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Pharmacology | Antibiotics: Cell Wall Synthesis | Part 1
 
22:16
Ninja Nerds! Join us for our pharmacology discussion where we begin our 4 part lecture series on antibiotics. During part 1 of this series, we will be showing how antibiotics target the cell wall synthesis and structure. ***PLEASE SUPPORT US*** PATREON | https://www.patreon.com/NinjaNerdScience ***EVERY DOLLAR HELPS US GROW & IMPROVE OUR QUALITY*** FACEBOOK | https://www.facebook.com/NinjaNerdScience INSTAGRAM | https://www.instagram.com/ninjanerdscience/ ✎ For general inquiries email us at: NinjaNerdScience@gmail.com
Просмотров: 13866 Ninja Nerd Science
ß-Lactams: Mechanisms of Action and Resistance
 
07:23
Developed and produced by http://www.MechanismsinMedicine.com Animation Description: This animation starts with the explanation of bacterial cell wall synthesis, the process targeted by ß-Lactams. Structurally, most bacteria consist of a cell membrane surrounded by a cell wall and, for some bacteria, an additional outer layer. Internal to the cell membrane is the cytoplasm which contains ribosomes, a nuclear region and in some cases granules and/or vesicles. Depending on the bacterial species, a number of different external structures may be found such as a capsule, flagella and pili. In gram negative bacteria, the gap between the cell membrane and the cell wall is known as the periplasmic space. Most gram positive bacteria do not possess a periplasmic space but have only periplasm where metabolic digestion occurs and new cell peptidoglycan is attached. Peptidoglycan, the most important component of the cell wall, is a polymer made of N-acetyl muramic acid alternating with N-acetyl glucosamine which are cross-linked by chains of four amino acids. The function of the bacterial cell wall is to maintain the characteristic shape of the organism and to prevent the bacterium from bursting when fluid flows into the organism by osmosis. Synthesis of peptidoglycan and ultimately the bacterial cell wall occurs in a number of stages. One of the first stages is the addition of 5 amino acids to N-acetyl muramic acid. Next, N-acetyl glucosamine is added to the N-acetyl muramic acid to form a precursor of peptidoglycan. This peptidoglycan precursor is then transported across the cell membrane to a cell wall acceptor in the periplasm. Once in the periplasm, the peptidoglycan precursors bind to cell wall acceptors, and undergo extensive crosslinking. Two major enzymes are involved in crosslinking: transpeptidase and D-alanyl carboxypeptidase. These enzymes are also known as penicillin binding proteins because of their ability to bind penicillins and cephalosporins. Eventually, several layers of peptidoglycan are formed all of which are crosslinked to create the cell wall. Gram positive bacteria have many more layers than gram negative bacteria and thus have a much thicker cell wall. Beta-lactam antibiotics include all penicillins and cephalosporins that contain a chemical structure called a beta-lactam ring. This structure is capable of binding to the enzymes that cross-link peptidoglycans. Beta-lactams interfere with cross-linking by binding to transpeptidase and D-alanyl carboxypeptidase enzymes, thus preventing bacterial cell wall synthesis. By inhibiting cell wall synthesis, the bacterial cell is damaged. Gram positive bacteria have a high internal osmotic pressure. Without a normal, rigid cell wall, these cells burst when subjected to the low osmotic pressure of their surrounding environment. As well, the antibiotic-penicillin binding protein complex stimulates the release of autolysins that are capable of digesting the existing cell wall. Beta-lactam antibiotics are therefore considered bactericidal agents. Bacterial resistance to beta-lactam antibiotics may be acquired by several routes. One of the most important mechanisms is through a process known as transformation. During transformation, chromosomal genes are transferred from one bacterium to another. When a bacterium containing a resistance gene dies, naked DNA is released into the surrounding environment. If a bacterium of sufficient similarity to the dead one is in the vicinity, it will be able to uptake the naked DNA containing the resistance gene. Once inside the bacterium, the resistance gene may be transferred from the naked DNA to the chromosome of the host bacteria by a process known as homologous transformation. Over time, the bacterium may acquire enough of these resistance genes to result in a remodelling of the segment of the host DNA. If this remodelled DNA segment codes for cross-linking enzymes (i.e. penicillin binding proteins), the result is the production of altered penicillin binding proteins. These altered penicillin binding proteins can still cross-link the peptidoglycan layers of the cell wall but have a reduced affinity for beta-lactam antibiotics thus rendering the bacterium resistant to the effects of penicillin and other beta-lactam agents. This transfer process has resulted in penicillin-resistant S. pneumoniae through the acquisition of genes from other naturally occurring penicillin-resistant Streptococcus species. A second important mechanism by which bacteria become resistant to beta-lactam antibiotics is by the production of enzymes capable of inactivating or modifying the drug before it has a chance to exert its effect on the bacteria. View animation to read more.
Просмотров: 668932 Mechanisms in Medicine
Pharmacology – ANTIBIOTICS – CELL WALL & MEMBRANE INHIBITORS (MADE EASY)
 
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Support us on Patreon: https://www.patreon.com/speedpharmacology Follow us on Facebook: https://www.facebook.com/SpeedPharmacology/ Get Speed Pharmacology Merch Here: https://teespring.com/stores/speed-pharmacology **************************************************************************************************** This is Part 1 of a 2-Part lecture on Antibiotics. Topics covered include: classification of antibiotics; cell wall structure of Gram-negative bacteria, Gram-positive bacteria, Mycobacteria; mechanism of action and side effects of Cell Wall Synthesis Inhibitors: Beta-lactams (Penicillins, Cephalosporins, Carbapenems, Monobactams), Beta-lactamases (Avibactam, Clavulanic acid, Sulbactam, Tazobactam), Fosfomycin, Cycloserine, Vancomycin, Bacitracin, Antimycobacterial drugs (Isoniazid, Ethambutol), mechanism of action and side effects of Cell Membrane Integrity Disruptors: Daptomycin, Polymyxins. Source of diagram at 6:49 : http://www.biomedcentral.com/1471-2180/11/16
Просмотров: 29656 Speed Pharmacology
Penicillin mode of action (cell wall biosynthesis inhibitors)
 
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This penicillin antibiotic video tutorial explains the mode of action of beta lactam antibiotics or the cell wall inhibitors like penicllin,ampicillin vancomycin antibiotics. For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html
Просмотров: 45377 Shomu's Biology
Bacterial cell wall synthesis
 
02:26
Creé este video con el Editor de video de YouTube (http://www.youtube.com/editor)
Просмотров: 53415 Gonzalo Jorquera Olave
Cell Wall Synthesis Inhibitors: Antibiotics – Antimicrobial Pharmacology | Lecturio
 
01:20
This video “Cell Wall Synthesis Inhibitors: Antibiotics” is part of the Lecturio course “Antimicrobial Pharmacology” ► WATCH the complete course on http://lectur.io/42 ► LEARN ABOUT: - Overview of cell wall synthesis - Antibacterial agents - Cell wall synthesis inhibitors ► THE PROF: Dr. Shukle is a board certified specialist in internal medicine. He performs over 150 special lectures across the nation each year with various audiences ranging from the general public, to nurses, to physicians, to medical specialists. His lectures are engaging, funny, and informative. ► LECTURIO is your single-point resource for medical school: Study for your classes, USMLE Step 1, USMLE Step 2, MCAT or MBBS with video lectures by world-class professors, recall & USMLE-style questions and textbook articles. Create your free account now: http://lectur.io/42 ► INSTALL our free Lecturio app iTunes Store: https://app.adjust.com/z21zrf Play Store: https://app.adjust.com/b01fak ► READ TEXTBOOK ARTICLES related to this video: Antibiotics – Types and Antibiotic Therapy http://lectur.io/antibioticsarticle ► SUBSCRIBE to our YouTube channel: http://lectur.io/subscribe ► WATCH MORE ON YOUTUBE: http://lectur.io/playlists ► LET’S CONNECT: • Facebook: https://www.facebook.com/lecturio.medical.education.videos • Instagram: https://www.instagram.com/lecturio_medical_videos • Twitter: https://twitter.com/LecturioMed
Просмотров: 2295 Lecturio Medical Videos
Penicillin Mechanism Of Action
 
03:10
Просмотров: 12814 Pharmacology Animation
Microbiology - Antibiotics Mechanisms of Action
 
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https://www.facebook.com/ArmandoHasudungan Support me: http://www.patreon.com/armando Instagram: http://instagram.com/armandohasudungan Twitter: https://twitter.com/Armando71021105
Просмотров: 369043 Armando Hasudungan
VANCOMYCIN Mechanism of Action
 
03:44
VANCOMYCIN Mechanism of Action Vancomycin is an antibiotic drug which is structurally classified as a glycopeptide. It mainly acts by prevention of cell-wall biosynthesis of bacteria. It is specially effective against gram-positive bacteria and has been known to be effective against resistant strains of MRSA. Vancomycin is known as the drug of last resort as it generally used when all other treatments have failed. However, bacteria have started developing resistance to vancomycin as well- leading to use of other antibiotics. Vancomycin acts by inhibiting cell wall synthesis of bacteria. Peptidoglycan layer of the cell wall is rigid due to its highly cross-linked structure. During the synthesis of the peptidoglycan layer of bacteria, new building blocks of peptidoglycan get inserted (i.e. monomers of N-acetylmuramic acid and N-acetylglucosamine) into the membrane.Vancomycin inhibit the synthesis of bacterial cell wall phospholipids as well as peptidoglycan polymerization in a time dependent fashion by binding to the D-ala-D-ala side chain of the precursor pentapeptide.This prevent the transglycosylation step in peptidoglycan polymerization . By doing so, vancomycin makes the peptidoglycan layer less rigid and more permeable. This causes cellular contents of the bacteria to leak out and eventually death of the bacteria. Mutations in the transpeptidase enzyme can lead to increased resistance to vancomycin.
Просмотров: 8211 Medinaz
Cell Wall Synthesis Inhibitors 1
 
29:17
Просмотров: 3950 Medicine
Pharmacology: Inhibitors of Cell Wall Synthesis
 
08:23
Please encourage us to like to our videos 👍👍 and subscribe to channel 🆘
Просмотров: 144 Department of Biology
Cell Wall Synthesis Inhibitors Antibiotics
 
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Classification of Cell Wall Synthesis Inhibitors. Antibiotics
Просмотров: 71 Faisal Mehboob Physiotherapist
Pharmacology Lessons: Beta lactams Antibiotics
 
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β-Lactam antibiotics (beta-lactam antibiotics) are a broad class of antibiotics, consisting of all antibiotic agents that contains a β-lactam ring in their molecular structures. This includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems. Most β-lactam antibiotics work by inhibiting cell wall biosynthesis in the bacterial organism and are the most widely used group of antibiotics.
Просмотров: 56979 Target PEBC PREP
Pharmacology – ANTIBIOTICS – NUCLEIC ACID & FOLIC ACID & PROTEIN SYNTHESIS INHIBITORS (MADE EASY)
 
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Support us on Patreon: https://www.patreon.com/speedpharmacology Follow us on Facebook: https://www.facebook.com/SpeedPharmacology/ Get Speed Pharmacology Merch Here: https://teespring.com/stores/speed-pharmacology **************************************************************************************************** This is Part 2 of a 2-Part lecture on Antibiotics. Topics covered include: mechanism of action and side effects of Nucleic Acid Synthesis Inhibitors: Metronidazole, Quinolones and Rifamycins; Protein Synthesis Inhibitors: Aminoglycosides, Tetracyclines, Glycylcyclines, Amphenicols, Macrolides, Ketolides, Lincosamides, Streptogramins and Oxazolidinones; Metabolic Pathway inhibitors: Sulfonamides and Trimethoprim.
Просмотров: 14958 Speed Pharmacology
VANCOMYCIN Quick Review with Mnemonic
 
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VANCOMYCIN - Quick review Vancomycin is a bactericidal glycoprotein that binds to the d-Ala-d-Ala terminal of the nascent peptidoglycan pentapeptide side chain and inhibits transglycosylation. Vancomycin is indicated for the treatment of serious or severe infections caused by susceptible strains of methicillin-resistant (beta-lactam-resistant) staphylococci. It is indicated for penicillin-allergic patients, for patients who cannot receive or who have failed to respond to other medications, including the penicillins or cephalosporins, and for infections caused by vancomycin-susceptible organisms that are resistant to other antimicrobials. Vancomycin is indicated for initial therapy when methicillin-resistant staphylococci are suspected, but after susceptibility data are available, therapy should be adjusted accordingly. Vancomycin is effective in the treatment of staphylococcal endocarditis. Its effectiveness has been documented in other infections due to staphylococci, including septicemia, bone infections, lower respiratory tract infections, skin and skin structure infections. When staphylococcal infections are localized and purulent, antibiotics are used as adjuncts to appropriate surgical measures. Vancomycin has been reported to be effective alone or in combination with an aminoglycoside for endocarditis caused by Streptococcus viridans or S. bovis. For endocarditis caused by enterococci (e.g., E. faecalis), vancomycin has been reported to be effective only in combination with an aminoglycoside. Vancomycin has been reported to be effective for the treatment of diphtheroid endocarditis. Vancomycin has been used successfully in combination with either rifampin, an aminoglycoside, or both in early-onset prosthetic valve endocarditis caused by S. epidermidis or diphtheroids. Specimens for bacteriologic cultures should be obtained in order to isolate and identify causative organisms and to determine their susceptibilities to vancomycin. To reduce the development of resistant bacteria and maintain the effectiveness of vancomycin and other antibacterials, vancomycin should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy. VANCOMYCIN Mechanism of Action Vancomycin is an antibiotic which is structurally classified as a glycopeptide. It mainly acts by prevention of cell-wall biosynthesis of bacteria. It is specially effective against gram-positive bacteria and has been known to be effective against resistant strains of MRSA. Vancomycin is known as the antibiotic of last resort as it generally used when all other treatments have failed. However, bacteria have started developing resistance to vancomycin as well- leading to use of other antibiotics. Vancomycin acts by inhibiting cell wall synthesis of bacteria. Peptidoglycan layer of the cell wall is rigid due to its highly cross-linked structure. During the synthesis of the peptidoglycan layer of bacteria, new building blocks of peptidoglycan get inserted (i.e. monomers of N-acetylmuramic acid and N-acetylglucosamine) into the membrane.Vancomycin inhibit the synthesis of bacterial cell wall phospholipids as well as peptidoglycan polymerization in a time dependent fashion by binding to the D-ala-D-ala side chain of the precursor pentapeptide.This prevent the transglycosylation step in peptidoglycan polymerization . By doing so, vancomycin makes the peptidoglycan layer less rigid and more permeable. This causes cellular contents of the bacteria to leak out and eventually death of the bacteria. Mutations in the transpeptidase enzyme can lead to increased resistance to vancomycin. Adverse Effects more than 10% Bitter taste (PO) Erythematous rash on face and upper body (IV; red neck or red man syndrome; related to infusion rate) Hypotension accompanied by flushing (IV) Nausea and vomiting (PO) 1-10% Chills (IV) Drug fever (IV) Eosinophilia (IV) Rash (IV) Fatique (PO) Peripheral edema (PO) Urinary tract infection (PO) Back pain (PO) Headache (PO) Reversible neutropenia (IV) Phlebitis (IV) less than 1% Nephrotoxicity Ototoxicity (especially with large doses) Stevens-Johnson syndrome Thrombocytopenia Vasculitis
Просмотров: 2888 Medinaz
Intro to Bacteria & Antibiotics: Non BL Cell Wall & Membrane Abx
 
08:36
4. Non BL Cell Wall & Membrane Abx This video is part of a comprehensive medical school microbiology, immunology & infectious diseases course. Your comments on videos will be key as we iterate content. If you are interested in implementing all or part of this course, we are happy to share and would only ask for your candid evaluation in return: https://stanfordmedicine.qualtrics.com/SE/?SID=SV_8i98rRk2XRCXQ45 If you are interested in collaborating with us, please contact: paulinebecker@stanford.edu This course was created collaboratively between Stanford, UW, Duke, UCSF, and University of Michigan and made possible by support from the Robert Wood Johnson Foundation.
Pharmacology | Antibiotics: Protein Synthesis | Part 3
 
13:55
Ninja Nerds! Join us for our pharmacology discussion where we continue our 4 part lecture series on antibiotics. During part 3 of this series, we will be talking about how antibiotics are targeting protein synthesis. ***PLEASE SUPPORT US*** PATREON | https://www.patreon.com/NinjaNerdScience ***EVERY DOLLAR HELPS US GROW & IMPROVE OUR QUALITY*** FACEBOOK | https://www.facebook.com/NinjaNerdScience INSTAGRAM | https://www.instagram.com/ninjanerdscience/ ✎ For general inquiries email us at: NinjaNerdScience@gmail.com
Просмотров: 5678 Ninja Nerd Science
Mechanism of Transpeptidase and Inhibition with Penicillin
 
13:18
Donate here: http://www.aklectures.com/donate.php Website video link: http://www.aklectures.com/lecture/structure-and-function-of-penicillin Facebook link: https://www.facebook.com/aklectures Website link: http://www.aklectures.com
Просмотров: 16125 AK LECTURES
Cell Wall Synthesis
 
17:42
More pharmacology content available at https://www.edukesh.com
Просмотров: 8038 EDUKESH
Pharma Tube - 79 - Chemotherapy - 2 - Cell Wall Inhibitors; Part I [HD]
 
01:22:45
فارما تيوب Pharma Tube هى سلسلة من الفيديوهات تحتوى على محاضرات فى علم الفارماكولوجى الأساسى والإكلينيكى يقدمها الصيدلى دهشان حسن دهشان الشرح من كتاب فارما جايد Pharma Guide Pharma Tube is a series of videos containing lectures about basic and clinical pharmacology which prepared from Pharma Guide book, by Pharmacist; Dahshan Hassan Dahshan. ** موضوعات هذة الحلقة: Cell Wall Inhibitors الجزء الأول Penicillins Classification of Penicillins Pharmacokinetics Mechanism of Action Mechanism of Resistance Side Effects A) Natural Penicillins - Penicillin G (Benzyl-penicillin) - Penicillin V (Phenoxy-methyl-penicillin) - Procaine Penicillin (Procaine Benzylpenicillin) - Benzathine Penicillin (Benzathine Benzylpenicillin) B) Penicillinase-Resistant (Antistaphylococcal) Penicillins - Methicillin - Nafcillin - Oxacillin - Cloxacillin - Dicloxacillin - Flucloxacillin C) Aminopenicillins - Ampicillin - Amoxicillin D) Broad Spectrum Penicillins (Aminopenicillins + β-lactamase Enzyme Inhibitors) - Ampicillin/Sulbactam - Sultamicillin - Co-Amoxiclav (Amoxicillin/ Clavulanate) E) Anti-Pseudomonal Penicillins - Carboxypenicillins; Ticarcillin and Carbenicillin - Ureidopenicillins; Piperacillin, Mezlocillin and Azlocillin - فقرة الصيدلية ******************** للإنضمام لفريق عمل مطورون كتاب فارما جايد .. إنضم الى جروب “Pharma Guide Developers” https://goo.gl/cxmhz8 لمعلومات أكثر عن الكتاب For more information about Pharma Guide book, click here https://goo.gl/izPQDe للتواصل مع المؤلف For contact with the author https://goo.gl/6qRWyN الآن متوفر تطبيق Pharma Tube وتطبيق Pharma Guide MCQs على جوجل بلاى لهواتف الأندرويد فقط Pharma Tube and Pharma Guide MCQs App are now available on Google Play for android devices هذه المحاضرات للمختصين في المجال الطبي، الصيادلة ، الأطباء ، أطباء الأسنان أو التمريض، وعلى الرغم من هذا فقد لا تتوافق مع النظم الصحية المعمول بها في بلدك فبرجاء مراجعتها أولاً. These lectures for specialists in the medical field, pharmacists, physicians, dentists or nurses and although this may not conform with applicable in your country health systems sure to first review. يمكنك تحميل تطبيق "فارما تيوب" أو "Pharma Tube" للهواتف الأندرويد من على جوجل بلاى للإستماع الى جميع الفيديوهات بكل سهولة دون معاناه فى البحث.
Просмотров: 15662 Dhshan Hassan Dhshan
cell wall synthesis inhibitors mechanism of action-1|By Muhammad Nasir Pharmacist
 
41:20
Introduction and complete mechanism of action of Call wall synthesis inhibitors|Cell Wall Synthesis | Antibiotics | Pharmacology|Structurally, most bacteria consist of a cell membrane surrounded by a cell wall and, for some bacteria, an additional outer layer. Internal to the cell membrane is the cytoplasm which contains ribosomes, a nuclear region and in some cases granules and/or vesicles. Depending on the bacterial species, a number of different external structures may be found such as a capsule, flagella and pili. In gram negative bacteria, the gap between the cell membrane and the cell wall is known as the periplasmic space. Most gram positive bacteria do not possess a periplasmic space but have only periplasm where metabolic digestion occurs and new cell peptidoglycan is attached. Peptidoglycan, the most important component of the cell wall, is a polymer made of N-acetyl muramic acid alternating with N-acetyl glucosamine which are cross-linked by chains of four amino acids. The function of the bacterial cell wall is to maintain the characteristic shape of the organism and to prevent the bacterium from bursting when fluid flows into the organism by osmosis. Synthesis of peptidoglycan and ultimately the bacterial cell wall occurs in a number of stages. One of the first stages is the addition of 5 amino acids to N-acetyl muramic acid. Next, N-acetyl glucosamine is added to the N-acetyl muramic acid to form a precursor of peptidoglycan. This peptidoglycan precursor is then transported across the cell membrane to a cell wall acceptor in the periplasm. Once in the periplasm, the peptidoglycan precursors bind to cell wall acceptors, and undergo extensive crosslinking. Two major enzymes are involved in crosslinking: transpeptidase and D-alanyl carboxypeptidase. These enzymes are also known as penicillin binding proteins because of their ability to bind penicillins and cephalosporins. Eventually, several layers of peptidoglycan are formed all of which are crosslinked to create the cell wall. Gram positive bacteria have many more layers than gram negative bacteria and thus have a much thicker cell wall. Beta-lactam antibiotics include all penicillins and cephalosporins that contain a chemical structure called a beta-lactam ring. This structure is capable of binding to the enzymes that cross-link peptidoglycans. Beta-lactams interfere with cross-linking by binding to transpeptidase and D-alanyl carboxypeptidase enzymes, thus preventing bacterial cell wall synthesis. By inhibiting cell wall synthesis, the bacterial cell is damaged. Gram positive bacteria have a high internal osmotic pressure. Without a normal, rigid cell wall, these cells burst when subjected to the low osmotic pressure of their surrounding environment. As well, the antibiotic-penicillin binding protein complex stimulates the release of autolysins that are capable of digesting the existing cell wall. Beta-lactam antibiotics are therefore considered bactericidal agents. https://pharmanotespdf.blogspot.com/ For inquiries email us at nsk59rph@gmail.com Follow us on https://web.facebook.com/nsk59rph/
Просмотров: 295 Muhammad Nasir Pharmacist
Antibiotics Targeting Bacterial Cell Wall Biosynthesis Part 1
 
13:03
In this video we look at the bacterial cell wall biosynthesis process and look at antibiotics which target cell wall biosynthesis.
Просмотров: 1868 Ben1994
Action Mechanism of Antibiotics
 
07:36
The Antibiotics target the Pathogens in different ways , and the most common target of Antibiotics is Cell wall. The following Cellular Processes are targeted by Antibiotics : 1.Transcription 2.Translation. 3.DNA Replication 4.Folate Synthesis. 5.Cell Wall Synthesis. They may either kill or inhibit the growth of bacteria. A limited number of antibiotics also possess anti-protozoal activity.Antibiotics are not effective against viruses such as the common cold or influenza, and their inappropriate use allows the emergence of resistant organisms.Drugs which inhibit viruses are termed antiviral drugs or antivirals rather than antibiotics. IMAGE CREDITS : www.pexels.com
Просмотров: 4276 Hussain Biology
Beta Lactam Antibiotic: Mechanism of Action (Penicillin)| Bhushan Science
 
14:55
β-lactam antibiotics (beta-lactam antibiotics) are a class of broad-spectrum antibiotics, consisting of all antibiotic agents that contain a beta-lactam ring in their molecular structures. This includes penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems. Most β-lactam antibiotics work by inhibiting cell wall biosynthesis in the bacterial organism and are the most widely used group of antibiotics. Share, Support, Subscribe!!! Please watch: "Beta Lactam Antibiotic: Mechanism of Action (Penicillin)| Bhushan Science |" https://youtu.be/sGpPgC7vOdw ► To Watch all our videos, click here – https://www.youtube.com/channel/UC3e7NIf2DOS79L9EKg3ESiA ► Subscribe to our channel, click here - https://www.youtube.com/channel/UC3e7NIf2DOS79L9EKg3ESiA
Просмотров: 3198 Bhushan Science
Cell wall inhibitors
 
00:44
Gram positive cocci with penicillin binding proteins being attacked by penicillin -- leading to cell membrane disruption and rupture of the bacterial wall Contact: medialab@cchmc.org
Просмотров: 3177 CCHMCMediaLab
Classes of antibiotics that target the cell envelope
 
05:55
This is a brief overview of classes of antibacterials that target the cell envelope β-lactams → mimic D-Ala-D-Ala to inhibit penicillin binding proteins (PBP) and thus block cell wall synthesis Subclasses: penicillins, cephalosporins, carbapenems, monobactams, clavams β-lactamases → antibiotic resistance mechanism to inactivate β-lactams, often by breaking ring ex: New Delhi Metallo-β-lactamase; extended spectrum β-lactamase (ESBL), good for cephalosporins PBPs in bacteria are blocked by antibiotic β-lactams, which the cell counters with β-lactamases, which can further be countered with clavulanic acid Glycopeptides → caps D-Ala-D-Ala to inhibit transglycosylation and block cell wall synthesis; ex: vancomycin Bacitracin → inhibits recycling of peptidoglycan carrier lipid Phosphomycin → blocks enzyme involved in peptidoglycan precursor synthesis (prevents NAG-NAM attachment) Cycloserine → blocks enzyme involved in peptidoglycan precursor synthesis (prevents NAM-peptide attachment) Isoniazid → inhibit mycolic acid synthesis (for Mycobacterium tuberculosis) Ethambutol → inhibit arabinotransferases (for Mycobacterium tuberculosis) Lipopeptides → forms pores in cytoplasmic membrane of gram positive bacteria, causing leakage I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor.
Просмотров: 1497 MedLecturesMadeEasy
Brandl's Basics: Protein synthesis inhibitors 1 - Mechanism of action
 
05:07
This video introduces the different classes of protein synthesis inhibitors and discusses their mechanism of action.
Просмотров: 5394 Katharina Brandl
VANCOMYCIN - What You Need to Know
 
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VANCOMYCIN - What You Need to Know Vancomycin is a bactericidal glycoprotein that binds to the d-Ala-d-Ala terminal of the nascent peptidoglycan pentapeptide side chain and inhibits transglycosylation. Vancomycin is indicated for the treatment of serious or severe infections caused by susceptible strains of methicillin-resistant (beta-lactam-resistant) staphylococci. It is indicated for penicillin-allergic patients, for patients who cannot receive or who have failed to respond to other drugs, including the penicillins or cephalosporins, and for infections caused by vancomycin-susceptible organisms that are resistant to other antimicrobial drugs. Vancomycin is indicated for initial therapy when methicillin-resistant staphylococci are suspected, but after susceptibility data are available, therapy should be adjusted accordingly. Vancomycin is effective in the treatment of staphylococcal endocarditis. Its effectiveness has been documented in other infections due to staphylococci, including septicemia, bone infections, lower respiratory tract infections, skin and skin structure infections. When staphylococcal infections are localized and purulent, antibiotics are used as adjuncts to appropriate surgical measures. Vancomycin has been reported to be effective alone or in combination with an aminoglycoside for endocarditis caused by Streptococcus viridans or S. bovis. For endocarditis caused by enterococci (e.g., E. faecalis), vancomycin has been reported to be effective only in combination with an aminoglycoside. Vancomycin has been reported to be effective for the treatment of diphtheroid endocarditis. Vancomycin has been used successfully in combination with either rifampin, an aminoglycoside, or both in early-onset prosthetic valve endocarditis caused by S. epidermidis or diphtheroids. Specimens for bacteriologic cultures should be obtained in order to isolate and identify causative organisms and to determine their susceptibilities to vancomycin. To reduce the development of drug-resistant bacteria and maintain the effectiveness of vancomycin and other antibacterial drugs, vancomycin should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy. VANCOMYCIN Mechanism of Action Vancomycin is an antibiotic drug which is structurally classified as a glycopeptide. It mainly acts by prevention of cell-wall biosynthesis of bacteria. It is specially effective against gram-positive bacteria and has been known to be effective against resistant strains of MRSA. Vancomycin is known as the drug of last resort as it generally used when all other treatments have failed. However, bacteria have started developing resistance to vancomycin as well- leading to use of other antibiotics. Vancomycin acts by inhibiting cell wall synthesis of bacteria. Peptidoglycan layer of the cell wall is rigid due to its highly cross-linked structure. During the synthesis of the peptidoglycan layer of bacteria, new building blocks of peptidoglycan get inserted (i.e. monomers of N-acetylmuramic acid and N-acetylglucosamine) into the membrane.Vancomycin inhibit the synthesis of bacterial cell wall phospholipids as well as peptidoglycan polymerization in a time dependent fashion by binding to the D-ala-D-ala side chain of the precursor pentapeptide.This prevent the transglycosylation step in peptidoglycan polymerization . By doing so, vancomycin makes the peptidoglycan layer less rigid and more permeable. This causes cellular contents of the bacteria to leak out and eventually death of the bacteria. Mutations in the transpeptidase enzyme can lead to increased resistance to vancomycin. Adverse Effects more than 10% Bitter taste (PO) Erythematous rash on face and upper body (IV; red neck or red man syndrome; related to infusion rate) Hypotension accompanied by flushing (IV) Nausea and vomiting (PO) 1-10% Chills (IV) Drug fever (IV) Eosinophilia (IV) Rash (IV) Fatique (PO) Peripheral edema (PO) Urinary tract infection (PO) Back pain (PO) Headache (PO) Reversible neutropenia (IV) Phlebitis (IV) less than 1% Nephrotoxicity Ototoxicity (especially with large doses) Stevens-Johnson syndrome Thrombocytopenia Vasculitis
Просмотров: 9894 Medinaz
Action Mechanism of Anti-biotics
 
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In this video we have discussed the Action mechanism of Anti- biotics. We know Bacteria being the Prokaryotic cell does all the metabolic activities like Protein synthesis , cell wall synthesis and other important functions , so basically these metabolic activities are targeted by these Anti- biotics and eliminate the Pathogens.
Просмотров: 1052 Hussain Biology
ANTIBIOTICS (part1)
 
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in this video cell wall synthesis inhibiting antibiotic penicillins have explained in detail.
Просмотров: 1414 EASY MEDICINE
Intro to Bacteria & Antibiotics: Protein Synthesis Inhibitors Pt.  I
 
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5. Protein Synthesis Inhibitors Pt. I This video is part of a comprehensive medical school microbiology, immunology & infectious diseases course. Your comments on videos will be key as we iterate content. If you are interested in implementing all or part of this course, we are happy to share and would only ask for your candid evaluation in return: https://stanfordmedicine.qualtrics.com/SE/?SID=SV_8i98rRk2XRCXQ45 If you are interested in collaborating with us, please contact: paulinebecker@stanford.edu This course was created collaboratively between Stanford, UW, Duke, UCSF, and University of Michigan and made possible by support from the Robert Wood Johnson Foundation.
Bacterial Cell Wall Synthesis
 
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Просмотров: 365 Lam Nguyen
normal Cell wall synthesis
 
01:12
Просмотров: 1163 Mohammed IRON
Cell Wall Synthesis Inhibitors 2
 
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Contents: - 1st Generation Cephalosporin : 1:50 - 2nd Generation Cephalosporin : 3:14 - 3rd Generation Cephalosporin : 5:45 - CARBAPENEM : 12:12 - MONOBACTAM : 16:10 - Daptomycin / Bacitracin : 20:00 - VANCOMYCIN : 21:50
Просмотров: 1962 Medicine
Cell Wall Synthesis Inhibitor Song
 
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This parody of Albert Hague's "Mr. Grinch" describes the pharmacology of monobactams, carbapenams, beta-lactamase inhibitors, daptomycin, fofsomycin, and vancomycin. All of these antibiotics are bacterial cell wall synthesis inhibitors. Lyrics are below. Lyrics: Monobactams are given By IM or IV sites. They are good in the CNS When meninges are inflamed. Gram minus rods Are their targets. They help aminoglycosides. Monobactam allergies Are like penicillin ones. Carbapenams parenteral Resist beta-lactamases. They go to All tissues in the body. Then they by renal excretion are gone. Carbapenam allergies Are like penicillin ones. They also cause GI distress, Headache, vertigo, tremor, confusion, and Seizures with renal failure. Iminipenem’s given with cilistatin. Beta-lactamase stoppers Need penicillins to act. They fight gram plus and minus And are oral or parenteral. They extend Antimicrobial spectra of the broad penicillins. Daptomycin fights germs that Resist vancomycin and May cause myopathy and allergic pneumonitis. It’s Stopped by surfactant. Fofsomycin stops peptidoglycan Synthesis and May cause vaginitis and GI distress. It’s used for Uncomplicated UTIs. Vancomycin inhibits Peptidoglycan’s making lines. It’s given by mouth or IV And is good in CSF with meningitis It can cause allergies or red man syndrome. Gram plus germs it fights.
Просмотров: 769 J.C. Sue
Pharmacology- CELL WALL SYNTHESIS INHIBITORS
 
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BY: Dr. Norraine Medina
Просмотров: 27 Maynard Villamil
How Antibiotics Work ?
 
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Antibiotics work by affecting things that bacterial cells have but human cells don't. For example, human cells do not have cell walls, while many types of bacteria do. The antibiotic penicillin works by keeping a bacterium from building a cell wall. The Antibiotics work at 3 levels,the first level is at Gene Expression of Bacteria,The gene expression of Bacteria is three step process where we see the flow of Information from DNA to RNA to Protein ,we see the DNA ,Transfers its information into mRNA molecules through a process called Transcription and from the information of mRNA molecule, the bacteria produces a Protein in the process of Translation. When both of the processes are stopped by Antibiotics the cell ceases to exist and also the DNA replication of Bacteria is halted by some Antibiotics…. Another novel, working of Antibiotics is that they Inhibit the cell wall synthesis of Bacteria……We humans don’t have cell wall in our cells ,,, so the cell wall becomes easy target of Antibiotics . And finally there are some antibiotics like Sulfa antibiotics that inhibit that inhibit the folate synthesis in Bacteria by competitive inhibition of enzymes. Antibiotics like Rifampicin , clindimycin , Beta Lactam , Pencillin and Chloramphenicol affect the bacteria growth and processes at various levels.
Просмотров: 1137 Hussain Biology
Peptidoglycan Biosynthesis [HD Animation]
 
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Peptidoglycan Biosynthesis Animation #Please → Like, comment, share and subscribe 👍🏻❤️
Просмотров: 8344 McGraw-Hill Animations
Antibiotics Targeting Bacterial Cell Wall Biosynthesis Part 5
 
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In this video we look at the bacterial cell wall biosynthesis process and look at antibiotics which target cell wall biosynthesis.
Просмотров: 587 Ben1994
50s ribosome inhibitor mode of action
 
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This antibiotic video tutorial explains the mode of action of 50s ribosome inhibitor antibiotics. These antibiotics are among protein biosynthesis inhibitors. For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html
Просмотров: 19423 Shomu's Biology
What is the mechanism of cephalosporins?
 
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ID: Pharmacology: Cephalosporins are bacteriocidal beta-lactam drugs that inhibit cell wall synthesis
Просмотров: 123 Flash-Med: Medical Questions and Answers
Drugs that weaken the bacterial cell wall
 
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Просмотров: 343 Cynthia Booher
Antibiotics - Protein synthesis inhibitor
 
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It highlights the target and mechanism of antibiotics belonging to class of protein synthesis inhibitor
Просмотров: 1649 Manish Aglawe
Simulations of Bacterial Cell Wall Synthesis
 
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Просмотров: 2480 Jensen Lab