bye - whiteblue

[ArchivalUser]

ML mechanism of hypocalcemia in a pt (60s, BMI 18, weight of 155 lb, disheveled, malnourished) with 20 yr hx of alcoholism, alcoholic hepatitis, jaundice, temporal wasting, scattered rhonchi heard throughout all lung fields, no abnormalities of cardiac exam, normal bowel sounds, liver span of 16, decrease sensation to pin prick and light touch over the feet, dec. deep tendon reflexes at the ankles? Lab shows: pos. occult blood stool, hemotocrit 33%; serum: Na 133. K 3.1, Cl 92, Mg 0.8, Ca 5.8, HCO3 26, BUN 6, Cr. 0.8; platelet count 145,000?
1. Renal resistance to PTH
2. Primary hyperparathyroidism
3. Impaired hydroxylation of vit D
4. Chronic metabolic acidosis
5. Hypomagnesemia

[ArchivalUser]

3.?

[ArchivalUser]

reasons please

[ArchivalUser]

whiteblue,
there is a cascade of vit D metabolism in the liver and kidney..In the liver it is hydrolysed to 25[OH] VIT D and the conversion of the active form occurs in the kidney as 1,25[OH]2 VIT D and this is regulated by parathyroidhormone. The patient's liver is in trouble. There is this alcoholic hepatitis. This problem in the liver impairs the hydroxylation of Vit D. Worthy of note is that VIT D increases the absorption of calcium in the small intestine. Deficiency of VIT D results in decrease serum level of calcium..
Let me digress a little bit. Sarcoidosis also results in high serum level of calcium. This is achieved, because sarcoidosis causes HYPERAVITAMINOSIS. Increase Vit D increases intestinal absorption of calcium leading to hypercalcemia...Alibism

[ArchivalUser]

alibi is right i---

but i thought hydroxylation problem of vit d occurs in the presence of hydroxylase deficiency, 1-25 chlecalcoferol in kidney --but of course it should occur in liver also because 25 hydroxylation occur there ,


but this question i thought it depicts malabsorption due to less bile and less absorption of fat soluble vit d and less absorption of calcium and hypocalcemia and hypomagnesimia--

but there is no choice for that --and hypomagnesimia does not cause hypocalcemia though it is another thing that both need to be corrected together


so i agree with alibi


please give answers --lingering too much is no way good --

thanks for an excellant question

[ArchivalUser]

djyoti,

I guess you forget what april17's note and have not diagnosed my disease - quick and very quick characteristics because you will see my post of disagreement right away if I have a different answer in mind or at hand!

[ArchivalUser]

Summary of albili™s note:
Dietary endogenous Vit D3 enters the liver where it is converted to 25-OH-Vit D which enters the kidneys to become 1,25 (OH)2 Vit D which causes an increase in Ca PO4 intestinal absorption ( 400 mg Ca2+/d, absorption of 30 -35%) and an increase in proximal tubular reabsorption of PO4

PTH:
Stimulates osteoclasts
Inc distal tubular reabsorption of Ca2+
Inc production of 1,25 (OH)2 vit D
Dec PO4 reabsorption

[ArchivalUser]

djyoti,

I guess you forget what april17's note says and you have not diagnosed my disease - "quick and very quick characteristics" because you will see my post of disagreement right away if I have a different answer in mind or at hand!