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Pharmacology II > CVS Drugs Part 1 > Flashcards

CVS Drugs Part 1 Flashcards

Antiplatelet/Antithrombotic Drugs & Anti-Arrhythmic Drugs

1
Q

First step in platelet aggregation

A

damage to endothelium causes platelets to become activated which cover and adhere to exposed subendothelial surface -> platelet adhesion

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2
Q

Second step of platelet aggregation

A

activated platelets release chemical mediators including thromboxane A2, ADP, serotonin, and PAF -> platelet activation

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3
Q

Third step of platelet aggregation

A

platelets are recruited forming platelet plug -> platelet aggregation

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4
Q

Intrinsic pathway factors

A

activation of factors XII, XI, IX, and VIII leading to activation of factor X

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5
Q

Extrinsic pathway factors

A

activation of factors III (tissue factor) and VII leading to activation of factor X

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6
Q

Common pathway factors

A

activation of factor X through extrinsic and intrinsic pathways leading to conversion of prothrombin (factor II) to thrombin (factor IIa), activation of factor XIII, and conversion of fibrinogen (factor I) to fibrin (factor Ia) resulting in fibrin clot formation

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7
Q

fibrinolysis

A

break down of a fibrin clot by plasmin after conversion of plasminogen to plasmin

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8
Q

Aspirin MOA

A

antiplatelet drug that irreversibly inhibits COX-1 enzyme inhibiting platelet aggregation (by inhibition of thromboxane A2 synthesis from prostaglandins)

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9
Q

Aspirin clinical indications

A
  • primary and secondary prevention of heart attack and stroke in patients previously diagnosed with CAD, DM, PVD, CVA, and TIA
  • in DAPT combined with P2Y12 ADP inhibitor (clopidogrel) recommended after CABG, PCI, stroke, and TIA (for 2 weeks)
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10
Q

Aspirin contraindications

A

intracranial, intramedullary, or posterior eye surgeries

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11
Q

Aspirin adverse effects

A

GI bleeding (especially in the elderly) and tinnitus

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12
Q

Clopidogrel MOA

A

antiplatelet drug that is an irreversible P2Y12 ADP receptor inhibitor causing inhibition of platelet activation

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13
Q

Clopidogrel clinical indications

A

1st line drug for prevention of atherosclerotic events in recent MI, CVA, unstable angina, ACS, and coronary angioplasty
- used in DAPT combined with aspirin for 1-6 months in BMS, 12 months in DES,12 months in ACS, and 10-21 days in TIA/minor ischemic strokes (not in major CVA d/t bleeding risk)

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14
Q

Clopidogrel contraindications

A

do not use during episodes of active bleeding, in patients with a history of bleeding, history of vascular disease including stable angina, prior TIA or stroke, and PAD

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15
Q

DAPT score associated with favorable benefit/risk ratio for prolonged DAPT

A

score of greater than or equal to 2

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16
Q

risk factors that increase DAPT score

A

tobacco smoking, diabetes, MI at presentation, prior PCI or MI, stent diameter <3 mm, paclitaxel-eluting stent, CHF or LVEF <30% (+2), and saphenous vein graft PCI (+2)

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17
Q

Clopidogrel pharmacokinetics

A

prodrug that is metabolized by CYP 2C19, onset = 2 hours (effects last 5 days)

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18
Q

clopidogrel drug interactions

A

omeprazole which inhibits CYP (if PPI needed, use pantoprazole)

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19
Q

Ticagrelor (Brilinta) MOA

A

only antiplatelet drug that is a reversible P2Y12 ADP receptor inhibitor

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20
Q

Ticagrelor pharmacokinetics

A

administered orally and is not metabolized by CYP (not a prodrug like clopidogrel), has fastest onset = 1-3 hours

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21
Q

Ticagrelor clinical indications

A
  • 2nd line for prevention of atherosclerotic events in recent MI, CVA, unstable angina, ACS, and coronary angioplasty
  • used in DAPT combined with aspirin
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22
Q

Prasugrel (Effient) MOA

A

antiplatelet drug that is an irreversible P2Y12 ADP receptor inhibitor with increased antiplatelet activity

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23
Q

Prasugrel clinical indications

A

used in combination with aspirin in ACS and after MI and stroke (not used routinely)

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24
Q

Prasugrel contraindications

A

increased risk of bleeding (especially >75 yo)

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25
Q

Ticlopidine MOA

A

antiplatelet drug that is an irreversible P2Y12 ADP receptor inhibitor causing inhibition of platelet activation

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26
Q

Ticlopidine clinical indications

A

TIA patients and patients with a prior history of stroke - no longer sold in the US due to life-threatening hematologic adverse effects (requires CBC every 2 weeks for 4 months)

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27
Q

Ticlopidine adverse effects

A

thrombocytopenia, agranulocytosis, and TTP

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28
Q

Ticagrelor adverse effects

A

increased aches and pains when combined with statins

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29
Q

Abciximab MOA

A

humanized monoclonal antibody that is an antiplatelet drug and GP IIb/IIIa receptor inhibitor that also binds to vWF and fibrinogen inhibiting platelet aggregation

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30
Q

Abciximab clinical indications

A

used in ACS patients who do not respond to conventional therapy within 24 hours and with aspirin and heparin during balloon angioplasty, coronary stent placement, and PCI to prevent further clot formation

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31
Q

Abciximab pharmacokinetics

A

administered IV and reaches peak effect after 30 minutes persisting 24 hours after stopping

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32
Q

Tirofiban MOA

A

antiplatelet drug and GP IIb/IIIa receptor inhibitor that also binds to vWF and fibrinogen inhibiting platelet aggregation

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33
Q

Tirofiban clinical indications

A

rarely used to reduce the rate of thrombotic CV events in NSTEMI with PCI

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34
Q

Tirofiban pharmacokinetics

A

administered IV with rapid onset and short duration of action (effects last 4-8 hours after IV stops), excreted in kidneys

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35
Q

Tirofiban contraindications

A

patients with history of bleeding including recent trauma or surgery, history of thrombocytopenia with previous tirofiban use, and history of bleeding diathesis

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36
Q

Tirofiban adverse effects

A

thrombocytopenia (must monitor aPTT)

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37
Q

Eptifibatide MOA

A

antiplatelet drug and GP IIb/IIIa receptor inhibitor that also binds to vWF and fibrinogen inhibiting platelet aggregation

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38
Q

Eptifibatide clinical indications

A

same as Tirofiban and interchangeable depending on insurance

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39
Q

Dipyridamole MOA

A

antiplatelet drug that inhibits adenosine deaminase and phosphodiesterase (and conversion of cAMP to AMP) inhibiting platelet aggregation and resulting in vasodilation

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40
Q

Dipyridamole clinical indications

A

rarely used but when used is in fixed combination with aspirin (Aggrenox) for secondary prevention of stroke - Clopidogrel and aspirin works as well and is safer

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41
Q

Cilostazol MOA

A

antiplatelet and vasodilatory drug that inhibits phosphodiesterase (and conversion of cAMP to AMP) inhibiting platelet aggregation and resulting in vasodilation

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42
Q

Cilostazol clinical indications

A

intermittent claudication (legs) in PVD (also increases HDL and decreases TG)

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43
Q

Cilostazol contraindications

A

heart failure

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44
Q

Cilostazol adverse effects

A

headache, GI upset, drug interactions due to metabolism by CYP

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45
Q

things to caution when prescribing antiplatelet drugs

A

patients taking other antithrombotic drugs, platelet-inhibiting supplements including fish oil, Dong quai, garlic, ginger, gincko, ginseng, and green tea

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46
Q

Unfractionated heparin MOA

A

indirect thrombin inhibitor that binds to and activates anti-thrombin creating a complex that leads to inactivation of thrombin (factor IIa) and intrinsic clotting factors IXa and Xa, inhibiting the formation of fibrin

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47
Q

Unfractionated heparin clinical indications

A

used in acute settings in treatment of PE, DVT, TIA, and ACS (MI) and sometimes used initially in the treatment of atrial fibrillation or prosthetic valves, and in hemodialysis and heart/lung bypass machine

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48
Q

Unfractionated heparin pharmacokinetics

A

administered IV or SC with rapid onset and short half life = 2 hours - must use lower dose with impaired kidney function

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49
Q

Unfractionated heparin contraindications

A

do not use with NSAIDs due to the risk of bleeding and renal dysfunction

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50
Q

Unfractionated heparin adverse effects

A

frequent bleeding, osteoporosis, hyperkalemia, transiently elevated transaminases, HIT (must monitor platelets and PTT)

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51
Q

Unfractionated heparin antidote

A

protamine sulfate (1 mg neutralizes 100 U heparin)

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52
Q

LMW heparin MOA

A

indirect thrombin inhibitor that binds to and activates anti-thrombin creating a complex that leads to inactivation of thrombin (factor IIa) and clotting factors IXa and Xa, inhibiting formation of fibrin

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53
Q

LMW heparin pharmacokinetics

A

administered SC with onset of 1-2 hours and half-life of 4 hours

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54
Q

LMW heparin contraindications

A

spinal or epidural catheters

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55
Q

Enoxaparin (Lovenox) clinical indications

A

a LMW heparin that is used in the treatment of DVT/PE and for DVT prophylaxis in knee and hip replacement surgeries as well as abdominal surgeries (safe in pregnancy), can also be used to bridge patients starting on warfarin until INR reaches satisfactory level

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56
Q

Enoxaparin adverse effects

A

peripheral edema, less HIT and osteoporosis compared with heparin

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57
Q

Dalteparin clinical indications

A

used primarily in patients with malignancy and more effective than warfarin in reducing recurrent embolic events

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57
Q

Dalteparin adverse effects

A

peripheral edema, less HIT and osteoporosis compared with heparin

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57
Q

Warfarin MOA

A

anticoagulant that inhibits Vitamin K, a co-factor in carboxylation/activation of clotting factors II, VII, IX, and X, inhibiting fibrin formation

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58
Q

Warfarin pharmacokinetics

A

administered orally, is absorbed rapidly and binds 99% to albumin, the onset of action is delayed (3-4 days) due to the time it takes to degrade clotting factors, metabolized by CYP enzymes, crosses the placenta

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59
Q

Warfarin clinical indications

A

used most commonly prophylactically to prevent thrombosis in atrial fibrillation, atrial flutter, prosthetic heart valves, and recurrent DVT, and perioperatively with TKA and THA, also used in the treatment of DVT/PE to prevent the thrombus from growing while body dissolves the fibrin plug

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60
Q

Warfarin adverse effects

A

bleeding

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61
Q

Warfarin antidote

A

Vitamin K infusion

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62
Q

Warfarin contraindications

A

pregnancy

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63
Q

recommended PT/INR for Warfarin

A

between 2-3 except for with mechanical heart valves which needs to be 2.5-3.5

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64
Q

Warfarin drug interactions

A

CYP inducers will reduce warfarin activity (Carbamazepine, Phenobarbital, Phenytoin, Rifampin, Vitamin K, Cholestyramine, Colestipol) and CYP inhibitors will increase warfarin activity and bleeding (Aspirin, Heparin, Antibiotics - decrease gut bacteria vitamin k production)

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65
Q

Foods rich in Vitamin K

A

asparagus, broccoli, Brussels sprouts, collard greens, kale, kiwi, lettuce, soybeans, spinach, Swiss chard

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66
Q

Dabigatran MOA

A

direct thrombin inhibitor = first warfarin alternative

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67
Q

Dabigatran clinical indications/advantages

A

used in prophylaxis of thrombosis similar to warfarin but with reduced drug/food interactions and risk for intracranial bleeding, superior to warfarin in patients with poor INR control - does not require INR monitoring

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68
Q

Dabigatran pharmacokinetics

A

administered orally, onset of action = 2-3 days (faster than warfarin)

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69
Q

Dabigatran adverse effects

A

more GI bleeding and heartburn than warfarin but less intracranial bleeding, discontinuation can cause rebound thrombosis

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70
Q

Dabigatran antidote

A

Idarucizumab (Praxbind)

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71
Q

Argatroban MOA

A

direct thrombin inhibitor that binds to thrombin and inhibits the conversion of fibrinogen to fibrin

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72
Q

Argatroban pharmacokinetics

A

administered IV only, must decrease dose in patients with hepatic impairment

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73
Q

Argatroban clinical indications

A

used as anticoagulant prophylaxis or treatment for HIT and also in PCI if a patient is at risk of HIT with heparin agent (must monitor ACT when being used)

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74
Q

Fondaparinux MOA

A

binds to and activates anti-thrombin causing direct inhibition of factor Xa (no direct effect on thrombin)

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75
Q

Fondaparinux clinical indications

A

used similar to a heparin in the treatment of DVT/PE and as DVT prophylaxis in orthopedic surgery, can be used as alternative to heparin in patients with history of HIT

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76
Q

Fondaparinux administration

A

SC injection

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77
Q

Rivaroxaban (Xarelto) MOA

A

direct inhibitor of factor Xa

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78
Q

Rivaroxaban clinical indications

A

used in prophylaxis and treatment of DVT/PE and stroke prevention in non-valvular atrial fibrillation

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79
Q

Rivaroxaban adverse effects

A

has the highest risk of the Xa inhibitors for GI bleeding and more liver/kidney toxicity but lower rates of serious and fatal bleeding than warfarin

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80
Q

Rivaroxaban administration

A

oral once daily

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81
Q

Apixaban (Eliquis) MOA

A

direct inhibitor of factor Xa

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82
Q

Apixaban clinical indications

A

used in prophylaxis of DVT/PE and stroke prevention in non-valvular atrial fibrillation, better than warfarin and safer than Rivaroxaban (DOC)

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83
Q

Apixaban adverse effects

A

less bleeding than warfarin

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84
Q

Apixaban administration

A

oral twice daily

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85
Q

Alteplase (tPA) MOA

A

endogenously activates the conversion of plasminogen to plasmin by activating protease and preferentially activates plasminogen bound to fibrin (avoiding systemic activation) which breaks down fibrin clots in arterial system

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86
Q

Alteplase clinical indications

A

administered IV for acute stroke, MI, and PE

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87
Q

Alteplase half-life

A

5 minutes

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88
Q

adverse effects of fibrinolytics

A

hemorrhage by destruction of therapeutic clots as well as pathologic clots is the biggest risk

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89
Q

Anistreplase MOA

A

purified human plasminogen and bacterial streptokinase that has been acylated to protect the enzyme active site which catalyzes the conversion of plasminogen to plasmin

90
Q

Anistreplase clinical indications

A

administered IV in the treatment of acute MI (not used much anymore)

91
Q

Urokinase clinical indications

A

treatment of acute PE (not used much anymore)

92
Q

Reteplase (r-PA)

A

genetically engineered smaller derivative of tPA administered IV for acute MI

93
Q

Tenecteplase (TNK-tPA)

A

genetically engineered smaller derivative of tPA with a higher affinity for fibrin than tPA

94
Q

Tenecteplase clinical indications

A

administered IV for acute MI

95
Q

Tenecteplase half-life

A

20-24 minutes

96
Q

Reteplase half-life

A

13-16 minutes

97
Q

Cardiac arrhythmia

A

an electrical activity that deviates from normal cardiac rhythm as a result of an abnormality in impulse formation and/or impulse conduction which can result in reduced cardiac output (occurs in over 80% of patients with an acute MI, 50% of anesthetized patients, and up to 25% of patients treated with digoxin)

98
Q

common causes of arrhythmias

A

ischemia, scarred tissue, hypoxia (sleep apnea), acidosis or alkalosis (sepsis), electrolyte disturbances, excessive catecholamine exposure (cocaine use), autonomic disturbances, and drug toxicities

99
Q

P wave on EKG

A

atrial depolarization followed by contraction

100
Q

QRS complex on EKG

A

ventricular depolarization followed by contraction

101
Q

T wave on EKG

A

ventricular repolarization followed by refilling

102
Q

Phase 0 of action potential

A

rapid influx of Na+ causing rapid depolarization

103
Q

Phase 2 of action potential

A

efflux of Ca2+ causing contraction of atrial or ventricular muscle and a relatively stable plateau in membrane potential

104
Q

Phase 3 of action potential

A

rapid efflux of K+ causing repolarization (drugs that delay repolarization prolong the ERP)

105
Q

Phase 4 of action potential

A

membrane potential remains stable (myocardium cells) or undergoes spontaneous depolarization where the membrane potential gradually rises until threshold potential is reached (SA node cells)

106
Q

Class Ia drugs effects on action potential

A

slow phase 0 depolarization in ventricular muscle fibers resulting in increased ERP and action potential duration

107
Q

Class Ib drugs effects on action potential

A

slow phase 0 depolarization and accelerate phase 3 repolarization in ventricular muscle fibers resulting in decreased ERP and action potential duration

108
Q

Class Ic drugs effects on action potential

A

markedly slow phase 0 of repolarization in ventricular muscle fibers and have no effect on ERP or action potential duration

109
Q

Class II drugs effects on action potential

A

slow phase 4 spontaneous depolarization resulting in decreased impulse automaticity, chronotropy, dromotropy, and inotropy of the myocardium and prolonged repolarization at the AV node

110
Q

Class III drugs effects on action potential

A

slow phase 3 repolarization resulting in increased ERP and action potential duration

111
Q

Class IV drugs effects on action potential

A

slow phase 4 spontaneous depolarization resulting in slowed conduction in the SA and AV node cells and decreased impulse automaticity and conduction in vascular smooth muscle and the myocardium

112
Q

Quinidine clinical indications/pharmacokinetics

A

Class Ia drug that is administered orally used uncommonly to convert atrial, AV junctional, and ventricular tachyarrhythmias to NSR or to prevent arrhythmias (historically used to treat malaria)

113
Q

Quinidine adverse effects

A

blurry vision, tinnitus, headache, vertigo (cinchonism), psychosis and also has some mild, alpha-adrenergic and anticholinergic actions

114
Q

Procainamide clinical indications/pharmacokinetics

A

Class Ia drug that is administered IV only and used uncommonly to treat acute atrial or ventricular arrhythmias or hemodynamically stable SMVT (largely replaced by amiodarone in clinical practice)

115
Q

Procainamide adverse effects

A

hypotension, lupus like syndrome

116
Q

Lidocaine clinical indications/pharmacokinetics

A

Class Ib drug that is administered IV only and used to terminate active ventricular tachycardia/ventricular fibrillation (ACLS) and in the prevention of ventricular fibrillation after cardioversion in setting of acute ischemia (not used in prevention due to risk of mortality)

117
Q

Lidocaine adverse effects

A

CNS changes - nystagmus, drowsiness, and slurred speech

118
Q

Mexiletine clinical indications

A

Class Ib drug that is used in chronic preventative treatment of ventricular arrhythmias in patients prone to VT

119
Q

Mexiletine adverse effects

A

nausea and vomiting, has a narrow therapeutic index

120
Q

Flecainide clinical indications/pharmacokinetics

A

Class Ic drug that is administered orally and used to treat patients with otherwise normal hearts who are prone to atrial fibrillation or flutter

121
Q

Flecainide adverse effects

A

blurry vision, nausea, may cause severe exacerbation of arrhythmia in patients with pre-existing VT and previous MI and ventricular ectopy

122
Q

Propafenone clinical indications

A

Class Ic drug that is used to control rhythm in atrial arrhythmia including atrial fibrillation and flutter and can be used to prevent paroxysmal SVT in patients with AVRT

123
Q

Propafenone adverse effects

A

has beta-blocking effects so can cause bronchospasms - use cautiously in asthmatics

124
Q

Beta-blockers anti-arrhythmic clinical indications/pharmacokinetics

A

administered oral or IV (except for Esmolol = IV only) and used to treat tachyarrhythmias caused by increased sympathetic activity - atrial flutter and fibrillation and AVNRT, also can be useful in preventing recurrent infarction and sudden death due to ventricular arrhythmias in patients recovering from acute MI

125
Q

Metoprolol clinical indications

A

cardioselective beta-blocker that is most widely used in the treatment of cardiac arrhythmias

126
Q

Esmolol clinical indications

A

very short-acting cardioselective beta-blocker with fast onset used IV to abort arrhythmias

127
Q

Class III drugs adverse effects on EKG

A

QT prolongation that increases the risk of torsades de pointes

128
Q

Amiodarone clinical indications

A

Class III drug that has features of all four drug classes administered oral or IV, used in the treatment of hemodynamically stable SMVT as well as pulseless VT/VF (ACLS), highly effective in the treatment and prevention of SVT, especially atrial fibrillation and also approved for prevention of recurrent ventricular arrhythmias in at-risk patients

129
Q

Amiodarone adverse effects

A

symptomatic bradycardia and heart block in patients with known sinus or AV nodal disease, peripheral vasodilation and hypotension, pulmonary fibrosis!! (required PFT monitoring), thyrotoxicity and hepatotoxicity!! (required LFT and TSH monitoring)

130
Q

Class Ia drugs adverse effects on EKG

A

QT prolongation and widened QRS complex

131
Q

Amiodarone contraindications

A

long-term treatment in YOUNGER patients

132
Q

Dronedarone clinical indications/pharmacokinetics

A

Class III drug that is administered orally and only used clinically to maintain NSR in patients with atrial arrhythmias, less effective than amiodarone

133
Q

Dronedarone contraindications

A

patients with symptomatic HF

134
Q

Sotalol clinical indications/pharmacokinetics

A

Class III drug that is a nonselective beta-blocker used to treat life-threatening ventricular arrhythmias (ACLS) and for cardioversion and maintenance of NSR in patients with atrial fibrillation (with telemetry in hospital setting)

135
Q

Sotalol contraindications

A

patients with long QT

136
Q

Verapamil clinical indications/pharmacokinetics

A

Class IV drug that is administered IV to terminate SVT and administered orally or IV for rate control in atrial fibrillation and atrial flutter (rarely able to covert atrial fibrillation/flutter to NSR)

137
Q

Diltiazem clinical indications/pharmacokinetics

A

Class IV drug that is administered orally or IV and used for managing supraventricular arrhythmias and rate control in atrial fibrillation/flutter (less side effects than with verapamil)

138
Q

Verapamil/Diltiazem adverse effects

A

HF, 3rd-degree AV block, bradycardia as well as hypotension

139
Q

Amiodarone half-life

A

25-110 days

140
Q

Amiodarone pharmacokinetics

A

administered orally or IV and metabolized by CYP3A4 so can interact with many drugs

141
Q

Digoxin MOA

A

inhibits the sodium/potassium-ATPase pump resulting in a shortened refractory period in atrial and ventricular myocardial cells and a prolonged refractory period/diminished conduction velocity in the AV node

142
Q

Digoxin clinical indications

A

used to control ventricular response rate in atrial fibrillation and atrial flutter but has a narrow therapeutic index (may be DOC for rate control in patients with heart failure and atrial fibrillation)

143
Q

Digoxin pharmacokinetics

A

administered orally or IV with loading dose prior to maintenance dosing, needs therapeutic level monitoring

144
Q

Digoxin adverse effects

A

at toxic doses, it may cause ectopic ventricular beats resulting in VT or VF

145
Q

Adenosine MOA

A

inhibits AV nodal conduction and increases AV nodal refractory period

146
Q

Adenosine clinical indications/pharmacokinetics

A

administered IV bolus and is DOC (very effective) for prompt conversion of paroxysmal SVT to NSR - duration of action = 10-15 seconds

147
Q

Adenosine adverse effects

A

flushing, SOB, and chest pain

148
Q

Atropine clinical indications

A

administered IV to abort life-threatening bradycardia due to medication toxicity/OD, 2nd-degree heart block, and complete heart block

149
Q

First-line treatment of Afib

A

rate control with CCB (Class IV) alone or in combination with beta-blocker (Class II), if heart failure is present- digoxin may be of value

150
Q

Rhythm control of Afib in patients with normal heart

A

DC cardioversion is the first choice therapy but an anti-arrhythmic agent like Flecainide (Class I) can be used as a form of cardioversion

151
Q

Rhythm control of Afib in patients with HF with low EF and/or hypertension

A

Amiodarone = first line

152
Q

Rhythm control of Afib in patients with CAD

A

Sotalol = first line

153
Q

Rhythm control of Afib in patients with mild HF (mild LVH, HFpEF) that do not convert to NSR with cardiac ablation or with established persistent Afib

A

Flecainide or Sotalol = first line, Amiodarone = second line

154
Q

Absolute refractory period (ARP)

A

time during which another stimulus will not lead to another AP (phases 0,1,2)

154
Q

Relative refractory period (RRP)

A

interval following ARP in which a 2nd stimulus is inhibited but not impossible (phases 2 and 3)

155
Q

Effective refractory period (ERP)

A

time in which a cell does not produce a new AP (phases 0,1,2,3)

156
Q

early afterdepolarizations (EADs)

A

disturbed impulses that occur during phase 3 of action potential and interfere with normal impulse formation

157
Q

delayed afterdepolarizations (DADs)

A

disturbed impulses that occur during phase 4 of the action potential and interfere with normal impulse formation

158
Q

EAD triggers

A

anything that causes QT prolongation (blockage of rapidly activating delayed rectifier potassium channels due to drugs or congenital syndrome), especially slow heart rates and hypokalemia, which can result in torsades de pointes (V Tach), tachycardia, and other arrhythmias

159
Q

DAD triggers

A

excess accumulation of intracellular calcium especially fast heart rates which can result in ventricular tachycardia, digitalis toxicity, excess catecholamines, and myocardial ischemia

160
Q

Torsades de pointes

A

disturbance of impulse formation caused by QT prolongation which can lead to ventricular tachycardia

161
Q

Wolff-Parkinson-White Syndrome

A

serious disturbance of impulse conduction caused by the failure of an impulse to die out after normal activation (typically due to an obstacle and availability of another circuit) and creating an additional repetitive impulse at the AV node

162
Q

Lipoproteins containing apo B-100

A

LDL, VLDL, and chylomicrons

163
Q

role of HDL

A

made up of mostly cholesterol and acts as a scavenger to take up cholesterol from peripheral tissues and triglycerides from degradation of VLDL - does not contain apo B-100

164
Q

role of VLDL

A

secreted by liver and functions to export triglycerides to peripheral tissues

165
Q

role of chylomicrons

A

formed in the intestine and function to carry triglycerides of dietary origin, unesterified cholesterol, and cholesteryl esters

166
Q

primary hyperlipidemia

A

genetically determined (familial; hereditary)

167
Q

secondary hyperlipidemia

A

acquired due to other conditions such as hypothyroidism, nephrotic syndrome, drugs, DM, alcohol, gout, chronic renal failure

168
Q

total cholesterol goal

A

less than or equal to 200

169
Q

triglycerides goal

A

less than or equal to 150

170
Q

LDL cholesterol goal

A

less than or equal to 100

171
Q

HDL cholesterol goal

A

greater than or equal to 60

172
Q

process of atherogenesis

A

LDL enters the intima of endothelium which becomes oxidized into proinflammatory lipids causing adhesion and entry of monocytes and T lymphocytes. Monocytes differentiate into macrophages and consume large amounts of LDL transforming into foam cells. The foam cells release growth factors that encourage atherosclerosis and creation of lipid pools.

173
Q

Statins MOA

A

competitive HMG CoA reductase inhibitors that prevent the synthesis of (mevalonate) cholesterol in the liver leading to a reduced intracellular supply of cholesterol which ultimately causes increased cell surface LDL receptors that bind and internalize circulating LDL-c reducing plasma cholesterol

174
Q

LDL-c effect of high intensity statins

A

lowers LDL-c by greater than or equal to 50%

175
Q

LDL-c effect of moderate intensity statins

A

lowers LDL-c by 30-49%

176
Q

LDL-c effect of low intensity statins

A

lowers LDL-c by less than or equal to 30%

177
Q

Statins clinical indications

A

used to lower the risk of atherosclerotic cardiovascular disease events by lowering plasma cholesterol levels in all types of hyperlipidemia

178
Q

Statins contraindications

A

pregnancy, lactation, active or chronic liver disease, red yeast rice, grapefruit juice

179
Q

Statins administration

A

administered orally usually taken at night (liver is most active at night)

180
Q

Statins adverse effects

A

elevated liver enzymes and liver toxicity (reversible when statin stopped), myopathy and rhabdomyolysis (CK levels above 150), photosensitivity, may increase levels of warfarin (check INR prior to initiating/changing doses), GI upset

181
Q

Atorvastatin and Rosuvastatin clinical indications

A

most potent statins used to lower triglycerides, LDL, and total cholesterol (Rosuvastatin reaches increased levels in Asians), atorvastatin metabolized by CYP

182
Q

Lovastatin clinical indications

A

low potency statin used mostly to lower LDL, metabolized by CYP

183
Q

Simvastatin clinical indications

A

medium potency statin used to lower triglycerides, LDL, and total cholesterol, metabolized by CYP - inhibitors may increase risk of rhabdomyolysis

184
Q

Pravastatin clinical indications

A

low to medium-potency statin (medium only at high doses)

185
Q

Statin preferred with renal impairment

A

Atorvastatin

186
Q

Niacin MOA

A

inhibits lipolysis in adipose tissue reducing production of free fatty acids and triglycerides - reduces VLDL secretion from liver lowering LDL-c plasma concentrations

187
Q

Niacin clinical indications

A

used to lower plasma levels of LDL-c, triglycerides, and lipoprotein(a), and is the most effective agent for increasing HDL-c in the treatment of familial hyperlipidemias and severe hypercholesterolemia, often used in combination with other agents

188
Q

Niacin contraindications

A

hepatic disease, active peptic ulcer, low BP, severe gout, and individuals with high uric acid levels (diabetics)

189
Q

Niacin adverse effects

A

intense cutaneous flush accompanied by uncomfortable feeling of warmth and pruritis, nausea, abdominal pain, hyperuricemia/gout, impaired glucose tolerance, hepatoxicity, and hypotension

190
Q

Gemfibrozil MOA

A

a fibrate that is a peroxisome proliferator-activated receptor-alpha agonist which decreases triglycerides by lowering VLDL levels and increases HDL levels (increases lipoprotein lipase activity)

191
Q

Gemfibrozil clinical indications

A

hypertriglyceridemia, type III hyperlipidemia, and low HDL

192
Q

Gemfibrozil contraindications

A

coadministration with statin therapy due to risk of myopathy, renal and hepatic dysfunction, pre-existing gallbladder disease or biliary cirrhosis

193
Q

Gemfibrozil adverse effects

A

GI upset, gallstones, myopathy, hepatic dysfunction, increased levels of warfarin

194
Q

Fenofibrate MOA

A

a fibrate that is a peroxisome proliferator-activated receptor-alpha agonist that decreases triglycerides (more effective than Gemfibrozil) by lowering VLDL levels and increases HDL levels (increases lipoprotein lipase activity)

195
Q

Fenofibrate adverse effects

A

GI upset, gallstones, myopathy, hepatic dysfunction, increased levels of warfarin (check INR)

195
Q

Fenofibrate contraindications

A

renal and hepatic dysfunction, pre-existing gallbladder disease or biliary cirrhosis

196
Q

Fenofibrate clinical indications

A

same as gemfibrozil - low HDL and hypertriglyceridemia, better than gemfibrozil when combined with statins

197
Q

Bile acid sequestrates MOA

A

bind bile acids in gut to form an insoluble complex preventing reabsorption in small intestine increasing the levels of cholesterol taken up to make new bile resulting in decreased serum level of cholesterol, upregulating LDL receptors (decreasing LDL)

198
Q

Bile acid sequestrates clinical indications

A

hyperlipidemias, elevated LDL, digitalis toxicity, and chronic pruritis

199
Q

Bile acid sequestrates contraindications

A

biliary cirrhosis, biliary obstruction, gallstones, hypertriglyceridemia, GI obstruction, coagulopathy, hypothyroid patients, prolonged use in renal disease, pregnancy/lactation

200
Q

Bile acid sequestrates adverse effects

A

constipation, bloating, nausea, flatulence, interferes with absorption of some drugs/fat-soluble vitamins (digoxin, warfarin, thyroid meds), can increase serum triglyceride concentration

201
Q

Colesevelam clinical indications

A

bile acid sequestrate that is used to treat hyperlipidemia and elevated LDL as well as type II diabetes in lowering glucose levels (fewer side effects than other bile acid sequestrates)

202
Q

Colestipol clinical indications

A

bile acid sequestrate that is used to treat hyperlipidemia and elevated LDL as well as adjunctive to diet and exercise in type II diabetes to improve glycemic control (do not use in type I diabetes or diabetic ketoacidosis)

203
Q

Ezetimibe (Zetia) MOA

A

selective inhibitor of absorption of dietary and biliary cholesterol in the small intestine

204
Q

Bile acid sequestrates pharmacokinetics

A

metabolized in small intestine and avoids the liver and kidneys

205
Q

Ezetimibe clinical indications

A

used usually in combo with statin to modestly lower LDL and in treatment of phytosterolemia

206
Q

Ezetimibe contraindications

A

severe hepatic insufficiency, pregnancy/lactation

207
Q

Ezetimibe adverse effects

A

hepatic dysfunction and myositis

208
Q

Ezetimibe pharmacokinetics

A

metabolized in the small intestine and liver with biliary and renal excretion

209
Q

Omega-3 fatty acids MOA

A

inhibit VLDL and triglyceride synthesis in the liver

210
Q

Omega-3 fatty acids clinical indications

A

lowering of triglycerides and used as adjunct to diet and exercise (not shown to reduce cardiovascular mortality)

211
Q

Omega-3 fatty acids contraindications

A

patients on anticoagulants, thrombolytics, or antiplatelets due to increased risk of bleeding, patients with a history of fish hypersensitivity

212
Q

Omega-3 fatty acids adverse effects

A

GI disturbances, increased bleeding risk

213
Q

drug with the largest lowering effect on LDL

A

statins then bile acid sequestrates

214
Q

drug with the largest increasing effect on HDL

A

niacin then fibrates

215
Q

drug with the largest lowering effect on triglycerides

A

fibrates then niacin

216
Q

drug to avoid in hypertriglyceridemia

A

bile acid sequestrates

217
Q

effects of combining statins with fibrates

A

increased risk for rhabdomyolysis

218
Q

reasons to use lipid-lowering drug combinations

A

significantly increased VLDL levels, both LDL and VLDL levels elevated initially, LDL or VLDL levels not normalized with single agent, elevated levels of lipo(a) or HDL deficiency coexists with other hyperlipidemia

219
Q

Evolocumab MOA

A

inhibits PCSK9 (a protein that binds to LDL receptors in the liver) resulting in decreased levels of circulating LDL in the blood

220
Q

Evolocumab clinical indications

A

used to decrease LDL when individuals have a genetic condition or in those with heart disease whose cholesterol has been difficult to control with other lipid-lowering medications

220
Q

Evolocumab pharmacokinetics

A

administered SC with half-life of 11-20 days

Pharmacology II (5 decks)

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