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�ݺ�ߣshows by User: tanukatnawer9 / http://www.slideshare.net/images/logo.gif �ݺ�ߣshows by User: tanukatnawer9 / Wed, 20 Jul 2022 12:31:47 GMT �ݺ�ߣShare feed for �ݺ�ߣshows by User: tanukatnawer9 ANTI MALARIAL.pptx /slideshow/anti-malarialpptx/252251536 8-220720123147-74ba0512
MALARIA It is an infectious disease of humans caused by parasitis protozoans belonging to the genus plasmodium. It is endemic in most parts of India and other tropical countries. As per WHO, malaria causes one death every minute globally and about 40,000 annual deaths in India. The disease is transmitted by the bite of an infected female Anopheles mosquito. Four species of protozoa plasmodium can cause malaria which are P. falciparum, P. vivax, P. ovale and P. malariae. INTRODUCTION These are the drugs which are used for the treatment, prophylaxis and prevention of relapses of malaria. The treatment of malaria is available since 17 century. During those times, the bark of Cinchona tree was used in the crude form. Later in 1820, quinine was isolated from the bark. Since 1920, quinine and other drugs are commercially available in the market OBJECTIVES IN USE OF ANTIMALARIAL DRUGS The various objectives are: To prevent clinical attack of malaria. To treat clinical attack of malaria. To completely eradicate the parasite from the patient’s body. To cut down human to mosquito transmission. THERAPEUTIC CLASSIFICATION 1. CAUSAL PROPHYLACTICS: (Destroy parasite in liver cells and prevent invasion of erythrocytes) e.g. primaquine, pyrimethamine 2.BLOOD SCHIZONTOCIDES SUPPRESIVES (destroy parasites in the RBC and terminate clinical attacks of malaria): e.g. chloroquine, quinine, mefloquine, halofantrine, pyrimethamine 3. TISSUE SCHIZONTOCIDES used to prevent relapse: act vivax and P. ovale that produce replapses. E.g. primaquine 4. GAMETOCIDAL DRUGS: primaquine, chloroquine, quinine. 1. CHLOROQUINE It acts as erythrocytic schizontocide against all species of plasmodia. The parasite disappears from peripheral blood in 1-3 days. It control the clinical attacks of malaria within 1-2 days. It doesn’t have any gametocidal activity. It is bitter in taste, so patient should be advised ‘not to chew the tablet’ it is used for the treatment of malaria during pregnancy: no teratogenic effects have been reported. MECHANISM OF ACTION Its gets concentrated in the infected RBCs and then is actively taken up by the susceptible plasmodia. The chloroquine binds to the heme and forms chloroquine heme complex. Complex inhibits the formation of hemozoin and also damages the Plasmodium memberane PHARMACOKINETICS It is well absorbed orally. 50% of the drug is plasma protein bound, gets concentrated in liver, spleen, kidneys, lungs, skin and leukocytes. The plasma half life is 3-10 days, whereas the terminal half life is 1-2 months. On prolonged use, it gets accumulated selectively in the retina and causes ocular toxicity. It is partially metabolized in liver and slowly excreted in urine. INDICATIONS ADVERSE EFFECTS Clinical drug of choice for malaria. Extraintestinal amoebiasis. Rheumatoid arthritis Infectious mononucleosis. Mil]]>
MALARIA It is an infectious disease of humans caused by parasitis protozoans belonging to the genus plasmodium. It is endemic in most parts of India and other tropical countries. As per WHO, malaria causes one death every minute globally and about 40,000 annual deaths in India. The disease is transmitted by the bite of an infected female Anopheles mosquito. Four species of protozoa plasmodium can cause malaria which are P. falciparum, P. vivax, P. ovale and P. malariae. INTRODUCTION These are the drugs which are used for the treatment, prophylaxis and prevention of relapses of malaria. The treatment of malaria is available since 17 century. During those times, the bark of Cinchona tree was used in the crude form. Later in 1820, quinine was isolated from the bark. Since 1920, quinine and other drugs are commercially available in the market OBJECTIVES IN USE OF ANTIMALARIAL DRUGS The various objectives are: To prevent clinical attack of malaria. To treat clinical attack of malaria. To completely eradicate the parasite from the patient’s body. To cut down human to mosquito transmission. THERAPEUTIC CLASSIFICATION 1. CAUSAL PROPHYLACTICS: (Destroy parasite in liver cells and prevent invasion of erythrocytes) e.g. primaquine, pyrimethamine 2.BLOOD SCHIZONTOCIDES SUPPRESIVES (destroy parasites in the RBC and terminate clinical attacks of malaria): e.g. chloroquine, quinine, mefloquine, halofantrine, pyrimethamine 3. TISSUE SCHIZONTOCIDES used to prevent relapse: act vivax and P. ovale that produce replapses. E.g. primaquine 4. GAMETOCIDAL DRUGS: primaquine, chloroquine, quinine. 1. CHLOROQUINE It acts as erythrocytic schizontocide against all species of plasmodia. The parasite disappears from peripheral blood in 1-3 days. It control the clinical attacks of malaria within 1-2 days. It doesn’t have any gametocidal activity. It is bitter in taste, so patient should be advised ‘not to chew the tablet’ it is used for the treatment of malaria during pregnancy: no teratogenic effects have been reported. MECHANISM OF ACTION Its gets concentrated in the infected RBCs and then is actively taken up by the susceptible plasmodia. The chloroquine binds to the heme and forms chloroquine heme complex. Complex inhibits the formation of hemozoin and also damages the Plasmodium memberane PHARMACOKINETICS It is well absorbed orally. 50% of the drug is plasma protein bound, gets concentrated in liver, spleen, kidneys, lungs, skin and leukocytes. The plasma half life is 3-10 days, whereas the terminal half life is 1-2 months. On prolonged use, it gets accumulated selectively in the retina and causes ocular toxicity. It is partially metabolized in liver and slowly excreted in urine. INDICATIONS ADVERSE EFFECTS Clinical drug of choice for malaria. Extraintestinal amoebiasis. Rheumatoid arthritis Infectious mononucleosis. Mil]]> Wed, 20 Jul 2022 12:31:47 GMT /slideshow/anti-malarialpptx/252251536 tanukatnawer9@slideshare.net(tanukatnawer9) ANTI MALARIAL.pptx tanukatnawer9 MALARIA It is an infectious disease of humans caused by parasitis protozoans belonging to the genus plasmodium. It is endemic in most parts of India and other tropical countries. As per WHO, malaria causes one death every minute globally and about 40,000 annual deaths in India. The disease is transmitted by the bite of an infected female Anopheles mosquito. Four species of protozoa plasmodium can cause malaria which are P. falciparum, P. vivax, P. ovale and P. malariae. INTRODUCTION These are the drugs which are used for the treatment, prophylaxis and prevention of relapses of malaria. The treatment of malaria is available since 17 century. During those times, the bark of Cinchona tree was used in the crude form. Later in 1820, quinine was isolated from the bark. Since 1920, quinine and other drugs are commercially available in the market OBJECTIVES IN USE OF ANTIMALARIAL DRUGS The various objectives are: To prevent clinical attack of malaria. To treat clinical attack of malaria. To completely eradicate the parasite from the patient’s body. To cut down human to mosquito transmission. THERAPEUTIC CLASSIFICATION 1. CAUSAL PROPHYLACTICS: (Destroy parasite in liver cells and prevent invasion of erythrocytes) e.g. primaquine, pyrimethamine 2.BLOOD SCHIZONTOCIDES SUPPRESIVES (destroy parasites in the RBC and terminate clinical attacks of malaria): e.g. chloroquine, quinine, mefloquine, halofantrine, pyrimethamine 3. TISSUE SCHIZONTOCIDES used to prevent relapse: act vivax and P. ovale that produce replapses. E.g. primaquine 4. GAMETOCIDAL DRUGS: primaquine, chloroquine, quinine. 1. CHLOROQUINE It acts as erythrocytic schizontocide against all species of plasmodia. The parasite disappears from peripheral blood in 1-3 days. It control the clinical attacks of malaria within 1-2 days. It doesn’t have any gametocidal activity. It is bitter in taste, so patient should be advised ‘not to chew the tablet’ it is used for the treatment of malaria during pregnancy: no teratogenic effects have been reported. ��MECHANISM OF ACTION�� Its gets concentrated in the infected RBCs and then is actively taken up by the susceptible plasmodia. The chloroquine binds to the heme and forms chloroquine heme complex. Complex inhibits the formation of hemozoin and also damages the Plasmodium memberane PHARMACOKINETICS It is well absorbed orally. 50% of the drug is plasma protein bound, gets concentrated in liver, spleen, kidneys, lungs, skin and leukocytes. The plasma half life is 3-10 days, whereas the terminal half life is 1-2 months. On prolonged use, it gets accumulated selectively in the retina and causes ocular toxicity. It is partially metabolized in liver and slowly excreted in urine. INDICATIONS ADVERSE EFFECTS Clinical drug of choice for malaria. Extraintestinal amoebiasis. Rheumatoid arthritis Infectious mononucleosis. Mil <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/8-220720123147-74ba0512-thumbnail.jpg?width=120&height=120&fit=bounds" /> MALARIA It is an infectious disease of humans caused by parasitis protozoans belonging to the genus plasmodium. It is endemic in most parts of India and other tropical countries. As per WHO, malaria causes one death every minute globally and about 40,000 annual deaths in India. The disease is transmitted by the bite of an infected female Anopheles mosquito. Four species of protozoa plasmodium can cause malaria which are P. falciparum, P. vivax, P. ovale and P. malariae. INTRODUCTION These are the drugs which are used for the treatment, prophylaxis and prevention of relapses of malaria. The treatment of malaria is available since 17 century. During those times, the bark of Cinchona tree was used in the crude form. Later in 1820, quinine was isolated from the bark. Since 1920, quinine and other drugs are commercially available in the market OBJECTIVES IN USE OF ANTIMALARIAL DRUGS The various objectives are: To prevent clinical attack of malaria. To treat clinical attack of malaria. To completely eradicate the parasite from the patient’s body. To cut down human to mosquito transmission. THERAPEUTIC CLASSIFICATION 1. CAUSAL PROPHYLACTICS: (Destroy parasite in liver cells and prevent invasion of erythrocytes) e.g. primaquine, pyrimethamine 2.BLOOD SCHIZONTOCIDES SUPPRESIVES (destroy parasites in the RBC and terminate clinical attacks of malaria): e.g. chloroquine, quinine, mefloquine, halofantrine, pyrimethamine 3. TISSUE SCHIZONTOCIDES used to prevent relapse: act vivax and P. ovale that produce replapses. E.g. primaquine 4. GAMETOCIDAL DRUGS: primaquine, chloroquine, quinine. 1. CHLOROQUINE It acts as erythrocytic schizontocide against all species of plasmodia. The parasite disappears from peripheral blood in 1-3 days. It control the clinical attacks of malaria within 1-2 days. It doesn’t have any gametocidal activity. It is bitter in taste, so patient should be advised ‘not to chew the tablet’ it is used for the treatment of malaria during pregnancy: no teratogenic effects have been reported. ��MECHANISM OF ACTION�� Its gets concentrated in the infected RBCs and then is actively taken up by the susceptible plasmodia. The chloroquine binds to the heme and forms chloroquine heme complex. Complex inhibits the formation of hemozoin and also damages the Plasmodium memberane PHARMACOKINETICS It is well absorbed orally. 50% of the drug is plasma protein bound, gets concentrated in liver, spleen, kidneys, lungs, skin and leukocytes. The plasma half life is 3-10 days, whereas the terminal half life is 1-2 months. On prolonged use, it gets accumulated selectively in the retina and causes ocular toxicity. It is partially metabolized in liver and slowly excreted in urine. INDICATIONS ADVERSE EFFECTS Clinical drug of choice for malaria. Extraintestinal amoebiasis. Rheumatoid arthritis Infectious mononucleosis. Mil

ANTI MALARIAL.pptx from NEHA BHARTI

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0 QUINOLONES.pptx /slideshow/quinolonespptx-252251512/252251512 6-220720122942-e6fd3542
These are synthetic antimicrobial having a quinolones structure. These are active against most of the gram negative bacteria. In 1960s the first membered of this group, Nalidixic acid, was introduced . Flouroquinolones have: High potency Expanded antimicrobial spectrum Better tissue penetration Good tolerability profile Very low resistance development 1. NALIDIXIC ACID It was the first member in quinolones. It was active against gram negative bacteria. It acts by inhibiting bacterial DNA gyrase. It is bacterial in nature. It is given orally. It attains good concentration in gut, lumen, hence useful in diarrhea. NALIDIXIC ACID CONTD… It is most commonly seen in children. And causes neurological toxicity present as headache, drowsiness and vertigo and contraindicated in infants and G6PD deficient patients. It is given in a dose of 0.5-1g TDS/QID 2. FLUOROQUINOLONES Fluoroquinolones are quinolones antimicrobials having one or more fluorine substituitions. The first generation fluoroquinolones have one fluoro substitution and were developed in 1980s. The second generation fluoroquinolones have additional fluoroquinolones have additional fluoro substitution, which extended the antimicrobial activity and were developed in 1990s. MECHANISM OF ACTION The fluoroquinolones inhibits the enzyme DNA gyrase in Gram-negative micro-organism and topoisomerase IV in gram positive micro-organism. This lead to the bactericidal effects of fluoroquinolones. RESISTANCE The resistance to fluoroquinolones develops when the bacteria produce a DNA gyrase or topoisomerase IV which have reduced affinity for fluoroquinolones or the bacteria produce efflux pumps across bacterial memberane which shunt out the fluoroquinolones from the bacterial cells. CLASSIFICATION FIRST GENERATION FLOUROQUINOLONES : Norfloxacin Ofloxacin Ciprofloxacin Pefloxacin SECOND GENERATION FLUOROQUINOLONES: Levofloxacin Moxifloxacin Lomefloxacin Gemifloxacin Sparfloxacin Prulifloxacin PHARMACOKINETICS These are given both by oral and intravenous route. These have good absorption, when given empty stomach and food delays the absorption. These drugs have good tissue penetrability. These are excreted in urine by glomerular filtration as well as tubular secretion. INDICATIONS Bacterial gastroenteritis Typhoid fever UTI Gonorrhoea Chancroid Bone, Soft tissue and gynaecological infections Respiratory infections Tuberculosis Gram negative septicemia and meningitis Conjuctivitis COMMON ADVERSE EFFECTS GI SYSTEM: Nausea, vomiting, bad taste and anorexia CNS: Headache, anxiety, insomnia, restlessness and impairment of concentrations. Skin: Rash, photosensitivity Contraindicated in pregnancy. They should be used in caution in children as a few cases of joint pain and swelling have been reported and a risk of cartilage damage is suspended. FIRST GENERATION FLUROQUINOLONES SECOND GENERATION FLUROQUINOLONES DRUG INTERACTIONS Antacids decrease the absorption]]>
These are synthetic antimicrobial having a quinolones structure. These are active against most of the gram negative bacteria. In 1960s the first membered of this group, Nalidixic acid, was introduced . Flouroquinolones have: High potency Expanded antimicrobial spectrum Better tissue penetration Good tolerability profile Very low resistance development 1. NALIDIXIC ACID It was the first member in quinolones. It was active against gram negative bacteria. It acts by inhibiting bacterial DNA gyrase. It is bacterial in nature. It is given orally. It attains good concentration in gut, lumen, hence useful in diarrhea. NALIDIXIC ACID CONTD… It is most commonly seen in children. And causes neurological toxicity present as headache, drowsiness and vertigo and contraindicated in infants and G6PD deficient patients. It is given in a dose of 0.5-1g TDS/QID 2. FLUOROQUINOLONES Fluoroquinolones are quinolones antimicrobials having one or more fluorine substituitions. The first generation fluoroquinolones have one fluoro substitution and were developed in 1980s. The second generation fluoroquinolones have additional fluoroquinolones have additional fluoro substitution, which extended the antimicrobial activity and were developed in 1990s. MECHANISM OF ACTION The fluoroquinolones inhibits the enzyme DNA gyrase in Gram-negative micro-organism and topoisomerase IV in gram positive micro-organism. This lead to the bactericidal effects of fluoroquinolones. RESISTANCE The resistance to fluoroquinolones develops when the bacteria produce a DNA gyrase or topoisomerase IV which have reduced affinity for fluoroquinolones or the bacteria produce efflux pumps across bacterial memberane which shunt out the fluoroquinolones from the bacterial cells. CLASSIFICATION FIRST GENERATION FLOUROQUINOLONES : Norfloxacin Ofloxacin Ciprofloxacin Pefloxacin SECOND GENERATION FLUOROQUINOLONES: Levofloxacin Moxifloxacin Lomefloxacin Gemifloxacin Sparfloxacin Prulifloxacin PHARMACOKINETICS These are given both by oral and intravenous route. These have good absorption, when given empty stomach and food delays the absorption. These drugs have good tissue penetrability. These are excreted in urine by glomerular filtration as well as tubular secretion. INDICATIONS Bacterial gastroenteritis Typhoid fever UTI Gonorrhoea Chancroid Bone, Soft tissue and gynaecological infections Respiratory infections Tuberculosis Gram negative septicemia and meningitis Conjuctivitis COMMON ADVERSE EFFECTS GI SYSTEM: Nausea, vomiting, bad taste and anorexia CNS: Headache, anxiety, insomnia, restlessness and impairment of concentrations. Skin: Rash, photosensitivity Contraindicated in pregnancy. They should be used in caution in children as a few cases of joint pain and swelling have been reported and a risk of cartilage damage is suspended. FIRST GENERATION FLUROQUINOLONES SECOND GENERATION FLUROQUINOLONES DRUG INTERACTIONS Antacids decrease the absorption]]> Wed, 20 Jul 2022 12:29:42 GMT /slideshow/quinolonespptx-252251512/252251512 tanukatnawer9@slideshare.net(tanukatnawer9) QUINOLONES.pptx tanukatnawer9 These are synthetic antimicrobial having a quinolones structure. These are active against most of the gram negative bacteria. In 1960s the first membered of this group, Nalidixic acid, was introduced . Flouroquinolones have: High potency Expanded antimicrobial spectrum Better tissue penetration Good tolerability profile Very low resistance development 1. NALIDIXIC ACID It was the first member in quinolones. It was active against gram negative bacteria. It acts by inhibiting bacterial DNA gyrase. It is bacterial in nature. It is given orally. It attains good concentration in gut, lumen, hence useful in diarrhea. NALIDIXIC ACID CONTD… It is most commonly seen in children. And causes neurological toxicity present as headache, drowsiness and vertigo and contraindicated in infants and G6PD deficient patients. It is given in a dose of 0.5-1g TDS/QID 2. FLUOROQUINOLONES Fluoroquinolones are quinolones antimicrobials having one or more fluorine substituitions. The first generation fluoroquinolones have one fluoro substitution and were developed in 1980s. The second generation fluoroquinolones have additional fluoroquinolones have additional fluoro substitution, which extended the antimicrobial activity and were developed in 1990s. MECHANISM OF ACTION The fluoroquinolones inhibits the enzyme DNA gyrase in Gram-negative micro-organism and topoisomerase IV in gram positive micro-organism. This lead to the bactericidal effects of fluoroquinolones. RESISTANCE The resistance to fluoroquinolones develops when the bacteria produce a DNA gyrase or topoisomerase IV which have reduced affinity for fluoroquinolones or the bacteria produce efflux pumps across bacterial memberane which shunt out the fluoroquinolones from the bacterial cells. CLASSIFICATION FIRST GENERATION FLOUROQUINOLONES : Norfloxacin Ofloxacin Ciprofloxacin Pefloxacin SECOND GENERATION FLUOROQUINOLONES: Levofloxacin Moxifloxacin Lomefloxacin Gemifloxacin Sparfloxacin Prulifloxacin PHARMACOKINETICS These are given both by oral and intravenous route. These have good absorption, when given empty stomach and food delays the absorption. These drugs have good tissue penetrability. These are excreted in urine by glomerular filtration as well as tubular secretion. INDICATIONS Bacterial gastroenteritis Typhoid fever UTI Gonorrhoea Chancroid Bone, Soft tissue and gynaecological infections Respiratory infections Tuberculosis Gram negative septicemia and meningitis Conjuctivitis COMMON ADVERSE EFFECTS GI SYSTEM: Nausea, vomiting, bad taste and anorexia CNS: Headache, anxiety, insomnia, restlessness and impairment of concentrations. Skin: Rash, photosensitivity Contraindicated in pregnancy. They should be used in caution in children as a few cases of joint pain and swelling have been reported and a risk of cartilage damage is suspended. FIRST GENERATION FLUROQUINOLONES SECOND GENERATION FLUROQUINOLONES DRUG INTERACTIONS Antacids decrease the absorption <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/6-220720122942-e6fd3542-thumbnail.jpg?width=120&height=120&fit=bounds" /> These are synthetic antimicrobial having a quinolones structure. These are active against most of the gram negative bacteria. In 1960s the first membered of this group, Nalidixic acid, was introduced . Flouroquinolones have: High potency Expanded antimicrobial spectrum Better tissue penetration Good tolerability profile Very low resistance development 1. NALIDIXIC ACID It was the first member in quinolones. It was active against gram negative bacteria. It acts by inhibiting bacterial DNA gyrase. It is bacterial in nature. It is given orally. It attains good concentration in gut, lumen, hence useful in diarrhea. NALIDIXIC ACID CONTD… It is most commonly seen in children. And causes neurological toxicity present as headache, drowsiness and vertigo and contraindicated in infants and G6PD deficient patients. It is given in a dose of 0.5-1g TDS/QID 2. FLUOROQUINOLONES Fluoroquinolones are quinolones antimicrobials having one or more fluorine substituitions. The first generation fluoroquinolones have one fluoro substitution and were developed in 1980s. The second generation fluoroquinolones have additional fluoroquinolones have additional fluoro substitution, which extended the antimicrobial activity and were developed in 1990s. MECHANISM OF ACTION The fluoroquinolones inhibits the enzyme DNA gyrase in Gram-negative micro-organism and topoisomerase IV in gram positive micro-organism. This lead to the bactericidal effects of fluoroquinolones. RESISTANCE The resistance to fluoroquinolones develops when the bacteria produce a DNA gyrase or topoisomerase IV which have reduced affinity for fluoroquinolones or the bacteria produce efflux pumps across bacterial memberane which shunt out the fluoroquinolones from the bacterial cells. CLASSIFICATION FIRST GENERATION FLOUROQUINOLONES : Norfloxacin Ofloxacin Ciprofloxacin Pefloxacin SECOND GENERATION FLUOROQUINOLONES: Levofloxacin Moxifloxacin Lomefloxacin Gemifloxacin Sparfloxacin Prulifloxacin PHARMACOKINETICS These are given both by oral and intravenous route. These have good absorption, when given empty stomach and food delays the absorption. These drugs have good tissue penetrability. These are excreted in urine by glomerular filtration as well as tubular secretion. INDICATIONS Bacterial gastroenteritis Typhoid fever UTI Gonorrhoea Chancroid Bone, Soft tissue and gynaecological infections Respiratory infections Tuberculosis Gram negative septicemia and meningitis Conjuctivitis COMMON ADVERSE EFFECTS GI SYSTEM: Nausea, vomiting, bad taste and anorexia CNS: Headache, anxiety, insomnia, restlessness and impairment of concentrations. Skin: Rash, photosensitivity Contraindicated in pregnancy. They should be used in caution in children as a few cases of joint pain and swelling have been reported and a risk of cartilage damage is suspended. FIRST GENERATION FLUROQUINOLONES SECOND GENERATION FLUROQUINOLONES DRUG INTERACTIONS Antacids decrease the absorption

QUINOLONES.pptx from NEHA BHARTI

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0 sulfonamides.pptx /slideshow/sulfonamidespptx/252251481 5-220720122745-269c6404
INTRODUCTION Sulfonamides were the first effective, synthetic antibacterial agents to be used systemically in man. They were introduced by Domagk in 1935 and in the next few years several of them were synthesized and widely used. Currently their role in therapeutics is limited because of their toxicity, development of resistance availability of safer drugs. CLASSIFICATION Short acting: Sulfisoxazole, Sulfadiazine Intermediate acting: Sulfamethoxazole Long-acting: Sulfamethoxypyridazine, sulfadoxine Poorly absorbed: Sulfasalazine Topical: Sulfacetamide, mefedine Silver sulfadiazine. ANTIBACTERIAL SPECTRUM It is wide spectrum antibiotic. It inhibits many gram positive and some gram negative bacteria including streptococci, H. influenza, Norcardia, E. coli, proteus, V. cholerae, some stains of staphylococci, gonococci, memingococci and pneumococci. They are also effective against Chlamydia, plasmodium falciparum and toxoplasma gondii. MECHANISM OF ACTION PABA (Para-aminobenzoic acid) Folic acid synthesis DIHYDROFOLIC ACID Bacteria synthesize their own folic acid from PABA with the help of the enzyme folic acid synthetase. Sulfonamides are structurally similar to PABA and competitively inhibiting the enzymes folic acid synthetase. They inhibit the enzyme folic acid synthase so folic acid is not synthesized (which is essential bacterial growth). PHARMACOKINETICS Sulfonamides are well absorbed, extensively bound to plasma proteins and are well distributed to all tissues. They are metabolized in the liver and excreted in urine. They can cross placental barriers. COMMON USES SYSTEMIC USES : sulfamethoxazole is used in combination with cotrimoxazolein many bacterial infections. It is the drug of choice in pneumocystitis in AIDS patient. Treatment of nocardiosis, toxoplasmosis, ulcerative colitis and rheumatoid arthritis. TOPICAL USES: ocular sulfacetamide sodium is used in trachoma/inclusion conjuctivitis. Topical silver sulfadiazine is used for preventing infection on burn surfaces. Mefinide is active in the presence of pus and against pseudomonas, clostridia which are not inhibited by topical sulfonamides. USES Because of the development of resistance and availability of better antimicrobials, which are more effective and less toxic, these are not commonly used now except in a few cases: UTI NOCARDIOSIS TOXOPLASMOSIS TRACHOMA AND INCLUSION CONJUCTIVITIS MALARIA TOPICAL ULCERATIVE COLLITIS Contraindication & Precautions: Children younger than 2yrs, Pregnant and breast feeding mother, Renal and hepatic diseases, Hypersensitivity to sulphonamides drug. Adverse effect: Fever, Rash, Nausea/vomiting, Aplastic Anemia. DRUG INTERACTIONS Sulphonamides can increasing the blood thinning effect of warfarin, possibly leading to abnormal bleeding. Increases blood level of potassium may occur when Sulfamethoxazole trimethoprim is combined with ACE inhibitors. Su]]>
INTRODUCTION Sulfonamides were the first effective, synthetic antibacterial agents to be used systemically in man. They were introduced by Domagk in 1935 and in the next few years several of them were synthesized and widely used. Currently their role in therapeutics is limited because of their toxicity, development of resistance availability of safer drugs. CLASSIFICATION Short acting: Sulfisoxazole, Sulfadiazine Intermediate acting: Sulfamethoxazole Long-acting: Sulfamethoxypyridazine, sulfadoxine Poorly absorbed: Sulfasalazine Topical: Sulfacetamide, mefedine Silver sulfadiazine. ANTIBACTERIAL SPECTRUM It is wide spectrum antibiotic. It inhibits many gram positive and some gram negative bacteria including streptococci, H. influenza, Norcardia, E. coli, proteus, V. cholerae, some stains of staphylococci, gonococci, memingococci and pneumococci. They are also effective against Chlamydia, plasmodium falciparum and toxoplasma gondii. MECHANISM OF ACTION PABA (Para-aminobenzoic acid) Folic acid synthesis DIHYDROFOLIC ACID Bacteria synthesize their own folic acid from PABA with the help of the enzyme folic acid synthetase. Sulfonamides are structurally similar to PABA and competitively inhibiting the enzymes folic acid synthetase. They inhibit the enzyme folic acid synthase so folic acid is not synthesized (which is essential bacterial growth). PHARMACOKINETICS Sulfonamides are well absorbed, extensively bound to plasma proteins and are well distributed to all tissues. They are metabolized in the liver and excreted in urine. They can cross placental barriers. COMMON USES SYSTEMIC USES : sulfamethoxazole is used in combination with cotrimoxazolein many bacterial infections. It is the drug of choice in pneumocystitis in AIDS patient. Treatment of nocardiosis, toxoplasmosis, ulcerative colitis and rheumatoid arthritis. TOPICAL USES: ocular sulfacetamide sodium is used in trachoma/inclusion conjuctivitis. Topical silver sulfadiazine is used for preventing infection on burn surfaces. Mefinide is active in the presence of pus and against pseudomonas, clostridia which are not inhibited by topical sulfonamides. USES Because of the development of resistance and availability of better antimicrobials, which are more effective and less toxic, these are not commonly used now except in a few cases: UTI NOCARDIOSIS TOXOPLASMOSIS TRACHOMA AND INCLUSION CONJUCTIVITIS MALARIA TOPICAL ULCERATIVE COLLITIS Contraindication & Precautions: Children younger than 2yrs, Pregnant and breast feeding mother, Renal and hepatic diseases, Hypersensitivity to sulphonamides drug. Adverse effect: Fever, Rash, Nausea/vomiting, Aplastic Anemia. DRUG INTERACTIONS Sulphonamides can increasing the blood thinning effect of warfarin, possibly leading to abnormal bleeding. Increases blood level of potassium may occur when Sulfamethoxazole trimethoprim is combined with ACE inhibitors. Su]]> Wed, 20 Jul 2022 12:27:45 GMT /slideshow/sulfonamidespptx/252251481 tanukatnawer9@slideshare.net(tanukatnawer9) sulfonamides.pptx tanukatnawer9 INTRODUCTION Sulfonamides were the first effective, synthetic antibacterial agents to be used systemically in man. They were introduced by Domagk in 1935 and in the next few years several of them were synthesized and widely used. Currently their role in therapeutics is limited because of their toxicity, development of resistance availability of safer drugs. CLASSIFICATION Short acting: Sulfisoxazole, Sulfadiazine Intermediate acting: Sulfamethoxazole Long-acting: Sulfamethoxypyridazine, sulfadoxine Poorly absorbed: Sulfasalazine Topical: Sulfacetamide, mefedine Silver sulfadiazine. ANTIBACTERIAL SPECTRUM It is wide spectrum antibiotic. It inhibits many gram positive and some gram negative bacteria including streptococci, H. influenza, Norcardia, E. coli, proteus, V. cholerae, some stains of staphylococci, gonococci, memingococci and pneumococci. They are also effective against Chlamydia, plasmodium falciparum and toxoplasma gondii. MECHANISM OF ACTION PABA (Para-aminobenzoic acid) Folic acid synthesis DIHYDROFOLIC ACID Bacteria synthesize their own folic acid from PABA with the help of the enzyme folic acid synthetase. Sulfonamides are structurally similar to PABA and competitively inhibiting the enzymes folic acid synthetase. They inhibit the enzyme folic acid synthase so folic acid is not synthesized (which is essential bacterial growth). PHARMACOKINETICS Sulfonamides are well absorbed, extensively bound to plasma proteins and are well distributed to all tissues. They are metabolized in the liver and excreted in urine. They can cross placental barriers. COMMON USES SYSTEMIC USES : sulfamethoxazole is used in combination with cotrimoxazolein many bacterial infections. It is the drug of choice in pneumocystitis in AIDS patient. Treatment of nocardiosis, toxoplasmosis, ulcerative colitis and rheumatoid arthritis. TOPICAL USES: ocular sulfacetamide sodium is used in trachoma/inclusion conjuctivitis. Topical silver sulfadiazine is used for preventing infection on burn surfaces. Mefinide is active in the presence of pus and against pseudomonas, clostridia which are not inhibited by topical sulfonamides. USES Because of the development of resistance and availability of better antimicrobials, which are more effective and less toxic, these are not commonly used now except in a few cases: UTI NOCARDIOSIS TOXOPLASMOSIS TRACHOMA AND INCLUSION CONJUCTIVITIS MALARIA TOPICAL ULCERATIVE COLLITIS Contraindication & Precautions: Children younger than 2yrs, Pregnant and breast feeding mother, Renal and hepatic diseases, Hypersensitivity to sulphonamides drug. Adverse effect: Fever, Rash, Nausea/vomiting, Aplastic Anemia. DRUG INTERACTIONS Sulphonamides can increasing the blood thinning effect of warfarin, possibly leading to abnormal bleeding. Increases blood level of potassium may occur when Sulfamethoxazole trimethoprim is combined with ACE inhibitors. Su <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/5-220720122745-269c6404-thumbnail.jpg?width=120&height=120&fit=bounds" /> INTRODUCTION Sulfonamides were the first effective, synthetic antibacterial agents to be used systemically in man. They were introduced by Domagk in 1935 and in the next few years several of them were synthesized and widely used. Currently their role in therapeutics is limited because of their toxicity, development of resistance availability of safer drugs. CLASSIFICATION Short acting: Sulfisoxazole, Sulfadiazine Intermediate acting: Sulfamethoxazole Long-acting: Sulfamethoxypyridazine, sulfadoxine Poorly absorbed: Sulfasalazine Topical: Sulfacetamide, mefedine Silver sulfadiazine. ANTIBACTERIAL SPECTRUM It is wide spectrum antibiotic. It inhibits many gram positive and some gram negative bacteria including streptococci, H. influenza, Norcardia, E. coli, proteus, V. cholerae, some stains of staphylococci, gonococci, memingococci and pneumococci. They are also effective against Chlamydia, plasmodium falciparum and toxoplasma gondii. MECHANISM OF ACTION PABA (Para-aminobenzoic acid) Folic acid synthesis DIHYDROFOLIC ACID Bacteria synthesize their own folic acid from PABA with the help of the enzyme folic acid synthetase. Sulfonamides are structurally similar to PABA and competitively inhibiting the enzymes folic acid synthetase. They inhibit the enzyme folic acid synthase so folic acid is not synthesized (which is essential bacterial growth). PHARMACOKINETICS Sulfonamides are well absorbed, extensively bound to plasma proteins and are well distributed to all tissues. They are metabolized in the liver and excreted in urine. They can cross placental barriers. COMMON USES SYSTEMIC USES : sulfamethoxazole is used in combination with cotrimoxazolein many bacterial infections. It is the drug of choice in pneumocystitis in AIDS patient. Treatment of nocardiosis, toxoplasmosis, ulcerative colitis and rheumatoid arthritis. TOPICAL USES: ocular sulfacetamide sodium is used in trachoma/inclusion conjuctivitis. Topical silver sulfadiazine is used for preventing infection on burn surfaces. Mefinide is active in the presence of pus and against pseudomonas, clostridia which are not inhibited by topical sulfonamides. USES Because of the development of resistance and availability of better antimicrobials, which are more effective and less toxic, these are not commonly used now except in a few cases: UTI NOCARDIOSIS TOXOPLASMOSIS TRACHOMA AND INCLUSION CONJUCTIVITIS MALARIA TOPICAL ULCERATIVE COLLITIS Contraindication & Precautions: Children younger than 2yrs, Pregnant and breast feeding mother, Renal and hepatic diseases, Hypersensitivity to sulphonamides drug. Adverse effect: Fever, Rash, Nausea/vomiting, Aplastic Anemia. DRUG INTERACTIONS Sulphonamides can increasing the blood thinning effect of warfarin, possibly leading to abnormal bleeding. Increases blood level of potassium may occur when Sulfamethoxazole trimethoprim is combined with ACE inhibitors. Su

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0 4. macrolide antibiotics.pptx /slideshow/4-macrolide-antibioticspptx/252251457 4-220720122544-355dba37
INTRODUCTION Erythromycin is the first member of group, and was isolated from a strain of Streptomyces erythreus in 1952. Rest drugs are semi-synthetic derivatives of erythromycin known as newer macrolides Some other drugs are dirithromycin, oleandomycin and troleandomycin. MECHANISM OF ACTION Macrolide antibiotics are bacteriostatic agents and inhibit the protein synthesis by binding reversibly to 50s ribosomal subunit of sensitive microorganism and interfere with translocation step in the protein synthesis. Gram positive bacteria's are 100 times more sensitive than gram negative bacteria's by these drugs. MECHANISM OF ACTION It is bacteriostatic at low concentration & bactericidal at high concentration Bactericidal property depends on the concentration, organism concerned and its rate of multiplication ANTI MICROBIAL SPECTRUM It is narrow spectrum antibiotic. These antibiotics are more active against gram positive cocci and inactive against most of the aerobic and enteric gram negative bacilli. In addition, Campylobacter, Legionella, Branhamella catarrhalis, G. vaginalis and Mycoplasma (which are not affected by pencillin are also highly susceptible to erythromycin) ANTI MICROBIAL SPECTRUM Moderately sensitive to H. influenza, B. pertussis, C. trachomatis, N. meningitidis and Rickettsiae Ineffective against Enterobacteriaceae, other gram negative bacilli. ERYTHROMYCIN This drug is acid labile, given as enteric coated tablets. Poorly absorbed when given empty stomach and has poor tissue penetration. DOSE: 250-500mg QID with half life of 1.5 hrs Indications: a drug of choice in atypical pneumonia, whooping cough and cancroids and as an alternative to penicillin in streptococcal pharyngitis, tonsillitis, mastoiditis. SIDE EFFECTS: Epigastric distress causing nausea, vomiting and diarrhea. Allergic reactions such as fever and skin eruption. CLARITHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration. Dose: 250-500mg BD with half life of 3-6 hrs at low dose and 3-9 hrs at high dose. Indications: upper and lower RTI, sinusitis, otitis media, atypical pneumonia, skin infections. And H. pylori infection and first line drug in combination regimens in AIDS infection Side effects: same as erythromycin but better gastric tolerance, reversible hearing loss at high doses. AZYTHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration Dose: 500mg OD with half life >50 hrs. Indications: pharyngitis, tonsillitis, sinusitis, otitis media pneumonias, chronic bronchitis. In the prophylaxis and treatment of AIDS infections. Side effects: nausea vomiting, diarrhea and abdominal pain. ROXITHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration DOSE: 150mg BD with half life of 12 hrs. Indications: alternative to erythromycin for respiratory, skin ]]>
INTRODUCTION Erythromycin is the first member of group, and was isolated from a strain of Streptomyces erythreus in 1952. Rest drugs are semi-synthetic derivatives of erythromycin known as newer macrolides Some other drugs are dirithromycin, oleandomycin and troleandomycin. MECHANISM OF ACTION Macrolide antibiotics are bacteriostatic agents and inhibit the protein synthesis by binding reversibly to 50s ribosomal subunit of sensitive microorganism and interfere with translocation step in the protein synthesis. Gram positive bacteria's are 100 times more sensitive than gram negative bacteria's by these drugs. MECHANISM OF ACTION It is bacteriostatic at low concentration & bactericidal at high concentration Bactericidal property depends on the concentration, organism concerned and its rate of multiplication ANTI MICROBIAL SPECTRUM It is narrow spectrum antibiotic. These antibiotics are more active against gram positive cocci and inactive against most of the aerobic and enteric gram negative bacilli. In addition, Campylobacter, Legionella, Branhamella catarrhalis, G. vaginalis and Mycoplasma (which are not affected by pencillin are also highly susceptible to erythromycin) ANTI MICROBIAL SPECTRUM Moderately sensitive to H. influenza, B. pertussis, C. trachomatis, N. meningitidis and Rickettsiae Ineffective against Enterobacteriaceae, other gram negative bacilli. ERYTHROMYCIN This drug is acid labile, given as enteric coated tablets. Poorly absorbed when given empty stomach and has poor tissue penetration. DOSE: 250-500mg QID with half life of 1.5 hrs Indications: a drug of choice in atypical pneumonia, whooping cough and cancroids and as an alternative to penicillin in streptococcal pharyngitis, tonsillitis, mastoiditis. SIDE EFFECTS: Epigastric distress causing nausea, vomiting and diarrhea. Allergic reactions such as fever and skin eruption. CLARITHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration. Dose: 250-500mg BD with half life of 3-6 hrs at low dose and 3-9 hrs at high dose. Indications: upper and lower RTI, sinusitis, otitis media, atypical pneumonia, skin infections. And H. pylori infection and first line drug in combination regimens in AIDS infection Side effects: same as erythromycin but better gastric tolerance, reversible hearing loss at high doses. AZYTHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration Dose: 500mg OD with half life >50 hrs. Indications: pharyngitis, tonsillitis, sinusitis, otitis media pneumonias, chronic bronchitis. In the prophylaxis and treatment of AIDS infections. Side effects: nausea vomiting, diarrhea and abdominal pain. ROXITHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration DOSE: 150mg BD with half life of 12 hrs. Indications: alternative to erythromycin for respiratory, skin ]]> Wed, 20 Jul 2022 12:25:44 GMT /slideshow/4-macrolide-antibioticspptx/252251457 tanukatnawer9@slideshare.net(tanukatnawer9) 4. macrolide antibiotics.pptx tanukatnawer9 INTRODUCTION Erythromycin is the first member of group, and was isolated from a strain of Streptomyces erythreus in 1952. Rest drugs are semi-synthetic derivatives of erythromycin known as newer macrolides Some other drugs are dirithromycin, oleandomycin and troleandomycin. MECHANISM OF ACTION Macrolide antibiotics are bacteriostatic agents and inhibit the protein synthesis by binding reversibly to 50s ribosomal subunit of sensitive microorganism and interfere with translocation step in the protein synthesis. Gram positive bacteria's are 100 times more sensitive than gram negative bacteria's by these drugs. MECHANISM OF ACTION It is bacteriostatic at low concentration & bactericidal at high concentration Bactericidal property depends on the concentration, organism concerned and its rate of multiplication ANTI MICROBIAL SPECTRUM It is narrow spectrum antibiotic. These antibiotics are more active against gram positive cocci and inactive against most of the aerobic and enteric gram negative bacilli. In addition, Campylobacter, Legionella, Branhamella catarrhalis, G. vaginalis and Mycoplasma (which are not affected by pencillin are also highly susceptible to erythromycin) ANTI MICROBIAL SPECTRUM Moderately sensitive to H. influenza, B. pertussis, C. trachomatis, N. meningitidis and Rickettsiae Ineffective against Enterobacteriaceae, other gram negative bacilli. ERYTHROMYCIN This drug is acid labile, given as enteric coated tablets. Poorly absorbed when given empty stomach and has poor tissue penetration. DOSE: 250-500mg QID with half life of 1.5 hrs Indications: a drug of choice in atypical pneumonia, whooping cough and cancroids and as an alternative to penicillin in streptococcal pharyngitis, tonsillitis, mastoiditis. SIDE EFFECTS: Epigastric distress causing nausea, vomiting and diarrhea. Allergic reactions such as fever and skin eruption. CLARITHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration. Dose: 250-500mg BD with half life of 3-6 hrs at low dose and 3-9 hrs at high dose. Indications: upper and lower RTI, sinusitis, otitis media, atypical pneumonia, skin infections. And H. pylori infection and first line drug in combination regimens in AIDS infection Side effects: same as erythromycin but better gastric tolerance, reversible hearing loss at high doses. AZYTHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration Dose: 500mg OD with half life >50 hrs. Indications: pharyngitis, tonsillitis, sinusitis, otitis media pneumonias, chronic bronchitis. In the prophylaxis and treatment of AIDS infections. Side effects: nausea vomiting, diarrhea and abdominal pain. ROXITHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration DOSE: 150mg BD with half life of 12 hrs. Indications: alternative to erythromycin for respiratory, skin <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/4-220720122544-355dba37-thumbnail.jpg?width=120&height=120&fit=bounds" /> INTRODUCTION Erythromycin is the first member of group, and was isolated from a strain of Streptomyces erythreus in 1952. Rest drugs are semi-synthetic derivatives of erythromycin known as newer macrolides Some other drugs are dirithromycin, oleandomycin and troleandomycin. MECHANISM OF ACTION Macrolide antibiotics are bacteriostatic agents and inhibit the protein synthesis by binding reversibly to 50s ribosomal subunit of sensitive microorganism and interfere with translocation step in the protein synthesis. Gram positive bacteria's are 100 times more sensitive than gram negative bacteria's by these drugs. MECHANISM OF ACTION It is bacteriostatic at low concentration & bactericidal at high concentration Bactericidal property depends on the concentration, organism concerned and its rate of multiplication ANTI MICROBIAL SPECTRUM It is narrow spectrum antibiotic. These antibiotics are more active against gram positive cocci and inactive against most of the aerobic and enteric gram negative bacilli. In addition, Campylobacter, Legionella, Branhamella catarrhalis, G. vaginalis and Mycoplasma (which are not affected by pencillin are also highly susceptible to erythromycin) ANTI MICROBIAL SPECTRUM Moderately sensitive to H. influenza, B. pertussis, C. trachomatis, N. meningitidis and Rickettsiae Ineffective against Enterobacteriaceae, other gram negative bacilli. ERYTHROMYCIN This drug is acid labile, given as enteric coated tablets. Poorly absorbed when given empty stomach and has poor tissue penetration. DOSE: 250-500mg QID with half life of 1.5 hrs Indications: a drug of choice in atypical pneumonia, whooping cough and cancroids and as an alternative to penicillin in streptococcal pharyngitis, tonsillitis, mastoiditis. SIDE EFFECTS: Epigastric distress causing nausea, vomiting and diarrhea. Allergic reactions such as fever and skin eruption. CLARITHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration. Dose: 250-500mg BD with half life of 3-6 hrs at low dose and 3-9 hrs at high dose. Indications: upper and lower RTI, sinusitis, otitis media, atypical pneumonia, skin infections. And H. pylori infection and first line drug in combination regimens in AIDS infection Side effects: same as erythromycin but better gastric tolerance, reversible hearing loss at high doses. AZYTHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration Dose: 500mg OD with half life >50 hrs. Indications: pharyngitis, tonsillitis, sinusitis, otitis media pneumonias, chronic bronchitis. In the prophylaxis and treatment of AIDS infections. Side effects: nausea vomiting, diarrhea and abdominal pain. ROXITHROMYCIN These drugs are acid stable, good absorption occurs when given empty stomach and has good tissue penetration DOSE: 150mg BD with half life of 12 hrs. Indications: alternative to erythromycin for respiratory, skin

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0 3. aminoglycosides.pptx /slideshow/3-aminoglycosidespptx/252251437 3-220720122357-5d068eef
INTRODUCTION Aminoglycosides are a class of antibiotics used mainly in the treatment of aerobic gram-negative bacilli infections, although they are also effective against other bacteria including Staphylococci and Mycobacterium tuberculosis. They are often used in combination with other antibiotics. Streptomycin – 1944 Actinomycetes – Streptomyces griseus Bactericidal antibiotics which is interfere with protein synthesis Used to treat aerobic Gram –ve bacteria Exhibit ototoxicity and nephrotoxicity MECHANISM OF ACTION These drugs inhibit protein synthesis in the bacteria, there permeability is increased and cell contents leak out and death of cell occurs. These drugs leave bactericidal action. CLINICAL USES Gram –ve bacillary infection – Septicaemia, pelvic & abdominal sepsis Bacterial endocarditis – enterococcal, streptococcal or staphylococcal infection of heart valves Pneumonias, Tuberculosis Tularemia Plague, Brucellosis Topical – Neomycin, Framycetin:- Infections of conjunctiva or external ear and also used it before surgery. COMMON INDICATIONS OF AMINOGLYCOSIDES Gram negative bacillary infections particularly septicemia, meningitis, UTI’s renal, pelvic and abdominal sepsis. Bacterial endocarditis: usually gentamicin is preferred as a part of regimen. Other infections such as tuberculosis, plague, brucellosis etc. Topical uses: neomycin, framycetin and sisomicin are used for various topical infections. NURSING IMPLICATIONS The renal function should be regularly monitored. Patients should be regularly enquired about any side effects. Patients should be warned for not driving or operating the machinery. Patient should be advised to take plenty of water during the course. Monitor the sign and symptoms of hearing loss. ]]>
INTRODUCTION Aminoglycosides are a class of antibiotics used mainly in the treatment of aerobic gram-negative bacilli infections, although they are also effective against other bacteria including Staphylococci and Mycobacterium tuberculosis. They are often used in combination with other antibiotics. Streptomycin – 1944 Actinomycetes – Streptomyces griseus Bactericidal antibiotics which is interfere with protein synthesis Used to treat aerobic Gram –ve bacteria Exhibit ototoxicity and nephrotoxicity MECHANISM OF ACTION These drugs inhibit protein synthesis in the bacteria, there permeability is increased and cell contents leak out and death of cell occurs. These drugs leave bactericidal action. CLINICAL USES Gram –ve bacillary infection – Septicaemia, pelvic & abdominal sepsis Bacterial endocarditis – enterococcal, streptococcal or staphylococcal infection of heart valves Pneumonias, Tuberculosis Tularemia Plague, Brucellosis Topical – Neomycin, Framycetin:- Infections of conjunctiva or external ear and also used it before surgery. COMMON INDICATIONS OF AMINOGLYCOSIDES Gram negative bacillary infections particularly septicemia, meningitis, UTI’s renal, pelvic and abdominal sepsis. Bacterial endocarditis: usually gentamicin is preferred as a part of regimen. Other infections such as tuberculosis, plague, brucellosis etc. Topical uses: neomycin, framycetin and sisomicin are used for various topical infections. NURSING IMPLICATIONS The renal function should be regularly monitored. Patients should be regularly enquired about any side effects. Patients should be warned for not driving or operating the machinery. Patient should be advised to take plenty of water during the course. Monitor the sign and symptoms of hearing loss. ]]> Wed, 20 Jul 2022 12:23:57 GMT /slideshow/3-aminoglycosidespptx/252251437 tanukatnawer9@slideshare.net(tanukatnawer9) 3. aminoglycosides.pptx tanukatnawer9 INTRODUCTION Aminoglycosides are a class of antibiotics used mainly in the treatment of aerobic gram-negative bacilli infections, although they are also effective against other bacteria including Staphylococci and Mycobacterium tuberculosis. They are often used in combination with other antibiotics. Streptomycin – 1944 Actinomycetes – Streptomyces griseus Bactericidal antibiotics which is interfere with protein synthesis Used to treat aerobic Gram –ve bacteria Exhibit ototoxicity and nephrotoxicity MECHANISM OF ACTION These drugs inhibit protein synthesis in the bacteria, there permeability is increased and cell contents leak out and death of cell occurs. These drugs leave bactericidal action. CLINICAL USES Gram –ve bacillary infection – Septicaemia, pelvic & abdominal sepsis Bacterial endocarditis – enterococcal, streptococcal or staphylococcal infection of heart valves Pneumonias, Tuberculosis Tularemia Plague, Brucellosis Topical – Neomycin, Framycetin:- Infections of conjunctiva or external ear and also used it before surgery. COMMON INDICATIONS OF AMINOGLYCOSIDES Gram negative bacillary infections particularly septicemia, meningitis, UTI’s renal, pelvic and abdominal sepsis. Bacterial endocarditis: usually gentamicin is preferred as a part of regimen. Other infections such as tuberculosis, plague, brucellosis etc. Topical uses: neomycin, framycetin and sisomicin are used for various topical infections. NURSING IMPLICATIONS The renal function should be regularly monitored. Patients should be regularly enquired about any side effects. Patients should be warned for not driving or operating the machinery. Patient should be advised to take plenty of water during the course. Monitor the sign and symptoms of hearing loss. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/3-220720122357-5d068eef-thumbnail.jpg?width=120&height=120&fit=bounds" /> INTRODUCTION Aminoglycosides are a class of antibiotics used mainly in the treatment of aerobic gram-negative bacilli infections, although they are also effective against other bacteria including Staphylococci and Mycobacterium tuberculosis. They are often used in combination with other antibiotics. Streptomycin – 1944 Actinomycetes – Streptomyces griseus Bactericidal antibiotics which is interfere with protein synthesis Used to treat aerobic Gram –ve bacteria Exhibit ototoxicity and nephrotoxicity MECHANISM OF ACTION These drugs inhibit protein synthesis in the bacteria, there permeability is increased and cell contents leak out and death of cell occurs. These drugs leave bactericidal action. CLINICAL USES Gram –ve bacillary infection – Septicaemia, pelvic & abdominal sepsis Bacterial endocarditis – enterococcal, streptococcal or staphylococcal infection of heart valves Pneumonias, Tuberculosis Tularemia Plague, Brucellosis Topical – Neomycin, Framycetin:- Infections of conjunctiva or external ear and also used it before surgery. COMMON INDICATIONS OF AMINOGLYCOSIDES Gram negative bacillary infections particularly septicemia, meningitis, UTI’s renal, pelvic and abdominal sepsis. Bacterial endocarditis: usually gentamicin is preferred as a part of regimen. Other infections such as tuberculosis, plague, brucellosis etc. Topical uses: neomycin, framycetin and sisomicin are used for various topical infections. NURSING IMPLICATIONS The renal function should be regularly monitored. Patients should be regularly enquired about any side effects. Patients should be warned for not driving or operating the machinery. Patient should be advised to take plenty of water during the course. Monitor the sign and symptoms of hearing loss.

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0 2. cephalosporins.ppt /slideshow/2-cephalosporinsppt/252251406 2-220720122057-9b4990b2
7-aminocephalosporanic acid has been modified by addition of different side chains to create a whole family of cephalosporin antibiotics. these have been conventionally divided into 5 generations Mechanism of action All cephalosporins are bactericidal. As penicillin it also inhibit the synthesis of bacterial cell wall and causing rapid cell lysis. Inhibition of transpeptidation (Transpeptidase enzymes then cross-link the chains to provide strength to the cell wall and enable the bacterium to resist osmotic lysis) Imperfect cell wall Osmotic drive Activation of autolysin enzymes Lysis of bacteria BACTERICIDAL CLASSIFICATION Based on antimicrobial spectrum Chronological sequence of development Divided into generations. First-generation agents Cephalexin (O) Cefadroxil (O) Cefazolin (i.m, i.v) Cefalothin (withdrawn) Exhibit good activity against gram-positive bacteria but modest activity against gram negative organisms. Most gram-positive cocci Strepto, Pneumo, Methicillin sens. Staph. are susceptible to first-generation cephalosporins Modest activity against E. coli, K. pneumoniae & Proteus mirabilis Second-generation agents Cefaclor (O) Ceforanide Cefuroxime (i.m , i.v) Cefoprozil Exhibit somewhat increased activity against gram negative organisms, but much less active than third generation agents. Less active against gram positive cocci & bacilli compared to first gen. drugs. Use declined Clinically replaced by 3rd & 4th generation drugs . Third-generation agents Cefotaxime Ceftriaxone Cefdinir Cefibuten Cefpodoxime Ceftizoxime Ceftazidime Cefoperazone (withdrawn) Highly augmented activity against gram-negative organisms Less active than first generation agents against gram positive cocci & anaerobes. All are highly resistant to β-lactamases from gram negative bacteria. Some inhibit psuedomonas as well; ceftazidime, cefoperazone(withdrawn) Some members of this group have enhanced ability to cross the blood-brain barrier eg. Ceftriaxone and are effective in treating meningitis caused by pneumococci, meningococci, H. influenzae and susceptible gram negative rods. Fourth-generation agents Cefpirome (im/iv) Cefepime (iv) Cefozopran (im) Highly active against G –ve organisms Similar to third gen drugs for g +ve bacteria The fourth generation drugs comparable to third generation but more resistant to hydrolysis by β-lactamases. Effective against bacterial infections resistant to earlier drugs Fifth-generation agents Ceftobiprole Ceftaroline Active against, g +ve cocci especially MRSA (Methicillin-resistant Staphylococcus aureus) It's tougher to treat than most strains of staphylococcus aureus -- or staph -- because it's resistant to some commonly used antibiotics. penicillin resistant S. pneumoniae and enterococci Adverse reactions Pain after im injection Thrombophlebitis of injected vein. Diarrhoea more common with oral Ceferadine P/E Cefoperazone (Banned) ]]>
7-aminocephalosporanic acid has been modified by addition of different side chains to create a whole family of cephalosporin antibiotics. these have been conventionally divided into 5 generations Mechanism of action All cephalosporins are bactericidal. As penicillin it also inhibit the synthesis of bacterial cell wall and causing rapid cell lysis. Inhibition of transpeptidation (Transpeptidase enzymes then cross-link the chains to provide strength to the cell wall and enable the bacterium to resist osmotic lysis) Imperfect cell wall Osmotic drive Activation of autolysin enzymes Lysis of bacteria BACTERICIDAL CLASSIFICATION Based on antimicrobial spectrum Chronological sequence of development Divided into generations. First-generation agents Cephalexin (O) Cefadroxil (O) Cefazolin (i.m, i.v) Cefalothin (withdrawn) Exhibit good activity against gram-positive bacteria but modest activity against gram negative organisms. Most gram-positive cocci Strepto, Pneumo, Methicillin sens. Staph. are susceptible to first-generation cephalosporins Modest activity against E. coli, K. pneumoniae & Proteus mirabilis Second-generation agents Cefaclor (O) Ceforanide Cefuroxime (i.m , i.v) Cefoprozil Exhibit somewhat increased activity against gram negative organisms, but much less active than third generation agents. Less active against gram positive cocci & bacilli compared to first gen. drugs. Use declined Clinically replaced by 3rd & 4th generation drugs . Third-generation agents Cefotaxime Ceftriaxone Cefdinir Cefibuten Cefpodoxime Ceftizoxime Ceftazidime Cefoperazone (withdrawn) Highly augmented activity against gram-negative organisms Less active than first generation agents against gram positive cocci & anaerobes. All are highly resistant to β-lactamases from gram negative bacteria. Some inhibit psuedomonas as well; ceftazidime, cefoperazone(withdrawn) Some members of this group have enhanced ability to cross the blood-brain barrier eg. Ceftriaxone and are effective in treating meningitis caused by pneumococci, meningococci, H. influenzae and susceptible gram negative rods. Fourth-generation agents Cefpirome (im/iv) Cefepime (iv) Cefozopran (im) Highly active against G –ve organisms Similar to third gen drugs for g +ve bacteria The fourth generation drugs comparable to third generation but more resistant to hydrolysis by β-lactamases. Effective against bacterial infections resistant to earlier drugs Fifth-generation agents Ceftobiprole Ceftaroline Active against, g +ve cocci especially MRSA (Methicillin-resistant Staphylococcus aureus) It's tougher to treat than most strains of staphylococcus aureus -- or staph -- because it's resistant to some commonly used antibiotics. penicillin resistant S. pneumoniae and enterococci Adverse reactions Pain after im injection Thrombophlebitis of injected vein. Diarrhoea more common with oral Ceferadine P/E Cefoperazone (Banned) ]]> Wed, 20 Jul 2022 12:20:57 GMT /slideshow/2-cephalosporinsppt/252251406 tanukatnawer9@slideshare.net(tanukatnawer9) 2. cephalosporins.ppt tanukatnawer9 7-aminocephalosporanic acid has been modified by addition of different side chains to create a whole family of cephalosporin antibiotics. these have been conventionally divided into 5 generations Mechanism of action All cephalosporins are bactericidal. As penicillin it also inhibit the synthesis of bacterial cell wall and causing rapid cell lysis. Inhibition of transpeptidation (Transpeptidase enzymes then cross-link the chains to provide strength to the cell wall and enable the bacterium to resist osmotic lysis) Imperfect cell wall Osmotic drive Activation of autolysin enzymes Lysis of bacteria BACTERICIDAL CLASSIFICATION Based on antimicrobial spectrum Chronological sequence of development Divided into generations. �First-generation agents � Cephalexin (O) Cefadroxil (O) Cefazolin (i.m, i.v) Cefalothin (withdrawn) Exhibit good activity against gram-positive bacteria but modest activity against gram negative organisms. Most gram-positive cocci Strepto, Pneumo, Methicillin sens. Staph. are susceptible to first-generation cephalosporins Modest activity against E. coli, K. pneumoniae & Proteus mirabilis Second-generation agents Cefaclor (O) Ceforanide Cefuroxime (i.m , i.v) Cefoprozil Exhibit somewhat increased activity against gram negative organisms, but much less active than third generation agents. Less active against gram positive cocci & bacilli compared to first gen. drugs. Use declined Clinically replaced by 3rd & 4th generation drugs . Third-generation agents Cefotaxime Ceftriaxone Cefdinir Cefibuten Cefpodoxime Ceftizoxime Ceftazidime Cefoperazone (withdrawn) Highly augmented activity against gram-negative organisms Less active than first generation agents against gram positive cocci & anaerobes. All are highly resistant to β-lactamases from gram negative bacteria. Some inhibit psuedomonas as well; ceftazidime, cefoperazone(withdrawn) Some members of this group have enhanced ability to cross the blood-brain barrier eg. Ceftriaxone and are effective in treating meningitis caused by pneumococci, meningococci, H. influenzae and susceptible gram negative rods. Fourth-generation agents Cefpirome (im/iv) Cefepime (iv) Cefozopran (im) Highly active against G –ve organisms Similar to third gen drugs for g +ve bacteria The fourth generation drugs comparable to third generation but more resistant to hydrolysis by β-lactamases. Effective against bacterial infections resistant to earlier drugs Fifth-generation agents Ceftobiprole Ceftaroline Active against, g +ve cocci especially MRSA (Methicillin-resistant Staphylococcus aureus) It's tougher to treat than most strains of staphylococcus aureus -- or staph -- because it's resistant to some commonly used antibiotics. penicillin resistant S. pneumoniae and enterococci Adverse reactions Pain after im injection Thrombophlebitis of injected vein. Diarrhoea more common with oral Ceferadine P/E Cefoperazone (Banned) <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/2-220720122057-9b4990b2-thumbnail.jpg?width=120&height=120&fit=bounds" /> 7-aminocephalosporanic acid has been modified by addition of different side chains to create a whole family of cephalosporin antibiotics. these have been conventionally divided into 5 generations Mechanism of action All cephalosporins are bactericidal. As penicillin it also inhibit the synthesis of bacterial cell wall and causing rapid cell lysis. Inhibition of transpeptidation (Transpeptidase enzymes then cross-link the chains to provide strength to the cell wall and enable the bacterium to resist osmotic lysis) Imperfect cell wall Osmotic drive Activation of autolysin enzymes Lysis of bacteria BACTERICIDAL CLASSIFICATION Based on antimicrobial spectrum Chronological sequence of development Divided into generations. �First-generation agents � Cephalexin (O) Cefadroxil (O) Cefazolin (i.m, i.v) Cefalothin (withdrawn) Exhibit good activity against gram-positive bacteria but modest activity against gram negative organisms. Most gram-positive cocci Strepto, Pneumo, Methicillin sens. Staph. are susceptible to first-generation cephalosporins Modest activity against E. coli, K. pneumoniae & Proteus mirabilis Second-generation agents Cefaclor (O) Ceforanide Cefuroxime (i.m , i.v) Cefoprozil Exhibit somewhat increased activity against gram negative organisms, but much less active than third generation agents. Less active against gram positive cocci & bacilli compared to first gen. drugs. Use declined Clinically replaced by 3rd & 4th generation drugs . Third-generation agents Cefotaxime Ceftriaxone Cefdinir Cefibuten Cefpodoxime Ceftizoxime Ceftazidime Cefoperazone (withdrawn) Highly augmented activity against gram-negative organisms Less active than first generation agents against gram positive cocci & anaerobes. All are highly resistant to β-lactamases from gram negative bacteria. Some inhibit psuedomonas as well; ceftazidime, cefoperazone(withdrawn) Some members of this group have enhanced ability to cross the blood-brain barrier eg. Ceftriaxone and are effective in treating meningitis caused by pneumococci, meningococci, H. influenzae and susceptible gram negative rods. Fourth-generation agents Cefpirome (im/iv) Cefepime (iv) Cefozopran (im) Highly active against G –ve organisms Similar to third gen drugs for g +ve bacteria The fourth generation drugs comparable to third generation but more resistant to hydrolysis by β-lactamases. Effective against bacterial infections resistant to earlier drugs Fifth-generation agents Ceftobiprole Ceftaroline Active against, g +ve cocci especially MRSA (Methicillin-resistant Staphylococcus aureus) It's tougher to treat than most strains of staphylococcus aureus -- or staph -- because it's resistant to some commonly used antibiotics. penicillin resistant S. pneumoniae and enterococci Adverse reactions Pain after im injection Thrombophlebitis of injected vein. Diarrhoea more common with oral Ceferadine P/E Cefoperazone (Banned)

2. cephalosporins.ppt from NEHA BHARTI

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0 CHEMOTHERAPY- PENICILLIN.pptx /slideshow/chemotherapy-penicillinpptx/252251338 1-220720121613-bba84773
DEFINITION CHEMOTHERAPY & ANTIBIOTICS CHEMOTHERAPY: Chemotherapy is the treatment of infections by substances which destroy or suppress bacteria and other microorganism. The substances / Agents used may natural synthetic or semi – synthetic in nature. ANTIBIOTICS: An antibiotic is a chemical substance produced by microorganism which prevents the growth of other microorganism or kills the other microorganism. These are natural substances CHEMOTHERAPY It is a method of therapy of infectious disease and cancer with chemical agents – chemotherapeutic medicines ANTIBIOTICS CLASSIFIED AS: According to the mode of action on Bacteria: According to the type of Bacteria: According to the effectiveness against microorganism: According to the mode of action on Bacteria: Bacteriostatic: These antibiotics inhibit the growth & multiplication of Bacteria. Eg. Tetracycline, Chloramphenicol, Sulphonamides, Dapsone, Erythromycin, Clindamycin. Bactericidal: These antibiotics destroy or kill all the Bacteria in the process of multiplication. Eg. Penicillin, Aminoglycosides, Cephalosporin, Fluoroquinolones, Rifampicin, Metronidazole etc. According to the type of Bacteria: Gram Positive: Some Antibiotics are effective mainly against Gram Positive Bacteria Eg. Penicillin. Gram Negative: Some Antibiotics are effective mainly against Gram Negative Bacteria Eg. Streptomycin. According to the effectiveness against microorganism: Broad Spectrum: The Antibiotics which acts against wide range of microorganisms. Eg. Tetracycline. Narrow Spectrum: These Antibiotics are useful against limited microorganisms. Eg. Erythromycin Toxic Effects: Gastrointestinal irritation, Nausea, Vomiting and diarrhea may occur when given by mouth. Skin sensitivity may develop with Penicillin or streptomycin causing rashes. Serious toxic effect may occur due to streptomycin on the vestibular & auditory nerve causing vertigo & deafness Drug Resistance: Many bacteria soon develops resistance to particular drug after a period of treatment, so that the bacteria will not respond to the same drug for example tubercle bacillus develops resistance to streptomycin quickly. Super infection: The antibiotics given by mouth kill the normal bacteria inhibiting the alimentary canal and permits the over growth of other insensitive organisms which can cause serious complications. Eg. Fungus cause thrush which may go to the lungs with fatal results. Hypersensitivity Reaction: Chemotherapeutic agents can cause Hypersensitivity reactions from mild rashes to serve anaphylactic shock. Eg. Penicillin & Sulphonamides. Vitamin Deficiency: Alteration in vitamin formation and absorption from the bowel take place . So there is deficiency of Vitamin B complex and Vitamin K. Anemia: In susceptible persons chloramphenicol may produce Aplastic anemia or agranulocytosis. (Action must be taken through proper history about previous drug reaction before administering penicillin sulphonamide and cephalosporin ]]>
DEFINITION CHEMOTHERAPY & ANTIBIOTICS CHEMOTHERAPY: Chemotherapy is the treatment of infections by substances which destroy or suppress bacteria and other microorganism. The substances / Agents used may natural synthetic or semi – synthetic in nature. ANTIBIOTICS: An antibiotic is a chemical substance produced by microorganism which prevents the growth of other microorganism or kills the other microorganism. These are natural substances CHEMOTHERAPY It is a method of therapy of infectious disease and cancer with chemical agents – chemotherapeutic medicines ANTIBIOTICS CLASSIFIED AS: According to the mode of action on Bacteria: According to the type of Bacteria: According to the effectiveness against microorganism: According to the mode of action on Bacteria: Bacteriostatic: These antibiotics inhibit the growth & multiplication of Bacteria. Eg. Tetracycline, Chloramphenicol, Sulphonamides, Dapsone, Erythromycin, Clindamycin. Bactericidal: These antibiotics destroy or kill all the Bacteria in the process of multiplication. Eg. Penicillin, Aminoglycosides, Cephalosporin, Fluoroquinolones, Rifampicin, Metronidazole etc. According to the type of Bacteria: Gram Positive: Some Antibiotics are effective mainly against Gram Positive Bacteria Eg. Penicillin. Gram Negative: Some Antibiotics are effective mainly against Gram Negative Bacteria Eg. Streptomycin. According to the effectiveness against microorganism: Broad Spectrum: The Antibiotics which acts against wide range of microorganisms. Eg. Tetracycline. Narrow Spectrum: These Antibiotics are useful against limited microorganisms. Eg. Erythromycin Toxic Effects: Gastrointestinal irritation, Nausea, Vomiting and diarrhea may occur when given by mouth. Skin sensitivity may develop with Penicillin or streptomycin causing rashes. Serious toxic effect may occur due to streptomycin on the vestibular & auditory nerve causing vertigo & deafness Drug Resistance: Many bacteria soon develops resistance to particular drug after a period of treatment, so that the bacteria will not respond to the same drug for example tubercle bacillus develops resistance to streptomycin quickly. Super infection: The antibiotics given by mouth kill the normal bacteria inhibiting the alimentary canal and permits the over growth of other insensitive organisms which can cause serious complications. Eg. Fungus cause thrush which may go to the lungs with fatal results. Hypersensitivity Reaction: Chemotherapeutic agents can cause Hypersensitivity reactions from mild rashes to serve anaphylactic shock. Eg. Penicillin & Sulphonamides. Vitamin Deficiency: Alteration in vitamin formation and absorption from the bowel take place . So there is deficiency of Vitamin B complex and Vitamin K. Anemia: In susceptible persons chloramphenicol may produce Aplastic anemia or agranulocytosis. (Action must be taken through proper history about previous drug reaction before administering penicillin sulphonamide and cephalosporin ]]> Wed, 20 Jul 2022 12:16:13 GMT /slideshow/chemotherapy-penicillinpptx/252251338 tanukatnawer9@slideshare.net(tanukatnawer9) CHEMOTHERAPY- PENICILLIN.pptx tanukatnawer9 DEFINITION �CHEMOTHERAPY & ANTIBIOTICS CHEMOTHERAPY: Chemotherapy is the treatment of infections by substances which destroy or suppress bacteria and other microorganism. The substances / Agents used may natural synthetic or semi – synthetic in nature. ANTIBIOTICS: An antibiotic is a chemical substance produced by microorganism which prevents the growth of other microorganism or kills the other microorganism. These are natural substances CHEMOTHERAPY It is a method of therapy of infectious disease and cancer with chemical agents – chemotherapeutic medicines ANTIBIOTICS CLASSIFIED AS: According to the mode of action on Bacteria: According to the type of Bacteria: According to the effectiveness against microorganism: According to the mode of action on Bacteria: Bacteriostatic: These antibiotics inhibit the growth & multiplication of Bacteria. Eg. Tetracycline, Chloramphenicol, Sulphonamides, Dapsone, Erythromycin, Clindamycin. Bactericidal: These antibiotics destroy or kill all the Bacteria in the process of multiplication. Eg. Penicillin, Aminoglycosides, Cephalosporin, Fluoroquinolones, Rifampicin, Metronidazole etc. According to the type of Bacteria: Gram Positive: Some Antibiotics are effective mainly against Gram Positive Bacteria Eg. Penicillin. Gram Negative: Some Antibiotics are effective mainly against Gram Negative Bacteria Eg. Streptomycin. According to the effectiveness against microorganism: Broad Spectrum: The Antibiotics which acts against wide range of microorganisms. Eg. Tetracycline. Narrow Spectrum: These Antibiotics are useful against limited microorganisms. Eg. Erythromycin Toxic Effects: Gastrointestinal irritation, Nausea, Vomiting and diarrhea may occur when given by mouth. Skin sensitivity may develop with Penicillin or streptomycin causing rashes. Serious toxic effect may occur due to streptomycin on the vestibular & auditory nerve causing vertigo & deafness Drug Resistance: Many bacteria soon develops resistance to particular drug after a period of treatment, so that the bacteria will not respond to the same drug for example tubercle bacillus develops resistance to streptomycin quickly. Super infection: The antibiotics given by mouth kill the normal bacteria inhibiting the alimentary canal and permits the over growth of other insensitive organisms which can cause serious complications. Eg. Fungus cause thrush which may go to the lungs with fatal results. Hypersensitivity Reaction: Chemotherapeutic agents can cause Hypersensitivity reactions from mild rashes to serve anaphylactic shock. Eg. Penicillin & Sulphonamides. Vitamin Deficiency: Alteration in vitamin formation and absorption from the bowel take place . So there is deficiency of Vitamin B complex and Vitamin K. Anemia: In susceptible persons chloramphenicol may produce Aplastic anemia or agranulocytosis. (Action must be taken through proper history about previous drug reaction before administering penicillin sulphonamide and cephalosporin <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/1-220720121613-bba84773-thumbnail.jpg?width=120&height=120&fit=bounds" /> DEFINITION �CHEMOTHERAPY & ANTIBIOTICS CHEMOTHERAPY: Chemotherapy is the treatment of infections by substances which destroy or suppress bacteria and other microorganism. The substances / Agents used may natural synthetic or semi – synthetic in nature. ANTIBIOTICS: An antibiotic is a chemical substance produced by microorganism which prevents the growth of other microorganism or kills the other microorganism. These are natural substances CHEMOTHERAPY It is a method of therapy of infectious disease and cancer with chemical agents – chemotherapeutic medicines ANTIBIOTICS CLASSIFIED AS: According to the mode of action on Bacteria: According to the type of Bacteria: According to the effectiveness against microorganism: According to the mode of action on Bacteria: Bacteriostatic: These antibiotics inhibit the growth & multiplication of Bacteria. Eg. Tetracycline, Chloramphenicol, Sulphonamides, Dapsone, Erythromycin, Clindamycin. Bactericidal: These antibiotics destroy or kill all the Bacteria in the process of multiplication. Eg. Penicillin, Aminoglycosides, Cephalosporin, Fluoroquinolones, Rifampicin, Metronidazole etc. According to the type of Bacteria: Gram Positive: Some Antibiotics are effective mainly against Gram Positive Bacteria Eg. Penicillin. Gram Negative: Some Antibiotics are effective mainly against Gram Negative Bacteria Eg. Streptomycin. According to the effectiveness against microorganism: Broad Spectrum: The Antibiotics which acts against wide range of microorganisms. Eg. Tetracycline. Narrow Spectrum: These Antibiotics are useful against limited microorganisms. Eg. Erythromycin Toxic Effects: Gastrointestinal irritation, Nausea, Vomiting and diarrhea may occur when given by mouth. Skin sensitivity may develop with Penicillin or streptomycin causing rashes. Serious toxic effect may occur due to streptomycin on the vestibular & auditory nerve causing vertigo & deafness Drug Resistance: Many bacteria soon develops resistance to particular drug after a period of treatment, so that the bacteria will not respond to the same drug for example tubercle bacillus develops resistance to streptomycin quickly. Super infection: The antibiotics given by mouth kill the normal bacteria inhibiting the alimentary canal and permits the over growth of other insensitive organisms which can cause serious complications. Eg. Fungus cause thrush which may go to the lungs with fatal results. Hypersensitivity Reaction: Chemotherapeutic agents can cause Hypersensitivity reactions from mild rashes to serve anaphylactic shock. Eg. Penicillin & Sulphonamides. Vitamin Deficiency: Alteration in vitamin formation and absorption from the bowel take place . So there is deficiency of Vitamin B complex and Vitamin K. Anemia: In susceptible persons chloramphenicol may produce Aplastic anemia or agranulocytosis. (Action must be taken through proper history about previous drug reaction before administering penicillin sulphonamide and cephalosporin

CHEMOTHERAPY- PENICILLIN.pptx from NEHA BHARTI

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0 Polycystic kidney disease /slideshow/polycystic-kidney-disease-144550441/144550441 polycystickidneydisease1-190509074225
definition types of Polycystic kidney disease complications of Polycystic kidney disease management for Polycystic kidney disease ]]>
definition types of Polycystic kidney disease complications of Polycystic kidney disease management for Polycystic kidney disease ]]> Thu, 09 May 2019 07:42:25 GMT /slideshow/polycystic-kidney-disease-144550441/144550441 tanukatnawer9@slideshare.net(tanukatnawer9) Polycystic kidney disease tanukatnawer9 definition types of Polycystic kidney disease complications of Polycystic kidney disease management for Polycystic kidney disease <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/polycystickidneydisease1-190509074225-thumbnail.jpg?width=120&height=120&fit=bounds" /> definition types of Polycystic kidney disease complications of Polycystic kidney disease management for Polycystic kidney disease

Polycystic kidney disease from NEHA BHARTI

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0 Hydronephrosis /slideshow/hydronephrosis-144549852/144549852 hydronephrosis-190509073914
definition of hydronephrosis, causes and types of hydronephrosis pathophysiology of hydronephrosis clinical manifestation and diagnostic test for hydronephrosis management ]]>
definition of hydronephrosis, causes and types of hydronephrosis pathophysiology of hydronephrosis clinical manifestation and diagnostic test for hydronephrosis management ]]> Thu, 09 May 2019 07:39:14 GMT /slideshow/hydronephrosis-144549852/144549852 tanukatnawer9@slideshare.net(tanukatnawer9) Hydronephrosis tanukatnawer9 definition of hydronephrosis, causes and types of hydronephrosis pathophysiology of hydronephrosis clinical manifestation and diagnostic test for hydronephrosis management <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/hydronephrosis-190509073914-thumbnail.jpg?width=120&height=120&fit=bounds" /> definition of hydronephrosis, causes and types of hydronephrosis pathophysiology of hydronephrosis clinical manifestation and diagnostic test for hydronephrosis management

Hydronephrosis from NEHA BHARTI

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0 NEPHRITIS /slideshow/nephritis/144549068 nephritis-190509073541
DEFINITION OF NEPHRITIS TYPES OF NEPHRITIS SUB TYPES OF NEPHRITIS PATHOPHYSIOLOGY OF NEPHRITIS SYMPTOMS OF NEPHRITIS MANAGEMENT OF NEPHRITIS]]>
DEFINITION OF NEPHRITIS TYPES OF NEPHRITIS SUB TYPES OF NEPHRITIS PATHOPHYSIOLOGY OF NEPHRITIS SYMPTOMS OF NEPHRITIS MANAGEMENT OF NEPHRITIS]]> Thu, 09 May 2019 07:35:41 GMT /slideshow/nephritis/144549068 tanukatnawer9@slideshare.net(tanukatnawer9) NEPHRITIS tanukatnawer9 DEFINITION OF NEPHRITIS TYPES OF NEPHRITIS SUB TYPES OF NEPHRITIS PATHOPHYSIOLOGY OF NEPHRITIS SYMPTOMS OF NEPHRITIS MANAGEMENT OF NEPHRITIS <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/nephritis-190509073541-thumbnail.jpg?width=120&height=120&fit=bounds" /> DEFINITION OF NEPHRITIS TYPES OF NEPHRITIS SUB TYPES OF NEPHRITIS PATHOPHYSIOLOGY OF NEPHRITIS SYMPTOMS OF NEPHRITIS MANAGEMENT OF NEPHRITIS

NEPHRITIS from NEHA BHARTI

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0 Nephrotic syndrome /slideshow/nephrotic-syndrome-144547255/144547255 nephroticsyndrome-190509072727
DEFINITION, CLASSIFICATION NEPHROTIC SYNDROME pathophysiology MANAGEMENT ]]>
DEFINITION, CLASSIFICATION NEPHROTIC SYNDROME pathophysiology MANAGEMENT ]]> Thu, 09 May 2019 07:27:26 GMT /slideshow/nephrotic-syndrome-144547255/144547255 tanukatnawer9@slideshare.net(tanukatnawer9) Nephrotic syndrome tanukatnawer9 DEFINITION, CLASSIFICATION NEPHROTIC SYNDROME pathophysiology MANAGEMENT <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/nephroticsyndrome-190509072727-thumbnail.jpg?width=120&height=120&fit=bounds" /> DEFINITION, CLASSIFICATION NEPHROTIC SYNDROME pathophysiology MANAGEMENT

Nephrotic syndrome from NEHA BHARTI

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0 Acute renal failure and chronic renal failure /slideshow/acute-renal-failure-and-chronic-renal-failure/144543797 acuterenalfailure2filesmerged-190509071023
DEFINITION, CAUSES, PHASES, PATHOPHYSIOLOGY, TREATMENT, MANGEMENT, EDUCATION]]>
DEFINITION, CAUSES, PHASES, PATHOPHYSIOLOGY, TREATMENT, MANGEMENT, EDUCATION]]> Thu, 09 May 2019 07:10:23 GMT /slideshow/acute-renal-failure-and-chronic-renal-failure/144543797 tanukatnawer9@slideshare.net(tanukatnawer9) Acute renal failure and chronic renal failure tanukatnawer9 DEFINITION, CAUSES, PHASES, PATHOPHYSIOLOGY, TREATMENT, MANGEMENT, EDUCATION <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/acuterenalfailure2filesmerged-190509071023-thumbnail.jpg?width=120&height=120&fit=bounds" /> DEFINITION, CAUSES, PHASES, PATHOPHYSIOLOGY, TREATMENT, MANGEMENT, EDUCATION

Acute renal failure and chronic renal failure from NEHA BHARTI

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0 Glaucoma /slideshow/glaucoma-120786570/120786570 glaucoma-181026045423
DEFINITION,EYE ANATOMY, Fluid Circulation, CAUSES AND RISK FACTORS, PATHOPHYSIOLOGY, CLASSIFICATIONS, DIAGNOSTIC EVALUATION, MANAGEMENT]]>
DEFINITION,EYE ANATOMY, Fluid Circulation, CAUSES AND RISK FACTORS, PATHOPHYSIOLOGY, CLASSIFICATIONS, DIAGNOSTIC EVALUATION, MANAGEMENT]]> Fri, 26 Oct 2018 04:54:23 GMT /slideshow/glaucoma-120786570/120786570 tanukatnawer9@slideshare.net(tanukatnawer9) Glaucoma tanukatnawer9 DEFINITION,EYE ANATOMY, Fluid Circulation, CAUSES AND RISK FACTORS, PATHOPHYSIOLOGY, CLASSIFICATIONS, DIAGNOSTIC EVALUATION, MANAGEMENT <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/glaucoma-181026045423-thumbnail.jpg?width=120&height=120&fit=bounds" /> DEFINITION,EYE ANATOMY, Fluid Circulation, CAUSES AND RISK FACTORS, PATHOPHYSIOLOGY, CLASSIFICATIONS, DIAGNOSTIC EVALUATION, MANAGEMENT

Glaucoma from NEHA BHARTI

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0 ABDELLAH’S THEORY /slideshow/abdellahs-theory-120088914/120088914 abdellahstheory-181020052756
BIOGRAPHY OF FAYE GLENN ABDELLAH, AS AN EDUCATOR AND RESEARCHER, INFLUENCED FAYE ANDELLAH IN THE DEVELOPMENT HER OWN MODEL OF NURSING, ABDELLAH’S TYPOLOGY OF 21 NURSING PROBLEMS, ASSUMPTION, CONCEPT, STEPS TO IDENTIFY THE CLIENT’S PROBLEM, 11 NURSING SKILLS, USE OF 21 PROBLEMS IN THE NURSING PROCESS AND LIMITATIONS]]>
BIOGRAPHY OF FAYE GLENN ABDELLAH, AS AN EDUCATOR AND RESEARCHER, INFLUENCED FAYE ANDELLAH IN THE DEVELOPMENT HER OWN MODEL OF NURSING, ABDELLAH’S TYPOLOGY OF 21 NURSING PROBLEMS, ASSUMPTION, CONCEPT, STEPS TO IDENTIFY THE CLIENT’S PROBLEM, 11 NURSING SKILLS, USE OF 21 PROBLEMS IN THE NURSING PROCESS AND LIMITATIONS]]> Sat, 20 Oct 2018 05:27:56 GMT /slideshow/abdellahs-theory-120088914/120088914 tanukatnawer9@slideshare.net(tanukatnawer9) ABDELLAH’S THEORY tanukatnawer9 BIOGRAPHY OF FAYE GLENN ABDELLAH, AS AN EDUCATOR AND RESEARCHER, INFLUENCED FAYE ANDELLAH IN THE DEVELOPMENT HER OWN MODEL OF NURSING, ABDELLAH’S TYPOLOGY OF 21 NURSING PROBLEMS, ASSUMPTION, CONCEPT, STEPS TO IDENTIFY THE CLIENT’S PROBLEM, 11 NURSING SKILLS, USE OF 21 PROBLEMS IN THE NURSING PROCESS AND LIMITATIONS <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/abdellahstheory-181020052756-thumbnail.jpg?width=120&height=120&fit=bounds" /> BIOGRAPHY OF FAYE GLENN ABDELLAH, AS AN EDUCATOR AND RESEARCHER, INFLUENCED FAYE ANDELLAH IN THE DEVELOPMENT HER OWN MODEL OF NURSING, ABDELLAH’S TYPOLOGY OF 21 NURSING PROBLEMS, ASSUMPTION, CONCEPT, STEPS TO IDENTIFY THE CLIENT’S PROBLEM, 11 NURSING SKILLS, USE OF 21 PROBLEMS IN THE NURSING PROCESS AND LIMITATIONS

ABDELLAH’S THEORY from NEHA BHARTI

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0 Nursing assessment and assessment of eye /slideshow/nursing-assessment-and-assessment-of-eye/120086370 nursingassessment-181020050239
examination of eye, Examination by ophthalmoscope, assessment of the functions of eye, . PUPILLARY RESPONSE, FUNCTIONAL EXAMINATION, test for Focusing power, confrontation test, Colour sense test and visual acuity testing procedure etc ]]>
examination of eye, Examination by ophthalmoscope, assessment of the functions of eye, . PUPILLARY RESPONSE, FUNCTIONAL EXAMINATION, test for Focusing power, confrontation test, Colour sense test and visual acuity testing procedure etc ]]> Sat, 20 Oct 2018 05:02:39 GMT /slideshow/nursing-assessment-and-assessment-of-eye/120086370 tanukatnawer9@slideshare.net(tanukatnawer9) Nursing assessment and assessment of eye tanukatnawer9 examination of eye, Examination by ophthalmoscope, assessment of the functions of eye, . PUPILLARY RESPONSE, FUNCTIONAL EXAMINATION, test for Focusing power, confrontation test, Colour sense test and visual acuity testing procedure etc <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/nursingassessment-181020050239-thumbnail.jpg?width=120&height=120&fit=bounds" /> examination of eye, Examination by ophthalmoscope, assessment of the functions of eye, . PUPILLARY RESPONSE, FUNCTIONAL EXAMINATION, test for Focusing power, confrontation test, Colour sense test and visual acuity testing procedure etc

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0 Bowel elimination /slideshow/bowel-elimination-99025570/99025570 boweleliminationbyme-180527062135
elimination, bowel elimination, physiology of elimination, process of bowel eliminaton factor impaired bowel, factors improve bowel elimination, alteration in bowel elimination, maintenance of bowel motility, assessment of bowel elimination, characteristics of feces, type of feces, methods for maintain the bowel elimination:- enemas, rectal suppositories and colostomies, types of colostomies, colostomy care]]>
elimination, bowel elimination, physiology of elimination, process of bowel eliminaton factor impaired bowel, factors improve bowel elimination, alteration in bowel elimination, maintenance of bowel motility, assessment of bowel elimination, characteristics of feces, type of feces, methods for maintain the bowel elimination:- enemas, rectal suppositories and colostomies, types of colostomies, colostomy care]]> Sun, 27 May 2018 06:21:35 GMT /slideshow/bowel-elimination-99025570/99025570 tanukatnawer9@slideshare.net(tanukatnawer9) Bowel elimination tanukatnawer9 elimination, bowel elimination, physiology of elimination, process of bowel eliminaton factor impaired bowel, factors improve bowel elimination, alteration in bowel elimination, maintenance of bowel motility, assessment of bowel elimination, characteristics of feces, type of feces, methods for maintain the bowel elimination:- enemas, rectal suppositories and colostomies, types of colostomies, colostomy care <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/boweleliminationbyme-180527062135-thumbnail.jpg?width=120&height=120&fit=bounds" /> elimination, bowel elimination, physiology of elimination, process of bowel eliminaton factor impaired bowel, factors improve bowel elimination, alteration in bowel elimination, maintenance of bowel motility, assessment of bowel elimination, characteristics of feces, type of feces, methods for maintain the bowel elimination:- enemas, rectal suppositories and colostomies, types of colostomies, colostomy care

Bowel elimination from NEHA BHARTI

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