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
Microbiology is the study of microorganisms.
The overall theme of the Microbiology course is to study the relationship between microbes and our lives.
Microorganisms (microbes) are organisms that are too small to be seen with the unaided eye, and usually require a microscope to be seen.
This relationship involves harmful effects such as diseases and food spoilage as well as many beneficial effects.
Direct Download Link ❤❤https://healthkura.com/antibacterial-agents/❤❤
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Antibacterial Agents/ antibiotics (Ocular Pharmacology)
PRESENTATION LAYOUT
Introduction to antimicrobial drugs
Classification of antimicrobial drugs
Antibacterial drugs:
- Classification
- Indications
- Side effects
Antibacterial Resistance
Antimicrobial drugs are chemotherapeutic drugs
Two categories: – Antibiotics : Antimicrobial drugs produced by microorganisms
– Synthetic drugs : Antimicrobial drugs synthesized in the lab
..............................................
For Further Reading
oTextbook of microbiology by Ananthanarayan & Paniker
o Essentials of Medical Pharmacology KD Tripathi
o Basic & Clinical Pharmacology by Bertram G. Katzung
o Ophthalmic Drugs by Graham Hopkins and Richard Pearson
o Internet
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
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
Microbiology is the study of microorganisms.
The overall theme of the Microbiology course is to study the relationship between microbes and our lives.
Microorganisms (microbes) are organisms that are too small to be seen with the unaided eye, and usually require a microscope to be seen.
This relationship involves harmful effects such as diseases and food spoilage as well as many beneficial effects.
Direct Download Link ❤❤https://healthkura.com/antibacterial-agents/❤❤
Dear viewers Check Out my other piece of works at ❤❤❤ https://healthkura.com ❤❤❤
Antibacterial Agents/ antibiotics (Ocular Pharmacology)
PRESENTATION LAYOUT
Introduction to antimicrobial drugs
Classification of antimicrobial drugs
Antibacterial drugs:
- Classification
- Indications
- Side effects
Antibacterial Resistance
Antimicrobial drugs are chemotherapeutic drugs
Two categories: – Antibiotics : Antimicrobial drugs produced by microorganisms
– Synthetic drugs : Antimicrobial drugs synthesized in the lab
..............................................
For Further Reading
oTextbook of microbiology by Ananthanarayan & Paniker
o Essentials of Medical Pharmacology KD Tripathi
o Basic & Clinical Pharmacology by Bertram G. Katzung
o Ophthalmic Drugs by Graham Hopkins and Richard Pearson
o Internet
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Antibiotics Resistance is a new issue in Microbiology-Medicine aspects, taken from Lange Review of Medical Microbiology, this purpose is for education only
Development of resistant Staphylococcus aureus over timeTim Plante
A module covering the development of antibiotic resistance in Staphylococcus aureus including the development of MRSA or methicillin resistant staph aureus.
Hospital acquired diseases have contributed enormously to the rising death toll of patients. I hope to bring closure on a scenario where you are most susceptible just when you think you are safe. Hospitals are safe havens to the sick people but silent killers lurk through the doors of even these safe havens.
To understand the mechanisms of antimicrobial action and the classification of antimicrobial drugs.
To explain the process of microbial resistance.
To understand the spread of resistant microbes.
Outlines the prevention of microbial resistance.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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 ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
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
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
2. A substance that is :
1. produced by or synthesized from other microorganisms,
such as molds.
2. capable of destroying or weakening certain
microorganisms, especially bacteria or fungi , that cause
infections or infectious diseases.
3. inhibit pathogens by interfering with essential intracellular
processes as protein synthesis .
NB : Antibiotics are derived from three sources: moulds or
fungi; bacteria; or synthetic or semi-synthetic compounds.
And they don’t kill viruses.
3. Cell wall inhibitors,
such as Penicillin and
Vancomycin.
Protein synthesis
inhibitors, such as
Aminoglycoside.
Inhibitors of nucleic acid
synthesis, such as
Fluoroquinolones(DNA)and
Rifampin(RNA)
Anti-metabolites,
such as the sulfa
drugs.
Cell Membrane Damaging
such as
PolymyxinB,Gramicidin and
Daptomycin.
4. Def. : Ability of a microorganism to withstand the effects of an antibiotic
through mutation or plasmid exchange between bacteria of the same species.
•Bacterium carries several resistance genes, it is called multiresistant or, informally, a
superbug.
•What are Causes of Resistance ?? :
1. Antibiotic overuse, abuse, and in some cases, misuse, due to incorrect diagnosis.
2. Antibiotic use in animal husbandry .
3. Increased Globalisation (Movement and contact of people).
4. hospital settings often give rise to
antibiotic resistant bacteria.
We are
prepared , are
you ??
5. Ex : Streptomyces
Natural
bacteria are ‘intrinsically’
resistant.
resistance can be due to :
1. some genes responsible
for resistance to its own
antibiotic.
2. lack a transport system or
a target for the antibiotics
3. increased efflux activity.
Acquired
sensitive to antibiotics, but
are liable to develop
resistance.
caused by mutations in
chromosomal genes.
acquisition of mobile
genetic elements, such as
plasmids or transposons,
which carry the antibiotic
resistance genes.
6. 1. Reduced drug accumulation: by decreasing drug
permeability ,increasing active efflux (pumping
out) of the drugs across the cell surface.
2. Enzymatic inactivation ((β-lactamase inactivate
penicillin G )).
3. Alteration or over-expression of the drug target.
4. Loss of enzymes involved in drug activation. This
mechanism is relatively new.
5. Alteration of metabolic pathway((sulfonamide-
resistant bacteria ))
7. Definition:
Is usually one that first appears three days after a patient is
admitted to a hospital or other health care facility.
Causes :
1. Contact with contaminated hands of hospital staff
2. Contact with contaminated surfaces such as door handles,
overbed tables and call bells .
3. Contact with contaminated equipment, such as stethoscopes
and blood pressure cuffs.
4. Urinary bladder catheterization and respiratory procedures.
5. Surgery and wounds and intravenous (IV) procedures.
Examples on Hospital-Acquired Infetions :
a) Staphylococcus aureus .
b) Enterococcus (urinary tract infections).
c) Pseudomonas aeruginosa .
d) Acinetobacter baumannii .
e) proteus species .
8. •According to the CDC(Center for Disease Control) , the most
common pathogens that cause nosocomial infections are
Staphylococcus aureus, Pseudomonas aeruginosa, and E. coli.
•The common nosocomial infections are urinary tract
infections, respiratory pneumonia, surgical site wound
infections, bacteremia, gastrointestinal and skin infections.
9. Enterococci are part of the normal intestinal
flora of humans and animals .
important pathogens responsible for serious
infections.
includes more than 17 species but only a few
cause clinical infections in humans.
capable of cellular respiration in both
oxygen-rich and oxygen-poor environments.
Causes urinary tract infections, bacterial
endocarditis, and meningitis.
10. MOA:
binds to the two D-alanine residues on the end of the peptide
chains No interaction with the cell wall cross-
linking enzyme inhibiting proper cell wall
synthesis.
Major side effects:
"Red man syndrome": RMS is characterized by :
flushing, erythema, and pruritus,
usually affecting the upper body,
neck, and face more than the lower body.
11. MOR:
D-alanine residue replaced by a D-lactate, so vancomycin cannot bind
vancomycin cannot bind stable cross links are
formed successfully (normal cell wall synthesis)
Six different types of vancomycin resistance are shown by
enterococcus(V.R.E) :
Van-A, Van-B, Van-C, Van-D, Van-E and Van-F. Of these, only Van-A,
Van-B and Van-C have been seen in general clinical practice, so far.
Van-A VRE is resistant to both vancomycin and teicoplanin.
Van-B VRE is resistant to vancomycin but sensitive to teicoplanin.
Van-C VRE is only partly resistant to vancomycin, and sensitive to
teicoplanin.
NB : In the US, Linezolid is commonly used to treat VRE, as teicoplanin
is not available.
Vancomycin is contraindicated in patients with known hypersensitivity
to this antibiotic
12. MOA :
via inhibition of protein synthesis by binding 23S
ribosomal RNA of the 50S subunit.
Major side effects:Diarrhea headache nausea.
MOR: point mutation , in which a guanine base is replaced
with thymine in base pair 2576 of the genes coding for
23S
ribosomal RNA.
Contraindications :
hypersensitivity to linezolid or any of the other product
components.
Or patients with carcinoid syndrome .
or in patients taking directly and indirectly acting
sympathomimetic agents, vasopressive agents
13. with the presence of bacterial motility and fimbriae
Urease production by Proteus may favor the
production of upper urinary tract infections (UTIs)
by organisms such as Proteus.
Treatment:
1st Usually used for UTIs Methenamine (anti-bacterial agent).
MOA:
Methenamine, an inactive weak base, slowly hydrolyzes in
acidic urine to ammonia and the nonspecific antibacterial
(formaldehyde).
Urinary formaldehyde concentrations may be bactericidal or
bacteriostatic.
14. 1. An allergic reaction (shortness of breath).
2. Lower back or side pain.
3. Blood in urine.
4. Painful or difficult urination.
MOR:
a. rod shaped bacterium has the ability to produce high levels
of urease,Urease hydrolyzes urea to ammonia (NH3).
b. makes the urine more alkaline stop Methenamine hydrolysis
and HCHO release
15. MOA :
inhibit the topoisomerase II leaving the two
nuclease domains intact leads to DNA
fragmentation.
Quinolones can enter cells easily via porins ,
therefore, are often used to treat intracellular
pathogens such as Legionella pneumophila and
Mycoplasma pneumoniae.
For many Gram-negative bacteria, DNA gyrase is
the target.
16. By three Mechanisms :
1. efflux pumps act to decrease
intracellular quinolone concentration.
2. Gram-negative bacteria, plasmid-mediated
resistance genes, produces proteins that bind to
DNA gyrase, protecting it from quinolones.
3. mutations at key sites in DNA gyrase or
topoisomerase IV can decrease binding affinity to
quinolones.
17. with patient takes drugs metabolized by CYP1A2 as they
leads to increased plasma concentrations of Quinolones drugs Thus,
leads to clinically significant adverse events of the coadministered
drug.
For your Knowledge :
Proteus is a genus of Gram-negative Proteobacteria.
Widely distributed in nature .
Found in decomposing animal
matter, in sewage, in manure soil,
and in human and animal feces.
They are opportunistic pathogens
responsible for urinary and septic infections,
often nosocomial.
18. Most common pathogen isolated from
patients who have been hospitalized longer
than 1 week.
frequent cause of nosocomial infections such
as pneumonia, urinary tract infections (UTIs),
and bacteremia.
complicated and can be life threatening.
19. administered intravenously and intramuscularly. Some are used in
topical preparations for wounds.
Oral administration can be used for gut decontamination (e.g., in
hepatic encephalopathy).
MOA:
act by binding to the aminoacyl site of 16S ribosomal RNA within
the 30S ribosomal subunit, leading to misreading of the genetic
code and inhibition of translocation.
20. Contraindications
Aminoglycosides should not be used in patients with:
a) previous vestibular or auditory toxicity due to an
aminoglycoside
b) serious hypersensitivity reaction to an
aminoglycoside
AMGs cross placenta ,not used in case of pregnancy
Major side effects:
a) Irreversible ototoxicity: loss of hearing, dizziness
b) Reversible nephrotoxicity.
c) Neuromuscular blockade may lead to respiratory
paralysis
21. increased
impermeability
across the cell wall
mechanism of this
type of resistance is
not known.
up-regulation of the
efflux system
(efflux pump)
isolated
Pseudomonas
aeruginosa
have been shown to
contain AMGs
modifying enzymes.
22. 2nd Treatment :
combination of an antipseudomonal beta-lactam
(eg, penicillin or cephalosporin) and an
aminoglycoside.
3rd Carbapenems (eg, imipenem, meropenem)
with antipseudomonal quinolones may be used in
conjunction with an aminoglycoside.
MOA: Carbapenems act as penicillins on cell wall
destruction of bacteria.
Major side effects:
1-GI distress and skin rashes.
2-CNS toxicity at very hight plasma lvl.
23. one of the leading causes of infections acquired in the
community and after surgery or hospital.
30% of individuals carry S. aureus in their nose, pharynx or
back of throat and on their skin.
presence of S. aureus does not always indicate infection.
S. aureus can survive from hours to months, on dry
environmental surfaces, depending on strain.
Although it is not always pathogenic, it is a common cause of
skin infections (e.g. boils), respiratory disease (e.g. sinusitis),
and food poisoning.
The emergence of antibiotic-resistant forms of pathogenic S.
aureus (e.g. MRSA(Methicillin-resistant S.A) is a worldwide
problem in clinical medicine.
24. 1st treatment of choice for S.aureus infection
is penicillins :
MOA:
By binding to specific penicillin-binding proteins
(PBPs) located inside the bacterial cell wall,
inhibits the third and last stage of bacterial cell
wall synthesis.
Cell lysis is then mediated by bacterial cell wall
autolytic enzymes such as autolysins; it is
possible that penicillin G interferes with an
autolysin inhibitor. (( increased effect))
25. MOR:
the bacterium produces the enzyme β-
lactamase or the enzyme penicillinase which
will hydrolyse the β-lactam ring of the
antibiotic, rendering the antibiotic ineffective.
Major side effects:
A. Hypersensitivity: difficulty breathing,
skin rash, hives, itching.
B. Stomach upset, diarrhea, nausea, and
vomiting.
26. like Methicilin or flucloxacillin or β-lactam antibiotics may be
co-administered with a β-lactamase inhibitor.
For example, Augmentin is made of amoxicillin, a β-lactam
antibiotic, and clavulanic acid, a β-lactamase inhibitor.
MOR:
modification in the mecA gene of the bacteria which codes for
an altered penicillin-binding protein leads to a lower affinity
for binding β-lactams (penicillins, cephalosporins and
carbapenems). This allows for resistance to all β-lactam
antibiotics.
3rd vancomycin is used.
27. MOA :
stop the growth and reproduction of bacteria by disrupting
translation of messenger RNA (mRNA) into proteins in the
ribosome.
MOR: The intrinsic resistance of most Gram-negative bacteria
to linezolid is due to the activity of efflux pumps, which
actively "pump" linezolid out of the cell faster than it can
accumulate.
Gram-positive bacteria usually develop resistance in which a
guanine base is replaced with thymine in base pair 2576 of
the genes coding for 23S ribosomal RNA .
28. Acinetobacter baumannii is a species of pathogenic bacteria
involved in most nosocomial infections.
Aerobic gram-negative bacterium resistant to
most antibiotics.
Ventilator-associated pneumonia (VAP) is a sub-type of
hospital-acquired pneumonia (HAP) which occurs in people
who are receiving mechanical ventilation.
Many of the typical symptoms of pneumonia will either be
absent or unable to be obtained in VAP why ??
Ans. : because People who are on mechanical ventilation are
often sedated and are rarely able to communicate.
The most important signs are fever, low body temperature,
new purulent sputum, and hypoxemia (decreasing amounts of
oxygen in the blood).
29. MOA :
inhibits bacterial wall synthesis like other B-lactam antibiotics. In
contrast to other B-lactams, it is highly resistant to degradation
by B-lactamases
MOR:
1. Resistance generally arises due to mutations in penicillin binding
proteins. or resistance to diffusion across the bacterial outer
membrane.
2. The most widespread B-lactamases with carbapenemase activity in
A. baumannii are carbapenem-hydrolysing class D beta-
lactamases (CHDLs) that are mostly specific for this species.
Unlike imipenem, it is stable to dehydropeptidase-1 and can
therefore be given without cilastatin.
30.
31.
32. Limiting the Spread of Drug Resistant
Bacteria:
A. Ensure that antibiotics are used only when
necessary.
B. Ensure that they are used for the
appropriate amount of time.(( Complete to
be fully effective and not breed resistance))
C. Third strategy for limiting drug resistance is
to use antibiotics combinations.
Development of New Antibiotics.
33. Phage Therapy.
Mobilisation of Host Defence Mechanisms,This
can be achieved through :
1. the mobilisation of innate immunity such as
defensins((They are small Cysteine-rich cationic
proteins, and function as host defense peptides
Cells of the immune system contain these
peptides to assist in killing phagocytosed
bacteria)).
2. through the development of vaccines, which
make antibiotics less necessary.