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Therapeutics III > CAD - Wendt > Flashcards

CAD - Wendt Flashcards

1
Q

What factors contribute to increased oxygen consumption?

A

Increased HR, contractility, afterload, and preload

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2
Q

What is afterload?

A

The pressure in the veins that the heart has to match to push blood through the body

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3
Q

What is preload?

A

The volume of blood that enters the heart during diastole

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4
Q

If veins are dilated preload is (increased/decreased)?

A

Decreased

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5
Q

If preload is (increased/decreased), oxygen consumption increases?

A

Increased

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6
Q

What are risk factors for angina?

A 
Age (>55 for men, >65 for women)
Cigarette smoking
Diabetes
HTN
Kidney disease
Obesity
Sedentary lifestyle
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7
Q

What two factors will increased coronary perfusion when they decrease?

A

HR and preload

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8
Q

How does preload increase the demand of the heart?

A

The heart has to stretch more to accommodate a larger blood volume

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9
Q

Why does a decreased HR increase coronary perfusion?

A

It allows the heart to spend more time in diastole, when blood can flow into coronary vessels

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10
Q

What are the 3 types of angina?

A 
Printzmetal's Variant
Chronic stable (fixed stenosis--narrowing of blood channel)
Unstable (from thrombus)
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11
Q

What causes stable angina?

A

Atherosclerosis which causes oxygen demand to exceed supply

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12
Q

What factors precipitate stable agnina?

A

Exertion, food, emotions (stress, anger, etc)

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13
Q

What are the characteristics of variant angina?

A

Sudden and transient constriction; often occurs at rest and at night; hard to diagnosis because vessels look healthy

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14
Q

Is variant angina supply ischemia or demand ischemia?

A

Supply–cardiac myocytes don’t receive enough oxygen

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15
Q

What are characteristics of unstable angina?

A

A sudden worsening of angina at rest

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16
Q

What causes unstable angina?

A

Thrombosis or plaque rupture

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17
Q

What treatment strategy is used for unstable angina?

A

Inhibit platelet function, dissolve clot

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18
Q

Which type of angina often comes before an MI?

A

Unstable angina

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19
Q

What drug classes are used to increase oxygen delivery?

A

Vasodilators (CCBs, nitrates)

Anti-thrombotics (anticoags, antiplatelets)

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20
Q

What drug classes are used to decrease oxygen demand?

A 
Vasodilators
Cardiac depressants (beta blockers, CCBs, HCN channel inhibitor)
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21
Q

How does vasodilation occur via NO?

A

Endothelial cells produce eNOS –> increased NO production –> NO –> moves to VSM –> causes vasodilation by activating cGMP –> MLCP–> dephosphorylates MLC –> can’t bind to actin –> vasodilation

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22
Q

What are the organic nitrate drugs?

A

Glyceryl trinitrate
Isosorbide mononitrate
Isosorbide dinitrate

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23
Q

Which of the nitrates is longest acting?

A

Isosorbide mononitrate

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24
Q

Which of the nitrates is shortest acting?

A

GNT

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25
Q

Which of the nitrates are used for angina prophylaxis?

A

5-ISMN, ISDN

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26
Q

Which of the nitrates develop tolerance?

A

All organic nitrates

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27
Q

What is the mechanism of GTN tolerance?

A

mtALDH is sulfated irreversibly to activate GTN–run out of the enzyme as it is permanently inactivated

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28
Q

How long does GTN tolerance last?

A

a few hours

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29
Q

Are organic nitrates more effective in the veins or the arteries? Why?

A

Veins

Veins are more flexible/able to dilate

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30
Q

How do CCBs work?

A

Decrease Ca influx in myocytes

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31
Q

What do CCBs do?

A

Dilate arteries and decrease HR

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32
Q

CCBs primarily effect (preload/afterload)?

A

Afterload (dilating arteries decreases BP)

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33
Q

Why do CCBs not affect veins as much?

A

Veins have a larger calcium store in SR; rely less on extracellular calcium

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34
Q

How do CCBs work?

A

Block Ca–Ca is needed to phosphorylate MLC (via CAM) to allow binding to actin and contraction. No Ca means no contraction –> dilation

35
Q

Which class of CCB is most effective for treating angina?

A

Dihydropyridines (effect vessels rather than heart)

36
Q

Beta blockers block ______ stimulation of myocardium to ___ HR and ____ coronary perfusion

A

Block epinephrine stimulation to lower HR and increase coronary perfusion

37
Q

How do beta blockers affect angina?

A

Reduce oxygen usage

38
Q

When during a heart beat is coronary perfusion highest?

39
Q

What is the MOA of beta blockers in VSM cells?

A

Blocks this pathway: Epinephrine binds to receptor –> increase in cAMP –> increase in PKA –> decrease in MLCK –> Relaxation (no binding with actin)

40
Q

What is the MOA of beta blockers in cardiac myocytes?

A

Blocks this pathway: Beta agonist binds to receptors –> active AC –> increased cAMP –> PKA –> Ca released from SR –> contraction in myocytes (CAM)

41
Q

What are the cardioselective Beta blockers?

A

Atenolol
Metoprolol
Acebutolol

42
Q

What are the non-selective beta blockers?

A

Propranolol
Carvedilol
Pindolol
Labetalol

43
Q

What patient population is it particularly important to use cardio-selective beta blockers?

A

Patients with COPD/asthma (non-cardioselective cause bronchiole constriction)

44
Q

What are the problems with nitrates, Beta blockers, and CCBs?

A

Reflex tachycardia
Increased preload
Constipation

45
Q

Which drug classes cause reflex tachycardia? Why?

A

Nitrates and DHP CCBs

They affect BP only - not heart

46
Q

What medications can be used to prevent reflex tachycardia?

A

Beta-blockers

47
Q

What medication causes an increase in preload?

A

Beta-blockers (by decreasing HR/contractility, filling time increases)

48
Q

What medication can prevent an increase in preload caused by Beta blockers?

A

Nitrates! (They dilate vessels, so more blood can be stored in them)

49
Q

Why are most angina drugs used in combinations?

A

To counteract the negative effect of one with the other

50
Q

What are the major side effects of non-specific beta-blockers?

A

LV dysfunction, bradycardia, bronchoconstriction

51
Q

What are the major side effects of nitrates?

A

Hypotension/Flushing headaches (from drop in BP)

52
Q

What are the major side effects of diltiazem?

A

generally well-tolerated–some flushing/HA, LV dysfunction, bradycardia

53
Q

What are the major side effects of DHPs?

A

Hypotension, flushing/HA

54
Q

What are the major side effects of verapamil?

A

LV dysfunction, bradycardia, GI ditress

55
Q

Which angina treatment option has the most potential for GI distress?

56
Q

Which angina treatment option has the most potential for hypotension/flushing/HA?

A

Nitrates, DHP CCBs

57
Q

Which angina treatment medications may cause bradycardia?

A

Beta-blocker, verapamil

58
Q

What do HCN Channels transport? Where?

A

Sodium into the cell in the SA Node

59
Q

How are HCN Channels activated?

A

Hyperpolarization

60
Q

What is an HCN Channel inhibitor?

A

Ivabradine

61
Q

How do HCN channels help treat angina?

A 
Slow HR (reduced oxygen consumption)
Prolong diastole and improve ventricular filling (increase perfusion)
62
Q

What can HCN channel inhibitors be used for?

A

Angina
Inappropriate sinus tachycardia
Heart failure

63
Q

What is a major benefit of ivabradine?

A

No hemodynamic abnormalities (no changes in blood pressure/vasculature)

64
Q

What is the NCX?

A

A channel that takes in Na and releases Ca - used to balance Ca concentrations

65
Q

When myocytes don’t have enough oxygen, they ____ sodium uptake, which decreases ______. This ____ Calcium flow and ___ heart function

A

increase sodium uptake; decreases sodium gradient. Increases calcium flow and increases heart function (b/c calcium stimulates heart)

66
Q

Which drug is an NCX blocker?

A

ranolazine

67
Q

What are side effects of ranolazine?

A

Dizziness and QT prolongation

68
Q

Does ranolazine affect blood pressure?

A

No–it is specific to myocytes

69
Q

What drugs are used in treating unstable angina?

A

ASA, heparin, P2Y12 antagonists

70
Q

Statins cause increased ____ receptors, more ____ deliver to the liver, and _____

A

LDL receptors; LDL; decreased plasma cholesterol

71
Q

What are the treatment goals of unstable angina?

A

Block thrombus formation

Dissolve existing thrombi

72
Q

What is the mechanism of action of aspirin?

A

Blocks platelet activation

73
Q

What is the mechanism of action of PSY12?

A

Blocks platelet activation

74
Q

What is the mechanism of action of GPIIb/IIIa antagonists?

A

Block platelet aggregation

75
Q

What is the mechanism of action of Heparin?

A

Inhibit thrombin formation (which is needed for fibrinogen formation, which causes platelet aggregation)

76
Q

Blocking ___ synthesis is key to antiplatelet activity of ASA

A

TXA2 (thromboxane)

77
Q

ASA irreversibly inactivates ____ through ____

A

COX-1; acetylation

78
Q

What class is clopidogrel?

A

PSY12: ADP Receptor inhibitor

79
Q

How long does clopidogrel’s action last?

A

Several days

80
Q

What is clopidogrel used for?

A

ACS, recent MI, stroke, PVD

81
Q

What 3 classes of medications are used to treat acute coronary syndrome?

A

Aspirin
P2Y12
GP IIb/IIIa inhibitors

82
Q

Which drugs are GP IIb/IIIa inhibitors?

A

eptifibatide
tirofiban
abciximab

83
Q

What is heparins structure?

A

Straight chain, polysaccharide

84
Q

How does heparin work?

A

Binds to AT-III, which increases plasma proteases

Therapeutics III (12 decks)

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