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Old 09-03-2011
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Default MCC of Hypocalcemia

"most common cause of hyocalcemia = albumin"

hey guys i have that written down in my notes...i forgot the reasoning behind it, or im not even sure if its a correct concept....anyone have an idea?
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Old 09-03-2011
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There's total calcium and free calcium. Calcium normally binds to albumin. In cases where there is loss of albumin let's say nephrotic syndrome, hypocalcemia will ensue. This only means that the total calcium is low but the free fraction calcium is the same and has not decreased. (which explains why the patient doesn't become symptomatic). Same goes for hyperalbuminemia and hypercalcemia. Always remember to adjust for albumin levels when interpreting calcium levels. Hope that helps
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Old 09-03-2011
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Quote:
Originally Posted by add1 View Post
There's total calcium and free calcium. Calcium normally binds to albumin. In cases where there is loss of albumin let's say nephrotic syndrome, hypocalcemia will ensue. This only means that the total calcium is low but the free fraction calcium is the same and has not decreased. (which explains why the patient doesn't become symptomatic). Same goes for hyperalbuminemia and hypercalcemia. Always remember to adjust for albumin levels when interpreting calcium levels. Hope that helps
thanks bro....i also had another question.....do you the concept behind ethanol hypoglycemia....in terms of why: (OAA >> malate and Pyruvate>>lactate cause decreased gluconeogenesis and increased fatty acids)?

thanks meng
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Buildup of NADH inhibits Gluconeogenesis, thus fasing hypoglycemia. How does it do this? Well, because there is excess NADH, Pyruvate is converted to lactate instead of Acetyl-CoA (in order to consume the NADH that is produced by alcohol metabolism). Although Acetyl-CoA is not directly a substrate for gluconeogenesis, it MUST be present for the first enzyme of gluconeogenesis to work. Since gluconeogenesis is impaired, you get fasting hypoglycemia. This hypoglyecemia then triggers the release of glucagon, which mobilizes fat stores via Hormone sensitive lipase. The fatty acids reach the liver and then cannot be sent out again because VLDL assembly is inhibited.
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Old 09-03-2011
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Originally Posted by dr_lizard View Post
Buildup of NADH inhibits Gluconeogenesis, thus fasing hypoglycemia. How does it do this? Well, because there is excess NADH, Pyruvate is converted to lactate instead of Acetyl-CoA (in order to consume the NADH that is produced by alcohol metabolism). Although Acetyl-CoA is not directly a substrate for gluconeogenesis, it MUST be present for the first enzyme of gluconeogenesis to work. Since gluconeogenesis is impaired, you get fasting hypoglycemia. This hypoglyecemia then triggers the release of glucagon, which mobilizes fat stores via Hormone sensitive lipase. The fatty acids reach the liver and then cannot be sent out again because VLDL assembly is inhibited.
thanks broski
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