Pathology Ch. 11 The Heart

Front 1

How much of an artery needs to be occluded to cause stable angina?

Back 1

>75% occlusion

Front 2

How does nitroglycerin work?

Back 2

It causes peripheral vasodilation, which reduces venous blood return. This reduces the work of the heart.

In large doses, it dilates coronary vessels to increase blood supply to myocardium.

Front 3

What's the best treatment for Prinzmetal's variant angina?

Back 3

Vasodilators like nitroglycerin or Calcium channel blockers

Do not administer beta blockers.

Front 4

What causes the majority of acute MIs?

Back 4

acute coronary artery thrombosis

Front 5

T/F: Thrombi must always be present to cause an MI.

Back 5

False. While most MI's are caused by thrombosis, a subendocardial infarction can be caused by severe diffuse coronary atherosclerosis that significantly limits coronary vessel perfusion. When this occurs over a long period of increased demand, it can cause necrosis of myocytes distal to epicardial vessels.

Front 6

Outline the steps of a typical MI.

Back 6

1) sudden disruption of atheromatous plaque(i.e. hemorrhage, erosion, ulceration, rupture or fissuring) which exposes subendothelial collagen and necrotic plaque contents.

2) platelets adhere, aggregate and become activated; they release TXA2, ADP, serotonin which cause aggregation.

3) Vasospasm; stimulated by platelet aggregation and mediator release.

4) extrinsic pathway of coagulation is activated and adds bulk to thrombus.

5) w/in minutes, the thrombus evolves to occlude vessel lumen.

Front 7

T/F: Some coronary artery occlusions clear spontaneously

Back 7

True.

They clear by lysis of thrombus or relaxation of vasospasm or incorporation into atherosclerotic plaques.

Front 8

Where does irreversible injury of ischemic myocytes first occur?

Back 8

The subendocardial zone.

Last area to receive blood from epicardial(coronary) vessels; high intraluminal pressure prevents perfusion.

Front 9

Define a transmural infarct

Back 9

>50% of myocardial wall thickness infarcted

Almost all transmural infarcts involve the left ventricle and/or ventricular septum.

Front 10

What artery supplies the posterior interventricular (posterior descending) artery in 90% of the population?

Back 10

Right coronary artery.

Front 11

T/F: MIs less than 12 hours old show gross changes of the heart.

Back 11

False.

But, you can see changes after 3 hours with special stains. Stain heart slices w/triphenyl tetrazolium chloride, which is a substrate for lactate dehydrogenase in viable heart. Areas of necrosis will stain pale white.

Front 12

How can you identify an infarct 12-24 hours after an MI?

Back 12

The infarct is grossly identified because it has a reddish blue discoloration from stagnant trapped blood.

Thereafter, the infarct becomes a tan yellow, soft, sharply delineated area.
By 10-14 days, there is a rim of hyperemic(vascular) granulation tissue.
After weeks, there is scarring.

Front 13

Microscopic changes of MI.

Back 13

coagulative necrosis can be detected 4-12 hours after infarction.

Wavy fibers present at edges of infarct; reflects stretching and buckling of noncontractile dead fibers. considered "soft" findings of acute MI.

Front 14

How does sublethal ischemia present?

Back 14

As myocyte vacuolization. These are large cleared intracellular spaces that contain water. Myocytes are still alive but poorly contractile.

Front 15

On what days are:

1) acute inflammation most prominent?
2) macrophages removing necrotic myocytes and neutrophil fragments?
3) infarcted zone is replaced by granulation tissue?

Back 15

1) 1-3 days after MI
2) 5-10 days after.
3) 2-3 weeks after.

Front 16

T/F: A myocardial infarction heals starting from the center.

Back 16

False. It heals from the borders toward the center bc ingrowth of new vessels begins from intact vessels at the margin of the infarct.

Front 17

Once a collagenous scar has formed and the MI has healed completely, can you tell how old the infarct is?

Back 17

No.

Front 18

How is reperfusion of an MI achieved?

Back 18

Via thrombolysis with tPa, balloon angioplasty and stenting, coronary artery bypass graft.

While reperfusion can salvage tissue, it can also cause reperfusion injury via oxygen free radicals generated by the infiltration leukocytes. Reperfusion injury causes hemorrhage and endothelial swelling that occludes capillaries and prevents local blood flow(called no-reflow).

Front 19

Myofibers of heart appear to have hypereosinophilic bands. What is the cause?

Back 19

The cause is reperfusion of irreversibly damaged myocytes after an MI. This presentation is called contraction band necrosis.

Front 20

"Silent" infarcts are common in what populations?

Back 20

Elderly, PT with diabetes mellitus

Front 21

Half of PT with an acute MI die w/in one hour and never reach the hospital. Cause of death?

Back 21

arrhythmias.

Poor prognostic factors: advanced age, female gender, diabetes mellitus, previous MI

Front 22

What % of PT develop complications after acute MI?

Back 22

75%.

Front 23

Prolonged cardiac hypertrophy due to HTN can result in myocyte contractile failure. How does heart failure due to HTN occur?

Back 23

cardiac hypertrophy is accompanied by changes in gene expression. this results in fetal isoforms of proteins that may be less functional or expressed in different amounts than the adult forms. Different intracellular handling of calcium can also impair contraction/relaxation.

Front 24

In long-standing systemic HTN, what happens to the left atrium?

Back 24

Left atrium enlarges and puts PT at risk for afib or CHF.

Front 25

In what conditions are PDAs common?

Back 25

PDAs very common in:
1)premature infants
2) maternal rubella infection.

Front 26

What 2 acquired valvular diseases account for 2/3s of all valve disease?

Back 26

acquired aortic stenosis and acquired mitral valve stenosis

Front 27

Calcific aortic stenosis

Back 27

most common degenerative valvular disease; most common aortic stenosis in U.S.

from age-associated "wear and tear"; in normal valves, begins in 70s-80s

Congenital bicuspid aortic valves are more prone to degenerative calcification. Begins earlier at age 40-50.

Front 28

Morphology of calcific aortic stenosis

Back 28

heaped-up calcified masses on the OUTflow side of the cusps (can view calcified mass from aortic aspect) that protrude into the sinuses of Valsalva and impede valve opening

early on, there is aortic vavle sclerosis, which is inconsequential; later on, cusps can become secondarily fibrosed and thickened

leads to L vent pressure overload and concentric hypertrophy

Front 29

What part of the valve does mitral valve calcification affect?

Back 29

The valve annulus. Usually asymptomatic unless calcifications encroach on adjacent conduction system.

Front 30

Clinical features of calcific aortic stenosis.

Back 30

valve orifice compromised 70-80% leading to L vent hypertrophy. The hypertrophied myocardium is ischemic(hypertensive heart disease) and angina can develop.

syncope can develop due to poor perfusion of brain; systolic and diastolic dysfunction leads to CHF and cardiac decompensation

onset of symptoms(CHF, angina, syncope) indicates exhausted cardiac compensation--> poor prognosis, surgery indicated; 50% mortality w/in 2 yrs of CHF inception

Front 31

Myxomatous mitral valve degeneration

Back 31

one or both mitral leaflets are "floppy" and prolapse

mitral valve prolapse- a primary form of myxomatous mitral degeneration affects women 7x more than men

Front 32

Morphology of myxomatous mitral valve degeneration

Back 32

thinning of the fibrosa layer of the valve and expansion of the middle spongiosa layer with increased deposition of myxomatous(mucoid) material results in ballooning of enlarged, redundant, thick and rubbery mitral leaflets;

concomitant tricuspid valve involvement is common (20-40% of cases)

Front 33

Pathogenesis of primary myxomatous mitral valve degeneration

(secondary causes would be IHD)

Back 33

from an intrinsic defect of connective tissue

commonly seen in Marfan syndrome (fibrillin-1 mutation)

Secondary myxomatous change results from "degenerative" changes in valve myofibroblasts responding to chronically aberrant hemodynamic forces

Front 34

Clinical features of mitral valve prolapse

Back 34

majority asymptomatic. a minority of PT will have palpitations, dyspnea, atypical chest pain.

midsystolic click caused by abrupt tension of valve leaflets and chordae tendinae as valve attempts to close

3% have severe complications- mitral regurge, CHF

All have increased risk infective endocarditis, sudden death from ventricular arrhythmias, stroke, systemic infarction from embolus formed in left atrium

Front 35

T/F: 70% of cases of Rheumatic Heart Disease involve the mitral valve.

Back 35

True. 25% involve mitral AND aortic valve. Tricuspid valve involved much less frequently.

Front 36

age of onset of calcific aortic stenosis in a congenitally bicuspid valve?

Back 36

50-60 yrs old.

calcific aortic stenosis of a normal valve occurs 70-80 yrs of age.