IATROGENIC DISORDERS

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A REVIEW ON DRUG INDUCED DISORDERS IN BRIEF

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IATROGENIC DISORDERS:

IATROGENIC DISORDERS BY M.RANGALAKSHMI NAIDU M.PHARMACY(PHARMACOLOGY) Ist SEMESTER SIMS COLLEGE OF PHARMACY

DEFINITION:

DEFINITION IATROGENIC is combination of two words “Iatro”, from the Greek “Iatro" Which means “physician "or “medicine and genic that is produced by. Iatrogenic induced in a patient by the treatment or comments of a physician OCCURANCE: Adverse effects of diagnostic procedures-mechanical procedures &diagnostic radiology Adverse effects of therapeutic regimen-Adverse drug reaction(ADR),Anaphylaxis 2

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DRUG INDUCED DISEASES DRUGS CUTANEOUS MANIFESTATIONS BARBITURATES,SULFONAMIDES,TETRACYCLINES,CYTOTOXIC DRUGS etc HAEMATOLOGICAL DISORDERS ORAL CONTACEPTIVES,PRIMAQUINE,ISONIAZIDE,etc GASTROINTESTINAL DISEASES PROPONOLOL,METHYDOPA,NSAIDS,CORTICOSTEROIDS,BROAD SPECTRUM ANTIBIOTICS HEPATIC DAMAGE CYCLOPHOSPHAMIDE,ACETAMINOPHEN,LOVASTATIN,etc RESPIRATORY DISORDERS ACE-INHIBITORS,BETA BLOCKERS,ACYCLOVIR,ANTI CANCER DRUGS,RESERPINE etc CARDIO VASCULAR DISEASES DIGITALIS,TRICYCLIC ANTI DEPRESSANTS,etc RENAL DISORDERS NSAIDS,CIS-PLATIN, AMINO GLYCOSIDES,etc PSYCHIATRIC SYNDROME PHENOTHIZENES,NIFIDIPINE,NTI CHOLINERGICS,NARCOTICS RHEUMATIC DISORDERS GROWTH HARMONES,CIMITIDINE,ANTI CONVULSANTS,ETHAM BUTOL, 3

Drug Induced renal disorder:

Drug Induced renal disorder Acute & chronic kidney disease commonly complicate drug therapy Potentially nephrotoxicmedications are constantly being released for use in clinical practice These drugs are often not tested in the patient populations who subsequently receive them Manifestations of drug-induced renal disorders Acute renal failure Chronic renal failure Nephrotic syndrome (Acute/Chronic) Fluid and Electrolyte disturbances Acid-base disorders 4

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DRUG INDUCED RENAL DISORDERS DRUGS FUNCTIONAL RENAL FAILURE NSAIDS,ACE-inhibitors,Diuretics,Interleukin-2,Amphotericin- B ACUTE TUBULAR NECROSIS Aminoglycosides,Rifampicin,NSAIDs,Cyclosporines,Cis-platin ACUTE INTERSTITIAL NEPHRITIS Pencillins,NSAIDs,Allopurinol,Thiazides,Sulphonamides HEMOLYTIC UREMIC SYNDROME Mitomycin-c,cyclosporin,Quinine,Cocaine,Clopidogrel ISOLATED PROTEINURIA WITH NEPHRITIC SYNDROME Gold.Heroin,Captopril,NSAIDs,IFN-alpha,D-pencillamine CHRONIC TUBULOINTERSTITIAL DISEASE NSAIDs,Thiazides,Lithium,Germanium,Chinese herb nephropathy RETROPERITONEAL FIBROSIS Methysergide,Hydralazine,Methyldopa 5

Drug-induce renal structural-functional changes:

Drug-induce renal structural-functional changes Proximal convoluted tubule (s1/s2 segment) Amino glycoside Cephaloridine Cadmium Cl K dichromate Renal vessel NSAIDs ACE Inhibitor Cyclosporin A Pappillae Phenacetin Interstitium Cephalosporin Cadmium NSAIDs Glomeruli Interferon- α Gold Penicillamine Proximal straight tubule (s3 segment) Cisplatin Mercuric Cl Dichlorovinyl -L- cysteine 6

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MECHNISM DISEASE DRUG PROSTAGLANDIN SYNTHESIS Hemodynamic effect NSAIDs/CNIs Podocytic injury, possible immune(T-cell)mediated MCD NSAIDs Podocyte injury, with phenotypic alterations FSGS pamidronate Inhibition of lysosomal enzymes PHOSPHOLIPIDOSIS Chloroquine Immune complex deposition MGN/lupus-like glomerulonephritis GOLD/PENCILLAMINE/HYDRALAZINE ANCA Crescentic / necrotising glomerulonephritis Infliximab / propylthiouracil Endothelial damage TMA CNIs/ Bevacizumab GLOMERULAR INJURY ANCA: antineutrophil cytoplasmic antibody; CNIs: calcineurin inhibitors; FSGS: focal and segmental glomerulosclerosis ; MCD: minimal change disease; MGN: membranous glomerulonephritis; NSAIDS: non-steroidal anti-inflammatory drugs; TMA: thrombotic microangiopathy 7

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VASCULAR INJURY MECHANISM DIESEASE DRUG Endothelial/ myocyte damage TMA CNIs Cell or antibody mediated Inflammatory vasculitis Various antibiotics Capillary /ischemic damage Analgesic nephropathy Combination analgesics CNIs: calcineurin inhibitors; TMA: thrombotic microangiopathy 8

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TUBULOINTERSTITIAL INJURY MECHANISM DIESEASE DRUG IMMUNE MEDIATED Acute or chronic tubulointerstitial nephritis Various antibiotics/NSAIDs Direct cellular toxicity ATN/ Nephrogenic diabetes insipidus Cisplatin / Lithium Changes in osmotic gradient across cell membrane Osmotic nephrosis Plasma volume expander/IVIG Cast formation obstructing tubules Tubulointerstitial nephritis/ATN Various drugs/ sirolimus Crystal deposition / Calcification Tubulo interstitial nephritis/ATN/ Nephrocalcinosis Dtiveiethylene glycol/ indinavir /oral sodium phosphate purgative ATN: acute tubular necrosis; IVIG: intravenous immune globulin 9

Prevention and management:

Prevention and management High risk patient must be identified Monitor SCr on 2 nd and 4 th day post procedure in all high risk patients Adequately hydration with 0.45% saline at (1.5 ml/kg/hr) starting 12 hr prior to the procedure and after the procedure Patient should be hemodynamically stable Minimize amount of contrast administered(<2ml/kg or max of 150ml) No benefit of mannitol and frusemide in preventing ARF but may increase risk of ARF Calcium blockers prevent renal ischemia during initial renal vasoconstrictory phase 10

DRUG INDUCED CARDIOVASCULAR DISEASES:

DRUG INDUCED CARDIOVASCULAR DISEASES Exacerbation of angina- alpha blockers Arrhythmias - digitalis, beta-adrenergic agents,tricyclic anti- depressants and quinine Cardiomyopathy – daunorubicin,emetine,lithium Hypo/hypertension – glucocorticoids and sympathomimetics Pericardial disease – emetine,procainamide and minoxidil Torsade de pointes - sparfloxacin 11

DRUG INDUCED ARRHYTHMIA:

DRUG INDUCED ARRHYTHMIA Prolongation of the QTc interval has been associated with proarrhythmia resulting from a potentially fatal form of polymorphic ventricular tachycardia called Torsade de pointes( TdP ) 12

TORSADES DE POINTES:

TORSADES DE POINTES Polymorphic ventricular tachycardia Resp. for - prolong repolarisation cardiac refractoriness by class III antiarrhythmic drugs, N on-cardiac drugs - delay cardiac repolarisation along with class III antiarrhythmics to cause TdP 13

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Blockade of I kr channels Increases intracellular K+ current and decreases net repolarizing current EARLY AFTER DEPOLARIZATION INCREASES ACTION POTENTIAL DURATION IN PURKINJEFIBRE AND M-CELLS RELATIVE TO EPI AND ENDOCARDIAL CELLS TRIGERRED ACTIVITY INCREASES HETEROGENITY (DISPERSSION )OF INTRA CARDIAC REPOLARIZATION UNIDIRECTIONAL BLOCK& INTRAMUCAL RE ENTRY CIRCUIT Torsades de pointes SUSTAINED DEGENRATES INTO VF AND CARDIAC ARREST NONSUSTAINED SYNCOPE MECHANISM 14

DRUGS THAT CAUSE QT PROLONGATION AND/OR TORSADES DE POINTES :

DRUGS THAT CAUSE QT PROLONGATION AND/OR TORSADES DE POINTES ANTI HISTAMINES – Second generation 1) TERFENADINE 2) ASTEMIZOLE COMBINATION – TERFINADINE + ASTEMAZOLE + CLASS III ANTI ARRHYTHMICS CO-administration – Anti arrhythmics,Anti-psychotics,Tricyclic anti depressants GROUP DRUG CLASS I A Quinidine,Disopyramide,Procinamide, CLASS III Sotolol,Amidorone CLASS III (INTRAVENOUS ANTI ARRYTHMICS) Ibutlide,Almokalant ANTI ARRHYTHMICS 15

ANTI MICROBIALS:

ANTI MICROBIALS MACROLIDES - Erythromycin,Clarithromycin Fluroquinolines - sproflaxacin Anti fungal - ketoconazole,itraconazole Anti malarial’s - Quinine,quinidine,Halofantrine TRICYCLIC ANTIDEPRESSANTS – Amitriptyline,Doxepin,Desipramine,Imiprmine,Clomipramine NEUROLEPTICS – Phenothiazine,Thioridazine,chlopromazine,Haloperidol ANTI PSYCHOTIC – Sertindole,Primozoide PROKINETICS - Cisaparide Other QT Prolonging Drugs That have been with drawn- Bepridil,Prenylamine ANTISPASMODIC AGENT - Terodiline 16

Prevention of Drug induced QT Prolongation:

Prevention of Drug induced QT Prolongation Avoiding QT prolonging drugs in patients with pre existing heart diseases Avoiding Concomitant administration of drugs that inhibit cyt p450 Drugs that prolong QT interval should ideally be listed and regularly updated in a National Drug Formulary 17

CURRENT STATEGIES TO REDUCE DRUG-ASSOCIATED ARRHYTHMIA:

CURRENT STATEGIES TO REDUCE DRUG-ASSOCIATED ARRHYTHMIA Reducing the risk of drug induced proarrhythmia by directing the clinicians through product labelling and through patient information package Computer assisted strategies – by Electronic prescribing Regulatory agencies 18

conclusion:

conclusion Given the large armamentarium of drugs available today judicious use of such drugs is required to prevent untoward side effects especially on such a vital organ .Identifying high risk patients and quick recognition of druginducedinjury-related syndrome with prompt cessation of the offending drug are the key to managing such a case before the injury causes permanent damage to the tissue. 19

REFERENCES:

REFERENCES Drug-induced Kidney Diseases NP Singh*, A Ganguli**, A Prakash** a review article Contemporary Reviews in Cardiovascular Medicine Drug -Induced Arrhythmia E . Kevin Heist , MD, PhD; Jeremy N. Ruskin , MD Drug induced QT prolongation and torsades de pointes Yee Guan Yap , A John Camm + Author Affiliations Department of Cardiological Sciences, St George’s Hospital Medical School, London, UK Correspondence to: Dr Yee Guan Yap Department of Cardiological Sciences, St George’s Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK; [email protected] Contd…. 20

PowerPoint Presentation:

Drug-induced Kidney Disease – Pathology and Current Concepts Alwin HL Loh,1 MBChB( Hons ), FRCPath , Arthur H Cohen,2,3MD Iatrogenic Disorders Lt Gen NR Krishnan, PHS ( Retd )*, Brig AS Kasthuri , VSM ( Retd )+MJAFI 2005; 61 : 2-6 DERMATOLOGY THERAPEUTICSACNE, PSORIASIS & DRUG INDUCED SKIN DISORDERS TH 5001 Therapeutics III - Fall 2003Tricia M. Berry,Pharm.D ., BCPSDecember 3, 2003 21

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