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Treat Hyperkalemia In Dka

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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 A Young Woman With Type 1 Diabetes Mellitus

A 32-year-old woman with multiple medical problems was brought to the emergency department with lethargy and weakness. The family noted progressive confusion and fatigue over 2 days, coupled with extreme weakness. The patient and family denied all other complaints as well as any traumatic or toxicologic events. The medical history included juvenile-onset diabetes mellitus, hypertension, renal insufficiency, and diabetic retinopathy with visual impairment; the patient used insulin and lisinopril as well as several other unknown medications. On examination, she was confused and lethargic but was aroused by stimuli and spoke coherently. Vital signs were: blood pressure, 188/106 mmHg; pulse, approximately 70 beats/min; respiratory rate, 24 breaths/min; temperature, 36.1°C (97°F); and oxygen saturation, 94% on room air; the ECG monitor demonstrated the rhythm strip in Figure 1. A bedside glucose test was 256 mg/dL. The remainder of the examination was unremarkable. Results of a 12-lead ECG are seen in Figure 2. Based upon the ECG findings noted in Figures 1 and 2, which of the following best describe the patient’s risk of an adverse event and the most appropriate management: A. Low 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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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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Popular Questions

  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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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]

Diabetic Ketoacidosis-induced Hyperkalemia

Abstract We report the biochemical data of 22 hospital admissions because of untreated diabetic ketoacidosis. Fifty percent of admitted patients showed an initial serum potassium between 4.6 and 6.0 mEq/1 whereas severe hyperkalemia (value>6.1 mEq/l) occurred in 32%. Initial potassium levels show a slight negative correlation with pH but a stronger correlation (p<0.001) was found between the initial serum potassium and glucose values. We suggest that hyperglycemia due to insulinopenia must be one of the factors in the pathogenesis of this hyperkalemia. Preview Unable to display preview. Download preview PDF. 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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