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Hyperkalemia is a condition defined as a serum potassium level greater than 5.0 mmol/L. The normal range is 3.5 to 5 mmol/L. Causes include a shift of potassium from intracellular to extracellular space, inadequate excretion by the kidneys, and excessive dietary intake. Clinical presentations include cardiac arrhythmias, weakness, and metabolic acidosis. Treatment involves emergency medications like calcium gluconate or insulin with glucose to shift potassium intracellularly, as well as kayexalate to bind potassium in the GI tract. Newer drugs like zirconium silicate work similarly by selectively trapping excess potassium in the GI tract without causing side effects.
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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.
Prateek
This document discusses hyperkalemia, beginning with potassium physiology and homeostasis. It explains that potassium is primarily intracellular and its concentration is regulated by the Na-K-ATPase pump. Factors that can cause hyperkalemia include a shift of potassium from intracellular to extracellular space due to metabolic acidosis, insulin deficiency, beta blockers, or drugs that inhibit Na-K-ATPase. Hyperkalemia can also be caused by reduced urinary potassium excretion due to decreased aldosterone, aldosterone resistance, or kidney impairment. Pseudohyperkalemia is an artificial laboratory finding not indicative of true hyperkalemia.
Hyperkalemia in children
This document discusses hyperkalemia, or high levels of potassium in the blood. It covers the normal physiology of potassium balance in the body, including intake through foods, absorption in the intestines, and excretion primarily through the kidneys under regulation of the hormone aldosterone. Causes of hyperkalemia include reduced kidney function, medications that interfere with potassium excretion, and conditions that cause a shift of potassium out of cells. The document provides details on evaluating, diagnosing, and classifying different severities of hyperkalemia based on serum potassium levels.
Hyperkalemia
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its levels are regulated by the kidneys, sodium-potassium pump, and aldosterone. Causes of hyperkalemia include intracellular shifts, decreased excretion, and excess intake. Clinical features range from asymptomatic to muscle weakness to arrhythmias. ECG changes correlate with potassium levels and include peaked T waves, PR prolongation, and eventually a sine wave pattern. Treatment focuses on antagonizing cardiac effects with calcium, driving potassium intracellularly with insulin/beta-agonists, and removing it through cation exchange resins, diuretics, or hemodialysis.
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.
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.
Hyperkalemia
This document discusses the management of hyperkalemia in chronic kidney disease (CKD). It notes that hyperkalemia is common in CKD patients, affecting 40-50% of those with end-stage renal disease, and is associated with increased mortality. The causes of hyperkalemia in CKD include increased intracellular shifting of potassium, decreased renal excretion, and medications that inhibit the renin-angiotensin-aldosterone system. The document outlines approaches for acute and chronic management of hyperkalemia in CKD, including calcium supplementation, insulin therapy, beta-agonists, cation exchange resins, and dialysis in severe cases. It emphasizes the importance of addressing both acute life-threatening rises in potassium as well
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.
Recommended
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.
Prateek
This document discusses hyperkalemia, beginning with potassium physiology and homeostasis. It explains that potassium is primarily intracellular and its concentration is regulated by the Na-K-ATPase pump. Factors that can cause hyperkalemia include a shift of potassium from intracellular to extracellular space due to metabolic acidosis, insulin deficiency, beta blockers, or drugs that inhibit Na-K-ATPase. Hyperkalemia can also be caused by reduced urinary potassium excretion due to decreased aldosterone, aldosterone resistance, or kidney impairment. Pseudohyperkalemia is an artificial laboratory finding not indicative of true hyperkalemia.
Hyperkalemia in children
This document discusses hyperkalemia, or high levels of potassium in the blood. It covers the normal physiology of potassium balance in the body, including intake through foods, absorption in the intestines, and excretion primarily through the kidneys under regulation of the hormone aldosterone. Causes of hyperkalemia include reduced kidney function, medications that interfere with potassium excretion, and conditions that cause a shift of potassium out of cells. The document provides details on evaluating, diagnosing, and classifying different severities of hyperkalemia based on serum potassium levels.
Hyperkalemia
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its levels are regulated by the kidneys, sodium-potassium pump, and aldosterone. Causes of hyperkalemia include intracellular shifts, decreased excretion, and excess intake. Clinical features range from asymptomatic to muscle weakness to arrhythmias. ECG changes correlate with potassium levels and include peaked T waves, PR prolongation, and eventually a sine wave pattern. Treatment focuses on antagonizing cardiac effects with calcium, driving potassium intracellularly with insulin/beta-agonists, and removing it through cation exchange resins, diuretics, or hemodialysis.
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.
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.
Hyperkalemia
This document discusses the management of hyperkalemia in chronic kidney disease (CKD). It notes that hyperkalemia is common in CKD patients, affecting 40-50% of those with end-stage renal disease, and is associated with increased mortality. The causes of hyperkalemia in CKD include increased intracellular shifting of potassium, decreased renal excretion, and medications that inhibit the renin-angiotensin-aldosterone system. The document outlines approaches for acute and chronic management of hyperkalemia in CKD, including calcium supplementation, insulin therapy, beta-agonists, cation exchange resins, and dialysis in severe cases. It emphasizes the importance of addressing both acute life-threatening rises in potassium as well
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.
hypokalemia, diagnosis and management
potassium homeostasis, hypokalemia and potassium correction, electrolyte imbalance, management of hypokalemia,potassium deficit
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.
POTTASIUM METABOLISM & APPROACH TO HYPERKALEMIA
This document discusses potassium metabolism and the approach to hyperkalemia. It begins with an introduction to potassium physiology and homeostasis. The kidney plays a key role in potassium excretion, reabsorbing 85-90% in the distal tubules where regulation occurs. Hyperkalemia is defined as a serum potassium over 5.5 mEq/L and can be caused by increased potassium load, impaired excretion, or transcellular shifting. Treatment focuses on stabilizing cardiac cells, rapidly lowering potassium levels, and enhancing elimination while addressing the underlying cause. Emergency therapies include calcium gluconate, insulin therapy, beta agonists, and sodium polystyrene sulfonate.
Hyperkalemia
This document discusses hyperkalemia, defined as a plasma potassium level above 5.5 mM. Causes include a shift of potassium from cells to plasma due to factors like acidosis, medications, or tissue breakdown. Symptoms range from cardiac arrhythmias to paralysis. Diagnosis involves blood tests. Treatment involves calcium to stabilize the heart, insulin or beta-agonists to shift potassium into cells, and resins, diuretics or dialysis to remove potassium from the body. The document provides details on treatment options, their mechanisms of action, dosages and cautions.
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.
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.
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.
A new perspective on hypokalemia
This document discusses hypokalemia from multiple perspectives. It begins by defining hypokalemia and describing its symptoms. Major causes of hypokalemia include renal and extra-renal losses. Renal losses can be further characterized by urinary potassium excretion and the transtubular potassium gradient. The document also discusses specific genetic disorders like Bartter's and Gitelman's syndrome that can cause hypokalemia. Treatment involves replacing potassium orally or intravenously depending on the severity. Factors like magnesium deficiency, diuretic use, and vomiting can also contribute to hypokalemia through urinary potassium losses.
Approach to management of 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 medications, or inadequate renal excretion due to reduced aldosterone levels or impaired kidney function. Symptoms range from none to muscle weakness or paralysis to cardiac arrhythmias. ECG changes include peaked T waves and prolonged PR interval. Treatment involves calcium to stabilize the heart, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins, diuretics or hemodialysis to remove excess potassium.
Potassium Disorders In-Service Presentation
Dave Porter presented on hyperkalemia and hypokalemia. Hyperkalemia is caused by conditions like kidney disease or medications and can lead to arrhythmias. Treatment depends on severity but may include calcium gluconate, insulin, or sodium bicarbonate. Hypokalemia is more common and can be caused by vomiting, diarrhea, or medications. It often has no symptoms but severe cases can cause heart problems. Treatment involves replacing potassium orally or intravenously depending on the situation. Both conditions need to be treated to keep potassium levels between 3.5-5.0 mEq/L.
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This document discusses two case studies of pediatric patients presenting with electrolyte abnormalities. Case 1 involves a 2-year-old boy named Rahul who was brought to the emergency department with diarrhea and dehydration. His lab work showed sodium of 131 mEq/L and potassium of 2 mEq/L, indicating hypokalemia. Case 2 involves a 7-year-old girl named Vinita who was admitted to the PICU for severe diabetic ketoacidosis. Her initial potassium was 4.4 mEq/L but the resident was concerned about potential hyperkalemia with further potassium supplementation. The document then reviews the causes, clinical manifestations, diagnosis, and management of hypo- and hyperkalemia in
Effects of hypo & hyper kalemia
The document discusses hyperkalemia, its effects on the electrocardiogram (ECG), and the role of calcium gluconate in reversing these effects. Hyperkalemia is a potentially lethal condition defined as a serum potassium level above 5 mEq/L. It can cause abnormal heart rhythms and cardiac arrest. On ECG, hyperkalemia presents as tall, peaked T waves and prolonged PR interval. Calcium gluconate works by antagonizing the effects of potassium at the cellular level and restoring the normal threshold potential, allowing action potentials to occur and reestablishing normal cardiac conduction. By rapidly shifting potassium into cells, calcium gluconate can quickly reverse the ECG changes and cardiac effects caused by hyperkalemia
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.
Hyperkalemia final
Hyperkalemia is defined as a serum potassium concentration greater than 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space, excessive potassium intake, or inadequate excretion. Pseudohyperkalemia is an artifactual increase. Treatment involves calcium to antagonize cardiac effects, insulin to shift potassium intracellularly, and cation exchange resins or dialysis to remove potassium from the body. The goal is to lower potassium levels urgently to prevent cardiac arrhythmias.
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.
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The document discusses adrenal glands and primary adrenal insufficiency. It describes the basic anatomy of the adrenal glands, their blood supply, embryology, and histology. It outlines primary adrenal insufficiency, including causes such as autoimmune disorders, infections, metastatic cancer, drugs that inhibit cortisol biosynthesis, and deposition diseases. Symptoms of primary adrenal insufficiency include fatigue, weight loss, nausea, muscle and joint pain, skin hyperpigmentation, and postural hypotension. Diagnosis involves tests to demonstrate inappropriate low cortisol secretion and treatment involves hydrocortisone replacement and mineralocorticoid replacement such as fludrocortisone.
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
Electrolyte imbalance
This document discusses electrolyte imbalances, specifically hypokalemia, hyperkalemia, and magnesium imbalance. It outlines the causes, clinical manifestations, and treatment considerations for anesthesia for each condition. Key points include decreased cardiac contractility and arrhythmias with hypokalemia, skeletal muscle weakness and cardiac effects with hyperkalemia, and uses of magnesium for conditions like preeclampsia and tetanus. Treatment involves oral or IV potassium replacement, calcium or sodium bicarbonate for hyperkalemia, and magnesium supplementation. Anesthetic implications are also addressed.
Hyperkalemia and other electrolytes disorders
This document provides an overview and guidelines for managing common electrolyte disorders like hyperkalemia, hypokalemia, and hypomagnesemia in hospitalized patients. It reviews the key steps in assessing the disorders, determining treatment approaches, selecting appropriate replacement methods and doses, and monitoring patients. The guidelines emphasize starting oral replacement when possible, calculating replacement based on estimated deficits, avoiding too rapid IV administration, and aggressively managing disorders in high-risk patients like those with diabetes or on IV diuretics.
Disorders of calcium metabolism
The document discusses disorders of calcium metabolism. It presents two clinical scenarios: a 59-year-old woman with hypercalcemia found on labs during a routine visit, and a 9-year-old boy admitted to the emergency department with acute pancreatitis and hypocalcemia after falling off his bike. It then outlines topics like the different forms of calcium, calcium homeostasis, regulation of calcium metabolism by parathyroid hormone, vitamin D, and calcitonin, and disorders like hypercalcemia, hypocalcemia, hyperparathyroidism, and hypoparathyroidism.
Reanimation(fluid & electrolyte)
The document provides information about fluid and electrolyte balance. It discusses the distribution and composition of body fluids, normal fluid exchange, and electrolyte disturbances including hypovolemia, hypervolemia, hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemia. It also covers parenteral fluid therapy including intravenous fluids, methods of calculating fluid transfusion rates, and management of fluid balance in surgical patients.
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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.
POTTASIUM METABOLISM & APPROACH TO HYPERKALEMIA
This document discusses potassium metabolism and the approach to hyperkalemia. It begins with an introduction to potassium physiology and homeostasis. The kidney plays a key role in potassium excretion, reabsorbing 85-90% in the distal tubules where regulation occurs. Hyperkalemia is defined as a serum potassium over 5.5 mEq/L and can be caused by increased potassium load, impaired excretion, or transcellular shifting. Treatment focuses on stabilizing cardiac cells, rapidly lowering potassium levels, and enhancing elimination while addressing the underlying cause. Emergency therapies include calcium gluconate, insulin therapy, beta agonists, and sodium polystyrene sulfonate.
Hyperkalemia
This document discusses hyperkalemia, defined as a plasma potassium level above 5.5 mM. Causes include a shift of potassium from cells to plasma due to factors like acidosis, medications, or tissue breakdown. Symptoms range from cardiac arrhythmias to paralysis. Diagnosis involves blood tests. Treatment involves calcium to stabilize the heart, insulin or beta-agonists to shift potassium into cells, and resins, diuretics or dialysis to remove potassium from the body. The document provides details on treatment options, their mechanisms of action, dosages and cautions.
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.
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.
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.
A new perspective on hypokalemia
This document discusses hypokalemia from multiple perspectives. It begins by defining hypokalemia and describing its symptoms. Major causes of hypokalemia include renal and extra-renal losses. Renal losses can be further characterized by urinary potassium excretion and the transtubular potassium gradient. The document also discusses specific genetic disorders like Bartter's and Gitelman's syndrome that can cause hypokalemia. Treatment involves replacing potassium orally or intravenously depending on the severity. Factors like magnesium deficiency, diuretic use, and vomiting can also contribute to hypokalemia through urinary potassium losses.
Approach to management of 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 medications, or inadequate renal excretion due to reduced aldosterone levels or impaired kidney function. Symptoms range from none to muscle weakness or paralysis to cardiac arrhythmias. ECG changes include peaked T waves and prolonged PR interval. Treatment involves calcium to stabilize the heart, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins, diuretics or hemodialysis to remove excess potassium.
Potassium Disorders In-Service Presentation
Dave Porter presented on hyperkalemia and hypokalemia. Hyperkalemia is caused by conditions like kidney disease or medications and can lead to arrhythmias. Treatment depends on severity but may include calcium gluconate, insulin, or sodium bicarbonate. Hypokalemia is more common and can be caused by vomiting, diarrhea, or medications. It often has no symptoms but severe cases can cause heart problems. Treatment involves replacing potassium orally or intravenously depending on the situation. Both conditions need to be treated to keep potassium levels between 3.5-5.0 mEq/L.
Hypokalemia - Approach and Management
Potassium - facts, Renal Handling.
Hypokalemia - Definition, causes, Approach to hypokalemia and its Management.
Hypokalemia and hyperkalemia indore pedicon 2014 final
This document discusses two case studies of pediatric patients presenting with electrolyte abnormalities. Case 1 involves a 2-year-old boy named Rahul who was brought to the emergency department with diarrhea and dehydration. His lab work showed sodium of 131 mEq/L and potassium of 2 mEq/L, indicating hypokalemia. Case 2 involves a 7-year-old girl named Vinita who was admitted to the PICU for severe diabetic ketoacidosis. Her initial potassium was 4.4 mEq/L but the resident was concerned about potential hyperkalemia with further potassium supplementation. The document then reviews the causes, clinical manifestations, diagnosis, and management of hypo- and hyperkalemia in
Effects of hypo & hyper kalemia
The document discusses hyperkalemia, its effects on the electrocardiogram (ECG), and the role of calcium gluconate in reversing these effects. Hyperkalemia is a potentially lethal condition defined as a serum potassium level above 5 mEq/L. It can cause abnormal heart rhythms and cardiac arrest. On ECG, hyperkalemia presents as tall, peaked T waves and prolonged PR interval. Calcium gluconate works by antagonizing the effects of potassium at the cellular level and restoring the normal threshold potential, allowing action potentials to occur and reestablishing normal cardiac conduction. By rapidly shifting potassium into cells, calcium gluconate can quickly reverse the ECG changes and cardiac effects caused by hyperkalemia
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.
Hyperkalemia final
Hyperkalemia is defined as a serum potassium concentration greater than 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space, excessive potassium intake, or inadequate excretion. Pseudohyperkalemia is an artifactual increase. Treatment involves calcium to antagonize cardiac effects, insulin to shift potassium intracellularly, and cation exchange resins or dialysis to remove potassium from the body. The goal is to lower potassium levels urgently to prevent cardiac arrhythmias.
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.
Adrenal glands t sg
The document discusses adrenal glands and primary adrenal insufficiency. It describes the basic anatomy of the adrenal glands, their blood supply, embryology, and histology. It outlines primary adrenal insufficiency, including causes such as autoimmune disorders, infections, metastatic cancer, drugs that inhibit cortisol biosynthesis, and deposition diseases. Symptoms of primary adrenal insufficiency include fatigue, weight loss, nausea, muscle and joint pain, skin hyperpigmentation, and postural hypotension. Diagnosis involves tests to demonstrate inappropriate low cortisol secretion and treatment involves hydrocortisone replacement and mineralocorticoid replacement such as fludrocortisone.
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
Electrolyte imbalance
This document discusses electrolyte imbalances, specifically hypokalemia, hyperkalemia, and magnesium imbalance. It outlines the causes, clinical manifestations, and treatment considerations for anesthesia for each condition. Key points include decreased cardiac contractility and arrhythmias with hypokalemia, skeletal muscle weakness and cardiac effects with hyperkalemia, and uses of magnesium for conditions like preeclampsia and tetanus. Treatment involves oral or IV potassium replacement, calcium or sodium bicarbonate for hyperkalemia, and magnesium supplementation. Anesthetic implications are also addressed.
Hyperkalemia and other electrolytes disorders
This document provides an overview and guidelines for managing common electrolyte disorders like hyperkalemia, hypokalemia, and hypomagnesemia in hospitalized patients. It reviews the key steps in assessing the disorders, determining treatment approaches, selecting appropriate replacement methods and doses, and monitoring patients. The guidelines emphasize starting oral replacement when possible, calculating replacement based on estimated deficits, avoiding too rapid IV administration, and aggressively managing disorders in high-risk patients like those with diabetes or on IV diuretics.
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Reanimation(fluid & electrolyte)
The document provides information about fluid and electrolyte balance. It discusses the distribution and composition of body fluids, normal fluid exchange, and electrolyte disturbances including hypovolemia, hypervolemia, hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemia. It also covers parenteral fluid therapy including intravenous fluids, methods of calculating fluid transfusion rates, and management of fluid balance in surgical patients.
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This document discusses potassium metabolism and the approach to hyperkalemia. It begins with an introduction to potassium physiology and homeostasis. The kidney plays a key role in potassium excretion, reabsorbing 85-90% in the distal tubules where regulation occurs. Hyperkalemia is defined as a serum potassium over 5.5 mEq/L and can be caused by increased potassium load, impaired excretion, or transcellular shifting. Treatment focuses on stabilizing cardiac cells, rapidly lowering potassium levels, and enhancing elimination while addressing the underlying cause. Emergency therapies include calcium gluconate, insulin therapy, beta agonists, and sodium polystyrene sulfonate.
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Approach to Hypokalemia.pptx
This document discusses hypokalemia, including its definition, prevalence, causes, clinical symptoms, diagnostic approach, and treatment. Some key points:
1. Hypokalemia is defined as a serum potassium level below 3.5 mEq/L and can be caused by decreased intake, redistribution into cells, or increased loss.
2. Clinical features include fatigue, weakness, constipation, cardiac arrhythmias, and in severe cases, paralysis.
3. Diagnosis involves considering the patient's medical history, medications, diet, and physical exam along with lab tests.
4. Treatment focuses on replacing potassium deficits, correcting the underlying cause, and preventing future episodes, using oral or
approach to hypokalemia.pptx
1. Hypokalemia, defined as a serum potassium level below 3.5 mEq/L, can result from reduced potassium intake, increased intracellular shifting of potassium, or increased renal or gastrointestinal losses.
2. The kidney plays a dominant role in potassium homeostasis by regulating urinary potassium excretion through principal and intercalated cells in the collecting duct. Diuretics like thiazides can cause hypokalemia by increasing sodium delivery to the distal tubule.
3. Gastrointestinal losses through vomiting or diarrhea, as well as conditions increasing mineralocorticoid activity, can also deplete total body potassium stores and result in hypokalemia. Close monitoring of potassium levels is important in
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Bartter syndrome is a genetic disorder characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hypercalciuria. It results from defects in sodium, chloride, and potassium transporters in the ascending loop of Henle. There are four main types based on the underlying molecular defects. The neonatal form presents in newborns with severe salt wasting, dehydration, and hypotension. Classic Bartter syndrome presents in older infants and children with muscle cramps, weakness, and growth failure due to chronic hypokalemia. Treatment involves potassium and sodium supplementation and potassium-sparing diuretics. With adequate treatment, long-term prognosis is generally good, though some may have chronic complications
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This document provides an overview of fluid therapy and electrolyte disturbances. It discusses the basic physiology of body fluids, including total body water content and distribution. It then covers various electrolyte abnormalities like hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemia. It also addresses acid-base balance disturbances and different intravenous fluid options for fluid resuscitation and maintenance.
1618256660403_hypokalemia and hyperkalemia.pptx
This document discusses hyperkalemia and hypokalemia in neonates. Hyperkalemia is defined as a serum potassium level greater than 5.5 mEq/L and can be caused by increased potassium load, impaired renal excretion, or transcellular shifts. It presents clinically with muscular or respiratory paralysis and arrhythmias. Treatment focuses on cardiac stabilization, shifting potassium intracellularly, enhancing excretion, and treating underlying causes. Hypokalemia is a serum potassium level below 3.5 mEq/L and can result from decreased intake, extrarenal losses, or tubular defects. It presents with muscle weakness and cardiac arrhythmias. Treatment involves replacing potassium orally or intravenously depending on severity
Potassium disorders-hypokalemia and hyperkalemia
This document summarizes potassium disorders including hypokalemia and hyperkalemia. It discusses the normal physiology of potassium regulation and mechanisms that can lead to imbalances. For hypokalemia, causes include decreased intake, redistribution into cells, and increased loss from the kidneys or gastrointestinal tract. Hyperkalemia can result from shifts of potassium into the extracellular space, inadequate renal excretion, and excessive potassium intake. Clinical features and treatment approaches focusing on antagonizing cardiac effects, redistributing potassium into cells, and removing excess potassium are outlined.
Electrolyte imbalance potassium
The document discusses potassium imbalance, focusing on hypokalemia and hyperkalemia, their causes, clinical effects, and treatment approaches. It provides details on potassium distribution and regulation in the body, factors that influence potassium levels, signs and symptoms of imbalance, and strategies for correcting deficiencies and excesses. The document is intended as an educational reference for medical professionals on electrolyte disorders related to potassium.
Understanding renal failure
Acute renal failure (ARF) is a sudden loss of kidney function that can be reversible. It is caused by renal cell damage from ischemia or toxic substances. ARF progresses through oliguric, diuretic, and recovery phases. Nursing management focuses on fluid and electrolyte balance, preventing infections, maintaining nutrition, and preserving neurologic function. Dialysis may be needed to correct electrolyte imbalances or other complications of ARF.
Acute renal failure in children
This document provides an overview of acute renal failure in children. It defines acute renal failure, discusses causes (pre-renal, intrinsic renal, post-renal), pathogenesis, laboratory findings, biomarkers, management including fluid resuscitation, diuretics, electrolyte abnormalities, nutrition, and indications for dialysis. Management is aimed at treating the underlying cause and maintaining fluid, electrolyte and acid-base balance until renal function recovers.
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.
POTASSIUM - ELECTROLYTE IMBALANCE (HYPERKALEMIA & HYPOKALEMIA).pdf
Hyperkalemia, causes, risk factors, pathophysiology, clinical manifestation, diagnostic evaluation, medical management, nursing management, Hypokalemia, causes, risk factors, pathophysiology, clinical manifestation, diagnostic evaluation, medical management, nursing management.
Inborn errors of bilirubin metabolism & wilson disease
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Clinical approach to patient with Hyperkalemia
Clinical approach to patient with Hyperkalemia
In internal medicine
Causes
Clinical findings
Complications
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Electrolytes Disturbances
This document discusses various electrolyte disturbances and their causes and effects. It covers sodium, potassium, magnesium, and trace elements. Key points include:
- Sodium is a major extracellular cation and is lost through sweat, GI tract, and urine. Hyponatremia can result from GI loss or inappropriate ADH secretion and causes neurological symptoms.
- Potassium is an important intracellular cation and is lost through the GI tract. Hypokalamia can result from GI loss and causes neuromuscular and cardiac issues.
- Magnesium is mainly stored in bone and muscles. Hypomagnesemia can block PTH and cause hypocalcemia and hypokalemia. It causes neurological
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- 2. -The normal serum level of potassium is 3.5 to 5 mmol/L -Daily Requirements 1-1.5 mmol/kg -Dietary sources include dried fruits; legumes; meats; poultry; fish; soy; bananas; citrus fruits; potatoes; tomatoes; broccoli; mushrooms; dark, leafy green vegetables
- 3. Potassium Regulation Review • Intracellular concentration about 150 mmol/L • The passive outward diffusion of K+ is the most important factor that generates the resting membrane potential. • Maintenance of steady state requires K+ ingestion = K+ excretion • Nearly all regulation of renal K+ excretion and total body K+ balance occurs in the distal nephron, via principal cells • Potassium secretion regulated by aldosterone and plasma K+ concentration
- 4. Potassium homeostasis This excess is (10%) excreted through the gut (90%) excreted through the kidneys - The most important site of regulation is the distal nephron, including the distal convoluted tubule, the connecting tubule, and the cortical collecting tubule -Gastrointestinal absorption is complete, resulting in daily excess intake of about 1 mmol/kg/d
- 6. DEFINITION • PLASMA [K+] >5.0 mEq/L • SEVERE HYPERKALEMIA – PLASMA [K+] >6mM
- 7. CAUSES OF HYPERKALEMIA 1.PSEUDO HYPERKALEMIA CELLULAR EFFLUX HERIDITARY DEFECTS IN RED CELL MEMBRANE TRANSPORT
- 8. 2. INTRA TO EXTRA CELLULAR SHIFT
- 9. 3. INADEQUATE EXCRETION A. Inhibition of the renin-angiotensin-aldosterone axis B. Decreased distal delivery C. Hyporeninemic hypoaldosteronism D. Renal resistance to mineralocorticoid E. Advanced renal insufficiency F. Primary adrenal insufficiency
- 12. Cardiac arrhythmias - sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and asystole. Secondary hyperkalemic paralysis Familial hyperkalemic periodic paralysis • Myopathic weakness during hyperkalemia • Induced by increased K+ intake or rest after heavy exercise. • Depolarization of skeletal muscle by hyperkalemia unmasks an inactivation defect in skeletal Na+ channels; • Autosomal dominant mutations in the SCN4A gene encoding this channel are the predominant cause. Metabolic acidosis.
- 13. DIAGNOSTIC APPPROACH • ASSESS NEED FOR EMERGENCY • MEDICATIONS • DIET • URINE OUTPUT • VOLUME STATUS
- 14. LAB INVESTIGATIONS • ELECTROLYTES • BUN • CREATININE • SERUM OSMOLARITY • CBC • URINARY pH
- 15. TTKG • > 6-7 • TTKG = [K+]URINE OSMOLserum [K+]SERUM OSMOLurine
- 17. ECG CHANGES
- 19. TREATMENT
- 20. NEWER DRUGS Phase 3 trial ZIRCONIUM SILICATE 9
- 21. • A MICROPOROUS ZIRCONIUM SILICATE COMPOUND. • ZS-9 CAN SELECTIVELY ENTRAP MONOVALENT CATIONS, INCLUDING EXCESS POTASSIUM AND AMMONIUM IONS, IN THE GI TRACT. • HOWEVER, IT DOES NOT SWELL IN THE GI TRACT, LIMITING GI SYMPTOMS. • THE DRUG COMES AS A FINE POWDER THAT DISSOLVES IN WATER AND IS TASTELESS.
- 22. THANK YOU
Editor's Notes
- Amount of K+ lost in stool typically 10% of dietary intake. This can increase to 60% of intake in CKD.