This document discusses antimycobacterial drugs used to treat tuberculosis. It begins by describing tuberculosis and how it is caused by Mycobacterium tuberculosis. It then discusses the various drugs used to treat tuberculosis, including their mechanisms of action, pharmacokinetics, adverse drug reactions, and classifications as first-line versus second-line treatments. Rifampin, isoniazid, pyrazinamide, and ethambutol are described as first-line treatments, while second-line treatments include drugs like capreomycin, fluoroquinolones, and cycloserine. The document concludes by discussing the different types of tubercular infections treated by these drugs.
1. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis and causes the chronic lung infection tuberculosis. It is treated using a combination of antibiotics over a long period of time to prevent drug resistance from developing.
2. First line antibiotics include isoniazid, rifampin, pyrazinamide, and ethambutol. Isoniazid and rifampin are highly effective at killing the bacteria while pyrazinamide and ethambutol prevent resistance. Treatment involves an initial phase to relieve symptoms followed by a continuous phase to fully eliminate the bacteria.
3. Drug resistance is a major problem, requiring longer and more toxic second line treatments. Factors like non-compliance
Tuberculosis is caused by Mycobacterium tuberculosis and is one of the world's most deadly infectious diseases. It primarily affects the lungs but can spread throughout the body. First line drugs used to treat tuberculosis include isoniazid, rifampin, pyrazinamide, and ethambutol. Isoniazid and rifampin are the most effective. Treatment requires combination drug therapy for an extended period of time to address both actively growing and dormant bacilli. Short course multidrug regimens introduced by the WHO have improved treatment completion rates. Problems in tuberculosis chemotherapy include the slow growth of mycobacteria and risk of resistance development with single drug therapy.
This document provides information about quinolones, including their classification, mechanism of action, and examples of specific quinolones. It discusses the classification of quinolones as first, second, third, or fourth generation. It also summarizes the mechanisms of action, pharmacokinetic properties, uses, and adverse effects of several common quinolones like ciprofloxacin, norfloxacin, ofloxacin, and moxifloxacin. Finally, it mentions some quinolones currently under clinical trials.
This document discusses various antimycobacterial drugs used to treat tuberculosis and leprosy. It describes the mechanisms of action, development of resistance, and importance of drug combinations for isoniazid, rifampin, ethambutol, pyrazinamide, streptomycin, fluoroquinolones, linezolid, bedaquiline, and dapsone. Resistance develops rapidly if these drugs are used alone rather than in combination regimens.
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.
This document discusses various antifungal drugs, including their mechanisms of action, classifications, and clinical uses. It covers major drug classes like azoles, polyenes, and echinocandins. Key drugs discussed include amphotericin B, which disrupts fungal cell membranes; azoles like fluconazole and itraconazole, which inhibit ergosterol synthesis; and echinocandins like caspofungin that target fungal cell wall synthesis. The document provides details on pharmacokinetics, mechanisms, resistance, administration routes and adverse effects of these important antifungal medications.
This document discusses mycobacterial infections, focusing on tuberculosis and leprosy. It provides details on the causative organisms, epidemiology, pathogenesis, classification of anti-tubercular drugs, mechanisms of action, resistance, treatment approaches, and drug-resistant tuberculosis. The main points covered are that tuberculosis is caused by Mycobacterium tuberculosis and is the leading infectious disease worldwide. Treatment involves a combination of first-line and second-line drugs administered for extended periods to prevent resistance and achieve cure. Drug-resistant tuberculosis including multi-drug resistant TB requires complex second-line drug regimens.
1. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis and causes the chronic lung infection tuberculosis. It is treated using a combination of antibiotics over a long period of time to prevent drug resistance from developing.
2. First line antibiotics include isoniazid, rifampin, pyrazinamide, and ethambutol. Isoniazid and rifampin are highly effective at killing the bacteria while pyrazinamide and ethambutol prevent resistance. Treatment involves an initial phase to relieve symptoms followed by a continuous phase to fully eliminate the bacteria.
3. Drug resistance is a major problem, requiring longer and more toxic second line treatments. Factors like non-compliance
Tuberculosis is caused by Mycobacterium tuberculosis and is one of the world's most deadly infectious diseases. It primarily affects the lungs but can spread throughout the body. First line drugs used to treat tuberculosis include isoniazid, rifampin, pyrazinamide, and ethambutol. Isoniazid and rifampin are the most effective. Treatment requires combination drug therapy for an extended period of time to address both actively growing and dormant bacilli. Short course multidrug regimens introduced by the WHO have improved treatment completion rates. Problems in tuberculosis chemotherapy include the slow growth of mycobacteria and risk of resistance development with single drug therapy.
This document provides information about quinolones, including their classification, mechanism of action, and examples of specific quinolones. It discusses the classification of quinolones as first, second, third, or fourth generation. It also summarizes the mechanisms of action, pharmacokinetic properties, uses, and adverse effects of several common quinolones like ciprofloxacin, norfloxacin, ofloxacin, and moxifloxacin. Finally, it mentions some quinolones currently under clinical trials.
This document discusses various antimycobacterial drugs used to treat tuberculosis and leprosy. It describes the mechanisms of action, development of resistance, and importance of drug combinations for isoniazid, rifampin, ethambutol, pyrazinamide, streptomycin, fluoroquinolones, linezolid, bedaquiline, and dapsone. Resistance develops rapidly if these drugs are used alone rather than in combination regimens.
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.
This document discusses various antifungal drugs, including their mechanisms of action, classifications, and clinical uses. It covers major drug classes like azoles, polyenes, and echinocandins. Key drugs discussed include amphotericin B, which disrupts fungal cell membranes; azoles like fluconazole and itraconazole, which inhibit ergosterol synthesis; and echinocandins like caspofungin that target fungal cell wall synthesis. The document provides details on pharmacokinetics, mechanisms, resistance, administration routes and adverse effects of these important antifungal medications.
This document discusses mycobacterial infections, focusing on tuberculosis and leprosy. It provides details on the causative organisms, epidemiology, pathogenesis, classification of anti-tubercular drugs, mechanisms of action, resistance, treatment approaches, and drug-resistant tuberculosis. The main points covered are that tuberculosis is caused by Mycobacterium tuberculosis and is the leading infectious disease worldwide. Treatment involves a combination of first-line and second-line drugs administered for extended periods to prevent resistance and achieve cure. Drug-resistant tuberculosis including multi-drug resistant TB requires complex second-line drug regimens.
Mycobacteria are slow-growing bacteria that cause tuberculosis (TB) and other diseases. TB is treated using a combination of antimicrobial drugs over several months to years to prevent drug resistance from emerging. First-line drugs include isoniazid, rifampin, ethambutol, and pyrazinamide. For drug-resistant TB, second-line drugs like fluoroquinolones, aminoglycosides, and others are used. Close monitoring of patients and directly observed therapy are important to ensure treatment is completed.
Quinolones and fluoroquinolones are a group of synthetic antibacterial agents that are mainly effective against gram-negative organisms. Nalidixic acid was the first member introduced in 1964 for urinary and gastrointestinal infections. Synthetic fluorinated analogs of nalidixic acid called fluoroquinolones were developed in the 1980s and have an extended spectrum and systemic effects. Fluoroquinolones are bactericidal and act by interfering with bacterial DNA replication through inhibition of DNA gyrase and topoisomerase enzymes. While effective, quinolones have limitations including low potency, resistance development, and side effects such as gastrointestinal issues.
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.
These are a class of antibiotics having a nucleus of four cyclic rings. The tetracyclines are primarily bacteriostatic; inhibit protein synthesis by binding to 30S ribosomes in susceptible organism.
Subsequent to such binding, attachment
of aminoacyl-t-RNA to the acceptor (A) site of
mRNA-ribosome complex. The carrier involved
in active transport of tetracyclines is absent in
the host cells. Moreover, protein synthesizing
apparatus of host cells is less susceptible to
tetracyclines. These two factors are responsible
for the selective toxicity of tetracyclines for
the microbes.
SlideShare On Chemotherapy of Antiviral Drugs (Pharmacology)Naveen K L
The document summarizes the pharmacology of antiviral drugs. It discusses the stages of viral replication and types of viruses. It then classifies antiviral drugs into different categories based on the virus they target such as anti-herpes viruses, anti-influenza viruses, anti-hepatitis viruses, and anti-retroviruses. For each category of antiviral drugs, it provides examples of drugs, their mechanisms of action, pharmacokinetics, uses, and adverse effects in concise detail. The document concludes by citing the reference used.
Antiprotozoal drugs classification,mechanism of action uses and adverse effectsMuhammad Amir Sohail
Antiprotozoal drugs are used to treat protozoal infections. They often have restricted activity against specific protozoa through interference with protozoal enzyme pathways. Treatment may not consistently clear infections and resistance is a growing problem. Some drugs have minimal side effects while others have effects that limit their use. Common antiprotozoal drugs include amprolium, fenbendazole, metronidazole, pyrimethamine/sulfadiazine combinations, and atovaquone which is used with azithromycin to treat babesiosis.
This document discusses various classes of antibiotics - polyenes and polypeptides. It provides details about Amphotericin B, Nystatin, Hamycin in the polyene class and Bacitracin, Polymyxin-B, Colistin/Polymyxin-E, and Dactinomycin/Actinomycin-D in the polypeptide class. It describes their origins, mechanisms of action, therapeutic uses, dosages and adverse effects.
This document summarizes antiviral drugs used to treat various viral infections. It discusses how viruses replicate inside host cells and highlights challenges in treating viral infections. It classifies antiviral drugs and describes their mechanisms of action, spectra, uses and limitations. Key drugs discussed include acyclovir for herpes viruses, ganciclovir for cytomegalovirus, oseltamivir for influenza, lamivudine/entecavir for hepatitis B, ribavirin for hepatitis C and respiratory syncytial virus, and interferons for hepatitis B and C. Adverse effects and pharmacokinetics of several drugs are also summarized.
This document presents information on antimicrobial resistance (AMR). It defines AMR as microorganisms becoming resistant to antimicrobial drugs like antibiotics, antivirals, and antimalarials. The document discusses factors that contribute to AMR, including overuse of antibiotics. It describes mechanisms of resistance such as mutations, plasmids, and enzymes that inactivate drugs. It recommends strategies to control AMR like prudent antibiotic use, developing new drugs, and reducing unnecessary use in animals. The conclusion emphasizes that AMR is a global threat that requires strategies to prevent further resistance development.
Macrolides are a group of antibiotics that contain a macrocyclic lactone ring and inhibit bacterial protein synthesis. They include erythromycin, clarithromycin, and azithromycin. Clarithromycin and azithromycin are semi-synthetic derivatives of erythromycin with improved acid stability and less gastrointestinal side effects. Macrolides are used to treat respiratory, skin, and sexually transmitted infections caused by bacteria, mycobacteria, and protozoa. Adverse effects include gastrointestinal upset and potential interactions with other drugs metabolized by cytochrome P450 enzymes.
Hello friends. In this PPT I am talking about anti-fungal drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
INTRODUCTION
Aminoglycosides are a class of antibiotics used mainly in the treatment of aerobic gram-negative bacilli infections, although they are also effective against other bacteria including Staphylococci and Mycobacterium tuberculosis.
They are often used in combination with other antibiotics.
Streptomycin – 1944
Actinomycetes – Streptomyces griseus
Bactericidal antibiotics which is interfere with protein synthesis
Used to treat aerobic Gram –ve bacteria
Exhibit ototoxicity and nephrotoxicity
MECHANISM OF ACTION
These drugs inhibit protein synthesis in the bacteria, there permeability is increased and cell contents leak out and death of cell occurs. These drugs leave bactericidal action.
CLINICAL USES
Gram –ve bacillary infection – Septicaemia, pelvic & abdominal sepsis
Bacterial endocarditis – enterococcal, streptococcal or staphylococcal infection of heart valves
Pneumonias, Tuberculosis
Tularemia
Plague, Brucellosis
Topical – Neomycin, Framycetin:- Infections of conjunctiva or external ear and also used it before surgery.
COMMON INDICATIONS OF AMINOGLYCOSIDES
Gram negative bacillary infections particularly septicemia, meningitis, UTI’s renal, pelvic and abdominal sepsis.
Bacterial endocarditis: usually gentamicin is preferred as a part of regimen.
Other infections such as tuberculosis, plague, brucellosis etc.
Topical uses: neomycin, framycetin and sisomicin are used for various topical infections.
NURSING IMPLICATIONS
The renal function should be regularly monitored.
Patients should be regularly enquired about any side effects.
Patients should be warned for not driving or operating the machinery.
Patient should be advised to take plenty of water during the course.
Monitor the sign and symptoms of hearing loss.
Minocycline is a broad-spectrum tetracycline antibiotic with a broader spectrum than other tetracyclines. It has a long half-life, resulting in higher serum levels than simple tetracyclines. Minocycline is highly lipid-soluble and penetrates tissues well but can cause more central nervous system side effects. Common uses include treating acne, skin infections, Lyme disease, and asthma. Potential side effects range from mild gastrointestinal issues to more serious allergic reactions and neuropsychiatric effects.
This document summarizes various aspects of antiviral drugs, including their classification, mechanisms of action, and use for specific viruses. It discusses drugs that target DNA viruses like herpes simplex virus and hepatitis B virus. These include nucleoside analogues like acyclovir and ganciclovir that inhibit viral DNA polymerase. It also covers drugs for influenza viruses like amantadine and oseltamivir that inhibit the viral M2 protein and neuraminidase enzyme. Antivirals for hepatitis C virus and human immunodeficiency virus are also outlined, such as interferons, ribavirin, protease inhibitors, and integrase inhibitors. The document provides brief descriptions of each drug's mechanism, pharmac
This document discusses antitubercular drugs used to treat tuberculosis. It describes how tuberculosis is a major health problem globally and in India. It outlines the classification of first-line and second-line antitubercular drugs, including their mechanisms of action and side effects. Key first-line drugs discussed are isoniazid, rifampin, pyrazinamide, and ethambutol. Considerations for treating tuberculosis in pregnant women, breastfeeding women, and AIDS patients are also covered. The document emphasizes the potency of rifampin and suitability of pyrazinamide for intracellular and acidic environments.
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.
Mycobacteria are slow-growing bacteria that cause tuberculosis (TB) and other diseases. TB is treated using a combination of antimicrobial drugs over several months to years to prevent drug resistance from emerging. First-line drugs include isoniazid, rifampin, ethambutol, and pyrazinamide. For drug-resistant TB, second-line drugs like fluoroquinolones, aminoglycosides, and others are used. Close monitoring of patients and directly observed therapy are important to ensure treatment is completed.
Quinolones and fluoroquinolones are a group of synthetic antibacterial agents that are mainly effective against gram-negative organisms. Nalidixic acid was the first member introduced in 1964 for urinary and gastrointestinal infections. Synthetic fluorinated analogs of nalidixic acid called fluoroquinolones were developed in the 1980s and have an extended spectrum and systemic effects. Fluoroquinolones are bactericidal and act by interfering with bacterial DNA replication through inhibition of DNA gyrase and topoisomerase enzymes. While effective, quinolones have limitations including low potency, resistance development, and side effects such as gastrointestinal issues.
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.
These are a class of antibiotics having a nucleus of four cyclic rings. The tetracyclines are primarily bacteriostatic; inhibit protein synthesis by binding to 30S ribosomes in susceptible organism.
Subsequent to such binding, attachment
of aminoacyl-t-RNA to the acceptor (A) site of
mRNA-ribosome complex. The carrier involved
in active transport of tetracyclines is absent in
the host cells. Moreover, protein synthesizing
apparatus of host cells is less susceptible to
tetracyclines. These two factors are responsible
for the selective toxicity of tetracyclines for
the microbes.
SlideShare On Chemotherapy of Antiviral Drugs (Pharmacology)Naveen K L
The document summarizes the pharmacology of antiviral drugs. It discusses the stages of viral replication and types of viruses. It then classifies antiviral drugs into different categories based on the virus they target such as anti-herpes viruses, anti-influenza viruses, anti-hepatitis viruses, and anti-retroviruses. For each category of antiviral drugs, it provides examples of drugs, their mechanisms of action, pharmacokinetics, uses, and adverse effects in concise detail. The document concludes by citing the reference used.
Antiprotozoal drugs classification,mechanism of action uses and adverse effectsMuhammad Amir Sohail
Antiprotozoal drugs are used to treat protozoal infections. They often have restricted activity against specific protozoa through interference with protozoal enzyme pathways. Treatment may not consistently clear infections and resistance is a growing problem. Some drugs have minimal side effects while others have effects that limit their use. Common antiprotozoal drugs include amprolium, fenbendazole, metronidazole, pyrimethamine/sulfadiazine combinations, and atovaquone which is used with azithromycin to treat babesiosis.
This document discusses various classes of antibiotics - polyenes and polypeptides. It provides details about Amphotericin B, Nystatin, Hamycin in the polyene class and Bacitracin, Polymyxin-B, Colistin/Polymyxin-E, and Dactinomycin/Actinomycin-D in the polypeptide class. It describes their origins, mechanisms of action, therapeutic uses, dosages and adverse effects.
This document summarizes antiviral drugs used to treat various viral infections. It discusses how viruses replicate inside host cells and highlights challenges in treating viral infections. It classifies antiviral drugs and describes their mechanisms of action, spectra, uses and limitations. Key drugs discussed include acyclovir for herpes viruses, ganciclovir for cytomegalovirus, oseltamivir for influenza, lamivudine/entecavir for hepatitis B, ribavirin for hepatitis C and respiratory syncytial virus, and interferons for hepatitis B and C. Adverse effects and pharmacokinetics of several drugs are also summarized.
This document presents information on antimicrobial resistance (AMR). It defines AMR as microorganisms becoming resistant to antimicrobial drugs like antibiotics, antivirals, and antimalarials. The document discusses factors that contribute to AMR, including overuse of antibiotics. It describes mechanisms of resistance such as mutations, plasmids, and enzymes that inactivate drugs. It recommends strategies to control AMR like prudent antibiotic use, developing new drugs, and reducing unnecessary use in animals. The conclusion emphasizes that AMR is a global threat that requires strategies to prevent further resistance development.
Macrolides are a group of antibiotics that contain a macrocyclic lactone ring and inhibit bacterial protein synthesis. They include erythromycin, clarithromycin, and azithromycin. Clarithromycin and azithromycin are semi-synthetic derivatives of erythromycin with improved acid stability and less gastrointestinal side effects. Macrolides are used to treat respiratory, skin, and sexually transmitted infections caused by bacteria, mycobacteria, and protozoa. Adverse effects include gastrointestinal upset and potential interactions with other drugs metabolized by cytochrome P450 enzymes.
Hello friends. In this PPT I am talking about anti-fungal drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
INTRODUCTION
Aminoglycosides are a class of antibiotics used mainly in the treatment of aerobic gram-negative bacilli infections, although they are also effective against other bacteria including Staphylococci and Mycobacterium tuberculosis.
They are often used in combination with other antibiotics.
Streptomycin – 1944
Actinomycetes – Streptomyces griseus
Bactericidal antibiotics which is interfere with protein synthesis
Used to treat aerobic Gram –ve bacteria
Exhibit ototoxicity and nephrotoxicity
MECHANISM OF ACTION
These drugs inhibit protein synthesis in the bacteria, there permeability is increased and cell contents leak out and death of cell occurs. These drugs leave bactericidal action.
CLINICAL USES
Gram –ve bacillary infection – Septicaemia, pelvic & abdominal sepsis
Bacterial endocarditis – enterococcal, streptococcal or staphylococcal infection of heart valves
Pneumonias, Tuberculosis
Tularemia
Plague, Brucellosis
Topical – Neomycin, Framycetin:- Infections of conjunctiva or external ear and also used it before surgery.
COMMON INDICATIONS OF AMINOGLYCOSIDES
Gram negative bacillary infections particularly septicemia, meningitis, UTI’s renal, pelvic and abdominal sepsis.
Bacterial endocarditis: usually gentamicin is preferred as a part of regimen.
Other infections such as tuberculosis, plague, brucellosis etc.
Topical uses: neomycin, framycetin and sisomicin are used for various topical infections.
NURSING IMPLICATIONS
The renal function should be regularly monitored.
Patients should be regularly enquired about any side effects.
Patients should be warned for not driving or operating the machinery.
Patient should be advised to take plenty of water during the course.
Monitor the sign and symptoms of hearing loss.
Minocycline is a broad-spectrum tetracycline antibiotic with a broader spectrum than other tetracyclines. It has a long half-life, resulting in higher serum levels than simple tetracyclines. Minocycline is highly lipid-soluble and penetrates tissues well but can cause more central nervous system side effects. Common uses include treating acne, skin infections, Lyme disease, and asthma. Potential side effects range from mild gastrointestinal issues to more serious allergic reactions and neuropsychiatric effects.
This document summarizes various aspects of antiviral drugs, including their classification, mechanisms of action, and use for specific viruses. It discusses drugs that target DNA viruses like herpes simplex virus and hepatitis B virus. These include nucleoside analogues like acyclovir and ganciclovir that inhibit viral DNA polymerase. It also covers drugs for influenza viruses like amantadine and oseltamivir that inhibit the viral M2 protein and neuraminidase enzyme. Antivirals for hepatitis C virus and human immunodeficiency virus are also outlined, such as interferons, ribavirin, protease inhibitors, and integrase inhibitors. The document provides brief descriptions of each drug's mechanism, pharmac
This document discusses antitubercular drugs used to treat tuberculosis. It describes how tuberculosis is a major health problem globally and in India. It outlines the classification of first-line and second-line antitubercular drugs, including their mechanisms of action and side effects. Key first-line drugs discussed are isoniazid, rifampin, pyrazinamide, and ethambutol. Considerations for treating tuberculosis in pregnant women, breastfeeding women, and AIDS patients are also covered. The document emphasizes the potency of rifampin and suitability of pyrazinamide for intracellular and acidic environments.
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 antitubercular drugs used to treat tuberculosis. It discusses first-line drugs like isoniazid, rifampin, pyrazinamide, ethambutol and streptomycin that are routinely used. It also discusses second-line drugs used when first-line drugs are ineffective or cannot be tolerated. The document describes the mechanisms of action, pharmacokinetics, resistance mechanisms and adverse effects of various antitubercular drugs. It also discusses treatment considerations for special populations like pregnant women, HIV patients and for chemoprophylaxis.
This document provides information on antitubercular drugs used to treat tuberculosis. It discusses first-line drugs like isoniazid, rifampin, pyrazinamide, ethambutol and streptomycin that are routinely used. It also discusses second-line drugs used when first-line drugs are ineffective or cannot be tolerated. The document describes the mechanisms of action, pharmacokinetics, resistance mechanisms and adverse effects of various antitubercular drugs. It also discusses treatment considerations for special populations like pregnant women, HIV patients and for chemoprophylaxis.
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.
1. Fungal infections are common in immunocompromised patients and those taking immunosuppressive drugs. They are harder to treat than bacterial infections.
2. There are two main types of fungal infections - superficial infections affecting the skin and mucous membranes, and deep infections affecting internal organs like the lungs and brain.
3. Major antifungal drug classes include azoles like fluconazole and itraconazole, polyenes like amphotericin B, and allylamines like terbinafine. They work by disrupting the fungal cell membrane or inhibiting fungal enzyme activity.
Tuberculosis is caused by Mycobacterium tuberculosis and treated using a combination of drugs over several months. The RNTCP in India aims to eliminate TB by 2025 through a strategy of detecting, treating, preventing, and building systems. First line drugs include isoniazid, rifampicin, pyrazinamide, and ethambutol while second line drugs are used to treat drug resistant forms of TB like MDR-TB and XDR-TB. Treatment involves a two month intensive phase using multiple drugs followed by a four month continuation phase with fewer drugs.
This document provides information on the classification, mechanisms of action, antimicrobial activity, mechanisms of resistance, pharmacokinetics, therapeutic uses and dosages, and adverse effects of various antimycobacterial agents used to treat diseases caused by mycobacteria such as tuberculosis. It discusses cell wall synthesis inhibitors including isoniazid, ethambutol, ethionamide, and cycloserine. It also discusses the cell membrane disruptor clofazimine and its mechanisms of action and antimicrobial activity.
This document discusses anti-tubercular drugs used to treat tuberculosis (TB), a chronic infectious disease caused mainly by Mycobacterium tuberculosis bacteria. It describes the first-line drugs isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin that are routinely used to treat TB. It explains their mechanisms of action, how drug resistance develops, pharmacokinetics, adverse effects, and interactions. The unique cell wall structure of mycobacteria that makes them intrinsically resistant to many drugs is also outlined.
The document provides an overview of aminoglycoside antibiotics including streptomycin, kanamycin, and gentamicin. It discusses their mechanisms of action, indications, absorption/excretion, adverse effects, dosages, and resistance. Aminoglycosides are mainly useful against aerobic Gram-negative bacteria and exhibit concentration-dependent killing. While effective, they can cause nephrotoxicity, ototoxicity, and neuromuscular blockade.
Anti mycobacterial drugs (tuberculosis drugs)Ravish Yadav
This document discusses anti-mycobacterial drugs used to treat tuberculosis. It begins by describing tuberculosis and how it is caused by the bacterium Mycobacterium tuberculosis. First-line drugs to treat tuberculosis are listed as isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin. Each drug's mechanism of action and potential resistance issues are then explained individually. Second-line drugs discussed include ethionamide, capreomycin, cycloserine, aminosalicylic acid, and fluoroquinolones. Common adverse drug reactions are also outlined.
This document discusses various non-steroidal immunosuppressant drugs used to treat non-infectious uveitis. It describes corticosteroid-sparing immunomodulatory therapy as necessary for patients who require high corticosteroid doses or have intolerances. The document categorizes immunomodulatory options and provides details on mechanisms of action, dosing regimens, and side effects of common agents including antimetabolites, calcineurin inhibitors, cytotoxic drugs, and biologic response modifiers.
Tuberculosis is caused by Mycobacterium tuberculosis and spreads via droplet infection, mainly affecting the lungs. There are several types including primary, secondary, and miliary tuberculosis. Treatment involves a combination of antibiotics classified as first-line (isoniazid, rifampin, ethambutol, pyrazinamide, streptomycin) or second-line drugs for resistant cases. The standard treatment regimen consists of a two month intensive phase with multiple antibiotics followed by a four month continuation phase with isoniazid and rifampin to prevent resistance. Directly observed therapy involves patients taking medications under supervision to improve adherence and cure rates.
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.
This document provides information on antifungal agents used to treat fungal infections. It discusses the types of fungal infections including superficial and deep infections caused by various fungi. It then classifies and describes various antifungal drugs including polyenes like amphotericin B, azoles like fluconazole and itraconazole, allylamines like terbinafine, and antimetabolites like flucytosine. It provides details on the mechanisms of action, pharmacokinetics, clinical uses and adverse effects of these major antifungal drug classes and agents.
This document discusses various immunizing agents, immunosuppressants, and hematopoietic drugs. It provides an overview of immunization including active and passive immunization. It also lists several common vaccines such as BCG, cholera, diphtheria, and pertussis vaccines. The document then discusses immunosuppressants including cytokine IL-2 inhibitors like cyclosporine and tacrolimus, inhibitors of cytokine gene expression like corticosteroids, and cytotoxic drugs. Finally, it covers several classes of hematopoietic drugs including platelet aggregation inhibitors like aspirin, thrombolytic drugs, and anticoagulants.
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 fungal infections (mycoses) in humans and antifungal treatments. It covers the major types of mycoses and their symptoms. It then describes several classes of antifungal agents including polyenes like amphotericin B and nystatin, azoles like fluconazole and itraconazole, allylamines like terbinafine, echinocandins like caspofungin, and others. It provides details on the mechanisms of action, spectra of activity, pharmacokinetics, uses, and precautions for many of the commonly used antifungal drugs. It also discusses systemic fungal infections, opportunistic infections, management principles, and drugs
6.antibiotics in oral and maxillofacial surgeryTejaswini498924
This document provides an overview of antibiotics used in oral and maxillofacial surgery. It begins with a brief history of antibiotics and chemotherapy. It then classifies antibiotics based on chemical structure, mechanism of action, spectrum of activity, and type of organism targeted. The document discusses principles for choosing and administering antibiotics, including achieving sufficient concentration at the infection site. It also covers antibiotic resistance, toxicity, and failure of chemotherapy. Finally, the document provides details on common classes of antibiotics like penicillins, cephalosporins, quinolones, macrolides, tetracyclines, and aminoglycosides.
Similar to anti mycobacterial and antileprotic drugs (20)
Immunosuppressants are drugs that inhibit immune responses and are used for organ transplantation and autoimmune diseases. The main classes of immunosuppressants discussed are calcineurin inhibitors like cyclosporine and tacrolimus which inhibit T-cell activation, mTOR inhibitors like sirolimus and everolimus, antiproliferative drugs like azathioprine and mycophenolate mofetil which inhibit lymphocyte proliferation, glucocorticoids which inhibit cytokine production, and biological agents that target specific components of the immune system such as TNF inhibitors. Each drug has a specific mechanism of action to suppress immune responses through different pathways.
Flow cytometry is a technique that uses laser-based technology to count, sort, and profile cells in a fluid mixture. A flow cytometer passes cells in single file through a laser, and measures light scatter and fluorescence to obtain quantifiable data on physical and chemical characteristics of cells. Key components include a fluidic system to hydrodynamically focus cells through the laser, an optics system using lasers and detectors to measure light signals, and an electronics system to convert these signals into electronic data that can be analyzed. Common applications include immunophenotyping, apoptosis measurement, and cell sorting.
The document discusses pharmacogenomics and how genetic variations can affect individual responses to drugs. It describes how pharmacogenomics examines genomic loci and biological pathways to determine drug variability. It also discusses pharmacogenetics which focuses on single gene variants. The document outlines some merits of pharmacogenomics like improving drug safety and personalized treatment. It then discusses various scenarios on how genetic polymorphisms can impact different drug metabolism pathways. Finally, it examines how specific genetic variations in drug metabolizing enzymes and transporters can influence drug pharmacokinetics and potential adverse effects.
Immunotherapeutics and Humanisation of antibodiesSanju Kaladharan
- Immunotherapeutics aim to activate the body's immune system to fight disease by triggering or mimicking immune responses. They include cytokines, monoclonal antibodies, antibody conjugates, and antibody-directed enzyme prodrug therapy.
- Monoclonal antibodies can directly induce cell death or block growth receptors. They also recruit immune cells through antibody-dependent cytotoxicity and complement-dependent cytotoxicity.
- Early monoclonal antibodies were murine but caused human anti-mouse antibody responses. Newer techniques generate chimeric antibodies by combining mouse and human portions or fully human antibodies from libraries or transgenic mice to reduce this immune response.
Biosimilars are biologic medicines that are developed to be similar to existing approved biologic medicines known as reference medicines. Biosimilars must demonstrate similarity to the reference medicine in terms of quality, safety and efficacy through comprehensive testing and analysis. While biosimilars may provide reduced costs and increased access to biologic treatments, they are more complex than traditional small molecule drugs due to differences in size, structure, manufacturing processes, and potential for immunogenicity. Thorough evaluation and regulation is required to ensure biosimilars are interchangeable for the reference product without compromising patient safety.
1. Hematopoietic drugs regulate the production of blood cells through hematopoietic growth factors and hematinics. Growth factors like erythropoietin and colony stimulating factors stimulate the production of red blood cells, granulocytes, and platelets.
2. Hematinics such as iron, vitamin B12, and folic acid are required for blood cell maturation and are used to treat anemias.
3. Recombinant forms of hematopoietic growth factors including erythropoietin, filgrastim, and sargramostim are used to treat chemotherapy-induced neutropenia and anemias.
This document discusses gene mapping and linkage mapping. It explains Mendel's law of independent assortment and how genes located on the same chromosome, called linked genes, are not always inherited independently. Linkage maps show the arrangement of genes along chromosomes based on how often they are inherited together. Recombination frequency during meiosis provides an estimate of how close together genes are physically located on a chromosome. Gene mapping through linkage analysis has helped locate genes responsible for several single-gene disorders and diseases.
Cell signaling occurs through four main categories: paracrine, autocrine, endocrine, and direct contact. Paracrine signaling involves short-range signals between nearby cells, such as synaptic signaling between neurons. Autocrine signaling allows cells to signal to themselves. Endocrine signaling uses the circulatory system to transmit long-range hormones from endocrine glands. Direct contact signaling transfers small molecules through gap junctions between cells. Intracellular signaling pathways transmit extracellular signals through phosphorylation cascades like the MAPK, JNK, p38, and PI3K pathways, ultimately influencing cell behavior.
This document discusses anticoagulants and antiplatelet drugs. It begins by describing how platelets activate and aggregate to form blood clots. It then discusses various classes of anticoagulant and antiplatelet drugs that prevent clot formation, including heparin and low molecular weight heparins, warfarin, and direct factor Xa and thrombin inhibitors. It also covers fibrinolytics that dissolve blood clots and antifibrinolytics that inhibit clot dissolution.
Enzymes are catalytic proteins that speed up biochemical reactions without being consumed themselves. They lower the activation energy needed for reactions to occur.
Structural
69
Structural proteins
Keratin
Example: Keratin in hair and nails provides strength and rigidity.
Function: Structure
A biosensor is an analytical device that uses a bioreceptor to detect a specific substance. It contains a bioreceptor, transducer, and processing system. Common bioreceptors include antibodies, enzymes, nucleic acids, cells, and molecularly imprinted polymers. The bioreceptor interacts with the target analyte and the transducer converts the interaction signal into an electrical signal that is processed. Examples of biosensors include glucose biosensors, which detect glucose using the enzyme glucose oxidase, and pregnancy tests, which detect human chorionic gonadotropin hormone using antibodies.
Cell viability and proliferation assays measure aspects of cellular health and function, such as membrane integrity, metabolic activity, and DNA synthesis. Common assays include MTT, which measures mitochondrial activity; ATP assays, which measure ATP concentration as a marker of viability; Sulforhodamine B, which binds cellular proteins to measure biomass; and propidium iodide staining, which detects compromised membranes. These assays are useful for screening drug toxicity and effects on cell growth.
This document describes a glucose uptake assay to analyze glucose transport activity in differentiated 3T3 L1 cells. The assay involves treating starved cells with insulin or plant extracts, then exposing the cells to a radioactive cocktail containing tagged glucose. Uptake of the tagged glucose is measured using liquid scintillation counting to analyze the effect of treatments on glucose uptake activity.
Hospital and its organisation, BUDGET AND pHARMACY AND tHERAPEUTIC COMMITTEESanju Kaladharan
Hospital administration oversees hospital operations and policies. Therapeutic services provide medical treatment to patients, including physical, occupational, speech and respiratory therapy. Diagnostic services determine the cause of illness through medical testing. Support services maintain hospital facilities and equipment. The pharmacy and therapeutics committee advises on drug selection and use to ensure cost-effective and quality patient care.
The document discusses hospital formularies, which are lists of approved medications used in hospitals. A pharmacy and therapeutics committee is responsible for developing and revising the formulary. This includes adding and removing drugs based on efficacy, safety, and cost. The formulary provides guidelines for procuring, prescribing, dispensing, and administering drugs in the hospital. It aims to promote rational and cost-effective drug use. Restrictions may be placed on certain drugs to ensure appropriate usage. Exceptions can be made for nonformulary drugs in special cases.
1. Gene regulation in prokaryotes and eukaryotes involves control at the levels of transcription and translation.
2. In prokaryotes, genes are often organized into operons and regulated through inducible and repressible operons controlled by regulatory proteins binding to operator and promoter sites. The lac and trp operons are examples of inducible and repressible operons, respectively.
3. In eukaryotes, gene expression is controlled through chromatin structure, transcriptional initiation, transcript processing and modification, transport, stability, and small RNA-mediated pathways. This allows for complex tissue-specific and developmental control of gene expression.
DNA replication is the process where a cell makes an identical copy of its DNA before cell division. It occurs in S phase of the cell cycle. DNA polymerase enzymes add nucleotides to each DNA strand based on complementary base pairing. This results in two identical DNA double helices, each with one original strand and one newly synthesized strand. In eukaryotes, DNA replication is more complex, involving multiple origins of replication and DNA polymerases. Mechanisms like proofreading and DNA repair help ensure high-fidelity copying of the genome.
The document summarizes key aspects of the cell cycle and cell division. It discusses the phases of the cell cycle including interphase and mitosis. It describes chromosome structure and duplication. It explains the process of mitosis and cytokinesis. It also discusses regulation of the cell cycle through checkpoints at the G1/S and G2/M transitions to ensure DNA integrity before cell division.
Pharmacogenomics is the study of how genetic variations affect individual responses to drugs. It examines genomic loci and biological pathways to determine variability in drug metabolism and effects. Pharmacogenetics focuses on clinical effects of single gene variants. Pharmacogenomics can improve drug safety, efficacy and discovery by tailoring treatments based on a person's genetics. It allows optimization of drug metabolism and dosing based on an individual's genetic profile. Variations in genes that encode drug targets, metabolizing enzymes, transporters and those associated with adverse drug reactions can impact drug responses. Pharmacogenomics aims to incorporate genetic insights to develop safer and more effective precision medicines.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
2. Tuberculosis
• Is prototype example of granulomatous
inflammation.
• It is a chronic specific inflammatory infectious
disease caused by Mycobacterium
tuberculosis in humans.
• Tuberculosis usually attacks the lungs but it
can also affect any parts of the body
9. MODE OF TRANSMISSION. :
• 1. Inhalation of organisms present in fresh cough droplets or in
dried sputum from an open case of pulmonary tuberculosis.
• 2. Ingestion of the organisms leads to development of tonsillar or
intestinal tuberculosis. This mode of infection of human tubercle
bacilli is from self-swallowing of infected sputum of an open case of
pulmonary tuberculosis, or ingestion of bovine tubercle bacilli from
milk of diseased cows.
• 3. Inoculation of the organisms into the skin may rarely occur
• from infected postmortem tissue.
• 4. Transplacental route results in development of congenital
tuberculosis in foetus from infected mother and is a rare mode of
transmission.
10. Five patterns of the TB disease are recognised:
i) Pulmonary disease produced by M. kansasii or M. avium
intracellulare.
ii) Lymphadenitis caused by M. avium-intracellulare or M.
scrofulaceum.
iii) Ulcerated skin lesions produced by M. ulcerans or M.
marinum.
iv) Abscesses caused by M.fortuitum or M. chelonae.
v) Bacteraemias by M. avium-intracellulare as seen in
immunosuppressed patients of AIDS.
11.
12. • Known as “Acid-fast bacilli" because of their
lipid-rich cell walls, which are relatively
impermeable to various basic dyes unless the
dyes are combined with phenol.
13.
14. Mycobacterium avium complex (MAC)
• consists of two species: M avium and M
intracellulare; because these species are
difficult to differentiate, they are also
collectively referred to as Mycobacterium
avium-intracellulare (MAI)
15. • The diagnosis is made by the following tests:
• i) Positive Mantoux skin test.
• ii) Positive sputum for AFB (on smear or culture).
• iii) Complete haemogram (lymphocytosis and raised
ERR).
• iv) Chest X-ray (characteristic hilar nodules and other
• parenchymal changes).
• v) Fine needle aspiration cytology of an enlarged
peripheral
• lymph node is quite helpful for confirmation of
diagnosis
16. • First line: These drugs have high
antitubercular efficacy as well as low toxicity;
are used routinely.
• Second line: These drugs have either low
antitubercular efficacy or higher toxicity or
both; and are used as reserve drugs.
17.
18. Rifampin (Rifampicin, R)
• It is a semisynthetic derivative of rifamycin B
obtained from Streptomyces mediterranei.
• Rifampin is bactericidal to M. tuberculosis
• It is well absorbed orally, (bioavailability is ~
70%), but food decreases absorption; rifampin
is to be taken in empty stomach.
19. MOA
• The rifamycins (rifampin, rifabutin, rifapentine) are bactericidal
and inhibit deoxyribonucleic acid (DNA)-dependent ribonucleic
acid (RNA) polymerase of mycobacteria (but not mammals). This
enzyme is composed of four subunits; rifamycins bind to the β-
subunit, which results in blocking the growing RNA chain .
• Mechanism of resistance
• Resistance is conferred by single mutations that tend to occur
(>95%) in an 81-base pair region of the rpoB gene that codes for the
β-subunit.
20.
21. ADR
• Hepatitis
• 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.
• Respiratory syndrome: breathlessness which may be
associated with shock and collapse.
• Purpura, haemolysis, shock and renal failure
22. isoniazid
• INH enters by passive diffusion
and is activated by katG to a
range of reactive species or
radicals and isonicotinic acid.
• These attack multiple targets,
including mycolic acid
synthesis, lipid peroxidation,
DNA, and NAD metabolism.
• Deficient efflux and
insufficient antagonism of INH-
derived radicals, such as
defective antioxidative
defense, may underlie the
unique susceptibility of M.
tuberculosis to INH.
23. • inhibition of synthesis of mycolic acids which are unique fatty acid
components of mycobacterial cell wall.
• The lipid content of mycobacteria exposed to INH is reduced.
• Two gene products labelled ‘InhA’ and ‘KasA’, which function in
mycolic acid synthesis are the targets of INH action.
• INH enters sensitive mycobacteria which convert it by a catalase-
peroxidase enzyme into a reactive metabolite.
• This then forms adduct with NAD that inhibits InhA and KasA.
• The reactive INH metabolite forms adduct with NADP as well which
inhibits mycobacterial DHFRase resulting in interruption of DNA
synthesis.
24. pharmacokinetics
• It is extensively metabolized in liver; most important pathway being
N-acetylation by NAT2.
• The rate of INH acetylation shows genetic variation. There are
• either:
• Fast acetylators (30–40% of Indians) t½ of INH 1 hr.
• Slow acetylators (60–70% of Indians) t½ of INH 3 hr.
• The proportion of fast and slow acetylators differs in different parts
of the world.
• However, acetylator status does not matter if INH is taken daily, but
biweekly regimens are less effective in fast acetylators. Isoniazid
induced peripheral neuritis is more common in slow acetylators.
25. ADR
• Dosedependant toxic effect like Peripheral neuritis and a variety
of neurological manifestations (paresthesias, numbness, mental
disturbances, rarely convulsions)
• These are due to interference with production of the active
coenzyme pyridoxal phosphate from pyridoxine, and its increased
excretion in urine
• Pyridoxine given prophylactically (10 mg/day) prevents the
neurotoxicity even with higher doses.
• INH induced hepatotoxicity
26. pyrazinamide
• Pyrazinamide is inactive at neutral pH but
tuberculostatic at acid pH.
• It is effective against the intracellular
organisms in macrophages because, after
phagocytosis, the organisms are contained in
phagolysosomes where the pH is low.
• Resistance develops rather readily, but cross-
resistance with isoniazid does not occur.
27. • PZA is converted to
pyrazinoic acid (POA) by the
enzyme encoded by pncA.
Its ability to kill M.
tuberculosis and not
other Mycobacteria species
may be due to a selective
defect in POA efflux in M.
tuberculosis.
• Proposed targets include
the mycobacterial fatty acid
synthase 1 and disruption of
mycobacterial membranes
by acidic action.
28. ADR
• Hepatotoxicity. Daily dose is limited to 25–30
mg/kg
• Hyperuricaemia is common and is due to
inhibition of uric acid secretion in kidney: gout
can occur.
• Hyperuricaemia is common and is due to
inhibition of uric acid secretion in kidney: gout
can occur.
29. Ethambutol
• Ethambutol is selectively tuberculostatic and
is active against MAC as well as some other
mycobacteria, but not other types of bacteria.
• Resistance emerges rapidly if the drug is used
alone.
• Ethambutol is given orally and is well
absorbed.
• It can reach therapeutic concentrations in the
CSF in tuberculous meningitis.
30. • MOA
• The mechanism of action of E is not fully understood, but it has
been found to inhibit arabinosyl transferases (encoded by embAB
genes) involved in arabinogalactan synthesis thereby interfering
with mycolic acid incorporation in mycobacterial cell wall.
• Mechanism of resistance
• Resistance to E develops slowly and is most commonly associated
with mutation in embB gene, reducing the affinity of the target
enzyme for E.
• No cross resistance with any other antitubercular drug has been
noted
31. ADR
• Safe during pregnancy
• Dose and duration dependant toxicities-Loss
of visual acuity/colour vision, field defects due
to optic neuritis
• nausea, rashes, fever, rarely peripheral
neuritis,Hyperuricemia
32. Streptomycin (S)
• an aminoglycoside antibiotic, acts by inhibiting bacterial protein
synthesis.
• It is given intramuscularly.
• Unwanted effects are ototoxicity (mainly vestibular) and
nephrotoxicity.
• acts only on extracellular bacilli (because of poor penetration into
cells)
• Donot cross CSF
• Develop resistance when used alone
• Due to low margin of safety -Use is restricted to a maximum
of 2 months. It is thus also labelled as a ‘supplemental’ 1st line
drug.
33. Second line drugs
• 1. Kanamycin (Km), Amikacin (Am)- similar to streptomycin
• 2. Capreomycin (Cm)
• 3. Fluoroquinolones (FQs)
• 4. Ethionamide (Eto) –similar to INH
• 5. Prothionamide (Pto)-similar to Eto
• 6. Cycloserine (Cs)
• 7. Terizidone-contain 2 molecules of cycloserine
• 8. Para-amino salicylic acid (PAS)-similar to sulphonamides
• 9. Thiacetazone (Thz)-not understood
• 10. Rifabutin
34. Capreomycin(Cm)
• It is a cyclic peptide antibiotic, chemically very
different from aminoglycosides, but with similar
mycobactericidal activity, ototoxicity and
nephrotoxicity.
• Unwanted effects include kidney damage and
injury to the auditory
• nerve, with consequent deafness and ataxia.
• The drug should not be given at the same time as
streptomycin or other drugs that may cause
deafness.
35. Cycloserine (Cs)
• This polypeptide antibiotic obtained from S.orchidaceus is an
analogue of D-alanine.
• Accordingly, it inhibits bacterial cell well synthesis by inactivating
the enzymes which racemize L-alanine and link two D-alanine
residues.
• Cs is tuberculostatic; given as intramuscular injection
• inhibits MAC as well as some other gram-positive bacteria,
• Given orally, it penetrates the CSF.
• ADR-headache and irritability to depression, convulsions and
psychotic states.
• Its use is limited to tuberculosis that is resistant to other
drugs.
36. Biology of tubercular infection
• (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 and to a lesser extent to R,
E and S.
• (b) Slow growing located intracellularly (inside macrophages) and
at inflamed sites where pH is low. They are particularly vulnerable
to Z, while H, R and E are less active, and S is inactive.
• (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.
37. Goals of therapy
• (a) Kill dividing bacilli
• b) Kill persisting bacilli
• (c) Prevent emergence of resistance
38. DOTS or Directly Observed Treatment
Short course
• 1. Sustained political and financial committment.
• 2.Diagnosis by quality ensured sputum-smear microscopy.
• 3.Standardized short-course anti-TB treatment (SCC) given under
direct and supportive observation (DOT).
• 4.A regular, uninterrupted supply of high quality anti-TB
drugs.
• 5. Standardized recording and reporting.
39.
40. Multidrug-resistant (MDR) TB
• MDR-TB is defined as resistance to both H and
R, and may be any number of other (1st line)
• drug(s).
• MDR-TB has a more rapid course with
• worse outcomes.
• Its treatment requires complex multiple 2nd
line drug regimens which are longer, more
expensive and more toxic.
41.
42. Extensively drug-resistant TB
• These are MDR-TB cases that are also resistant
to FQs as well as one of the injectable 2nd line
drugs and may be any number of other drugs.
• The bacilli thus are resistant to at least 4 most
effective cidal drugs, viz. H,R,FQ and one of
Km/Am/Cm.
43. Mycobacterium avium complex (MAC)
infection
• MAC is an opportunistic pathogen which causes disseminated and
multifocal disease in immunocompromized (HIV-AIDS) patients.
• The disease develops when cell mediated immunity is markedly
depressed, i.e. when CD4 count drops to <50 cells/μL, HIV-RNA load
is high and other opportunistic infections
46. • Leprosy is a chronic, progressive bacterial
infection caused by the
bacterium Mycobacterium leprae.
• It primarily affects the nerves of the
extremities, the lining of the nose, and the
upper respiratory tract.
• Leprosy produces skin sores, nerve damage,
and muscle weakness.
47. Leprosy is caused by a slow-growing type of bacteria
called Mycobacterium leprae (M. leprae)
Also known as Hansen's disease, after the scientist ho
discovered M. leprae in 1873
It primarily affects the skin and the peripheral nerves
Long Incubation period (3 – 5 years)
49. The simplest, oldest, cheapest
MOA: Leprostatic even at low concentration
Chemically related to Sulfonamides – same mechanism –
inhibition of incorporation of PABA into folic acid (folic acid
synthase)
Specificity to M leprae – affinity for folate synthase
Activity: Used alone – resistance – MDT needed
Resistance – Primary and Secondary (mutation of folate synthase
– lower affinity)
However, 100 mg/day – high MIC -500 times and continued to be
effective to low and moderately resistant Bacilli (low % of resistant
patient) Persisters. Also has antiprotozoal action (Falciparum
and T. gondii)
50. Pharmacokinetics: Complete oral absorption and high
distribution (less CNS penetration) Half life 24-36 Hrs, but
cumulative
70% bound to plasma protein – concentrated in Skin, liver, muscle
and kidney
Acetylated and glucoronidated and sulfate conjugated –
enterohepatic circulation
ADRs: Generally Well tolerated drug
Haemolytic anaemia (oxidizing property) - G-6-PD are
more susceptible
Gastric - intolerance, nausea, gastritis
Methaemoglobinaemia, paresthesia, allergic rashes, FDE,
phototoxicity, exfoliative dermatitis and hepatotoxicity etc.
51. Active against protozoa
Combined with pyrimethamine alternative to
sulfadoxine-pyrimethamine for P.falciparum and
toxoplasma gondii infection
Active against Pneumocystis jirovecii
Also has anti-inflammatory property
52. Symptoms: Fever, malaise, lymph node enlargement,
desquamation of skin, jaundice and anemia
Starts after 4- 6 weeks of therapy, more common with
MDT
Management: stopping of Dapsone, corticosteroid
therapy
Dapsone contraindications: Severe anaemia and G-6-
PD deficiency
53. Phenazine dye – antileprotic, anti-inflammatory and
Bacteriostatic
MOA:
Interference with template function of DNA
Alteration of membrane structure and transport
Disruption of mitochondrial electron transport
Monotherapy causes resistance in 1 – 3 years
Dapsone resistants respond to Clofazimine
Kinetics: absorbed orally (70%) and gets deposited in
subcutaneous tissues – as crystals
Half life – 70 days
54. ADRs: well tolerated
Skin: Reddish-black discolouration of skin,
discolouration of hair and body secretions
Dryness of skin and troublesome itching,
phototoxicity, conjunctival pigmentation
GIT: Nausea, anorexia, abdominal pain and loose
stool (early and late) – dreaded enteritis
Contraindication: Early pregnancy, liver and kidney
diseases
55. Rifampicin: Cidal. 99.99% killed in 3-7 days, skin
symptoms regress within 2 months
Included in MDT to shorten the duration of
treatment and also to prevent resistance
No toxic dose as single dose only Should
not be used in ENL and Reversal
phenomenon
Ofloxacin: all fluoroquinolones except ciprofloxacin are
active. Used as alternative to Rifampicin
Minocycline: Lipophillic - enters M leprae. Less marked
effect than Rifampicin
56. Anti leprotic and anti tubercular
It is a fast acting drug than dapsone
But it is more expensive and more toxic
It is orally effective and it is administered daily
Poorly tolerated –hepatotoxicity
250mg/day
57. Only macrolide with activity against M. leprae
Less bactericidal than rifampin
Monotherapy- 500mg daily/ 8wks- 99.9% killing
Synergistic action with minocycline
Used in alternative MDT regimen
MINOCYCLINE
High lipophilicity –penetrates into M.leprae
100mg/day
Antileprotic activity rif>mino >Clari
8 wks treatment
58. The acute exacerbation which occurs during the course of leprosy
is called as lepra reaction
It occursin LL type- after starting with chemotherapy and
intercurrent infections
Jerish Hexheimer (Arthus) type reaction due to release of
antigens from killed bacilli
May be mild severe or life threatening
ENL- erythema Nodosum Leprosum
Treatment-clofazimine -200mg
Dapsone temporary withdrawal
Severe reaction- prednisone-40-60 mg.. Tapered in 2-3 months
Thalidomide –alternative to prednisolone in ENL
59. TT and BL cases
Manisfestation of delayed hypersensitivity to M.leprae
antigens
Cutaneous ulceration, multiple nerve involvement
with tender nerves
Treatment-Clofazimine/ corticosteroids