Nutrient drug interaction

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Nutrient drug interaction

  1. 1. FOOD-DRUG INTERACTIONPRESENTED BY:DEEPIKA BARANWALPhD SCHOLAR
  2. 2. DEFINITION Drug-nutrient interaction: the result ofthe action between a drug and a nutrientthat would not happen with the nutrient orthe drug alone. Food-drug interaction: a broad term thatincludes drug-nutrient interactions and theeffect of a medication on nutritional status.
  3. 3. Food-Drug Interaction For example, a drug that causes chronic nausea ormouth pain may result in poor intake and weightloss.
  4. 4. BENEFITS OF MINIMISING DRUGINTERACTION Medications achieve their intended effects. Patients do not discontinue their drug. The need for additional medication is minimized. Fewer caloric or nutrient supplements are required. Adverse side effects are avoided. Optimal nutritional status is preserved. Accidents and injuries are avoided. Disease complications are minimized. The cost of health care services is reduced. There is less professional liability. Licensing agency requirements are met.
  5. 5. DRUG EFFECTS ON FOOD INTAKEIncreased appetite (antihistamines,psychotropic drugs and steroids)Decreased appetite(amphetamines, insulinand alcohol)Taste changes(chelating agents anddiuretics)Nausea (cardiac glycosides )Bulking effects (methylcellulose and otherdietary fiber products)
  6. 6. DRUG EFFECTS ON NUTRIENTABSORPTION AND METABOLISM Increased nutrient absorption (cimetidineand ranitidine) Decrease nutrientabsorption(colchicine, alcohol, laxatives, antibiotic neomycin) Mineral depletion (diuretics, chelatingagents, alcohol, antacids, aspirin) Vitamin depletion(vitamin antagonists, oralcontraceptives)
  7. 7. OUTCOMES OF DRUG AND NUTRIENTINTERACTIONS BENEFICIAL EFFECTS:Infectious disease controlControl of cancerPrevention of thrombosesTreatment of metabolic diseasePrevention of acute drug toxicity
  8. 8. To be continued :ADVERSE EFFECTS:Loss of drug efficacyDrug- induced nutritional deficienciesToxic reactionsBlocked feeding tubes
  9. 9. Table 1. Drug Induced Nutritional DeficienciesDRUG AFFECTEDNUTRIENTSPOSSIBLEMECHANISMEFFECTANORECTIC DRUGS(amphetamines)All nutrients Anorexia Decreased food intakeANTACIDS Phosphates Decreased absorption OsteomalaciaANTIEPILECTICDRUGS(phenytion ,phenobarbitone,primidone,valproic acid)FolateVitamin DVitamin EZincSeleniumVitamin KDecreased absorptionEnzyme inductionExcess utilization ?ChelationPeroxide damage?Megaloblastic anemiaOsteomalaciaHaemolysisAnorexia , celebellardysfunctionHepatotoxicityHemorrhageANTIFOLATE DRUGS(e.g. methotrexate,pyrimethamine,trimethamine,trimethoprim)Folate Dihydrofolate reductaseinhibitionMegaloblastic anemia,cytopeniaBIGUANIDES(phenformin,metformin)Vitamin B12 Decreased absorption Megaloblastic anemia
  10. 10. To be continued:DRUG AFFECTEDNUTRIENTSPOSSIBLEMECHANISMEFFECTCHOLESTYRAMINE Fat , vitaminA,D,K,B12,folate ironComplex formationbleeding, steatorrhoeaAnaemia ,osteomalaciaCOLCHICINE Fat, β-carotene, Na,K,vitamin B12Mucosal damage Anaemia , lethargyCORTICOSTEROIDS Calcium Decreased Ca, vitaminD metabolismBone disordersCOUMARINANTICOGULANTSVitamin K ? HemorrhageDIURETICS Zn , Ca, K, Mg Urinary loss depression Weakness , electrolyteimbalanceFRUSEMIDE Thiamin Urinary loss Cardiac muscleweaknessGLUTETHIMIDE Calcium Enzyme induction,altered calciummetabolismWeakness, osteopenia
  11. 11. To be continued:DRUG AFFECTEDNUTRIENTSPOSSIBLEMECHANISMEFFECTHARMONALCONTRACEPATIVESSTEROIDSRiboflavin , Folate Enzyme induction,decreased absorption,competition for bindingof the enzymesMetabolic errors,depressionHYDRALAZINE Pyridoxine Complex formation Peripheral neuropathyISONIAZED (INH) Pyridoxine Complex formation Peripheral neuropathy,Convulsions, psychatricmanifestationLAXATIVE (MINERALOILS)Vitamin D Enzyme inhibition OsteopeniaLEVODOPA Nicotinic acid Competitive inhibitioncoenzyme and vitaminB6 deficiencyPellagraNEOMYCIN Vitamin A,D,E,K,B12,Ca,pyridoxineMal-absorption,complex formation,Mucosal damage,binding of bile saltsOsteomalacia,Peripheral neuropathy
  12. 12. To be continued:DRUG AFFECTEDNUTRIENTSPOSSIBLEMECHANISMEFFECTPARA – AMINOSALICYCLIC (PAS)Vitamin B12 decreased absorption Megaloblastic anaemiaD-PENICILLAMINE Pyridoxine ,Zn, Cu Complex formation Peripheral neuropathy,AnemiaPOTASSIUMCHLORIDEVitamin B12 decreased ileal Ph Decreased absorptionRIFAMPCIN Vitamin D Enzyme induction OsteomalaciaSALICYLATES Vitamin C, Folate Increased excretion,decreased uptakeAnemia ,infectionNEOMYCIN Vitamin A,D,E,K,B12,Ca,pyridoxineMal-absorption,complex formation,Mucosal damage,binding of bile saltsOsteomalacia,Peripheral neuropathySULPHASALAZINE Folate Mucosal block Decreased absorptionTETRACYCLINE Iron , vitamin C Chelation Decreased absorption
  13. 13. TYPES:1. Pharmacodynamic Interactions: whichaffect the pharmacologic action of thedrug.1. Pharmacokinetic Interaction: whichaffect the movement of the druginto, around, out of the body.
  14. 14. PHARMACODYNAMICSPharmaco-dynamics is the study of the biochemicaland physiologic effects of a drug. The mechanism of action, e.g. how a drug works Often the drug molecule binds to a receptor, enzyme,or ion channel, producing a physiological response
  15. 15. PHARMACOKINETICSPharmacokinetics is the study of thetime course of a drug in the bodyinvolving absorption, distribution,metabolism (biotransformation), andexcretion of the drug.
  16. 16. ABSORPTION : Absorption is the process of the movement of the drug from the siteof administration to the blood-stream. This process is dependent on the (1) route of administration, (2) the chemistry of the drug and its ability to cross biologicmembranes, (3.) the rate of gastric emptying & gastrointestinal movement, and (4.) the quality of product formulation Food, food components and nutritional supplements can interferewith the absorption process, especially when the drug isadministered orally.
  17. 17. Absorption Swallowing Disintegration tablet swells breaks up Dissolution reactions with acid faster when ionized Absorption most post pyloric in basic environment require non-ionized state
  18. 18. Food Interactions with Absorption Milk products alter pH Metals chelate some medications Some foods compete for same absorption sites Food speeds GI speed – reduced absorption Degree of significance is important
  19. 19. DISTRIBUTION:Distribution occurs when the drug leaves thesystemic circulation and moves to various parts ofthe body Drugs in the bloodstream are often bound toplasma proteins; only unbound drugs can leave theblood and affect target organs Low serum albumin can increase availability ofdrugs and potentiate their effects
  20. 20. Metabolism (biotransformation) Primarily in the liver; cytochrome P-450 enzymesystem facilitates drug metabolism; metabolismgenerally changes fat soluble compounds to watersoluble compounds that can be excreted Foods or dietary supplements that increase or inhibitthese enzyme systems can change the rate or extent ofdrug metabolism
  21. 21. Metabolism – Interaction with food Cytochrome P-450 inGI, liver Grapefruit juicemade from frozenconcentrate will alterthis enzyme Many drugs for AIDS,HTN Effects occur 24 hoursafter ingestion
  22. 22. EXCRETION Drugs are eliminated from the body as anunchanged drug or metabolite Renal excretion the major route of elimination;affected by renal function and urinary pH Some drugs eliminated in bile and other bodyfluids
  23. 23. Excretion Urine acidity willchange drugexcretion Cranberry juicewill alter pH andcause higherdissolution. Thisoccurs withsulfonamides Lime juice is mostacidic
  24. 24. PHARMACOGENOMICS Genetically determined variations that arerevealed solely by the effects of drugs Affect only a subset of people Examples include G6PD (glucose-6-phosphatedehydrogenase) enzyme deficiency, warfarinresistance, and slow inactivation of isoniazid(IHN) or phenelzine
  25. 25. SLOW INACTIVATION OF ISONIAZID OR PHENEIZINE: Increases the risk of pyridoxinedeficiency and peripheralneuropathy. Slow inactivation ofphenelzine, a monoamineoxidase inhibitor (MAOI),increases the risk forhypertensive crisis if foodshigh in tyramine areconsumed.
  26. 26. G6PD (GLUCOSE-6-PHOSPHATEDEHYDROGENASE) ENZYME DEFICIENCY It can lead to : Neonatal jaundice, hemolytic anemia oracute hemolysis. It is also called favism. Drugs included: aspirin, sulfonamides andantimalerial drugs caused hemolysis and acuteanemia. Food –drug interactions in G6PD deficiency :Ingestion of fava beansVitamin CVitamin K
  27. 27. Warfarin Anticoagulant used to reduce strokes Inactivated by Vitamin K - broccoli Enteral nutrition products contain Vitamin K. Warfarin activity drops when nutrition given Study shows warfarin binds to protein at pH 8

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