Transcript Gross cut surface Lung acute pulmonary congestion and edema

• The left frame shows marked narrowing as
seen by angiography. The right frame
shows the histology of the narrowed area.
There is marked thickening of the wall due
to fibrosis of the intima. This results from
coronary atherosclerosis, The red mass in
the narrowed lumen is a postmortem clot.
• What is the difference between a
postmortem clot and a thrombus?
What is the difference 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.
DESCRIBE THE LESION
• The lumen of the coronary artery is
completely occluded by a dark red
thrombus.
• What are the most common and the
most important cause of arterial
thrombosis ?
• What are the components of thrombus?
Fibrin, platelets, and red cells.
• What are the various fates of thrombi?
Propagation, embolism, dissolution, and
organization with recanalization.
Which of these fates is clinically most
significant in the arterial circulation vs. the
venous circulation?
• The most significant problem with arterial
thrombi is propagation leading to luminal
obstruction, resulting in infarction of the tissue
supplied. Important examples include
myocardial and cerebral infarction.
• In contrast, the most significant problem with
venous thrombi is the possibility of potentially
fatal embolization into the pulmonary circulation
• What are the major similarities between a myocardial and a
cerebral infarct?
• The major similarity is in the etiology. Both types of infarcts are
commonly caused by thrombotic occlusion of the arteries
supplying them. Thrombi usually form on the same underlying
disease process (ie, atherosclerotic arterial disease).
• What are the major differences between a myocardial and a
cerebral infarct?
• A myocardial infarct typically features coagulative necrosis,
which heals by fibrosis and leaves behind a fibrous scar. In
contrast, a cerebral infarct is typically liquefactive necrosis, in
which dead tissue is digested without being replaced by
fibrosis, leaving behind a cystic, cavitary lesion.
• What is the mechanism of formation of hemorrhagic infarcts in
brain?
• Brain infarcts can be pale or hemorrhagic. Hemorrhagic
infarcts are due to arterial occlusion followed by reperfusion.
Examples are embolic occlusion followed by fragmentation of
emboli or occlusive vasospasm that later is relieved.
Liver, chronic passive venous
congestion
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This condition is caused by resistance or obstruction to the
outflow of venous blood from the liver, as may occur in
chronic right heart failure (congestive heart failure).
The area surrounding the central veins (centrizonal) becomes
intensely congested, and the hepatocytes in the central zone
may even become necrotic due to hypoxia.
These centrilobular areas are seen as the dark red spots on
the 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 the
periportal to the central zones, and hence the centrilobular
areas are more vulnerable to hypoxia than are the peripheral
hepatocytes.
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 failure
of 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).
Gross
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Lung
acute
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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 the
left side of the heart
• (----- name some causes-------------).
• Pooling of blood in the lung capillaries and associated
microhemorrhages produce a dark brown discoloration,
noted here.
• In addition, septal fibrosis causes the lung to become
stiff. The fibrosis causes the lung to feel firm to the touch;
also, the fibrosis causes the cut edges to be raised or to
stand up. This gross appearance is also called brown
induration of the lung.
• What is the brown pigment that is derived from
hemoglobin?
• Hemosiderin.
• What is the pathogenesis of pulmonary edema?
• Left ventricular failure (eg, caused by a
myocardial infarct) causes pump failure, and
secondarily there is impaired flow of blood from
the lung to the left atrium. This causes increased
hydrostatic pressure in pulmonary alveolar
capillaries and subsequent transudation of fluid
into alveoli.
• How does this type of edema differ from that seen in
acute inflammation?
• The fluid in pulmonary edema is a transudate (ie, it is
protein poor, has low specific gravity, and does not
contain inflammatory cells). Edema in inflammation is an
exudate.
• What effect would such a histologic picture have on
gaseous exchange in the lung?
• It would be markedly impaired
• What might the symptoms be?
• Dyspnea, orthopnea, paroxysmal nocturnal dyspnea,
and cough.
• 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 may
embolize systemically and cause infarcts,
abscesses, or septicemia .
• Could this person develop a cerebral infarct?
What would be the appearance of such an
infarct of the brain?
• This patient could develop a cerebral infarct
from embolization. The infarct would be an area
of liquefactive necrosis along with an acute
inflammatory response to the bacteria in the
embolus, resulting in brain abscess formation.