Unit 1: HEMODYNAMIC DISORDERS (Hyperemia, stasis, hemorrhage, edema)

Hyperemia is blood volume increase within the organ

There are arterial & venous Hyperemia, General & local, Acute & chronic
Classification of local arterial hyperemia: a) inflammatory;
b) postischemic; c) vocational (syn. Decompression); d) angionevrotic; e) collateral;
g) with arteriovenous fistula. Chronic venous hyperemia as venous congestion is one of the most
important part in the clinical picture. It occurs systematically in nutmeg liver, the kidney & the
spleen or the lungs. It occurs locally in nutmeg liver. Pathogenesis: the right- sided heart failure (or
congestive right heart failure) leads to chronic passive congestion with nutmeg liver, cyanotic
induration of the kidneys, cyanotic induration of the spleen (syn. congestive splenomegaly).
Congestion of capillary beds is closely related to the development of edema, so congestion & edema
are common to occur together.
Hemorrhage is blood outcome from the vessel or the heart.
There are three mechanisms of bleeding: 1 per rhexin- with rupture of the vessel; 2 per
diapedesin- with hyperpermobility of the small vessels (capillaries, arterioles, venules); 3 per
diabrosin- with erosion (corrosive) of the vascular wall (pus, enzymes of the tumor, gastric juice).
Classification of hemorrhage: 1) According to the vessel & heart: 1 venous, 2 arterial, 3capillaries,
4 parenchymal, 5 flow from cardiac chambers.
2) According to the site: 1 external, 2 internal: a) into the organ; b) into the body cavity.
1definition: external hemorrhage is the blood outflow to environment.
EXTERNAL hemorrhage: 1 nasal hemorrhage – epistaxis; 2 blood vomiting -
hematemesis; 3 irregular bleeding between the periods – metrorrhagia;
4 the presence of blood in the urine – hematuria;
5 tarry stool as a sign of bleeding in the gastrointestinal tract- melena; 6 the presence of blood in
the phlegm- hemapthoe.
INTERNAL hemorrhages within the organs are 1 hemorrhagic infiltration;
2 hematoma; 3 petechii; 4 ecchymosi (see abridged dictionary of medical terms).
The types of the internal hemorrhage into the body cavities are: 1 hemothorax;
2 hemopericardium; 3 hemoperitoneum; 4 hemarthrosis.
Hemorrhagic diathesis is an increased tendency to hemorrhage within lots of organs.
Microsamples:
1 Nutmeg liver (chronic venous hyperemia in the liver) H & E design
2 Brown induration of the lung H & E; Pearls stain
3 Hemorrhagic infiltration within the brain H & E des
4 Intravascular microcirculatory blood Stasis within the brain H & E des
5 Collateral hyperemia of esophageal veins H & E
Macrosamples:
1 Nutmeg liver
2 Brown induration of the lung
3 Collateral hyperemia of esophageal veins
4 Inflammatory hyperemia of the appendix
5 Cyanotic induration of the kidney
6 Hematoma within the brain
7 Chronic ulcer of the stomach

1 №8 NUTMEG LIVER H & E des

Microscopically: the central vein and the vascular sinusoids of the centrilobular regions of the liver
are distended with blood. The central hepatocytes become atrophic
 secondary to chronic hypoxia. The peripheral hepatocytes suffer due to less severe hypoxia, fatty
changes develop.
Grossly: The central regions of the hepatic lobule become red-blue, surrounded by
a zone of uncongested liver substance descriptively referred to as nutmeg liver.
The liver is some what enlarged, firm with smooth surface.
The nutmeg liver is a chronic venous hyperemia (passive congestion) in the liver.
Definition: a chronic venous hyperemia (passive congestion) is the increase of venous blood
volume within the organ resulting from impaired venous return from a tissue.
Etiology: for nutmeg liver, it is right-sided heart failure, less common in the obstruction of the
inferior vena cava; for nutmeg liver there is also obstruction of the hepatic vein with Chiari-Budd
syndrome.
Morphogenesis: passive venous congestion – atrophy of hepatocytes- sclerosis- portal (nutmeg)
cirrhosis of the liver.
Result of chronic venous hyperemia (chronic passive congestion) of the liver is in
portal (nutmeg) cirrhosis of the liver.
Diseases: 1 chronic lung diseases (pneumosclerosis, chronic bronchitis, emphysema);
2 congenital heart diseases; 3 heart valvular diseases (mitral stenosis and insufficiency);
3 cardiomyopathy; 4 postinfarction cardiosclerosis.
Clinical signs: Chronic passive congestion is the passive hyperemia in affected parts of vein as
venous blood flow is impaired. An increase of deoxygenated hemoglobin in blood increases with
cyanosis as the blue tint with hypoxia of surrounding tissues is
noted. Physician palpates the soft, firm liver.
2 №21 BROWN INDURATION OF THE LUNG H & E; Pearls’ stain. des
Microscopically: The pulmonary alveolar capillaries are congested (chronic venous hyperemia).
With persistent elevation of pulmonary venous pressure, the capillaries may become tortuous and
rupture to produce in small hemorrhage into alveolar spaces. Alveolar macrophages phagocytosis of
red blood cells is noted and eventually becomes filled with hemosiderin. Persistence of septal edema
induces fibrosis within the alveolar walls.
Hemosiderin contains iron revealed by Pearls’ stain.
Grossly: The lungs become dark brown firm and short air is noted.
Classifications: see above
Etiology: Left-sided heart failure.
Diseases: 1 heart valvular diseases (mitral stenosis, insufficiency); 2 cardiomyopathy;
3 postinfarction cardiosclerosis; 4 arterial hypertension.
Pathogenesis of chronic venous hyperemia or chronic passive congestion within the
lungs: It occurs as hyperemia of the lung which capillary bed between alveoli with
diapedesis of erythrocytes within alveolar spaces. Erythrocytes are destructed with
formation of hemosiderin (hemoglobinogenic pigment), accumulated into siderophages. Chronic
hypoxia, mechanical and resorption lymph insufficiency and sclerogenic affect of SH-ferritin
composed hemosiderin lead to diffuse sclerosis of the lung.
Results are in progressive hemosiderosis and pneumosclerosis
Clinical signs: 1rusty sputum; 2 shortness of breath.

3 №16A HEMORRHAGIC INFILTRATION WITHIN THE BRAIN H&E des

Microscopically: Blood saturates within the cerebral tissue without its destruction.
This type of the intraorganic hemorrhage is named hemorrhagic infiltration.
Grossly: Another type of the intraorganic hemorrhage is referred to as hematoma.
Hematoma is the cavity filled with Blood with drawn from the cerebral tissue.
 Definition: hemorrhagic infiltration is the blood saturation of the tissue.
The mechanisms of their formation is rupture of the vessels (Latin term is per rhexin)
Diseases: Essential and symptomatic Arterial hypertension; Atherosclerosis; Aneurisms;
Tumor; Leukemia; Trauma; Sepsis; Rheumatism; DIC-syndrome; Typhus fever
Result of hemorrhage into the brain may be a cyst.
Clinical signs: neuralgic symptoms or death of the patient many occur.

4 № 9 INTRAVASCULAR MICROCIRCULATORY BLOOD STASIS

WITHIN THE BRAIN H & E des
Microscopically: erythrocytes slug & adhesion into vascular lumen is noted.
Definition: stasis is the cessation of the natural blood stream in a living organism Pathogenesis:
blood stasis is characterized by location slowing the circulation with
increasing permeability of the microvasculature walls and the concentration of red cells in small
vessels with increased viscosity of the blood and dilated small vessels.
Stages: prestasis; stasis; poststasis.
Results: 1 the restoration of the blood stream into small vessels; 2 thromboses:
3 diapedesis.
Clinical signs: a pain of the organ.
5 № 10 COLLATERAL HYPEREMIA OF ESOPHAGUS VIENS H & E
Microscopically: The veins of the submucous membrane of the esophagus are enlarged thinned
with blood esophageal varices.
Grossly: There are esophageal varices showing dilated submucosal veins.
Definition: This is collateral local venous hyperemia as an adaptive compensatory process, when
the general vessel is obstructive.
Pathogenesis: Increased resistance to portal blood flow is named portal hypertension.
With the rise in portal system pressure, bypasses develop wherever the systemic and portal
circulations share capillary beds.
There are three collateral anastomoses (or portosystemic shunts): 1 esophageal; 2 abdominal; 3 rectal.
Abdominal wall collaterals appear as dilated subcutaneous veins extending from the umbilicus
toward the rib margins are the so- called Medusa’s head (caput medusae).
Diseases are hepatic cirrhosis or portal vein thrombosis.
Result for esophageal varices may be in external massive hemorrhage after variceal rupture.
Clinical signs: hematemesis, melena.
Inflammatory hyperemia of the appendix
Grossly: the inflamed appendix is red, swollen. This is a manifestation of the local
arterial hyperemia.
Cyanotic induration of the kidney
Grossly: the kidney is somewhat enlarged, solid and cyanotic. This is a manifestation of
the general chronic venous hyperemia.
Hemorrhage into the brain as hematoma
Grossly: there is a cavity filled with clotted blood enclosed within a cerebral tissue.

Chronic ulcer of the stomach

Grossly: The peptic ulcer of the stomach has a vessel in its base.
Vascular lumen is closed by thrombus. This is the sign of former external hemorrhage
named melena with erosion fallow of the vascular wall by gastric juice.
Mechanisms are the so- called per diabrosin.