

Sodium nitroprusside

Back 48

*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

Front 49

Thiosulfate

Back 49

*combines w/ CN to form thiocyanate which is excreted renally

Front 50

methylene blue

Back 50

*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

Front 51

Furosemide

Back 51

*act on Loop of Henle to inhibit Na/K/2 Cl cotransporter causes a saluresis

Front 52

Isosorbide dinitrate

Back 52

*donate NO to dilate venules dec preload

Front 53

Lisinopril

Back 53

*ACE inhibitors block Ang I from being converted to Ang II

Front 54

Valsartan

Back 54

*ARB block binding of Ang II to its receptor AT1

Front 55

Isosorbide dinitrate + hydralazine

Front 56

Eplerenone

Back 56

*aldosterone receptor antagonists

Front 57

Carvedilol

Back 57

*blocks beta 1, beta 2 & alpha 1 adrenoceptors

Front 58

Digoxin

Back 58

*direct positive inotropic effect

Front 59

Morphine

Back 59

*dec SNS activity by analgesic effects & inhibition of carotid baroreflex

Front 60

Dopamine

Back 60

*low dose= stimulates D1 receptors in renal arterioles causing venodilation

Front 61

Dobutamine

Back 61

*stim beta 1 & beta 2 receptors

Front 62

Milrinone

Back 62

*inhibits type III PDEase inc cAMP in cardiac myocytes

Front 63

Nitroglycerin

Back 63

*given iv infusion

Front 64

Sodium nitroprusside

Back 64

*rapidly converted to NO which causes balanced vasodilation

Front 65

Rosuvastatin, Pravastatin, Atorvastatin, Lovastatin

Back 65

*increase hepatic LDL receptor expression via the sterolstat (inhibits HMG CoA Reductase); ; *atorvastatin, simvastatin, lovastatin & rosuvastatin are the most potent of the statins

Front 66

Ezetimibe

Back 66

*increased hepatic LDL receptor production via the sterolstat; (blocks the protein mediated transporter which absorbs dietary chol from the GI tract)

Front 67

Cholestyramine; Colestipol; Colesevelan

Back 67

*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)

Front 68

Niacin

Back 68

*AKA Vit B3; *MOA is unknown

Front 69

Gemfibrozil

Back 69

*activation of lipoprotein lipase especially in skeletal muscle

Front 70

Fenofibrate

Back 70

*activation of lipoprotein lipase especially in skeletal muscle

Front 71

Topical Nitroglycerin (glyceryl trinitrate); Isosorbide dinitrate; Isosorbide mononitrate

Back 71

*NO donor that preferentially dilates veins

Front 72

Sublingual NTG

Back 72

*sublingual admin allows all of absorbed NTG to reach heart via the SVC & thus be distributed to both arteries & veins via CO

Front 73

Diltiazem

Back 73

*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract

Front 74

Verapamil

Back 74

*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract

Front 75

Amlodipine; (a dyhydropyridine)

Back 75

*calcium channel blockers block the L-type calcium channels in VSM, AV & SA node & myocardial cells w/o calcium, the muscles won’t contract

Front 76

Aspirin

Back 76

*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

Front 77

Abciximab; Tirofiban

Back 77

*blocks the IIb/IIIa receptors which allow fibrinogen to bind platelets together blocks platelet aggregation caused by any factor

Front 78

Ticlopidine; Clopidogrel

Back 78

*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

Front 80

Heparin

Back 80

*blocks adhesion of platelets by maintaining the electronegativity of the damaged vascular wall prevents platelet adhesion, aggregation & the “release” rxn

Front 81

Heparin

Back 81

*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

Front 82

Dalteparin; Enoxaparin

Back 82

*LMW heparins that primarily inhibit activated factor 10

Front 83

Danaproid

Back 83

*non-heparin glycosaminoglycan heparan ; *promtes binding of ATIII to factor Xa

Front 84

Lepirudin

Back 84

*direct inhibitor of thrombin (IIa)

Front 85

Protamine sulfate

Back 85

*see comparison chart

Front 86

Warfarin

Back 86

*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

Front 87

Phytonadione

Back 87

*see comparison chart

Front 88

Alteplase

Back 88

*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

Front 89

Streptokinase

Back 89

*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

Front 90

Aminocaproic acid

Back 90

*see comparison chart

Front 91

Quinidine

Back 91

Class IA; *blocks Na & K channels, blocks alpha receptors & muscarinic receptors

Front 92

Procainamide

Back 92

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

Front 93

Lidocaine

Back 93

Class IB; *only affects the ventricles!; *blocks Na channels; *dec ERP & APD of fast fibers

Front 94

Atenolol; Propanolol; Esmolol

Back 94

Class II; *blockade of cardiac beta receptors

Front 95

Amiodarone

Back 95

Class III; *blocks inward Na & outward K channels; *non-competitive alpha & beta blockade

Front 96

Dofetilide

Back 96

Class III; *delays repolarization; -blocks outward repol K current; -delayed repol inc APD & ERP in fast fibers

Front 97

Sotalol

Back 97

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)

Front 98

Verapamil; Diltiazem

Back 98

Class IV; *blockade of calcium channels in slow fibers, esp AV node

Front 99

Digoxin

Back 99

*acts centrally to inc efferent vagal activity; *dec symp outflow at therapeutic window; *inc dp/dt via partial inhibition of the Na/K ATPase

Front 100

Adenosine

Back 100

*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

Front 101

Hydrochlorothiazide

Back 101

*not known, but fall in BP is dependent on maintaining a neg Na balance b/c high salt intake reverses the anti-HTN effect

Front 102

Captopril; Enalapril; Lisinopril

Back 102

*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**

Front 103

Losartan; Valsartan

Back 103

*Angiotensin II receptor antagonists (ARB); *competitively block the AT1 receptor ; **no effect on bradykinin metabolism

Front 104

Nifedipine; Amlodipine; Felodipine

Back 104

*calcium channel blockers block L type Ca channels in VSM & cardiac muscle

Front 105

Atenolol; Metoprolol; Propanolol; Timolol

Back 105

*beta-blockers; *dec TPR by unknown mechanism

Front 106

Labetolol

Back 106

*blocks beta 1 in heart; *blocks alpha 1 in arterioles & venules; *partial agonist at beta 2

Front 107

α-methyldopa

Front 108

Clonidine

Back 108

*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

Front 109

Hydralazine

Back 109

*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established

Front 110

Minoxidil

Back 110

*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established

Front 111

Diazoxide

Back 111

*relax arteriolar VSM by dec availability of intracellular Ca for excitation-contraction coupling mech by which they effect this change has not been established

Front 112

Sodium nitroprusside

Back 112

*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

Front 113

Thiosulfate

Back 113

*combines w/ CN to form thiocyanate which is excreted renally

Front 114

Nitrite+thiosulfate+; methylene blue

Back 114

*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;

Front 115

Furosemide

Back 115

*act on Loop of Henle to inhibit Na/K/2 Cl cotransporter causes a saluresis

Front 116

Isosorbide mononitrate; Isosorbide dinitrate

Back 116

*donate NO to dilate venules dec preload

Front 117

Captopril; Enalapril; Lisinopril

Back 117

*ACE inhibitors block Ang I from being converted to Ang II; *”balanced vasodilators”

Front 118

Losartan; Valsartan

Back 118

*ARB block binding of Ang II to its receptor AT1; *”balanced vasodilators”

Front 119

Isosorbide dinitrate + hydralazine

Front 120

Spironolactone; Eplerenone

Back 120

*aldosterone receptor antagonists

Front 121

Carvedilol

Back 121

*blocks beta 1, beta 2 & alpha 1 adrenoceptors

Front 122

Digoxin

Back 122

*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

Front 123

Morphine

Back 123

*dec SNS activity by analgesic effects & inhibition of carotid baroreflex

Front 124

Dopamine

Back 124

*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

Front 125

Dobutamine

Back 125

*stim beta 1 & beta 2 receptors

Front 126

Milrinone

Back 126

*inhibits type III PDEase inc cAMP in cardiac myocytes

Front 127

Nitroglycerin

Back 127

*given iv infusion; *converted to NO vasodilation

Front 128

Sodium nitroprusside

Back 128

*rapidly converted to NO which causes balanced vasodilation