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  #1  
Old 11-02-2012
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Arrow Billy Step 1 Questions # 72

A 75-year-old woman trips on the carpet in her home and falls to the floor. She immediately has marked pain in the right hip. On physical examination, there is shortening of the right leg and marked pain with any movement. A radiograph shows a right femoral neck fracture. The fracture is repaired. Six months later, a dual-energy x-ray absorptiometry (DEXA) scan of
the patient's left hip and lumbar vertebrae shows a bone mineral density 2 standard deviations below the young adult reference range. Which of the following processes contributes most to development of these findings?


□ (A) Decreased osteoprotegrin production
□ (B) Decreased sensitivity of osteoblasts to dihydroxycholecalciferol
□ (C) Decreased secretion of interleukin-1, interleukin-6, and tumor necrosis factor-α by monocytes
□ (D) Increased sensitivity of bone to the effects of parathyroid hormone
□ (E) Mutation in the fibroblast growth factor receptor 3 gene
□ (F) Synthesis of chemically abnormal osteoid
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  #2  
Old 11-02-2012
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not at all sure just a random guess..........B

osteoporosis.........

changing my answer to A(confused between these 2)


thanks

Last edited by venky2600; 11-02-2012 at 04:48 PM.
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  #3  
Old 11-02-2012
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Quote:
Originally Posted by billy View Post
A 75-year-old woman trips on the carpet in her home and falls to the floor. She immediately has marked pain in the right hip. On physical examination, there is shortening of the right leg and marked pain with any movement. A radiograph shows a right femoral neck fracture. The fracture is repaired. Six months later, a dual-energy x-ray absorptiometry (DEXA) scan of
the patient's left hip and lumbar vertebrae shows a bone mineral density 2 standard deviations below the young adult reference range. Which of the following processes contributes most to development of these findings?


□ (A) Decreased osteoprotegrin production
□ (B) Decreased sensitivity of osteoblasts to dihydroxycholecalciferol
□ (C) Decreased secretion of interleukin-1, interleukin-6, and tumor necrosis factor-α by monocytes
□ (D) Increased sensitivity of bone to the effects of parathyroid hormone
□ (E) Mutation in the fibroblast growth factor receptor 3 gene
□ (F) Synthesis of chemically abnormal osteoid
I would choose B) Decreased sensitivity of osteoblasts to dihydroxycholecalciferol
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  #4  
Old 11-02-2012
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Osteoprotogerin normally prevents the bone resorption by osteoclasts.............i think this is a case of senile osteoporosis and i go with Answer AA.................
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Old 11-02-2012
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stuck b/w A and B
wuld go with A....
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Old 11-02-2012
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not sure guessing its A
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  #7  
Old 11-03-2012
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Default my answer :)

(B) Decreased sensitivity of osteoblasts to dihydroxycholecalciferol

I was thinking about A) also but I think that in this case we're dealing with a senile osteoporosis where the main issue is a decreased activity of osteoblasts.

A) would result in increased activation/differentiation of osteoclasts which is an issue in celiac sprue osteoporosis and postmenopausal osteoporosis..

nice question looking forward to seeing the answer!
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Old 11-03-2012
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Quote:
Originally Posted by billy View Post
A 75-year-old woman trips on the carpet in her home and falls to the floor. She immediately has marked pain in the right hip. On physical examination, there is shortening of the right leg and marked pain with any movement. A radiograph shows a right femoral neck fracture. The fracture is repaired. Six months later, a dual-energy x-ray absorptiometry (DEXA) scan of
the patient's left hip and lumbar vertebrae shows a bone mineral density 2 standard deviations below the young adult reference range. Which of the following processes contributes most to development of these findings?


□ (A) Decreased osteoprotegrin production
□ (B) Decreased sensitivity of osteoblasts to dihydroxycholecalciferol
□ (C) Decreased secretion of interleukin-1, interleukin-6, and tumor necrosis factor-α by monocytes
□ (D) Increased sensitivity of bone to the effects of parathyroid hormone
□ (E) Mutation in the fibroblast growth factor receptor 3 gene
□ (F) Synthesis of chemically abnormal osteoid
senile osteoporosis
increased activity of osteoclast, osteoblast.
So,(B) Decreased sensitivity of osteoblasts to dihydroxycholecalciferol
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Old 11-03-2012
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Correct Answer A is correct

With advancing age, the ability of osteoblasts to divide and to lay down osteoid is reduced as osteoclast activity increases, giving rise to accelerated bone loss known as osteoporosis. Differentiation of stromal progenitor cells into osteoclasts requires binding of RANK ligand on osteoblasts to RANK receptor on osteoclast precursors and stimulation by
M-CSF produced by osteoblasts. Osteoprotegrin (OPG) is a “decoy receptor” for RANK ligand that slows osteoclast formation and action. When osteoblasts produce less OPG, bone loss is accelerated. Marrow stromal cells produce WNT proteins that bind to osteoblast receptors, activating β-catenin and OPG production. Postmenopausal osteoporosis is
characterized by hormone-dependent acceleration of bone loss. Estrogen deficiency results in increased secretion of interleukin-1, interleukin-6, and tumor necrosis factor-α by monocytes-macrophages. These cytokines act by increasing the levels of RANK and RANK-L, and decreasing the levels of osteoprotegerin. In older women, bone loss is accelerated by reduced synthesis and increased resorption. Nonhormonal drugs such as alendronate are designed to reduce osteoclast resorption of bone. There are no age-associated changes in the sensitivity to vitamin D or parathyroid hormone action or composition of osteoid. Fibroblast growth factor receptor 3 gene mutations occur in dwarfism syndromes, such as
achondroplasia
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  #10  
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@billy - thanks for the question! I did qs on this issue from different sources and some of their explanations are contradictory

so according to your explanation does it mean that both in postmenopausal and senile osteoporosis there's a decrease in osteoblasts activity and hence (due to loss of inhibition of RANK/RANK-L) increase in osteoclasts activity?

I'm asking bc in Goljan RR they discuss separately those two issues but give vague info about senile osteoporosis patomechanism.
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  #11  
Old 11-04-2012
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Osteoblasts and activated T cells in the bone marrow produce the RANKL cytokine. RANKL binds to RANK expressed by osteoclasts and osteoclast precursors to promote osteoclast differentiation. Osteoprotegerin is a soluble decoy receptor that inhibits RANKL-RANK by binding and sequestering RANKL.
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  #12  
Old 11-05-2012
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Quote:
Originally Posted by billy View Post
Osteoblasts and activated T cells in the bone marrow produce the RANKL cytokine. RANKL binds to RANK expressed by osteoclasts and osteoclast precursors to promote osteoclast differentiation. Osteoprotegerin is a soluble decoy receptor that inhibits RANKL-RANK by binding and sequestering RANKL.
@billy - thanks for the info dude, I'm familiar with that concept but that doesn't really answer my question..
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