MHD: Ischemic Heart Disease Flashcards Preview

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Flashcards in MHD: Ischemic Heart Disease Deck (38):
1

What is the leading cause of death/disability in the US?

Heart disease

2

What is heart failure?

A progressive condition where the heart is unable to pump blood sufficiently to meed the demand of tissues

3

What is the difference between systolic and diastolic heart failure?

In systolic heart failure, the heart is unable to properly contract to eject blood out. Diastolic failure has to do with stiffened ventricles that are unable to properly relax.

4

Which side of the hear is most often involved with heart failure: left, right or both?

Both. Usually left sided heart failure leads to right sided heart failure causing biventricular failure.

5

How is aortic stenosis related to diastolic heart failure?

Stenosis causes LV hypertrophy, which makes the LV stiffer leading to diastolic failure due to decreased filling

6

Where does blood "back up" into in right sided heart failure?

Portal venous circulation leading to peripheral edema, ascites, portal hypertension

7

Where does blood "back up" into in left sided heart failure?

Pulmonary circulation

8

What is the main cause of right heart failure?

Left heart failure

9

What is cor pulmonale?

Right heart failure without left heart failure, usually caused by lung disease, pulmonary hypertension

10

What condition has the same risk factors as ischemic heart disease?

Atherosclerosis
-hypertension, hyperlipidemia, diabetes, smoking, increased age, male gender

11

What are the 4 clinical presentations of ischemic heart disease?

Angina pectoris
Acute myocardial infarction
Chronic ischemic heart disease/heart failure
Sudden cardiac death

12

What are the 3 types of angina pectoris?

Stable, unstable, and Prinzmetal variant

13

Describe stable angina pectoris

Stenosis (>75% reduction) due to coronary artherosclerosis prevents adequate O2 supply during increased cardiac demand.
Presents as chest pressure on exertion that goes away with rest

14

Describe unstable angina pectoris

Caused by atherosclerotic plaque disruption (fissure/ulceration of fibrotic cap) that triggers platelet activation, aggregation and vasospasm
Partially occluding thrombus causes chest pain, even at rest.

15

Describe the composition of vulnerable plaques

Lipid rich with thin fibrous caps

16

True or false: stable and unstable angina can cause myocardial infarction

False. Both stable and unstable angina cause ischemia, not infarction.

17

What is prinzmetal variant angina?

Caused by coronary artery spasm that is unrelated to physical activity, heart rate, blood pressure.
Responds to vasodilators

18

Describe the pathogenesis of myocardial infarction

Plaque disruption leads to platelet adhesion, aggregation, activation, vasospasm and coagulation.
An occlusive thrombus forms leads to a true infarct

19

How quickly after occlusion does myocardial infarction become irreversible?

After 30 minutes, damage is irreversible, coagulative necrosis begins

20

What is a transmural infarction

An infarction involving the full thickness of the myocardial wall

21

Describe the location of a non-transmural infarct

Usually subendocardial infarction
The endocardium is most susceptible to ischemic damage due to distance from coronary arterial O2 supply

22

Describe the gross/microscopic changes associated with MI after 1/2-4 hours

No gross or microscopic changes

23

Describe the gross/microscopic changes associated with MI after 4-12 hours

Coagulation necrosis begins, is visible histologically as eosinophilic cytoplasm, pyknotic nuclei.
No gross changes visible.

24

Describe the gross/microscopic changes associated with MI after 12-24 hours

Gross changes visible: dark mottling due to hemorrhage into infarcted tissues
Ongoing coagulation necrosis, pyknosis of nuclei

25

Describe the gross/microscopic changes associated with MI after 1-3 days

Gross: mottled tissue
Histology: loss of nuclei and myocytes, neutorphils infiltrating

26

Describe the gross/microscopic changes associated with MI after 3-7 days

Gross: yellow appearing tissue
Histology: myocytes disintegrated via phagocytosis

27

Describe the gross/microscopic changes associated with MI after 7-10 days

Histology: granulation tissue begins to form

28

Describe the gross/microscopic changes associated with MI after 10-14 days

Histology: granulation tissue formed (mature collagen visible on trichrome stain)

29

Describe the gross/microscopic changes associated with MI after 2-8 weeks

Scar formation visible on trichrome stain (blue-stained collagen) and gross specimen (white scarring)

30

Describe the clinical presentation of myocardial infarction

Crushing substernal chest pain, dyspnea, diaphoresis
Tachycardia, pulmonary congestion, edema
Silent in 10-15% of patients

31

What laboratory tests are used to detect recent MI?

Creatinine kinase and troponin

32

What is the classical EKG finding of MI?

ST segment elevation

33

List the treatments of MI

Aspirin and other antiplatelet drugs
Heparin
Thrombolytic therapy
Beta blockers
ACE inhibitors
Nitrates
Oxygen

"A BATH, NO?"

34

What mechanisms are responsible for reperfusion injury?

Free radical production
Myocyte hypercontracture, increased Ca
Leukocyte aggregation
Mitochondrial dysfunction

35

What is cardiogenic shock?

A major complication of MI in which the heart is no longer able to supply enough blood to the rest of the body

36

What is an arrhythmia?

A disturbance of electrical conduction that can be caused by MI

37

Describe the vulnerable state of the heart following an MI that leads to myocardial rupture

3-7 days following infarction, the myocytes are dead and neutrophils have invaded. Neither provide any support, which makes the wall very weak

38

What is sudden cardiac death?

Fatal arrhythmia due to structural heart disease. Almost always related to sever atherosclerotic heart disease, not acute infarction