(pdf) Factors Precipitating Hypokalemia In Diabetic Patients: A Cross Sectional Study
Factors Precipitating Hypokalemia in Diabetic Patients: A Cross Sectional Study.pdf Background: Hypokalemia is a very common electrolyte imbalance in diabetic patients which leads to substantial morbidity and mortality. Severe hypokalemia is associated with life- threatening arrhythmias and sudden cardiac death. There are no adequate studies regarding the incidence and factors precipitating hypokalemia in Bangladeshi diabetic subjects. Objective: The objective of this study was to find out the factors precipitaing hypokalemia in diabetic patients. Materials and Methods: A total 95 admitted diabetic patients with hypokalemia were studied. Specimens were collected from all adult diabetic patients with serum potassium level <3.5 mmol/L irrespective of cause of admission. Informations were obtained in a semistructured data collection form and analyzed. Results: Most of the subjects (61.1%) belonged to the age group of 60 years and above, 31.5% to the age group 4059 years and 7.4% belonged to the age group of 2039 years. Sixty one (64.2%) patients were females and 34 (35.8%) were males. In 63.2% cases, vomiting was found as a factor causing hypokalemia in the diabetic patients. Other common factors precipitaing hypokalemia were diarrhea (42.1%), inadequate diet (9.5%), severe hyperglycemia (3,2%), diabetic ketoacidosis (6.3%) and drugs especially diuretics (18.9%), bronchodilators (6.3%) and steroids (5.3%). The commonest comorbidity associated with diabetes was hypertension. Conclusion: In this study the commonest precipitating factor causing hypokalemia was vomiting. Majority of hypokalemic patients were female and of older age group. When hypokalemia is identified, the underlying precipitating factor should be sought and the disorder treated. Diuretics should be used wit Continue reading >>
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Causes Of Hypokalemia In Adults
INTRODUCTION Hypokalemia is a common clinical problem. Potassium enters the body via oral intake or intravenous infusion, is largely stored in the cells, and then excreted in the urine. Thus, decreased intake, increased translocation into the cells, or, most often, increased losses in the urine, gastrointestinal tract, or sweat can lead to a reduction in the serum potassium concentration (table 1). This topic will review the major causes of hypokalemia. The evaluation and treatment of hypokalemia are discussed separately. (See "Evaluation of the adult patient with hypokalemia" and "Clinical manifestations and treatment of hypokalemia in adults".) DECREASED POTASSIUM INTAKE Potassium intake is normally 40 to 120 mEq per day, most of which is then excreted in the urine. The kidney is able to lower potassium excretion to a minimum of 5 to 25 mEq per day in the presence of potassium depletion . Thus, decreased intake alone rarely causes significant hypokalemia. This was demonstrated in a study of normal individuals in whom lowering potassium intake to 20 mEq per day was associated with a reduction in serum potassium from 4.1 mEq/L at baseline to 3.5 mEq/L . However, a low potassium intake can contribute to the severity of potassium depletion when another cause of hypokalemia is superimposed, such as diuretic therapy. INCREASED ENTRY INTO CELLS More than 98 percent of total body potassium is intracellular, chiefly in muscle [3,4]. The normal distribution of potassium between cells and the extracellular fluid is primarily maintained by the Na-K-ATPase pump in the cell membrane [3,4]. Increased activity of the Na-K-ATPase pump and/or alterations in other potassium transport pathways can result in transient hypokalemia due to increased potassium entry into cells. Continue reading >>
Hypokalemia During Treatment Of Diabetic Ketoacidosis: Clinical Evidence For An Aldosterone-like Action Of Insulin - Sciencedirect
Hypokalemia during Treatment of Diabetic Ketoacidosis: Clinical Evidence for an Aldosterone-Like Action of Insulin Get rights and content To investigate whether the development of hypokalemia in patients with diabetic ketoacidosis (DKA) treated in the pediatric critical care unit (PCCU) could be caused by increased potassium (K+) excretion and its association with insulin treatment. In this prospective observational study of patients with DKA admitted to the PCCU, blood and timed urine samples were collected for measurement of sodium (Na+), K+, and creatinine concentrations and for calculations of Na+ and K+ balances. K+ excretion rate was expressed as urine K+-to-creatinine ratio and fractional excretion of K+. Of 31 patients, 25 (81%) developed hypokalemia (plasma K+ concentration <3.5 mmol/L) in the PCCU at a median time of 24 hours after therapy began. At nadir plasma K+ concentration, urine K+-to-creatinine ratio and fractional excretion of K+ were greater in patients who developed hypokalemia compared with those without hypokalemia (19.8 vs 6.7, P = .04; and 31.3% vs 9.4%, P = .004, respectively). Patients in the hypokalemia group received a continuous infusion of intravenous insulin for a longer time (36.5 vs 20 hours, P = .015) and greater amount of Na+ (19.4 vs 12.8 mmol/kg, P = .02). At peak kaliuresis, insulin dose was higher in the hypokalemia group (median 0.07, range 0-0.24 vs median 0.025, range 0-0.05 IU/kg; P = .01), and there was a significant correlation between K+ and Na+ excretion (r = 0.67, P < .0001). Hypokalemia was a delayed complication of DKA treatment in the PCCU, associated with high K+ and Na+ excretion rates and a prolonged infusion of high doses of insulin. Continue reading >>
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Hypokalemia is generally defined as a serum potassium level of less than 3.5 mEq/L (3.5 mmol/L). Moderate hypokalemia is a serum level of 2.5-3.0 mEq/L, and severe hypokalemia is a level of less than 2.5 mEq/L. Hypokalemia is a potentially life-threatening imbalance that may be iatrogenically induced. Hypokalemia may result from inadequate potassium intake, increased potassium excretion, or a shift of potassium from the extracellular to the intracellular space. Increased excretion is the most common mechanism. Poor intake or an intracellular shift by itself is a distinctly uncommon cause, but several causes often are present simultaneously. (See Etiology.) Gitelman syndrome is an autosomal recessive disorder characterized by hypokalemic metabolic alkalosis and low blood pressure. See the image below. Signs and symptoms Patients are often asymptomatic, particularly those with mild hypokalemia. Symptoms that are present are often from the underlying cause of the hypokalemia rather than the hypokalemia itself. The symptoms of hypokalemia are nonspecific and predominantly are related to muscular or cardiac function. Complaints may include the following: Weakness and fatigue (most common) Psychological symptoms (eg, psychosis, delirium, hallucinations, depression) Physical findings are often within the reference range. Abnormal findings may reflect the underlying disorder. Severe hypokalemia may manifest as bradycardia with cardiovascular collapse. Cardiac arrhythmias and acute respiratory failure from muscle paralysis are life-threatening complications that require immediate diagnosis. See Presentation for more detail. Diagnosis In most cases, the cause of hypokalemia is apparent from the history and physical examination. First-line studies include measurement of urine pota Continue reading >>
What Is The Connection Between Diabetes And Potassium?
Usually, your body processes the food you eat and turns it into a sugar called glucose. Your body uses glucose for energy. Insulin is a hormone your pancreas produces. Your body uses the insulin to help move glucose into cells throughout your body. If you have diabetes, your body is unable to produce or use insulin efficiently. Type 1 diabetes isn’t preventable, but you can prevent type 2 diabetes. Type 2 diabetes, or adult-onset diabetes, usually occurs in people ages 35 and older. Potassium is an electrolyte and mineral that helps keep your bodily fluids at the proper level. Your body can do the following if your fluids are in check: contract your muscles without pain keep your heart beating correctly keep your brain functioning at its highest capability If you don’t maintain the right level of potassium, you can experience a variety of symptom that include simple muscle cramps to more serious conditions, such as seizures. According to recent research, there may be a link between type 2 diabetes and low potassium levels. Although people recognize that potassium affects diabetes, research is ongoing to determine why this may happen. Researchers in one study at Johns Hopkins University School of Medicine linked low levels of potassium with high levels of insulin and glucose in people who were otherwise healthy. Low levels of potassium with high levels of insulin and glucose are both traits doctors associate with diabetes. One 2011 study found that people taking thiazides to treat high blood pressure experienced a loss of electrolytes, such as potassium. Researchers noted that this loss might increase a person’s risk of developing diabetes. And along with that, researchers have also linked potassium levels to high blood pressure. Even though low potassium may incre Continue reading >>
Potassium As A Link Between Insulin And The Renin-angiotensin-aldosterone System.
Abstract PURPOSE: To focus on the interactions between insulin secretion, glucose tolerance and insulin sensitivity on the one hand and the renin-angiotensin-aldosterone system on the other. EFFECTS ON INSULIN: Insulin is a potent stimulus for hypokalaemia, sparing body potassium from urinary excretion by transporting it into cells. Potassium also appears to play a key role in the antinatriuretic effect of insulin. Insulin-induced hypokalaemia increases plasma renin and angiotensin II levels while decreasing the serum aldosterone concentration. In turn, the renin-angiotensin-aldosterone system affects glucose tolerance by modulating plasma potassium levels, which act as a stimulus for glucose-induced insulin release. EFFECTS OF ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITION: Interference with the renin-angiotensin-aldosterone system by ACE inhibition blunts the hypokalaemic response to insulin, thereby improving glucose-induced insulin release and oral glucose tolerance. ACE inhibition, however, does not cause major changes in insulin sensitivity. POTASSIUM AND BLOOD PRESSURE: Plasma potassium levels are inversely related to blood pressure, both in population surveys and in intervention studies. In addition, in patients with essential hypertension, the level of plasma potassium appears to predict the blood pressure response to ACE inhibition. SUMMARY: Potassium metabolism is an important link between carbohydrate metabolism and the renin-angiotensin-aldosterone system by way of a double-feedback mechanism. Through the potential effects on blood pressure control, plasma levels of potassium represent a link between insulin and blood pressure in humans. Continue reading >>
Why Doesn't Regular Insulin Therapy Cause Hypokalemia In Patients With Diabetes Mellitus? - Quora
Why doesn't regular insulin therapy cause hypokalemia in patients with diabetes mellitus? aMdy OofybgFyGIBs ANQDwVwumjkcmIZkAsDWDuacvXokTydYhGNQYxwovlz Did you know that unlike searching on DuckDuckGo, when you search on Google, they keep your search history forever? That means ... Originally Answered: Why doesn't regular insulin therapy cause hypokalemia in patient with diabetes mellitus? Hypokalemia is low potassium. Your potassium level is maintained within a range. As part of your electrolytes that move in and out of the cells as needed. Insulin reduces serum K+ from ECF to ICF mainly because insulin increases the activity of the sodium-potassium pump. insulin is the first-line defense against hyperkalemia. a rise in plasma k+ stimulates insulin release by the pancreatic beta cell. insulin, in turn, enhances cellular potassium uptake, returning plasma k+ towards normal. the enhanced cellular uptake of k+ that results from increased insulin levels is thought to be largely... Read More Loading Originally Answered: Why doesn't regular insulin therapy cause hypokalemia in patient with diabetes mellitus? Hypokalemia is low potassium. Your potassium level is maintained within a range. As part of your electrolytes that move in and out of the cells as needed. Insulin reduces serum K+ from ECF to ICF mainly because insulin increases the activity of the sodium-potassium pump. insulin is the first-line defense against hyperkalemia. a rise in plasma k+ stimulates insulin release by the pancreatic beta cell. insulin, in turn, enhances cellular potassium uptake, returning plasma k+ towards normal. the enhanced cellular uptake of k+ that results from increased insulin levels is thought to be largely due to the ability of insulin to stimulate activity of the sodium potassium atpas Continue reading >>
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Diabetes Mellitus And Electrolyte Disorders
Go to: Abstract Diabetic patients frequently develop a constellation of electrolyte disorders. These disturbances are particularly common in decompensated diabetics, especially in the context of diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. These patients are markedly potassium-, magnesium- and phosphate-depleted. Diabetes mellitus (DM) is linked to both hypo- and hyper-natremia reflecting the coexistence of hyperglycemia-related mechanisms, which tend to change serum sodium to opposite directions. The most important causal factor of chronic hyperkalemia in diabetic individuals is the syndrome of hyporeninemic hypoaldosteronism. Impaired renal function, potassium-sparing drugs, hypertonicity and insulin deficiency are also involved in the development of hyperkalemia. This article provides an overview of the electrolyte disturbances occurring in DM and describes the underlying mechanisms. This insight should pave the way for pathophysiology-directed therapy, thus contributing to the avoidance of the several deleterious effects associated with electrolyte disorders and their treatment. Keywords: Glucose, Osmotic diuresis, Hyponatremia, Hyperkalemia, Hypomagnesemia Core tip: Diabetic patients frequently develop a constellation of electrolyte disorders. These patients are often potassium-, magnesium- and phosphate-depleted, especially in the context of diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. Diabetes is linked to both hypo- and hyper-natremia, as well as to chronic hyperkalemia which may be due to hyporeninemic hypoaldosteronism. This article provides an overview of the electrolyte disturbances occurring in diabetes and describes the underlying mechanisms. This insight should pave the way for pathophysiology-direct Continue reading >>
Insulin And Potassium
Insulin has a number of actions on the body besides lowering your blood glucose levels. Insulin suppresses the breakdown and buildup of glycogen, which is the storage form of glucose, it blocks fat metabolism and the release of fatty acids, and it puts potassium into the cells by activating the sodium-potassium cellular channels. Insulin stimulates the uptake of glucose and potassium in all cells of the body but primarily fuels the muscle cells as well as some of the fat cells. In type 2 diabetes or metabolic syndrome (a form of metabolic disease), insulin is not functioning up to its normal level. The cells of the body become resistant to insulin and the blood sugar levels are elevated. The serum potassium (K+) level is a reflection of the total body stores of potassium, although it can be inaccurate in some conditions that affect the distribution of potassium in the body’s cells. The plasma potassium level determines the resting potential of the cells of the body. A person can have low potassium (hypokalemia) or high potassium (hyperkalemia), both of which are asymptomatic conditions that can be serious as they both cause heart arrhythmias. The Relationship between Insulin and Potassium Shortly after insulin was discovered, scientists revealed that insulin had something to do with the potassium levels in both the cells and in the blood. The insulin is the hormone in the body that keeps the potassium level in the blood within the normal range. When insulin is decreased, the potassium level rises and can rise even further if you eat something high in potassium, such as salt substitutes and bananas. When the potassium level is high, it causes the pancreas to release insulin in order to counteract the effects of high potassium levels. When you eat something that is high Continue reading >>
Hypokalemia & Diabetes
According to a 2011 national diabetes fact sheet from the Centers for Disease Control and Prevention, over 25 million people, or 8.3 percent of the United States population, have diabetes. Diabetes is the condition that results from the lack of insulin production or from insulin resistance; in diabetes, there is abnormal metabolism of glucose, which results in elevated blood glucose levels. Diabetes is associated with dysregulation of potassium, but several studies suggest that hypokalemia may mediate the development of diabetes. Video of the Day According to "Davidson's Principles & Practice of Medicine," hypokalemia, or low blood potassium, is defined as blood potassium levels below 3.5 millimoles per liter, or mmol/L, of blood. Potassium facilitates the function of insulin in the delivery of glucose to cells; when insulin binds to its receptors on the cell membrane, it causes potassium to flow into the cells. As levels of insulin increase in the blood, more potassium is driven into cells; therefore, hyperinsulinemia, or high blood insulin, is commonly associated with hypokalemia. Hypokalemia and Diabetes Studies Since a clear relationship exists between insulin and potassium, researchers have speculated the possibility of potassium's involvement in the development of diabetes. According to a 2008 article in the journal "Hypertension," several studies have collectively demonstrated a strong inverse relationship between blood glucose levels and potassium levels during the use of thiazides diuretics; therefore, as potassium levels decrease, blood glucose levels should increase. This inverse relationship between glucose and potassium, concurs with the notion that total body potassium has a role in determining person's sensitivity to insulin. In diabetics, excessive use o Continue reading >>
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Hyperkalemia (high Blood Potassium)
How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>
Physiologic Effects Of Insulin
Stand on a streetcorner and ask people if they know what insulin is, and many will reply, "Doesn't it have something to do with blood sugar?" Indeed, that is correct, but such a response is a bit like saying "Mozart? Wasn't he some kind of a musician?" Insulin is a key player in the control of intermediary metabolism, and the big picture is that it organizes the use of fuels for either storage or oxidation. Through these activities, insulin has profound effects on both carbohydrate and lipid metabolism, and significant influences on protein and mineral metabolism. Consequently, derangements in insulin signalling have widespread and devastating effects on many organs and tissues. The Insulin Receptor and Mechanism of Action Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane. The insulin receptor is a tyrosine kinase. In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor. The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response. Several intracellular proteins have been identified as phosphorylation substrates for the insulin receptor, the best-studied of which is insulin receptor substrate 1 or IRS-1. When IRS-1 is activa Continue reading >>
What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?
What causes potassium and sodium loss in diabetic ketoacidosis (DKA)? Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. This loss is not mirrored in serum potassium levels, which may be low, within the reference range, or even high. Potassium loss is caused by a shift of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis. Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis. Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia. Sodium also is lost in the urine during the osmotic diuresis. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5 Continue reading >>
Hypokalemia: Video, Anatomy, Definition & Function | Osmosis
Rishi Desai, MD, MPH , Tanner Marshall, MS , Tanner Marshall, MS , Jake Ryan , Tanner Marshall, MS With hypokalemia, hypo- means under and -kal- refers to potassium, and -emia refers to the blood, so hypokalemia means lower than normal potassium levels in the blood, generally under 3.5 mEq/L. Now, total body potassium can essentially be split into two componentsintracellular and extracellular potassium, or potassium inside and outside cells, respectively. The extracellular component includes both the intravascular space, which is the space within the blood and lymphatic vessels and the interstitial spacethe space between cells where you typically find fibrous proteins and long chains of carbohydrates which are called glycosaminoglycans. Now, the vast majority, around 98%, of all of the bodys potassium is intracellular, or inside of the cells. In fact, the concentration of potassium inside the cells is about 150 mEq/L whereas outside the cells its only about 4.5 mEq/L. Keep in mind that these potassium ions carry a charge, so the difference in concentration also leads to a difference in charge, which establishes an overall electrochemical gradient across the cell membrane . And this is called the internal potassium balance. This balance is maintained by the sodium-potassium pump, which pumps 2 potassium ions in for every 3 sodium ions out, as well as potassium leak channels and inward rectifier channels that are scattered throughout the membrane. This concentration gradient is extremely important for setting the resting membrane potential of excitable cell membranes, which is needed for normal contraction of smooth, cardiac, and skeletal muscle . Also, though, in addition to this internal potassium balance, theres also an external potassium balance, which refers to the Continue reading >>
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes. DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>