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Chapter Three Hemodynamic Disorders
Normal fluid homeostasis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Hyperemia: Arterial hyperemia Venous hyperemia Section A
[object Object],Hyperemia Normal blood fluid Hyperemia Congestion
Physiological:  exercise Pathological : Inflammatory Post-ischemic   ,[object Object],[object Object]
 
[object Object],[object Object],[object Object],[object Object],Morphology of hyperemia
[object Object],[object Object],Systemic  —cardiac failure ,[object Object],-L. heart failure -R. heart failure Pulmonary cong. Systemic cong. 1. External pressure 2. Internal occlusion  Local
Pulmonary congestion Edema Hemorrhage Heart failure cells Brown induration
[object Object],[object Object],Morphology
Acute pulmonary congestion
Chronic pulmonary congestion
 
Liver congestion Atrophy Fatty change Nutmeg liver Centrilobular necrosis liver cirrhosis
[object Object],Central veins and hepatic sinuses of the centrilobular regions are distended with blood.
 
[object Object],[object Object],[object Object]
[object Object],“  Nutmeg  liver”
 
Cardiac cirrhosis of the liver in the longstanding cases
 
Thrombosis Thrombus  Section B
[object Object],[object Object]
Normal hemostatic process
 
 
 
[object Object],[object Object],[object Object]
[object Object],Pro- and anticoagulant activities of endothelial cells
Platelet adhesion and aggregation
[object Object],The coagulation cascade
Fibrinolytic system
THREE INFLUENCES OF THROMBOSIS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],Pro- and anticoagulant activities of endothelial cells
Endothelial injury ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Alterations in normal blood flow ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Hypercoagulable states Primary (genetic): Antithrombin III deficiency Protein C deficiency Protein S deficiency Other combined deficiency
Hypercoagulable states Secondary (acquired): High risk: Prolonged bed rest or immobilization. Myocardial infarction.  Tissue damage  (surgery, fractures, burns).  Cardiac failure.  Cancer.  Acute leukemia.  DIC.  Thrombotic thrombocytopenia.
Hypercoagulable states Secondary (acquired): Low risk: Atrial fibrillation.  Cardiomyopathy.  Nephrotic syndrome.  Hyperlipidemia.  Late pregnancy/postdelivery.  Oral contraceptives.  Lupus anticoagulant.  Sickle cell anemia.  Smoking.  Thrombocytosis.
 
 
[object Object],[object Object],[object Object],[object Object],Types of thrombus
White thrombus Site: heart valve ,  artery Component: Platelet, fibrin
Mixed thrombus Site:  heart chamber, vein Component: Platelet, fibrin,RBC
 
Mural thrombosis
Mural thrombosis
RED THROMBUS
Fibrinous thrombi are visible within parts of capi. of the glomerulus ,[object Object]
[object Object],[object Object],[object Object],[object Object],Fate of thrombus
 
Organization and recanalization of thrombus During organization, the thrombus dissolved and blood could flow again.
 
[object Object],[object Object],[object Object],[object Object],[object Object],Effects of thrombosis
[object Object],[object Object],Section C
[object Object],[object Object],[object Object]
Types of embolus ,[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],Fat embolism
[object Object],[object Object],[object Object],[object Object],Fat embolism
[object Object]
 
Etiology: Intravenous therapeutic procedures Obstetric procedures Chest wall injury Decompression sickness (nitrogen) Air embolism ,[object Object],[object Object]
AMNIOTIC FLUID EMBOLISM Incidence:  1/50 000 deliveries Mortality rate:  80% Clinical onset:  Sudden severe dyspnea, cyanosis, hypotensive shock, DIC
 
 
 
 
 
 
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Motional pathway of embolus:
 
[object Object]
 
THROMBOEMBOLISM ,[object Object],[object Object],[object Object],Pulmonary 1.Large emboli (5%):
 
2.Small emboli (60-80%): ,[object Object],[object Object],[object Object],[object Object]
3. Between the extremes of large and  small emboli (10-15%): Pulmonary hemorrhage. 4. Multiple  small emboli: Pulmonary hypertension and vascular sclerosis.
Systemic embolism I .  80-85% from heart, secondary to myocardial infarction. II .  5-10% from auricular thrombi associated  with rheumatic  heart disease and atrial  fibrillation. III .  5% from the dilated cardiac chamber  of myocarditis /  cardiomyopathy. VI .  Less common sources: Debris from ulcerative atheromata,  or thrombi in aneurysms, infectious endocarditis,  prosthetic valves, paradoxical emboli. V .   Unknown.
[object Object],[object Object],Section D
infarct/infarction ,[object Object],[object Object]
Intrinsic occlusion for example, thrombosis,  embolism expansion of atheroma Vasospasm Extrinsic compression for example, twisting of the vessels Etiology
INFARCTION ,[object Object],[object Object],[object Object],[object Object],[object Object],Morphology of infarct
 
 
 
 
[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],The myocardial cells shows coagulative necrosis with the outline of the myocardium. In the margin of the infarct there are numerous inflammatory exudation and connective tissue.
white infarct/anemic  infarct ,[object Object],[object Object]
 
 
 
 
Venous occlusions Loose tissues Tissues with dual circulations Tissues previously congested Blood flow reestablished Red infarct/hemorrhagic infarct
The  alteration of blood in pulmonary embolism
[object Object]
 
 
 
 
Hemorrhage ,[object Object]

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Hemodynamic Disorders

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