Sandbox : anmol: Difference between revisions

Latest revision as of 17:32, 14 January 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2]

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 __NOTOC__
-{{Hyperparathyroidism}}
 {{CMG}}; {{AE}} {{Anmol}}
+==Tables==
+{| class="wikitable"
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+!Diagnosis
+!Lab findings
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-=Pathophysiology=
-==Pathophysiology==
-*GSD type 1 results due to defects in either hydrolysis or transport of glucose-6-phosphate
-*GSD type 1a is due to the deficiency of glucose-6-phosphatase enzyme (G6Pase).
-*GDS type 1b is due to defect in glucose-6-phosphate transporter (T1 deficiency).
-*G6Pase is primarily expressed in expressed primarily in the gluconeogenic the liver and kidney. It is also expressed to a lesser extent in the intestine and pancreas.
-*Glucose-6-phosphatase catalyzes the conversion of glucose-6-phosphate to glucose during glycogenolysis and gluconeogenesis.
-*This defects hinders the conversion of glucose-6 phosphate to glucose in organs.The inability of  glucose-6-phosphate to leave cells leads to hypoglycemia.
-==Genetics==
-*80% Cases of GSD 1 are of GSD type 1a.
-*G6Pase gene is located on chromosome locus 17q21.
-*GSD type 1 follows autosomal recessive pattern.
 ==References==
 {{reflist|2}}