Mineral and bone disorders commonly accompany chronic kidney disease due to imbalances in calcium, phosphorus, parathyroid hormone, and vitamin D levels as kidney function declines. Treatment for secondary hyperparathyroidism and hyperphosphatemia in CKD involves controlling dietary intake, using phosphate binders such as calcium-based or non-calcium-based options, and medications like calcimimetics, calcitriol, or vitamin D analogs to regulate mineral levels and reduce cardiovascular risks from CKD-MBD. The 2017 KDIGO guidelines updated recommendations around phosphate management and treatment thresholds in earlier CKD stages based on newer evidence.
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting more than 3 months. Management of CKD involves controlling comorbidities like hypertension and diabetes, and nutritional management including restricting protein and salt intake. Treatment of complications includes managing anemia with iron or ESAs, controlling mineral and bone disorder with phosphate binders, vitamin D analogs, and calcimimetics, and treating secondary hyperparathyroidism.
This document provides a summary of a presentation on the management of anemia and mineral bone disorders in chronic kidney disease. It defines anemia and its causes in CKD, including relative erythropoietin deficiency and iron deficiency. It outlines the evaluation, treatment, and monitoring of anemia in CKD patients, including the use of iron supplementation, erythropoiesis-stimulating agents, and blood transfusions. It also describes chronic kidney disease-mineral bone disorder, including abnormalities in calcium, phosphorus, PTH, and vitamin D metabolism. It discusses the pathogenesis and types of CKD-MBD, including high turnover bone disease and adynamic bone disease, and their treatment through dietary phosphorus restrictions,
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common complication in chronic kidney disease caused by reduced kidney function and mineral metabolism abnormalities. This leads to high phosphate, activation of parathyroid hormone, and bone abnormalities from renal osteodystrophy to vascular calcification. Treatment focuses on controlling phosphate levels through binders like sevelamer and cinacalcet to reduce parathyroid hormone in order to prevent bone disease and fractures while minimizing cardiovascular risks.
This document discusses calcium homeostasis and disorders, including hypercalcemia and hyperparathyroidism. It provides details on the roles of parathyroid hormone (PTH), vitamin D, and calcitonin in regulating calcium levels. It examines causes of hypercalcemia such as primary hyperparathyroidism, malignancy, and vitamin D toxicity. Guidelines for treatment of asymptomatic primary hyperparathyroidism with surgery or medication are reviewed based on calcium levels, bone mineral density, kidney stones, and age. Non-surgical treatments including vitamin D supplementation and cinacalcet are also discussed.
This document discusses dietary guidelines for kidney health. It notes that kidneys play a key role in nutrient homeostasis and that loss of kidney function disrupts this. For chronic kidney disease (CKD) patients, guidelines recommend a daily protein intake of 0.6-0.8g/kg, limiting fat intake to 30% of calories, and restricting sodium and phosphorus intake. While protein restriction may slow CKD progression, large trials like MDRD found little overall benefit. A plant-based, low-protein diet that is low in phosphorus and sodium may be most suitable for CKD patients. Focusing on overall dietary patterns like the DASH diet may be more practical than individual nutrient restrictions.
This document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD). It begins with an overview of the key components involved in CKD-MBD, including calcium, phosphorus, parathyroid hormone, vitamin D, fibroblast growth factor 23, and magnesium. The document then presents two clinical cases involving patients with CKD and discusses treatment options based on their lab results. It also covers the roles of vitamin D and magnesium in vascular pathology and mortality in CKD patients. Guidelines for the treatment of secondary hyperparathyroidism from KDIGO are also summarized.
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting more than 3 months. Management of CKD involves controlling comorbidities like hypertension and diabetes, and nutritional management including restricting protein and salt intake. Treatment of complications includes managing anemia with iron or ESAs, controlling mineral and bone disorder with phosphate binders, vitamin D analogs, and calcimimetics, and treating secondary hyperparathyroidism.
This document provides a summary of a presentation on the management of anemia and mineral bone disorders in chronic kidney disease. It defines anemia and its causes in CKD, including relative erythropoietin deficiency and iron deficiency. It outlines the evaluation, treatment, and monitoring of anemia in CKD patients, including the use of iron supplementation, erythropoiesis-stimulating agents, and blood transfusions. It also describes chronic kidney disease-mineral bone disorder, including abnormalities in calcium, phosphorus, PTH, and vitamin D metabolism. It discusses the pathogenesis and types of CKD-MBD, including high turnover bone disease and adynamic bone disease, and their treatment through dietary phosphorus restrictions,
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a common complication in chronic kidney disease caused by reduced kidney function and mineral metabolism abnormalities. This leads to high phosphate, activation of parathyroid hormone, and bone abnormalities from renal osteodystrophy to vascular calcification. Treatment focuses on controlling phosphate levels through binders like sevelamer and cinacalcet to reduce parathyroid hormone in order to prevent bone disease and fractures while minimizing cardiovascular risks.
This document discusses calcium homeostasis and disorders, including hypercalcemia and hyperparathyroidism. It provides details on the roles of parathyroid hormone (PTH), vitamin D, and calcitonin in regulating calcium levels. It examines causes of hypercalcemia such as primary hyperparathyroidism, malignancy, and vitamin D toxicity. Guidelines for treatment of asymptomatic primary hyperparathyroidism with surgery or medication are reviewed based on calcium levels, bone mineral density, kidney stones, and age. Non-surgical treatments including vitamin D supplementation and cinacalcet are also discussed.
This document discusses dietary guidelines for kidney health. It notes that kidneys play a key role in nutrient homeostasis and that loss of kidney function disrupts this. For chronic kidney disease (CKD) patients, guidelines recommend a daily protein intake of 0.6-0.8g/kg, limiting fat intake to 30% of calories, and restricting sodium and phosphorus intake. While protein restriction may slow CKD progression, large trials like MDRD found little overall benefit. A plant-based, low-protein diet that is low in phosphorus and sodium may be most suitable for CKD patients. Focusing on overall dietary patterns like the DASH diet may be more practical than individual nutrient restrictions.
This document discusses chronic kidney disease-mineral and bone disorder (CKD-MBD). It begins with an overview of the key components involved in CKD-MBD, including calcium, phosphorus, parathyroid hormone, vitamin D, fibroblast growth factor 23, and magnesium. The document then presents two clinical cases involving patients with CKD and discusses treatment options based on their lab results. It also covers the roles of vitamin D and magnesium in vascular pathology and mortality in CKD patients. Guidelines for the treatment of secondary hyperparathyroidism from KDIGO are also summarized.
The pathogenesis of CKD-MBD is complex, involving disruptions in mineral homeostasis and hormone levels as kidney function declines. Key factors include hyperphosphatemia, decreased calcitriol levels, and hypocalcemia. This leads to elevated PTH levels as the parathyroid glands respond to low calcium and calcitriol. Over time, the parathyroid glands become resistant due to downregulation of receptors. Progressive CKD also impairs the kidneys' ability to regulate phosphate, exacerbating hyperphosphatemia and CKD-MBD.
This document defines chronic kidney disease and provides details on its classification, causes, pathogenesis, complications, presentation, diagnosis, risk factors, slowing progression, and long-term management. Chronic kidney disease is defined as abnormalities of the kidneys lasting more than three months, as indicated by kidney damage or decreased GFR. It is classified based on cause, GFR level, and albuminuria level. Common causes in children include congenital anomalies, obstructive uropathy, glomerulonephritis, and inherited disorders. Risk factors for CKD and strategies for slowing progression are also outlined. Long-term management focuses on nutrition, growth promotion, managing mineral bone disease, anemia, and infections. Dialysis or transplant
1. Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting more than 3 months, including decreased glomerular filtration rate (GFR) <60 mL/min/1.73m2 or markers of kidney damage.
2. Dietary management of CKD involves restricting sodium, potassium, phosphorus, and fluid intake depending on the stage of disease. Protein intake is usually moderately restricted.
3. Common complications of CKD include anemia, bone mineral disorders, cardiovascular disease, electrolyte abnormalities, acidosis, and hypertension. Treatment involves controlling risk factors and managing complications through diet, medications, dialysis or transplant.
This document provides information on chronic kidney disease (CKD) diagnosis and management. It discusses common clinical features of CKD, which are often vague until late stages. It outlines the approach to investigating patients, including lab tests and imaging studies. Management focuses on slowing progression, treating complications, and timely planning for renal replacement therapy if needed. Goals include controlling risk factors like hypertension and diabetes, treating anemia, bone disease, and other issues. Dialysis criteria include refractory symptoms, complications, or glomerular filtration rate below 10 ml/min/1.73m2.
This document presents the case of a 50-year-old female diabetic patient referred for evaluation of renal impairment. Her creatinine had risen from 1.3 to 3.8 over the past year. She has a history of diabetes, hypertension, and diabetic retinopathy. On examination, she has lower limb edema. Tests show anemia, hyperkalemia, and high HbA1c. The provisional diagnosis is chronic kidney disease likely due to her long-standing diabetes, with complications of hyperkalemia and uncontrolled diabetes. The plan is to control her blood sugar and potassium, restrict diet, and regularly monitor her kidney function and diabetes.
This case study describes a 41-year-old male patient with chronic kidney disease who is undergoing hemodialysis treatment. His medical history, social history, physical exam findings, laboratory results, medications, and dietary intake are presented. The patient's lab results show abnormalities including high phosphorus and potassium levels. His current diet does not meet the nutritional recommendations for dialysis patients. The case study involves assessing the patient's diet, creating a sample meal plan meeting his needs, and addressing risks such as secondary hyperparathyroidism resulting from his chronic kidney disease.
Hyperparathyroidism involves the dysregulation of calcium homeostasis. Normally, calcium levels are tightly controlled within a narrow range through absorption in the gut, distribution between extracellular and intracellular spaces, and renal handling. This balance involves hormones like parathyroid hormone (PTH), vitamin D, and fibroblast growth factor 23. Chronic kidney disease can lead to secondary hyperparathyroidism as the kidneys lose function regulating calcium, phosphate, vitamin D, and PTH. Longstanding secondary hyperparathyroidism can progress to tertiary hyperparathyroidism where the parathyroid glands become autonomous. Treatment focuses on dietary phosphate control, phosphate binders, vitamin D analogs, calcimimetics, and parathy
CKD-MBD is a systemic disorder of mineral and bone metabolism due to chronic kidney disease. It is characterized by abnormalities in calcium, phosphorus, PTH, or vitamin D levels and bone abnormalities. The pathogenesis involves elevated PTH levels, hyperphosphatemia, decreased calcitriol activity, and hypocalcemia. Treatment focuses on controlling phosphate levels through diet, phosphate binders, and dialysis; maintaining normal calcium levels; and treating secondary hyperparathyroidism through calcimimetics and vitamin D analogues. The goal is to prevent skeletal and extraskeletal complications like fractures, vascular calcification, and calciphylaxis.
This document discusses diabetic kidney disease and nephropathy. Diabetic nephropathy is the leading cause of renal failure, with 50% of dialysis patients having diabetes. Risk factors include poor blood glucose control, long diabetes duration, hypertension, and family history. Symptoms include protein in urine, high blood pressure, and declining renal function. Screening for microalbuminuria is important. Strict glycemic control and keeping blood pressure below 130/80 can prevent or slow progression. Treatment involves diet, medication, fluid management, and potentially renal replacement therapies like hemodialysis if kidney function declines severely.
a precise presentation over CKD made for house officers/medical interns . It focuses over signs and symptoms and in-hospital management of resulting problems , material taken majorly from medscape, CMDT and oxford hand book
The document defines chronic kidney disease (CKD) and provides guidelines for evaluating and managing CKD according to the KDIGO 2012 Clinical Practice Guideline. It defines CKD based on glomerular filtration rate (GFR) and albuminuria categories. It recommends evaluating CKD severity annually and monitoring for progression. It provides guidance on managing complications of CKD like anemia, bone disease, and cardiovascular risk. It also addresses medication management, specialist referral indications, and timing the initiation of renal replacement therapy.
Parathyroid hormone (PTH) regulates calcium homeostasis. Primary hyperparathyroidism is caused by overproduction of PTH by one or more abnormal parathyroid glands. It can cause increased bone resorption and loss of bone mineral density. Surgical removal of the abnormal gland(s) is the only cure. Secondary and tertiary hyperparathyroidism are caused by chronic kidney disease and long-term renal failure which disrupt normal calcium regulation, leading to PTH overproduction. They are treated medically or with subtotal parathyroidectomy. New localization techniques and medications are improving diagnosis and management.
Nutrition therapy work shop dawly second part 2017FarragBahbah
This document provides information on nutrition for patients with chronic kidney disease (CKD) and those undergoing dialysis. It discusses recommendations for calories, protein, carbohydrates, fat, sodium, fluids, phosphorus, calcium, potassium and micronutrients. It notes that dialysis can impact nutrition by causing losses of certain nutrients and affecting appetite and food intake. Dietary goals for patients on dialysis include managing blood pressure and glucose as well as intake of minerals and fluids.
Hypercalcemia is a condition where there are abnormally high levels of calcium in the blood. It affects around 0.5-1% of the general population. The most common causes are primary hyperparathyroidism and hypercalcemia caused by malignancy, which together account for 90% of cases. Symptoms range from none to neurological effects like confusion, weakness, and coma. Treatment involves rehydration, calcitonin, bisphosphonates, and dialysis for severe cases. Ongoing treatment aims to prevent recurrence by addressing the underlying cause when possible.
Hypercalcemia is a condition where there are abnormally high levels of calcium in the blood. It affects around 0.5-1% of the general population. The two most common causes are primary hyperparathyroidism and hypercalcemia caused by malignancy, which together account for 90% of cases. Symptoms range from none to neurological effects like confusion, weakness, and coma. Treatment involves rehydration, calcitonin, bisphosphonates, and dialysis for severe cases. Ongoing treatment aims to prevent recurrence by addressing the underlying cause when possible.
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
Management of anemia in chronic kidney disease -Boushra Alsaoor
This document provides an overview of the management of anemia in chronic kidney disease. It defines anemia according to WHO criteria and notes that nearly 90% of CKD patients with a GFR below 30 mL/min have anemia. The main causes of anemia in CKD are decreased erythropoietin production and a shorter red blood cell lifespan. Treatment with erythropoiesis-stimulating agents or ESAs like epoetin and darbepoetin can help increase hemoglobin levels and improve outcomes. The goals of ESA therapy are to raise hemoglobin by 1-2 g/dL per month until it reaches 10-11.5 g/dL without exceeding 13 g/dL. Iron supplementation is
The AALL1331 trial compared blinatumomab to chemotherapy as consolidation therapy after re-induction in pediatric patients with first relapse B-cell acute lymphoblastic leukemia. The open-label, randomized controlled trial found that blinatumomab significantly improved disease-free survival compared to chemotherapy, with 3-year disease-free survival rates of 45% for blinatumomab versus 27% for chemotherapy. Blinatumomab was generally well-tolerated though adverse events included cytokine release syndrome and neurotoxicity. The results support using blinatumomab as consolidation therapy to bridge pediatric B-ALL patients to hematopoietic stem cell transplant.
Coronary artery disease remains the leading cause of death in the US. Acute coronary syndromes are caused by a sudden reduction in coronary blood flow due to atherosclerosis. There are three presentations of ACS: unstable angina, NSTEMI, and STEMI. Treatment involves stabilizing the patient, risk stratification, and determining reperfusion strategy which may involve fibrinolysis, PCI, or CABG. Long term management focuses on preventative therapies including antiplatelets, statins, beta blockers, ACE inhibitors, and other secondary prevention medications.
The pathogenesis of CKD-MBD is complex, involving disruptions in mineral homeostasis and hormone levels as kidney function declines. Key factors include hyperphosphatemia, decreased calcitriol levels, and hypocalcemia. This leads to elevated PTH levels as the parathyroid glands respond to low calcium and calcitriol. Over time, the parathyroid glands become resistant due to downregulation of receptors. Progressive CKD also impairs the kidneys' ability to regulate phosphate, exacerbating hyperphosphatemia and CKD-MBD.
This document defines chronic kidney disease and provides details on its classification, causes, pathogenesis, complications, presentation, diagnosis, risk factors, slowing progression, and long-term management. Chronic kidney disease is defined as abnormalities of the kidneys lasting more than three months, as indicated by kidney damage or decreased GFR. It is classified based on cause, GFR level, and albuminuria level. Common causes in children include congenital anomalies, obstructive uropathy, glomerulonephritis, and inherited disorders. Risk factors for CKD and strategies for slowing progression are also outlined. Long-term management focuses on nutrition, growth promotion, managing mineral bone disease, anemia, and infections. Dialysis or transplant
1. Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting more than 3 months, including decreased glomerular filtration rate (GFR) <60 mL/min/1.73m2 or markers of kidney damage.
2. Dietary management of CKD involves restricting sodium, potassium, phosphorus, and fluid intake depending on the stage of disease. Protein intake is usually moderately restricted.
3. Common complications of CKD include anemia, bone mineral disorders, cardiovascular disease, electrolyte abnormalities, acidosis, and hypertension. Treatment involves controlling risk factors and managing complications through diet, medications, dialysis or transplant.
This document provides information on chronic kidney disease (CKD) diagnosis and management. It discusses common clinical features of CKD, which are often vague until late stages. It outlines the approach to investigating patients, including lab tests and imaging studies. Management focuses on slowing progression, treating complications, and timely planning for renal replacement therapy if needed. Goals include controlling risk factors like hypertension and diabetes, treating anemia, bone disease, and other issues. Dialysis criteria include refractory symptoms, complications, or glomerular filtration rate below 10 ml/min/1.73m2.
This document presents the case of a 50-year-old female diabetic patient referred for evaluation of renal impairment. Her creatinine had risen from 1.3 to 3.8 over the past year. She has a history of diabetes, hypertension, and diabetic retinopathy. On examination, she has lower limb edema. Tests show anemia, hyperkalemia, and high HbA1c. The provisional diagnosis is chronic kidney disease likely due to her long-standing diabetes, with complications of hyperkalemia and uncontrolled diabetes. The plan is to control her blood sugar and potassium, restrict diet, and regularly monitor her kidney function and diabetes.
This case study describes a 41-year-old male patient with chronic kidney disease who is undergoing hemodialysis treatment. His medical history, social history, physical exam findings, laboratory results, medications, and dietary intake are presented. The patient's lab results show abnormalities including high phosphorus and potassium levels. His current diet does not meet the nutritional recommendations for dialysis patients. The case study involves assessing the patient's diet, creating a sample meal plan meeting his needs, and addressing risks such as secondary hyperparathyroidism resulting from his chronic kidney disease.
Hyperparathyroidism involves the dysregulation of calcium homeostasis. Normally, calcium levels are tightly controlled within a narrow range through absorption in the gut, distribution between extracellular and intracellular spaces, and renal handling. This balance involves hormones like parathyroid hormone (PTH), vitamin D, and fibroblast growth factor 23. Chronic kidney disease can lead to secondary hyperparathyroidism as the kidneys lose function regulating calcium, phosphate, vitamin D, and PTH. Longstanding secondary hyperparathyroidism can progress to tertiary hyperparathyroidism where the parathyroid glands become autonomous. Treatment focuses on dietary phosphate control, phosphate binders, vitamin D analogs, calcimimetics, and parathy
CKD-MBD is a systemic disorder of mineral and bone metabolism due to chronic kidney disease. It is characterized by abnormalities in calcium, phosphorus, PTH, or vitamin D levels and bone abnormalities. The pathogenesis involves elevated PTH levels, hyperphosphatemia, decreased calcitriol activity, and hypocalcemia. Treatment focuses on controlling phosphate levels through diet, phosphate binders, and dialysis; maintaining normal calcium levels; and treating secondary hyperparathyroidism through calcimimetics and vitamin D analogues. The goal is to prevent skeletal and extraskeletal complications like fractures, vascular calcification, and calciphylaxis.
This document discusses diabetic kidney disease and nephropathy. Diabetic nephropathy is the leading cause of renal failure, with 50% of dialysis patients having diabetes. Risk factors include poor blood glucose control, long diabetes duration, hypertension, and family history. Symptoms include protein in urine, high blood pressure, and declining renal function. Screening for microalbuminuria is important. Strict glycemic control and keeping blood pressure below 130/80 can prevent or slow progression. Treatment involves diet, medication, fluid management, and potentially renal replacement therapies like hemodialysis if kidney function declines severely.
a precise presentation over CKD made for house officers/medical interns . It focuses over signs and symptoms and in-hospital management of resulting problems , material taken majorly from medscape, CMDT and oxford hand book
The document defines chronic kidney disease (CKD) and provides guidelines for evaluating and managing CKD according to the KDIGO 2012 Clinical Practice Guideline. It defines CKD based on glomerular filtration rate (GFR) and albuminuria categories. It recommends evaluating CKD severity annually and monitoring for progression. It provides guidance on managing complications of CKD like anemia, bone disease, and cardiovascular risk. It also addresses medication management, specialist referral indications, and timing the initiation of renal replacement therapy.
Parathyroid hormone (PTH) regulates calcium homeostasis. Primary hyperparathyroidism is caused by overproduction of PTH by one or more abnormal parathyroid glands. It can cause increased bone resorption and loss of bone mineral density. Surgical removal of the abnormal gland(s) is the only cure. Secondary and tertiary hyperparathyroidism are caused by chronic kidney disease and long-term renal failure which disrupt normal calcium regulation, leading to PTH overproduction. They are treated medically or with subtotal parathyroidectomy. New localization techniques and medications are improving diagnosis and management.
Nutrition therapy work shop dawly second part 2017FarragBahbah
This document provides information on nutrition for patients with chronic kidney disease (CKD) and those undergoing dialysis. It discusses recommendations for calories, protein, carbohydrates, fat, sodium, fluids, phosphorus, calcium, potassium and micronutrients. It notes that dialysis can impact nutrition by causing losses of certain nutrients and affecting appetite and food intake. Dietary goals for patients on dialysis include managing blood pressure and glucose as well as intake of minerals and fluids.
Hypercalcemia is a condition where there are abnormally high levels of calcium in the blood. It affects around 0.5-1% of the general population. The most common causes are primary hyperparathyroidism and hypercalcemia caused by malignancy, which together account for 90% of cases. Symptoms range from none to neurological effects like confusion, weakness, and coma. Treatment involves rehydration, calcitonin, bisphosphonates, and dialysis for severe cases. Ongoing treatment aims to prevent recurrence by addressing the underlying cause when possible.
Hypercalcemia is a condition where there are abnormally high levels of calcium in the blood. It affects around 0.5-1% of the general population. The two most common causes are primary hyperparathyroidism and hypercalcemia caused by malignancy, which together account for 90% of cases. Symptoms range from none to neurological effects like confusion, weakness, and coma. Treatment involves rehydration, calcitonin, bisphosphonates, and dialysis for severe cases. Ongoing treatment aims to prevent recurrence by addressing the underlying cause when possible.
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
Management of anemia in chronic kidney disease -Boushra Alsaoor
This document provides an overview of the management of anemia in chronic kidney disease. It defines anemia according to WHO criteria and notes that nearly 90% of CKD patients with a GFR below 30 mL/min have anemia. The main causes of anemia in CKD are decreased erythropoietin production and a shorter red blood cell lifespan. Treatment with erythropoiesis-stimulating agents or ESAs like epoetin and darbepoetin can help increase hemoglobin levels and improve outcomes. The goals of ESA therapy are to raise hemoglobin by 1-2 g/dL per month until it reaches 10-11.5 g/dL without exceeding 13 g/dL. Iron supplementation is
The AALL1331 trial compared blinatumomab to chemotherapy as consolidation therapy after re-induction in pediatric patients with first relapse B-cell acute lymphoblastic leukemia. The open-label, randomized controlled trial found that blinatumomab significantly improved disease-free survival compared to chemotherapy, with 3-year disease-free survival rates of 45% for blinatumomab versus 27% for chemotherapy. Blinatumomab was generally well-tolerated though adverse events included cytokine release syndrome and neurotoxicity. The results support using blinatumomab as consolidation therapy to bridge pediatric B-ALL patients to hematopoietic stem cell transplant.
Coronary artery disease remains the leading cause of death in the US. Acute coronary syndromes are caused by a sudden reduction in coronary blood flow due to atherosclerosis. There are three presentations of ACS: unstable angina, NSTEMI, and STEMI. Treatment involves stabilizing the patient, risk stratification, and determining reperfusion strategy which may involve fibrinolysis, PCI, or CABG. Long term management focuses on preventative therapies including antiplatelets, statins, beta blockers, ACE inhibitors, and other secondary prevention medications.
This document summarizes the background, objectives, methods, and endpoints of the MENDS2 trial, a randomized controlled trial comparing dexmedetomidine to propofol for sedation in mechanically ventilated adults with sepsis. The trial aims to test whether dexmedetomidine results in better short-term outcomes, such as fewer days of delirium or coma and more ventilator-free days, and long-term outcomes like survival and cognition at 6 months compared to propofol. The trial plans to enroll approximately 420 patients and randomize them 1:1 to receive either dexmedetomidine or propofol infusion titrated to light sedation. The primary outcome is the number of days alive
This document summarizes the epidemiology, pathophysiology, presentation, diagnosis and treatment of acute decompensated heart failure (ADHF). Some key points:
1. ADHF is a leading cause of hospitalization and mortality worldwide, with high readmission rates. Risk factors include non-adherence to medications and acute infections.
2. Presentation depends on the degree of pulmonary congestion and systemic perfusion. Diagnosis is made clinically based on symptoms and objective data like chest x-ray and BNP levels.
3. Initial treatment focuses on relieving congestion with diuretics. Vasodilators may be used in hypertensive patients. Inotropes and vasopress
Parkinson's disease is a neurodegenerative disorder characterized by three key points:
1) Loss of dopaminergic neurons in the substantia nigra leads to decreased dopamine in the striatum and motor symptoms like bradykinesia.
2) Accumulation of alpha-synuclein protein is involved in the pathogenesis and motor symptoms result from disinhibition of movement circuits due to dopamine deficiency.
3) Treatment involves dopamine replacement therapy using levodopa although long term use can cause motor fluctuations and dyskinesias which other drugs aim to reduce.
ASandler Patient Case Presentation_OK_ESBL bacteremia.pptxAnnaSandler4
An 88-year-old female presented with abdominal pain and altered mental status. She has a history of ESBL bacteremia. Blood and urine cultures were obtained and empiric meropenem started. The ID physician is considering switching to piperacillin/tazobactam to reduce carbapenem use. Piperacillin/tazobactam is active against some ESBLs but its efficacy in bacteremia is uncertain. Studies show carbapenems are associated with better outcomes than other antibiotics for ESBL bacteremia due to their reliable activity against these resistant organisms. More evidence is needed before safely using alternative agents like piperacillin/tazobactam for ESBL b
1. The document discusses uncomplicated versus complicated urinary tract infections (UTIs). Uncomplicated UTIs are confined to the bladder, while complicated UTIs extend beyond the bladder.
2. Common organisms that cause uncomplicated UTIs include Escherichia coli and other gram-negative rods. Complicated UTIs can be caused by a broader range of bacteria, including multidrug-resistant organisms.
3. Treatment for uncomplicated UTIs involves oral antibiotics like nitrofurantoin, trimethoprim-sulfamethoxazole, or fluoroquinolones. Complicated UTIs may require intravenous antibiotics like piperacillin-tazobactam or
This randomized controlled trial evaluated the effect of dapagliflozin versus placebo on worsening heart failure or cardiovascular death in patients with heart failure and an ejection fraction above 40%. It found that dapagliflozin reduced the risk of the primary composite outcome compared to placebo, both in the overall population and in those with an ejection fraction under 60%. Dapagliflozin also reduced the risk of worsening heart failure alone. There was no significant difference in cardiovascular death or adverse events between the groups. The authors concluded that dapagliflozin lowered the risk of worsening heart failure or cardiovascular death regardless of ejection fraction.
The document summarizes guidelines for the treatment of heart failure. Key points include:
- The 2022 guidelines recommend the use of sacubitril/valsartan (ARNi) as initial treatment for HFrEF, and suggest SGLT2 inhibitors may also be used as initial treatment.
- For HFpEF, SGLT2 inhibitors are recommended based on evidence that empagliflozin reduces hospitalizations. Other medications like ARNi, MRAs, and BB may also be considered but require further study.
- Treatment focuses on guideline-directed medical therapy including ACEi/ARB, BB, MRAs, and diuretics, with addition of other drugs like SGLT2
Final mab DI question presentation.docxAnnaSandler4
This document discusses monoclonal antibody treatments for COVID-19, including:
- Monoclonal antibodies bind to the spike protein of SARS-CoV-2 to block viral attachment and entry into cells. Several monoclonal antibodies have received emergency use authorization for treatment or prevention of COVID-19.
- For treatment, authorized monoclonal antibodies include bebtelovimab, sotrovimab, and casirivimab/imdevimab. For pre-exposure prevention, authorized options are tixagevimab/cilgavimab. Post-exposure prevention includes tixagevimab/cilgavimab and bamlanivimab/etesevimab.
- The document provides details
The document discusses community-acquired pneumonia (CAP), including its pathophysiology as an acute infection of the pulmonary tissue acquired outside of the hospital. It provides details on the diagnosis, presentation, and treatment of CAP, noting that typical bacteria include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Empiric antibiotic treatment options for CAP are outlined depending on a patient's risk factors, comorbidities, and severity of illness.
The ENVISAGE-TAVI trial compared edoxaban to warfarin for stroke prevention in patients with atrial fibrillation following transcatheter aortic valve replacement (TAVR). The trial randomized 1426 patients 1:1 to edoxaban 60 mg daily or dose-adjusted warfarin. The primary endpoint was a composite of death, myocardial infarction, ischemic stroke, systemic embolism, valve thrombosis or major bleeding (net adverse clinical events). Edoxaban was found to be noninferior to warfarin for the primary endpoint with a hazard ratio of 0.82 (95% CI 0.65-1.04). Rates of major bleeding were also similar between the groups. The
This document summarizes the background, objectives, and methods of the MENDS2 trial, a triple-blind randomized controlled trial comparing dexmedetomidine to propofol for sedation in mechanically ventilated adults with sepsis. The trial aims to test if dexmedetomidine results in better short-term outcomes like fewer days of delirium or coma and longer-term outcomes like mortality at 90 days compared to propofol. Over 400 patients will be randomly assigned to receive either dexmedetomidine or propofol infusion titrated to light sedation levels. The primary outcome is the number of days alive without delirium or coma during the 14-day intervention period. Secondary outcomes include ventil
1. Sepsis and septic shock result from an excessive host response to infection that can lead to life-threatening organ damage and failure. It affects over 30 million people worldwide annually, resulting in 6 million deaths. Treatment involves early recognition, source control, antibiotics, fluid resuscitation, vasopressor support, and monitoring for organ dysfunction.
2. Norepinephrine is usually the first-line vasopressor to restore blood pressure in septic shock. Additional agents like vasopressin may be needed if the target blood pressure is not achieved with norepinephrine alone. Corticosteroids can be considered if shock is not responsive to fluids and vasopressors.
3. Broad-spectrum
This document summarizes a case study involving a 19-year old male (EG) who was admitted to the ICU following a high-speed motorcycle accident and subsequent traumatic brain injury. EG remains intubated and sedated, with elevated heart rate, temperatures, and signs of sympathetic hyperactivity. The attending physician asks the clinical pharmacist about evidence for using propranolol to treat EG's sympathetic hyperactivity. The pharmacist then reviews the pathophysiology and presentation of paroxysmal sympathetic hyperactivity, current treatment options including beta blockers like propranolol, and a literature review on the use of beta blockers including propranolol in traumatic brain injury patients.
This document discusses diabetic ketoacidosis (DKA), a life-threatening complication of diabetes caused by a lack of insulin. It provides details on the pathophysiology, presentation, diagnosis, and treatment of DKA. Treatment involves rapidly correcting dehydration and electrolyte abnormalities with intravenous fluids, replenishing potassium, and administering insulin to lower blood glucose levels and reverse ketosis. The main goals of treatment are to resuscitate the patient, replete fluids and electrolytes, and reverse the metabolic acidosis through insulin administration.
Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition caused by infection, injury or other insults that leads to hypoxemia. It is characterized by diffuse alveolar damage and impaired gas exchange. ARDS has a mortality rate ranging from 27-45% depending on severity. Treatment involves lung-protective ventilation with low tidal volumes, conservative fluid management, prone positioning in severe cases, paralysis and consideration of steroids in refractory cases. Refractory ARDS may be treated with extracorporeal membrane oxygenation.
The study evaluated the efficacy and safety of rivaroxaban compared to vitamin K antagonists for stroke prevention in patients with rheumatic heart disease-associated atrial fibrillation (RHD-AF). Over 4565 patients from 24 countries were randomized to receive either rivaroxaban 20 mg daily or a vitamin K antagonist such as warfarin, with a mean follow up of 3.1 years. The primary outcome occurred in 560 patients (8.21% per year) in the rivaroxaban group and 446 patients (6.49% per year) in the vitamin K antagonist group, showing rivaroxaban to be less effective with a hazard ratio of 1.25. There were no significant
This document summarizes a study evaluating the role of rivaroxaban after revascularization for peripheral vascular disease. The VOYAGER PAD trial was a double-blind randomized controlled trial comparing rivaroxaban 2.5 mg twice daily plus aspirin to aspirin alone in over 8,000 patients with symptomatic peripheral artery disease who had undergone recent revascularization. The study found that rivaroxaban plus aspirin significantly reduced the risk of major adverse limb or cardiovascular events compared to aspirin alone, with acceptable bleeding risk. This suggests that rivaroxaban may be a suitable alternative to warfarin for preventing complications after peripheral revascularization.
Can Allopathy and Homeopathy Be Used Together in India.pdfDharma Homoeopathy
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Mental Benefits: Explains the psychological advantages, including stress reduction, improved mood, and better sleep.
Tips for Staying Active:
Encourages consistency, variety in exercises, setting realistic goals, and finding enjoyable activities to maintain motivation.
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Integrating Nutrition and Exercise: Suggests meal planning and incorporating physical activity into daily routines.
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1. 1
Stage eGFR
G1 >/= 90
G2 60-89
G3a 45-59
G3b 30-44
G4 15-29
G5 < 15
G5D < 15 + dialysis
Substance Ca Phos.
PTH
1, 25 dihydroxyvitamin
D (calcitriol)
Background
Anna Sandler
Mineral and Bone Disorder in CKD
PharmD Candidate, 2023
Physiology and Pathophysiology: When tight control is disrupted
Mineral and bone disorders (MBDs) commonly accompany
chronic kidney disease (CKD)
Associated with:
o Imbalance of calcium (Ca), phosphorous, parathyroid
hormone (PTH) and vitamin D
CKD-MBD has been linked to cardiovascular mortality1
o Disruptions in mineral homeostasis
o Vascular calcification
2017: > 60% of CV deaths in dialysis patients
The kidney responds to signals from the parathyroid
gland
The parathyroid gland has a calcium-sensing receptor
(CaSR) that allows it to control serum Ca levels
In response to low Ca levels, the PTH gland stimulates the
kidney to reabsorb Ca from the blood
The kidney produces more activated vitamin D to increase
intestinal Ca absorption
Renal failure
Phosphorous Calcitriol
Secondary Hyperparathyroidism
Drug Target
CaSR
1: Hyperphosphatemia, vascular calcification, and elevated fibroblast growth factor 23 (FGF23) seen in CKD are
associated with increased CV morbidity and mortality. Mortality in CKD patients on dialysis is approximately 20
times higher than that of the general population.
In renal failure, the tight control is lost
o Impaired excretion of phosphorous
o Decreased production of calcitriol
o Decreased sensitivity of CaSR
2. 2
High Phos +Low Vit.
D + Decreased CaSR
Hyperparathyroidism Renal osteodystrophy
Abnormality Levels Presentation
Hypercalcemia >10.5mg/dL (total
normal 8.5-10.5
mg/dL)
Vascular
calcifications, chronic
hypertension
Hyperphosphatemia >4.5 mg/dL (normal
2.8-4.5 mg/dL)
Vascular
calcifications, chronic
hypertension
Renal
osteodystrophy
PTH > ~55-65 pg/mL
(high-turnover)
Bone pain, fractures,
deformities
Presentation and Diagnosis
General Approach to Treatment
Based on metabolic abnormality
and severity of kidney dysfunction
o Secondary
hyperparathyroidism
o Hyperphosphatemia
o Decreased calcitriol
Tailor treatment to stage of CKD and
whether patients are on dialysis
o Many recommendations for
stages G3a-G5 and G5D
Ca/Vit D balance Hyperparathyoridism
Hyperphosphatemia
General
considerations
Presentation based on metabolic abnormality
and severity of disease
Big victim: Bones!
Detectable biomarkers:
o Increased Fibroblast growth factor 23
(FGF23)
Gold standard for diagnosis and classification for
bone disease:
o Bone biopsy (not always feasible)
More common:
o Ca, Phosphorous, PTH, bone-specific
alkaline phosphatase levels + radiograph
Renal osteodystrophy
Increased bone turnover Low bone turnover
2017 KDIGO Guideline
Updates
3. 3
Drug Type Initial dosing and titration Pearls, AEs, monitoring
Calcium
carbonate
(Tums)
Calcium-
containing
500-100 mg elemental Ca TID
with meals, increase by 500 mg
increments per meal
40% elemental Ca
Binds to phosphate in GI tract to create
soluble complexes
Monitor: Ca*P product
AEs: constipation, calcifications
Calcium
acetate
(Phos-Lo)
Calcium-
containing
1334 mg TID with meals
Increase by 667 mg per meal
25% elemental Ca
May be more efficient > carbonate
Sevelamer
(Renvela,
Renagel)
Non-calcium
containing
800-1600 mg3
PO TID
depending on initial
phosphorous levels. Increase or
decrease by 400-800 mg/meal
if phos. Levels are < 3.5 mg/dL
or > 5.5 mg/dL respectively
Nonabsorbable cationic polymer that binds
phosphate through ion exchange
HCl salt (Renagel): Potential metabolic
acidosis
AEs: bowel obstruction, colitis, dysphagia4
Watch out for DDIs
Sucroferric
oxyhydroxide
(Velphoro)
Non-calcium
containing
2.5 g TID or 500 mg (elemental)
TID. Titrate in increments of
500 mg of iron/day beginning
week 1.
For eGFR < 15
AEs: diarrhea, nausea, constipation,
vomiting, dark stools
Monitoring: Iron hemostasis, Ca, phos,
PTH, drug-drug interactions
Lanthanum Non-calcium
containing
1500 mg daily with meals
increased by 750 mg daily
every 2-3 weeks
Chewable tablet, lower pill burden
Hyperphosphatemia
Treatment:
o Dietary restriction
Preventing > treating may be of value in stages G3a to G5D
Normal phosphate levels may not be an indication to start phosphate-lowering
therapies
o Phosphate-reducing agents: persistent elevations > 5.5 mg/dL despite dietary restriction
Calcium-containing or non-calcium-containing
Avoid if Ca*P product >/= 55
Non-dialysis:
o Moderate dietary restriction (~ 900 mg/day)
o Phosphate-reducing agents per criteria noted above
Dialysis:
o Some clinicians may couple dietary restriction with medications
o Refractory: Consider decreasing PTH with calcimimetics, calcitriol, or vitamin D
analogs
Non-calcium
containing >
calcium containing
due to potential
mortality benefits2
2: A meta-analysis by Jamal 2013 revealed a decreasing tend in all-cause mortality in CKD patients
receiving non-Ca based agents compared with those receiving Ca-based agents.
3: Dose adjustment when switching between phosphate-binders: 667 mg calcium acetate ~ 800 mg
sevelamer
4: Use caution in patients with swallowing or GI motility disorders, or after major GI surgery
5: Binders may decrease absorption of many oral medications, so separation of administration is
recommended
Major points: Take with meals, evaluate for drug-drug
interactions5 What about
aluminum
hydroxide or
calcium citrate?
4. 4
High PTH
G3a-G5
Address
modifiable risk
factors
Vit D, phos, Ca
Vitamin D
supplements
Severe and
progressive + G4-
G5
Calcimimetics,
calcitriol, Vitamin
D analogs
G5D
Maintain iPTH 2-9
X UNL
Calcimimetics,
calcitriol, Vitamin
D analogs
Secondary
hyperparathyroidism
Treat High
Phosphorous
first
Dietary Binders
Maintain Ca
and Vit D
levels
Treat high
PTH
Phos < 5.5 +
Ca < 9.5
Calcitriol
Vitamin D
analogs
Inadequate
reduction of
PTH
Add
calcimimetic
Secondary hyperparathyroidism
KDIGO guidelines do not recommend
routine use of calcitriol or vit. D
analogs in CKD stage G3 to G5!
By increasing sensitivity to the
CaSR, what do we predict will
happen to calcium levels?
By providing vitamin D what
do we predict will happen to
the calcium and phosphorous
levels?
5. 5
Drug Class Initial dosing and titration Pearls, AEs, monitoring
Cinacalcet Calcimimetic 30 mg PO once daily,
increase every 2-4 weeks
in 30 mg increments up to
180 mg once daily as
needed to maintain PTH
levels
Increases sensitivity of CaSR to calcium
to reduce PTH levels
AEs: hypotension,
hypoparathyroidism, nausea, vomiting,
hyperkalemia,
Avoid if Ca < 8.4 mg/dL
Monitoring: s/sx hypocalcemia, PTH,
Ca, especially with CYP3A4 inhibitors
or CYP2D6 substrates, or those with
seizure disorders6
Monotherapy may be inadequate to
control hyper PTH in advanced disease
May be beneficial in older individuals
at higher CV risk (EVOLVE trial7
)
Calcitriol Active vitamin
D derivative
Dialysis, oral: 0.25 mcg
once daily, increase by
0.25 mcg increments daily
at 4-8 week intervals up to
0.5-1 mcg/day
Non-dialysis, oral: 0.25
mcg once daily or less
frequently/week
Avoid if Ca > 10.2, or phos > 5.5
Monitoring: Ca, Phos,
Doxercalciferol Synthetic
vitamin D
analog
Dialysis: 10 mcg 3
times/week at dialysis, no
more frequently than
every other day, titrate by
2.5 mcg/dose at 8-week
intervals
Non-dialysis G3-G5,
Oral: 1 mcg once daily,
titrate dose by 0.5
mcg/dose at 2-week
intervals
Monitoring: Ca, Phos,
AEs: edema, headache, malaise,
dizziness, anemia, constipation, n/v
Use caution in patients with hepatic
impairment
Drug Table
6: Ca reductions lead to lowering of the seizure threshold; therefore, Ca levels need to be closely monitored
7: Despite a nonsignificant reduction seen in the unadjusted primary endpoint of all-cause mortality, nonfatal MI, unstable
angina hospitalization, CHF, or peripheral vascular events, a significant treatment-age interaction (P = 0.03), led to
speculation that cinacalcet may be effective in older dialysis patients. Significant risk reduction in the primary endpoint was
also demonstrated in the > 65 years old subgroup.
What are some s/sx of
hypocalcemia?
6. 6
Topic 2017 2009 Rationale
G3a-G5D: Phosphate
levels
Lower TOWARDS the
normal range
Maintain in the normal
range
Lack of data to support
maintaining phosphate
in the normal range
provides benefit to
G3a-G4 patients and
some safety concerns8
G3a-G5D: Phosphate-
lowering treatment
Decision to start should be
based on progressively or
persistently elevated serum
phosphate
Suggest using in the
treatment of
hyperphosphatemia
Data does not currently
support “preventive”
phosphate-lowering
treatment
Additional considerations
o Need for further randomized controlled trials
o Comparing phosphate-lowering strategies
and safety/efficacy in stages G3a-G4
o More studies in children
o Individualizing dialysate Ca concentrations in CKD
G5D to optimize Ca and phosphate balance,
improving bone metabolism and reducing
accelerated arteriosclerosis and CV mortality
Comparing the 2017 and 2009 KDIGO guideline recommendations for adults with CKD
8: There was some concern about vascular calcifications in a 2012 study by Block et al who evaluated the effects of
phosphate binders in moderate CKD.
7. 7
1. Block GA, Kilpatrick RD, Lowe KA, Wang W, Danese MD. CKD–Mineral and Bone Disorder and
Risk of Death and Cardiovascular Hospitalization in Patients on Hemodialysis. CJASN.
2013;8(12):2132-2140. doi:10.2215/CJN.04260413
2. Block GA, Wheeler DC, Persky MS, et al. Effects of phosphate binders in moderate CKD. J Am Soc
Nephrol. 2012;23(8):1407-1415. doi:10.1681/ASN.2012030223
3. Jamal SA, Vandermeer B, Raggi P, et al. Effect of calcium-based versus non-calcium-based
phosphate binders on mortality in patients with chronic kidney disease: an updated systematic
review and meta-analysis. Lancet. 2013;382(9900):1268-1277. doi:10.1016/S0140-
6736(13)60897-1
4. Ketteler M, Block GA, Evenepoel P, et al. Executive summary of the 2017 KDIGO Chronic
Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what’s changed and
why it matters. Kidney Int. 2017;92(1):26-36. doi:10.1016/j.kint.2017.04.006
5. Shah A, Aeddula NR. Renal Osteodystrophy. In: StatPearls. StatPearls Publishing; 2022. Accessed
September 24, 2022. http://www.ncbi.nlm.nih.gov/books/NBK560742/
6. Sprague SM, Martin KJ, Coyne DW. Phosphate Balance and CKD–Mineral Bone Disease. Kidney
International Reports. 2021;6(8):2049-2058. doi:10.1016/j.ekir.2021.05.012
7. The EVOLVE Trial Investigators. Effect of Cinacalcet on Cardiovascular Disease in Patients
Undergoing Dialysis. N Engl J Med. 2012;367(26):2482-2494. doi:10.1056/NEJMoa1205624
8. Toussaint N, Cooney P, Kerr PG. Review of dialysate calcium concentration in hemodialysis.
Hemodial Int. 2006;10(4):326-337. doi:10.1111/j.1542-4758.2006.00125.x
Picture Links:
https://www.imdb.com/title/tt0460627/
https://www.parathyroid.com/blog/what-do-our-parathyroid-glands-do
https://www.netmeds.com/health-library/post/kidney-disease-signs-symptoms
https://www.pinterest.com/pin/783978247613644996/
https://www.freseniusmedicalcare.asia/en/healthcare-professionals/acute-therapies/crrt-fluids
UpToDate Link:
https://www.uptodate.com/contents/overview-of-chronic-kidney-disease-mineral-and-bone-
disorder-ckd-
mbd?search=mineral%20bone%20disease&source=search_result&selectedTitle=1~150&usage_t
ype=default&display_rank=1#
References