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Pharmacology Unit 4 > Angina I and II > Flashcards

Angina I and II Flashcards

1
Q

Name some factors that cause vasodilation.

A

Shear stress, nitrates, NE (Beta 2 receptor), ACh

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2
Q

Name some factors that cause vasoconstriction

A

NE (alpha 1 receptor), TXA2, 5-HT, Endothelin.

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3
Q

Define Angina

A

A clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back and/or arm that is aggravated by exertion or emotional stress and relieved by nitroglycerin.

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4
Q

What, in simple terms, causes angina?

A

Myocardial oxygen demand greater than coronary oxygen supply.

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5
Q

How do increased heart rate and increased myocardial contractility affect myocardial oxygen demand?

A

They increase demand.

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6
Q

With what conditions is angina associated?

A

CAD of at least one epicardial artery. May also occur with valvular heart disease, hypertrophic cardiomyopathy, and uncontrolled hypertension.

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7
Q

What are the metabolic effects of myocardial ischemia?

A
  • Switch from aerobic to anaerobic cellular respiration.
  • Glycolysis is inadequate.
  • ATP and creatine phosphate levels fall.
  • Intra- and extracellular acidosis develops.
  • Extracellular potassium, lactate, phosphate, and fatty acid levels rise.
  • Intracellular LCFAs accumulate as well.
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8
Q

Which metabolic effect of ischemia is the most important contributor to electrophysiologic changes?

A

Hyperkalemia.During the plateau phase of the action potential, increased permeability to potassium results in an outward leakage of K+.

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9
Q

How do free fatty acids increase during myocardial ischemia?

A

Sympathetic activity is triggered by ischemia, causing liposomal phospholipase activity with subsequent phospholipid breakdown.

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10
Q

What is an injury current?

A

A gradient between ischemic and normal cells due to altered polarization.

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11
Q

Describe the diastolic injury current in terms of phase, voltage difference, and current flow.

A
  • Occurs during phase 4.-
    Ischemic cells are less negative than normal cells.
  • Current flows from ischemic to normal cells.
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12
Q

Why are ischemic cells more negative than normal cells during phase 2 and 3 of the action potential?

A

The ischemic cells have shorter action potentials with less depolarization.

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13
Q

Describe the systolic injury current in terms of phase, voltage difference, and current flow.

A

Current flows from normal cells to ischemic cells during phase 2 and 3 of the action potential because ischemic cells are more negative. (Current flows from positive to negative). This is the injury current the lecture said to focus on.

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14
Q

What is the non-invasive way to diagnose myocardial ischemia?

A

Stress testing: 6 to 12 minutes on a treadmill for patients who can exercise (Bruce protocol). Valid if 85% of max heart rate is achieved. At least 1 mm of horizontal or downsloping ST depression must be seen to diagnose ischemia.

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15
Q

How do you calculate the predicted max heart rate?

A

220 - age.

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16
Q

When do you need to use imaging?

A

If the baseline EKG is abnormal.

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17
Q

What does echocardiography test?

A

The normality of wall motion.

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18
Q

What are the chemical stress test agents and how do they work?

A
  • Dobutamine: directly stimulates Beta-1 receptors (positive inotropic and chronotropic effects).- Adenosine or dipyramidole: coronary vasodilators (dipyramidole prevents cellular uptake and degradation of adenosine).
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19
Q

What must you worry about with adenosine and dipyramidole?

A

Coronary steal may occur. Less stenotic coronary arteries are more responsive to vasodilation, thus taking increased blood away from ischemic areas.

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20
Q

What does electron beam CT scanning do?

A

Identifies the presence of calcium in the coronaries. Most useful in predicting the absence of coronary disease.

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21
Q

What are the risk factors for CAD?

A
  • Lipid abnormalities
  • Smoking
  • Diabetes Mellitus
  • Hypertension
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22
Q

Name the 7 antiplatelet drugs.

A
  • Aspirin
  • Ticlopidine
  • Clopidogrel
  • Prasugrel
  • Ticagrelor
  • Dipyramidole
  • Cilostazol
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23
Q

What is the mechanism of action of aspirin?

A

Irreversible COX inhibitor –> inhibit TXA2 production –> prevent platelet aggregation for the life of each platelet

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24
Q

What is the mechanism of action of ticlopidine?

A

Inhibition of platelet aggregation induced by ADP, reduction of blood viscosity via decreased plasma fibrinogen and increased RBC deformity.

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25
Q

What are the side effects of ticlopidine?

A

Neutropenia and (rarely) TTP.

26
Q

How does Clopidogrel prevent platelet aggregation?

A

Selectively and irreversibly inhibits the binding of ADP to its platelet receptors (blocks activation of the GPIIb/IIIa complex) to prevent aggregation of platelets.

27
Q

How does Prasugrel work?

In what patient group is Prasugrel indicated?

A

Irreversibly binds the P2Y12 receptor (a GPCR for ADP). Primarily given in patients who have received PCI (stent) treatment for ACS.

28
Q

How does Prasugrel match up to Clopidogrel in terms of efficacy and side effects?

Prasugrel is limited to what patients?

A

Prasugrel is more efficacious in reduction of mortality from cardiovascular causes, but increased risk of serious/fatal bleeding.

(For each life saved with increased efficacy, one is lost to fatal bleeding.)

Prasugrel is limited to patients < 75 years who weight > 60kg, and have no history of stroke or TIA.

29
Q

How does Ticagrelor block ADP receptors?

Why does it have a fast onset of action?

A

It blocks ADP receptors reversibly at a site other than the ADP binding site.

It does not require hepatic activation.

30
Q

How does Ticagrelor match up to Clopidogrel in terms of efficacy and side effects?

A

Like Prasugrel, Ticagrelor has better efficacy than clopidogrel but a greater risk of bleeding events.

Note: doses of aspirin greater than 100mg of decrease the efficacy of Ticagrelor. Also, ticagrelor has faster action than clopidogrel and prasugrel, and is dosed 2x/day due to fast elimination.

31
Q

How does Dipyramidole work?

A

Increases intracellular platelet cAMP (inhibits phosphodiesterase, activates adenylate cyclase, and inhibits uptake of adenosine from vascular endothelium and RBC).

32
Q

Why is the use of Dipyramidole and Cilostazol limited?

A

They vasodilate coronary arteries, enhancing exercise-induced ischemia.

33
Q

How does Citostazol work?

A

It inhibits phosphodiesterase and increases cAMP, inhibiting platelet aggregation.

34
Q

How do the -statins work?

A

They inhibit HMG-COA receptors to decrease LDL cholesterol. They decrease the risk of adverse ischemic events in patients with established CAD.

35
Q

How does the renin-angiotensin-aldosterone system work?

A
  • Renin cleaves angiotensinogen into angiotensin I.- ACE in the lung capillaries cleaves angiotensin I into angiotensin II.- Angiotensin II is a potent vasoconstrictor and promotes aldosterone synthesis.- Aldosterone increases renal reuptake of sodium and water.- Overall, this increases blood pressure.
36
Q

Which glomerular vessel is most constricted by angiotensin II?

A

The efferent arteriole.

37
Q

What is the other name for ACE?

A

Kininase II. This is because it degrades bradykinin, a potent vasodilator, into inactive metabolites. Inhibition of bradykinin degradation causes cough in 10 to 30% of patients on ACEIs.

38
Q

What is the life-threatening side effect that rarely occurs with ACEIs and angiotensin receptor blockers (ARBs)?

A

Angioedema: swelling of the skin around the mouth, mucosa of the mouth, throat, and tongue.

39
Q

How does the reduction in blood pressure in patients with on ACEIs dosed for angina compare to their outcomes?

A

Reduction of mortality far exceeds the minimal decrease in blood pressure (2 to 3 mmHg) seen in most of these patients such that another mechanism must be at play to account for the dramatic effects.

40
Q

Name the ACEIs. Which is the shortest acting?

A
  • Captopril (shortest acting)
  • Enalapril
  • Lisinopril
  • Ramipril
  • Quinapril
  • Fosinopril
41
Q

What are the side effects of ACEIs?

A
  • Dry cough (10-30%)- Hypotension- Hyperkalemia (via decreased aldosterone)- angioedema (rare)
42
Q

What are the effects of blocking beta 2 receptors?

A
  • Small degree of peripheral vasoconstriction.- Bronchospasm
43
Q

How do beta blockers reduce myocardial ischemia?

A

They are negative chronotropic and negative inotropic agents which reduce myocardial oxygen demand.

44
Q

What class of anti-arrhythmics are beta blockers?

A

Class II. They decrease SA node automaticity, decrease conduction velocity, and decrease aberrant pacemaker activity. They increase action potential duration and increase the effective refractory period.

45
Q

Name some commonly used beta blockers and any special indications mentioned. Which are beta 1 selective?

A
  • Metoprolol*
  • Atenolol*
  • Propanolol (rarely used for CAD. 2nd line for migraines).
  • Carvedilol (used in heart failure and patients with diabetes mellitus)
  • Bisoprolol* (1x/day. Used in heart failure and LV dysfunction)*beta-1 selective.
46
Q

When should you not use beta blockers?

A
  • Severe bradycardia- High degree A/V block- Sick sinus syndrome (alternating brady- and tachycardia)
  • Unstable LV failureCaution with:- Asthma/bronchospastic disease
  • Severe depression (esp. propanolol)
  • Peripheral vascular disease (Raynaud)Long term role of beta blockers is unclear based on most recent studies.
47
Q

What are the side effects of beta blockers?

A
  • Fatigue
  • Decreased exercise tolerance
  • Lethargy
  • Insomnia
  • Worsening claudication
  • Impotence
48
Q

What is the mechanism of action of nitrates?

A

They vasodilate independent of endothelium by enhancing intracellular production of nitric oxide (NO)

49
Q

What are the effects of nitric oxide (NO)?

A

NO activates smooth muscle guanylyl cyclase to form cGMP.cGMP inhibits calcium entry into the cell, resulting in smooth muscle relaxation.This increases myocardial oxygen delivery and relieves coronary vasospasm in the absence of CAD (Prinzmetal’s angina). Veins dilate as well to reduce preload and ventricular pressure (which enhances diastolic blood flow in the myocardium and decreased myocardial oxygen demand).NO also inhibits platelet aggregation and inhibits leukocyte-endothelial interactions (anti-inflammatory).

50
Q

How are nitrates delivered?

A

Sublingually or via nasal spray.Or, 3-4x/day oral isosorbide dinitrate, 1x//day isosorbide mononitrate (Imdur), or 2x/day isosorbide mononitrate (Ismo).Transdermal oinments and patches are also available in acute settings, but ointments are messy and patients may be allergic to the patch adhesive.

51
Q

When are nitrates contraindicated?

A
  • When you don’t want to decrease the pre-load- Hypertrophic cardiomyopathy- Severe aortic stenosis
  • When you don’t want to vasodilate- Significant hypotension
  • When you want to use Viagra- Use of phosphodiesterase inhibitors (e.g. Viagra) inhibits cGMP degradation, thereby prolonging the effects of nitrates and causing massive vasodilation with hypotensive shock.
52
Q

Whar are some side effects of nitrates?

A
  • Tolerance: depletion of tissue sulfhydryl groups or scavenging of NO by superoxides (peroxynitrate also inhibits guanylyl cyclase). This is countered by infrequent dosing with nitrate free periods (8 to 12 hours).- Headaches (CNS vasodilation)- Hypotension (vasodilation and decreased preload)- Bradycardia from reflex vagal stimulation (Bezold-Jarisch reflex).
53
Q

How do calcium channel blockers work?

A

They reduce transmembrane flux of calcium to aid smooth muscle relaxation and thus vasodilation. They are also negative inotropic agents.

54
Q

What are the two types of calcium channel blockers and what drugs fall into these categories?

A

Vasoselective dihydropyridines (more likely to be used in CAD than non-dihydropyridines)- Nifedipine- Amlodipine - Felodipine- IsradipineNon-dihydropyridines- Verapamil (myocardial selective)- Diltiazem (intermediate between verapamil and dihydropyridines)

55
Q

What type of angina do dihydropyridines treat best?

A

Prinzmetal’s angina (coronary vasospasm).

56
Q

How does nifedipine compare to the second generation dihydropyridines?

A

It has more side effects. In particular, it has some negative inotropic effects whereas the others do not.

57
Q

How do the non-dihydropyridines compare to the dihydropyridines?

A

The non-dihydropyridines are negative inotropic agents which decrease myocardial contractility and conduction velocity, decreasing heart rate. Verapamil is less effective as a systemic vasodilator.

58
Q

When are calcium channel blockers contraindicated?

A
  • Overt decompensated heart failure.- Bradycardia, sinus nose dysfunction, high degree A/V block (for non-dihydropyridines).
59
Q

What are some side effects of calcium channel blockers?

A
  • Hypotension
  • Worsening heart failure
  • Peripheral edema (least in amlodipine)
  • Constipation
  • Headache
  • Flushing
  • Bradycardia
  • A/V block
60
Q

What are the pharmacologic interventions in an acute ischemic setting?

A
  • Aspirin (162 to 325mg)- Not usually other antiplatelet drugs (risk of bleeding yields surgery contraindication for 5 days after use).
  • Heparin (if unstable angina or Non-STEMI). (Heparin activates antithrombin III)
  • GPIIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban)- Thrombolytics (if STEMI) (plasminogen activators)
  • Nitroglycerin (IV)
  • Beta-blockers
  • ACEIs
  • stains may also be used.

Pharmacology Unit 4 (9 decks)

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