2. 1 By ASS.Prof.Naglaa Samier CIRCULATORY DISTURBANCE

3.  Impaction of an embolus in BV.  Embolus: Undissolved material circulating in blood stream. Types and effects: 1.Thrombotic embolism:  Impaction of an embolus in BV.  Embolus: Undissolved material circulating in blood stream. Types and effects: 1.Thrombotic embolism: Detached thrombus or fragmented thrombus Septic Aseptic When impacted Pyaemic abscess Go into the lung Different organs SmallLarge Ischaemic necrosis Or infarction Ischaemic necrosis Or infarction If has Ch V.C lung If has Ch V.C lung No infarction Infarction Extensive pulm. Embolism ± death If no C.V.C If RT. Heart side origin or Venous If lt. heart side origin or Arterial

4. Septic embolus When impacted Pyaemic abscess

5. Go into the lung SmallLarge If has Ch V.C lung If has Ch V.C lung No infarction Extensive pulm. Embolism ± death If no C.V.C If RT. Heart side origin or Venous Aseptic embolus Aseptic embolus

6. Aseptic embolus Different organs Ischaemic necrosis Or infarction Ischaemic necrosis Or infarction If lt. heart side origin or Arterial

7. 2.Tumour embolism  metastases 3.Parasitic emboli  parasitic lesion when impacted: A.Ova of bilh. In L.I  liver  fibrosis. B.Larva of E. Granulosus in I.  liver hydatid cyst. C.Vegetative form of E.H from I.  liver  amaebic abscess. 2.Tumour embolism  metastases 3.Parasitic emboli  parasitic lesion when impacted: A.Ova of bilh. In L.I  liver  fibrosis. B.Larva of E. Granulosus in I.  liver hydatid cyst. C.Vegetative form of E.H from I.  liver  amaebic abscess.

8. 4.Fat emboli: A.Trauma to bone marrow during surgery  fat emboli  usually no effect. B.Subcutaneous tissue following trauma  emboli. 4.Fat emboli: A.Trauma to bone marrow during surgery  fat emboli  usually no effect. B.Subcutaneous tissue following trauma  emboli.

9. 5.Air emboli: Causes: 1.Chest wall injury and injuries involving neck vein /artificial pneumothorax / intravenous infusion 2. Obstetric procedures e.g. tubal insufflation Generally 100 ml of air is required to produce a clinical effect. Gas bubbles can obstruct vascular flow as frothy masses producing ischemic necrosis or can reach the right ventricle, mix with blood and interfere with ventricular contraction leading to right side heart failure and death. Gas bubbles in cerebral vessels

10. Decompression Sickness: In deep seas (high atmospheric pressure), there is high amount of dissolved air mainly nitrogen in blood& body tissues of divers thus if they come up quickly (rapid decrease of pressure), this large amount of dissolved nitrogen will be released from tissues and bubble out of solution to form gas emboli producing mechanical obstruction wherever they lodge.

11. 6.Amniotic fluid: Post labour ±  amniotic fluid embolism. 6.Amniotic fluid: Post labour ±  amniotic fluid embolism. Causes: It is a serious complication of labor and the immediate postpartum period. It is caused by infusion of amniotic fluid and its contents into the maternal circulation through a tear in the placental membranes and rupture of uterine veins that are drained through the systemic veins and reach the pulmonary microcirculation.

12. These elements induce marked pulmonary edema and diffuse alveolar damage. (dyspnea, cyanosis and shock) disseminated intravascular coagulopathy develops (DIC) due to release of thrombogenic substances from amniotic fluid producing systemic micro thrombi and multiple infarctions wherever they are formed followed by severe bleeding disorder (consumption coagulopathy).

13. Pulmonary artery occluded by fetal tissue (squames) & amniotic fluid

14. Results of Arterial Obstruction Results of Arterial Obstruction The effect depends on:  Nature of vascular supply:  Collateral supply resist infarction  Double blood supply resist infarction  End artery infarction  Rate of development of occlusion  Vulnaribilty to ischemia  Oxygen content of blood

15. Def. decrease arterial. Bl. S. to a tissue in relation to its demand. Types and effects Partial arterial occlusion Complete occlusion Atheroma Thrombosis – embolism - Arterial spasm - Proliferative intimal change Cause: Ischaemic atrophy of parenchymatous cells (e.g H. brain. kid.) Ischaemic atrophy of parenchymatous cells (e.g H. brain. kid.) Fibrosis Failure to remove waste products  intermittent pain. (e.g. coronary ischaemia  angina. P.) (L.L. atherosc.  intermittent claudication)  intermittent pain. (e.g. coronary ischaemia  angina. P.) (L.L. atherosc.  intermittent claudication) Cause: Poor anastomosis (end artery) Diseased collateral Diseased collateral Efficient collateral Efficient collateral Ischaemic necrosis (infarction) Ischaemic necrosis (infarction) Ischaemic necrosis (infarction) No effect

17. Def. : Ischaemic necrosis produced by loss or marked reduction of arterial blood S. (necrotic tissue called infarct). Types: Def. : Ischaemic necrosis produced by loss or marked reduction of arterial blood S. (necrotic tissue called infarct). Types: 1) Acc. to vascularity of the tissue Hemorrhagic Pale  Organs having double blood supply e.g., lung  Organs having anastomotic circulation as S.I.  Organs having double blood supply e.g., lung  Organs having anastomotic circulation as S.I.  Organs having end artery. e.g., heart, kidney, spleen. 2) Acc. to nature of tissue Coagulative necrosis Liqufactive necrosis  (Only in CNS)

18. Gross:  Infarcts wedge shaped  Base directed towards the S.  Apex towards the hilum Microscopic:  Coagulative necrosis  Surrounded by congested vessels  At margin area of acute inflame, odema, congestion Healing: Replaced by granulation tissue fibrosis Effects clinical: 1.Fever, leucocytosis and  ESR due to abs. of autolysed products of necrotic area 2.Liberation of serological enzymes e.g. LDH, SGOT. in myocardial Infarction Gross:  Infarcts wedge shaped  Base directed towards the S.  Apex towards the hilum Microscopic:  Coagulative necrosis  Surrounded by congested vessels  At margin area of acute inflame, odema, congestion Healing: Replaced by granulation tissue fibrosis Effects clinical: 1.Fever, leucocytosis and  ESR due to abs. of autolysed products of necrotic area 2.Liberation of serological enzymes e.g. LDH, SGOT. in myocardial Infarction end Wedge- shaped infarct Occluded vessel at apex apex base

19. Myocardial Infarction

20. The outline is preserved with loss of nuclei. The nuclei seen here are of the inflammatory cells The infarcted area is replaced by fibrous tissue but still is infiltrated with inflammatory cells.

21. Myocardial Infarction Acute pale myocardial infarction surrounded by a congested rim Old myocardial infarction with collagenous (fibrotic ) scar

22. Cerebral Infarction Frontal lobe infarction (liquefactive necrosis) &cyst formation Macrophages (on the left) are cleaning up the dead area

23. Lung Infarction The alveolar wall are necrotic & the alveolar spaces are filled with blood. The rest of the lung may show chronic venous congestion. Triangular area (wedge) with its base outside, firm and deep red in colour

24. Infarction of Kidney Pale infarction Coagulative necrosis Congested edge

26. Infarction of Spleen Multiple infarcts Triangular infarction, note the congested outer rim Inflammatory cells at the periphery

27. Infarction of Intestine Early ischaemic changes The loops are congested, oedematous & haemorrhagic Early changes appear as necrosis of surface epithelium with marked congestion of the whole wall.