Pathomorphology of systemic and local violation of blood circulation презентация

Main groups of the hemodynamic disturbances
violations of the blood volume (filling):
hyperemia or congestion
anemia or ischemia
violations of vessel’s wall permeability:
bleeding (hemorrhage)
edema (plazmorraghie)
violation of blood circulation:
stasis
sladge-phenomenon
thrombosis
embolism

Reasons of circulatory disturbances
Heart failure:
of the myocardium (pump function failure)
obstruction of blood outflow (valvular disease)
Vascular changes:
constrictions caused by vascular spasm
dilatations of vessels
obstructions of vessels
abnormal arterial-venous communications
rupture of vessel’s wall
increased vascular permeability
Blood disturbances, such as changes in the volume, composition, viscosity, or coagulation ability of blood.
Multi-systemic organ failure (shock or sepsis).

Classification of blood circulation disorders
According to the time of development: а) acute
chronic
According to the prevalence of process:
а) general (systemic) - disorders of heart function
local (region) - disorder of vascular function in
one area, that leads to structural changers
According to the type of violation of blood
circulation:
а) hyperemia (congestion) – arterial or vein
ischemia (anemia) – general or local
stasis – stopping of blood circulation in micro-
vessels

Types of systemic violations of
blood circulation
Shock
Acute disorders of blood circulation at acute arrhythmia and myocardial insufficiency
De-compensation of heart function

Systemic disorders of blood circulation
Reasons of development:
Violations of heart rhythm and pump function.
Violation of capacity of vascular system at: а) violation of neuro-endocrin function
loss of tone under influence of vascular-paralytic
metabolites
surplus of arterial-vein shunting in skin, lungs, kidney
violation of antigravity functions of body muscles.
Violation of Volume of Blood Circulation (VBC = plasma
+ proteins of plasma + blood cells). Reasons of violation:
а) bleeding
transudation
stagnation or expiration of lymph
vascular de-hydrotation (extra cells).
Violations of microcirculation of blood in tissue.

Shock
It is a clinical state of
cardiovascular collapse that develops under influence of extra-powerful stimuli and characterized by disturbances in CNS function, metabolism and microcirculatory system, resulting in destructive changes of the organs and tissues

Classification of shock according
to etiology and pathogenesis
Hypo-volemic at:
blood loss, trauma, peritonitis, cholera
Cardiogenic at:
vascular and myocardium insufficiency
obstruction of outflow (pulmonary embolism)
Septic – caused by bacterial toxins
Anaphylactic – immediate reaction of hypersensitivity
Neurogenic – drugs intoxications
Shock, at hormonal insufficiency (thyrotoxic,
myxedema)

Stages of shock
Compensation (non-progressive) – it is stage of
centralization of blood circulation:
а) blood come out from organs-depots
arteriole-venous shunting began in skin,
lungs, kidneys
increased concentration of adrenalin and
noradrenalin (tachycardia, spasm of arteriole)
Progressive de-compensative stage – it is violations of microcirculation in tissue that leads to acute poly-organ insufficiency
Stage of hemodynamic de-compensation (irreversible) – firm vasodilatation, loss of sensitiveness to medicines

Shock morphology
Main pathological processes at shock:
DIC (disseminated intravascular coagulation)
syndrome
Hemorrhagic diathesis
Liquid cadaver blood - blood is localized in micro-vessels and does not convolve, redistribution of blood in the vascular circulation (empty heart cavity and large vessels).
Microscopically:
Generalized spasm of the vessels
Microthrombosis
Increased vascular permeability in
microcirculatory system
Hemorrhages, degenerations and necrosis that are connected with hypoxia and effect of toxins

Shock changes in organs
а) Lungs – acute swollening of interstitial, lungs mass is increased in 2-3 times, a foamy liquid flows down from the surface of the cut with the admixture of dark blood – serouse- hemorrhagic edema - Large moist lungs
Kidneys – degeneration and necrosis in proximal canals is observed. During 2-3 days necrosis of cortex substances develops (symmetrical type) – Acute cortical necrosis of kidney (Shock kidney)
Liver – centro-lobular necrosis (hypoxic necrosis’s of central departments of lobules). Color of marble crumb.
GIT – acute gastric and intestine ulcers because of violation of micro-circulation in the wall of intestine.

It is a consequence of widespread activation of the coagulation system through endothelial injury and/or release of thromboplastic substances into circulation. Reasons of development:
infections
trauma
neoplasia
obstetric complications
Morphology:
Small fibrin thrombi are formed in small arteries of brain, heart, lungs, kidneys, and other organs and produce ischemic tissue damage
Disseminated intravascular coagulation(DIC)

Reasons of death
⮚Acute respiratory insufficiency
⮚Acute kidney insufficiency
⮚Acute liver and renal insufficiency
⮚Perforation of intestine, peritonitis

PATHOLOGY OF BLOOD FILLING
Hyperemia
Arterial
General
Ishemia
General
Vein
Local
Local
Physiological
Pathological
neuroparalitical
collateral
post-anemic
vacant
inflammatory
hyperemia at arterio-venosis swish
Cyanotic induration of extremities at the thrombosis
Syndrome of
portal hypertension
Budd-Chiari syndrome
Syndrome of sub- clavicular vein (SCV)

Hyperemia
Hyperemia may be caused by:
an increased supply of blood from the arterial system - active hyperemia. In hyperemia, increased inflow results in erythema.
by impaired exit of blood through venous vessels - passive hyperemia or congestion. In congestion, diminished outflow leads to a capillary swollen resulting in cyanosis.

Generalized passive hyperemia (Congestion)
Acute passive congestion is clinical consequence of acute left or right ventricular failure.
Chronic passive congestion - is generalized increasing in venous pressure at:
Chronic heart failure (left- and right- sided), results in slower blood flow and a consequent increase in blood volume in many organs, including liver, spleen, and kidneys.
Congestive heart failure secondary to coronary artery disease and hypertension, and right-sided failure due to pulmonary disease.

Regional vein hyperemia
It is a local vein plethora, observed at difficulty of outflow of vein blood from the organ or part of the body
Types:
Swollening and indurations of extremities at the thrombosis of veins of lower extremities.
Syndrome of portal hypertension – violation of blood outflow from the portal vein system:
а) increasing and stagnation of blood in the portal vessels
compensate of porto-caval anastomosis
isolated ascites without hydrotorax and hydropericardium (ascites-peritonitis)
Budd-Chiari syndrome – violation of blood outflow
through the hepatic vein
Syndrome of sub-clavicular vein (SCV) – at the
thrombosis of SCV (after catheterization)

Arterial plethora
Arterial plethora (active hyperemia) is promoted blood- involving of organ or tissue because of arising up of arterial blood inflow. Can be:
Physiologic - at increased functional demand of heart and skeletal muscle during exercise.
Pathological
Types, according to distribution:
general - is observed at the increased volume of circulatory blood or number of red cells. In such cases are marked red coloring of skin and mucous membranes and high arterial pressure
local – at inflammation or at different reasons.

Bleeding
Bleeding (hemorrhage) — it is coming out of blood from the blood vessel or cavity of heart to the surrounding outpace (outward bleeding) or into the tissue or cavity of body (inlaying bleeding).

BLEEDING
Internal
Into serous cavities
Hemopericardium
Hemoperitoneum
Hemarthrosis
Hemothorax
Into the tissue
Hematoma
Petechiae
Purpura
Ecchymosis
Hemorrhagic infiltration
External
hemoptoa
bleeding from nose
(epistaxis)
vomiting by blood (hemotenesis)
selection of blood with excrement (melaena)
bleeding from uterus
(metrorrhagia)

Reasons of bleeding:
Break down of vessel wall
Erosion of vessel wall
Increased permeability of vessel wall
Outcomes:
dissolution of blood
formation of cyst in place of hemorrhage
encapsulation or germination of hematoma by the connective tissue
joining of infection and suppuration

Thrombosis – It is rolling up of blood in the vessels or chambers of heart during life. Formation of a clotted mass of blood in the non-interrupted cardiovascular system. Basis of thrombosis is the physiological process of rolling up.
Thrombosis refers to the formation of a thrombus – it is aggregate of coagulated blood containing platelets, fibrin, and cellular elements.

Virchow triad in thrombosis
Endothelial integrity is the single most important factor,
Local blood flow and/or coagulability;
Abnormal blood flow (stasis or turbulence)
The elements of the triad may act independently or may
combine to cause thrombus formation.

Thrombosis macroscopically
It is necessary to distinguish a blood clot from the postmortem clot:
A thrombus is related closely to the wall of blood vessel, and postmortem clot lies freely.
A thrombus has dim, sometimes even rough surface (lines of Zahn), and at postmortem clot surface is smooth.
A thrombus has fragile consistency, while
consistency of postmortem clot is jam-like.

Classification of thrombus, according to
composition
red blood clot – red coloring, quickly appears and consists of red cells mainly
white – yellow-white color, slowly appears in arteries, leucocytes prevail in composition
mixed
hyaline – in the vessels of different tissue, plasma proteins prevail in composition above the cells of blood.

Classification according to the relation
to vessel’s walls
obstructive, that means, that a vessel is closed by mass of blood clot
near-wall
spherical blood clots - in the chambers of heart and in aneurism
dilatational
thromb-endocarditis – at the damage of
endocardium
axial – with the longitudinal axis (head,
body, tail)

Outcomes
1. organization - germination by the connecting
tissue
2. petrification - deposition of calcium salts in the
blood clot (in vein)
3. dissolution - aseptic autolysis
4. medicinal fibrinolisis
5. re-canalization of blood clot
6. propagandation
7. infected of blood clot with set about its particles
on organs with forming of abscesses
8. embolization

Outcomes of thrombosis
Arterial thrombi occlude the vessel and lead to ischemic necrosis of tissue (infarct).
1.Thrombosis of a coronary or cerebral artery results:
myocardial infarct (heart attack)
cerebral infarct (stroke),
2. End-arteries that are affected by atherosclerosis and often suffer
thrombosis:
mesenteric arteries (intestinal infarction),
renal arteries (kidney infarcts),
arteries of the leg (gangrene).