hemodynamic ppt 2.pptx.pdf

Hemodynamic disturbance Lec. Dr. Asma Mohammadsheet Alhialy M.B.Ch.B MSc.(Histopath) CABHS(surgical path.) Pathology Department/Ninevah University/Collage of Medicine  Thrombosis The pathological counterpart of hemostasis is thrombosis--> formation of a solid or semi...

Hemodynamic disturbance Lec. Dr. Asma Mohammadsheet Alhialy M.B.Ch.B MSc.(Histopath) CABHS(surgical path.) Pathology Department/Ninevah University/Collage of Medicine  Thrombosis The pathological counterpart of hemostasis is thrombosis--> formation of a solid or semi sold mass from the blood constituents within the vascular system during life due to inappropriate activation of hemostasis. This mass is called a (thrombus).  Pathogenesis of a thrombus There are three predisposing factors for thrombus formation(Virchow’s traid). 1- Endothelial injury. 2-Stasis or turbulence of blood flow. 3-Blood hypercoagulability( changes in composition of blood). 1-Endothelial injury: A. Mechanical injury: such as, pressure, rupture or torsion of the vessel. B. Degeneration of vascular endothelium at the site of atherosclerosis, aneurysm, endothelium covering a myocardial infarction. C-Inflammatory processes as in phlebitis, arteries and inflammation of heart valves. Endothlial injury lead to exposure of subenothelial ECM---> adhesion of platalets. 2- Alteration in normal blood flow: Turbulence--->arterial and cardiac thrombosis Stasis---> venous thrombosis Stasis and turbulent therefore lead to thrombus formation by; 1- endothelial injury. 2-disrupt laminar flow and bring platelets into contact with endothelium. 3- prevent dilution of activated clotting factors by fresh blood. 2-retard the inflow of clotting factors inhibitors & permitt building of thrombus. 3- promote endothelial cell activation---> local thrombosis, leukocyte adhesion...etc. 3- Blood hypercoagulability. a-primary causes(genetic):antithrombinIII defeciency, protein C defeciency...... b-secondary causes(aquired): immobilization, MI, HF, tissue damage, burns, OCCP, sickle cell anaemia, leukemia, smoking...... Virchow’s traid Fate of Thrombus 1- Propagation 2-Embolization 3-Dissolution 4- Organization and re- canalization. 5- Calcification. Thrombi are significant because; 1-They cause obstruction of vessels. 2-They are possible source of emboli. Morphology of thrombus Grossly and microscopically: have apparent laminations( lines of Zahn),producing by alternating pale layers of platelets admixed with some fibrin and darker layers of red cells. Arterial thrombi are usually occlusive, are firmly attached to the wall and are gray white and friable. Venous thrombi are almost invariably occlusive, less firmly attached to the wall and are red. Post mortem clots are gelatinous, dark red, usually not attached to the wall and lack lines of Zahn. Mural thrombi, are those attached are the wall of the heart chambers or in the aortic lumen. Vegetations, are thrombi formed on heart valves.  laminated thrombus in a dilated abdominal aortic aneurysm with numerous friable thrombi superimposed on advanced atherosclerotic lesions of more proximal aorta. vegetations on heart valves showing lines of zahn Mural thrombi inside the left and right ventricular apices overlying white fibrous scar. Coronary artery was opened longitudinally in autopsy, showing dark red cord like mass Diagnosis : coronary artery thrombus "lines of Zahn" are alternating pale pink bands of platelets with fibrin and red bands of RBC's forming a true thrombus. There is a pink red recent thrombus ( RBC, platelets, and fibrin) occluding a narrowed atherosclerotic coronary artery with numerous identifiable cholesterol clefts Diagnosis: complicated atheroma with thrombus  Disseminated intravascular coagulation(DIC) DIC is a sudden or insidious onsets of widespread fibrin thrombi formation in the micro- circulation associated with rapid consumption of platelets and coagulation Proteins (consumption coagulopathy) that results in activation of fibrinolytic mechanisms---->serious bleeding disorders. DIC is not a primary disease but rather a potential complication of many conditions have in common, the wide spread activation of thrombin(obstetrical complications, infections, massive tissue injury).  Embolism is a detached intravascular solid, liquid, or gaseous mass, carried by blood to a site distant from its point of origin Types of emboli - Thrombo-emboli - Fat and bone. marrow - Gas (air, nitrogen) - Athero-emboli - Tumor fragments - Foreign body (bullet). Pulmonary Thrombo-Embolism In most instances, deep leg vein thrombi are the source, depending on the size of the embolus, it; - may occlude main pulmonary artery - may impact across the bifurcation (saddle embolus) - may pass into the smaller arterioles - may enter the systemic circulation (para-doxical embolism). Clinical consequences of pulmonary embolism 1-most pulmonary emboli are silent 2- sudden death (acute corpulmonale) 3- obstruction of medium-size arteries> pulmonary hemorrhage 4 - obstruction of small endarterioles> infarction 5 - multiple emboli over time> chronic corpulmonale This is the microscopic appearance of a pulmonary embolus (PE) in a major pulmonary artery branch ( RBC, platelets, and fibrin forming lines of Zahn). Diagnosis: pulmonary thromboembolism. This pulmonary thromboembolus is occluding the main pulmonary artery. (gross)  Systemic Thrombo-Emboli they can originate from: - Intra-cardiac mural thrombi(89%of emboli). - Aortic aneurysm - Thrombi on ulcerated atherosclerotic plaques - Fragmentation of valvular vegetations. - Paradoxical emboli -15% are of unknown origin Main sites involved in embolism: - Lower extremities (75%) - Brain (10%) - Intestines - Kidneys - Spleen - Upper extremities Fat Embolism May result from - Fractures of long bones(most common). - Soft tissue trauma and burns(rare). Clinical features - Pulmonary insufficiency - Neurologic symptoms - Anemia - Thrombocytopenia - Symptoms appear within 1 to 3 days  Decompression Sickness Gas Embolism Type of gas embolism in people who are exposed to sudden changes in Air may enter the circulation during; atmospheric pressure (deep sea divers) - Obstetric procedures If air is breathed at high pressure, high - Chest wall injury amount of gas (nitrogen), is dissolved *More than100 cc is required to have a clinical effect in the blood and tissue *The bubbles produce physical obstruction to If the diver ascends (depressurizes) vessels>infarction too rapidly, nitrogen expands in tissues and bubbles out of solution in the blood to form gas emboli Clinically, the diver suffers from; 1- Muscle and joint pain. 2- Respiratory distress. 3- Infarctions in various tissue. Amniotic fluid embolism: is a grave but uncommon complication of labor). The underlying cause is the infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins. Clinically; sudden severe dyspnea, cyanosis, hypotensive shock, seizure and coma. If the patient survive, pulmonary oedema and DIC developed.  Ischemia It is inadequate blood supply to an area of a tissue. Causes of ischemia : 1- 99% it result from thrombotic or embolic mechanism. 2- complicated atheroma. i.e. atheroma with subsequent hemorrhage. 3-twisting of blood vessel. 4-compression from out side by tumor or by entrapment in a hernial sac. 5- venous obstruction can occur in a varicose vein. Effect of ischemia: Variable depend on the adequacy of collateral circulation , if a good collateral is present it will produce little or no effect but if the collateral circulation is poor, it will lead to functional disturbances or even cell death. Ischemia in the heart can lead to chest pain (angina) , while in lower limb ,it produce intermittent claudication (pain in the calf muscle during exercise ).  INFARCTION INFARCTION is defined as; Ischemic necrosis due to occlusion of either artery or vein Causes of infarction: -Thrombosis or embolism (99%) - Local vasospasm - Expansion of atheroma - Extrinsic compression of a vessel (tumor, twisting, edema, hernia) - Traumatic rupture of vessel Morphology: Infarction has a wedge shape , the apex at the site of occluded blood vessels & the periphery of the organ forming the base which is poorly defined. The dominant histological characteristic of infarcts is ischemic coagulative necrosis. With time the edge become more defined by a narrow zone of hyperemia due to inflammation & pale infarction become more paler & sharply defined while red infarction it become more firm & brown. Septic infarcts--> abscess is formed.  Morphology of infarcts Red Infarcts( hemorrhegic): occur in the following situations; 1- venous occlusion(testis, ovaries). 2- loose tissue 3-tissue with dual circulation 4- previously congested tissue. 5- re-established blood flow. White infarcts ( anemic): occur following arterial occlusion in solid organs with end arterial circulation and by time change into scar tissue.  Factors that influence Infarct development The consequences of vascular occlusion can range from no effect, to death of tissue or even the individual. The factors that influences the outcome include; 1-The anatomy of the vascular supply i.e. presence or absence of an alternative blood supply can determine whether the occlusion of a blood vessel can cause damage. lungs have dual blood supply from the pulmonary and bronchial arteries.so obstruction of pulmonary artery will not cause severe damage until the brochial artery is also blocked. While kidney and spleen have end- arterial circulation so any arterial obstruction---> infarction of these tissues. 2-rate of development of occlusion slowly developing occlusion will allow time for collateral circulation to open e.g. in coronary arteries anastomosis. 3- vulnerability to hypoxia: neurons undergo irreversible damage when deprived of their blood supply for 3-4 min. Myocardial cells can withstand ischemia for 20-30 min only. In contrast to the fibroblast within the myocardium which can remain viable for hours after ischemia. 4- oxygen content of blood. Low blood O2 ---> increase extent and vulnerability of infarction.  Shock is pathological state of life- threatening hypoperfusion of vital organs and cellular hypoxia, due to diminished Causes of Shock and its types cardiac output or reduced effective circulating blood volume resulting in---> Hypotension --->Impaired tissue perfusion --->Cellular hypoxia. Initially, cellular injury is reversible; but if shock is sustained>cell death.  Stages of shock I. Stage of Compensation (initial nonprogressive stage ) Decreased cardiac output cause reflex sympathetic stimulation, which increases the heart rate (tachycardia) and causes peripheral vasoconstriction that maintains blood pressure in vital organs (brain and myocardium). Vasoconstriction in renal arterioles decreases the pressure and rate of glomerular filtration ---> resulting in decreased urine output (oliguria). II. Stage of Impaired Tissue Perfusion (progressive stage ). Prolonged excessive vasoconstriction, impairs tissue perfusion and oxygenation. Impaired tissue perfusion; Promotes anaerobic glycolysis, leading to production of lactic acid and lactic acidosis. Produces cell necrosis, which is most apparent in the kidney; causing acute renal tubular necrosis and acute renal failure.  In the lung, hypoxia causes acute alveolar damage with intraalveolar edema, hemorrhage, and formation of hyaline fibrin membranes (shock lung, or adult respiratory distress syndrome [ARDS] In the liver, anoxic necrosis of the central region of hepatic lobules may occur. Ischemic necrosis of the intestine is important because it is frequently associated with hemorrhage or release of bacterial endotoxins that further aggravate the shock state. III. Stage of Decompensation ► As shock progresses, decompensation occurs. ► Widespread vasodilation and stasis result and lead to a progressive fall in blood pressure to a critical level. ► Cerebral hypoxia causes brain dysfunction (loss of consciousness). ► Myocardial hypoxia leads to further diminution of cardiac output, and death may occur rapidly.  Morphological changes in shock Changes are those of hypoxic injury, Most particularly involved organs, (brain, heart, lungs, kidneys, adrenals, gastro-intestinal tract) Clinical features: - In hypovolemic and cardiogenic shock, the patient presents with:. Hypotension. Weak rapid pulse. Cool, clammy, and cyanotic skin -In septic shock, the skin initially is warm and flushed Prognosis -Varies with the cause of shock and its duration;age of patient *The best is in young with hypovolemic shock *The worst is in an old with cardiogenic shock or with septic shocke Thank you