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While you will have a high serum potassium, your total body potassium will be low due to very low intracellular potassium (which is where the majority of the body's potassium is usually).
This is why you give potassium to patients with DKA
Why do you not get an increased bicarbonate concentration?
Bicarb acts as a buffer and binds up excess H+ in DKA
In other words, DKA a is a cause of metabolic acidosis. Hallmark of MA is low bicarb.
Also INsulIN shifts K+ INto cells. Insulin is used as a treatment for hyperkalemia. This person has DKA thus low Insulin so shes expected to have hyperkalemia because insulin isn't shiting K+ into cells. Theres also the DKA acidosis too.
I know Insulin cause shift K+ into cells due to closing of ATP-sensitive K channels (blocking K from leaving)? Does it increase K in the cells by another mechanism?
@dentist - Insulin stimulates the Na+-K+-ATPase pump, this drives K+ into the cell (Source: Amboss)
Another mechansim = acidosis causes hyperkalemia due to H+/K+ antiporters. H+ is high in blood so shifts into cells via this antiporter, which shifts K+ out. --potassium section of acid/base chapter in Costanzo physiology
super high blood glucose; super high glucose spillage into urine; lots of peeing = volume depleted (“osmotic diuresis”)
because insulin normally stimulates Na/K ATPase, which sequesters K inside cell. lack of insulin means that there will be more K outside of the cell causing hyperkalemia. however, you are still total body K depleted due to osmotic diuresis. so the hyperkalemia is mainly due to a shift of K from the intracellular (where the vast majority of your K is inside your body is) to the extracellular space.
*where the vast majority of your K is inside your body
Nevermind, thought about this more: DKA causes an anion gap acidosis (hence normal chloride and elevated keto-anions).