Circulatory disturbances.

Arterial and venous hyperemia.

Edema. Bleeding and
hemorrhage.

Adequacy of bloodstream
is provided with:

1) Adequate

function of heart;

2) Continuity
3) Balance

of vascular wall;

between coagulative and

anticoagulative blood systems.

Types of circulatory disturbances:

1)

2)

3)

Vascularity disturbances (hyperemia,

ischemia);
Vascular wall permeability disturbance
(hemorrhage, bleeding);
Disturbance of rheological blood
properties (stasis, thrombosis,
embolism, sludge-phenomenon, DICsyndrome [disseminated intravascular
coagulation]).

Hyperemia
1)
2)

Arterial;
Venous.

Arterial hyperemia
Increase of hyperemia
through increase of
arterial blood flow.
But blood outflow is not
changed.

Arterial hyperemia
By localization:
general;
local.

General arterial hyperemia

It is specified by 2 factors:
1) Increase

of erythrocyte
quantity erythremia;
2) Increase of blood volume
plethora.

Local arterial hyperemia

Physiological:
Reflex or emotional;
Working?
2) Pathological:
Angioneurotic is developed at
overstimulation of vasodilator nerve or
paralysis of vasoconstrictive nerve (as
a result of trauma, neuritis);
Vacatnaya? occurs under the
conditions of low barometric pressure;
1)

At arteriovenous abnormality/commumication:
is developed under anastomosis/fistula between
artery and vein, at vascular malformation in
pia;
Collateral occurs at the obstruction of the
basic arterial trunk by thrombus or embolus. It
is a kind of compensatory and adaptive
process.
Inflammatory at any inflammation. It is also a
kind of compensatory and adaptive process.
Hyperemia after anemia

All types of arterial local

hyperemia are developed
briefly and that is why
structural changed do not
occur in organs and tissues.

Anatomical manifestations
Redness

of skin, mucous, and

organs;
Increase of arterial blood
pressure;
Increase of body temperature.

Value of arterial hyperemia

It

has often compensatory and

adaptive character.
Structural change does not
occur in the organs.

Venous hyperemia
It is an increased
vascularity/blood filling of
organ or tissue as a result
of venous blood outflow
disturbance
Blood inflow is not changed.

By distribution:
General;
Local.

By course:
Acute;
Chronic.

Causes:
of general venous hyperemia:
Cardiac insufficiency;
of local:
Thromboses in veins;
Compression of veins (adhesion,
cicatrix/scar, tumor, fluid)

Anatomical manifestations
Organ

is
enlarged;
is sclerosed;
of dark-red or
dark-blue
(cyanotic)
colour.

Morphological changes in the

tissues
Vascular permeability is increased
under the development of hypoxia; as
a result the edema and diapedesis of
erythrocytes are developed. There is
primarily fatty dystrophy in
parenchymatous cells
So, microscopically: plethoric (fullblooded) veins, edema of stroma,
diapedetic hemorrhage, dystrophic
changes of parenchymatous cells.

Chronic course:
- at the place of hemorrhage
hemosiderin is formed;
- in stroma the connective tissue is
developed;
- in parenchymatous cells atrophy is
developed along with dystrophy.

Effects/consequences:

At acute course the process is reversible;

At chronic course atrophy of parenchyma
and sclerosis of stroma with outcome into
cirrhosis.

Organopathology:

Nutmeg liver;
Brown [pigment] induration of lungs;
The kidneys, spleen, skin - cyanotic
induration.

Brown induration of lungs

Primarily the edema is developed in the
lungs; the fluid is stored/accumulated in the
lumen of alveoli.
Subsequently the diapedesis of erythrocytes
occurs in the lumen of alveoli; the
erythrocytes are caught with macrophages;
and hemosiderin is formed.
The connective tissue is developed in
alveolar septum because of hypoxia and the
septum becomes thicken. The lungs obtain
dense consistency.

Nutmeg liver
At disturbance of venous blood outflow the
central vein is dilated and plethoric/fullblooded. Hyperemia comes to sinusoids which
become enlarged and constrict hepatocytes (as
a result they are atrophied). All centre of
lobule/clove has red colour. On the lobule
periphery the hepatocytes are subjected to
fatty dystrophy, and the liver in these
department has yellow-brown colour.
Alternation of red and yellow-brown colors
makes a parti/multicolored view of liver and
looks like the nutmeg.
Outcome nutmeg cirrhosis.

Dark spots (plethoric/full-blooded centers of lobules) on yellow

background (dystrophy) of general venous hyperemia
manifestation

Cyanotic induration
At the beginning the edema is
developed, then enlargement of
connective tissue occurs. Under these
process the organs obtain dense
consistency, and under the dilated
plethric veins cyanotic edema.
Outcome cyanotic induration.

Bleeding blood issue from

heart cavity or vascular lumen

into environment or tissues and
body cavities.
Internal;
External.

Mechanisms of bleeding
1.

Rupture of vascular wall:

Medianecrosis of aorta;
Syphilitic meseorthite?;
Rupture of enlarged organs (liver,
spleen);
Aneurysm of heart, aorta, cerebral
artery;
Traumatic rupture.

Mechanisms of bleeding
2. Erosion of wall:
In

inflammation focuses;
At ulceration;
At fallopian pregnancy;
In zone of necrosis.

Mechanisms of bleeding
3.

Diapedesis

through/across the uninjured

vascular wall with higher permeability
At hypertonic disease;
At vasculitis/angiitis;
At infections (typhus, scarlatina/scarlet fever,
sepsis/septicemia);
At diseases of hemopoietic [blood-forming]
organs;
DIC-syndrome (disseminated intravascular
coagulation);
In hypoxic states.

Hemorrhage blood accumulation in

the tissues.

Types of hemorrhage
1)

2)
3)

4)

Petechia or petechial [punctate]

hemorrhage fine/small dot
hemorrhage on mucous and skin.
Mechanism diapedesis.
Bruise (fruise) flat-bed
hemorrhage.
Hemorrhagic infiltration blood
impregnates muscles and fatty
tissue.
Hematoma haemorrhage
following the tissue
destruction.

Outcomes of hemorrhage
1)
2)

3)

4)

Resorption / resolution;
Organization (encapsulation)
displacement of blood with
connective tissue;
Formation of cyst (in the
brain);
Suppuration / purulence.

Effects / consequences of
bleeding and hemorrhage:
depend on:
Rate of blood loss;
Volume
of
blood
hemorrhage;
Localization.

loss

and

Disturbance of interstitial [tissue]

content
Transsudate hydropic fluid (transparent,
contains less 2% proteins).
Edema fluid is accumulated in the tissues.
Hydrops/dropsy transsudate is stored in
the cavities.
Anasarca / hydrosarca fluid
accumulation in the tissues, organs, and
cavities (hydrothorax, hydropericardium).

Mechanisms of edema development

1)

2)

3)

4)

Increase of hydrostatic pressure

(congestive edema);
Decrease of colloid-osmotic pressure
(oncotic edema);
Membranogenic edema (disturbance
of Na balance);
Lymphogenous edema at
disturbance of lymph outflow.