The most common mode of action for antibiotics is the inhibition of cell wall synthesis. Antibiotics that inhibit cell wall synthesis work because of the fact that most eubacteria have peptidoglycan-based cell walls but mammals do not. Growth is prevented by inhibiting peptidoglycan synthesis. Thus these antibiotics only work for actively growing bacteria. The cell wall of new bacteria that grew in the presence of cell-wall-synthesis inhibitors is deprived of peptidoglycan. These bacteria will be subjected to osmotic lysis.In addition, gram-negative bacteria generally are less susceptible to inhibitors of cell wall synthesis than are gram-positive bacteria. In the former cell wall synthesis inhibitors fail to reach the cell wall because they are blocked by the gram-negative outer membrane.Penicillin is the classic example of an inhibitor of cell wall synthesis. Other examples include: ampicillin, bacitracin, carbapenems, cephalosporin, methicillin, oxacillin and vancomycin
The presentation include semisynthetic penicillin introduction and classification.
Contents
Semisynthetic penicillins- Introduction
Classification
Acid-resistant alternative to Penicillin G
Penicillinase- resistant penicillins
Extended spectrum penicillins
Tetracyclines slide contains full information about uses, adverse effect, marketed preparation, precaution, route of drug administration, antimicrobial spectrum, mechanism of action, pharmacokineticks and pharmacodynamics of tetracyclines. This slide is very helpful for pharmacy and pharmacology student for the study about tetracyclines.
A protein synthesis inhibitor is a substance that stops or slows the growth or proliferation of cells by disrupting the processes that lead directly to the generation of new proteins. All of the antibiotics that target bacterial protein synthesis do so by interacting with the bacterial ribosome and inhibiting its function. The ribosome might not seem like a very good target for selective toxicity, because all cells, including our own, use ribosomes for protein synthesis.The good thing is that bacteria and eukaryotes have ribosomes that are structurally different. Bacteria have so-called 70S ribosomes and eukaryotes have 80S ribosomes. No, not '70s and '80s ribosomes, although that would be pretty entertaining. The S stands for 'Svedberg unit,' and it refers to the rate at which particles sediment down into the tube during high-speed ultracentrifugation. Basically, it tells us about the ribosome's molecular weight and shape.
70S and 80S ribosomes are different enough that antibiotics can specifically target one and not the other. Let's take a closer look at the bacterial 70S ribosome and see where some different kinds of antibiotics act on it. Remember that ribosomes are made of RNA and protein and that they have two subunits, one large and one small.
The bacterial 70S ribosome's subunits are the 50S subunit and the 30S subunit. Yes, I know, 50 + 30 = 80, not 70, but this is not a math mistake. Using the Svedberg unit to measure ribosomes means that things don't always add up perfectly, because rates of sedimentation are not additive like molecular weights are.
Before we get into the specifics of how antibiotics inhibit bacterial ribosomes, let's briefly review how ribosomes work. First, a tRNA loaded with a particular amino acid enters the ribosome at the A site. The tRNA's anticodon has to match the codon, or group of three nucleotides on the mRNA. Then, at the P site of the ribosome, a peptide bond forms between the previous amino acid and the new amino acid. Finally, the empty tRNA exits at the E site. This process repeats for the whole length of the mRNA, and the polypeptide chain continues to grow.
The presentation include semisynthetic penicillin introduction and classification.
Contents
Semisynthetic penicillins- Introduction
Classification
Acid-resistant alternative to Penicillin G
Penicillinase- resistant penicillins
Extended spectrum penicillins
Tetracyclines slide contains full information about uses, adverse effect, marketed preparation, precaution, route of drug administration, antimicrobial spectrum, mechanism of action, pharmacokineticks and pharmacodynamics of tetracyclines. This slide is very helpful for pharmacy and pharmacology student for the study about tetracyclines.
A protein synthesis inhibitor is a substance that stops or slows the growth or proliferation of cells by disrupting the processes that lead directly to the generation of new proteins. All of the antibiotics that target bacterial protein synthesis do so by interacting with the bacterial ribosome and inhibiting its function. The ribosome might not seem like a very good target for selective toxicity, because all cells, including our own, use ribosomes for protein synthesis.The good thing is that bacteria and eukaryotes have ribosomes that are structurally different. Bacteria have so-called 70S ribosomes and eukaryotes have 80S ribosomes. No, not '70s and '80s ribosomes, although that would be pretty entertaining. The S stands for 'Svedberg unit,' and it refers to the rate at which particles sediment down into the tube during high-speed ultracentrifugation. Basically, it tells us about the ribosome's molecular weight and shape.
70S and 80S ribosomes are different enough that antibiotics can specifically target one and not the other. Let's take a closer look at the bacterial 70S ribosome and see where some different kinds of antibiotics act on it. Remember that ribosomes are made of RNA and protein and that they have two subunits, one large and one small.
The bacterial 70S ribosome's subunits are the 50S subunit and the 30S subunit. Yes, I know, 50 + 30 = 80, not 70, but this is not a math mistake. Using the Svedberg unit to measure ribosomes means that things don't always add up perfectly, because rates of sedimentation are not additive like molecular weights are.
Before we get into the specifics of how antibiotics inhibit bacterial ribosomes, let's briefly review how ribosomes work. First, a tRNA loaded with a particular amino acid enters the ribosome at the A site. The tRNA's anticodon has to match the codon, or group of three nucleotides on the mRNA. Then, at the P site of the ribosome, a peptide bond forms between the previous amino acid and the new amino acid. Finally, the empty tRNA exits at the E site. This process repeats for the whole length of the mRNA, and the polypeptide chain continues to grow.
Mechanism of action of major antibiotic classes including betal lactam agents, aminoglycosides, macrolides, tetracyclines, quinolons, vancomycin, oxazolidionons. Detailed review and illustrations
Definition
History
Chemistry
Properties
Classification & its Generation
Pharmacokinetics
Mechanism of action
Indication
Contraindication
Therapeutic use
Adverse effect
Resistance
Comparison with penicillin
Market preparation
12.COMPREHENSIVE OFANTIMICROBIAL AGENTS AND CHEMOTHERAPY ( CLASSIFICATION AND...Saminathan Kayarohanam
Antimicrobial Agents and Chemotherapy (AAC) features interdisciplinary studies that build our understanding of the underlying mechanisms and therapeutic applications of antimicrobial and antiparasitic agents and chemotherapy.
Mechanism of action of major antibiotic classes including betal lactam agents, aminoglycosides, macrolides, tetracyclines, quinolons, vancomycin, oxazolidionons. Detailed review and illustrations
Definition
History
Chemistry
Properties
Classification & its Generation
Pharmacokinetics
Mechanism of action
Indication
Contraindication
Therapeutic use
Adverse effect
Resistance
Comparison with penicillin
Market preparation
12.COMPREHENSIVE OFANTIMICROBIAL AGENTS AND CHEMOTHERAPY ( CLASSIFICATION AND...Saminathan Kayarohanam
Antimicrobial Agents and Chemotherapy (AAC) features interdisciplinary studies that build our understanding of the underlying mechanisms and therapeutic applications of antimicrobial and antiparasitic agents and chemotherapy.
Tuberculosis treatment refers to the medical treatment of the infectious disease tuberculosis (TB).
The standard "short" course treatment for TB is isoniazid (along with pyridoxal phosphate to obviate peripheral neuropathy caused by isoniazid), rifampicin (also known as rifampin in the United States), pyrazinamide, and ethambutol for two months, then isoniazid and rifampicin alone for a further four months. The patient is considered to be free of living bacteria after six months (although there is still a relapse rate of up to 7%). For latent tuberculosis, the standard treatment is six to nine months of daily isoniazid alone or three months of weekly (12 doses total) of isoniazid/rifapentine combination. If the organism is known to be fully sensitive, then treatment is with isoniazid, rifampicin, and pyrazinamide for two months, followed by isoniazid and rifampicin for four months. Ethambutol need not be used.
Immunosuppressant are drugs or medicines that lower the body's ability to reject a transplanted organ. Another term for these drugs is anti-rejection drugs. There are 2 types of immunosuppressants: Induction drugs: Powerful antirejection medicine used at the time of transplant.
The quinolones are a family of synthetic broad-spectrum antibacterial drugs. Quinolones, and derivatives, have also been isolated from natural sources and can act as natural antimicrobials and/or signalling molecules.
Antifolates are drugs that antagonise (that is, block) the actions of folic acid (vitamin B9). Folic acid's primary function in the body is as a cofactor to various methyltransferases involved in serine, methionine, thymidine and purine biosynthesis.
This slide have the information about chemotherapy:- the treatment of disease by means of chemicals that have a specific toxic effect upon the disease-producing microorganisms or that selectively destroy cancerous tissue.Also include the drug resistance:-Drug resistance is the reduction in effectiveness of a drug such as an antimicrobial.
This is lecturer notes on pharmacology & toxicology for B.V.Sc & A.H. Seventh semester students.This may useful for other institute veterinary students.Please send your comment and suggestion;jibachhashah@gmail.com,mob.9845024121
This presentation provides a comprehensive introduction to antibiotics, exploring their historical significance, classifications, and essential role in modern medicine. Attendees will gain a profound understanding of the diverse mechanisms through which antibiotics act to combat bacterial infections.
Outline:
Introduction to Antibiotics
Definition and historical context
Significance in treating bacterial infections
Classification of Antibiotics
Broad-spectrum vs. narrow-spectrum antibiotics
Classes: penicillins, cephalosporins, tetracyclines, etc.
Mechanisms of Antibiotic Action
Inhibition of cell wall synthesis (e.g., penicillins)
Disruption of protein synthesis (e.g., macrolides)
Inhibition of nucleic acid synthesis (e.g., quinolones)
Interference with metabolic pathways (e.g., sulfonamides)
Selective Toxicity
Understanding the concept and importance
How antibiotics target bacterial structures without harming human cells
Resistance to Antibiotics
Factors contributing to antibiotic resistance
Consequences and global impact
Case Studies
Examples of well-known antibiotics and their mode of action
Real-world applications and success stories
Future Trends and Challenges
Emerging technologies in antibiotic development
Strategies to address antibiotic resistance
Conclusion
Recap of key points
Emphasis on the critical role antibiotics play in public health
This presentation aims to provide a solid foundation for understanding antibiotics and their mode of action, catering to both beginners and those looking to deepen their knowledge in the field. Through engaging visuals and clear explanations, you will have a heightened awareness of the vital role antibiotics play in preserving human health while being mindful of the challenges posed by antibiotic resistance.
Myself Gaurav Chaudhary, Assistant Professor, I.T.S. College of Pharmacy.
The Slideshare contains complete Notes of Unit-1 Medicinal Chemistry-III BP601T
It contains the Classification, stereochemistry chemical degradation, and Structure-activity relationship of Antibiotics(Penicillin, Cephalosporins, Monobactum, Aminoglycosides).
The study material is authentic.
Similar to 2.ANTIBIOTIC (CELL WALL INHIBITORS) (20)
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
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It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
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3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
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2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
2. 2
NUM CONTENT SLIDE
1 OVERVIEW OF PENICILLIN 4
2 DEFINITIONS 5
3 THE SPECTRUM OF ANTIBIOTIC ACTIVITY 6
4 COMMON BACTERIA BY SITE OF INFECTION 7,8
5 DRUG,PRIMARY EFFECTS,SPECTRUM AND SIDE EFFECTS 9
6 GENERAL MECHANISAM OF ANTIBIOTICS 10
7 CLASSIFICATION OF CELL WALL INHIBITORS 11
8 CLASSIFICATION OF PENICILLIN 12-14
9 STRUCTURAL FEATURES OF β-LACTAM ANTIBIOTICS 15
10 MECHANISM OF ACTION OF PENICILLINS 16,17
11 ADVERSE EFFECTS OF PENICILLINS 18,19
12 THERAPEUTIC APPLICATIONS 20-22
13 INTRODUCTION TO CEPHALOSPORINS 23
14 THERAPEUTIC APPLICATIONS OF CEPHALOSPORINS 24
3. 3
LEARNING OUTCOME
1. Able to understand and describe various definition
related to antibiotics
2. Describe the common bacteria, types of infection and
the treatment.
3. Abele to demonstrate the general mechanism of
antibiotics and classification of cell wall inhibitors.
4. Able to describe the penicillin mechanism and
adverse effects.
5. Able to understand the therapeutic application of cell
wall inhibitors.
4. 4
1. OVERVIEW OF PENICILLIN
Antibiotics or Antibacterials are a type of antimicrobial used in
the treatment and prevention of bacterial infection. They may
either kill or inhibit the growth of bacteria.
The penicillin is naturally produced by fungi of the
genus Penicillium.
Penicillin is a common antibiotic, used to treat bacterial infections.
Penicillin was discovered by Scottish scientist Sir Alexander
Flemingin 1928.
Bactericidal An antimicrobial drug that can eradicate an infection in
the absence of host defense mechanisms; kills bacteria.
Bacteriostatic An antimicrobial drug that inhibits microbial growth
but requires host defense mechanisms to eradicate the infection;
does not kill bacteria.
Beta-lactam antibiotics Drugs with structures containing a beta-
lactam ring: includes the penicillins, cephalosporins and
carbapenems. This ring must be intact for antimicrobial action.
Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
5. 2. DEFINITIONS
5
Beta-lactamases Bacterial enzymes (penicillinases,
cephalosporinases) that hydrolyze the beta-lactam ring of certain
penicillins and cephalosporins.
Beta-lactam inhibitors Potent inhibitors of some bacterial beta-
lactamases used in combinations to protect hydrolyzable
penicillins from inactivation.
Penicillin-binding proteins (PBPs) Bacterial cytoplasmic
membrane proteins that act as the initial receptors for penicillins
and other beta-lactam antibiotics.
Peptidoglycan Chains of polysaccharides and polypeptides that
are cross-linked to form the bacterial cell wall.
Selective toxicity More toxic to the invader than to the host; a
property of useful antimicrobial drugs.
Transpeptidases Bacterial enzymes involved in the cross-
linking of linear peptidoglycan chains, the final step in cell wall
synthesis.
Con…Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
6. 6
3.THE SPECTRUM OF ANTIBIOTIC ACTIVITY
6Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
15. 15
PENICILLINS
The penicillin's are among the most
widely effective antibiotics and also
the least toxic drugs known, but
increased resistance has limited
their use.
Members of this family differ from
one another in the R substituent
attached to the 6-aminopenicillanic
acid residue.
The nature of this side chain affects
the antimicrobial spectrum, stability
to stomach acid, and susceptibility to
bacterial degradative enzymes (β-
lactamases).
9.STRUCTURAL FEATURES OF Β -LACTAM ANTIBIOTICS
Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
16. 10. MECHANISM OF ACTION OF PENICILLINS
16
1.Penicillin-binding proteins:
Penicillins inactivate numerous proteins on the bacterial cell membrane.
These penicillin-binding proteins (PBPs) are bacterial enzymes involved
in the synthesis of the cell wall and in the maintenance of the
morphologic features of the bacterium.
2.Inhibition of transpeptidase:
Penicillins inhibit this transpeptidase-catalyzed reaction, thus hindering
the formation of cross-links essential for cell wall integrity. As a result of
this blockade of cell wall synthesis.
3.Production of autolysins:
Many bacteria, particularly the gram-positive cocci, produce degradative
enzymes (autolysins) that participate in the normal remodeling of the
bacterial cell wall.
Con…
16
Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
17. 17
1- Penicillin (or other cell wall synthesis inhibitor) is
added to the growth medium.
2- The cell begins to grow, but is unable to synthesize
new cell wall.
3- cytoplasm covered by plasma membrane begins to
squeeze out through the gap(s) in the cell wall.
4- Cell wall integrity is further violated. The cell
continues to increase in size, but is unable to "pinch
off" the extra cytoplasmic material into two daughter
cells .
5- The loss of the cell wall also causes the cell to lose
control over its shape, Finally, the fact that the cell
disrupts homeostasis, which usually leads to the cell's
death
10. MECHANISM OF ACTION OF PENICILLINS
Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
23. 13. INTRODUCTION TO CEPHALOSPORINS
23
These β-lactam antibiotics are also fungal products and
have bactericidal activity due to inhibition of
transpeptidase.
The cephalosporins are β-lactam antibiotics that are closely
related both structurally and functionally to the penicillins.
Most cephalosporins are produced semisynthetically by the
chemical attachment of side chains to 7-
aminocephalosporanic acid.
Cephalosporins are acid stable, but many are poorly
absorbed.
Cephalosporins are penicillinase-resistant.
Cephalosporins are broad-spectrum antibacterials.
Cephalosporins are mostly well tolerated.
All can cause allergic reactions, some cause renal injury,
alcohol intolerance, and bleeding (vitamin K antagonism).
Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
The frequency of cross-allergenicity between the two groups of drugs is
uncertain but is probably around 5–10%.
Cephalosporins that contain a methylthiotetrazole group (eg, cefamandole, cefmetazole, cefotetan, cefoperazone) frequently cause hypoprothrombinemia and bleeding disorders. Administration of vitamin K1, 10 mg twice weekly, can prevent this.