Hypertensive Nephrosclerosis
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Hypertensive Nephrosclerosis is the second leading cause of Chronic Renal Disease in Adults worldwide
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Acute kidney injury
The document discusses acute kidney injury (AKI), including its causes, diagnosis, and management. It provides details on prerenal, intrinsic, and postrenal forms of AKI. For prerenal AKI, management focuses on correcting the underlying cause, such as volume depletion, and restoring intravascular volume through fluid resuscitation. For intrinsic AKI, identifying and removing nephrotoxic agents is important. Dialysis may be needed for severe AKI with fluid/electrolyte imbalance or uremia.
renal tubular acidosis (RTA)
metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance.
Diabetic nephropathy
This document discusses the stages, diagnosis, prevention, and management of diabetic nephropathy. It begins with objectives and defining diabetic nephropathy as persistent albuminuria and declining kidney function. Risk factors include poor blood sugar and blood pressure control, smoking, and family history. Screening involves measuring the albumin-creatinine ratio annually after diagnosis. Prevention focuses on patient education, glycemic control, blood pressure management, and smoking cessation. Treatment includes ACE inhibitors or ARBs to slow progression even in normotensive patients, with referral to a nephrologist for advanced kidney disease.
Hyponatremia and hypernatremia
This document discusses hyponatremia and hypernatremia. It begins by explaining sodium regulation and the physiological basis of serum sodium concentration. It then defines and describes the types and causes of hyponatremia, including hypovolemic, euvolemic, and hypervolemic hyponatremia as well as pseudo hyponatremia. Specific conditions like SIADH are explained in detail. The clinical features, diagnosis, and treatment of hyponatremia are outlined. Hypernatremia is also defined and its causes such as net water loss or hypertonic sodium gain are summarized. The clinical features of hypernatremia are said to be predominantly neurologic.
secondary hypertension
This case report describes a 17-year-old male college student presenting with occipital headache, blurred vision, and vomiting for two days. His history revealed similar complaints three months prior when he was diagnosed with hypertension but did not take medications regularly. On examination, his blood pressure was elevated at 210/120 mmHg and fundoscopy showed grade 1 hypertensive retinopathy. Investigations showed abnormal renal function and echocardiogram revealed left ventricular hypertrophy. CT brain showed findings suggestive of posterior reversible encephalopathy syndrome. Based on his history of poorly controlled hypertension, family history, examination findings, and investigation results, he was diagnosed with secondary hypertension likely due to chronic kidney disease.
diabetic nephropathy
This document discusses diabetic nephropathy, which is kidney damage caused by diabetes. It begins with an introduction on the increasing prevalence of diabetes in India and how about 25-40% of diabetics develop end stage renal disease or chronic kidney disease. The natural history of kidney disease progression through 5 stages is described from early increased filtration to end stage requiring dialysis or transplant. Risk factors, screening methods, management including controlling blood glucose and blood pressure, and treatment options like dialysis and transplant are covered.
Approach to a Patient with Acute kidney injury
This document discusses acute kidney injury (AKI), including its definition, epidemiology, causes, diagnosis, and treatment approaches. It provides details on:
- AKI definitions including RIFLE and KDIGO criteria.
- Common causes of AKI including pre-renal, intrinsic renal, and post-renal etiologies.
- Diagnostic evaluation including blood and urine tests, imaging, and biomarkers.
- General treatment principles including fluid resuscitation, eliminating nephrotoxins, and initiating renal replacement therapy.
- Specific approaches for pre-renal, intrinsic renal, and post-renal AKI as well as infections, nephrotoxins, and complications.
Acute kidney injury
This is a presentation meant for medical students and other medical practitioners who need to have background information on Acute Kidney Injury
Recommended
Acute kidney injury
The document discusses acute kidney injury (AKI), including its causes, diagnosis, and management. It provides details on prerenal, intrinsic, and postrenal forms of AKI. For prerenal AKI, management focuses on correcting the underlying cause, such as volume depletion, and restoring intravascular volume through fluid resuscitation. For intrinsic AKI, identifying and removing nephrotoxic agents is important. Dialysis may be needed for severe AKI with fluid/electrolyte imbalance or uremia.
renal tubular acidosis (RTA)
metabolic acidosis develops because of defects in the ability of the renal tubules to perform the normal functions required to maintain acid-base balance.
Diabetic nephropathy
This document discusses the stages, diagnosis, prevention, and management of diabetic nephropathy. It begins with objectives and defining diabetic nephropathy as persistent albuminuria and declining kidney function. Risk factors include poor blood sugar and blood pressure control, smoking, and family history. Screening involves measuring the albumin-creatinine ratio annually after diagnosis. Prevention focuses on patient education, glycemic control, blood pressure management, and smoking cessation. Treatment includes ACE inhibitors or ARBs to slow progression even in normotensive patients, with referral to a nephrologist for advanced kidney disease.
Hyponatremia and hypernatremia
This document discusses hyponatremia and hypernatremia. It begins by explaining sodium regulation and the physiological basis of serum sodium concentration. It then defines and describes the types and causes of hyponatremia, including hypovolemic, euvolemic, and hypervolemic hyponatremia as well as pseudo hyponatremia. Specific conditions like SIADH are explained in detail. The clinical features, diagnosis, and treatment of hyponatremia are outlined. Hypernatremia is also defined and its causes such as net water loss or hypertonic sodium gain are summarized. The clinical features of hypernatremia are said to be predominantly neurologic.
secondary hypertension
This case report describes a 17-year-old male college student presenting with occipital headache, blurred vision, and vomiting for two days. His history revealed similar complaints three months prior when he was diagnosed with hypertension but did not take medications regularly. On examination, his blood pressure was elevated at 210/120 mmHg and fundoscopy showed grade 1 hypertensive retinopathy. Investigations showed abnormal renal function and echocardiogram revealed left ventricular hypertrophy. CT brain showed findings suggestive of posterior reversible encephalopathy syndrome. Based on his history of poorly controlled hypertension, family history, examination findings, and investigation results, he was diagnosed with secondary hypertension likely due to chronic kidney disease.
diabetic nephropathy
This document discusses diabetic nephropathy, which is kidney damage caused by diabetes. It begins with an introduction on the increasing prevalence of diabetes in India and how about 25-40% of diabetics develop end stage renal disease or chronic kidney disease. The natural history of kidney disease progression through 5 stages is described from early increased filtration to end stage requiring dialysis or transplant. Risk factors, screening methods, management including controlling blood glucose and blood pressure, and treatment options like dialysis and transplant are covered.
Approach to a Patient with Acute kidney injury
This document discusses acute kidney injury (AKI), including its definition, epidemiology, causes, diagnosis, and treatment approaches. It provides details on:
- AKI definitions including RIFLE and KDIGO criteria.
- Common causes of AKI including pre-renal, intrinsic renal, and post-renal etiologies.
- Diagnostic evaluation including blood and urine tests, imaging, and biomarkers.
- General treatment principles including fluid resuscitation, eliminating nephrotoxins, and initiating renal replacement therapy.
- Specific approaches for pre-renal, intrinsic renal, and post-renal AKI as well as infections, nephrotoxins, and complications.
Acute kidney injury
This is a presentation meant for medical students and other medical practitioners who need to have background information on Acute Kidney Injury
Acute kidney injury(AKI)
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
tubulointerstitial diseases-
This document discusses tubulo-interstitial pathology and chronic glomerulonephritis. It defines acute pyelonephritis, its causes and morphology. It describes chronic pyelonephritis and reflux nephropathy, including forms of chronic pyelonephritis and their gross and microscopic morphology. It also discusses drug-induced tubulo-interstitial nephritis, analgesic nephropathy, causes of chronic glomerulonephritis, and interpreting morphology of chronic glomerulonephritis.
hypernatremia
Hypernatremia is defined as a plasma sodium concentration >145 mEq/L. It is usually caused by a water deficit rather than sodium gain. Common causes include impaired thirst, diarrhea, insensible losses from fever/ventilation, and renal losses from osmotic diuresis or diabetes insipidus. Symptoms range from none in chronic cases to neurologic issues like altered mental status. Treatment involves gradually correcting the sodium level by about 10-12 mEq/L/day using oral or IV water while monitoring for complications like cerebral edema. Replacing volume deficits and identifying underlying causes are also important.
Acute liver failure
Acute liver failure (ALF) is a rare condition defined as a rapid deterioration of liver function resulting in altered mental status and coagulopathy in individuals without pre-existing liver disease within 26 weeks. It carries a high mortality and often affects young persons. The document discusses the causes, clinical presentation, complications, diagnosis, and management of ALF including supportive care, specific treatments, liver transplantation, and prognosis.
Chronic kidney disease, Hemodialysis
The document discusses chronic kidney disease (CKD) and provides guidelines for its treatment and management. It defines CKD as abnormalities of kidney structure or function for over 3 months. It then lists markers used to diagnose CKD and common causes including diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. The document concludes by outlining treatment recommendations for CKD, including controlling blood pressure and protein intake, and monitoring mineral metabolism.
Acute kidney injury defnition, causes,
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
Diabetic nephropathy
This document provides an overview of diabetic kidney disease. It discusses how diabetes is the leading cause of chronic kidney disease and end-stage renal disease. It covers the diagnosis of diabetic kidney disease based on albuminuria and decreased estimated glomerular filtration rate. Risk factors, pathogenesis, natural history, and management strategies such as glycemic control, blood pressure control, angiotensin inhibition, and reducing proteinuria are described in detail. The roles of various drug classes and lifestyle modifications in slowing the progression of diabetic kidney disease are also summarized.
Acute Kidney Injury in Children
This document presents a seminar on acute kidney injury (AKI) in children. It defines AKI and describes the RIFLE and AKIN criteria for classifying it. Common causes of pediatric AKI include pre-renal issues like dehydration, intrinsic renal problems like acute tubular necrosis, and post-renal obstruction. Clinical features depend on the etiology. Management involves treating life-threatening complications, fluid/electrolyte balance, nutrition support, and addressing the underlying disorder. Outcomes vary according to cause but have improved with advanced care; prevention emphasizes hydration and avoiding nephrotoxins.
Acute kidney injury
Acute Kidney Injury (AKI) is a common complication, affecting 5-7% of hospital admissions and 30% of intensive care unit patients. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Biomarkers like cystatin C and kidney injury molecule 1 can help detect AKI earlier than creatinine. Treatment involves fluid resuscitation, eliminating nephrotoxins, and renal replacement therapy for complications like electrolyte imbalances or uremia. Outcomes depend on the underlying cause, with pre-renal and post-renal AKI having a better prognosis than intrinsic renal injury.
Acute Kidney Injury
the presentation highlights on the approach of a patient with AKI: i.e History, physical findings, investigations
Hypernatremia
Hypernatremia is a serum sodium level over 145 mEq/L, occurring in 1% of hospitalized patients with high mortality regardless of acute or chronic onset. It can be caused by hypovolemia due to fluid losses exceeding intake, euvolemia from excess skin and lung losses, or hypervolemia from concentrated saline or mineralocorticoid excess. Symptoms include GI issues, dry skin and mucosa, neurologic changes like restlessness and seizures, and cardiovascular abnormalities depending on volume status. Treatment involves gradually decreasing sodium levels with hypotonic fluids and restricting dietary sodium intake.
Approach to a patient with hyponatremia (2) (1)
The document discusses hyponatremia, which refers to a low serum sodium level. It begins by defining hyponatremia and providing normal sodium levels. It then covers the frequency, age and sex predispositions, physiology/pathophysiology, types and causes. The types include hypovolemic, euvolemic, hypervolemic, redistributive, and pseudohyponatremia. Common causes are discussed like SIADH, heart failure, cirrhosis. The clinical approach involves assessing volume status, labs like sodium, osmolality, urine sodium. Management depends on the type and involves restricting free water intake or using hypertonic saline in severe cases to slowly correct the
Approach to Rapidly Progressive Glomerulonephritis RPGN
Clinical approach to Rapidly Progressive Renal failure and Rapidly Progressive Glomerulonephritis. Diagnosing crescentic Glomerulonephritis and Pauci immune vasculitis syndromes - churg strauss, wegeners and good pasture syndromes
Renal Hypertension
Renal hypertension is high blood pressure caused by kidney disease. It can be caused by renal stenosis where the renal arteries narrow, decreasing blood flow to the kidneys, or chronic glomerulonephritis where inflammation damages the glomeruli. This causes increased renal vascular resistance and decreased glomerular filtration, stimulating the renin-angiotensin system which increases blood pressure. Investigations include blood and urine tests, ultrasound, CT scan, and biopsy. Treatments depend on the cause but may include angioplasty, stenting, medications, or controlling blood pressure and protein intake.
INTERNAL MEDICINE - Secondary Hypertension
The document discusses secondary hypertension, defining it as elevated blood pressure due to an underlying disorder. The most common causes of secondary hypertension include renal parenchymal diseases, primary aldosteronism, Cushing's syndrome, pheochromocytoma, and renovascular hypertension. It provides details on the definition, causes, signs and symptoms, diagnostic tests, treatment options, and prognosis for each of these common causes of secondary hypertension.
Anemia in Chronic Kidney DIsease
Anemia is a common complication of chronic kidney disease that can cause fatigue. While the kidneys normally produce erythropoietin to stimulate red blood cell production, CKD patients have relative erythropoietin deficiency. This leads to anemia which, if left untreated, can negatively impact quality of life and cardiovascular health. Erythropoiesis-stimulating agents and iron supplementation are used to treat anemia in CKD, though the appropriate hemoglobin target level remains an area of ongoing research and debate given risks identified with higher targets in some studies.
Chronic Kidney Disease in Pediatrics
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.
Lupus nephritis
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
Hepatorenal syndrome
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
Acute decompensated heart failure
This document discusses the management of acute decompensated heart failure (ADHF). It outlines assessing patients for ADHF through clinical signs and symptoms, initial investigations including ECG, labs, and imaging. Treatment involves immediate relief of symptoms through intensive monitoring and care, identifying precipitating causes, stabilizing the patient, and modifying medical therapy which may include diuretics, vasodilators, inotropes, and managing underlying conditions. Goals include symptom relief, hemodynamic monitoring, addressing congestion or hypoperfusion, and developing discharge plans.
Diseases involving blood vessels of the kidney
1) Nearly all renal diseases secondarily involve the renal blood vessels, with the main diseases affecting the kidneys' blood vessels being benign nephrosclerosis, malignant nephrosclerosis, and thrombotic microangiopathies.
2) Benign nephrosclerosis is characterized by hyaline thickening of small arteries and arterioles causing ischemic atrophy, while malignant nephrosclerosis features hyperplastic "onion skin" thickening of arterioles and fibrinoid necrosis.
3) Thrombotic microangiopathies include hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, characterized by microangiopathic hemolytic anemia
Hypertension and kidney
This document summarizes hypertension and its relationship to the kidneys. It discusses how essential hypertension is mainly caused by abnormal sodium retention and genetic predisposition. It also notes that low birth weight can result in fewer nephrons and later hypertension. The kidneys play a key role in maintaining blood pressure through pressure natriuresis, which allows excess salt to be excreted by inhibiting reabsorption when blood pressure is high. For patients with essential hypertension, diuretics are often the first choice of treatment since salt retention is a major factor, but they can cause side effects like hyponatremia and gout. The document emphasizes monitoring blood pressure and kidney function for patients on antihypertensive medications.
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Acute kidney injury(AKI)
Acute kidney injury (AKI) is a potentially life-threatening
syndrome that occurs primarily in hospitalized patients
and frequently complicates the course of critically ill
patient.
Acute Kidney Injury is is (abrupt) reduction in kidney functions as evidence by changed in laboratory values; serum creatinine, blood urea nitrogen(BUN)and urine output
tubulointerstitial diseases-
This document discusses tubulo-interstitial pathology and chronic glomerulonephritis. It defines acute pyelonephritis, its causes and morphology. It describes chronic pyelonephritis and reflux nephropathy, including forms of chronic pyelonephritis and their gross and microscopic morphology. It also discusses drug-induced tubulo-interstitial nephritis, analgesic nephropathy, causes of chronic glomerulonephritis, and interpreting morphology of chronic glomerulonephritis.
hypernatremia
Hypernatremia is defined as a plasma sodium concentration >145 mEq/L. It is usually caused by a water deficit rather than sodium gain. Common causes include impaired thirst, diarrhea, insensible losses from fever/ventilation, and renal losses from osmotic diuresis or diabetes insipidus. Symptoms range from none in chronic cases to neurologic issues like altered mental status. Treatment involves gradually correcting the sodium level by about 10-12 mEq/L/day using oral or IV water while monitoring for complications like cerebral edema. Replacing volume deficits and identifying underlying causes are also important.
Acute liver failure
Acute liver failure (ALF) is a rare condition defined as a rapid deterioration of liver function resulting in altered mental status and coagulopathy in individuals without pre-existing liver disease within 26 weeks. It carries a high mortality and often affects young persons. The document discusses the causes, clinical presentation, complications, diagnosis, and management of ALF including supportive care, specific treatments, liver transplantation, and prognosis.
Chronic kidney disease, Hemodialysis
The document discusses chronic kidney disease (CKD) and provides guidelines for its treatment and management. It defines CKD as abnormalities of kidney structure or function for over 3 months. It then lists markers used to diagnose CKD and common causes including diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. The document concludes by outlining treatment recommendations for CKD, including controlling blood pressure and protein intake, and monitoring mineral metabolism.
Acute kidney injury defnition, causes,
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
Diabetic nephropathy
This document provides an overview of diabetic kidney disease. It discusses how diabetes is the leading cause of chronic kidney disease and end-stage renal disease. It covers the diagnosis of diabetic kidney disease based on albuminuria and decreased estimated glomerular filtration rate. Risk factors, pathogenesis, natural history, and management strategies such as glycemic control, blood pressure control, angiotensin inhibition, and reducing proteinuria are described in detail. The roles of various drug classes and lifestyle modifications in slowing the progression of diabetic kidney disease are also summarized.
Acute Kidney Injury in Children
This document presents a seminar on acute kidney injury (AKI) in children. It defines AKI and describes the RIFLE and AKIN criteria for classifying it. Common causes of pediatric AKI include pre-renal issues like dehydration, intrinsic renal problems like acute tubular necrosis, and post-renal obstruction. Clinical features depend on the etiology. Management involves treating life-threatening complications, fluid/electrolyte balance, nutrition support, and addressing the underlying disorder. Outcomes vary according to cause but have improved with advanced care; prevention emphasizes hydration and avoiding nephrotoxins.
Acute kidney injury
Acute Kidney Injury (AKI) is a common complication, affecting 5-7% of hospital admissions and 30% of intensive care unit patients. The top causes of AKI in India are diarrheal diseases, sepsis, malaria, drug toxicity, and hospital-acquired injuries. Biomarkers like cystatin C and kidney injury molecule 1 can help detect AKI earlier than creatinine. Treatment involves fluid resuscitation, eliminating nephrotoxins, and renal replacement therapy for complications like electrolyte imbalances or uremia. Outcomes depend on the underlying cause, with pre-renal and post-renal AKI having a better prognosis than intrinsic renal injury.
Acute Kidney Injury
the presentation highlights on the approach of a patient with AKI: i.e History, physical findings, investigations
Hypernatremia
Hypernatremia is a serum sodium level over 145 mEq/L, occurring in 1% of hospitalized patients with high mortality regardless of acute or chronic onset. It can be caused by hypovolemia due to fluid losses exceeding intake, euvolemia from excess skin and lung losses, or hypervolemia from concentrated saline or mineralocorticoid excess. Symptoms include GI issues, dry skin and mucosa, neurologic changes like restlessness and seizures, and cardiovascular abnormalities depending on volume status. Treatment involves gradually decreasing sodium levels with hypotonic fluids and restricting dietary sodium intake.
Approach to a patient with hyponatremia (2) (1)
The document discusses hyponatremia, which refers to a low serum sodium level. It begins by defining hyponatremia and providing normal sodium levels. It then covers the frequency, age and sex predispositions, physiology/pathophysiology, types and causes. The types include hypovolemic, euvolemic, hypervolemic, redistributive, and pseudohyponatremia. Common causes are discussed like SIADH, heart failure, cirrhosis. The clinical approach involves assessing volume status, labs like sodium, osmolality, urine sodium. Management depends on the type and involves restricting free water intake or using hypertonic saline in severe cases to slowly correct the
Approach to Rapidly Progressive Glomerulonephritis RPGN
Clinical approach to Rapidly Progressive Renal failure and Rapidly Progressive Glomerulonephritis. Diagnosing crescentic Glomerulonephritis and Pauci immune vasculitis syndromes - churg strauss, wegeners and good pasture syndromes
Renal Hypertension
Renal hypertension is high blood pressure caused by kidney disease. It can be caused by renal stenosis where the renal arteries narrow, decreasing blood flow to the kidneys, or chronic glomerulonephritis where inflammation damages the glomeruli. This causes increased renal vascular resistance and decreased glomerular filtration, stimulating the renin-angiotensin system which increases blood pressure. Investigations include blood and urine tests, ultrasound, CT scan, and biopsy. Treatments depend on the cause but may include angioplasty, stenting, medications, or controlling blood pressure and protein intake.
INTERNAL MEDICINE - Secondary Hypertension
The document discusses secondary hypertension, defining it as elevated blood pressure due to an underlying disorder. The most common causes of secondary hypertension include renal parenchymal diseases, primary aldosteronism, Cushing's syndrome, pheochromocytoma, and renovascular hypertension. It provides details on the definition, causes, signs and symptoms, diagnostic tests, treatment options, and prognosis for each of these common causes of secondary hypertension.
Anemia in Chronic Kidney DIsease
Anemia is a common complication of chronic kidney disease that can cause fatigue. While the kidneys normally produce erythropoietin to stimulate red blood cell production, CKD patients have relative erythropoietin deficiency. This leads to anemia which, if left untreated, can negatively impact quality of life and cardiovascular health. Erythropoiesis-stimulating agents and iron supplementation are used to treat anemia in CKD, though the appropriate hemoglobin target level remains an area of ongoing research and debate given risks identified with higher targets in some studies.
Chronic Kidney Disease in Pediatrics
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.
Lupus nephritis
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
Hepatorenal syndrome
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
Acute decompensated heart failure
This document discusses the management of acute decompensated heart failure (ADHF). It outlines assessing patients for ADHF through clinical signs and symptoms, initial investigations including ECG, labs, and imaging. Treatment involves immediate relief of symptoms through intensive monitoring and care, identifying precipitating causes, stabilizing the patient, and modifying medical therapy which may include diuretics, vasodilators, inotropes, and managing underlying conditions. Goals include symptom relief, hemodynamic monitoring, addressing congestion or hypoperfusion, and developing discharge plans.
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Approach to Rapidly Progressive Glomerulonephritis RPGN
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Diseases involving blood vessels of the kidney
1) Nearly all renal diseases secondarily involve the renal blood vessels, with the main diseases affecting the kidneys' blood vessels being benign nephrosclerosis, malignant nephrosclerosis, and thrombotic microangiopathies.
2) Benign nephrosclerosis is characterized by hyaline thickening of small arteries and arterioles causing ischemic atrophy, while malignant nephrosclerosis features hyperplastic "onion skin" thickening of arterioles and fibrinoid necrosis.
3) Thrombotic microangiopathies include hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, characterized by microangiopathic hemolytic anemia
Hypertension and kidney
This document summarizes hypertension and its relationship to the kidneys. It discusses how essential hypertension is mainly caused by abnormal sodium retention and genetic predisposition. It also notes that low birth weight can result in fewer nephrons and later hypertension. The kidneys play a key role in maintaining blood pressure through pressure natriuresis, which allows excess salt to be excreted by inhibiting reabsorption when blood pressure is high. For patients with essential hypertension, diuretics are often the first choice of treatment since salt retention is a major factor, but they can cause side effects like hyponatremia and gout. The document emphasizes monitoring blood pressure and kidney function for patients on antihypertensive medications.
Nephrosclerosis
This document discusses two types of nephrosclerosis: benign and malignant. Benign nephrosclerosis is caused by thickening of renal arterioles over time from aging, hypertension, or diabetes. It can cause scarring and loss of renal function. Malignant nephrosclerosis involves a worsening of hypertension that damages renal vessels, causing ischemia and sudden loss of function. The pathology involves fibrinoid necrosis and intimal thickening of arteries. Aggressive treatment of high blood pressure is needed to prevent permanent kidney damage in malignant nephrosclerosis.
Acclerated Hypertension
The document discusses accelerated hypertension and provides recommendations for treatment. It notes that the target for reducing mean arterial blood pressure within 24-48 hours is a 25% decrease. Proper treatment is important to prevent multi-organ damage that can result from accelerated hypertension.
Nephrotic And Nephritic Syndrome 2008
This document defines and compares nephrotic syndrome and nephritic syndrome. It provides details on various causes of glomerular disease including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, IgA nephropathy, lupus nephritis, anti-GBM disease, and rapidly progressive glomerulonephritis. Evaluation of glomerular disease involves history, exam, urinalysis, and complement levels with renal biopsy used to confirm specific diagnoses.
Hypertensive crisis
Hypertensive crisis is defined as a systolic blood pressure over 180 mmHg and/or diastolic blood pressure over 120 mmHg that can lead to end organ damage. It is classified as either a hypertensive emergency, requiring immediate medical treatment to prevent permanent organ damage, or a hypertensive urgency where treatment is still needed but not as immediately. Common causes of hypertensive crisis include uncontrolled essential hypertension, pregnancy-related conditions like preeclampsia, renal disease, endocrine disorders, drug or substance use, and neurological issues.
CKD MBD - Think Outside The Box - Case Scenarios Snapshots - Dr. Gawad
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HTN and kidney
The document discusses hypertension and its effects on the kidney. It begins by defining normal blood pressure regulation and the role of the kidney in long-term blood pressure control. It then discusses the epidemiology of hypertension globally and in various countries. The document also covers the epidemiology of chronic kidney disease, how hypertension affects the kidney and can lead to hypertensive nephropathy, and how chronic kidney disease in turn affects blood pressure. It concludes by outlining blood pressure targets and treatment strategies for patients with hypertension and chronic kidney disease.
Hypertensive crisis
This document discusses hypertensive crisis, including its definition, clinical presentation, management, and targets of organ damage. It presents a case study of a patient with chest tightness and shortness of breath who is found to have severely high blood pressure and signs of organ damage. The diagnosis is hypertensive emergency. Treatment involves rapid intravenous blood pressure reduction in the hospital. Guidelines recommend lowering mean arterial pressure no more than 25% within the first hour for hypertensive emergencies. Exceptions are made for certain conditions like ischemic stroke and aortic dissection that require more aggressive blood pressure control.
Malignant hypertension
Malignant hypertension is a rare but serious form of high blood pressure characterized by a sudden onset of very high blood pressure along with damage to the eyes and kidneys. It occurs when blood pressure in the arteries rises quickly to severely high levels, with diastolic pressure often over 130 mmHg. Common causes include essential hypertension, kidney disease, and pregnancy-related issues. Symptoms may include blurred vision, chest pain, seizures, reduced urine output, and headaches. Diagnosis involves examining physical signs of organ damage and testing for complications affecting the eyes, kidneys, heart, and brain. Treatment aims to lower blood pressure gradually over hours to days to avoid dangerous drops, using short-acting intravenous drugs like nitroprusside
Uremic Pruritus - A life annoying problem - Dr. Gawad
Uremic pruritus is a common problem for patients with kidney disease that significantly impacts quality of life. The document discusses the prevalence, diagnosis, management, and pathophysiology of uremic pruritus based on evidence from multiple studies. Control of calcium, phosphorus and PTH levels can help reduce pruritus. Pregabalin is often used as first-line treatment, with other options including topical moisturizers, UVB phototherapy, pentoxifylline, and drugs targeting opioid and calcium channels if initial treatments are ineffective. Further research is still needed due to limitations and inconsistencies in current studies.
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Mgt of htn crisis by gelaye
The document provides information on the management of hypertensive crisis. It begins with outlines of topics covered which include introduction, etiology, pathophysiology, clinical evaluation, workup, and management. It then goes into further detail on these topics. The key points are:
1) Hypertensive crisis is defined as a sudden rise in blood pressure that causes end organ damage and is classified as either a hypertensive urgency or emergency.
2) Common causes include poorly controlled essential hypertension and renal disease.
3) Rapid evaluation is needed to identify end organ damage to the heart, kidneys, brain, or vasculature.
4) Treatment involves slowing lowering blood pressure, usually over hours
Hrs ashraf omar
Hepatorenal Syndrome (HRS) is a functional kidney failure that occurs in patients with cirrhosis and advanced liver disease. It is characterized by severe abnormalities in renal blood flow regulation and renal function. There are two main types - type 1 is a rapidly progressive form and type 2 is a slower progressive form. The pathogenesis involves splanchnic vasodilation leading to renal vasoconstriction. Diagnosis requires meeting criteria related to kidney function tests and ruling out other causes. Treatment aims to reverse renal failure through use of vasoconstrictors like terlipressin or octreotide to relieve renal vasoconstriction until liver transplantation.
Oedema
This document discusses edema, including its definition, pathophysiology, common causes, and approaches to diagnosis and management. Edema is caused by increased hydrostatic pressure, decreased colloid osmotic pressure, or increased capillary permeability. Common causes include heart failure, cirrhosis, nephrotic syndrome, and pregnancy. The case scenario describes a patient with fatigue, swelling, and liver enlargement, suggesting heart failure as the most likely diagnosis. Diagnostic testing may include chest x-rays, echocardiograms, and lab tests. Treatment involves reversing the underlying cause, restricting dietary sodium, and using diuretic medications.
Hypertension.pptx
This document discusses the diagnosis and treatment of essential hypertension. It outlines key steps in physical examination for hypertension including blood pressure measurement. It describes target organ damage hypertension can cause such as heart, brain, kidney and retinal damage. Instrumental tests for diagnosing and monitoring hypertension are discussed, including electrocardiograms, home blood pressure monitoring, and ambulatory blood pressure monitoring. Lifestyle changes for treatment include salt restriction. Pharmacotherapy options for treating hypertension include RAAS blockers, diuretics, beta blockers, calcium channel blockers, and others. Core drug treatment strategies are outlined, along with the use of single-pill combination therapies.
HTN CRISIS SEMINER.pptx
This document discusses hypertensive crisis and provides details on its etiology, pathophysiology, clinical evaluation, and management. It defines hypertensive crisis as an acute severe elevation in blood pressure of usually over 180/120 mmHg that may be associated with end organ dysfunction. It further categorizes hypertensive crisis into hypertensive urgency and hypertensive emergency based on the presence or absence of end organ damage. The document outlines the various causes, mechanisms, clinical assessment approach, and goals of treatment for hypertensive crisis, with an emphasis on preventing further organ damage while maintaining tissue perfusion.
Cardiovascular Pathophysiology- Hypertension
This document summarizes cardiovascular pathophysiology related to hypertension. It defines hypertension and provides a clinical classification system. It describes the etiology and pathogenesis of both primary (essential) and secondary hypertension. For primary hypertension, it discusses genetic and environmental risk factors and the role of the renin-angiotensin-aldosterone system. For secondary hypertension, it covers renal, endocrine, neurogenic and other causes. It also outlines the pathological changes that can occur in the heart, blood vessels and kidneys as well as the clinical features of primary versus secondary hypertension.
Ckd prevention
This document discusses chronic kidney disease (CKD), including its pathophysiology, risk factors, and treatment strategies to slow progression. It notes that CKD progression involves both hemodynamic and non-hemodynamic mechanisms, such as activation of the renin-angiotensin-aldosterone system leading to inflammation and fibrosis. Blocking the RAAS through ACE inhibitors, ARBs, and blood pressure control has been shown to slow CKD progression by reducing proteinuria, glomerular hypertension, and inflammation. The document reviews several landmark clinical trials that established the renoprotective effects of RAAS inhibition in diabetic and non-diabetic kidney diseases.
Hypertension
This document discusses hypertension (high blood pressure), including its causes, symptoms, diagnosis, and treatment. It defines hypertension and describes its classification. It also outlines lifestyle modifications and medications that are used to treat hypertension. The goals of treatment are to lower blood pressure and prevent target organ damage to the heart, brain, kidneys and eyes. Nursing care focuses on educating patients, monitoring for side effects, ensuring compliance with treatment, and evaluating treatment effectiveness.
HYPERTENSION
Hypertension, or high blood pressure, is a common health problem that typically has no symptoms until late stages. It contributes to diseases like heart disease and stroke. The document defines hypertension as a diastolic pressure over 90 mm Hg or systolic over 140 mm Hg. While the causes are unknown for most people (essential hypertension), it can be secondary to other conditions. Complications involve damage to the heart, blood vessels, brain, kidneys and eyes. Evaluation of patients with hypertension aims to identify risk factors, secondary causes, and evidence of organ damage.
cirrhosis 1 (1).pptx
This document summarizes cirrhosis and its complications. It defines cirrhosis as a diffuse process characterized by liver necrosis and fibrosis. Cirrhosis can result from various infections, toxins like alcohol, and genetic or autoimmune conditions. Cirrhosis leads to portal hypertension and vascular shunts. When portal pressure exceeds 10-12 mmHg, complications like ascites and variceal bleeding occur. Two pulmonary complications are hepatopulmonary syndrome, involving intrapulmonary vascular dilation causing hypoxemia, and portopulmonary hypertension. Renal dysfunction includes hepatorenal syndrome. Hepatic encephalopathy is a serious neuropsychiatric complication with fluctuating symptoms ranging from mild impairment to coma.
Cardiorenal syndrome
1) Cardiorenal syndrome commonly occurs in patients with acute decompensated heart failure and is associated with poor outcomes. It involves a complex interaction between hemodynamic alterations and activation of neurohormonal systems that affects both the heart and kidneys.
2) There are five types of cardiorenal syndrome classified based on the inciting cardiac or renal event and the affected secondary organs. Type 1 is acute cardiorenal syndrome due to acute worsening of cardiac function leading to kidney injury.
3) Loop diuretics are the mainstay of treatment for congestion in heart failure but aggressive diuresis may worsen kidney function. Other therapies discussed include inotropic agents, vasopressin antagonists
27 beans acute renal-failure
Mr. Henle hasn't urinated in the night and may have acute renal failure (ARF). Key things to assess include urine output measured over the last few hours and days, symptoms, vital signs, and labs. ARF has multiple potential etiologies including prerenal from hypoperfusion, postrenal from obstruction, and intrinsic renal disease. Management involves treating the underlying cause, supporting the kidneys, and addressing complications like fluid overload and electrolyte abnormalities. Outcomes depend on severity and patient factors, with mortality around 50% for ARF.
Htn
This document discusses hypertension (high blood pressure) and its mechanisms, causes, and effects. It defines hypertension and explains that it doubles the risk of cardiovascular diseases by increasing cardiac output and peripheral resistance. Primary causes of hypertension include increased vascular volume from sodium intake, activation of the sympathetic nervous system, and the renin-angiotensin-aldosterone system. Secondary causes include renal disease, obesity, sleep apnea, pheochromocytoma, Cushing's syndrome, and others. The document outlines approaches to evaluating patients for hypertension through history, physical exam, and laboratory tests to identify underlying conditions and target organ damage.
Hypertensive Emergencies
This document discusses hypertensive emergencies, which are severe cases of high blood pressure that result in acute organ damage. It defines categories of hypertensive states and provides details on etiology, pathophysiology, presentation, workup, and treatment of hypertensive emergencies. Treatment involves identifying the affected organ system and gradually lowering blood pressure over hours to days to prevent further organ injury, using intravenous medications like nitroprusside, labetalol, or nicardipine depending on the situation. Specific guidance is provided for rapidly lowering blood pressure in conditions like hypertensive encephalopathy, intracerebral hemorrhage, and ischemic stroke.
HYPERTENSIVE CRISIS
A 76-year-old male is admitted to the ICU for recovery after lung surgery. His BP is 168/96 mmHg without end-organ damage, so this represents a hypertensive urgency rather than emergency. Fundoscopic exam is not needed for this transient postoperative hypertension. Starting IV antihypertensives or consulting a hypertension specialist are not necessary actions at this time. The patient should be reassessed later since there is no end-organ damage currently.
Hypertensive crisis
A 76-year-old male is admitted to the ICU for recovery after lung surgery. His BP is 168/96 mmHg without end-organ damage, so this represents a hypertensive urgency rather than emergency. Fundoscopic exam is not needed for this transient postoperative hypertension. Starting IV antihypertensives or consulting a hypertension specialist are not necessary actions at this time. The patient should be reassessed later since there is no end-organ damage currently.
CARDIAC COMPLICATIONS & ITS MANAGEMENT OF CKD
Uremic cardiomyopathy is the primary manifestation of cardiac complications in patients with chronic kidney disease. It results from the combined effects of pressure and volume overload on the heart from conditions like hypertension as well as the uremic state itself. This leads to left ventricular hypertrophy initially as an adaptive response but later maladaptive changes like cardiomyocyte death, fibrosis, and dilated cardiomyopathy if left unmanaged. Early initiation of hemodialysis, preferably non-conventional daily or nocturnal dialysis, can help halt progression of uremic cardiomyopathy while kidney transplantation has been shown to reverse it.
Generalized oedema
This document discusses the clinical approach to a patient presenting with generalized edema. It defines edema and discusses mechanisms that can cause fluid accumulation. The main causes of generalized edema are cardiac (congestive heart failure), renal (nephrotic syndrome), hepatic (liver cirrhosis), nutritional (malnutrition), allergic reactions, and drugs. Investigations and treatment focus on identifying the underlying cause and using diuretics and fluid restriction to increase excretion of sodium and water. Diuretic classes - thiazides, loops, and potassium-sparing - are described along with their mechanisms, indications, side effects and contraindications. Diuretic resistance and its management are also covered.
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Management of hypertension and hypertensive emergencies
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Hypertensive Nephrosclerosis
- 2. CHIEF COMPLIANTS 1. Vomiting x 1/12 2. Fever x 1/12 3. Muscle Cramps x 1/12 4. SOB x 1/52 37 year old Male referred to GPHC from Private Institution two days old
- 3. History of Presenting Illness COMPLAINTS DETAILS VOMITING Gradual Onset, 20 episodes/24hr, Bitter yellow fluid to meals, no associated GI Symptoms FEVER Intermittent, Associated with Productive Cough, Rx ASA CRAMPS Hands and Legs would contract, no fasciculation, paraesthesia SOB Lying down, ease with sitting, chest pains on inspiration, 2 pillow orthopnoea, PND once weekly
- 4. Past Medical History Uncontrolled HTN x 7/12 PSHx – nil Family Hx – DM, HTN SHx – Alcohol 0, Smoking 0, Driver Drug Hx – ASA for Fever Allergies – nil Blood Transfusions – nil Trauma - nil
- 5. Review of Systems Neuro – Blurred Vision CVS – Palpitation, Angina on exertion GU – Frequency, dysuria MS – Joint Pains Derm- Itching on Hands and Abdomen
- 6. Physical Examination VITAL S HR=74, RR= 20, BP= 210/120 , SPO2 = 97% RA HEENT MM – Pale and Moist RESP BAE, decreased BS to base, Creps to Base CVS S1, S2, M0 ABD Globous, depressible, non tender, no organomegaly, BS+ EXT Nx4, no pretibial oedema CNS GCS 15/15
- 7. Impressions 37 year old Male with PMHx of Uncontrolled Hypertension presents with symptoms of Uraemia, possible diagnosis of Chronic Renal Disease secondary to HTN
- 9. Background The term hypertensive nephrosclerosis has traditionally been used to describe a clinical syndrome characterized by long-term essential hypertension, hypertensive retinopathy, left ventricular hypertrophy, minimal proteinuria, and progressive renal insufficiency. In 2009, hypertensive nephrosclerosis (HN) accounted for 28% of patients reaching end-stage renal disease (ESRD). HN is the leading cause of ESRD in Africans (46%) and the second leading cause of ESRD worldwide.
- 10. Pathophysiology Two pathophysiologic mechanisms have been proposed for the development of hypertensive nephrosclerosis. (1) Glomerular Ischemia- chronic hypertension results in narrowing of preglomerular arteries and arterioles, with a consequent reduction in glomerular blood flow. (2) glomerular hypertension and glomerular hyperfiltration - Initial Hypertension leads to glomerular endothelial damage and sclerosis, subsequently in an attempt to compensate for the loss of renal function, the remaining nephrons undergo vasodilation of the preglomerular arterioles and experience an increase in renal blood flow and glomerular filtration. The result is glomerular hypertension, glomerular hyperfiltration, and progressive glomerular sclerosis.
- 11. Clinical Presentation HISTORY In most patients, hypertension is present for many years (usually >10 y), with evidence of periods of accelerated or poorly controlled BP. Patients may present with symptoms of Uremia Nausea Vomiting Fatigue Anorexia Weight loss Muscle cramps Pruritus Mental status changes Visual disturbances Increased thirst
- 12. Clinical Presentation PHYSICAL evidence of hypertension-related target organ damage includes hypertensive changes in the retinal vessels and signs of left ventricular hypertrophy.
- 13. Diagnostic Steps Blood Tests CBC, BUN, Cr, Electrolytes, Glucose Urine Analysis Microalbuminuria ( 0.5 to 1g / 24hr) Ultrasound of Kidneys kidney size is usually symmetric and may be normal or modestly reduced. ECG LVH RENAL BIOPSY Diagnsotic, Myointimal hypertrophy of the interlobular arteries, hyaline degeneration, and sclerosis of afferent arterioles are the most characteristic findings of hypertensive nephrosclerosis.
- 14. Management Blood Pressure Control ideal BP of <130/80 mmHg for patients with hypertensive nephropathy Several antihypertensive medications, including thiazide diuretics, beta-blockers, ACE inhibitors, ARBs, and calcium channel blockers, in principle, can be used as initial monotherapy in patients with hypertension. Uremia and CRD PD or Hemodialysis Fluid restriction Epo and iron supplements for anemia
- 15. Prognosis The optimal BP goal to slow the progression of renal failure in patients with hypertensive nephrosclerosis currently is unknown. Evidence for the beneficial effect of hypertension treatment on patients with hypertensive nephrosclerosis is lacking, and many questions regarding the ability of these drugs to protect renal function in the long term remain unanswered. hypertensive nephropathy accounts for more than one-third of patients on hemodialysis and the annual mortality rate for patients on hemodialysis is 23.3%. Haemodialysis is recommended for patients who progress to end- stage kidney disease (ESKD) and hypertensive nephropathy is the second most common cause of ESKD after diabetes.
- 16. References http://emedicine.medscape.com/article/244342- overview Harrisons Principles of Internal Medicine