This document summarizes the pathophysiology of acute and chronic renal failure. It describes how acute renal failure is characterized by a rapid decline in glomerular filtration rate over hours to weeks, leading to retention of waste products and oliguria. The main causes of acute renal failure are prerenal failure due to hypoperfusion, intrinsic renal failure due to direct kidney damage, and postrenal failure due to urinary tract obstruction. Chronic renal failure develops over months to years and is caused by a gradual loss of kidney function, leading to accumulation of waste products and complications like metabolic bone disease, anemia, and cardiovascular disease.
The document discusses the pathophysiology of acute and chronic renal failure. It defines acute renal failure (ARF) as a rapid decline in glomerular filtration rate over hours to weeks, leading to retention of waste products. ARF is classified into three types: prerenal, intrinsic renal, and postrenal (obstruction). Prerenal ARF is caused by hypoperfusion from factors like hypovolemia, low cardiac output, or increased renal vascular resistance. Intrinsic renal ARF is caused by issues like glomerulonephritis, acute tubular necrosis from ischemia or nephrotoxins, or interstitial nephritis. Chronic renal failure develops over time as the kidneys are
The kidneys perform several important functions including removing waste, regulating electrolytes and blood pressure, activating vitamin D, and stimulating red blood cell production. Acute renal failure refers to a sudden, usually reversible loss of kidney function over days or weeks and is commonly caused by decreased blood flow to the kidneys (pre-renal) or direct kidney damage (intrinsic). Pre-renal acute renal failure, which accounts for 60-70% of cases, is often due to low blood volume from causes like bleeding, burns, or diarrhea. It can typically be reversed by restoring blood volume and pressure through fluid resuscitation.
The document discusses acute renal failure (ARF), which refers to a sudden and usually reversible loss of renal function that develops over days or weeks. ARF can be pre-renal, intrinsic renal, or post-renal in cause. Reversible pre-renal ARF occurs when haemodynamic disturbances like hypotension produce acute dysfunction that can be rapidly reversed by treating the underlying cause and restoring renal perfusion. Left untreated, pre-renal ARF can progress to established acute tubular necrosis. Proper diagnosis involves assessing the cause, signs of poor perfusion, and urine and blood tests. Management focuses on correcting the underlying problem and restoring blood volume through fluids.
This document discusses acute and chronic renal failure. It defines acute renal failure as a rapid onset of renal dysfunction characterized by oliguria or anuria and increased metabolic waste products in the blood. Causes include pre-renal issues reducing blood flow, intra-renal kidney tissue diseases, and post-renal urinary obstruction. Chronic renal failure is a progressive and irreversible deterioration of renal function due to kidney parenchyma damage, ultimately resulting in death. It discusses diseases causing glomerular or tubulointerstitial damage and the four stages of chronic renal failure. Clinical features of both include fluid, electrolyte, and acid-base imbalances leading to primary uraemic manifestations and secondary extra-renal symptoms
Acute renal failure (ARF), now called acute kidney injury (AKI), is defined as a rapid decline in renal function over 48 hours characterized by increased serum creatinine and urea. It can be prerenal from decreased renal perfusion, intrinsic renal from direct kidney damage, or postrenal from urinary tract obstruction. The causes of ARF vary by region and healthcare access. Prerenal ARF is most common and usually reversible with volume restoration. Intrinsic ARF is often ischemic or toxic acute tubular necrosis. Postrenal ARF requires relief of obstruction. ARF is associated with electrolyte abnormalities and increased mortality. Management focuses on treating the underlying cause, preventing complications through fluid and electrolyte
This document discusses acute renal failure (ARF), including its causes, classification, pathophysiology, clinical features, investigations, and management. ARF is defined as the rapid onset of renal impairment resulting in the accumulation of nitrogenous waste products. It can be prerenal, intrinsic, or postrenal. Management involves prevention through proper fluid balance and monitoring, as well as conservative treatment and renal replacement therapy if needed. Symptoms include dyspnea, hypertension, arrhythmias, and neurological symptoms like confusion.
04 Differential Diagnosis Of Acute Renal Failureguest2379201
The document provides an overview of the differential diagnosis of acute renal failure (ARF). It discusses various causes that can lead to prerenal ARF including volume depletion, liver disease, heart failure, renal arterial disease, perinatal issues in newborns. It also covers intrinsic renal failure due to tubular diseases, interstitial diseases, glomerular diseases, vascula diseases, and nephrotoxins. Post-renal ARF due to urinary tract obstruction is also summarized. The document provides details on evaluation and laboratory findings that can help in differential diagnosis of ARF.
04 Differential Diagnosis Of Acute Renal FailureDang Thanh Tuan
The document provides an overview of the differential diagnosis of acute renal failure (ARF). It discusses various causes that can lead to prerenal ARF including volume depletion, liver disease, heart failure, renal arterial disease, hemorrhage, and asphyxia in newborns. Intrinsic renal failure can be caused by tubular diseases, interstitial diseases, glomerular diseases, or vascula diseases. Acute tubular necrosis is described as the most common cause. Post-renal ARF can result from urinary tract obstruction. Laboratory findings that can aid in diagnosis are also summarized.
The document discusses the pathophysiology of acute and chronic renal failure. It defines acute renal failure (ARF) as a rapid decline in glomerular filtration rate over hours to weeks, leading to retention of waste products. ARF is classified into three types: prerenal, intrinsic renal, and postrenal (obstruction). Prerenal ARF is caused by hypoperfusion from factors like hypovolemia, low cardiac output, or increased renal vascular resistance. Intrinsic renal ARF is caused by issues like glomerulonephritis, acute tubular necrosis from ischemia or nephrotoxins, or interstitial nephritis. Chronic renal failure develops over time as the kidneys are
The kidneys perform several important functions including removing waste, regulating electrolytes and blood pressure, activating vitamin D, and stimulating red blood cell production. Acute renal failure refers to a sudden, usually reversible loss of kidney function over days or weeks and is commonly caused by decreased blood flow to the kidneys (pre-renal) or direct kidney damage (intrinsic). Pre-renal acute renal failure, which accounts for 60-70% of cases, is often due to low blood volume from causes like bleeding, burns, or diarrhea. It can typically be reversed by restoring blood volume and pressure through fluid resuscitation.
The document discusses acute renal failure (ARF), which refers to a sudden and usually reversible loss of renal function that develops over days or weeks. ARF can be pre-renal, intrinsic renal, or post-renal in cause. Reversible pre-renal ARF occurs when haemodynamic disturbances like hypotension produce acute dysfunction that can be rapidly reversed by treating the underlying cause and restoring renal perfusion. Left untreated, pre-renal ARF can progress to established acute tubular necrosis. Proper diagnosis involves assessing the cause, signs of poor perfusion, and urine and blood tests. Management focuses on correcting the underlying problem and restoring blood volume through fluids.
This document discusses acute and chronic renal failure. It defines acute renal failure as a rapid onset of renal dysfunction characterized by oliguria or anuria and increased metabolic waste products in the blood. Causes include pre-renal issues reducing blood flow, intra-renal kidney tissue diseases, and post-renal urinary obstruction. Chronic renal failure is a progressive and irreversible deterioration of renal function due to kidney parenchyma damage, ultimately resulting in death. It discusses diseases causing glomerular or tubulointerstitial damage and the four stages of chronic renal failure. Clinical features of both include fluid, electrolyte, and acid-base imbalances leading to primary uraemic manifestations and secondary extra-renal symptoms
Acute renal failure (ARF), now called acute kidney injury (AKI), is defined as a rapid decline in renal function over 48 hours characterized by increased serum creatinine and urea. It can be prerenal from decreased renal perfusion, intrinsic renal from direct kidney damage, or postrenal from urinary tract obstruction. The causes of ARF vary by region and healthcare access. Prerenal ARF is most common and usually reversible with volume restoration. Intrinsic ARF is often ischemic or toxic acute tubular necrosis. Postrenal ARF requires relief of obstruction. ARF is associated with electrolyte abnormalities and increased mortality. Management focuses on treating the underlying cause, preventing complications through fluid and electrolyte
This document discusses acute renal failure (ARF), including its causes, classification, pathophysiology, clinical features, investigations, and management. ARF is defined as the rapid onset of renal impairment resulting in the accumulation of nitrogenous waste products. It can be prerenal, intrinsic, or postrenal. Management involves prevention through proper fluid balance and monitoring, as well as conservative treatment and renal replacement therapy if needed. Symptoms include dyspnea, hypertension, arrhythmias, and neurological symptoms like confusion.
04 Differential Diagnosis Of Acute Renal Failureguest2379201
The document provides an overview of the differential diagnosis of acute renal failure (ARF). It discusses various causes that can lead to prerenal ARF including volume depletion, liver disease, heart failure, renal arterial disease, perinatal issues in newborns. It also covers intrinsic renal failure due to tubular diseases, interstitial diseases, glomerular diseases, vascula diseases, and nephrotoxins. Post-renal ARF due to urinary tract obstruction is also summarized. The document provides details on evaluation and laboratory findings that can help in differential diagnosis of ARF.
04 Differential Diagnosis Of Acute Renal FailureDang Thanh Tuan
The document provides an overview of the differential diagnosis of acute renal failure (ARF). It discusses various causes that can lead to prerenal ARF including volume depletion, liver disease, heart failure, renal arterial disease, hemorrhage, and asphyxia in newborns. Intrinsic renal failure can be caused by tubular diseases, interstitial diseases, glomerular diseases, or vascula diseases. Acute tubular necrosis is described as the most common cause. Post-renal ARF can result from urinary tract obstruction. Laboratory findings that can aid in diagnosis are also summarized.
04 Differential Diagnosis Of Acute Renal FailureDang Thanh Tuan
The document provides an overview of the differential diagnosis of acute renal failure. It discusses prerenal, intrinsic renal, and postrenal causes of acute renal failure. Prerenal causes include volume depletion, advanced liver disease, congestive heart failure, and renal arterial disease. Intrinsic renal causes include tubular diseases, interstitial diseases, glomerular diseases, and vascula diseases. Postrenal causes involve urinary obstruction.
Acute renal failure (ARF) is a sudden decrease in kidney function that results in the buildup of waste products in the blood. It can be caused by decreased blood flow to the kidneys, direct kidney damage, or urinary tract obstruction. The most common type is prerenal ARF due to low blood volume or pressure. Symptoms include thirst, dizziness, and reduced urine output. Treatment focuses on correcting the underlying cause, managing fluid balance and dialysis if needed. ARF is usually reversible but can last weeks depending on the severity of the initial insult.
Acute renal failure (ARF) is defined as a rapid decline in kidney function over days or weeks. It can be caused by pre-renal factors that decrease blood flow to the kidneys, intrinsic renal disease, or post-renal obstruction of urine flow. ARF is characterized by rising levels of blood urea and creatinine, decreased urine output, and a decline in glomerular filtration rate. Diagnosis involves laboratory tests of blood and urine as well as imaging studies like ultrasound. Complications of ARF include electrolyte imbalances, pulmonary edema, bleeding, and metabolic acidosis. Prevention focuses on avoiding dehydration in high-risk patients and using caution with nephrotoxic drugs.
This document provides an overview of common renal disorders, including acute renal failure (ARF), chronic renal failure, nephrotic syndrome, nephrolithiasis, and renal tubular acidosis. ARF is characterized by a rapid decline in glomerular filtration rate and is divided into prerenal, intrinsic renal, and postrenal types. Chronic renal failure is usually caused by diabetes or glomerulonephritis and results in metabolic abnormalities and uremic syndrome. Nephrotic syndrome involves proteinuria, hypoalbuminemia, edema, and hyperlipidemia due to increased glomerular permeability. Nephrolithiasis is caused by supersaturation of urine leading to stone formation,
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 acute kidney injury (AKI), including its definition, classification, causes, diagnostic evaluation and management. AKI can be prerenal, intrinsic renal or postrenal. Prerenal AKI is due to reduced renal blood flow and reversible. Intrinsic renal AKI involves direct kidney damage from factors like ischemia or toxins. Postrenal AKI is due to urinary tract obstruction. Evaluation includes urine and blood tests. Management focuses on treating the underlying cause, maintaining fluid/electrolyte balance and preventing complications through supportive care and possibly dialysis.
Acute renal failure (ARF) is the sudden loss of kidney function, causing a build up of waste products in the blood. It can be oliguric or non-oliguric depending on urine output. ARF has three main causes - prerenal from low blood flow, intrinsic kidney damage, or postrenal from urinary obstruction. Management involves fluid management, electrolyte control, antibiotics for infection, and possibly dialysis. Nurses monitor patients closely and prevent complications through infection control and skin care.
Renal failure is divided into acute renal failure (ARF) and chronic renal failure (CRF). ARF is characterized by rapid onset of renal dysfunction and increased waste products in the blood. It can be caused by issues with blood flow (pre-renal), the kidneys themselves (intra-renal), or urine outflow (post-renal). CRF is a progressive loss of renal function that eventually leads to end-stage kidney disease. It is caused by damage to the glomeruli or tubulointerstitial tissues and develops over four stages with declining kidney function and increasing symptoms of uraemia.
The document summarizes renal functions, morphology, anatomy, urine formation, and clinical assessment of renal function. It describes the categories of acute renal failure as prerenal, intrinsic renal, or postrenal. Prerenal azotemia is caused by decreased effective blood volume or impaired renal blood flow and is reversible. Intrinsic renal azotemia directly involves the renal parenchyma, commonly from acute tubular necrosis or glomerulonephritis. Postrenal azotemia results from bilateral ureteric obstruction. Laboratory findings and urinalysis can help distinguish the three categories.
This document discusses acute renal failure (ARF) and its causes, definitions, and classifications. It describes the key components of the nephron and how ARF results from a reduction in glomerular filtration rate (GFR). ARF can be classified as pre-renal, renal, or post-renal based on its underlying cause and pathophysiology. The most common type of renal ARF is acute tubular necrosis (ATN), which results from intrinsic injury to the renal tubules.
This document provides an overview of acute and chronic renal failure. It defines renal failure as loss of kidney function and describes how acute renal failure has a sudden onset and is potentially reversible, while chronic failure progresses slowly over months or years. The major causes, symptoms, and metabolic consequences of both acute and chronic renal failure are discussed. Laboratory findings and management approaches for acute renal failure are also outlined. The document contrasts the features of acute versus chronic renal failure and describes problems related to end-stage renal disease as well as dialysis options.
The kidneys filter blood and regulate fluid levels in the body by selectively reabsorbing or secreting solutes. Urine passes from the kidneys through ureters into the bladder, then through the urethra. The kidneys contain nephrons which filter blood and reabsorb or excrete products. Hematuria, the presence of blood in urine, can indicate issues ranging from minor infections to serious conditions like cancer and requires medical evaluation.
Acute renal failure is a sudden loss of kidney function over hours to days that results in oliguria or anuria and the buildup of waste products like BUN and creatinine in the blood. It can be caused by prerenal factors like decreased blood flow or direct kidney damage. Treatment focuses on restoring blood flow and removing waste until the kidneys can recover. Chronic kidney disease is progressive and irreversible, resulting in permanent kidney damage and uremia if untreated with dialysis or transplant.
Acute renal failure is characterized by rapid onset of renal dysfunction and increased metabolic waste products in the blood. It can be caused by pre-renal issues which decrease blood flow to the kidneys, intra-renal issues involving direct kidney damage, or post-renal issues obstructing urine flow. Symptoms include electrolyte imbalances, decreased urine output, and buildup of waste products in the blood. Treatment focuses on supporting blood volume and pressure, correcting fluid and electrolyte levels, and using dialysis to filter waste if the kidneys are no longer functioning properly.
Acute renal failure (ARF) is characterized by a rapid decline in renal function and the accumulation of metabolic waste products in the blood. It can be caused by pre-renal issues that decrease blood flow to the kidneys, intra-renal kidney damage, or post-renal urinary tract obstruction. Chronic renal failure (CRF) is the gradual, irreversible loss of kidney function that can result from glomerular diseases or tubulointerstitial diseases and progresses through stages from decreased function to end-stage kidney disease. The clinical manifestations of CRF include primary uraemic effects like metabolic acidosis as well as secondary extra-renal effects that impact multiple organ systems.
Chronic renal failure is an irreversible deterioration in renal function that develops over years. It initially only causes biochemical abnormalities but eventually leads to uraemia and loss of kidney excretory, metabolic and endocrine functions. The most common causes are diabetes, hypertension, and glomerulonephritis. As kidney function declines, patients experience widespread effects including anaemia, acidosis, cardiovascular disease, bone disease, muscle problems, neuropathy, endocrine abnormalities, bleeding issues, and increased susceptibility to infection.
1. Acute renal failure (ARF) and chronic renal failure (CRF) were defined. ARF is abrupt in onset and often reversible, while CRF develops over time and is generally irreversible.
2. There are three main types of ARF - pre-renal from decreased blood flow, intrinsic/intra-renal from kidney damage, and post-renal from urinary tract obstruction.
3. Causes, pathophysiology, signs and symptoms, and diagnostic tests for ARF were outlined, along with the multiple phases ARF can progress through. Management of fluid, electrolyte, and acid-base imbalances was also discussed.
Acute renal failure (ARF) is defined as a rapid loss of kidney function over hours to days. It occurs when the kidneys are unable to excrete daily toxins due to damage. To properly diagnose ARF, a thorough history, physical exam, and lab tests are required to determine the cause (pre-renal, intrinsic, post-renal) and severity. Treatment involves fluid resuscitation, electrolyte management, treating the underlying cause, and potentially renal replacement therapies like dialysis. The goal of treatment is to reverse ARF and restore kidney function if possible.
Asthma is a chronic inflammatory lung disease that causes narrowing of the airways. It affects over 300 million people worldwide. The hallmark symptoms of asthma include wheezing, coughing, chest tightness, and shortness of breath. Asthma is caused by a combination of genetic and environmental factors that lead to airway inflammation and constriction. Common triggers include allergens, viruses, exercise, and air pollution. Diagnosis involves lung function tests to measure airflow limitation and its improvement with bronchodilator medication. Treatment focuses on reducing symptoms with bronchodilators and preventing exacerbations with anti-inflammatory drugs like corticosteroids.
04 Differential Diagnosis Of Acute Renal FailureDang Thanh Tuan
The document provides an overview of the differential diagnosis of acute renal failure. It discusses prerenal, intrinsic renal, and postrenal causes of acute renal failure. Prerenal causes include volume depletion, advanced liver disease, congestive heart failure, and renal arterial disease. Intrinsic renal causes include tubular diseases, interstitial diseases, glomerular diseases, and vascula diseases. Postrenal causes involve urinary obstruction.
Acute renal failure (ARF) is a sudden decrease in kidney function that results in the buildup of waste products in the blood. It can be caused by decreased blood flow to the kidneys, direct kidney damage, or urinary tract obstruction. The most common type is prerenal ARF due to low blood volume or pressure. Symptoms include thirst, dizziness, and reduced urine output. Treatment focuses on correcting the underlying cause, managing fluid balance and dialysis if needed. ARF is usually reversible but can last weeks depending on the severity of the initial insult.
Acute renal failure (ARF) is defined as a rapid decline in kidney function over days or weeks. It can be caused by pre-renal factors that decrease blood flow to the kidneys, intrinsic renal disease, or post-renal obstruction of urine flow. ARF is characterized by rising levels of blood urea and creatinine, decreased urine output, and a decline in glomerular filtration rate. Diagnosis involves laboratory tests of blood and urine as well as imaging studies like ultrasound. Complications of ARF include electrolyte imbalances, pulmonary edema, bleeding, and metabolic acidosis. Prevention focuses on avoiding dehydration in high-risk patients and using caution with nephrotoxic drugs.
This document provides an overview of common renal disorders, including acute renal failure (ARF), chronic renal failure, nephrotic syndrome, nephrolithiasis, and renal tubular acidosis. ARF is characterized by a rapid decline in glomerular filtration rate and is divided into prerenal, intrinsic renal, and postrenal types. Chronic renal failure is usually caused by diabetes or glomerulonephritis and results in metabolic abnormalities and uremic syndrome. Nephrotic syndrome involves proteinuria, hypoalbuminemia, edema, and hyperlipidemia due to increased glomerular permeability. Nephrolithiasis is caused by supersaturation of urine leading to stone formation,
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 acute kidney injury (AKI), including its definition, classification, causes, diagnostic evaluation and management. AKI can be prerenal, intrinsic renal or postrenal. Prerenal AKI is due to reduced renal blood flow and reversible. Intrinsic renal AKI involves direct kidney damage from factors like ischemia or toxins. Postrenal AKI is due to urinary tract obstruction. Evaluation includes urine and blood tests. Management focuses on treating the underlying cause, maintaining fluid/electrolyte balance and preventing complications through supportive care and possibly dialysis.
Acute renal failure (ARF) is the sudden loss of kidney function, causing a build up of waste products in the blood. It can be oliguric or non-oliguric depending on urine output. ARF has three main causes - prerenal from low blood flow, intrinsic kidney damage, or postrenal from urinary obstruction. Management involves fluid management, electrolyte control, antibiotics for infection, and possibly dialysis. Nurses monitor patients closely and prevent complications through infection control and skin care.
Renal failure is divided into acute renal failure (ARF) and chronic renal failure (CRF). ARF is characterized by rapid onset of renal dysfunction and increased waste products in the blood. It can be caused by issues with blood flow (pre-renal), the kidneys themselves (intra-renal), or urine outflow (post-renal). CRF is a progressive loss of renal function that eventually leads to end-stage kidney disease. It is caused by damage to the glomeruli or tubulointerstitial tissues and develops over four stages with declining kidney function and increasing symptoms of uraemia.
The document summarizes renal functions, morphology, anatomy, urine formation, and clinical assessment of renal function. It describes the categories of acute renal failure as prerenal, intrinsic renal, or postrenal. Prerenal azotemia is caused by decreased effective blood volume or impaired renal blood flow and is reversible. Intrinsic renal azotemia directly involves the renal parenchyma, commonly from acute tubular necrosis or glomerulonephritis. Postrenal azotemia results from bilateral ureteric obstruction. Laboratory findings and urinalysis can help distinguish the three categories.
This document discusses acute renal failure (ARF) and its causes, definitions, and classifications. It describes the key components of the nephron and how ARF results from a reduction in glomerular filtration rate (GFR). ARF can be classified as pre-renal, renal, or post-renal based on its underlying cause and pathophysiology. The most common type of renal ARF is acute tubular necrosis (ATN), which results from intrinsic injury to the renal tubules.
This document provides an overview of acute and chronic renal failure. It defines renal failure as loss of kidney function and describes how acute renal failure has a sudden onset and is potentially reversible, while chronic failure progresses slowly over months or years. The major causes, symptoms, and metabolic consequences of both acute and chronic renal failure are discussed. Laboratory findings and management approaches for acute renal failure are also outlined. The document contrasts the features of acute versus chronic renal failure and describes problems related to end-stage renal disease as well as dialysis options.
The kidneys filter blood and regulate fluid levels in the body by selectively reabsorbing or secreting solutes. Urine passes from the kidneys through ureters into the bladder, then through the urethra. The kidneys contain nephrons which filter blood and reabsorb or excrete products. Hematuria, the presence of blood in urine, can indicate issues ranging from minor infections to serious conditions like cancer and requires medical evaluation.
Acute renal failure is a sudden loss of kidney function over hours to days that results in oliguria or anuria and the buildup of waste products like BUN and creatinine in the blood. It can be caused by prerenal factors like decreased blood flow or direct kidney damage. Treatment focuses on restoring blood flow and removing waste until the kidneys can recover. Chronic kidney disease is progressive and irreversible, resulting in permanent kidney damage and uremia if untreated with dialysis or transplant.
Acute renal failure is characterized by rapid onset of renal dysfunction and increased metabolic waste products in the blood. It can be caused by pre-renal issues which decrease blood flow to the kidneys, intra-renal issues involving direct kidney damage, or post-renal issues obstructing urine flow. Symptoms include electrolyte imbalances, decreased urine output, and buildup of waste products in the blood. Treatment focuses on supporting blood volume and pressure, correcting fluid and electrolyte levels, and using dialysis to filter waste if the kidneys are no longer functioning properly.
Acute renal failure (ARF) is characterized by a rapid decline in renal function and the accumulation of metabolic waste products in the blood. It can be caused by pre-renal issues that decrease blood flow to the kidneys, intra-renal kidney damage, or post-renal urinary tract obstruction. Chronic renal failure (CRF) is the gradual, irreversible loss of kidney function that can result from glomerular diseases or tubulointerstitial diseases and progresses through stages from decreased function to end-stage kidney disease. The clinical manifestations of CRF include primary uraemic effects like metabolic acidosis as well as secondary extra-renal effects that impact multiple organ systems.
Chronic renal failure is an irreversible deterioration in renal function that develops over years. It initially only causes biochemical abnormalities but eventually leads to uraemia and loss of kidney excretory, metabolic and endocrine functions. The most common causes are diabetes, hypertension, and glomerulonephritis. As kidney function declines, patients experience widespread effects including anaemia, acidosis, cardiovascular disease, bone disease, muscle problems, neuropathy, endocrine abnormalities, bleeding issues, and increased susceptibility to infection.
1. Acute renal failure (ARF) and chronic renal failure (CRF) were defined. ARF is abrupt in onset and often reversible, while CRF develops over time and is generally irreversible.
2. There are three main types of ARF - pre-renal from decreased blood flow, intrinsic/intra-renal from kidney damage, and post-renal from urinary tract obstruction.
3. Causes, pathophysiology, signs and symptoms, and diagnostic tests for ARF were outlined, along with the multiple phases ARF can progress through. Management of fluid, electrolyte, and acid-base imbalances was also discussed.
Acute renal failure (ARF) is defined as a rapid loss of kidney function over hours to days. It occurs when the kidneys are unable to excrete daily toxins due to damage. To properly diagnose ARF, a thorough history, physical exam, and lab tests are required to determine the cause (pre-renal, intrinsic, post-renal) and severity. Treatment involves fluid resuscitation, electrolyte management, treating the underlying cause, and potentially renal replacement therapies like dialysis. The goal of treatment is to reverse ARF and restore kidney function if possible.
Asthma is a chronic inflammatory lung disease that causes narrowing of the airways. It affects over 300 million people worldwide. The hallmark symptoms of asthma include wheezing, coughing, chest tightness, and shortness of breath. Asthma is caused by a combination of genetic and environmental factors that lead to airway inflammation and constriction. Common triggers include allergens, viruses, exercise, and air pollution. Diagnosis involves lung function tests to measure airflow limitation and its improvement with bronchodilator medication. Treatment focuses on reducing symptoms with bronchodilators and preventing exacerbations with anti-inflammatory drugs like corticosteroids.
Asthma is a chronic disease characterized by inflammation of the airways causing coughing, wheezing, chest tightness, and difficulty breathing. It is usually caused by allergic triggers like pollen, dust mites, or animal dander that lead to bronchospasms and airway obstruction. Diagnosis involves patient history, physical exam, pulmonary function tests, and allergy testing. Treatment includes bronchodilators, corticosteroids, leukotriene modifiers, and monoclonal antibodies to reduce inflammation and prevent symptoms.
Ischaemic heart disease is caused by an imbalance between the heart's supply and demand for oxygenated blood, usually due to atherosclerosis narrowing the coronary arteries. The main symptoms are chest pain or discomfort known as angina. There are different types of angina that vary based on their triggers and patterns. Diagnosis involves tests like ECG, echocardiogram, stress tests and angiography. Treatment options include medications to reduce demands on the heart like nitrates, beta-blockers, and calcium channel blockers, as well as interventions like angioplasty, stents and bypass surgery.
Atherosclerosis is a disease where plaque builds up in the arteries. Over time, the plaque hardens and narrows the arteries, limiting blood flow. Risk factors include age, family history, smoking, high blood pressure, high cholesterol, diabetes, and obesity. Complications arise when blood flow is reduced to organs like the heart, brain, kidneys, and limbs, potentially causing heart attacks, strokes, chronic kidney disease, or poor circulation. Treatment focuses on lifestyle changes and medications to control risk factors and symptoms.
This document provides an outline for a lecture on hypertension. It begins with objectives to understand hypertension's etiology, risk factors, and complications. It then covers definitions of hypertension, classifications based on cause and clinical features, risk factors, pathogenesis, regulation of blood pressure, vascular changes in hypertension, and complications affecting the heart, blood vessels, kidneys, eyes, and brain. The lecture topics include primary and secondary causes, benign vs malignant hypertension, endocrine factors influencing blood pressure, and target organ damage.
Hypertension and its pathophysiology.pptxImtiyaz60
The document discusses hypertension and the heart. It provides details on:
- The structure and layers of the heart, including the myocardium and pericardium.
- The path of blood through the heart, from the vena cava and atria to the ventricles, valves, and out the aorta to the body.
- Additional details are given on heart size, location in the thoracic cavity, and the double-walled pericardium surrounding and protecting the heart.
This document discusses various appetite stimulants, digestants, and carminatives. It describes how appetite is influenced by several factors in the hypothalamus and gut-brain pathways. Common appetite stimulants mentioned include lemon pickles, bitter orange peel, and soups containing aromatic oils. Some medications can increase appetite but also have side effects. The document also discusses various digestive enzymes and bile acids that may aid digestion, though evidence for their efficacy is limited. Finally, it outlines several common carminative herbs and spices that can relieve gas and bloating.
Anti Ulcer drugs pharmacology and classificationImtiyaz60
This document summarizes drugs used to treat peptic ulcers. It discusses the anatomy and physiology of gastric acid secretion regulated by histamine, acetylcholine, and gastrin. It describes prostaglandins' protective role in the stomach and how H2 receptor blockers and proton pump inhibitors work to suppress acid secretion. H2 blockers competitively inhibit histamine receptors, while PPIs irreversibly inactivate the proton pump. Common medications discussed include cimetidine, ranitidine, famotidine, omeprazole, and lansoprazole. The goals of anti-ulcer therapy are relieving pain, promoting healing, and preventing complications and relapse.
Ginger and asafoetida are plants with medicinal properties. Ginger is native to Southeast Asia and cultivated in many tropical regions. It has buff-colored rhizomes with an aromatic odor and taste. Chemical constituents include volatile oils and phenolic compounds that give ginger its flavor and pharmacological effects. Asafoetida is an oleo-gum-resin obtained from Ferula plants. It occurs in tear or mass forms, has an intense odor, and chemical tests detect umbelliferone. Both ginger and asafoetida have traditional uses as carminatives, expectorants, and to treat conditions like nausea, flatulence, and asthma. They can be subject to adulteration
Leprosy is caused by Mycobacterium leprae. It primarily affects the skin and peripheral nerves, causing hypopigmented patches and thickening of nerves. There are two main forms - tuberculoid leprosy, which causes localized lesions, and lepromatous leprosy, which involves multiple organs. Diagnosis involves skin smears and biopsies to identify acid-fast bacilli. Treatment involves multidrug chemotherapy regimens containing dapsone, rifampicin, and clofazimine. Prevention focuses on contact tracing, chemoprophylaxis, isolation during reactions, and rehabilitation.
Tuberculosis (TB) is a chronic bacterial infection caused by Mycobacterium tuberculosis that typically forms granulomas in the lungs. It is treatable with a combination of anti-TB drugs over a 6-12 month period to kill both actively replicating and dormant bacilli. Diagnosis involves physical exam, chest x-ray, tuberculin skin test, and sputum culture. Risk factors include HIV infection, poverty, and crowded living conditions.
Stroke is the 5th leading cause of death in the US. There are three main types of stroke: ischemic, hemorrhagic, and transient ischemic attacks (TIAs). Ischemic strokes, which account for 85% of cases, occur when a blood clot blocks an artery supplying blood to the brain. Hemorrhagic strokes occur when a brain artery ruptures due to conditions like hypertension. TIAs are temporary and cause no permanent damage but indicate risk for future strokes. Symptoms of stroke appear suddenly and include face drooping, arm weakness, speech difficulties, and severe headache. Diagnostic tests help determine the type and location of stroke. Lifestyle changes and medical treatment can help prevent strokes.
The thyroid gland is located in the neck below the larynx. It produces thyroid hormones including thyroxine (T4) and triiodothyronine (T3) which increase metabolism in nearly every organ system. Iodine is necessary for thyroid hormone production. Disorders include hypothyroidism, where thyroid hormone production is inadequate, and hyperthyroidism, where production is excessive. Graves' disease is an autoimmune cause of hyperthyroidism. Cretinism results from untreated congenital hypothyroidism and causes severe physical and mental impairment.
Inflammatory bowel disease (IBD) represents a group of chronic disorders that cause prolonged inflammation of the digestive tract. The two main types are ulcerative colitis, which causes inflammation and ulcers in the lining of the large intestine, and Crohn's disease, which is a chronic inflammatory disease that can affect any part of the gastrointestinal tract from mouth to anus. IBD is treated through a combination of medications, dietary changes, and sometimes surgery, with the goals of inducing and maintaining remission of symptoms, preventing complications, and avoiding surgery if possible. Treatments include aminosalicylates, corticosteroids, immunosuppressants, biologics that target tumor necrosis factor, and antimicrobial agents.
Tannins are polyphenolic compounds found in many plants. They are classified as hydrolysable tannins, condensed tannins, or pseudo-tannins. Hydrolysable tannins are hydrolyzed by acids into gallic acid or ellagic acid, while condensed tannins are more resistant to hydrolysis. Tannins are extracted using mixtures of polar and non-polar solvents due to their high molecular weight. Identification tests for tannins include the gelatin test, Goldbeater's skin test, and reactions with ferrous sulfate or ferric chloride that produce colors. Pterocarpus marsupium, or Bijasal, is a plant source of k
This document discusses various drug classes used in the treatment of heart failure, including their mechanisms and effects. Diuretics reduce preload on the heart by reducing extracellular fluid volume through natriuresis. Vasodilators such as nitroglycerin and ACE inhibitors reduce preload and afterload by dilating blood vessels. Nesiritide is a natriuretic peptide that causes vasodilation and natriuresis. β-blockers improve outcomes in heart failure by inhibiting the deleterious effects of sympathetic activation on the heart.
Tuberculosis (TB) is a bacterial infection caused by Mycobacterium tuberculosis that most commonly infects the lungs. It can be treated with antibiotics. TB is spread through airborne droplets when an infected person coughs or sneezes. While latent TB means the immune system has contained the infection and the person is not infectious, active TB means the person is sick and can spread the disease. Standard TB treatment involves a combination of antibiotics like isoniazid, rifampin and ethambutol over a period of 6-9 months.
The document discusses infectious diseases and infectious agents. It covers host barriers to infection like the skin, respiratory system, gastrointestinal tract, and urogenital tract. It describes how these barriers can fail and allow infection. It also discusses the different classes of infectious agents including bacteria, viruses, fungi and parasites. The document outlines the different types of inflammatory responses infections can cause like suppurative inflammation, granulomatous inflammation, and cytopathic responses. It covers how microbes can evade the immune system and the various ways infections can be transmitted.
The document defines key terms related to the electrophysiology of the heart such as action potential, membrane potential, refractory period, and threshold potential. It then describes the four phases of the cardiac action potential: Phase 0 involves stimulation and sodium/calcium influx causing depolarization; Phase 1 involves partial repolarization through ion efflux; Phase 2 involves a plateau phase through continued ion fluxes; Phase 3 involves full repolarization through ion efflux slower than depolarization. Phase 4 is the interval between repolarizations. The cardiac action potential triggers mechanical contraction. An electrocardiogram detects and records the summed action potentials to analyze patterns like the P, QRS, and T waves related to atrial depolarization, ventricular depolarization
THE SACRIFICE HOW PRO-PALESTINE PROTESTS STUDENTS ARE SACRIFICING TO CHANGE T...indexPub
The recent surge in pro-Palestine student activism has prompted significant responses from universities, ranging from negotiations and divestment commitments to increased transparency about investments in companies supporting the war on Gaza. This activism has led to the cessation of student encampments but also highlighted the substantial sacrifices made by students, including academic disruptions and personal risks. The primary drivers of these protests are poor university administration, lack of transparency, and inadequate communication between officials and students. This study examines the profound emotional, psychological, and professional impacts on students engaged in pro-Palestine protests, focusing on Generation Z's (Gen-Z) activism dynamics. This paper explores the significant sacrifices made by these students and even the professors supporting the pro-Palestine movement, with a focus on recent global movements. Through an in-depth analysis of printed and electronic media, the study examines the impacts of these sacrifices on the academic and personal lives of those involved. The paper highlights examples from various universities, demonstrating student activism's long-term and short-term effects, including disciplinary actions, social backlash, and career implications. The researchers also explore the broader implications of student sacrifices. The findings reveal that these sacrifices are driven by a profound commitment to justice and human rights, and are influenced by the increasing availability of information, peer interactions, and personal convictions. The study also discusses the broader implications of this activism, comparing it to historical precedents and assessing its potential to influence policy and public opinion. The emotional and psychological toll on student activists is significant, but their sense of purpose and community support mitigates some of these challenges. However, the researchers call for acknowledging the broader Impact of these sacrifices on the future global movement of FreePalestine.
A Free 200-Page eBook ~ Brain and Mind Exercise.pptxOH TEIK BIN
(A Free eBook comprising 3 Sets of Presentation of a selection of Puzzles, Brain Teasers and Thinking Problems to exercise both the mind and the Right and Left Brain. To help keep the mind and brain fit and healthy. Good for both the young and old alike.
Answers are given for all the puzzles and problems.)
With Metta,
Bro. Oh Teik Bin 🙏🤓🤔🥰
Elevate Your Nonprofit's Online Presence_ A Guide to Effective SEO Strategies...TechSoup
Whether you're new to SEO or looking to refine your existing strategies, this webinar will provide you with actionable insights and practical tips to elevate your nonprofit's online presence.
Gender and Mental Health - Counselling and Family Therapy Applications and In...PsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
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إضغ بين إيديكم من أقوى الملازم التي صممتها
ملزمة تشريح الجهاز الهيكلي (نظري 3)
💀💀💀💀💀💀💀💀💀💀
تتميز هذهِ الملزمة بعِدة مُميزات :
1- مُترجمة ترجمة تُناسب جميع المستويات
2- تحتوي على 78 رسم توضيحي لكل كلمة موجودة بالملزمة (لكل كلمة !!!!)
#فهم_ماكو_درخ
3- دقة الكتابة والصور عالية جداً جداً جداً
4- هُنالك بعض المعلومات تم توضيحها بشكل تفصيلي جداً (تُعتبر لدى الطالب أو الطالبة بإنها معلومات مُبهمة ومع ذلك تم توضيح هذهِ المعلومات المُبهمة بشكل تفصيلي جداً
5- الملزمة تشرح نفسها ب نفسها بس تكلك تعال اقراني
6- تحتوي الملزمة في اول سلايد على خارطة تتضمن جميع تفرُعات معلومات الجهاز الهيكلي المذكورة في هذهِ الملزمة
واخيراً هذهِ الملزمة حلالٌ عليكم وإتمنى منكم إن تدعولي بالخير والصحة والعافية فقط
كل التوفيق زملائي وزميلاتي ، زميلكم محمد الذهبي 💊💊
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A Visual Guide to 1 Samuel | A Tale of Two HeartsSteve Thomason
These slides walk through the story of 1 Samuel. Samuel is the last judge of Israel. The people reject God and want a king. Saul is anointed as the first king, but he is not a good king. David, the shepherd boy is anointed and Saul is envious of him. David shows honor while Saul continues to self destruct.
2. Acute renal failure (ARF)
• Rapid decline in glomerular filtration rate
(hours to weeks)
• Retention of nitrogenous waste products
– occurs in 5% of all hospital admission and
up to 30% of admission to intensive care
units
3. • Oliguria (urine output <400 ml/d) is
frequent
• ARF is usually asymptomatic and is
diagnosed when screening of hospitalized
patients reveals a recent increase in
serum blood urea nitrogen and creatinine
4. ARF
• May complicate a wide range of diseases
which for purposes of diagnosis and
management are conveniently divided into 3
categories:
1. Disorders of renal perfusion
– kidney is intrinsically normal (prerenal azotemia,
prerenal ARF) (~55%)
2. Diseases of renal parenchyma
– (renal azotemia, renal ARF) (~40%)
3. Acute obstruction of the urinary tract
– (postrenal azotemia, postrenal ARF) (~5%)
7. ARF
• usually reversible
• a major cause of in-hospital morbidity
and mortality due to the serious nature
of the underlying illnesses and the high
incidence of complications
8. ARF – etiology and pathophysiology
Prerenal azotemia (prerenal ARF)
– Due to a functional response to renal
hypoperfusion.
– Is rapidly reversible upon restoration of
renal blood flow and glomerular
ultrafiltration pressure.
– Renal parenchymal tissue is not damaged.
– Severe or prolonged hypoperfusion may
lead to ischemic renal parenchymal injury
and intrinsic renal azotemia
10. Major causes of prerenal ARF
2. Low cardiac output
• Diseases of myocardium, valves, and pericardium,
arrhythmias, tamponade
• Other: pulmonary hypertension, pulmonary embolus
3. Increased renal systemic vascular resistance
ratio
• Systemic vasodilatation: sepsis, vasodilator therapy,
anesthesia, anaphylaxis
• Renal vasoconstriction: hypercalcemia,
norepinephrine, epinephrine
• Cirrhosis with ascites
11. • Prerenal azotemia (prerenal ARF)
– Due to a functional response to renal
hypoperfusion
hypovolemia
mean arterial pressure
detection as reduced stretch by arterial (e.g.
carotid sinus) and cardiac baroreceptors
trigger a series of neurohumoral responses to
maintain arterial pressure:
• activation of symptahetic nervous system
• RAA
• releasing of vasopresin (AVP, ADH) and endothelin
12. • Prerenal azotemia (prerenal ARF)
– Is rapidly reversible upon restoration of renal
blood flow and glomerular ultrafiltration
pressure
norepinephrine
angiotensin II
ADH
endothelin
vasoconstriction in musculocutaneous and
splanchnic vascular beds
reduction of salt loss through sweat glands
thirst and salt appetite stimulation
renal salt and water retention
16. • Renal azotemia (renal ARF)
– Most cases are caused either by ischemia
secondary to renal hypoperfusion
ischemic ARF
– or toxins nephrotoxic ARF
Ischemic and nephrotoxic ARF are
frequently associated with necrosis of
tubule epithelial cells – this syndrome is
often referred to as acute tubular necrosis
(ATN)
17. Ischemic ARF
– Renal hypoperfusion from any cause may
lead to ischemic ARF if severe enough to
overwhelm renal autoregulatory and
neurohumoral defence mechanisms
– It occurs not frequently after
cardiovascular surgery, trauma,
hemorrhage, sepsis or dehydration
19. Ischemic ARF
• Mechanisms by which renal hypoperfusion and
ischemia impair glomerular filtration include
– Reduction in glomerular perfusion and filtration
– Obstruction of urine flow in tubules by cells and debris
(including casts) derived from ischemic tubule
epithelium
– Backleak of glomerular filtrate through ischemic tubule
epithelium
– Neutrophil activation within the renal vasculature and
neutrophil-mediated cell injury may contribute
22. Fate of an injured proximal tubule cell after an ischemic
episode depends on the extent and duration of ischemia
23. • Renal hypoperfusion leads to ischemia of
renal tubule cells particularly the terminal
straight portion of proximal tubule (pars
recta) and the thick ascending limb of the
loop of Henle
• These segments traverse corticomedullary
junction and outer medulla, regions of the
kidney that are relatively hypoxic compared
with the renal cortex, because of the unique
counterurrent arrangement of the
vasculature
24. Nephrotoxic ARF
– The kidney is particularly susceptible to
nephrotic injury by virtue of its
• Rich blood supply (25 % of CO)
• Ability to concentrate toxins in medullary
interstitium (via the renal countercurrent
mechanism)
• Renal epithelial cells (via specific transporters)
25. • Radiocontrast agents
• Mechanisms: intrarenal vasoconstriction and
ischemia triggered by endothelin release from
endothelial cells, direct tubular toxicity
Intraluminal precipitation of protein or uric acid
crystals
• Rhabdomyolysis and hemolysis can cause ARF,
particularly in hypovolemic or acidotic individuals
– Rhabdomyolysis and myoglobinuric ARF may occur with
traumatic crush injury
• Muscle ischemia (e.g. arterial insufficiency, muscle
compression, cocaine overdose), seizures, excessive
exercise, heat stroke or malignant hyperthermia,
alcoholism, and infections (e.g. influenza, legionella),
etc.
26. • ARF due to hemolysis is seen most commonly
following blood transfusion reactions
• The mechanisms by which rhabdomyolysis and
hemolysis impair GFR are unclear, since neither
hemoglobin nor myoglobin is nephrotoxic when
injected to laboratory animals
• Myoglobin and hemoglobin or other compounds
release from muscle or red blood cells may cause
ARF via direct toxic effects on tubule epithelial
cells or by inducing intratubular cast formation;
they inhibit nitric oxide and may trigger intrarenal
vasoconstriction
27. Postrenal azotemia (postrenal ARF)
Major causes
1. Ureteric
calculi, blood clot, cancer
2. Bladder neck
neurogenic bladder, prostatic hyperplasia,
calculi, blood clot, cancer
3. Urethra
stricture
28. Mechanisms:
• During the early stages of obstruction (hours
to days), continued glomerular filtration lead
to increase intraluminal pressure upstream
to the obstruction, eventuating in gradual
distension of proximal ureter, renal pelvis,
and calyces and a fall in GFR
30. Chronic renal failure (CRF)
• Many forms of renal injury progress inexoraly
to CRF
• Reduction of renal mass causes structural
and functional hypertrophy of remaining
nephrons
• This compensatory hypertrophy is due to
adaptive hyperfiltration mediated by
increases in glomerular capillary pressures
and flows
31. Chronic renal failure (CRF) - causes
• Glomerulonephritis – the most common
cause in the past
• Diabetes mellitus
• Hypertension
• Tubulointerstitial nephritis
– are now the leading causes of CRF
32. Consequences of sustained reduction in
GFR
• GFR – sensitive index of overall renal
excretory function
• GFR retention and accumulation of
the unexcreted substances in the body
fluids
–A – urea, creatinine
–B – H+, K+, phosphates, urates
–C – Na+
34. Uremia
Is clinical syndrome that results from profound
loss of renal function
Cause(s) of it remains unknown
Refers generally to the constellation of signs and
symptoms associated with CRF, regardless of
cause
Presentations and severity of signs and symptoms
of uremia vary and depend on
the magnitude of reduction in functioning renal
mass
rapidity with which renal function is lost
35. Uremia – pathophysiology and
biochemistry
• The most likely candidates as toxins in uremia
are the by–products of protein and amino acid
metabolism
– Urea – represents some 80% of the total nitrogen
excreted into the urine
– Guanidino compunds: guanidine, creatinine,
creatin, guanidin-succinic acid)
– Urates and other end products of nucleic acid
metabolism
– Aliphatic amines
– Peptides
– Derivates of the aromatic amino acids: tryptophan,
tyrosine, and phenylalanine
36. Uremia – pathophysiology and
biochemistry
• The role of these various substances in the
pathogenesis of uremic syndrome is unclear
• Uremic symptoms correlate only in a rough
and inconsistent way with concentrations of
urea in blood
• Urea may account for some of clinical
abnormalities: anorexia, malaise, womiting,
headache
37. Tubule transport in reduced nephron
mass
• Loss of renal function with progressive renal disease is
usually attended by distortion of renal morphology and
architecture
• Despite this structural disarray, glomerular and tubule
functions often remain as closely integrated (i.e.
glomerulotubular balance) in the normal organ, at least
until the final stages of CRF
• A fundamental feature of this intact nephron hypothesis
is that following loss of nephron mass, renal function is
due primarily to the operation of surviving healthy
nephrons, while the diseased nephrons cease functioning
38. Tubule transport in reduced nephron
mass
• Despite progressive nephron destruction, many of the
mechanisms that control solute and water balance
differ only quantitatively, and not qualitatively, from
those that operate normally.
40. Tubule transport of sodium and water -1
• In most patients with stable CRF, total-body Na+ and
water content are increased modestly, although ECF
volume expansion may not be apparent
• Excessive salt ingestion contributes to
– congestive heart failure
– hypertension
– ascites
– edema
• Excessive water ingestion
– hyponatremia
– weight gain
41. Tubule transport of sodium and water - 2
• Patient with CRF have impaired renal mechanisms
for conserving Na+ and water
• When an extrarenal cause for fluid loss is present
(vomiting, diarrhea, fever), these patients are prone
to develop ECF volume depletion
– depletion of ECF volume results in deterioration of
residual renal function
42. Potassium homeostasis
• Most CRF patients maintain normal serum K+
concentrations until the final stages of uremia
– due to adaptation in the renal distal tubules and colon, sites
where aldosteron serve to enhance K+ secretion
• Oliguria or disruption of key adaptive mechanisms
(abrupt lowering of arterial blood pH), can lead to
hyperkalemia
• Hypokalemia is uncommon
– poor dietary K+ intake + excessive diuretic therapy +
increased GIT losses
43. Metabolic acidosis
• Metabolic acidosis of CRF is not due to
overproduction of endogenous acids but is
largely a reflection of the reduction in renal
mass, which limits the amount of NH3 (and
therefore HCO3
-
) that can be generated
44. Phosphate, calcium and bone
• Hypocalcemia in CRF results from the
impaired ability of the diseased kidney to
synthesize 1,25-dihydroxyvitamin D, the
active metabolite of vitamin D
• Hyperphosphatemia due to GFR
45. Phosphate, calcium and bone
• PTH
• disordered vitamin D metabolism
• chronic metabolic acidosis - bone is large reservoir
of alkaline salts –calcium phospate, calcium carbonate;
dissolution of this buffer source probably contributes to:
renal and metabolic osteodystrophy:
a number of skeletal abnormalities,
including osteomalcia, osteitis fibrosa,
osteosclerosis
49. Hematologic abnormalities
• Normochromic normocytic anemia
– Erythropoiesis is depressed
• Effects of retained toxins
• Diminished biosynthesis of erythropoietin – more
important
• Aluminium intoxication – microcytic anemia
• Fibrosis of bone marrow due to hyperparathyreoidism
• Inadequate replacement of folic acid
50. Hematologic abnormalities
• Abnormal hemostasis
– Tendency to abnormal bleeding
• From surgical wounds
• Spontaneously into the GIT, pericardial sac, intracranial
vault, in the form of subdural hematoma or intracerebral
hemorrhage
– Prolongation of bleeding time
• platelet factor III activity – correlates with plasma
levels of guanidinosuccinic acid
51. Hematologic abnormalities
• Leucocyte function impairment
– uremic serum
– coexisting acidosis
– hyperglycemia
– protein-calorie malnutrition
– serum and tissue hyperosmolarity (due to
azotemia)
enhanced susceptibility to infection
52. Hematologic abnormalities
Anemia is normochromic and normocytic with a low reticulocyte count
Uremic milieu
Reduction in
renal mass
erythropoetin
erythropoesis
Red blood cell mass
Red blood
cell survival
Platelet dysfunction
Bleeding tendency
53. Neuromuscular abnormalities
• CNS
– inability to concentrate
– drowsiness
– insomnia
– mild behavioral changes
– loss of memory
– errors in judgment
+ neuromuscular irritability including hiccups
cramps
fasciculations
twitching of
muscles
early symptoms of uremia
55. Neuromuscular abnormalities
• Peripheral neuropathy
– Sensory nerve involvement exceeds motor, lower
extremities are involved more than the uppe, and
the distal portions of the extremities more than
proximal
– The restless legs syndrome is characterized by
ill-definedsensations of discomfort in the feet and
lower legs and frequent leg movement
– Later motor nerve involvement follow ( deep
tendon reflexes, etc.)
56. Gastrointestinal abnormalities
– anorexia
– hiccups
– nausea
– vomiting
Uremic fetor, a uriniferous odor to the breath, derives
from the breakdown of urea in saliva to ammonia and is
associated with unpleasant taste sensation
Uremic gastroenteritis (late stages of CRF)
Peptic ulcer
gastric acidity
hypersecretion of gastrin
Secondary hyperparathyreoidism
early manifestation of uremia
?
57. Lipid metabolism
• Hypertriglyceridemia and high-density lipoprotein
cholesterol are common in uremia, whereas cholesterol
levels in plasma are usually normal
• Whether uremia accelerates triglyceride production by
the liver and intestine is unknown
• the enhancement of lipogenesis by insulin may
contribute to increased triglyceride synthesis
• The rate of removal of triglycerides from the circulation,
which depends in large part on enzyme lipoprotein
lipase, is depressed in uremia
• The high incidence of premature atherosclerosis in
patients on chronic dialysis