Презентация на тему: Antimicrobial drugs

Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
SULFONAMIDES
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
QUINOLONES
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Antimicrobial drugs
Literature
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Первый слайд презентации: Antimicrobial drugs

Disinfectants and Antiseptics Antibacterial chemotherapeutic drugs

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Antimicrobial drugs have antimicrobial properties. They are divided into 2 groups: Disinfectants and Antiseptics (drugs are used locally) Antibacterial chemotherapeutic drugs are applied resorptively. Type of action: Bacteriostatic : drugs delay the growth and reproduction of bacterial cells. Bactericidal: drugs cause cell death.

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Disinfectants and Antiseptics Disinfection denotes the inactivation or killing of pathogens (protozoa, bacteria, fungi, viruses) in the human environment (instruments, equipment, premises, dishes, patients’ excrements). They provide a rapidly developing effect. They are applied at bactericidal concentration and aimed at the prevention of the spread of infection.

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Phenol was the first antiseptics. Phenol coefficient (the ratio between the concentration of phenol and the antiseptic under test, in which both substances provide equal antimicrobial effect) is a common measure of antiseptic activity.

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Antisepsis refers to the reduction by chemical agents of germ numbers on skin and mucosal surfaces. Agents for chemical disinfection ideally should cause rapid, complete, and persistent inactivation of all germs, but at the same time exhibit low toxicity (systemic toxicity, tissue irritancy, antigenicity) and be non-deleterious to inanimate materials. But anticeptics are highly toxic and can cause side effects: local irritant and cauterizing effect. At higher concentrations they are disinfectants.

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Disinfectants come from various chemical classes, including oxidants, halogens or halogen-releasing agents, alcohols, aldehydes, organic acids, phenols, cationic surfactants (detergents) and formerly also heavy metals. The basic mechanisms of action involve denaturation of proteins, inhibition of enzymes, or a dehydration. Effects are dependent on concentration and contact time. Activity spectrum. Disinfectants inactivate bacteria (gram-positive > gram-negative > mycobacteria), less effectively their sporal forms, and a few (e.g., formaldehyde) are virucidal.

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Applications Skin “disinfection.” (Reduction of germs before injections or surgical procedures). Useful agents include: alcohols ( ethanol ) 7 0–90%; iodine-releasing agents like povidone, cationic surfactants, and mixtures of these. Minimal contact times should be at least 15 s on skin. Mucosal disinfection: Germ counts can be reduced by PVP iodine or chlorhexidine (contact time 2 min), although not as effectively as on skin.

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Wound disinfection can be achieved with hydrogen peroxide or with potassium permanganate, as well as PVP iodine, chlorhexidine, and biguanidines. Hygienic and surgical hand disinfection: is required after a suspected contamination, before surgical procedures. Alcohols, mixtures of alcohols and phenols, cationic surfactants, or acids are available for this purpose. Admixture of other agents prolongs duration of action and reduces inflammation

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Disinfection of instruments: Instruments that cannot be heat- or steam sterilized can be precleaned and then disinfected with aldehydes and detergents. Surface (floor) disinfection employs aldehydes combined with cationic surfactants and oxidants or, more rarely, acidic or alkalizing agents.

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Chemotherapeutic drugs inhibit/kill the infecting organism and have no/minimal effect on the recipient. They can be divided: Antibiotics are produced by microorganisms. Synthetic drugs. These drugs influence specific microorganism and have wide therapeutic window. They suppress the growth of or kill other microorganisms at very low concentrations. They are used for the treatment and prevention of diseases, for the treatment of infection carries.

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Basic principles of chemotherapy Early start of treatment. Determination of the causative agent, its sensitivity to the drug. The use of optimum doses. Accounting pharmacokinetics of the drug: the degree of absorption, distribution, features of excretion, duration of action. Accounting for toxicity of drugs. Carrying out a full course of treatment (5-10 days). If necessary – the possibility of combining drugs.

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Слайд 15: SULFONAMIDES

Sulfonamides were the first antimicrobial agents (AMAs) effective against pyogenic bacterial infections. All sulfonamides are derivatives of sulfanilamide. Individual members differ in the nature of N1 substitution, which governs solubility, potency and pharmacokinetic property. A free amino group in the para-position (N4) is required for antibacterial activity.

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Sulfonamides are primarily bacteriostatic against many gram-positive and gram-negative bacteria. However, bactericidal concentrations may be attained in urine. Sensitivity patterns among microorganisms have changed from time-to-time and place-to-place. Those still sensitive are: Strepto с. pyogenes, Haemophilus Influenzae, Vibrio cholerae, Staph. aureus, gonococci, meningococci, pneumococci, Escherichia coli, Shigella, Chlamydiae, Actinomyces, Nocardia and Toxoplasma. Anaerobic bacteria are not susceptible now.

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1. Preparations used for their systemic action: Short acting (4–8 hr): Sulfadiazine, sulfadimidine Intermediate acting (8–12 hr): Sulfamethoxazole Long acting (12-24 days): Sulfamethoxypyrazine, sulfadimethoxine With a very long-term action (more 7 days): Sulfadoxine, sulfalene 2. D. acting in the intestinal lumen: phthalylsulphathiazole 3. D. for topical use: sulfacetamide sodium, silver sulfadiazine

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The mechanism is connected with their competitive antagonism with para-aminobenzoic acid (PABA). Sulfonamides block dihydropteroate synthetase also. They inhibit the union of PABA with pteridine residue to form dihydropteroic acid which conjugates with glutamic acid to produce dihydrofolic acid. They inhibit bacterial folate synthase → FA is not formed and a number of essential metabolic reactions suffer. Human cells also require FA, but they utilize preformed FA supplied in diet and are unaffected by sulfonamides.

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Sulfonamides are rapidly and nearly completely absorbed from G.I.T. Extent of plasma protein binding differs considerably (10–95%) among different members. The highly protein bound members are longer acting. Sulfonamides are widely distributed in the body—enter serous cavities easily. The free form of sulfadiazine attains the same concentration in CSF as in plasma. They cross placenta freely. The primary pathway of metabolism of sulfonamides is acetylation primarily in liver. The acetylated derivative is inactive, but can contribute to the adverse effects. It is generally less soluble in acidic urine than the parent drug—may precipitate and cause crystalluria.

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Sulfonamides are excreted mainly by the kidney through glomerular filtration. Both renal tubular secretion and reabsorption occur. The more lipid-soluble members are highly reabsorbed in the tubule, therefore are longer acting. Phthalylsulphathiazole is not absorbed from GIT and acts there. So it can be used for the treatment of intestinal infections.

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Side effects: Nausea, vomiting and epigastric pain. Crystalluria. Precipitation in urine can be minimized by taking plenty of fluids and by alkalinizing the urine in which sulfonamides and their acetylated derivatives are more soluble. Hypersensitivity reactions (rashes, urticaria and drug fever). Photosensitization. Hepatitis, unrelated to dose. Haemolysis can occur in G-6-PD deficient individuals with high doses of sulfonamides.

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USES : suppressive therapy of chronic urinary tract infection; ear, throat, nose infections; gum infection; malaria and toxoplasmosis. Ocular sulfacetamide sod. (10–30%) is a cheap alternative in trachoma and conjunctivitis, Topical silver sulfadiazine is used for preventing infection on burn surfaces.

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The fixed dose combination of trimethoprim and sulfamethoxazole is called cotrimoxazole. Trimethoprim selectively inhibits bacterial dihydrofolate reductase (DHFRase).

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Individually, both sulfonamide and trimethoprim are bacteriostatic, but the combination becomes bacteriocidal against many organisms. Spectrum of action of trimethoprim and sulfonamides overlap considerably. Additional organisms covered by the combination are— Salmonella typhi, Serratia, Klebsiella, Enterobacter, Yersinia enterocolitica, Pneumocystis and many sulfonamide-resistant strains of Staph. aureus, Strep. pyogenes, Shigella, enteropathogenic E. coli, H.influenzae, gonococci and meningococci.

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Uses Urinary tract infections (acute cystitis, prostatitis); Respiratory tract infection caused by gram positive cocci and H. influenzae; Bacterial diarrhoeas and dysentery caused by E. coli, Shigella, nontyphoid Salmonella, and Y. enterocolitica; Pneumonia in neutropenic and AIDS patients caused by Pneumocystis jiroveci; Chancroid.

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Side effects of cotrimoxazole Nausea, vomiting, stomatitis, headache and Folate deficiency (megaloblastic anaemia). Cotrimoxazole should not be given during pregnancy. Trimethoprim is an antifolate, there is theoretical teratogenic risk. Neonatal haemolysis and methaemoglobinaemia can occur if it is given near term.

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Слайд 29: QUINOLONES

1.Quinolones (without F) Nalidixic acid 2.First generation fluoroquinolones Norfloxacin, Ofloxacin, Ciprofloxacin, Pefloxacin 3. Second generation fluoroquinolones Levofloxacin, Lomefloxacin, Prulifloxacin, Moxifloxacin

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Nalidixic acid It is active against gram-negative bacteria ( E. coli, Proteus, Klebsiella, Enterobacter, Shigella but not Pseudomonas). It acts by inhibiting bacterial DNA gyrase and is bactericidal. Resistance to nalidixic acid develops rather rapidly. Nalidixic acid is absorbed orally, highly plasma protein bound and partly metabolized in liver: one of the metabolites is active. It is excreted in urine. T½ ~8 hrs.

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Nalidixic acid is primarily used as a urinary antiseptic. It has also been employed in diarrhoea caused by Proteus, E. coli, Shigella or Salmonella. Adverse effects: g.i. upset and rashes; headache, drowsiness, vertigo, visual disturbances, occasionally seizures (especially in children); phototoxicity; haemolysis.

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FLUOROQUINOLONES These preparations exhibit a bactericidal effect. Mechanism of action is associated with the inhibition of bacterial enzymes – topoisomerases II (DNA- gyrase) and IV. This impairs DNA replication and RNA formation. All this interferes with bacterial growth and division.

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The spectrum of action of First generation fluoroquinolones Highly susceptible : Neisseria gonorrhoeae; N. meningitidis; E. coli; K. pneumoniae; Enterobacter; H. influenzae; Salmonellas; Campylobacter; Shigella; Yersinia enterocolitica; Proteus; Vibrio cholerae Moderately susceptible: Pseudomonas aeruginosa; Legionella; Staph. Aureus (including few MRSA); Brucella; Listeria; Bacillus anthracis; Mycobact. tuberculosis Organisms which have shown low/variable susceptibility are: Streptococci, Mycoplasma, Chlamydia. Notable resistant bacteria are: Bacteroides fragilis, Clostridia, anaerobic cocci.

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The spectrum of action of 2 generation fluoroquinolones They are more active against gram-positive bacteria. They suppress Streptococci, Staphylococci, listeria, Corinebacteria, Enterococci, Pneumococci, Chlamydia, Mycoplasma, Ureaplasma, anaerobic microorganism. Their bactericidal activity against gram-negative bacteria is also maintained.

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Pharmacokinetics: Drugs are absorbed from the gastrointestinal tract at 60-100%, They bind to proteins of blood. They penetrate the tissues and body fluids, in the cells very well. They can pass through the BBB. They are excreted in the active form by the kidneys. They are prescribed 1-2 times a day. There are drugs for intravenous and topical use.

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Uses Urinary tract infections; Gonorrhoea; Chancroid; Bacterial gastroenteritis: dysentery, salmonellosis, cholera; Typhoid; Bone (osteomyelitis, joint infections), soft tissue, gynecological and wound infections;

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Respiratory infections (2nd generation FQs is better); Tuberculosis; Septicaemias; Conjunctivitis; Meningitis

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Side effects Dyspeptic disorders (nausea, vomiting, anorexia, diarrhea); Allergic reactions (rash, itching), photosensitization; Dizziness, headache, insomnia, mood changes, convulsions; Anemia, thrombocytopenia; Tendovaginitis, myalgia, arthralgia ; Dysbacteriosis ; Impaired liver and kidney function. Contraindications: to pregnant women and children under 2 years of age due to the risk of damage to cartilaginous tissue.

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Derivative of 8-hydroxyquinoline – Nitroxoline Mechanism: reducing the activity of enzymes due to the formation of complexes with metals. Type: bacteriostatic or bactericidal depending on the dose; Spectrum: enterobacteria (Escherichia, Shigella, Klebsiella, some Proteus strains), protozoa (amoeba, Giardia), the fungus Candida.

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Pharmacokinetics. Nitroxoline is administered orally 4 times a day. It is well absorbed from the digestive tract. It penetrates into the tissue badly, is excreted in the urine unchanged, staining it in yellow Indications: urinary tract infections Side effects: dyspepsia, allergies, neuritis

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Nitrofuran derivatives Nitrofural : antiseptic Furazolidon : intestinal infections, giardiasis, Trichomonas colpitis Nifuroxazide: intestinal infections. Nitrofurantoin (Furadonin), Furazidin (Furagin): uroinfection. Spectrum: Gram-negative bacteria: Escherichia coli, Shigella, Salmonella, Klebsiella Cocci (entero-, staphylo-,strepto-, meningo-, gonorrhea) Vibrio cholerae, Giardia, Trichomonas

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Mechanism: The restoration of the nitro group to the amino group under the influence of reductase microbial cells. The formation of complexes with nucleic acids, Disruption of the respiratory mechanisms of microorganisms. Increase in the body's resistance to infections. The decline in the production of toxins. Type of action: bacteriostatic or bactericidal

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Pharmacokinetics They are absorbed from the digestive tract at 30 (furazolidon) – 50 %. They penetrate the lymph, bile. They accumulate in the bile. They go through the placenta, they go through the BBB badly. They are excreted by the kidneys in different forms. They are used 3-4 times a day.

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Side effects Dyspeptic disorders: nausea, vomiting, diarrhea; Cholestasis; disorders of liver function; Allergic reaction; Headache, dizziness; Hemolytic anemia, methemoglobinemia in children up to a year; Arterial hypertension;

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Nitroimidazoles Metronidazole, Tinidazole, Ornidazole Spectrum: Entamoeba histolytica, Trichomonas vaginalis, lamblia, Bact. fragilis, Fusobacterium, Clostridium perfringens, Cl. difficile, Helicobacter pylori, Campylobacter, peptococci, spirochetes and anaerobic Streptococci enterobacteria in the presence of Bac.fragilis.

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Mechanism of action Metronidazole is selectively toxic to anaerobic and microaerophilic microorganisms. After entering the cell by diffusion, its nitro group is reduced by certain redox proteins to a highly reactive nitro radical which exerts cytotoxicity. The nitro radical of metronidazole acts as an electron sink which competes with the biological electron acceptors of the anaerobic organism for the electrons generated by the pyruvate (pyruvate oxidation). The energy metabolism of anaerobes that have no mitochondria is disrupted. Aerobic environment attenuates cytotoxicity of metronidazole by inhibiting its reductive activation.

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They are almost completely absorbed from the small intestines; little unabsorbed drug reaches the colon. They are widely distributed in the body, attaining therapeutic concentration in vaginal secretion, semen, saliva and CSF. Metabolism occurs in liver primarily by oxidation and glucuronide conjugation followed by renal excretion. Plasma t½ of Metronidazole is 8 hrs; Plasma t½ of Tinidazole 12 hr; Plasma t½ of Ornidazole 12–14 hr.

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Indications for uses Amoebiasis Giardiasis Trichomonas vaginitis Anaerobic bacterial infections ( after colorectal or pelvic surgery, appendicectomy, brain abscesses and endocarditis) Pseudomembranous enterocolitis (Cl. Difficile) Acute necrotizing ulcerative gingivitis ( fusobacteria, spirochetes and bacteroides) Helicobacter pylori gastritis/peptic ulcer Guinea worm infestation

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Side effects Anorexia, nausea, metallic taste and abdominal cramps are the most common. Less frequent side effects are—headache, glossitis, dryness of mouth and dizziness. Allergic reactions ( urticaria, flushing, heat, itching, rashes) Prolonged administration may cause peripheral neuropathy and CNS effects. Seizures have followed very high doses. Leucopenia is likely with repeated courses. Thrombophlebitis of the injected vein occurs if the solution is not well diluted. They are contraindicated in neurological disease, first trimester of pregnancy

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OXAZOLIDINONE - Linezolid It is active against Staphylococcus aureus, penicillin-resistant Streptococci, M. tuberculosis, Corynebacterium, Listeria, Clostridia and Bact. fragilis. It is primarily bacteriostatic, but can exert cidal action against some streptococci, pneumococci and B. fragilis. Gram-negative bacteria are not affected.

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Linezolid inhibits bacterial protein synthesis by acting at an early step. Linezolid is rapidly and completely absorbed orally, partly metabolized nonenzymatically and excreted in urine. Linezolid given orally or i.v. is used for uncomplicated and complicated skin and soft tissue infections, pneumonias, bacteraemias and other drug-resistant gram-positive infections Side effects: dyspepsia, diarrhea, constipation, insomnia, dizziness, rash.

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Quinoxaline derivatives – quinoxidine and dioxidine Spectrum: Proteus, Pseudomonas aeruginosa, intestinal bacteria, cocci, Clostridium, bacteroids. Application: orally, IV and locally in the case of the inefficiency of other drugs in severe pleurisy, lung abscesses, peritonitis, pyelonephritis. Complications: dyspepsia, headache, dizziness, allergic reactions, chills, intestinal candidiasis, convulsions, carcinogenesis, teratogenicity.

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Последний слайд презентации: Antimicrobial drugs: Literature

1. Tripathi K.D. Essentials of Medical Pharmacology. Eighth Edition. -2019.- Jaypee Brothers Medical Publishers. The Health Sciences Publisher. -New Delhi. London. Panama 2. D.A.Kharkevich. Pharmacology. Textbook for medical students. Translation of 12 th edition of Russion textbook “Pharmacology” (2017). – М., ГЭОТАР - Медиа, 2017. 3. Review of pharmacology. Gobind Rai Garg, Sparsh Gupta. 13 th edition. - 2019.- Jaypee Brothers Medical Publishers. The Health Sciences Publisher. -New Delhi. London. Panama 4. Whalen Karen. Lippincott Illustrated Reviews : Pharmacology. Sixth Edition. - Wolters Kluwer. - 2015.-Philadelphia 5. Color Atlas of Pharmacology. 2nd edition, revised and expanded. Heinz Lüllmann.- 2000 Thieme 6. Pharmacology Examination & Board Review. Tenth Edition. Trevor Anthony J., Katzung Bertram G., Kruidering -Hall Marieke, Susan B. Masters. - a LANGE medical book. - 2013.-New York 7. Medical Pharmacology at a Glance. Eighth Edition. Neal Michael J. – 2016. John Wiley & Sons, Ltd. 8. USMLE Step 1. Lecture Notes. Pharmacology. Lionel P.Raymon and others.- Kaplan Medical.Inc. -2009

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