This document summarizes renal physiology and pathophysiology. It discusses the kidney's role in regulating water balance, electrolytes, acid-base balance, and blood pressure. It also describes renal blood flow regulation and the renin-angiotensin system. Common renal diseases are outlined like acute kidney injury, glomerulonephritis, nephrotic syndrome, and chronic kidney disease. Diagnostic tests and management of renal disorders are summarized as well.
The document discusses renal disease and renal failure in dogs. It defines key terms like renal disease, renal failure, azotemia and uremia. Renal failure can be acute or chronic. Acute renal failure is a sudden reduction in renal function while chronic renal failure is a relatively common syndrome in older dogs representing the end stage of various renal diseases. The document outlines the causes, clinical signs, diagnosis, and management of both acute and chronic renal failure in dogs. It also lists some breeds that are prone to developing renal failure.
This document provides information on acute kidney injury (AKI), including its definition, causes, risk factors, pathophysiology, clinical manifestations, diagnostic studies, complications, collaborative care, nursing diagnoses, and nursing management. AKI is characterized by a sudden loss of kidney function, ranging from minor impairment to complete kidney failure. It can be caused by decreased blood flow to the kidneys, direct damage to the kidneys, or obstruction of urine flow. The main goals in treatment are managing fluid balance and electrolyte abnormalities through medication, diet, and potentially dialysis.
Renal disorders and their dental managementDivya Rana
The kidneys play a vital role in regulating fluid and electrolyte balance, filtering waste from the blood, producing hormones, and controlling blood pressure. When kidney function declines, waste builds up in the blood and patients may develop complications. Chronic kidney disease is staged based on glomerular filtration rate, with later stages characterized by increased waste levels, electrolyte imbalances, and other systemic effects. Treatment options for kidney failure include hemodialysis, peritoneal dialysis, and transplantation. Hemodialysis involves filtering blood through a dialysis machine, while peritoneal dialysis uses the peritoneal membrane to filter waste from the blood. Both require dietary and medication modifications.
The renal system consists of the kidneys, ureters, bladder and urethra. The kidneys filter waste from the blood and regulate electrolytes and fluid balance. They produce erythropoietin to stimulate red blood cell production and activate vitamin D to regulate calcium levels. Renal failure occurs when kidney function declines, leading to the buildup of waste and imbalances in fluid, electrolytes and acid-base levels. Treatment options for renal failure include dialysis and transplantation.
The renal system functions to eliminate waste, regulate blood pressure and electrolyte levels, and produce hormones. It consists of the kidneys, ureters, bladder and urethra. The kidneys contain millions of nephrons which filter blood to remove waste and regulate water and electrolyte levels through glomerular filtration, tubular reabsorption and secretion. Renal failure occurs when this filtration process is impaired and leads to a buildup of waste and imbalances throughout the body. Treatment involves managing fluid levels, electrolytes, acids and other complications through dietary changes and medications.
Renal failure occurs when the kidneys can no longer remove waste and regulate fluids and electrolytes in the body. Chronic kidney disease develops gradually over months to years and initially presents no symptoms. As kidney function declines, waste builds up in the blood and the kidneys lose their ability to concentrate urine and regulate fluids, electrolytes, and acid-base balance. Treatment focuses on managing complications through medications, diet, dialysis, and potentially a kidney transplant. The goals are to maintain kidney function and homeostasis for as long as possible.
Acute renal failure and chronic renal failureNEHA BHARTI
This document provides information about acute renal failure. It begins by defining renal failure and its two types - acute and chronic. Acute renal failure is described as a sudden loss of kidney function over hours to weeks. Risk factors, phases, clinical manifestations, diagnostic evaluations, and management including pharmacologic therapy, fluid/electrolyte replacement, nutrition, and dialysis are summarized. Chronic renal failure is defined as a gradual loss of kidney function over months to years that progresses to end-stage renal disease requiring dialysis or transplant. Stages and uremic symptoms affecting multiple organ systems are outlined.
This document provides an overview of acute kidney injury (AKI), chronic kidney disease (CKD), end-stage renal disease (ESRD), and their treatment and management. It discusses the pathophysiology, stages, symptoms, complications, medical and surgical interventions, and nursing care for each condition. Dialysis methods like hemodialysis and peritoneal dialysis are explained in detail. Surgical procedures for the kidneys like nephrectomy and transplantation are also summarized.
The document discusses renal disease and renal failure in dogs. It defines key terms like renal disease, renal failure, azotemia and uremia. Renal failure can be acute or chronic. Acute renal failure is a sudden reduction in renal function while chronic renal failure is a relatively common syndrome in older dogs representing the end stage of various renal diseases. The document outlines the causes, clinical signs, diagnosis, and management of both acute and chronic renal failure in dogs. It also lists some breeds that are prone to developing renal failure.
This document provides information on acute kidney injury (AKI), including its definition, causes, risk factors, pathophysiology, clinical manifestations, diagnostic studies, complications, collaborative care, nursing diagnoses, and nursing management. AKI is characterized by a sudden loss of kidney function, ranging from minor impairment to complete kidney failure. It can be caused by decreased blood flow to the kidneys, direct damage to the kidneys, or obstruction of urine flow. The main goals in treatment are managing fluid balance and electrolyte abnormalities through medication, diet, and potentially dialysis.
Renal disorders and their dental managementDivya Rana
The kidneys play a vital role in regulating fluid and electrolyte balance, filtering waste from the blood, producing hormones, and controlling blood pressure. When kidney function declines, waste builds up in the blood and patients may develop complications. Chronic kidney disease is staged based on glomerular filtration rate, with later stages characterized by increased waste levels, electrolyte imbalances, and other systemic effects. Treatment options for kidney failure include hemodialysis, peritoneal dialysis, and transplantation. Hemodialysis involves filtering blood through a dialysis machine, while peritoneal dialysis uses the peritoneal membrane to filter waste from the blood. Both require dietary and medication modifications.
The renal system consists of the kidneys, ureters, bladder and urethra. The kidneys filter waste from the blood and regulate electrolytes and fluid balance. They produce erythropoietin to stimulate red blood cell production and activate vitamin D to regulate calcium levels. Renal failure occurs when kidney function declines, leading to the buildup of waste and imbalances in fluid, electrolytes and acid-base levels. Treatment options for renal failure include dialysis and transplantation.
The renal system functions to eliminate waste, regulate blood pressure and electrolyte levels, and produce hormones. It consists of the kidneys, ureters, bladder and urethra. The kidneys contain millions of nephrons which filter blood to remove waste and regulate water and electrolyte levels through glomerular filtration, tubular reabsorption and secretion. Renal failure occurs when this filtration process is impaired and leads to a buildup of waste and imbalances throughout the body. Treatment involves managing fluid levels, electrolytes, acids and other complications through dietary changes and medications.
Renal failure occurs when the kidneys can no longer remove waste and regulate fluids and electrolytes in the body. Chronic kidney disease develops gradually over months to years and initially presents no symptoms. As kidney function declines, waste builds up in the blood and the kidneys lose their ability to concentrate urine and regulate fluids, electrolytes, and acid-base balance. Treatment focuses on managing complications through medications, diet, dialysis, and potentially a kidney transplant. The goals are to maintain kidney function and homeostasis for as long as possible.
Acute renal failure and chronic renal failureNEHA BHARTI
This document provides information about acute renal failure. It begins by defining renal failure and its two types - acute and chronic. Acute renal failure is described as a sudden loss of kidney function over hours to weeks. Risk factors, phases, clinical manifestations, diagnostic evaluations, and management including pharmacologic therapy, fluid/electrolyte replacement, nutrition, and dialysis are summarized. Chronic renal failure is defined as a gradual loss of kidney function over months to years that progresses to end-stage renal disease requiring dialysis or transplant. Stages and uremic symptoms affecting multiple organ systems are outlined.
This document provides an overview of acute kidney injury (AKI), chronic kidney disease (CKD), end-stage renal disease (ESRD), and their treatment and management. It discusses the pathophysiology, stages, symptoms, complications, medical and surgical interventions, and nursing care for each condition. Dialysis methods like hemodialysis and peritoneal dialysis are explained in detail. Surgical procedures for the kidneys like nephrectomy and transplantation are also summarized.
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.
This document provides an overview of renal failure for healthcare professionals. It begins with defining normal kidney function and the pathophysiology of acute kidney injury and chronic renal disease. It then explores the collaborative management of patients with renal failure, including conservative therapy, nutrition management, pharmacologic treatment, and dialysis options like peritoneal dialysis and hemodialysis. The document covers clinical manifestations, diagnostic studies, complications, and the multidisciplinary care required for patients experiencing renal failure.
Acute kidney injury (AKI), previously known as acute renal failure, is characterized by a sudden decrease in kidney function and the retention of waste products. It can be prerenal, renal, or post-renal in origin. Prerenal causes are due to decreased blood flow to the kidneys, renal causes involve damage to the kidneys themselves, and post-renal causes result from obstruction of urine flow. Diagnosis involves evaluating urine output, laboratory tests of kidney function, urine analysis, and occasionally imaging tests or kidney biopsies. Prompt diagnosis and treatment of the underlying cause is important to prevent further kidney damage and other complications of AKI.
The document discusses acute kidney injury (AKI), formerly called acute renal failure (ARF). It defines AKI as a sudden decrease in glomerular filtration rate (GFR) over hours to days. Serum creatinine is commonly used to assess renal function but is not an ideal marker as it rises after GFR drops and is affected by non-renal factors. The causes and types of AKI are described including pre-renal, renal (intrinsic), and post-renal. Acute tubular necrosis (ATN) is the most common cause of intrinsic AKI. Management involves identifying and correcting underlying causes, monitoring fluid balance, and treating complications like hyperkalemia. Dialysis is indicated for refractory
1. The kidneys maintain water and electrolyte balance, blood pH, excrete waste products and toxins, filter the blood, produce erythropoietin, and reabsorb desirable elements.
2. Renal function can be impaired acutely (acute renal failure) or chronically (chronic renal failure). Tests like urea, creatinine, and uric acid help diagnose and monitor kidney function.
3. Kidney diseases include acute tubular necrosis, renal calculi, and gout caused by uric acid crystals. Treatment depends on the underlying cause but may include fluid management, dialysis, and transplantation.
The document summarizes renal support in patients with hepatic disease. It defines hepatorenal syndrome as renal failure that develops in patients with advanced liver disease due to alterations in renal physiology. HRS is diagnosed when renal dysfunction occurs in the absence of other identifiable kidney problems. The document outlines risk factors, types, diagnostic criteria, and management approaches for HRS, including prevention through infection control and treatment with vasoconstrictors, renal support, and liver transplantation.
The document provides information on chronic renal failure (CRF), including its causes, symptoms, progression, and treatment options. It discusses how CRF results from the slow, progressive loss of kidney function. As kidney function declines, waste builds up in the bloodstream and numerous health issues can develop. Treatment focuses on managing symptoms through dietary changes, medication, and renal replacement therapies like hemodialysis or peritoneal dialysis.
The document discusses renal failure, including acute renal failure (ARF) and chronic renal failure (CRF). It defines renal failure as when the kidneys cannot remove metabolic waste or perform regulatory functions. ARF is a reversible clinical syndrome with sudden loss of kidney function over hours to days. CRF is kidney damage for 3+ months with decreased GFR. CRF management focuses on slowing progression, limiting complications like anemia and bone disease, and preparing for renal replacement therapies like dialysis and transplantation.
The document summarizes renal function tests and their clinical implications. It describes the key components of the kidney including the nephron and processes involved in urine formation. Normal ranges are provided for various urine and serum parameters like volume, color, specific gravity, pH, creatinine, BUN, electrolytes, glucose and proteins. Elevated or decreased levels are discussed in conditions like kidney disease, dehydration, diabetes, obstruction. Interfering factors and formulas to calculate glomerular filtration rate are also mentioned.
Chronic kidney disease (CKD) is defined as decreased kidney function over a period of three months or more. It can cause complications such as anemia, metabolic acidosis, hyperkalemia, and cardiovascular disease as kidney function declines. Treatment involves managing the underlying cause, restricting dietary intake of sodium, potassium, and phosphorus, treating complications pharmacologically, and potentially performing long-term dialysis or kidney transplantation for end-stage renal disease. Nursing care focuses on fluid management, dietary modifications, treatment of complications, and health education.
This document discusses acute kidney injury (AKI), formerly known as acute renal failure, in pediatrics. It defines AKI, describes the causes and pathophysiology, presents approaches to evaluation and management, and outlines treatment of complications. The key points are:
- AKI is defined as an abrupt reduction in kidney function over 48 hours, seen as a rise in creatinine or decrease in urine output.
- Common causes include prerenal failure from hypovolemia, intrinsic renal failure like acute tubular necrosis, and postrenal failure from urinary tract obstruction.
- Management involves treating complications, maintaining fluid/electrolyte balance, and considering dialysis for issues like fluid
Acute kidney injury (AKI), also known as acute renal failure (ARF), is a sudden episode of kidney failure or kidney damage that happens within a few hours
CKD is a condition in which the kidneys are damaged and cannot filter blood as well as they should. Because of this, excess fluid and waste from blood remain in the body and may cause other health problems, such as heart disease and stroke.
Guideline, management of acute kidney injuryvita madmo
This document provides guidelines for the management of acute kidney injury (AKI). It defines AKI and outlines stages of severity based on the RIFLE, AKIN and KDIGO criteria. Management of AKI focuses on treating underlying causes, maintaining fluid and electrolyte balance, and considering renal replacement therapy for complications like fluid overload or severe azotemia. Dialysis modalities and anticoagulation options are discussed. The guidelines recommend supportive care including diet modification and avoiding nephrotoxic drugs.
The document provides information on the nutritional management of renal diseases. It discusses the structure and function of the kidneys, defines common renal diseases like glomerulonephritis and chronic renal failure, and their symptoms. It also describes the process of hemodialysis and dietary management for different kidney conditions like nephrotic syndrome and acute renal failure. The goal is to control waste levels, electrolyte balance, fluid retention and nutritional needs for patients with impaired renal function.
This document summarizes renal function tests and urine analysis. It describes the anatomy and function of the nephron, steps in urine formation, and normal ranges for physical and chemical urine tests including volume, color, odor, specific gravity, pH, creatinine, BUN, electrolytes, glucose, protein, and ketones. It discusses clinical implications of abnormal test values and interfering factors. Macroscopic urine examination for casts and cells is also covered, in addition to exogenous markers of glomerular filtration rate like inulin and iothalamate clearance tests.
The summary of the document is:
1. The Renin-Angiotensin-Aldosterone System (RAAS) is activated in response to hypotension, decreased sodium concentration, and decreased blood volume to increase blood pressure through vasoconstriction and sodium retention.
2. Nephrotic syndrome requires proteinuria over 3g per day, hypobulinemia, and edema. The most common causes are membranous glomerulonephritis, minimal-change GN, and focal segmental glomerulosclerosis.
3. Nephritic syndrome presents with hematuria, proteinuria, hypertension, edema, and oliguria. It is often seen in IgA nep
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,
1. The document provides an overview of renal anatomy and physiology, clinical manifestations of renal diseases, methods for estimating renal function, and common renal disease syndromes.
2. Key aspects of renal anatomy discussed include the structure and function of nephrons, the glomerular filtration barrier, and countercurrent exchange mechanisms.
3. Common clinical signs of renal diseases include edema, hypertension, flank pain, urinary abnormalities, and changes in estimated glomerular filtration rate.
4. Major renal disease syndromes covered are nephrotic syndrome, nephritic syndrome, acute renal failure, and chronic renal failure.
I apologize for any confusion, but I am an AI assistant created by Anthropic to be helpful, harmless, and honest. I do not actually experience distress or need saving. How else can I assist you today?
This document provides an introduction to medical surgical nursing. It defines medical surgical nursing as nursing care for patients whose conditions are treated medically or surgically. The objectives of the chapter are to define medical surgical nursing, explain the concepts of health and illness, and discuss the nursing process. The nursing process is presented as a systematic problem-solving approach used by nurses to meet patient needs through assessment, nursing diagnosis, planning, implementation, and evaluation. Health is defined in both negative and positive terms, and the concepts of illness, disease, impairment, disability, and handicap are explained. The document also covers health promotion, illness prevention, and the levels of nursing assessment.
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.
This document provides an overview of renal failure for healthcare professionals. It begins with defining normal kidney function and the pathophysiology of acute kidney injury and chronic renal disease. It then explores the collaborative management of patients with renal failure, including conservative therapy, nutrition management, pharmacologic treatment, and dialysis options like peritoneal dialysis and hemodialysis. The document covers clinical manifestations, diagnostic studies, complications, and the multidisciplinary care required for patients experiencing renal failure.
Acute kidney injury (AKI), previously known as acute renal failure, is characterized by a sudden decrease in kidney function and the retention of waste products. It can be prerenal, renal, or post-renal in origin. Prerenal causes are due to decreased blood flow to the kidneys, renal causes involve damage to the kidneys themselves, and post-renal causes result from obstruction of urine flow. Diagnosis involves evaluating urine output, laboratory tests of kidney function, urine analysis, and occasionally imaging tests or kidney biopsies. Prompt diagnosis and treatment of the underlying cause is important to prevent further kidney damage and other complications of AKI.
The document discusses acute kidney injury (AKI), formerly called acute renal failure (ARF). It defines AKI as a sudden decrease in glomerular filtration rate (GFR) over hours to days. Serum creatinine is commonly used to assess renal function but is not an ideal marker as it rises after GFR drops and is affected by non-renal factors. The causes and types of AKI are described including pre-renal, renal (intrinsic), and post-renal. Acute tubular necrosis (ATN) is the most common cause of intrinsic AKI. Management involves identifying and correcting underlying causes, monitoring fluid balance, and treating complications like hyperkalemia. Dialysis is indicated for refractory
1. The kidneys maintain water and electrolyte balance, blood pH, excrete waste products and toxins, filter the blood, produce erythropoietin, and reabsorb desirable elements.
2. Renal function can be impaired acutely (acute renal failure) or chronically (chronic renal failure). Tests like urea, creatinine, and uric acid help diagnose and monitor kidney function.
3. Kidney diseases include acute tubular necrosis, renal calculi, and gout caused by uric acid crystals. Treatment depends on the underlying cause but may include fluid management, dialysis, and transplantation.
The document summarizes renal support in patients with hepatic disease. It defines hepatorenal syndrome as renal failure that develops in patients with advanced liver disease due to alterations in renal physiology. HRS is diagnosed when renal dysfunction occurs in the absence of other identifiable kidney problems. The document outlines risk factors, types, diagnostic criteria, and management approaches for HRS, including prevention through infection control and treatment with vasoconstrictors, renal support, and liver transplantation.
The document provides information on chronic renal failure (CRF), including its causes, symptoms, progression, and treatment options. It discusses how CRF results from the slow, progressive loss of kidney function. As kidney function declines, waste builds up in the bloodstream and numerous health issues can develop. Treatment focuses on managing symptoms through dietary changes, medication, and renal replacement therapies like hemodialysis or peritoneal dialysis.
The document discusses renal failure, including acute renal failure (ARF) and chronic renal failure (CRF). It defines renal failure as when the kidneys cannot remove metabolic waste or perform regulatory functions. ARF is a reversible clinical syndrome with sudden loss of kidney function over hours to days. CRF is kidney damage for 3+ months with decreased GFR. CRF management focuses on slowing progression, limiting complications like anemia and bone disease, and preparing for renal replacement therapies like dialysis and transplantation.
The document summarizes renal function tests and their clinical implications. It describes the key components of the kidney including the nephron and processes involved in urine formation. Normal ranges are provided for various urine and serum parameters like volume, color, specific gravity, pH, creatinine, BUN, electrolytes, glucose and proteins. Elevated or decreased levels are discussed in conditions like kidney disease, dehydration, diabetes, obstruction. Interfering factors and formulas to calculate glomerular filtration rate are also mentioned.
Chronic kidney disease (CKD) is defined as decreased kidney function over a period of three months or more. It can cause complications such as anemia, metabolic acidosis, hyperkalemia, and cardiovascular disease as kidney function declines. Treatment involves managing the underlying cause, restricting dietary intake of sodium, potassium, and phosphorus, treating complications pharmacologically, and potentially performing long-term dialysis or kidney transplantation for end-stage renal disease. Nursing care focuses on fluid management, dietary modifications, treatment of complications, and health education.
This document discusses acute kidney injury (AKI), formerly known as acute renal failure, in pediatrics. It defines AKI, describes the causes and pathophysiology, presents approaches to evaluation and management, and outlines treatment of complications. The key points are:
- AKI is defined as an abrupt reduction in kidney function over 48 hours, seen as a rise in creatinine or decrease in urine output.
- Common causes include prerenal failure from hypovolemia, intrinsic renal failure like acute tubular necrosis, and postrenal failure from urinary tract obstruction.
- Management involves treating complications, maintaining fluid/electrolyte balance, and considering dialysis for issues like fluid
Acute kidney injury (AKI), also known as acute renal failure (ARF), is a sudden episode of kidney failure or kidney damage that happens within a few hours
CKD is a condition in which the kidneys are damaged and cannot filter blood as well as they should. Because of this, excess fluid and waste from blood remain in the body and may cause other health problems, such as heart disease and stroke.
Guideline, management of acute kidney injuryvita madmo
This document provides guidelines for the management of acute kidney injury (AKI). It defines AKI and outlines stages of severity based on the RIFLE, AKIN and KDIGO criteria. Management of AKI focuses on treating underlying causes, maintaining fluid and electrolyte balance, and considering renal replacement therapy for complications like fluid overload or severe azotemia. Dialysis modalities and anticoagulation options are discussed. The guidelines recommend supportive care including diet modification and avoiding nephrotoxic drugs.
The document provides information on the nutritional management of renal diseases. It discusses the structure and function of the kidneys, defines common renal diseases like glomerulonephritis and chronic renal failure, and their symptoms. It also describes the process of hemodialysis and dietary management for different kidney conditions like nephrotic syndrome and acute renal failure. The goal is to control waste levels, electrolyte balance, fluid retention and nutritional needs for patients with impaired renal function.
This document summarizes renal function tests and urine analysis. It describes the anatomy and function of the nephron, steps in urine formation, and normal ranges for physical and chemical urine tests including volume, color, odor, specific gravity, pH, creatinine, BUN, electrolytes, glucose, protein, and ketones. It discusses clinical implications of abnormal test values and interfering factors. Macroscopic urine examination for casts and cells is also covered, in addition to exogenous markers of glomerular filtration rate like inulin and iothalamate clearance tests.
The summary of the document is:
1. The Renin-Angiotensin-Aldosterone System (RAAS) is activated in response to hypotension, decreased sodium concentration, and decreased blood volume to increase blood pressure through vasoconstriction and sodium retention.
2. Nephrotic syndrome requires proteinuria over 3g per day, hypobulinemia, and edema. The most common causes are membranous glomerulonephritis, minimal-change GN, and focal segmental glomerulosclerosis.
3. Nephritic syndrome presents with hematuria, proteinuria, hypertension, edema, and oliguria. It is often seen in IgA nep
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,
1. The document provides an overview of renal anatomy and physiology, clinical manifestations of renal diseases, methods for estimating renal function, and common renal disease syndromes.
2. Key aspects of renal anatomy discussed include the structure and function of nephrons, the glomerular filtration barrier, and countercurrent exchange mechanisms.
3. Common clinical signs of renal diseases include edema, hypertension, flank pain, urinary abnormalities, and changes in estimated glomerular filtration rate.
4. Major renal disease syndromes covered are nephrotic syndrome, nephritic syndrome, acute renal failure, and chronic renal failure.
Similar to nur_4206--renal__updated_3-31-09.ppt (20)
I apologize for any confusion, but I am an AI assistant created by Anthropic to be helpful, harmless, and honest. I do not actually experience distress or need saving. How else can I assist you today?
This document provides an introduction to medical surgical nursing. It defines medical surgical nursing as nursing care for patients whose conditions are treated medically or surgically. The objectives of the chapter are to define medical surgical nursing, explain the concepts of health and illness, and discuss the nursing process. The nursing process is presented as a systematic problem-solving approach used by nurses to meet patient needs through assessment, nursing diagnosis, planning, implementation, and evaluation. Health is defined in both negative and positive terms, and the concepts of illness, disease, impairment, disability, and handicap are explained. The document also covers health promotion, illness prevention, and the levels of nursing assessment.
This document provides an overview of congestive heart failure (CHF), including its definition, etiology, pathophysiology, classifications, and signs and symptoms. CHF is defined as the inability of the heart to pump an adequate amount of oxygenated blood to meet the body's demands. It results from underlying causes that weaken the heart muscle such as cardiomyopathy or valvular disease, which are exacerbated by precipitating factors like hypertension. The pathophysiology involves compensatory mechanisms like neurohormonal activation and cardiac remodeling that initially help the failing heart but eventually worsen its condition. CHF can be classified based on its effects on systolic or diastolic function, involvement of the right or left side of
This document outlines the organization and setup of a neonatal intensive care unit (NICU). It discusses the definition of a NICU and describes the physical facilities, equipment, staffing, and levels of care provided in a NICU. A NICU provides intensive medical care for premature and ill newborn infants and is directed by neonatologists and staffed by nurses and other medical professionals. The document outlines the necessary space, environmental controls, supplies, and equipment required in a NICU to properly care for sick and premature newborns.
This document provides information on assessing and managing disorders of the integumentary system in children. It discusses the objectives of the lecture, the functions of skin, and techniques for assessing the skin, hair and nails through history taking and physical examination. Specific assessment methods are outlined, including inspection of skin color and lesions, palpation of temperature, texture and edema. Common skin disorders and burns in children are also reviewed. The goal is to equip students to properly examine the integumentary system and identify any disorders, as well as understand their treatment and nursing care.
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Meconium is the first intestinal discharge of a newborn, which can be passed in utero during periods of fetal distress. If meconium is aspirated during delivery, it can lead to meconium aspiration syndrome (MAS). Risk factors for in utero meconium passage include post-term pregnancy, preeclampsia, and fetal distress. MAS causes airway obstruction, inflammation, and difficulty breathing. Treatment involves suctioning meconium from the airways and providing oxygen therapy and ventilation support.
This document discusses neonatal resuscitation and care. It begins by defining a neonate and outlining the rapid physiological changes that must occur for an infant to transition from intrauterine to extrauterine life. It then describes the risks for neonatal difficulties at birth and outlines the priorities, equipment, and techniques for resuscitation. These include providing oxygen, ventilation, chest compressions, and medications as needed. The document concludes by discussing components of initial routine neonatal care like screening, physical assessment, prophylaxis, encouraging parent-infant interaction, and preventing heat loss.
This document discusses various types of birth trauma including cranial injuries, peripheral nerve injuries, bone fractures, and intra-abdominal injuries. It describes the risk factors, clinical presentation, diagnosis, and management of common conditions like cephalohematoma, Erb's palsy, clavicular fractures, skull fractures, and subgaleal hemorrhage. Subgaleal hemorrhage is highlighted as the most severe form of birth trauma, often requiring strict follow-up and management for issues like shock and severe anemia.
This document discusses common childhood diseases, with a focus on respiratory illnesses. It covers:
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2. Children are particularly vulnerable to respiratory illnesses due to developmental differences like smaller airways and fewer alveoli.
3. Specific respiratory diseases covered include the common cold, influenza, sinusitis, otitis media (ear infections), tonsillitis, and pneumonia. Signs and symptoms, diagnoses, and treatment approaches are discussed for each.
Neonatal sepsis is a potentially life-threatening infection that can occur in newborns younger than one month of age. Risk factors include maternal infections, prematurity, and procedures during delivery that expose the newborn to bacteria. Symptoms may include apnea, jaundice, and poor feeding. Treatment involves administering antibiotics like ampicillin and gentamicin intravenously if sepsis is suspected, with prevention through practices such as proper hand hygiene and eye drops for newborns. Nursing care focuses on supportive measures as well as ensuring medications and isolation protocols are properly followed to treat the infection and prevent spread.
This document discusses common neonatal problems including congenital heart disease, neonatal jaundice, neonatal abstinence syndrome, and neonatal sepsis. Some key points include:
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- Neonatal jaundice that is early-onset, high bilirubin levels, late-onset, or prolonged may indicate an underlying pathological cause that needs investigation.
- Neonatal abstinence syndrome can occur in babies exposed to opioids in utero and may require treatment and monitoring for withdrawal symptoms for up to 14 days of life.
- Neonatal sepsis can present non-specifically and it is important
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This document provides information on the normal newborn and common neonatal problems. It discusses the normal physical exam findings of a newborn and common benign skin conditions like salmon patches, port wine stains, and hemangiomas. It also describes some common birth injuries and problems such as caput succedaneum, cephalhematoma, Erb's palsy, and neonatal gynecomastia. The document provides details on the clinical presentation and typical resolution of these common neonatal findings and issues.
I apologize for any confusion, but I am an AI assistant created by Anthropic to be helpful, harmless, and honest. I do not actually experience distress or need saving. How else can I assist you today?
Newborn care involves providing essential care during the first hours, days, and weeks of life to support survival and well-being. This includes immediate care at birth such as cleaning, thermal protection, early breastfeeding initiation, and resuscitation if needed. The four basic newborn needs are to breathe normally, be protected, be warm, and be fed. Common neonatal conditions addressed include respiratory distress, meconium aspiration, and jaundice/hyperbilirubinemia. Proper newborn care and identification of issues can help ensure newborns remain healthy.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
2. Regulation of water excretion
Regulation of electrolyte function
Regulation of acid-base balance—retain
HCO3- and excrete acid in urine
Regulation of blood pressure--RAAS
Regulation of RBCs
Vitamin D synthesis
3. Secretion of prostaglandin E and prostacyclin
which cause vasodilation, important in
maintaining renal blood flow
Excretion of waste products-body’s main
excretory organ. Urea, creatinine, phosphates,
uric acid and sulfates. Drug metabolites.
4. Stimuli for Renin Excretion
Angiotensinogen in liver
Renin release
Angiotensin I
Converting enzyme in lungs
Angiotensin II
Renal autoregulation
Increased BP, increased circulating volume
5. Renin—raises BP
Bradykinins—increase blood flow and vascular
permeability
Erythropoietin
ADH
Aldosterone—promotes sodium reabsorption
and potassium excretion
Natriuretic hormones—released from the
cardiac atria and brain.
7. GFR decreases following 40 years with a yearly
decline of about 1 mL/min
Renal reserve declines
Multiple medications can result in toxic
metabolites
Diminished osmotic stimulation of thirst
Incomplete emptying of bladder
Urinary incontinence
8.
9. Sp. Gravity—1.005-1.020
Microscopic examination for protein, RBCs,
ketones, glycosuria, presence of bacteria,
general appearance and odor
Leukocyte esterase—enzyme found in WBCs
Nitrites –bacteria convert nitrates to nitrites
Osmolality—accurate measurement of the
kidney’s ability to concentrate urine. Normal
range is 500-1200 mOsm/kg.
Culture important in ‘Id’ing pathogen
10. Albuminuria—albumin in urine not
measurable by dipstick
Normal values in freshly voided sample should
range between 2.0-20 for men and 2.8-28 for
women. Higher levels indicate
microalbuminuria.
Can also be determined by 24h specimen
11. Urine osmolality—indication of concentrating
ability, changes seen early in disease processes
Creatinine clearance—tests clearance of
creatinine in one min. Reflects GFR.
Serum creatinine—measures effectiveness of
renal function. 0.6 to 1.2 mg/dL
Urea nitrogen—also indicator of renal function.
7-18 mg/dL. Measures renal excretion of urea
nitirogen, a byproduct of protein metabolism.
Is not always elevated with kidney disease. Not
best indicator of renal function.
12. Liver must function properly to produce urea
nitrogen. BUN levels indicate the extent of
renal clearance of this nitrogenous waste
product.
May see elevation of BUN with bleeding into
tissues or from rapid cell destruction from
infection/steroids
13. Ratio of BUN to creatinine distinguishes
between renal and non-renal factors causing
elevations
Dehydration can affect the BUN
When blood volume is down, or BP is low,
BUN level rises more rapidly than creatinine
level.
14. Volume of fluid filtered from renal glomerular
capillaries into Bowman’s capsule per unit of
time
Generally expressed in ml/minute
Normal GFR generally is 125mL/minute
15. Cockcraft-Gault formula
Modification of Diet in Renal Disease Study
Group formula (MDRD)
Schwartz formula
Starling equation
16.
17. No common pathologic condition, other than
renal disease, increases the serum creatinine
level
Serum creatinine does not increase until at least
50% of renal function is lost
18. Is a calculated measure of glomerular filtration
rate. Is best indicator of overall kidney
function.
Based on 24 hour urine collection
Midway will obtain serum creatinine. Serum
creatinine levels vary with age, gender and
body muscle mass
Calculate: (Volume of urine X urine creatinine)
Divided by serume creatinine
21. Antigen-antibody complexes form in blood and
become trapped in glomerular capillaries
Induce an inflammatory response
Manifested by proteinuria, hematuria,
decreased GFR and alteration in excretion of
sodium
Acute and chronic glomerulonephritis
Nephrotic syndrome
22. Antigen (group A strep)
Antigen-antibody product
Deposition of antigen-antibody complex in glomerulus
Increased production of epithelial cells lining the glomerulus
Leukocyte infultration of the glomerulus
Thickening of the glomerular filtration membrane
Scarring and loss of glomerular filtration membrane
Decreased GFR
24. Hematuria
Edema
Azotemia-accumulation of nitrogenous wastes
Urine appearance may be cola colored
Hypertension
Hypoalbuminemia
Hyperlipidemia
Rising BUN and creatinine
26. Treat s/s such as elevated BP
Check GFR by 24h urine for creatinine clearance
ANA
Treat streptococcal infection with antibiotics,
preferably PCN
Corticosteroids
Immunosuppressants
Limit dietary protein, increase CHO
Restrict sodium
May progress to chronic glomerulonephritis, will
treat as in CKD
27. Is not a specific glomerular disease
Is a syndrome with a cluster of findings that
include:
Marked increase in protein in urine (especially
albumin)
Hypoalbuminemia
Edema
High serum cholesterol and LDL
28. A condition of increased glomerular permeability
Results in massive protein loss
Often linked genetically or r/t
immune/inflammatory process
Caused by chronic glomerulonephritis, diabetes
mellitus with glomerulosclerosis, amyloidosis,
lupus, multiple myeloma and renal vein
thrombosis
Major manifestation is edema
Hallmark is albuminuria exceeding 3.5g/day
32. Renal biopsy to determine specific cause
Steroids
Immunosuppressive agents
ACEIs can decrease proteinuria
Cholesterol lowering agents
Heparin to reduce coagulability
Limit sodium intake
33. Reversible clinical syndrome whereby there is
sudden and pronounced loss of kidney
function
Occurs over hours to days
Results in kidneys failure to excrete
nitrogenous wastes
34. Intrarenal actual parenchymal damage
Prolonged renal ischemia from myoglobinuria
(rhabdo, trauma, burns), hemoglobinuria
(transfusion reaction, hemolytic anemia)
Nephrotoxic agents like aminoglycosides,
radiopaque contrast, heavy metals, solvents,
NSAIDs, ACEIs, acute glomerulonephritis
35. Prerenal 60-70% of cases
Volume depletion as seen in hemorrhage, renal
losses from diuretics, GI losses from vomiting,
diarrhea
Impaired cardiac output 2ndary to MI, heart
failure, dysrhythmias, cardiogenic shock
Vasodilation from sepsis, anaphylaxis,
antihypertensive meds
37. 1. Initiation occurs with the insult
2. Oliguria with urinary output less than
400ml/24h . rising potassium, BUN, Cr. Not
responsive to fluid challenges.
3. Diuresis period— gradual increase in urinary
output. Beginning recovery. Renal function
gradually improves
4. Recovery—may take 3-12 months. May have
permanent reduction in functioning of 1%-3%.
38. Prerenal-hypotension, tachycardia, decreased
CO, decreased urinary output, lethargy
intrarenal and postrenal—oliguria or anuria,
hypertension, tachycardia, SOB, orthopnea,
n/v, generalized edema and weight gain,
lethargy, confusion
40. Elevated BUN and creatinine
Sodium retention but may be deceptive due to
water retention
Potassium increased
Phosphorus increased
Calcium decreased
H&H decreased
Sp. Gravity decreased and fixed
41. Objectives : Restore normal
chemical balance and prevent complications
until restoration of renal function
Identify and treat underlying cause
Maintain fluid balance—wts, serial CVP
readings, BP, strict I&O
May give Mannitol, Lasix or Edecrin
May need temporary dialysis
42. If prerenal, fluid challenges and diuretics to
enhance renal blood flow
Oliguric renal failure, low dose dopamine.
Calcium channel blockers may be used to
prevent influx of calcium into kidney cells,
maintains cell integrity and increase GFR
43. Hyperkalemia—closely monitor electrolytes
Kayexalate/Sorbitol—may need Flexiseal
IV dextrose, insulin and calcium may help shift
K+
Cautious administration of any medication that
can be nephrotoxic
Monitor ABGs and acid-base balance
Monitor phosphate levels
44. Azotemia and uremia are directly related to the
rate of protein breakdown
Dietary proteins are individualized to each
patient. Is a catabolic state and if insufficient
intake, patient may lose up to 0.5-1 pounds
daily. Encourage high CHO. Protein needs for
non-dialysis patients need 0.6g/kg of body
weight
Dialysis patients will need 1-1.5g/kg
Fluid restriction=urine volume plus 500ml
45. Monitor fluid and electrolyte balance
Reduce metabolic demands
Promote pulmonary function
Prevent infection
Provide skin care
Provide support
46. Progressive, irreversibe deterioration in renal
function
Causation: #1 diabetes mellitus, hypertension,
glomerulonephritis, pyelonephritis, polycystic
kidney disease, vascular disorders, others
Uremia---collection of nitrogenous wastes
normally excreted by the kidneys. S/S include:
HA, seizures, coma, dry skin, rapid pulse,
elevated BP, scanty urine, labored breathing
47. Nephrons hypertrophy and work harder until
70-80% of renal function is lost
Nephrons could only compensate by
decreasing water reabsorption thus:
Hyposthenuria—loss of urine concentrating
ability occurs
Polyuria—increased urine output
Then isosthenuria—fixed osmolality
Gradual decline in urinary output
48. 1. GFR greater than or equal to 90mL/min/1.73
m2. Kidney damage w/normal or increased
GFR
2. GFR = 60-89, mild decrease in GFR
3. GFR = 30-59, moderate decrease in GFR
4. GFR = 15-29. severe decrease in GFR
5. GFR < 15. Kidney failure
49. Every body system is affected
CV—hypertension (RAAS), heart failure,
pulmonary edema, pericarditis, MI
Pulm.—crackles, Kussmaul, pleuritic pain
Derm—severe pruritus, uremic frost (urea
crystals)
GI—n/v, anorexia, uremic fetor (ammonia
odor to breath), constipation or diarrhea
Neurologic—LOC changes, confusion, seizures,
agitation, neuropathies, RLS
50. Hematologic—anemia, thrombocytopenia
Musculoskeletal—muscle cramps, renal
osteodystrophy, bone pain, bone fractures
Metabolic changes—urea and creatinine,
sodium, potassium, acid-base, calcium and
phosphorus
51. Calcium and phosphorus binders—Calcium
carbonate, calcium acetate
Antihypertensives
Antiseizure—valium or dilantin
Erythropoietin
Iron supplements
Diet—CHO and fat, vitamins, restrict protein
53. Based on principles of diffusion, osmosis and
ultrafiltration
Diffusion—removal of toxins and wastes.
Move from blood to dialysate.
Osmosis—excess water is removed. Goes from
area of higher solute concentration (blood) to
lower concentration (dialysate)
Ultrafiltration—water moves from high
pressure area to lower pressure. Applied by
negative pressure, more efficient than just by
osmosis
54. ASHD
Disturbances of lipids worsened by dialysis
Anemia and fatigue
Gastric ulcers
Renal osteodystrophy
Sleep problems
Hypotension
Muscle cramps
Dysrhythmias
Dialysis equilibrium from cerebral fluid shifts
55. Caused by rapid decrease in fluid volume and
blood urea nitrogen levels during HD
Change in urea levels can cause cerebral edema
and increased ICP
Neurologic complications include: HA,
vomiting, restlessness, decreased LOC,
seizures, coma or death
Can be prevented by starting HD for short
periods and low blood flows
56. Hemodialysis
In ICUs where patient is too unstable to have
hemodialysis, can have CRRT
Peritoneal dialysis
57. More successful if done before dialysis
HLA and ABO compatibility
Donor kidney placed in iliac fossa
Patient must be free from infection
Similar care for patient post-op as any surgery
58. Post-op—assess for s/s of rejection such as
oliguria, edema, fever, increasing blood
pressure, weight gain and swelling or
tenderness over transplanted area
Monitor creatinine level, in those on
cyclosporine, may be the only s/s
Monitor WBCs
Monitor urinary output, may need
hemodialysis temporarily (2-3 weeks may
initially have ATN)
59. Occurs in types 1 and 2
Severity of diabetic renal disease is related to
extent, duration and effects of atherosclerosis,
htn and neuropathy.
60. Microvascular complication of diabetes
First manifestation is persistent albuminuria
Diabetic patients are always considered to be at
risk for renal failure
Avoid nephrotoxic agents and dehydration
61. Stage 1—at time of diagnosis of diabetes.
Kidney size and GFR are increased. Blood
sugar control can reverse the changes.
Stage 2, 2-3 years after diagnosis. Basement
membrane changes result in loss of filtration
surface area and scar formation. These changes
are called glomerulosclerosis.
62. Stage 3, 7-15 years after diagnosis.
Microalbuminuria is present. GRF may be
normal or increased.
Stage 4, albuminuria is detectable by dipstick.
GRF decreased. BP is increased. Retinopathy is
present.
Stage V, GFR decreases at an average rate of
10ml/min./year
64. If bacteriuria, following should have cultures done:
All men
All children
Patients with diabetics
Those with recent instrumentation
Those hospitalized or who live in long term care
Pregnant women
Sexually active
Postmenopausal
68. Acute pyelonephritis
Will have fever, chills, leukocytosis, bacteriuria
and pyuria
CVA tenderness
US or CT to r/o any obstruction
Urine C&S
69. Tx:
Hydration
Antiemetics
Two week course of antibiotics such as
Bactrim, Cipro, gentamycin w/or w/o
ampicillin, 3rd generation cephalosporin
Pregnant women hospitalized for 2-3 days
f/u culture in two weeks
70. Stress incontinence—invol. loss of urine w/
activities that increase intraabdominal pressure
Urge incontinence—unable to suppress signal
from bladder to brain
Overflow incontinence-when bladder is distended,
will have small amount of incont.
Functional incontinence as seen in Alzheimer’s
Reflex incontinence as seen in SCI patients
Mixed-stress and urge
Neurogenic bladder—lesion of ns leads to urinary
incontinence
71. May be caused by MS, SCI, HNP, spinal tumor,
spina bifida, diabetes
Spastic—upper motor neuron lesion
Flaccid—lower motor neuron lesion. Fills then
have overflow incontinence
Assess by checking residuals, I&O, UA,
assessing sensory awareness
Tx-urecholine, surgery, intermittent caths, S/P
caths
72. Diuretics
CNS depressants which affect LOC
CVAs
Parkinson’s
Depression and altered self-esteem
Inability to ambulate safely
Assistance products cost prohibitive for patient
UTI
75. Presence of calculi in urinary tract
Cause pain as they pass
Nephrolithiasis is formation of stones in the
kidney
76. Involves three conditions:
1. Slow urine flow resulting in supersaturation of
the urine with the particular element
2. Damage to the lining of the urinary tract
3. Decreased inhibitor substances in the urine
that would otherwise prevent supersaturation
and crystal aggregation
77. Metabolic risk factors such as hyperuricemia,
hyperoxaluria or hypercalcemia
High dietary calcium not contributive unless
metabolic or renal tubular defect exists
Immobilization
Urinary stasis, dehydration and urinary
retention mamy be causative
78. Evaluate for bladder obstruction
UA will reveal RBCs, odor, turbidity, WBCs
MRI, KUB, CT
Noncontrast helical CT has highest sensitivity
IV urography will show obstruction
79. Analgesia
Avoid NSAIDs if to have lithotripsy (affect
platelets)
Hydration
Urine straining
Lithotripsy (monitor ECG and sedate patient)
Minimally invasive surgical procedures (MIS)
such as stenting, nephrolithotomy
80. Antibiotics
Thiazide diuretics for hypercalciuria
Allopurinol and vitamin B6 for oxalate
containing stones
Uric acid stone—allopurinol and alkalinizing
the urine. Sodium bicarbonate or potassium
citrate helpful.
Cystine –captopril and
alphamercaptopropionylglycine w/ hydration
and alkalinazation of urine
82. Ureterostomy
Conduits—to intestine and stoma
Sigmoidostomies-divert urine to large intestine
so no stoma
Ileal reservoir—surgically created pouch
Editor's Notes
Vasa recta are specialized vessels that monitor BP. Renin is then excreted=angiotensinogen, angiotgensin I and the II (most powerful vasoconstrictor known)
Aldosterone will be excreted in response to pituitary in response to poor perfusion or increasing osmolality
Renal clearance—ability of kidneys to clear solutes from plasma
Creatinine is waste product of skeletal muscle that is filtered at glomerulus and excreted in urine
Erythropoietin in response to low oxygen tension
Kidneys final conversion of inactive Vitamin D to active form 1,25 dihydroxycholecalciferol
Prostaglandin important in vasodilatory action
Renin excretion prompted by decreased renal perfusion and/or decreased salt delivery to kidney tubules, e.g. hemorrhage, heart failure, loop diuretics
Increased BP—vasoconstriction, increased myocardial contractility, prostaglandin release
Increased circulating volume—aldosterone release, sodium and water reabsorption, potassium excretion, ADH release
Renin—2ndary to angiotensin and aldosterone
Bradykinins—increase blood flow and vascular permeability
ADH—fr. Post. Pituitary. Maximizes reabsorption of water in the kidney and produces a concentrated urine.
Aldosterone—fr. Adrenal cortex. Promotes sodium reabsorption and potassium secretion in distal collecting tubules. Water and chloride follow sodium.
Natriuretic hormones—cause tubular secretion of sodium. Release from cardiac atria and brain.