Transcript Gross cut surface Lung acute pulmonary congestion and edema

What is the organ?
Describe What do you see.
Gross
Heart, view of the
tricuspid valve
from the right
atrium The valve
are obscured by
the presence of
large irregular
and friable
masses of
thrombi, also
called
vegetations
The vegetations are formed due to an underlying damage to the valvular
endocardium (endocarditis) by organisms (bacteria, fungi) that gain access to
the venous circulation, (in intravenous drug abusers via use of nonsterile
needles). The microorganisms reach the tricuspid valve, causing
inflammation (endocardial injury), thus allow infected thromboi (or
vegetations) to form.
Describe what do you see.
low-power
micrograph Heart,
coronary artery Angiography &
radiograph The left
frame shows marked
narrowing as seen
by angiography. The
right shows the
histology of the
narrowing.
There is marked thickening of the intima due to coronary atherosclerosis( it is a
disease of the intima and the process is characterized by lipid deposition in the
intimal layer followed by laying down of collagen and calcification).. The red
mass in the narrowed lumen is a postmortem clot.
What therapeutic agent can be used to lyse the
clots in coronary vessels?
How do the various natural anticoagulants act?
• Thrombolysis can be accomplished by
tissue plasminogen activator (t-PA) or
streptokinase.
• both cause fibrinolysis by generating
plasmin.
Describe what do you see
Gross, cross
section
Coronary artery,
right, with
thrombus
The lumen of the coronary artery is completely occluded by a dark red
thrombus. Thrombosis in general results from damage to the endothelium.
The most common and the most important cause of arterial thrombosis is
atherosclerosis.
Describe what do you see
Low power
Heart,
coronary
artery
thrombosis
A fresh thrombus is attached to the damaged endothelium. In some parts
of the thrombus, there is formation of new capillary channels. This
process, called recanalization, can restore blood flow. Note that the media
is thinned, secondary to compression by the thickened intima.
-What are other causes of arterial
thrombosis?
Arterial thrombosis is caused by injury to
the endothelium. In addition to
*atherosclerosis,
*vasculitis
*trauma.
-What is the thrombus made of?
Fibrin, platelets, and red cells
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.
What causes arterial thrombosis?
..venous thrombosis?
Arterial thrombosis is caused by
endothelial damage (eg, atherosclerosis or
vasculitis);
venous thrombosis is caused by stasis
(sluggishness) of blood flow.
Both types of vessels are affected in
hypercoagulable states such as
antithrombin or protein C deficiency.
-What conditions predispose to venous
thrombosis?
Venous stasis caused by prolonged immobilization
(eg, in hospitalized patients after surgery) or by
congestive heart failure.
-What is the most common symptom
associated with such venous thrombi?
There are no symptoms in about 50% of cases.
Local pain and edema occur in the remaining cases.
What are the various fates of
thrombi?
Propagation,
Embolism,
Dissolution,
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 is the most common symptom of
pulmonary embolism?
• There are usually no symptoms. Most
pulmonary emboli (60-80%) are clinically
silent because of their small size and
because of the dual blood flow through the
bronchial circulation.
• With time, these emboli organize and are
incorporated into the vessel wall.
How and when does pulmonary
thromboembolism cause sudden death?
If more than 60% of the pulmonary
circulation is obstructed by emboli, the
patient is at a high risk of sudden death
due to acute right heart failure (cor
pulmonale) or shock (cardiovascular
collapse).
When does pulmonary thromboembolism
result in infarction?
• The possibility of developing pulmonary
infarction is higher in a previously
diseased lung, especially in the setting of
sluggish bronchial arterial flow or prior
pulmonary congestion due to left heart
failure.
What is the risk of recurrence of
pulmonary thromboembolism?
• In general, the patient who has had one
pulmonary embolus is at a higher risk of
having more.
Describe what do you see
• 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.
High power Lung, infarct
Gross, cut surface Lung, pulmonary infarct
Why are some infarcts red and
others pale?
• Red infarcts result from hemorrhage into the
necrotic area. This is likely to occur in tissues
that have a loose texture and dual blood
supply (eg, lung)
• By contrast, pale infarcts occur in compact
tissues and those in which the collaterals do
not readily refill the necrotic area (eg, heart).
Gross
cut surface
Lung acute
pulmonary
congestion
and edema
u
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,
a
s
s
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e
n
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n
c
a
s
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s
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f
l
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Medium power
Lung, acute
pulmonary
congestion
and edema
The alveolar septa are
prominent, due to marked
congestion of the capillaries.
The alveolar lumens contain
pale-staining edema fluid.
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.
• Pulmonary edema in other cases may also
result from damage to alveolar capillaries (eg,
in adult respiratory distress syndrome).
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.
Lymphedem
a, filaria
infection –
Clinical
presentation
Breast,
lymphedema
secondary to
breast
carcinoma –
Clinical
presentation
Gross, cut
surface
Lung,
chronic
passive
congestion
–
High power
Lung,
chronic
passive
venous
congestion
Lung, chronic passive venous
congestion
• 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.
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 causes enlargement of the
liver, edema, and fullness of the
neck veins in patient with
ischemic heart disease?
patient with ischemic heart disease can
develop 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, cut
surface
Spleen,
chronic
passive
congestio
n (case of
heart
failure)
Why did a patient infected by gramnegative bacteria develop shock?
The patient infectived with with gram-negative
Bactria will develop septicemia. The shock will result
from release from the bacteria of endotoxins that
triggered the release of inflammatory mediators
such as IL-1 and tumor necrosis factor (TNF).
TNF plays an important role in the development of
septic shock by promoting the release of IL-1, IL-6,
IL-8, and nitric oxide, thus initiating a cytokine
cascade. These mediators, in low to moderate
quantities, may lead to local inflammation and
systemic effects, such as fever. When present in
higher quantities, however, they promote the
development of shock by causing systemic
vasodilation, impaired myocardial contractility, and
widespread endothelial injury, which may lead to
DIC.
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.
Gross
outer & cut
sufaces
Kidney,
renal
tubular
necrosis
due to
shock
High power
Kidney
acute
tubular
necrosis
due to
shock
Gross coronal
section Brain,
cortical laminar
necrosis
Compare the
thinned and
discolored
cerebral cortex
on the left side to
the relatively
preserved cortex
on the right side