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Aldosterone In Dka

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A Renal Mechanism Limiting The Degree Of Potassium Loss In Severely Hyperglycemic Patients

Potassium (K) secretion in the cortical ‘distal nephron’ was assessed in vivo in 29 consecutive patients presenting with diabetic ketoacidosis (DKA) or the hyperglycemic hyperosmolar syndrome (HHS). The only selection criteria applied were that the electrolytes and osmolality be measured in the urine on admission. Five patients with DKA and 3 patients with HHS were reported in detail as plasma aldosterone levels were also measured in these patients on admission. K secretion in the ‘cortical distal nephron’ was assessed by a semiquantitative index, the transtubular K concentration gradient (TTKG). TTKG values less than 6.0, consistent with less than maximal renal K secretion, were found in 28 of 29 patients despite the presence of hyperkalemia and/or stimuli for renin and aldosterone release. Plasma aldosterone levels on admission were very elevated in 4 patients, at the upper end of the usual normal range in 3 and in the low part of the normal range in 1 patient. Treatment with intravenous saline, KC1 and insulin corrected the fluid and electrolyte abnormalities in the plasma over 24–48 h. Concurrently, plasma aldosterone levels fell, but the TTKG rose; this suggests that 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

  4. -> Continue reading
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What is hyperaldosteronism? Hyperaldosteronism is a condition in where the adrenal glands produce too much of the hormone aldosterone. Find more videos at http://osms.it/more. Study better with Osmosis Prime. Retain more of what youre learning, gain a deeper understanding of key concepts, and feel more prepared for your courses and exams. Sign up for a free trial at http://osms.it/more. Subscribe to our Youtube channel at http://osms.it/subscribe. Get early access to our upcoming video releases, practice questions, giveaways and more when you follow us on social: Facebook: http://osms.it/facebook Twitter: http://osms.it/twitter Instagram: http://osms.it/instagram Thank you to our Patreon supporters: Alex Wright Omar Berrios Osmosis's Vision: Empowering the worlds caregivers with the best learning experience possible.

Hyperaldosteronism In Ketoacidosis And In Poorly Controlled Non-ketotic Diabetes

Summary PLASMA aldosterone concentrations were measured in 14 patients in diabetic ketoacidosis and in 20 patients with poorly controlled non-ketotic diabetes, both before treatment and again when metabolic control was achieved. Plasma aldosterone was above normal in 12 of 14 patients in ketoacidosis and there was a highly significant fall in mean plasma aldosterone concentration when metabolic control improved. Plasma aldosterone concentration in ketoacidosis was significantly related to plasma angiotensin //, arterial pH and indirect indices of dehydration. Plasma aldosterone was also above normal before treatment in 7 of 20 patients with poorly controlled non-ketotic diabetes. When metabolic control improved there was a small but significant reduction in mean plasma aldosterone concentration. However, plasma aldosterone and angiotensin were not significantly related in these patients. It is concluded that ketoacidosis is usually associated with marked hyper-aldosteronism. Poorly controlled nonketotic diabetes is sometimes associated with mild aldosterone excess, which may contribute to the potassium wasting associated with poorly controlled diabetes. 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

  4. -> Continue reading
read more
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Please watch: "LEARN HEART SOUNDS IN 20 MINUTES!!!" https://www.youtube.com/watch?v=NrdZh... -~-~~-~~~-~~-~- Watch over 120 hours of Medical Videos at http://www.ftplectures.com Diabetic ketoacidosis is an emergency complication that leads to ketoacidosis, elevated blood glucose and lack of insulin.

Hyperkalaemia

Clinical Cases Causes of HYPERkalaemia Serum potassium levels above the normal range (3.5-5.0 mmol/L) 1) Increased potassium intake (rare) Oral (potassium supplements) IV (transfusion of stored blood, supplement infusions) 2) Increased production Tissue injury Rhabdomyolysis, tumour lysis syndrome Burns, ischaemia, haemolysis Intense physical activity 3) Decreased renal excretion Renal failure (ARF and CRF) Aldosterone (Mineralocorticoid acting on collecting duct to reabsorb Na and excrete K and maintain intravascular volume) Hypoaldosteronism, Addison’s, Chronic active hepatitis Obstructive uropathy 4) Transcellular shift Acidosis: Metabolic acidosis (DKA, mineral acid overdose) HYPERglycaemia Respiratory acidosis 5) Fictitious (Pseudohyperkalaemia) Laboratory error Haemolysis of sample, clenched fist, ischaemic tourniquet Leucocytosis, thrombocytosis 6) Drugs causing hyperkalaemia Transcellular Suxamethonium, Beta blockers, phenylephrine Aldosterone inhibition ACE inhibitors, Angiotensin II blockers Heparin, spironolactone, Beta blockers Increased aldosterone resistance (Trimethoprim, amiloride) Inhibition Na/K/ATPase (Digoxin) Potassium supplements and IV additives (Increase e 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

  4. -> Continue reading
read more

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