Discrepancy in antibiotics dosing

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Miss Arm

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First, I apologize for my previous post which appeared as seeking medical advice, but it was not my intention to break the rule here.

I was not asking why we need a higher dose for certain medical condition, but I was wondering why the commonly used dosing for the condition is not mentioned in the drug fact. Did you learn the knowledge about the drug usage from special drug information publications that are not available to the public or from experience?

Thank you all the pharmasists and pharmacy students!
 
If the reference is based on package insert, then it can only list FDA approved indication and dosing.

But the practice of medicine goes beyond the FDA indication where practitioners go off label more often than not.

If you're really curious about Infectious Disease, read this...tho it'll probably be little over your head since you're a pre-pharm.

http://www.idsociety.org/Content.aspx?id=9088
 
First, I apologize for my previous post which appeared as seeking medical advice, but it was not my intention to break the rule here.

I was not asking why we need a higher dose for certain medical condition, but I was wondering why the commonly used dosing for the condition is not mentioned in the drug fact. Did you learn the knowledge about the drug usage from special drug information publications that are not available to the public or from experience?

Thank you all the pharmasists and pharmacy students!

I learned most of the unlabeled use of a drug through experience at the pharmacy and internships. But if you think about how the drug mechanism works, sometimes you can figure out the unlabeled use. For example, propranolol is for chest pain, but how does it work? It dilates the blood vessels. So because it dilates the blood vessels, it will decrease the blood pressure. As a result, by decreasing blood pressure, you can use this to decrease anxiety of a patient. I hope this makes sense to you. :xf:
 
I learned most of the unlabeled use of a drug through experience at the pharmacy and internships. But if you think about how the drug mechanism works, sometimes you can figure out the unlabeled use. For example, propranolol is for chest pain, but how does it work? It dilates the blood vessels. So because it dilates the blood vessels, it will decrease the blood pressure. As a result, by decreasing blood pressure, you can use this to decrease anxiety of a patient. I hope this makes sense to you. :xf:

The anti-anginal effect is mainly due to negative chronotropic and inotropic effects (decreasing myocardial O2 demand)...not vasodilitation. The anxiolytic portion has nothing to do with blood pressure; propranolol crosses the BBB and interferes with sympathetic activity. Beta blockers that don't cross the BBB have no effect on anxiety.
 
I learned most of the unlabeled use of a drug through experience at the pharmacy and internships. But if you think about how the drug mechanism works, sometimes you can figure out the unlabeled use. For example, propranolol is for chest pain, but how does it work? It dilates the blood vessels. So because it dilates the blood vessels, it will decrease the blood pressure. As a result, by decreasing blood pressure, you can use this to decrease anxiety of a patient. I hope this makes sense to you. :xf:


Wow..this is a pretty bad advice...

understanding the MOA is important but this is certainly not the way to learn unlabeled use of antimicrobials. That's like saying "if you understand the mechanism of combustion engine, you'll know how fast a car can move."

The b-blocker example is pretty bad too..
 
Technically, propranolol is not for "chest pain" and the decrease in blood pressure is not how it relieves angina.. it's the bradycaric effect and the decrease O2 demand.

I think we need a pathophysio lesson on Myocardial Infarction and/or Ischemic Angina here...

Mikey..draw us a diagram of how a clot dams the blood flow.. :meanie:
 
Technically, propranolol is not for "chest pain" and the decrease in blood pressure is not how it relieves angina.. it's the bradycaric effect and the decrease O2 demand.

I think we need a pathophysio lesson on Myocardial Infarction and/or Ischemic Angina here...

Mikey..draw us a diagram of how a clot dams the blood flow.. :meanie:


I'll sign up for that class, especially if I get to see more of WVU's MS Paint skills. Seriously Z, if you have time, I'm sure the forum denizens would appreciate your effort. I know I enjoyed the kinetics discussion from a couple of months ago.
 
I'll sign up for that class, especially if I get to see more of WVU's MS Paint skills. Seriously Z, if you have time, I'm sure the forum denizens would appreciate your effort. I know I enjoyed the kinetics discussion from a couple of months ago.

Flattery will get you everywhere.

Here goes...a layman's explanation of MI.

Coronary Artery Disease refers to atherosclerotic build up of plaque and hardening of in coronary arteries. Plaque gives a misrepresentation of the hardening as being soft but quite the opposite. The build up in the arterial walls is quite hard..like a piece of rock.

Here lies the problem...if you've seen a beating heart, you know the vigor and the dynamic movement which can trigger a tear in coronary artery surrounding the build up.

Think about it...piece of hard pebble constantly rubbing against soft artery. The tear causes bleeding.. and bleeding results in a clot. Duh..

The clot now blocks the blood flow to oxygen hungry myocardial muscle tissues.. ouch. That ladies and gentlemen.. is what causes the chest pain which can lead to an infarction.

Treatment options?

Will someone else chime in ?

If you've processed MI admission orders...you know by heart what's used..
 
Thanks Z. I haven't processed MI admission orders, but I'll go with MONA, then think about thrombolytics if the criteria are met.
 
Flattery will get you everywhere.

Here goes...a layman's explanation of MI.

Coronary Artery Disease refers to atherosclerotic build up of plaque and hardening of in coronary arteries. Plaque gives a misrepresentation of the hardening as being soft but quite the opposite. The build up in the arterial walls is quite hard..like a piece of rock.

Here lies the problem...if you've seen a beating heart, you know the vigor and the dynamic movement which can trigger a tear in coronary artery surrounding the build up.

Think about it...piece of hard pebble constantly rubbing against soft artery. The tear causes bleeding.. and bleeding results in a clot. Duh..

The clot now blocks the blood flow to oxygen hungry myocardial muscle tissues.. ouch. That ladies and gentlemen.. is what causes the chest pain which can lead to an infarction.

Treatment options?

Will someone else chime in ?

If you've processed MI admission orders...you know by heart what's used..

Young Padawan's initial gut instinct suggests the option of nitroglycerin tabs sublingually- Nitro will reduce the heart muscle's need for O2, and thus ischemia can be avoided. We could also reduce the brutal pumping force of the heart with Tenormin or Blocadren.

:xf:


@ Pianopooh: I suggest that anxiety's root cause is not blood pressure and that your advice is terrible. There are several recent studies demonstrating a link between anxiety disorder NOS and HTN, absolutely, but you've got the causation incorrect. The propensity of AD-NOS to precipitate HTN is the correct order, not HTN--->Anxiety. Dr. Simon Bacon did one of the more memorable studies on this, perhaps you should look it up. =] I know, Propronalol can be used to help alleviate stage fright or whatever... but having worked in mental health, I can say that if the anxiety one is experiencing is related to an excess of Norepinephrine, Propranolol might be really useful, such as in PTSD treatment, but all that is totally inconclusive as we stand now. And, as a general rule, HTN does not cause anxiety.
 
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Young Padawan's initial gut instinct suggests the option of nitroglycerin tabs sublingually- Nitro will reduce the heart muscle's need for O2, and thus ischemia can be avoided. We could also reduce the brutal pumping force of the heart with Tenormin or Blocadren.

:xf:


@ Pianopooh: I suggest that anxiety's root cause is not blood pressure and that your advice is terrible. There are several recent studies demonstrating a link between anxiety disorder NOS and HTN, absolutely, but you've got the causation incorrect. The propensity of AD-NOS to precipitate HTN is the correct order, not HTN--->Anxiety. Dr. Simon Bacon did one of the more memorable studies on this, perhaps you should look it up. =] I know, Propronalol can be used to help alleviate stage fright or whatever... but having worked in mental health, I can say that if the anxiety one is experiencing is related to an excess of Norepinephrine, Propranolol might be really useful, such as in PTSD treatment, but all that is totally inconclusive as we stand now. And, as a general rule, HTN does not cause anxiety.

I was never this smart in school....

wanna add a lil somethin for the pain and prevention of more clots?
 
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Yep, I was waiting for someone to put the smack down.

To answer the OPs question. There are no secret or special publications not available to the public. They may not be readily accesable but they are not secret.

You learn from experience. How do you think they figured out how or why to use a medication off label?

The first time I saw Amoxacillin dosed at 90mg/kg per day I did like every other pharmacist has done. I called the Doctor because it was double what the package insert said. I got a really cool ER doc who faxed me a page from the American Academy of Pediatrics which discussed why high dose therapy was needed for acute otitis media. I still have it.

Experience is the best teacher.
 
I was never this snart in school....

wanna add a lil somethin for the pain and prevention of more clots?

I wasn't trying to be snarky/smart-ass... well, not to you. Maybe to the Piano person but I think s/he deserved it. To your question I was really just curious if that would be a viable option.

I'll take a stab at it. For clotting, definitely a VitK antagonist, we could try Coumadin and for pain we could use a Ca-chan blocker, like Calblock? Something tells me that a typical Opioid like Hydrocod+APAP wouldn't be indicated for this kind of pain. Of course I'm probably wrong. =/
 
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I wasn't trying to be snarky/smart-ass... well, not to you. Maybe to the Piano person but I think s/he deserved it. To your question I was really just curious if that would be a viable option.

I'll take a stab at it. For clotting, a VitK antagonist, we could try Coumadin and for pain we could use a Ca-chan blocker, like Calblock? Something tells me that a typical Opioid like Hydrocod+APAP wouldn't be indicated for this kind of pain. Of course I'm probably wrong. =/


Dood...don't you read typo. I meant "smart"...... I was typing on my phone while driving... sorry.
 
I'll take a stab at it. For clotting, a VitK antagonist, we could try Coumadin and for pain we could use a Ca-chan blocker, like Calblock? Something tells me that a typical Opioid like Hydrocod+APAP wouldn't be indicated for this kind of pain. Of course I'm probably wrong. =/

Some wrong...some not quite too wrong...
 
Yep, I was waiting for someone to put the smack down.

To answer the OPs question. There are no secret or special publications not available to the public. They may not be readily accesable but they are not secret.

You learn from experience. How do you think they figured out how or why to use a medication off label?

The first time I saw Amoxacillin dosed at 90mg/kg per day I did like every other pharmacist has done. I called the Doctor because it was double what the package insert said. I got a really cool ER doc who faxed me a page from the American Academy of Pediatrics which discussed why high dose therapy was needed for acute otitis media. I still have it.

Experience is the best teacher.


You butting in again?? dood...
 
Hey I commented on the OPs original question. I stayed out of your little side topic.

Seriously? Typing while driving? You have a serious SDN addiction. I suggest immediate treatment.

Or he has an attention-deficit like 90% of people aged 20-35.

Driving is boring, especially if you're on the freeway. For me it's drive 100 mph+ or send some texts at 70. (Gross exaggeration alert).

I'm totally down with posting on SDN while driving as long as it's done with caution!
 
Fl
Will someone else chime in ?

Don't forget the inflammation factor. I really think this will be the MOA for statins effects on reducing the likelihood of MI's both primarily and secondarily. I think (though I have no information to back it up) that there is an inflammatory process in the vessel walls that is the primary cause of the problem....

As for beta blockers and nitrates for that matter, they reduce MOD. Period. Even NTG does not increase MOS. They reduce MOD. NTG is best because it effects preload (by reducing venous return) and afterload, while isosorbide only effects afterload.
 
Thanks for your input everyone. This is my understanding of the beta blocker propranolol, and also from what I have put together from notes. I will consider all of your input, thanks again.
 
So without getting too much into the pharmacotherapy as to how you'd treat an MI - basically remember that you want to do two main things:

1) Decrease myocardial oxygen demand (via heart rate, muscle contractility and wall tension)
2) Increase oxygen supply (via blood flow and stabilizing the plaque)

I'm sure Z will cover how you'd go about doing this, but I figured I'd throw in a different angle to the conversation, which is how radiopharmaceuticals become involved.

Essentially, there're 3 types of nuclear cardiac imaging studies:

1) Avid infarct imaging: you're looking for actual defects (dead muscle tissue) resulting from the MI. You can do this using Tc-99m labeled Pyrophosphate. After an MI, calcium accumulates in the tissue, which the PYP will bind to. When the patient is imaged, you will actually see areas of dead muscle, and the extent of heart damage. The trick here though is that drug delivery to the area requires blood flow, obviously. An old infarct with no blood flow to the area will not appear on the scan. As a result, imaging must be done maximum 2 weeks after the actual MI – with maximum uptake about 2 to 3 days post MI.

2) Myocardial perfusion imaging: here you're comparing an image of the patient's heart when it's at "rest" and one where it's "stressed" (either chemically or physically). If the two images of the patient's heart look different comparatively, this indicates ischemia (low blood flow to the heart – but NOT necessarily cell death). If both images at rest and stress are the same, it indicates the patient has indeed had an MI. This is by far the most common study we prepare doses for at my pharmacy (and any nuclear pharmacy); and the findings from this will ultimately help to decide how/how aggressive the patient is treated. There are 3 radiopharmaceuticals out there for these types of studies: Thallium, Tc-99m Sestamibi (for which very recently there are 2 generic manufacturers making), and Tc-99m Tetrofosmin.

3) Cardiac function studies: here you're trying to determine how well the heart is pumping blood. So the drugs we use to do this won't be taken up by the heart tissue, but will remain in the blood itself. You can look at the heart wall motion, as well as calculate a gated ejection fraction (percent of blood that's pumped out of the heart after each contraction). These types of studies will help determine the patient's prognosis after MI.

So there you go! Quick and dirty version of how what I do comes into play! 😉
 
This thread has become boring...I'm leaving..I have hot pink maribou and shackles to tie into another wooly bugger..
 
Thanks for your input everyone. This is my understanding of the beta blocker propranolol, and also from what I have put together from notes. I will consider all of your input, thanks again.


ehhhh we didn't mean to be so harsh... but we'll beat up your instructors for you...
 
ehhhh we didn't mean to be so harsh... but we'll beat up your instructors for you...



Spiriva Promised us a full, pharmacotherapeutic explanation of MI treatment due to CAD and I'm not leaving until we get one! :meanie:
 
This thread has become boring...I'm leaving..I have hot pink maribou and shackles to tie into another wooly bugger..

Z, what happened? Put down your hot pink malibu barbie in shackles and educate some folks!
 
Does anyone else love saying the names of Beta Blockers or am I the only one?

I get a thrill whenever I get to say PROPRANO-LAWL!

Yeah... maybe it'll subside soon.
 
Clopidogrel 300 for some...ASA 325 for all.

NSTEMI/UA, titrate nitro for pain. Bring in for PCI (if indicated), use eptifibatide (debatable now).

STEMI...lots of morphine for pain and reperfuse with reteplase or PCI.

Are you going to drop that Plavix dose eventually?
I might just keep on both ASA and clopidogrel. If insurance allows. I hate to see any resistance to either agent.....
 
Correct is like pregnant. It's a binary state. Either the answer is correct or it's not...😕

Sometimes correct is conditional. Under one condition a statement maybe correct. Under others it may be incorrect. I suppose what you're saying is if he didn't specify the conditions under which his statement would be correct that it is therefore incorrect as it is false or at least misleading when applied as a general rule.
 
Sometimes correct is conditional. Under one condition a statement maybe correct. Under others it may be incorrect. I suppose what you're saying is if he didn't specify the conditions under which his statement would be correct that it is therefore incorrect as it is false or at least misleading when applied as a general rule.

If the person did not supply the conditioning documentation then the statement is incorrect. An answer is always conditional on the question. The answer is "2" is conditional on the question. If the question is 2+2 or if it 3+3.

Answers are either correct or incorrect....
 
It's sad that as smart as you all think you are. You guys still count pills by 5 and get yelled at by some high school drop outs on a daily basis.
 
It's sad that as smart as you all think you are. You guys still count pills by 5 and get yelled at by some high school drop outs on a daily basis.

Do you have a different opinion than what we've offered here? I'd love to hear it from someone as enlightened as you.
 
oh no no no... I don't wanna offend you pharmacology geeks. Just stating the fact that's all. How many of your customer actually cares what the hell is ionotropic vs. chronotropic effect? Just put the pills in the bottle already.
 
oh no no no... I don't wanna offend you pharmacology geeks. Just stating the fact that's all. How many of your customer actually cares what the hell is ionotropic vs. chronotropic effect? Just put the pills in the bottle already.

I use unit-dose, no need for bottles even. So much easier!
 
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