Leprosy
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Leprosy

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Leprosy Leprosy Presentation Transcript

  • Presented byD.VIJAY KUMAR 09DG1R0013 1
  • WHAT IS CHEMOTHERAPY Chemotherapy can be defined as the use of chemicals in infectious diseases to destroy microorganisms without damaging the host tissues 2
  • Basic principle of chemotherapyThe chemical agent should be toxic topathogenic micro organism and minimaleffect on host cell.The selective toxicity is important for thesedrugs. 3
  • BIOCHEMICAL REACTIONS OF ALLBACTERIAL CELLSClass 1:- Energy productionClass2:- Growth and servivalClass3:- Replication These reactions are potential targets for attack by antibacterial drugs. 4
  • BIOCHEMICAL REACTIONS AS POTENTIAL TARGETSClass 1 : These reactions are poor targets , for two reasons . First ,there is no difference between bacteria and humans cells in the mechanism for obtaining energy from glucose . second , even though selective toxic to ATP synthesis in the bacteria. It could be used alternative sources like lactate and amino acids . 5
  •  Class 2 : These reactions are good targets because folic acid bio synthesis pathway takes place only in bacteria not in human cells. But folic acid is required in the synthesis of nucleic acid in both human cells and bacterial cells. 6
  • FOLIC ACID SYNTHESIS PABA sulfonamide Dihydropterate synthetase DHFATrimethoprim Dihydrofolate reductase THFA5-flurouracil Thymidylate synthetase THYMIDYLATES DNA 7
  • class 3 : These reactions are particularly best targets for selective toxicity. There are very distinct differences between mammalian cells and parasitic cells. That are : The synthesis of peptidoglycan Protein synthesis Nucleic acid synthesis 8
  • What is Leprosy Leprosy, also known as Hansens disease (HD), is a chronic disease caused by the bacteria Mycobacterium leprae 9
  • Signs and symptoms Neuropathic pain Skin lesions are the primary external sign. It causing permanent damage to the skin, nerves, limbs, and eyes. Collapsed nose. 10
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  • Depending on clinical features, leprosy is classified as: Indeterminate leprosy (IL) Tuberculoid leprosy (TT) Borderline tuberculoid leprosy (BT) Lepromatous leprosy (LL) 12
  • Stages of leprosy:1st stage: bacteria enters through skin, the skin sensation become dull and smallpatches develop. In this stage the bacteria multiply in the axoplasm of nerve fiberscausing tingling sensations.2nd stage: skin becomes thick and wrinkled, ears become swollen, nodules areformed in skin of nose and throat. These nodules discharge fluid which is highlyinfectious.3rd stage: the bacteria burst out of the nerve cell and go to peripheral tissues andbegin to proliferarate. This results in deformities in hands, feet, face and toes etc. 13
  • TREATMENT Pre-modern treatment : Chaulmoogra oil Modern treatment : Dapsone Rifampicin Clofazimine 14
  • Chaulmoogra oil A common pre-modern treatment of leprosy was chaulmoogra oil. The oil has long been used in India as an Ayurvedic medicine for the treatment of leprosy and various skin conditions. It has also been used in China and Burma 15
  • DAPSONE Dapsone (diamino-diphenyl sulfone) is an antibacterial most commonly used in combination with rifampicin and clofazimine as multidrug therapy (MDT) for the treatment of Mycobacterium leprae infections leprosy 16
  • SYNTHESIS OF DAPSONE:4,4-Dinitrodiphenyl sulfide Dapsone sulfone 17
  • MECHANISM OF ACTION Dapsone is chemically related to the sulfonamides. It acts by inhibition of folic acid synthesis 18
  • PABADAPSONE Dihydropterate synthetase DHFA Dihydrofolate reductase THFA Thymidylate synthetaseTHYMIDYLATES DNA 19
  • PHARMACOKINETICS : Dapsone is given orally and is well absorbed and widely distributed through body water and all tissues. The plasma half-life is 24-48hrs. It is metabolised in the liver and excreted through urine. 20
  • Unwanted effects : Methaemoglobinaemia Hepatotoxicity Photo sensitivity Haemolytic anaemia Nausea and vomiting. 21
  • RIFAMPICIN: Rifampicin is rapidly bactericidal to Mycobacterium leprae . It can be conveniently given once a monthly. It is used in combination with dapsone in multidrug therapy (MDT) Rifampicin given alone, bacteria develops resistance . 22
  • Mechanism of action: Rifampicin inhibits bacterial DNA-dependent RNA synthesis by inhibiting bacterial DNA- dependent RNA polymerase enzyme. 23
  • Pharmacokinetics: Rifampicin is given orally and is widely distributed in the tissues and body fluids. Rifampicin is easily absorbed from the gastrointestinal tract because its ester functional group is quickly hydrolyzed in the bile. Plasma half-life is 1-5 hrs. , Though urinary elimination accounts for only about 30% of the drug excretion. About 60% to 65% is excreted through the feces. 24
  • UNWANTED EFFECTS: Orange colour of body fluids. Hepatotoxicity- liver failure in severe cases Respiratory problems- breathlessness Cutaneous - flushing, , rash, redness and watering of eyes. Abdominal - nausea, vomiting, abdominal cramps with or without diarrhoea. Flu-like symptoms - fever, headache. 25
  • CLOFAZIMINE: Clofazimine is a fat-soluble riminophenazine dye used in combination with rifampicin and dapsone as multidrug therapy (MDT) for the treatment of leprosy. It has been used investigationally in combination with other antimycobacterial drugs to treat Mycobacterium- avium infections in AIDS patients 26
  • CLOFAZIMINE:Systematic (IUPAC) nameN,5-bis(4-chlorophenyl)-3-(propan-2-ylimino)-3,5-dihydrophenazin-2-amine 27
  • Mechanism of action: Clofazimine works by binding to the guanine bases of bacterial DNA, thereby blocking the template function of the DNA and inhibiting bacterial proliferation. 28
  • Pharmacokinetics: Clofazimine is given orally and is widely distributed in the tissues and body fluids. But clofazimine has a very long half life of about 70 days. It is metabolised in the liver and excreted through urine. 29
  • Unwanted effects: Reddish colour of urine. Clofazimine produces pink to brownish skin pigmentation in 75-100% of patients within a few weeks, as well as similar discoloration of most body fluids and secretions. These discolorations are reversible but may take months to years to disappear. 30
  •  H.P.RANG & M.M. DALE, TEXT BOOK OF PHARMACOLOGY,5th EDITION ,PG NO: 620-653 K.D.TRIPATHI,TEXT BOOK OF PHARMACOLOGY,PG NO:335-41 R.S.SATOSKAR, PHARMACOLOGY AND PHARMACOTHERAPEUTICS,21ST EDITION,PG NO:755- 59 SALIL K BHATTACHARYA, PARANTAPA SEN, ARUNABHA RAY, PHARMACOLOGY,SECOND EDITION,PG NO:413-416 Padmaja Udaykumar,, textbook of Medical Pharmacology, Second Edition, Pg no:337-343 http://www.Uic.edu/pharmacy http://www.Suite101.com http://www.aac.asm.org http://www.pathmicro.med.sc.edu http://www.quizlet.com http://www.merckmanuals.com 31
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