Hemodynamics - Hyperemia

4,290 views 25 slides Jan 12, 2017
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About This Presentation

Disorders of perfusion - hyperemia, congestion, hemorrhage


Slide Content

DISORDERS OF PERFUSION Dr. J yothi Reshma S Tutor Dept of Pathology HYPEREMIA, CONGESTION, HEMORRHAGE HEMODYNAMICS - 2

ACTIVE HYPEREMIA Active hyperemia : increased supply of blood from the arterial system Physiologic response to increased functional demand Eg : heart and skeletal muscle during exercise, inflammation Neurogenic and hormonal influences Reactive hyperemia - temporary interruption of blood supply (ischemia) - histamine

PASSIVE HYPEREMIA Passive hyperemia or congestion : impaired exit of blood through venous pathways Increased hydrostatic pressure - edema . L ack of blood flow - chronic hypoxia - ischemic tissue injury and scarring. Capillary rupture - small hemorrhages - catabolism of extravasated red cells - hemosiderin-laden macrophages - Chronic venous congestion (CVC)

Consequences of Impaired Venous Outflow Increased intravascular pressure Stasis HAEMORRHAGE NECROSIS CONGESTION OEDEMA HYPOXIA FIBROSIS Capillary rupture Acute Chronic

CVC LUNG Enlarged, heavy Fibrosis + iron = firm brown lung - brown induration

CVC LUNG Alveolar congestion Intra-alveolar hemorrhage Hemosiderin-laden macrophages in the lung - congestive heart failure – heart failure cells

LIVER - ORGANIZATION

CVC LIVER Distension - central vein and sinusoids Centrilobular area is at the distal end of the hepatic blood supply - ischemic necrosis Periportal hepatocytes - better oxygenated because of proximity to hepatic arterioles — fatty change.

CVC LIVER – NUTMEG LIVER Dark foci of centrilobular congestion surrounded by paler zones of unaffected peripheral portions of the lobules

CVC LIVER – M/S C entrilobular hemorrhage H emosiderin-laden macrophages H epatocyte dropout and necrosis

CVC SPLEEN Gross : enlarged and tense M /s: Diffuse splenic fibrosis - iron-containing, fibrotic and calcified foci of old hemorrhage Gamna -Gandy bodies E xcessive functional activity— hypersplenism - hematologic abnormalities - thrombocytopenia

CVC SPLEEN Gamna -Gandy bodies

SUMMARY GROSS MICROSCOPY Enlarged Reddish blue - cyanosed C/s : oozing of blood Firm : fibrosis Capsule : thickened Capillary (sinusoids) : dilated , congested – blood Septa : thickened Fibrotic bands Hemosiderin laden macrophages : special names (lung, spleen) PATHOGENESIS

HEMORRHAGE E scape of blood from the vasculature into surrounding tissues, a hollow organ or body cavity, or to the outside ETIOLOGY, TYPES, CONSEQUENCES

HEMATOMA L ocalized hemorrhage - within a tissue or organ

PETECHIAE Pinpoint hemorrhages - <3mm - skin or conjunctiva Rupture - capillary or arteriole C oagulopathies or vasculitis

PURPURA Diffuse superficial hemorrhages in the skin Up to 1 cm in diameter

ECCHYMOSIS L arge superficial hemorrhage in the skin > 1cm P urple – green – yellow (progressive oxidation of bilirubin released from the hemoglobin of degraded erythrocytes)

Hemothorax , hemopericardium , hemarthrosis , hemoperitoneum

COMPREHENSION QUESTIONS A 40-year-old woman dies after a long history of an illness characterized by dyspnea , orthopnea , hepatomegaly, distended neck veins, and peripheral edema . The cut surface of the liver as it appears at autopsy is shown in the first panel. The second panel shows the microscopic appearance of the liver. What is the most likely cause of these findings?

A 36-year-old man dies during cardiac surgery . He had a history of long-standing rheumatic heart disease with mitral stenosis. At autopsy, the pathologist reports findings consistent with mitral stenosis and noted the presence of “heart failure cells.” This finding results from (A) activation of the coagulation cascade. (B) chronic passive congestion of the lungs. (C) hypoxic myocardial injury. (D) myocardial hyperemia .

EXAMPLE OF ECCHYMOSIS

T H A N K Y O U