الجمعة، 10 يناير 2014

MCQs In Calcium Hemeostasis

Q 1

Which of the following statements about calcium homeostasisis incorrect?

a. Approximately 45% of serum calcium is bound to protein.
b. Parathyroid hormone stimulates bone resorption via its actions on osteoblasts.
c. Activated vitamin D inhibits the enzyme 1a-hydroxylase.
d. The daily calcium requirement for a teenage girl is 800 mg per day.
e. Wholemeal bread increases the dietary calcium absorption.

The Answer :

E

Wholemeal bread increases dietary calcium absorption. Calcium is available in milk and dairy products, as well as in fortified white and brown flour. It is also well absorbed from vegetables such as broccoli. 

Absorption is, however, reduced in the presence of phytates, which are present in wholegrain cereals, unleavened bread and pulses. Oxalates in spinach and rhubarb also impair absorption. 

Activated vitamin D inhibits the enzyme 1a-hydroxylase via negative feedback mechanisms.

 The recommended calcium intake for a teenage girl is 800 mg per day; reference nutrient intake levels vary according to age.

Mature osteoclasts do not appear to have parathyroid hormone receptors.

 PTH has several actions on bone, some direct and some indirect. In bone, PTH receptors are
located on osteoblasts but not on osteoclasts. Initially and transiently, PTH causes an increase in
bone formation by a direct action on osteoblasts. (This brief action is the basis for the usefulness of intermittent synthetic PTH administration in the treatment of osteoporosis.) In a second, longlasting
action on osteoclasts, PTH causes an increase in bone resorption. This second action on osteoclasts
is indirect and mediated by cytokines released from osteoblasts; these cytokines then increase the
number and activity of the bone-resorbing osteoclasts.

Thus, the bone-forming cells, osteoblasts, are required for the bone-resorbing action of PTH
on osteoclasts.

The initial event in bone degradation is the attachment of osteoclasts to the bone surface following their recruitment. PTH binding to osteoblasts triggers the synthesis of ODF, also known as RANKL or osteoprotegerin ligand.

 PTH stimulates the expression of this cell membrane protein in osteoblastic cells. Th is ligand binds to the ODF receptor (receptor activator of nuclear factor-κB [ RANK] ) expressed on the hemopoietic osteoclastic precursors and stimulates their diff erentiation into functional osteoclasts. Th ese 2 cell surface proteins, RANK expressed on osteoclast precursor cells and its partner RANKL expressed on osteoblasts, are the key regulators of osteoclast formation and function.

Activation by RANKL increases the expression of specifi c genes leading to osteoclast maturation. When an osteoclast precursor encounters an osteoblast, the resulting interaction between RANK and RANKL stimulates the osteoclast precursor to mature into a fully diff erentiated, bone-resorbing osteoclast.

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A 14-year-old girl presented to A&E with acute abdominal pain and vomiting. Questioning uncovered a history of thirst, polyuria, lethargy and malaise, increasing over the previous few weeks. This had led to her missing several weeks of schooling. One year previously, she had been given a diagnosis of Osgood–Schlatter’s disease after presenting with bilateral knee pain. She had improved with physiotherapy
but was still troubled by frequent bone pains. She had reached all developmental milestones as expected and had been otherwise well. Her paternal uncle was diabetic, but there was no other family history of note.
On examination, this was a slim girl who appeared mildly dehydrated. Her abdomen was soft and non-tender with normal bowel sounds and no masses. She was afebrile, and there were no other relevant findings.
No surgical cause could be found for her symptoms. She was normoglycaemic on both bedside and laboratory blood glucose analysis (5.4 mmol/l, reference fasting range 3.4–5.5 mmol/l), and a urine dipstick test showed protein+, blood+ and ketones negative.

Blood testing revealed these values (reference range in brackets):
Na 148 mmol/l (135–145 mmol/l);
K 3.7 mmol/l (3.5–5.3 mmol/l);
urea 8.6 mmol/l (2.0–6.0 mmol/l);
creatinine 85 mmol/l (30–90 mmol/l);
total Ca2+ 2.92 mmol/l (2.15–2.55 mmol/l);
PO4 1.06 mmol/l (1.0–1.8 mmol/l);
alkaline phosphatase 170 IU/l (100–400 IU/l);
albumin 25 g/l (24–48 g/l).


CASE :

Question 2

What is this girl’s calcium level when corrected for serum albumin (corrected calcium reference range
2.2–2.7 mmol/l)?
a. 3.22 mmol/l
b. 3.54 mmol/l

c. 2.85 mmol/l
d. 3.85 mmol/l

e. 4.22 mmol/l.

Question 3

What is your first-line treatment for this girl’s symptomatic hypercalcaemia?

a. Sodium bicarbonate infusion
b. 0.9% saline infusion
c. Oral prednisolone
d. Bisphosphonate infusion
e. Furosemide.