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What Causes High Potassium In Dka?

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What is DIABETIC KETOACIDOSIS? What does DIABETIC KETOACIDOSIS mean? DIABETIC KETOACIDOSIS meaning - DIABETIC KETOACIDOSIS definition - DIABETIC KETOACIDOSIS explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... 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. About 4% of people with type 1 diabetes in United Kingdom develop DKA a 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 universally fatal. The risk of death with adequate and timely treatment is currently around 1–4%. Up to 1% of children with DKA develop a complication known as cerebral edema. The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as "Kussmaul respiration"). The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of people; this tends to originate from erosion of the esophagus. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness). On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate.....

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 l Continue reading >>

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  1. nurseprnRN

    The hypokalemia comes when the patient gets treated with insulin, driving the glucose and K+ into the cells. The kidneys can't (and won't) move so much out through urine with the excess glucose to make for hypokalemia.

  2. Esme12

    There can be a brief period of hypoglycemia in the early stages of an elevated blood sugar (polyuria)....but by the time "ketoacidosis" sets in the Serum potassium is elevated but the cellular potassium is depleted (all that shifting that goes on)
    Diabetic ketoacidosis

  3. April2152

    So pretty much what we would observe clinically is hyperkalemia because the osmotic duiresis does not move serum potassium significantly?

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What is KETOACIDOSIS? What does KETOACIDOSIS mean? KETOACIDOSIS meaning - KETOACIDOSIS definition - KETOACIDOSIS explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and ß-hydroxybutyrate. Ketoacidosis is a pathological metabolic state marked by extreme and uncontrolled ketosis. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased. In extreme cases ketoacidosis can be fatal. Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct by-product of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover. Ketosis may also smell, but the odor is usually more subtle due to lower concentrations of acetone. Treatment consists most simply of correcting blood sugar and insulin levels, which will halt ketone production. If the severity of the case warrants more aggressive measures, intravenous sodium bicarbonate infusion can be given to raise blood pH back to an acceptable range. However, serious caution must be exercised with IV sodium bicarbonate to avoid the risk of equally life-threatening hypernatremia. Three common causes of ketoacidosis are alcohol, starvation, and diabetes, resulting in alcoholic ketoacidosis, starvation ketoacidosis, and diabetic ketoacidosis respectively. In diabetic ketoacidosis, a high concentration of ketone bodies is usually accompanied by insulin deficiency, hyperglycemia, and dehydration. Particularly in type 1 diabetics the lack of insulin in the bloodstream prevents glucose absorption, thereby inhibiting the production of oxaloacetate (a crucial molecule for processing Acetyl-CoA, the product of beta-oxidation of fatty acids, in the Krebs cycle) through reduced levels of pyruvate (a byproduct of glycolysis), and can cause unchecked ketone body production (through fatty acid metabolism) potentially leading to dangerous glucose and ketone levels in the blood. Hyperglycemia results in glucose overloading the kidneys and spilling into the urine (transport maximum for glucose is exceeded). Dehydration results following the osmotic movement of water into urine (Osmotic diuresis), exacerbating the acidosis. In alcoholic ketoacidosis, alcohol causes dehydration and blocks the first step of gluconeogenesis by depleting oxaloacetate. The body is unable to synthesize enough glucose to meet its needs, thus creating an energy crisis resulting in fatty acid metabolism, and ketone body formation.

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath od Continue reading >>

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  1. nurseprnRN

    The hypokalemia comes when the patient gets treated with insulin, driving the glucose and K+ into the cells. The kidneys can't (and won't) move so much out through urine with the excess glucose to make for hypokalemia.

  2. Esme12

    There can be a brief period of hypoglycemia in the early stages of an elevated blood sugar (polyuria)....but by the time "ketoacidosis" sets in the Serum potassium is elevated but the cellular potassium is depleted (all that shifting that goes on)
    Diabetic ketoacidosis

  3. April2152

    So pretty much what we would observe clinically is hyperkalemia because the osmotic duiresis does not move serum potassium significantly?

  4. -> Continue reading
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The effect of hyperkalemia on Resting Membrane Potential. 1. Introduction: a. Hyperkalemia: Increased K+ level in the blood Increase extracellular potassium level. b. The Equilibrium potential for K+ is -90 mV. c. The resting membrane potential is maintained by the ion that has the highest conductance through its membrane during resting. In this case, K+ has the highest conductance at rest. Therefore, K+ electrochemical gradient has the most effect the membrane potential. The resting membrane potential tends to move towards K+ equilibrium potential. d. Normally, there are more potassium inside the cell (more intracellular potassium) than they are outside of the cell (less extracellular potassium) e. In this video, I will talk about the resting membrane potential of cardiac myocytes with is around -90mV. The high conductance of K+ through the leak channels in its membrane brings the resting membrane potential towards its equilibrium potential. 1. So on the left is the normal cell. As you can see that there are leak channels on the cell membrane for both Na+ and K+, however, there are much more leak channels K+ than for Na+. Therefore, the conductance for K+ is much greater than for Na+. For this reason, K+ is the main ion that is used to maintain resting membrane potential. a. Under normal condition, resting membrane potential is around -90mV and there are more potassium inside the cell (more intracellular K+) than outside of the cell. K+ is freely moving into and out of the cell through the leak channel to maintain this electrochemical gradient at resting and there are no net movement of the ion into or out of the cell (intra or extracellularly). 2. However, when there is hyperkalemia. An increase level of potassium in the blood, which means that there is an increased level of potassium outside of the cell (extracellularly). Now the chemical gradient for K+ has been changed, and that change cause a change in the resting membrane potential. Since we have disrupted the chemical equilibrium for K+ ion, with more K+ outside the cell the net flow of K+ will be into the cell until a new electrochemical gradient has been established. Thus, there will be more K+ inside the cell. More positive ion inside the cell causes the cell to become less negative (depolarize). Under normal condition, the resting membrane potential of cardiac myocyte is around -90mV. A patient with hyperkalemia, their new resting membrane potential maybe -85mV or -80mV, the cells have been depolarized (less negative) because K+ is trapped inside. ======================= I tried my best to explain these concepts to the best of my knowledge and made it as simple as possible. I hope that you might find them helpful while you are reviewing your materials for your steps! Good luck to you all! ====================== DISCLAIMER: THE AUTHOR DISCLAIMS ANY LIABILITY, LOSS, INJURY, OR DAMAGE INCURRED AS A CONSEQUENCE DIRECTLY OR INDIRECTLY OF THE USE AND APPLICATION OF ANY OF THE CONTENT AND MATERIAL CONTAINED IN THIS VIDEO. ALTHOUGH THE INFORMATION IN THIS VIDEO HAS BEEN CAREFULLY REVIEWED FOR CORRECTNESS, THE AUTHOR CANNOT ACCEPT ANY RESPONSIBILITY FOR ANY ERRORS OR OMISSIONS THAT MAY BE MADE. THE AUTHOR MAKES NO WARRANTY. EXPRESS OR IMPLIED. AS TO THE COMPLETENESS, CURRENCY OR ACCURACY OF THE CONTENTS OF THIS VIDEO. THE INFORMATION CONTAINED IN THIS VIDEO SHOULD NOT BE CONSTRUED AS SPECIFIC INSTRUCTIONS FOR INDIVIDUAL PATIENTS, MANUFACTURER'S PRODUCT INFORMATION AND PACKAGE INSERTS SHOULD BE REVIEWED FOR CURRENT INFORMATION. INCLUDING CONTRAINDICATIONS. DOSAGES. AND PRECAUTIONS. USMLEAID123. This is video is made and uploaded exclusively for USMLEAID123, any reuploading is prohibited and will be reported to Youtube as copyright infringement.

Hyperkalemia In Diabetic Ketoacidosis - Sciencedirect

Volume 299, Issue 3 , March 1990, Pages 164-169 Author links open overlay panel MilfordFulopMD Get rights and content Patients with diabetic ketoacidosis tend to have somewhat elevated serum K+ concentrations despite decreased body K+ content. The hyperkalemia was previously attributed mainly to acidemia. However, recent studies have suggested that organic acidemias (such as that produced by infusing beta-hydroxybutyric acid) may not cause hyperkalemia. To learn which, if any, routinely measured biochemical indices might correlate with the finding of hyperkalemia in diabetic ketoacidosis, we analyzed the initial pre-treatment values in 131 episodes in 91 patients. Serum K+correlated independently and significantly (p < 0.001) with blood pH (r = 0.39), serum urea N (r = 0.38) and the anion gap (r = 0.41). The mean serum K+ among the men was 5.55 mmol/ 1, significantly higher than among the women, 5.09 mmol/1 (p < 0.005). Twelve of the 16 patients with serum K+ 6.5 mmol/1 were men, as were all eight patients with serum K+ 7.0 mmol/1. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/1) than the women (11.2 mmol/1, p < 0.01). Continue reading >>

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  1. metalmd06

    Does acute DKA cause hyperkalemia, or is the potassium normal or low due to osmotic diuresis? I get the acute affect of metabolic acidosis on potassium (K+ shifts from intracellular to extracellular compartments). According to MedEssentials, the initial response (<24 hours) is increased serum potassium. The chronic effect occuring within 24 hours is a compensatory increase in Aldosterone that normalizes or ultimatley decreases the serum K+. Then it says on another page that because of osmotic diuresis, there is K+ wasting with DKA. On top of that, I had a question about a diabetic patient in DKA with signs of hyperkalemia. Needless to say, I'm a bit confused. Any help is appreciated.

  2. FutureDoc4

    I remember this being a tricky point:
    1) DKA leads to a decreased TOTAL body K+ (due to diuresis) (increase urine flow, increase K+ loss)
    2) Like you said, during DKA, acidosis causes an exchange of H+/K+ leading to hyperkalemia.
    So, TOTAL body K+ is low, but the patient presents with hyperkalemia. Why is this important? Give, insulin, pushes the K+ back into the cells and can quickly precipitate hypokalemia and (which we all know is bad). Hope that is helpful.

  3. Cooolguy

    DKA-->Anion gap M. Acidosis-->K+ shift to extracellular component--> hyperkalemia-->symptoms and signs
    DKA--> increased osmoles-->Osmotic diuresis-->loss of K+ in urine-->decreased total body K+ (because more has been seeped from the cells)
    --dont confuse total body K+ with EC K+
    Note: osmotic diuresis also causes polyuria, ketonuria, glycosuria, and loss of Na+ in urine--> Hyponatremia
    DKA tx: Insulin (helps put K+ back into cells), and K+ (to replenish the low total potassium
    Hope it helps

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