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Disturbances of
microcirculation
.
DEPARTMENT OF PATHOLOGICAL PHYSIOLOGY
 Peripheral circulation includes the movement of blood
in the smaller arteries and veins
 Microcirculation system includes the movement of
blood in the arterioles, precapillaries, capillaries,
postcapillaries, venules and arterioles, capillary
shunts, as well as in lymph capillaries and movement
of intercellular fluid. It enables the exchange of
substances between blood and tissues. It’s
components are
 Microhemocirculation
 Microlumphocirculation
 Movement of intercellular fluid
Microcirculatory disturbances
Intravascular disturbances – occur during
disorders of laminar flow and reological
properties of the blood (sludge, stasis)
Vascular disturbances - occur during increasing
of permeability of the vessel walls (diapedesis of
red blood cells)
Extravascular disturbances – occur during
edema, scar, tumor growing outside of vessels.
Transcapillary transport
The types of microcirculatory
disturbances
Arterial
hyperemia
Venous
hyperemia
Ischemia
Stasis Thrombosis Embolie
Arterial hyperemia –
increase blood supply to an organ or tissue
due to increased blood flow through the
arteries and arterioles
Types of arterial hyperemia
Physiological (occurs during functional
hyperactivity of organs and tissues)
Pathological (occurs during burns,
inflammation, nervous and endocrine
disorders)
Mechanisms of arterial hyperemia
Neurogenic
mechanism
Neurotonic
Neuroparalytic
Humoral
mechanism
Myoparalytic
Arterial hyperemia
Signs: Redness of the skin and mucous
membranes, increased tissue tension,
increased vascular pulsation
Outcome: leads to improved metabolism,
can lead to the spread of infection and
hemorrhage.
Venous hyperemia –
Increase of amount of venous blood in
organs and tissues as a result of
disturbance of venous outflow.
Venous Hyperemia
Causes: diseases of heart, respiratory
system
Signs: - Cyanosis of the skin and mucous
membranes
Edema - increase in size of organ
 Expansion of vascular lumen
Venous stasis
Venous Hyperemia
Outcome:
- Hypoxia, acidosis
- Edema, dystrophy, fibrosis on the
parenchymal organs
- Development of ascites
- Formation of thrombus
ISCHEMIA -
reduction of blood supply to an organ or tissue
due to decreased blood inflow through the
arteries
The mechanisms of ischemia
Reflex spasm of arterioles (angiospastic)
Compression of arterioles from outside
Obstruction of arterioles inside
Redistributive of blood in the body
ISCHEMIA
Causes:
- Angiospasm
- Blood clots, emboli, atherosclerotic plaque
- Compression of the vessels by tumor -
compression
Signs :
- Colorless (pale color) of the tissue and organ
- Slow blood flow
- Weak pulsation of the arteries
Outcome: Hypoxia, acidosis, necrosis of
tissue, infarction
INFARCT. Types of infarct
 White infarct- blood does not flow in the ischemic area, it
develops in organs with weak developed collateral
circulation (spleen).
Red infarct - in the area of ​​ischemia the blood
flows through the collaterals, they dilates and
red blood cells passage out of the vessels in the
necrotic tissue (lung, intestine)
White infarct surrounded by the red border -
on the periphery of the infarction blood vessels
dilated and causes there hemorrhage (heart,
kidney)
OUTCOME of INFARCT
Coagulative necrosis (necrotic area
became hard – often in cardiac
muscle, kidney)
Colliquative necrosis (necrotic area
became soft – often in brain)
THROMBOSIS
The process of blood clotting (in vivo) in
the vessel lumen (or in the cavity of the
heart) preventing partial or complete
blood flow
Virchow Triad –(three main
reasons of thrombosis)
Formation of thrombus
Coagulation cascade
The stages of thrombi formation
Vascular stage - vascular wall damage leads
to the vasospasm; from damaged cells leak
out biologically active substances that alter the
properties of platelets
Thrombocytic stage – in the damaged area
of vessel wall accumulates platelets that
adhere to the wall (Gp Ib), glued together (Gp
IIb-IIIa) and destructed; from these cells leak
out thrombocytic factors of blood clotting.
Plasmatic stage - plasma clotting factors
activates; fibrinogen is converted into fibrin,
blood cells accumulates on the fibrin fibers.
The types of thrombi
White thrombi- consist of leukocytes,
platelets and fibrin
Red thrombi- consist of leukocytes,
platelets, fibrin and erythrocytes
 Mixed thrombi- have a white head and
mixed body, red tail
 Hyaline thrombi - consist of
decomposed blood cells and precipitated
plasma proteins – but rarely fibrin
fibers
The types of thrombi
Small thrombi on the vessel’s wall –
those diminish the lumen of vessel.
Obstructive – those lead to the
completely occlusion of the lumen of
vessel.
OUTCOME of THROMBOSIS
Aseptically autolysis – occurs in small thrombi
Septic autolysis – occurs under influence of
pyrogenic bacteria. Thrombi breakdown with
spreading of infection in all organism (sepsis)
Organization, canalization and vascularization
of thrombi – thrombi replaced by the connective
tissue (organization), then the cavities form in the
middle of the thrombus and between the thrombus
and the walls of the vessel (canalization), the
cavities encapsulated by endothelium and filled
with blood as a result the blood flow through the
vessel (vascularization).
Detachment of thrombi – thromboembolism –
Outcome of thrombosis
EMBOLISM
Occlusion of blood vessels with bits of
matter carried by the blood or lymph and
usually foreign to the blood stream.
The types of emboli
 Air emboli – forms during damage of large vessels
 Gaseous emboli– in caisson disease, in divers
 Thromboemboli – occur during varicosis of veins,
atherosclerosis
 Fat emboli– occur during fractures of bones
 Cellular or tissue emboli – formed as a result of
destruction of malignant tumors
 Bacterial emboli – may develop during severe infection
processes
 Foreign body emboli – bullet fragments
 Amniotic water emboli – may occur during childbirth
Thromboembolia of pulmonary
artery
Disturbance of lymph
circulation
Mechanical- (includes : organic changes- squeezinf of lymph vessels by tumor and
 functional --- spasm in lymph vessel
Dynamic (increasing of filtration from arterioles as a result of hypoproteinemia
leads to overwhelm straining of lymph circulation)
Resorptional ( when oncotic pressure increases in interstistial spase
reobsorbsion of fluid decreases from here to vascular lumen become unable)
Chronic lymph stasis
(elephantiasis)

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4.Microcirculatiomicrocirculation presentation

  • 2.
  • 3.  Peripheral circulation includes the movement of blood in the smaller arteries and veins  Microcirculation system includes the movement of blood in the arterioles, precapillaries, capillaries, postcapillaries, venules and arterioles, capillary shunts, as well as in lymph capillaries and movement of intercellular fluid. It enables the exchange of substances between blood and tissues. It’s components are  Microhemocirculation  Microlumphocirculation  Movement of intercellular fluid
  • 4. Microcirculatory disturbances Intravascular disturbances – occur during disorders of laminar flow and reological properties of the blood (sludge, stasis) Vascular disturbances - occur during increasing of permeability of the vessel walls (diapedesis of red blood cells) Extravascular disturbances – occur during edema, scar, tumor growing outside of vessels.
  • 6. The types of microcirculatory disturbances Arterial hyperemia Venous hyperemia Ischemia Stasis Thrombosis Embolie
  • 7. Arterial hyperemia – increase blood supply to an organ or tissue due to increased blood flow through the arteries and arterioles
  • 8.
  • 9. Types of arterial hyperemia Physiological (occurs during functional hyperactivity of organs and tissues) Pathological (occurs during burns, inflammation, nervous and endocrine disorders)
  • 10. Mechanisms of arterial hyperemia Neurogenic mechanism Neurotonic Neuroparalytic Humoral mechanism Myoparalytic
  • 11. Arterial hyperemia Signs: Redness of the skin and mucous membranes, increased tissue tension, increased vascular pulsation Outcome: leads to improved metabolism, can lead to the spread of infection and hemorrhage.
  • 12. Venous hyperemia – Increase of amount of venous blood in organs and tissues as a result of disturbance of venous outflow.
  • 13. Venous Hyperemia Causes: diseases of heart, respiratory system Signs: - Cyanosis of the skin and mucous membranes Edema - increase in size of organ  Expansion of vascular lumen Venous stasis
  • 14. Venous Hyperemia Outcome: - Hypoxia, acidosis - Edema, dystrophy, fibrosis on the parenchymal organs - Development of ascites - Formation of thrombus
  • 15. ISCHEMIA - reduction of blood supply to an organ or tissue due to decreased blood inflow through the arteries
  • 16. The mechanisms of ischemia Reflex spasm of arterioles (angiospastic) Compression of arterioles from outside Obstruction of arterioles inside Redistributive of blood in the body
  • 17. ISCHEMIA Causes: - Angiospasm - Blood clots, emboli, atherosclerotic plaque - Compression of the vessels by tumor - compression Signs : - Colorless (pale color) of the tissue and organ - Slow blood flow - Weak pulsation of the arteries Outcome: Hypoxia, acidosis, necrosis of tissue, infarction
  • 18. INFARCT. Types of infarct  White infarct- blood does not flow in the ischemic area, it develops in organs with weak developed collateral circulation (spleen). Red infarct - in the area of ​​ischemia the blood flows through the collaterals, they dilates and red blood cells passage out of the vessels in the necrotic tissue (lung, intestine) White infarct surrounded by the red border - on the periphery of the infarction blood vessels dilated and causes there hemorrhage (heart, kidney)
  • 19. OUTCOME of INFARCT Coagulative necrosis (necrotic area became hard – often in cardiac muscle, kidney) Colliquative necrosis (necrotic area became soft – often in brain)
  • 20. THROMBOSIS The process of blood clotting (in vivo) in the vessel lumen (or in the cavity of the heart) preventing partial or complete blood flow
  • 21. Virchow Triad –(three main reasons of thrombosis)
  • 24. The stages of thrombi formation Vascular stage - vascular wall damage leads to the vasospasm; from damaged cells leak out biologically active substances that alter the properties of platelets Thrombocytic stage – in the damaged area of vessel wall accumulates platelets that adhere to the wall (Gp Ib), glued together (Gp IIb-IIIa) and destructed; from these cells leak out thrombocytic factors of blood clotting. Plasmatic stage - plasma clotting factors activates; fibrinogen is converted into fibrin, blood cells accumulates on the fibrin fibers.
  • 25. The types of thrombi White thrombi- consist of leukocytes, platelets and fibrin Red thrombi- consist of leukocytes, platelets, fibrin and erythrocytes  Mixed thrombi- have a white head and mixed body, red tail  Hyaline thrombi - consist of decomposed blood cells and precipitated plasma proteins – but rarely fibrin fibers
  • 26. The types of thrombi Small thrombi on the vessel’s wall – those diminish the lumen of vessel. Obstructive – those lead to the completely occlusion of the lumen of vessel.
  • 27. OUTCOME of THROMBOSIS Aseptically autolysis – occurs in small thrombi Septic autolysis – occurs under influence of pyrogenic bacteria. Thrombi breakdown with spreading of infection in all organism (sepsis) Organization, canalization and vascularization of thrombi – thrombi replaced by the connective tissue (organization), then the cavities form in the middle of the thrombus and between the thrombus and the walls of the vessel (canalization), the cavities encapsulated by endothelium and filled with blood as a result the blood flow through the vessel (vascularization). Detachment of thrombi – thromboembolism –
  • 28.
  • 30. EMBOLISM Occlusion of blood vessels with bits of matter carried by the blood or lymph and usually foreign to the blood stream.
  • 31.
  • 32. The types of emboli  Air emboli – forms during damage of large vessels  Gaseous emboli– in caisson disease, in divers  Thromboemboli – occur during varicosis of veins, atherosclerosis  Fat emboli– occur during fractures of bones  Cellular or tissue emboli – formed as a result of destruction of malignant tumors  Bacterial emboli – may develop during severe infection processes  Foreign body emboli – bullet fragments  Amniotic water emboli – may occur during childbirth
  • 34.
  • 35. Disturbance of lymph circulation Mechanical- (includes : organic changes- squeezinf of lymph vessels by tumor and  functional --- spasm in lymph vessel Dynamic (increasing of filtration from arterioles as a result of hypoproteinemia leads to overwhelm straining of lymph circulation) Resorptional ( when oncotic pressure increases in interstistial spase reobsorbsion of fluid decreases from here to vascular lumen become unable)