Edema
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Edema is an increase in fluid volume in the tissues caused by several factors including increased capillary permeability, hydrostatic pressure, and decreased oncotic pressure. The main types are disseminated edema affecting multiple areas and local edema affecting a specific site. Disseminated edema can be caused by conditions like cardiac failure, nephritic disorders, liver failure, and malnutrition. Local edema includes traumatic, inflammatory, venous, and lymphatic edema. The pathogenesis involves a balance between hydrostatic forces driving fluid out of capillaries and oncotic forces pulling fluid back in.
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Edema
PATHOGENESIS OF EDEMA, TYPES OF EDEMA: Renal edema, Cardiac edema, Pulmonary edema, Cerebral edema, Hepatic edema, Nutritional edema, Myxoedema.
edema pathology
Edema is an abnormal accumulation of fluid in the spaces between cells. There are two main types of edema - generalized edema, where fluid collects in multiple areas of the body, and localized edema, where fluid is confined to a specific body part. Generalized edema can be caused by conditions like congestive heart failure, nephrotic syndrome, and cirrhosis of the liver. Localized edema has causes such as trauma, infection, lymphatic obstruction, and venous obstruction.
Hemolytic anemia and post hemorrhagic syndrome
Hemolytic anemia is a condition where red blood cells are destroyed faster than the body can replace them, leading to anemia. It can be caused by intrinsic issues with red blood cells themselves or extrinsic factors like infections, medications, autoimmune disorders, or enlarged organs destroying healthy cells. Symptoms include paleness, fatigue, fever, and abdominal pain. Diagnosis involves blood tests measuring red blood cell counts and liver function. Treatment options depend on the underlying cause but may include blood transfusions, immunosuppressants, corticosteroids, or spleen removal. Posthemorrhagic anemia develops after acute blood loss and is treated by addressing the cause of bleeding with fluids, transfusions, or surgery along
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The pathogenesis of liver cirrhosis and fibrosis
This document summarizes the pathogenesis of liver cirrhosis and fibrosis. It begins with an introduction to liver disease as a major health problem worldwide. It then discusses the epidemiology of cirrhosis, noting its 10th and 12th leading causes of death in the US. The document outlines the classification of cirrhosis based on nodule size, and describes the key events in the pathogenesis of fibrosis, including hepatic stellate cell activation and cytokine signaling pathways. Morphological features of cirrhosis seen on microscopy and complications like portal hypertension are also summarized. The document concludes by stating hepatic fibrogenesis involves both resident and recruited cell types, and advances may help develop effective antifibrotic therapies.
Infraction - Dr. Abhinav Golla MD. Pathology
1. An infarction is an area of ischemic necrosis in an organ resulting from reduced blood supply, usually due to arterial obstruction.
2. The main causes of infarction are thromboembolism and atherosclerosis, which interrupt arterial blood flow. This leads to localized tissue death from coagulative necrosis.
3. Pathologically, infarcts appear pale and wedge-shaped, with inflammation at the borders and eventual scar formation. Location and outcomes vary by organ, such as potentially lethal myocardial infarction or non-lethal splenic infarction.
Polycythemia vera
Polycythemia Vera is a chronic myeloproliferative disorder characterized by an overproduction of red blood cells from bone marrow due to a mutation in the JAK2 gene. This leads to thickening of the blood and complications like blood clots and spleen enlargement. It is diagnosed through blood tests showing increased red blood cells. While there is no cure, treatment focuses on reducing blood cell counts through regular blood removal and medications to suppress bone marrow production and stimulate the immune system.
Hemodynamics congestion & hyperemia
This document discusses various hemodynamic disorders including edema, hyperemia, congestion, and hemorrhage. It defines each term and describes the microscopic findings associated with congestion in different organs. Edema is an increase in fluid in the interstitial space, while hyperemia and congestion both refer to increased blood volume in a tissue. Hyperemia is an active process of arteriolar dilation, while congestion is passive due to impaired venous outflow. Congestion of the liver, lungs, spleen, and kidneys can result in centrilobular necrosis, thickening of alveolar septa, enlargement and fibrosis of the spleen, and mild changes to the kidneys respectively. Hem
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Edema
PATHOGENESIS OF EDEMA, TYPES OF EDEMA: Renal edema, Cardiac edema, Pulmonary edema, Cerebral edema, Hepatic edema, Nutritional edema, Myxoedema.
edema pathology
Edema is an abnormal accumulation of fluid in the spaces between cells. There are two main types of edema - generalized edema, where fluid collects in multiple areas of the body, and localized edema, where fluid is confined to a specific body part. Generalized edema can be caused by conditions like congestive heart failure, nephrotic syndrome, and cirrhosis of the liver. Localized edema has causes such as trauma, infection, lymphatic obstruction, and venous obstruction.
Hemolytic anemia and post hemorrhagic syndrome
Hemolytic anemia is a condition where red blood cells are destroyed faster than the body can replace them, leading to anemia. It can be caused by intrinsic issues with red blood cells themselves or extrinsic factors like infections, medications, autoimmune disorders, or enlarged organs destroying healthy cells. Symptoms include paleness, fatigue, fever, and abdominal pain. Diagnosis involves blood tests measuring red blood cell counts and liver function. Treatment options depend on the underlying cause but may include blood transfusions, immunosuppressants, corticosteroids, or spleen removal. Posthemorrhagic anemia develops after acute blood loss and is treated by addressing the cause of bleeding with fluids, transfusions, or surgery along
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This document provides an overview of shock, including its history, definition, pathogenesis, stages, classification, and treatment. It discusses the various types of shock - hypovolemic (hemorrhagic), cardiogenic, obstructive, and distributive (septic, anaphylactic, neurogenic). For hypovolemic shock, it outlines the stages, compensatory mechanisms, assessment including vital signs and labs, and classification based on percentage of blood loss. Treatment of hypovolemic shock involves initial and late resuscitation, with goals of hemodynamic stabilization while avoiding over-resuscitation and permissive hypotension when possible.
The pathogenesis of liver cirrhosis and fibrosis
This document summarizes the pathogenesis of liver cirrhosis and fibrosis. It begins with an introduction to liver disease as a major health problem worldwide. It then discusses the epidemiology of cirrhosis, noting its 10th and 12th leading causes of death in the US. The document outlines the classification of cirrhosis based on nodule size, and describes the key events in the pathogenesis of fibrosis, including hepatic stellate cell activation and cytokine signaling pathways. Morphological features of cirrhosis seen on microscopy and complications like portal hypertension are also summarized. The document concludes by stating hepatic fibrogenesis involves both resident and recruited cell types, and advances may help develop effective antifibrotic therapies.
Infraction - Dr. Abhinav Golla MD. Pathology
1. An infarction is an area of ischemic necrosis in an organ resulting from reduced blood supply, usually due to arterial obstruction.
2. The main causes of infarction are thromboembolism and atherosclerosis, which interrupt arterial blood flow. This leads to localized tissue death from coagulative necrosis.
3. Pathologically, infarcts appear pale and wedge-shaped, with inflammation at the borders and eventual scar formation. Location and outcomes vary by organ, such as potentially lethal myocardial infarction or non-lethal splenic infarction.
Polycythemia vera
Polycythemia Vera is a chronic myeloproliferative disorder characterized by an overproduction of red blood cells from bone marrow due to a mutation in the JAK2 gene. This leads to thickening of the blood and complications like blood clots and spleen enlargement. It is diagnosed through blood tests showing increased red blood cells. While there is no cure, treatment focuses on reducing blood cell counts through regular blood removal and medications to suppress bone marrow production and stimulate the immune system.
Hemodynamics congestion & hyperemia
This document discusses various hemodynamic disorders including edema, hyperemia, congestion, and hemorrhage. It defines each term and describes the microscopic findings associated with congestion in different organs. Edema is an increase in fluid in the interstitial space, while hyperemia and congestion both refer to increased blood volume in a tissue. Hyperemia is an active process of arteriolar dilation, while congestion is passive due to impaired venous outflow. Congestion of the liver, lungs, spleen, and kidneys can result in centrilobular necrosis, thickening of alveolar septa, enlargement and fibrosis of the spleen, and mild changes to the kidneys respectively. Hem
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SHOCK - PATHOPHYSIOLOGY, TYPES, APPROACH, TREATMENT.
1. Shock is defined as a state of poor tissue perfusion and cellular metabolism due to circulatory failure and hypoperfusion.
2. The main causes of shock include hypovolemic, cardiogenic, septic, anaphylactic, neurogenic, and respiratory etiologies.
3. The pathophysiology of shock involves a low cardiac output state leading to vasoconstriction and redistribution of blood flow away from non-vital organs to preserve perfusion of vital organs. Persistent shock can progress to cellular damage, organ dysfunction, and death.
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Polycythemia
Polycythemia is a condition characterized by an abnormal increase in the red blood cell count. There are two types: relative polycythemia, caused by a decrease in plasma volume leading to a higher concentration of red blood cells; and absolute polycythemia, caused by overproduction of red blood cells in the bone marrow. Polycythemia vera is a specific myeloproliferative disorder and type of absolute polycythemia caused by a mutation in the JAK2 gene, leading to uncontrolled red blood cell production. Symptoms include headaches, dizziness, and blood flow issues from hyperviscosity. Treatment involves phlebotomy to reduce red blood cell counts and medications to control bone marrow
Anaemia pathology ppt
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Oedema new edited
Edema is an excessive accumulation of fluid in the interstitial spaces or body cavities. There are several types and causes of edema. Cardiac edema is caused by congestive heart failure which increases venous pressure and hydrostatic pressure, pulling fluid from blood vessels into tissues. Renal edema can be caused by nephritic syndrome which causes salt and water retention, or nephrotic syndrome which decreases plasma protein levels. Hepatic edema manifests as ascites and is caused by portal hypertension or low plasma proteins in conditions like liver cirrhosis. Pulmonary edema can result from left heart failure or inflammation while cerebral edema includes cytotoxic edema from cell injury or vesogenic edema from blood brain barrier disruption.
Anemia and types of Anemia Chapter 14 pdf JAPYEE, K Sembulingam
https://www.youtube.com/channel/UCrrAABI7QDRCJ1yMrQCip_w/videos
Anemia and types of Anemia Chapter 14 pdf JAPYEE, K Sembulingam
INTRODUCTION
CLASSIFICATION
SIGNS AND SYMPTOMS
CLASSIFICATION OF ANEMIA
Anemia is classified by two methods:
1. Morphological classification
2. Etiological classification.
Morphological classification of anemia
Normocytic normochromic
Normocytic hypochromic
Macrocytic hypochromic
Microcytic hypochromic
ETIOLOGICAL CLASSIFICATION
1. Hemorrhagic anemia
2. Hemolytic anemia
3. Nutrition deficiency anemia
4. Aplastic anemia
5. Anemia of chronic diseases.
SIGNS AND SYMPTOMS OF ANEMIA
Edema
CONTENTS:
GENERAL
NORMAL FLUID CIRCULATION
EDEMA- INTRODUCTION
CAUSES
CLASSIFICATION
MAJOR TYPES
NOTE- Fonts may appear weird because the original fonts are different from the ones visible here.
Edema
Edema is the accumulation of excessive body fluid in interstitial spaces or serous cavities due to diseases rather than being a disease itself. It can be classified based on its range (generalized vs local) or cause (renal, hepatic, cardiac, etc.). Edema develops due to an imbalance in fluid exchange between plasma and tissues or due to renal sodium and water retention. Causes include increased capillary pressure, decreased plasma proteins, obstructed lymphatics, increased capillary permeability, and renal issues. Edema fluid characteristics depend on capillary permeability and it can be pitting or recessive with distribution influenced by factors like gravity. Edema generally harms tissues but may help dilute toxins in
3 hemorrhage
This document discusses hemorrhage, or extravasation of blood due to rupture of blood vessels. Hemorrhage can occur through capillaries due to chronic congestion or hemorrhagic diatheses, or through rupture of a large artery or vein due to vascular injury, trauma, atherosclerosis, or neoplastic erosion of the vessel wall. Manifestations of hemorrhage depend on the size, extent, and location of bleeding and can include hematomas, petechiae, purpura, ecchymoses, and accumulations of blood in body cavities. The clinical significance of hemorrhage depends on the volume and rate of blood loss, with losses over 20% potentially resulting in hemorrh
Renovascular disorders
This document provides an overview of renovascular disorders (RVD), including:
1. RVD can be classified based on the anatomic location of vascular pathology in the renal arteries, arterioles/microvasculature, or veins.
2. Common causes of RVD include atherosclerotic renal artery stenosis (ARAS), fibromuscular dysplasia, thromboembolic occlusion, and atheroembolic disease.
3. Clinical manifestations of RVD vary and can include hypertension, renal failure, and flash pulmonary edema depending on the extent and timing of vascular occlusion.
4. Diagnosis involves imaging modalities like MRI, CT, ultrasound and angiography. Treatment may
nephritic and nephrotic syndrome
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
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Shock is a life-threatening condition defined by inadequate tissue perfusion and oxygen delivery. It can be caused by hypovolemia, cardiac dysfunction, or vasodilation. The main symptoms include low blood pressure, fast heart rate, fast breathing, and decreased urine output. Untreated shock can lead to organ failure and death. Treatment focuses on restoring circulating volume and oxygen delivery through fluid resuscitation, vasopressors, and treating the underlying cause. Prompt recognition and treatment are essential for recovery.
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Disseminated Intravascular Coagulation
DEFINITION
TYPES
PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS
DIFFERENTIAL DIAGNOSIS
DIAGNOSIS
TREATMENT
REFERENCES
HYPERAEMIA & CONGESTION
This document discusses chronic venous congestion (CVC) and its effects on various organs. It describes how CVC results in localized blood volume increase within dilated vessels. It then summarizes the gross and microscopic findings of CVC in the lungs, liver, spleen, and kidneys. The lungs show brown induration and thickened alveolar septa. The liver has a nutmeg appearance and centrilobular necrosis. The spleen exhibits congestion and fibrosis. The kidneys demonstrate mild degenerative changes. Hemorrhage and its causes, effects based on amount/speed of blood loss are also outlined.
Chronic pyelonephritis
Chronic pyelonephritis is a chronic inflammation of the renal tubules and interstitium that occurs due to recurrent urinary tract infections and scarring. It most commonly affects children with congenital anomalies or spinal cord injuries and is the leading cause of end-stage renal disease. It is typically caused by either chronic obstructive pyelonephritis due to obstruction of urine outflow, or reflux nephropathy caused by vesicoureteral reflux allowing urine to flow back into the kidneys. Symptoms may include fever, flank pain, and symptoms of chronic renal failure like hypertension. The condition can lead to complications like proteinuria, focal glomerulosclerosis, and papillary necrosis.
Edema
Edema is the abnormal accumulation of fluid in the interstitial spaces of tissues. It can occur locally or systemically. There are several mechanisms that can cause edema, including increased hydrostatic pressure, decreased plasma oncotic pressure, lymphatic obstruction, and sodium/water retention. Localized edema can be caused by inflammation, venous obstruction, or decreased plasma proteins. Systemic edema is often seen in conditions like congestive heart failure and nephrotic syndrome. Symptoms of edema include swelling, skin indentation, and weight gain.
AMYLOIDOSIS
This document provides an overview of amyloidosis, including:
- Amyloidosis is characterized by extracellular deposition of misfolded proteins that form insoluble fibrils, damaging tissues.
- There are different types classified by the misfolded protein involved, including AL, AA, and rare forms.
- Organs commonly affected include the kidney, heart, GI tract, and nerves.
- Diagnosis involves biopsy of affected tissues and staining with Congo red to identify amyloid deposits.
- Prognosis depends on type and organ involvement, with generalized amyloidosis having a poor prognosis of around 2 years.
Approach to edema
Edema is swelling caused by excess fluid trapped in your body's tissues. Although edema can affect any part of your body, you may notice it more in your hands, arms, feet, ankles and legs.
Edema can be the result of medication, pregnancy or an underlying disease — often congestive heart failure, kidney disease or cirrhosis of the liver.
Taking medication to remove excess fluid and reducing the amount of salt in your food often relieves edema. When edema is a sign of an underlying disease, the disease itself requires separate treatment.
Edema
The document discusses edema, which is an increase in fluid volume in body tissues. It notes that 75% of body weight is water, with 50% being intracellular volume, 20% interstitial volume, and 5% intravascular volume. Edema can be local, such as pulmonary or cerebral edema, or disseminated, involving an increase in interstitial fluid volume. The pathogenesis of edema involves capillary permeability, hydrostatic pressure, oncotic pressure, tissue resistance, lymphatic drainage, and renal/hormonal factors.
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Hypertension and kidney
This document summarizes hypertension and its relationship to the kidneys. It discusses how essential hypertension is mainly caused by abnormal sodium retention and genetic predisposition. It also notes that low birth weight can result in fewer nephrons and later hypertension. The kidneys play a key role in maintaining blood pressure through pressure natriuresis, which allows excess salt to be excreted by inhibiting reabsorption when blood pressure is high. For patients with essential hypertension, diuretics are often the first choice of treatment since salt retention is a major factor, but they can cause side effects like hyponatremia and gout. The document emphasizes monitoring blood pressure and kidney function for patients on antihypertensive medications.
SHOCK - PATHOPHYSIOLOGY, TYPES, APPROACH, TREATMENT.
1. Shock is defined as a state of poor tissue perfusion and cellular metabolism due to circulatory failure and hypoperfusion.
2. The main causes of shock include hypovolemic, cardiogenic, septic, anaphylactic, neurogenic, and respiratory etiologies.
3. The pathophysiology of shock involves a low cardiac output state leading to vasoconstriction and redistribution of blood flow away from non-vital organs to preserve perfusion of vital organs. Persistent shock can progress to cellular damage, organ dysfunction, and death.
Inflammation
Definition of inflammation, Causes, Signs of inflammation, Types of inflammation, Triple response, Phagocytosis, Transudate or Exudate, Difference between transudate and exudate, Granuloma and Granulomatous inflammation
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Polycythemia is a condition characterized by an abnormal increase in the red blood cell count. There are two types: relative polycythemia, caused by a decrease in plasma volume leading to a higher concentration of red blood cells; and absolute polycythemia, caused by overproduction of red blood cells in the bone marrow. Polycythemia vera is a specific myeloproliferative disorder and type of absolute polycythemia caused by a mutation in the JAK2 gene, leading to uncontrolled red blood cell production. Symptoms include headaches, dizziness, and blood flow issues from hyperviscosity. Treatment involves phlebotomy to reduce red blood cell counts and medications to control bone marrow
Anaemia pathology ppt
This document provides an overview of hematopoiesis, erythropoiesis, and anemia. It discusses where blood cell formation occurs, the lifespan and production rate of red blood cells, and how hypoxia stimulates erythropoietin production. It defines anemia, lists global and country prevalence data, and compensatory mechanisms. It describes classifications of anemia including morphological and etiological, and covers causes such as blood loss, bone marrow disorders, nutritional deficiencies, and hemolytic anemias. Laboratory evaluation of anemia and peripheral blood smear findings are also summarized.
Oedema new edited
Edema is an excessive accumulation of fluid in the interstitial spaces or body cavities. There are several types and causes of edema. Cardiac edema is caused by congestive heart failure which increases venous pressure and hydrostatic pressure, pulling fluid from blood vessels into tissues. Renal edema can be caused by nephritic syndrome which causes salt and water retention, or nephrotic syndrome which decreases plasma protein levels. Hepatic edema manifests as ascites and is caused by portal hypertension or low plasma proteins in conditions like liver cirrhosis. Pulmonary edema can result from left heart failure or inflammation while cerebral edema includes cytotoxic edema from cell injury or vesogenic edema from blood brain barrier disruption.
Anemia and types of Anemia Chapter 14 pdf JAPYEE, K Sembulingam
https://www.youtube.com/channel/UCrrAABI7QDRCJ1yMrQCip_w/videos
Anemia and types of Anemia Chapter 14 pdf JAPYEE, K Sembulingam
INTRODUCTION
CLASSIFICATION
SIGNS AND SYMPTOMS
CLASSIFICATION OF ANEMIA
Anemia is classified by two methods:
1. Morphological classification
2. Etiological classification.
Morphological classification of anemia
Normocytic normochromic
Normocytic hypochromic
Macrocytic hypochromic
Microcytic hypochromic
ETIOLOGICAL CLASSIFICATION
1. Hemorrhagic anemia
2. Hemolytic anemia
3. Nutrition deficiency anemia
4. Aplastic anemia
5. Anemia of chronic diseases.
SIGNS AND SYMPTOMS OF ANEMIA
Edema
CONTENTS:
GENERAL
NORMAL FLUID CIRCULATION
EDEMA- INTRODUCTION
CAUSES
CLASSIFICATION
MAJOR TYPES
NOTE- Fonts may appear weird because the original fonts are different from the ones visible here.
Edema
Edema is the accumulation of excessive body fluid in interstitial spaces or serous cavities due to diseases rather than being a disease itself. It can be classified based on its range (generalized vs local) or cause (renal, hepatic, cardiac, etc.). Edema develops due to an imbalance in fluid exchange between plasma and tissues or due to renal sodium and water retention. Causes include increased capillary pressure, decreased plasma proteins, obstructed lymphatics, increased capillary permeability, and renal issues. Edema fluid characteristics depend on capillary permeability and it can be pitting or recessive with distribution influenced by factors like gravity. Edema generally harms tissues but may help dilute toxins in
3 hemorrhage
This document discusses hemorrhage, or extravasation of blood due to rupture of blood vessels. Hemorrhage can occur through capillaries due to chronic congestion or hemorrhagic diatheses, or through rupture of a large artery or vein due to vascular injury, trauma, atherosclerosis, or neoplastic erosion of the vessel wall. Manifestations of hemorrhage depend on the size, extent, and location of bleeding and can include hematomas, petechiae, purpura, ecchymoses, and accumulations of blood in body cavities. The clinical significance of hemorrhage depends on the volume and rate of blood loss, with losses over 20% potentially resulting in hemorrh
Renovascular disorders
This document provides an overview of renovascular disorders (RVD), including:
1. RVD can be classified based on the anatomic location of vascular pathology in the renal arteries, arterioles/microvasculature, or veins.
2. Common causes of RVD include atherosclerotic renal artery stenosis (ARAS), fibromuscular dysplasia, thromboembolic occlusion, and atheroembolic disease.
3. Clinical manifestations of RVD vary and can include hypertension, renal failure, and flash pulmonary edema depending on the extent and timing of vascular occlusion.
4. Diagnosis involves imaging modalities like MRI, CT, ultrasound and angiography. Treatment may
nephritic and nephrotic syndrome
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
Types of Shock
Shock is a life-threatening condition defined by inadequate tissue perfusion and oxygen delivery. It can be caused by hypovolemia, cardiac dysfunction, or vasodilation. The main symptoms include low blood pressure, fast heart rate, fast breathing, and decreased urine output. Untreated shock can lead to organ failure and death. Treatment focuses on restoring circulating volume and oxygen delivery through fluid resuscitation, vasopressors, and treating the underlying cause. Prompt recognition and treatment are essential for recovery.
Coagulative Necrosis + Morphology
- Coagulative Necrosis / summarized
- Description of the GROSS appearance of Coagulative necrosis.
- Description of the MICROSCOPIC appearance of Coagulative necrosis.
Hemolytic anemia
This document discusses hemolytic anemia and focuses on sickle cell disease. It defines hemolytic anemia as increased destruction of red blood cells outside the bone marrow. Key diagnostic findings include increased reticulocyte count, hyperbilirubinemia, decreased haptoglobin, and increased lactate dehydrogenase. Hemolytic anemias are classified as hereditary defects within red blood cells or acquired external causes. Sickle cell disease results from a hereditary hemoglobinopathy and causes chronic hemolytic anemia. Complications include infections, acute chest syndrome, stroke, leg ulcers, splenic sequestration, and retinopathy. Diagnosis is made by finding sickle cells on peripheral smear and abnormal hem
Disseminated Intravascular Coagulation
DEFINITION
TYPES
PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS
DIFFERENTIAL DIAGNOSIS
DIAGNOSIS
TREATMENT
REFERENCES
HYPERAEMIA & CONGESTION
This document discusses chronic venous congestion (CVC) and its effects on various organs. It describes how CVC results in localized blood volume increase within dilated vessels. It then summarizes the gross and microscopic findings of CVC in the lungs, liver, spleen, and kidneys. The lungs show brown induration and thickened alveolar septa. The liver has a nutmeg appearance and centrilobular necrosis. The spleen exhibits congestion and fibrosis. The kidneys demonstrate mild degenerative changes. Hemorrhage and its causes, effects based on amount/speed of blood loss are also outlined.
Chronic pyelonephritis
Chronic pyelonephritis is a chronic inflammation of the renal tubules and interstitium that occurs due to recurrent urinary tract infections and scarring. It most commonly affects children with congenital anomalies or spinal cord injuries and is the leading cause of end-stage renal disease. It is typically caused by either chronic obstructive pyelonephritis due to obstruction of urine outflow, or reflux nephropathy caused by vesicoureteral reflux allowing urine to flow back into the kidneys. Symptoms may include fever, flank pain, and symptoms of chronic renal failure like hypertension. The condition can lead to complications like proteinuria, focal glomerulosclerosis, and papillary necrosis.
Edema
Edema is the abnormal accumulation of fluid in the interstitial spaces of tissues. It can occur locally or systemically. There are several mechanisms that can cause edema, including increased hydrostatic pressure, decreased plasma oncotic pressure, lymphatic obstruction, and sodium/water retention. Localized edema can be caused by inflammation, venous obstruction, or decreased plasma proteins. Systemic edema is often seen in conditions like congestive heart failure and nephrotic syndrome. Symptoms of edema include swelling, skin indentation, and weight gain.
AMYLOIDOSIS
This document provides an overview of amyloidosis, including:
- Amyloidosis is characterized by extracellular deposition of misfolded proteins that form insoluble fibrils, damaging tissues.
- There are different types classified by the misfolded protein involved, including AL, AA, and rare forms.
- Organs commonly affected include the kidney, heart, GI tract, and nerves.
- Diagnosis involves biopsy of affected tissues and staining with Congo red to identify amyloid deposits.
- Prognosis depends on type and organ involvement, with generalized amyloidosis having a poor prognosis of around 2 years.
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Anemia and types of Anemia Chapter 14 pdf JAPYEE, K Sembulingam
Anemia and types of Anemia Chapter 14 pdf JAPYEE, K Sembulingam
Similar to Edema
Approach to edema
Edema is swelling caused by excess fluid trapped in your body's tissues. Although edema can affect any part of your body, you may notice it more in your hands, arms, feet, ankles and legs.
Edema can be the result of medication, pregnancy or an underlying disease — often congestive heart failure, kidney disease or cirrhosis of the liver.
Taking medication to remove excess fluid and reducing the amount of salt in your food often relieves edema. When edema is a sign of an underlying disease, the disease itself requires separate treatment.
Edema
The document discusses edema, which is an increase in fluid volume in body tissues. It notes that 75% of body weight is water, with 50% being intracellular volume, 20% interstitial volume, and 5% intravascular volume. Edema can be local, such as pulmonary or cerebral edema, or disseminated, involving an increase in interstitial fluid volume. The pathogenesis of edema involves capillary permeability, hydrostatic pressure, oncotic pressure, tissue resistance, lymphatic drainage, and renal/hormonal factors.
Edema congestion 15th.pdf
Slide Note: Edema Congestion
Title: Edema Congestion: Understanding the Mechanisms and Clinical Implications
Introduction:
Edema congestion is a pathological condition characterized by the abnormal accumulation of fluid within tissues or body cavities, leading to swelling and impaired tissue function. It is a complex physiological process that can arise due to various underlying factors and may manifest in different regions of the body. Understanding the mechanisms and clinical implications of edema congestion is crucial for healthcare professionals to effectively diagnose, manage, and treat patients presenting with this condition.
I. Mechanisms of Edema Congestion:
A. Increased Capillary Hydrostatic Pressure:
- Elevated pressure within the capillaries due to factors such as venous obstruction, heart failure, or localized inflammation.
- Higher hydrostatic forces cause an excessive filtration of fluid from the capillaries into the interstitial spaces, contributing to tissue swelling.
B. Decreased Plasma Oncotic Pressure:
- Reduction in plasma protein levels, particularly albumin, results in decreased oncotic pressure.
- Lower oncotic pressure leads to reduced fluid reabsorption from the interstitial spaces back into the capillaries, exacerbating fluid accumulation.
C. Lymphatic Obstruction or Insufficiency:
- Impaired lymphatic drainage due to lymphatic vessel obstruction, surgical intervention, or congenital malformations.
- Inadequate lymphatic clearance results in the retention of interstitial fluid, leading to edema.
D. Sodium and Water Retention:
- Dysregulation of sodium and water balance in conditions like kidney dysfunction, cirrhosis, or hormonal imbalances.
- Sodium retention leads to increased osmotic pressure, causing water to accumulate in the interstitial spaces.
II. Clinical Implications:
A. Peripheral Edema:
- Swelling predominantly in the extremities, commonly observed in conditions such as heart failure, deep vein thrombosis, or venous insufficiency.
- Patients may experience discomfort, reduced mobility, and skin changes due to chronic edema.
B. Pulmonary Edema:
- Accumulation of fluid in the lungs, often resulting from heart failure, acute respiratory distress syndrome (ARDS), or pneumonia.
- Respiratory compromise, cough, and shortness of breath are common symptoms requiring urgent medical intervention.
C. Cerebral Edema:
- Swelling within the brain due to trauma, stroke, or tumors.
- Potentially life-threatening, as it can lead to increased intracranial pressure, neurological deficits, and herniation.
D. Ascites:
- Edema within the peritoneal cavity, commonly associated with liver cirrhosis, malignancies, or congestive heart failure.
- Abdominal distension, discomfort, and respiratory compromise are typical manifestations.
III. Diagnostic Approach:
A. Clinical Examination:
- Careful assessment of the patient's medical history, physical symptoms, and risk factors.
Edema
Edema is excess fluid in the interstitial compartment. It results from an imbalance between hydrostatic pressure pushing fluid into the interstitium, oncotic pressure pulling fluid back into blood vessels, and lymphatic drainage removing interstitial fluid. Common causes of edema include increased hydrostatic pressure from conditions like heart failure, decreased oncotic pressure from low albumin, and impaired lymphatic drainage or sodium retention. Edema can occur systemically or in body cavities and tissues, and causes symptoms depending on its location.
1 edema
The document discusses edema and fluid balance in the body. It describes the normal circulation of fluid between blood and tissues, mediated by hydrostatic and oncotic pressures. Edema occurs when there is increased hydrostatic pressure, decreased oncotic pressure, increased capillary permeability, or impaired lymphatic drainage. Specific types of edema discussed include cardiac, hepatic, pulmonary, cerebral, and lymphatic edema. Sites of common edema and clinical significance are also reviewed.
Patofisiologi edema
Oedema, or swelling, is caused by an abnormal accumulation of fluid in the interstitial tissue spaces. There are two main types - localized oedema affecting an organ or limb, and generalized oedema known as anasarca. The physiology of oedema involves a balance between hydrostatic pressure pushing fluid out of blood vessels and oncotic pressure pulling fluid back in. Disruptions to this balance that can cause oedema include decreased oncotic pressure, increased hydrostatic pressure, lymphatic obstruction, and increased capillary permeability. Common causes of oedema include cardiac, renal, and hepatic diseases.
Hemodynamics 1
This document summarizes hemodynamic disorders and edema. It defines edema as abnormal excessive accumulation of fluid in tissues and serous cavities. Edema can be localized or generalized depending on its cause and distribution. The key mechanisms of edema formation are increased hydrostatic pressure, decreased plasma oncotic pressure, lymphatic obstruction, and sodium and water retention. Specific types of edema like pulmonary edema, cerebral edema, hepatic edema, and renal edema are also discussed. The document compares the characteristics of transudate and exudate fluids and provides diagrams to illustrate the pathogenesis of different types of edema.
1. hemodynamic disorders edema, congestion.pptx
This document discusses various hemodynamic disturbances including congestion, hemorrhage, and edema. It defines these conditions and describes their morphological features. Congestion is a passive increase in blood volume due to impaired outflow, causing tissues to appear cyanotic or red-brown. Hemorrhage can be external or internal, and results from vessel rupture. Edema is the accumulation of fluid in interstitial spaces or cavities, and can be localized or generalized. It results from increased hydrostatic pressure, decreased oncotic pressure, lymphatic obstruction, sodium retention, or inflammation. The morphology of congestion, hemorrhage and edema in various organs is described.
Edema
Edema can be caused by increased hydrostatic pressure, decreased plasma oncotic pressure, or lymphatic obstruction. Increased hydrostatic pressure can result from heart failure, liver cirrhosis, or venous obstruction. Decreased plasma oncotic pressure occurs when albumin is lost, such as in nephrotic syndrome, or not produced sufficiently, as in liver disease or malnutrition. Lymphatic obstruction leads to localized edema and can be caused by infection, cancer, or surgery. Edema fluid accumulation in tissues can impair function and be life-threatening in the lungs or brain.
Haemorrhage & shock
This document provides an overview of hemorrhage (blood loss) including its definition, classification, pathophysiology, causes, clinical features, investigations, management in oral surgery, fluid resuscitation, and hemostasis. Hemorrhage is classified based on its source, time of occurrence, whether it is visible or not, and clinical signs. Mechanisms of hemostasis include vasoconstriction, platelet plug formation, and coagulation pathways. Methods to achieve hemostasis include mechanical, chemical, and thermal approaches. Proper fluid resuscitation and hemostasis are important for managing blood loss during and after oral surgery.
4. Hemodynamic disorders (Edema, Hemorrhage, thrombosis, embolism)(1).ppt
Hemodynamic disorders (Edema, Hemorrhage, thrombosis, embolism)
6.HEMODYNAMICS.pptx
1. Hemodynamic disorders include edema, hemostasis, thrombosis, embolism, and shock. Edema is excess fluid in tissues and can result from increased capillary pressure, decreased plasma proteins, lymphatic obstruction, sodium retention, or increased capillary permeability.
2. Hemostasis and thrombosis involve the vascular wall, platelets, and coagulation cascade. Thrombosis occurs when the clotting process is inappropriately activated, forming clots in uninjured vessels.
3. Embolism occurs when a detached mass such as a thrombus is carried by the bloodstream to obstruct vessels elsewhere. Pulmonary embolism is a common type that arises from deep vein
hemodynamics disorder pathophysiology .pptx
This document provides an overview of hemodynamics disorders and outlines various pathologies including edema, hyperemia, congestion, hemorrhage, hemostasis, thrombosis, embolism, and infarction. It discusses the normal balance of fluid movement across capillaries and how various pathologic conditions can disrupt this balance and cause edema. Key concepts covered include the Starling forces, categories of edema, factors influencing thrombosis, and the coagulation cascade. Morbidities associated with cardiovascular diseases are also briefly mentioned.
4.oedema,thrombosis,embolism
Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel or heart chamber. There are three main types of thrombi based on composition and location. Thrombosis occurs due to endothelial injury, abnormal blood flow, and hypercoagulability. Thrombi form at sites of injury or turbulence in arteries and heart chambers, and at sites of stasis in veins. Microscopically, thrombi appear laminated with alternating pale and dark layers. Thrombosis can occur in any blood vessel and lead to complications such as embolism if parts of the thrombus break off.
Edema pathogenesis,causes, approach.pptx
This document discusses edema, including its causes, pathophysiology, and clinical presentations. It defines edema as excess interstitial fluid clinically evident. Edema develops from a net movement of fluid from blood vessels to interstitial space due to increased hydrostatic pressure, impaired lymphatic drainage, decreased oncotic pressure, or capillary damage. Activation of the renin-angiotensin-aldosterone system and arginine vasopressin system can cause sodium and water retention leading to edema. Different diseases like heart failure, renal disease, and liver cirrhosis are discussed in relation to their pathophysiologic mechanisms of edema formation.
Oedema
This document discusses hemodynamic disorders and edema. It defines edema as an excessive accumulation of fluid in tissues or body cavities. Edema can occur when there is an increase in hydrostatic pressure, decrease in plasma osmotic pressure, lymphatic obstruction, or sodium and water retention. The document outlines Starling's forces that normally maintain fluid balance and describes how imbalances in these forces can lead to edema. Causes, clinical signs, pathology, and consequences of edema are also summarized.
6.HEMODYNAMICS.pptx
Edema, hemostasis, thrombosis, embolism, and shock are hemodynamic disorders that can occur due to issues with fluid distribution and blood flow regulation in the body. Edema is excess fluid in tissues, usually caused by increased capillary pressure, decreased plasma proteins, lymphatic obstruction, sodium retention, or increased capillary permeability. Thrombosis is the formation of clots in blood vessels due to endothelial injury, stasis or turbulence of blood flow, or hypercoagulability. Embolism occurs when a thrombus or other mass breaks off and is carried by the bloodstream, potentially blocking vessels. Shock is a state of circulatory failure causing inadequate cellular perfusion.
Pathophysiology of edema
This document discusses the pathophysiology of edema. It defines edema as swelling caused by excess fluid in the interstitial spaces between tissues. Edema can be classified as transudate or exudate based on protein content, and as localized or generalized based on location. The key mechanisms that can cause edema are increased hydrostatic pressure, reduced plasma oncotic pressure, lymphatic obstruction, and sodium and water retention. The movement of fluid between blood vessels and tissues is normally regulated by the balance of hydrostatic and oncotic pressures according to Starling's forces, but imbalances in these forces can result in excess fluid accumulation in the tissues and cause edema.
Circulatory disorders
This document discusses several circulatory disorders including hyperemia, congestion, hemorrhage, and thrombosis. Hyperemia and congestion both involve increased blood volume in tissues but have different mechanisms. Hyperemia is an active process of arteriolar dilation while congestion is a passive process resulting from impaired venous outflow. Hemorrhage is defined as blood escaping from vessels, and can be classified by site, size, vessel type, and timing relative to trauma. Thrombosis is the formation of blood clots and can result from endothelial injury, abnormal blood flow like stasis or turbulence, or a hypercoagulable state of the blood.
Similar to Edema (20)
4. Hemodynamic disorders (Edema, Hemorrhage, thrombosis, embolism)(1).ppt
4. Hemodynamic disorders (Edema, Hemorrhage, thrombosis, embolism)(1).ppt
Edema
- 1. 1 EDEMA
- 2. 2 75 % of total body weight is water - 50 % - Intracellular volume - 20 % - Interstitial volume - 5 % - Intravascular volume
- 3. 3 Increasing of fluid volume in tissues. -It is usually used to define the increasing of extracellular and extravascular fluid volume EDEMA
- 4. 4 EDEMA – Local (Pulmonary, cerebral, pharyngeal - Disseminated (Increasing of interstitial fluid volume)
- 5. 5 Intraperitoneal - Ascites Intrapleural - Hydrothorax
- 6. 6 PATHOGENESIS OF EDEMA 1) Capillary permeability 2) Hydrostatic pressure of intracapillary fluid 3) Oncotic pressure of intracapillary fluid 4) Oncotic pressure of interstitial fluid 5) Tissue resistance 6) Lymphatic drainnage 7) Renal hormonal factors 8) Atrial natriüretic peptide
- 7. 7 Capillary permeability Water, electrolytes,gases – Diffusion Proteins - Filtration Chemical, bacterial, thermal, mechanical factors may cause the increasing of permeability – inflamatory edema / angioedema
- 8. 8 Hydrostatic pressure: It forces the blood fluid pass into the tissues through the capillary wall. It is 32 mmHg at the arteriolar end of the capillary, and 12 mmHg at the venule hand.
- 9. 9 Oncotic pressure: Formed by plasma proteins (especially albumin) It tries to keep the fluid in the capillary The oncotic pressure of the capillary is 24 mmHg.
- 10. 10 Plasma protin content > İnterstitial protein content → Plasma oncotic pressure > ınterstitial oncotic pressre Effective oncotic pressure = Plasma oncotic pressure – Interstitium oncotic pressure Effective oncotic pressure decreases: - As the decreasing of plasma oncotic pressure ( cirrhosis, malnutrition, nephrotic syndrome, protein loosing ent.) - As the increasing of interstitium oncotic pressure (Increasing of permeability – inflamatory / allergy)
- 11. 11 Arteriolar end: Hydrostatic pressure > Oncotic pressure ⇒ Fluid passes into interstitium Venule end: Oncotic pressure > Hydrostatic pressure ⇒ Fluid returns capillary bed * The increase of pressure at the venule end ⇒Fluid cannot return capillary and stay at the interstitium
- 12. 12 Oncotic pressure of the interstitium: The amount of protein is nearly 0.3 % g / dl and it is not so important
- 13. 13 Lymph drainege: Some of the fluid in the interstitium and a few amount of protein diffused into interstitium is carried by lymph vessels. Obstruction of the vessels causes edema.
- 14. 14 RENAL HORMONAL MECHANISM Decreasing of stroke volume Increasing of ADH Decreasing of kidney blood perfusion Reabsorbtion of water Poor perfusion of juxta glomerular in tubules of kidneys aparatus Secretion of renin
- 15. 15 Renin Angiotensinogen Angiotensin I Converting enzyme Angiotensin II
- 16. 16 Angiotensin II: 1) Causes vasoconstriction 2) Increases the secretion of aldosteron from adrenal gland ( seconder hyperaldosteronism) – İncreases sodium reabsorbtion in distal tubules
- 17. 17 ATRIAL NATRURETIC PEPTIDE -Secreted by the secretory granules in the atrium -Secretion is stimulated by atrial enlargement ( plasma volume increases) -Increases diuresis and sodium output. -Causes vasodilatation -Inhibits renin and angiotensin release
- 19. 19 Disseminated Edema • Edema due to cardiac failure • Nephritic edema • Nephrotic edema • Edema caused by liver failure • Nutritional edema (inadequate intake) • Protein loss through gastrointestinal system • Edema due to endocrine pathologies • Edema during pregnancy
- 20. 20 Local edema - Traumatic - Inflammatory edema - Obstriction of venous circulation - Thrombophlebitis - Compression of veins -Lymphatic edema -Angioneurotic edema
- 21. 21 Cardiac Insufficiency - Blood volume per minute decreases ⇒ Water is conserved by renal and hormonal mechanisms - Hydrostatic pressure increases
- 22. 22 Nephritic Edema Mild and hard edema is seen in acute glomerulonephritis Glomerular filtration decreases, but tubular reabsorbtion is not disturbed. (glomerulotubular inbalance) Capillaritis (generalized capillary disorder)
- 23. 23 Nephrotic Edema -It is very soft and in anasarca type -Low oncotic pressure due to protein loss -Secondary hyperaldosteronism
- 24. 24 Cirrhotic Edema • It is usually seen with ascites • Albumin synthesis in liver decreases • Some blood proteins are excreted in feces due to portal hypertension • Aldosteron breakdown in liver decreases ; secretion by adrenal gland increases (secondary hyperaldosteronism)
- 25. 25 Nutritional edema • Kwashiworker • Malabsobtion Syndromes • Gastrectomy • Cancer
- 26. 26 Edema due to endocrine pathologies • Mixedema • Premenstrual edema • Pregnancy
- 27. 27 Iatrogenic Edema • Mineralocorticoid • Corticosteroid • Androgen • ADH
- 28. 28 Inflammatory Edema Due tu increased permeability - Microorganisms - Connective tissue disorders
- 29. 29 Venous Edema • Thrombophlebitis: Local inflamations cause thrombus ⇒ venous obstriction -Large and hard edema - Erythema, hotness,pain • Compression of veins -Ganglion, tumor,ascites • Edema related to varices High hydrostatic pressure in veins
- 30. 30 Lymphatic Edema • Due to obstruction of lymph vessels,plasma proteins cannot be taken from the interstitium
- 31. 31 Angioneurotic Edema (Quincke’s edema) Vessels insubcutaneous tissue enlarge due to local histamine discharge and extravasation from capillaries occurs -Food allergy -Drug allergy -Infections -Emotional
- 32. References • Anand IS et al: Studies of body water andsodium, renal function, , hemadynamic indexes, and plasma hormones in untreated congestive heart failure. Circulation 1989;80:299 • Abassi Z et al: Control of extracelluler fluid volume and the pathophysiology of edema formation . The kidney. 7th ed, BM Brenner (ed). Philedelphia, Saunders, 2004 ; pp777,856. • Braunwald E:Edema in the Harrison’s Principles of Internal Medicine, 16 th edition, Braunwald (ed). USA McGraw –Hill Companies,2005, pp212-216 • Braunwald E:Edema in the Harrison’s Principles of Internal Medicine, 14th edition, Braunwald (ed). USA McGraw –Hill Companies, 1998, pp210-214 • Chertow GM: Approach to the patient with edema . Cardiolgy for the Primary Care Phsician. Braunwald E,Goldman L (eds) 2nd ed, Philedelphia, Saunders, 2003, pp 117- 128. 32