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Enzymes and chemicals involved in digestion,probiotic enzyme digestive care,enzymes for digestion in small intestine youtube,nova probiotics reviews 2014 - Test Out

When we put that favorite meal of ours into our mouth, it would not be useful to the body without the food getting digested and absorbed. Digestion in humans is achieved by the mechanical breakdown of large food components so that the chemical process of digestion can proceed efficiently and effectively. The esophagus (oesophagus) is a narrow collapsible muscular tube that connects the pharynx and the stomach. The stomach is a big bean-shaped muscular bag that seats in the upper left side of our abdomen.
The liver produces bile - that greenish bitter liquid that gives a greenish colour to the content of a vomit.
The pancreas is a j-shaped gland that lies within the curve of the duodenum, just behind the stomach.
The following are the main enzymes and chemicals known to be involved in the digestive process in humans.
The full process of digestion of food in humans involves a step by step sequence which we will explain here. Appendix Pain Location - Where Appendicitis Pain Starts From And Stays Jul 05, 16 12:14 PMSee the appendix pain location as depicted in the pictures here. Sharp twangs on lower right side of abdomen Jul 01, 16 06:26 PMI'm 35 years old and for about the last 3 months have been suffering with sharp twangs of pain in my lower right side of stomach.
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Digestion is the process where the complex chemical make up in the food we eat is broken down into simpler components that our body can absorb and use to maintain health and proper functions. There is no clear separation in real time between the physical and chemical process of digestion. Without it, food cannot be transferred from the mouth through the throat into the esophagus and stomach.
Eating and digestion would be very very difficult without these silent lubrication and digestive factory in our mouth.
It does not only act as a storage sac for the food we consume, it also works as a powerful mixer of the food. Bile helps to break fats in our diet into smaller water soluble substance in a process known as emulsification. It is one of the most important glands in the body, producing vital chemicals like insulin and glucagon that helps in the regulation of blood glucose. It is here that the pancreas releases the pancreatic juice that helps digestion.Irritation of the wall of the duodenum leads to ulcer forming here - duodenal ulcer and can cause significant abdominal pain. Once the process of digestion is complete, the indigestible remnant of the ingested material passes on to the colon. For clarity, we shall use an example of ingestion of a meal of fried chicken and roasted potato. The incisors help to cut food items that does not require significant jaw power, like cutting off banana or biscuit or potatoes.
The inner lining of the wall of the stomach contains glands that produce different chemicals including strong acids that help sterilize our food as well as aid digestion. The small intestines produces the intestinal juice called succus entericus Succus entericus contains sodium bicarbonate that helps create the right environment for enzyme function, mucus that helps in further lubrication of the food material as it passes down the gut and a host of powerful enzymes including trypsin, chymotrypsin, maltase, lactase, sucrase and enteropeptidases.
Here, the food is held for a while to allow anaerobic digestion take place by the activities of the good bacteria of gut.
This is an enzyme produced by the salivary glands that helps break down starch  into less complex carbohydrate. This case demonstrates why it is important that health care practitioners report ADRs to the Food and Drug Administration (FDA).
Each of these glands or organs produce unique types of chemicals called enzymes and emulsifiers and lubricants to aid digestion.To help us understand the human digestive process more clearly, let us take a look at the different organs involved in this process, including fluids, enzymes, emulsifiers and lubricants that are released and involved in digestion.
The canine teeth helps to tear meat off bones, or cut through tough material that the incisors may not be able to handle. The tongue has powerful sensors that helps identify parts of a mouthful of food that requires further chewing and positioning it for further chewing. Though this part of the digestive tract acts mainly as a conduit, it also help protects the airways from being clogged with food.If the muscles of the pharynx are weak (like following a strike), it leads to choking when eating or drinking. The enzyme pepsin is produced in the stomach and it helps with protein breakdown, as well as several other chemicals like gastrin, cholecystokinins, substance P etc that helps in both digestion and fine regulation of other parts of our digestive system. It is stored in the gallbladder, a small pear shaped sac attached to the under surface of the liver.When the gallbladder gets clogged (by stones or sludge) it can lead to right upper abdominal pain or biliary colic.
It produces the pancreatic juice that contains pancreatic amylase (responsible for the breakdown of starch), protease (for the break down of proteins and pancreatic lipase (for the breakdown of lipids or fats).Poor functioning of the pancreas would lead to diabetes and or bulky, floating strong odorous feces. These enzymes help in further digestion and break down of milk and other forms of protein and smaller molecules of sugars .
These good bacteria ferment plant parts that would otherwise be impossible to breakdown by human enzymes.Some of the breakdown products are then quickly absorbed, and what is left mixes with mucus produced by the colon. Select it and click on the button to choose it.Then click on the link if you want to upload up to 3 more images. We shall then put together and follow the sequence in which they act and bring about digestion. This is because the pharynx can no longer close effectively and protect the wind pipe or trachea from food going down the throat. The stomach also acts as a surface for the absorption of certain food items and alcohol into the blood stream.Certain drugs (like aspirin, ibuprofen, diclofenac, almodipine), and chemicals like alcohol can cause the irritation of the wall of the stomach leading to upper abdominal pain, bloating, feeling of nausea and vomiting. The small intestine also provide a very large surface area for the absorption of digested food material.
Water is absorbed from this mix and the remnant is passed down the rectum and anus as feces.
We will then examine several well-recognized types of drug interactions that are the causes of preventable adverse reactions. This section will focus primarily on cytochrome P450-mediated drug interactions, although other types of interactions will also be included, as well as examples of drug-drug, drug-diet, and drug-herbal interactions.
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Let's see each of the organs that bring about digestion and exactly what each of these organs does.
They also help to provide the right working environment for the chemicals and enzymes in the gastric juice produced by the stomach.Pepsinogen. The emphasis will be on current knowledge that can help healthcare providers predict possible drug interactions.
Please consider upgrading your browser software or enabling style sheets (CSS) if you are able to do so. This will be followed by a discussion of ADR reporting via the FDA’s MedWatch program.
Pepsin helps in the breakdown of protein in the food material within the stomach.Cholecystokinin (also called pancreozymin) itself is not a digestive enzyme. However, it is produced within the stomach cells and it causes the release of the pancreatic enzymes in response to the presence of food in the stomach. What a marvel of ingenious design!The process of digestion continues with the chyme passing down the remaining length of the small intestines, where over 90% of absorption occurs. Recognition and reporting of this arrhythmia in association with terfenadine, astemizole (Hismanal), cisapride (Propulsid), grepafloxacin (Raxar), and mibefradil (Posicor) ultimately led to the removal of these medications from the market.1Monahan BP, Ferguson CL, Cleave ES, Lloyd BK, Troy J, Cantilena LR. It also causes a strong contraction of the gallbladder and release of bile for the emulsification of fats in our food.Bile. This is a green bitter liquid produced in the liver in response to the hormone hepatocrinin and  stored in the gallbladder. On the eighth day of terfenadine therapy the patient began a self-medicated course of ketoconazole (Nizoral—an azole antifungal) at 200 mg twice-a-day for vaginal candidiasis. Without this action of reducing fat into tiny small globules, it will be impossible for enzymes - which are water soluble, to mix with and digest fat in our food.
Bile is released into the duodenum by the contraction of the gallbladder in response to stimulation by the hormone, cholecystokinin.Pancreatic Juice.
Upon admission to the hospital the patient was noted to have a QTc interval of 655 milliseconds (normal is less than 440 milliseconds). During the hospitalization the patient experienced near syncopal episodes associated with torsades de pointes noted on telemetry.After discontinuing the medications, the QTc interval normalized. It contains enzymes that helps in the breakdown of carbohydrates (pancreatic amylase), Proteins (proteases) and fats (lipases).
She had no further episodes of torsades de pointes, and she was discharged with no recurrence of syncope.1Monahan BP, Ferguson CL, Cleave ES, Lloyd BK, Troy J, Cantilena LR. It also contains sodium bicarbonate, which helps to create the right working environment for the pancreatic enzymes.Intestinal juice. Ketoconazole has not been associated with development of torsades de pointes when used by itself. How did ketoconazole interact with terfenadine to cause QT prolongation and torsades de pointes in this patient? It contains a number of enzymes (trypsin, chymotrypsin, maltase, lactase, sucrase and enteropeptidases) as mentioned above, as well as lubricating mucus and bicarbonate. That question will be answered during the course of this module.1Monahan BP, Ferguson CL, Cleave ES, Lloyd BK, Troy J, Cantilena LR. The Institute of Medicine reported in January of 2000 that from 44,000 to 98,000 deaths occur annually from medical errors.1 Of this total, an estimated 7,000 deaths occur due to ADRs.
Incidence of adverse drug reactions in hospitalized patients: A meta-analysis of prospective studies. Again, methodological constraints limit making completely accurate estimates, but one estimate of the cost of drug-related morbidity and mortality is $136 billion annually,1 which is more than the total cost of cardiovascular or diabetic care in the United States. This will allow us to make the most appropriate choices in prescribing and avoiding preventable ADRs.1Schappert SM.


Ambulatory care visits to physician offices, hospital outpatient departments, and emergency departments: United States,1997. However, some drugs cause serious ADRs at very low frequencies and would require many more exposures to detect the reaction. For example, bromfenac (Duract) was a non-steroidal anti-inflammatory agent (NSAID) that was removed from the market in 1998, less than 1 year after it was introduced. Bromfenac caused serious hepatotoxicity in only 1 in 20,000 patients taking the drug for longer than 10 days.1 To reliably detect the toxic effects of a drug with a 1 in 20,000 adverse drug reaction frequency, the new drug application database would have to include 100,000 patient exposures.
A drug that is tested in a few thousand people 11 may have an excellent safety profile in those few thousand patients.
However, within a short time after entering the market, the drug may be administered to several million patients. The complete safety profile of a new drug will be defined only after it has been approved and is in use on the market.1Friedman MA, Woodcock J, Lumpkin MM, Shuren JE, Hass AE, Thompson LJ. However, the temporal relationship of a reaction with regard to the administration of a new medication can be helpful. Also, biological plausibility (asking if the drug’s mechanism of action makes this possible or likely) can also be helpful. A health care provider does not have to be absolutely certain that a drug caused a reaction. In the example case in this module, a single report ultimately led to the removal of terfenadine from the market.
This report potentially saved many lives and led to a better understanding of the mechanism involved in causing torsades de pointes.
Almost all drugs are now evaluated prior to being released on the market for their potential to induce cardiac arrhythmias, also as a result of this single case report.1Figueiras A, Tato F, Fontainas J, Gestal-Otero JJ. Each of these drugs has value in the pharmaceutical marketplace, and each has value to patients. Although the respondents were very concerned about suffering from pain and the cost of filling prescriptions, they were most concerned about being given the wrong drug or that a drug interaction would occur.
The public in general has a much greater level of concern about ADRs than most health care providers would suspect. These data demonstrate that drug interactions and reactions are not only a concern to health care providers but to patients as well.1American Society of Health Systems Pharmacists.
Bethesda, MD.Types of Drug InteractionsThe previous slides have reviewed information about the magnitude of adverse drug reactions and the burden they place on the health care system.
How much do drug interactions contribute to the total number of preventable ADRs? Again, estimates of the numbers of patients injured due to drug interactions vary widely.
2Raschetti R,  Morgutti M, Menniti-Ippolito F, Belisari A, Rossignoli A, Longhini P, et al. Suspected adverse drug events requiring emergency department visits or hospital admissions. More significant is the fact that, although this information is avail-able, it is not uniformly or optimally incorporated into decision making. A fundamental understanding of the clinical pharmacology of drug interactions and a framework for avoiding preventable drug interactions remains critically important.
Thus we need to overlay technologic solutions on a base that is strong in basic principles of clinical pharmacology and drug interactions. Incorporation of up-to-date computerized databases is valuable, and frequent consultation with other members of the healthcare team, such as nurses and pharmacists, is essential.1Bates DW, Leape LL, Cullen DJ ,Laird N, Petersen LA, Teich JM et al.
Effect of computerized physician order entry and a team intervention on prevention of serious medication errors. Contraindicated use of cisapride: impact of food and drug administration regulatory action. Both slow the heart rate by different mechanisms, and the combination is relatively contraindicated because heart block can result. Because of this interaction many textbooks and computer pro-grams warn against concomitant use of any beta-blocker and any calcium channel blocker. This creates a great deal of confusion and distrust of drug interaction warnings, because most health care providers know that drugs in these two classes are often employed successfully and safely in patients with hypertension.The next few slides will review some of the mechanisms for drug interactions in more detail. Several examples of drug interactions that occur prior to drug administration are listed here. When phenytoin is added to solutions of dextrose, a precipitate forms and the phenytoin falls to the bottom of the IV bag as an insoluble salt. Amphotericin is still used widely as a urinary bladder perfusion to treat aggressive fungal infections.
If it is administered in saline, the drug precipitates and can erode through the bladder wall if not removed. The clinical presentation of such cases is an acute abdomen due to perforation of the bladder.1 Lastly, it is recommended that aminoglycosides not be co-mixed in IV fluids with betalactam antibiotics. Women taking iron supplements often do not consider them as a medicines, and should be specifically questioned about whether they are taking iron if they are to be prescribed a quinolone or azithromycin.
Drugs such as ketoconazole (Nizoral) and delavirdine (Rescriptor) require an acidic environment to be in the non-charged form that is preferentially absorbed.
The previously cited examples have subsequently been shown to be due to inhibition of elimination, not plasma protein displacement.Drug MetabolismThe next few slides will focus on drug metabolism.
Some important preventable drug interactions are due to their effects on drug metabolizing enzymes, resulting in either inhibition (reduced activity) of the enzyme or induction (increased activity) of the enzyme. Of the remaining drugs, some are converted to metabolites that retain the same activity as the parent. An example of this is fexofenadine (Allegra), the active metabolite of terfenadine that has equal potency at the histamine receptor and now is on the market and used clinically for allergic rhinitis. On the other hand, if the parent drug needs to be metabolized to the active compound and metabolism is inhibited, then a therapeutic failure could result. Induction of drug metabolizing enzymes could similarly result in a subtherapeutic effect by reducing drug levels below that required for efficacy.1Woosley RL, Chen Y, Freiman JP, Gillis RA. In addition to cytochrome P450, there are other enzymes in microsomes such as flavin monooxygenase (termed FMO3).
Since Phase II reactions generally result in conjugation of a drug to a water-soluble group like a sugar, peptide (glutathione) or sulfur group, and, because there is a large excess of these groups in well nourished cells, these reactions are rarely rate-limiting. In contrast, the Phase I reactions carried out by cytochrome P450 enzymes, flavin monooxygenases, and reductases are more frequently rate-limiting. These are the target of clinically significant drug interactions, such as the inhibition of cyclosporine metabolism by erythromycin.Six cytochrome P450 isoforms have been well characterized in terms of drug metabolism in humans. The predominant enzymes responsible for Phase I reactions are those involving the microsomal mixed function oxidation system. These enzymes are companions and part of a cascade that shuttles electrons from molecular oxygen to oxidize drugs. Because many drugs are metabolized principally by these enzymes, important interactions between drugs can be predicted by using a list of drugs that are inhibitors or inducers of that enzyme. This simplifies the search for interacting drugs and provides a framework for prediction of interactions.
Next we will review how these enzymes are named.Cytochrome P450s were named by molecular biologists and protein chemists. Because of this great sensitivity, small changes in amino acid sequence can result in huge changes in substrate specificity for the cytochrome P450 enzymes.
For example, 2C19 is the principal metabolic enzyme for omeprazole (Prilosec) metabolism, but a closely related enzyme, 2C9, has no catabolic effect on omeprazole.
Thus, little functional similarity is imparted by the similarity in amino acid sequence on which this nomenclature is based. However, as will be seen later, there is some concordance between classes of drugs and the P450 family that metabolizes them.
The focus of the subsequent slides will be to outline the role of the cytochrome P450 isozymes in metabolism of commonly used drugs and to identify tools that can be used in clinical practice to avoid cytochrome P450-mediated drug interactions.The graph on the left lists the major isoforms of CYP450 and their relative roles in drug metabolism (not relative amounts found in the liver) based upon the number of drugs that are known to be metabolized by that particular isozyme. CYP2D6 accounts for less than 2% of the total content of P450 in the liver, but as shown on the left, is responsible for the metabolism of a large fraction of drugs. A large amount of cytochrome P450 has not yet been characterized.There is tremendous variability between individuals in terms of expression of cytochrome P450 isozymes. Interindividual variations in human liver cytochrome P-450 enzymes involved in the oxidation of drugs, carcinogens and toxic chemicals: studies with liver microsomes of 30 Japanese and 30 Caucasians. As a result, the enzyme may be absent or have low, or no, metabolizing activity for drugs that are usually metabolized by that enzyme.
If the mutation is relatively common (more than 1%) it creates a polymorphism—this is a trait that has genetic variation that results in more than a single population being represented in greater than 1% of the total population. On the graph, PM means poor metabolizer, EM means extensive metabolizer, which is the normal or usual phenotype, and URM means ultra-rapid metabolizer.
Ultra-rapid metabolizers usually do not appear as a separate distribution in most phenotypic data but are important because a usual dose of drug in these people will be cleared more quickly than in the rest of the population and will result in lower blood levels of the drug and, perhaps, less therapeutic effect. For CYP2D6, it is known that these individuals have very high activity because they have multiple copies of the CYP2D6 gene (up to13 copies have been reported).Second, people that have usual drug metabolizing ability (EM) can become phenotypic poor metabolizers if they are given a substance (drug or food as we will see later) that inhibits the enzyme. If this occurs, metabolism of any drug that is a substrate for that isozyme will be metabolized more quickly resulting in lower plasma concentrations of the drug. Also, if the drug is metabolized to a toxic compound, the toxic metabolite may accumulate to higher levels.The P450 isozymes will now be reviewed in more detail.
The laminated card in the pocket of the module can be used as a reference for the next few slides.CYP3A is responsible for metabolizing the greatest number of marketed drugs. These include a wide range of important medications including cyclosporine and HIV protease inhibitors, as well as cisapride (Propulsid) and the no longer marketed non-sedating antihistamines terfenadine (Seldane) and astemizole (Hismanal). Although CYP3A is not polymorphic in its distribution (it doesn’t have a distinctly separate population as seen on the previous graph), its activity varies over 50-fold in the general population. Terfenadine, one of the first non-sedating antihistamines, is metabolized by CYP3A to fexofenadine. When the CYP3A-mediated metabolism of terfenadine is inhibited by ketoconazole, as in the case described, terfenadine accumulates to high levels.


At these high levels, terfenadine is a blocker of potassium channels in the heart.2 Potassium channels are important for repolarization of the heart. Once these channels are blocked, QT interval on the electrocardiogram can be prolonged and torsades de pointes can  develop, as was seen in this case. This important enzyme has been the basis for most of the fatal drug interactions that have gained so much publicity in recent years. For terfenadine, as well as astemizole and cisapride, recognition and reporting of torsades de pointes in association with the drug and its interactions ultimately led to withdrawal of these drugs from the market.The vast majority of drugs that may cause cardiac arrhythmias by prolonging the QT interval are metabolized by cytochrome P450 3A. While the biological basis for this remains unclear, it does make it easier to remember!Also note that CYP3A is found in the liver and also in the GI tract.
Drugs that are substrates of CYP3A can be extensively metabolized in the GI tract, and ,in fact, the GI tract is responsible for a large part of the metabolism that was formerly attributed totally to the liver! Inhibition of GI tract CYP3A also results in higher plasma levels of substrate drugs.1Thummel KE, Wilkinson GR.
Azole antifungal drugs, in general, are potent inhibitors of CYP3A, although fluconazole is a weak inhibitor and inhibits CYP3A only at high doses.
All the macrolide antibiotics, except azithromycin, are also potent inhibitors of this cytochrome P450 isoform.
The role of grapefruit juice in drug interactions will be discussed later.Several commonly used drugs have been characterized as inducers of CYP3A.
Use of these drugs could potentially result in lack of therapeutic efficacy of a CYP3A substrate.
Study of CYP2D6 has led to understanding the failure of codeine to relieve pain in some patients.
Codeine itself is much less active as an analgesic, but causes nausea and other adverse effects.
These include quinidine3 as well as haloperidol and some other antipsychotics.4,5 The well-described pharmacokinetic interaction between selective serotonin reputake inhibitor (SSRI) antidepressants and tricyclic antidepressants appears to be due to the fact that fluoxetine and paroxetine are both potent inhibitors of CYP2D66,7 and render patients metabolically equivalent to people who do not have the enzyme. This increases the plasma levels of tricyclic antidepressants and increases the potential for side effects. In contrast, patients co-prescribed fluoxetine or paroxetine with codeine may experience no analgesic benefit, since codeine requires CYP2D6 for metabolism to morphine.1Caraco Y, Sheller J, Wood AJ. Pharmacogenetic determination of the effects of codeine and prediction of drug interactions. Frequent distribution of ultrarapid metabolizers of debrisoquine in an ethiopian population carrying duplicated and multiduplicated functional CYP2D6 alleles. Potent inhibition of CYP2D6 by haloperidol metabolites: stereoselective inhibition by reduced halo-peridol. Effect of antipsychotic drugs on human liver cytochrome P-450 (CYP) isoforms in vitro: preferential inhibition of CYP2D6. Effect of adjunctive paroxetine on serum levels and side-effects of tricyclic antidepressants in depressive inpatients. It is the major enzyme responsible for metabolism of many of the non-steroidal anti-inflammatory drugs (NSAIDs), including the second generation cyclooxygenase-2 (COX-2) specific inhibitors. A number of other important medications have their metabolism primarily catalyzed by CYP2C9. An important drug metabolized by this enzyme is warfarin (Coumadin), and almost all inter-patient variability in warfarin levels and anticoagulant effects can be explained on the basis of CYP2C9 activity (not the differences in protein binding as originally thought).The azole antifungal agent fluconazole (Diflucan) is a potent inhibitor of CYP2C9. Contrasting effects of fluconazole and ketoconazole on phenytoin and testosterone disposition in man. This enzyme metabolizes many anticonvulsants, diazepam (Valium), omeprazole (Prilosec) and several of the tricyclic antidepressants. Asians have reduced clearance of diazepam compared to Caucasians,1 and, in fact, a survey of Asian and Western physicians demonstrated the use of lower doses of diazepam in Asians.2 Asian patients may have a lower omeprazole dosage requirement for effective treatment of Helicobacter pylori.
Do Oriental psychiatric patients receive different dosages of psychotropic medication when compared with occidentals. Effect of genetic differences in omeprazole metabolism on cure rates for Helicobacter pylori infection and peptic ulcer.
Effect of genotypic differences in CYP2C19 on cure rates for Helicobacter pylori infection by triple therapy with a proton pump inhibitor, amoxicillin, and clarithromycin. Effects of ketoconazole on the polymorphic 4-hydroxylations of S-mephenytoin and debrisoquine. Comparison of the interaction potential of a new proton pump inhibitor, E3810,versus omeprazole with diazepam in extensive and poor metabolizers of S-mephenytoin 4'-hydroxylation. Inhibition of cytochrome P450 (CYP450) isoforms by isoniazid: potent inhibition of CYP2C19 and CYP3A.
The clearance of theophylline, imipramine, propranolol and clozapine are all increased by smoking.
Thus, people who smoke may require higher doses of some of the medications that are substrates of CYP1A2.
In contrast, a smoker would require a decrease in theophylline dosage if, for example, smoking were discontinued and the enzyme no longer induced. Ciprofloxacin increases serum clozapine and N-desmethylclozapine: a study in patients with schizophrenia. An evaluation of the quinolone-theophylline interaction using the Food and Drug Administration spontaneous reporting system. Fortunately there are aids to help health care providers to anticipate and prevent drug interactions, such as the tool shown here. This table includes a listing of the 6 major cytochrome P450 isozymes involved in drug metabolism and the drugs that are metabolized by them.
We recommend using this or another table as a quick reference for detection of potential drug interactions.If 2 drugs are metabolized by the same cytochrome P450 isozyme, it is very possible that competitive inhibition could lead to higher than usual levels of either or both of the drugs. If a drug is metabolized by a specific cytochrome P450 and is taken with an inhibitor or inducer of that isozyme, an interaction is also likely.The following are examples of how to use this card. Suppose your patient is taking amiodarone and you want to add a statin agent to decrease the patient’s cholesterol (follow red circles and arrows above).
We also note that lovastatin and simvastatin are metabolized by CYP3A and that if given with amiodarone (which is inhibiting the enzyme) a toxic level of the statin may occur. Another example would be if your patient were taking an HIV protease inhibitor and wants to take St.
At the website, it is possible to easily obtain the reference for a given drug by clicking on the drug. The website hyperlinks to PubMed and searches for a list of the relevant publications.In addition to the drug-drug interactions just reviewed, drug-disease interactions can occur. Severe liver disease can be associated with reduced metabolic clearance and higher plasma levels of drugs extensively metabolized by the liver.1 Although liver disease reduces drug clearance on average, the change is relatively small and usually not clinically relevant except in patients with near terminal liver disease. Pharmacokinetics of theophylline in hyperthyroid and hypothyroid patients with chronic obstructive pulmonary disease. Higher incidence of elevated body temperature or increased C-reactive protein level in asthmatic children showing transient reduction of theophylline metabolism.
One of the early observations was the reduced absorption of tetracycline when taken with milk products.
The chelation of tetracycline by calcium prevents it from being absorbed from the intestines. Dietary sources of vitamin K, such as spinach or broccoli, may increase the dosage requirement for warfarin by a pharmacodynamic antagonism of its effect.
Grapefruit juice contains a bioflavonoid that inhibits CYP3A and blocks the metabolism of many drugs.
This was first described for felodipine (Plendil)2 but has now been observed with several drugs.3 This interaction can lead to reduced clearance and higher blood levels when the drugs are taken simultaneously with grapefruit juice. Grapefruit juice increases felodipine oral availability in humans by decreasing intestinal CYP3A protein expression. Compared with water, there is an increase in felodipine plasma concentrations, as well as a decrease in systolic and diastolic blood pressure.
This demonstrates a potentially clinically significant effect of the grapefruit juice-felodipine interaction.1Dresser GK, Bailey DG, Carruthers SG. It is therefore important that health care providers obtain a complete drug history that includes herbal remedies and other natural products and dietary supplements and that they be alert to potential interactions.1Piscitelli SC, Burstein AH, Chaitt D, Alfaro RM, Falloon J. Pharmacokinetic interaction of digoxin with an herbal extract from St John’s wort (Hypericum perforatum). John’s wort, a 57% reduction was observed in the indinavir area under the plasma concentration-time curve (AUC), indicative of reduced exposure to indinavir. The potential for loss of therapeutic efficacy due to this interaction suggests the importance of taking a complete medication history.
This history should include questions about herbal therapy and other natural products as well as over-the-counter medications.1Piscitelli SC, Burstein AH, Chaitt D, Alfaro RM, Falloon J. The first goal is to increase awareness of drug, device and other medical product induced disease and the importance of reporting.The second goal of MedWatch is to clarify what should (and should not) be reported.
This is important both in improving the quality of individual reports and enabling the FDA and the manufacturer to focus on the most significant reactions. Introducing MedWatch: a new approach to reporting medication and device adverse effects and product problems. It is therefore important to develop a stepwise approach to preventing adverse reactions due to drug interactions.First, taking a good medication history is essential. Studies show that the rate of adverse drug reactions increases exponentially in patients taking 4 or more medications.1 Importantly, some categories of drugs are especially at high risk for interactions. Depending upon the practice setting, this may be a clinical pharmacologist, a hospital pharmacist, a specially trained office staff nurse, or the nearby pharmacist in community practice.Fifth, use one of the computerized databases available. Palm Pilot) and can be configured to automatically update each time you synchronize with the desktop computer.



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