This document discusses antitubercular drugs and the treatment of tuberculosis in India. It begins by introducing TB as an airborne infection caused by Mycobacterium tuberculosis that commonly affects the lungs. It then discusses the milestones of India's antitubercular programs from 1962 to the present. The document categorizes first- and second-line antitubercular drugs and discusses the mechanisms and characteristics of several major drugs including isoniazid, rifampin, pyrazinamide, ethambutol, streptomycin, and bedaquiline. It provides details on their pharmacokinetics, mechanisms of action, resistance, indications, and adverse effects.
This document provides guidelines for tuberculosis management under the Revised National Tuberculosis Control Program (RNTCP) in India. It discusses Delhi's high TB incidence rate and key risk factors. It outlines diagnostic tools and algorithms for presumptive pulmonary, extra-pulmonary, pediatric, and drug-resistant TB. It also describes case definitions, classification by anatomical site and drug resistance, and drug sensitive TB treatment regimens. Key points covered include the national guidance on regimens, fixed-dose drug combinations, daily dosage schedules, managing treatment adherence through ICT-based monitoring, and pediatric dispersible formulations.
Tricyclic antidepressants have been used since the 1950s and include compounds with three rings. They are the largest group of drugs used to treat depression. Overdoses can be life-threatening due to their rapid absorption and effects on the central nervous system, cardiovascular system, and respiratory system. Treatment for overdoses involves stabilizing the patient, reducing drug absorption, increasing elimination, treating seizures and arrhythmias, and observing the patient for at least 6 hours if symptoms resolve before discharge.
This document provides an overview of the management of drug-resistant tuberculosis (DR-TB). It defines different types of DR-TB including mono-resistant TB, poly-resistant TB, multidrug-resistant TB (MDR-TB), and extensively drug-resistant TB (XDR-TB). It discusses the epidemiology, mechanisms of drug resistance, clinical features, diagnosis, and treatment regimens for MDR-TB and XDR-TB according to WHO guidelines. The treatment regimens involve the use of second-line drugs including fluoroquinolones, aminoglycosides, ethionamide, cycloserine, linezolid, and others. Strict adherence to treatment is important to prevent the development
Diagnosis and management of tuberculosis with revised rntcpDrPrincePrakash
The document provides guidelines for the diagnosis and management of tuberculosis (TB) according to the Revised National Tuberculosis Control Programme (RNTCP). It discusses definitions of TB cases, classification based on treatment history, diagnostic methods, treatment regimens for pulmonary and extra-pulmonary TB, management of drug-resistant TB, and follow-up procedures. Key changes in the recent guidelines include introducing a daily treatment regimen for both new and previously treated TB cases, as well as additional guidance for diagnosing and treating multi-drug resistant TB.
Benzodiazepines are commonly prescribed sedative-hypnotic agents that were introduced in 1960. They are used for conditions like anxiety, insomnia, alcohol withdrawal, and seizures by enhancing the effects of the inhibitory neurotransmitter GABA. While generally safe, benzodiazepines can cause side effects with prolonged use or overdose like dependence, withdrawal symptoms, and respiratory depression. The effects of different benzodiazepines vary based on their ability to cross the blood-brain barrier and metabolism, with short-acting agents having faster onsets but shorter durations of action.
This document provides guidelines for tuberculosis management under the Revised National Tuberculosis Control Program (RNTCP) in India. It discusses Delhi's high TB incidence rate and key risk factors. It outlines diagnostic tools and algorithms for presumptive pulmonary, extra-pulmonary, pediatric, and drug-resistant TB. It also describes case definitions, classification by anatomical site and drug resistance, and drug sensitive TB treatment regimens. Key points covered include the national guidance on regimens, fixed-dose drug combinations, daily dosage schedules, managing treatment adherence through ICT-based monitoring, and pediatric dispersible formulations.
Tricyclic antidepressants have been used since the 1950s and include compounds with three rings. They are the largest group of drugs used to treat depression. Overdoses can be life-threatening due to their rapid absorption and effects on the central nervous system, cardiovascular system, and respiratory system. Treatment for overdoses involves stabilizing the patient, reducing drug absorption, increasing elimination, treating seizures and arrhythmias, and observing the patient for at least 6 hours if symptoms resolve before discharge.
This document provides an overview of the management of drug-resistant tuberculosis (DR-TB). It defines different types of DR-TB including mono-resistant TB, poly-resistant TB, multidrug-resistant TB (MDR-TB), and extensively drug-resistant TB (XDR-TB). It discusses the epidemiology, mechanisms of drug resistance, clinical features, diagnosis, and treatment regimens for MDR-TB and XDR-TB according to WHO guidelines. The treatment regimens involve the use of second-line drugs including fluoroquinolones, aminoglycosides, ethionamide, cycloserine, linezolid, and others. Strict adherence to treatment is important to prevent the development
Diagnosis and management of tuberculosis with revised rntcpDrPrincePrakash
The document provides guidelines for the diagnosis and management of tuberculosis (TB) according to the Revised National Tuberculosis Control Programme (RNTCP). It discusses definitions of TB cases, classification based on treatment history, diagnostic methods, treatment regimens for pulmonary and extra-pulmonary TB, management of drug-resistant TB, and follow-up procedures. Key changes in the recent guidelines include introducing a daily treatment regimen for both new and previously treated TB cases, as well as additional guidance for diagnosing and treating multi-drug resistant TB.
Benzodiazepines are commonly prescribed sedative-hypnotic agents that were introduced in 1960. They are used for conditions like anxiety, insomnia, alcohol withdrawal, and seizures by enhancing the effects of the inhibitory neurotransmitter GABA. While generally safe, benzodiazepines can cause side effects with prolonged use or overdose like dependence, withdrawal symptoms, and respiratory depression. The effects of different benzodiazepines vary based on their ability to cross the blood-brain barrier and metabolism, with short-acting agents having faster onsets but shorter durations of action.
Anti Tubercular Drugs - Mechanism of Action and Adverse effects Thomas Kurian
A brief outline of the mechanism of action and adverse effects of anti tubercular drugs
Only First line and second line drugs are dealt with.First line drugs may be useful for MBBS students and the rest is directed for postgraduate students.
Hope you find it useful.
This document discusses tuberculosis (TB) management in special situations. It provides WHO guidelines for TB treatment regimens based on category of TB, including doses and duration of treatment. It also summarizes TB treatment considerations for pregnancy, breastfeeding, infants, liver disease, renal disease, HIV co-infection, and other groups. Key recommendations include safe drugs to use in pregnancy, dose adjustments for liver and renal impairment, and extending TB treatment duration for certain high-risk patients.
Quinolones are a class of synthetic broad-spectrum antimicrobials. First generation quinolones like norfloxacin and ciprofloxacin are effective against gram-negative bacteria and are used to treat uncomplicated UTIs. Later generations have enhanced activity against pseudomonas and anaerobes. Quinolones work by inhibiting DNA gyrase in bacteria. They are well-absorbed orally, achieve high tissue concentrations, and have a low resistance risk. Common adverse effects include nausea, diarrhea, headache and phototoxicity. Quinolones can prolong the QT interval and interact with divalent cations. They are used to treat respiratory, gastrointestinal, skin and joint infections.
This document discusses monoclonal antibody treatments for asthma, focusing on omalizumab. It defines asthma and describes its symptoms and classifications. It explains the role of IgE in asthma and the mechanism of action of omalizumab, which inhibits IgE binding to prevent mast cell degranulation. It covers the pharmacokinetics, dosing, safety, and indications of omalizumab. It also briefly mentions other monoclonal antibodies in development for treating asthma, such as mepolizumab, anti-TNF antibodies, and antibodies targeting IL-13, TIM-1, and tissue kallikrein 1.
This document discusses multidrug-resistant tuberculosis (MDR-TB) and extensively drug-resistant tuberculosis (XDR-TB). It defines MDR-TB as tuberculosis resistant to at least isoniazid and rifampicin, and defines XDR-TB as MDR-TB additionally resistant to fluoroquinolones and injectable second-line drugs. It also discusses mechanisms of drug resistance development, clinical factors promoting resistance, testing methods, categories of antituberculosis drugs, and public health responsibilities regarding treatment and prevention of drug-resistant tuberculosis.
Management of Opioid Analgesic OverdoseSun Yai-Cheng
This document summarizes the management of opioid analgesic overdoses. It notes that opioid overdoses can have life-threatening effects on multiple organ systems. The duration of action varies between opioid formulations and an overdose can prolong intoxication. Prescriptions for opioid analgesics in the US increased 700% from 1997-2007. Opioid overdoses lead to over 27,500 health care facility admissions in 2010. Clinical signs of overdose include respiratory depression, apnea, miosis, and stupor. Naloxone is the antidote and works by reversing opioid receptor activity but has a shorter duration than many opioids. Higher and repeated naloxone doses may be needed for long-acting opioids like
The document provides information on the management of chloroquine resistant malaria. It discusses the life cycle of malaria parasites, various antimalarial drugs including their mechanisms of action and treatment of chloroquine sensitive and resistant malaria. It summarizes that malaria is caused by Plasmodium parasites and transmitted by Anopheles mosquitoes. It affects over 500 million people annually, especially children in developing countries. Resistance to chloroquine, previously the first-line treatment, has emerged and led to the use of alternative antimalarial drugs.
MDR-TB is tuberculosis that is resistant to at least isoniazid and rifampicin, the two most effective anti-TB drugs. It is not cured by standard short-course chemotherapy and develops due to incorrect treatment, irregular drug supply, noncompliance, or lack of supervision and follow-up. Treating MDR-TB is difficult, requiring treatment for at least two years with more toxic and expensive second-line drugs and hospitalization of isolated patients to prevent further spread. DOTS-Plus utilizes longer multi-drug treatment regimens to prevent development and transmission of MDR-TB.
This presentation deals with important pathophysiological steps involved with HIV infection, the various classes of drugs used in treatment of this condition, along with WHO-guidelines for treatment regimen(depending on various ages & conditions).
Newer drugs have also been mentioned and emphasized upon.
The document provides an overview of updates to India's National Tuberculosis Elimination Programme (NTEP) guidelines in 2020. It summarizes the history of tuberculosis programs in India since 1997 and key changes introduced in 2020, including renaming the program from the Revised National Tuberculosis Control Programme to NTEP. It outlines case definitions, diagnostic algorithms, treatment guidelines for drug-sensitive and drug-resistant tuberculosis, and definitions of treatment outcomes. The guidelines emphasize making every attempt to microbiologically confirm TB diagnoses and introduce changes like daily drug dosing and expanding the use of molecular diagnostic tests like CBNAAT.
This document provides information about anti-tuberculosis therapy. It begins by listing the learning objectives, which include describing primary and secondary anti-tuberculosis drugs, the phases of TB treatment, mechanisms of action and side effects of drugs, defining multi-drug resistant TB, and the role of vaccines in prevention. It then discusses specifics of TB as a global health problem, treatment regimens, first and second-line drugs, mechanisms of action of isoniazid and rifampin, and side effects of isoniazid. The document aims to educate about best practices for treating TB through use of combination drug therapy.
This document provides treatment guidelines for tuberculosis. It outlines the aims of TB treatment as curing the patient, preventing death from active or relapsed TB, decreasing transmission, and preventing drug resistance. It describes the initial and continuation phases of treatment for new and previously treated cases. It also defines different types of TB cases and provides recommended drug regimens and dosages depending on the category of TB patient. Isoniazid, rifampicin, pyrazinamide, and ethambutol are first-line oral drugs, while streptomycin and thioacetazone are also mentioned. BCG vaccination guidelines are also briefly covered.
The document summarizes quinolones and fluoroquinolones. Quinolones are a family of synthetic broad-spectrum antibacterial drugs that prevent bacterial DNA from duplicating. Fluoroquinolones are derived from quinolones and have an even broader spectrum. They are classified into generations based on their spectrum, with later generations having increased gram-positive and atypical coverage. Fluoroquinolones are generally well-absorbed, penetrate tissues deeply, and have few drug interactions or side effects, making them preferred drugs. However, their overuse has led to increasing antimicrobial resistance.
This document provides information on Mycobacterium tuberculosis, the bacteria that causes tuberculosis (TB). It discusses the physiology and structure of M. tuberculosis, how it is transmitted, diagnosed, and its typical appearance under microscopy. The document also categorizes and describes the mechanisms and uses of both first- and second-line anti-tuberculosis drugs, including isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin from the first line and ethionamide, cycloserine, and thiacetazone from the second line. It addresses drug-resistant TB and the different groupings of alternative drugs used to treat multi- and extensively drug-resistant strains.
This document discusses iron poisoning from excessive iron intake. Sources of excess iron include supplements, red meat, pollution, and occupational exposure. Too much iron can replace other minerals, cause inflammation, form toxic iron oxide, and stimulate bacterial growth. It affects organs like the pancreas, liver and kidneys. Acute poisoning causes stomach pain and organ damage while chronic poisoning risks diabetes, cancer and nervous system diseases. Treatment involves chelating agents and iron antagonists while a fatal dose is over 50mg/kg of elemental iron.
This PPT covers drug therapy for tuberculosis. It includes classification of antitubercular drugs, chemotherapy for tuberculosis, strategies for addressing resistance and pharmacotherapy of antitubercular drugs
This document discusses antimycobacterial drugs used to treat tuberculosis and other mycobacterial infections. It first provides an overview of mycobacteria and the diseases they cause. The main drugs discussed are isoniazid, rifampin, and other rifamycins. Isoniazid and rifampin are critical first-line drugs for tuberculosis treatment. Isoniazid targets mycolic acid synthesis while rifampins inhibit RNA transcription. The document outlines the mechanisms, spectra, resistance, pharmacokinetics, and adverse effects of these important antimycobacterial agents.
Anti Tubercular Drugs - Mechanism of Action and Adverse effects Thomas Kurian
A brief outline of the mechanism of action and adverse effects of anti tubercular drugs
Only First line and second line drugs are dealt with.First line drugs may be useful for MBBS students and the rest is directed for postgraduate students.
Hope you find it useful.
This document discusses tuberculosis (TB) management in special situations. It provides WHO guidelines for TB treatment regimens based on category of TB, including doses and duration of treatment. It also summarizes TB treatment considerations for pregnancy, breastfeeding, infants, liver disease, renal disease, HIV co-infection, and other groups. Key recommendations include safe drugs to use in pregnancy, dose adjustments for liver and renal impairment, and extending TB treatment duration for certain high-risk patients.
Quinolones are a class of synthetic broad-spectrum antimicrobials. First generation quinolones like norfloxacin and ciprofloxacin are effective against gram-negative bacteria and are used to treat uncomplicated UTIs. Later generations have enhanced activity against pseudomonas and anaerobes. Quinolones work by inhibiting DNA gyrase in bacteria. They are well-absorbed orally, achieve high tissue concentrations, and have a low resistance risk. Common adverse effects include nausea, diarrhea, headache and phototoxicity. Quinolones can prolong the QT interval and interact with divalent cations. They are used to treat respiratory, gastrointestinal, skin and joint infections.
This document discusses monoclonal antibody treatments for asthma, focusing on omalizumab. It defines asthma and describes its symptoms and classifications. It explains the role of IgE in asthma and the mechanism of action of omalizumab, which inhibits IgE binding to prevent mast cell degranulation. It covers the pharmacokinetics, dosing, safety, and indications of omalizumab. It also briefly mentions other monoclonal antibodies in development for treating asthma, such as mepolizumab, anti-TNF antibodies, and antibodies targeting IL-13, TIM-1, and tissue kallikrein 1.
This document discusses multidrug-resistant tuberculosis (MDR-TB) and extensively drug-resistant tuberculosis (XDR-TB). It defines MDR-TB as tuberculosis resistant to at least isoniazid and rifampicin, and defines XDR-TB as MDR-TB additionally resistant to fluoroquinolones and injectable second-line drugs. It also discusses mechanisms of drug resistance development, clinical factors promoting resistance, testing methods, categories of antituberculosis drugs, and public health responsibilities regarding treatment and prevention of drug-resistant tuberculosis.
Management of Opioid Analgesic OverdoseSun Yai-Cheng
This document summarizes the management of opioid analgesic overdoses. It notes that opioid overdoses can have life-threatening effects on multiple organ systems. The duration of action varies between opioid formulations and an overdose can prolong intoxication. Prescriptions for opioid analgesics in the US increased 700% from 1997-2007. Opioid overdoses lead to over 27,500 health care facility admissions in 2010. Clinical signs of overdose include respiratory depression, apnea, miosis, and stupor. Naloxone is the antidote and works by reversing opioid receptor activity but has a shorter duration than many opioids. Higher and repeated naloxone doses may be needed for long-acting opioids like
The document provides information on the management of chloroquine resistant malaria. It discusses the life cycle of malaria parasites, various antimalarial drugs including their mechanisms of action and treatment of chloroquine sensitive and resistant malaria. It summarizes that malaria is caused by Plasmodium parasites and transmitted by Anopheles mosquitoes. It affects over 500 million people annually, especially children in developing countries. Resistance to chloroquine, previously the first-line treatment, has emerged and led to the use of alternative antimalarial drugs.
MDR-TB is tuberculosis that is resistant to at least isoniazid and rifampicin, the two most effective anti-TB drugs. It is not cured by standard short-course chemotherapy and develops due to incorrect treatment, irregular drug supply, noncompliance, or lack of supervision and follow-up. Treating MDR-TB is difficult, requiring treatment for at least two years with more toxic and expensive second-line drugs and hospitalization of isolated patients to prevent further spread. DOTS-Plus utilizes longer multi-drug treatment regimens to prevent development and transmission of MDR-TB.
This presentation deals with important pathophysiological steps involved with HIV infection, the various classes of drugs used in treatment of this condition, along with WHO-guidelines for treatment regimen(depending on various ages & conditions).
Newer drugs have also been mentioned and emphasized upon.
The document provides an overview of updates to India's National Tuberculosis Elimination Programme (NTEP) guidelines in 2020. It summarizes the history of tuberculosis programs in India since 1997 and key changes introduced in 2020, including renaming the program from the Revised National Tuberculosis Control Programme to NTEP. It outlines case definitions, diagnostic algorithms, treatment guidelines for drug-sensitive and drug-resistant tuberculosis, and definitions of treatment outcomes. The guidelines emphasize making every attempt to microbiologically confirm TB diagnoses and introduce changes like daily drug dosing and expanding the use of molecular diagnostic tests like CBNAAT.
This document provides information about anti-tuberculosis therapy. It begins by listing the learning objectives, which include describing primary and secondary anti-tuberculosis drugs, the phases of TB treatment, mechanisms of action and side effects of drugs, defining multi-drug resistant TB, and the role of vaccines in prevention. It then discusses specifics of TB as a global health problem, treatment regimens, first and second-line drugs, mechanisms of action of isoniazid and rifampin, and side effects of isoniazid. The document aims to educate about best practices for treating TB through use of combination drug therapy.
This document provides treatment guidelines for tuberculosis. It outlines the aims of TB treatment as curing the patient, preventing death from active or relapsed TB, decreasing transmission, and preventing drug resistance. It describes the initial and continuation phases of treatment for new and previously treated cases. It also defines different types of TB cases and provides recommended drug regimens and dosages depending on the category of TB patient. Isoniazid, rifampicin, pyrazinamide, and ethambutol are first-line oral drugs, while streptomycin and thioacetazone are also mentioned. BCG vaccination guidelines are also briefly covered.
The document summarizes quinolones and fluoroquinolones. Quinolones are a family of synthetic broad-spectrum antibacterial drugs that prevent bacterial DNA from duplicating. Fluoroquinolones are derived from quinolones and have an even broader spectrum. They are classified into generations based on their spectrum, with later generations having increased gram-positive and atypical coverage. Fluoroquinolones are generally well-absorbed, penetrate tissues deeply, and have few drug interactions or side effects, making them preferred drugs. However, their overuse has led to increasing antimicrobial resistance.
This document provides information on Mycobacterium tuberculosis, the bacteria that causes tuberculosis (TB). It discusses the physiology and structure of M. tuberculosis, how it is transmitted, diagnosed, and its typical appearance under microscopy. The document also categorizes and describes the mechanisms and uses of both first- and second-line anti-tuberculosis drugs, including isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin from the first line and ethionamide, cycloserine, and thiacetazone from the second line. It addresses drug-resistant TB and the different groupings of alternative drugs used to treat multi- and extensively drug-resistant strains.
This document discusses iron poisoning from excessive iron intake. Sources of excess iron include supplements, red meat, pollution, and occupational exposure. Too much iron can replace other minerals, cause inflammation, form toxic iron oxide, and stimulate bacterial growth. It affects organs like the pancreas, liver and kidneys. Acute poisoning causes stomach pain and organ damage while chronic poisoning risks diabetes, cancer and nervous system diseases. Treatment involves chelating agents and iron antagonists while a fatal dose is over 50mg/kg of elemental iron.
This PPT covers drug therapy for tuberculosis. It includes classification of antitubercular drugs, chemotherapy for tuberculosis, strategies for addressing resistance and pharmacotherapy of antitubercular drugs
This document discusses antimycobacterial drugs used to treat tuberculosis and other mycobacterial infections. It first provides an overview of mycobacteria and the diseases they cause. The main drugs discussed are isoniazid, rifampin, and other rifamycins. Isoniazid and rifampin are critical first-line drugs for tuberculosis treatment. Isoniazid targets mycolic acid synthesis while rifampins inhibit RNA transcription. The document outlines the mechanisms, spectra, resistance, pharmacokinetics, and adverse effects of these important antimycobacterial agents.
Leprosy
Tuberculosis
TYB pharmacy
Pharmacology semester VI notes
Pharmacology VI semester
Pharmacology notes
Third year B pharmacy pharmacology notes
Pharmacology unit 3 notes
Pharmacology VI semester notes
This document discusses antimycobacterial drugs used to treat tuberculosis and other mycobacterial infections. It provides information on various first-line drugs including isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin. It notes that combinations of two or more drugs are required to treat mycobacterial infections due to slow growth and potential drug resistance. Treatment must be prolonged, typically for months to years, to eliminate both actively dividing and dormant bacteria. Second-line drugs are discussed for treatment of multi-drug resistant infections. Worldwide tuberculosis statistics and drug regimens are also summarized.
Tuberculosis is caused by Mycobacterium tuberculosis bacteria and spreads through droplets from the lungs. It can affect the lungs or other parts of the body. There are first and second line drugs used to treat TB, including isoniazid, rifampin, pyrazinamide, and ethambutol. These drugs work by inhibiting cell wall synthesis or RNA polymerase and can have side effects like hepatitis or peripheral neuritis. Resistance can develop if treatment is not properly adhered to.
This document discusses chemotherapy for tuberculosis, including first-line and second-line antitubercular drugs. It describes the classification, mechanisms of action, pharmacokinetics, and adverse effects of isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin as first-line drugs. It also mentions that the goals of antitubercular chemotherapy are to kill dividing bacilli, kill persisting bacilli, and prevent emergence of drug resistance. The document assigns discussing the mechanisms, adverse effects, and uses of second-line drugs including kanamycin, amikacin, capreomycin, fluoroquinolones, and ethionamide.
This document discusses chemotherapy for tuberculosis, including first-line and second-line antitubercular drugs. It describes the classification, mechanisms of action, pharmacokinetics, and adverse effects of isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin as first-line drugs. It also mentions that the goals of antitubercular chemotherapy are to kill dividing bacilli, kill persisting bacilli, and prevent emergence of drug resistance. The document assigns discussing the mechanisms, adverse effects, and uses of second-line drugs including kanamycin, amikacin, capreomycin, fluoroquinolones, and ethionamide.
This document provides information on tuberculosis (TB) and its management. It discusses how India has a high burden of TB cases, accounting for 27% of global cases. It also notes that multidrug-resistant TB (MDR-TB) has been reported in over 120 countries. Diagnosis involves bacteriological tests and radiography. Treatment involves a combination of first-line drugs like isoniazid and rifampin, as well as preventive measures and vaccination with BCG. Drug resistance is a major challenge, with estimates of MDR-TB and extensively drug-resistant TB cases on the rise in India.
This document provides information on various anti-tuberculosis drugs including isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin. It discusses the mechanisms of action, pharmacokinetics, interactions, dosing, and adverse effects of each drug. It also provides historical context on the development of anti-tuberculosis treatments and classifications of first and second-line drugs.
This document discusses various antitubercular agents used to treat tuberculosis. It begins with a brief overview of Mycobacterium tuberculosis and the goals of antitubercular chemotherapy. It then provides a history of the development of major antitubercular drugs and their mechanisms of action. The remainder of the document discusses the first-line drugs isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin as well as several second-line drugs, outlining their mechanisms of action, pharmacokinetics, uses, and adverse drug reactions. It emphasizes the importance of multi-drug therapy to target different subpopulations of the bacteria.
This document discusses antitubercular agents used to treat tuberculosis. It begins by describing the peculiar features of M. tuberculosis bacteria and the goals of anti-tuberculosis chemotherapy. The first-line drugs discussed are isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin. Their mechanisms of action, pharmacokinetics, adverse drug reactions, and dosing are summarized. The document also discusses second-line drugs and newer agents used to treat drug-resistant tuberculosis. It emphasizes the importance of multi-drug therapy to prevent the emergence of drug resistance.
This document discusses anti-tubercular drugs. It begins by describing tuberculosis and its transmission. It then discusses the classification of anti-TB drugs into 1st line essential, 1st line supplemental, and 2nd line drugs. The individual drugs discussed in detail include isoniazid, rifampicin, ethambutol, pyrazinamide, and streptomycin. It covers their mechanisms of action, mechanisms of resistance, pharmacokinetics, dosages, adverse effects, and interactions. Treatment categories and regimens are also summarized.
Tuberculosis is caused by infection with Mycobacterium tuberculosis. It infects over a billion people worldwide and kills millions each year. A combination of drugs, including isoniazid, rifampin, pyrazinamide, and ethambutol or streptomycin, are used to treat tuberculosis. Isoniazid and rifampin are the most effective drugs but multi-drug therapy is required to prevent resistance. Both drugs have bactericidal effects and penetrate tissues well but can cause adverse reactions like hepatitis which requires monitoring during treatment.
Tuberculosis is completely curable disease now a days but one should follow the treatment regimens correctly .so for under graduate MBBS students it is clearly explained with animations.Hope you all this will be helpful.
- Mycobacterium infections like tuberculosis are difficult to treat due to their lipid-rich cell walls and ability to reside intracellularly. Combination drug therapy is required to prevent resistance.
- Common first-line drugs include isoniazid, rifampin, pyrazinamide, and ethambutol. Second-line alternatives include ethionamide, capreomycin, cycloserine, aminoglycosides, and fluoroquinolones.
- Each drug has a unique mechanism of action and potential adverse effects that require monitoring like hepatitis, neuropathy, and optic neuritis. Combination therapy and treatment duration aims to kill both actively growing and dormant bacilli.
This document discusses anti-tubercular drugs used to treat tuberculosis. It begins by stating tuberculosis is a major health problem, especially in developing countries, with over 1/3 of the world's population infected. It then discusses the goals and components of India's Revised National Tuberculosis Control Programme (RNTCP) to control and treat TB. The document primarily focuses on first-line anti-tubercular drugs, describing their mechanisms of action, resistance, administration, interactions, and adverse effects. Key drugs discussed include isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin.
This document discusses anti-tuberculosis drugs and their use in treating tuberculosis (TB) and leprosy. It outlines the first-line drugs used to treat TB, including isoniazid, rifampin, ethambutol, pyrazinamide, and streptomycin. It describes their mechanisms of action, therapeutic uses, and potential adverse effects. The document also discusses second-line drugs and treatment regimens for both active and latent TB. Finally, it covers the drugs used to treat leprosy, including dapsone, clofazimine, and rifampin.
CHEMOTHERAPY OF TUBERCULOSIS AND LEPROSY.POWERPOINT.pptxSamuelAgboola11
This document provides information on the chemotherapy of tuberculosis and leprosy. It defines tuberculosis and leprosy, and describes their causative organisms. It discusses first and second line drugs used to treat tuberculosis, including isoniazid, rifampicin, ethambutol, pyrazinamide, and streptomycin. It describes the dosages and unwanted effects of these drugs. It also discusses multidrug-resistant tuberculosis. For leprosy, it discusses the drugs used, including dapsone, rifampin, and clofazimine, and the WHO recommendations for treatment of multibacillary and paucibacillary leprosy.
The document discusses antimycobacterial drugs used to treat tuberculosis and leprosy. It begins by outlining the challenges of treating infections caused by slow-growing mycobacteria, including their intrinsic resistance. It then describes the goals and principles of TB therapy, including using multi-drug regimens to prevent resistance. The first-line drugs for TB, including isoniazid, rifampin, pyrazinamide, and ethambutol are discussed in detail. Treatment regimens for both adults and children are provided. The document also covers definitions and treatment approaches for drug-resistant TB. Finally, it concludes with an overview of drugs used to treat leprosy such as dapsone, rifamp
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Top 10 Best Ayurvedic Kidney Stone Syrups in India
Antitubercular drugsnew
1. ANTITUBERCULAR DRUGS
A D I T I M A I T R A
S E N I O R R E S I D E N T
P H A R M A C O L O G Y D E P A R T M E N T
C N M C H
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INTRODUCTION
TB is caused by Mycobacterium Tuberculosis which affects most commonly
the lungs .
TB is an airborne bacterial infection
Transmission occurs through inhalation of droplet nuclei
This chronic granulomatous disease – major health problem
1/3rd of world`s population is infected of which only 10-15% develop the
disease
India – 2.3 million patients were suffering from India (highest contributor)
2018
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MILESTONES OF ANTI TB PROGRAMME IN INDIA
• National Tuberculosis Programme of India – 1962
•Revised National Tuberculosis Control Programme launched in 1997
•Nation wide coverage of DoT therapy 2006
•Notifiable disease 2012 -web-based TB notification system NIKSHAY was established to provide platform for
notification from both public and private sectors.
•Revised treatment guidelines 2016,2019
•NATIONAL STRATEGIC PLAN (NST) FOR TUBERCULOSIS ELIMINATION 2017–2025 – Decline burden, morbidity,
motality and elimination. DTPB Approach is- detect – treat – prevent-build
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ANTI TUBERCULAR DRUG CLASSIFICATION
1st line:High efficacy , low toxicity - routinely used
Oral:
A. Isoniazid (H)
B. Rifampicin (R)
C. PyrazinamideZ
D. Ethambutol (E)
Intramuscular:
Streptomycin (S)
2nd line- Low antitubercular efficacy and/or higher toxicity –
reserve drugs:
Oral-thiacetazone, PAS, Ehionamide, Cycloserine,
Rifabutin,Rifapentine
Injectable-kanamycin, capreomycin, amikacin,
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ALTERNATE CLASSIFICATION-WHO 2010,RNTCP 2016
Group I: most potent , best tolerated oral drugs used routinely.
Group II: potent and bactericidal, but injectable
Group III: bactericidal oral drugs; drug resistant TB should receive
one FQ.
Group IV: less effective, bacteriostatic/more toxic oral drugs for
resistant TB.
Group V: are drugs with uncertain efficacy; not recommended for
MDR-TB; may be used in extensively resistant TB (XDR-TB).
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SUBPOPULATIONS OF TB BACILLI
(a)Rapidly growing with high bacillary load as in the wall of a cavitary lesion where oxygen tension is
high and pH is neutral. These bacilli are highly susceptible to H
(b) Slow growing located intracellularly (inside macrophages) and at inflamed sites where pH is low.
They are particularly vulnerable to Z
(c) Spurters found mostly within caseous material where oxygen tension is low but pH is neutral: the
bacilli grow intermittently with occasional spurts of active metabolism. R is most active on this
subpopulation.
(d) Dormant some bacilli remain totally inactive for prolonged periods. No antitubercular drug is
significantly active against them.
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Isoniazid (Isonicotinic acid hydrazide, H)
Essential component – unless resistance or intolerability issue
Tuberculocidal – fast multiplying organisms
Acts on Extracellular as well as intracellular
Active in acidic and alkaline medium
Acts by Oxygen dependent pathway
MOA:
Inhibition of synthesis of mycolic acid – unique fatty acid in
mycobacterial cell wall – lipid content of mycobacteria reduced
Genes “InhA” and “KasA” are targets for INH action
INH enters mycobacteria – converts to active metabolite by catalase
peroxidase (KatG) enzyme
Adducts with NAD and inhibits “InhA” and “KasA” Also adducts with
NADPH – DHFRase inhibition – no DNA
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ISONIAZID ( cont.)
Pharmacokinetics:
Complete oral absorption – only impaired if isoniazid is taken with
high-fat meals
Penetrates all tissues, cavities, meninges, placenta
Extensively metabolized in liver; most important pathway being N-
acetylation by NAT2 & it is genetically determined. The rate of INH
acetylation shows genetic variation. There are either:
1. Fast acetylators: (30–40% of Indians) t½ of INH 1 hr.
2. Slow acetylators: (60–70% of Indians) t½ of INH 3 hr.
Acetylator status does not matter if INH is taken daily.
Isoniazid induced peripheral neuritis is more common in slow
acetylators
Excretion is through glomerular filtration and secretion, predominantly
as metabolites
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ISONIAZID ( cont.)
Resistance:
1 in 106 tubercle bacilli is inherently resistant- if given alone
Mutation of KatG ,“InhA” and “KasA”
Efflux of INH and its concentrating mechanism
Drug Interactions :
Aluminium hydroxide inhibits INH absorption.
INH retards phenytoin, carbamazepine, diazepam, theophylline and warfarin metabolism
by
inhibiting CYP2C19 and CYP3A4,
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ISONIAZID ADR: -
Most important dose-dependent toxic effects- Peripheral neuritis & variety
of neurological manifestations (paresthesias, numbness, mental
disturbances, rarely convulsions)
Pyridoxine given prophylactically (10 mg/day) prevents the neurotoxicity.
INH neurotoxicity is treated by pyridoxine 100 mg/day.
Prophylactic pyridoxine must be given to diabetics, chronic alcoholics,
malnourished, pregnant, lactating and HIV infected patients, but routine
use is not mandatory.
INH reacts with pyridoxal to form a hydrazine- inhibits generation of active
coenzyme pyridoxal phosphate. Due to formation of hydrazones, the renal
excretion of pyridoxine compounds is increased- produces a pyridoxine
deficiency state
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ISONIAZID ADR: -
Hepatitis, a major adverse effect of INH [MCQ]
Rare in children, but more common in older people and
in alcoholics (chronic alcoholism induces CYP2E1 which
generates the hepatotoxic metabolite).
INH hepatotoxicity is due to dose-related damage to
liver cells, but is reversible on stopping the drug.
Other -lethargy, rashes, fever, acne and arthralgia.
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Rifampin (Rifampicin, R)
Obtained from Streptomyces mediterranei.
Rifampin is bactericidal to M. tuberculosis, Staph. aureus, N. meningitidis,
H. influenzae, E. coli, Klebsiella, Pseudomonas, Proteus and Legionella.
Acts best on slowly or intermittently dividing ones (spurters)
Both extra- and intracellular organisms are affected
Only drug acts against dormant bacteria
MOA-
• Rifampin interrupts RNA synthesis
•R binds to β subunit of mycobacterial DNA-dependent RNA polymerase
(encoded by rpoB gene ) → Blocks polymerizing function
•The basis of selective toxicity is that mammalian RNA polymerase does not
avidly bind rifampin.
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Rifampin (Rifampicin, R)
RESISTANCE:
• incidence of resistant bacilli is less than 10–7
•unusual to have primary rifampin resistant tubercular infection [India only2%] .
•resistance due to mutation in the rpoB gene- reducing its affinity for the drug.
INDICATION:
1. TB [can be used safely in renal dysfunction ]mcq
2. Leprosy
3. Prophylaxis of Meningococcal and H. influenzae meningitis and carrier state.
4. Second/third choice drug for MRSA, diphtheroids and Legionella infections.
5. Combination of doxycycline and rifampin - brucellosis.
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Pharmacokinetics
I well absorbed orally, (bioavailability is ~ 70%) - food decreases absorption- R to be taken in empty stomach
It is widely distributed -penetrates intracellularly, enters tubercular cavities, caseous masses, placenta,
meninges( largely pumped out from CNS by P-glycoprotein). t½ of rifampin is variable (2–5 hours)
It is metabolized in liver to an active deacetylated metabolite which is excreted mainly in bile, some in urine also.
Rifampin and its desacetyl derivative undergo enterohepatic circulation.
Drug Interactions
Rifampin is a microsomal enzyme inducer—↑CYP450
isoenzymes(CYP3A4, CYP2D6 CYP1A2 and CYP2C)- ↑ its own metabolism
as well as that of many drugs
Contraceptive failures have occurred. It is advisable to switch over to an
oral contraceptive containing higher dose (50 μg) of estrogen or use
alternative method of contraception
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RIFAMPICIN ADVERSE REACTION
Hepatitis, a major adverse dose-related effect(infrequent with < 600 mg/ day
dose)
Generally occurs in patients with preexisting liver disease- Development of
jaundice requires discontinuation of the drug—then it is reversible.
Cutaneous syndrome: flushing, pruritus + rash (especially on face and scalp),
redness and watering of eyes.,
Flu syndrome: with chills, fever, headache, malaise and bone pain.
Abdominal syndrome: nausea, vomiting, abdominal cramps with or without
diarrhoea. Urine and secretions may become orange-red— but this is harmless.
Serious but rare reactions:
Respiratory syndrome: breathlessness which may be associated with shock and
collapse
Purpura, haemolysis, shock and renal failure.
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•Rifabutin related to rifampin in structure and mechanism of action
•Less active against M tuberculosis, and more active against MAC
•Only place of rifabutin in the treatment of TB is as a substitute for R - to ↓drug interactions due to
strong enzyme inducing property of R. (Rifabutin is a much weaker inducer of CYP enzymes than
R) Esp important in HIV coinfected patients of TB who receive a protease inhibitor (PD) and/or a
non-nucleoside reverse transcriptase inhibitor (NNRTI) whose metabolism is markedly induced by R
rendering them ineffective. The primary indication of rifabutin is for prophylaxis and treatment of
MAC infection( 300 mg/day)in HIV-AIDS patients
•ADR: gastrointestinal intolerance, rashes ,granulocytopenia, myalgia and uveitis
RIFABUTIN
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Rifampin congener,
t1/2 of rifapentine (13-15 hr) is longer than that of rifampin, so that it can
be given once or twice weekly.
Only indication of rifapentine (600 mg once/twice weekly) is in the
continuation phase of treatment of TB, as a substitute of daily rifampin. It
is not suitable for use during the intensive phase.
Once weekly rifapentine combined with INH has also been employed to
treat latent TB.
RIFAPENTIN
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Pyrazinamide (Z)
Chemically similar to INH
More active in acidic medium.
More lethal to intracellularly located bacilli and to those at sites showing an inflammatory response
By killing the residual intracellular bacilli it has good ‘sterilizing’ activity. Its inclusion has enabled duration of
treatment to be shortened and risk of relapse to be reduced.
Mechanism of action:
It converted inside the mycobacterial cell into an active
metabolite pyrazinoic acid (POA)by an enzyme
(pyrazinamidase) encoded by the pncA gene.
POA gets accumulated in acidic medium and probably
inhibits mycolic acid synthesis, but by interacting with a
different fatty acid synthase. Pyrazinoic acid - disrupt
mycobacterial cell membrane and its transport function.
Resistance : mostly due to mutation in the pncA gene.
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PK:
absorbed orally, widely distributed, has good penetration in CSF( highly useful
in meningeal TB) extensively metabolized in liver and excreted in urine.
plasma t½ is 6–10 hours.
ADR:
Hepatotoxicity is the most important dose related adverse effect.
Less common in the Indian population than in western countries.
Daily dose is now limited to 25–30mg/kg which produces only a low incidence
of hepatotoxicity. It is contraindicated in patients with liver disease.
Safety during pregnancy is uncertain.
Hyperuricaemia is common & due to inhibition of uric acid secretion in kidney
Other :abdominal distress, arthralgia, flushing, rashes, fever and loss of
diabetes control: repeated blood glucose monitoring is warranted in diabetics.
Pyrazinamide (Z)
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ETHAMBUTOL ( E )
Ethambutol is selectively tuberculostatic
Fast multiplying bacilli are more susceptible.
Hasten the rate of sputum conversion and to prevent development of resistance(primary purpose)
Mechanism of action of E –
Resistance develops slowly and is most commonly associated with mutation in embB gene.
It is safe during pregnancy. It is not hepatotoxic.
Ethambutol is used in MAC infection as well
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ETHAMBUTOL ( E )
SIDE EFFECTS :
Loss of visual acuity/colour vision, field defects due to optic neuritis
- most important ( due to effect on amacrine & bipolar cells of
retina) [mcq]
Dose and duration of therapy dependent toxicity.
Early recognition & stoppage of the drug-visual toxicity reversible.
Patients should be instructed to stop the drug at the first indication
of visual impairment. Young children now allowed with due
precaution.
Contraindicated in patients with optic neuritis.
other S/E:
nausea, rashes, fever, rarely peripheral neuritis , hyperuricemia
Caution required in patients with renal disease.
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STREPTOMYCIN (S)
Aminoglycoside antibiotic, tuberculocidal, labelled as a
‘supplemental’ 1st line drug.
Acts only on extracellular bacilli (because of poor penetration
into cells). It penetrates tubercular cavities, but does not cross to
the CSF.
Resistance developed rapidly when streptomycin was used alone
It is not hepatotoxic
lower margin of safety (ototoxicity and nephrotoxicity)
Contraindicated in pregnancy
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BEDAQUILINE
Diaaryl quinoline acts by a novel mechanism-targets mycobacterial ATP synthase, and enzyme
essential for supply of energy to mycobacterium TB
Use of BDQ for MDR-TB reduced the time for sputum to become culture negative .
Exhibits strong bactericidal and sterilizing activity against M. tuberculosis by killing both rapidly
multiplying as well as dormant bacilli
Bedaquiline (BDQ) MOA: inhibits mycobacterial ATP synthase-limiting energy production within
mycobacterial cell. The human ATP synthase is 20,000 fold less sensitive to BDQ than is the
mycobacterial enzyme.[mcq]
Resistance to BDQ primarily by mutation of ATP synthase enzyme & by acquisition of BDQ efflux
from the bacilli. no cross resistance between BDQ and any 1 line or 2nd line anti-TB drug occurs.
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Bedaquiline PK: well absorbed orally; fatty meal improves absorption, highly plasma protein bound ,extensively
distributed in tissues.
Metabolism occurs in liver, mainly by CYP3A4 - drug interactions occur with CYP3A4 inducers and inhibitors.
The terminal t½ of BDQ is very long ( 160 days), probably due to redistribution from tissues.
It is excreted mainly in faeces.
Recommendations regarding use of BDQ are:
It should be used only for pulmonary MDR-TB adults (18 yr)
Women patients should be nonpregnant and willing to remain so during BDQ use
Cardiac fitness desirable
BDQ dose: maximum of 24 weeks in a dose of 400 mg/day for 2 weeks followed by 200 mg 3 times a week for the next
22 weeks.
Adverse effects of BDQ : nausea, headache. arthralgia and prolongation of QT interval, hepatotoxicity(with other QT
prolonging drug)
BEDAQUILINE
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DELAMANID
Nitroimidazole class drug-new drug
MOA: blocks mycolic acid synthesis & release NO
DOSE: 100mg BD for 24 weeks
INDICATION: MDR, XDR, MIXED PATTERN RESISTANT TB
ADR: QT prolongation, GI disturbances
recommendations regarding use of delamanid are:
It should be used only for pulmonary MDR-TB adults (18 yr)
Women patients should be nonpregnant and willing to remain so during BDQ use
Cardiac screening
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Presumptive TB cases ( previously k/a suspected )
Presumptive pulmonary TB refers to a person with any of the symptoms or signs suggestive of TB:
• cough >2 weeks, • fever >2 weeks, • significant weight loss, • haemoptysis, • any abnormalities in chest X-ray
Presumptive TB cases in paediatric patients, where loss of body weight is defined that loss of >5% body weight as
compared to highest weight recorded in the last 3 months. The history of unexplained or no weight gain in the past 3
months and symptomatic child contact with any form of active TB in the last 2 years may be significant.
Presumptive DRTB cases as follows:
• TB patients who have failed treatment with first-line anti-tubercular drugs (ATD)
• Paediatric TB non-responder
• TB patients who are contacts of DRTB
• TB patients who are found positive on any follow-up sputum smear examination during treatment with first-line ATD
• Previously treated TB cases
• TB patients with HIV co-infection.
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Goals Of Antitubercular Chemotherapy
(a) Kill dividing bacilli- patient is non-contagious to the community: transmission of TB is
interrupted,affords quick symptom relief.
(b) Kill persisting bacilli To effect cure and prevent relapse.
(c) Prevent emergence of resistance - bacilli remain susceptible to the drugs.
PHASES OF TB TREATMENT:
All regimens have an initial intensive phase with 4–5 drugs lasting 2–3 months aimed to
rapidly kill the bacilli, bringing about sputum conversion and afford fast symptomatic relief.
This is followed by a continuation phase with 2–3 drugs lasting 4–5 months during which the
remaining bacilli are eliminated so that relapse does not occur.
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CASE DEFINITIONS
1.Microbiologically confirmed TB case -presumptive TB patient with biological specimen positive for
acid-fast bacilli, or positive for mycobacterium TB on culture, or positive for TB through Quality
Assured Rapid Diagnostic molecular test.
2. Clinically diagnosed TB case -presumptive TB patient who is not microbiologically confirmed, but has
been diagnosed with active TB by a clinician on the basis of X-ray abnormalities, histopathology or
clinical signs with a decision to treat the patient with a full course of anti-TB treatment.
Microbiologically confirmed or clinically diagnosed cases of TB are classified according to
1. Anatomical site of disease
2. History of previous TB
3. Drug resistance.
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CLASSIFICATION – BASED ON HISTORY OF THE
PREVIOUS TREATMENT
1. New case – A TB patient who has never had treatment for TB or has taken ATD for <1 month.
2 Previously treated patients have received one month or more ATD in the past. This may be:
(a) Recurrent TB case – A TB patient previously declared as successfully treated
(cured/treatment completed) and who is subsequently found to be microbiologically confirmed
TB case is a recurrent TB case. (Previously called relapse.)
(b) Treatment after failure – Patients are those who have previously been treated for TB and
whose treatment failed at the end of their most recent course of treatment. (Previously, it was
called failure)
3. Treatment after loss to follow-up – A TB patient previously treated for TB for one month or
more and who was declared lost to follow-up in their most recent course of treatment and
subsequently found microbiologically confirmed TB cases. (Previously called treatment after
default)
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CLASSIFICATION ON THE BASIS OF DRUG RESISTANCE
1. Mono resistance (MR) – A TB patient whose biological specimen is resistant to one first-line anti-TB
drug only.
2. Poly resistance (PDR) – A TB patient whose biological specimen is resistant to more than one
first-line anti-TB drug, other than both INH and Rifampicin.
3. Multi-drug resistance (MDR) – A TB patient whose biological specimen is resistant to both INH and
Rifampicin with or without resistance other first-line ATD, based on results from a Quality Assured
Laboratory. (No changes.)
4. Rifampicin resistance (RR) – Resistance to Rifampicin detected by phenotypic or genotypic methods
with or without resistant to other ATD excluding INH. Patient with RR should be managed as if they
are in MDR TB case.
5. Extensive drug resistance (XDR) – MDR TB case whose biological specimen was resistant to a
Fluroquinolone (FQ) and a second-line injectable ATD from a Quality Assured Laboratory. (No
changes.)
33. NEW GUIDELINES
For new TB cases
• Treatment in IP will consist of 8 weeks of INH, Rifampicin, Pyrazinamide and Ethambutol in daily dosages as
per four weight bands categories
• There will be no need for extension of IP
• Only Pyrazinamide will be stopped in CP while the other three drugs will be continued for another 16 weeks
as daily dosages.
For previously treated cases:
• IP will be of 12 weeks, where injection Streptomycin will be stopped after 8 weeks and the remaining four
drugs in daily dosages as per weight band for another 4 weeks
• No need of extension of IP
• At the start of CP, Pyrazinamide will be stopped while rest of the drugs will be continued for another 20
weeks as daily dosages.
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NEW GUIDELINES
Management of extra-pulmonary TB (new guidelines) –
• The CP in both new and previously treated cases may be extended 3–6 months in certain TB such as
a) CNS
b) skeletal
c) disseminated TB
d) based on clinical decision of the treating physicians
Extension beyond 3 months will only be on recommendation of experts of concerned field.
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MDR/RR TB cases (without additional resistance)
Treatment regimen for MDR TB contains 6–9 months of IP with Kanamycin, Levofoxacin, Ethambutol,
Pyrazinamide, Ethionamide and Cycloserine and 18 months of CP with Levofoxacin, Ethambutol, Ethionamide
and Cycloserine (no change).
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But if INH resistance is not known or DST result shows sensitivity to INH, then addition of INH
in the regimen of ATD is to be done. (New addition)
Appropriate modification of the treatment regimen can be done in case of additional resistance.
If isoniazid resistance is found, the use of isoniazid depends on:
1. If high-level resistance detected by liquid culture – omit INH.
2. If low-level resistance detected by LC – add high dose INH.
3. If LPA reports INH resistance by Kat G mutation – omit INH.
4. If LPA reports INH resistance by INH A mutation – add high dose INH.
MDR/RR TB cases (without additional resistance)
39.
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Tuberculosis In AIDS Patients
• When CD4 count is <150 cells/μL, extrapulmonary and dual TB is more commonly encountered.
• Adverse reactions to anti-TB drugs are more common in HIV patients.
• All HIV positive TB patients should also receive cotrimoxazole preventive therapy at least throughout the
anti-TB regimen - to reduce mortality, probably by preventing Pneumocystis jirovecii and other infections
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Isoniazid Preventive Therapy (IPT) for PLHIVs
(a) Adult and adolescents living with HIV should be screened for TB and those who are unlikely to
have active TB should be offered IPT
(b) Children with HIV who have no TB symptoms and who are unlikely to have active TB on
symptom-based
screening should be offered IPT regardless of their age
(c) All children with HIV who have successfully completed treatment for TB disease should
receive IPT.
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Chemoprophylaxis
Purpose - to prevent progression of latent tubercular infection to active disease. This is indicated only in :
(a) Contacts of open cases who show recent Mantoux conversion.
(b) Children with positive Mantoux and a TB patient in the family.
(c) Neonate of tubercular mother.
(d) Patients of leukaemia, diabetes, silicosis, or those who are HIV positive but are not anergic, or are on
corticosteroid therapy who show a positive Mantoux.
(e) Patients with old inactive disease who are assessed to have received inadequate therapy.
The standard drug for chemoprophylaxis of TB is H 300 mg (10 mg/kg in children) daily for 6 months. This is
as effective in HIV patients as in those with normal immune function. The CDC (USA) recommends 4 months R
prophylaxis in case H cannot be used.
The RNTCP recommend that MDRTB contacts should be watched without giving any prophylactic medication,
and treated promptly if they develop active disease.
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Tuberculosis In Pregnant Women
WHO and British Thoracic Society consider H, R, E and Z to be safe to the foetus and recommend the
standard 6 month (2HRZE + 4HR) regimen for pregnant women with TB.
S is contraindicated because it is ototoxic to the foetus.
Z is not recommended in the USA (due to lack of adequate teratogenicity data).
RNTCP 2016 Guidelines: consider Z to be safe & recommend full course TB therapy
Treatment of TB should not be withheld or delayed because of pregnancy.
All pregnant women being treated with INH should receive pyridoxine 10–25 mg/day.
All 1st line drug are compatible with breastfeeding – full course should be given- breastfeeding should be
continued.
Infant receive 6 month INH preventive therapy – rule out active TB followed by BCG vaccination.
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Role of corticosteroids
Corticosteroids should not be ordinarily used in tubercular patients.
They may be used under adequate chemotherapeutic cover:
(a) In seriously ill patients (miliary or severe pulmonary TB) to buy time for drugs to act.
(b) When hypersensitivity reactions occur to anti tubercular drugs.
(c) In meningeal/renal/pericardial TB or pleural effusion—to reduce exudation, prevent its organisation and
strictures, etc.
(d) In AIDS patients with severe manifestations of tuberculosis.
Corticosteroids are contraindicated in intestinal tuberculosis because silent perforation can occur.(MCQ)
Corticosteroids, if given, should be gradually withdrawn when the general condition of the patient improves.
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Mycobacterium avium
complex (MAC) infection
MAC is an opportunistic pathogen which causes disseminated and
multifocal disease in immunocompromized(HIV-AIDS) patients.
Develops when - CD4 count drops to <50 cells/μL, HIV-RNA load is
high , presence of other opportunistic infections (P. jirovecii, etc.)
Duration of therapy:
Intensive phase - dependent on the response-till CD4 count rises
> 100 cells/μL and symptomatic relief -may take 2–6 months.
Maintenance therapy is continued till a and CD4 count stays > 100
cell/μL for at least 6 months.
All patients must simultaneously receive HAART for the HIV
infection.
Prophylaxis of MAC infection: Protect the AIDS patient from
developing active MAC disease during the period CD4 count
remains below 50 cell/μL.
Prophylaxis of MAC infection- A single drug is used.
azithromycin 1200 mg/week / clarithromycin 500 mg
twice a day-preferred drugs.
Rifabutin 300 mg/day – can also be used.
Duration - continued till the simultaneously instituted
HAART achieves complete suppression of HIV
replication, CD4 count rises above 100 cell/μL and
stays there for at least 3 months.
50. Aditi
Maitra
• Face mask might serve dual purpose if it becomes a mandatory part of our lives post
COVID 19 pandemic.
• It not only curbs the spread of COVID 19, but also has been reported to reduce the
spread of TB & achieve the goal of END TB by 2025
COVID 19 ERA LEGACY