1. A patient history and physical examination are crucial for assessing the cause of acute kidney injury (AKI). Laboratory tests can help distinguish between pre-renal, intrinsic renal, and post-renal causes of AKI.
2. Common causes of intrinsic AKI include acute tubular necrosis, acute interstitial nephritis, and glomerular diseases. Acute tubular necrosis can be ischemic or nephrotoxic in origin.
3. Evaluation of AKI involves renal function tests, urine analysis, fractional excretion of sodium, and other tests. Imaging such as ultrasound or CT scan may be used when the underlying cause is unclear.
The document discusses various endocrine emergencies including diabetic ketoacidosis (DKA), hypoglycemia, and thyroid storm. It provides details on the causes, symptoms, diagnostic criteria and treatment approaches for each condition. DKA results from lack of insulin and needs urgent treatment including rehydration, insulin administration, and electrolyte correction. Hypoglycemia can be caused by too much insulin or too little food intake and requires glucose administration. Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires treatments to correct the hyperthyroidism and address any precipitating factors.
This document provides an overview of acute pancreatitis including its anatomy, epidemiology, pathophysiology, etiology, clinical presentation, workup, severity scoring, treatment, prognosis, and complications. It begins with definitions of the pancreas' anatomy and functions. It then discusses the disease's worldwide incidence, risk factors, presentations, diagnostic criteria, hematological and radiological evaluations, and key findings on imaging studies like CT scans. The document provides a comprehensive review of acute pancreatitis.
Benign prostatic hyperplasia (BPH) is a common condition in aging men where the prostate gland enlarges. This can cause lower urinary tract symptoms like frequent urination, weak urine stream, and urgency. BPH is caused by changes in hormone levels as men age and cannot be prevented. Treatment options include medications to shrink the prostate or relax muscles, heat therapies, and surgery. Transurethral resection of the prostate (TURP) is a common surgical procedure that uses an electrified loop to cut away prostate tissue through the urethra. Potential complications include bleeding, infection, and a condition called TURP syndrome if too much irrigating fluid is absorbed during surgery. Careful fluid
This document discusses nephrolithiasis (kidney stones). It begins by providing background on the prevalence and costs of kidney stones. It then describes the types of stones (calcium, uric acid, struvite, cystine, drug-induced), risk factors, clinical presentation including renal colic, methods of diagnosis using imaging, and medical management focusing on pain control and increasing fluid intake to pass stones. It concludes by outlining principles of preventing recurrent stones through increasing urine volume and specific measures for preventing calcium stones, the most common type, which involve addressing hypercalciuria.
This document discusses hypercalcemia and hypocalcemia. It defines hypercalcemia as a serum calcium level above 10.1 mg/dL and lists various causes including excessive PTH production, hypercalcemia of malignancy from PTHrP or bone metastases, excessive vitamin D production, and increased bone resorption. Symptoms can include neuropsychiatric issues, GI symptoms, ECG changes, and kidney stone formation. Evaluation involves correcting for albumin and measuring PTH to determine the cause. Treatment depends on the underlying condition but may include IV fluids, bisphosphonates, glucocorticoids, or gallium nitrate. Hypocalcemia is then discussed, outlining causes such as hy
This document discusses hypercalcemia and hypocalcemia, including their causes, symptoms, and management. Hypercalcemia can be caused by hyperparathyroidism, certain malignancies, vitamin D toxicity, and other conditions. Symptoms range from none in mild cases to fatigue, nausea, and cognitive issues in severe cases. Treatment focuses on rehydration, bisphosphonates, calcitonin, surgery, and addressing the underlying cause. Hypocalcemia is usually asymptomatic but can cause tingling and seizures in severe cases. It is often caused by hypoparathyroidism, vitamin D deficiency, or tumor lysis syndrome. Treatment involves calcium and vitamin D supplementation to address the deficiency. Laboratory tests are important to
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
The document discusses various endocrine emergencies including diabetic ketoacidosis (DKA), hypoglycemia, and thyroid storm. It provides details on the causes, symptoms, diagnostic criteria and treatment approaches for each condition. DKA results from lack of insulin and needs urgent treatment including rehydration, insulin administration, and electrolyte correction. Hypoglycemia can be caused by too much insulin or too little food intake and requires glucose administration. Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires treatments to correct the hyperthyroidism and address any precipitating factors.
This document provides an overview of acute pancreatitis including its anatomy, epidemiology, pathophysiology, etiology, clinical presentation, workup, severity scoring, treatment, prognosis, and complications. It begins with definitions of the pancreas' anatomy and functions. It then discusses the disease's worldwide incidence, risk factors, presentations, diagnostic criteria, hematological and radiological evaluations, and key findings on imaging studies like CT scans. The document provides a comprehensive review of acute pancreatitis.
Benign prostatic hyperplasia (BPH) is a common condition in aging men where the prostate gland enlarges. This can cause lower urinary tract symptoms like frequent urination, weak urine stream, and urgency. BPH is caused by changes in hormone levels as men age and cannot be prevented. Treatment options include medications to shrink the prostate or relax muscles, heat therapies, and surgery. Transurethral resection of the prostate (TURP) is a common surgical procedure that uses an electrified loop to cut away prostate tissue through the urethra. Potential complications include bleeding, infection, and a condition called TURP syndrome if too much irrigating fluid is absorbed during surgery. Careful fluid
This document discusses nephrolithiasis (kidney stones). It begins by providing background on the prevalence and costs of kidney stones. It then describes the types of stones (calcium, uric acid, struvite, cystine, drug-induced), risk factors, clinical presentation including renal colic, methods of diagnosis using imaging, and medical management focusing on pain control and increasing fluid intake to pass stones. It concludes by outlining principles of preventing recurrent stones through increasing urine volume and specific measures for preventing calcium stones, the most common type, which involve addressing hypercalciuria.
This document discusses hypercalcemia and hypocalcemia. It defines hypercalcemia as a serum calcium level above 10.1 mg/dL and lists various causes including excessive PTH production, hypercalcemia of malignancy from PTHrP or bone metastases, excessive vitamin D production, and increased bone resorption. Symptoms can include neuropsychiatric issues, GI symptoms, ECG changes, and kidney stone formation. Evaluation involves correcting for albumin and measuring PTH to determine the cause. Treatment depends on the underlying condition but may include IV fluids, bisphosphonates, glucocorticoids, or gallium nitrate. Hypocalcemia is then discussed, outlining causes such as hy
This document discusses hypercalcemia and hypocalcemia, including their causes, symptoms, and management. Hypercalcemia can be caused by hyperparathyroidism, certain malignancies, vitamin D toxicity, and other conditions. Symptoms range from none in mild cases to fatigue, nausea, and cognitive issues in severe cases. Treatment focuses on rehydration, bisphosphonates, calcitonin, surgery, and addressing the underlying cause. Hypocalcemia is usually asymptomatic but can cause tingling and seizures in severe cases. It is often caused by hypoparathyroidism, vitamin D deficiency, or tumor lysis syndrome. Treatment involves calcium and vitamin D supplementation to address the deficiency. Laboratory tests are important to
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
Choledocholithiasis refers to stones in the common bile duct. Stones can form primarily in the bile duct or secondarily migrate from the gallbladder. Primary stones are rare and caused by infections, anomalies, or genetic defects. Secondary stones are more common, originating from gallstones. Stones may be asymptomatic or cause abdominal pain, jaundice, and other symptoms by blocking bile flow. Diagnosis involves blood tests, imaging like MRCP or ERCP. Treatment options include nonsurgical ERCP or shockwave lithotripsy, or surgical procedures like choledochotomy with or without T-tube placement.
The document outlines various procedures and treatments for gastrointestinal bleeding including:
1) Establishing IV access and administering fluids, blood transfusions, vasopressors, antibiotics, and performing endoscopy for diagnosis and treatment.
2) Endoscopic procedures include band ligation, coagulation, and injection therapies to stop active bleeding.
3) Long term management involves eliminating risk factors, treating H. pylori infections, and using proton pump inhibitors.
This document discusses acute pancreatitis, including its causes, signs and symptoms, diagnosis, and treatment. It notes that acute pancreatitis results in sudden upper abdominal pain due to pancreatic inflammation. Patients often present to the emergency room with severe abdominal pain. It requires hospital admission for medical management including fluid resuscitation, nutritional support, and pain management. Causes include gallstones, alcohol abuse, medications, infections, and trauma. Diagnosis involves elevated serum amylase and lipase levels as well as imaging tests like abdominal CT or MRI. Treatment focuses on fluid replacement, nutritional support, treating any infections, and pain control.
1. The document discusses various lumbar masses including colonic masses like pericolic abscesses from diverticulitis or carcinoma, retroperitoneal sarcomas, adrenal tumors, renal cysts, hydronephrosis, infections, trauma, and renal cell carcinoma.
2. It provides details on the presentation, investigations, and management of these different pathological conditions involving the lumbar area and kidneys.
3. Masses may present as pain, fever, masses, or abnormalities found on imaging studies. Evaluation involves tests like ultrasound, CT, MRI, and treatment depends on the specific diagnosis and includes antibiotics, surgery, chemotherapy, or radiation.
The document discusses evaluation and treatment of hypokalemia. It states that the urine potassium-to-creatinine ratio is usually less than 13 mEq/g creatinine with hypokalemia caused by transcellular shifts, GI losses, diuretic use, or poor diet, and is higher with renal potassium wasting. Oral or IV potassium replacement should be based on severity, with mild cases receiving tablets and moderate cases receiving higher doses orally or IV. Severe hypokalemia under 2.5 mEq/L or with symptoms requires IV replacement at 10-20 mmol/hour depending on the route and ECG monitoring. Guidelines recommend KCl infusion in non-dextrose solutions under
This document discusses the approach to vomiting. It defines nausea, vomiting, and regurgitation. There are five classes of stimuli that can provoke nausea and vomiting, including toxins in the GI tract, absorbed toxins, visceral pathologies, CNS stimuli, and vestibular stimuli. The major pathways involved in emesis are the vagal afferents, area postrema, vestibular system, and amygdala. A thorough history and physical exam is important. Investigations help identify potential causes. Management involves rehydration, correcting electrolyte imbalances, treating the underlying cause, and considering antiemetics in some cases. Complications can include dehydration, aspiration pneumonia, and
The document discusses acute cholangitis, including its pathogenesis, clinical manifestations, diagnostic criteria, severity assessment, imaging, and management. Regarding diagnostic criteria, it summarizes that Charcot's triad has low sensitivity for diagnosing acute cholangitis compared to the Tokyo Guidelines 2007 and 2013 criteria. It also notes that the Tokyo Guidelines 2007 criteria for severity assessment were insufficient and have been revised in subsequent guidelines to better distinguish mild from moderate cases in the initial diagnosis.
The document discusses acute kidney injury (AKI), including its causes, diagnosis, and management. It provides details on prerenal, intrinsic, and postrenal forms of AKI. For prerenal AKI, management focuses on correcting the underlying cause, such as volume depletion, and restoring intravascular volume through fluid resuscitation. For intrinsic AKI, identifying and removing nephrotoxic agents is important. Dialysis may be needed for severe AKI with fluid/electrolyte imbalance or uremia.
Tumor lysis syndrome and hypercalcemia of malignancyGaurav Kumar
This document discusses hypercalcemia and tumor lysis syndrome. It defines hypercalcemia as calcium levels above normal physiological range. The main causes of hypercalcemia include parathyroid disorders, malignancy, vitamin D abnormalities, and renal failure. Symptoms range from mild to severe depending on calcium level. Tumor lysis syndrome occurs when large numbers of cancer cells break down rapidly, releasing electrolytes. This can cause hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia, potentially leading to renal failure. The document outlines evaluation, treatment and prevention of both conditions.
Chronic pancreatitis is a progressive inflammatory disease of the pancreas characterized by irreversible destruction of pancreatic tissue. It commonly causes severe abdominal pain and can lead to exocrine and endocrine insufficiency over time. The most common causes are alcohol consumption and smoking. Diagnosis involves pancreatic function tests, imaging like CT or MRCP to identify changes in the pancreas and pancreatic duct. Treatment focuses on managing pain, treating underlying causes, nutrition support, and in some cases endoscopic or surgical interventions. The prognosis is often poor with declining health and function over time and an increased risk of pancreatic cancer with longstanding disease.
This document discusses thyrotoxicosis and hyperthyroidism. It begins by covering thyroid physiology including iodine metabolism and thyroid hormone synthesis. It then discusses the causes and clinical manifestations of Graves' disease (diffuse toxic goiter), toxic multinodular goiter, and toxic adenoma. Diagnostic tests and treatment options including antithyroid drugs, radioactive iodine therapy, and surgery are described for hyperthyroidism. Thyroid storm, a medical emergency, is also summarized.
Balanoposthitis is inflammation of the glans penis and foreskin in uncircumcised males. It is commonly caused by infections, particularly Candida albicans or other fungi. Other causes include viruses like HSV, bacteria like Gardnerella vaginalis, irritants, trauma, fixed drug eruptions, premalignant conditions, and various cutaneous and mucocutaneous diseases. Symptoms include papules, pustules, vesicles, erosions, edema, phimosis, and foul discharge. Diagnosis involves examination, tests like KOH mounts or cultures, and biopsies. Treatment involves hygiene, antibiotics, antifungals, corticosteroids, circumcision for severe
Parathyroid Cancer – Symptoms and Treatment.pdfMeghaSingh194
Parathyroid cancer, or parathyroid carcinoma, is a rare form of cancer that affects the four parathyroid glands found in the neck. These glands are responsible for producing parathyroid hormone, which regulates the body’s calcium levels. Let's explore more: https://www.southlakegeneralsurgery.com/parathyroid-cancer-symptoms-and-treatment/
This document defines interstitial cystitis (IC) and bladder pain syndrome (BPS) as chronic bladder pain and discomfort perceived to be related to the urinary bladder. It discusses the epidemiology, etiology, signs and symptoms, diagnosis, and treatment of IC/BPS. Regarding treatment, it emphasizes conservative therapies like behavioral modification, physical therapy, and oral medications first before more invasive options like intravesical therapies, cystoscopy, neuromodulation, or in rare cases, surgery. The goal is to avoid surgery if possible and use multiple simultaneous treatments for best outcomes.
Acute calculous cholecystitis is caused by obstruction of the cystic duct by a gallstone. Symptoms include biliary colic, fever, and right upper quadrant pain. Ultrasound and hepatobiliary scintigraphy can diagnose thickened gallbladder walls and obstruction. Treatment involves early laparoscopic cholecystectomy for mild cases, or initial conservative treatment with antibiotics and potential percutaneous cholecystostomy for severe cases presenting with sepsis, with delayed cholecystectomy once the patient improves. Guidelines recommend early surgery for mild disease and initial medical management for severe acute cholecystitis.
Dr. Mohd Anuar Bin Awang and Dr. Ainin Tasneem Bt Abdul Rafa presented on fluid and electrolyte balance. They discussed total body water distribution, fluid compartments, principles of fluid therapy, and common electrolyte imbalances including sodium, potassium, calcium, and their causes and management. Maintaining proper fluid and electrolyte balance is crucial as changes can occur due to surgery, trauma, or medical conditions and require careful monitoring and replacement as needed.
This document discusses the thyroid gland and various thyroid conditions. It begins by explaining what the thyroid gland does, producing hormones that regulate metabolism. It then discusses different types of goiters (enlargement of the thyroid gland), including diffuse goiter, multi-nodular goiter, and solitary thyroid nodules. For each condition, it covers causes, symptoms, diagnostic evaluation, and treatment approaches. Key points are that toxic goiters are rarely malignant, solitary nodules need evaluation to exclude cancer, and surgery is rarely needed for autoimmune or inflammatory thyroid diseases.
This document discusses complications of acute pancreatitis, with a focus on pseudocyst and pancreatic necrosis. It summarizes that pseudocysts are fluid collections contained by a well-defined capsule that can develop after acute or chronic pancreatitis. Complications include infection, rupture, enlargement, and erosion into blood vessels. Diagnosis involves imaging and labs. Treatment depends on symptoms and includes drainage or resection. Pancreatic necrosis involves death of pancreatic tissue and can become infected. Interventions like drainage may be needed if necrosis is infected or causing other issues. Both conditions are serious complications of acute pancreatitis.
Renal replacement therapy replaces the normal filtering function of the kidneys using modalities like hemodialysis, peritoneal dialysis, or renal transplantation. Peritoneal dialysis uses the peritoneal membrane for diffusion and ultrafiltration of solutes and fluid, while hemodialysis uses an external dialyzer to filter the blood via diffusion and convection. Both therapies aim to control uremia, electrolyte abnormalities, and fluid balance. Choice of modality depends on factors like age, cardiovascular status, and expertise available. Continuous renal replacement therapy is preferred for critically ill patients who are hemodynamically unstable.
This document provides an overview of acute kidney injury (AKI). It defines AKI and notes its worldwide epidemiology. The main causes of AKI are discussed as pre-renal, renal, and post-renal. The pathophysiology of each type is explained. Clinical presentation depends on the cause but may include elevated creatinine and reduced urine output. Staging of AKI is outlined using KDIGO criteria. Investigations and management aim to identify and treat the underlying cause while maintaining fluid and electrolyte balance. Complications include fluid overload and metabolic disturbances. Prognosis depends on severity and comorbidities.
AKI, CKD, and ESRD are conditions involving the kidneys. AKI is a sudden loss of kidney function that develops over days or weeks and is often reversible. It is caused by prerenal factors like low blood pressure or intrinsic renal damage. Common causes include sepsis, low fluid intake, and medications. Diagnosis is based on increases in BUN and creatinine and decreased urine output. Treatment focuses on identifying and treating the underlying cause while managing fluid, electrolyte and acid-base imbalances. Long term kidney damage can progress to CKD or end stage renal disease requiring renal replacement therapies.
Choledocholithiasis refers to stones in the common bile duct. Stones can form primarily in the bile duct or secondarily migrate from the gallbladder. Primary stones are rare and caused by infections, anomalies, or genetic defects. Secondary stones are more common, originating from gallstones. Stones may be asymptomatic or cause abdominal pain, jaundice, and other symptoms by blocking bile flow. Diagnosis involves blood tests, imaging like MRCP or ERCP. Treatment options include nonsurgical ERCP or shockwave lithotripsy, or surgical procedures like choledochotomy with or without T-tube placement.
The document outlines various procedures and treatments for gastrointestinal bleeding including:
1) Establishing IV access and administering fluids, blood transfusions, vasopressors, antibiotics, and performing endoscopy for diagnosis and treatment.
2) Endoscopic procedures include band ligation, coagulation, and injection therapies to stop active bleeding.
3) Long term management involves eliminating risk factors, treating H. pylori infections, and using proton pump inhibitors.
This document discusses acute pancreatitis, including its causes, signs and symptoms, diagnosis, and treatment. It notes that acute pancreatitis results in sudden upper abdominal pain due to pancreatic inflammation. Patients often present to the emergency room with severe abdominal pain. It requires hospital admission for medical management including fluid resuscitation, nutritional support, and pain management. Causes include gallstones, alcohol abuse, medications, infections, and trauma. Diagnosis involves elevated serum amylase and lipase levels as well as imaging tests like abdominal CT or MRI. Treatment focuses on fluid replacement, nutritional support, treating any infections, and pain control.
1. The document discusses various lumbar masses including colonic masses like pericolic abscesses from diverticulitis or carcinoma, retroperitoneal sarcomas, adrenal tumors, renal cysts, hydronephrosis, infections, trauma, and renal cell carcinoma.
2. It provides details on the presentation, investigations, and management of these different pathological conditions involving the lumbar area and kidneys.
3. Masses may present as pain, fever, masses, or abnormalities found on imaging studies. Evaluation involves tests like ultrasound, CT, MRI, and treatment depends on the specific diagnosis and includes antibiotics, surgery, chemotherapy, or radiation.
The document discusses evaluation and treatment of hypokalemia. It states that the urine potassium-to-creatinine ratio is usually less than 13 mEq/g creatinine with hypokalemia caused by transcellular shifts, GI losses, diuretic use, or poor diet, and is higher with renal potassium wasting. Oral or IV potassium replacement should be based on severity, with mild cases receiving tablets and moderate cases receiving higher doses orally or IV. Severe hypokalemia under 2.5 mEq/L or with symptoms requires IV replacement at 10-20 mmol/hour depending on the route and ECG monitoring. Guidelines recommend KCl infusion in non-dextrose solutions under
This document discusses the approach to vomiting. It defines nausea, vomiting, and regurgitation. There are five classes of stimuli that can provoke nausea and vomiting, including toxins in the GI tract, absorbed toxins, visceral pathologies, CNS stimuli, and vestibular stimuli. The major pathways involved in emesis are the vagal afferents, area postrema, vestibular system, and amygdala. A thorough history and physical exam is important. Investigations help identify potential causes. Management involves rehydration, correcting electrolyte imbalances, treating the underlying cause, and considering antiemetics in some cases. Complications can include dehydration, aspiration pneumonia, and
The document discusses acute cholangitis, including its pathogenesis, clinical manifestations, diagnostic criteria, severity assessment, imaging, and management. Regarding diagnostic criteria, it summarizes that Charcot's triad has low sensitivity for diagnosing acute cholangitis compared to the Tokyo Guidelines 2007 and 2013 criteria. It also notes that the Tokyo Guidelines 2007 criteria for severity assessment were insufficient and have been revised in subsequent guidelines to better distinguish mild from moderate cases in the initial diagnosis.
The document discusses acute kidney injury (AKI), including its causes, diagnosis, and management. It provides details on prerenal, intrinsic, and postrenal forms of AKI. For prerenal AKI, management focuses on correcting the underlying cause, such as volume depletion, and restoring intravascular volume through fluid resuscitation. For intrinsic AKI, identifying and removing nephrotoxic agents is important. Dialysis may be needed for severe AKI with fluid/electrolyte imbalance or uremia.
Tumor lysis syndrome and hypercalcemia of malignancyGaurav Kumar
This document discusses hypercalcemia and tumor lysis syndrome. It defines hypercalcemia as calcium levels above normal physiological range. The main causes of hypercalcemia include parathyroid disorders, malignancy, vitamin D abnormalities, and renal failure. Symptoms range from mild to severe depending on calcium level. Tumor lysis syndrome occurs when large numbers of cancer cells break down rapidly, releasing electrolytes. This can cause hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia, potentially leading to renal failure. The document outlines evaluation, treatment and prevention of both conditions.
Chronic pancreatitis is a progressive inflammatory disease of the pancreas characterized by irreversible destruction of pancreatic tissue. It commonly causes severe abdominal pain and can lead to exocrine and endocrine insufficiency over time. The most common causes are alcohol consumption and smoking. Diagnosis involves pancreatic function tests, imaging like CT or MRCP to identify changes in the pancreas and pancreatic duct. Treatment focuses on managing pain, treating underlying causes, nutrition support, and in some cases endoscopic or surgical interventions. The prognosis is often poor with declining health and function over time and an increased risk of pancreatic cancer with longstanding disease.
This document discusses thyrotoxicosis and hyperthyroidism. It begins by covering thyroid physiology including iodine metabolism and thyroid hormone synthesis. It then discusses the causes and clinical manifestations of Graves' disease (diffuse toxic goiter), toxic multinodular goiter, and toxic adenoma. Diagnostic tests and treatment options including antithyroid drugs, radioactive iodine therapy, and surgery are described for hyperthyroidism. Thyroid storm, a medical emergency, is also summarized.
Balanoposthitis is inflammation of the glans penis and foreskin in uncircumcised males. It is commonly caused by infections, particularly Candida albicans or other fungi. Other causes include viruses like HSV, bacteria like Gardnerella vaginalis, irritants, trauma, fixed drug eruptions, premalignant conditions, and various cutaneous and mucocutaneous diseases. Symptoms include papules, pustules, vesicles, erosions, edema, phimosis, and foul discharge. Diagnosis involves examination, tests like KOH mounts or cultures, and biopsies. Treatment involves hygiene, antibiotics, antifungals, corticosteroids, circumcision for severe
Parathyroid Cancer – Symptoms and Treatment.pdfMeghaSingh194
Parathyroid cancer, or parathyroid carcinoma, is a rare form of cancer that affects the four parathyroid glands found in the neck. These glands are responsible for producing parathyroid hormone, which regulates the body’s calcium levels. Let's explore more: https://www.southlakegeneralsurgery.com/parathyroid-cancer-symptoms-and-treatment/
This document defines interstitial cystitis (IC) and bladder pain syndrome (BPS) as chronic bladder pain and discomfort perceived to be related to the urinary bladder. It discusses the epidemiology, etiology, signs and symptoms, diagnosis, and treatment of IC/BPS. Regarding treatment, it emphasizes conservative therapies like behavioral modification, physical therapy, and oral medications first before more invasive options like intravesical therapies, cystoscopy, neuromodulation, or in rare cases, surgery. The goal is to avoid surgery if possible and use multiple simultaneous treatments for best outcomes.
Acute calculous cholecystitis is caused by obstruction of the cystic duct by a gallstone. Symptoms include biliary colic, fever, and right upper quadrant pain. Ultrasound and hepatobiliary scintigraphy can diagnose thickened gallbladder walls and obstruction. Treatment involves early laparoscopic cholecystectomy for mild cases, or initial conservative treatment with antibiotics and potential percutaneous cholecystostomy for severe cases presenting with sepsis, with delayed cholecystectomy once the patient improves. Guidelines recommend early surgery for mild disease and initial medical management for severe acute cholecystitis.
Dr. Mohd Anuar Bin Awang and Dr. Ainin Tasneem Bt Abdul Rafa presented on fluid and electrolyte balance. They discussed total body water distribution, fluid compartments, principles of fluid therapy, and common electrolyte imbalances including sodium, potassium, calcium, and their causes and management. Maintaining proper fluid and electrolyte balance is crucial as changes can occur due to surgery, trauma, or medical conditions and require careful monitoring and replacement as needed.
This document discusses the thyroid gland and various thyroid conditions. It begins by explaining what the thyroid gland does, producing hormones that regulate metabolism. It then discusses different types of goiters (enlargement of the thyroid gland), including diffuse goiter, multi-nodular goiter, and solitary thyroid nodules. For each condition, it covers causes, symptoms, diagnostic evaluation, and treatment approaches. Key points are that toxic goiters are rarely malignant, solitary nodules need evaluation to exclude cancer, and surgery is rarely needed for autoimmune or inflammatory thyroid diseases.
This document discusses complications of acute pancreatitis, with a focus on pseudocyst and pancreatic necrosis. It summarizes that pseudocysts are fluid collections contained by a well-defined capsule that can develop after acute or chronic pancreatitis. Complications include infection, rupture, enlargement, and erosion into blood vessels. Diagnosis involves imaging and labs. Treatment depends on symptoms and includes drainage or resection. Pancreatic necrosis involves death of pancreatic tissue and can become infected. Interventions like drainage may be needed if necrosis is infected or causing other issues. Both conditions are serious complications of acute pancreatitis.
Renal replacement therapy replaces the normal filtering function of the kidneys using modalities like hemodialysis, peritoneal dialysis, or renal transplantation. Peritoneal dialysis uses the peritoneal membrane for diffusion and ultrafiltration of solutes and fluid, while hemodialysis uses an external dialyzer to filter the blood via diffusion and convection. Both therapies aim to control uremia, electrolyte abnormalities, and fluid balance. Choice of modality depends on factors like age, cardiovascular status, and expertise available. Continuous renal replacement therapy is preferred for critically ill patients who are hemodynamically unstable.
This document provides an overview of acute kidney injury (AKI). It defines AKI and notes its worldwide epidemiology. The main causes of AKI are discussed as pre-renal, renal, and post-renal. The pathophysiology of each type is explained. Clinical presentation depends on the cause but may include elevated creatinine and reduced urine output. Staging of AKI is outlined using KDIGO criteria. Investigations and management aim to identify and treat the underlying cause while maintaining fluid and electrolyte balance. Complications include fluid overload and metabolic disturbances. Prognosis depends on severity and comorbidities.
AKI, CKD, and ESRD are conditions involving the kidneys. AKI is a sudden loss of kidney function that develops over days or weeks and is often reversible. It is caused by prerenal factors like low blood pressure or intrinsic renal damage. Common causes include sepsis, low fluid intake, and medications. Diagnosis is based on increases in BUN and creatinine and decreased urine output. Treatment focuses on identifying and treating the underlying cause while managing fluid, electrolyte and acid-base imbalances. Long term kidney damage can progress to CKD or end stage renal disease requiring renal replacement therapies.
This document provides an overview of acute kidney injury (AKI). It discusses the definition, epidemiology, etiology, pathophysiology, diagnosis and treatment of AKI. Some key points:
- AKI accounts for 5-7% of acute care hospital admissions and 30% of ICU admissions, with mortality rates as high as 50%. It can worsen chronic kidney disease and increase the risk of end-stage renal disease.
- Causes include pre-renal issues like hypovolemia, renal issues like acute tubular necrosis, and post-renal issues like obstruction. Diagnosis involves history, physical exam, lab tests of kidney function and imaging.
- Treatment focuses on optimizing
This document provides an overview of acute renal failure (ARF), also known as acute kidney injury (AKI). It defines ARF, discusses epidemiology and etiology. For etiology, it distinguishes between pre-renal, renal, and post-renal causes of ARF and lists examples for each. It describes the clinical features, diagnosis, and management of ARF, including treatment and indications for renal replacement therapy. ARF is generally reversible if the underlying cause is addressed promptly. Differentiating between pre-renal, renal and post-renal ARF involves considering history, physical exam findings, lab tests and urine analysis.
This document provides an overview of acute kidney injury (AKI), formerly known as acute renal failure. It discusses the definition, epidemiology, diagnostic criteria, etiology, pathophysiology, diagnostic evaluation, urine and blood findings, complications, supportive management including nutrition and monitoring, indications for hemodialysis, timing of dialysis initiation, and prognosis. AKI is characterized by sudden impairment of kidney function and retention of waste products. It commonly occurs in hospitalized patients, especially those in the intensive care unit. The most widely used diagnostic criteria are from KDIGO. Common causes include acute tubular necrosis, prerenal azotemia, and acute injury superimposed on chronic kidney disease. Supportive care focuses on fluid
Acute renal failure (ARF), also known as acute kidney injury (AKI), can have various causes including pre-renal, renal, and post-renal factors. The definition includes an abrupt decline in kidney function over 48 hours seen through rises in creatinine or decreases in urine output. Evaluation involves assessing volume status, obtaining urine and blood tests, and ultrasound. Treatment focuses on identifying and treating the underlying cause, providing supportive care like fluid management, and potentially initiating renal replacement therapy for complications such as fluid overload or electrolyte imbalances. Prognosis depends on the severity and underlying etiology of the AKI.
Nephritis is a inflammation of kidney .
It is classified into various types like lupus nephritis ,interstitial nephritis , glomerulonephritis ,pyelonephritis.
Lupus nephritis is an inflammation of kidney due to autoimmune disorder named as lupus .
It is inflammation of lower urinary tract .
This document discusses acute renal failure (ARF), also known as acute kidney injury (AKI). It defines ARF, discusses its epidemiology and causes. The main causes of ARF are pre-renal (decreased blood flow/volume), renal (damage within the kidneys), and post-renal (obstruction of urine flow). The most common form of intrinsic ARF is acute tubular necrosis, often due to ischemia or nephrotoxins. Diagnosis involves lab tests of kidney function and urine analysis. Treatment focuses on identifying and reversing the underlying cause, maintaining fluid/electrolyte balance, and potentially initiating renal replacement therapy like dialysis.
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.
22 - Acute and chronic kidney failure.pptxStewardBwalya1
Most medical students graduate without knowing the diagnosis and management of acute and chronic kidney failure. Renal units requires you to have a thorough knowledge. So this presentation will assist you to have such knowledge
Acute kidney injury (AKI), formerly called acute renal failure (ARF), is defined as an abrupt decline in renal function over hours to weeks. It is commonly caused by decreased renal blood flow, direct kidney damage, or urine flow obstruction. AKI is diagnosed through increased levels of blood urea nitrogen and creatinine and confirmed by kidney imaging and biopsy if needed. Treatment focuses on reversing the underlying cause, managing complications like fluid overload, and providing renal replacement therapy like hemodialysis if severe. The prognosis depends on the cause, with community-acquired AKI having a better prognosis than hospital-acquired AKI which is often part of multi-organ failure.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be caused by primary kidney disease or secondary systemic diseases. Treatment involves identifying the underlying cause, managing symptoms like edema, and preventing complications. The first-line treatment is prednisone to induce remission, with diuretics used to reduce edema. Patients are monitored for relapses and infections, with additional immunosuppressants used in resistant cases.
Acute tubular necrosis is damage and necrosis of the renal tubule epithelial cells, usually caused by ischemia or nephrotoxic drugs. It presents with muddy brown casts or renal tubular cells in the urine and increased creatinine and BUN. Management involves treating the underlying cause, stopping nephrotoxic drugs, managing fluid balance and electrolyte abnormalities, and considering dialysis for refractory complications like fluid overload or uremia. Prognosis depends on the severity of the initial injury and development of complications.
Acute kidney injury (AKI) is a deterioration of renal function over hours to days resulting in failure to excrete waste and maintain homeostasis. [1] There are over 35 AKI definitions showing its complexity. [2] It can be classified as oliguric/non-oliguric or prerenal, renal, postrenal. [3] Prerenal and acute tubular necrosis account for most hospital AKI cases. [4] Management involves diagnosis through tests and imaging, and treatment focusing on fluid balance, electrolytes, and potentially renal replacement therapy. [5] The prognosis remains poor especially in critically ill patients, as currently the condition can only be supported but not cured. [6
Acute kidney injury (AKI) is the abrupt reduction of renal function over a period of less than 3 months. It can be caused by decreased renal blood flow (prerenal), direct kidney injury (renal), or urinary tract obstruction (postrenal). AKI has systemic effects and increases the risk of complications like fluid overload, electrolyte imbalances, and metabolic acidosis. Treatment involves restoring renal perfusion, treating the underlying cause, managing complications supportively or with renal replacement therapy, and preventing further kidney injury. AKI increases mortality, hospital stay, and risk of progressing to chronic kidney disease.
Oncological Emergencies are the group of conditions that occur as a direct or indirect results of cancer or its treatment that are potentially life-threatening.
after definition it consist of classification and descriptive explanation of each disease and in the end NURSES ROLE
DECODING THE RISKS - ALCOHOL, TOBACCO & DRUGS.pdfDr Rachana Gujar
Introduction: Substance use education is crucial due to its prevalence and societal impact.
Alcohol Use: Immediate and long-term risks include impaired judgment, health issues, and social consequences.
Tobacco Use: Immediate effects include increased heart rate, while long-term risks encompass cancer and heart disease.
Drug Use: Risks vary depending on the drug type, including health and psychological implications.
Prevention Strategies: Education, healthy coping mechanisms, community support, and policies are vital in preventing substance use.
Harm Reduction Strategies: Safe use practices, medication-assisted treatment, and naloxone availability aim to reduce harm.
Seeking Help for Addiction: Recognizing signs, available treatments, support systems, and resources are essential for recovery.
Personal Stories: Real stories of recovery emphasize hope and resilience.
Interactive Q&A: Engage the audience and encourage discussion.
Conclusion: Recap key points and emphasize the importance of awareness, prevention, and seeking help.
Resources: Provide contact information and links for further support.
Letter to MREC - application to conduct studyAzreen Aj
Application to conduct study on research title 'Awareness and knowledge of oral cancer and precancer among dental outpatient in Klinik Pergigian Merlimau, Melaka'
We are one of the top Massage Spa Ajman Our highly skilled, experienced, and certified massage therapists from different corners of the world are committed to serving you with a soothing and relaxing experience. Luxuriate yourself at our spas in Sharjah and Ajman, which are indeed enriched with an ambiance of relaxation and tranquility. We could confidently claim that we are one of the most affordable Spa Ajman and Sharjah as well, where you can book the massage session of your choice for just 99 AED at any time as we are open 24 hours a day, 7 days a week.
Visit : https://massagespaajman.com/
Call : 052 987 1315
Comprehensive Rainy Season Advisory: Safety and Preparedness Tips.pdfDr Rachana Gujar
The "Comprehensive Rainy Season Advisory: Safety and Preparedness Tips" offers essential guidance for navigating rainy weather conditions. It covers strategies for staying safe during storms, flood prevention measures, and advice on preparing for inclement weather. This advisory aims to ensure individuals are equipped with the knowledge and resources to handle the challenges of the rainy season effectively, emphasizing safety, preparedness, and resilience.
R3 Stem Cell Therapy: A New Hope for Women with Ovarian FailureR3 Stem Cell
Discover the groundbreaking advancements in stem cell therapy by R3 Stem Cell, offering new hope for women with ovarian failure. This innovative treatment aims to restore ovarian function, improve fertility, and enhance overall well-being, revolutionizing reproductive health for women worldwide.
Unlocking the Secrets to Safe Patient Handling.pdfLift Ability
Furthermore, the time constraints and workload in healthcare settings can make it challenging for caregivers to prioritise safe patient handling Australia practices, leading to shortcuts and increased risks.
Chandrima Spa Ajman is one of the leading Massage Center in Ajman, which is open 24 hours exclusively for men. Being one of the most affordable Spa in Ajman, we offer Body to Body massage, Kerala Massage, Malayali Massage, Indian Massage, Pakistani Massage Russian massage, Thai massage, Swedish massage, Hot Stone Massage, Deep Tissue Massage, and many more. Indulge in the ultimate massage experience and book your appointment today. We are confident that you will leave our Massage spa feeling refreshed, rejuvenated, and ready to take on the world.
Visit : https://massagespaajman.com/
Call : 052 987 1315
Hypertension and it's role of physiotherapy in it.Vishal kr Thakur
This particular slides consist of- what is hypertension,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is summary of hypertension -
Hypertension, also known as high blood pressure, is a serious medical condition that occurs when blood pressure in the body's arteries is consistently too high. Blood pressure is the force of blood pushing against the walls of blood vessels as the heart pumps it. Hypertension can increase the risk of heart disease, brain disease, kidney disease, and premature death.
Let's Talk About It: Breast Cancer (What is Mindset and Does it Really Matter?)bkling
Your mindset is the way you make sense of the world around you. This lens influences the way you think, the way you feel, and how you might behave in certain situations. Let's talk about mindset myths that can get us into trouble and ways to cultivate a mindset to support your cancer survivorship in authentic ways. Let’s Talk About It!
3. Introduction
• Acute kidney injury (AKI)
• previously called acute renal failure (ARF)
• is an abrupt and usually reversible decline in the glomerular filtration rate (GFR).
This results in an elevation of serum blood urea nitrogen (BUN), creatinine, and
other metabolic waste products that are normally excreted by the kidney.
4. Introduction
• Acute kidney injury (AKI) has been observed in 9 % of
hospitalized patients and in more than 50 % of patients in
the intensive care unit.
• The two major causes of AKI that occur in the hospital are
prerenal disease and acute tubular necrosis (ATN).
Together, they account for approximately 65 to 75 % of
cases of AKI.
5. KDIGO
• The Kidney Disease: Improving Global Outcomes
• Before diagnosing and classifying AKI, one should assess and optimize volume
status and exclude obstruction
• The KDIGO guidelines define AKI as follows :
• Increase in serum creatinine by ≥0.3 mg/dL (≥26.5 micromol/L) within 48 hours, OR
• Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to
have occurred within the prior seven days, OR
• Urine volume <0.5 mL/kg/hour for six hours.
6. Staging criteria (KDIGO)
AKI
Stage 1
Increase in serum creatinine to 1.5 to 1.9 times
baseline
increase in serum creatinine by ≥0.3 mg/dL (≥26.5
micromol/L)
reduction in urine output to <0.5 mL/kg/hour for 6 to
12 hours
Stage 2
Increase in serum creatinine to 2.0 to 2.9 times
baseline
reduction in urine output to <0.5 mL/kg/hour for ≥12
hours.
Stage 3
Increase in serum creatinine to 3.0 times baseline
increase in serum creatinine to ≥4.0 mg/dL (≥353.6
micromol/L)
reduction in urine output to <0.3 mL/kg/hour for ≥24
hours
anuria for ≥12 hours
the initiation of renal replacement therapy
in pt. <18 years, decrease in estimated glomerular
filtration rate (eGFR) to <35 mL/min/1.73 m2.
OR OR
OR
OR
OR
OR
OR
OR
16. 2.A. AcuteTubular Necrosis
Nephrotoxic
Exogenous
Endogenous
•Crystal-induced :
•high cellular turnover (ie, uric acid, calcium phosphate), in certain
malignancies or the treatment of malignancies
Pigments :
-Myoglobinuria (heme protein found in muscle) e.g Rhabdomyolysis.
-Hemoglobinuria most often is associated with transfusion reactions.
Monoclonal :
Multiple Myloma ( Ig light chains )
17. • Recent surgery, hypotension, sepsis, muscle necrosis, or volume depletion, as well as exposure
to nephrotoxic agents.
• Myalgias,Generalized weakness, Darkened urine H/O recent trauma or infection
(Rhabdomyolysis)
• Several of those may be present Simultaneously, which increases the risk and severity of ATN.
• pre-existing medical conditions or medication use (eg, diabetes mellitus, multiple myeloma,
nonsteroidal anti-inflammatory drugs)
2.A. AcuteTubular Necrosis History
18. • Muscle tenderness due to rhabdomyolysis
• Abdominal distension may raise the concern of intra-abdominal hypertension and
compartment syndrome
• Hypovolemia (eg, low jugular venous pressure, loss of skin turgor, orthostatic
hypotension, dry mucous membranes, tachycardia).
2.A. AcuteTubular Necrosis Exam
23. • Medication use, rash, arthralgias, fever, infectious illness.
• Rifampin, PPI and NSAIDs less commonly associated with fever, rash, and eosinophilia.
• Nonspecific signs and symptoms.
• Symptoms of nephrotic syndrome :
• Face / body swelling ( started around eyes and legs , then generalized) , foamy urine , fatigue
, loss of appetite.
• Mostly seen in pt.AIN induced by NSAID.
2.B. Acute Interstitial Nephritis History :
24. • In most patients, no characteristic findings exist.
• Fever , Rash
• Nephrotic Syndrome: In AIN induced by NSAID
• Edema, Ascites
• Pleural effusions.
• Hematuria and hypertension manifest in a minority of patients.
• Some patients present with hypertension, although others may be normotensive or
hypotensive.
2.B. Acute Interstitial Nephritis Exam :
25. 2.C. Glomerulus diseases History
• Hematuria, Oliguria
• Triad of sinusitis, pulmonary infiltrates, and nephritis (Wegener granulomatosis)
• Nausea and vomiting, abdominal pain, and purpura (Henoch-Schönlein purpura)
• Rash , Arthralgias (SLE)
• Hemoptysis (Goodpasture syndrome)
• arthritis, uveitis, sinusitis
• Constitutional symptoms : weight loss, fatigue, loss of appetite.
• Infection : hepatitis C virus infection, HIV.
• Edema ( peripheral or periorbital ).
26. • Hypertension
• Altered level of consciousness (malignant hypertension or hypertensive encephalopathy)
• Edema ( peripheral or periorbital ).
• Crackles (ie, if pulmonary edema)
• Elevated jugular venous pressure
• Arthritis , rash , pallor
• Others : pharyngitis, impetigo, weight gain, oral ulcers
2.C. Glomerulus Diseases Exam
27. 2.D.VascularAKI History
• The presence of a condition requiring anticoagulation
• History of polyarthritis nodosa PAN
• Medical history: (thrombotic thrombocytopenic purpura, hemolytic uremic syndrome,
malignant hypertension, disseminated intravascular coagulation, HELLP , scleroderma
renal crises ) can lead to TMA then this can lead to AKI.
• History of vascular surgery
• Recent history of arterial catheterization
28. • Funduscopic examination retinal hemorrhages, exudates, and
papilledema (showing severe hypertension).
• Progressive skin tightness and induration, tightening of the skin
in the face, hyperpigmentation and
hypopigmentation (scleroderma).
• Livedo reticularis (e.g PAN ,TTP ).
• Abdominal bruit (e.g PAN).
2.D.VascularAKI Exam
Livedo reticularis
29. 3. Post- renal AKI History
• Obstructive Symptoms (BPH):Hesitancy , intermittency ,
weak urine stream, straining, sensation of incomplete
bladder.
• Irritative Symptoms (BPH): Nocturia , urgency ,
frequency.
• Urinary Stones: Hematuria, abdominal pain, dysuria.
• Malignancy : Smoking , male , FHx of bladder cancer h/o
irritative or obstructive symptoms.
• Medications
31. MCQ 1
• A 65-year-old female patient suffering from diabetes mellitus presents with complaints of
decreased urination, nausea, fatigue, and swelling in her legs. One week ago, she was
started on medication for the treatment of her urinary tract infection.Today, her blood tests
show elevated blood urea nitrogen (BUN) and serum creatinine levels.Which of the
following medications most likely precipitated her current symptoms?
A. Insulin
B. Amoxicillin
C. Ceftriaxone
D.Trimethoprim/sulfamethoxazole
32. Answer is D
• The patient’s symptoms indicate renal dysfunction. Sulfamethoxazole is a nephrotoxic drug that
can result in acute kidney injury (AKI).
• Sulfonamide containing medications, such as trimethoprim/sulfamethoxazole, are nephrotoxic
and can cause intrinsic renal impairment that decreases creatinine clearance.
• Sulfonamide containing medication can result in the buildup of crystals that block renal tubules.
• This leads to the mechanical blocking of tubules and ureters. Hematuria, oliguria, and anuria
may follow.Ceftriaxone and amoxicillin are unlikely to cause damage to renal function.
33. A PATIENT HISTORY AND PHYSICAL
EXAMINATION, WITH AN EMPHASIS ON
ASSESSINGTHE PATIENT’SVOLUME STATUS,
ARE CRUCIAL
34. Investigation
Work up
Lab
CBC & diff
Fractional
excretion
of NA
Renal
function
test
Urine
output
Urine
analysis
dipstick
Microscopic
exam
Serology
Urine
osmolality
Imaging
CT scan
U/S
others
Renal
biopsy
35. Laboratory findings
• PRE-RENAL
• ↓Urine volume (Oliguric)
• Except in diuretic s use , which will acutely raise
the urine volume while the diuretic is acting.
• Fraction excretion of NA is < 1%
• Fractional excretion of urea ≤ 35%
• this is helpful incase the pre-renal AKI is due to
diuretics use.
• BUN/CR >20
• urine osmolality > 500 mosmol/kg
• Urinalysis
• Bland sediments , Transparent Hyaline casts
36. Cont.
• INTRINSIC
1. AcuteTubular Necrosis
• Urine volume : either oliguric or non-oliguric.
• Fraction excretion of NA is > 2%
• Fractional excretion of urea > 50%
• BUN/CR < 20
• urine osmolality <450 mosmol/kg (almost all cases) & usually < 350
mosmol/kg
• Urinalysis
• Bland sediments
• Pigmented granular muddy brown casts
• ± RBCs & protein (from the tubular damage)
38. Cont.
2. Acute interstitial nephritis
• Urinalysis
• WBCs
• WBC casts
• ± RBCs
• Negative Urine culture.
• Urine Eosinophil
• In case of Antibiotic induced AIN
• Lymphocytes
• In case of NSAID induced AIN
40. Cont.
• POST RENAL
• Urine volume : anuria (urine output <50 to 100 mL/day) is
rare.
• Anuria is most often seen in two conditions: shock and
complete bilateral urinary tract obstruction.
• Urinalysis
• Normal urine analysis.
• ± Non dysmorphic RBCs,WBCs , crystals.
• RBCs Casts.
41. Imaging
• Imaging is generally performed in patients with AKI when the underlying cause is not clear.
• Assess For Urinary Tract Obstruction.
• Patients who have an obvious cause of AKI do not require imaging, at least initially.
• (U/S) most commonly used.
• safe, easy to perform, and sensitive for obstruction.
• (CT) scan without contrast is generally preferred among patients with possible urolithiasis.
• (MRI) with gadolinium should be avoided.
42. Other
• RENAL BIOPSY
1. Is reserved for patients whom prerenal and postrenal causes ofAKI have been excluded
and the cause of intrinsic renal injury is unclear.
2. When clinical assessment and labs suggest a diagnosis that requires confirmation before
starting disease specific therapy (e.g., Immunosuppressive medications).
3. Need to be performed urgently in patients with (oliguria who have rapidly worseningAKI ,
hematuria, and red blood cell casts, anemia, hymoptysis ). In this setting the biopsy may
support the initiation of special therapies, such as plasmapheresis if goodpasture
syndrome is present.
43. Cont.
• RENAL BIOPSY
4. Renal biopsy may need to be performed urgently in patients with oliguria who
have rapidly worsening acute kidney injury, hematuria, and red blood cell casts.
5. Patients who have a characteristic urinalysis for AIN but are not being treated
with a drug known to cause AIN.
6. Patients who are being treated with a drug known to cause AIN but do not have a
characteristic urinalysis.
7. Diagnosis of AIN to be uncertain.
44. Management
• collaboration among primary care physicians,
nephrologists, hospitalists, and other subspecialists
participating in the care of the patient.
• management is primarily SUPPORTIVE.
• Patients with acute kidney injury generally should be
hospitalized unless the condition is mild and clearly
resulting from an easily reversible cause.
45. General management
• Volume depletion in pre-renal AKI
• IV fluids isotonic solutions (e.g., Normal saline) are preferred over hyper
oncotic solutions.
• MAP goal greater than 65 mm hg is reasonable.
• May require the use of vasopressors in patients with persistent hypotension.
• Renal-dose dopamine is associated with poorer outcomes & it is no longer
recommended.
46. Cont.
• Correction of electrolyte imbalances (e.g Severe hyperkalemia):
• 5 to 10 units of regular insulin.
• Dextrose 50% given intravenously.
• Calcium gluconate (10 mL of 10% solution infused intravenously over five minutes)
to stabilize the membrane and reduce the risk of arrhythmias.
• In patients without ECG evidence of hyperkalemia, calcium gluconate is not necessary.
• Dietary intake of potassium should be restricted.
47. Cont.
• Diuretics:
• The main indication for use of diuretics is management of volume overload.
• diuretics do not improve morbidity, mortality, or renal outcomes, and should
not be used to prevent or treat acute kidney injury in the absence of volume
overload.
48. Cont.
• Medications:
• All medications that may potentially affect renal function by direct toxicity or by
hemodynamic mechanisms should be discontinued, if possible.
• Avoidance of iodinated contrast media and gadolinium is important and, if imaging
is needed, noncontract studies are recommended.
• The dosages of essential medications should be adjusted.
49. Cont.
• Corticosteroids :
• Some studies show a benefit to kidney function recovery after AIN with using corticosteroids,
particularly if started within 1 to 2 weeks of diagnosis.
• So, short course of prednisolone should be considered in most patients whose kidney function does
not improve rapidly after drug withdrawal, unless corticosteroid therapy is contraindicated.
• This should be undertaken with the results of a kidney biopsy confirming the diagnosis of AIN and
excluding other possible diagnoses.
• Corticosteroids should be continued for 1 to 1.5 months as much of the recovery of kidney function is
expected in this period.
50. • Indications (when conditions are refractory to conservative management):
• Acid base disturbance : refractory acidemia
• Certain poisonings and intoxications: (metformin, valproic acid, methanol, ethylene glycol, lithium,
salicylates, barbiturates, thallium, theophylline).
• Electrolyte disorder: ↑K, ↑Ca, ↑PO4, tumor lysis syndrome.
• Overload: refractory hypervolemia ( e.g CHF, Pulmonary edema )
• Uremic: pericarditis or pleuritis, uremic encephalopathy
• No mortality benefit to early initiation of RRT
Renal ReplacementTherapy (RRT)
51. • A 65-year-old woman who lives in a nursing home is brought to the emergency department due to a day of
lethargy and confusion. She is febrile and disoriented. Past medical history includes diabetes mellitus and
hypertension. During the hospitalization, she received gentamicin sulfate 3 mg/kg every 8 hours to treat a life-
threatening infection. Following the administration of this drug, the patient became more irritable and vomited
several times. Fluid balance indicates a blood urea nitrogen of 46 mg/dL, creatinine of 2.6 mg/dL, sodium of 148
mEq/L, and potassium of 4.8 mEq/L. Which of the following is the most appropriate next step in the management
of this patient?
A. Discontinue gentamicin and initiate volume repletion
B. Continue current care with close observation
C. Add IV cephalosporin
D. Repeat urine analysis
MCQ 2
52. • Kidney damage is a problem in 10-25% of people who receive aminoglycosides,
and gentamicin is one of the most nephrotoxic drugs of this class.
• Oftentimes, acute nephrotoxicity is reversible, but it may be fatal.
• Fluid resuscitation is vital in the treatment of acute kidney injury due to
nephrotoxic agents.
Answer is A
53. Management Key Recommendations
• Adequate fluid balance should be maintained in patients with acute kidney injury by using
isotonic solutions (e.g., normal saline) instead of hyperoncotic solutions (e.g., dextrans,
hydroxyethyl starch, albumin). (C)
• Balanced crystalloids are preferred over 0.9% sodium chloride for fluid resuscitation in
critically and non-critically ill patients. (B)
54. Management Key Recommendations
• There is no difference in 90-day mortality between early initiation of renal
replacement therapy and delayed initiation. (B)
• High-dose statins lower the risk of contrast media induced acute kidney
injury in patients undergoing coronary angiography or percutaneous
intervention compared with lower-dose statins. (A)
55. Management Key Recommendations
• KIDO recommends not using diuretics to preventAKI. (1B)
• KIDO suggests not using diuretics to treat AKI, except in the management
of volume overload. (2C)
56. Management Key Recommendations
• KIDO recommends not using low-dose dopamine to prevent or treat AKI.
(1A)
• KIDO suggests not using fenoldopam to prevent or treat AKI. (2C)
57. Management Key Recommendations
• KIDO suggests not using atrial natriuretic peptide (ANP) to prevent AKI.
(2C)
• KIDO suggests not using atrial natriuretic peptide (ANP) to treat AKI. (2B)
61. Non-Emergency
department
URGENT
NEPHROLOGY
REFERRAL
Initial interventions fail to substantially improve the kidney injury.
•AKI occurs as a complication of treatment of an unrelated
condition and future treatment depends upon nephrology input
(such as AKI occurring as a complication of chemotherapy)
Glomerulonephritis (GN) is strongly suspected (such as in a patient
withAKI, hematuria, and proteinuria).
Referral
62. To Emergency
department
Patients with stage 2 or 3 AKI as per the KDIGO criteria.
Patients with AKI of any stage seen in a resource-limited
outpatient setting where the initial diagnostic evaluation
(eg, renal ultrasound to rule out urinary tract obstruction)
or interventions (eg, intravenous fluid administration)
Patients with stage 1 AKI
Unclear etiology
Unknown duration or trajectory of elevated
creatinine
Here is concern that the condition may not
be rapidly reversible with simple
interventions
If they have a concomitant, uncontrolled
comorbid condition
Referral
63. • Patients with acute kidney injury are more
likely to develop:
• Chronic kidney disease in the future
• Higher risk of end-stage renal disease
• Higher risk for premature death.
Prognosis
64. Follow up ( post AKI )
• It Is Important For Primary Care PhysiciansTo Identify PatientsWhoAre At High Risk Of
DevelopingAKI.
• ThoseAt Highest Risk Include:
• Adults OlderThan 75Years.
• PersonsWith Diabetes.
• Preexisting Chronic Kidney Disease.
• PersonsWith Medical Problems Such As Cardiac Failure, Liver Failure.
• Sepsis.
• ThoseWhoAre ExposedTo Contrast Agents.
• Who Are Undergoing Cardiac Surgery.
65. Cont.
• F/U 3 months after hospitalization is reasonable if renal function is recovered (90% or
greater from baseline).
• F/U at 3 weeks and then again at 3 months for patients with a slower recovery.
• Blood pressure, weight, serum creatinine level, and GFR should be measured at each
visit.
• Nephrology consultation is recommended if the estimated GFR remains less than 60
mL per minute per 1.73 m2.
• The optimal duration of monitoring after acute kidney injury is unclear
67. • A 62-year-old man with hypertension, hypercholesterolemia, and benign prostatic hypertrophy (BPH)
presents to his physician with increasing muscle aches in his thighs and shoulders and complains of
tea-colored urine.These symptoms started about 10 days ago. He has been drinking plenty of fluids as
a new diet, specifically grapefruit juice. On routine laboratory evaluation, his serum transaminases are
elevated to nearly three times the normal limit, serum creatinine is 1.4 mg/dL (baseline 1.2 mg/dL),
urinalysis reveals 1+ proteinuria. His only medications are lisinopril, simvastatin, and a baby aspirin.
of the following is the most likely diagnosis in this patient?
A. Drug-induced hepatitis from long-term simvastatin
B. Postrenal azotemia and proteinuria due to BPH
C. Acute kidney injury secondary to aspirin and lisinopril
D. Hepatic enzyme inhibition leading to elevated circulating drug levels
MCQ 3
68. • Grapefruit juice inhibits the cytochrome P450 3A4 system that metabolizes simvastatin.
• This patient has rhabdomyolysis from increased circulating levels of simvastatin. Simvastatin
may increase transaminases, but associated cases of hepatitis and liver failure are very rare.
• The combination of aspirin and lisinopril has not been shown to cause acute kidney injury; a
creatinine level of 0.2 mg/dL above baseline levels does not confer acute kidney injury.
• Moderate proteinuria and a mild elevation in serum creatinine do not constitute postrenal
azotemia and proteinuria due to BPH in this patient.
Answer is D
71. Summary
1-The two major causes of acute kidney injury (AKI) developing in the hospital are prerenal disease and acute
tubular necrosis (ATN).
2- Causes of AKI can be divided to ( pre-renal, intrinsic and post renal) .
3- KDIGO system staging AKI into three stages using SCR and urine output.
4-The FeNa is typically less than 1 % in prerenal disease and above 2 % in ATN.
5- A patient history and physical examination, with an emphasis on assessing the patient’s volume status, are
crucial.
6- Not recommended to use low dose dopamine to treat or prevent AKI.
7- Not recommended to use diuretics to prevent or treat AKI unless there is volume overload.
72. 8- Management of acute kidney injury involves fluid resuscitation, avoidance of nephrotoxic
medications and contrast media exposure, and correction of electrolyte imbalances
9- F/U 3 months after hospitalization is reasonable if renal function is recovered (90% or greater
from baseline).
10- F/U at 3 weeks and then again at 3 months for patients with a slower recovery.
11- Recognition of risk factors (e.g., older age, sepsis, hypovolemia/shock, cardiac surgery, infusion
of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver
failure) is important.
Summary
73. References:
• KDIGO Clinical PracticeGuidelines for Acute Kidney Injury.
• AmericanAcademyOf Family Physicians.
• Royal Collage of General Practitioners.
• Toronto Notes Book 34th Edition.
• Pocket Medicine 7th Edition.
• Case files 4th edition.
• BMJ Best Practice.
• Medscape.
• Uptodate.
• Statpearls.
Editor's Notes
Other two classification systems
RIFLE which depends on either GFR system or UO
And report the changes in 7 days
But other system is AKIN which no relay on GFR and report the changed in 48 h.
Third system is KDIGO system which is more recent and much preferred which depend on Cr and UO
1-Distributive shock : septic shock , neurogenic shock and anaphylactic shock
In sepsis Wbc release nitric oxide this will lead to dilation of the blood vessel and increase in size or diameter
This will lead decrease vascular resistance so less force to pump the blood
Then decrease in blood pressure all over the body
Decrease tissue perfusion
Including kidney
2-abdominal compartment syndrome :
-organ dysfunction caused by intra-abdominal hypertension (IAH). ACS is defined as a sustained IAP >20 mm Hg associated with organ dysfunction/failure.
-Intra-abdominal pressure (IAP) is approximately <5
-IAH is graded as follows: Grade I: IAP 12-15 mm Hg; Grade II: IAP 16-20 mm Hg; Grade III: IAP 21-25 mm Hg; Grade IV: IAP >25 mm Hg.
-chronic abdominal compartment syndrome include the following:
Peritoneal dialysis,Morbid obesity, Cirrhosis, Intra-abdominal mass.
acute:
Penetrating trauma, Intraperitoneal hemorrhage ,Pancreatitis, Rupture of abdominal aortic aneurysm , Perforated peptic ulcer.
3- CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of 1 organ may induce acute or chronic dysfunction of the other.
4-Hepatorenal syndrome (HRS) is the development of renal failure in patients with advanced chronic liver disease [1] and, occasionally, fulminant hepatitis, who have portal hypertension and ascites. Estimates indicate that at least 40% of patients with cirrhosis and ascites will develop HRS during the natural history of their disease.
-chirrosis > increase hepatic resistance > portal hypertention> vascular conditions, architectural changes in the liver are associated with a deficient nitric oxide (NO) production
(deficient nitric oxide (NO) production, which results in an increased vascular tone with a further increase in hepatic resistance and portal pressure)
the splanchnic (and systemic) circulation experiences a relative excess in regional NO generation> reduction of circulating vascular volume and renal perfusion> To compensate for the lower effective intravascular volume > , activation of the renin-angiotensin system and sympathetic nervous system plus secretion of antidiuretic hormone result in> sodium and water retention coupled with renal vasoconstriction, reduced renal blood flow, and ultimately renal hypoperfusion
5- hypercalcemia MAS starts with the development of hypercalcemia, which causes vasoconstriction of the afferent renal arterioles, thus decreasing the glomerular filtration rate (GRF) [5]; this leads to renal insufficiency which further exacerbates the ability of the kidney to excrete calcium, resulting in increasingly higher serum calcium levels. Hypercalcemia also leads to the activation of the calcium–sensing receptor in the medullary thick ascending limb which results in natriuresis and volume depletion
clots : gross hematuria and acute renal failure following percutaneous renal biopsy
Afferent arteriolar vasoconstriction can be caused by the following:
Hypercalcemia
Drugs - NSAIDs, amphotericin B, calcineurin inhibitors, norepinephrine, radiocontrast agents
Hepatorenal syndrome
Hepatorenal : is a hipatic problem leads to renal problem via vasoconstriction > the problem starts within the liver (chirrosis, fulminant liver failure) lead the liver to secrete vasodilator material like Nitric oxide can cause vasodilation this will lead to hypotension the most affected organ is kidneys
Then when it comes to the kidney the kidney will sisnce the hypotention and as aresponce will make efferent vasocontruction by Rinin Angiotensin system ( will make salt and water retention then. Leads to scitis , efferent vasoconstriction)
Vomiting occurs if the level of obstruction is proximal. Increasing small-bowel distention leads to increased intraluminal pressures. This can cause compression of mucosal lymphatics, leading to bowel wall lymphedema. With even higher intraluminal hydrostatic pressures, increased hydrostatic pressure in the capillary beds results in massive third spacing of fluid, electrolytes, and proteins into the intestinal lumen. The fluid loss and dehydration that ensue may be severe and contribute to increased morbidity and mortality.
causes of intra-abdominal hypertension, defined as repeated intra-abdominal pressures > 12 mm Hg. The presence of organ dysfunction in this setting due to compressive symptoms now confirms a diagnosis of abdominal compartment syndrome.
Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) in the renal category.
In contrast to a prerenal etiology, acute kidney injury caused by acute tubular necrosis does not improve with adequate repletion of intravascular volume and blood flow to the kidneys. Both ischemic and nephrotoxic acute tubular necrosis can resolve over time
It is a well-defined three-part sequence of initiation, maintenance, and recovery:
initiation phase is characterized by an acute decrease in glomerular filtration rate (GFR) to very low levels, with a sudden increase in serum creatinine and blood urea nitrogen (BUN) concentrations.
The maintenance phase is characterized by a sustained severe reduction in GFR that persists for a variable length of time, most commonly 1-2 weeks
recovery phase, in which tubular function is restored, is characterized by an increase in urine volume (if oliguria was present during the maintenance phase) and by a gradual decrease in BUN and serum creatinine to their preinjury levels.
The tubule cell damage and cell death that characterize ATN usually result from an acute ischemic or toxic event
Treatment :
The goals of management are avoidance of further kidney damage, treatment of underlying conditions, and aggressive treatment of complications.
There is no specific therapy for ATN apart from supportive care
The goals of management are avoidance of further kidney damage, treatment of underlying conditions, and aggressive treatment of complications.
Elimination of Nephrotoxins
Dialysis
Diet
KDIGO guidelines for AKI/ATN suggests the following dietary measures, although most are supported with limited evidence [24] :
Total energy intake of 20–30 kcal/kg/d
Avoid restriction of protein intake
Administer 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without need for dialysis and 1.0–1.5 g/kg/d in patients with AKI on renal replacement and up to a maximum of 1.7 g/kg/d in patients on continuous renal replacement therapy (CRRT) and in hypercatabolic patients.
Entreral nutrition is preferential than parenteral
Increase uric acid : ,myelo , lymphoprolifrative dis / tumor lysis syndrome (after initial chemotherapy ) when large amount of tumer content released into the circulation.
Rabdomyalysis :
Rhabdomyolysis is a syndrome caused by injury to skeletal muscle and involves leakage of large quantities of potentially toxic intracellular contents into plasma.
Causes:
Trauma and muscle compression
blunt trauma or crush injury
High-voltage electrical injury
Heat stroke
Extensive burns
Infection
Drugs and myotoxins
Ethanol/ Methanol/ Ethylene glycol/Heroin/Methadone/Barbiturates/Cocaine/Statins/Antihistamines (particularly in children)/Salicylates
Symptoms:
Myalgias
Generalized weakness
Darkened urine
Acute interstitial nephritis (AIN) is a renal lesion that typically causes a decline in renal function and is characterized by an inflammatory infiltrate in the kidney interstitium.
NSAID including selective COX-2 inhebitors
Drug induced AIN is not a dose dependent
Several studies shown association between PPIs and AIN
In exception to NSAID < 1% are seen with nephrotic syndrome.
Thrombotic Microangiopathy
What is it?
Thrombotic microangiopathies (TMA) are clinical syndromes defined by the presence of hemolytic anemia (destruction of red blood cells), low platelets, and organ damage due to the formation of microscopic blood clots in capillaries and small arteries. The kidneys are commonly affected, although virtually any organ may be involved.
PAN:
Classic polyarteritis nodosa (PAN or c-PAN) is a systemic vasculitis characterized by necrotizing inflammatory lesions that affect medium-sized and small muscular arteries, preferentially at vessel bifurcations. These lesions result in microaneurysm formation, aneurysmal rupture with hemorrhage, thrombosis, and, consequently, organ ischemia or infarction
The glomerular filtration rate (GFR) may fall to very low levels in patients with acute intrinsic kidney injury (AKI). However, a low GFR is not necessarily associated with a parallel reduction in urine output, which can vary from oliguria (<400 to 500 mL/day) to normal values (eg, 1 to 2 L/day).
Reaching a pathological diagnosis is important because minimal-change disease, focal glomerulosclerosis, and membranous nephropathy have different treatment options and prognoses. It is important to differentiate minimal-change disease presenting in adults from focal glomerulosclerosis, as the former has an excellent response to steroids. Another entity called immunoglobulin M (IgM) nephropathy falls in between the two and has an intermediate response to steroids.
Minimal-change disease (MCD), also known as lipoid nephrosis or nil disease, arises from a histopathologic lesion in the glomerulus and is characterized by intense proteinuria leading to edema and intravascular volume depletion. [1] It is the most common single form of nephrotic syndrome in children, but it can also occur in adults.
Goodpasture syndrome :
Symptoms include the following:
Constitutional symptoms (eg, malaise, chills and fever, arthralgias) may precede or develop concurrently with pulmonary or renal manifestations
Hemoptysis is the presenting symptom when the disease affects the lungs. The level of hemoptysis may vary and, in a small percentage of patients, may be absent. Other pulmonary symptoms include cough, dyspnea, and shortness of breath
Massive pulmonary hemorrhage leading to respiratory failure may occur
Chest pain is present in less than half of the patients
Renal manifestations include hematuria, edema, high blood pressure and eventually uremia
Significant anemia may result from persistent intrapulmonary bleeding
Urinalysis findings are characteristic of acute glomerulonephritis, usually demonstrating low-grade proteinuria, gross or microscopic hematuria, and red blood cell casts.
Other studies show a benefit to kidney function recovery after AIN with using corticosteroids, particularly if started within 1 to 2 weeks of diagnosis. [10] [30] [31] Based on these data, a short course of prednisolone should be considered in most patients whose kidney function does not improve rapidly after drug withdrawal, unless corticosteroid therapy is contraindicated. [32] This should be undertaken with the results of a kidney biopsy confirming the diagnosis of AIN and excluding other possible diagnoses. Corticosteroids should be continued for 1 to 1.5 months as much of the recovery of kidney function is expected in this period
BMJ best practice
Blood urea nitrogen (BUN), serum or plasma
8 to 20 mg/dL ; 2.9 to 7.1 mmol/L (SI)
Creatinine, serum
Female: 0.50 to 1.10 mg/dL; 44 to 97 micromol/L (SI)
Male: 0.70 to 1.30 mg/dL ; 62 to 115 micromol/L (SI)
Blood urea nitrogen (BUN), serum or plasma
8 to 20 mg/dL ; 2.9 to 7.1 mmol/L (SI)
Creatinine, serum
Female: 0.50 to 1.10 mg/dL; 44 to 97 micromol/L (SI)
Male: 0.70 to 1.30 mg/dL ; 62 to 115 micromol/L (SI)
Colloids (e.g. starches, dextrans, or gelatins , human albumin ) volume expanders
Balanced crystalloid solutions (e.g., lactated Ringer). Balanced crystalloids have a sodium, potassium, and chloride content closer to that of extracellular fluid and, when given intravenously, have fewer adverse effects on acid-base balance.
Fenoldopam : is a medication that is used to treat hypertensive crises
Selective dopamine recepetor agonist.
ANP is a hormone workd on diuresis
And it vasodilate afferent and vasoconstrict efferent arteriol thus will increase the GFR and increase urine volume
Mannitol, acting as an osmotic diuretic, is thought to increase urinary flow and reduce myoglobin cast obstruction in renal tubules. isotonic sodium chloride solution (0.9% NaCl) with 1 ampule of sodium bicarbonate administered at 100 mL/h. Sodium bicarbonate is used with care because it may potentiate hypocalcemia. The IV bicarbonate concentration is often adjusted to achieve a urine pH higher than 6.5-7.0. This level of alkalization inhibits precipitation of myoglobin and hemoglobin in the tubules
Pathogenesis of kidney injury :
The exact mechanism of kidney involvement is unclear
postulated mechanisms include sepsis leading to cytokine storm syndrome ( increase level of cyctokines in body in responce to virus thus leads to multiorgan damage ) or direct cellular injury due to the virus.