Diabetes biochemistry

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ddw2013

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A 10-year-old boy is brought to the emergency department because of vomiting for 6 hours. He has had excessive
thirst and excretion of large amounts of urine for 3 weeks. His pulse is 120/min, and respirations are 32/min.
Physical examination shows sunken eyes and diminished skin turgor. Serum studies show hyperglycemia, ketosis,
and metabolic acidosis. Urine studies show glucose and ketones. Which of the following sets of hepatic findings is
most likely in this patient?
Phosphoprotein
Protein Kinase A Phosphatase cAMP
(A) ↑ ↑ ↓
(B) ↑ ↓ ↑
(C) ↑ ↓ ↓
(D) ↓ ↑ ↑
(E) ↓ ↓ ↑
(F) ↓ ↓ ↓
I understand phosphatase should decrease.
Why PKA and cAMP are increased? Is this because of epinephrine's effect?
In type 1 DM, the glucagon should decrease (? I am not sure). Glucagon activates PKA-cAMP. So even there is more epinephrine, the PKA-cAMP may still be normal.
 
Diabetic ketoacidosis is basically a starvation response that has gone off the tracks without the inhibitory effects of insulin, so glucagon should be elevated as well as its downstream signaling constituents.
 
A 10-year-old boy is brought to the emergency department because of vomiting for 6 hours. He has had excessive
thirst and excretion of large amounts of urine for 3 weeks. His pulse is 120/min, and respirations are 32/min.
Physical examination shows sunken eyes and diminished skin turgor. Serum studies show hyperglycemia, ketosis,
and metabolic acidosis. Urine studies show glucose and ketones. Which of the following sets of hepatic findings is
most likely in this patient?
Phosphoprotein
Protein Kinase A Phosphatase cAMP
(A) ↑ ↑ ↓
(B) ↑ ↓ ↑
(C) ↑ ↓ ↓
(D) ↓ ↑ ↑
(E) ↓ ↓ ↑
(F) ↓ ↓ ↓
I understand phosphatase should decrease.
Why PKA and cAMP are increased? Is this because of epinephrine's effect?
In type 1 DM, the glucagon should decrease (? I am not sure). Glucagon activates PKA-cAMP. So even there is more epinephrine, the PKA-cAMP may still be normal.
Which q bank is this question from?
 
Anyone else find it interesting that glucagon isn't released when a diabetic is hypoglycemic; but that it does increase during diabetic ketoacidosis when they are hyperglycemic... anybody have a good understanding of why this is??
 
Anyone else find it interesting that glucagon isn't released when a diabetic is hypoglycemic; but that it does increase during diabetic ketoacidosis when they are hyperglycemic... anybody have a good understanding of why this is??
Intracellular glucose =/= serum glucose. DKA hyperglycemia is marked by a shortage of intracellular glucose which leads to decreased energy production. As far as the inside of the cell is concerned, there's no glucose to be found anywhere in the body so it starts pumping out glucagon and stress hormones to break down glycogen and protein stores to increase serum glucose. However, because there is still an insulin shortage, the glucose can't be transported into the cell, so the whole pathway is continually stimulated and further increases the serum glucose concentration.
 
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