1. Hemodynanic Disorders Abnormalities of Blood Supply
Chanpter 3
Hemodynanic Disorders
Abnormalities of Blood Supply
Department of Pathology ,
Bengbu medical college
Ge Xia

2. Section D Infarction Definition classification of infarction
morphology of infarct
Factors that influence development of an infarct
Evolution of infarcts

3. 一、Definition
Infarction is the development of an area of localized necrosis in a tissue resulting from sudden reduction of its blood supply.

4. tissue undergo necrosis.
●parenchymal cells and in interstitial
tissue undergo necrosis.
● Infarction is most commonly due to
arterial obstruction by thrombosis or
embolism.
● More rarely, obstruction of venous
drainage results in infarction.
（v回流受阻导致梗死）

5. Infarction parenchymal Cells and interstitial tissue undergo necrosis.
due to arterial obstruction by thrombosis or embolism
Artery bloodstream
Infarction

6. 二、classification of infarction
The appearance of an infarction varies with the site.
Various classification schemes方案 are used.

7. classification of infarction
pale versus red infarction
solid versus liquefied infarction
Sterile versus septic infarction

8. （一）..pale versus red:

9. 1、Pale (white, anemic) infarcts
● Causes:
Pale infarcts occur as result of arterial obstruction , that lack significant collateral circulation. The continuing venous drainage of blood from the ischemic tissue accounts for the pallor of such infarcts.

10. Sites:
solid organs ： heart 、kidney、spleen、brain

11. 2、Red (or hemorrhagic) infarcts:
Site:
Red infarcts are found in tissue that have a double blood supply-e.g, lung . Liver. intestine that have collateral vessels permitting some continued flow into the area although the amount is not sufficient to prevent infarction.

12. double blood supply：
lung ：
bronchal artery and pulmonary artery
Liver.
hepatic artery and portal vein
intestine：
mesenteric vein and mesenteric artery

13. Red infarcts may also occur in tissue if dissolution or fragmentation of the occluding thrombus permits reestablishment of arterial flow to the infarcted area. .

14. Color of infarcted area：
●The infarct is red
● because of extravasation (外渗)of blood in the infarcted area from necrotic small vessels

16. （二）.solid versus liquefied

17. 1、Sites of solid infarct :
solid infarct occure
Heart ,spleen, kidney,
infarction usually produces coagulative necrosis of cells. leading to a solid infarct. Because more protein

18. kidney in coagulative necrosis

19. 2、Sites of liquefied necrosis :
Brain-----liquefied necrosis of cells leads to the formation of a fluid mass in the area of infarction.
the end result is frequently a cystic cavity

20. Why is liquefied
necrosis
in the brain tissue?
Because of content multitude of the wet and phospholipids

21. Is this organ ? What is pathological changes ?
cystic cavity
Is this organ ? What is pathological changes ?

22. (三）.Sterile versus septic
Most infarction are Sterile
septic infarcts are Characterized by secondary bacterial infection of the necrosis tissue

23. septic infarcts occur:
microorganisms are present in the occluding thrombus or emboli, e.g. emboli in acute infective endocarditis
infarction occurs in a tissue (e.g. intestine) that normally contains bacteria
bacteria from the blood-stream cause secondary infection (this is unusual because blood is normally sterile)

24. Characterized of septic infarction
septic infarction are characterized by acute inflammation that frequently converts the infarct to an abscess.
Secondary bacterial infection of an infarct may also result in gangrene (e.g. in the intestine )

25. 三、morphology of infarcts
gross

26. gross --Shape of infarct in kidney spleen and lung
Infarcts in kidney, spleen, and lung are wedge-shaped,
the occluded artery situated near the apex of the wedge
the base of the infarct located on the surface of the organ.

27. The characteristic shape of infarcts in these organs is due to the symmetric dichotomous分支branching pattern of the arteries supplying them.

28. 肾脏血流分布图 profile of blood flow in the kidney
如树枝样分布: like branch sample

29. wedge-shaped base of located on the surface of th organ. base apex
Occluded
artery situated
occluded artery situated

30. gross -------Shape of infarct in cerebral and myocardial
The shape of cerebral and myocardial infarcts is irregular and determined by the distribution of the occluded artery and the limits of collateral arterial supply

31. Left coronary
artery
right coronary
artery

32. myocardial infarcts is irregular

33. left ventricular wall sectional to offer: yellow brown myocardial infarction;
surrounding congestion to offer red

35. gross -------Shape of intestinal infarction
Intestinal infarcts develop in loops of bowel in accordance with与一致 the pattern of arterial supply.
The most common infarcts of the intestine occur in the small intestine as a result of occlusion of the superior mesenteric artery.

36. Histological changes:
The dominant histologic characteristic of infarction is ischemic coagulative necrosis.
if the vascular occlusion has occurred shortly (minutes to hours) before the death of the patient, no demonstrable histologic changes may be evident;

37. Histological changes:
even if the patient survives 12 to 18 hours; the only change present may be a hemorrhagic suffusion.

38. Histological changes:
An inflammation response begins to develop along the margins of infarcts within a few hours and is usually well defined within 1 to 2 days.
Inflammation at these sites is incited by the necrotic tissue

39. inflammatory cells in the infarct area

40. Histological changes:
ultimately, in all forms of infarcts, there is gradual degradation分解作用 of the dead tissue with phagocytosis of the tissue debris by recruited补充 inflammatory cells.

41. Histological changes:
Eventually, the inflammatory response is followed by a reparative response beginning in the preserved margins.
some parenchymal regeneration may occur at the periphery where the underlying stromal architecture has been spared.

42. Histological changes:
most infarcts are ultimately replaced by scar tissue.
The brain is an exception例外
like other causes of necrosis ischemic tissue injury in the central nervous system results in liquefactive necrosis.(液化性坏死)

43. 四、Venous infarction Causes： superior sagittal sinus thrombosis上矢状窦
renal vein thrombosis,
superior mesenteric vein thrombosis.
total occlusion of all venous drainage from a tissue occurs

44. 四、Venous infarction Results: severe edema, congestion, hemorrhage,
progressive increase in tissue hydrostatic pressure流体静压.
When tissue hydrostatic pressure increases sufficiently, arterial blood flow into the tissue is obstructed, leading to ischemia and infarction.

45. 四、Venous infarction Special types of venous infarction occur in：
strangulation绞窄,
constriction of the neck of a hernial sac results in infarction of the contents of the sac;
intestine torsion,
where twisting of the pedicle of an organ , most commonly the testis, results in venous obstruction and hemorrhagic infarction.

46. 四、Venous infarction
Venous infarcts are always hemorrhagic infarction

48. Red infarction
in lung

49. 五、Factors that influence development of an infarct
The consequences of a vascular occlusion can range from no or minimal effect, all the way up to death of a tissue or even the individual . The major determinants are as follows:
血管阻塞的后果不同，影响极弱，一直到组织甚至人死亡，主要取决如下

50. A、Nature of the vascular supply
The availability有效 of alternative blood supply is the most important factor in determining whether occlusion of a vessel will cause damage.
For example:

51. Lung Pulmonary artery bronchial artery Dual blood supply
obstruction of small pulmonary arterioles does not cause infarction in an otherwise healthy individual with an intact bronchial circulation

52. portal vein circulation
hepatic artery
Liver,
Dual circulation
portal vein circulation
relatively resistant to infarction.

53. obstruction of such vessels generally cause infarction
In contrast,
renal and splenic circulation are end-arterial
obstruction of such vessels
generally cause infarction

54. B 、rate of development of occlusion
slowly developing occlusions are less likely to cause infarction
because they provide time for the development of alternative pathways旁路 of flow.
for example

55. ▲interconnect 互相连接the three major coronary arteries in the heart.
▲ If one of the coronaries is only slowly occluded ( e.g. atherosclerotic plaque),flow within this collateral circulation may increase sufficiently to prevent infarction ,even through the major coronary artery is eventually occluded

56. C 、vulnerability to hypoxia
The susceptibility of a tissue to hypoxia influences the linkelihood of infarction.
Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes.

57. C 、vulnerability to hypoxia
Myocardial cells are also quite sensitive and die after only 20 to 30 minutes of ischemia.
fibroblasts within myocardium remain viable after many hours of ischemia.

58. D、oxygen content of blood
The partial pressure of oxygen in blood also determines the outcome of vascular occlusion.
血液中部分氧分压也决定血管阻塞结果
Partial flow obstruction of a small vessel in an anemic or cyanotic partial might lead to tissue infarction. 在贫血性

59. D、oxygen content of blood
Whereas it would be without effect under conditions of normal oxygen tension. In this way, congestive heart failure, with compromised flow and ventilation, could cause infarction in the setting of an otherwise in consequential blockage.

60. 六、Evolution of infarcts
An infarct is irreversible tissue injury characterized by necrosis of both parenchymal cells and the connective tissue framework

61. 六、Evolution of infarcts
Necrosis induces an acute inflammatory response in the surrounding tissue,
with congestion and neutrophil emigration.
Lysosomal enzymes from neutrophils then cause lysis of the infracted area,
macrophages phagocytose the liquefied debris.
growth of granulation tissue occurs.

62. 六、Evolution of infarcts
Collagen production by fibroblasts in the granulation tissue ultimately leads to scar formation.
Because of contraction, the resulting scar is much smaller than the area of the original infarct.
Cytokines released by chronic inflammation cells are partly responsible for stimulating fibrosis and neovascularization.

63. 六、Evolution of infarcts
Evolution of a cerebral infarct differs from the above .
Necrotic cells undergo liquefaction because of their enzyme content.
Liquefied brain cells are phageocytosed by special macrophages(microglia),
The infarct area is converted into a fluid-filled cystic cavity that becomes walled off by proliferation of reactive astrocytes.

64. 六、Evolution of infarcts
The rate of evolution of an infarct and the time required for complete healing vary with size.
A small infarct may heal within 1-2weeks,
healing of a large infarct may take 6-8 weeks or longer.

65. 六、Evolution of infarcts
Evaluation of the gross and microscopic changes in an infracted area enables the pathologist to assess the age of an infarct, which is an important consideration at autopsy in establishing the sequence of events that caused death.

66. thank you
goou bye