MMT: ischemic heart disease Flashcards

1
Q

What is ischemic heart disease?

A

Poor circulation to the heart or parts of the heart results in insufficient oxygen supply followed by tissue death in the heart.

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2
Q

What is the #1 preventable factor in cardiac ischemia?

A

Smoking

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3
Q

What is the main pathogenic mechanism of ischemic heart disease?

A

Atherosclerosis

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4
Q

What are some risk factors for atherosclerosis?

A

High LDL, high C reactive protein, high homocysteine, HTN, smoking, other lifestyle factors.

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5
Q

What are the types of ischemia?

A

Stable angina, variant angina.

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6
Q

Describe stable angina.

A

Chest pain that is brought on by exertion and relieved by rest. This is due to limited flow creating hypoxic conditions during times of higher oxygen demand. It can be treated by increasing oxygen supply/decreasing oxygen demand.

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7
Q

Describe variant angina.

A

Vasospasms in the coronary arteries cause a transient reduction in diameter that limits oxygen supply. This varies with circadian rhythm and often occurs at rest in morning hours. This can be managed by increasing oxygen supply and reversing vasospasm.

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8
Q

Describe unstable angina.

A

Obstruction of a coronary artery due to a plaque rupture limits oxygen supply, resulting in new and severe chest pain at rest. Treatment includes increasing oxygen supply, then decreasing demand followed by other therapies.

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9
Q

What are the types of acute coronary syndrome?

A

Unstable angina, STEMI, and NSTEMI.

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10
Q

Describe NSTEMI.

A

Non-ST segment elevation MI results from a complete occlusion of a minor artery or partial occlusion of a major one.

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11
Q

NSTEMI results in __ thickness damage to heart muscle.

A

Partial

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12
Q

Describe STEMI.

A

ST elevated MI results from the complete occlusion of a major coronary artery.

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13
Q

STEMI results in __ thickness damage to heart muscle.

A

Full

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14
Q

___ is the more common form of a heart attack.

A

NSTEMI

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15
Q

What is the major factor of oxygen supply that can be controlled with drugs?

A

Coronary flow; this can be done with vasodilators and antithrombic drugs.

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16
Q

What are some factors that increase myocardial oxygen demand?

A

Contractility, HR, afterload, increased ventricle diameter, increased calcium.

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17
Q

What are common ways of uncovering cardiac ischemia? Why?

A

Cold and exertional stress; these will increase contractility which will increase oxygen demand.

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18
Q

What is the rationale behind organic nitrate drugs?

A

Nitrate groups break off the structure, resulting in vasodilation and thus increased oxygen supply, as well as lowered calcium via cGMP/PKG pathways. This response is very dose dependent.

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19
Q

What are the target ischemias of nitrate drugs?

A

Stable angina and can be used in combination with other drugs for various ischemic treatments.

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20
Q

What are the MOAs of organic nitrate drugs?

A
  1. PKG phosphorylates voltage gated calcium channels to limit influx. 2. PKG phosphorylates and opens calcium activated potassium channels to hyperpolarize VSMCs and further reduce calcium influx. 3. PKG activates a phosphatase that dephosphorylates MLC to cause relaxation.
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21
Q

NO dilates __ at low doses and __ at high doses.

A

Veins; arteries.

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22
Q

How do organic nitrates impact preload or afterload in different doses?

A

They lower preload at low doses and lower afterload at higher doses. At low doses, the venodilation results in less blood returning to the heart and thus lowered preload. At higher doses, arterial dilation lowers resistance, resulting in a lowered afterload.

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23
Q

What are the major examples of organic nitrates?

A

Nitroglycerin, isosorbide mononitrate, and isosorbide dinitrate.

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24
Q

Which organic nitrate has a high first pass metabolism?

A

Nitroglycerin.

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25
Q

Which organic nitrate has the highest stability against hepatic breakdown?

A

Isosorbide mononitrate.

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26
Q

What is an issue with organic nitrates?

A

Nitrate tolerance; continuous use can lead to a tolerance. To combat this, people using a patch can wear it during activity and take it off during sleep.

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27
Q

What are adverse effects of organic nitrates?

A

Tolerance, headache, reflex tachycardia, acute withdrawal.

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28
Q

What are contraindications of organic nitrates?

A

Interaction with sildenafil (PDE5 inhibitors) and those with low BP.

29
Q

In what instances do you use sublingual organic nitrates?

A

One or fewer attacks per week and for emergency relief.

30
Q

In what instances do you use sustained release organic nitrates?

A

Two or more attacks per week and for vasodilation for all day activities.

31
Q

What are the benefits of combining nitrates and beta blockers?

A

Tachycardia is limiting and contractility is decreased.

32
Q

What is the rationale behind beta adrenergic drugs?

A

They reduce oxygen demand by blocking catecholamine activity. This lowers contractility and heart rate, reducing demand.

33
Q

What are the major examples of beta-adrenergic blockers for ischemic heart disease?

A

Metoprolol, atenolol, propranolol.

34
Q

What are the uses of beta blockers in terms of cardiac ischemia?

A

Prophylaxis for exertional angina, can reduce exercise-induced ST depression, and improves capacity for daily activities.

35
Q

When are beta blockers not effective?

A

During acute angina attacks.

36
Q

Why are B1 selective blockers preferred for cardiac ischemia?

A

If B2 is blocked, alpha1 activity rules and causes more constriction and potentially more ischemia. Thus, selecting for just B1 is best.

37
Q

In cardiac ischemia, when would non-selective beta blockers be used?

A

If a patient has angina and hypertension.

38
Q

What are SEs of beta blockers?

A

Bradycardia, fatigue, bronchoconstriction, nightmares, ED.

39
Q

What are symptoms of BB toxicity?

A

Severe bradycardia, hypotension, bronchospasm, and heart failure.

40
Q

What ischemias can calcium channel blockers be used to treat?

A

Stable angina, variant angina, HTN.

41
Q

Compare non dihydropyridines with dihydropyridines in terms of their effects.

A

Non-DHPs have a larger effect decreasing myocardial contractility, while DHPs have high vascular selectivity and lead to increased coronary blood flow.

42
Q

What are the examples of non-DHPs?

A

Verapamil and diltiazem.

43
Q

What tissue do non-DHP CCBs select for?

A

Nodal tissue.

44
Q

What are the cautions for non-DHPs?

A
  1. Caution for additive effect with BBs. 2. Verapamil may cause AV block.
45
Q

What are the examples of DHPs?

A

Amlodipine and nifedipine.

46
Q

What tissue do DHP CCBs select for?

A

Vascular smooth muscle cells.

47
Q

What side effect is common with nifedipine?

A

Reflex tachycardia.

48
Q

What are the major side effects of non-DHPs?

A

Hypotension and bradyarrhythmia.

49
Q

What are specific side effects of verapamil?

A

Congestive heart failure and constipation.

50
Q

What are major side effects of DHPs?

A

Reflex tachycardia, gingival hyperplasia, flushing, peripheral edema.

51
Q

What are the contraindications of DHPs?

A

High dose may worsen unstable angina due to increased reflex tachycardia.

52
Q

What is the main sodium channel blocker?

A

Ranolazine.

53
Q

What is the MOA of ranolazine?

A

There can be increased Na/Ca exchange due to defective late phase exchangers that lead to excess calcium that can lead to myocardial dysfunction in angina. Ranolazine inhibits the late sodium current to limit calcium influx.

54
Q

What are the cardiac effects of ranolazine?

A

Increased relaxation, decreased wall stress, and coronary blood flow.

55
Q

What biochemical process does ranolazine block?

A

Fatty acid oxidation.

56
Q

What endocrine condition can ranolazine help?

A

Diabetes via reducing glucagon release.

57
Q

What are the target ischemias of ranolazine?

A

Stable angina.

58
Q

Describe clinical use of ranolazine.

A

Given if all other antianginal therapies fail. Can be given with beta blockers.

59
Q

What are contraindications of ranolazine?

A

Can cause torsades in those with long QT and may impact those with renal impairment.

60
Q

Describe statins in treating cardiac ischemia.

A

They reduce cardiac events by reducing atheromas and stabilizing plaques; they’re pretty much always recommended in cases of angina.

61
Q

Describe ACEi in treating cardiac ischemia.

A

They reduce oxygen demand by decreasing workload. This is via downregulating sympathetic activity, reducing salt and water retention, and causing some vasodilation to increase oxygen supply.

62
Q

What is the function of drug eluting stents?

A

They prevent re-stenosis to widen arteries; they may have paclitaxel and sirolimus.

63
Q

What are the treatment combinations for stable angina?

A
  1. Nitrates 2. CCB or BB 3. Nitrates + BB 4. Nitrates + CCB + BB.
64
Q

What are the treatment combinations for unstable angina?

A
  1. Antiplatelet 2. BB 3. BB + nitrates 4. CCBs 5. Ranolazine 6. Stenting.
65
Q

What is the immediate treatment for MI?

A

Antiplatelet, nitrates, oxygen, BB, morphine for pain.

66
Q

What is the lifelong treatment following MI?

A

Statins, aspirin, BB, ACEi.

67
Q

What medication(s) do we not want to use in variant angina?

A

Propranolol.

68
Q

What medications are used in variant angina?

A

CCB + nitrates, statins.

69
Q
A