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Pharmacology – ANTIBIOTICS – CELL WALL & MEMBRANE INHIBITORS (MADE EASY)
 
16:05
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: 45031 Speed Pharmacology
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: 17543 Ninja Nerd Science
ß-Lactams: Mechanisms of Action and Resistance
 
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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: 692854 Mechanisms in Medicine
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: 48198 Shomu's Biology
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: 2662 Lecturio Medical Education
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: 386194 Armando Hasudungan
Bacterial cell wall synthesis
 
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Creé este video con el Editor de video de YouTube (http://www.youtube.com/editor)
Просмотров: 59767 Gonzalo Jorquera Olave
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: 2032 Medicine
Cell Wall Synthesis Inhibitors 1
 
29:17
Просмотров: 4112 Medicine
Cell Wall Synthesis
 
17:42
More pharmacology content available at https://www.edukesh.com
Просмотров: 10492 EDUKESH
Drugs that weaken the bacterial cell wall
 
11:11
Просмотров: 369 Cynthia Booher
Protein Synthesis Inhibition [HD Animation]
 
02:31
Antibiotics Protein Synthesis Inhibition HD Animation #Please → Like, comment, share and subscribe 👍🏻❤️
Просмотров: 4795 McGraw-Hill Animations
Penicillin Mechanism of Action animation video
 
03:10
Penicillin pass through porins of gram negative bacterial cell wall. The penicillin then binds to penicillin binding protein linked the cell membrane to be activated. Active penicillin binds to and inactivate transpeptidase enzyme. As a result peptidoglycans NAM and NAG sugars are not cross-linked and the cell wall collapse
Просмотров: 18181 Pharmacology Animation
Pharmacology: Inhibitors of Cell Wall Synthesis
 
08:23
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Просмотров: 185 Department of Biology
Microbials and Antibiotics: Part 2
 
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Table of Contents: 00:00 - Microbes and Antimicrobials – A systematic approach to antibiotics (Part 2) 00:26 - 01:36 - Antibiotics 02:01 - 1. Cell wall synthesis inhibitors 02:58 - 2. Bacterial Translation Drugs 05:54 - Aminoglycosides 05:54 - Aminoglycosides 08:13 - Aminoglycosides continued 10:33 - Tetracyclines continued 11:37 - Chloramphenicol 14:18 - Macrolides 14:18 - Macrolides 15:23 - Macrolides 16:01 - Clindamycin 17:25 - Linezolid 17:49 - 3. Nucleic acid synthesis inhibitors 18:42 - Folic acid synthesis inhibitors 18:47 - 20:10 - Folic acid synthesis inhibitors 21:04 - 21:04 - Clinical uses of folic acid synthesis inhibitors 22:53 - Folic acid synthesis inhibitors 24:29 - Direct inhibitors of nucleic acid synthesis 26:02 - Quinolones continued 27:00 - 4. Unclassified drugs 28:05 - Antibiotics
Просмотров: 1711 Dushyant Iyer
Protein Synthesis Inhibitors antibiotics animation video
 
02:20
Protein synthesis inhibitors antibiotics targets various steps in ribosomal protein synthesis. Bacterial ribosome is composed of two subunits; 30s and 50s subunits that unite together to form 70s complex. Tetracycline inhibits the binding of tRNA to 30s subunit. Aminoglycosides bind to and distort 30s subunit. Chloramphenicol inhibit the elongation of amino acids sequences. Macrolides inhibit the sliding of mRNA in the ribosome.
Просмотров: 2449 Pharmacology Animation
Peptidoglycan Biosynthesis [HD Animation]
 
02:45
Peptidoglycan Biosynthesis Animation #Please → Like, comment, share and subscribe 👍🏻❤️
Просмотров: 13586 McGraw-Hill Animations
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: 346 Muhammad Nasir Pharmacist
VANCOMYCIN Mechanism of Action
 
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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: 9688 Medinaz
Cell Wall Synthesis Inhibitors Antibiotics
 
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Classification of Cell Wall Synthesis Inhibitors. Antibiotics
Просмотров: 110 Muhammad Faisal
Action Mechanism of Antibiotics
 
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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: 4901 Hussain Biology
Pharmacology | Antibiotics: Protein Synthesis | Part 3
 
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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: 7426 Ninja Nerd Science
Antibiotics Targeting Bacterial Cell Wall Biosynthesis Part 1
 
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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: 1906 Ben1994
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: 776 J.C. Sue
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.
Pharmacology – ANTIBIOTICS – DNA, RNA, 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: 23169 Speed Pharmacology
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: 17563 Dhshan Hassan Dhshan
ANTIBIOTICS (part1)
 
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in this video cell wall synthesis inhibiting antibiotic penicillins have explained in detail.
Просмотров: 2349 EASY MEDICINE
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: 3608 Medinaz
PROTEIN SYNTHESIS INHIBITOR : ANTIBIOTICS | PHARMACOLOGY | GPAT-2019
 
14:02
Visit our website :- http://www.gdc4gpat.com Download GDC App:- https://goo.gl/uaGsY2 Join GDC Online Test:- http://www.gdconlinetest.in/ FACEBOOK- https://www.facebook.com/GPATDISCUSSION/ INSTAGRAM- https://www.instagram.com/gpat_discus... TWITTER- https://twitter.com/GPAT_Discussion Dr. Puspendra Classes Videos:- https://www.youtube.com/user/puspendra007
Просмотров: 1157 GPAT DISCUSSION CENTER
Simulations of Bacterial Cell Wall Synthesis
 
19:19
Просмотров: 2598 Jensen Lab
Bacterial Cell Wall Synthesis
 
00:44
Просмотров: 399 Lam Nguyen
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
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How antibiotics work , Part 2 - Everything You Need To Know - Dr. Nabil Ebraheim
 
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Dr. Ebraheim’s educational animated video describes how the antibiotic works. •Cell wall: 1.Penicillins 2.Cephalosporins 3.vancomycin Inhibit the cell wall synthesis by blocking the cross-linking. The penicillin-binding protein enzymes are involved in the cross-linking. Beta-lactams have a ring that binds to the enzyme and prevents the cell wall synthesis. When beta-lactam inhibits the cell wall synthesis, this will cause damage to the bacterial cell. If you are allergic to penicillin or cephalosporins, you may be given clindamycin or vancomycin. Vancomycin may be given if methicillin-resistant Staphylococcus aureus (MRSA) is suspected or encountered (vancomycin is essential in the treatment of MRSA). Patients allergic to clindamycin may be given Cipro. The penicillin-binding protein is involved. mecA gene allows a bacterium to be resistant to antibiotics. This is how MRSA develops. The bacteria produce an altered penicillin-binding protein that can do the cross-linking but has no affinity to Beta-lactam antibiotics. It renders the bacteria resistant to the effects of penicillin and cephalosporins. Vancomycin is used in these cases. The transformation from one bacteria to another. Plasmid. Three main mechanisms by which resistant genes can be transferred: 1.Conjugation: the bacteria may conjugate their DNA from one bacteria to the other through transformation via a sex pilus. 2.Transformation 3.Transduction There is another mechanism which produces an enzyme that will inactivate the drugs before it reaches the bacteria. This is beta-lactamase which is capable of destroying the beta-lactam antibiotics. The bata-lactam ring of the antibiotics is destroyed and will not be able to bind to the wall. •Cell membrane: polymyxin. Polymyxin will increase the cell wall permeability. •Folic acid synthesis: sulfonamides, trimethoprim. •Nucleic acid synthesis: •DNA synthesis inhibitors: 1- Fluoroquinolones: ciprofloxacin (gyrase). DNA gyrase is responsible for removing the superhelical twist so that DNA replication can proceed. The fluoroquinolones inhibit the DNA gyrase. Using cirpo may contribute to the condition of Achilles tendon rupture. 2- Metronidazole (direct effect on DNA). Bacteriocidal that creates free oxygen radicals that are metabolic bi-products which disrupt the DNA. Can be used to treat pseudomembranous colitis c.diff. RNA polymerase inhibitors: rifampin. RNA polymerase is an enzyme that produces messenger RNA. The synthesis of messenger RNA is called transcription. Messenger RNA is DNA dependant and uses it as a template. Rifampin targets and inactivates the RNA polymerase bacterial enzyme. Rifampin works against staph infection and the Mycobacterium tuberculosis (TB). Staphylococcus aureus that is phagocytosed by the macrophages causes them to become intracellular (antibiotics cannot reach). 30S: 1.tetracyclines (doxycycline): avoided in children less than 12 years (impaired growth, and teeth discoloration) may be used to treat Lyme disease. 2.aminoglycosides (gentamycin): possible problems with ears or kidneys. It is used to treat ope fractures type III. 50S: 1.Clindamycin: may cause pseudomembranous colitis (c.diff). monitor patients who are taking warfarin (Coumadin). It can wipe out the bacteria flora from the gut (intestinal bacteria secrete vitamin K). usually used if the patient is allergic to penicillins or Ancef. Clindamycin creates C/diff that is helped by antibiotics. Use cirpo if allergy to clindamycin or flagyl if c.diff is created. Clindamycin will achieve the highest concentration in bone. 2.macrolides (erythromycin): be aware of Coumadin interaction. 3.Zyvox (linezolid): used in resistant gram-positive bacteria 4.chloramphenicol: watch out for anaplastic anemia. Other points of interest •When you add antibiotics to the cement, the maximum effect occurs at 2 weeks and there will be no effect at 8 weeks. •Panton-Valentine Leukocidin (PVL) is a cytotoxin produced by Staphylococcus aureus and this toxin may cause necrotizing fasciitis or necrosis of the tissues. It is usually found in the community-acquired cases of MRSA. There will be more complex infection. More incidence of DVT and PE. Become a friend on facebook: http://www.facebook.com/drebraheim Follow me on twitter: https://twitter.com/#!/DrEbraheim_UTMC Donate to the University of Toledo Foundation Department of Orthopaedic Surgery Endowed Chair Fund: https://www.utfoundation.org/foundation/home/Give_Online.aspx?sig=29
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Beta Lactam Antibiotic: Mechanism of Action (Penicillin)| Bhushan Science
 
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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
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Bacterial Cell Envelope, Gram Positive and Gram Negative Bacteria
 
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Donate here: http://www.aklectures.com/donate.php Website video link: http://www.aklectures.com/lecture/bacterial-cell-envelope-gram-positive-and-gram-negative-bacteria Facebook link: https://www.facebook.com/aklectures Website link: http://www.aklectures.com
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Mechanism of Transpeptidase and Inhibition with Penicillin
 
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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
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Antibiotics that target bacterial nucleic acids
 
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This is a brief overview of antibiotics that target bacterial nucleic acids Sulfonamides (e.g. sulfamethoxazole (smx)) Bacteriostatic alone, bactericidal when used with tmp Inhibits DHPS protein that makes precursor to tetrahydrofolate synthesis, which is crucial for nucleic acid synthesis Resistance conferred by (1) spontaneous mutation in dhps, (2) acquisition of alternative DHPS, or (3) increased PABA production Trimethoprim (tmp) Bactericidal, combination with sulfonamides is synergistic (both drugs used at lower doses) Inhibits DHFR, the enzyme that makes tetrahydrofolate Quinolones/Fluoroquinolones (e.g. nalidixic acid (1st gen) and ciprofloxacin (2nd gen)) Bactericidal; inhibit DNA gyrase and topoisomerase IV Resistance conferred by (1) mutation in target proteins, (2) decreased uptake, (3) increased efflux, and (4) cross resistance with other antibiotics Rifamycins (e.g. rifampin) Bacteriostatic or bactericidal depending on dosage Bind to RNA polymerase to inhibit mRNA synthesis (transcription) Resistance conferred by RNA polymerase mutations Nitroimidazoles (e.g. metronidazole) Bactericidal against anaerobic microbes Damages DNA that is already made; must be activated by microbial enzymes (prodrugs) I created this presentation with Google Slides. Image were created or taken from Wikimedia Commons I created this video with the YouTube Video Editor.
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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.
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normal Cell wall synthesis
 
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Peptidoglycan Synthesis
 
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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.
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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.
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Classes of antibiotics that target the cell envelope
 
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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.
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