Approach to Hypokalemia
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This document provides an approach to treating hypokalemia. It discusses taking a history of the patient and examining them physically and through laboratory tests and ECG. Clinical features of hypokalemia include neuromuscular and gastrointestinal issues as well as arrhythmias and metabolic alkalosis. Drugs like loop diuretics can cause hypokalemia. The document outlines treatment of hypokalemia through oral or IV potassium supplementation depending on severity, monitoring potassium levels, and treating underlying causes. Severe hypokalemia can lead to complications like QT prolongation and arrhythmias.
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Approach to hypokalemia
This document discusses the approach to hypokalemia, including its definition, prevalence, physiology, causes, symptoms, diagnosis, and treatment. Hypokalemia is defined as a plasma potassium level below 3.5 mEq/L and can range from mild to severe. It affects around 14% of outpatients and is more common in hospitalized patients. Potassium levels are tightly regulated and most potassium is found intracellularly. Causes of hypokalemia include low intake, redistribution into cells, and increased loss due to renal or extra-renal factors. Clinical symptoms depend on severity and may include fatigue, weakness, constipation or arrhythmias. Treatment involves replacing potassium stores orally or intravenously
Hypokalemia
This document discusses hypokalemia, defined as a serum potassium level below 3.6 mEq/L. It notes that potassium is critical for nerve impulse transmission and muscle function. The major causes of hypokalemia include decreased intake, intracellular shifts, non-renal losses like vomiting/diarrhea, and renal losses due to drugs like diuretics. Clinical features range from muscle weakness to cardiac arrhythmias. Diagnosis involves evaluating electrolytes, ECG changes, urine studies, and considering underlying causes. Treatment focuses on replacing potassium losses and correcting the underlying etiology.
Hyperkalemia
Hyperkalemia is defined as a plasma potassium level above 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space due to acidosis or tissue damage. Other causes include reduced renal excretion due to medications like ACE inhibitors or renal failure. Symptoms range from none to muscle weakness to cardiac arrhythmias. Treatment involves calcium to antagonize cardiac effects, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins or dialysis to remove excess potassium.
Potassium; Hypokalemia and hyperkalemia
Renal regulation of potassium balance is critical for maintaining normal potassium levels. The kidneys excrete most of the daily potassium intake and reabsorb potassium in the proximal tubule. In the distal tubule and collecting duct, aldosterone stimulates potassium secretion. Hyperkalemia occurs when potassium levels shift from cells to extracellular fluid or potassium excretion is decreased. Hypokalemia is usually caused by increased potassium excretion due to mineralocorticoid excess or drugs like diuretics. Both conditions can cause cardiac arrhythmias.
ACUTE MANAGEMENT OF Hyperkalemia
This document discusses hyperkalemia, or high levels of potassium in the blood. It begins by listing the normal potassium range and then describes some common causes of hyperkalemia, including the release of potassium from cells due to conditions like rhabdomyolysis or tumor lysis syndrome, and decreased renal excretion of potassium due to renal failure or medications. Clinical manifestations of hyperkalemia are then outlined, such as weakness, paralysis, arrhythmias, and ECG changes including peaked T waves. The document concludes by presenting two case histories of patients with hyperkalemia and CKD and recommends treatment approaches starting with calcium gluconate for cardiac instability and then other options to increase potassium excretion or remove it through dialysis if
Approach to Hypokalemia
This document discusses the approach to hypokalemia. It begins by distinguishing between renal and extrarenal causes of hypokalemia based on urinary potassium levels and the transtubular potassium gradient. It then reviews various endocrine causes of hypokalemia related to the renin-angiotensin-aldosterone system. Primary aldosteronism is discussed in more detail, including criteria for diagnosis, screening methods such as the aldosterone-renin ratio, and distinctions between forms with and without an adrenal tumor. Tests for evaluating renal tubular function like the urine anion gap and methods for diagnosing renal tubular acidosis are also summarized.
Hypokalemia - Approach and Management
Potassium - facts, Renal Handling.
Hypokalemia - Definition, causes, Approach to hypokalemia and its Management.
Hypokalemia & Hyperkalemia PPT (2)
This document discusses potassium levels in the blood and factors that can cause hypokalemia (low potassium) or hyperkalemia (high potassium). It begins by stating the normal range for potassium in blood is 3.5-5 mEq/L. It then provides multiple potential causes for abnormal potassium levels including medications, diet, vomiting/diarrhea, kidney disease, and cellular shifts of potassium between extracellular and intracellular fluid. Mnemonics are also presented to help remember key points. Assessment findings and complications associated with hypo- and hyperkalemia like arrhythmias and muscle weakness are described.
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Approach to hypokalemia
This document discusses the approach to hypokalemia, including its definition, prevalence, physiology, causes, symptoms, diagnosis, and treatment. Hypokalemia is defined as a plasma potassium level below 3.5 mEq/L and can range from mild to severe. It affects around 14% of outpatients and is more common in hospitalized patients. Potassium levels are tightly regulated and most potassium is found intracellularly. Causes of hypokalemia include low intake, redistribution into cells, and increased loss due to renal or extra-renal factors. Clinical symptoms depend on severity and may include fatigue, weakness, constipation or arrhythmias. Treatment involves replacing potassium stores orally or intravenously
Hypokalemia
This document discusses hypokalemia, defined as a serum potassium level below 3.6 mEq/L. It notes that potassium is critical for nerve impulse transmission and muscle function. The major causes of hypokalemia include decreased intake, intracellular shifts, non-renal losses like vomiting/diarrhea, and renal losses due to drugs like diuretics. Clinical features range from muscle weakness to cardiac arrhythmias. Diagnosis involves evaluating electrolytes, ECG changes, urine studies, and considering underlying causes. Treatment focuses on replacing potassium losses and correcting the underlying etiology.
Hyperkalemia
Hyperkalemia is defined as a plasma potassium level above 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space due to acidosis or tissue damage. Other causes include reduced renal excretion due to medications like ACE inhibitors or renal failure. Symptoms range from none to muscle weakness to cardiac arrhythmias. Treatment involves calcium to antagonize cardiac effects, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins or dialysis to remove excess potassium.
Potassium; Hypokalemia and hyperkalemia
Renal regulation of potassium balance is critical for maintaining normal potassium levels. The kidneys excrete most of the daily potassium intake and reabsorb potassium in the proximal tubule. In the distal tubule and collecting duct, aldosterone stimulates potassium secretion. Hyperkalemia occurs when potassium levels shift from cells to extracellular fluid or potassium excretion is decreased. Hypokalemia is usually caused by increased potassium excretion due to mineralocorticoid excess or drugs like diuretics. Both conditions can cause cardiac arrhythmias.
ACUTE MANAGEMENT OF Hyperkalemia
This document discusses hyperkalemia, or high levels of potassium in the blood. It begins by listing the normal potassium range and then describes some common causes of hyperkalemia, including the release of potassium from cells due to conditions like rhabdomyolysis or tumor lysis syndrome, and decreased renal excretion of potassium due to renal failure or medications. Clinical manifestations of hyperkalemia are then outlined, such as weakness, paralysis, arrhythmias, and ECG changes including peaked T waves. The document concludes by presenting two case histories of patients with hyperkalemia and CKD and recommends treatment approaches starting with calcium gluconate for cardiac instability and then other options to increase potassium excretion or remove it through dialysis if
Approach to Hypokalemia
This document discusses the approach to hypokalemia. It begins by distinguishing between renal and extrarenal causes of hypokalemia based on urinary potassium levels and the transtubular potassium gradient. It then reviews various endocrine causes of hypokalemia related to the renin-angiotensin-aldosterone system. Primary aldosteronism is discussed in more detail, including criteria for diagnosis, screening methods such as the aldosterone-renin ratio, and distinctions between forms with and without an adrenal tumor. Tests for evaluating renal tubular function like the urine anion gap and methods for diagnosing renal tubular acidosis are also summarized.
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Potassium - facts, Renal Handling.
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Hypokalemia & Hyperkalemia PPT (2)
This document discusses potassium levels in the blood and factors that can cause hypokalemia (low potassium) or hyperkalemia (high potassium). It begins by stating the normal range for potassium in blood is 3.5-5 mEq/L. It then provides multiple potential causes for abnormal potassium levels including medications, diet, vomiting/diarrhea, kidney disease, and cellular shifts of potassium between extracellular and intracellular fluid. Mnemonics are also presented to help remember key points. Assessment findings and complications associated with hypo- and hyperkalemia like arrhythmias and muscle weakness are described.
2disorders of potassium balance 2
The document discusses disorders of potassium balance, including hypokalemia (low potassium levels) and hyperkalemia (high potassium levels). It covers the normal regulation and distribution of potassium in the body, causes and manifestations of hypokalemia and hyperkalemia, ECG changes associated with each, and their treatment approaches.
Potassium disorders , comprehensive & practical approach .
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.
Management of Hyperkalemia
This document discusses the management of hyperkalemia. It begins with a case study of a 77-year-old male presenting with dehydration and unresponsiveness. It then covers the physiology and causes of hyperkalemia, how to evaluate patients for hyperkalemia through history, clinical exam and labs, acute management including calcium, insulin, beta-agonists and loop diuretics, and chronic management including diet, medications and dialysis. The key points are that hyperkalemia can cause life-threatening cardiac issues and needs to be rapidly treated to stabilize the cardiac membrane and shift potassium intracellularly in emergency situations.
Hyperkalemia
Hyperkalemia can be caused by high potassium intake, redistribution of potassium from cells, or low renal potassium excretion. It may be drug-induced or related to decreased renal function, hypoaldosteronism, decreased circulating volume, or pseudohyperkalemia. Clinical manifestations range from weakness to cardiac arrhythmias. Emergent therapy includes calcium to stabilize membranes, insulin with glucose to shift potassium into cells (unless glucose is over 175 mg/dL), and potassium-binding resins. Additional workup may include ECG, chemistry panel, creatinine kinase, TTKG, and hemodialysis for severe cases.
Hypokalemia diagnosis, causes and treatment
This document discusses the approach to hypokalemia. It begins by covering the pathophysiology of potassium homeostasis and how small changes in potassium levels can have profound effects. It then discusses factors that can modify cellular potassium distribution like acid-base status, hormones, exercise and more. Treatment of hypokalemia involves decreasing potassium losses, replenishing stores, addressing any toxicities, and determining the underlying cause. Oral and intravenous potassium replacement is discussed as well as monitoring requirements and administration rates.
Hyperkalemia and its management
This document discusses hyperkalemia, including its definition, causes, clinical manifestations, and treatment. It provides details on potassium regulation and homeostasis in the body. The main causes of hyperkalemia are a shift of potassium from intracellular to extracellular space, excessive potassium intake, and decreased renal potassium excretion. Symptoms range from weakness to cardiac arrhythmias. Treatment involves calcium gluconate for cardiac issues, insulin with glucose to shift potassium intracellularly, sodium bicarbonate for acidosis, and diuretics or dialysis to increase renal excretion.
Magnesium Homeostasis and disorders
This document discusses magnesium disorders and hypomagnesemia. It begins by providing background on magnesium, including where it is stored in the body and its many functions. It then discusses the causes, clinical manifestations, diagnosis, and treatment of hypomagnesemia. Hypomagnesemia can be caused by renal magnesium wasting due to drugs, diseases, or genetic disorders, or by extrarenal losses from poor nutrition, malabsorption, diarrhea, or sweat losses. Symptoms affect the cardiovascular, neuromuscular, skeletal, and central nervous systems. Treatment involves identifying and addressing the underlying cause, as well as oral or parenteral magnesium supplementation.
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- It affects 14-15% of US adults and prevalence increases with age. The leading causes are hypertension and diabetes.
- As CKD progresses, surviving nephrons undergo hypertrophy which can lead to sclerosis and loss of filtration surface area over time. Tubulointerstitial fibrosis also contributes to declining kidney function.
- The renin-angiotensin-
Potassium imbalance and management
This document discusses potassium imbalance and its management. It provides reference ranges for normal serum electrolyte levels including potassium. It then discusses causes, classifications, signs, and treatments for both hyperkalemia and hypokalemia. For hyperkalemia, it outlines approaches for managing severe cases including using calcium, insulin, beta-agonists, and dialysis. For hypokalemia it discusses causes like drugs and investigations to identify the cause before outlining oral and IV supplementation approaches.
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This document defines hypercalcemia and discusses its causes, evaluation, clinical presentation, and management. The main causes are parathyroid hormone dependent (primary hyperparathyroidism, tertiary hyperparathyroidism) and independent (malignancy, vitamin D related, endocrinopathies). Evaluation involves history, exam, and labs. Acute management is rehydration and medications to increase calcium excretion. Long term management depends on the underlying cause and may involve surgery, bisphosphonates, glucocorticoids, or ketoconazole.
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Potassium Imbalance
The document discusses potassium metabolism and disorders of potassium levels. It covers:
1) Normal potassium metabolism and regulation by the kidneys, factors that influence renal secretion/excretion.
2) Causes and pathophysiology of hypokalemia and hyperkalemia, including excessive renal/gastrointestinal loss or intake, shifts between intracellular/extracellular fluid.
3) Effects of abnormal potassium levels on neuromuscular and cardiac function, including changes in membrane potential and electrical activity.
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This document discusses calcium homeostasis and hypercalcemia. It notes that calcium is critical for many physiological functions and is mainly stored in bones. Hypercalcemia can be caused by primary hyperparathyroidism, vitamin D excess, certain malignancies, and other conditions. The diagnostic approach involves distinguishing between hyperparathyroidism and hypercalcemia of malignancy based on lab tests. Treatment focuses on rehydration, increasing calciuresis, and decreasing bone resorption or intestinal calcium absorption using medications like calcitonin, bisphosphonates, glucocorticoids, or dialysis depending on the severity of hypercalcemia.
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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
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This document discusses electrolyte disorders and their management. It covers water and sodium metabolism including hypo- and hypernatremia. It also discusses potassium disorders including hypo- and hyperkalemia. The key mechanisms and renal regulation of electrolytes are explained. Treatment approaches are outlined depending on the electrolyte abnormality and patient volume status. Symptoms, causes, and management strategies are provided for common electrolyte disorders.
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2disorders of potassium balance 2
The document discusses disorders of potassium balance, including hypokalemia (low potassium levels) and hyperkalemia (high potassium levels). It covers the normal regulation and distribution of potassium in the body, causes and manifestations of hypokalemia and hyperkalemia, ECG changes associated with each, and their treatment approaches.
Potassium disorders , comprehensive & practical approach .
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.
Management of Hyperkalemia
This document discusses the management of hyperkalemia. It begins with a case study of a 77-year-old male presenting with dehydration and unresponsiveness. It then covers the physiology and causes of hyperkalemia, how to evaluate patients for hyperkalemia through history, clinical exam and labs, acute management including calcium, insulin, beta-agonists and loop diuretics, and chronic management including diet, medications and dialysis. The key points are that hyperkalemia can cause life-threatening cardiac issues and needs to be rapidly treated to stabilize the cardiac membrane and shift potassium intracellularly in emergency situations.
Hyperkalemia
Hyperkalemia can be caused by high potassium intake, redistribution of potassium from cells, or low renal potassium excretion. It may be drug-induced or related to decreased renal function, hypoaldosteronism, decreased circulating volume, or pseudohyperkalemia. Clinical manifestations range from weakness to cardiac arrhythmias. Emergent therapy includes calcium to stabilize membranes, insulin with glucose to shift potassium into cells (unless glucose is over 175 mg/dL), and potassium-binding resins. Additional workup may include ECG, chemistry panel, creatinine kinase, TTKG, and hemodialysis for severe cases.
Hypokalemia diagnosis, causes and treatment
This document discusses the approach to hypokalemia. It begins by covering the pathophysiology of potassium homeostasis and how small changes in potassium levels can have profound effects. It then discusses factors that can modify cellular potassium distribution like acid-base status, hormones, exercise and more. Treatment of hypokalemia involves decreasing potassium losses, replenishing stores, addressing any toxicities, and determining the underlying cause. Oral and intravenous potassium replacement is discussed as well as monitoring requirements and administration rates.
Hyperkalemia and its management
This document discusses hyperkalemia, including its definition, causes, clinical manifestations, and treatment. It provides details on potassium regulation and homeostasis in the body. The main causes of hyperkalemia are a shift of potassium from intracellular to extracellular space, excessive potassium intake, and decreased renal potassium excretion. Symptoms range from weakness to cardiac arrhythmias. Treatment involves calcium gluconate for cardiac issues, insulin with glucose to shift potassium intracellularly, sodium bicarbonate for acidosis, and diuretics or dialysis to increase renal excretion.
Magnesium Homeostasis and disorders
This document discusses magnesium disorders and hypomagnesemia. It begins by providing background on magnesium, including where it is stored in the body and its many functions. It then discusses the causes, clinical manifestations, diagnosis, and treatment of hypomagnesemia. Hypomagnesemia can be caused by renal magnesium wasting due to drugs, diseases, or genetic disorders, or by extrarenal losses from poor nutrition, malabsorption, diarrhea, or sweat losses. Symptoms affect the cardiovascular, neuromuscular, skeletal, and central nervous systems. Treatment involves identifying and addressing the underlying cause, as well as oral or parenteral magnesium supplementation.
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This document discusses cirrhosis and its complications over two parts. Part I covers what cirrhosis is, its etiologies, clinical presentations, physical exam findings, laboratory tests, liver biopsy, and prognosis for different etiologies. Part II covers complications of cirrhosis including portal hypertension, variceal bleeding, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatopulmonary syndrome, and hepatocellular carcinoma screening and treatment. Liver transplantation is also discussed as a treatment option.
Approach to CKD
This document provides an overview of chronic kidney disease (CKD) including definitions, epidemiology, pathophysiology, risk factors, and genetics. Some key points include:
- CKD is defined as kidney damage or glomerular filtration rate <60 mL/min/1.73m2 for ≥3 months.
- It affects 14-15% of US adults and prevalence increases with age. The leading causes are hypertension and diabetes.
- As CKD progresses, surviving nephrons undergo hypertrophy which can lead to sclerosis and loss of filtration surface area over time. Tubulointerstitial fibrosis also contributes to declining kidney function.
- The renin-angiotensin-
Potassium imbalance and management
This document discusses potassium imbalance and its management. It provides reference ranges for normal serum electrolyte levels including potassium. It then discusses causes, classifications, signs, and treatments for both hyperkalemia and hypokalemia. For hyperkalemia, it outlines approaches for managing severe cases including using calcium, insulin, beta-agonists, and dialysis. For hypokalemia it discusses causes like drugs and investigations to identify the cause before outlining oral and IV supplementation approaches.
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Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Hypercalcemia
This document defines hypercalcemia and discusses its causes, evaluation, clinical presentation, and management. The main causes are parathyroid hormone dependent (primary hyperparathyroidism, tertiary hyperparathyroidism) and independent (malignancy, vitamin D related, endocrinopathies). Evaluation involves history, exam, and labs. Acute management is rehydration and medications to increase calcium excretion. Long term management depends on the underlying cause and may involve surgery, bisphosphonates, glucocorticoids, or ketoconazole.
Lactic Acidosis
Lactic acidosis occurs when there is an imbalance between the production and use of lactic acid in the body. It can be caused by tissue hypoxia (type A) or other non-hypoxic factors like malignancy, liver disease, or drugs (type B). The document discusses the pathophysiology of lactic acidosis including lactate metabolism, cytokine effects, and the Warburg effect seen in cancer. Treatment focuses on resolving the underlying cause, with sodium bicarbonate used cautiously and alternatives like hemodialysis considered to correct acidosis and remove lactate when needed.
Potassium Imbalance
The document discusses potassium metabolism and disorders of potassium levels. It covers:
1) Normal potassium metabolism and regulation by the kidneys, factors that influence renal secretion/excretion.
2) Causes and pathophysiology of hypokalemia and hyperkalemia, including excessive renal/gastrointestinal loss or intake, shifts between intracellular/extracellular fluid.
3) Effects of abnormal potassium levels on neuromuscular and cardiac function, including changes in membrane potential and electrical activity.
Approach to a patient with hyponatremia (2) (1)
The document discusses hyponatremia, which refers to a low serum sodium level. It begins by defining hyponatremia and providing normal sodium levels. It then covers the frequency, age and sex predispositions, physiology/pathophysiology, types and causes. The types include hypovolemic, euvolemic, hypervolemic, redistributive, and pseudohyponatremia. Common causes are discussed like SIADH, heart failure, cirrhosis. The clinical approach involves assessing volume status, labs like sodium, osmolality, urine sodium. Management depends on the type and involves restricting free water intake or using hypertonic saline in severe cases to slowly correct the
Renal tubular acidosis
Renal tubular acidosis topic is clearly explained for the benefit of both UG and PG students of medicine and biochemistry students.
Hyponatremia (1)
Hyponatremia, defined as a plasma sodium concentration below 135 mM, is a common electrolyte disorder seen in up to 22% of hospitalized patients. It is usually caused by water retention due to increased secretion of antidiuretic hormone (ADH) and/or increased renal sensitivity to ADH combined with free water intake. Hyponatremia can be categorized as hypovolemic, euvolemic, or hypervolemic based on clinical history and volume status. Treatment involves correcting the underlying cause and raising the plasma sodium concentration slowly to avoid complications like osmotic demyelination syndrome which can result from overly rapid correction.
Approach to Hypercalcemia
This document discusses calcium homeostasis and hypercalcemia. It notes that calcium is critical for many physiological functions and is mainly stored in bones. Hypercalcemia can be caused by primary hyperparathyroidism, vitamin D excess, certain malignancies, and other conditions. The diagnostic approach involves distinguishing between hyperparathyroidism and hypercalcemia of malignancy based on lab tests. Treatment focuses on rehydration, increasing calciuresis, and decreasing bone resorption or intestinal calcium absorption using medications like calcitonin, bisphosphonates, glucocorticoids, or dialysis depending on the severity of hypercalcemia.
Hypokalemia
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
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This document discusses the approach to diagnosing and treating hypercalcemia. It reviews calcium metabolism and the role of parathyroid hormone. Symptoms of hypercalcemia are described for the neurological, gastrointestinal, skeletal, renal, and cardiovascular systems. Causes of hypercalcemia include primary hyperparathyroidism, malignancy, granulomatous diseases, vitamin D toxicity, and certain drugs. The diagnostic approach involves measuring PTH, phosphorus, vitamin D, and PTH-rP levels. Treatment options aim to increase calcium excretion or decrease bone resorption/absorption and include IV fluids, calcitonin, bisphosphonates, glucocorticoids, loop diuretics, and dial
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This document reviews the approach to diagnosis and treatment of hypercalcemia. It begins by describing calcium metabolism and the role of parathyroid hormone and vitamin D. Symptoms of hypercalcemia are then outlined affecting the central nervous system, gastrointestinal tract, skeleton, kidneys, and cardiovascular system. Causes of hypercalcemia including primary hyperparathyroidism, malignancy, granulomatous diseases, and medications are discussed. The document concludes by outlining treatments to reduce calcium levels including intravenous fluids, calcitonin, bisphosphonates, glucocorticoids, loop diuretics, and dialysis.
2.1. Heart Failure.ppt
Heart failure is defined as the inability of the heart to pump enough blood to meet the body's needs. It can be caused by conditions that overload or restrict the heart. The main symptoms are shortness of breath, fatigue, and fluid retention. Treatment focuses on managing symptoms with diuretics, ACE inhibitors, beta-blockers, and controlling underlying conditions. Prognosis depends on the severity and cause of heart failure.
ECG: Hypokalemia
1. A 52-year-old male presented with loose stools and vomiting for 4 days. Examination found hypokalemia.
2. ECG showed ST segment depression in V3-V6 and prominent U waves, consistent with changes seen in hypokalemia.
3. The patient was diagnosed with hypokalemia likely caused by gastrointestinal potassium losses from diarrhea, as indicated by his symptoms and laboratory findings. Treatment involved potassium supplementation and treatment of the underlying condition causing the diarrhea.
Emergent haemodialysis
Acute renal replacement therapy (RRT) is indicated for acute kidney injury (AKI) with severe complications such as hyperkalemia, acidosis, or fluid overload. Other indications include toxic ingestions that can be cleared by RRT like toxic alcohols, lithium, and salicylates. RRT may also be used to manage severe electrolyte imbalances other than from AKI, including sodium levels less than 110 or greater than 160 mmol/L, and hyperthermia over 40°C.
ACUTE KIDNEY INJURY.pptx
1. Acute kidney injury (AKI) is the sudden deterioration of renal function that can range from mild to severe. It is a global problem associated with high morbidity and mortality.
2. AKI is classified based on location of injury (pre-renal, intrinsic, post-renal), urine output, and severity of decline in renal function. Common causes include sepsis, nephrotoxins, and decreased renal perfusion.
3. Management involves treating the underlying cause, maintaining fluid/electrolyte balance, and potentially renal replacement therapy for complications like fluid overload or severe electrolyte imbalances. Outcomes depend on factors like age, cause, and need for dialysis.
Renal Presentation
The document provides an overview of nephrology topics including the objectives, anatomy and physiology of the kidney, acute kidney injury (AKI), chronic kidney disease (CKD), and relevant investigations and treatments. Specifically, it discusses the glomerular filtration barrier, nephron structure, renal transport mechanisms, causes and management of pre-renal, intrinsic, and post-renal AKI, stages of CKD, and key investigations for differentiating AKI etiologies. Notable exclusions are listed.
hyperkalamia
Hyperkalemia can be caused by increased potassium intake, redistribution of potassium from cells into the bloodstream, or decreased excretion of potassium by the kidneys. Clinical manifestations range from weakness to cardiac arrhythmias. Treatment involves membrane stabilization with calcium, shifting potassium into cells with insulin and glucose or sodium bicarbonate, and removing potassium from the body with loop diuretics, potassium-binding resins, or hemodialysis. Glucose should be given with insulin to treat hyperkalemia only if blood sugar is below 175 mg/dL.
Hyperkalemia
Hyperkalemia is a life-threatening electrolyte imbalance where potassium levels are elevated. The case discusses a 52-year-old man with diabetes and hypertension who developed quadriparesis due to severe hyperkalemia. His hyperkalemia was caused by multiple factors, including insulin deficiency from uncontrolled diabetes, acidosis, renal dysfunction from medications like an ACE inhibitor and spironolactone, and decreased distal delivery of sodium and water due to his kidney issues. He was treated with dialysis to rapidly lower his potassium level and remove the implicated medications causing his hyperkalemia.
Anesthesia for Torsion testis patient in tumor lysis-final.pptx
Join us for a compelling presentation on 'Anesthesia for Torsion Testis in the Context of Tumor Lysis.' Delve into the delicate balance of anesthetic management for patients facing the dual challenge of testicular torsion and tumor lysis syndrome.
Acute renal failure
Acute renal failure is a sudden decline in kidney function that results in the buildup of waste products in the blood. It can be caused by decreased blood flow to the kidneys, obstruction of urine outflow, or direct damage to the kidneys. Symptoms include decreased urine output, fluid retention, electrolyte imbalances, and accumulation of waste products. Treatment focuses on restoring fluid and electrolyte balance, preventing complications, and addressing the underlying cause of kidney injury through medical management or renal replacement therapy if needed. Nursing care is aimed at monitoring fluid status, preventing infections, improving nutrition, and managing complications of acute renal failure.
Renal Principles
The document discusses renal and kidney function including:
1. The functions of the kidney including regulation of fluid balance, electrolytes, acid-base balance, and hormone production.
2. The structure of the nephron and how it filters blood to form urine through processes like glomerular filtration and reabsorption.
3. Factors that influence kidney function like the renin-angiotensin-aldosterone system and how different drugs can impact renal excretion and dosing considerations in renal failure.
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Approach to Hypokalemia
- 1. Approach to a patient with HYPOKALEMIA -P.shanmuga sundaram
- 2. APPROACH • History of the patient • Clinical features • Physical Examination • Investigation - Laboratory test - ECG • Treatment
- 3. HISTORY • Diarrhoea • Periodic weakness • Medications (eg: laxatives, diuretics, antibiotics) • Diet and Dietary habits (eg: licorice ) • Arrhythmia
- 4. CLINICAL FEATURES • Neuromuscular: Fatigue, myalgia, and muscular weakness of the lower extremities. – Smooth muscle involvement – Constipation, ileus, urinary retention – progressive weakness, hypoventilation (due to respiratory muscle involvement), and eventually complete paralysis • Impaired ability of kidneys to concentrate urine – Polyuria, urine with low osmolality, polydipsia • GI manifestations: – Anorexia, nausea, vomiting – Constipation, Abdominal distension, paralytic ileus • CVS – Arrhythmias • Metabolic alkalosis
- 5. Drugs causing hypokalemia • Loop diuretics (eg:furosemide) • Thiazide diuretics (eg:hydrochlorothiazide) • Antifungal • Amphotericin B • cisplatin
- 6. PHYSICAL EXAMINATION Check for • Blood pressure(hyper, hypotension) • Volume status(hypovolaemia) • Signs of -hyperthyroidism -cushing’s syndrome
- 7. INVESTIGATION • Laboratory test - electrolytes - BUN - urinary pH - creatinine - osmolality • ECG • Hormones
- 8. ELECTROLYTES • Serum potassium level normal 3.5-5.5 mMol/L hypokalemia < 3.5 mMol/L mild 3.0 – 3.3 mMol/L moderate 2.5 – 3.0 mMol/L severe <2.5 mMol/L • Urinary pH - Hypokalemic , alkaline (metabolic alkalosis)
- 12. Blood pressure
- 13. Blood pressure
- 14. • Creatinine Urinary K+: creatinine > 13 mMol/g of creatinine • HORMONES that decreases the ECF K+ are -insulin -aldosterone -thyroid hormone
- 15. ECG Changes in Hypokalemia Early changes: • Flattening or inversion of T waves • Prominent U waves • ST segment depression • Prolonged QT interval Severe Potassium depletion: • Prolonged PR interval • Decreased voltage of QRS • Widening of QRS complex • Ventricular arrhythmia
- 16. The ecg changes are due to DELAYED VENTRICULAR REPOLARIZATION Diagnosis is therefore based on ST segment, T wave & U wave abnormalities
- 18. Treatment • Correct volume depletion & Rx of underlying etiology • serum K+ drops by approximately 0.27 mM for every 100-mmol reduction in total-body stores • If mild hypokalemia - start oral K+ supplementation • If severe hypokalemia – Start I.V K+ infusion – At Rate of < 20 mEq/hr Potassium infusion – In peripheral vein < 40 mEq/L – In central vein < 60 mEq/L • Monitor K+ during therapy • Search for & Rx hypomagnesemia
- 19. Treatment Contd... • Preparations Available – Various salts of K+ : Cl- , HCO3 - , Phosphate & Gluconate salts – KCl : More effective in hypokalemia with metabolic alkalosis (e.g. Diuretic usage, Diarrhea) – KHCO3 / K Citrate : Hypokalemia & metabolic acidosis (e.g. RTA)
- 20. Etiology to be corrected • Discontinue diuretics/laxatives • Use potassium-sparing diuretics if diuretic therapy is required (eg, severe heart failure) • Treat diarrhea or vomiting • Administer H2 blockers to patients receiving nasogastric suction • Control hyperglycemia if glycosuria is present
- 21. complication severe hypokalemia QT prolongation torsades di pointes ventricular fibrillation
- 22. Thank you