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Aldosterone In Dka

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The Renin Angiotensin Aldosterone Reflex

We are going to talk about the homeostatic reflex mentioned as the following things in a textbook: renin-angiotensin system (RAS) renin-angiotensin-aldosterone system (RAAS) renin-angiotensin-aldosterone pathway (RAA pathway) Don’t let these words scare you! We’re going to follow a pattern here. Renin leads to Angiotensin being released which eventually leads to Aldosterone being released. We’re going to explain all that in detail. We begin with the kidney. The kidney is an endocrine gland (since it secretes several hormones) and it excretes two hormones we are going to learn about: renin (renal means kidney) and erythropoietin (brand name Procrit). The cells that secrete renin are called Juxtaglomerular (J-G) cells. Three triggers that cause JG cells to secrete Renin into the blood stream: A drop in blood pressure, A decrease in blood sodium levels, An increase in blood potassium levels. That triggers this hormonal homeostatic reflex. A homeostatic reflex is there to compensate or correct for a stress. Examples of homeostatic reflexes: The RAA pathway ensures that it will correct for all three of these triggers. It makes this a very important reflex because it controls your 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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