64974 hemodynamic tutorial ee 07

8/11/2019 64974 Hemodynamic Tutorial EE 07

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The left frame shows marked narrowing asseen by angiography. The right frameshows the histology of the narrowed area.

There is marked thickening of the wall dueto fibrosis of the intima. This results fromcoronary atherosclerosis, The red mass inthe narrowed lumen is a postmortem clot.

What is the d if ference between a

postmor tem clot and a thrombus?


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What is the d if ference between a

postmortem clot and a

thrombus?

Postmortem clots are not attached to

endothelium; they are gelatinous, rubbery,dark red at the ends and yellowish

elsewhere. Thrombi are attached to

endothelium and are traversed by pale

grey fibrin strands that can be seen on cut

section; they are more firm but fragile.


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DESCRIBE THE LESION


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The lumen of the coronary artery is

completely occluded by a dark red

thrombus.

What are the most common and the

mos t important cause of arter ial

th rombos is ?


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What are the components of thrombus?

Fibrin, platelets, and red cells.

What are the var ious fates o f thrombi?Propagation, embolism, dissolution, and

organization with recanalization.


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Which of these fates is cl in ical ly m os tsignif icant in the arterial circulat ion vs. thevenous ci rcu lat ion?

The most significant problem with arterialthrombi is propagationleading to luminalobstruction, resulting in infarction of the tissuesupplied. Important examples include

myocardial and cerebral infarction. In contrast, the most significant problem with

venousthrombi is the possibility of potentiallyfatal embolizationinto the pulmonary circulation


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What are the major s imi lar i t ies between a m yoc ardial and acerebral in farct?

The major similarity is in the etiology. Both types of infarcts arecommonly caused by thrombotic occlusion of the arteriessupplying them. Thrombi usually form on the same underlyingdisease process (ie, atherosclerotic arterial disease).

What are the major dif ferences between a myocardial and acerebral in farct?

A myocardial infarct typically features coagulative necrosis,which heals by fibrosis and leaves behind a fibrous scar. Incontrast, a cerebral infarct is typically liquefactive necrosis, inwhich dead tissue is digested without being replaced byfibrosis, leaving behind a cystic, cavitary lesion.

What is the mechanism of formation of h emorrhagic infarcts inbra in?

Brain infarcts can be pale or hemorrhagic. Hemorrhagicinfarcts are due to arterial occlusion followed by reperfusion.Examples are embolic occlusion followed by fragmentation ofemboli or occlusive vasospasm that later is relieved.


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Liver, chronic passive venous

congestion

This condition is caused by resistance or obstruction to theoutflow of venous blood from the liver, as may occur inchronic right heart failure (congestive heart failure).

The area surrounding the central veins (centrizonal) becomesintensely congested, and the hepatocytes in the central zonemay even become necrotic due to hypoxia.

These centrilobular areas are seen as the dark red spots onthe cut surface.

The alternating pale areas represent the periportal

hepatocytes, which have sustained a lesser degree of hypoxia.This gross appearance is also called nutmeg liver.

Remember that in the hepatic lobules, blood flows from theperiportal to the central zones, and hence the centrilobularareas are more vulnerable to hypoxia than are the peripheralhepatocytes.


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What caused enlargement of the

liver, edema, and fullness of the

neck veins in this patient?

This patient had ischemic heart disease due

to coronary thrombosis. This led to failureof the left ventricle and, eventually, of the

right ventricle, giving rise to congestive

heart failure. Because of impaired venous

return to the heart, the neck veins become

distended, the liver becomes enlarged,

and fluid collects in interstitial spaces

(edema).


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Grosscut

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Lungacute

pulmonary

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edema


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Lung, chronic passive venous

congestion - Gross This is caused by any chronic condition that retards the

outflow of pulmonary venous blood from the lungs to theleft side of the heart

(----- name some causes-------------).

Pooling of blood in the lung capillaries and associatedmicrohemorrhages produce a dark brown discoloration,noted here.

In addition, septal fibrosis causes the lung to becomestiff. The fibrosis causes the lung to feel firm to thetouch; also, the fibrosis causes the cut edges to beraised or to stand up. This gross appearance is alsocalled brown induration of the lung.


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What is the brown pigment that is derived fromhemoglobin?

Hemosiderin.

What is the pathogenesis of pulmonary edema?

Left ventricular failure (eg, caused by amyocardial infarct) causes pump failure, andsecondarily there is impaired flow of blood fromthe lung to the left atrium. This causes increased

hydrostatic pressure in pulmonary alveolarcapillaries and subsequent transudation of fluidinto alveoli.


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How does this type of edema differ from that seen inacute inflammation?

The fluid in pulmonary edema is a transudate (ie, it isprotein poor, has low specific gravity, and does not

contain inflammatory cells). Edema in inflammation is anexudate.

What effect would such a histologic picture have ongaseous exchange in the lung?

It would be markedly impaired

What might the symptoms be?

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea,and cough.


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What are the major morphologic changes in

multiple organ failure in a patient who dies of

shock? Kidneys: Acute tubular necrosis.

Brain:Laminar cortical necrosis.

Lungs: Shock lung (diffuse alveolar damage)

with hyaline membranes (seen mainly in septic

shock).

Heart: Foci of necrosis, hemorrhage,

contraction band necrosis. GI: Hemorrhages. Liver: Central hemorrhagic necrosis, fatty

change.


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What is the name of that type of thrombi?

Vegetations.

What complications may arise from this lesion?

Infected vegetations on the mitral valve mayembolize systemically and cause infarcts,abscesses, or septicemia .

Could this person develop a cerebral infarct?What would be the appearance of such aninfarct of the brain?

This patient could develop a cerebral infarctfrom embolization. The infarct would be an area

of liquefactive necrosis along with an acuteinflammatory response to the bacteria in theembolus, resulting in brain abscess formation.

64974 hemodynamic tutorial ee 07

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