This document discusses common pathologies of the kidney by describing four basic morphological components of the kidney (glomeruli, tubules, interstitium, blood vessels) and how diseases can affect each component. It then focuses on specific pathologies including glomerular diseases like acute proliferative glomerulonephritis, rapidly progressive glomerulonephritis, nephritic syndrome, nephrotic syndrome, and membranoproliferative glomerulonephritis. For each disease, it discusses pathogenesis, morphology under light microscopy, immunofluorescence, and electron microscopy.
Glomerular diseases are a heterogeneous group of kidney disorders that can be primary, secondary, or hereditary in nature. They involve pathological changes to the glomeruli, such as injury to the mesangial cells, endothelial cells, basement membrane, or podocytes. This can lead to clinical manifestations like proteinuria, hematuria, edema, hypertension, and renal failure. The mechanisms of glomerular injury are complex, often involving the immune system through immune complex deposition, complement activation, or cytotoxic antibodies. Glomerular diseases have diverse clinical presentations and outcomes depending on the specific cause and severity of involvement.
Glomerulonephritides are diseases of the glomeruli that constitute major problems in nephrology. The glomerulus consists of a network of capillaries surrounded by epithelial cells. Glomerular diseases can be primary or secondary to other systemic diseases. The pathogenesis involves immune mechanisms such as deposition of immune complexes or antibodies reacting with antigens in the glomerulus. This causes inflammation and injury through activation of complement and recruitment of leukocytes. Conditions like minimal-change disease and focal segmental glomerulosclerosis are common causes of nephrotic syndrome, characterized by massive proteinuria and edema.
Nodular glomerulosclerosis (GN) can be caused by long-standing diabetes mellitus, monoclonal immunoglobulin deposition disease, amyloidosis, or healed immune complex glomerulonephritides. Histologically, it is characterized by nodular mesangial expansion and thickening of peripheral capillary loops. Idiopathic nodular GN is a diagnosis of exclusion when no underlying cause is identified.
This document provides information on various glomerular diseases. It begins by defining glomerulonephritis as inflammation of the glomeruli. The main types of primary glomerular diseases discussed include minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy. For each disease, the document covers pathogenesis, morphology, and clinical manifestations. It provides detailed descriptions of the histologic alterations and immune mechanisms involved in the different glomerular diseases.
Glomerulus and nephrotic & nephritic syndromeessamramdan
This document provides an overview of kidney diseases focusing on glomerular diseases and nephrotic syndrome. It discusses the structure of the kidney and glomerulus. Glomerular diseases are often immunologically mediated involving circulating immune complexes or antibodies reacting within the glomerulus. Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Primary causes include minimal change disease, membranous glomerulonephritis, and focal segmental glomerulosclerosis. Minimal change disease appears normal by light microscopy but shows diffuse foot process effacement by electron microscopy. Membranous glomerulonephritis involves subepithelial immune deposits along the glo
This document discusses glomerular and cystic renal diseases. It begins with an overview of glomerular anatomy and mechanisms of glomerular injury, including immune complex deposition and various immune mechanisms that can cause damage. It then discusses specific diseases like minimal change disease, focal segmental glomerulosclerosis (FSGS), and membranous glomerulonephritis that present as nephrotic syndrome. For minimal change disease and FSGS, it provides the definitions, morphology, epidemiology, clinical characteristics, treatment and examples of case presentations. It emphasizes that minimal change disease appears normal by light microscopy but shows foot process effacement by electron microscopy, while FSGS shows segmental sclerosis of some glomeruli
Glomerulonephritis (GN) refers to a group of kidney diseases characterized by damage to the glomeruli. There are many potential causes of GN, including both immune-mediated mechanisms like deposition of immune complexes or antibodies, and non-immune factors like hypertension. This can lead to inflammation in the glomeruli and injury to the filtration barrier. Pathological features are classified based on patterns of involvement seen on biopsy. Treatment involves controlling risk factors like blood pressure and use of corticosteroids, immunosuppressants, or plasmapheresis depending on the underlying etiology and severity.
most of the glomerular diseases , either primary or secondary..touching all the aspects including light microscopy, electron microscopy and immunoflourescence.
Glomerular diseases are a heterogeneous group of kidney disorders that can be primary, secondary, or hereditary in nature. They involve pathological changes to the glomeruli, such as injury to the mesangial cells, endothelial cells, basement membrane, or podocytes. This can lead to clinical manifestations like proteinuria, hematuria, edema, hypertension, and renal failure. The mechanisms of glomerular injury are complex, often involving the immune system through immune complex deposition, complement activation, or cytotoxic antibodies. Glomerular diseases have diverse clinical presentations and outcomes depending on the specific cause and severity of involvement.
Glomerulonephritides are diseases of the glomeruli that constitute major problems in nephrology. The glomerulus consists of a network of capillaries surrounded by epithelial cells. Glomerular diseases can be primary or secondary to other systemic diseases. The pathogenesis involves immune mechanisms such as deposition of immune complexes or antibodies reacting with antigens in the glomerulus. This causes inflammation and injury through activation of complement and recruitment of leukocytes. Conditions like minimal-change disease and focal segmental glomerulosclerosis are common causes of nephrotic syndrome, characterized by massive proteinuria and edema.
Nodular glomerulosclerosis (GN) can be caused by long-standing diabetes mellitus, monoclonal immunoglobulin deposition disease, amyloidosis, or healed immune complex glomerulonephritides. Histologically, it is characterized by nodular mesangial expansion and thickening of peripheral capillary loops. Idiopathic nodular GN is a diagnosis of exclusion when no underlying cause is identified.
This document provides information on various glomerular diseases. It begins by defining glomerulonephritis as inflammation of the glomeruli. The main types of primary glomerular diseases discussed include minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy. For each disease, the document covers pathogenesis, morphology, and clinical manifestations. It provides detailed descriptions of the histologic alterations and immune mechanisms involved in the different glomerular diseases.
Glomerulus and nephrotic & nephritic syndromeessamramdan
This document provides an overview of kidney diseases focusing on glomerular diseases and nephrotic syndrome. It discusses the structure of the kidney and glomerulus. Glomerular diseases are often immunologically mediated involving circulating immune complexes or antibodies reacting within the glomerulus. Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Primary causes include minimal change disease, membranous glomerulonephritis, and focal segmental glomerulosclerosis. Minimal change disease appears normal by light microscopy but shows diffuse foot process effacement by electron microscopy. Membranous glomerulonephritis involves subepithelial immune deposits along the glo
This document discusses glomerular and cystic renal diseases. It begins with an overview of glomerular anatomy and mechanisms of glomerular injury, including immune complex deposition and various immune mechanisms that can cause damage. It then discusses specific diseases like minimal change disease, focal segmental glomerulosclerosis (FSGS), and membranous glomerulonephritis that present as nephrotic syndrome. For minimal change disease and FSGS, it provides the definitions, morphology, epidemiology, clinical characteristics, treatment and examples of case presentations. It emphasizes that minimal change disease appears normal by light microscopy but shows foot process effacement by electron microscopy, while FSGS shows segmental sclerosis of some glomeruli
Glomerulonephritis (GN) refers to a group of kidney diseases characterized by damage to the glomeruli. There are many potential causes of GN, including both immune-mediated mechanisms like deposition of immune complexes or antibodies, and non-immune factors like hypertension. This can lead to inflammation in the glomeruli and injury to the filtration barrier. Pathological features are classified based on patterns of involvement seen on biopsy. Treatment involves controlling risk factors like blood pressure and use of corticosteroids, immunosuppressants, or plasmapheresis depending on the underlying etiology and severity.
most of the glomerular diseases , either primary or secondary..touching all the aspects including light microscopy, electron microscopy and immunoflourescence.
- Systemic lupus erythematosus (SLE) is a multi-system autoimmune disease characterized by tissue damage from antibody and complement deposition, leading to periods of disease exacerbation and remission.
- It predominantly affects females of childbearing age and is more prevalent in non-whites. Major features include the presence of autoantibodies against nuclear and other antigens, immune complex deposition in organs like the kidney and skin, and depression of serum complement levels during disease flares.
- The disease has genetic, hormonal, and environmental risk factors and results from a loss of self-tolerance leading to hyperactive B and T cells that produce pathogenic autoantibodies against self-ant
This document outlines the objectives and content for two pathology lectures on renal glomerular syndromes including nephrotic syndrome and nephritic syndrome. The lectures will cover the clinical presentation and pathological findings of key renal diseases like minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, acute post-streptococcal glomerulonephritis, lupus nephritis, IgA nephropathy, and rapidly progressive glomerulonephritis. The lectures will discuss kidney biopsy techniques and the role of light microscopy, immunofluorescence and electron microscopy in the diagnosis of renal diseases. Key pathological mechanisms like the location of immune deposits and pathogenesis of glomerular
Approach to the patient with Glomerular Disease.Sufindc
The document discusses the approach to patients with glomerular disease. It describes the structure and function of the glomerulus and capillaries. Common causes of glomerular disease include genetic mutations, infections, autoimmunity, hypertension, and diabetes. Key clinical syndromes are nephritic syndrome, nephrotic syndrome, basement membrane syndrome, glomerular-vascular syndrome, and infectious disease-associated syndrome. The initial workup involves a history, physical exam, urinalysis, and blood tests to help classify the glomerular disease.
This document summarizes various types of renal failure including acute renal failure and chronic kidney disease. It discusses the etiology, pathogenesis and phases of acute tubular necrosis. It also covers chronic glomerulonephritis and specific conditions like membranous nephropathy, membranoproliferative glomerulonephritis, focal segmental glomerulosclerosis, IgA nephropathy, and diabetic nephropathy. The document provides details on urine analysis findings, histopathology techniques like immunofluorescence and electron microscopy in the evaluation of renal diseases.
The document discusses several glomerular diseases characterized by a mesangioproliferative pattern of injury including mesangial proliferative GN, lupus nephritis class II, IgA nephropathy, resolving post-infectious GN, fibrillary GN, immunotactoid glomerulopathy, early diabetic glomerulosclerosis, and minimal change disease. For each disease, the document describes histopathological findings on light microscopy, immunofluorescence, and electron microscopy.
This document discusses the immunological mechanism leading to glomerulonephritis, or inflammation of the glomeruli in the kidneys. It first defines glomerulonephritis and explains that it occurs when the glomeruli are damaged and unable to properly filter blood and remove excess fluids. It then describes how Type III hypersensitivity, or immune-complex mediated hypersensitivity, can cause membranous glomerulonephritis. In Type III reactions, antigen-antibody complexes are formed in the blood and deposited in tissues like the kidney glomeruli, activating the complement system and attracting neutrophils that cause tissue injury. Examples of diseases that can lead to glomerulonephritis this way include
Membranous glomerulopathy is a slowly progressive disease that most commonly affects people between 30-50 years old. It is the second most common cause of nephrotic syndrome in adults. There are primary and secondary types, with 85% being primary/idiopathic and the remainder being secondary to conditions like autoimmune diseases, infections, drugs, or tumors. It is caused by immune complex formation in the glomerulus resulting from antibodies binding to antigens in the glomerular basement membrane. On pathology, it shows diffuse thickening of the glomerular basement membrane. Treatment involves immunosuppressive drugs and anti-proteinuria measures, with prognosis being one-third spontaneous remission, one-third progression
This document discusses the histopathological features of several types of crescentic glomerulonephritis (GN), including anti-glomerular basement membrane (GBM) disease, pauci-immune GN, immune complex-mediated GN, lupus nephritis class IV, IgA nephropathy, and post infectious GN. Key findings include fibrinoid necrosis, crescent formation, immune complex deposition patterns on immunofluorescence, and electron-dense deposits, effacement of foot processes, and basement membrane abnormalities on electron microscopy. The diseases are distinguished by their pathogenic mechanisms and specific immune staining and ultrastructural characteristics.
Membranous GN
MOST COMMON cause is idiopathic (85%); peak age 30-50; male:female, 2:1
May be secondary to:
Drugs-captopril, penicillamine, gold, mercury, trimethadione, NSAIDS
Infections-malaria (P. malariae), leprosy, schistosomiasis, syphilis, hepatitis B and C, filariasis, hydatid disease and enterococcal endocarditis
Diseases-malignancy (Carcinoma of breast, lung, colon, stomach, and esophagus) melanoma, renal cell CA, SLE, sarcoidosis, diabetes, thyroiditis, sickle cell anemia, Crohn’s disease
Glomerulonephritis is inflammation of the glomeruli in the kidney. It can be caused by inherited factors, immune system attacks, metabolic issues, or abnormal protein deposition. There are several classifications based on histopathology and presentations. Nephrotic syndrome involves injury to the podocytes and features massive proteinuria. Minimal change disease is a common cause in children characterized by podocyte foot process effacement. Focal segmental glomerulosclerosis often presents in adults with nephrotic syndrome. Membranous nephropathy can be primary or secondary to other conditions. Nephritic syndrome typically involves hematuria and modest proteinuria with preserved kidney function. Immunoglobulin A nephropathy and
The document discusses glomerulonephritis, which refers to diseases of the glomeruli in the kidneys mediated by immune mechanisms. It can present as either a nephritic or nephrotic syndrome. Nephritic syndrome is characterized by hematuria, hypertension, and variable proteinuria, while nephrotic syndrome presents with massive proteinuria (>3.5 g/day), edema, hyperlipidemia, and sometimes a hypercoagulable state. The pathogenesis involves immune complex deposition or T-cell mediated responses targeting antigens in the glomerular basement membrane or mesangium. Treatment aims to control symptoms and slow disease progression using immunosuppressants or ACE inhibitors depending on the specific type
lectureoncellinjury and adaptation-170214073507.pptxvandana thakur
This document discusses cell injury and cellular adaptation. It begins by defining cell injury and discussing its causes, including hypoxia, physical and chemical agents, and infections. It then covers the pathogenesis and outcomes of cell injury, including reversible and irreversible injury. It also discusses the types of cellular adaptation to injury, including atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia. The document concludes by comparing the morphologies of reversible and irreversible injury, such as necrosis, apoptosis, and calcification.
Nephrotic syndrome is a kidney disorder characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is mostly seen in children and is usually caused by minimal change disease or focal segmental glomerulosclerosis. Treatment involves corticosteroids, which are effective in resolving symptoms in 80% of children. Relapses are common and managed with additional courses of steroids. The document provides details on the definition, causes, pathology, clinical manifestations, investigations, and management of nephrotic syndrome.
This is about glomerulonephritis and all that you need to know. It contains different images illustrating this subject matter, well defined outline, different aspect of glomerulonephritis, which include acute and chronic glomerulonephritis, nephritic and nephrotic syndrome, investigations, how to diagnose glomerulonephritis, treatment and important discussions on Glomerulonephritidis. It is a presentation you need to check out.
This document provides an overview of cell injury and cellular adaptation. It discusses the various causes of cell injury including hypoxia, infections, physical and chemical insults. The pathogenesis and morphological changes associated with reversible and irreversible cell injury are described. Cellular responses and adaptations to injury like atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia are also covered. The key morphological features of necrosis and apoptosis are highlighted.
references
20th edition of Harrison's T.B. OF INTERNAL MEDICINE
Blood and Lymphatic Cancer: Targets and Therapy
Advances in the diagnosis and management
of lymphoma
Zachary H Word1
Matthew J Matasar1,2
This document provides information on cell injury and cellular adaptation. It discusses the causes of cell injury including hypoxia, infections, physical and chemical insults. The pathogenesis and outcomes of cell injury are described, including reversible and irreversible injury. Cellular responses like atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia are defined. The morphology of reversible and irreversible injury is outlined, focusing on changes seen in necrosis and apoptosis.
Glomerulonephritis refers to inflammation of the glomeruli in the kidney. It can be caused by various factors like infections, autoimmune diseases, or genetic conditions. Patients may experience symptoms like blood or protein in the urine. Diagnosis involves urinalysis, kidney biopsy, and tests for antibodies. Treatment depends on the underlying cause and severity of symptoms, but often includes medications to reduce inflammation and protect kidney function. The prognosis can range from spontaneous remission to progressive kidney damage and failure.
Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis characterized by thickening of the glomerular basement membrane, proliferation of mesangial cells and capillary loops, and activation of the complement system. There are two main types - type I is caused by immune complex deposition and type II (dense deposit disease) results from abnormal alternative complement pathway regulation leading to dense material deposition in the glomerular basement membrane. MPGN follows a progressive clinical course and can lead to end stage renal disease within 10 years if left untreated. Treatment aims to slow disease progression and control symptoms.
1. Leukemia is the unregulated proliferation of leukocytes in the bone marrow, leaving little room for normal cell production. It can vary in duration from weeks to years depending on type.
2. The main types are acute myeloid leukemia, acute lymphoblastic leukemia, chronic myeloid leukemia, and chronic lymphocytic leukemia. Acute leukemias involve more primitive cells and rapid progression while chronic leukemias involve more mature cells and slower progression.
3. Treatment involves chemotherapy in remission induction, consolidation, and maintenance phases to destroy the leukemic cells while preserving normal stem cells. The goal is to reduce blast cells to less than 5% in the bone marrow. Allogenic bone marrow
Rumaiya, a 10-month-old girl, presented with not growing well, leg swelling, fever, and diarrhea. She had severe malnutrition with pneumonia and dehydration. Her management included rehydration, broad-spectrum antibiotics, vitamin and mineral supplements, specialized formula feeding, and counseling parents on proper care and feeding. She was to be followed up closely to monitor her recovery.
This document summarizes a clinical meeting discussing a 3-month-old male patient, Ayan, who presented with jaundice, pale stool, and dark urine since 20 days of life. On examination, he was mildly pale and icteric with hepatomegaly but no other abnormalities. Investigations showed evidence of cholestasis. Ultrasound found an enlarged liver without a visualized gallbladder. Liver biopsy was compatible with biliary atresia. The final diagnosis was neonatal cholestasis due to biliary atresia. The treatment plan involved supportive care, ursodeoxycholic acid, phenobarbital, fat-soluble vitamin supplementation, and consideration of Kasai operation or liver
- Systemic lupus erythematosus (SLE) is a multi-system autoimmune disease characterized by tissue damage from antibody and complement deposition, leading to periods of disease exacerbation and remission.
- It predominantly affects females of childbearing age and is more prevalent in non-whites. Major features include the presence of autoantibodies against nuclear and other antigens, immune complex deposition in organs like the kidney and skin, and depression of serum complement levels during disease flares.
- The disease has genetic, hormonal, and environmental risk factors and results from a loss of self-tolerance leading to hyperactive B and T cells that produce pathogenic autoantibodies against self-ant
This document outlines the objectives and content for two pathology lectures on renal glomerular syndromes including nephrotic syndrome and nephritic syndrome. The lectures will cover the clinical presentation and pathological findings of key renal diseases like minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, acute post-streptococcal glomerulonephritis, lupus nephritis, IgA nephropathy, and rapidly progressive glomerulonephritis. The lectures will discuss kidney biopsy techniques and the role of light microscopy, immunofluorescence and electron microscopy in the diagnosis of renal diseases. Key pathological mechanisms like the location of immune deposits and pathogenesis of glomerular
Approach to the patient with Glomerular Disease.Sufindc
The document discusses the approach to patients with glomerular disease. It describes the structure and function of the glomerulus and capillaries. Common causes of glomerular disease include genetic mutations, infections, autoimmunity, hypertension, and diabetes. Key clinical syndromes are nephritic syndrome, nephrotic syndrome, basement membrane syndrome, glomerular-vascular syndrome, and infectious disease-associated syndrome. The initial workup involves a history, physical exam, urinalysis, and blood tests to help classify the glomerular disease.
This document summarizes various types of renal failure including acute renal failure and chronic kidney disease. It discusses the etiology, pathogenesis and phases of acute tubular necrosis. It also covers chronic glomerulonephritis and specific conditions like membranous nephropathy, membranoproliferative glomerulonephritis, focal segmental glomerulosclerosis, IgA nephropathy, and diabetic nephropathy. The document provides details on urine analysis findings, histopathology techniques like immunofluorescence and electron microscopy in the evaluation of renal diseases.
The document discusses several glomerular diseases characterized by a mesangioproliferative pattern of injury including mesangial proliferative GN, lupus nephritis class II, IgA nephropathy, resolving post-infectious GN, fibrillary GN, immunotactoid glomerulopathy, early diabetic glomerulosclerosis, and minimal change disease. For each disease, the document describes histopathological findings on light microscopy, immunofluorescence, and electron microscopy.
This document discusses the immunological mechanism leading to glomerulonephritis, or inflammation of the glomeruli in the kidneys. It first defines glomerulonephritis and explains that it occurs when the glomeruli are damaged and unable to properly filter blood and remove excess fluids. It then describes how Type III hypersensitivity, or immune-complex mediated hypersensitivity, can cause membranous glomerulonephritis. In Type III reactions, antigen-antibody complexes are formed in the blood and deposited in tissues like the kidney glomeruli, activating the complement system and attracting neutrophils that cause tissue injury. Examples of diseases that can lead to glomerulonephritis this way include
Membranous glomerulopathy is a slowly progressive disease that most commonly affects people between 30-50 years old. It is the second most common cause of nephrotic syndrome in adults. There are primary and secondary types, with 85% being primary/idiopathic and the remainder being secondary to conditions like autoimmune diseases, infections, drugs, or tumors. It is caused by immune complex formation in the glomerulus resulting from antibodies binding to antigens in the glomerular basement membrane. On pathology, it shows diffuse thickening of the glomerular basement membrane. Treatment involves immunosuppressive drugs and anti-proteinuria measures, with prognosis being one-third spontaneous remission, one-third progression
This document discusses the histopathological features of several types of crescentic glomerulonephritis (GN), including anti-glomerular basement membrane (GBM) disease, pauci-immune GN, immune complex-mediated GN, lupus nephritis class IV, IgA nephropathy, and post infectious GN. Key findings include fibrinoid necrosis, crescent formation, immune complex deposition patterns on immunofluorescence, and electron-dense deposits, effacement of foot processes, and basement membrane abnormalities on electron microscopy. The diseases are distinguished by their pathogenic mechanisms and specific immune staining and ultrastructural characteristics.
Membranous GN
MOST COMMON cause is idiopathic (85%); peak age 30-50; male:female, 2:1
May be secondary to:
Drugs-captopril, penicillamine, gold, mercury, trimethadione, NSAIDS
Infections-malaria (P. malariae), leprosy, schistosomiasis, syphilis, hepatitis B and C, filariasis, hydatid disease and enterococcal endocarditis
Diseases-malignancy (Carcinoma of breast, lung, colon, stomach, and esophagus) melanoma, renal cell CA, SLE, sarcoidosis, diabetes, thyroiditis, sickle cell anemia, Crohn’s disease
Glomerulonephritis is inflammation of the glomeruli in the kidney. It can be caused by inherited factors, immune system attacks, metabolic issues, or abnormal protein deposition. There are several classifications based on histopathology and presentations. Nephrotic syndrome involves injury to the podocytes and features massive proteinuria. Minimal change disease is a common cause in children characterized by podocyte foot process effacement. Focal segmental glomerulosclerosis often presents in adults with nephrotic syndrome. Membranous nephropathy can be primary or secondary to other conditions. Nephritic syndrome typically involves hematuria and modest proteinuria with preserved kidney function. Immunoglobulin A nephropathy and
The document discusses glomerulonephritis, which refers to diseases of the glomeruli in the kidneys mediated by immune mechanisms. It can present as either a nephritic or nephrotic syndrome. Nephritic syndrome is characterized by hematuria, hypertension, and variable proteinuria, while nephrotic syndrome presents with massive proteinuria (>3.5 g/day), edema, hyperlipidemia, and sometimes a hypercoagulable state. The pathogenesis involves immune complex deposition or T-cell mediated responses targeting antigens in the glomerular basement membrane or mesangium. Treatment aims to control symptoms and slow disease progression using immunosuppressants or ACE inhibitors depending on the specific type
lectureoncellinjury and adaptation-170214073507.pptxvandana thakur
This document discusses cell injury and cellular adaptation. It begins by defining cell injury and discussing its causes, including hypoxia, physical and chemical agents, and infections. It then covers the pathogenesis and outcomes of cell injury, including reversible and irreversible injury. It also discusses the types of cellular adaptation to injury, including atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia. The document concludes by comparing the morphologies of reversible and irreversible injury, such as necrosis, apoptosis, and calcification.
Nephrotic syndrome is a kidney disorder characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is mostly seen in children and is usually caused by minimal change disease or focal segmental glomerulosclerosis. Treatment involves corticosteroids, which are effective in resolving symptoms in 80% of children. Relapses are common and managed with additional courses of steroids. The document provides details on the definition, causes, pathology, clinical manifestations, investigations, and management of nephrotic syndrome.
This is about glomerulonephritis and all that you need to know. It contains different images illustrating this subject matter, well defined outline, different aspect of glomerulonephritis, which include acute and chronic glomerulonephritis, nephritic and nephrotic syndrome, investigations, how to diagnose glomerulonephritis, treatment and important discussions on Glomerulonephritidis. It is a presentation you need to check out.
This document provides an overview of cell injury and cellular adaptation. It discusses the various causes of cell injury including hypoxia, infections, physical and chemical insults. The pathogenesis and morphological changes associated with reversible and irreversible cell injury are described. Cellular responses and adaptations to injury like atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia are also covered. The key morphological features of necrosis and apoptosis are highlighted.
references
20th edition of Harrison's T.B. OF INTERNAL MEDICINE
Blood and Lymphatic Cancer: Targets and Therapy
Advances in the diagnosis and management
of lymphoma
Zachary H Word1
Matthew J Matasar1,2
This document provides information on cell injury and cellular adaptation. It discusses the causes of cell injury including hypoxia, infections, physical and chemical insults. The pathogenesis and outcomes of cell injury are described, including reversible and irreversible injury. Cellular responses like atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia are defined. The morphology of reversible and irreversible injury is outlined, focusing on changes seen in necrosis and apoptosis.
Glomerulonephritis refers to inflammation of the glomeruli in the kidney. It can be caused by various factors like infections, autoimmune diseases, or genetic conditions. Patients may experience symptoms like blood or protein in the urine. Diagnosis involves urinalysis, kidney biopsy, and tests for antibodies. Treatment depends on the underlying cause and severity of symptoms, but often includes medications to reduce inflammation and protect kidney function. The prognosis can range from spontaneous remission to progressive kidney damage and failure.
Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis characterized by thickening of the glomerular basement membrane, proliferation of mesangial cells and capillary loops, and activation of the complement system. There are two main types - type I is caused by immune complex deposition and type II (dense deposit disease) results from abnormal alternative complement pathway regulation leading to dense material deposition in the glomerular basement membrane. MPGN follows a progressive clinical course and can lead to end stage renal disease within 10 years if left untreated. Treatment aims to slow disease progression and control symptoms.
1. Leukemia is the unregulated proliferation of leukocytes in the bone marrow, leaving little room for normal cell production. It can vary in duration from weeks to years depending on type.
2. The main types are acute myeloid leukemia, acute lymphoblastic leukemia, chronic myeloid leukemia, and chronic lymphocytic leukemia. Acute leukemias involve more primitive cells and rapid progression while chronic leukemias involve more mature cells and slower progression.
3. Treatment involves chemotherapy in remission induction, consolidation, and maintenance phases to destroy the leukemic cells while preserving normal stem cells. The goal is to reduce blast cells to less than 5% in the bone marrow. Allogenic bone marrow
Rumaiya, a 10-month-old girl, presented with not growing well, leg swelling, fever, and diarrhea. She had severe malnutrition with pneumonia and dehydration. Her management included rehydration, broad-spectrum antibiotics, vitamin and mineral supplements, specialized formula feeding, and counseling parents on proper care and feeding. She was to be followed up closely to monitor her recovery.
This document summarizes a clinical meeting discussing a 3-month-old male patient, Ayan, who presented with jaundice, pale stool, and dark urine since 20 days of life. On examination, he was mildly pale and icteric with hepatomegaly but no other abnormalities. Investigations showed evidence of cholestasis. Ultrasound found an enlarged liver without a visualized gallbladder. Liver biopsy was compatible with biliary atresia. The final diagnosis was neonatal cholestasis due to biliary atresia. The treatment plan involved supportive care, ursodeoxycholic acid, phenobarbital, fat-soluble vitamin supplementation, and consideration of Kasai operation or liver
This study aimed to evaluate myocardial injury in children with unoperated congenital heart diseases using cardiac troponin I levels. The study found an 80% incidence of elevated cTnI levels in children with CHDs, indicating a high prevalence of myocardial injury. Univariate analysis revealed significant correlations between higher cTnI levels and hemodynamic factors like higher pulmonary to systemic blood flow and pressure ratios. The study concludes that cTnI is a useful marker for detecting myocardial injury in children with unoperated CHDs.
This document provides details from a clinical meeting regarding a patient named Rafin. Rafin is a 4 year old male who has been experiencing seizures since age 1. He also has delays in development including lack of neck control or ability to sit. The document describes Rafin's history, examination, assessments, diagnoses of spastic quadriplegic cerebral palsy with microcephaly and global developmental delays, and proposed management including nutrition, medications, therapies and follow up.
The document provides information on a continuing medical education session on childhood immunization, including the presenters and topics to be covered such as the history of vaccination, types of vaccines and vaccination, immunization schedules in Bangladesh, vaccine-preventable diseases under surveillance, and addressing issues like dropouts and those left out of vaccination programs.
This document summarizes a study comparing clinical features of infants with biliary atresia who were cytomegalovirus immunoglobulin M positive versus negative. The study found no significant differences in clinical presentation, lab values, or liver histology between the two groups. Of the 43 infants studied, 20 (42%) were CMV IgM positive. The study concludes that CMV does not appear to be a direct cause of biliary atresia based on the lack of differences observed between the CMV positive and negative groups.
This document provides guidelines for assessing and treating dehydration in infants and children. It defines mild, moderate and severe dehydration based on clinical signs. It provides formulas for calculating fluid and electrolyte deficits and replacements based on the degree and type of dehydration (isonatremic, hyponatremic or hypernatremic). Examples are given for calculating maintenance and replacement fluids and electrolytes over 24-48 hours depending on the scenario. The document emphasizes slow correction of sodium levels to avoid complications.
This document provides information about renal biopsy procedures and pathological interpretation of renal biopsy specimens. It discusses the history and indications for renal biopsy. It describes the procedure, including contraindications, complications, and post-biopsy care. It explains how biopsies are evaluated with light microscopy, immunofluorescence, and electron microscopy. Key terms used to describe histological lesions in the glomeruli, tubules, interstitium, and blood vessels are defined. The document emphasizes the importance of integrating clinical and pathological findings for an accurate diagnosis.
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
Assessment and Planning in Educational technology.pptxKavitha Krishnan
In an education system, it is understood that assessment is only for the students, but on the other hand, the Assessment of teachers is also an important aspect of the education system that ensures teachers are providing high-quality instruction to students. The assessment process can be used to provide feedback and support for professional development, to inform decisions about teacher retention or promotion, or to evaluate teacher effectiveness for accountability purposes.
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
The simplified electron and muon model, Oscillating Spacetime: The Foundation...RitikBhardwaj56
Discover the Simplified Electron and Muon Model: A New Wave-Based Approach to Understanding Particles delves into a groundbreaking theory that presents electrons and muons as rotating soliton waves within oscillating spacetime. Geared towards students, researchers, and science buffs, this book breaks down complex ideas into simple explanations. It covers topics such as electron waves, temporal dynamics, and the implications of this model on particle physics. With clear illustrations and easy-to-follow explanations, readers will gain a new outlook on the universe's fundamental nature.
2. Introductions
Kidney diseases can be described by dividing them into
four basic morphological components.
1.Glomeruli.
2.Tubules.
3.Interstitium.
4.Blood vessels.
3. Most glomerular diseases are immunologically mediated, on the other
hand tubular and interstitial disorders are frequently caused by toxic or
infectious agents.
Primary disorders of the blood vessels inevitably affects all the
structure supplied by these vessels.
In chronic kidney disease all four basic components are damaged
ultimately.
4. Pathologic Responses of the Glomerulus to Injury
Various types of glomerulopathies are characterized by one or more of
four basic tissue reactions:
i. Hypercellularity
ii. Basement Membrane Thickening
iii. Hyalinosis
iv. Sclerosis
5. Hypercellularity
Some inflammatory diseases of the
glomerulus are characterized by an increase in
the number of cells in the glomerular tufts.
This hypercellularity results from one or more
of the following:
1.Proliferation of mesangial or endothelial
cells.
2. Infiltration of leukocytes.
3. Formation of crescents.
6. 1. Proliferation of mesangial or endothelial cells and Infiltration of
leukocytes includes
• Neutrophils
• Monocytes and
• In some diseases, lymphocytes.
The combination of infiltration of leukocytes and swelling and proliferation
of mesangial and/or endothelial cells is often referred to as endocapillary
proliferation
7. 3. Formation of crescents
• These are accumulations of cells composed of proliferating glomerular
epithelial cells (predominately parietal but including some visceral cells)
and infiltrating leukocytes.
• The epithelial cell proliferation that characterizes crescent formation
occurs following an immune/inflammatory injury involving the capillary
walls.
• Plasma proteins leak into the urinary space, where it is believed that
exposure to pro-coagulants such as tissue factor leads to fibrin deposition
include multiple proinflammatory cytokines.
8. • Activation of coagulation factors such as thrombin is suspected of being
a trigger for crescent formation, but the actual mechanisms are still
unknown.
• Molecules that have been implicated in recruitment of leukocytes into
crescents.
10. II- Basement Membrane Thickening:
• By light microscopy, this change appears as thickening of the capillary
walls, best seen in sections stained with periodic acid-Schiff (PAS).
• By electron microscopy , such thickening takes one of three forms:
• 1. Deposition of amorphous electron-dense material, most often immune
complexes on the
Endothelial side of the basement membrane or
Epithelial side of the basement membrane or
Within the basement membrane (GBM) itself.
11. 2. Fibrin, amyloid, cryoglobulins, and abnormal fibrillary proteins may also
deposit in the GBM.
3. Increased synthesis of the protein components of the basement occurs in
diabetic glomerulosclerosis.
4. Formation of additional layers of basement membrane matrices, which
most often occupy subendothelial locations and may range from poorly
organized matrix to fully duplicated lamina densa, as occurs in
Membranoproliferative glomerulonephritis.
13. Hyalinosis
• Hyalinosis denotes the accumulation of material that is homogeneous
and eosinophilic by light microscopy.
• Hyaline is an extracellular, amorphous material composed of plasma
proteins that have insudated from the circulation into glomerular
structures.
• When extensive, these deposits may obliterate the capillary lumens of the
glomerular tuft.
14. • Hyalinosis is usually a consequence of endothelial or capillary wall
injury and typically the end result of various forms of glomerular
damage.
• Sclerosis: It is characterized by deposition of extracellular collagenous
matrix and may be confined to mesangial areas.
15. Mediators of glomerular injury
• The mediators both cells & molecules are the usual suspects involved in
acute & chronic inflammation.
Cells:
1.Neutrophils & monocytes infiltrate the glomerulus in certain types of
glomerulonephritis.
2.Macrophage & T lymphocytes, which infiltrate the glomerulous in
antibody & cell mediated reactions.
3.Platelet may aggregate in the glomerulous during immune mediated
injury.
16. 4. Resident glomerular cells, particularly mesangial cells, can be
stimulated to produce several inflammatory mediators including reactive
oxygen species, cytokines, chemokines, growth factors, NO,endothelin.
Soluble mediators
1. Complement activation leads to the generation of chemotactic products
& formation of C5b-C9(the membrane attack complex). C5b-C9 causes
cell lysis & also stimulates mesangial cells to produce oxidant, protease &
other mediator.
17. 2.Eicosanoids,NO,angiotensin & endothelin are involved in the
hemodynamic changes.
3.Cytokine mainly IL-1 & TNF also cause glomerular injury.
4.Coagulation system is also a mediator of glomerular damage.
18. Immune mechanism of glomerular injury:
Antibody mediated injury.
In situ immune complex deposition
1. Fixed intensive tissue antigen
2. Planted antigen: May be exogenous & endogeneous.
Circulating immune complex deposition: May be endogeneous &
exogeneous.
Cell mediated immune injury.
Activation of alternative complement pathway.
24. Tubular and Interstitial Disease
• Acute Kidney injury (Acute Tubular Necrosis)
• Tubulo Interstitial Nephritis-
Pyelonephritis and Urinary Tract Infection
Acute Pyelonephritis
Chronic pyelonephritis and reflex nephropathy
25. Vascular Diseases:
• Benign Nephrosclerosis
• Malignant Hypertension and Accelerated
Nephrosclerosis
• Renal Artery Stenosis
• Thrombotic Microangiopathies and Other vascular
Disorder
26. Cystic Disease of Kidney:
• AD (Adult) polycystic Kidney disease
• AR (Childhood) Polycystic Kidney disease
• Cystic diseases of Renal Medula
Medulary Sponge Kidney
and Medulary Cystic Disease
• Acquired (Dialysis Associated) Cystic disease
• Simple Cysts
27. Tumors of the Kidney
• Benign tumors
Renal Papillary Adenoma
Angiomyolipoma
Oncocytoma
• Malignant Tumors
Renal cell carcinoma(AdenoCarcinoma)
Urothelial Carcinomas of the renal pelvis
28. Nephritic Syndrome
• It is characterized by inflammation of glomeruli.
Acute Proliferative(Post streptococcal) glomerulonephritis: It
usually appears 1 to 4 weeks after a streptococcal infection of
the pharynx(1-2weeks) or skin(3 to 4 weeks).It is caused by
nephritogenic strains of group A B-hemolytic streptococci; M
protein,strains 1, 4,12,25 & 49 are the most common.
29. Glomerular injury in PSGN result from deposition of immune complexes
in the glomerular capillaries. These immune complexes result in
activation of complement, infiltration of neutrophils, proliferation of
glomerular cells & expansion of mesangial matrix.
Molecular mimicry between streptococcal antigens & normal glomerular
antigens that reacts with antibodies against streptococcal antigens.
30. Morphology:
Light microscope: Enlarged hypercellular glomeruli is caused by
1.Infiltration by leukocytes- both neutrophil and monocyte.
2. Proliferation of endothelial and mesangial cell
3. In severe cases crescent formation
Immunofluorescence microscopy: Granular deposition of IgG,C3 and
occasionally IgM in the mesangium and along the GBM.It may be focal or
diffuse.
31. • Electron microscopic findings: Discrete, amorphous, electron
dense deposit on the epithelial side of the membrane(like
humps).Subendothelial deposits are also commonly seen,
typically early in the disease course.
33. Rapidly Progressive (Crescentic) Glomerulonephritis
• It is a syndrome associated with severe glomerular injury but does not
denote a specific etiologic from of GN.
• Pathogenesis: Although no single mechanism can explain all cases but in
most cases the glomerular injury is immunologically mediated.
• Several distinct pathogenic mechanisms describe below:
• 1.Anti-GBM antibody mediated disease-characterized by linear deposits
of IgG &,in many cases C3 in the GBM.
34. • 2.Diseases caused by immune complex deposition.RPGN can be a
complication of any of the immune complex nephritis,including;
PIGN,lupus nephritis,IgA nephropathy & HSP.
• 3.Pauci-immune RPGN-defined by the lack of detectable anti-GBM
antibodies or immune complexes by immunefluorescence & electron
microscopy.Most patients with this type of RPGN have circulating
antineutrophil cytoplasmic antibodies(ANCAs) that produce cytoplasmic
or perinuclear staining pattern & are known to play a role in some
vasculitis.
35. • Morphology: The kidneys are enlarged and pale, often with petechial
hemorrhage on the cortical surface.
• Light microscope: 1. Glomeruli often so focal and segmental necrosis and
show diffuse or focal endothelial and mesangial proliferation.
2. Crescents are formed by proliferation of parietal cells
and migration of monocytes and macrophage into the urinary space.
Neutrophil and lymphocyte may be present.
3. Fibrin strands are frequently prominent between the
cellular layer in the crescents.
36. Immunofluorescence microscopy:
Granular immune deposit, in case of Goodpasture syndrome- linear
GBM fluorescence for Ig and complement.
In pauci immune cases Little or no deposition of immune reactant.
Electron microscopic findings: show rupture in GBM, that allows
leukocytes, plasma protein. Coagulation factor , complement to reach the
urinary space, where they trigger crescent formation.
37. Nephrotic Syndrome:
• Caused by a derangement in glomerular capillary wall resulting in
increased permeability to plasma protein. The manifestation of the
syndrome include-massive proteinuria, hypoabuminemia, generalized
edema & hyperlipidemia.
• Causes of nephrotic syndrome:
• Primary glomerular diseases
• Minimal change disease.
• Membranous nephropathy
• Focal segmental glomerulosclorosis
• Membranoproliferative glomerulonephritis & dense deposit disease
• Others proliferative glomerulonephritides.
39. Minimal change disease:
• This relatively benign disorder is characterized by diffuse effacement of
foot processes of visceral epithelial cells(podocytes),detectable only by
electron microscopy, in glomeruli that appear virtually normal by light
microscopy.
It is most frequent cause of NS.
• Pathogenesis:
The absence of immune deposit of glomerulus exclude classic immune
complex mechanism.
According to current hypothesis it involves some immune dysfunction
that results damage visceral epithelial cells & causes proteinuria.
40. Morphology:
Light microscope:
Glomeruli are normal
Immunofluorescence microscopy:
Show no Ig or complement deposit.
Electron microscopic findings: The GBM appears normal and no
electron dense material deposited. The principal lesion is the visceral
epithelial cells which show a uniform and diffuse effacement of foot
processes.
42. Membranous Nephropathy
• Membranous nephropathy is characterized by diffuse thickening of the
glomerular capillary wall due to the accumulation of deposits containing Ig
along the subepithelial side of the basement membrane. .
• 75% of cases are primary. The remaining cases occur in association with
other diseases referred to as secondary.
• The most notable of these associations are-
1.Drugs-Penicillamine,gold,captopril,NSAID.
2.Malignant tumour-Carcinoma of colon & lungs, melanoma.
3.SLE-
4.Infections-Hepatitis-B,C,Syphilis,Malaria.
.
43. • Pathogenesis: It is a form of chronic immune complex mediated disease.
Primary membranous nephropathy ,thought to be of unknown cause. It is
now considered to be an autoimmune disease linked to certain HLA
alleles such as HLA DQA1 & caused in most cases by antibodies to a
renal autoantigen.
44. Morphology:
Light microscope: The glomeruli either appear normal in the early stages of
the disease or exhibit uniform, diffuse thickening of the glomerular capillary
wall.
Immunofluorescence microscopy: Granular deposits contain both
immunoglobulin and complement. As the disease progresses segmental
sclerosis may occur.
Electron microscopic findings: Irregular electron dense thickening is
seen.Deposit containing immune complex between the GBM and the
overlying epithelial cells, with effacement of podocyte foot processes. These
appear as irregular spike protruding from the GBM.
45. Focal Segmental Glomerulosclerosis:
• It is the common cause of nephrotic syndrome in adults.
• Pathogenesis: The characteristic degeneration & focal disruption of
visceral cells with effacement of foot processes. Epithelial damage is the
hallmark of FSGS. Different mechanisms are responsible for such
epithelial damage including circulating factors and genetically determined
defects affecting components of the slit diaphragm complex.
The first relevant gene NPHS1 maps to chromosome 19q13 & encode the
protein nephrin.
A distinctive pattern of autosomal recessive FSGS result from mutation in
the gene NPHS2 maps to chromosome 1q25-q31.
46. Morphology
Light microscope:
1. Focal & segmental lesions may involve only a minority of the
glomeruli.
2.In the sclerotic segment there is collapse of capillary loops, increase in
matrix & segmental deposition of plasma protein along the capillary wall.
Lipid droplets & foam cells are often present.
Immunofluorescence microscopy:Ig M & C3 may be present in the
sclerotic areas & in the mesangium. In addition pronounced hyalinosis &
thickening of afferent arterioles may be found. In time it leads to total
sclerosis of glomeruli with tubular atrophy & interstitial fibrosis.
Electron microscopy: Both sclerotic & nonsclerotic areas show diffuse
effacement of foot processes & may also be focal detachment of epithelial
cells & denudation of the underlying GBM.
47. Membranoproliferative Glomerulonephritis:
• It is considered a pattern of immune mediated injury rather than a specific
disease.
• MPGN into two groups-
• 1.Type-I:deposition of immune complexes containing IgG & complement.
2.Type-II:Dense deposit disease,in which excessive activation of alternative
complement pathway. Decrease serum C3 but normal C1 & C4.
• Pathogenesis:
There is evidence of immune complexes in the glomerulus & activation of
both classical & alternative complement pathway.The antigen involved in
idiopathic MPGN are unknown.In many cases they are belived to be protein
derived from infectious agent such as Hepatitis B,C virus.
48. Morphology
Light microscopy:
The glomeruli are large & hypercellular. Lobular appearance of glomeruli is
due to the proliferating mesangial cells & increased mesagial matrix.
The GBM is thickened & shows a double contour or tram-track appearance
due to duplication of GBM.
Electron microscopy:
In type I MPGN , discrete subendothelial electron dense deposit are present.
In type II ,lamina densa of the GBM is transform into a irregular ribbon like
homogeneous extremely electron dense material of unknown compostion.
Immunofluorescence:
Ig G & C3 are deposited in a granular pattern & early complement
component(C1q & C4 ) are often present.
49.
50. IgA nephropathy(Berger Dz):
It is characterized by the presence of prominent Ig A deposit in the
mesangium. It is the most common type of glomerulonephropathies
worldwide.
• Pathogenesis:
It is a hereditary or acquired defect in the normal formation or attachment
of galactose containing sugar chain to the hinge region of the IgA molecule.
The glomerular deposit consist predominantly IgA molecule with
aberrant glycosylation. The deposited IgA & IgA immune complexes
activate mesangial cell to proliferate, increase amount of ECM & secrete
numerous cytokines & growth factor.
These causes,inflammation of glomeruli & activation of complement
pathway. Hence the presence of C3 & the absence of C1q & C4 in glomeruli
are typical of this disorder.
51. Morphology
Light microscope:
The glomeruli may be normal or may show mesengial widening due to
cell proliferation ,accumulation of matrix or immune- deposit &
endocapillary proliferation, segmental proliferation.
Immunofluorescence:
Mesangial deposition of IgA with C3 & properdin & lesser amount of
IgG & IgM.
Electron microscope :
Electron dense deposit predominantly in the mesangium & sparse
capillary wall deposit may be found.
52. Hereditary Nephritis
• It refers to a group of heterogeneous familial renal diseases associated
with mutations in collagen genes that manifest primarly with glomerular
injury.
• Alport syndrome:
When it is fully developed is manifested by hematuria with progression
to CRF ,accompanied by nerve deafness & eye disorders.
• Pathogenesis :
The disease manifestations are due to mutation in one of several
genes coding for subunit of the collagen IV molecules, which resulting
in defective assembly of type IV collagen which is crucial for the
function of GBM ,lens of eye & cochlea.
53. Morphology:
Electron microscope:
The GBM shows irregular foci of thickening alternating with
attenuation & splitting & lamination of the lamina densa which produce
basket-weave appearance.
Immunofluorescence:
Absent or borderline basement membrane lesion due to antibodies to
α3,4 & 5 collagen fail to stain.
54. Chronic Glomerulonephritis:
• Chronic GN refers to end stage glomerular disease that may result from
specific types of GN or may develop from without antecedent history of any
of the well recognized forms of acute GN.
• Morphology:
The kidneys are symmetrically contracted and have diffusely granular
cortical surface.
On section:
The cortex is thinned & increase in pelvic fat.
The glomerular histology depends on the stage of the disease. In early
stage the glomeruli show evidence of primary disease.
Eventually causes obliteration of glomeruli, increase mesagial matrix,
arterial & arteriolar sclorosis may be conspicuous.
55. Acute Tubular Injury/Necrosis:
• It is a clinicopathologic entity characterized clinically by acute renal
failure & often, but not invariably, morphologic evidence of tubular injury,
in the form of necrosis of tubular epithelial cell.
• Pathogenesis: The critical events in both ischemic & nephrotoxic .ATI are
believed to be.
1.Tubular cell injury:
Tubular epithelial cells are sensitive to ischemia & are also vulnerable to
toxin. Ischemia causes structural & functional alteration in epithelial cells,
resulting in abnormal ion transport across the cell.
2.Disturbence in blood flow.
56. Morphology:
It is characterized by focal tubular epithelial
necrosis at multiple point along the nephron with large skip areas
in between often accompanied by rupture of basement membrane
& occlusion of tubular lumens by casts.
57. Pyelonephritis:
Morphology:
Acute pyelonephritis:
The hallmark of acute pylonephritis are patchy interstitial suppurative
inflammation, intratubular aggregates of neutrophils, neutrophilic tubulitis
& tubular necrosis. The suppuration may occur as discrete focal abscesses
or large wedge like areas & can involve one or both kidneys.
Chronic pyelonephritis:
The hallmark of chronic pyelonephritis are course discrete
corticomedullary scar overlying dilated, blunted or deformed calyces &
flattening of papillae.
58. • It is one of the most common diseases of the kidney & is defined as
inflammation affecting the tubules, interstitium & renal pelvis.
• Pathogenesis:
Acute pylonephritis is generally caused by bacterial infection &
associated with UTI. Mostly caused by the Gm (-) bacilli that are normal
inhabitants of the intestinal tract.
The microbes move from the bladder to the kidneys by following
mechanisms-
1. Urinary tract obstruction & stasis of urine
2. Vesicoureteral reflux.
3. Intrarenal reflux.
60. Autosomal Recessive (Childhood) polycystic kidney Disease:
• Autosomal recessive (childhood) polycystic kidney disease is genetically
distinct from adult polycystic kidney disease.
Perinatal, neonatal, infantile & juvenile subcategories have been defined,
depending on the time of presentation & presence of associated hepatic lesions.
• Genetics & pathogenesis:
In most cases, the disease is caused by mutations of the PKHD1 gene,
which maps to chromosome region 6p21-p23.The PKHD1 gene encodes
fibrocystin.
61. Morphology:
The kidneys are enlarged & have a smooth external appearance.
On cut section:
Numerous small cysts in the cortex & medulla give the kidney a sponge
like appearance. Dilated elongated channels are present at right angle to
the cortical surface, completely replacing the medulla & cortex.
On microscopic examination:
There is cylindrical or sacular dilatation of all collecting tubules.The
cyst have a uniform lining of cuboidal cells.
62. Autosomal dominant(Adult) polycystic kidney
Disease
• Autosomal dominant(adult) polycystic kidney disease is a hereditary
disorder characterized by multiple expanding cyst on both kidneys that
ultimately destroy the renal parenchyma & cause renal failure.
• Genetics:
A wide range of different mutations occur in the PKD1 & PKD2 genes. The
PKD1 gene is located on chromosome 16p13.3.It encode large integral
membrane protein named polycystin1.
The PKD2 gene located on chromosome 4q21 & encode polycystin 2.
• Pathogenesis:
The pathogenesis of disease is not established, but currently favored
hypothesis places the cilia chromosome complex of tubular epithelial cells at
the center of the disorder .
63. Morphology:
The kidneys are bilaterally enlarged & enormous sizes.
On microscopic examination:
Functioning nephrons are dispersed between the cyst.
The cyst may be filled with a clear serous fluid or with turbid, red to
brown, sometimes hemorrhagic.
Occasionally, papillary epithelial formations & polyps project into
the lumen.
65. Renal Artery Stenosis:
• Unilateral renal stenosis is responsible for 2% to 5% of hypertension.
• Pathogenesis:
HTN secondary to renal artery stenosis is caused by increased production of
renin from the ischemic kidney.
The most common cause of renal artery stenosis is narrowing at the region of
the renal artery by an atheromatous plaque. This occurs more frequently in men,
& the increases with advancing age & DM.
• Morphology:
There is fibromascular dysplasia of the renal artery. Fibromascular thickening
that may involve the intima, the media, or the adventitia.
The ischemic kidney is reduced in size & shows signs of diffuse ischemic
atrophy ,with crowded glomeruli, atrophic tubules, interstitial fibrosis & focal
inflammatory infiltrates.
66. Neoplasm of the kidney:
• Both benign & malignant neoplasms occur in the kidney. Malignant
neoplasms are of great importance clinically. The most common malignant
tumor is renal cell carcinoma, followed by Wilms tumor which is found in
children.
• Morphology:
Renal cell carcinomas may arise any portion or the kidney, but more
commonly affect the pole. Clear cell carcinoma mostly arise from proximal
tubular epithelium.
They are bright yellow gray white spherical mass that distort the renal
outline. There are large areas of gray-white necrosis & foci of hemorrhagic
discoloration.
67. The growth patterns varies from solid to trabecular or tubular.
Papillary carcinoma composed of cuboidal or low columnar
cells arranged in papillary formations. Interstitial foam cells are
common in the papillary cores. Psammoma bodies may be
present.
69. Bladder Neoplasm
Bladder cancer accounts for approximately 7% of cancers.
Pathogenesis: Several acquired genetic alterarions have been observed in
urothelial carcinoma,many of which lead to constitutive activation of growth
receptor signaling casecade.
Morphology: The appearance of urothelial tumors varies from papillary to
nodular or flat.
Papillary carcinoma 1.Low grade papillary carcinoma: The cells are evenly
spaced(i.e maintain polarity) & cohesive.There is mild degree of nuclear
atypia consisting of scattered hyperchromatic nuclei,infrequent mitotic
figure predominantly toward the base.
70. • 2.High grade papillary carcinoma: Contain dyscohesive cells with large
hyperchromatic nuclei.Some of the cells are highly anaplastic.Atypical
mitotic figure are frequent.Architecturally,there is disarray & loss of
polarity.
• 3.Carcinoma insitu(flat urothelial carcinoma):Presence of cytologically
malignant cells within a flat urothelium.
71.
72. Cystitis
• The common etiologic agents of cystitis are the coliforms or
example.E.coli,proteus enterobacter. Womens are more likely to develop
cystitis as a result of their shorter urethra. Tuberculous cystitis is almost
always a sequel to renal TB.
• Morphology: Most cases of cystitis produce nonspecific acute or
chronic inflammation of the bladder.
• In acute cystitis: There is hyperemia of the mucosa & neutrophilic
infiltrate,sometimes associated with exudate.
• In chronic cystitis : Mononuclear cells are infiltrated.