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Cardio > Anti-lipid, Anti-platelet, and anti-HTN drugs > Flashcards

Anti-lipid, Anti-platelet, and anti-HTN drugs Flashcards

1
Q

Dabigitran

A

Direct-acting thrombin inhibitor (oral)

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2
Q

Fondaparinux

A

Indirect-acting Xa-inhibitor (SubQ)

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3
Q

P2Y12 inhibitors - describe MoA and name drugs

A

targets ADP receptor and prevents platelets from using energy Clopidogrel, prasugrel, ticagrel

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4
Q

Side effects of B1 and B2 antag

A

B - need to be careful w/ diabetes b/c messes up insulin B2 - watch for asthma/COPD due to bronchioconstriction

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5
Q

name an a2 agonist and describe MoA/use

A

clonidine, HTN, acts presynaptically in anti-sympathetic ways

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6
Q

Eptifibatide

A

GpIIb/IIIa inhibitor These are the receptors for fibrin, which prevents fibrinogen bridges from forming (prevents platelet plug)

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7
Q

What are the fibric acid derivatives (FADs)? What are they mainly used for?

A

Gemfibrozil and fenofibrate Lowering TAGs

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8
Q

Bivalirudin

A

Direct-acting thrombin inhibitor (IV)

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9
Q

Niacin MoA + side effects

A

reduces secretion of VLDL and reduces the amount of lipid in circulation flushing, pruritus, insulin resistance (not used very often)

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10
Q

Furosemide

A

Loop diuretic inhibits Na/K/Cl symporter hypokalemia, alkalosis **preferred during pregnancy compared to other diuretics

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11
Q

Hydochlorothiazide

A

thiazide diuretic inhibits Na/Cl symporter hypokalemia, alkalosis

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12
Q

Apixaban

A

Direct-acting Xa-inhibitor (oral)

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13
Q

What are toxicities associated w/ statins?

A
  1. birth defects (use BABAs during pregnancy) 2. hepatotoxicity 3. myopathy (rhabdomyolysis) 4. drug-drug interactions (esp w/ amlodipine)
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14
Q

What drugs can you use in the case of HIT?

A

Direct-acting thrombin inhibitors

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15
Q

Anti-thrombin (FII) drugs, direct and indirect

A

Direct: Argatroban (IV) Bivalirudin (IV) Dabigtran (oral) Indirect: U. heparin (IV) Warfarin

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16
Q

What is a cholesterol absorption inhibitor? How does it work?

A

Ezetimibe 1. blocks absorption from GI tract (blocks NPCI receptor) 2. also stimulates LDL receptor to absorb more from bloodstream

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17
Q

Alirocumab MoA

A

cholesterol absorption stimulator; stimulates LDL receptor to increase the amount of LDL absorbed into the liver; does this by blocking PCSK9; PCSK9 promotes the breakdown of the LDL receptor, so alirocumab stabilizes against degradation

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18
Q

Abciximab

A

GpIIb/IIIa inhibitor These are the receptors for fibrin, which prevents fibrinogen bridges from forming (prevents platelet plug)

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19
Q

What drugs would you use to treat angina and HTN at same time?

A

B blockers or CCBx

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20
Q

Captopril

A

ACEi

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21
Q

B blockers used for HTN + selectivity

A

atenolol (B1), metoprolol (B1), carvedilol (a1, B1-3)

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22
Q

Name the loop diuretics, MoA, and side effects

A

furosemide inhibits Na/K/Cl symporter; hypokalemia, alkalosis; **preferred during pregnancy compared to other diuretics

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23
Q

Prasugrel

A

P2Y12 inhibitor (targets ADP receptor)

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24
Q

What does a direct versus indirect thrombin inhibitor mean?

A

Indirect-acting drugs use antithrombin to impact thrombin (or inhibit Vit K reductase in case of warfarin) **includes indirect anti-Xa drugs like Fondaparinux and Enoxaparin Direct-acting drugs directly bind to thrombin (Factor II)

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25
Q

ACE inhibitor MoA, drugs + side effects

A

captopril and lisinopril prevent conversion of angiotensin I to II by inhibiting ACE angiodema and cough (due to build-up of bradykinin), hyperkalemia, be careful w/ first trimester of pregnancy

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26
Q

Name the thiazides, MoA and side effects

A

Hydrochlorothiazide and chlorthalidone inhibits Na/Cl symporter hypokalemia, alkalosis

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27
Q

What are statins best used for? What can you combine them with?

A

Lowering LDL and TAGs Many other anti-lipid drugs, esp ezetimibe

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28
Q

Clopidogrel

A

P2Y12 inhibitor (targets ADP receptor)

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29
Q

Enoxaparin

A

Indirect-acting Xa-inhibitor (SubQ)

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30
Q

Name the statins and their MoA

A

atorvastatin, rosuvastatin, simvustatin, pravastain, lovastain inhibit HMG CoA reductase (rate-limiting step of cholesterol synthesis, increase uptake of LDL)

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31
Q

Parenteral indirect-acting anti-thrombotic drugs

A

FII+FXa Unfractionated heparin FXa Fondaparinux Enoxaparin

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32
Q

What’s the MoA of FADs?

A
  1. directly stimulate LDL receptor (draw out of circulation) 2. stimulate lipoprotein lipase (decreases TAGs in circulation) 3. promotes breakdown of FFAs
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33
Q

What is the MoA of BABAs?

A

increase elimination of bile acids, drawing more out of the liver (only way to excrete cholesterol) also increases LDL receptors to pull more LDL out of bloodstream

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34
Q

Tirofiban

A

GpIIb/IIIa inhibitor These are the receptors for fibrin, which prevents fibrinogen bridges from forming (prevents platelet plug)

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35
Q

diltiazem

A

non-DHP CCBx

36
Q

nifedipine

A

DHP CCBx

37
Q

Endoxaban

A

Direct-acting Xa-inhibitor (oral)

38
Q

Side effects of warfarin

A

birth defects, increased bleeding risk when combined w/ other medications (e.g. FADs, NSAIDs, amiodarone), variation in Vit K in diet can be a challenge

39
Q

What are the GpIIb/IIIa inhibitors?

A

Abciximab, eptifibatide, tirofiban

40
Q

Name the K+ sparing drugs, MoA, and side effects

A

2 MoA: 1. aldosterone receptor antagonists: spironolactone, eplerenone (both = steroid hormones) 2. Enac blockers: triamterene;

spironolactone similar to estradiol so leads to gynecomastia

41
Q

carvedilol selectivity

A

a1, B1, 2, 3

42
Q

ARB MoA, drugs + side effects

A

losartan, valsartan blocks receptor of angio II (prevents aldosterone/RAAS system effects) risk of hyperkalemia and arrhythmia, be careful w/ first trimester

43
Q

Losartan

A

ARB

44
Q

What are the categories of anti-platelet drugs?

A

COX 1/2 inhibitors, P2Y12 inhibitors, GpIIb/IIIa inhibitors

45
Q

Colestipol + side effects

A

BABA - increase elimination of bile acids, drawing more out of the liver (only way to excrete cholesterol) also increases LDL receptors to pull more LDL out of bloodstream Use during pregnancy, severe GI tox

46
Q

Valsartan

A

ARB

47
Q

3 types of diuretics for HTN

A
  1. loop diruetics 2. thiazides 3. K-sparing
48
Q

Oral indirect-acting anti-thrombotic drugs

A

Warfarin (vitamin K reductase inhibitor)

49
Q

clonidine

A

a2 agonist, used for HTN

50
Q

How do GpIIb/IIIa inhibitors work and when are they used?

A

These are the receptors for fibrin, which prevents fibrinogen bridges from forming (prevents platelet plug) angioplasty and stent placement

51
Q

nimodipine

A

DHP CCBx

52
Q

When are statins usually taken?

A

Often at night (not all)

53
Q

Which HTN drugs lead to hyperkalemia and hypokalemia?

A

Hyper: ACE inhibitors and ARBs Hypo: loop diuretics and thiazides

54
Q

What are the Vitamin K-dependent factors?

A

2, 7, 9, 10 protein C and S

55
Q

Lisinopril

A

ACEi

56
Q

diazoxide

A

hyperpolarizes smooth muscle cells and inhibits contraction parenteral; used for hypertensive emergencies

57
Q

Argatroban

A

Direct-acting thrombin inhibitor (IV)

58
Q

Chlorathalidone

A

thiazide diuretic inhibits Na/Cl symporter hypokalemia, alkalosis

59
Q

Rivaroxaban

A

Direct-acting Xa-inhibitor (oral)

60
Q

prazosin

A

a1 antagonist, relaxes VSM and is used for HTN orthostatic hypertension

61
Q

Tacagrelor

A

P2Y12 inhibitor (targets ADP receptor)

62
Q

What should you combine ezetimibe w/ and why?

A

Statins so that HMG CoA reductase doesn’t increase synthesis of cholesterol

63
Q

When should you take BABAs?

A

1 hour before other drugs or 3 hours after (can interfere w/ absorption)

64
Q

What other effects do statins have?

A

Cardioprotective effects such as: 1. increases in NO 2. stabilizing plaques and decrease risk of thrombosis 3. decrease inflammation 4. decrease platelet activation and VTE risk

65
Q

FXa drugs (direct and indirect)

A

Direct apixaban (oral) rivaroxaban (oral) endoxaban (oral) No parenteral drugs Indirect: Fondaparinux (SubQ) Enoxaparin (SubQ)

66
Q

Spironolactone

A

K-sparing diuretic, aldosterone receptor antagonist gynecomastia

67
Q

Parenteral direct-acting anti-thrombotic drugs

A

Argatroban and bivalirudin

68
Q

Oral direct-acting anti-thrombotic drugs

A

FII Dabigitran FXa Apixiban Rivaroxaban Endoxaban

69
Q

Name the vasodilator MoAs (column 2 on drug chart) and name side effects

A
  1. cGMP levels - relaxation 2. K+ openers - hyper polarize cells and inhibit contraction 3. Ca channel blockers Gingival enlargement (not sure if for all?)
70
Q

What’s a comorbidity you should consider for ACE inhibitors + ARBs?

A

Is protective against diabetic nephropathy compared to other drugs

71
Q

amlodipine

A

DHP CCBx

72
Q

How do COX 1/2 inhibitors work and what’s an important anti-platelet?

A

Aspirin Targets thromboxane, decreases platelet aggregation and activation Use for unstable angina, stroke, and MI

73
Q

Which statins interact poorly w/ amlodipine?

A

atorvastatin, simvustatin, lovastatin

74
Q

Ezetimibe MoA

A
  1. blocks absorption from GI tract (blocks NPCI receptor) 2. also stimulates LDL receptor to absorb more from bloodstream
75
Q

Eplerenone

A

K-sparing diuretic, aldosterone receptor antagonist

76
Q

hydralazine

A

changes cGMP levels and induces vascular relaxation

77
Q

What is a cholesterol absorption stimulator? How does it work?

A

Alirocumab stimulates LDL receptor to increase the amount of LDL absorbed into the liver; does the by blocking PCSK9 PCSK9 promotes the breakdown of the LDL receptor, so alirocumab stabilizes against degradation

78
Q

Fenofibrate MoA + side effects

A

FAD 1. directly stimulate LDL receptor (draw out of circulation) 2. stimulate lipoprotein lipase (decreases TAGs in circulation) 3. promotes breakdown of FFAs Watch for drug-drug interactions (statins, warfarin, etc.)

79
Q

What are the BABAs? When should you use them? Toxicities?

A

Colestipol Use during pregnancy Can cause severe GI tox

80
Q

Which statins are highly effective?

A

Atorvastatin and rosouvastatin

81
Q

Side effects of a1 antagonists

A

orthostatic hypotension (prazosin)

82
Q

Triamterene

A

K-sparing diuretic, Enac blocker

83
Q

Gemfibrozil MoA + side effects

A

FAD 1. directly stimulate LDL receptor (draw out of circulation) 2. stimulate lipoprotein lipase (decreases TAGs in circulation) 3. promotes breakdown of FFAs Watch for drug-drug interactions (statins, warfarin, etc.)

84
Q

What are side effects of FADs?

A

Myopathy (especially when used in combo w/ statins… FADs decrease statin absorption in liver which increases serum levels of statins and contribute to myopathy) Also increases bleeding risk from warfarin (does same thing as it does w/ statins and increases amount in bloodstream)

85
Q

Name the 2 types of Ca channel blockers and the drugs that fall into both

A

Both reduce strength of contraction non-DHPs (also anti rhythmics) verapamil, diltiazem DHPs amlodipine, nifedipine, nimodipine

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