8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 1/53

 

Question 1 Say some thing about calcitonin

Calcitonin Injections - Discussion - National Osteoporosis ... https://www.inspire.com/groups/national.../ calcitonin-injections/  

National Osteoporosis

Foundation Support Community 

  Home  

  New  

  Recommended  

  Discussions  

  Journals  

  Members  

  About  

  Join  

  All   Active 

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 2/53

  Recommended   Topics   Start a discussion 

Calcitonin Injections

By JilleWhite · May 28, 2008 at 12:24 am · 16 replies

In Osteoporosis medications 

  Recommend  Problem 

More options 

  Shared with the public Why do they not seem to use Calcitonin Injections as an option anymore? I did this in the

beginning of my diagnosis (16 years ago) & saw significant increase. Am curious and have

been revisiting the thought since I seem to be losing bone mass again.

Jill

Explore topics in this post 

16 replies

  Oldest first  Newest first 

By MotherGoose 

Reply 85488

May 28, 2008 at 7:06 am

  Report post 

Calcitonin is now given by nasal spray. This is a more user friendly method of

administration. (This medication cannot be given orally).

Lucy Buckley PT aka Mother Goose

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 3/53

 

By JilleWhite 

Reply 85646

May 28, 2008 at 12:21 pm

  Report post 

Lucy ~ I also did the nasal spray years ago, but did not have the same positive effects as I

did with the injections. Do studies show that they should have the same effects, or do you

know?

Jill

By Donnalc 

Reply 356836 · In reply to 85488 by MotherGoose

April 17, 2009 at 5:10 pm

  Report post 

Calcitriol can be taken orally.

Donnalc

By Donnalc 

Reply 356838

April 17, 2009 at 5:11 pm

  Report post Calcitriol can be taken orally.

Donnalc

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 4/53

 

By MotherGoose 

Reply 357248 · In reply to 356836 by Donnalc

April 18, 2009 at 6:40 am

  Report post 

Calcitonin and calcitriol are not the same thing.

Lucy Buckley PT aka Mother Goose

By Donnalc 

Reply 358673 · In reply to 357248 by MotherGoose

April 19, 2009 at 7:51 pm

  Report post 

In what way are they different? In the need to know.

Donnalc

By MotherGoose 

Reply 358975 · In reply to 358673 by Donnalc

April 20, 2009 at 6:56 am

  Report post 

Calcitriol is another name for Vitamin D.

Calcitonin is a hormone that suppresses bone resorption and is a 32 amino acid peptide.Lucy Buckley PT aka Mother Goose

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 5/53

By rmchavin (Inactive)

Reply 421711

June 13, 2009 at 12:27 pm

  Report post 

Dear JilleWhite:

You wanted to know why calcitonin is not used much more frequently than it actually is for

treating severe osteoporosis. Believe it or not, that's a very good question. The only bad

things I could find about calcitonin are from non-scientific websites such as

these: http://www.drugs.com/sfx/calcitonin-side-

effects.htmlhttp://www.drugs.com/mtm/calcitonin-nasal.html http://www.rxlist.com/miacalcin-

drug.htm I remember my medical doctor telling me he almost never prescribes calcitonin

because it was inconvenient and could cause a reaction. However, the PubMed research

studies on calcitonin all say only very positive things about calcitonin and never anything

negative about calcitonin. For example,

these:http://www.ncbi.nlm.nih.gov/pubmed/8935399http://www.ncbi.nlm.nih.gov/pubmed/18

713548http://www.ncbi.nlm.nih.gov/pubmed/18071651 Perhaps you could do us a favor?

You might want to try natural salmon calcitonin and you could report back to everybody at

NOF Inspire regarding how well your experience went.

By slansing 

Reply 422423

June 14, 2009 at 12:48 am

  Report post 

My sister just had a bone scan this week after a year on calcitonin nasal spray. She's gone

all the way from osteo back to just shy of normal! My doctor had pooh poohed my question

about calcitonin last year, but now I'm seriously interested! I was planning to start some

research, so this discussion is really valuable.

By letshope 

Reply 422727

June 14, 2009 at 11:27 am

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 6/53

  Report post 

i was wondering about injections since i've never done well with anything administered in a

nasal spray since i'm prone to chronic sinus infections.

is the natural salmon cacitonin an injection as well?

By carmk5 

Reply 422799

June 14, 2009 at 12:46 pm

  Report post 

Hi,When I was first diagnosed ten years ago with Osteo, my primary doctor prescribed

Calcitonin. I was not able to tolerate it. It made me dizzy and it inflamed my nasal passages.

I was on it for a month, then she switched me to Fosomax. I wish I could try the injections of

Calcitonin to see if it makes a difference but from everything I have learned, they just don't

do it anymore.

Carmen

By willamette 

Reply 423055

June 14, 2009 at 6:03 pm

  Report post 

Hi

I used Calcitonin for about 9 months. It gave me such severe constipation, I had to stop

using it. Also thinning hair. I am afraid to take anything else, because i have so many

problems with my teeth. Will see my doctor in August, to see whats next.

I tried all kinds of things for the constipation, but nothing worked.

Any suggestions to help????

Thanks Marla

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 7/53

 

By rmchavin (Inactive)

Reply 423070 · In reply to 423055 by willamette

June 14, 2009 at 6:24 pm

  Report post 

Dear willamette:

The best way to counteract constipation is with psyllium husk capsules. Psyllium husk,

which is grown in and imported from India, is rapidly increasing in popularity in the U.S.,

Europe, Japan, and elsewhere. The capsules are more convenient and are better able to be

taken every 2 hours than the psyllium husk powder, which is cheaper but less convenient.

Metamucil is mostly just psyllium husk plus aspartame (Equal/Nutrasweet). I buy mypsyllium husk capsules from Sam's Club at a very good price. The second best way to fight

constipation is with prunes. Plums and prunes contain a specific constipation-fighting

chemical, dihydrophenylisatin, which no other fruit or vegetable contains in any meaningful

quantity. The third best way to fight constipation is with ground flaxseed meal. Pour boiling

hot water over it and eat it five minutes later. Both prunes and flaxseed meal are high in

calories, while psyllium husk is low in calories. All 3 of the above solutions for constipation

have many additional health benefits. The medical doctors prescribe softgels containing

docusate sodium to treat constipation. It works but takes a long time - too long. Also,

docusate sodium has no other health benefit and can cause side effects.

By willamette 

Reply 423303

June 14, 2009 at 10:34 pm

  Report post 

To rmchacin

Thank you I will definately try the psylliun husk capsules. Do you take them every two

hours.? I know as long as I take the calcitonin, I will need to take something.

This could be a lifesaver for me.

Thank you again.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 8/53

 

By rmchavin (Inactive)

Reply 423394 · In reply to 423303 by willamette

June 15, 2009 at 2:08 am

  Report post 

Dear willamette:

The instructions say to conveniently swallow about six psyllium husk capsules per day

depending on the severity of your constipation. Six to eight capsules per day should be

enough for successfully treating most cases of constipation. However, there is no harm in

swallowing twelve or more capsules per day as long as you never swallow more than two

capsules per 20 minutes. Never swallow more than one capsule at a time. Always drink atleast a half cup of fluid together with one capsule. As a practical matter, it's too inconvenient

to keep watching the clock. Therefore, just leave a whole bunch of capsules out in the open

where it won't collect dust. (One good place would be inside your refrigerator where they

won't collect dust). Just swallow one capsule every time you realize that you want to drink

some fluid and enough time has transpired since your last swallowing of one capsule. You

might want to try to estimate how many capsules you normally end up swallowing each day

using this method. If your constipation is extremely severe, you might want to combine

psyllium husk capsules with prunes, ground flaxseed meal, and/or docusate sodium (now

available at Sam's Club without a prescription). In extremely rare cases, constipation can be

caused by colorectal cancer so it's a good idea to obey the American Cancer Society and

schedule a colonoscopy once every ten years starting at age 50. Swallowing probiotic

(acidophilus) capsules might help slightly.

By willamette 

Reply 424533

June 15, 2009 at 8:13 pm

  Report post 

Dear rmchavin

Thank you so much for your help

I did have a colonoscopy, so I am ok there.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 9/53

 

I will try this. I hope it works. Will keep you posted.

I really appreciate you response to me.

Calcitonin vs. Parathyroid Hormone [Archive] - Student Doctor ... forums.studentdoctor.net › ... › MCAT Study Question Q&A 

Student Doctor Network Forums > Pre-Medical Forums > MCAT Discussions > MCAT Study Question Q&A >Calcitonin vs. Parathyroid HormonePDA 

View Full Version : Calcitonin vs. Parathyroid Hormone 

Revilla06-06-2008, 01:35 PMI was under the impression calcitonin increased Ca and PTH decreased it, but my review book is exactly theopposite. Can someone verify that calcitonin decreases Ca while PTH increases it?

Andrew401006-06-2008, 01:37 PMCalcitonin decreases the blood calcium level whereas PTH increases it.

cwfergus06-06-2008, 01:38 PMNope Calcitonin reduces Ca2+ concentrations, PTH will increase it

iA-MD201306-06-2008, 01:41 PM

Calcitonin decreases the blood calcium level whereas PTH increases it.

Nope Calcitonin reduces Ca2+ concentrations, PTH will increase itThey are both correct :thumbup:

supertrooper6606-06-2008, 01:48 PMI was under the impression calcitonin increased Ca and PTH decreased it, but my review book is exactly theopposite. Can someone verify that calcitonin decreases Ca while PTH increases it?

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 10/53

that's what my book says, too. calcitonin decreases blood Ca and PTH increases it. that's coming fromkaplan.

i hate the hormones. not sure how many of them we really need to know. seems like the more obscureones, like the ones you listed, would be included in a passage instead. ones like the catecholamines,aldosterone, and vasopressin i would assume you should know, though. no way I can prove that, tho!

Revilla06-06-2008, 02:36 PMThanks guys! I've had it backwards in my head this whole time.

DrMattOglesby06-06-2008, 02:49 PMI always had trouble with these two hormones.the things to remember are:

Parathyroid gets rid of Ca2+ from the bones and sends it to the bloodstream.Calcitonin will tone up the bones by depositing Ca2+ from the bloodstream into the bones.

Alliteration is a fun game everyone can play!

Revilla06-08-2008, 04:16 PMSo that's where I was confused! Calcitonin increases Ca+2 in the bones by taking it from the bloodstreamand Parathyroid increases Ca+2 in the blood stream by taking it from the bones.

nityking06-08-2008, 04:23 PMyou GOT IT! Since production of Estrogen/Progestrone decreases siginificantly in post-menopausal women,they cause increase osteoclast activity to increase blood calcium and decrease osteoblast activity (to formbones). Thus they are at high risk of suffering from osteoperosis than men! Now you would ask then why dothey have to take regular Calcium pills if their blood Ca2+ will be technically higher? They are not higher cuzhigher blood Ca2+ causes increase in its excretion by kidneys so they are still deficient of Ca2+ regardlessof decrease in bone resorption.

facetguy06-09-2008, 11:55 AMCalcitonin "puts the bone-in"! (i.e., puts the calcium INTO the bone). PTH does the opposite.

DrMattOglesby06-09-2008, 12:02 PMloli love how everybody pretty much said the same thing in their reply to this thread <i'm guilty too>! As if more people saying the correct answer made it MORE accurate. Almost as if its correct by generalconsensus. :hardy:

facetguy06-09-2008, 01:08 PMloli love how everybody pretty much said the same thing in their reply to this thread <i'm guilty too>! As if 

more people saying the correct answer made it MORE accurate. Almost as if its correct by generalconsensus. :hardy:

I learned that little mnemonic over 15 years ago and it continues to stick, so I thought I'd share it here.

BloodySurgeon06-09-2008, 01:20 PMAlso another idea to keep in mind would be to understand how other systems work with PTD and Calcitonin.Bone is made up of inorganic mineral hydroxyapatite that includes Calcium and Phosphates. So whathappens to the phosphates after the calcium is removed? Where does the calcium and phosphates go? How

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 11/53

does Vitamin D promote strong bones? How does calcium get to the bones from the blood? What isosteoclast vs. osteoblast? Osteocytes? If you can answer all these, then you will have a betterunderstanding of how calicium homeostasis works. Search these on wikipeda and you will find your answers.

*hint* the small intestine and the kidneys play a role.

nityking

06-20-2008, 03:33 PMtricky question on AAMC: Bone formation involves not only the use of Ca and PO43- but also hydroxylmolecules combined with them two. There was a discrete question on it and guessed the wrong one OH- :(instead of Potassium, which doesn't not belong to bone matrix. Was thinking of hematopoetic stem cells inthe bones and K+ is a major intracellular ion. Too much knowledge + over thinking = bad for MCAT

Farcus06-20-2008, 03:58 PMremember this

When I think of calcitonin I think of something strong... if something is strong it needs a lot of Calcium in

the bones, and thus a DECREASE in Ca2+ in bloodstream. I think of bloodstream as soft plushy weak sauce

:).

Questions from Achiever 1 [Archive] - Student Doctor Network Forums forums.studentdoctor.net › ... › DAT Discussions

Student Doctor Network Forums > Dental Forums [ DDS / DMD ] > DAT Discussions > Questions fromAchiever 1PDA 

View Full Version : Questions from Achiever 1 

Shinpe07-30-2009, 01:41 AM

So I have a couple of things in the survey of natural sciences I couldn't figure out from Achiever's test 1solutions:

1. In question 6's solution it says that osteoblasts deposit Ca2+ in response to Calcitonin's presence. I knowCalcitonin lowers blood calcium but I thought it does so by reducing osteoclast activity, confirmed by

wikipedia. But does anyone have other resources confirming what Achiever is claiming?

2. In quesiton 38, it's asking "The maximum number of chromosome combinations among the gametes of adiploid organism (2n =10) is"

and then in the answer it says since the haploid has 5 chromosomes, it's 2^5. Can some one explain thisquesiton? I don't get the question, yet alone the answer lol.

3. In OC question 72, it is asking which compound is not aromatic. There are two possibilities I think. One isthe cyclooctene (8-C ring with 4 pi bonds), which is anti-arommatic and I agree. But another option is a

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 12/53

three-C ring cation. Where there is a double bond between two of the carbons and the third has a positivecharge. Then it says it passes Huckel's rule, so it's arommatic, but isn't the other requirements foraromaticity that it is planar and all carbons have a pair of pi-electrons on them? I don't feel like that issatisfied here. Any thoughts?

4. In 82, it's adding HBr to an alkene in presence of hv and says that it is anti-mark since a free radicalwould form. I get it that radicals add anti-mark, but don't u need Br2 instead of HBr? I mean wouldnt HBr

dissociate completely in water anywayz (well it doesn't say what the solvent is, but anywayz) or wouldn'tthe bond be too polar for an equal split?

Thanks in advance for answers.

Shinpe07-30-2009, 11:41 AM

Any comments???

Sepx07-30-2009, 12:23 PM

1. In question 6's solution it says that osteoblasts deposit Ca2+ in response to Calcitonin's presence. I knowCalcitonin lowers blood calcium but I thought it does so by reducing osteoclast activity, confirmed bywikipedia. But does anyone have other resources confirming what Achiever is claiming?

I don't have achiever, i don't understand your other questions, except the bio one and a ochem one.The stimulus is the raising of Ca in the blood, then thyroid hormone secretes calcitonin. NOW, calicitoninlowers the Ca in two ways, one by increasing deposition of Ca on to bones. Ca deposition on to bones("making bones") is done by osteoblast, therefore increase osteoblast activity.Another thing calcinotin does is REDUCING Ca uptake in kidney.

If you have campbell, got to endocrine chapter, look for figure about controling blodd calcium: PTH vsCalcitonin. they are antogonistic.

4. In 82, it's adding HBr to an alkene in presence of hv and says that it is anti-mark since a free radicalwould form. I get it that radicals add anti-mark, but don't u need Br2 instead of HBr? I mean wouldnt HBrdissociate completely in water anywayz (well it doesn't say what the solvent is, but anywayz) or wouldn'tthe bond be too polar for an equal split?

You need to hit the text book on this one, you getting rxns confused. Study the mechanism for both, theyare diffrent.They are both electrophilic addition rxns though and there is no carobocation rearengement in either one!(but if you additng HBr w/o peroxide, there could be rearengement, always check!)

>addition of HBr w/ peroxide is anti mark addition of Br radical to alkene.

>but addition of Br2 (or Cl2), adds two bromide (chloride) to the alkene.>also Addition of Br2 with presensence of water results in formation of Halohyrine (alcohol with a halogen).

Sepx07-30-2009, 12:24 PM

oops i meant thyroid gland* :D

Sepx07-30-2009, 12:30 PM

also meant halohydrine..sorry about the typos...

Shinpe07-30-2009, 12:54 PM

Yeah I just had read somewhere (I think kaplan and forsure wiki) that Calcitonin lowers blood Calcium butLOWERING Osteoclast activity (bone resorption) as opposed to increasing bone deposition by osteoblasts. Iguess Campbell does say in the figure "stimulates calcium deposition in bones" which I guess must be doneby osteoblasts, but it never mentions it in the text of the chapter, weird.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 13/53

 For that second one, I looked, and I guess you need trace concentrations of HBr, usually delieverd by NBS,to be able to do the radical electrophilic addition, but I guess I should have just taken the hv hint and gonewith radical.

Here are the pictures for the other Orgo question. One is cyclooctatetraene, which is anti-aromatic, and the

other is the carbocation of cyclopropene. Take the second figure and add a positive charge to the carbon ontop.

cyclooctatetraenehttp://upload.wikimedia.org/wikipedia/commons/2/2a/Cyclooctatetraene.png

Cyclopropene (add a + charge to the top C)http://upload.wikimedia.org/wikipedia/commons/e/eb/Cyclopropene-2D-skeletal.png

Shinpe07-30-2009, 01:06 PM

And question number 2 is word for word out of Achiever, I really don't have any idea WTF it's talking about.

pauly1123507-30-2009, 01:11 PM

3. the cyclopropene is aromatic because it does not have any sp3 carbons and it follows the 4n +2 rulewhere n is equal to zero. Aromatic must NOT have any sp3 carbons and by putting a + charge on the topcarbon it signifies that it is rather sp2.

Shinpe07-30-2009, 01:24 PM

So having a pair of pi electrons is not a definite requirement? although I guess I could see that drawingresonance structures will put that double bond on each bond so it is really shared with all of them.

Thanks

Shinpe07-30-2009, 06:45 PM

1. In question 6's solution it says that osteoblasts deposit Ca2+ in response to Calcitonin's presence. I knowCalcitonin lowers blood calcium but I thought it does so by reducing osteoclast activity, confirmed by

wikipedia. But does anyone have other resources confirming what Achiever is claiming?

I don't have achiever, i don't understand your other questions, except the bio one and a ochem one.The stimulus is the raising of Ca in the blood, then thyroid hormone secretes calcitonin. NOW, calicitoninlowers the Ca in two ways, one by increasing deposition of Ca on to bones. Ca deposition on to bones("making bones") is done by osteoblast, therefore increase osteoblast activity.Another thing calcinotin does is REDUCING Ca uptake in kidney.

If you have campbell, got to endocrine chapter, look for figure about controling blodd calcium: PTH vsCalcitonin. they are antogonistic.

Ok so this was on my nerve. I found 5-6 places online that said calcitonin decrease blood calcium byinhibiting bone resorption by lowering osteoclast activity. I also went through my old physiology book and itsays the same thing. So I'm pretty sure it lowers blood calcium by lowering osteoclast activity. Since bone isconstantly being deposited and resorbed, this has the same net effect as depositing calcium from blood ontobones. The Campbell book doesn't say anything about osteoblasts/osteoclasts, just says "calcium depositedonto bone" due to calcitonin, so maybe they just didn't wanna go through that much detail. Well afterall, theexact opposite effect of PTH would be to decrease osteoclast activity, not increase osteoblast activity, perse. Anywayz, I'm kinda convinced that it lowers osteoclast activity, unless you guys have any otherresources that say otherwise???

Am I being too anal??? lol

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 14/53

 

And I guess no one has an answer for that second question yet? I really have zero clue ......

Orgolover07-30-2009, 09:54 PM

question 2 solution.

well the question first i guess, cause it was a worded a little funny.

They want to know if 2n = 10, how many different combination of chromosomes can you have in a gametecell. This is kind of QR related, but not too bad. So if 2n = 10 that means that there are 5 pairs of homologous chromosomes, and when they align, each member of the 5 pairs can go either way; right or leftyielding 2 options. since 5 pairs have 2 options each, there are 5^2 possible gamete combinations.

hope this helps.

Shinpe07-30-2009, 09:57 PM

question 2 solution.well the question first i guess, cause it was a worded a little funny.

They want to know if 2n = 10, how many different combination of chromosomes can you have in a gamete

cell. This is kind of QR related, but not too bad. So if 2n = 10 that means that there are 5 pairs of homologous chromosomes, and when they align, each member of the 5 pairs can go either way; right or leftyielding 2 options. since 5 pairs have 2 options each, there are 5^2 possible gamete combinations.

hope this helps.

I trust you meant 2^5 in your last statement, but here comes another question then, wouldn't there becrossing over and all those good stuff happening at prophase I? The 4 chromatids resulting from eachchromosome are all different, right? So at the end you have really 4 options for each chromosome, shouldn'tthat make it 4^5 possible ways???

Orgolover07-30-2009, 10:07 PM

Agreed. it is 2^5 ( ... and also 1 am in the morn- forgive me).

I believe there would be crossing over, but it seems that this question seems to ignore that. I thought of itas how many combinations of chromosomes coming from the dad and mom are there. Perhaps its better tothink of them like that. So even though there is crossing over, they treat the ones from dad the same, andthe ones from mom the same.

ALSO. I recall thinking the same thing and realizing that 32 is the largest option choice they offer. ... so nobrainer. Although I do agree with you, crossing over is fun stuff. First time i heard it, i thought of that oldshow on upn, "crossing over" guy tells over messages to relatives of dead people.yes. all this goes through my head during topscore exam ! ! ! ;)

txchexmex07-30-2009, 10:19 PM

For what its worth, Destroyer also says that calcitonin lowers osteoclast activity

Shinpe07-30-2009, 10:21 PM

Agreed. it is 2^5 ( ... and also 1 am in the morn- forgive me).

I believe there would be crossing over, but it seems that this question seems to ignore that. I thought of itas how many combinations of chromosomes coming from the dad and mom are there. Perhaps its better tothink of them like that. So even though there is crossing over, they treat the ones from dad the same, andthe ones from mom the same.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 15/53

ALSO. I recall thinking the same thing and realizing that 32 is the largest option choice they offer. ... so nobrainer. Although I do agree with you, crossing over is fun stuff. First time i heard it, i thought of that oldshow on upn, "crossing over" guy tells over messages to relatives of dead people.yes. all this goes through my head during topscore exam ! ! ! ;)

How I guessed was that it has to have something to do with the haploid number (5) and the only thing outof 2,4,8,16,32 that has anything to do with 5 is 32. I hope actual DAT questions are this easy to guess lol.

But yea I think if a question like this came up on the test, it should really be 4^5, crossing over doesn't liketo be taken lightly ;p

Shinpe07-30-2009, 10:23 PM

For what its worth, Destroyer also says that calcitonin lowers osteoclast activity

So that's where else I had seen it lol. I also asked my friend and she looked it up in her endocrinology bookand confirmed this, that's why it's used as a drug against osteoporosis.

Orgolover09-03-2009, 09:56 PM

girls are icky... don't trust them.

The Official "Lessons Learned from MCAT Studying" Thread [Archive ... forums.studentdoctor.net › ... › Pre-Medical Forums › MCAT Discussions 

Student Doctor Network Forums > Pre-Medical Forums > MCAT Discussions > The Official "Lessons Learned fromMCAT Studying" ThreadPDA 

View Full Version : The Official "Lessons Learned from MCAT Studying" Thread 

ADeadLois04-21-2006, 08:48 AM

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 16/53

I'm feeling very contemplative about by MCAT studying experience, so I've decided to summarize some of what Ilearned from the experience. I hope I'll be able to post this in 30+ MCAT tips above, but for know, it'll stay downhere.

1. Believe in EK, but don't rely too much on Audio Osmosis

After sampling a bit of Kaplan, TPR, and EK, I have come to the conclusion that EK makes the best MCAT prepmaterial, bar none. The books cover what you need to know, and are written in such a way that you willremember the material. However, don't go too nuts about Audio Osmosis. It's a great product, but it's not"complete MCAT preparation" as they boast on the CDs. It's good for going over material when you're walking toclass or in the car, but it's not substitute for book studying and practice problem. It's worth buying however,because even though it's pricey, you can very likely get most of the money back if you re-sell it on Amazon oreBay.

However, one thing to keep in mind is that EK also thinks they are the best. I don't know the exact stats, but I'mrather confident that they are still 3rd to Kaplan and TPR in total profitability and popularity. They thusovercompensate by putting down other test prep companies. However, I still think Kaplan and TPR havetremendous value, if only for their wealth of practice material. EK likes to boast that they are the best, but don'tlimit yourself to what they have to say.

1A. If you only buy one MCAT prep book, make it EK's 101 Passages in Verbal Reasoning.

And do all of them. My scores on practice tests went up significantly because of this book. Use whatever strategyyou are most comfortable with, just make sure you practice with this book. There really isn't much more to sayabout verbal than that.

2. Get AAMC practice tests however you can.

This has been beaten to death on this forum, so I won't go into too much detail. However, one thing I shouldmention: Kaplan gives AAMC material to college libraries. I discovered this before nearly spending $40 on AAMC9. Kaplan claims it's only for Kaplan students, but I was able to get the AAMC material on reserve with only myschool ID. This isn't true for all colleges, but it's worth looking into. I have a feeling they do this with schools thatare far away from Kaplan centers.

3. Take as many Kaplan Full-Lengths as you can, even those dreaded PS sections.

For the most part, Kaplan Full-Lengths are not representative of the actual MCAT, but that doesn't mean they arenot worth doing. They make the PS sections super hard for a reason. I took AAMC 8 PS and thought it was abreeze. It really boosts your confidence when you take an AAMC test after a Kaplan Full-Length. Trust me onthis.

4. Ignore other people's scoring trends posted in this forum.

Everyone is different. Getting hyped about other people's performance just make you more anxious and lessconfident.

5. If you don't like studying in groups, don't feel obligated to.

I hate studying in groups. It just makes me nervous that other people know more than me. If you are in the same

boat, don't feel that you're at a disadvantage if you're not in a study group. This is just a matter of personalpreference.

And the most important lesson I learned...

6. Studying for the MCAT is not about learning the material. It's about building confidence.

A little vague, but very true. No matter how long you study, you will not know everything. Instead, you should betrying to study so that you have the right attitude going into the test. This means taking practice tests, and not

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 17/53

stressing out. It's tough to grasp at first, but I think this is the most crucial element to MCAT studying.

mangos304-21-2006, 09:43 AM

What did you do to improve on verbal?? You said you took a lot of practice tests, but what did you learn to do/notdo after doing all that practice? To me, it just seems like half luck most of the time.

Mr. Tee04-21-2006, 09:52 AM

What did you do to improve on verbal?? You said you took a lot of practice tests, but what did you learn to do/notdo after doing all that practice? To me, it just seems like half luck most of the time.

Since VR is multiple choice, that means that only ONE choice will be correct, and the others will be categoricallyincorrect. It's your objective to find out why those answer choices are incorrect. Over time, your gut feel will bedeveloped and you'd already be subconsciously analyzing why those answer choices are incorrect.

Taking practice tests is good for honing speed and rhythm. You have to read at a decent pace and think throughthe questions rather quickly if you want to finish the VR section. The main thing is to dissect the questions so thatyou know what they're really asking for.

Nutmeg04-21-2006, 12:04 PM

6. Studying for the MCAT is not about learning the material. It's about building confidence.

A little vague, but very true. No matter how long you study, you will not know everything. Instead, you should betrying to study so that you have the right attitude going into the test. This means taking practice tests, and notstressing out. It's tough to grasp at first, but I think this is the most crucial element to MCAT studying.I heartily concur. :thumbup:

QuantumMechanic04-21-2006, 12:18 PM

:thumbup: :thumbup: :thumbup: :thumbup: :thumbup: :thumbup:

Excellent post, OP!

This is my exact advice to friends studying for the MCAT. Its funny how they write off EK (especially verbal 101:laugh: :laugh: :laugh: ) as not being as good, in the end they aren't going to score as highly as I did (which was

solely due to EK and AAMC practice tests).

EMH04-21-2006, 12:24 PM

Great post, only thing I would add is go over your practice tests soon after taking them, so you can determinewhy you got problems right and wrong. This is how you develop that feel for the MCAT. Kind of being able to pickout a good wrong answer.

41@3104-21-2006, 05:23 PM

6. Studying for the MCAT is not about learning the material. It's about building confidence.

Wow, great post. Since I've been back at school as a post-bac, I've always said the same thing to myself beforeevery exam:

"You know enough to ace this test. You knew enough a month ago. Relax."

Most of us on this forum have studied for this, and most of us know our calcitonin from our Delta G. At this point,its just mind over matter. I'm gonna kill this test.

Good luck everyone.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 18/53

-S

txguy04-21-2006, 05:34 PM

Nice post...........especially #6...........

good luck :luck:

-tx

I'm feeling very contemplative about by MCAT studying experience, so I've decided to summarize some of what Ilearned from the experience. I hope I'll be able to post this in 30+ MCAT tips above, but for know, it'll stay downhere.

1. Believe in EK, but don't rely too much on Audio Osmosis

After sampling a bit of Kaplan, TPR, and EK, I have come to the conclusion that EK makes the best MCAT prepmaterial, bar none. The books cover what you need to know, and are written in such a way that you willremember the material. However, don't go too nuts about Audio Osmosis. It's a great product, but it's not"complete MCAT preparation" as they boast on the CDs. It's good for going over material when you're walking toclass or in the car, but it's not substitute for book studying and practice problem. It's worth buying however,

because even though it's pricey, you can very likely get most of the money back if you re-sell it on Amazon oreBay.

However, one thing to keep in mind is that EK also thinks they are the best. I don't know the exact stats, but I'mrather confident that they are still 3rd to Kaplan and TPR in total profitability and popularity. They thusovercompensate by putting down other test prep companies. However, I still think Kaplan and TPR havetremendous value, if only for their wealth of practice material. EK likes to boast that they are the best, but don'tlimit yourself to what they have to say.

1A. If you only buy one MCAT prep book, make it EK's 101 Passages in Verbal Reasoning.

And do all of them. My scores on practice tests went up significantly because of this book. Use whatever strategyyou are most comfortable with, just make sure you practice with this book. There really isn't much more to sayabout verbal than that.

2. Get AAMC practice tests however you can.

This has been beaten to death on this forum, so I won't go into too much detail. However, one thing I shouldmention: Kaplan gives AAMC material to college libraries. I discovered this before nearly spending $40 on AAMC9. Kaplan claims it's only for Kaplan students, but I was able to get the AAMC material on reserve with only myschool ID. This isn't true for all colleges, but it's worth looking into. I have a feeling they do this with schools thatare far away from Kaplan centers.

3. Take as many Kaplan Full-Lengths as you can, even those dreaded PS sections.

For the most part, Kaplan Full-Lengths are not representative of the actual MCAT, but that doesn't mean they arenot worth doing. They make the PS sections super hard for a reason. I took AAMC 8 PS and thought it was abreeze. It really boosts your confidence when you take an AAMC test after a Kaplan Full-Length. Trust me onthis.

4. Ignore other people's scoring trends posted in this forum.

Everyone is different. Getting hyped about other people's performance just make you more anxious and lessconfident.

5. If you don't like studying in groups, don't feel obligated to.

I hate studying in groups. It just makes me nervous that other people know more than me. If you are in the sameboat, don't feel that you're at a disadvantage if you're not in a study group. This is just a matter of personal

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 19/53

preference.

And the most important lesson I learned...

6. Studying for the MCAT is not about learning the material. It's about building confidence.

A little vague, but very true. No matter how long you study, you will not know everything. Instead, you should betrying to study so that you have the right attitude going into the test. This means taking practice tests, and notstressing out. It's tough to grasp at first, but I think this is the most crucial element to MCAT studying.

WAOZA04-21-2006, 06:14 PM

Here are my lessons:

1. Most of the answers are in the passages.

2. The verbal section is an open book test. Also, because you cannot study for that part of the test, it is acrapshoot.

3. As other people have stated, this test is mostly about confidence.

4. Kaplan's Full Length Physical Science Sections are insanity, but if you can master those, the AAMC Phy SciSections are cake.

sweetstuff2504-21-2006, 07:36 PM

 just thinking about EK gives a level of confidence. i just feel good with their books. :)

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 20/53

 

Question 13www.guideline.gov/content.aspx?id=3876 - 227k 

Guideline Title

Management of osteoporosis. A national clinical guideline.

Bibliographic Source(s)

Scottish Intercollegiate Guidelines Network (SIGN). Management of osteoporosis. A national clinical

guideline. Edinburgh (Scotland): Scottish Intercollegiate Guidelines Network (SIGN); 2003 Jun. 45 p. (SIGN

publication; no. 71). [149 references] 

Guideline Status

This is the current release of the guideline.

The guideline was reaffirmed by the developer in 2007.

Any amendments to the guideline will be noted on Scottish Intercollegiate Guidelines Network (SIGN) Web site  .

-

Scope 

-

Methodology 

-

Recommendations 

-

Evidence Supporting the Recommendations 

-

-

Qualifying Statements 

-

Implementation of the Guideline 

-

Institute of Medicine (IOM) National Healthcare QualityReport Categories 

-

Identifying Information and Availability 

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 21/53

Benefits/Harms of Implementing the Guideline

Recommendations 

-

Contraindications 

-

Disclaimer 

Back to top 

Scope

Disease/Condition(s)

Osteoporosis

Note: The guideline does not address corticosteroid induced osteoporosis.

Guideline Category

Diagnosis

Management

Risk Assessment

Treatment

Clinical Specialty

Family Practice

Geriatrics

Internal MedicineObstetrics and Gynecology

Orthopedic Surgery

Preventive Medicine

Intended Users

Advanced Practice Nurses

Allied Health Personnel

Dietitians

Nurses

Patients

Physical Therapists

Physician Assistants

Physicians

Guideline Objective(s)

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 22/53

  To ensure the timely identification of those individuals at highest risk of osteoporosis, as well as those

who already have the disease

  To explore the treatment options that can be used in these patients to reduce their increased risk of 

further fractures with the aim of achieving "secondary prevention of fracture"

Target Population

Individuals at high risk for, or who currently have, osteoporosis, including women and men over 50who present with fractures (that occur in the absence of major trauma, such as road traffic accidents)

Interventions and Practices Considered

Risk Assessment 

1.  Assessment of risk factors including history of falls/fracture, age, sex, ethnicity, reproductive factors,

family history, weight, smoking history, alcohol use, exercise, diet, and risk scores

Diagnosis 

1.  Techniques for measuring bone mineral density, including:

  Dual-energy X-ray absorptiometry (DEXA or DXA)

  Peripheral dual-energy X-ray absorptiometry (pDXA) (not recommended)

  Peripheral quantitative computed tomography (pQCT) (not recommended)

  Single photon absorptiometry (SPA)(not recommended)

  Single-energy X-ray absorptiometry (SEXA or SXA) (not recommended)

  Radiograph absorptiometry

2.  Techniques discussed but not specifically recommended:

  Quantitative ultrasound (QUS) to assess bone quality and structure  Biochemical markers such as resorption markers to assess bone turnover

  Quantitative computed tomography (QCT)

Treatment 

 Non-pharmacological 

1.  Exercise

2.  Calcium + vitamin D

3.  Interventions discussed but not specifically recommended:

  Fluoridation of water  Use of ipriflavone

  Elimination of caffeine

Pharmacological 

1.  Bisphosphonates (alendronate, etidronate, risedronate)

2.  Hormone replacement therapy (considered but not recommended)

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 23/53

3.  Raloxifene

4.  Calcitonin

Major Outcomes Considered

  Fracture rates and risk  Fracture related morbidity

Back to top 

Methodology

Methods Used to Collect/Select the Evidence

Searches of Electronic Databases

Description of Methods Used to Collect/Select the Evidence

The evidence base for this guideline was synthesised in accordance with Scottish IntercollegiateGuidelines Network (SIGN) methodology. A systematic review of the literature was carried out usingan explicit search strategy devised in collaboration with members of the guideline development group.Searches were restricted to systematic reviews, meta-analyses, randomised controlled trials, andlongitudinal studies. Internet searches were carried out on the websites of the Canadian PracticeGuidelines Infobase, the UK Health Technology Assessment Programme, the US National GuidelinesClearinghouse, and the US Agency for Healthcare Research and Quality. Searches were also carriedout on the search engines Google and OMNI, and all suitable links followed up. Database searcheswere carried out on Cochrane Library, Embase 1993 to 2000, and Medline 1990 to 2000. Searcheswere later updated to June 2001.

The main searches were supplemented by material identified by individual members of thedevelopment group. All selected papers were evaluated using standard methodological checklistsbefore conclusions were considered as evidence.

2007 Currency Review Process 

A scoping search for new evidence was carried out in 2007. The search was designed to identifyguidelines, health technology appraisals, Cochrane reviews and other systematic reviews relevant tothe contents of the guideline.

Search terms included MeSH headings for the condition specified and any common variations as freetext, plus terms for the interventions and care processes discussed in the guideline.

Sources Searched  

  Guidelines: National Institute for Health and Clinical Excellence (NICE), National Library for Health

guidelines finder, National Guideline Clearinghouse (NGC), Guidelines International Network (GIN)

Web site.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 24/53

  Technology appraisals: NICE, UK HTA database (Southampton), INAHTA database

  Cochrane review: Cochrane library

  Other good quality systematic reviews: UK HTA database (Southampton), DARE

SIGN provided a summary of new evidence and how it might influence a potential update to the

guideline. A Committee of 15 individuals provided feedback on the summary of new evidence (GPs3, Academics 2, Physicians 1, Rheumatologists 1, Biochemists 1, Other 7). A standard template wasused for responses. The Committee was asked to:

  Comment on assessment of the impact of the new evidence and its likely effect on recommendations

  List any additions to the remit of the guideline that might be beneficial

  Indicate preferred option for review (no update, full update, selective update, withdrawal)

Number of Source Documents

Not stated

Methods Used to Assess the Quality and Strength of the Evidence

Weighting According to a Rating Scheme (Scheme Given)

Rating Scheme for the Strength of the Evidence

Levels of Evidence 

1++: High quality meta-analyses, systematic reviews of randomised controlled trials (RCTs), or RCTswith a very low risk of bias

1+: Well-conducted meta-analyses, systematic reviews of RCTs, or RCTs with a low risk of bias

1-: Meta-analyses, systematic reviews of RCTs, or RCTs with a high risk of bias

2++: High quality systematic reviews of case control or cohort or studies; high quality case control orcohort studies with a very low risk of confounding or bias and a high probability that the relationshipis causal

2+: Well conducted case control or cohort studies with a low risk of confounding or bias and amoderate probability that the relationship is causal

2-: Case control or cohort studies with a high risk of confounding or bias and a significant risk that therelationship is not causal

3: Non-analytic studies, e.g. case reports, case series

4: Expert opinion

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 25/53

Methods Used to Analyze the Evidence

Review of Published Meta-Analyses

Systematic Review with Evidence Tables

Description of the Methods Used to Analyze the Evidence

The Scottish Intercollegiate Guidelines Network (SIGN) carries out comprehensive systematicreviews of the literature using customized search strategies applied to a number of electronicdatabases and the Internet. This is often an iterative process whereby the guideline development groupwill carry out a search for existing guidelines and systematic reviews in the first instance and, after theresults of this search have been evaluated, the questions driving the search may be redefined andfocused before proceeding to identify lower levels of evidence.

Once papers have been selected as potential sources of evidence, the methodology used in each studyis assessed to ensure its validity. SIGN has developed checklists to aid guideline developers to

critically evaluate the methodology of different types of study design. The result of this assessmentwill affect the level of evidence allocated to the paper, which in turn will influence the grade of recommendation it supports.

Additional details can be found in the companion document titled "An Introduction to the SIGNMethodology for the Development of Evidence-based Clinical Guidelines" (Edinburgh [UK]: ScottishIntercollegiate Guidelines Network. [SIGN publication; no. 50]). Available from the SIGN Website  .

Methods Used to Formulate the Recommendations

Expert Consensus

Description of Methods Used to Formulate the Recommendations

The process for synthesising the evidence base to form graded guideline recommendations isillustrated in the companion document titled "An Introduction to the SIGN Methodology for theDevelopment of Evidence-based Clinical Guidelines." (Edinburgh [UK]: Scottish IntercollegiateGuidelines Network. [SIGN publication; no. 50], available from the SIGN Web site  .

Evidence tables should be compiled, summarizing all the validated studies identified from thesystematic literature review relating to each key question. These evidence tables form an importantpart of the guideline development record and ensure that the basis of the guideline developmentgroup's recommendations is transparent.

In order to address how the guideline developer was able to arrive at their recommendations given theevidence they had to base them on, SIGN has introduced the concept of considered judgement.

Under the heading of considered judgement, guideline development groups are expected tosummarise their view of the total body of evidence covered by each evidence table. This summary

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 26/53

view is expected to cover the following aspects:

  Quantity, quality, and consistency of evidence

  Generalisability of study findings

  Applicability to the target population of the guideline

  Clinical impact (i.e., the extent of the impact on the target patient population, and the resources needto treat them.)

Guideline development groups are provided with a pro forma in which to record the main points fromtheir considered judgement. Once they have considered these issues, the groups are asked tosummarise their view of the evidence and assign a level of evidence to it, before going on to derive agraded recommendation.

The assignment of a level of evidence should involve all those on a particular guideline developmentgroup or subgroup involved with reviewing the evidence in relation to each specific question. Theallocation of the associated grade of recommendation should involve participation of all members of 

the guideline development group. Where the guideline development group is unable to agree on aunanimous recommendation, the difference of opinion should be formally recorded and the reason fordissent noted.

The recommendation grading system is intended to place greater weight on the quality of the evidencesupporting each recommendation, and to emphasise that the body of evidence should be considered asa whole, and not rely on a single study to support each recommendation. It is also intended to allowmore weight to be given to recommendations supported by good quality observational studies whererandomised controlled trials (RCTs) are not available for practical or ethical reasons. Through theconsidered judgement process guideline developers are also able to downgrade a recommendationwhere they think the evidence is not generalisable, not directly applicable to the target population, or

for other reasons is perceived as being weaker than a simple evaluation of the methodology wouldsuggest.

On occasion, there is an important practical point that the guideline developer may wish to emphasisebut for which there is not, nor is their likely to be, any research evidence. This will typically be wheresome aspect of treatment is regarded as such sound clinical practice that nobody is likely to questionit. These are marked in the guideline as "good practice points." It must be emphasized that these arenot an alternative to evidence-based recommendations, and should only be used where there is noalternative means of highlighting the issue.

Rating Scheme for the Strength of the Recommendations

The grade of recommendation relates to the strength of the evidence on which the recommendation isbased. It does not reflect the clinical importance of the recommendation.

A: At least one meta-analysis, systematic review of randomised controlled trials (RCTs), or RCTrated as 1++ and directly applicable to the target population; or  

A body of evidence consisting principally of studies rated as 1+, directly applicable to the target

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 27/53

population, and demonstrating overall consistency of results

B: A body of evidence including studies rated as 2++, directly applicable to the target population, anddemonstrating overall consistency of results; or  

Extrapolated evidence from studies rated as 1++ or 1+

C: A body of evidence including studies rated as 2+, directly applicable to the target population anddemonstrating overall consistency of results; or  

Extrapolated evidence from studies rated as 2++

D: Evidence level 3 or 4; or  

Extrapolated evidence from studies rated as 2+

Cost Analysis

Cost Effectiveness of Diagnostic Approaches 

Only three relevant economic papers on the use of dual-energy X-ray absorptiometry (DXA) scanningwere identified. These all involved modelling, rather than incorporation of economic evaluation intoclinical trials.

There is some evidence that for relatively expensive medication, such as bisphosphonates, treatmentprogrammes with prior bone density screening are likely to be more cost-effective than those withoutand, in some circumstances, become cost saving.

One recent paper concluded that diagnosis and treatment of women at risk of osteoporosis would bemade more cost effective by targeting treatment to those with the lowest bone measurement results.Inclusion of another assessment, such as a risk profile, may improve the cost effectiveness of diagnosis.

Cost Effectiveness of Treatment 

A recent Health Technology Assessment (HTA) examined the cost utility and cost effectiveness of different treatments for established osteoporosis. This study compared treatments using the cost perquality-adjusted life-year (QALY). It used a threshold of £30,000 or less per quality-adjusted life-year

to represent cost effectiveness. Using an economic model developed by the authors, at age 50 yearsonly hormone replacement therapy (HRT) and calcium plus vitamin D were likely to be consideredcost-effective (assuming that the agent would decrease the risk of non-vertebral fractures at this age).In older age groups a wider range of treatments, including hormone replacement therapy, calciumwith or without vitamin D and bisphosphonates were considered cost effective.

This Health Technology Assessment demonstrates that age is an important determinant of costeffectiveness since the risk of fractures increases with age. High costs of intervention are associated

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 28/53

with poorer cost effectiveness since, in general, the variation in cost is greater than any provenvariation in efficacy.

Method of Guideline Validation

External Peer ReviewInternal Peer Review

Description of Method of Guideline Validation

A national open meeting is the main consultative phase of Scottish Intercollegiate GuidelinesNetwork (SIGN) guideline development, at which the guideline development group presents its draftrecommendations for the first time. The national open meeting for this guideline was held in February2002 and was attended by 328 representatives of all the key specialties relevant to the guideline. Thedraft guideline was also available on the SIGN website for a limited period at this stage to allow thoseunable to attend the meeting to contribute to the development of the guideline. The comments

received from the national open meeting were considered when the guideline was redrafted for peerreview.

The guideline was also reviewed in draft form by independent expert referees, who were asked tocomment primarily on the comprehensiveness and accuracy of interpretation of the evidence basesupporting the recommendations in the guideline.

As a final quality control check, the guideline is reviewed by an Editorial Group comprising therelevant specialty representatives on SIGN Council to ensure that the peer reviewers' comments havebeen addressed adequately and that any risk of bias in the guideline development process as a wholehas been minimised.

Each member of the guideline development group then approved the final guideline for publication.

Back to top 

Recommendations

Major Recommendations

 Note from the Scottish Intercollegiate Guidelines Network (SIGN) and National Guideline

Clearinghouse (NGC): In addition to these evidence-based recommendations, the guideline

development group also identifies points of best clinical practice in the original guideline document. 

The strength of recommendation grading (A-D) and level of evidence (1++, 1+, 1-, 2++, 2+, 2-, 3, 4)are defined at the end of the "Major Recommendations" field.

Risk Factors for Osteoporosis 

B - Patients who have suffered one or more fragility fractures should be priority targets forinvestigation and treatment of osteoporosis.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 29/53

C - Use of family history in assessing risk of osteoporosis should include maternal, paternal, andsister history.

C - Family history should include not only a given diagnosis of osteoporosis but also kyphosis andlow trauma fracture after age 50.

B - Smokers should be considered at greater risk of osteoporosis than non-smokers, and advised tostop, for this and other reasons.

Measurement, Diagnosis and Monitoring 

B - Conventional radiographs should not be used for the diagnosis or exclusion of osteoporosis.

B - When plain films are interpreted as "severe osteopaenia" it is appropriate to suggest referral fordual-energy X-ray absorptiometry (DXA).

A  – Bone mineral density (BMD) should normally be measured by DXA scanning performed on twosites, preferably anteroposterior spine and hip.

B - Repeat measurements should only be performed if they influence treatment.

C - If DXA investigations are repeated, anteroposterior (AP) spine and total hip measurements shouldbe used to follow response to treatment.

C - Following a DXA scan of the hip, the annual hip fracture risk (or 10 year fracture risk) should beincluded in the DXA report.

C - Where lateral spine scans acquired with fan-beam DXA are available, visual assessment should beused to assess prevalent vertebral fractures.

B - Evidence of existing vertebral deformity should be used to modify the hip fracture risk estimatedfrom age, sex, and BMD.

A - Biochemical markers of bone turnover should have no role in the diagnosis of osteoporosis or inthe selection of patients for BMD measurement.

Non-pharmacological Interventions 

B - High intensity strength training is recommended as part of a management strategy forosteoporosis.

B - Low impact weight bearing exercise is recommended as part of a management strategy forosteoporosis.

A - Postmenopausal women should aim for a dietary intake of 1,000 mg calcium per day.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 30/53

B - Ipriflavone should not be used as a sole therapy for fracture reduction in patients withosteoporosis.

Pharmacological Management 

For postmenopausal women with multiple vertebral fractures

A - To reduce fracture risk at all sites: treatment with oral risedronate (5 mg daily or 35 mg onceweekly + calcium + vitamin D).

A - To reduce vertebral fracture risk: treatment with intermittent cyclical etidronate (400 mg daily for14 days + 500 mg calcium daily for 76 days, repeating 3 monthly cyclical therapy).

For postmenopausal women with osteoporosis determined by axial DXA and with a history of at leastone vertebral fracture

A - To reduce fracture risk at all sites: treatment with oral alendronate (10 mg daily or 70 mg onceweekly + calcium + vitamin D).

A - To reduce vertebral fracture risk: treatment with oral raloxifene (60 mg daily + calcium + vitaminD).

B - To reduce vertebral fracture risk: treatment with intranasal calcitonin (200 IU daily + calcium +vitamin D).

For postmenopausal women with osteoporosis determined by axial DXA, with or without previousnon-vertebral fracture

A - To reduce fracture risk at all sites: treatment with either oral alendronate (10 mg daily or 70 mgonce weekly + calcium + vitamin D) or oral risedronate (5 mg daily or 35 mg once weekly + calcium+ vitamin D).

A - To reduce vertebral fracture risk: treatment with oral raloxifene (60 mg per day + calcium +vitamin D).

For frail, elderly (aged 80+ years) women with a diagnosis of osteoporosis, with or without previousnon-vertebral fractures

A - To reduce fracture risk at all sites, elderly women who have suffered multiple vertebral fracturesor who have had osteoporosis confirmed by DXA scanning should be considered for treatment witheither oral risedronate (5 mg daily or 35 mg once weekly+ calcium + vitamin D) or oral alendronate(10 mg daily or 70 mg once weekly + calcium + vitamin D).

A - To reduce hip fracture risk, frail elderly women who are housebound should receive oral calcium1,000 to 1,200 mg daily + 800 IU vitamin D.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 31/53

For men with a diagnosis of osteoporosis determined by axial DXA with or without previousosteoporotic fracture

A - To reduce fracture risk at all sites, men with low BMD and/or a history of one or more vertebralfractures or one non-vertebral osteoporotic fracture should be treated with oral alendronate (10 mg +

500mg calcium + 400 IU vitamin D daily).

Definitions:

Grades of Recommendation 

A: At least one meta-analysis, systematic review of randomised controlled trials (RCTs), or RCTrated as 1++ and directly applicable to the target population; or  

A body of evidence consisting principally of studies rated as 1+, directly applicable to the targetpopulation, and demonstrating overall consistency of results

B: A body of evidence including studies rated as 2++, directly applicable to the target population, anddemonstrating overall consistency of results; or  

Extrapolated evidence from studies rated as 1++ or 1+

C: A body of evidence including studies rated as 2+, directly applicable to the target population anddemonstrating overall consistency of results; or  

Extrapolated evidence from studies rated as 2++

D: Evidence level 3 or 4; or  

Extrapolated evidence from studies rated as 2+

Levels of Evidence 

1++: High quality meta-analyses, systematic reviews of randomised controlled trials (RCTs), or RCTswith a very low risk of bias

1+: Well-conducted meta-analyses, systematic reviews of RCTs, or RCTs with a low risk of bias

1-: Meta-analyses, systematic reviews of RCTs, or RCTs with a high risk of bias

2++: High quality systematic reviews of case control or cohort studies; high quality case control orcohort studies with a very low risk of confounding or bias and a high probability that the relationshipis causal

2+: Well conducted case control or cohort studies with a low risk of confounding or bias and amoderate probability that the relationship is causal

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 32/53

2-: Case control or cohort studies with a high risk of confounding or bias and a significant risk that therelationship is not causal

3: Non-analytic studies, e.g. case reports, case series

4: Expert opinion

Clinical Algorithm(s)

An algorithm is provided in the original guideline document for the management of glucocorticoid-induced osteoporosis in men and women.

Back to top 

Evidence Supporting the Recommendations

Type of Evidence Supporting the Recommendations

The type of supporting evidence is identified and graded for each recommendation (see "MajorRecommendations").

Back to top 

Benefits/Harms of Implementing the Guideline Recommendations

Potential Benefits

  Reduction in the incidence of fractures

  Alleviation of fracture related morbidity

  Prevention of subsequent fractures

  Identification of risk factors to provide targeted treatment

Potential Harms

All bisphosphonates can potentially be associated with gastrointestinal side effects. Foraminobisphosphonates such as alendronate, this can on rare occasions present as oesophagealulceration. The risk of these symptoms can be lessened by the avoidance of lying flat within 30minutes of ingestion or by using the once weekly preparations.

Back to top 

Contraindications

Contraindications

Previous history of venous thromboembolism (VTE) contraindicates oral hormone replacementtherapy (HRT) or raloxifene.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 33/53

Back to top 

Qualifying Statements

Qualifying Statements

  This guideline is not intended to be construed or to serve as a standard of medical care. Standards of care are determined on the basis of all clinical data available for an individual case and are subject to

change as scientific knowledge and technology advance and patterns of care evolve. These

parameters of practice should be considered guidelines only. Adherence to them will not ensure a

successful outcome in every case, nor should they be construed as including all proper methods of 

care or excluding other acceptable methods of care aimed at the same results.

  The ultimate judgement regarding a particular clinical procedure or treatment plan must be made by

the doctor in light of the clinical data presented by the patient and the diagnostic and treatment

choices available. However, it is advised that significant departures from the national guideline or any

local guidelines derived from it should be fully documented in the patient’s case notes at the time the

relevant decision is taken.

Back to top 

Implementation of the Guideline

Description of Implementation Strategy

Implementation of national clinical guidelines is the responsibility of each National Health System(NHS) Trust and is an essential part of clinical governance. It is acknowledged that every Trustcannot implement every guideline immediately on publication, but mechanisms should be in place toensure that the care provided is reviewed against the guideline recommendations and the reasons forany differences assessed and, where appropriate, addressed. These discussions should involve both

clinical staff and management. Local arrangements may then be made to implement the nationalguideline in individual hospitals, units and practices, and to monitor compliance. This may be done bya variety of means including patient-specific reminders, continuing education and training, andclinical audit.

The National Osteoporosis Society (NOS) has produced an Osteoporosis Framework setting outstandards for osteoporosis services in Scotland. This framework has been endorsed by the Chief Medical Officer.

The key recommendations from the National Osteoporosis Society framework document are:

  Include prevention of osteoporotic fractures in the local Health Improvement Plan (HIP)  Identify lead clinicians in primary and secondary care to develop a local osteoporosis programme

based on this framework. Each Local Health Cooperative, Primary Care, and Acute Trust should have a

lead clinician for osteoporosis.

  Each Health Board should have a consultant in Public Health to assist in coordinating this osteoporosis

strategy between primary and secondary care.

  Establish a local osteoporosis advisory group to facilitate multidisciplinary implementation of this

framework.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 34/53

  Use a selective case-finding approach to target treatment at individuals at high risk.

  Provide access to adequate levels of diagnostic and specialist services - e.g. a Local Health Care Co-

operative serving a population of 50,000 would require approximately 500 dual-energy X-ray

absorptiometry (DXA) scans per year.

  Promote the use of care pathways and audit to improve standards of care.

  Monitor performance to assess health impact.

Key points for audit are identified in the original guideline document.

Implementation Tools

Clinical Algorithm

Patient Resources

Quick Reference Guides/Physician Guides

For information about availability, see the Availability of Companion Documents and Patient Resources fields

below.

Back to top 

Institute of Medicine (IOM) National Healthcare Quality Report Categories

IOM Care Need

Living with Illness

IOM Domain

Effectiveness

Patient-centeredness

Back to top 

Identifying Information and Availability

Bibliographic Source(s)

Scottish Intercollegiate Guidelines Network (SIGN). Management of osteoporosis. A national clinical

guideline. Edinburgh (Scotland): Scottish Intercollegiate Guidelines Network (SIGN); 2003 Jun. 45 p. (SIGN

publication; no. 71). [149 references] 

Adaptation

Not applicable: The guideline was not adapted from another source.

Date Released

2003 Jun (reaffirmed 2007)

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 35/53

Guideline Developer(s)

Scottish Intercollegiate Guidelines Network - National Government Agency [Non-U.S.]

Source(s) of Funding

Scottish Executive Health Department

Guideline Committee

Not stated

Composition of Group That Authored the Guideline

Guideline Development Group: Dr Tricia Donald (Chair ), General Practitioner, Edinburgh; Dr JohnEnnis (Secretary), General Practitioner, Edinburgh; Dr Lisa Mackenzie (Methodologist), SpR

Rheumatology, Glasgow Royal Infirmary; Dr Graham Beastall, Clinical Biochemist, Glasgow RoyalInfirmary; Dr Lucy Caird, Consultant Gynaecologist, Raigmore Hospital, Inverness; Dr ClareCampbell, General Practitioner, Broxburn; Dr Donald Farquhar, Consultant Geriatrician, St. John’s

Hospital, Livingston; Dr Ailsa Gebbie, Community Gynaecologist, Edinburgh; Mr Alberto Gregori,Consultant Orthopaedic Surgeon, Hairmyres Hospital, East Kilbride; Dr Jim Hannan, Physicist,Western General Hospital, Edinburgh; Mr Robin Harbour, Quality & Information Director, ScottishIntercollegiate Guidelines Network; Ms Janice Harris, Senior Pharmacist, Royal Victoria Hospital,Edinburgh; Dr Andrew Jamieson, Consultant Physician, Queen Margaret Hospital, Dunfermline; DrJustus Krabshuis, Highland Data Ltd; Ms Ann Lees, Health Planning Manager (Health Economist),Argyll and Clyde Acute Hospitals National Health System Trust; Dr Alastair McLellan, ConsultantEndocrinologist, Western Infirmary, Glasgow; Ms Alice Mitchell, Health Visitor, Glasgow; Dr Sarah

Mitchell, Physiotherapist, Glasgow Royal Infirmary; Dr Caroline Morrison, Public Health Consultant,Greater Glasgow Health Board, Dr Anne Payne, Lecturer in Clinical Nutrition and Dietetics, GlasgowCaledonian University; Dr Colin Perry (Methodologist), Specialist Registrar (Endocrinology),Glasgow Royal Infirmary; Dr Nigel Raby, Consultant Radiologist, Western Infirmary, Glasgow;Professor David Reid, Consultant Rheumatologist, Foresterhill, Aberdeen; Dr Mary Scott, GeneralPractitioner, Dunfermline; Mrs Anne Simpson, National Osteoporosis Society Coordinator forScotland

Financial Disclosures/Conflicts of Interest

All members of the Scottish Intercollegiate Guidelines Network (SIGN) guideline development

groups are required to complete a declaration of interests, both personal and non-personal. A personalinterest involves payment to the individual concerned (e.g., consultancies or other fee-paid work commissioned by or shareholdings in the pharmaceutical industry); a non-personal interest involvespayment which benefits any group, unit, or department for which the individual is responsible (e.g.,endowed fellowships or other pharmaceutical industry support). Details of the declarations of interestof any guideline development group member(s) are available from the SIGN executive.

Guideline Status

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 36/53

This is the current release of the guideline.

The guideline was reaffirmed by the developer in 2007.

Any amendments to the guideline will be noted on Scottish Intercollegiate Guidelines Network 

(SIGN) Web site  .

Guideline Availability

Electronic copies: Available from the Scottish Intercollegiate Guidelines Network (SIGN) Web site:

  HTML format 

  Portable Document Format (PDF) 

Availability of Companion Documents

The following are available:

  Quick reference guide: Management of osteoporosis. A national clinical guideline. Scottish

Intercollegiate Guidelines Network, 2003. 2 p. Available in Portable Document Format (PDF) from the

Scottish Intercollegiate Guidelines Network (SIGN) Web site  .

  SIGN 50: A guideline developer’s handbook. Edinburgh (Scotland): Scottish Intercollegiate Guidelines

Network. (SIGN publication; no. 50). Available from the SIGN Web site  .

  Appraising the quality of clinical guidelines. The SIGN guide to the AGREE (Appraisal of Guidelines

Research & Evaluation) guideline appraisal instrument. Edinburgh (Scotland): Scottish Intercollegiate

Guidelines Network, 2001. Available from the SIGN Web site  .

Patient Resources

The following is available:

  Information for discussion with patients and carers. In: Management of osteoporosis. A national

clinical guideline. Edinburgh (Scotland): Scottish Intercollegiate Guidelines Network (SIGN); 2003 Jun.

45 p. (SIGN publication; no. 71).

Electronic copies: Available from the Scottish Intercollegiate Guidelines Network (SIGN) Web site .

Please note: This patient information is intended to provide health professionals with information toshare with their patients to help them better understand their health and their diagnosed disorders. Byproviding access to this patient information, it is not the intention of NGC to provide specific medicaladvice for particular patients. Rather we urge patients and their representatives to review this materialand then to consult with a licensed health professional for evaluation of treatment options suitable forthem as well as for diagnosis and answers to their personal medical questions. This patientinformation has been derived and prepared from a guideline for health care professionals included onNGC by the authors or publishers of that original guideline. The patient information is not reviewed

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 37/53

by NGC to establish whether or not it accurately reflects the original guideline's content.

NGC Status

This NGC summary was completed by ECRI on April 26, 2004. The information was verified by the

guideline developer on July 15, 2004. The information was reaffirmed by the guideline developer in2007 and updated by ECRI Institute on March 29, 2010. This summary was updated by ECRIInstitute on December 10, 2010 following the U.S. Food and Drug Administration (FDA) advisory onBisphosphonates.

Copyright Statement

Scottish Intercollegiate Guidelines Network (SIGN) guidelines are subject to copyright; however,SIGN encourages the downloading and use of its guidelines for the purposes of implementation,education, and audit.

Users wishing to use, reproduce, or republish SIGN material for commercial purposes must seek priorapproval for reproduction in any medium. To do this, please contact sara.twaddle@nhs.net. 

Additional copyright information is available on the SIGN Web site  .

Back to top 

Disclaimer

NGC Disclaimer

The National Guideline Clearinghouse™ (NGC) does not develop, produce, approve, or endorse the

guidelines represented on this site.

Read full disclaimer... 

  Other Sections▼ 

Abstract

Osteoporosis or osteopenia occurs in about 44 million Americans, resulting in 1.5 millionfragility fractures per year. The consequences of these fractures include pain, disability,depression, loss of independence, and increased mortality. The burden to the healthcare system,in terms of cost and resources, is tremendous, with an estimated direct annual USA healthcareexpenditure of about $17 billion. With longer life expectancy and the aging of the baby-boomergeneration, the number of men and women with osteoporosis or low bone density is expected torise to over 61 million by 2020. Osteoporosis is a silent disease that causes no symptoms until afracture occurs. Any fragility fracture greatly increases the risk of future fractures. Most patients

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 38/53

with osteoporosis are not being diagnosed or treated. Even those with previous fractures, who areat extremely high risk of future fractures, are often not being treated. It is preferable to diagnoseosteoporosis by bone density testing of high risk individuals before the first fracture occurs. If osteoporosis or low bone density is identified, evaluation for contributing factors should beconsidered. Patients on long-term glucocorticoid therapy are at especially high risk for

developing osteoporosis, and may sustain fractures at a lower bone density than those not takingglucocorticoids. All patients should be counseled on the importance of regular weight-bearingexercise and adequate daily intake of calcium and vitamin D. Exposure to medications that causedrowsiness or hypotension should be minimized. Non-pharmacologic therapy to reduce the non-skeletal risk factors for fracture should be considered. These include fall prevention throughbalance training and muscle strengthening, removal of fall hazards at home, and wearing hipprotectors if the risk of falling remains high. Pharmacologic therapy can stabilize or increasebone density in most patients, and reduce fracture risk by about 50%. By selecting high risk patients for bone density testing it is possible to diagnose this disease before the first fractureoccurs, and initiate appropriate treatment to reduce the risk of future fractures.Keywords: osteoporosis, management, treatment, bone density testing, DXA, glucocorticoid,

fracture, risk 

  Other Sections▼ 

BackgroundOsteoporosis is a silent disease that causes no symptoms until a fracture occurs. It is a majorpublic health concern, with about 44 million American men and women, or 55% of thepopulation age 50 and over, having osteoporosis or low bone density that can lead to fractures[1]. About 80% of osteoporosis occurs in women and 20% in men. The prevalence is increasing,with over 61 million expected to have osteoporosis or low bone density by 2020. About 30% of Caucasian women age 50 and over have osteoporosis, when defined as a T-score of less than -2.5at the spine, hip, or mid-forearm [2]. In men age 50 and older, the prevalence of osteoporosis isabout 19% [3]. There are about 1.5 million fragility fractures in the USA each year, with 700,000vertebral fractures, 300,000 hip fractures, 250,000 wrist fractures, and 250,000 at other skeletalsites. The lifetime risk of fracture is substantial. Population data from Rochester, Minnesota,estimate that at the age of 50, a Caucasian woman has about a 40% lifetime risk and a Caucasianman a 13% lifetime risk of fracture of fracture at hip, spine, or distal forearm [4]. In Malmö,Sweden, the lifetime risk of fracture of the hip, spine, forearm or proximal humerus at age 50was reported to be 46% in women and 22% in men [5]. The Dubbo study found that at the age 60there was a residual lifetime fracture risk of 56% for women and 29% for men, assuming averagelife expectancy [6]. A woman's risk of hip fracture is equal to her combined risk of breast,uterine, and ovarian cancer [7]. Fractures of the spine and hip are associated with an increasedrisk of chronic pain, deformity, depression, disability, and death. About 50% of those with a hipfracture will be permanently unable to walk without assistance and 25% will require long-termcare [8]. The mortality rate five years after a fracture of the hip or a clinical vertebral fracture isabout 20% greater than expected [9], with men having higher mortality rates than women, evenwhen standardized for age [10]. The direct cost of osteoporotic fractures in the USA was about$17 billion per year in 2001 [11], extrapolated from 1995 figures using the Medical Index of theConsumer Price Index, with this value expected to rise greatly in future years.

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 39/53

  Other Sections▼ 

Bone density and bone strengthOsteoporosis is defined as "a skeletal disease characterized by compromised bone strengthpredisposing a person to an increased risk of fracture. Bone strength primarily reflects the

integration of bone density and quality." [12] Bone mineral density (BMD) correlates very wellwith fracture risk, with the relative risk of fracture approximately doubling (range 1.6 – 2.6) forevery standard deviation decrease in BMD, depending on the skeletal site measured and the typeof fracture [13]. Many devices and technologies are available for measuring BMD. Dual-energyX-ray absorptiometry (DXA) is the method used to diagnose osteoporosis according to criteriaestablished by the World Health Organization [14] [Table [Table11].

Table 1 Classification of Bone Mineral Density (World HealthOrganization) [14].

Non-BMD factors that may alter bone strength include bone turnover, architecture (size andshape, or bone geometry), microarchitecture, damage accumulation, matrix properties,mineralization, and mineral properties. These factors and probably many others that have not yetbeen well-defined are collectively called "bone quality" or "bone qualities." Accumulatingknowledge regarding bone qualities offers insight into the pathophysiology of osteoporosis andmetabolic bone disease, and helps in understanding the mechanisms of action of bone-activedrugs. However, with the exception of bone turnover markers and bone geometry, none of theseare these presently have clinical applications.The adult skeleton is in a constant state of remodeling, a process whereby bone and bone matrix(mostly composed of type 1 collagen) is continually being removed by osteoclasts in discretepackets, or bone remodeling units, followed by osteoblast-mediated bone formation and

mineralization. With high bone turnover states, such as occurs with estrogen deficiency in theearly postmenopausal years, there are more bone remodeling units resulting in a greater numberof "stress-risers," or weakened areas of bone. A stress-riser in bone is analogous to a scored lineon a sheet of glass, where the glass is more likely to break than in an area that is not scored.Ultimately, thinning and perforation of trabecular structures may occur, as well as impairedmineralization. High bone turnover, which is detected clinically by the finding of elevatedmarkers of bone resorption, has been shown to be an independent risk factor for fracture [15].Small bones, as in individuals with a small frame or in women compared to men, are weakerthan large bones. This is consistent with the engineering concept that a tubular structure, such asa long bone, has a greater ability to resist bending forces as the diameter increases. Longer hipaxis length (the distance from the lateral surface of the greater trochanter to the inner surface of 

the pelvis, along the axis of the femoral neck), larger femoral neck-shaft angle (the anglebetween the axis of the femoral neck and the femoral shaft), and wider femoral neck diameter(the width of the femoral neck at its narrowest portion) are associated with increased risk of hipfracture [16]. This may explain, in part, the lower risk of hip fracture in Chinese and Japanesewomen compared to Caucasians, despite similar BMD. A larger vertebral body is less likely tofracture than a smaller one, even with the same BMD, since a larger cross-sectional area hasgreater resistance to compressive forces [17].

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 40/53

Bone microarchitecture, best evaluated by bone biopsy, concerns bone properties at themicroscopic level, such as the spatial distribution of trabecular rods and plates, trabecularthickness and connectivity, cortical thickness and cortical porosity. The horizontal trabeculae,which stabilize the load-bearing vertical trabeculae, are subject to thinning and perforation inpatients with osteoporosis, resulting in loss of bone strength and increased fracture risk [18]. The

number, size, and distribution of cortical porosities may play a role in determining bone strength[19].Damage accumulation, such as the increasing number of microfractures with advancing age,occurs at multiple skeletal sites in some, but perhaps not all individuals [20]. While this hasadverse effects on the biomechanical properties of bone, the relationship between microfracturesand clinical fractures is not clear, and the significance of increased microdamage accumulationwith antiresorptive therapy is not known.Bone matrix is the noncalcified portion of bone, 90% of which is composed of type 1 collagen. Itprovides elasticity and flexibility to bone. Inherited and acquired disorders of the collagen fibrils,crosslinking, or non-collagenous proteins may have serious consequences on bone strength andfracture risk. Mild forms of metabolic bone disease with abnormal collagen, such as osteogenesis

imperfecta and Ehlers-Danlos syndrome, may sometimes masquerade as postmenopausalosteoporosis.Mineralization is responsible for stiffness, or mechanical rigidity, of bone. Too much(osteopetrosis) or too little (osteomalacia) bone mineral can have adverse effects on bonestrength. Mineralization takes place in two phases: the primary, or active bone formation phase,occurring over a period of months, and the secondary, or slow phase, which takes years. Thesecond phase, which may be responsible for as much as 50% of bone mineralization, isincomplete in high bone turnover states. The rapid increase in BMD over the first 6 – 12 monthsof bisphosphonate therapy is due to "filling of the remodeling space" associated with the firstphase of mineralization, while the slower increase in BMD over the following years is due toincreased secondary mineralization allowed by the reduced rate of bone turnover [21]. Even thesize and distribution of hydroxyapatite crystals may affect the mechanical properties of bone,with animal studies suggesting that a mix of small and large crystals are stronger than only largecrystals or only small crystals [22].

  Other Sections▼ 

Clinical risk factorsConsideration of risk factors can provide helpful information for patient management. It isenlightening to distinguish risk factors for osteoporosis from risk factors for fracture, risk factorsfor hip fracture from risk factors for vertebral fracture, and skeletal risk factors for fracture fromnon-skeletal ones, since the clinical implications will vary accordingly. For example, risk factorsfor osteoporosis, such as advanced age, small stature, or family history, are commonly used inselecting patients for bone density testing, and may determine whether the test is covered byinsurance. Clinical risk factors for osteoporosis are not a substitute for bone density testing, andin fact cannot accurately predict which individual patients have low bone density [23]. Risk factors for fracture, which overlap risk factors for osteoporosis but are not totally the same, canhelp determine which patients require medical intervention. Skeletal risk factors for fracture,such as low bone density or high bone turnover, may be treated with pharmacologic agents. Non-skeletal risk factors for fracture, such as poor balance and high risk for falling, require other

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 41/53

types of intervention, such as balance training and hip protectors. Advancing age is a risk factorfor osteoporosis and fractures for which there is no antidote. Good nutrition, regular weight-bearing exercise, and avoidance of cigarette smoking, alcohol excess and bone-toxic drugs canmaximize the genetic potential for skeletal integrity. Validated risk factors for fracture also varyaccording to the type of fracture, with many more risk factors identified for hip fracture than for

vertebral fracture. A list of common skeletal and nonskeletal risk factors for hip fracture is inTable Table2.2. The best validated risk factors for vertebral fracture are low BMD, advancingage, and previous fracture.

Table 2 Selected Skeletal and Nonskeletal Risk Factors for Hip Fracture[15,48].

Long-term glucocorticoid therapyA meta-analysis of 66 BMD studies and 23 fracture studies showed that oral glucocorticoidtreatment with more than prednisolone 5 mg per day or equivalent leads to a decrease in BMDand increased risk of fracture [24]. The increase in fracture risk begins within 3 – 6 months of starting glucocorticoids, decreases soon after stopping, and is independent of age, sex, orunderlying disease. Analysis of the United Kingdom General Practice Research Database (UKGPRD) of 244,235 patients on oral glucocorticoid therapy showed that a low dose (less than 2.5mg per day) was associated with an increased risk of vertebral and nonvertebral fractures, anddoses greater than 2.5 mg per day were associated with increased risk of vertebral, nonvertebral,and hip fractures [25]. Fracture risk was dose-dependent, increasing dramatically as the doseincreased. The fracture risk associated with glucocorticoid therapy appears to be related toaverage daily dose rather than cumulative dose, suggesting that the adverse skeletal effects areacute rather than chronic [26]. Some [27], but not all [28], studies have shown that patients onglucocorticoid therapy fracture at a higher BMD than patients not on glucocorticoid therapy,suggesting problems with bone quality that are independent of BMD, and that perhaps treatment

thresholds should be more aggressive for glucocorticoid patients. A UK GPRD study of 170,818patients on inhaled glucocorticoids showed increased risk of vertebral, nonvertebral, and hipfractures compared to controls, but suggested that the risk increase may have been due to theunderlying respiratory disease rather than the inhaled glucocorticoids [29]. A meta-analysis of 27studies showed that inhaled glucocorticoids (triamcinolone, budesonide, beclomethasone) indoses over 1.5 mg per day (0.75 mg per day for fluticasone propionate) may be associated with asignificant reduction in bone density [30]. In a 2-year randomized placebo-controlled trial of inhaled fluticasone in asthma patients, there was no significant change in BMD with doses of 0.176 mg per day [31]. There is no convincing evidence that intranasal glucocorticoids innormally prescribed doses have any clinically significant adverse effect on skeletal integrity [32],although some studies have demonstrated suppression of the hypothalamic-pituitary-adrenal axis

[33]. Further study is needed to define the impact of intranasal glucocorticoid formulation, dose,and combination with oral or inhaled glucocorticoids on the development of bone disease. Theprevalence of glucocorticoid-induced osteoporosis is often difficult to determine due to theconfounding effects of comorbidities and polypharmacy. A study of general practice patients inIceland showed that 26% of those treated with oral glucocorticoids for more than 3 months werediagnosed with osteoporosis, and 20% had a history of fragility fractures [34]. Thepathophysiology of glucocorticoid-induced osteoporosis is multifactorial, and includes 1.)impairment of osteoblast, osteocyte, and osteoclast function, leading to decreased bone turnover

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 42/53

and reduced microfracture repair; 2.) disordered calcium metabolism, with reduced intestinalabsorption, increased renal excretion, and possible secondary hyperparathyroidism; and 3.)decreased synthesis of sex hormones [35].

  Other Sections▼ 

DiagnosisBone density testingA clinical diagnosis of osteoporosis may be made in the presence of a fragility fracture, providedother causes of fracture have been ruled-out. A fragility fracture is any fracture occurring aftertrivial trauma, such as falling from the standing position, coughing, bending, or reaching. Mostfractures in adults, except those from major trauma, such as auto accident or falling off a ladder,are fragility fractures. The preferable method of diagnosing osteoporosis is by bone densitytesting, before the first fracture has occurred. The WHO criteria may be used to classify BMD,expressed as T-score, as normal, osteopenia, or osteoporosis.A T-score is the standard deviation (SD) variance of the patient's BMD compared to a healthy

young-adult reference population. It is calculated according to the following formula, with BMDand SD expressed as g/cm2:

This formula shows that the T-score is dependent on factors other than the patient's BMD, andthat a change in the mean or SD of the reference population can result in a different T-score. Forexample, if the mean young-adult BMD in the reference population is higher, the T-score willdecrease, and if the SD is lower, the T-score will increase. This is a clinically import concept,since the reference population may vary according to the manufacturer of the instrument, thesoftware version installed, or the region of interest being measured. For this reason, comparisonof serial DXA studies should always be done with absolute BMD values in g/cm2, and not with

T-scores.A Z-score is the standard deviation (SD) variance of the patient's BMD compared to an age- andsex-matched reference population, and should not be used to diagnose osteoporosis. It iscalculated according to the same formula as the T-score, except that the reference population isage- and ethnicity-matched instead of young-adult matched.The WHO classification system was originally devised as a public health tool for evaluating theprevalence of osteoporosis in populations of postmenopausal women. It was not intended for usein the diagnosis of osteoporosis in individual patients. However, in the absence of a betteryardstick, it quickly came to be used in that fashion. The T-score cut-off of -2.5 for diagnosingosteoporosis was selected because it identified approximately 30% of postmenopausal Caucasianwomen as having osteoporosis, which is roughly the same as the lifetime risk of clinical fragility

fractures in this population. The WHO criteria apply to BMD measurement by DXA of the spine,hip and forearm in postmenopausal women and in men age 65 and older [36]. At the presenttime, the WHO criteria should not be used with BMD measurement devices other than DXA, norfor measurement at skeletal sites other than spine, hip, and forearm. Perhaps in the future, withstandardization of reference databases, and acquisition of device-specific data on prevalence of osteoporosis and fracture risk, the diagnosis of osteoporosis will be made with devices other thanDXA.Who should be tested?

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 43/53

Bone density testing should be considered in anyone at risk for osteoporosis, or being monitoredfor treatment of osteoporosis, provided that the results of the test are likely to play a role inpatient management decisions. Of all the published guidelines of indications for bone densitytesting, the most comprehensive are those of the International Society for Clinical Densitometry(ISCD) [36], listed in Table Table33. 

Table 3 Indications for Bone Density Testing [36] (Official Position of the International Society for Clinical Densitometry).

  Other Sections▼ 

Evaluation of low bone densityIt is prudent to have a high index of suspicion for contributing factors in every patient with lowdensity. A T-score of -2.5 or below is not always osteoporosis. It could be metabolic bonedisease, such as osteomalacia, or a localized bone disorder, such as a bone cyst in the measuredskeletal site. A postmenopausal woman with osteoporosis does not always have postmenopausalosteoporosis. She could have malabsorption due to undiagnosed celiac disease, or possiblymultiple myeloma. Table Table44 lists diseases, conditions, and medications commonlyassociated with low bone density. In every patient with low BMD, it is reasonable to considermeasuring a complete blood count, serum calcium, phosphorous, creatinine, alkalinephosphatase, liver enzymes, and thyroid stimulating hormone. Tests that are often helpfulinclude a 24-hour urine for calcium, celiac antibodies, and in older patients, a serum and urineprotein electrophoresis. In selected patients, a serum intact parathyroid hormone level, urinary

free cortisol (or other tests to rule out Cushing's syndrome), or additional studies may be helpful.Table 4 Causes of Low Bone Mineral Density.

  Other Sections▼ 

Prevention and treatmentNonpharmacologic therapyNonpharmacologic therapy can be divided into the categories of nutrition, lifestyle, and fallprevention. These represent the foundation for the management of osteoporosis, without whichpatients are unlikely to achieve the full benefit of pharmacologic therapy. Calcium and vitamin Dsupplementation have been shown to increase BMD [37] and reduce the risk of fractures [38] inprospective trials. The average American diet is deficient in calcium, and many Americans havean insufficient daily intake of vitamin D. The National Osteoporosis Foundation recommends

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 44/53

that all adults have a daily intake of at least 1200 mg elemental calcium with diet plussupplements, and 400 – 800 IU vitamin D per day for patients at risk of deficiency [39].Lifestyle intervention for osteoporosis includes regular weight-bearing exercise and avoidance of unhealthy behavior, such as cigarette smoking and excess alcohol intake. Patients with low BMDand high risk for falling may benefit from additional measures, such as muscle strengthening, fall

prevention, balance training, Tai Chi, extra care with the dosing of certain drugs (e.g., sedatives,hypnotics, antihypertensives, anticonvulsants), nightlights, handrails, grab-bars, removal of slippery carpets and dangerous obstacles at home, correction of impaired eyesight and hearing,and the wearing of hip protectors.The decision to treatSince the goal of treatment is to prevent fractures, selection of patients for drug treatment shouldbe based on level of fracture risk. Current guidelines for initiation of pharmacologic therapy[Table [Table5]5] are based on T-score or T-score plus clinical risk factors. While theseguidelines are a helpful for appropriate patient populations, over-reliance on T-scores alone mayunderestimate or overestimate absolute fracture risk and lead to inappropriate therapy. Forexample, a healthy 30 year-old premenopausal woman with a T-score (or Z-score) of -2.1

probably has a low 5 – 10 year absolute fracture risk and would probably not benefit frompharmacologic therapy, while an elderly man or woman with a T-score of -1.4 and a history of fragility fracture is at high risk for future fracture and could expect a significant reduction infracture risk with therapy. Efforts are currently underway to develop a standardized methodologyfor calculating and expressing absolute fracture risk, which is arguably the best way of establishing therapeutic thresholds. Personal issues and non-skeletal effects of medications arealso important to consider in the decision to treat and drug selection [Table [Table66] 

Table 5 Indications for Pharmacologic Therapy.

Table 6 Nonskeletal Effects of Pharmacologic Therapy.

Pharmacologic therapyThe medications that are FDA-approved for the management of osteoporosis may be divided intoantiresorptive agents (estrogen, alendronate, risedronate, and calcitonin) and anabolic agents, of which there is now only one-teriparatide. These agents can be expected to stabilize or increaseBMD [Table [Table7]7] and reduce fracture risk by approximately 50% in most patients. All of the FDA-approved medications have been shown to reduce the risk of vertebral fractures, whileonly estrogen, alendronate, and risedronate have reduced the risk of hip fractures in prospectiveclinical trials. [Table [Table88] 

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 45/53

 

Table 7 Bone Density Response to Therapy.

Table 8 Fracture Risk Reduction in Response to Therapy.

The Women's Health Initiative was the first large prospective randomized placebo-controlled

trial to show reduction of hip fracture, vertebral fracture, and other nonvertebral fractures withconjugated equine estrogen (CEE) plus medroxyprogesterone acetate (MPA) [40] and CEE alone[41]. However, the study was stopped before its planned completion date due to increased risk of adverse events. Considering the small but significant increase in the risk of breast cancer, stroke,coronary heart disease, and venous thromboembolic disease with CEE plus MPA, and theincrease risk of stroke with CEE alone, it is likely that estrogen will not be used as a drug of firstchoice for the treatment of osteoporosis, and that its main use will be for the control of menopausal symptoms. The bisphosphonates, alendronate and risedronate, are both proven toreduce the risk of hip fractures, and may be good choices in elderly patients and any patientswith high risk of hip fracture. Raloxifene and calcitonin are useful agents where reduction of hipfracture risk is not a primary concern, with the added benefit that raloxifene may reduce the risk 

of breast cancer and calcitonin may have an analgesic effect in patients with acute painfulvertebral fractures. Teriparatide, human recombinant 1 – 34 parathyroid hormone, is approved foruse in women and men at high risk for fracture. Despite its greater expense and theinconvenience of daily subcutaneous injections for a 2-year course of therapy, this agent is awelcome addition to the pharmacologic armamentarium for selected patients. Current evidencesuggests that there is no added benefit to combining teriparatide with alendronate, but giving abisphosphonate following a course of treatment with teriparatide may serve to preserve the bonemass previously gained. Combination therapy in general is discouraged, since there are nostudies showing that it offers additional benefit in terms of fracture risk reduction.Glucocorticoid-induced osteoporosis (GIO)Long-term term glucocorticoid therapy may have devastating consequences in terms of loss of 

bone density and increased fracture risk. Any patient being started on oral glucocorticoid therapywith the intent to treat for more than 3 months should be considered for bone density testing andbone-protective medication. Table Table99 shows the guidelines of the American College of Rheumatology for the prevention and treatment of GIO [42].

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 46/53

 

Table 9 Management of Glucocorticoid-Induced Osteoporosis [42].

Monitoring treatmentThe ultimate indicator of efficacy for osteoporosis therapy is reduction of fracture risk. Inclinical trials, this is done by comparing fractures rates in a group receiving active medicationcompared to placebo. For individual patients in clinical practice, BMD is normally used as asurrogate measurement of changes in bone strength and fracture risk in response to therapy. Anincrease or stabilization of BMD is associated with reduction in fracture risk [43], although othermeasures of bone qualities, particularly changes in bone turnover markers [44], are correlated tochanges in fracture risk as well. Patients started on pharmacologic therapy are typically retestedin 1 – 2 years in order to be sure there has been no loss of BMD, and retested at longer intervals

once response to therapy has been shown. Patients at very high risk for bone loss, such as thoseon glucocorticoid therapy, may need to be tested as often as every 6 months, until stability of bone mass has been demonstrated.Discontinuation of treatmentIt is intuitive that pharmacologic therapy should be continued as long as fracture risk is high, andstopped when that is no longer the case. Prolonged therapy adds to patient cost andinconvenience, and possibly increases the risk of drug toxicity due to longer exposure. Clinicaltrials and knowledge of drug mechanisms of action are helpful in predicting the likely outcomeof discontinuation, and suggestive of appropriate measures for follow-up. Discontinuingestrogen, raloxifene, or calcitonin therapy is likely to be associated with rapid loss of therapeuticeffect and subsequent bone loss due to sex hormone deficiency and/or aging. Therefore, patients

at high risk for fracture who stop these drugs should probably soon be started on another anti-fracture drug. Bisphosphonates, having a strong affinity for bone and a long bone half-life, havebeen shown to have persistence of suppression of bone turnover for months to years aftercessation of therapy. This suggests that patients who have been taking an oral bisphosphonatesfor years may continue to benefit from drug effects for a long time after discontinuation, with theduration of persistent effect varying according to the pharmacological properties of thebisphosphonate used. With teriparatide, there is evidence that discontinuation may be quicklyfollowed by bone loss, which can be prevented by initiating bisphosphonate therapy.NonrespondersIn clinical trials, the overwhelming majority of patients treated for osteoporosis withantiresorptive or anabolic medication stabilize or increase BMD and benefit from a reduction in

fracture risk. In clinical practice, approximately 10% of elderly patients treated with abisphosphonate have been shown to lose BMD [45], defined as a BMD decrease more than theLeast Significant Change (LSC) at a 95% level of confidence, a value that can be calculated foreach bone densitometry center. Medical evaluation of these BMD losers revealed a previouslyunrecognized contributing factor, or secondary cause of osteoporosis in about 50%. Althoughthere is no universal consensus on the definition of non-response to therapy, definingnonresponse in terms of BMD loss more than the LSC is a useful tool in clinical practice, and iscause for further medical investigation. Common causes for nonresponse include poor adherence

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 47/53

(not taking medication or not taking it correctly), calcium or vitamin D deficiency, andcomorbidities (diseases, conditions or medication that impair drug effect or are associated withosteoporosis) [46].When to refer to an osteoporosis specialistThe care of osteoporosis patients crosses all medical specialty lines. Primary care specialists and

most medical subspecialists may justifiably claim the right to manage osteoporosis in theirpatients, and do it well. In a small percentage of patients with unusual clinical presentations,intolerance to standard medications, or poor response to therapy, additional expertise may berequired. Table Table1010 shows established guidelines for referral to an osteoporosis specialist[47].

Table 10 When to Refer to an Osteoporosis Specialist [47].

  Other Sections▼ 

SummaryOsteoporosis is a common disorder of low bone strength due to a combination of factors thatinclude low BMD, high bone turnover, altered microarchitecture, geometry, damageaccumulation, and mineralization, leading to increased risk of fractures. The consequences of fragility fractures are serious-disability, loss of independence, chronic pain, and increasedmortality. Patients on long-term oral glucocorticoid therapy, even at low doses, are at increasedrisk for fracture. Inhaled glucocorticoids in sufficiently high doses may increase fracture risk.

Intranasal glucocorticoids, in doses normally prescribed, do not appear to have clinicallysignificant adverse skeletal effects. BMD testing is the most important clinical tool fordiagnosing high risk patients before the first fracture occurs, allowing for timely and appropriatemedical intervention to strengthen bones and reduce the risk of fracture.Competing interestsGrant / Research Support: Merck, Eli Lilly, Novartis, Aventis, Amgen, Pfizer, Kyphon, Wyeth-Ayerst, Roche, GE Lunar, Procter & Gamble.Consultant, Advisory Board, or Speakers' Bureau: Merck, Eli Lilly, Novartis, Procter & Gamble,Aventis, Kyphon, Roche, Wyeth-Ayerst, GE Lunar.Authors' contributionsThe author is solely responsible for all content of this review.

AcknowledgementsSpecial thanks to Lance A. Rudolph, MD, for manuscript review and editing.

  Other Sections▼ 

References

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 48/53

1.  Foundation National Osteoporosis. America's Bone Health: The State of Osteoporosisand Low Bone Mass in Our Nation. National Osteoporosis Foundation; 2002.

2.  Melton LJ., III How many women have osteoporosis now? J Bone Miner Res.1995;10:175 – 177. [PubMed] 

3.  Melton LJ,III, Atkinson EJ, O'Connor MK, O'Fallon WM, Riggs BL. Bone density and

fracture risk in men. J Bone Miner Res. 1998;13:1915 – 1923. [PubMed] 4.  Melton LJ,III, Chrischilles EA, Cooper C, Lane AW, Riggs BL. Perspective. How manywomen have osteoporosis? J Bone Miner Res. 1992;7:1005 – 1010. [PubMed] 

5.  Kanis JA, Johnell O, Oden A, Sembo I, Redlund-Johnell I, Dawson A, De Laet C,Jonsson B. Long-term risk of osteoporotic fracture in Malmo. Osteoporos Int.2000;11:669 – 674. doi: 10.1007/s001980070064. [PubMed] [Cross Ref ] 

6.  Jones G, Nguyen T, Sambrook PN, Kelly PJ, Gilbert C, Eisman JA. Symptomaticfracture incidence in elderly men and women: the Dubbo Osteoporosis EpidemiologyStudy (DOES) Osteoporos Int. 1994;4:277 – 282. [PubMed] 

7.  Fast Facts on Osteoporosis. National Institutes of Health Osteoporosis and Related BoneDisease National Resource Center; 1996.

8.  Riggs BL, Melton LJ, 3rd. The worldwide problem of osteoporosis: insights afforded byepidemiology. Bone. 1995;17 (5 Suppl):505S – 511S. doi: 10.1016/8756-3282(95)00258-4. [PubMed] [Cross Ref ] 

9.  Cooper C, Atkinson EJ, Jacobsen SJ, O'Fallon WM, Melton LJ,III. Population-basedstudy of survival after osteoporotic fractures. Am J Epidemiol. 1993;137:1001 – 1005.[PubMed] 

10. Center JR, Nguyen TV, Schneider D, Sambrook PN, Eisman JA. Mortality after all majortypes of osteoporotic fracture in men and women: an observational study. Lancet.1999;353:878 – 882. doi: 10.1016/S0140-6736(98)09075-8. [PubMed] [Cross Ref ] 

11. Ray NF, Chan JK, Thamer M, Melton LJ,III. Medical expenditures for the treatment of osteoporotic fractures in the United States in 1995: Report from the national osteoporosisfoundation. J Bone Miner Res. 1997;12:24 – 35. [PubMed] 

12. Klibanski A, Adams-Campbell L, Bassford T, Blair SN, Boden SD, Dickersin K, GiffordDR, Glasse L, Goldring SR, Hruska K, Johnson SR, McCauley LK, Russell WE,Osteopor NIH Consensus Dev Panel. Osteoporosis prevention, diagnosis, and therapy.JAMA. 2001;285:785 – 795. [PubMed] 

13. Marshall D, Johnell O, Wedel H. Meta-analysis of how well measures of bone mineraldensity predict occurrence of osteoporotic fractures. BMJ. 1996;312:1254 – 1259. [PMCfree article] [PubMed] 

14. Osteoporosis WHO Study Group on Assessment of Fracture Risk and its Application toScreening for Postmenopausal. Assessment of fracture risk and its application toscreening for postmenopausal osteoporosis. Geneva, World Health Organization; 1994.(Technical report series 843).

15. Garnero P, Hausherr E, Chapuy M-C, Marcelli C, Grandjean H, Muller C, Cormier C,Breart G, Meunier PJ, Delmas PD. Markers of bone resorption predict hip fracture inelderly women: The EPIDOS prospective study. J Bone Miner Res. 1996;11:1531 – 1538.[PubMed] 

16. Gnudi S, Malavolta N, Testi D, Viceconti M. Differences in proximal femur geometrydistinguish vertebral from femoral neck fractures in osteoporotic women. Br J Radiol.2004;77:219 – 223. doi: 10.1259/bjr/79551075. [PubMed] [Cross Ref ] 

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 49/53

17. Myers ER, Wilson SE. Biomechanics of osteoporosis and vertebral fracture. Spine.1997;22 (24 Suppl):25S – 31S. doi: 10.1097/00007632-199712151-00005. [PubMed] [Cross Ref ] 

18. Heaney RP. Pathophysiology of osteoporosis. Endocrinol Metabol Clin North Am.1998;27:255 – 265.

19. Bell KL, Loveridge N, Power J, Garrahan N, Meggitt BF, Reeve J. Regional differencesin cortical porosity in the fractured femoral neck. Bone. 1999;24:57 – 64. doi:10.1016/S8756-3282(98)00143-4. [PubMed] [Cross Ref ] 

20. Burr D. Microdamage and bone strength. Osteoporos Int. 2003;14(Suppl 5):67 – 72. doi:10.1007/s00198-003-1476-2. [PubMed] [Cross Ref ] 

21. Delmas PD. How does antiresorptive therapy decrease the risk of fracture in women withosteoporosis? Bone. 2000;27:1 – 3. doi: 10.1016/S8756-3282(00)00301-X. [PubMed] [Cross Ref ] 

22. Boskey A. Bone Mineral Crystal Size. Osteoporos Int. 2003;14(Suppl 5):S16 – S21.23. Watts NB, Pols H, Ringe JD, Roux C, Horlait S, van de Langerijt L, Cahall DI, Delmas

PD. Detection of "unexpected" osteoporosis: insights from the "IMPACT" trial. Arthritis

Rheum. 2001;44:S256.24. van Staa TP, Leufkens HGM, Cooper C. The epidemiology of corticosteroid-inducedosteoporosis: a meta-analysis. Osteoporos Int. 2002;13:777 – 787. doi:10.1007/s001980200108. [PubMed] [Cross Ref ] 

25. van Staa TP, Leufkens HGM, Abenhaim L, Zhang B, Cooper C. Use of oralcorticosteroids and risk of fractures. J Bone Miner Res. 2000;15:993 – 1000. [PubMed] 

26. van Staa TP, Leufkens HGM, Abenhaim L, Zhang B, Cooper C. Oral corticosteroids andfracture risk: relationship to daily and cumulative dosing. Rheumatology. 2000;39:1383 – 1389. doi: 10.1093/rheumatology/39.12.1383. [PubMed] [Cross Ref ] 

27. Luengo M, Picado C, Del Rio L, Montserrat JM, Setoain J. Vertebral fractures in steroiddependent asthma and involutional osteoporosis: a comparative study. Thorax.1991;46:803 – 806. [PMC free article] [PubMed] 

28. Selby PL, Halsey JP, Adams KRH, Klimiuk P, Knight SM, Pal B, Stewart IM, SwinsonDR. Corticosteroids do not alter the threshold for vertebral fracture. J Bone Miner Res.2000;15:952 – 956. [PubMed] 

29. van Staa TP, Leufkens HGM, Cooper C. Use of inhaled corticosteroids and risk of fractures. J Bone Miner Res. 2001;16:581 – 588. [PubMed] 

30. Lipworth BJ. Systemic adverse effects of inhaled corticosteroid therapy, a systematicreview and meta-analysis. Arch Intern Med. 1999;159:941 – 955. doi:10.1001/archinte.159.9.941. [PubMed] [Cross Ref ] 

31. Kemp JP, Osur S, Shrewsbury SB, Herje NE, Duke SP, Harding SM, Faulkner K, CrimCC. Potential effects of fluticasone propionate on bone mineral density in patients withasthma: a 2-year randomized, double-blind, placebo-controlled trial. Mayo Clin Proc.2004;79:458 – 466. [PubMed] 

32. Allen DB. Systemic effects of intranasal steroids: an endocrinologist's perspective. JAllergy Clin Immunol. 2000;106:S179 – S190. doi: 10.1067/mai.2000.110038. [PubMed] [Cross Ref ] 

33. Wolthers OD. Systemic activity versus systemic adverse effects of nasal glucocorticoidsin the treatment of allergic rhinitis. Acta Paediatr. 2000;89:1158 – 1161. doi:10.1080/080352500750027493. [PubMed] [Cross Ref ] 

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 50/53

34. Gudbjornsson B, Juliusson UI, Gudjonsson FV. Prevalence of long term steroid treatmentand the frequency of decision making to prevent steroid induced osteoporosis in dailyclinical practice. Ann Rheum Dis. 2002;61:32 – 36. doi: 10.1136/ard.61.1.32. [PMC freearticle] [PubMed] [Cross Ref ] 

35. Patschan D, Loddenkemper K, Buttgereit F. Molecular mechanisms of glucocorticoid-

induced osteoporosis. Bone. 2001;29:498 – 505. doi: 10.1016/S8756-3282(01)00610-X.[PubMed] [Cross Ref ] 36. Leib ES, Lewiecki EM, Binkley N, Hamdy RC. Official positions of the International

Society for Clinical Densitometry. J Clin Densitom. 2004;7:1 – 6. doi: 10.1385/JCD:7:1:1.[PubMed] [Cross Ref ] 

37. Dawson-Hughes B, Harris SS, Krall EA, Dallal GE. Effects of calcium and vitamin Dsupplementation on bone density in men and women 65 years of age and older. N Engl JMed. 1997;337:670 – 676. doi: 10.1056/NEJM199709043371003. [PubMed] [Cross Ref ] 

38. Chapuy MC, Arolt ME, Duboeuf F, Brun J, Crouzet B, Arnaud S, Delmas PD, MeunierPJ. Vitamin D3 and calcium to prevent hip fractures in elderly women. N Engl J Med.1992;327:1637 – 1642. [PubMed] 

39. Foundation National Osteoporosis. Physician's guide to prevention and treatment of osteoporosis. Washington, D.C, National Osteoporosis Foundation; 2003.40. Investigators Writing Group for the Women's Health Initiative. Risks and benefits of 

estrogen plus progestin in healthy postmenopausal women. JAMA. 2002;288:321 – 333.[PubMed] 

41. Anderson GL, Limacher M, Assaf AR, Bassford T, Beresford SA, Black H, Bonds D,Brunner R, Brzyski R, Caan B, Chlebowski R, Curb D, Gass M, Hays J, Heiss G,Hendrix S, Howard BV, Hsia J, Hubbell A, Jackson R, Johnson KC, Judd H, KotchenJM, Kuller L, LaCroix AZ, Lane D, Langer RD, Lasser N, Lewis CE, Manson J,Margolis K, Ockene J, O'Sullivan MJ, Phillips L, Prentice RL, Ritenbaugh C, Robbins J,Rossouw JE, Sarto G, Stefanick ML, Van Horn L., Wactawski-Wende J, Wallace R,Wassertheil-Smoller S. Effects of conjugated equine estrogen in postmenopausal womenwith hysterectomy: the Women's Health Initiative randomized controlled trial. JAMA.2004;291:1701 – 1712. [PubMed] 

42. Osteoporosis American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced. Recommendations for the prevention and treatment of glucocorticoid-inducedosteoporosis. Arthritis Rheum. 2001;44:1496 – 1503. doi: 10.1002/1529-0131(200107)44:7<1496::AID-ART271>3.0.CO;2-5. [PubMed] [Cross Ref ] 

43. Wasnich RD, Miller PD. Antifracture efficacy of antiresorptive agents are related tochanges in bone density. J Clin Endocrinol Metab. 2000;85:231 – 236. doi:10.1210/jc.85.1.231. [PubMed] [Cross Ref ] 

44. Riggs BL, Melton LJ,III. Bone turnover matters: The raloxifene treatment paradox of dramatic decreases in vertebral fractures without commensurate increases in bonedensity. J Bone Miner Res. 2002;17:11 – 14. [PubMed] 

45. EM Lewiecki, LA Rudolph. How common is loss of bone mineral density in elderlyclinical practice patients receiving oral bisphosphonate therapy for osteoporosis? J BoneMiner Res. 2002;17(Suppl 2):S367.

46. Lewiecki EM. Nonresponders to osteoporosis therapy. J Clin Densitom. 2003;6:307 – 314.doi: 10.1385/JCD:6:4:307. [PubMed] [Cross Ref ] 

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 51/53

47. Hodgson SF, Watts NB, Bilezikian JP, Clarke BL, Gray TK, Harris DW, JohnstonCC,Jr., Kleerekoper M, Lindsay R, Luckey MM, McClung MR, Nankin HR, Petak SM,Recker RR, Anderson RJ, Bergman DA, Bloomgarden ZT, Dickey RA, Palumbo PJ,Peters AL, Rettinger HI, Rodbard HW, Rubenstein HA, AACE Osteoporosis Task Force.American Association of Clinical Endocrinologists medical guidelines for clinical

practice for the prevention and treatment of postmenopausal osteoporosis: 2001 edition,with selected updates for 2003. Endocrine Practice. 2003;9:544 – 564. [PubMed] 48. Cummings SR, Nevitt MC, Browner WS, Stone K, Fox KM, Ensrud KE, Cauley J, Black 

D, Vogt TM. Risk factors for hip fracture in white women. Study of OsteoporoticFractures Research Group. N Engl J Med. 1995;332:767 – 773. doi:10.1056/NEJM199503233321202. [PubMed] [Cross Ref ] 

Articles from Clinical and Molecular Allergy : CMA are provided here courtesy of BioMed Central 

Question 1 EFFO

Follow: Join the Word of the Day Mailing List 

Share: This page:Share:

On this page

Word Browser  

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 52/53

Advertisement (Bad banner? Please let us know) 

Ads by Google

Bloodline Calculator

Your Bloodline Champions Calculator for traits and gems build!

www.bloodlinecalculator.com

Foreign Direct InvestmentFDI - Economist Intelligence Unit report on investing in Ireland

www.mop.ie/fdi

Ethiopia

Find Hotels, Compare Rates, Read Reviews & More. Try TripAdvisor!

www.TripAdvisor.com

QROPS - Overseas Pension

WINNER- Best QROPS Provider 2011 QROPS, New Low Charges

www.overseaspension.com

Acronym Definition

EFFO European Foundation for Osteoporosis and Bone Disease

EFFO European Forum for OS-9

submit new definition

Copyright 1988-2008 AcronymFinder.com, All rights reserved.

How to thank TFD for its existence? Tell a friend about us, add a link to this page, add the

site to iGoogle, or visit webmaster's page for free fun content. 

Link to this page:<a href=

 

Please bookmark with social media, your votes are noticed and appreciated:

Ads by Google

Aviation consultants

Independant aviation consultants Strong track record Airport-Airline

www.atlanticbridgeaviation.com

Looking for Your Friend?

Find Your Friend on Facebook. Sign Up Free Now!

www.Facebook.com

Scholarship for African

Free College Scholarship to Student From Africa, UK USA Germany France

Scholarship-Positions.com/Africa

Flight Planning Support

Affordable flight support for small and private operators

www.lancelotfs.aero

8/2/2019 Wondifraw Document Question 1 Say Some Thing About Calcitonin

http://slidepdf.com/reader/full/wondifraw-document-question-1-say-some-thing-about-calcitonin 53/53

 

www.ncbi.nlm.nih.gov/pmc/articles/PMC493281/ -

Management of osteoporosisE Michael Lewiecki 1 1New Mexico Clinical Research & Osteoporosis Center, 300 Oak St. NE, Albuquerque, NewMexico 87106, USACorresponding author.

E Michael Lewiecki: LEWIECKI@aol.com Received May 12, 2004; Accepted July 14, 2004.This article has been cited by other articles in PMC.