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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.
 

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could you please explain the mechanism of low K in HHNKC?
It is believed that the main cause of increased serum Potassium level in diabetic ketoacidosis is the acidosis that shifts the K to the ECF.
Since we rarely have acidosis in hyperosmolar hyperglycemic non ketotic coma then the serum Potassium level truly reflects the body store of Potassium (which is depleted because of the diuresis) therefore you always have hypokalemia in HHNKC and it's usually safe to start Potassium supplementation right away in the treatment.
In DKA, you have to be careful. Because you may have increased ECF K level and giving K before shifting it back to the cells (via insulin) may further increase the hyperkalemia endangering cardiac myocytes functioning.
 

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Why acidosis is absent in HHS ??!

Why don't we have acidosis in the non ketotic coma?
"The absence of acidosis in HHS is not completely understood. Presumably, the insulin deficiency is only relative and less severe than in DKA. Lower levels of counter regulatory hormones and free fatty acids have been found in HHS than in DKA insome studies. It is also possible that the liver is less capable of ketone body synthesis or that the insulin/glucagon ratio does not favor ketogenesis."

HARRISON'S PRINCIPLES OF Internal Medicine
 

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In DKA there is excessive H+ in the body as acidosis , so body wants to compensate this acidosis in exchange of K+, by efflux of K+ and influx of H+ in cell causes thru H+-K+ pump causes hyperkalamia in DKA .....
Function of insulin is to transport K+ inside the cell , so in treatment of DKA insulin should be used cautiously and K+ level should be monitored closely as insulin dose in DKA Rx may cause sudden hypokalamia , which may cause life threatening arrythmia ........
DKA = hyperkalamia
DKA Rx = hypokalamia ( may cause) due to exogenous insulin
 

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why hyperosmolar coma isvnot associated with acidosis

hyperosmolar coma is generally associated with type2 DM .. that is there is insulin resistance... in type1 there is insulin deficiency.. hence in type1 insulin deficiency low insulin leads to low activity of acetyl coa carboxylase hence low malonyl coA.. malonylcoA causes turning off of the enzyme carnitine acyl transferase CAT1..here there is low malonylcoA hence high activity of CAT1...This CAT1 catalyses the transfer of acyl groups from coA to carnitine and this is the main step in ketone formation..,thus ketones r formed.. acetone,acetoacetic acid and beta hydroxy butyric acic.. these causes acidosis

in type2 DM there is no insulin deficiency so all this doesn't happen and ketones are not formed...there is only relative insulin deficiency caused due to concomitant illnesses like sepsis or myocardial infarction etc. but insulin levels r enuf to suppress lipolysis n ketone formation prevention. hence the problem is hyperosmolarity and this leads to polyuria /dipsia n leads to loss of electrolytes in urine and dehydration///
 

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k+

k+ in DKA depends.. we shud assign treatment on the basis of serum k+... serum k+ cud be normal or increased.. increased becoz of insulin deficiency leading to extracellular shift of k+.. but becoz k+ is lost in urine the total k+ shud be low but serum k+ cud be high or normal..

hence we shud monitor the serum k+ n administer it along with the iv fluid infusion..
replacement of k+ generally is not necessary.. it again depends on levels... if k+ is more than 5meq its not necessary... if it is b/w 3.5 to 5 administer k+ along with the iv fluid infusion 20 to 30 millimoles administered along with the iv fluid infusion..if less than 3mmol then give abt 40mmol k+ in the iv fluid infusion...
always monitor serum k+ and ecg if necessary...target k+ shud be b/w 4 to 5mmol...
and k+ supplementation is always done in the second step of management and not first 2 to 3 hours..its given only after 4 hours in generals after the vitals of the patient are stabilized
 

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great

This is the best discussion I've ever seen in a usmle forum so far. You guys are terrific, I love like this website.
Keep it up :happy:
 

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HHNKC is also having K shift out of the cell

It is believed that the main cause of increased serum Potassium level in diabetic ketoacidosis is the acidosis that shifts the K to the ECF.
Since we rarely have acidosis in hyperosmolar hyperglycemic non ketotic coma then the serum Potassium level truly reflects the body store of Potassium (which is depleted because of the diuresis) therefore you always have hypokalemia in HHNKC and it's usually safe to start Potassium supplementation right away in the treatment.
In DKA, you have to be careful. Because you may have increased ECF K level and giving K before shifting it back to the cells (via insulin) may further increase the hyperkalemia endangering cardiac myocytes functioning.
The potassium level in HHS (hyperglycemic hyperosmolar state) is also falsely high. This is because the hyperosmolar state promotes water movement out of the cell into the ECF, this water movement may pull potassium ions with it; a phenomenon called (solvent drag). Moreover, you also have a state of insulin deficiency in HHNKC which also promotes the shift of K from ICF to the ECF.
So like DKA, in HHNKC we should also be careful.
 

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The potassium level in HHS (hyperglycemic hyperosmolar state) is also falsely high. This is because the hyperosmolar state promotes water movement out of the cell into the ECF, this water movement may pull potassium ions with it; a phenomenon called (solvent drag). Moreover, you also have a state of insulin deficiency in HHNKC which also promotes the shift of K from ICF to the ECF.
So like DKA, in HHNKC we should also be careful.
You are right, but it seems that the effect of acidosis is stronger than the factors mentioned that's why K is always recommended in HHNKA but not always recommended in in DKA.
 
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