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Why Do You Have Hyperkalemia In Diabetic Ketoacidosis?

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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

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin Continue reading >>

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  1. hippocampus

    What are the potassium level abnormalities associated with DKA (during diagnosis and treatment.)

  2. ahassan

    During DKA, the total body K is low bcz of osmotic diuresis, BUT the serum k conc. is raised bcz of the lack of insulin action, which allows k to shift out of the cells. So hyperkalemia.
    During treatment, k is shifted into the cells, which may lead to profound hypokalemia n death if not treated, so during therapy you have to adjust KCL conc. depending on blood K levels.

  3. tomymajor

    In DKA--> K level may be high or normal so we dont add k from the start of ttt
    But : In HHNKC---> K level is low from the start so we give k from start of ttt

  4. -> Continue reading
read more
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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.

Abstract 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 less than 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/l, significantly higher than among the women, 5.09 mmol/l (p less than 0.005). Twelve of the 16 patients with serum K+ greater than or equal to 6.5 mmol/l were men, as were all eight patients with serum K+ greater than or equal to 7.0 mmol/l. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/l) than the women (11.2 mmol/l, p less than 0.01). The greater tendency to hyperkal Continue reading >>

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Popular Questions

  1. hippocampus

    What are the potassium level abnormalities associated with DKA (during diagnosis and treatment.)

  2. ahassan

    During DKA, the total body K is low bcz of osmotic diuresis, BUT the serum k conc. is raised bcz of the lack of insulin action, which allows k to shift out of the cells. So hyperkalemia.
    During treatment, k is shifted into the cells, which may lead to profound hypokalemia n death if not treated, so during therapy you have to adjust KCL conc. depending on blood K levels.

  3. tomymajor

    In DKA--> K level may be high or normal so we dont add k from the start of ttt
    But : In HHNKC---> K level is low from the start so we give k from start of ttt

  4. -> Continue reading
read more
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This animated video presentation is about potassium regulation and the pathophsyiology of hyperkalemia to make it easy to follow and understand the causes and the management of Hyperkalemia. email : [email protected]

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Lack of insulin, thus no proper metabolism of glucose, ketones form, pH goes down, H+ concentration rises, our body tries to compensate by exchanging K+ from inside the cells for H+ outside the cells, hoping to lower H+ concentration, but at the same time elevating serum potassium. Most people are seriously dehydrated, so are in acute kidney failure, thus the kidneys aren’t able to excrete the excess of potassium from the blood, compounding the problem. On the other hand, many in reality are severely potassium depleted, so once lots of fluid so rehydration and a little insulin is administered serum potassium will plummet, so needs to be monitored 2 hourly - along with glucose, sodium and kidney function - to prevent severe hypokalemia causing fatal arrhythmias, like we experienced decades ago when this wasn’t so well understood yet. In practice, once the patient started peeing again, we started adding potassium chloride to our infusion fluids, the surplus potassium would be peed out by our kidneys so no risk for hyperkalemia. Continue reading >>

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Popular Questions

  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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