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in NIDDM how the ketoacidosis occur?
any ideas?
good luck.


Fat use ...HMG-CoA path... AcetoAcetylCoA...


Ketacidosis usually occurs in Type I since there is enough insulin in Type II to prevent ketoacidosis
The ketones occur from increased oxidation of fatty acids
Also I "think" since potassium and phosphate are lost in the urine more H ion is absorbed.


agrre with u mjl1717.
ketones i understand why they occur but stil thinking on your answer for acidosis.
thanx for reply.


Yes santa clara, that last sentence concerning K and H ion exchange was strictly attempted extrapolation and "trying" to put it a together with renal physio :oops:




pls read this and i read it on one web site.

and after that tell me also how it happened. i m also trying to undestand.

The absence of insulin, the primary anabolic hormone, means that tissues such as muscle, fat, and liver do not take up glucose. Counterregulatory hormones, such as glucagon, growth hormone, and catecholamines, enhance triglyceride breakdown into free fatty acids and gluconeogenesis, which is the main cause for the elevation in serum glucose in DKA. Beta-oxidation of these free fatty acids leads to increased formation of ketone bodies. Overall, metabolism in DKA shifts from the normal fed state characterized by carbohydrate metabolism to a fasting state characterized by fat metabolism.

Secondary consequences of the primary metabolic derangements in DKA include an ensuing metabolic acidosis as the ketone bodies produced by beta-oxidation of free fatty acids deplete extracellular and cellular acid buffers. The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, and water as well as ketones and glucose. Commonly, the total body water deficit is 10%, and the potassium deficit is 5 mEq per kg of body weight. The total body potassium deficit may be masked by the acidosis, which sustains an increased serum potassium level. The potassium level can drop precipitously once rehydration and insulin treatment start. Urinary loss of ketoanions with brisk diuresis and intact renal function also may lead to a component of hyperchloremic metabolic acidosis


This is my interpertation:
In DKA the counterregulatory hormones enhance fatty acid metabolism and gluconeogenesis*
*Ketones produced by beta oxidation of FFA deplete buffers.
*Also Hyperglycemia induced osmotic diuresis depletes Na, K ,PO4, H20,
ketones and glucose.

The total body K deficit may be masked by acidosis which sustains an increase in serum K.
The K level can drop once rehydration and insulin Rx is started.

Urinary loss of ketoanions with brief diuresis and intact renal function also may lead to a componet of hyperchloremic metabolic acidosis

Key words for IDDM are: nonenzymatic glycosylation
osmotic damage

Key words for DKA are: ketones that eventually deplete buffers
ketones produced by beta oxidation of FFA
*Gluconeogenesis-hyperglycemia thru osmotic
diuresis also depletes buffers ions, ketones,etc
**Total body K deficit can be masked by hyperkalemic metabolic acidosis
which sustains an increase in serum K!

Santaclara that was a good tutorial- I think many will get something out of that. :idea:


i agree with ur post above sataclara. Acidosis is due to exces production of organic acids (ie ketone bodies)


thanx mjl1717.
godd luck for exams.


in type I DM> decreased glucose utilization, hyperglycemi, increased fattyacid oxidation
1)Increased fatty acid oxidation leads toexcessive production of ketone bodys >KETOACIDOSIS
2)Acetoacetic and 3-hydroxybutyric acids DISSOCIATES at body pH and release H+ >METABOLIC ACIDOSIS

Combinationof them is called KETOACIDOSIS


The main substance that cuse DKA in type 1 and not 2 is malonyl coA

type 1 no insunline-->dec Malonyl COA -->enhance FA oxidation-->DKA

type 2 insuline-->increased Mal coA--->inc FA synthesis, and decreased oxidation----> no DKA

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