Circulatory disorder , status, thrombosis.

Blood circulation disease and there type prevention method.

1. Circulatory disorders: Circulatory disorders:
stasis, thrombosis, stasis, thrombosis,
embolism. embolism.
DIC-syndrome. ShockDIC-syndrome. Shock
Diveyeva Gulnara Damirovna
DEPARTMENT OF PATHOLOGICAL ANATOMY

2. Stasis – (from lat. stasis-stop) - a sharp slowdown and stop
of blood flow in the vessels of the microcirculatory, mainly
in the capillaries.
Cause: - venous congestion (congestive stasis)
- ischemia (ischemic stasis)
- a result of the action of infections (for example,
malaria, typhoid fever)
- various chemical and physical agents on the tissue
(high temperature, cold)
- leading to a violation of the innervation of the
microcirculatory
- in infectious-allergic and autoimmune (rheumatic
diseases) diseases, etc.

3. Blood stasis is characterized by stopping the blood in
the capillaries and venules with the expansion of the
lumen and the adhesion of red blood cells in
homogeneous columns – this distinguishes stasis from
venous hyperemia. Hemolysis and blood clotting do
not occur.
Significance: in the surrounding tissues develop
hypoxia, then plasmorrhea, swelling, oedema.
Prolonged stasis may be complication of thrombosis.
Outcomes: positive (resolution), negative
(thrombosis, necrobiosis and necrosis)

4. Stasis in the vessels of the brain

5. Stasis must be differentiated from the "sludge
phenomenon". Sludge is a phenomenon of
red blood cells sticking together not only in
capillaries, but also in vessels of various
calibers, including veins and arteries. This
syndrome is also called intravascular
aggregation of red blood cells and is observed
in a variety of infections, intoxications due to
increased adhesion of red blood cells, changes
in their charge.

6. Sludge phenomenon

7. Thrombosis (from the Greek. thrombosis-
clotting) – in vivo blood clotting in the lumen of
the vessel or the cavities of the heart. The mass
of blood products is called as a thrombus.
Blood clotting is observed in the vessels after
death (post-mortem blood clotting). And the
dense masses of blood that fall out are called a
postmortem blood clot.

8. Differences between a clot and a postmortem clot:
1)the blood clot is attached to the vessel wall, rough, corrugated,
dense consistency, dry, dark-red color
2)the postmortem clot is loose, soft, elastic, smooth, glance, free
lying, white-red color

9. Diseases where the risk of thrombosis
is increased
1)Long-term bed rest (after surgery)
2)Chronic Heart Failure
3)Atherosclerosis
4)Malignant tumor
5) The state of hypercoagulability
(congenital and acquired)
6)Pregnancy

10. Pathogenesis factors (Virchow’s triad):
1) damage to the vessel wall – particularly the
endothelium, is the main cause of arterial and
intracardiac thrombosis;
2) disordered blood flow – relative stasis is
important in initiating thrombus in slow-
flowing blood such as in veins. Turbulent
blood flow predisposes to thrombus formation
in arterial vessels and the heart;

11. Pathogenesis factors (Virchow’s triad):
3) abnormally enhanced haemostatic
properties of the blood – increased platelet
concentration or stickiness, or factors
promoting blood clotting or diminished
fibrinolysis contribute to both arterial and
venous thrombosis. Changes in blood viscosity
such as occur in dehydration, major illness,
disseminated carcinoma and the postoperative
state are included in this category.

12. Morphological stages of thrombosis:
1) Agglutination of platelets
2) Coagulation of fibrinogen with the
formation of fibrin
3) Agglutination of red blood cell
4) The precipitation of plasma proteins

15. The morphology of the thrombus
1) relative to the vessel wall (thrombus may partially
or completely occlude a vessel lumen):
a) obstructing (the lumen of the vessel is almost
completely closed)
b) parietal (most of the lumen is free)
2) by structure and appearance:
a) white
b) red
c) mixed
d) hyaline

16. White thrombus - formed slowly with rapid blood flow
(often in the arteries), consists of platelets, fibrin and white
blood cells.
Red thrombus -formed quickly with a slow blood flow
(usually in the veins), consists of red blood cells, platelets
and fibrin.
Mixed thrombus - formed more often in the veins, heart
cavity or aneurysms, and contains elements of red and white
thrombus. In a mixed thrombus differentiated head (attached
to the endothelium, has a structure of white thrombus), body
(mixed thrombus) and tail (lying freely in the lumen of the
vessel, has a structure of red thrombus)

17. Parietal mixed and
red obstructing
thrombus

18. Compound thrombus of the artery (№12)– H&E
The thrombus is adherent to the arterial wall and is seen
occluding most of the lumen. It shows lines of fibrin meshwork,
leucocytes with haemolysed red cells and plasma proteins. From the
blood vessel wall determined connective tissue growth and fissures
and new formed small vessels (vascularization).
Denote:
1) Blood vessel wall
а) zone of safe intima
(endothelium cells)
b) zone of vessel wall
defect
2) Thrombus
a) fibrin strides
b) agglutinated Tc
c) leucocytes
d) haemolysed red cells

19. Outcomes of thrombosis
1) Positive:
a) aseptic autolysis
b) the organization (can be accompanied by
recanalization and vascularization)
c) calcification (in the veins, there are stones
– phlebolites)
2) Negative:
a) septic autolysis with the development of
septicopyemia
b) disengage the thrombus with the
development of thromboembolic events
c) progression

20. Organization of a thrombus with the formation
of new vessels (revascularization)

21. Clinical significance
Thrombosis -> ischemia -> infarction
Thrombosis -> thromboembolism ->
infarction

23. An embolus (from the Greek Emballon-to throw inside) is
a detached intravascular solid, liquid, or gaseous mass that
is carried by the blood to a site distant from its point of
origin.
Pathways to move emboli:
Orthograde embolism (by blood flow)
Retrograde embolism (against blood flow)
Paradoxical embolism (from the right heart to the
left, bypassing the lungs, for defects in the interventricular
or atrial septum)

25. Types of embolism
1)Thromboembolism
2)Microbial
3)Tissue
4)Air
5)Gas
6)Fat
7)Foreign body

26. Fat embolism
* Develops when drops of fat enter the blood flow:
•In case of traumatic bone marrow injury (fractures of long
tubular bones),
•Crushing subcutaneous fat,
•After intravenous administration of oil solutions.
* Fat drops obturate capillaries of the lungs and through
arteriovenous anastomoses enter a large circle blood
circulation, obturate the capillaries of the kidneys, brain and
other organ
* Fat droplets can be revealed by sudan III staining in
interalveolar septae capillaries
* Outcomes: acute pulmonary insufficiency, brain capillaries
obturation with multiple brain hemorrhages

28. Fat embolism of
the lung’s vessels

29. Air embolism
* Develops air enters the blood flow:
• after the wounds of the veins of the neck (negative
pressure)
• after childbirth and abortion,
• through the sclerotized lung,
• with occasional intravenous injection air together with the
drug substance.
•Air bubbles in the blood cause embolism of capillaries of
a lung; when air bubbles reach a large circle blood
circulation embolism of capillaries the brain can develop
•Air embolism can be detected on the autopsy by release of
air from the right heart after puncturing it underwater and a
foamy blood in the cavities of the heart.

31. Gas embolism
* Typical for caisson disease=decompression
sickness: develops with rapid decompression
(transfer from increased pressure to normal
atmospheric pressure or from normal to decreased).
* Released nitrogen bubbles (located at high
blood pressure in the dissolved state) cause
blockage of the brain and spinal cord, liver,
kidneys and other body’s parts capillaries , which
is accompanied by the appearance in them small
foci of ischemia and necrosis.

32. Foreign bodies embolism
Catheters, bullets, as well as crystals of cholesterol from ulcerating
atherosclerotic plaques

33. Microbial embolism
* Bacteria, fungi, protozoa circulate in the blood
and obturate the capillaries lumen.
* Often, bacterial emboli are formed in purulent
melting of thrombus – thrombobacterial embolism.
* At the site of occlusion of the vessel with
bacterial emboli formed metastatic abscesses.

34. An example of bacterial
embolism may embolic
purulent nephritis (often
found in septicopyemia):
•The kidney is
enlarged in size,
•Cortex and medulla
show multiple small
yellowish foci (purulent
inflammation).

35. Microbial (bacterial)
embolism

36. Tissue embolism
• May occur when tissue is destroyed due to
trauma or pathological process leading to the
inflow of pieces of tissue (cells) into the blood.
• Embolism of amniotic fluid in woman in
labor may be accompanied by the development of
DIC syndrome and lead to death.
• Embolism of malignant tumor cells lies in
the tumor metastasis: in organs numerous tumor
nodes round in shape are revealed, often with a
dip in the center (necrosis).

37. Tissue embolism

38. Tissue embolism of the pulmonary vessels (№155) – H&E
Masses of malignant epithelial cells (tumor cells) are seen in
the lymph vessels. The tumor cells are obturated vessel lumen and
infiltrated vessel wall into surrounded tissue.
Denote:
1) Lung tissue elements:
a) alveolus
b) septa
c) vessels
2) Tissue embolism:
a) atypical neoplastic
cells in vessel space

39. Thromboembolism
Detachment of a blood clot fragment and its transfer by
blood flow is the most common cause of embolism
Arterial embolism
•Cause: thrombi formed in left heart ventricle (with
endocarditis, heart defects, myocardial infarction,
arrhythmia, etc.) and in the aorta (or large arteries)
atherosclerosis
•Outcomes:
* Ischemic infarctions in different organs

40. Venous (Pulmonary) embolism
(PE)
Causes: blood clots in 1) deep veins of the lower extremities,
2) pelvic veins,
3) right atrium
Outcomes:
1) thromboembolism of medium/small-sized
pulmonary artery leads to the development of hemorrhagic pulmonary
infarction
2) heart arrest and death (In the genesis of death in PE,
closure of the lumen of the vessel (of main pulmonary artery, zone
bifurcation (saddle embolus)) with the development of acute right
ventricular failure, as well as pulmonary-coronary reflex
(Kitaev’sreflex): spasm of the bronchi, branches of the pulmonary
artery and coronary arteries

44. Pulmonary embolism

45. Thromboembolism of small-sized pulmonary artery
(hemorrhagic pulmonary infarction)

46. Lung hemorrhagic infarction (№14) – H&E
In the lung tissue determined three zones. First zone - the
ischemic necrosis of the lung parenchyma in the affected area of
hemorrhages i.e. the alveolar walls, bronchioles and vessels in the
infracted zone show outlines but loss of nuclear and cytoplasmic
detals. Margin of the infarct shows inflammatory infiltrate, initially
by neutrophils and later their place is taken by macrophages and
hemosiderin.
Denote:
1) Infarction sings:
a) necrotic zone diffusely
infiltrated by blood
b) demarcation inflammation
c) save lung tissue with
edema and plethoric
vessels

47. Thromboembolic syndrome
(systemic thrombosis) develops
when blood clots forming in the
arterial part of the large circle of
blood circulation, followed by
the development of arterial
thromboembolism. The main
significance of thromboembolic
syndrome is multiple infarctions
in different organs
(simultaneously in the heart,
brain, liver, spleen, kidneys,
lungs, etc)

48. Causes of arterial thromboembolism
in the large circulatory system
1) Intracardiac blood clots (80-85%):
a) myocardial infarction or aneurysm
b) rheumocarditis (fragmentation of a valvular
vegetation)
c) cardiomyopathy
d) pathology of the valves
2) Extracardiac thrombus:
a) aortic aneurysms
b) thrombi on ulcerated atherosclerotic plaques
3) Cryptogenic

49. Shock - circulatory collapse, accompanied by
hypoperfusion of tissues and a decrease in their
oxygenation
Causes of shock:
- decreased cardiac output
- common peripheral vasodilation

50. Types of shock:
- hypovolemic
-cardiogenic
-septic
-vascular
Stages of shock:
-non-progressive
-progressive
- irreversible

51. Shock morphology
•Kidney:
• Necrotic nephrosis (acute renal failure)
•Lungs:
• Adult Respiratory Distress Syndrome (ARDS).
• Foci of atelectasis,
• Serous hemorrhagic edema with accumulation of fibrin
in lumen of the alveoli (hyaline membranes),
• Stasis and thrombi in microcirculatory vessels.
•Liver:
• Centrolobular necrosis.
•Brain:
• Foci of necrosis,
• Minor hemorrhages.
•Gastrointestinal tract:
• Hemorrhages.

52. Shock kidney
(necrotic nephrosis)

53. Disseminated intravascular
coagulation (DIC, consumption
coagulopathy, defibrination,
thrombohemorrhagic syndrome, intravascular
microcoagulation, etc.) is characterized by
activation of coagulation factors, which leads
to microthrombus in the vessels of the small
vessels of the whole organism, the
expenditure of clotting factors (activation of
fibrinolysis) leads to massive hemorrhage
(bleeding)

54. Pathogenetic types DIC
1) with a predominance of procoagulant
hemostasis (massive flow of procoagulants
into the blood flow during premature placental
abruption, intrauterine fetal death, amniotic
fluid embolism, metastatic cancer,
intravascular hemolysis, extensive trauma,
crushing syndrome)

55. 2) with a predominance of vascular-platelet
hemostasis (generalized vascular wall damage
or effects on platelets in infectious, autoimmune
diseases, transplantation organs and tissues)
3) with the same activity of procoagulant and
vascular-platelet parts (extracorporeal blood
circulation, extensive burns, acute leukemia,
shock, monoclonal paraproteinemia, erythremia,
thrombocytemia)

56. Stages of DIC
I stage (hypercoagulation)
-- It is characterized by intravascular
aggregation of blood cells, disseminated blood
coagulation with the formation of multiple blood
clots in microvesselsof various organs and tissues.
-- As a rule, it is short-term, duration up to 8 -
10 min.
-- Clinically manifests as a shock.

57. II stage (consumption coagulopathy)
•Characterized by a significant decreased amount of
platelets and fibrinogen, spent on the formation of
thrombi.
•There is a transition from hyper - to
hypocoagulation, manifesting by hemorrhagic
syndrome.
•Removal of active coagulation factors from the
blood stream is due to phagocytosis, so the presence
of fibrin in cytoplasm of macrophages and
neutrophils is confirmation of this stage.

58. III stage (pronounced hypocoagulation and activation
fibrinolysis)
-- There is a lysis of previously formed microthrombi
and often the degradation of circulating clot factors
-- Developing hyperplasminemia leads to the
appearance of readily soluble and fibrin-containing
complexes, fibrin degradation products, and fibrin-
monomer looses its ability to polymerize.
-- It usually develops 2 to 8 hours after the onset of
DIC.
-- Complete blood incoagulability, severe bleeding
and hemorrhage, microangiopathic hemolytic anemia are
noted.

59. IV stage (restorative (residual manifestations):
--Dystrophic, necrotic and hemorrhagic lesions of
organs and tissues.
--In most cases, there is a reverse development of
tissue changes.
--In severe cases of DIC syndrome, lethality is 50%
due to acute polyorganic insufficiency.
-- In newborns, especially premature born, mortality
is 75 -90% (due to imperfect fibrinolytic system,
insufficient synthesis of liver clotting factors, etc.)

60. Pathomorphologic changes.
Basic morphologic changes DIC are
microthrombus, necrosis and hemorrhages.
Hemorrhages develop as results coagulopathies and
fibrinolysis, necrosis – as results stoppage blood flowing
(widespread microthrombosis). Composition and structure
microthrombus differ from thrombus in large vessels.
Microthrombus may be fibrinal, hyaline, globylar,
plateletal, leucocytal (white), erythrocytal (red)

61. Morphology of DIC
• Morphology and morphogenesis of DIC syndrome are
due to a number of factors, among which an important
role play:
• The main disease,
• DIC triggering mechanisms,
• Time,
• Treatment measures
• Regardless of the combination of these factors, the
main morphological manifestations of DIC syndrome
are:
• Microthrombi,
• Necrosis,
• Hemorrhages.

62. Morphology of DIC
Multiple microthrombi in the vessels of
microcirculatory vessels:
• Fibrin clots:
• Detected most often and in the largest quantity.
• Consist of fibrin with single red blood cells.
• Hyaline thrombi,
• White (leukocytic) thrombi,
• Red (erythrocyte) blood clots.

63. Morphology of DIC
Lungs:
• Serous-hemorrhagic edema,
• Fibrin and hyaline thrombi,
• Sludge and agglutination of erythrocytes,
• Multiple hemorrhages,
• Small hemorrhagic infarctions (in some cases),
• Hyaline membranes (consisting of fibrin).
Kidney:
• Dystrophy of the proximal and distal convoluted tubules
epithelium,
• In severe cases, necrotic nephrosis (necrosis tubular
epithelium, tubulorhexis, symmetrical focal and total
corticonecrosis),
• Multiple hemorrhages, incl. subcapsular,
• Multiple microtrombi.

64. Liver:
• Dystrophic and necrotic changes in hepatocytes (up to
centrolobular necrosis),
• Fibrin thrombi in the central veins,
• Filaments of fibrin lying freely in sinusoids.
Adrenal glands:
• Dystrophy with loss of lipids and necrosis of cells in
cortex and medulla,
• Multiple microthrombi,
• Extensive hemorrhage (Waterhouse –Friderixen
syndrome).
Pancreas:
• Edema,
• Hemorrhages,
• Microthrombi,
• In severe cases, pancreatic necrosis.

65. Skin:
• Multiple petechial hemorrhages,
• Rarely -extensive hemorrhages (ecchymosis),
• Small necrotic foci (in some cases).
Gastrointestinal tract:
• Multiple small hemorrhages,
• Erosions and acute ulcers.
Spleen:
• Small-scale hemorrhages in parenchyma and capsule
• Hyaline and fibrin thrombi in small arteries and veins
• Fibrin fibers in sinusoids
Myocardium and brain (rarely affected):
• Single microtrombi
• Dystrophic changes
• Edema