Clincal Pharmacy: answer a question, pose a question

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No problem.

The Claritin-D commercial states that the company is true to its formulation and it doesn't want to change its pseudoephrine formulation to PE. However, what is the true reason as to why it can't switch to PE?

Loratadine is a qd-BID formula - it lasts 12-24 hours (5 vs 10 mg). So far, phenylephrine is not available in an extended relief form. So PE has to be taken every 4 hours, which wouldn't work for the Claritin-D "all day relief" advertisement.

I don't have a question of my own to post right now🙂
 
So PE has to be taken every 4 hours, which wouldn't work for the Claritin-D "all day relief" advertisement.

That is right! Loratidine is long acting while PE is short acting so they can't go together.
 
Why shouldn't you use the sig: "Apply one patch daily"? What would happen if the patient actually followed that sig?
 
It doesn't involve taking the patch off, so they would just keep putting patches on.

My question: Would Fosamax cause a 10 lb weight gain in a patient? It should be noted that this patient has hypothyroidism, however, your recent TSH levels were in range. What would you tell her?
 
Why shouldn't you use the sig: "Apply one patch daily"? What would happen if the patient actually followed that sig?

Because patients can be stupid and might not realize to take off the first patch.
 
It doesn't involve taking the patch off, so they would just keep putting patches on.

My question: Would Fosamax cause a 10 lb weight gain in a patient? It should be noted that this patient has hypothyroidism, however, your recent TSH levels were in range. What would you tell her?

I would tell the patient to stop taking Fosamax; osteoporosis was not considered a disease until Fosamax was in Phase II trials, huge surprise (what we like to call disease mongering). We'd also be able to see if it caused the weight gain. Seems reasonable to me.

Can anyone tell me if there is actual data to support using statins for primary prevention of coronary artery disease? If your answer is yes, provide a link.
 
I would tell the patient to stop taking Fosamax; osteoporosis was not considered a disease until Fosamax was in Phase II trials, huge surprise (what we like to call disease mongering). We'd also be able to see if it caused the weight gain. Seems reasonable to me.

Can anyone tell me if there is actual data to support using statins for primary prevention of coronary artery disease? If your answer is yes, provide a link.


According to Lexi-comp, Fosamax weight gain is not an ADR. Instead of stoping her Fosamax (her T-scores were -2.9) you would need to find out if her exercise or eating habits had changed any. There is probably a more probable cause of her weight gain than the Fosamax. This was a prime example of a case from our patient care lab.
 
According to Lexi-comp, Fosamax weight gain is not an ADR. Instead of stoping her Fosamax (her T-scores were -2.9) you would need to find out if her exercise or eating habits had changed any. There is probably a more probable cause of her weight gain than the Fosamax. This was a prime example of a case from our patient care lab.

Can you tell me how the T-score was created and when? Has alendronate ever been proven to prevent hip fractures or death? These are the important things right?

And don't wikipedia the T-score real quick, be honest, you quoted a value, but do you know anything about where it comes from???
 
According to Lexi-comp, Fosamax weight gain is not an ADR..

Hopefully by the time you finish pharmacy school, you will realize that Lexicomp is not the ultimate arbiter of adverse events. Actually it is not even close.
 
Hopefully by the time you finish pharmacy school, you will realize that Lexicomp is not the ultimate arbiter of adverse events. Actually it is not even close.

:meanie::meanie:

What do you know...lowly resident!!!
 
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That's pretty freaking tricky. According to my notes from the GINA Expert Panel 3, the equivalent medium daily doses of budesonide and fluticasone are around 400-800mcg and 250-500mcg/day, giving us roughly a 40:25 (or 8:5) budesonide:fluticasone ratio.

As to formoterol and salmeterol, my notes say that 12mcg of formoterol is equivalent to 50mcg of salmeterol (a 12:50 ratio). Both of these are generally dosed BID (up to 24 mcg qd for formoterol and up to 100mcg qd of salmeterol).

The problem lies in the formulation of the inhalers. Symbicort comes in two strengths: 80/4.5 and 160/4.5. The Advair Diskus comes in three strengths (colors): 100/50, 250/50 and 500/50 (the HFA comes as 45/21, 115/21, and 230/21.) There just isn't a mathematical way to get ~400/12 dose of symbicort equal to a 250/50 dose of advair. The closest way to get equivalent doses would be 2 puffs BID of the 160/4.5 Symbicort to 1 puff BID Advair (I know that this is actually "considered" to be equivalent, but it isn't exactly).

Soooo... even though I may be off the mark for Epic's question, I'll pose one of my own (probably pretty easy): What, if any, drug therapy alternatives are there to hydralazine for preeclampsia or gestational hypertension?


Thank you... this is a good analysis.

btw.. I don't have an answer.
 
Can you tell me how the T-score was created and when? Has alendronate ever been proven to prevent hip fractures or death? These are the important things right?

And don't wikipedia the T-score real quick, be honest, you quoted a value, but do you know anything about where it comes from???

The t-score comes from Bone Mineral Density Scans. It is quoted in standard deviations from women in their 30 which is the peak time for bone density. A t-score of -1 to -2.5is considered osteopenia according to the WHO classification and a t-score of below -2.5 is considered osteoporosis.

Alendronate has not been proven to prevent hip fractures and death however, it has been proven to stabilize t-scores in women.

And I know that lexi-comp is not a complete source of ADRs. However, can you automatically say something is cause by a medication if you don't take into account other independent factors that could be causing it?

BTW, thanks, your questions helped me study for my therapeutics exam.
 
:meanie::meanie:

What do you know...lowly resident!!!

Hey, this was something I realized well before I graduated from school, I was giving this guy the benefit of the doubt. Like I have always said, I have made it through pharmacy school rotations and most of a PGY1 year without the help of a palm pilot. Med students use palm pilots for drug information, pharmacists should be able to do better.
 
I am sorry I didn't answer your question about when the t-score was created. I honestly don't know the answer that question. Maybe you can give me some insight.
 
The t-score comes from Bone Mineral Density Scans. It is quoted in standard deviations from women in their 30 which is the peak time for bone density. A t-score of -1 to -2.5is considered osteopenia according to the WHO classification and a t-score of below -2.5 is considered osteoporosis.

Alendronate has not been proven to prevent hip fractures and death however, it has been proven to stabilize t-scores in women.

And I know that lexi-comp is not a complete source of ADRs. However, can you automatically say something is cause by a medication if you don't take into account other independent factors that could be causing it?

BTW, thanks, your questions helped me study for my therapeutics exam.

So, what does a T-score actually provide information on (i.e. what type of bone)? If it doesn't prevent hip fractures or death, then who cares about normalizing a T-score? This is what we call a surrogate marker of efficacy, not really much information on whether patients actually derive any benefit from these drugs, right?

Do you know anything about the WHO panel that was put together to define the T-score? Do you think any of them were financially tied to Merck? Do you think this presents a problem, a dangerous conflict of interest perhaps?
 
So, what does a T-score actually provide information on (i.e. what type of bone)? If it doesn't prevent hip fractures or death, then who cares about normalizing a T-score?

Do you know anything about the WHO panel that was put together to define the T-score? Do you think any of them were financially tied to Merck? Do you think this presents a problem, a dangerous conflict of interest perhaps?

The most common sites that you get t-scores from are hip, wrist, and lumbar.
I am going out on a limb here, and saying that if bone density is stabilized (which would be indicated by the stabilization of the t-scores)-then the likelihood of hip fractures decreases. It has been shown that once you start losing BMD then you are at a higher risk for fractures.
I don't know anything about the WHO panel that put together the definition of the T-Score. If they were financially tied to Merck it would be a conflict of interest. However, I don't how dangerous it would be.

However, I don't understand why you seem so against prevention/treatment of osteoporosis.
 
Hey, this was something I realized well before I graduated from school, I was giving this guy the benefit of the doubt. Like I have always said, I have made it through pharmacy school rotations and most of a PGY1 year without the help of a palm pilot. Med students use palm pilots for drug information, pharmacists should be able to do better.


If I don't pick on you...who will..
 
The most common sites that you get t-scores from are hip, wrist, and lumbar.
I am going out on a limb here, and saying that if bone density is stabilized (which would be indicated by the stabilization of the t-scores)-then the likelihood of hip fractures decreases. It has been shown that once you start losing BMD then you are at a higher risk for fractures.
I don't know anything about the WHO panel that put together the definition of the T-Score. If they were financially tied to Merck it would be a conflict of interest. However, I don't how dangerous it would be.

However, I don't understand why you seem so against prevention/treatment of osteoporosis.

The T-score measures cortical bone, is this the part that has much to do with the strength of the bone? Are there several studies that show that regular exercise prevents fractures several orders greater than any bisphosphonate? (This is a rhetorical question, and the bisphosphonates do not prevent clinically important fractures, so it cannot really be answered)
 
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However, I don't how dangerous it would be.

However, I don't understand why you seem so against prevention/treatment of osteoporosis.

You do not think it would be dangerous if Merck paid investigators/"experts" were charged with creating a measure by which a drug Merck was developing would be prescribed. The T-score as it stands basically classifies every woman in the country in her mid-fifties as having osteopenia and every woman in the country in her mid-sixties as having osteoporosis (so of course you have to treat, we need to get that T-score up). Do you think this is a coincidence. I actually do not.
 
Did I put this thread to rest? Where is WVU, he wanted us to keep this thing going.
 
Beta-blockers used to be contraindicated in CHF...but then they became recommended. Why do beta-blockers work in heart failure? It's something that doesn't make much sense on the surface...

Had a test on this on Monday. Short answer - Beta-blockers work in HF because the negative effects of excess sympathetic drive outweigh the risks of decreased inotropy. But they still have to be dosed/titrated pretty carefully.

Long answer:
The benefits include decreased cardiac remodeling, a reduction in activity of the renin-angiotension-aldosterone system, decreased O2 demand, decreased afterload, and a "reset" of beta receptor ratio (beta-1 receptors are downregulated in HF - the beta-blockers help make the ratio normal again). Plus, if you use a non-selective beta blocker like Coreg you can get some alpha-1 blockade, which can promote vasodilation ==> decreased preload.

I haven't been studying enough on arrhrythmias yet, but my question is, if amiodarone is such a toxic/nasty drug, why do they use it during ACLS (acute cardiac life support?)
 
Beta-blockers used to be contraindicated in CHF...but then they became recommended. Why do beta-blockers work in heart failure?

systolic HF (decrease contractility) results primarily from systolic HTN and ischemic heart Dx. Beta blockers decrease HR, cardiac contractility & CO when first initiated but when start w/a low dose followed by gradual titration upward of certain βBs to high dose (use carvedilol for pts who also have high BP; metoprolol ER for pts who also have low BP or pulmonary Dx) results in cardiac beta receptors upregulation and compensatory tachycardia and excessive catecholamine release is halted.
 
Beta-blockers used to be contraindicated in CHF...but then they became recommended. Why do beta-blockers work in heart failure? It's something that doesn't make much sense on the surface...

Well, no one even took a shot at my initial question regarding statins, but I wasn't expecting a good one anyway.
 
Well, no one even took a shot at my initial question regarding statins, but I wasn't expecting a good one anyway.

There are a few studies out there with built-in primary prevention patients. PROSPER, ALLHAT, Airforce/Texas, WOSCOPS. I didn't like WOSCOPS though...the baseline between the two groups was just way off. The LDL for the Pravastatin group was significantly higher to begin with...so of course it's going to show a reduction. As for PROSPER...didn't show a reduction in MI/stroke in the primary prevention patients (but it did in secondary). Same with ALLHAT. And ADR reporting in these studies is pretty weak...who's to say you're not offsetting possible benefits with statin therapy with a serious ADR?

So, I'd say the answer is no...I haven't seen anything conclusive anyways. Curious to see what JUPITER comes up with though with the inflammation angle (in relatively healthy patients). Even though it's funded by AstraZeneca and I'm not a fan of Crestor.
 
Beta-blockers used to be contraindicated in CHF...but then they became recommended. Why do beta-blockers work in heart failure? It's something that doesn't make much sense on the surface...


Over my career I've learned that we don't know the true answers to a lot of medical questions and just take guesses. BB usage in HF is a perfect example.

This is why I know they work, they did "body count" trials with carvedilol, metoprolol and bisoprolol.

At the end of the study periods there were more live bodies in the bb groups than placebo groups therefore we know they work. It's why I only give credit to clinical outcome trials. Other trials don't mean much to me, just ask how Pfizer how a drug that raises HDL actually increases mortality......

All the other answers given are just hypothesis and we still don't know a lot about the "TRUE" mechanisms/benefits/changes in physiology.


But for the right answer, Let me go ask my dermatologist who makes 300K a year, he knows everything and is much smarter than a lowly pharmacist such as myself.
 
How would you dose a patient who is 180 kg on Vancomycin with an abdominal wound?
 
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There are a few studies out there with built-in primary prevention patients. PROSPER, ALLHAT, Airforce/Texas, WOSCOPS. I didn't like WOSCOPS though...the baseline between the two groups was just way off. The LDL for the Pravastatin group was significantly higher to begin with...so of course it's going to show a reduction. As for PROSPER...didn't show a reduction in MI/stroke in the primary prevention patients (but it did in secondary). Same with ALLHAT. And ADR reporting in these studies is pretty weak...who's to say you're not offsetting possible benefits with statin therapy with a serious ADR?

So, I'd say the answer is no...I haven't seen anything conclusive anyways. Curious to see what JUPITER comes up with though with the inflammation angle (in relatively healthy patients). Even though it's funded by AstraZeneca and I'm not a fan of Crestor.

That's actually pretty good, much better than I anticipated (ok, really good considering your ultimate answer was "no," which is correct).
 
There are a few studies out there with built-in primary prevention patients. PROSPER, ALLHAT, Airforce/Texas, WOSCOPS. I didn't like WOSCOPS though...the baseline between the two groups was just way off. The LDL for the Pravastatin group was significantly higher to begin with...so of course it's going to show a reduction. As for PROSPER...didn't show a reduction in MI/stroke in the primary prevention patients (but it did in secondary). Same with ALLHAT. And ADR reporting in these studies is pretty weak...who's to say you're not offsetting possible benefits with statin therapy with a serious ADR?

So, I'd say the answer is no...I haven't seen anything conclusive anyways. Curious to see what JUPITER comes up with though with the inflammation angle (in relatively healthy patients). Even though it's funded by AstraZeneca and I'm not a fan of Crestor.


You sell statins?
 
Hey! It's my turn to ask a question. I gotta think of one that you'll actually have to think about or look into to answer. :meanie:

I know everything. If I don't know....it's not important and I don't need to know..
 
I know everything. If I don't know....it's not important and I don't need to know..

Ok. Here's one for you (and you should know every drug that comes into your hospitals!). What are some of the clinical differences between Metastron and Quadramet.

Props to anyone who wants to look into it though 😉
 
why would a pharmacy department concern themselves with radioactive IV analgesic?

One is made by GE and the other by Cytogen. Thank you google.


Seems like quadramet is a shorter acting agent.. with a lower incidence of bone marrow toxicity.
 
180kg? Do we know their height?
I don't think height is needed because vanco is usually dosed on actual body weight, not a dosing body weight. (10-15 mg/kg?)

But I would want to know renal function/creatinine clearance to figure out a dosing interval.

This is probably a lame answer...I'm recalling what they did in the ICU on my last rotation.
 
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I don't think height is needed because vanco is usually dosed on actual body weight, not a dosing body weight. (10-15 mg/kg?)

But I would want to know renal function/creatinine clearance to figure out a dosing interval.

This is probably a lame answer...I'm recalling what they did in the ICU on my last rotation.

Incorrect.
 
why would a pharmacy department concern themselves with radioactive IV analgesic?

One is made by GE and the other by Cytogen. Thank you google.


Seems like quadramet is a shorter acting agent.. with a lower incidence of bone marrow toxicity.

Why wouldn't you want to know about bone met palliation therapy? And bone marrow toxicity...that's right up your alley.

Can you image them?
 
Why wouldn't you want to know about bone met palliation therapy? And bone marrow toxicity...that's right up your alley.

Can you image them?

because it's pushed by lowly drug reps who don't bring lunch to pharmacy but instead hang out with radio peeps.
 
What is the role of antibiotic prophylaxis in patients with neutropenic fever?
 
because it's pushed by lowly drug reps who don't bring lunch to pharmacy but instead hang out with radio peeps.

You're right...no food/drinks in the restricted area.

But whattya' know. Next time the patient's WBCs are tanking and they got a dose of Metastron, you may be able to figure it out. I thought you couldn't "learn you no more"!
 
What is the role of antibiotic prophylaxis in patients with neutropenic fever?

afebrile or febrile?

For afrebrile.... bactrim for PCP

For febrile...use of prophylaxis abx reduces GCSF usage.

Do we need to get into Antifungal and antiviral too?
 
You're right...no food/drinks in the restricted area.

But whattya' know. Next time the patient's WBCs are tanking and they got a dose of Metastron, you may be able to figure it out. I thought you couldn't "learn you no more"!

Are you serious....

quadramet is palliative and a radiotracer...hence imaging is possible.

You have to ask a question that stimulates "thinking"
 
Are you serious....

quadramet is palliative and a radiotracer...hence imaging is possible.

You have to ask a question that stimulates "thinking"

Ehhh. Strontium is reactor produced but it's only a beta emitter. We can't image betas. But it bombards the bone met...3 mm deep (think bone marrow toxicity). Samarium is beta andddd gamma. Nice 100ish keV. So we can image it! Patient actually gets to "see" that the pain's getting better. And the betas penetrate about half of what Metastron does. Completely renally excreted...so whatever doesn't stick is gone in a few hours.

That got you thinking a little?
 
Ehhh. Strontium is reactor produced but it's only a beta emitter. We can't image betas. But it bombards the bone met...3 mm deep (think bone marrow toxicity). Samarium is beta andddd gamma. Nice 100ish keV. So we can image it! Patient actually gets to "see" that the pain's getting better. And the betas penetrate about half of what Metastron does. Completely renally excreted...so whatever doesn't stick is gone in a few hours.

That got you thinking a little?

boring..😴😴


:meanie:
 
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