This document discusses antibiotics, including their sources, roles, mechanisms of action, and classifications. It describes the main types and classes of antibiotics, focusing on their targets in bacteria and how they inhibit critical processes like cell wall synthesis, protein synthesis, membrane function, and nucleic acid synthesis. Key points include: antibiotics can be naturally produced by microorganisms or synthetically produced, and are classified based on their structure, function, and spectrum of activity. The major classes discussed are inhibitors of cell wall synthesis (beta-lactams, glycopeptides, fosfomycins), protein synthesis (aminoglycosides, macrolides, tetracyclines), membrane function (polymyxins), antimetabolites
This document provides a summary of beta lactam and other cell wall- and membrane-active antibiotics. It discusses the history, structure, mechanisms of action, and classifications of penicillins and cephalosporins. It describes how these antibiotics inhibit the final step of bacterial cell wall synthesis and provides examples of specific antibiotics, their spectra of activity, and dosages. Adverse effects and mechanisms of resistance are also summarized.
This document summarizes beta lactam antibiotics and other cell wall-active antibiotics. It discusses the history, structure, mechanisms of action, and classifications of penicillins. It provides details on specific penicillins including their spectra of activity, pharmacokinetics, dosages and adverse effects. The document covers key classes of beta lactam antibiotics including penicillins, cephalosporins, carbapenems, and other cell wall synthesis inhibitors.
Antibiotics are chemical substances that kill or inhibit the growth of microorganisms. They can be classified based on their source (natural, semisynthetic, synthetic), spectrum of activity (broad or narrow), or mechanism of action. Common mechanisms include inhibition of cell wall synthesis, protein synthesis, nucleic acid synthesis, and cell membrane function. Examples provided include penicillins, cephalosporins, carbapenems, glycopeptides, aminoglycosides, macrolides, quinolones, sulfonamides, and metronidazole.
This document discusses the classification and mechanisms of action of antibiotics. It covers several key topics:
1. Antibiotics can be classified based on their chemical structure or mechanism of action. Major classes include beta-lactams, quinolones, sulfonamides, and glycopeptides.
2. Antibiotics have selective toxicity toward bacteria and not the host. Their therapeutic index and whether they are bactericidal or bacteriostatic are important properties.
3. Antibiotics can inhibit protein synthesis, nucleic acid synthesis, cell wall synthesis, or disrupt the bacterial cell membrane. They have different targets within each of these pathways.
4. Resistance can arise through mutation, acquisition of
1. The document discusses various antibiotics and their mechanisms of action on bacterial cells, focusing on how they inhibit important metabolic processes.
2. Key antibiotic classes are described that inhibit cell wall synthesis, protein synthesis, DNA replication, and folic acid biosynthesis. Examples like penicillins, aminoglycosides, fluoroquinolones, and sulfonamides are provided.
3. The major sites of antibiotic action discussed are the bacterial cell wall, cytoplasmic membrane, DNA, ribosomes, and metabolic pathways. How each antibiotic class interferes with these sites is explained.
This document discusses the classification and mechanisms of action of antibiotics. It covers several key points:
1) Antibiotics are classified based on their chemical structure and mechanism of action, including classes like β-lactams, quinolones, sulfonamides, and glycopeptides.
2) Antibiotics can have bactericidal or bacteriostatic effects and act by inhibiting protein synthesis, nucleic acid synthesis, cell wall synthesis, or by disrupting the cell membrane.
3) Resistance can develop through mutations altering the antibiotic target, acquisition of extrachromosomal DNA conferring resistance, or efflux pump mechanisms expelling antibiotics.
This document provides a summary of beta lactam and other cell wall- and membrane-active antibiotics. It discusses the history, structure, mechanisms of action, and classifications of penicillins and cephalosporins. It describes how these antibiotics inhibit the final step of bacterial cell wall synthesis and provides examples of specific antibiotics, their spectra of activity, and dosages. Adverse effects and mechanisms of resistance are also summarized.
This document summarizes beta lactam antibiotics and other cell wall-active antibiotics. It discusses the history, structure, mechanisms of action, and classifications of penicillins. It provides details on specific penicillins including their spectra of activity, pharmacokinetics, dosages and adverse effects. The document covers key classes of beta lactam antibiotics including penicillins, cephalosporins, carbapenems, and other cell wall synthesis inhibitors.
Antibiotics are chemical substances that kill or inhibit the growth of microorganisms. They can be classified based on their source (natural, semisynthetic, synthetic), spectrum of activity (broad or narrow), or mechanism of action. Common mechanisms include inhibition of cell wall synthesis, protein synthesis, nucleic acid synthesis, and cell membrane function. Examples provided include penicillins, cephalosporins, carbapenems, glycopeptides, aminoglycosides, macrolides, quinolones, sulfonamides, and metronidazole.
This document discusses the classification and mechanisms of action of antibiotics. It covers several key topics:
1. Antibiotics can be classified based on their chemical structure or mechanism of action. Major classes include beta-lactams, quinolones, sulfonamides, and glycopeptides.
2. Antibiotics have selective toxicity toward bacteria and not the host. Their therapeutic index and whether they are bactericidal or bacteriostatic are important properties.
3. Antibiotics can inhibit protein synthesis, nucleic acid synthesis, cell wall synthesis, or disrupt the bacterial cell membrane. They have different targets within each of these pathways.
4. Resistance can arise through mutation, acquisition of
1. The document discusses various antibiotics and their mechanisms of action on bacterial cells, focusing on how they inhibit important metabolic processes.
2. Key antibiotic classes are described that inhibit cell wall synthesis, protein synthesis, DNA replication, and folic acid biosynthesis. Examples like penicillins, aminoglycosides, fluoroquinolones, and sulfonamides are provided.
3. The major sites of antibiotic action discussed are the bacterial cell wall, cytoplasmic membrane, DNA, ribosomes, and metabolic pathways. How each antibiotic class interferes with these sites is explained.
This document discusses the classification and mechanisms of action of antibiotics. It covers several key points:
1) Antibiotics are classified based on their chemical structure and mechanism of action, including classes like β-lactams, quinolones, sulfonamides, and glycopeptides.
2) Antibiotics can have bactericidal or bacteriostatic effects and act by inhibiting protein synthesis, nucleic acid synthesis, cell wall synthesis, or by disrupting the cell membrane.
3) Resistance can develop through mutations altering the antibiotic target, acquisition of extrachromosomal DNA conferring resistance, or efflux pump mechanisms expelling antibiotics.
- Penicillins are a major class of antibiotics that were the first discovered from the mold Penicillium. They work by inhibiting the final step of bacterial cell wall synthesis through binding to penicillin-binding proteins. This disrupts cell wall formation and causes cell lysis.
- There are different generations/classes of penicillins that vary in their spectra of activity and resistance to bacterial beta-lactamases. Oral forms are absorbed from the gastrointestinal tract while injectable forms provide more sustained drug levels. Adverse effects include hypersensitivity reactions and gastrointestinal issues.
The document provides an overview of medical microbiology and bacteriology. It discusses various gram-positive and gram-negative cocci and their associated diseases. It then reviews the sites of antibiotic action in bacteria, including inhibition of cell wall synthesis by beta-lactams, cell membrane disruption by polymyxins, DNA inhibition by quinolones and metronidazole, inhibition of transcription by actinomycin D and rifampin, and inhibition of translation in the bacterial ribosome by various antibiotics classes that bind to the 30S or 50S subunits. It also discusses competitive antagonistic antibiotics that inhibit metabolic pathways like isoniazid, sulfonamides, and trimethoprim.
The document summarizes key information about penicillin, including its history of discovery, structure, mechanisms of action, resistance, pharmacokinetics, uses, and adverse effects. Penicillin was the first antibiotic discovered from mold and works by inhibiting bacterial cell wall synthesis. It binds to penicillin-binding proteins and inhibits the final transpeptidation step in peptidoglycan synthesis, disrupting cell wall formation.
This document defines chemotherapy and provides information on antimicrobial drugs. It discusses the mechanisms of action, spectra, and examples of various classes of antibacterial, antiviral, antifungal, antiparasitic, and antihelminthic drugs. The key classes covered include sulfonamides, fluoroquinolones, penicillins, cephalosporins, aminoglycosides, tetracyclines, chloramphenicol, macrolides, and more. It also addresses bacterial resistance mechanisms, drug combinations, and treatment of specific infections like HIV.
This document discusses antimicrobial agents and antibiotic resistance. It defines antimicrobial agents as chemicals that treat infectious diseases by inhibiting or killing pathogens. Ideal antimicrobial agents kill or inhibit pathogens without harming the host. The document then discusses different classes of antibiotics including their sources, mechanisms of action, and examples. It covers antibiotics that inhibit cell wall synthesis, cell membrane function, protein synthesis, and nucleic acid synthesis. The document concludes by discussing intrinsic and acquired antibiotic resistance in bacteria.
This document discusses the history and definitions of antibiotics and chemotherapeutic agents. It begins by defining antibiotics as chemical substances produced by microorganisms that inhibit other microorganisms at low concentrations. The document then summarizes the history of antibiotics, including the discoveries of Paul Ehrlich, Gerhard Domagk, Alexander Fleming, and Selman Waksman. It also outlines the ideal properties of antimicrobial drugs and describes various antibiotic mechanisms of action, including inhibition of protein synthesis, DNA/RNA synthesis, and cell wall synthesis. The clinical uses and susceptibility testing of antibiotics are briefly discussed.
This document discusses objectives and research questions related to determining the minimum inhibitory concentration (MIC) values for various bacteria using antibiotic susceptibility testing. It aims to identify how disc susceptibility tests can be used in the antibiotic drug discovery process. It also provides background on bacterial cell anatomy, classifications of antibiotics by their mechanisms of action including targeting cell walls, protein biosynthesis, DNA replication, and folic acid metabolism. Mechanisms of antibiotic resistance for bacteria include reduced outer membrane permeability, efflux pumps, target molecule modification, and enzymatic inactivation or modification of antibiotics.
1. The document discusses various classes of beta-lactam antibiotics including penicillins, cephalosporins, carbapenems, and their structure, classification, mechanism of action, clinical uses, and key points.
2. Penicillins are the most widely used beta-lactam antibiotics and work by inhibiting the synthesis of peptidoglycan in bacterial cell walls. Cephalosporins are broader spectrum and more resistant to beta-lactamases than penicillins.
3. Carbapenems have a very broad antibacterial spectrum and high resistance to beta-lactamases, making them effective against many drug-resistant bacteria.
biosynthesis of the cell wall and antibioticsSafaFallah
the cell wall description and the difference between the gram positive and negative bacteria and the structure of peptidoglycan and the biosynthesis of the cell wall (peptidoglycan) in bacteria and the end is with some groups of antibiotics that inhibit the synthesis of peptidoglycan in different ways and targets the bacteria.
This document discusses antimicrobials and antimicrobial resistance. It covers several topics:
1. It defines antimicrobial compounds and describes their importance in treating infections and medical procedures. However, it notes the need to understand resistance mechanisms.
2. It describes several classes of antibiotics including beta-lactams, aminoglycosides, fluoroquinolones, macrolides, tetracyclines, and glycopeptides. It explains their mechanisms of action.
3. It discusses antimicrobial susceptibility testing methods including manual, semi-automated, and automated methods and covers topics like interpretive criteria and quality control.
4. It mentions the diminishing pipeline of new drugs and drivers of antimicrobial
This document discusses various classes of antibiotics and their mechanisms of action. It describes five main mechanisms: inhibition of cell wall synthesis, inhibition of cell membrane function, inhibition of protein synthesis, and inhibition of nucleic acid synthesis. For each mechanism, it provides examples of antibiotic classes that act through that mechanism, such as beta-lactams that inhibit cell wall synthesis and aminoglycosides that inhibit protein synthesis. It also describes the sources, spectra of activity, and modes of action for many individual antibiotic drugs.
medicines used to treat bacterial infectionsbahati_jr
This document summarizes different classes of anti-bacterial agents based on their mechanism of action. It discusses four main classes: 1) cell wall synthesis inhibitors like beta-lactams and vancomycin, 2) inhibitors of cell membrane function like polymyxins, 3) inhibitors of nucleic acid synthesis like sulfonamides and quinolones, and 4) inhibitors of protein synthesis like aminoglycosides, tetracyclines, chloramphenicol, and macrolides. Specific drugs in each class are described along with their mechanisms, spectra of activity, routes of administration, and common side effects.
This document discusses cephalosporins, a class of antibiotics. It begins with a brief history, noting their discovery from fungi in 1948. It describes their chemistry, including their beta-lactam ring structure similar to penicillin. Generations of cephalosporins are defined based on their antimicrobial spectrum and chronological development. The document outlines the pharmacokinetics and pharmacodynamics of cephalosporins, including their mechanism of action inhibiting bacterial cell wall synthesis and development of antimicrobial resistance. It summarizes the first through fifth generations in terms of their structures, spectra of activity, and clinical uses.
This document discusses antimicrobial agents and antibiotics. It defines antimicrobial agents as chemicals that treat infectious diseases by inhibiting or killing pathogens. Ideal antimicrobial agents kill or inhibit pathogens, are not harmful to the host, cause no allergic reactions, and remain effective after storage and in tissues. The document then discusses different classes of antibiotics based on their source, mechanism of action, and targets, including cell wall synthesis inhibitors like penicillin and vancomycin, protein synthesis inhibitors like tetracyclines and chloramphenicol, and nucleic acid synthesis inhibitors like sulfonamides. It also addresses resistance acquisition through intrinsic, mutational or acquired genetic means.
This document discusses antimicrobial agents and antibiotics. It defines antimicrobial agents as chemicals that treat infectious diseases by inhibiting or killing pathogens. Ideal qualities of antimicrobial agents are listed. Antibiotics are defined as substances derived from microorganisms or produced synthetically that destroy or limit microbial growth. Various classifications of antibiotics are described based on their source, spectrum of activity, route of administration, and mechanism of action. The major mechanisms of action discussed are inhibition of cell wall synthesis, cell membrane function, protein synthesis, and nucleic acid synthesis. Bacterial resistance both intrinsic and acquired is also summarized.
The document provides an overview of antibiotics, including their mechanisms of action, targets in bacterial cells, and factors to consider when choosing an antibiotic. It discusses several classes of antibiotics in detail, including beta-lactams (penicillins, cephalosporins, monobactams, and carbapenems), summarizing their spectrum of activity, side effects, bioavailability, metabolism, and resistance mechanisms. The document is intended to teach medical students about appropriate antibiotic usage and selection.
Beta-lactam antibiotics like penicillin and cephalosporins act by inhibiting the synthesis of peptidoglycan in the bacterial cell wall. They do this by binding to penicillin-binding proteins and blocking the final cross-linking step of peptidoglycan synthesis. Bacteria can develop resistance through beta-lactamase production or modifications of penicillin-binding proteins. Newer drugs and beta-lactamase inhibitors have been developed to counteract resistance mechanisms. Common side effects include diarrhea and hypersensitivity reactions.
Penicillin and other beta-lactam antibiotics work by inhibiting the penicillin-binding proteins (PBPs) involved in bacterial cell wall synthesis. This disrupts cell wall formation and causes cell lysis and death. While effective against many gram-positive and some gram-negative bacteria, resistance can develop through beta-lactamase production or modifications of PBPs. Different penicillins have varying spectra of activity, pharmacokinetic properties, and resistance profiles that determine their clinical applications.
This document discusses different classes of diuretic drugs, including their mechanisms of action, examples, and side effects. The main classes covered are:
1. Salidiuretics (thiazides) such as hydrochlorothiazide which increase sodium and chloride excretion in the distal renal tubules.
2. Loop diuretics such as furosemide which act on the ascending limb of Henle's loop to increase excretion of sodium, chloride, magnesium and calcium.
3. Carbonic anhydrase inhibitors like acetazolamide which inhibit the enzyme carbonic anhydrase in the kidneys and other tissues.
4. Potassium-sparing diuretics including sp
Three types of anti-diabetic drugs are discussed:
1) Drugs that enhance insulin secretion like sulfonylureas and meglitinide analogues.
2) Biguanides like metformin that overcome insulin resistance.
3) Miscellaneous drugs that include alpha-glucosidase inhibitors and SGLT2 inhibitors.
The document provides details on the mechanisms of action, examples of drugs, and side effects of the different classes of anti-diabetic medications.
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Similar to antibioticsmechanismsofactions-150428084652-conversion-gate02.pdf
- Penicillins are a major class of antibiotics that were the first discovered from the mold Penicillium. They work by inhibiting the final step of bacterial cell wall synthesis through binding to penicillin-binding proteins. This disrupts cell wall formation and causes cell lysis.
- There are different generations/classes of penicillins that vary in their spectra of activity and resistance to bacterial beta-lactamases. Oral forms are absorbed from the gastrointestinal tract while injectable forms provide more sustained drug levels. Adverse effects include hypersensitivity reactions and gastrointestinal issues.
The document provides an overview of medical microbiology and bacteriology. It discusses various gram-positive and gram-negative cocci and their associated diseases. It then reviews the sites of antibiotic action in bacteria, including inhibition of cell wall synthesis by beta-lactams, cell membrane disruption by polymyxins, DNA inhibition by quinolones and metronidazole, inhibition of transcription by actinomycin D and rifampin, and inhibition of translation in the bacterial ribosome by various antibiotics classes that bind to the 30S or 50S subunits. It also discusses competitive antagonistic antibiotics that inhibit metabolic pathways like isoniazid, sulfonamides, and trimethoprim.
The document summarizes key information about penicillin, including its history of discovery, structure, mechanisms of action, resistance, pharmacokinetics, uses, and adverse effects. Penicillin was the first antibiotic discovered from mold and works by inhibiting bacterial cell wall synthesis. It binds to penicillin-binding proteins and inhibits the final transpeptidation step in peptidoglycan synthesis, disrupting cell wall formation.
This document defines chemotherapy and provides information on antimicrobial drugs. It discusses the mechanisms of action, spectra, and examples of various classes of antibacterial, antiviral, antifungal, antiparasitic, and antihelminthic drugs. The key classes covered include sulfonamides, fluoroquinolones, penicillins, cephalosporins, aminoglycosides, tetracyclines, chloramphenicol, macrolides, and more. It also addresses bacterial resistance mechanisms, drug combinations, and treatment of specific infections like HIV.
This document discusses antimicrobial agents and antibiotic resistance. It defines antimicrobial agents as chemicals that treat infectious diseases by inhibiting or killing pathogens. Ideal antimicrobial agents kill or inhibit pathogens without harming the host. The document then discusses different classes of antibiotics including their sources, mechanisms of action, and examples. It covers antibiotics that inhibit cell wall synthesis, cell membrane function, protein synthesis, and nucleic acid synthesis. The document concludes by discussing intrinsic and acquired antibiotic resistance in bacteria.
This document discusses the history and definitions of antibiotics and chemotherapeutic agents. It begins by defining antibiotics as chemical substances produced by microorganisms that inhibit other microorganisms at low concentrations. The document then summarizes the history of antibiotics, including the discoveries of Paul Ehrlich, Gerhard Domagk, Alexander Fleming, and Selman Waksman. It also outlines the ideal properties of antimicrobial drugs and describes various antibiotic mechanisms of action, including inhibition of protein synthesis, DNA/RNA synthesis, and cell wall synthesis. The clinical uses and susceptibility testing of antibiotics are briefly discussed.
This document discusses objectives and research questions related to determining the minimum inhibitory concentration (MIC) values for various bacteria using antibiotic susceptibility testing. It aims to identify how disc susceptibility tests can be used in the antibiotic drug discovery process. It also provides background on bacterial cell anatomy, classifications of antibiotics by their mechanisms of action including targeting cell walls, protein biosynthesis, DNA replication, and folic acid metabolism. Mechanisms of antibiotic resistance for bacteria include reduced outer membrane permeability, efflux pumps, target molecule modification, and enzymatic inactivation or modification of antibiotics.
1. The document discusses various classes of beta-lactam antibiotics including penicillins, cephalosporins, carbapenems, and their structure, classification, mechanism of action, clinical uses, and key points.
2. Penicillins are the most widely used beta-lactam antibiotics and work by inhibiting the synthesis of peptidoglycan in bacterial cell walls. Cephalosporins are broader spectrum and more resistant to beta-lactamases than penicillins.
3. Carbapenems have a very broad antibacterial spectrum and high resistance to beta-lactamases, making them effective against many drug-resistant bacteria.
biosynthesis of the cell wall and antibioticsSafaFallah
the cell wall description and the difference between the gram positive and negative bacteria and the structure of peptidoglycan and the biosynthesis of the cell wall (peptidoglycan) in bacteria and the end is with some groups of antibiotics that inhibit the synthesis of peptidoglycan in different ways and targets the bacteria.
This document discusses antimicrobials and antimicrobial resistance. It covers several topics:
1. It defines antimicrobial compounds and describes their importance in treating infections and medical procedures. However, it notes the need to understand resistance mechanisms.
2. It describes several classes of antibiotics including beta-lactams, aminoglycosides, fluoroquinolones, macrolides, tetracyclines, and glycopeptides. It explains their mechanisms of action.
3. It discusses antimicrobial susceptibility testing methods including manual, semi-automated, and automated methods and covers topics like interpretive criteria and quality control.
4. It mentions the diminishing pipeline of new drugs and drivers of antimicrobial
This document discusses various classes of antibiotics and their mechanisms of action. It describes five main mechanisms: inhibition of cell wall synthesis, inhibition of cell membrane function, inhibition of protein synthesis, and inhibition of nucleic acid synthesis. For each mechanism, it provides examples of antibiotic classes that act through that mechanism, such as beta-lactams that inhibit cell wall synthesis and aminoglycosides that inhibit protein synthesis. It also describes the sources, spectra of activity, and modes of action for many individual antibiotic drugs.
medicines used to treat bacterial infectionsbahati_jr
This document summarizes different classes of anti-bacterial agents based on their mechanism of action. It discusses four main classes: 1) cell wall synthesis inhibitors like beta-lactams and vancomycin, 2) inhibitors of cell membrane function like polymyxins, 3) inhibitors of nucleic acid synthesis like sulfonamides and quinolones, and 4) inhibitors of protein synthesis like aminoglycosides, tetracyclines, chloramphenicol, and macrolides. Specific drugs in each class are described along with their mechanisms, spectra of activity, routes of administration, and common side effects.
This document discusses cephalosporins, a class of antibiotics. It begins with a brief history, noting their discovery from fungi in 1948. It describes their chemistry, including their beta-lactam ring structure similar to penicillin. Generations of cephalosporins are defined based on their antimicrobial spectrum and chronological development. The document outlines the pharmacokinetics and pharmacodynamics of cephalosporins, including their mechanism of action inhibiting bacterial cell wall synthesis and development of antimicrobial resistance. It summarizes the first through fifth generations in terms of their structures, spectra of activity, and clinical uses.
This document discusses antimicrobial agents and antibiotics. It defines antimicrobial agents as chemicals that treat infectious diseases by inhibiting or killing pathogens. Ideal antimicrobial agents kill or inhibit pathogens, are not harmful to the host, cause no allergic reactions, and remain effective after storage and in tissues. The document then discusses different classes of antibiotics based on their source, mechanism of action, and targets, including cell wall synthesis inhibitors like penicillin and vancomycin, protein synthesis inhibitors like tetracyclines and chloramphenicol, and nucleic acid synthesis inhibitors like sulfonamides. It also addresses resistance acquisition through intrinsic, mutational or acquired genetic means.
This document discusses antimicrobial agents and antibiotics. It defines antimicrobial agents as chemicals that treat infectious diseases by inhibiting or killing pathogens. Ideal qualities of antimicrobial agents are listed. Antibiotics are defined as substances derived from microorganisms or produced synthetically that destroy or limit microbial growth. Various classifications of antibiotics are described based on their source, spectrum of activity, route of administration, and mechanism of action. The major mechanisms of action discussed are inhibition of cell wall synthesis, cell membrane function, protein synthesis, and nucleic acid synthesis. Bacterial resistance both intrinsic and acquired is also summarized.
The document provides an overview of antibiotics, including their mechanisms of action, targets in bacterial cells, and factors to consider when choosing an antibiotic. It discusses several classes of antibiotics in detail, including beta-lactams (penicillins, cephalosporins, monobactams, and carbapenems), summarizing their spectrum of activity, side effects, bioavailability, metabolism, and resistance mechanisms. The document is intended to teach medical students about appropriate antibiotic usage and selection.
Beta-lactam antibiotics like penicillin and cephalosporins act by inhibiting the synthesis of peptidoglycan in the bacterial cell wall. They do this by binding to penicillin-binding proteins and blocking the final cross-linking step of peptidoglycan synthesis. Bacteria can develop resistance through beta-lactamase production or modifications of penicillin-binding proteins. Newer drugs and beta-lactamase inhibitors have been developed to counteract resistance mechanisms. Common side effects include diarrhea and hypersensitivity reactions.
Penicillin and other beta-lactam antibiotics work by inhibiting the penicillin-binding proteins (PBPs) involved in bacterial cell wall synthesis. This disrupts cell wall formation and causes cell lysis and death. While effective against many gram-positive and some gram-negative bacteria, resistance can develop through beta-lactamase production or modifications of PBPs. Different penicillins have varying spectra of activity, pharmacokinetic properties, and resistance profiles that determine their clinical applications.
Similar to antibioticsmechanismsofactions-150428084652-conversion-gate02.pdf (20)
This document discusses different classes of diuretic drugs, including their mechanisms of action, examples, and side effects. The main classes covered are:
1. Salidiuretics (thiazides) such as hydrochlorothiazide which increase sodium and chloride excretion in the distal renal tubules.
2. Loop diuretics such as furosemide which act on the ascending limb of Henle's loop to increase excretion of sodium, chloride, magnesium and calcium.
3. Carbonic anhydrase inhibitors like acetazolamide which inhibit the enzyme carbonic anhydrase in the kidneys and other tissues.
4. Potassium-sparing diuretics including sp
Three types of anti-diabetic drugs are discussed:
1) Drugs that enhance insulin secretion like sulfonylureas and meglitinide analogues.
2) Biguanides like metformin that overcome insulin resistance.
3) Miscellaneous drugs that include alpha-glucosidase inhibitors and SGLT2 inhibitors.
The document provides details on the mechanisms of action, examples of drugs, and side effects of the different classes of anti-diabetic medications.
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X-linked diseases are caused by mutations on the X chromosome. There are two main types: X-linked dominant and X-linked recessive diseases. X-linked dominant diseases affect both males and females and are passed from father to all daughters. X-linked recessive diseases mainly affect males and a carrier mother will pass the disease to all sons. Common X-linked diseases include color blindness, hemophilia, and Duchenne muscular dystrophy. While there are some treatment options, prevention through not having children or prenatal gene therapy may be the best approach for inherited X-linked conditions.
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Rheumatoid arthritis is a chronic inflammatory disease that commonly causes pain, stiffness, and swelling in the joints. It is characterized by symmetrical inflammation of multiple joints that can lead to joint deformity and damage over time. While there is no cure, treatment aims to reduce inflammation and pain, slow joint damage, and improve quality of life through medications, surgery, exercise, and splinting of joints.
This document discusses complications that can arise from fractures, classified as either immediate, early, or late complications. Immediate complications include hypovolemic shock from blood loss. Early local complications involve injuries to soft tissues, blood vessels, organs, nerves. Conditions like haemarthrosis, compartment syndrome, and infections are also discussed. Systemic early complications include fat embolism, DVT, ARD, pneumonia and sepsis. Late complications result from imperfect fracture healing and include non-union, malunion, avascular necrosis and osteoarthritis. Treatment options focus on relieving pressure, debriding tissues, and stabilizing fractures with fixation and bone grafts.
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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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.
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.
2. What are Antibiotics?
Antibiotics: chemical substances produced by
microorganisms that inhibits the growth or kills other
microorganisms
Antimicrobial agents: chemical substances from a
biological source or produced by chemical synthesis
that kills or inhibits the growth of microorganisms.
3. Sources of Antibiotics
Natural : mainly fungal sources (e.g Benzylpenicillin
and Gentamycin)
Semi synthetic: chemically altered natural compound
(e.g Ampicillin & Amikacin).
Synthetic: chemically designed in the lab (e.g
Moxifloxacin and Norfloxacin).
4. What are the Roles of Antibiotics?
Bacteriostatic effect: To inhibit multiplication
@ [drug] = MIC minimal inhibitory concentration.
Bactericidal effect: To kill (destroy) the bacteria
population
@ [drug] = MBC minimal bactericidal concentration.
There is a much closer relationship between the MIC
and MBC values for bactericidal drugs than for
bacteriostatic drugs.
5. Principle of Selective toxicity: What
is an ideal Antibacterial?
Selective target – target unique
Bactericidal – kills
Narrow spectrum – does not kill normal flora
High therapeutic index – ratio of toxic level to
therapeutic level
Few adverse reactions – toxicity, allergy
Various routes of administration – IV, IM, oral
Good absorption
Good distribution to site of infection
Emergence of resistance is slow
6. Antibiotics classification
Antibiotics are usually classified based on their structure , Function and/or spectrum of
activity
1. Structure - molecular structure.
ß-Lactams - Beta-lactam ring
Aminoglycosides - vary only by side chains attached to basic structure
2. Function - how the drug works, its mode of action.
5 functional groups
These are all components or functions necessary for bacterial growth
Targets for antibiotics:
Inhibitors of cell wall synthesis
Inhibitors of protein synthesis
Inhibitors of membrane function
Anti-metabolites
Inhibitors of nucleic acid synthesis
3. Spectrum of Activity:
Narrow spectrum
Broad Spectrum
In these discussions, we will primarily use the functional classification, but will point out where
8. Inhibitors of Cell Wall Synthesis:
The Penicillins
1928 - Alexander Fleming
Bread mold (Penicillin notatum) growing on petri dish
1939 - Florey, Chain, and Associates
Began work on isolating and synthesizing large amounts
of Penicillin.
1944 - Used in WWII to treat infections
Late 1940’s - available for general use in US
Penicillins as well as cephalosporins are called beta-lactam
antibiotics and are characterized by three fundamental
structural requirements:
the fused beta-lactam structure (shown in the blue
and red rings,
a free carboxyl acid group (shown in red bottom
right),
one or more substituted amino acid side chains
(shown in black).
The lactam structure can also be viewed as the
covalent bonding of pieces of two amino acids -
cysteine (blue) and valine (red).
The beta-lactam nucleus itself is the chief structural
requirement for biological activity;
metabolic transformation or chemical alteration of this
portion of the molecule causes loss of all significant
antibacterial activity Figure 1: beta lactam structure
10. Mechanism of Actions of Beta
lactams
All penicillin derivatives produce their bacteriocidal
effects by inhibition of bacterial cell wall synthesis.
Specifically, the cross linking of peptides on the
mucosaccharide chains is prevented. If cell walls are
improperly made cell walls allow water to flow into the
cell causing it to burst.
11. Bacteria Cell Wall Synthesis
The cell walls of bacteria are essential for their normal
growth and development.
The peptidoglycan (which provide rigid mechanical
stability) is composed of glycan chains, which are
linear strands of two alternating amino sugars (N-
acetylglucosamine and N-acetylmuramic acid) that are
cross-linked by peptide chains. (NAG-NAM).
In gram-positive microorganisms, the cell wall is 50 to
100 molecules thick, but it is only 1 or 2 molecules
thick in gram-negative bacteria
12. Bacteria Cell Wall Synthesis (cont)
The biosynthesis of the peptidoglycan involves about 30 bacterial enzymes and
may be considered in three stages.
The first stage is precursor formation in the cytoplasm. The product, uridine diphosphate
(UDP)-acetylmuramyl-pentapeptide, called a "Park nucleotide“.
The last reaction in the synthesis of this compound is the addition of a dipeptide, D-
alanyl-D-alanine.
The second stage, UDP-acetylmuramyl-pentapeptide and UDP-acetylglucosamine are
linked to form a long polymer.
The third and final stage involves the completion of the cross-link. This is accomplished by
a transpeptidation reaction that occurs outside the cell membrane. The transpeptidase
itself is membrane bound. The terminal glycine residue of the pentaglycine bridge is
linked to the fourth residue of the pentapeptide (D-alanine), releasing the fifth residue
(also D-alanine).
Penicillin binds at the active site of the transpeptidase enzyme that cross-links the
peptidoglycan strands. It does this by mimicking the D-alanyl-D-alanine residues that
would normally bind to this site. Penicillin irreversibly inhibits the enzyme transpeptidase
by reacting with a serine residue in the transpeptidase. This reaction is irreversible and so
the growth of the bacterial cell wall is inhibited.
13. Bacteria Cell Wall Synthesis (cont):
The PBPs and Binding of Penicillins
Related targets of penicillins and cephalosporins collectively termed penicillin-
binding proteins (PBPs)
PBPs functions are diverse: catalyze the transpeptidase reaction, maintam
shape, forms septums during division, Inhibit autolytic enzymes.
Binding to PBPs results in:
Inhibition of transpeptidase: transpeptidase catalyzes the cross-linking
of the pentaglycine bridge with the fourth residue (D-Ala) of the
pentapeptide. The fifth reside (also D-Ala) is released during this reaction.
Spheroblasts are formed.
Structural irregularities: binding to PBPs may result in abnormal
elongation, abnormal shape, cell wall defects.
14. Figure 3. The transpeptidase reaction in Staphylococcus
aureus that is inhibited by penicillins and cephalosporins.
15. Figure 4. Comparison of the structure and composition of
gram-positive and gram-negative cell walls.
16. Other Inhibitors of Cell Wall
Synthesis:
Glycopeptide
Include two compounds with similar structures;
Vancomycin and Teicoplanin
Teicoplanin not FDA approved in the U.S.
Both are of high molecular weight (1500-2000 daltons)
Glycopeptides have a complex chemical structure
Inhibit cell wall synthesis at a site different than the
beta-lactams
All are bactericidal
All used for Gram-positive infections. (No Gram-
negative activity)
Pharmaceutical research and development has been
very active in this area recently resulting in new
antimicrobials and classification
In Gram-Positives: The drugs enter without any problem
because peptidoglycan does not act as a barrier for the
diffusion of these molecules.
In Gram-Negatives: Glycopeptides are of high molecular
weight (1500-2000 daltons), stopping them from passing
through the porins of gram-negative bacteria (i.e.,
glycopeptides have no activity against Gram-negatives).
Vancomyci
n
17. Other Inhibitors of Cell Wall
Synthesis:
Glycopeptide
MOA
Glycopeptides inhibit the final cell wall stage of the
peptidoglycan synthesis process
The ‘pocket-shaped’ glycopeptide binds the D-ala-D-ala
terminal of the basic sub-unit theoretically waiting to be
incorporated into the growing peptidoglycan
Because it is so bulky, the glycopeptide inhibits the action of
the glycosyltransferases and transpeptidases (which act as a
kind of “cement”) - blocks pentaglycine from joining
molecules, thereby blocking peptidoglycan growth.
Glycopeptides are bactericidal, but slow-acting
18. Other Inhibitors of Cell Wall
Synthesis:
Fosfomycins
Spectrum of Action
Fosfomycin: Acts to inhibit cell wall synthesis at a stage
earlier than the penicillins or cephalosporins. FDA
approved 1996.
It is a broad spectrum agent
Mode of Action:
Inhibits the first step of the peptidoglycan synthesis
process (Actual step of inhibition is not completely
understood)
19. 2. Inhibitors of Protein Synthesis
Aminoglycosides -(Bactericidal) : Gentamicin, Tobramycin, Amikacin
MLSK (Macrolides, Lincosamides, Streptogramins, Ketolides) (Bacteriostatic) –
Erythromycin, Clindamycin, Quinupristin-Dalfopristin (Synercid), Clarithromycin,
Azithromycin, Telithromycin
Tetracyclines (Bacteriostatic) – Tetracycline, Doxycycline, Minocycline
Glycylcyclines - Tigecycline
Phenocols (Bacteriostatic), Chloramphenicol
Oxazolidinones – Linezolid (Bactericidal for Streptococci; Bacteriostatic for Enterococcus
and Staphylococci)
Ansamycins - Rifampin
(Bacteriostatic or Bactericidal depending on organism and concentration)
20. Inhibitors of Protein Synthesis
These classes interferes with ribosomes
Most are bacteriostatic
Resistance to tetracycline and Macrolide is common.
22. Tetracyclines
Analogs; Doxycycline Minocycline, and Tigecycline
Enter microorganisms in part by passive diffussion, and in
part by active transport
Binds to 30S subunits & blocks the binding of amino acyl
tRNA to the acceptor site on the mRNA-ribosome complex.
Active against; many gram+ve & gram –ve, rickettsiae,
chlamydiae, mycoplasmas.
23. Macrolides
Characterized by Macrocyclic lactone rings + deoxy sugars
Prototype: Erythromycin (from streptomyces erythreus)
Semisynthetic derivatives: clarithramycin , ketolides and azithromycin
Inhibit 50S ribosomal RNA near peptidyl transferase centre, thereby preventing peptide
chain elongation by blocking of polypeptide exit tunnel. As a result,m pepidyl tRNA is
dissociated from the ribosome
Active against: pneumococci, streptococci, staphylococci, H. Pyroli, Ricketssia spp,
chlamydia spp
Hemophilus influenza and Campylobacter are less susceptible
Resistances: Usually plasmic encoded, reduced permeability of membrane, active efflux,
or by production of esterases (by enterobaceriaceae) that hydrolyzes macrolides
Action of clindamycin and streptogramins is related to that of erythromycin
24. Chloramphenicol
Chloramphenicol binds reversibly to the 50S subunit
of the bacterial ribosome and inhibit peptide bond
formation
Bacteriostatic broad-spectrum antibiotic that is active
against both aerobic and anaerobic gram +ve & gram -
ve organisms.
It is active also against Rickettsiae but not Chlamydiae.
Clinically significant resistance is due to production of
chloramphenicol acetyltransferase, a plasmid-encoded
enzyme that inactivates the drug.
25. MOA of MLSK
Translation:
1.Initiation 2. Elongation 3Termination
Figure 6: MOA OF MLSK (Macrolides, Lincosamides,
Streptogramins, Ketolides)
26. 3. Inhibitors of Membrane
Function
Lipopeptides
Polymyxins (A,B,C,D, and E)
• Polymyxin B and E can be used therapeutically
• Polymyxin B – derived from Bacillus polymyxa var.
aerosporus
• Polymyxin E – derived from Bacillus polymyxa var.
colistinus = Colistin. Colistin exsists as two forms:
Colistin sulfate – intestinal infections, topical, powders, media
Colistimethate sodium – most active, effective form
Cyclic Lipopeptides
• All Bactericidal
27. Polymyxin Mode of Action
Target =Membrane phospholipids (lipopolysaccharides (LPS) and
lipoproteins)
1. Outer and Cytoplasmic Membrane Effect:
Polymyxins are positively charged molecules (cationic) which are attracted to the
negatively charged bacteria.
The negative charge of bacteria is due to LPS in the outer membrane and the
peptidoglycan (notably the teichoic acid).
The antibiotic binds to the cell membrane, alters its structure and makes it more
permeable. This disrupts osmotic balance causing leakage of cellular molecules,
inhibition of respiration and increased water uptake leading to cell death.
The antibiotic acts much like a cationic detergent and effects all membranes similarly.
Toxic side effects are common.
Little or no effect on Gram-positives since the cell wall is too thick to permit access to the
membrane.
Gram-positives are naturally resistant.
28. 4. Antimetabolites
Folate Pathway Inhibitors:
Sulfonamides, Trimethoprim/Sulfamethoxazole
The drug resembles a microbial substrate and competes with
that
substrate for the limited microbial enzyme
The drug ties up the enzyme and blocks a step in metabolism
Figure 7: Competitive Antagonism
29. Synthesis of Tetrahydrofolic Acid
Humans do not
synthesize folic acid.
Good selective target
Sulfonamides
(sulfadiazine,
sulfamethoxazole,
sulfadoxine)
Bacteriostatic
Introduced in 1930’s –
first effective systemic
antimicrobial agent
Used for treatment of
acute, uncomplicated
UTI’s
Trimethoprim/Sulfamethoxaz
ole
TMP/SXT is bactericidal
Broad spectrum
Synergistic action
Figure 8: synthesis of THF
30. Anti-metabolite (conts)
The combination SXT (thrimethoprim-sulfamethoxazole)
is synergistic and the association provides a bactericidal
effect
Natural Resistance
Enterococcus – low level and poorly expressed
S. pneumoniae
Ps. aeruginosa (impermeability)
31. 5. Inhibitors of Nucleic Acid
Synthesis (Qunolones & Furanes)
Quinolones:
Humans do synthesize DNA - shared process with
bacteria
Do tend to see some side effects with Quinolones
Some drugs withdrawn from market quickly
All are bactericidal
32. Quinolones
Mode of Action
Small and hydrophilic, quinolones have no problem
crossing the outer membrane.
They easily diffuse through the peptidoglycan and the
cytoplasmic membrane and rapidly reach their target.
Target = Topoisomerases (DNA-gyrase)
Rapid bactericidal activity
33. Quinolones inhibit DNA synthesis
Mode of Action
A typical E. coli’s chromosome is 1400 microns long (1 micron in diameter
when supercoiled), enough to fit in the E. coli’s bacterial cells which is 2-3
microns long
The bacterial chromosome consists of a single circle of DNA
DNA is double-stranded forming a left-handed double helix
All topoisomerases ( which are involved in DNA replication,
transcription and recombination) can relax DNA but only gyrase which
carry out DNA supercoiling.
The main quinolone target is the DNA gyrase which is responsible for
cutting one of the chromosomal DNA strands at the beginning of the
supercoiling process. The nick is only introduced temporarily and later
the two ends are joined back together (i.e., repaired).
• The quinolone molecule forms a stable complex with DNA gyrase
thereby inhibiting its activity and preventing the repair of DNA cuts
34. Resistance to Quinolones
Natural Resistance
Gram Positives – 1st generation quinolones
S.pneumoniae – decreased activity to Ofloxacin and
Ciprofloxacin
Ps. aeruginosa – decreased activity to Norfloxacin and
Ofloxacin
35. Furanes
Nitrofurantoin
Mode of Action:
The drug works by damaging bacterial DNA.
In the bacterial cell, nitrofurantoin is reduced by flavoproteins (nitrofuran
reductase). These reduced products are are highly active and attack ribosomal
proteins, DNA, respiration, pyruvate metabolism and other macromolecule
within the cell.
It is not known which of the actions of nitrofurantoin is primarily responsible
for its bactericidal acitivity.
Natural Resistance:
Pseudomonas and most Proteus spp. are naturally resistant.
37. Bibliography
Katzung, B.G. Basic and Clinical Pharmacology, 12th
Edition, Chapters 44 and 45, p774-783. D
Avis, B. D., Chen, L. L. & Tai, P. C. Misread protein creates
membrane channels: an essential step in the bactericidal
action of aminoglycosides. Proc. Natl Acad. Sci. USA 83,
6164–6168 (1986).
Wise, E. M. Jr & Park, J. T. Penicillin: its basic site of action
as an inhibitor of a peptide cross-linking reaction in cell
wall mucopeptide synthesis. Proc. Natl Acad. Sci. USA 54,
75–81 (1965).
Davis, B. D. Mechanism of bactericidal action of
aminoglycosides. Microbiol. Rev. 51, 341–350 (1987).