Micro Specimens 1-7 Concluding 1

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Hemodynamic disorders part (II)

Hemodynamic disorders II

I. Microspecimens:

№ 4. Recent red thrombus in the vein. (H-E. stain). Indications:


1. Vein wall.
2. Thrombus within the lumen of the vessel:
a) fibrin strands;
b) hemolyzed erythrocytes.

Cross section through the vein, the lumen is obturated by a thrombus, consisting of a network
of filaments and homogeneous, eosinophilic masses of fibrin, in which there are figurative
elements of the blood, predominantly hemolysed erythrocytes. The thrombus adheres to the
vessel intima.

№ 140. Lymphatic vessels celluar (cancerous) embolism. (H-E. stain). Indications:


1. Dilated lymphatic vessel.
2. Embolus (cancer cells) in the lymph vessel lumen.
3. Vein.
4. Pulmonary alveoli.

Pulmonary lymphatic vessels, which accompany blood vessels, are dilated, in their lumen are
present clusters of cancer cells (cell emboli).
1

№ 4. Recent red thrombus in the vein. (H-E. stain).


2
4
1

№ 140. Lymphatic vessels cellular (cancerous) embolism. (H-E. stain).


№ 101. Microbial embolism of the renal vessels. (H-E. stain). Indications:
1. Microbial emboli in glomerular capillary lumen.
2. Focus of microbial necrosis around emboli.
3. Clusters of neutrophils (abscess).
4. Unchanged glomerulus.

In some glomeruli there are clusters of microbes (microbial emboli), of intensely


basophilic color ( look like ink spots), around which necrotic changes (karyolysis) and
agglomerations of neutrophilic leukocytes (metastatic abscesses) are determined; microbial
emboli are also observed in the lumen of some arterioles and veins; In some microspecimens
microbial masses are found in the lumen of the collecting tubules in the medullary layer of
the kidney.

№ 13. Diapedesis hemorrhage in the brain. (H-E. stain). Indications:


1. Clusters of erythrocytes (hemorrhagic focus).
2. Blood vessel.
3. The brain tissue.

In the cerebral tissue, agglomerations of red blood cells (haemorrhagic foci) are observed,
arranged in shape of rings around small blood vessels; the integrity of the blood vessel
walls is preserved.
4

2 3

№ 101. Microbial embolism of the renal vessels. (H-E. stain).


2
1

№ 13. Diapedesis hemorrhage in the brain. (H-E. stain).


II. Macrospecimens:

№ 3. Parietal thrombus in the abdominal aorta.

The intima of the aorta is irregular, rough, with multiple protrusions of the wall (atherosclerotic plaques) and
ulcerations, covered with atheromatous masses of yellow color; there is a parietal thrombus, adherent to the intima
of red-dark color, dense consistency, irregular surface.

№ 37. Thromboembolism of pulmonary artery.

In the common trunk of the pulmonary artery or at the level of the bifurcation, fragments of dark red cylindrical
thrombi of 0.5-1.0 cm diameter are observed, which do not adhere to the vessel wall (thromboemboli); at the level
of the bifurcation the thrombus obstructs the lumen of both pulmonary arteries, having the appearance of "rider in
the saddle".

№ 42. Metastases of cancer into lung.


In the lung under the pleura and on the section, there are multiple whitish-gray tumor nodules, round or oval in
shape, up to 3-5 cm in diameter, well delimited by the adjacent tissue.

№ 85. Purulent embolic nephritis (metastatic abscess into the kidney).


The kidney is enlarged in size, under the capsule there are multiple disseminated foci of purulent inflammation, of
yellowish color, with a diameter of 0.5-1.0 cm, which protrude on the surface of the organ - metastatic abscesses.

№ 121. Cerebral hemorrhage (parenchymal hematoma).


In the brain, there is an accumulation of dark red coagulated blood (hematoma), the adjacent brain tissue is
softened, of a flaccid consistency.
№ 3. Parietal thrombus in the abdominal aorta.
№ 37. Thromboembolism of pulmonary artery.
№ 42. Metastases of cancer into lung.
№ 85. Purulent embolic nephritis (metastatic abscess into the kidney).
№ 121. Cerebral hemorrhage (parenchymal hematoma).
Virchow triad in
thrombosis.
Arterial thrombosis.
Spherical thrombus in the right
atrium.

Chronic cardiac aneurysm with thrombosis.


Parietal thrombi in the abdominal aorta in Parietal thrombus in the
atherosclerosis. iliac vein.
Deep vein thrombosis of the lower limbs.
Thrombus in course of
organization. (H-E stain).
Recanalized thrombus.
(H-E stain).
Consequences of thrombosis.
Pulmonary artery thromboembolism.
Paradoxical embolism Congenital heart defect: defect
scheme. of the interventricular septum.
Cancer metastases in the lung.

Cancer metastases in the liver.


Hemorrhage (per diabrosin)
in tubal pregnancy.

Fatal intracerebral
hemorrhage
(per rhexis).
Petechial hemorrhages in the
epicardium of the heart. Hemopericardium.

Per
diapedesis

Per
rhexis
Hemorrhage
Definition:
“Extravasation of blood due to vessel rupture”
Types: (depending on the site, extent and
location)
External
Internal
Hematoma: ‘Blood within the tissue’
(small; like a Bruise, or sufficiently large as to
be fatal)
Causes of hemorrhage:
- vascular diseases with rupture (atherosclerosis,
arteritis, aneurysms, etc.).

- low platelets (below 10-15,000/cu mm);


coagulopathy (factors less than 10% activity);

- ulcers, tumors, coagulation factors, infarcts,


trauma.
Types of hemorrhage: acute vs. chronic
petechia (-ae) - 1 to 2 mm. hemorrhages, usually
indicating either platelet disorder or capillary fragility
ecchymosis (-es) - hemorrhages measuring > 1 cm.,
often indicating coagulation factor abnormality
purpura - ecchymotic and petechial hemorrhages into
skin
hemopericardium - blood into pericardium
hemothorax - blood into thoracic cavity (ies)
hemoperitoneum - blood into peritoneal cavity
hematochezia - bright red blood per rectum
melena - dark black blood per rectum
hematuria - blood, gross or microscopic, in urine
hemoptysis - coughing up of blood
hematemesis - vomiting up of blood
Hemorrhage
Petechiae:
 Minute 1-2 mm
 Into skin, mucous membrane, or
serosal surfaces
 Causes: Locally increased
intravascular pressure, low platelet
count, defect in platelet function,
and deficiency of clotting factors.
Petechial hemorrhages of colonic mucosa
as a consequence of thrombocytopenia
Hemorrhage
Purpura:
 Slightly larger ≥ 3mm
 All causes of Petechiae, plus
 Secondary to trauma, vascular
inflammation, and increased
vascular fragility
Hemorrhage
Ecchymoses:
(Subcutaneous hematoma; Bruises)
 Larger > 1-2 cm
 Characteristically seen after
trauma
 Exacerbation of any of the
aforementioned conditions
Hemorrhage
Ecchymoses:
(Colours changes in hematoma)
 Hemoglobin (Red-blue)
 Bilirubin (Blue-green)
 Hemosiderin (Gold-brown)
Petechiae & Ecchymoses
Fatal intracerebral
hemorrhage
Hemorrhage:
Ectopic pregnancy
One complication of a transmural myocardial infarction is rupture of
the myocardium. This is most likely to occur in the first week between
3 to 5 days following the initial event, when the myocardium is the
softest.
Here are petechial
hemorrhages seen on
the epicardium of the
heart.
Subarachnoid
Haemorrhage:
Thrombosis: Intravascular
coagulation
THROMBUS solidified blood inside the
vascular space in a living organism.

Composed of fibrin, platelets, and rbc's


Hemostatic plug formation
endothelial injury
platelet aggregation
fibrin meshwork

Location of thrombi: Arteries, veins, heart


chambers, heart valves

Types of thrombi: Arterial vs. venous; bland


vs. septic
Virchow triad in thrombosis.
Endothelial integrity is the single most important factor. Note that injury
to endothelial cells can affect local blood flow and/or coagulability;
abnormal blood flow (stasis or turbulence) can, in turn, cause endothelial
injury. The elements of the triad may act independently or may combine to
cause thrombus formation.
Diagrammatic representation of the
normal hemostatic process
Diagrammatic representation of
the normal hemostatic process
Platelets adhere to exposed
extracellular matrix (ECM)
via von Willebrand factor
(vWF) and are activated,
undergoing a shape change
and granule release;
released adenosine
diphosphate (ADP) and
thromboxane A2 (TxA2)
lead to further platelet
aggregation to form the
primary hemostatic plug.
Diagrammatic representation of the normal
hemostatic process

Local activation of
the coagulation
cascade (involving
tissue factor and
platelet
phospholipids)
results in fibrin
polymerization,
"cementing" the
platelets into a
definitive
secondary
hemostatic plug.
Diagrammatic
representation of the
normal hemostatic process
Counter -
regulatory
mechanisms, such as
release of tissue
type plasminogen
activator (t-PA)
(fibrinolytic) and
thrombomodulin
(interfering with the
coagulation
cascade), limit the
hemostatic process
to the site of injury.
Mural
thrombi.
Sites of Thrombosis
in heart (atria , ventricles & on valves); in arteries ; in veins ; and
in capillaries.

Large mural
thrombus on top of Left atrial mural thrombus in a
myocardial infarction case of rheumatic mitral stenosis
Venous Thrombi:
Fates
 Organization
 Ingrowth of cells
into thrombus with
incorporation into
wall
 Resolution
 It goes away
 Embolization
 Travels from its
site of origin to a
distal part of
circulation
VENOUS THROMBI FATES
Arterial Thrombi
Morphology  Adherent masses of
blood that demonstrate
areas of pale
alternating with areas
of red
 Lines of Zahn
Coronary
Atheorsclerosis
Coronary
Thrombosis
With Infarction
Arterial Thrombi
Morphology
Arterial Thrombi
Outcome

 Similar to venous thrombi


 Resolution
 Organization/Incorporation/Recanalization
 Embolization (arterial)
 Propagation
Atherosclerosis
Aorta
Ruptured aneurism
Nephrosclerosis
Aorta Dissecting Aneurisms:
Coronary Narrowing in
Atherosclerosis:
Low-power view of a
thrombosed artery.
A, H&E-stained section. B, Stain for elastic tissue. The original
lumen is delineated by the internal elastic lamina (arrows)
and is totally filled with organized thrombus, now
punctuated by a number of small recanalized channels.
Embolism & Thromboembolism
Embolism:
 Abnormal solid mass carried in blood.
 Source – destination
 Types.
 Thromboembolism - atherosclerosis
 Fat - Fractures
 Tumor - cancers
 Gas – ‘Caisson disease’
 Liquid – Amniotic fluid in new born.
 Rapid onset of infarction –vs. Thrombosis
Pulmonary
Thromboembolism
 20-25 per 100,000
hospitalized patients
 May be fatal if 60% of
pulmonary circulation is
obstructed (acute cor
pulmonale)
 Saddle PE straddles the
bifurcation of the main PA
 Sequelae: Sudden death,
clinically silent – resolution –
organization, shortness of
breath, pulmonary infarction
 Pathogenesis: Deep venous
thrombi usual cause –often
following immobilization-bed
rest from hospitalization
Fat Embolism
Bone marrow
embolus in the
pulmonary
circulation.

Fat embolus in a
glomerulus
Thrombo-
embolism
PARADOXICAL EMBOLI

 EMBOLI WHICH
TRAVEL FROM
VENOUS TO
ARTERIAL
CIRCULATION
VIA A
COMMUNICATIO
N BETWEEN
ARTERIAL AND
VENOUS
CIRCULATION

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