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EXERCISE 8: FLUID AND HEMODYNAMIC DERANGEMENTS

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HISTOLOGIC DESCRIPTION

EDEMA

Slide 25. A10-1OC2. A07-5202. Pulmonary edema


An important feature in these slides is the presence of pale pink material within the alveolar
spaces (fluid or transudate), Take note that the alveolar septae are intact with no evidence of
necrosis. Extravasated red blood cells and congested capillaries can be appreciated.

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Slide 19. Acute suppurative meningitis


The specimen was taken from a child who died of bacterial meningitis. Note that the
subarachnoid space is densely Infiltrated with PMN's. There is vasodilation and congestion with
fluid exudation (seen as pink staining material). Necrosis of neuronal and glial elements is not
seen in this section.

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EXERCISE 8: FLUID AND HEMODYNAMIC DERANGEMENTS

ACTIVE CONGESTION

Slide 3541/201. External hemorrhoids


This section of hemorrhoidal tissue shows congested blood-filled vessels. There is also a
thrombus within a dilated vein. Look for the area where the thrombus has contracted and a space
is formed.

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Slide 2873B/210 Hemorrhoids


This section shows hemorrhoidal tissue with congested and thrombosed blood vessels. Look for
the thrombus which has contracted and has undergone partial recanalization.

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EXERCISE 8: FLUID AND HEMODYNAMIC DERANGEMENTS
Slide 30. Interstitial pneumonitis
In this disease, the fluid collects first in the alveolar walls and not inside the alveolar spaces. The
peribronchial walls are also infiltrated with lymphocytes and plasma cells
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PASSIVE CONGESTION

Slide 27. Liver. Chronic passive congestion


The section was taken from a patient who died of congestive (chronic) cardiac failure. Chronic
passive congestion of the liver occurs when these is right-sided heart failure either from chronic
lung disease with pulmonary hypertension (cor pulmonale) or chronic passive congestion of the
lungs progressing into right sided heart failure or the presence of congenital heart disease with
left to right shunts. Note that the central veins are dilated. Sinusoids are engorged and congested
and there is fatty change of hepatocytes, especially those located in the areas near central veins.

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EXERCISE 8: FLUID AND HEMODYNAMIC DERANGEMENTS
Slide #28. Chronic passive congestion. Spleen
Take note of the presence of Gamma-Gandy bodies) or siderofibrotic nodules (hemosiderin plus
fibrosis). These appear as yellow-brown splinters. This condition occurs in the setting of portal
hypertension

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Slide #26, 193. Chronic passive congestion. Lung


Sections show hemosiderin-laden macrophages (brown pigment) inside alveolar spaces. The
darker brown-black pigment is carbon (anthracotic pigment).

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EXERCISE 8: FLUID AND HEMODYNAMIC DERANGEMENTS

Slide 2010-DM/215. Diaphragmatic muscle, hemorrhage


Hemorrhage is the escape of blood from a blood vessel and extravasation of red blood cells into
tissue. This may be due to a wide number of causes, one of which is trauma. Note the presence
of red blood cells extravasated into skeletal muscle.

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Slide 3552-C. Endometriosis


Endometriosis is the growth of implanted endometrial tissue outside the uterus. This tissue
responds to cyclic hormonal changes and periodically bleeds. Old or previous hemorrhage is
evident with the presence of hemosiderin-laden macrophages (brown pigment).

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EXERCISE 8: FLUID AND HEMODYNAMIC DERANGEMENTS

THROMBOSIS

Slide 162-A. Lung thrombosis and infarction


Take note of the presence of a thrombus obstructing the pulmonary artery. Examine the thrombus
and the presence of Lines of Zahn. The area supplied by the artery has undergone coagulative
necrosis and this is seen as a paler staining area. The outlines of the alveoli are still appreciable.
This condition is commonly manifested as sudden onset of dyspnea, cyanosis and chest pain.
What are the predisposing factors to the development of thrombosis and thromboembolism?

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Slide #31. Lung, pulmonary thromboembolism


The section of lung was taken from a 62-year old male patient who died of pulmonary embolism
with infarction. He had undergone surgery for an enlarged prostate. Varicose veins were also
present. Third day post-op, he complained of severe dyspnea and chest pain and became
cyanotic. He died three hours later. On autopsy, there was reddish consolidation of both right and
left lungs and blood oozed from the alveoli. There was fibrin coating the pleural surfaces of the
lower lobes & bases. Dissection showed the presence of a massive embolus located in the
bifurcation of the main pulmonary artery which extended into its right & left branches and into the
succeeding smaller branches.

This slide shows two emboli located within the lumens of two medium-sized arteries located near
a bronchus showing an embolic mass composed of fibrin in which leukocytes and erythrocytes
are enmeshed. One shows Lines of Zahn. Adjacent lung tissue is unremarkable. Some
anthracotic pigment is noted in the interstitium.

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EXERCISE 8: FLUID AND HEMODYNAMIC DERANGEMENTS

Slide D21. Thrombosis


Shown in this slide are sections of blood vessels with thrombi in varying stages. Recall the
different outcomes of a thrombus. Look for the thrombus undergoing reçanalization.

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INFARCTION

Slide #12, Renal infarct


Take note of the demarcation between the normal and the infarcted area. Examination of the
infarcted area shows loss of cellular detail of the tubular epithelial cells, increase in eosinophilia
and loss of most nuclei. Neutrophilic and mononuclear cell infiltration is seen between the necrotic
tubules. At the periphery of the area Is moderate congestion, some erythrocytic diapedesis or
hemorrhage, which also exhibits congestion and hydropic changes

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EXERCISE 8: FLUID AND HEMODYNAMIC DERANGEMENTS
Slide 13. Splenic infarct
The infarcted area is markedly eosinophilic and consists of “tombstones” of necrotic cells. This
area is surrounded by hemosiderin-laden macrophages and early fibrosis. Viable splenic tissue is
seen in the periphery. Take note that the infarcted area appears pale pink, in contrast to the
viable area.

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Slide 217. Myocardial infarction


The myocardial fibers appears pale pink and many are devoid of nuclei. The outlines of the cells
are still intact.

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Slide # 30. Ileum, infarct


Because of the looseness of GIT tissue, any ischemia that occurs, whether due to mesenteric
arterial occlusion or mechanical obstruction compromising arterial supply, may lead to the
development of an infarct which is red and hemorrhagic rather than pale or anemic as what would
occur in solid organs. The entire wall of the ileum is edematous due to the escape of plasma into
tissues with many extravasated red blood cells seen from the mucosal layer to the serosal wall.
Most of the mucosa no longer shows glandular structures but only ghost outlines of villi. Blood
vessels in the submucosa and muscularis are dilated and congested.

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TIPS AND GUIDE QUESTIONS


1. Give three differences between and anemic (pale) infarct and a hemorrhagic (red) infarct.
2. What is the source of emboli which give rise to pulmonary embolism and infarction?
3. Study the mechanisms by which a thrombus forms within the lumen of a blood vessel.
4. Why is fracture of long bones closely associated with fat embolism?
5. What is amniotic fluid embolism?
6. Once a thrombus has formed within the lumen of a blood vessel, what are the possible
changes in this thrombus (outcomes or fate of the thrombus)?
7. Where is the fluid located in pulmonary edema? Is this fluid an exudate or transudate?
8. Study the etiology, pathogenesis and clinical course of pulmonary edema. What makes it a
serious condition?
9. What are "heart failure cells"?
10. What are the causes of chronic passive congestion of the lungs? Of the liver?
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