Let's learn the pharmacology related to nephrotic syndrome - features of nephrotic syndrome with underlying mechanisms, objectives of treatment, and management of the nephrotic syndrome.
This document discusses chronic kidney disease (CKD) in pediatrics. It defines CKD as kidney damage lasting at least 3 months as determined by structural abnormalities and/or a glomerular filtration rate below 60 mL/min/1.73m2. The stages of CKD are described based on GFR. Common causes in children include congenital abnormalities and glomerulonephritis. The pathogenesis involves hyperfiltration injury and other factors like proteinuria that accelerate kidney damage. Management aims to address complications through careful monitoring, nutrition, treatment of mineral bone disorders, and controlling blood pressure and electrolyte abnormalities.
Inroduction
Nephrotic syndrome is one of the bcommon cause of hospitalization among children.
Incidence of the condition is 2 to7 per1000.
It is more common in male child.
Mean age of occurrence is 2 to 5 years.
It is a symptom complex manifested by massive oedema, hypoalbuminemia, marked albuminuria and hyperlipidemia
Classification
Congenital nephrotic syndrome
Idiopathic or primary nephrotic syndrome
Secondary nephrotic syndrome
Congenital nephrotic syndrome
It is rare but serious and fatal problem usually associated with other congenital abnormalities of kidney.
It is inherited as autosomal recessive disease.
Severe renal insufficiency and urinary infections along with this condition result is poor prognosis.
Idiopathic or primary nephrotic syndrome
It is the most common type(about 90%) and regarded as autoimmune phenomenon as it responds to immunosuppressive therapy.
Subgroup of this type◦ Minimal change nephrotic syndrome(85%)◦ Proliferative nephrotic syndrome(5%)◦ Focal sclerosis nephrotic syndrome(10%)
Nephrotic syndrome may be caused by primary (idiopathic) renal disease or by a variety of secondary causes. Patients present with marked edema, proteinuria, hypoalbuminemia, and often hyperlipidemia.
Nephrotic syndrome is a primary glomerular disease characterized by the following:
Marked increase in protein in the urine (proteinuria)
Decrease in albumin in the blood (hypoalbuminemia)
Edema (The swelling (edema), can be most noticeable on the face, around the eyes, around the feet and ankles, and in the belly area (or the abdomen).
High serum cholesterol and low-density lipoproteins (hyperlipidemia)
Nephrotic syndrome is a clinical disorder characterized by marked increase of protein in the urine ( proteinuria ), decrease in albumin in the blood (hypoalbuminemia ),edema, & excess lipids in the blood ( hyperlipidemia )
Pathophysiology
Nephrotic syndrome can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus.
Although generally considered a disorder of childhood, nephrotic syndrome does occur in adults, including the elderly. Causes include:
Chronic glomerulonephritis
Diabetes mellitus with intercapillary glomerulosclerosis
Amyloidosis of the kidney
Systemic lupus erythematosus
Multiple myeloma and renal vein thrombosis.
NSAIDs
Pre eclampsia
Nephrotic syndrome is defined by nephrotic range proteinuria, edema, hyperlipidemia, and hypoalbuminemia. It results from increased glomerular permeability allowing protein loss in the urine. The most common causes are minimal change disease in children and membranous nephropathy in adults. Treatment involves diuretics, albumin, steroids, and steroid-sparing immunosuppressants depending on disease severity and steroid responsiveness. Prognosis is generally good but depends on underlying pathology.
This document provides information on rapidly progressive glomerulonephritis (RPGN), including definitions, classifications, pathogenesis, clinical features, pathology, treatment, and epidemiology of the main types. It discusses anti-glomerular basement membrane glomerulonephritis, immune complex-mediated RPGN, and pauci-immune RPGN. The pathology and clinical presentation of each type is described. Treatment typically involves immunosuppression with corticosteroids and cyclophosphamide along with plasmapheresis in severe cases.
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
1. Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. The majority of cases in children are idiopathic or minimal change disease.
2. Secondary causes include systemic diseases, infections, medications, and genetic conditions.
3. Treatment involves corticosteroids as first line, with recurrence being common in minimal change disease. Kidney biopsy may be needed to identify secondary causes or steroid resistance.
This document discusses chronic kidney disease (CKD) in pediatrics. It defines CKD as kidney damage lasting at least 3 months as determined by structural abnormalities and/or a glomerular filtration rate below 60 mL/min/1.73m2. The stages of CKD are described based on GFR. Common causes in children include congenital abnormalities and glomerulonephritis. The pathogenesis involves hyperfiltration injury and other factors like proteinuria that accelerate kidney damage. Management aims to address complications through careful monitoring, nutrition, treatment of mineral bone disorders, and controlling blood pressure and electrolyte abnormalities.
Inroduction
Nephrotic syndrome is one of the bcommon cause of hospitalization among children.
Incidence of the condition is 2 to7 per1000.
It is more common in male child.
Mean age of occurrence is 2 to 5 years.
It is a symptom complex manifested by massive oedema, hypoalbuminemia, marked albuminuria and hyperlipidemia
Classification
Congenital nephrotic syndrome
Idiopathic or primary nephrotic syndrome
Secondary nephrotic syndrome
Congenital nephrotic syndrome
It is rare but serious and fatal problem usually associated with other congenital abnormalities of kidney.
It is inherited as autosomal recessive disease.
Severe renal insufficiency and urinary infections along with this condition result is poor prognosis.
Idiopathic or primary nephrotic syndrome
It is the most common type(about 90%) and regarded as autoimmune phenomenon as it responds to immunosuppressive therapy.
Subgroup of this type◦ Minimal change nephrotic syndrome(85%)◦ Proliferative nephrotic syndrome(5%)◦ Focal sclerosis nephrotic syndrome(10%)
Nephrotic syndrome may be caused by primary (idiopathic) renal disease or by a variety of secondary causes. Patients present with marked edema, proteinuria, hypoalbuminemia, and often hyperlipidemia.
Nephrotic syndrome is a primary glomerular disease characterized by the following:
Marked increase in protein in the urine (proteinuria)
Decrease in albumin in the blood (hypoalbuminemia)
Edema (The swelling (edema), can be most noticeable on the face, around the eyes, around the feet and ankles, and in the belly area (or the abdomen).
High serum cholesterol and low-density lipoproteins (hyperlipidemia)
Nephrotic syndrome is a clinical disorder characterized by marked increase of protein in the urine ( proteinuria ), decrease in albumin in the blood (hypoalbuminemia ),edema, & excess lipids in the blood ( hyperlipidemia )
Pathophysiology
Nephrotic syndrome can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus.
Although generally considered a disorder of childhood, nephrotic syndrome does occur in adults, including the elderly. Causes include:
Chronic glomerulonephritis
Diabetes mellitus with intercapillary glomerulosclerosis
Amyloidosis of the kidney
Systemic lupus erythematosus
Multiple myeloma and renal vein thrombosis.
NSAIDs
Pre eclampsia
Nephrotic syndrome is defined by nephrotic range proteinuria, edema, hyperlipidemia, and hypoalbuminemia. It results from increased glomerular permeability allowing protein loss in the urine. The most common causes are minimal change disease in children and membranous nephropathy in adults. Treatment involves diuretics, albumin, steroids, and steroid-sparing immunosuppressants depending on disease severity and steroid responsiveness. Prognosis is generally good but depends on underlying pathology.
This document provides information on rapidly progressive glomerulonephritis (RPGN), including definitions, classifications, pathogenesis, clinical features, pathology, treatment, and epidemiology of the main types. It discusses anti-glomerular basement membrane glomerulonephritis, immune complex-mediated RPGN, and pauci-immune RPGN. The pathology and clinical presentation of each type is described. Treatment typically involves immunosuppression with corticosteroids and cyclophosphamide along with plasmapheresis in severe cases.
Management Of Nephrotic Syndrome
Objectives
To briefly review the definition & etiology of nephroticsyndrome.
To understand the terminology pertaining to clinical course of nephroticsyndrome.
To understand the management of nephroticsyndrome:Specific management & Supportive care and management of complications
Management of congenital nephrotic syndrome
1. Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. The majority of cases in children are idiopathic or minimal change disease.
2. Secondary causes include systemic diseases, infections, medications, and genetic conditions.
3. Treatment involves corticosteroids as first line, with recurrence being common in minimal change disease. Kidney biopsy may be needed to identify secondary causes or steroid resistance.
This document discusses acute nephritic syndrome, specifically acute post-streptococcal glomerulonephritis (PSGN). It notes that PSGN classically presents after a streptococcal throat or skin infection with hematuria, proteinuria, hypertension, and edema. Investigations may show elevated anti-streptococcal antibodies. On biopsy, there is diffuse mesangial proliferation with immune complex deposition. Management involves controlling symptoms while the infection resolves spontaneously in 6-8 weeks. Complications include hypertension, renal failure, and rarely chronic kidney disease.
This document discusses nephrotic syndrome, which is characterized by proteinuria, hypoalbuminemia, and edema. It defines nephrotic syndrome and outlines its causes, which include genetic, secondary, and idiopathic factors. The pathophysiology involves disturbances in the immune system and mutations affecting glomerular filtration. Clinical features and laboratory findings are provided for different types. Management involves treating symptoms, infections, and relapses with corticosteroids and immunosuppressants. Complications include edema, infections, thrombosis, and renal failure. Prognosis depends on response to steroids, with minimal change disease having a good prognosis and focal segmental glomerulosclerosis having poorer outcomes.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be primary, caused by diseases of the kidney itself, or secondary, caused by systemic illnesses that affect the kidneys. The most common primary causes are minimal-change disease in children and membranous glomerulonephritis in adults. Secondary causes include diabetes, lupus, and infections. Treatment involves controlling edema with diuretics, treating underlying conditions, and using steroids, immunosuppressants, or ACE inhibitors depending on disease type and severity.
Nephrotic syndrome is characterized by nephrotic range proteinuria, hypoalbuminemia, hyperlipidemia, and edema. It can be primary, caused by diseases limited to the kidney, or secondary, caused by diseases involving other organ systems. Primary causes include minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Management involves treating any underlying causes, controlling edema and hyperlipidemia, and using corticosteroids or other immunosuppressive drugs to induce remission in frequent relapsers or steroid-dependent patients.
This document defines acute kidney injury (AKI), formerly known as acute renal failure (ARF), and discusses its causes, diagnosis, and management. AKI is defined based on increases in serum creatinine and decreases in urine output. The main causes of AKI are pre-renal (decreased renal blood flow), renal (intrinsic kidney injury), and post-renal (urinary tract obstruction). Common etiologies include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis. Diagnosis involves laboratory and imaging tests. Management focuses on treating the underlying cause, fluid management, and potentially renal replacement therapy. Prognosis depends on the severity and reversibility of the kidney injury
The document discusses different types of kidney diseases and disorders:
- It describes the normal anatomy and histology of the kidney, including structures like the glomerulus.
- Nephrotic syndrome is discussed, which is characterized by proteinuria and low albumin levels, causing fluid retention and edema. Investigations include urine tests and kidney biopsies.
- Different glomerular diseases are described based on their pathology, including membranous glomerulonephritis, minimal change disease, focal segmental glomerulosclerosis (FSGS), and membranoproliferative glomerulonephritis. Their features on light microscopy, immunofluorescence and electron microscopy are provided.
- IgA nep
Pediatric urinary tract infections (UTIs) are common in children, especially girls under the age of 1. Left untreated, UTIs can cause renal scarring and long-term kidney damage. Diagnosis involves urine tests to check for white blood cells and bacteria. Treatment depends on symptoms and severity but often involves antibiotics and hydration. Follow up is important to monitor for recurrent UTIs and issues like vesicoureteral reflux, as both increase risk of permanent kidney damage if not addressed.
This document discusses glomerular disease and glomerulonephritis. It begins by defining glomerular disease and glomerulonephritis, noting that glomerulonephritis is a type of glomerular disease involving inflammation of the glomeruli. It then discusses the main clinical presentations of glomerular disease, including nephrotic syndrome, acute glomerulonephritis, and asymptomatic urinary abnormalities. The causes, symptoms, investigations, and management of various glomerular diseases are subsequently outlined. Throughout, examples are provided of specific diseases like post-streptococcal glomerulonephritis, membranous nephropathy, and crescentic glomerulone
Acute kidney injury (AKI), formerly known as acute renal failure, is defined as a sudden deterioration of kidney function resulting in the inability to maintain fluid and electrolyte homeostasis. It can be caused by prerenal issues affecting blood flow to the kidneys, intrinsic renal parenchymal damage, or postrenal urinary tract obstruction. The incidence of AKI varies globally and it commonly occurs in critically ill children with coexisting conditions. Etiologies include pre-renal causes like decreased intravascular volume, intrinsic renal diseases affecting glomeruli or tubules, and post-renal obstruction. Diagnosis involves lab tests of kidney and liver function as well as imaging studies. Treatment focuses on fluid management, electrolyte
This document discusses diabetes mellitus (DM), specifically in children. It defines DM as a chronic metabolic disorder characterized by hyperglycemia resulting from defects in insulin secretion or action. Type 1 DM is described as an autoimmune disease resulting in absolute insulin deficiency, while Type 2 DM is associated with insulin resistance. Signs and symptoms, classification, incidence rates, diagnosis, treatment involving insulin therapy, nutrition management, and exercise are covered. Nursing care focuses on education, emotional support, and ensuring safety.
Acute poststreptococcal glomerulonephritis (APSGN) is characterized by sudden edema, hematuria, proteinuria, and hypertension 1-4 weeks after a streptococcal infection. Histologically, there is diffuse proliferation of glomerular cells and leukocytes. It is caused by immune complexes forming in response to certain M protein serotypes of streptococcus. On microscopy, there are subepithelial immune deposits, complement activation, and inflammation, appearing as "humps". Patients typically experience malaise, fever, nausea, and hematuria after a sore throat. Laboratory findings include elevated antibody titers and low complement levels. Most children fully recover with conservative care, while a small percentage progress
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
This document provides information on diabetes including definitions, epidemiology, diagnosis, etiologic classifications, physiology, presentation, investigations, management, treatment, insulin types, and special considerations for pediatric diabetes. It defines diabetes as a metabolic disorder characterized by hyperglycemia caused by insulin deficiency or resistance. Key points include that type 1 diabetes is an autoimmune condition resulting in absolute insulin deficiency, while type 2 involves insulin resistance with relative deficiency. Diagnosis requires hyperglycemic symptoms and blood glucose criteria. Management involves a multidisciplinary team, medical treatment including insulin administration and nutrition management, and screening for acute and long-term complications.
The most common type of diabetes in children and teens is type 1 diabetes, also called juvenile diabetes. With type 1 diabetes, the pancreas does not produce insulin. Type 2 diabetes used to be called adult-onset diabetes but is becoming more common in children due to increases in obesity. Children with type 2 diabetes are at high risk if they are overweight, have a family history of diabetes, or are not physically active. Lifestyle changes like maintaining a healthy weight, being physically active, eating smaller portions of healthy foods, and limiting screen time can lower the risk of type 2 diabetes in children. Children with type 2 diabetes may be managed through diet and exercise alone, but some patients will need oral medications or insulin. Children with type
1) Poststreptococcal glomerulonephritis (PSGN) is an acute inflammation of the renal glomeruli that occurs after infection with certain strains of Streptococcus.
2) It is characterized by hematuria, edema, hypertension, and oliguria.
3) The pathogenesis involves molecular mimicry between streptococcal antigens and renal antigens, resulting in the trapping of immune complexes in the glomeruli.
This document provides an overview of the assessment and management of genitourinary dysfunction in children. It discusses topics such as urinary tract infections, glomerulonephritis, nephrotic syndrome, renal failure, dialysis, transplantation, and Wilms' tumor. Nursing priorities include thorough assessment, administering appropriate antibiotic therapy, managing complications, providing patient and family education, and preventing infections through aseptic technique.
This document discusses glomerular disease and nephrotic syndrome. It begins by defining nephrotic syndrome and describing the structure of the glomerulus. It then covers the main causes of nephrotic syndrome including minimal change disease, membranous glomerulonephritis, and focal segmental glomerulosclerosis. Investigations, prognosis, complications, and treatment approaches are also summarized. The document provides histological classifications and details on each of the primary causes of nephrotic syndrome.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
- Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is usually caused by primary glomerular disease but can be secondary to other medical conditions.
- Diagnosis requires proteinuria >3.5g/day and hypoalbuminemia <2.5g/dL. Management involves salt and fluid restriction, diuretics, ACE inhibitors to reduce proteinuria, and corticosteroids which induce remission in 80-90% of adults. Frequent relapses or steroid resistance may require additional immunosuppressive drugs. Complications include infection, thromboembolism, and renal failure.
This document discusses acute nephritic syndrome, specifically acute post-streptococcal glomerulonephritis (PSGN). It notes that PSGN classically presents after a streptococcal throat or skin infection with hematuria, proteinuria, hypertension, and edema. Investigations may show elevated anti-streptococcal antibodies. On biopsy, there is diffuse mesangial proliferation with immune complex deposition. Management involves controlling symptoms while the infection resolves spontaneously in 6-8 weeks. Complications include hypertension, renal failure, and rarely chronic kidney disease.
This document discusses nephrotic syndrome, which is characterized by proteinuria, hypoalbuminemia, and edema. It defines nephrotic syndrome and outlines its causes, which include genetic, secondary, and idiopathic factors. The pathophysiology involves disturbances in the immune system and mutations affecting glomerular filtration. Clinical features and laboratory findings are provided for different types. Management involves treating symptoms, infections, and relapses with corticosteroids and immunosuppressants. Complications include edema, infections, thrombosis, and renal failure. Prognosis depends on response to steroids, with minimal change disease having a good prognosis and focal segmental glomerulosclerosis having poorer outcomes.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be primary, caused by diseases of the kidney itself, or secondary, caused by systemic illnesses that affect the kidneys. The most common primary causes are minimal-change disease in children and membranous glomerulonephritis in adults. Secondary causes include diabetes, lupus, and infections. Treatment involves controlling edema with diuretics, treating underlying conditions, and using steroids, immunosuppressants, or ACE inhibitors depending on disease type and severity.
Nephrotic syndrome is characterized by nephrotic range proteinuria, hypoalbuminemia, hyperlipidemia, and edema. It can be primary, caused by diseases limited to the kidney, or secondary, caused by diseases involving other organ systems. Primary causes include minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Management involves treating any underlying causes, controlling edema and hyperlipidemia, and using corticosteroids or other immunosuppressive drugs to induce remission in frequent relapsers or steroid-dependent patients.
This document defines acute kidney injury (AKI), formerly known as acute renal failure (ARF), and discusses its causes, diagnosis, and management. AKI is defined based on increases in serum creatinine and decreases in urine output. The main causes of AKI are pre-renal (decreased renal blood flow), renal (intrinsic kidney injury), and post-renal (urinary tract obstruction). Common etiologies include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis. Diagnosis involves laboratory and imaging tests. Management focuses on treating the underlying cause, fluid management, and potentially renal replacement therapy. Prognosis depends on the severity and reversibility of the kidney injury
The document discusses different types of kidney diseases and disorders:
- It describes the normal anatomy and histology of the kidney, including structures like the glomerulus.
- Nephrotic syndrome is discussed, which is characterized by proteinuria and low albumin levels, causing fluid retention and edema. Investigations include urine tests and kidney biopsies.
- Different glomerular diseases are described based on their pathology, including membranous glomerulonephritis, minimal change disease, focal segmental glomerulosclerosis (FSGS), and membranoproliferative glomerulonephritis. Their features on light microscopy, immunofluorescence and electron microscopy are provided.
- IgA nep
Pediatric urinary tract infections (UTIs) are common in children, especially girls under the age of 1. Left untreated, UTIs can cause renal scarring and long-term kidney damage. Diagnosis involves urine tests to check for white blood cells and bacteria. Treatment depends on symptoms and severity but often involves antibiotics and hydration. Follow up is important to monitor for recurrent UTIs and issues like vesicoureteral reflux, as both increase risk of permanent kidney damage if not addressed.
This document discusses glomerular disease and glomerulonephritis. It begins by defining glomerular disease and glomerulonephritis, noting that glomerulonephritis is a type of glomerular disease involving inflammation of the glomeruli. It then discusses the main clinical presentations of glomerular disease, including nephrotic syndrome, acute glomerulonephritis, and asymptomatic urinary abnormalities. The causes, symptoms, investigations, and management of various glomerular diseases are subsequently outlined. Throughout, examples are provided of specific diseases like post-streptococcal glomerulonephritis, membranous nephropathy, and crescentic glomerulone
Acute kidney injury (AKI), formerly known as acute renal failure, is defined as a sudden deterioration of kidney function resulting in the inability to maintain fluid and electrolyte homeostasis. It can be caused by prerenal issues affecting blood flow to the kidneys, intrinsic renal parenchymal damage, or postrenal urinary tract obstruction. The incidence of AKI varies globally and it commonly occurs in critically ill children with coexisting conditions. Etiologies include pre-renal causes like decreased intravascular volume, intrinsic renal diseases affecting glomeruli or tubules, and post-renal obstruction. Diagnosis involves lab tests of kidney and liver function as well as imaging studies. Treatment focuses on fluid management, electrolyte
This document discusses diabetes mellitus (DM), specifically in children. It defines DM as a chronic metabolic disorder characterized by hyperglycemia resulting from defects in insulin secretion or action. Type 1 DM is described as an autoimmune disease resulting in absolute insulin deficiency, while Type 2 DM is associated with insulin resistance. Signs and symptoms, classification, incidence rates, diagnosis, treatment involving insulin therapy, nutrition management, and exercise are covered. Nursing care focuses on education, emotional support, and ensuring safety.
Acute poststreptococcal glomerulonephritis (APSGN) is characterized by sudden edema, hematuria, proteinuria, and hypertension 1-4 weeks after a streptococcal infection. Histologically, there is diffuse proliferation of glomerular cells and leukocytes. It is caused by immune complexes forming in response to certain M protein serotypes of streptococcus. On microscopy, there are subepithelial immune deposits, complement activation, and inflammation, appearing as "humps". Patients typically experience malaise, fever, nausea, and hematuria after a sore throat. Laboratory findings include elevated antibody titers and low complement levels. Most children fully recover with conservative care, while a small percentage progress
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
This document provides information on diabetes including definitions, epidemiology, diagnosis, etiologic classifications, physiology, presentation, investigations, management, treatment, insulin types, and special considerations for pediatric diabetes. It defines diabetes as a metabolic disorder characterized by hyperglycemia caused by insulin deficiency or resistance. Key points include that type 1 diabetes is an autoimmune condition resulting in absolute insulin deficiency, while type 2 involves insulin resistance with relative deficiency. Diagnosis requires hyperglycemic symptoms and blood glucose criteria. Management involves a multidisciplinary team, medical treatment including insulin administration and nutrition management, and screening for acute and long-term complications.
The most common type of diabetes in children and teens is type 1 diabetes, also called juvenile diabetes. With type 1 diabetes, the pancreas does not produce insulin. Type 2 diabetes used to be called adult-onset diabetes but is becoming more common in children due to increases in obesity. Children with type 2 diabetes are at high risk if they are overweight, have a family history of diabetes, or are not physically active. Lifestyle changes like maintaining a healthy weight, being physically active, eating smaller portions of healthy foods, and limiting screen time can lower the risk of type 2 diabetes in children. Children with type 2 diabetes may be managed through diet and exercise alone, but some patients will need oral medications or insulin. Children with type
1) Poststreptococcal glomerulonephritis (PSGN) is an acute inflammation of the renal glomeruli that occurs after infection with certain strains of Streptococcus.
2) It is characterized by hematuria, edema, hypertension, and oliguria.
3) The pathogenesis involves molecular mimicry between streptococcal antigens and renal antigens, resulting in the trapping of immune complexes in the glomeruli.
This document provides an overview of the assessment and management of genitourinary dysfunction in children. It discusses topics such as urinary tract infections, glomerulonephritis, nephrotic syndrome, renal failure, dialysis, transplantation, and Wilms' tumor. Nursing priorities include thorough assessment, administering appropriate antibiotic therapy, managing complications, providing patient and family education, and preventing infections through aseptic technique.
This document discusses glomerular disease and nephrotic syndrome. It begins by defining nephrotic syndrome and describing the structure of the glomerulus. It then covers the main causes of nephrotic syndrome including minimal change disease, membranous glomerulonephritis, and focal segmental glomerulosclerosis. Investigations, prognosis, complications, and treatment approaches are also summarized. The document provides histological classifications and details on each of the primary causes of nephrotic syndrome.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
- Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is usually caused by primary glomerular disease but can be secondary to other medical conditions.
- Diagnosis requires proteinuria >3.5g/day and hypoalbuminemia <2.5g/dL. Management involves salt and fluid restriction, diuretics, ACE inhibitors to reduce proteinuria, and corticosteroids which induce remission in 80-90% of adults. Frequent relapses or steroid resistance may require additional immunosuppressive drugs. Complications include infection, thromboembolism, and renal failure.
Nephrotic syndrome is characterized by proteinuria (>3.5g/24hr), hypoalbuminemia, edema, and other issues. The proteinuria is caused by damage to the glomerular filtration barrier, and the other symptoms are secondary effects of protein loss in the urine. Nephrotic syndrome has potential complications including edema, hyperlipidemia, hypercoagulability, and infection risk. Management involves identifying the underlying cause, treating that cause if possible, controlling proteinuria with ACE inhibitors, and managing complications like edema and hyperlipidemia. Steroids are often used but renal biopsy is usually needed first in adults to guide treatment.
Nephrotic syndrome is characterized by proteinuria, low protein levels, edema, and high cholesterol. It is caused by increased permeability of the glomerular basement membrane, allowing protein to pass into the urine. Symptoms include edema, fatigue, and abdominal pain. Laboratory tests show protein in the urine, low serum protein and albumin levels, and elevated cholesterol. Treatment focuses on restricting salt and protein intake, using diuretics to control edema, and treating the underlying cause, often by using corticosteroids or other immunosuppressive drugs. The prognosis depends on the cause, with minimal change disease often responding well to treatment.
Nephrotic syndrome is a kidney disorder characterized by protein in the urine, low albumin levels, edema, and high cholesterol. It can be caused by primary kidney diseases or secondary to other systemic illnesses. The main primary causes are minimal-change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Treatment involves corticosteroids, diuretics, ACE inhibitors, and managing symptoms and complications like infection and hyperlipidemia. Long-term monitoring is also important.
Nephrotic syndrome is a kidney disorder characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be caused by primary kidney diseases or secondary to conditions like lupus erythematosus. The pathophysiology involves damage to the glomerular filtration barrier, allowing protein leakage. This causes hypoalbuminemia and edema. Treatment depends on the underlying cause but may include corticosteroids, diuretics, ACE inhibitors, and managing complications like infection and hyperlipidemia.
Nephrotic syndrome is a kidney disorder characterized by protein in the urine, low blood protein levels, high cholesterol levels, and swelling. It is caused by damage to the glomeruli in the kidneys. The main types are minimal change disease, focal segmental glomerulosclerosis, and membranoproliferative glomerulonephritis. Nephrotic syndrome is primarily treated through dietary changes, diuretics to reduce swelling, and corticosteroids to reduce protein in the urine. The standard treatment is prednisone or prednisolone over 12 weeks, with dosage adjustments made for relapses. Complications can include infections, blood clots, and renal failure if left untreated.
Nephrotic syndrome is a kidney disorder characterized by protein in the urine, low albumin levels, edema, and high cholesterol. It is caused by various conditions that damage the glomeruli such as chronic glomerulonephritis, diabetes, infections, drugs, and allergens. Symptoms include edema, fatigue, proteinuria, and hyperlipidemia. Diagnosis involves urinalysis, urine protein tests, and blood work. Treatment focuses on managing edema, treating underlying causes, and controlling cholesterol. Complications can include blood clots, malnutrition, high blood pressure, and kidney damage or failure if left untreated.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be caused by primary glomerular diseases like minimal change disease, membranous nephropathy, and focal segmental glomerulosclerosis or secondary to conditions like diabetes, infections, drugs, and amyloidosis. Treatment involves managing edema, lipids, and the underlying cause. Kidney biopsy is needed to identify the specific glomerular lesion causing nephrotic syndrome and guide treatment.
The document provides an overview of glomerulonephritis including its anatomy, epidemiology, etiology, pathophysiology, clinical presentation, diagnosis, and treatment. The glomerulus filters blood and allows small molecules to pass through while excluding larger ones like proteins. Glomerulonephritis can be caused by immune system abnormalities and is a common cause of kidney failure. Symptoms depend on whether the nephrotic or nephritic syndrome is present. Treatment involves controlling symptoms, reducing proteinuria and blood pressure, and using immunosuppressants.
Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is caused by conditions that damage the glomerulus, increasing permeability to plasma proteins. Primary causes include minimal change disease, membranous glomerulonephritis, and focal segmental glomerulosclerosis. Secondary causes can be infections, connective tissue diseases, and cancers. Treatment focuses on reducing proteinuria with ACE inhibitors or NSAIDs, managing edema and hyperlipidemia, and treating the underlying condition, often with corticosteroids, cyclophosphamide, or cyclosporine.
Parenteral nutrition (PN) can result in numerous complications if not carefully monitored. Mechanical complications include injuries from catheters. Metabolic complications involve issues like hyperglycemia, hepatic dysfunction, and refeeding syndrome. Infections from catheters are also common. Close monitoring of patients on PN is necessary to check for metabolic and clinical issues and manage complications. Careful attention to nutrient levels and other medical factors can help reduce risks.
Nephrotic syndrome is defined by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is caused by damage to the glomerular basement membrane that increases pore size and protein leakage. Loss of protein like albumin leads to edema as serum oncotic pressure decreases. Steroids are first line treatment but some patients are steroid resistant. Kidney biopsy guides treatment, which may include immunosuppressants for steroid resistant forms. Complications include infection, hypercoagulability, and renal failure.
Nephrotic syndrome is characterized by nephrotic-range proteinuria (>3g/day), low serum albumin, and edema. It is caused by loss of albumin in the urine leading to lower plasma protein levels and sodium retention in the kidneys. This causes edema. Complications include infection, hyperlipidemia, hypocalcemia, hypercoagulability, and hypertension. Diagnosis involves urinalysis showing proteinuria, low serum albumin, and sometimes a renal biopsy. Treatment focuses on preventing blood clots, lowering lipids, and managing fluid retention and edema with diuretics.
This document discusses nephrotic syndrome, which is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia due to damage to the glomerular capillary membrane. This allows excess plasma proteins to leak into the urine. Causes include glomerulonephritis, diabetes, lupus, amyloidosis, sarcoidosis, cancer, drugs, and infections. Symptoms include edema, fatigue, weight gain, and hyperlipidemia. Treatment focuses on controlling edema and symptoms, treating underlying causes, and preventing infection. Nursing care centers around monitoring fluid status and intake, preventing infection, and managing cognitive effects of uremia.
Nephrotic syndrome is characterized by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. The most common cause is minimal change disease. Treatment involves corticosteroids as initial therapy, with cyclophosphamide or other immunosuppressants used for frequent relapses or steroid resistance. Supportive care focuses on managing edema, diet, and preventing infections, which are a major complication. Kidney biopsy may be needed to identify underlying renal pathology or guide treatment decisions.
A 19-year-old man presented with red urine, periorbital and pretibial edema. He was diagnosed with tonsillitis 3 weeks prior. Examination found hypertension and crackles in both lung bases. Urine analysis showed proteinuria and dysmorphic red blood cells. The most likely diagnosis is poststreptococcal glomerulonephritis resulting from the recent streptococcal infection. Treatment involves controlling hypertension, edema and complications through diuretics and sodium restriction. Renal biopsy showed diffuse proliferative glomerulonephritis with neutrophils and immune deposits consistent with poststreptococcal glomerulonephritis.
This document provides an overview of plantar fasciitis. It begins with an applied anatomy section and defines plantar fasciitis as pain in the heel and bottom of the foot that is worse with first steps in the morning or after periods of rest. A clinical case is presented of a 37-year old obese female with right heel pain for 8 months. Differentials for heel pain are discussed. The document then covers the history, examination, investigations and treatment approaches for plantar fasciitis, emphasizing conservative management options.
This document provides an overview of necrotizing fasciitis. It begins with a historical background noting the earliest descriptions in the 5th century BC and increased rates in the mid-1980s. It then outlines the presentation, including risk factors like diabetes and trauma, signs of pain out of proportion, fever, and skin changes. Diagnosis involves clinical examination, lab tests, and imaging. Treatment requires aggressive surgical debridement, antibiotics, and resuscitation. Prognosis depends on speed of diagnosis and treatment, with mortality rates around 30% overall but higher for polymicrobial infections.
Let's learn about the relevant anatomy & physiology associated with glaucoma- the angle of the anterior chamber, physiology of aqueous humor circulation, and many more. Happy Learning!
Intraocular lenses (IOLs) are used to restore vision after cataract surgery by replacing the crystalline lens. Sir Harold Ridley first proposed using acrylic plastic lenses for cataracts after observing aircraft plastic fragments in soldiers' eyes did not trigger rejection. IOLs are either single or multi-piece, made of acrylic or silicone, and placed in the anterior or posterior chamber of the eye. Their power is calculated using the SRK formula based on axial length and corneal curvature. Complications can include posterior capsular opacification, calcification, and degradation.
Let's study diplopia along with the relevant anatomy & function of extraocular muscles, pathophysiology, compensatory head position, and few case-based scenarios. Happy Learning!
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Clubbing, characterized by widening of the nail bed angle beyond 180 degrees, is caused by megakaryocytes and platelet fragments entering the systemic circulation from the lungs or heart due to damage or shunting. In the fingertips, these cells release growth factors that increase blood flow and connective tissue, causing clubbing. Clubbing is seen in pulmonary disorders where the capillaries are damaged, as well as cyanotic heart defects with right-to-left shunts and endocarditis where cells bypass or break off from the heart.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
2. LEARNING OBJECTIVE
• To list the features of nephrotic syndrome with their
underlying mechanisms.
• To define the objectives of treatment of nephrotic
syndrome.
• To describe the management of nephrotic syndrome.
3. NEPHROTIC SYNDROME
Feature Mechanism Consequence
Proteinuria
(> 3.5 g/day )
-Structural damage to glomerular
basement membrane
-Loss of size & charge barrier
-Hypoalbuminemia
Hypoalbuminemia
(<3 g/dl)
-Massive proteinuria
-High catabolism of reabsorbed
albumin (proximal tubule of kidney)
-Reduced oncotic pressure
-Edema
Sodium retention - Secondary hyperaldosteronism -Edema
Hypercholesterolemia -Increased hepatic lipoprotein
synthesis in response to
hypoalbuminemia
-Atherosclerosis
Hypercoagulability -Urinary loss of antithrombin III,
protein C and S
-Increased serum fibrinogen level
-Venous
thromboembolism
Infection -Urinary loss of immunoglobulin -Pneumococcal infection
4. OBJECTIVES OF TREATMENT OF
NEPHROTIC SYNDROME
• To identify the underlying cause and reverse it (if
possible).
• To reduce proteinuria.
• To reduce edema formation.
• To reduce blood cholesterol level.
• To restrict dietary sodium.
5. OBJECTIVES OF TREATMENT OF
NEPHROTIC SYNDROME
• To prevent complications like
- hypercoagulability
- infection
- acute kidney disease
• To maintain electrolyte balance.
• To maintain quality of life.
7. Management of edema
Dietary sodium restriction
Thiazide diuretics ( Bendroflumethiazide)
Furosemide with amiloride -
If unresponsive to thiazide
Parenteral route if resistance to oral diuretic
-Nephrotic patient may malabsorb diuretics owing
to gut mucosal edema
8. Management of proteinuria
Normal protein diet intake
- High protein diet (80-90 g/day) increases
proteinuria
ACE inhibitors and/or angiotensin II antagonist
- Reduces glomerular efferent arteriolar resistance
- Reduces intraglomerular capillary pressure
- Reduces protein filtration
9. Management of hypercholesterolemia
Lipid lowering drugs
- HMG CoA reductase inhibitors, fibrates
Restrict saturated and trans-fatty acids in diet
Management of hypercoagulability
Prolonged bed rest avoided
- Thromboembolism very common in nephrotic syndrome
Long term prophylactic anticoagulant
- In absence of any contraindications
10. Management of infection
Early detection and aggressive treatment of infection
- Rather than long term antibiotic prophylaxis
Pneumococcal vaccine given
- Pneumococcal infections particularly common
11. REFERENCES
• Davidson’s Principles & Practice of Medicine; 21st
Edition ; page no. 481
• KUMAR & CLARK CLINICAL MEDICINE; 6th
EDITION ; Page no.901-903
• HARRISON’S Principles of INTERNAL
MEDICINE; 17th Edition ; Page no. 1210