W12circulatory Disturbance
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Circulatory disturbances Workshop 12
• • • •
Pulmonary edema Chronic passive congestion - lung Chronic passive congestion - liver Cerebral hemorrhage by erythrodiapedesis
Edema • Edema represents the increase of fluid in interstitium and preformed cavities • Transudate = fluid with density <1012, with a reduced protein content
Pulmonary edema •
Appears in acute left cardiac failure.
•
Microscopy (histologic section through the lung) The alveolar walls are thickened by: Parieto-alveolar capillary distension and Interstitial edema The alveolar lumen: An eosinophilic, fine granular material, (transudate) that replaces partially or totally the air content.
-
-
Passive congestion
• The passive congestion represents the increase of the blood volume in a tissue or organ (by dilation of the venous and capillary network) as a result of decreased blood return).
Chronic passive congestion of the lung • • -
• -
Appears in the chronic left cardiac failure. Microscopy (histologic section through the lung) The alveolar wall is thickened by distension of parieto-alveolar capillaries. The alveolar lumen: microhemorrhage (intra-alveolar erythrocytes) prodused by erythrodiapedesis or rupture of capillaries) siderrophages - hemosidderin leiden macrophages (heart failure cells) transudate
In evolution: Hemossiderin accumulation Brown induration Parieto-alveolar fibrosis
Chronic passive congestion of the lung
(Perls stain) •
Perls stain = diferentiate the hemosiderin from anthracotic pigment. The hemosiderin is staining in blue
•
In the alveolar lumen we can see macrophages that contain a granular blue pigment.
Chronic passive congestion of the liver •
Appears in chronic right cardiac failure.
• Microscopy (histological section through the liver)
The centrolobular veins and the adjacent synusoid capillaries are distended and filled with blood. The centrolobular hepatocytes – atrophy by compression and hemorrhagic necrosis The mediolobular hepatocytes – steatosis (anoxia) The periportal hepathocytes normal
Haemorrhage • Extravasation of blood from normal conducts (heart and vessels during life)
Cerebral haemorrhage by erithrodiapedesis • Microscopy (histological
section through the white cerebral substance microhemorrhage – small hemorrhagic foci centred by congestive capillaries with intact endotelium Erithrocytes form a ring around cerebral capillaries produced by erythrodiapedesis (extravasation of erythrocytes from vessel lumen)
Circulatorry disturbance Workshop 13
• Recent arterial thrombosis • Recent renal infarction • Pulmonary hemorrhagic infarction
THROMBOSIS • Represents the process of blood coagulation in heart and vessels during life.
Recent artherial thrombosis •
•
The artherial thrombosis is produced in artheries with altered endothelium by different lessions (atherosclerosis) Microscopy (transversal section through a muscular arthery) The vascular lumen is obliterated by a recent thrombus, adherent to the wall. The thrombus is constituted from an eosinophilic fibrin network, erithrocytes and leukocytes. The wall is thickened due to a plaque of atherosclerosis.
INFARCTION • Is an aria of circumscribed necrosis determined by sudden interruption of blood flow in a tissue or organ • Classification: White infarction (anemic) is produced in solid organs with terminal, anastomotical, unfunctional circulation, (heart, kidney, spleen, brain) Red infarction (hemorrhagic) is produced in organs with loose structure, with double circulation (lung, liver, intestine)
Recent renal infarction •
•
White infarction (anemic) is produced in the kidney due to obstruction of a renal branch
arthery by an embolus or occlusive thrombus Microscopy (histological section through the kidney) ischemic, structural, coagulative necrosis the glomeruli and tubes are intense eosinophilic, without nuclei with preserved cellular limits.
Pulmonary hemorrhagic infarction •
The hemorrhagic infarction is produced in organs with loose structure and double circulation by: obstruction of a pulmonary arthery by an embolus in the presence of pulmonary stasis
•
Microscopy (histological section through the lung) Large area of structural, coagulative necrosis, with preservation of lung structure The alveolar walls are necrotic with homogeneous, eosinophilic appearance and without nuclei The alveolar lumen contains a mass of erithrocytes The adjacent pulmonary parenchyma presents lung stasis
•
•
• • • •
Pulmonary edema Chronic passive congestion - lung Chronic passive congestion - liver Cerebral hemorrhage by erythrodiapedesis
Edema • Edema represents the increase of fluid in interstitium and preformed cavities • Transudate = fluid with density <1012, with a reduced protein content
Pulmonary edema •
Appears in acute left cardiac failure.
•
Microscopy (histologic section through the lung) The alveolar walls are thickened by: Parieto-alveolar capillary distension and Interstitial edema The alveolar lumen: An eosinophilic, fine granular material, (transudate) that replaces partially or totally the air content.
-
-
Passive congestion
• The passive congestion represents the increase of the blood volume in a tissue or organ (by dilation of the venous and capillary network) as a result of decreased blood return).
Chronic passive congestion of the lung • • -
• -
Appears in the chronic left cardiac failure. Microscopy (histologic section through the lung) The alveolar wall is thickened by distension of parieto-alveolar capillaries. The alveolar lumen: microhemorrhage (intra-alveolar erythrocytes) prodused by erythrodiapedesis or rupture of capillaries) siderrophages - hemosidderin leiden macrophages (heart failure cells) transudate
In evolution: Hemossiderin accumulation Brown induration Parieto-alveolar fibrosis
Chronic passive congestion of the lung
(Perls stain) •
Perls stain = diferentiate the hemosiderin from anthracotic pigment. The hemosiderin is staining in blue
•
In the alveolar lumen we can see macrophages that contain a granular blue pigment.
Chronic passive congestion of the liver •
Appears in chronic right cardiac failure.
• Microscopy (histological section through the liver)
The centrolobular veins and the adjacent synusoid capillaries are distended and filled with blood. The centrolobular hepatocytes – atrophy by compression and hemorrhagic necrosis The mediolobular hepatocytes – steatosis (anoxia) The periportal hepathocytes normal
Haemorrhage • Extravasation of blood from normal conducts (heart and vessels during life)
Cerebral haemorrhage by erithrodiapedesis • Microscopy (histological
section through the white cerebral substance microhemorrhage – small hemorrhagic foci centred by congestive capillaries with intact endotelium Erithrocytes form a ring around cerebral capillaries produced by erythrodiapedesis (extravasation of erythrocytes from vessel lumen)
Circulatorry disturbance Workshop 13
• Recent arterial thrombosis • Recent renal infarction • Pulmonary hemorrhagic infarction
THROMBOSIS • Represents the process of blood coagulation in heart and vessels during life.
Recent artherial thrombosis •
•
The artherial thrombosis is produced in artheries with altered endothelium by different lessions (atherosclerosis) Microscopy (transversal section through a muscular arthery) The vascular lumen is obliterated by a recent thrombus, adherent to the wall. The thrombus is constituted from an eosinophilic fibrin network, erithrocytes and leukocytes. The wall is thickened due to a plaque of atherosclerosis.
INFARCTION • Is an aria of circumscribed necrosis determined by sudden interruption of blood flow in a tissue or organ • Classification: White infarction (anemic) is produced in solid organs with terminal, anastomotical, unfunctional circulation, (heart, kidney, spleen, brain) Red infarction (hemorrhagic) is produced in organs with loose structure, with double circulation (lung, liver, intestine)
Recent renal infarction •
•
White infarction (anemic) is produced in the kidney due to obstruction of a renal branch
arthery by an embolus or occlusive thrombus Microscopy (histological section through the kidney) ischemic, structural, coagulative necrosis the glomeruli and tubes are intense eosinophilic, without nuclei with preserved cellular limits.
Pulmonary hemorrhagic infarction •
The hemorrhagic infarction is produced in organs with loose structure and double circulation by: obstruction of a pulmonary arthery by an embolus in the presence of pulmonary stasis
•
Microscopy (histological section through the lung) Large area of structural, coagulative necrosis, with preservation of lung structure The alveolar walls are necrotic with homogeneous, eosinophilic appearance and without nuclei The alveolar lumen contains a mass of erithrocytes The adjacent pulmonary parenchyma presents lung stasis
•
•
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