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All cardio Flashcards

1
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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2
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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3
Q

Name the classes that increase refractory period (including those that increase APD and those that do not)

A

APD increased: IA (because of K+), III

No change in APD: IB, IC, adenosine

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4
Q

Bivalirudin

A

Direct-acting thrombin inhibitor (IV)

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5
Q

Name the thiazides, MoA and side effects

A

Hydrochlorothiazide and chlorthalidone inhibits Na/Cl symporter hypokalemia, alkalosis

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6
Q

what makes vasculature different than other structures in the body? What receptors does it have? What dominates?

A

No parasympathetic receptors; mediated by a1 and B2 a1 dominates so constriction typically wins

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7
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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8
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

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9
Q

Rank the relative strength of Na channel blockers

A

IC (flecainide and propafenone) = strongest

IA (procainamide) = middle

IB (lidocaine) = weakest

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10
Q

FXa drugs (direct and indirect)

A

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

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11
Q

What is a1’s primary role? Where are these located/how do the receptors work?

A

SM contraction (sympathetic) eye and bladder contraction - in conjunction w/ B2

Also very important for vascular constriction and dilation (a1 dominates so constriction typically wins dominates)

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12
Q

name an a2 agonist and describe how it works + a cardio application

A

clonidine - a2 agonist so it inhibits NE from presynaptic neuron and counterintuitively blocks sympathetic signals - use for HTN

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13
Q

what is the role of a2?

A

inhibits NE from presynaptic neuron and postsynaptically induces smooth muscle contraction like a1 COUNTERINTUITIVELY: blocks sympathetic signals

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14
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

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15
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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16
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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17
Q

Propafenone

A

IC Na+ blocker (strong)

Don’t use in pts w/ structural abnormalities

Increases threshold potential (decreases automaticity), increases RP (no increase in APD), and decreases conduction velocity

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18
Q

Which drugs should you avoid using w/ patients who have structural abnormalities?

A

Class IC drugs because they bind tightly to Na+ and are proarrhythmic

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19
Q

Parenteral direct-acting anti-thrombotic drugs

A

Argatroban and bivalirudin

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20
Q

Losartan

A

ARB

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21
Q

Name the drugs that decrease conduction velocity

A

IA, IC, Class II, Class IV, adenosine

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22
Q

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

A

Gemfibrozil and fenofibrate Lowering TAGs

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23
Q

What are the GpIIb/IIIa inhibitors?

A

Abciximab, eptifibatide, tirofiban

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24
Q

Name Class III side effects

A

All K+ blockers besides for Amiodarone: prolong QT and association w/ Torsades (including Procainamide)

Amiodarone - prolongs QT but no Torsades (has multiple mechanisms); hypo/hyperthyroidism or blue skin/tongue tint

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25
Q

B1-selective only drugs

A

metropolol and atenolol (also called selective B blockers) - both used for HTN, metoprolol used for HF

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26
Q

What drugs can you use in the case of HIT?

A

Direct-acting thrombin inhibitors

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27
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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28
Q

B blockers used for HTN + selectivity

A

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

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29
Q

Name the classes that decrease automaticity for antiarrhythmics

A

All classes

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30
Q

name an a1 antagonist and describe how it works

A

prazosin counters SM contraction by blocking a1 and leads to vasodilation, thus decreasing BP

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31
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

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32
Q

what receptors are used by GI and what are their effects?

A

M3 and B2; M3 = contraction, B2 = relaxation for GI

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33
Q

amlodipine

A

DHP CCBx

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34
Q

Valsartan

A

ARB

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35
Q

Name the 3 broad mechanisms/goals of antiarrhythmics

A
  1. decrease automaticity
  2. increase refractory period (can increase APD or have no impact on APD)
  3. can slow conduction velocity
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36
Q

Parenteral indirect-acting anti-thrombotic drugs

A

FII+FXa Unfractionated heparin FXa Fondaparinux Enoxaparin

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37
Q

What is B1’s primary role?

A

stimulates SA/AV nodes

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38
Q

What is the main difference between epi and NE sensitivity’s to receptors?

A

NE has low affinity for B2 (this was emphasized in the ANS and cardio lecture)

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39
Q

Lisinopril

A

ACEi

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40
Q

Name the class II anti-arrhythmic drugs and describe their mechanism

A

B-blockers (B1 antagonists)

Block epi and NE, decrease sympathetic reseponse, DECREASE PHASE 4 SLOPE

Atenolol, metoprolol, carvediol, propanolol

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41
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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42
Q

a 1, 2, B 1, 2 - selective agonist

A

epinephrine (broncodilation, SM relaxation, among other impacts)

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43
Q

Lidocaine

A

Weak Na+ block with unclear mechanism (beyond increasing threshold potential)

Decreases automaticity, increases RP w/ no increase in APD

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44
Q

epinephrine

A

a1/2, B 1/2 - selective agonist

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45
Q

diazoxide

A

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

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46
Q

Chlorathalidone

A

thiazide diuretic inhibits Na/Cl symporter hypokalemia, alkalosis

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47
Q

Solatol

A

Class III K+ blocker

Increases APD

Prolongs QT and is associated w/ Torsades

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48
Q

propanolol

A

B1/2/3 - selective antagonist (B blocker), decreases cardiac output

Anti-arrhythmic (decreases Phase 4 slope)

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49
Q

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

A

B blockers or CCBx

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50
Q

B1 antagonists

A

metoprolol, atenolol, carvedilol, propandolol (B blockers)

Primarily works by decreasing the slope of Phase 4 depolarization and decreasing HR

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51
Q

how is a2 different from other receptors?

A

effects of a2 work on presynaptic neuron (inhibits the release of NE from presynaptic neuron, but postsynaptically, a2 induces smooth muscle contraction like a1)

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52
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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53
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

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54
Q

Side effects of a1 antagonists

A

orthostatic hypotension (prazosin)

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55
Q

What is B2’s primary role?

A

SM relaxation (sympathetic) for GI, lungs, salivary glands, etc.

In eye and bladder, used in conjunction w/ a1

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56
Q

Flecainide

A

IC Na+ blocker (strong)

Don’t use in pts w/ structural abnormalities

Increases threshold potential (decreases automaticity), increases RP (no increase in APD), and decreases conduction velocity

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57
Q

Rivaroxaban

A

Direct-acting Xa-inhibitor (oral)

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58
Q

Procainamide

A

Class IA, Na+ K+ blocker

Associated w/ Torsades

Reduces automaticity (Increases threshold potential), increases refractory period, and decreases conduction velocity

Moderate Na+ block

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59
Q

What role do M3 and B2 play in the uterus?

A

M3 - contractions, B2, relaxation (L+D plus menstrual applications)

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60
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.)

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61
Q

What mechanisms should you try to use for structural defects/reeentry

A

Increase the refractory period, decrease conduction velocity

62
Q

Ivabradine (didn’t really discuss this in class but it’s on the drug chart)

A

If (HCN) channel inhibitor

63
Q

3 types of diuretics for HTN

A
  1. loop diruetics 2. thiazides 3. K-sparing
64
Q

non-selective parasympathetic antagonist used to increase cardiac output or to dilate eyes

A

Atropine

65
Q

atenolol

A

B1 antagonist, B blocker (decreases cardiac output)

Anti-arrhythmic (decreases Phase 4 slope)

Also used for HTN

66
Q

Diltiazem

A

Class IV Ca++ channel blocker (non-DHP)

Slows nodal depolarization (decreases automaticity), decreases conduction velocity

Also used for HTN

67
Q

Verapamil

A

Class IV Ca++ channel blocker (non-DHP)

Slows nodal depolarization (decreases automaticity), decreases conduction velocity

Also used for HTN

68
Q

Describe how adenosine works

A

Increases max diastolic potential (cell is more negative between action potentials)

Opens K+ channels, slows CA influx, is a nodal agent

69
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

70
Q

What receptors are used by salivary glands and what are their effects? **what do you need to remember about the sympathetic receptor in this case?

A

for salivation - M3 = watery, B2 = thick (sympathetic) **note B2’s primary role is SM relaxation, not induction of secretion

71
Q

Enoxaparin

A

Indirect-acting Xa-inhibitor (SubQ)

72
Q

dobutamine

A

B1 agonist, increases cardiac output

Use in cases of cardiogenic shock (acute HF) to increase CO (also use milrinone, mentioned in HF lecture - phosphodiesterase 3 antagonist)

Routine use of ionotropes does not improve mortality (may shorten life)

73
Q

metropolol

A

B1 antagonist, B blocker (decreases cardiac output)

Anti-arrhythmic (decreases Phase 4 slope)

Also used for HTN and HF

74
Q

Amiodarone

A

Class III K+ blocker

Increases APD

Prolongs QT but not associated w/ Torsades

Hyper/hypothyroidism, blue skin/tongue tint

75
Q

nifedipine

A

DHP CCBx

76
Q

Eplerenone

A

K-sparing diuretic, aldosterone receptor antagonist

77
Q

carvedilol

A

a1, B1/2/3 (nonselective) antagonist (B blocker), decreases cardiac output

Anti-arrhythmic (decreases Phase 4 slope)

Also used for HTN and HF

78
Q

Isoproterenol

A

B1 and B2 agonist synthetic drug similar to dobutamine (discussed in ANS and cardio lecture)

79
Q

Oral indirect-acting anti-thrombotic drugs

A

Warfarin (vitamin K reductase inhibitor)

80
Q

what role do the following play in urinary control? a1, M3, and B2

A

M3 - parasympathetic control (contraction - detrusor) B2 - sympathetic control (relaxation - detrusor) a1 - sympathetic control (contraction - internal urethral sphincter) somatic control - external urethral sphincter (nicotinic receptor)

81
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

82
Q

Name the Class I anti-arrhythmic drugs + subclasses, and describe their mechanism

A

Na+ channel blockers - increase threshold potential and make it harder to depolarize

Slow resetting of NA+ channels

IA - Procainamide

IB lidocaine

IC flecainide, propafenone

83
Q

What are M3’s primary roles?

A

SM contraction, secretion (parasympathetic)

84
Q

What are the categories of anti-platelet drugs?

A

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

85
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

86
Q

When should you be careful with ACE inhibitors?

A

During pregnancy - teratogenic during 1st trimester (messes up fetus’s blood supply)

87
Q

B1 agonist, name and function

A

dobutamine, increases cardiac output

88
Q

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

A

Is protective against diabetic nephropathy compared to other drugs

89
Q

When should you take BABAs?

A

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

90
Q

Spironolactone

A

K-sparing diuretic, aldosterone receptor antagonist gynecomastia

Used for HF

91
Q

clonidine

A

a2 agonist, used for HTN

92
Q

name an a2 agonist and describe MoA/use

A

clonidine, HTN, acts presynaptically in anti-sympathetic ways

93
Q

What type of muscle does not fire action potentials?

A

Vascular smooth muscle (under involuntary control - hormones, ANS neurotransmitters like adrenergic receptors, local stimuli)

94
Q

Argatroban

A

Direct-acting thrombin inhibitor (IV)

95
Q

prazosin

A

a1 antagonist - counters SM contraction and leads to vasodilation, decreasing BP; used for HTN

can cause orthostatic hypotension

96
Q

Triamterene

A

K-sparing diuretic, Enac blocker

97
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

98
Q

Eptifibatide

A

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

99
Q

Dronedaron

A

Class III K+ blocker

Increases APD

Prolongs QT and is associated w/ Torsades

100
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

101
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)

102
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

103
Q

Dabigitran

A

Direct-acting thrombin inhibitor (oral)

104
Q

Prasugrel

A

P2Y12 inhibitor (targets ADP receptor)

105
Q

describe mediators of urinary control

A

parasympathetic control - detrusor muscle (M3), contracts to put pressure on bladder during times of rest; sympathetic control - detrusor muscle (B2) - relaxes during times of stress (decreasing urge to urinate) sympathetic control - urethra (a1) - contracts during times of stress (also so you don’t pee yourself) but is inhibited when at rest; external sphincter - somatic control

106
Q

What are the Vitamin K-dependent factors?

A

2, 7, 9, 10 protein C and S

107
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?)
108
Q

Atropine

A

non-selective parasympathetic antagonist (indirect) used to increase cardiac output (tx bradycarida) or to dilate eyes

Decreases Phase 4 slope by blocking ACh receptors (increases threshold)

109
Q

nimodipine

A

DHP CCBx

110
Q

P2Y12 inhibitors - describe MoA and name drugs

A

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

111
Q

Dofelitide

A

Class III K+ blocker

Increases APD

Prolongs QT and is associated w/ Torsades

112
Q

Apixaban

A

Direct-acting Xa-inhibitor (oral)

113
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)

114
Q

name an a1 agonist and describe how it works

A

phenylephrine; increases BP by increasing vascular constriction Activates voltage-gated Ca++ channels, increases SR release (increases contraction)

115
Q

What should you combine ezetimibe w/ and why?

A

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

116
Q

Describe the differences between direct and indirect acting parasympathetic drugs; give an example of an indirect drug

A

Direct - target the receptor (mAchR) - Ach mimics indirect - target acetylcholinesterase (AchE) in the synapse, AchE inhibitors atropine = indirect

117
Q

Ezetimibe MoA

A
  1. blocks absorption from GI tract (blocks NPCI receptor) 2. also stimulates LDL receptor to absorb more from bloodstream
118
Q

Clopidogrel

A

P2Y12 inhibitor (targets ADP receptor)

119
Q

Which statins are highly effective?

A

Atorvastatin and rosouvastatin

120
Q

describe how phenylephrine works

A

a1 agonist; increases BP by increasing vascular constriction

121
Q

Endoxaban

A

Direct-acting Xa-inhibitor (oral)

122
Q

Tirofiban

A

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

123
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

124
Q

Which statins interact poorly w/ amlodipine?

A

atorvastatin, simvustatin, lovastatin

125
Q

hydralazine

A

changes cGMP levels and induces vascular relaxation

Used for HF

126
Q

How should you try to modify abnormal impulse formation

A

decrease automaticity (can target nodal rate or myocytes with premature beats)

127
Q

Captopril

A

ACEi

128
Q

Name the Class IV drugs and describe their mechanism

A

Diltiazem and verapamil (non-DHPs)

Slow AV/SA depolarization (similar to class I except nodally focused)

129
Q

Tacagrelor

A

P2Y12 inhibitor (targets ADP receptor)

130
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

131
Q

What is M2’s role?

A

parasympathetic control; slows SA/AV node

132
Q

Which HTN drugs lead to hyperkalemia and hypokalemia?

A

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

133
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

134
Q

Name the Class III antiarrhythmics and describe their mechanism

A

K+ blockers

Increase AP duration (increase refractory period and slow repol)

Amiodarone, dronedaron, dofelitide, solatol

135
Q

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

A

Colestipol Use during pregnancy Can cause severe GI tox

136
Q

Hydochlorothiazide

A

thiazide diuretic inhibits Na/Cl symporter hypokalemia, alkalosis

137
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.)

138
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

139
Q

Adenosine

A

Antiarrhythmic

Makes cell more depolarized at baseline (increases max diastolic potential)

Slows Ca++ influx, opens K+ channels

Works through all 3 paths

140
Q

Oral direct-acting anti-thrombotic drugs

A

FII Dabigitran FXa Apixiban Rivaroxaban Endoxaban

141
Q

Furosemide

A

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

142
Q

Fondaparinux

A

Indirect-acting Xa-inhibitor (SubQ)

143
Q

When are statins usually taken?

A

Often at night (not all)

144
Q

carvedilol selectivity

A

a1, B1, 2, 3

145
Q

What drugs do you use for HF? Contraindications?

A

Entresto; ACEi or ARB (contra to ACEi: angiodema, advanced renal disease), B blockers (metoprolol or carvdedilol; contra = bronchospasm or acute HF or bradycardia), aldosterone antagnoists (spirolactone and eplerenone - contra= hyperkalemia or advanced renal disease); use other diruetics for symptom control w/ wet HF

146
Q

Good review of uses of specific B blockers for reference

A
147
Q

Digitalis/digoxin

A

Inhibits Na+ export via Na/K+ ATPase, promoting Ca++ retention and increased inotropy (contractility)

Narrow therapeutic window before toxicity (including arrhythmias, confusion, seizures, visual disturbances, N/V, etc)

148
Q

What are considerations related to diurertics in HF that you should keep in mind?

A

May be toxic to kidneys, have no mortality benefit; helpful to reduce the amount of fluid in a “wet” patient to get them out of pulmonary edema zone

Use loop diurertics (e.g. furosemide) for HF (aldosterone antag aka K-sparing diuretics often used as first-line treatment due to mortality benefit)

Thiazides rarely used in HF

149
Q

Isosorbibe mononitrate + hydralazine (BiDil)

A

Drug controversially used only for African American/Black patients in HF… interesting tie-ins w/ social medicine as pointed out by Dr. Saunders early in the semster

See actual BiDil ad w/ Snoop Dogg (and this article for more info: https://www.healthaffairs.org/doi/abs/10.1377/hlthaff.W5.455?journalCode=hlthaff)

150
Q

Summarize HF drugs that improve mortality and those that improve symptoms

A

Cardio (3 decks)

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