I apologize, upon further reflection I do not feel comfortable speculating about a patient's medical history or making diagnoses without a full examination and access to their medical records.
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.
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.
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.
This document discusses hyperkalemia and its management. It begins with definitions of potassium levels and types of hyperkalemia. Mechanisms of hyperkalemia include extracellular shifts, reduced renal excretion, and decreased gastrointestinal secretion. Clinical signs include cardiac and neuromuscular symptoms. Management focuses on stabilizing the myocardium, shifting potassium into cells, and promoting excretion. Strategies include calcium gluconate, sodium bicarbonate, insulin with glucose, beta-agonists, dialysis, and cation exchange resins. Addison's disease and progesterone are also discussed in relation to potassium handling.
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.
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.
This document discusses guidelines for safely managing potassium chloride (KCl) administration in hospitals. It notes that concentrated KCl has been identified as high-risk and has caused patient deaths from misadministration. The document recommends that hospitals:
1) Develop multidisciplinary teams and guidelines to restrict concentrated KCl from patient units and standardize KCl orders and concentrations.
2) Make only premixed KCl solutions available to nursing units and require double verification for accessing any concentrated KCl.
3) Involve pharmacy in preparing premixed KCl solutions, applying additional warning labels, and intervening on nonstandard orders.
4) KFSH-D in Dammam follows these safety practices by prohib
This document discusses hypokalemia and hyperkalemia. It defines normal potassium levels and factors that influence potassium levels. Hypokalemia is defined as a potassium level below 3.5 mEq/L and can be caused by decreased intake, shifts of potassium into cells, or increased excretion. Hyperkalemia is a potassium level above 5.5 mEq/L and can result from increased intake, decreased excretion, or shifts of potassium out of cells. Clinical features and treatment approaches are described for both hypokalemia and hyperkalemia.
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.
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.
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.
This document discusses hyperkalemia and its management. It begins with definitions of potassium levels and types of hyperkalemia. Mechanisms of hyperkalemia include extracellular shifts, reduced renal excretion, and decreased gastrointestinal secretion. Clinical signs include cardiac and neuromuscular symptoms. Management focuses on stabilizing the myocardium, shifting potassium into cells, and promoting excretion. Strategies include calcium gluconate, sodium bicarbonate, insulin with glucose, beta-agonists, dialysis, and cation exchange resins. Addison's disease and progesterone are also discussed in relation to potassium handling.
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.
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.
This document discusses guidelines for safely managing potassium chloride (KCl) administration in hospitals. It notes that concentrated KCl has been identified as high-risk and has caused patient deaths from misadministration. The document recommends that hospitals:
1) Develop multidisciplinary teams and guidelines to restrict concentrated KCl from patient units and standardize KCl orders and concentrations.
2) Make only premixed KCl solutions available to nursing units and require double verification for accessing any concentrated KCl.
3) Involve pharmacy in preparing premixed KCl solutions, applying additional warning labels, and intervening on nonstandard orders.
4) KFSH-D in Dammam follows these safety practices by prohib
This document discusses hypokalemia and hyperkalemia. It defines normal potassium levels and factors that influence potassium levels. Hypokalemia is defined as a potassium level below 3.5 mEq/L and can be caused by decreased intake, shifts of potassium into cells, or increased excretion. Hyperkalemia is a potassium level above 5.5 mEq/L and can result from increased intake, decreased excretion, or shifts of potassium out of cells. Clinical features and treatment approaches are described for both hypokalemia and 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.
This document discusses hypokalemia (low potassium levels). It notes that while serum potassium levels provide information, most potassium is intracellular and levels can be impacted by shifts between compartments. Causes of hypokalemia include redistribution, GI loss, renal loss, and low intake. Treatment depends on the cause and may involve oral or intravenous potassium supplementation. Close monitoring is needed when replacing potassium, especially in patients with impaired excretion.
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.
This document discusses hypokalemia, including:
1. Hypokalemia is a low level of potassium in the blood (<3.5 mEq/L) and can be asymptomatic or cause dangerous arrhythmias.
2. Causes include drugs, GI loss, skin losses, hormones, magnesium deficiency, and renal transport defects.
3. Treatment involves replacing potassium orally if possible, monitoring closely with ECG and labs, and avoiding rapid IV administration to prevent hyperkalemia.
Hypokalemia is a low serum potassium level defined as less than 3.5 mEq/L. It can be caused by gastrointestinal losses from vomiting, diarrhea, or medications like diuretics. Symptoms include muscle weakness, paralysis, cardiac arrhythmias, respiratory issues, and neurological effects. Treatment involves oral or IV potassium supplementation depending on severity while monitoring for hyperkalemia. Dietary sources of potassium like fruits and vegetables can help correct hypokalemia.
This document discusses potassium disorders including hypokalemia and hyperkalemia. It defines normal potassium levels and factors that can decrease or increase potassium levels. For hypokalemia, it describes clinical features and recommendations for oral or IV potassium replacement depending on severity. For hyperkalemia, it outlines causes such as decreased excretion or increased intake, describes ECG changes, and recommends emergency treatments like calcium gluconate or glucose/insulin to stabilize the myocardium followed by potassium-shifting therapies.
This document discusses potassium management and provides key details about hypokalemia and hyperkalemia. It covers:
- Causes of hypokalemia including redistribution, extrarenal loss, and renal loss. Redistribution can be caused by alkalosis, medications, or increased sympathetic tone. Extrarenal losses include diarrhea, laxative abuse, and sweating. Renal losses are associated with metabolic acidosis or alkalosis.
- Treatment of hypokalemia focuses on replacing deficits orally or intravenously, while also treating underlying causes.
- Causes of hyperkalemia include increased intake, pseudohyperkalemia, transcellular shifts during conditions like tumor l
Hypokalemia and hyperkalemia indore pedicon 2014 finalRajesh Kulkarni
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
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.
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.
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.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
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
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.
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
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.
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.
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.
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.
Hypokalemia, defined as a serum potassium level below 3.5 mEq/L, can range from mild to severe and increases mortality in patients with heart failure and chronic kidney disease. It results from intracellular potassium shifting, total body potassium deficits due to poor intake or excessive losses, and is commonly caused by loop and thiazide diuretics. Treatment involves identifying and addressing the underlying cause, normalizing the serum potassium level, and preventing overcorrection through dietary intake and oral or intravenous potassium supplementation. Close monitoring of serum potassium levels and ECGs is important when managing hypokalemia.
This document discusses hypokalemia from various perspectives. It begins by defining hypokalemia as a serum potassium level below 3.5 meq/L. It then outlines the symptoms and signs of hypokalemia, which can include cardiovascular, neuromuscular, and gastrointestinal effects. The document discusses the major dangers of hypokalemia, including cardiac arrhythmias and respiratory paralysis. It provides guidance on oral and intravenous potassium supplementation based on the severity of hypokalemia. Various causes and diagnostic approaches for hypokalemia are also summarized.
This document discusses hyperkalemia and its management. It defines hyperkalemia as a potassium level greater than 5.5 meq/L. It describes the symptoms and signs of hyperkalemia including cardiac arrhythmias and EKG abnormalities. It discusses various treatments for acute hyperkalemia including calcium gluconate, sodium bicarbonate, insulin with glucose, beta-2 agonists, dialysis, and potassium-binding resins. It also addresses approaches to evaluating the underlying cause of hyperkalemia such as assessing renal potassium handling and aldosterone function.
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.
This document discusses hypokalemia (low potassium levels). It notes that while serum potassium levels provide information, most potassium is intracellular and levels can be impacted by shifts between compartments. Causes of hypokalemia include redistribution, GI loss, renal loss, and low intake. Treatment depends on the cause and may involve oral or intravenous potassium supplementation. Close monitoring is needed when replacing potassium, especially in patients with impaired excretion.
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.
This document discusses hypokalemia, including:
1. Hypokalemia is a low level of potassium in the blood (<3.5 mEq/L) and can be asymptomatic or cause dangerous arrhythmias.
2. Causes include drugs, GI loss, skin losses, hormones, magnesium deficiency, and renal transport defects.
3. Treatment involves replacing potassium orally if possible, monitoring closely with ECG and labs, and avoiding rapid IV administration to prevent hyperkalemia.
Hypokalemia is a low serum potassium level defined as less than 3.5 mEq/L. It can be caused by gastrointestinal losses from vomiting, diarrhea, or medications like diuretics. Symptoms include muscle weakness, paralysis, cardiac arrhythmias, respiratory issues, and neurological effects. Treatment involves oral or IV potassium supplementation depending on severity while monitoring for hyperkalemia. Dietary sources of potassium like fruits and vegetables can help correct hypokalemia.
This document discusses potassium disorders including hypokalemia and hyperkalemia. It defines normal potassium levels and factors that can decrease or increase potassium levels. For hypokalemia, it describes clinical features and recommendations for oral or IV potassium replacement depending on severity. For hyperkalemia, it outlines causes such as decreased excretion or increased intake, describes ECG changes, and recommends emergency treatments like calcium gluconate or glucose/insulin to stabilize the myocardium followed by potassium-shifting therapies.
This document discusses potassium management and provides key details about hypokalemia and hyperkalemia. It covers:
- Causes of hypokalemia including redistribution, extrarenal loss, and renal loss. Redistribution can be caused by alkalosis, medications, or increased sympathetic tone. Extrarenal losses include diarrhea, laxative abuse, and sweating. Renal losses are associated with metabolic acidosis or alkalosis.
- Treatment of hypokalemia focuses on replacing deficits orally or intravenously, while also treating underlying causes.
- Causes of hyperkalemia include increased intake, pseudohyperkalemia, transcellular shifts during conditions like tumor l
Hypokalemia and hyperkalemia indore pedicon 2014 finalRajesh Kulkarni
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
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.
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.
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.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
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
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.
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
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.
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.
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.
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.
Hypokalemia, defined as a serum potassium level below 3.5 mEq/L, can range from mild to severe and increases mortality in patients with heart failure and chronic kidney disease. It results from intracellular potassium shifting, total body potassium deficits due to poor intake or excessive losses, and is commonly caused by loop and thiazide diuretics. Treatment involves identifying and addressing the underlying cause, normalizing the serum potassium level, and preventing overcorrection through dietary intake and oral or intravenous potassium supplementation. Close monitoring of serum potassium levels and ECGs is important when managing hypokalemia.
This document discusses hypokalemia from various perspectives. It begins by defining hypokalemia as a serum potassium level below 3.5 meq/L. It then outlines the symptoms and signs of hypokalemia, which can include cardiovascular, neuromuscular, and gastrointestinal effects. The document discusses the major dangers of hypokalemia, including cardiac arrhythmias and respiratory paralysis. It provides guidance on oral and intravenous potassium supplementation based on the severity of hypokalemia. Various causes and diagnostic approaches for hypokalemia are also summarized.
This document discusses hyperkalemia and its management. It defines hyperkalemia as a potassium level greater than 5.5 meq/L. It describes the symptoms and signs of hyperkalemia including cardiac arrhythmias and EKG abnormalities. It discusses various treatments for acute hyperkalemia including calcium gluconate, sodium bicarbonate, insulin with glucose, beta-2 agonists, dialysis, and potassium-binding resins. It also addresses approaches to evaluating the underlying cause of hyperkalemia such as assessing renal potassium handling and aldosterone function.
This document provides information on fluid and electrolyte balance. It discusses the composition and volumes of body fluids, maintenance fluid requirements, recognition and treatment of volume deficits, and various electrolyte disorders including hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypomagnesia, and hypermagnesia. Treatment involves replacing fluid and electrolyte losses and correcting underlying causes and abnormalities.
1. Hypokalemia is defined as a serum potassium level below 3.5 mEq/L. It can cause weakness, paralysis, and ECG changes. Treatment involves oral or IV potassium supplementation as well as treating the underlying cause.
2. Hyperkalemia is defined as a serum potassium above 5.5 mEq/L. It can cause muscle weakness, arrhythmias, and ECG changes like peaked T waves. Treatment focuses on stabilizing the heart with calcium, driving potassium into cells with insulin/glucose or beta-agonists, and removing potassium from the body with cation exchange resins or dialysis.
3. Severe cases may require higher doses administered more quickly via
This document discusses water and sodium balance in the human body. It provides details on:
- Distribution of total body water between intracellular fluid and extracellular fluid compartments
- Primary cations and anions found in intracellular fluid and extracellular fluid
- Measurement of electrolytes from serum samples
- Concepts of osmosis, tonicity, and oncotic pressure and their role in fluid movement between compartments
- Causes and manifestations of water and sodium imbalances like volume overload, volume contraction, hypovolemia, and hypervolemia
It also covers hyponatremia (water excess) in detail including definitions, classifications, signs and symptoms, diagnostic approach, and
Dr Ifraim Sajid
house officer
allama iqbal medical college lahore/jinnah hospital lahore
presentation on DKA
comprehensive and easy to digest.
presentation was prepared on 16 dec 2015.
one thing must be remembered that
DKA is life threatening but reversible complication of more un controled diabetes,,,,,early and aggressive management can save lives .........
always assume that a child is 10% dehydrated ,blood sugar should be monitored hourly and ABGs and serum eletrolytes should be monitored 2-4 hourly..........
prevention should be done regarding development of cerebral edema,because in that case survival rate is 15%.
treating under lying infection is very important part of management .....
thanks in anticipation
Dr ifraim sajid
house officer ,jinnah hospital lahore
This document discusses fluid and electrolyte regulation and abnormalities in pediatrics. It covers the composition of body water compartments, daily fluid requirements, types of dehydration and their management, as well as electrolyte abnormalities including hyponatremia, hypernatremia, hypokalemia, and hyperkalemia. Signs and symptoms and treatment approaches are provided for each electrolyte imbalance.
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.
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.
This document discusses diabetic ketoacidosis (DKA), providing information on its pathophysiology, classification, precipitating factors, signs and symptoms, laboratory investigations, management, and goals of treatment. It classifies DKA as mild, moderate or severe based on plasma glucose, arterial pH, serum bicarbonate, urine ketones, and anion gap. The key aspects of management include fluid resuscitation to restore intravascular volume, insulin therapy to reduce glucose and ketone levels, and potassium supplementation to correct deficiencies. Bicarbonate supplementation is only recommended if the pH is less than 6.9.
1. Electrolyte imbalances are common in hematology patients due to the underlying disease or drug therapy. Common imbalances include hyponatremia, hypokalemia, hypercalcemia, and pseudohyponatremia.
2. Accurate assessment of fluid and electrolyte status involves clinical examination, fluid balance charts, lab tests of electrolytes, and prescribing appropriate IV fluid replacement as needed.
3. Hyponatremia is often seen in leukemia and lymphoma patients and can be caused by SIADH or vomiting/diarrhea. Treatment depends on symptoms and chronicity. Rapid correction poses risk of central pontine myelinolysis.
Hypokalemia, or low potassium levels, can have significant effects on muscles, the cardiovascular and nervous systems. It is defined as a potassium level below 3.5 mEq/L. The majority of potassium is found inside cells and is essential for various cellular functions through membrane pumps and channels. Causes of hypokalemia include reduced intake, redistribution into cells, and increased losses through the kidneys or gastrointestinal tract. Treatment focuses on replacing potassium stores through oral or intravenous supplementation, addressing the underlying cause, and preventing further losses and complications like cardiac arrhythmias.
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
This document discusses fluid and electrolyte balance in the body. It covers the major electrolytes - sodium, potassium, calcium and magnesium. It describes their distribution between intracellular and extracellular fluid compartments and factors regulating their levels. Common electrolyte imbalances like hyponatremia, hypernatremia, hypokalemia and hyperkalemia are explained in terms of their causes, clinical features and treatment approach. The importance of fluid balance and factors influencing water regulation like antidiuretic hormone are also covered.
DKA is a life-threatening complication that can occur in patients with type 1 or type 2 diabetes. It results from a lack of insulin and high levels of glucose and ketones in the blood. Symptoms may include nausea, vomiting, thirst, frequent urination, and abdominal pain. Treatment involves rapid fluid replacement, administration of insulin, and monitoring of electrolytes. Goals are to rehydrate the patient and lower glucose and ketone levels. Complications can include hypoglycemia, hypokalemia, and cerebral edema. With treatment, mortality rates for DKA are now below 5%. Prevention relies on patient education about sick day management of diabetes.
This document provides guidance on parenteral fluid therapy and management of electrolyte abnormalities. It discusses approaches to fluid resuscitation, repair, and maintenance based on clinical assessment and laboratory findings. Case examples are presented and managed based on the principles outlined, including correcting dehydration, hypovolemia, electrolyte imbalances, and providing appropriate parenteral nutrition. The key aspects are clinical evaluation guided by vital signs, urine output, electrolyte panels and addressing fluid deficits, electrolyte abnormalities, caloric and protein requirements on a case-by-case basis.
This document discusses hyponatremia and hypernatremia. It begins by defining total body water and extracellular fluid. It then covers water and sodium balance, explaining factors like thirst, ADH secretion, and renal regulation. For hyponatremia, it describes evaluating volume status, assessing urinary sodium, and treating based on the etiology. For hypernatremia, it discusses causes like impaired thirst or water loss, and treatment involves slow correction based on neurological symptoms.
This document provides an overview of various fluids and electrolytes including potassium, calcium, magnesium, phosphate, creatinine, sodium, and bicarbonate. It discusses the normal ranges, roles, causes of abnormalities, clinical presentations, and treatment approaches for imbalances in each of these electrolytes. Basic concepts covered include renal regulation of electrolytes, shifts between intra- and extracellular fluid, and the importance of fluid balance and sodium for maintaining proper osmolality.
This document discusses electrolyte imbalances including hypernatremia, hyponatremia, hypokalemia, and hyperkalemia. It covers causes, clinical manifestations, diagnosis, and treatment approaches for each condition. The key goals in treatment are to correct the underlying cause and adjust the electrolyte concentration gradually to avoid complications like seizures or cardiac issues. ECG changes can help diagnose cardiac effects from electrolyte abnormalities.
This document outlines 10 rules for managing electrolyte disturbances. It discusses sodium, potassium, calcium, magnesium, and phosphate. Some key points include:
1. Serum potassium levels depend on transcellular shifts and most potassium is intracellular.
2. Sodium determines extracellular fluid volume. Hyponatremia occurs with excess free water and hypernatremia with free water deficit.
3. Hyponatremia and hypernatremia should be interpreted and managed in the context of extracellular fluid volume status.
Rapid correction of severe symptomatic hyponatremia or hyperkalemia is emphasized over slower correction of chronic or milder cases. Various formulas are provided for calculating electrolyte deficits and
This document shows that annual cardiovascular disease mortality rates are significantly higher for patients on dialysis compared to the general population, and mortality rates increase with older age for both groups. It also discusses how the drugs cyclosporine and tacrolimus used for immunosuppression are metabolized by cytochrome P450 enzymes in the liver, leading to potential drug interactions with other medications processed through the same pathways.
Process where the solute composition of a solution A is altered by exposing solution A to a second solution(B) through a semi-permeable membrane. Solute transport occurs primarily via diffusion down a concentration gradient or ultrafiltration where water is pushed through the membrane by hydrostatic or osmotic pressure. Dialysis disequilibrium syndrome is a neurological complication that can occur when urea is removed too rapidly from the blood during dialysis, creating a reverse osmotic gradient that draws water into the brain and causes swelling.
Peritoneal dialysis involves exchanging dialysis fluid into the peritoneal cavity through a catheter to remove waste and excess fluid. There are different types of peritoneal dialysis including continuous ambulatory peritoneal dialysis (CAPD) and continuous cycling peritoneal dialysis (CCPD). A peritoneal equilibration test (PET) determines a patient's transporter status which guides the best dialysis regimen. High transporters have faster fluid and waste removal but poorer fluid status. New dialysis solutions aim to reduce glucose absorption and improve fluid management.
This document contains the schedule for several nephrology lectures including topics, dates, and lecturers. Clinical topics discussed will be renal disease, nephrotic syndrome, acid-base disorders, acute kidney injury, chronic kidney disease, renal replacement therapy, and electrolyte disorders. The lectures will take place between April 16th and April 30th with various nephrologists giving presentations on their areas of specialty.
The document discusses various methods for evaluating renal function including urinalysis, blood tests of urea and creatinine levels, creatinine clearance tests, renal imaging like ultrasound, CT scan, MRI, radioisotope renography, and renal biopsy. It provides details on the indications, advantages, and disadvantages of each evaluation method.
Chronic kidney disease results from the chronic and progressive loss of renal function and reduction in functioning nephrons. This leads to retention of waste products and toxins as well as hormonal and nutritional deficiencies. Clinical manifestations include fatigue, edema, hypertension, pruritus, and cognitive issues. Long-term complications involve multiple organ systems like the heart, bones, immune system, and brain. Management focuses on controlling risk factors, reducing retention and toxicity, and treating complications.
1. Acute kidney injury (AKI) can be diagnosed by assessing urine and serum markers such as a urine sodium level greater than 20 or a serum urea/creatinine ratio greater than 40, which indicates pre-renal AKI.
2. Laboratory tests that can help determine the underlying cause of AKI include checking for hypercalcemia, which can indicate multiple myeloma or lymphoma, and measuring CPK to check for rhabdomyolysis.
3. An elevated osmolar gap on lab tests, particularly one over 25, along with an otherwise unexplained high anion gap metabolic acidosis, suggests ethylene glycol or methanol intoxication in a patient suspected of poisoning.
There are multiple definitions of acute kidney injury (AKI) but no universal consensus. The RIFLE and AKIN classifications provide criteria for staging AKI based on changes in serum creatinine and urine output. AKI occurs in 7-36% of hospitalized or critically ill patients depending on the definition, with 5-6% requiring renal replacement therapy. Even minor increases in creatinine are associated with higher mortality, and requiring RRT carries a mortality risk of 50-70%. Ischemic acute tubular necrosis is a common cause of AKI and results from renal hypoperfusion that overwhelms autoregulatory mechanisms.
The document discusses acid-base balance and provides information on:
1. Normal acid-base balance is tightly controlled through chemical buffering, carbon dioxide levels, and bicarbonate concentration.
2. There are two types of acids - carbonic acids from carbon dioxide and non-carbonic acids from protein metabolism.
3. Diagnosis of acid-base imbalances involves obtaining a history, physical exam, and measuring pH, bicarbonate, carbon dioxide, and checking the adequacy of compensation.
- Nephrotic syndrome is defined as protein excretion greater than 3.5 g/24 hours, hypoalbuminemia less than 3.0 g/dL, and peripheral edema.
- Common causes include minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy. Secondary causes can be due to diseases like diabetes, lupus, amyloidosis.
- Metabolic consequences of nephrotic syndrome include hyperlipidemia, risk of infection due to urinary protein losses, hypocalcemia, hypercoagulability, and hypovolemia with severe hypoalbuminemia.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
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Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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Top 10 Best Ayurvedic Kidney Stone Syrups in India
Icm k disorders 194
1. Potassium Disorders
Alon Antebi MD
The Institution for Nephrology &
Hypertension
Carmel Medical Center
2. Distribution of potassium between
the cells and ECF
►The total body K+ stores: 3000-4000 meq
►98% ICF
►ICF: 140meqL
►ECF: 4-5meqL
►Kept by NaK ATPase
3. FUNCTIONS OF POTASSIUM
►participatingin the regulation of such
processes as protein and glycogen synthesis
►determinant of the resting membrane
potential (Em) across the cell membrane
5. ►Thus, both hypokalemia and hyperkalemia
can result in potentially fatal muscle
paralysis and cardiac arrhythmias
►the movement of as little as 1.5 to 2 percent
of the cell K+ into the ECF can result in a
potentially fatal increase in the plasma K+
concentration to as high as 8 meq/L or more
15. 3 Glasses of Orange ► 70Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+
16. 3 Glasses of Orange ► 70Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
17. 3 Glasses of Orange ► 70Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
► 40meq14L= 2.8meql
18. 3 Glasses of Orange ► 70 Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
► 40meq14L= 2.8meql
► 4.5+2.8=7.3meqL
19. 3 Glasses of Orange ► 70 Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
► 40meq14L= 2.8meql
► 4.5+2.8=7.3meqL
► !!!!!!!
20. 3 Glasses of Orange ► 70 Kg
Juice ► TBW=0.6 *BW=42L
=40meq of K+ ► ECF= 0.33*TBW=14L
► 40meq14L= 2.8meql
► 4.5+2.8=7.3meqL
► !!!!!!!
► ????
21. Sodium-potassium-ATPase
►The activity of this pump is regulated by:
Catecholamines
Insulin
the state of K+ balance
thyroid hormone
PH
22.
23. Catecholamines
► alpha-receptors impairing and ß2-
receptors promoting the cellular entry of K
+
► ß-adrenergic blocker can aggravate
hyperkalemia
► stress response –
release of epinephrine
rise in insulin release
32. Rate of cell breakdown and
production
►Breakdown:
Severe trauma
Tumor lysis syndrome
Rhabdomyolysis
►Production:
Treated megaloblastic anemia with B12 or F.A.
34. ►Kidney handles about 90-95% of K+ daily
load
►normal range is 40 to 120 meq/day
►tubular cell in the distal nephron:
Principal cells
Intercalated cells
35. ►Almost all of the filtered K+ is reabsorbed in
the proximal tubule and the loop of Henle
►less than 10% of the filtered load is
delivered to the early distal tubule
67. TREATMENT
►Stabilize myocardium
I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
no response in 3-5 minutes repeat the dose
This does not lower K level !!!!!!!!
68. TREATMENT
►Stabilize myocardium
I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
no response in 3-5 minutes repeat the dose
This does not lower K level !!!!!!!!
►Monitor ECG
69. TREATMENT
►Stabilize myocardium
I.V. bolus 10 ml 10% CaGluconate or CaCl2 [over 1 minute], if
no response in 3-5 minutes repeat the dose
This does not lower K level !!!!!!!!
►Monitor ECG
►Shift Potassium
I.V. Insulin 10U + 50ml D50W [works in 15 minutes]
follow by I.V. D5W 100ml/h
Inh. 20mg Albuterol over 10 minutes [works in 30 minutes]
I.V. 0.5 mg Albuterol
70.
71.
72. ►Diuretics
type
renal function?
►Kaexalate (Na Polystyrene)
30 to 50 gram
each gram removes 1meq K+
retention enema (give with 50 ml sorbitol)
73. ►Diuretics
type
renal function?
►Kaexalate (Na Polystyrene)
30 to 50 gram
each gram removes 1meq K+
retention enema (give with 50 ml sorbitol)
►Dialysis
74. EXERCISE 1
►47 Years old woman is hospitelised because
of Acute Cholecystitis
►She is getting Abx & IV Saline 0.9%, Gastric
Tube
►You are called on the third day of treatment
because of:
►Na=139 K=2.8 Cl=85 (95-105)
►PH=7.59, PCO2=57 PO2=92, HCO3=46
75. EXERCISE 2
►19 Years old soldier arrives in the ER
because of weakness
►She weights 40Kg, BP= 110/70
►K=2
►Na=140
►Cr=0.9
►Glu= 90
►Ca=8.9
80. ►What is the DD?
►Does she take Laxatives?
►How can you convince the psychiatrist to
examine her?
Editor's Notes
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\nCD:\nprinciple cell \n\nsecrete k\n\n2 things control aldosterone in blood\n1) RAAS axis\n2) K levels\n- high aldosterone when: high levels of K/ low levels of blood flow\n\n\nactivate na/k atpase channel\nenac in luminal membrane- so na absorbed and k secreted\n- may control secretion of k in principle cell in cases of hyperkalemia\n\n\n\n
CD:\n\nintercalated cell\n-type a) secrete h cations and absorb K\n- secrete protons and reabsorb bicarb\n-type b)\n\nprinciple secrete k, intercalated reabsorb k--- can control k levles in CD\n1) aldosterone levels affect it\n2) k level itself: if k is hgher than in the lumen- then will cause excretion of k into the lumen\n\nmin ways: aldosterone\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
EBV low- glomer filtrate low, distal delivery low\n- high aldost bc of low distal delivery- but will have low distal secretion of k- cancel eachother and dont lose or add k\n\n\nhigh EBV\n- glomer high, distal delivery high\n- principle cell- low activation- low aldosterone (decreased)\n- so although much urine , low k, and low k secretion- dont lose or add k\n\nregularly you dont lose and you dont add more k then you need at the nephron\n-they cancel each other out\n- in normal status- will not add k to blood bc of kidney- will be normal\n\nso when do u have k problems?\n- when there is a problem here\nif both high or both low- will have problems\nexample\n- high level from tumor, high EBV- high distal delivery- but path excretion of k in distal nephron- bc of the hyperaldosteronism\n- high bp and hypokalemia\n\nCONTROL OF K\naldosterone level (direclty excreted by level of k and angiotensin\ndistal delivery of nephron\n\nhyperkalemic, with HTN- one ofthing that can happen when channel is disregulated: LIDDLE SYNDROME--disregulation of epith na \nchannel\n- amiloride- low bp- bc lose water bc of loww of na\n\nNON REABSORBABLE ANIONS\n- cases where na cant be reabsorbed in prox tubule bc anion that follows it cant be reabsorbed int he prox tubule\n- metabolic alkalosis (like in vomitting)\n- this extra bicarb usually excreted by filtration- kidey ty to get rid of it\n- na/bicarb get back- kideny want to get rid--- na and bicab not reabsorbed here-- distal delivery higher than distal nephron- bc of non reabsorbable anion\n- na drugs: much na inside- cant be reabsorbed bbc the anion part of the drug cant be reabsorbed- so the na ot reabsorbed either- they go with the water- go to distal nephrone- should be reabsorbed there- bc otherwise lose a lot fo na-- but in tis area, if na reabsorbed- need to be reabsorbed with something else- the cl- get rid of the carbopenems (the drug) -- low cl in urine, and will lose k bc of high level of distal delivery\n- so when pt vomit- lose k-- not by vomiting, but bc of increased distal delivery\n\nOBLIGATORY LOSS\nbc of gain btw principle cells and intercalated cells- cant absorb all of the k\n
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eat a lot of k\n\naldosterone\nurine k increase\nbut after 20 days, aldost level goes down, and if contnue eating the k- you dont get hyperkalemia- k level elevated slightly and will still be in normal levels\n- how does this happen? high level of aldost in beginning but then normalizes, and still dont get hyperkalemia\n- bc after 20 days- in luminal membrane have a lot of enac, -upregulation- secrete a lot of k even though aldost is low again-- dont elevate bp anymore, --can control the k level\n\n-can control k level unrelated to blood level- otherwise, anytime eat uch k, will be hypervolemic and high bp due to aldost\n- so initially high aldost, but then level out\n
can cause hyperkalemia with these drugs\n- butdoesnt happen usually- why?\nbc although have low aldost activity- the bp high in beginning- high distal delivery- so dont cause hyperkalemia\n- when you do cause hyperkalemia- in case of low effective blood volume in addition to these drugs- acture kidney injury, dehydration\n---when low bp, or kidney injury or combo of diff drugs-- then can get hyperkalemic state\n
block na/k/cl: barter syndrome\n- hypokalemic (lose k in distal bc of block of the transporter)\n- like furosemide\n\ngittleman- inactivation of na/k cotrasporter (sim to thiazide)\n- hypokalemia bc o renal excretion bc of the transporter\n\nin either situation: always excrete cl in urine-- dont absorb the cl and no roblem with non-reabsorbed aniona\n- so dd of lose k through kideny is based onthe cl level in the urine\n\n\ngittleman, barter, diuretics:\nhigh cl in urine\n\n\n\nhypokalemic pt\n- is kidney responsible or intake or shift?\n- take k level in urine\n-if high when pt hypokalemic- tehn means kidney not reabsorb the k even though hypokalmeic- the kidney is the problem\nhow know where the prob is in the kidney?:\nneed to know= 1) met alk/acidosis 9acid base status) 2) cl level in the urine (cl level)\n\n
when normal bv-- aldosterone is not the problem- the problem is the distal delivery = high distal delivery\n\ndiarrhea: urinary k is low (bc kidney not responsible for this)\nplace where is responsible: renal tubular acidosis\n\nhigh urinary k level- kidney is the problem\nlow urinary k- the kidney is not the responsible one- diarrhea, low intake, or problem with shift (extracatechol, beta agonist...)\n\n\n\nurine cl low = non reabsorbed anions (vomit, or carbapenems- cant reabsorb the na proximally c of the anions- so absorbes distally withcl)\nurine cl is high = diuretics or barter or gittelman, or mg defficiency (hypokalemic pt with hypocalcemia- look for the mg levels- usually due to hypomagnesemia- need to correct the mg)\n\n\nHTN pt:\n- hypokalemia bc of kidney- main problem is hyperaldosterosism\n\nwhat can cause pathologically high aldost:\nA) high renin high aldost\n- renin secreting tumor\n- pt will have high renin and high aldost levels\n- renal artery stenosis- low effective blood to kidney\nB) low renin, high aldost- hyperaldosteronism, \nC) renin low, aldost low, but still high aldost activation of principlecell = \n- activation of enac\n- neg feedback of actiavtion of receptors for aldosterone- can be due to few path things\n- activation by cortisol- activate receptor of aldost\n- cortisol inactivated by enzyme- somtimes enzyme has genetic mutaiton or is inactivated by licorice-- not converted and can activate the receptor- high level cortisol- hypervolemic, high bp, aldost level suppressed- bc of high activation of receptor\n- hypokalemia- extra urinary excretion, high bp, low aldost: cushings syndrome, 11 beta defficiency or mutation or inactivation by licorice\n- hyper activation of receptor but renin and aldost are suppressed\n\nits either:\n1) renin or 2) aldosterone or 3) activation of receptor by something lese\n\n
hypokalemia cause tachy\nhyperkalemia cause brady \n
acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
acid base balance NEEDED for dx\n-look at:\n1) acid base\n2) urinary electrolytes: k and cl\n3) bp\n
intake not usually effect- but if have other problems will (like if dont have kidney, or low effective blood volume- no filtration, no distal deli ery- no excretion)\n\n\neither extreme situation- ate so much k ( rare)\ndont have kidney (kidney failure) - most common\nhave kidney but fail bc of low ebv - most common\nor hypoaldosteronism (rare)\nsome drugs that block raas axis and cause low aldost - most common\n\n\nhigh k in lab- not really higjh k in blood\n- lab problem (hemolysis)\n.......\n\nmetabolic acidosis- shift of k from inside cells to outside\n\n
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heparin suppress aldost secretion from adrenal gland\n
pts on dialysis shoulndt eat these\n
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not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
not respond to dieretics, or kaexalate, or shit frombeta agonist.... = dialysis\n
high pco2 \nhigh hco3\nhypokalemic\n\nhypokal\nalkylotic\nlow bp/normal bp\n\ngastric tube- doesnt absorb anything from the gastric outlet to the gut (similar to idea of vomitting)\n- metabolic alkalosis, kidney try to get rid of bicarb- non-absorb anion- high distal delivery- increased excretion of k\n\n- high urinary k\n- low urinary cl\n\n
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high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n
high ph\n\nmetabolic alkalosis\n\nyoung woman, wants to lose weight\ndiuretics or laxative or throws up\n\nlaxatives: prob not diarrhea- bc met alkalosis- so prob not laxatives (and would k to be low in urine- bc lose via GIT and not kidney)\nvomitting: prob not, bc cl hould be low in urine\ndiuretic: met alk, high k in urine, high cl in urine = gittleman, diuretics, (not barter, not mg- bc mg normal (not low)\n\nlook for diuretics in the urine\n\n\n\n\n\n