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Carafate, or sucralfate will bind up ciprofloxacin, norfloxacin, and phenytoin. The Carafate or sucralfate and ciprofloxacin doesn’t work to separate them by two to three hours. They’ve done some studies looking at it and they still found about 95% to 98% absorption of ciprofloxacin even with dosage separation of three hours. So what I would tell you is that with the expense of ciprofloxacin, please don’t do that to your patient. The expense is about 70-some dollars for a prescription of ciprofloxacin, depending on the dose, and the last thing in the world I as a patient would want to do is to have them take it and then sort of just dump it back into the sewage system rather than gain much benefit from it. So that’s one of those interactions that you really want to avoid. Pick something different to use.
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What about bacterial drug metabolism? U. bacterium lentum is one of the primary bacteria in the gut and it can cause some problems for us with the drugs that need to be metabolized in the gut in order to be put into the active form. Tetracycline and penicillin have been shown to cause potential contraceptive failure, breakthrough bleeding and pregnancy in patients who are taking oral contraceptives and then receive tetracycline or penicillin. I have to tell you that this an area that is extremely difficult to study. There are … if there’s a drug on the market that’s been on the market long enough to have something published about it in case report form, there’s a case report implicating that it caused oral contraceptive failure in the literature. I think the problems are actually two-fold. No patient likes to come in and say, “Yeah, I guess I didn’t take my oral contraceptive just as I was supposed to.” It’s easier to say, “I think this antibiotic caused the problem.” And also it’s almost impossible to really study it because women who are taking oral contraceptives are obviously taking them because they don’t want to become pregnant and they are not going to be very enthusiastic about enrolling in a study where we say to them, “Okay, you’re taking an oral contraceptive. Would you mind taking this antibiotic and let’s just see if you get pregnant?” There are pretty big implications to asking someone to do that so we don’t have clinical trials to really give us definite answers, so we just have to go on case reports. There are lots and lots of case reports on tetracycline and penicillin on causing oral contraceptive failure. I can tell you that it appears that short course – 7 to 10 days of erythromycin or trimethoprim sulfamethoxazole – appears to be safe. It’s my practice and it’s my advice to you that the patients needs to be told that antibiotics can cause oral contraceptive failure. If you really don’t want to get pregnant I would advise that you use an additional form of contraception during this cycle and let them make the decision. I guess my motto in this situation is that it’s really better to be safe than sorry. I wish I could give you absolute answers on this one but there just really are not any out there.
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Protein binding? This is an area of drug/drug interaction that … there’s a lot published on it, however the body – the magnificent organism that it is – has its own compensatory process that when changes in free concentrations of drugs happen, the body eliminates that extra drug as long as we haven’t given another drug to block its natural excretion process. So there aren’t a whole lot of really clinically significant drug/drug interactions, but you’ll hear tons and tons of “Oh, this drug is highly protein bound, and so is this drug.” So I’ve chosen to talk about it. An example – although not one that really applies much to use in humans anymore – is the use of phenylbutazone in combination with warfarin. Phenylbutazone is almost exclusively used in racehorses anymore. But phenylbutazone and warfarin are both very highly protein bound and they will compete for protein binding sites and phenylbutazone will block the excretion of warfarin. Order cialis professional online. So in this situation you do have a situation where you can have problems with increases in bleeding. What I would suggest to you is that if you have a situation where you are concerned about the potential for increase in serum concentrations due to an interaction of highly protein bound drugs, that you monitor free serum concentrations. And you can do that. That’s what you are really concerned about, is like free phenytoin levels. What is the free fraction of this drug? And that will tell you. That will help you gauge whether or not you have the potential for toxicity.
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Altered metabolism? We can do that through blood flow or through enzyme function either by increasing or decreasing both of those. When we talk about enzyme induction we talk about increasing enzymatic binding sites. The thing that is important to remember about that is that when we are increasing actual binding sites, there is the requirement for protein synthesis. What’s the big deal about that? The importance of that is that that does not happen overnight. It does not happen in 24 hours. It doesn’t happen in 48 hours. It probably takes two to three weeks before you see the maximal effect. The reason that I make a big deal out of this is that a lot of time I think what happens is we think, “Oh, well this drug can increase the serum concentration of this drug. I’ll bring them back in three or four days and check the serum concentration and see where it is.” We do that and we see that it’s okay and we send them out and we don’t think three weeks down the road. We kind of forget that end step because everything looked great. Now I’m not saying bringing them back in four days or five days or even a week is inappropriate. I think that’s very appropriate. But keep in mind, if they are getting up there close to the upper end of the therapeutic range that you are going to want to check again. Because there’s a possibility that they could become toxic further out. So just keep in mind that it takes longer for the full effect to be realized than what you may have previously thought. Also there’s some data to suggest that perhaps the elderly may be a little less sensitive to this type of an interaction than the general population. Mostly because some of them are malnourished and may have a lesser ability to synthesize proteins.

The first type, or the first sub-category if you will, within the pharmacokinetic is altered absorption through gastric pH. We know that the H2 receptor antagonists increase gastric pH. Cimetidine, ranitidine and also famotidine and nizatidine all will do that and with those drugs they will cause an increase in aspirin absorption. Now you may think, what difference does that really make? Well, for the patient who is taking aspirin for occasional aches and pains or headaches or whatever, it really makes no difference. Or taking one aspirin a day for cardiovascular protection. Viagra professional – erectile dysfunction treatment. Increased absorption of that really isn’t going to make any difference at all. However, if you have a patient who is using it for true antiinflammatory purposes, at big time doses maybe for rheumatoid arthritis or something like that, it may make a big difference. It may be enough that it would push them over the edge to potential aspirin toxicity with ringing in the ears and that sort of thing. So this is one of those situations where you really need to… it really depends on the situation of the patient. Also, these drugs are known to decrease the absorption of iron and again this is a situation where you need to look at why is the patient taking iron? If the patient is taking it as part of a multivitamin just because they think that’s the healthy thing to do, and it’s kind of used as a dietary supplement, if they absorb a little bit less than they would have previously, again, clinically it’s not going to make any difference. However, if they have iron-deficiency anemia that you are trying to treat, that’s going to be significant. And increased doses may need to be used or you may just see a slower response, and those sorts of things.
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Now with ketoconazole I can’t come up with a reason why somebody would take ketoconazole unless you were really trying to treat a fungal infection, so in every situation that I can come up with, the interaction between the H2 receptor antagonist and ketoconazole will always be clinically significant. So if possible, you need to find some other way to treat peptic ulcer disease in those patients who are receiving ketoconazole.
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What about increasing gastric emptying rate? Metoclopramide and cisapride can do that as well as the antacids. This is a graphic representation of 11 patients who were receiving digoxin therapy. We have here serum digoxin concentrations and along here kind of their regimen of therapy. If you’ll take a look here, for all practical purposes, the serum concentrations for all 11 patients were within that therapeutic range at the beginning. Metoclopramide was added to the regimen and in every situation those serum concentrations decreased. Some of them fell below what we would consider therapeutic. Some fell but still stayed within that range. And then when metoclopramide was discontinued and digoxin was added on, put back on board, it … the nearest you can tell from the scanty graph that they’ve provided us with here is that all of those patients returned back to baseline, or nearly back to baseline. What the authors concluded was that digoxin speeded up transit through the GI tract. Digoxin is a very insoluble product and we know that. It needs gastric acid to go into solution, so if you hurry it on through less of it goes into solution so there’s less of it to be absorbed. A couple of things I want to point out for you is that first of all, this is done with digoxin tablets. It’s only the tablets that have to go into solution. So if your patient is receiving Lanoxicaps, which are those liquid-filled gelatin capsules, this interaction doesn’t … it’s not affected by that because it’s already in solution so gastric acid is not important in that situation. Also the digoxin elixir, the digoxin elixir, again it’s a solution so it’s those patients who are taking tablets this is pertinent. Obviously the IV is not an issue either.
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What about decreasing gastric emptying rate? We know that anticholinergics and all those drugs that have anticholinergic-type side effects slow down the gut. That’s why they get constipated. Also narcotic analgesics. You will see just the opposite with the digoxin. The digoxin tablets. They are there in the gut for a longer period time, more goes into solution so there’s more to be absorbed. So you will see patients with an increase in their serum levels.
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And then those drugs that are acid sensitive. Drugs like penicillin, Pen VK also ampicillin and erythromycin. Those drugs are acid sensitive hence the reason we attempt to tell patients to take them on an empty stomach. Erythromycin is a real problem because it causes such GI upset that patients sometimes can’t even take it if they take it with food. But the theory behind that is that it is acid sensitive and if they take it with food they will absorb less. But that’s better than not being able to keep it down at all. Cheap amoxicillin
Complex and chelate formation. This basically is when you have two drugs given together and they bind each other up in the gut and never are absorbed. This happens with the antacids and dairy products when iron and tetracycline and ciprofloxacin are given. Activated charcoal we use specifically for that purpose. To bind drugs in the gut in overdose situations, so it is not absorbed. Cholestyramine really poses us a lot of problems with drug/drug interactions because if you look at the drugs it interacts with, it interacts with digoxin, thyroxine and Warfarin. Just about every patient who is on cholestyramine is on one of those other three, if not on two or all three of them. So this can be a real problem for us. Basically what we usually tell patients is to separate the dosing by two to three hours. The tablet medication they can take and then in two to three hours they can do the cholestyramine or vice-versa. The problem with that is that then you end up with your patient having to increase the number of administration times each day that they have to remember to take medication. So it can be avoided, and there’s a solution to it, but it requires that extra effort by the patient which is sometimes difficult to get from them.

Lets move on to some more specific examples with the drug/drug interactions. The first ones we are going to talk about are the pharmacodynamic drug/drug interactions. We talked about that and kind of told you what that was. That’s when you have two or more drugs when given together that have action at the same receptor site and because of their actions given simultaneously you have a change in the effect that you see. This type of interaction, undoubtedly, they are the most common interactions, they are the most logical. They are very obvious when you stop and think about them. The first example would be direct receptor effects. An example might be the administration of a beta agonist in combination with a beta antagonist or a beta blocker. Seeing antagonism of the desired effect. If you have someone, an asthmatic or a COPD, that receives a beta agonist on a routine basis and then they have an MI or hypertension and you add a beta blocker to their therapy, you may exacerbate their symptoms of COPD or asthma. The one thing that I want to caution you about is that when – you may think, well I’ll use a cardio-selective beta blocker and avoid that problem – and in some situations you can. But keep in mind that as you titrate that dose up of that beta blocker, even if it is cardio-selective, you will begin to get spill-over relatively early. If you have a patient that’s really sensitive to those effects, you can exacerbate symptoms even with a cardio-selective product.
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What about indirect receptor effects? This might be a situation where you have a diabetic patient who is receiving a hypoglycemic agent, whether it be an oral hypoglycemic or whether it be insulin, and you administer a beta antagonist to that patient or a beta blocker. There is a possible increased risk of hypoglycemia in that patient for a couple of reasons. First of all, beta blockers block the patients response with the ability to respond to hypoglycemia through breakdown of glycogen in the liver. It kind of blunts that effect so they don’t respond quite as early. Secondly, beta blockers will block all but one of the signs and symptoms of hypoglycemia. It will block all the typical ones of nervousness, agitation, maybe tremor. The symptom that it does not block is sweating. The reason it does not block sweating is that, if you remember way back to pharmacology, sweating is a parasympathetic response. So it’s controlled by the cholinergic side of things. So if the patient is someone who can be educated and you feel comfortable with their ability to begin to recognize hypoglycemia by sweating as the primary symptom, and not the symptoms that they may have been used to, this combination still can be used relatively safely.
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Another example would the use of basically any antihypertensive in combination with primarily the tricyclic antidepressant-type drugs and/or ethynyl thiazine and the resulting consequence of orthostatic hypotension. All of those drugs can cause orthostatic hypotension so if you add them together you get an increased risk of orthostasis.
Fluid and electrolyte disturbances, again this is going to be fairly obvious to you. Spironolactone, a potassium-sparing diuretic when it’s used in combination either with a potassium supplement or with an ACE inhibitor can potentially result in hyperkalemia. The one thing that I would suggest to you is that there are some reports out there that suggest that that response may be more than additive. So it may be greater than what you anticipate but I haven’t seen any reports yet that will call it truly synergistic but they just sort of suggest that it may be more than additive. So that may be something to keep your eye on.
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Now I think you would probably agree with me that those were all relatively obvious and things that you knew already. So what we are going to spend the rest of the time concentrating on are the pharmacokinetic drug/drug interactions and they are the ones that are, in my opinion, a lot of times much more difficult to anticipate. They are the ones where you start to see differences within the same classes of drugs, differences in effects of the drugs. So we’ll spend the rest of the morning talking about those. Again, the pharmacokinetic drug/drug interactions are when you have two or more drugs that are given at the same time, altering the serum concentrations of one or more of those drugs resulting in a change in the actual effect that is seen. Viagra oral jelly.

The pharmacokinetic drug/drug interactions actually start over on this side, on the left side, and move all the way through to the right side. And that is when you have drugs administered simultaneously and because of something that happens – either through absorption or distribution or metabolism – you have a change in the plasma concentration of one or both of those drugs. Then, because of that change in the plasma concentration, you have a change in how it acts at the receptor site and thus a change in effect.
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Because of the way pharmacokinetic drug/drug interactions happen, or have changes in serum concentrations, we need to think about where those interactions happen. Basically they can happen in any step of the process that a drug goes through. From the time that it’s ingested to the time that it’s eliminated from the body. So it can happen in the gastrointestinal tract, it can happen because of changes in tissue or protein binding, it can happen in metabolism and it can also happen in excretion. So anywhere along that – we use the pneumogram of ADME, absorption, distribution, metabolism, and excretion – anywhere along that ADME path you can have the drug/drug interactions occurring.
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Okay, so what drugs in which patients do we need to be most concerned about? The drugs that we are most concerned about are those drugs which affect a vital process. What do I mean by a vital process? Well, those would things like seizure-threshold, cardiovascular rhythm, blood coagulation status, and respiratory function and also the drugs that have a narrow therapeutic index. How might you know if they have a narrow therapeutic index? The drugs that have narrow therapeutic indexes are the ones that we routinely monitor serum concentrations of. If you think about it, it’s really nice because it goes hand-in-hand with those drugs that affect a vital process. We monitor anticonvulsant levels, we monitor antiarrhythmic levels, we monitor theophylline levels and we don’t necessarily monitor warfarin and heparin levels but we monitor coagulation status. So those two things go really hand-in-hand and those are the drugs that we need to be most concerned about. As far as which patients; the patients that are critically ill, basically just because they happen to be on the greatest number of drugs. Probability will tell you that as a patient’s number of drugs increase, so does the likelihood that they would be on drugs that interact. Also the elderly patients. Again, because the elderly tend to have more disease processes going on and also tend to be on a greater number of medications.
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Pitfalls and literature evaluation. I just want to make a couple of comment about this. The first being inappropriate extrapolation. Basically what I mean by that is that if you happen to run across a case report in one of the journals that you are perusing, and it makes a comment about an interaction happening between verapamil, as a calcium channel blocker, and another drug. One thing that you want to be very careful about is not to assume that because verapamil interacts with a given drug that all of the calcium channel blockers interact with that drug. Because that’s not the case in many situations. It is in some but it’s not in all, and vice versa. You wouldn’t want to assume that because verapamil didn’t interact, that all of the calcium channel blockers would not interact. You need to be somewhat specific in trying to assimilate that information. Also I list excessive reliance on experience. This is kind of a touchy one and it gets more and more touchy the longer I’m out of school because you gather more and more experience and it’s really nice to draw upon experience. But again, you have to remember with the drug/drug interactions that there is a tremendous amount of inter-patient variability and just because you cold use theophylline and the ciprofloxacin together in one patient and there was not a problem, that does not mean that at some point you may not run into the problem. So you don’t want to discount the drug/drug interactions too quickly.
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Clinically important drug/drug interactions. A drug/drug interaction is a pharmacologic response which cannot be explained by the action of a single drug alone, but rather it is due to two or more drugs acting simultaneously. I made absolutely no comments as to whether or not it was beneficial or harmful. The reason for that is because there are situations actually where we do use drugs in combination, because they interact and they do have a beneficial effect to our patients. It really demonstrates this point very clearly, and that is the use of probenecid which actually inhibits the excretion of amoxicillin or ampicillin through the kidneys and it would prolong antibiotic serum concentrations, thereby increasing the efficacy of ampicillin or amoxicillin when treating Neisseria gonorrhea. Now we know that Neisseria has developed a tremendous resistance to ampicillin and amoxicillin so we don’t use it anymore for that purpose. But it used to be the sole treatment and we got increased benefit by adding probenecid just because it prevented excretion and it stuck around for a longer period of time.
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The ones that we are most concerned about and the ones that I will spend the most time talking about today are those that are harmful. Obviously we are not in the business of trying to do harm to our patients, and when it’s the harmful ones it’s the ones that we don’t anticipate. Because they are harmful, drug/drug interactions that result of adverse outcomes are put in the category of adverse drug reactions and they are reported that way to the FDA. An example, and one that we will spend some more time talking about later on is the example of ciprofloxacin when it’s added to that regimen of a patient receiving theophylline, resulting in dramatically increased serum theophylline levels.
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So what types of drug/drug interactions are there? Well, there’s the pharmaceutical, pharmacodynamic and pharmacokinetic. Let me explain a little bit further. The pharmaceutical drug/drug interactions simply are nothing more than when you take two clear solutions, mix them together, and you end up with a solution that’s developed a precipitate. This is the type of interaction that we repeatedly get asked questions about from the nursing staff. “Can we run drug A through the line that has drug B running through it? Are they compatible?” It’s based primarily on pH-type properties. A good example of two solutions that you would not want to run through the lines together would be when you think about when we used to do codes and we would push sodium bicarb kind of one of the standard algorithms. And then you may need to push calcium chloride. You wanted to make sure you flushed that line really well because if you didn’t and then you pushed calcium chloride you would get essentially chalk forming in your lines with a line that would then be unusable. So that’s an example of pharmaceutical drug/drug interactions. There are tremendous references out there that can be used, if you have interest in that. I’m sure the pharmacist would be willing to share that with you. This is really all I’m going to say about pharmaceutical drug/drug interactions.
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What we are going to spend the rest of the morning talking about are the ones that are more clinically oriented. If you want to take a look at the right had side of the slide here, it is the pharmacodynamic drug/drug interactions. And pharmacodynamic drug/drug interactions happen when you have two drugs that have action at the same receptor site. Or the same site of action. Now they can antagonize one another or they can both be agonists, but because of their same effect at the same receptor site, you end up with a different effect than what you might have anticipated.

3. Parenteral iron. Parenteral iron in the form of iron-dextran may be given intramuscularly or intravenously, but does not lead to a more rapid hematologic response than oral iron and rare anaphylactic reactions have been reported. In general it should be reserved for individuals with malabsorption or intractable non-compliance with oral therapy.
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4. Blood transfusion. Blood transfusion should be avoided if at all possible, but may be necessary for individuals with anemia so severe as to cause cardiorespiratory embarrassment; in this case it should be given as packed red cells with a potent diuretic administered concomitantly.

D. Prevention of iron deficiency. Iron deficiency is such a prevalent problem that it is appropriate to approach prevention on a population basis. Efforts to increase heme protein in the diet may be useful, especially for young children after weaning. Iron supplementation with a therapeutic iron preparation to improve the iron status of a segment of the population in a relatively short period of time is beneficial in pregnant women and may be considered for infants, school children, and groups of workers. Iron fortification, the addition of iron to a common food to increase the iron intake of the population as a whole, is practiced in western countries by adding iron to flour and likely would be of benefit in developing countries.
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E. Differential diagnosis of microcytic anemia. Other causes of a microcytic hypochromic anemia include thalassemias, lead poisoning, hereditary sideroblastic anemia, and the anemia of chronic inflammation.