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MHD/Pharm Block 4 > MHD: Ischemic Heart Disease > Flashcards

MHD: Ischemic Heart Disease Flashcards

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1
Q

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

A

Heart disease

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2
Q

What is heart failure?

A

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

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3
Q

What is the difference between systolic and diastolic heart failure?

A

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.

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4
Q

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

A

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

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5
Q

How is aortic stenosis related to diastolic heart failure?

A

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

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6
Q

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

A

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

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7
Q

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

A

Pulmonary circulation

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8
Q

What is the main cause of right heart failure?

A

Left heart failure

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9
Q

What is cor pulmonale?

A

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

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10
Q

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

A

Atherosclerosis

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

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11
Q

What are the 4 clinical presentations of ischemic heart disease?

A

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

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12
Q

What are the 3 types of angina pectoris?

A

Stable, unstable, and Prinzmetal variant

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13
Q

Describe stable angina pectoris

A

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

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14
Q

Describe unstable angina pectoris

A

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.

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15
Q

Describe the composition of vulnerable plaques

A

Lipid rich with thin fibrous caps

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16
Q

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

A

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

17
Q

What is prinzmetal variant angina?

A

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

18
Q

Describe the pathogenesis of myocardial infarction

A

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

19
Q

How quickly after occlusion does myocardial infarction become irreversible?

A

After 30 minutes, damage is irreversible, coagulative necrosis begins

20
Q

What is a transmural infarction

A

An infarction involving the full thickness of the myocardial wall

21
Q

Describe the location of a non-transmural infarct

A

Usually subendocardial infarction

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

22
Q

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

A

No gross or microscopic changes

23
Q

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

A

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

24
Q

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

A

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

25
Q

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

A

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

26
Q

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

A

Gross: yellow appearing tissue
Histology: myocytes disintegrated via phagocytosis

27
Q

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

A

Histology: granulation tissue begins to form

28
Q

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

A

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

29
Q

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

A

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

30
Q

Describe the clinical presentation of myocardial infarction

A

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

31
Q

What laboratory tests are used to detect recent MI?

A

Creatinine kinase and troponin

32
Q

What is the classical EKG finding of MI?

A

ST segment elevation

33
Q

List the treatments of MI

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

“A BATH, NO?”

34
Q

What mechanisms are responsible for reperfusion injury?

A

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

35
Q

What is cardiogenic shock?

A

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

36
Q

What is an arrhythmia?

A

A disturbance of electrical conduction that can be caused by MI

37
Q

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

A

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

38
Q

What is sudden cardiac death?

A

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

MHD/Pharm Block 4 (25 decks)

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