Edema

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Edema Localized Systemic Local disturbance of fluid exchange mechanism Increased retention of body sodium and water Causes – inflammation, allergic reaction, venous obstruction, lymphatic obstruction Causes – congestive heart failure, renal disease, hypoproteinemia – protein loss in urine-kidney disease, decreased protein synthesis- liver disease, decreased protein intake-malnutrition Edema deposits in ankles in upright and sacral region in bedridden Whole body edema is anasarca Hyperemia Congestion Active process Passive process Increased blood blow (inflammation, exercise) Decreased venous outflow (obstructed vein-local, CHF- general) Erythematous and warmer (rubor, calor) Cyanotic (bluer), increase in deoxygenated blood, chronicityhypoxianecrosis Crazy workoutmaybe transudateno edema unless lymphatics are blocked Increased hydrostatic pressuretransudatecapillary rupture Congestion Acute Edema Chronic Edema Acute Pulmona ry Edema Sudden left ventricular failure, increase hydrostatic pressure, engorgement of capillary beds (transudate formation) Chronic Pulmona ry Edema Persistent, less severe hydrostatic pressure, alveolar wallsthicken and fibrotic, macrophāges – heart failure cells

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pathology edema medical school notes

Transcript of Edema

Edema

LocalizedSystemic

Local disturbance of fluid exchange mechanismIncreased retention of body sodium and water

Causes inflammation, allergic reaction, venous obstruction, lymphatic obstructionCauses congestive heart failure, renal disease, hypoproteinemia protein loss in urine-kidney disease, decreased protein synthesis-liver disease, decreased protein intake-malnutrition

Edema deposits in ankles in upright and sacral region in bedriddenWhole body edema is anasarca

HyperemiaCongestion

Active processPassive process

Increased blood blow (inflammation, exercise)Decreased venous outflow (obstructed vein-local, CHF-general)

Erythematous and warmer (rubor, calor)Cyanotic (bluer), increase in deoxygenated blood, chronicityhypoxianecrosis

Crazy workoutmaybe transudateno edema unless lymphatics are blockedIncreased hydrostatic pressuretransudatecapillary rupture

Congestion

Acute EdemaChronic Edema

Acute Pulmonary EdemaSudden left ventricular failure, increase hydrostatic pressure, engorgement of capillary beds (transudate formation) capillaries rupture, frothy pink edemaChronic Pulmonary EdemaPersistent, less severe hydrostatic pressure, alveolar wallsthicken and fibrotic, macrophges heart failure cells (hemosiderin from RBC)

Acute Liver CongestionSecondary to shock or hepatic vein thrombosis, central vein and sinusoids distended with blood, centrilobular hepatocytes more vulnerable to injuryChronic Liver CongestionRight ventricular failure, hepatic lobule zonal changes, chronic hypoxia appears as fatty change, centrilobular hepatocyteshypoxicnecrosis small foci of hemorrhage, hemosiderin filled macrophages, red areas-congestion and hemorrhage, yellow areas-viable parenchyma (nutmeg liver), advanced cases-fibrosis-cardiac cirrhosis, but no actual cirrhosis, since no regeneration nodules, only fibrosis

Bleeding to DeathClotting to Death

Trauma, major surgery, hemophiliaStroke, MI, thrombosis

ThrombusBlood Clot

Coagulation cascade and platelet activationCoagulation cascade only

Develops in heart and vascular system Develops in extravascular areas (hematoma), in vitro (test tube), vessels after death (post mortem clot)

Often attached to underlying endotheliumNot attached to underlying endothelium

Displays orderly layering of platelets and fibrinDisplays randomly oriented fibrin with passively entrapped platelets and RBCsPost-mortem clot shows sedimentation effect, fibrin, entrapped RBCs settle out, leaving WBCs, plasma to form upper clot layer

Result of activation/inactivation of coagulation cascade and platelet activation (major role)Result of activation of coagulation cascade platelet activating (minor role)