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Diabetes Hypokalemia

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Hypokalemia & Diabetes

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 >>

Factors Precipitating Hypokalemia In Diabetic Patients: A Cross Sectional Study

Factors Precipitating Hypokalemia In Diabetic Patients: A Cross Sectional Study

Bangladesh Journals OnLine (BanglaJOL) is a service to provide access to Bangladesh published research, and increase worldwide knowledge of indigenous scholarship. Read more . Professor, Department of Medicine, Bangladesh Institute of Health Sciences (BIHS) & Hospital, Dhaka Consultant, Department of Endocrinology, BIHS & Hospital, Dhaka Registrar, Department of Medicine, BIHS & Hospital, Dhaka Medical Officer, Department of Medicine, BIHS & Hospital, Dhaka Professor, Department of Biochemistry, Enam Medical College, Savar, Dhaka Factors Precipitating Hypokalemia in Diabetic Patients: A Cross Sectional Study Sheikh Salahuddin Ahmed, Fazle Nur, Md Rahamat Ullah, Abdullah Al Mamun, Md Aminul Haque Khan Background: Hypokalemia is a very common electrolyte imbalance in diabetic patients which leads to substantial morbidity and mortality. Severe hypokalemia is associated with lifethreatening 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 di Continue reading >>

Nephrogenic Diabetes And Hypokalemia

Nephrogenic Diabetes And Hypokalemia

SDN members see fewer ads and full resolution images. Join our non-profit community! Does anyone know how a decrease in potassium can cause nephrogenic diabetes insipidus? Does anyone know how a decrease in potassium can cause nephrogenic diabetes insipidus? decr aldosterone secondary to hypokalemia, but to the extent of diabetes insipidus...? It's because of decreased responsiveness of the collecting tubules to ADH, which is possibly due to decreased aquaporin 2 expression and/or decreased activity of the Na-K-Cl pump in the TAL (which would diminish the corticopapillary gradient necessary for free water absorption). The entire mechanism is not completely understood. I've never heard of hypokalaemia directly causing nephrogenic DI. Where did you read that? Are you referring to the 8th edition? Which page? (It's not that I don't believe you. But it's important that I read up on it.) It's because of decreased responsiveness of the collecting tubules to ADH, which is possibly due to decreased aquaporin 2 expression and/or decreased activity of the Na-K-Cl pump in the TAL (which would diminish the corticopapillary gradient necessary for free water absorption). The entire mechanism is not completely understood. You're right about the kidney not being responsive to high levels of ADH but my question is what triggers the release of ADH in the first place? I know that hypokalemic patients eventually develop hypertension (must be a chronic imbalance). I just can't connect the dots... Continue reading >>

Hypokalemia | Diabetes And Endocrinology Institute Of Tampa

Hypokalemia | Diabetes And Endocrinology Institute Of Tampa

Hypokalemia is a serious condition in which the potassium level in a patients blood has become abnormally low, usually due to prescribed diuretics or antibiotics, an underlying illness such as kidney disease, overuse of laxatives or as a complication of diabetes. It is not usually due to a dietary insufficiency, though patients who have had severe diarrhea or vomiting may have lost too much potassium as a result. When hypokalemia is diagnosed via a blood test, your physician may prescribe potassium supplements and will otherwise look to address the underlying illness that caused it. Occasionally, intravenous potassium may be necessary to treat a severe case; otherwise, it may just be a matter of switching you to a potassium-sparing diuretic medication. At Diabetes and Endocrine Institute of Tampa, our specialists are very aware of the signs, symptoms and potential complications of hypokalemia and closely monitor patients who are at high risk of developing this condition. We are a destination resource for the treatment of all manner of metabolic and endocrine disorders and are accepting new patients and referrals, so contact us at 813.615.7620 if we can be of assistance to you or your loved one. Continue reading >>

Hyperkalemia (high Blood Potassium)

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 >>

Autophagic Degradation Of Aquaporin-2 Is An Early Event In Hypokalemia-induced Nephrogenic Diabetes Insipidus

Autophagic Degradation Of Aquaporin-2 Is An Early Event In Hypokalemia-induced Nephrogenic Diabetes Insipidus

Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus Scientific Reports volume 5, Articlenumber:18311 (2015) Hypokalemia (low serum potassium level) is a common electrolyte imbalance that can cause a defect in urinary concentrating ability, i.e., nephrogenic diabetes insipidus (NDI), but the molecular mechanism is unknown. We employed proteomic analysis of inner medullary collecting ducts (IMCD) from rats fed with a potassium-free diet for 1 day. IMCD protein quantification was performed by mass spectrometry using a label-free methodology. A total of 131 proteins, including the water channel AQP2, exhibited significant changes in abundance, most of which were decreased. Bioinformatic analysis revealed that many of the down-regulated proteins were associated with the biological processes of generation of precursor metabolites and energy, actin cytoskeleton organization, and cell-cell adhesion. Targeted LC-MS/MS and immunoblotting studies further confirmed the down regulation of 18 selected proteins. Electron microscopy showed autophagosomes/autophagolysosomes in the IMCD cells of rats deprived of potassium for only 1 day. An increased number of autophagosomes was also confirmed by immunofluorescence, demonstrating co-localization of LC3 and Lamp1 with AQP2 and several other down-regulated proteins in IMCD cells. AQP2 was also detected in autophagosomes in IMCD cells of potassium-deprived rats by immunogold electron microscopy. Thus, enhanced autophagic degradation of proteins, most notably including AQP2, is an early event in hypokalemia-induced NDI. Hypokalemia (low serum potassium level) is a very common electrolyte imbalance encountered in clinical medicine, occurring as a result of poor nutritional status, gas Continue reading >>

Hypokalemia | Diabetes Forum The Global Diabetes Community

Hypokalemia | Diabetes Forum The Global Diabetes Community

Diabetes Forum The Global Diabetes Community Find support, ask questions and share your experiences. Join the community I was 1.5 for the hypokalemia which apparently is life threatening I was in hospital on couple of different drips? I'm wondering tho once you get your numbers back to a safe place is this likely to happen again? It was pretty scary and my heart felt like it was going to explode. If you are having a hypo then adrenaline released in response to the hypo, and excess insulin in situ which caused the hypo, can stimulate the uptake of potassium from the bloodstream causing hypokalemia. Low potassium is thought to play a part in dead in bed syndrome because it causes long QT waves and cardiac arrhythmia. If you are having a hypo then adrenaline released in response to the hypo, and excess insulin in situ which caused the hypo, can stimulate the uptake of potassium from the bloodstream causing hypokalemia. Low potassium is thought to play a part in dead in bed syndrome because it causes long QT waves and cardiac arrhythmia. Oh really whow ok thank you very much for that. Are some people more prone to getting it tho than others or can it just happen when having a hypo? Off the Coke an working hard now to be healthy It's a roller coaster but I'm being positive about the ride Hope your well and you health is in an ausom place Apparently hypokalemia can be caused by several medications taken by diabetics, and also can occur as a result of a ketogenic diet. My levels of K dropped while i was doing keto,and GP advised a supplement and eating bananas. I had problems with a diuretic I was using, and most of my heart and blood meds were either contraindicated or had the symptoms listed as a side effect. Googling the condition will not show these other med interactions Continue reading >>

Glucose Intolerance With Hypokalemia: Failure Of Short-term Potassium Depletion In Normal Subjects To Reproduce The Glucose And Insulin Abnormalities Of Clinical Hypokalemia

Glucose Intolerance With Hypokalemia: Failure Of Short-term Potassium Depletion In Normal Subjects To Reproduce The Glucose And Insulin Abnormalities Of Clinical Hypokalemia

The mechanism by which potassium deficiency per se impairs glucose tolerance was studied in seven subjects who were potassium depleted experimentally (mean depletion = 326 mEq.). In five subjects studied using the oral glucose tolerance test, all showed impairment during the potassium depletion phase compared to the predepletion control period, and four of five subjects showed improvement with potassium repletion. The four subjects with impaired glucose tolerance compared to both control periods showed a delay in the initial phase of total immunoreactive insulin release. None of the five subjects showed a significant variation in the per cent proinsulin-like component from the potassium depletion phase to either control period. Two subjects studied using the intravenous glucose tolerance test showed no impairment of glucose tolerance with potassium depletion, and no evidence of insulin resistance was found following the injection of 0.05 U. per kilogram of insulin. These two subjects did manifest impaired growth hormone responses to the hypoglycemic stimulus, however. Potassium depletion per se impairs glucose tolerance. The defect is mild; severe glucose intolerance, alterations in total immunoreactive insulin, and plasma insulin components seen in clinical hypokalemic states involve a complex interplay between potassium deficiency and the primary disease state. Continue reading >>

Hypokalemia

Hypokalemia

Hypokalemia, also spelled hypokalaemia, is a low level of potassium (K+) in the blood serum.[1] Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels below 3.5 mmol/L defined as hypokalemia.[1][2] Mildly low levels do not typically cause symptoms.[3] Symptoms may include feeling tired, leg cramps, weakness, and constipation.[1] It increases the risk of an abnormal heart rhythm, which are often too slow, and can cause cardiac arrest.[1][3] Causes of hypokalemia include diarrhea, medications like furosemide and steroids, dialysis, diabetes insipidus, hyperaldosteronism, hypomagnesemia, and not enough intake in the diet.[1] It is classified as severe when levels are less than 2.5 mmol/L.[1] Low levels can also be detected on an electrocardiogram (ECG).[1] Hyperkalemia refers to a high level of potassium in the blood serum.[1] The speed at which potassium should be replaced depends on whether or not there are symptoms or ECG changes.[1] Mildly low levels can be managed with changes in the diet.[3] Potassium supplements can be either taken by mouth or intravenously.[3] If given by intravenous, generally less than 20 mmol are given over an hour.[1] High concentration solutions (>40 mmol/L) should be given in a central line if possible.[3] Magnesium replacement may also be required.[1] Hypokalemia is one of the most common water–electrolyte imbalances.[4] It affects about 20% of people admitted to hospital.[4] The word "hypokalemia" is from hypo- means "under"; kalium meaning potassium, and -emia means "condition of the blood".[5] Play media Video explanation Signs and symptoms[edit] Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure,[6] and can provoke the development of an abnormal heart rhythm. Se Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Diabetes Mellitus And Electrolyte Disorders

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 >>

Bartter's Syndrome With Type 2 Diabetes Mellitus - Sciencedirect

Bartter's Syndrome With Type 2 Diabetes Mellitus - Sciencedirect

Volume 72, Issue 2 , February 2009, Pages 88-90 Bartter's Syndrome with Type 2 Diabetes Mellitus Author links open overlay panel Ting-TingSeea Siu-PakLeeb We report a rare case of Bartter's syndrome in a 35-year-old woman with type 2 diabetes mellitus. The patient presented with leg weakness, fatigue, polyuria and polydipsia. Hypokalemia, metabolic alkalosis, and high renin and aldosterone concentrations were present, but the patient was normotensive. Gitelman's syndrome was excluded because of the presence of hypercalciuria, secondary hyperparathyroidism and bilateral nephrocalcinosis. The patient's condition improved upon administration of a prostaglandin synthetase inhibitor (acemetacin), oral potassium chloride and potassium-sparing diuretics. Five months later, the patient discontinued acemetacin because of epigastric discomfort; at the same time, severe hypokalemia and hyperglycemia developed. Glucagon stimulation and water deprivation tests were performed. Type 2 diabetes mellitus with nephrogenic diabetes insipidus was diagnosed. To avoid further gastrointestinal complications, the patient was treated with celecoxib, a selective cyclooxygenase 2 inhibitor. This case serves as a reminder that Bartter's syndrome is associated with various metabolic derangements including nephrogenic diabetes insipidus, nephrocalcinosis and diabetes mellitus. When treating Bartter's syndrome, it is also prudent to remember that the long-term use of nonsteroidal anti-inflammatory drugs and potassium-sparing diuretics may result in serious adverse reactions. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>

(pdf) Factors Precipitating Hypokalemia In Diabetic Patients: A Cross Sectional Study

(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 >>

Why Doesn't Regular Insulin Therapy Cause Hypokalemia In Patient With Diabetes Mellitus?

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 atpase located in cell plasma membranes. the insulin induced cellular uptake of potassium is not dependent on the uptake of glucose caused by insulin. insulin deficiency allows a mild rise in plasma k+ chronically and makes the subject to severe hyperkalemia if a potassium load is given. conversely, potassium deficiency may cause decreased insulin release. thus plasma potassium and insulin participate in a feedback control mechanism. Continue reading >>

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