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controlled. The tolerance levels may be set at much higher RSD in trace analyses where instruments are operated at higher levels of sensitivity and achieving 100% recovery of the analyte may be difficult. Intermediate precision Intermediate precision expresses within-laboratory variation of precision when the analysis is carried out by different analysts, on different days and with different equipment. Obviously a laboratory will want to cut down the possibility for such variations being large and thus it will standardise on particular items of equipment, particular methods of data handling, and make sure that all their analysts are trained to the same standard. Reproducibility Reproducibility expresses the precision between laboratories. Such a trial would be carried out when a method was being transferred from one part of a company to another. The data obtained during such method transfer does not usually form part of the marketing dossier submitted in order to obtain a product licence. For new methodologies a popular method for surveying the performance of a method is to carry out a round robin trial, where many laboratories are asked to carry out qualitative and quantitative analysis of a sample where the composition is only known to those organising the trial. Accuracy As described above, methods may be precise without being accurate. The determination of accuracy in the assay of an unformulated drug substance is relatively straightforward. The simplest method is to compare the substance being analysed with a reference standard analysed by the same procedure. The reference standard is a highly characterised form of the drug which has been subjected to extensive analysis including a test for elemental composition. The methods for determining the accuracy of an assay of a formulated drug are less straightforward. The analytical procedure may be applied to: a drug formulation prepared on a small scale so that the amount of drug in the formulation is more precisely controlled than in a bulk process; a placebo formulation spiked with a known amount of drug or the formulated drug spiked with a known amount of drug. The accuracy of the method may also be assessed by comparison of the method with a previously established reference method such as a pharmacopoeial method. Accuracy should be reported as percent recovery in relation to the known amount of analyte added to the sample or as the difference between the known amount and the amount determined by analysis. In general, at least five determinations, at 80, 100 and 120% of the label claim for drug in the formulated product, should be carried out in order to determine accuracy. Standard operating procedure (SOP) for the assay of paracetamol tablets The terms defined above are perhaps best illustrated by using the example of the simple assay that we mentioned before. The assay in Box 1.4 is laid out in the style of a standard operating procedure (SOP). This particular section of the operating proce]]>
controlled. The tolerance levels may be set at much higher RSD in trace analyses where instruments are operated at higher levels of sensitivity and achieving 100% recovery of the analyte may be difficult. Intermediate precision Intermediate precision expresses within-laboratory variation of precision when the analysis is carried out by different analysts, on different days and with different equipment. Obviously a laboratory will want to cut down the possibility for such variations being large and thus it will standardise on particular items of equipment, particular methods of data handling, and make sure that all their analysts are trained to the same standard. Reproducibility Reproducibility expresses the precision between laboratories. Such a trial would be carried out when a method was being transferred from one part of a company to another. The data obtained during such method transfer does not usually form part of the marketing dossier submitted in order to obtain a product licence. For new methodologies a popular method for surveying the performance of a method is to carry out a round robin trial, where many laboratories are asked to carry out qualitative and quantitative analysis of a sample where the composition is only known to those organising the trial. Accuracy As described above, methods may be precise without being accurate. The determination of accuracy in the assay of an unformulated drug substance is relatively straightforward. The simplest method is to compare the substance being analysed with a reference standard analysed by the same procedure. The reference standard is a highly characterised form of the drug which has been subjected to extensive analysis including a test for elemental composition. The methods for determining the accuracy of an assay of a formulated drug are less straightforward. The analytical procedure may be applied to: a drug formulation prepared on a small scale so that the amount of drug in the formulation is more precisely controlled than in a bulk process; a placebo formulation spiked with a known amount of drug or the formulated drug spiked with a known amount of drug. The accuracy of the method may also be assessed by comparison of the method with a previously established reference method such as a pharmacopoeial method. Accuracy should be reported as percent recovery in relation to the known amount of analyte added to the sample or as the difference between the known amount and the amount determined by analysis. In general, at least five determinations, at 80, 100 and 120% of the label claim for drug in the formulated product, should be carried out in order to determine accuracy. Standard operating procedure (SOP) for the assay of paracetamol tablets The terms defined above are perhaps best illustrated by using the example of the simple assay that we mentioned before. The assay in Box 1.4 is laid out in the style of a standard operating procedure (SOP). This particular section of the operating proce]]> Sun, 05 Jan 2025 18:37:48 GMT /slideshow/physical-and-chemical-properties-of-drug-molecules-1-pdf/274652772 yisihakchalachew@slideshare.net(yisihakchalachew) Physical and Chemical Properties of Drug Molecules (1).pdf yisihakchalachew controlled. The tolerance levels may be set at much higher RSD in trace analyses where instruments are operated at higher levels of sensitivity and achieving 100% recovery of the analyte may be difficult. Intermediate precision Intermediate precision expresses within-laboratory variation of precision when the analysis is carried out by different analysts, on different days and with different equipment. Obviously a laboratory will want to cut down the possibility for such variations being large and thus it will standardise on particular items of equipment, particular methods of data handling, and make sure that all their analysts are trained to the same standard. Reproducibility Reproducibility expresses the precision between laboratories. Such a trial would be carried out when a method was being transferred from one part of a company to another. The data obtained during such method transfer does not usually form part of the marketing dossier submitted in order to obtain a product licence. For new methodologies a popular method for surveying the performance of a method is to carry out a round robin trial, where many laboratories are asked to carry out qualitative and quantitative analysis of a sample where the composition is only known to those organising the trial. Accuracy As described above, methods may be precise without being accurate. The determination of accuracy in the assay of an unformulated drug substance is relatively straightforward. The simplest method is to compare the substance being analysed with a reference standard analysed by the same procedure. The reference standard is a highly characterised form of the drug which has been subjected to extensive analysis including a test for elemental composition. The methods for determining the accuracy of an assay of a formulated drug are less straightforward. The analytical procedure may be applied to: a drug formulation prepared on a small scale so that the amount of drug in the formulation is more precisely controlled than in a bulk process; a placebo formulation spiked with a known amount of drug or the formulated drug spiked with a known amount of drug. The accuracy of the method may also be assessed by comparison of the method with a previously established reference method such as a pharmacopoeial method. Accuracy should be reported as percent recovery in relation to the known amount of analyte added to the sample or as the difference between the known amount and the amount determined by analysis. In general, at least five determinations, at 80, 100 and 120% of the label claim for drug in the formulated product, should be carried out in order to determine accuracy. Standard operating procedure (SOP) for the assay of paracetamol tablets The terms defined above are perhaps best illustrated by using the example of the simple assay that we mentioned before. The assay in Box 1.4 is laid out in the style of a standard operating procedure (SOP). This particular section of the operating proce <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/physicalandchemicalpropertiesofdrugmolecules1-250105183748-94d0104f-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> controlled. The tolerance levels may be set at much higher RSD in trace analyses where instruments are operated at higher levels of sensitivity and achieving 100% recovery of the analyte may be difficult. Intermediate precision Intermediate precision expresses within-laboratory variation of precision when the analysis is carried out by different analysts, on different days and with different equipment. Obviously a laboratory will want to cut down the possibility for such variations being large and thus it will standardise on particular items of equipment, particular methods of data handling, and make sure that all their analysts are trained to the same standard. Reproducibility Reproducibility expresses the precision between laboratories. Such a trial would be carried out when a method was being transferred from one part of a company to another. The data obtained during such method transfer does not usually form part of the marketing dossier submitted in order to obtain a product licence. For new methodologies a popular method for surveying the performance of a method is to carry out a round robin trial, where many laboratories are asked to carry out qualitative and quantitative analysis of a sample where the composition is only known to those organising the trial. Accuracy As described above, methods may be precise without being accurate. The determination of accuracy in the assay of an unformulated drug substance is relatively straightforward. The simplest method is to compare the substance being analysed with a reference standard analysed by the same procedure. The reference standard is a highly characterised form of the drug which has been subjected to extensive analysis including a test for elemental composition. The methods for determining the accuracy of an assay of a formulated drug are less straightforward. The analytical procedure may be applied to: a drug formulation prepared on a small scale so that the amount of drug in the formulation is more precisely controlled than in a bulk process; a placebo formulation spiked with a known amount of drug or the formulated drug spiked with a known amount of drug. The accuracy of the method may also be assessed by comparison of the method with a previously established reference method such as a pharmacopoeial method. Accuracy should be reported as percent recovery in relation to the known amount of analyte added to the sample or as the difference between the known amount and the amount determined by analysis. In general, at least five determinations, at 80, 100 and 120% of the label claim for drug in the formulated product, should be carried out in order to determine accuracy. Standard operating procedure (SOP) for the assay of paracetamol tablets The terms defined above are perhaps best illustrated by using the example of the simple assay that we mentioned before. The assay in Box 1.4 is laid out in the style of a standard operating procedure (SOP). This particular section of the operating proce
Physical and Chemical Properties of Drug Molecules (1).pdf from yisihakchalachew
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Calcium Supplementation Calcium generally maintains or increases BMD slightly, but its effects are less than those of other therapies. There are insufficient data to support using calcium and vitamin D supplementation to reduce fracture incidence. Because the fraction of calcium absorbed decreases with increasing dose, maximum single doses of 600 mg or less of elemental calcium are recommended. Calcium carbonate is the salt of choice because it contains the highest concentration of elemental calcium (40%) and is typically least expensive. It should be ingested with meals to enhance absorption in an acidic environment. Calcium citrate (21% calcium) has acid-independent absorption and need not be taken with meals. It may have fewer GI side effects than calcium carbonate. Tricalcium phosphate contains 38% calcium, but calcium-phosphate complexes could limit overall calcium absorption. It may be useful in patients with hypophos- phatemia that cannot be resolved with increased dietary intake. Constipation is the most common calcium-related adverse reaction; treat with increased water intake, dietary fiber (given separately from calcium), and exercise. Calcium carbonate can sometimes cause flatulence or upset stomach. Calcium causes kidney stones rarely. Calcium can decrease the oral absorption of some drugs including iron, tetracyclines, quinolones, bisphosphonates, and thyroid supplements. Vitamin D Supplementation Vitamin D supplementation using 700800 units per day significantly reduces the incidence of both hip and nonvertebral fractures with small increases in BMD. Supplementation is usually provided with daily nonprescription cholecalciferol (vitamin D3 ) products. Higher-dose prescription of ergocalciferol (vitamin D2 ) regimens given weekly, monthly, or quarterly may be used for replacement and maintenance therapy. The RDAs in Table 3-1 should be achieved through food and supplementation. Current guidelines recommend treating patients with osteoporosis to a 25-hydroxyvi - tamin D concentration of at least 20 ng/mL (mcg/L; 50 nmol/L) or 3050 ng/mL. Because the half-life of vitamin D is about 1 month, recheck the vitamin D concentra- tion after about 3 months of therapy. Medications that can induce vitamin D metabolism include rifampin, phenytoin, barbiturates, valproic acid, and carbamazepine. Vitamin D absorption can be decreased by cholestyramine, colestipol, orlistat, and mineral oil. Vitamin D can enhance the absorption of aluminum; therefore, aluminum-containing products should be avoided to prevent aluminum toxicity. Bisphosphonates Bisphosphonates (Table 3-2) mimic pyrophosphate, an endogenous bone resorption inhibitor. Therapy leads to decreased osteoclast maturation, number, recruitment, bone adhesion, and life span. Incorporation into bone gives bisphosphonates long biologic half-lives of up to 10 years. Bisphosphonates consistently increase BMD and reduce fracture risk, with differenc]]>
Calcium Supplementation Calcium generally maintains or increases BMD slightly, but its effects are less than those of other therapies. There are insufficient data to support using calcium and vitamin D supplementation to reduce fracture incidence. Because the fraction of calcium absorbed decreases with increasing dose, maximum single doses of 600 mg or less of elemental calcium are recommended. Calcium carbonate is the salt of choice because it contains the highest concentration of elemental calcium (40%) and is typically least expensive. It should be ingested with meals to enhance absorption in an acidic environment. Calcium citrate (21% calcium) has acid-independent absorption and need not be taken with meals. It may have fewer GI side effects than calcium carbonate. Tricalcium phosphate contains 38% calcium, but calcium-phosphate complexes could limit overall calcium absorption. It may be useful in patients with hypophos- phatemia that cannot be resolved with increased dietary intake. Constipation is the most common calcium-related adverse reaction; treat with increased water intake, dietary fiber (given separately from calcium), and exercise. Calcium carbonate can sometimes cause flatulence or upset stomach. Calcium causes kidney stones rarely. Calcium can decrease the oral absorption of some drugs including iron, tetracyclines, quinolones, bisphosphonates, and thyroid supplements. Vitamin D Supplementation Vitamin D supplementation using 700800 units per day significantly reduces the incidence of both hip and nonvertebral fractures with small increases in BMD. Supplementation is usually provided with daily nonprescription cholecalciferol (vitamin D3 ) products. Higher-dose prescription of ergocalciferol (vitamin D2 ) regimens given weekly, monthly, or quarterly may be used for replacement and maintenance therapy. The RDAs in Table 3-1 should be achieved through food and supplementation. Current guidelines recommend treating patients with osteoporosis to a 25-hydroxyvi - tamin D concentration of at least 20 ng/mL (mcg/L; 50 nmol/L) or 3050 ng/mL. Because the half-life of vitamin D is about 1 month, recheck the vitamin D concentra- tion after about 3 months of therapy. Medications that can induce vitamin D metabolism include rifampin, phenytoin, barbiturates, valproic acid, and carbamazepine. Vitamin D absorption can be decreased by cholestyramine, colestipol, orlistat, and mineral oil. Vitamin D can enhance the absorption of aluminum; therefore, aluminum-containing products should be avoided to prevent aluminum toxicity. Bisphosphonates Bisphosphonates (Table 3-2) mimic pyrophosphate, an endogenous bone resorption inhibitor. Therapy leads to decreased osteoclast maturation, number, recruitment, bone adhesion, and life span. Incorporation into bone gives bisphosphonates long biologic half-lives of up to 10 years. Bisphosphonates consistently increase BMD and reduce fracture risk, with differenc]]> Thu, 02 Jan 2025 19:40:18 GMT /slideshow/pharmacotherapeutics-i-diagnostic-test-1-pptx/274594377 yisihakchalachew@slideshare.net(yisihakchalachew) Pharmacotherapeutics I Diagnostic test (1).pptx yisihakchalachew Calcium Supplementation Calcium generally maintains or increases BMD slightly, but its effects are less than those of other therapies. There are insufficient data to support using calcium and vitamin D supplementation to reduce fracture incidence. Because the fraction of calcium absorbed decreases with increasing dose, maximum single doses of 600 mg or less of elemental calcium are recommended. Calcium carbonate is the salt of choice because it contains the highest concentration of elemental calcium (40%) and is typically least expensive. It should be ingested with meals to enhance absorption in an acidic environment. Calcium citrate (21% calcium) has acid-independent absorption and need not be taken with meals. It may have fewer GI side effects than calcium carbonate. Tricalcium phosphate contains 38% calcium, but calcium-phosphate complexes could limit overall calcium absorption. It may be useful in patients with hypophos- phatemia that cannot be resolved with increased dietary intake. Constipation is the most common calcium-related adverse reaction; treat with increased water intake, dietary fiber (given separately from calcium), and exercise. Calcium carbonate can sometimes cause flatulence or upset stomach. Calcium causes kidney stones rarely. Calcium can decrease the oral absorption of some drugs including iron, tetracyclines, quinolones, bisphosphonates, and thyroid supplements. Vitamin D Supplementation Vitamin D supplementation using 700800 units per day significantly reduces the incidence of both hip and nonvertebral fractures with small increases in BMD. Supplementation is usually provided with daily nonprescription cholecalciferol (vitamin D3 ) products. Higher-dose prescription of ergocalciferol (vitamin D2 ) regimens given weekly, monthly, or quarterly may be used for replacement and maintenance therapy. The RDAs in Table 3-1 should be achieved through food and supplementation. Current guidelines recommend treating patients with osteoporosis to a 25-hydroxyvi - tamin D concentration of at least 20 ng/mL (mcg/L; 50 nmol/L) or 3050 ng/mL. Because the half-life of vitamin D is about 1 month, recheck the vitamin D concentra- tion after about 3 months of therapy. Medications that can induce vitamin D metabolism include rifampin, phenytoin, barbiturates, valproic acid, and carbamazepine. Vitamin D absorption can be decreased by cholestyramine, colestipol, orlistat, and mineral oil. Vitamin D can enhance the absorption of aluminum; therefore, aluminum-containing products should be avoided to prevent aluminum toxicity. Bisphosphonates Bisphosphonates (Table 3-2) mimic pyrophosphate, an endogenous bone resorption inhibitor. Therapy leads to decreased osteoclast maturation, number, recruitment, bone adhesion, and life span. Incorporation into bone gives bisphosphonates long biologic half-lives of up to 10 years. Bisphosphonates consistently increase BMD and reduce fracture risk, with differenc <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/pharmacotherapeuticsidiagnostictest1-250102194019-ca6fdf98-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Calcium Supplementation Calcium generally maintains or increases BMD slightly, but its effects are less than those of other therapies. There are insufficient data to support using calcium and vitamin D supplementation to reduce fracture incidence. Because the fraction of calcium absorbed decreases with increasing dose, maximum single doses of 600 mg or less of elemental calcium are recommended. Calcium carbonate is the salt of choice because it contains the highest concentration of elemental calcium (40%) and is typically least expensive. It should be ingested with meals to enhance absorption in an acidic environment. Calcium citrate (21% calcium) has acid-independent absorption and need not be taken with meals. It may have fewer GI side effects than calcium carbonate. Tricalcium phosphate contains 38% calcium, but calcium-phosphate complexes could limit overall calcium absorption. It may be useful in patients with hypophos- phatemia that cannot be resolved with increased dietary intake. Constipation is the most common calcium-related adverse reaction; treat with increased water intake, dietary fiber (given separately from calcium), and exercise. Calcium carbonate can sometimes cause flatulence or upset stomach. Calcium causes kidney stones rarely. Calcium can decrease the oral absorption of some drugs including iron, tetracyclines, quinolones, bisphosphonates, and thyroid supplements. Vitamin D Supplementation Vitamin D supplementation using 700800 units per day significantly reduces the incidence of both hip and nonvertebral fractures with small increases in BMD. Supplementation is usually provided with daily nonprescription cholecalciferol (vitamin D3 ) products. Higher-dose prescription of ergocalciferol (vitamin D2 ) regimens given weekly, monthly, or quarterly may be used for replacement and maintenance therapy. The RDAs in Table 3-1 should be achieved through food and supplementation. Current guidelines recommend treating patients with osteoporosis to a 25-hydroxyvi - tamin D concentration of at least 20 ng/mL (mcg/L; 50 nmol/L) or 3050 ng/mL. Because the half-life of vitamin D is about 1 month, recheck the vitamin D concentra- tion after about 3 months of therapy. Medications that can induce vitamin D metabolism include rifampin, phenytoin, barbiturates, valproic acid, and carbamazepine. Vitamin D absorption can be decreased by cholestyramine, colestipol, orlistat, and mineral oil. Vitamin D can enhance the absorption of aluminum; therefore, aluminum-containing products should be avoided to prevent aluminum toxicity. Bisphosphonates Bisphosphonates (Table 3-2) mimic pyrophosphate, an endogenous bone resorption inhibitor. Therapy leads to decreased osteoclast maturation, number, recruitment, bone adhesion, and life span. Incorporation into bone gives bisphosphonates long biologic half-lives of up to 10 years. Bisphosphonates consistently increase BMD and reduce fracture risk, with differenc
Pharmacotherapeutics I Diagnostic test (1).pptx from yisihakchalachew
]]> 7 0 https://cdn.slidesharecdn.com/ss_thumbnails/pharmacotherapeuticsidiagnostictest1-250102194019-ca6fdf98-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 drug therapy in specific patient groups.pptx /slideshow/drug-therapy-in-specific-patient-groups-pptx/274453021 drugtherapyinspecificpatientgroups-241228055241-5053d7ab
Osteoporosis is a bone disorder characterized by low bone density, impaired bone architecture, and compromised bone strength predisposing to fracture. PATHOPHYSIOLOGY Bone loss occurs when resorption exceeds formation, usually from a high bone turnover when the number or depth of bone resorption sites greatly exceeds the ability of osteoblasts to form new bone. Accelerated bone turnover can increase the amount of immature bone that is not adequately mineralized. Men and women begin to lose bone mass starting in the third or fourth decade because of reduced bone formation. Estrogen deficiency during menopause increases osteoclast activity, increasing bone resorption more than formation. Men are at a lower risk for developing osteoporosis and osteoporotic fractures because of larger bone size, greater peak bone mass, increase in bone width with aging, fewer falls, and shorter life expectancy. Male osteoporosis results from aging or secondary causes. Age-related osteoporosis results from hormone, calcium, and vitamin D deficiencies; decreased production or function of cytokines; decreased body water; less exercise; and other factors that result in accelerated bone turnover and reduced osteoblast formation. Drug-induced osteoporosis may result from systemic corticosteroids, excessive thyroid hormone replacement, antiepileptic drugs (eg, phenytoin, phenobarbital), depot medroxyprogesterone acetate, and other agents. CLINICAL PRESENTATION Many patients are unaware that they have osteoporosis and only present after fracture. Fractures can occur after bending, lifting, or falling or independent of any activity. The most common fractures involve vertebrae, proximal femur, and distal radius (wrist or Colles fracture). Vertebral fractures may be asymptomatic or present with moderate to severe back pain that radiates down a leg. The pain usually subsides after 24 weeks, but residual back pain may persist. Multiple vertebral fractures decrease height and sometimes curve the spine (kyphosis or lordosis). Patients with a nonvertebral fracture frequently present with severe pain, swelling, and reduced function and mobility at the fracture site. DIAGNOSIS The World Health Organization (WHO) Fracture Risk Assessment Tool (FRAX tool) uses the following risk factors to predict the percent probability of fracture in the next 10 years: age, race/ethnicity, sex, previous fragility fracture, parent history of hip fracture, body mass index, glucocorticoid use, current smoking, alcohol (3 drinks per day), rheumatoid arthritis, and select secondary causes with femoral neck or total hip bone mineral density (BMD) data optional. The Garvan calculator uses four risk factors (age, sex, low-trauma fracture, and falls) with the option to also use BMD. It calculates 5- and 10-year risk estimates of any osteoporotic/fragility fracture and hip fracture. This tool corrects some disadvantages of FRAX because it includes falls and the numb]]>
Osteoporosis is a bone disorder characterized by low bone density, impaired bone architecture, and compromised bone strength predisposing to fracture. PATHOPHYSIOLOGY Bone loss occurs when resorption exceeds formation, usually from a high bone turnover when the number or depth of bone resorption sites greatly exceeds the ability of osteoblasts to form new bone. Accelerated bone turnover can increase the amount of immature bone that is not adequately mineralized. Men and women begin to lose bone mass starting in the third or fourth decade because of reduced bone formation. Estrogen deficiency during menopause increases osteoclast activity, increasing bone resorption more than formation. Men are at a lower risk for developing osteoporosis and osteoporotic fractures because of larger bone size, greater peak bone mass, increase in bone width with aging, fewer falls, and shorter life expectancy. Male osteoporosis results from aging or secondary causes. Age-related osteoporosis results from hormone, calcium, and vitamin D deficiencies; decreased production or function of cytokines; decreased body water; less exercise; and other factors that result in accelerated bone turnover and reduced osteoblast formation. Drug-induced osteoporosis may result from systemic corticosteroids, excessive thyroid hormone replacement, antiepileptic drugs (eg, phenytoin, phenobarbital), depot medroxyprogesterone acetate, and other agents. CLINICAL PRESENTATION Many patients are unaware that they have osteoporosis and only present after fracture. Fractures can occur after bending, lifting, or falling or independent of any activity. The most common fractures involve vertebrae, proximal femur, and distal radius (wrist or Colles fracture). Vertebral fractures may be asymptomatic or present with moderate to severe back pain that radiates down a leg. The pain usually subsides after 24 weeks, but residual back pain may persist. Multiple vertebral fractures decrease height and sometimes curve the spine (kyphosis or lordosis). Patients with a nonvertebral fracture frequently present with severe pain, swelling, and reduced function and mobility at the fracture site. DIAGNOSIS The World Health Organization (WHO) Fracture Risk Assessment Tool (FRAX tool) uses the following risk factors to predict the percent probability of fracture in the next 10 years: age, race/ethnicity, sex, previous fragility fracture, parent history of hip fracture, body mass index, glucocorticoid use, current smoking, alcohol (3 drinks per day), rheumatoid arthritis, and select secondary causes with femoral neck or total hip bone mineral density (BMD) data optional. The Garvan calculator uses four risk factors (age, sex, low-trauma fracture, and falls) with the option to also use BMD. It calculates 5- and 10-year risk estimates of any osteoporotic/fragility fracture and hip fracture. This tool corrects some disadvantages of FRAX because it includes falls and the numb]]> Sat, 28 Dec 2024 05:52:41 GMT /slideshow/drug-therapy-in-specific-patient-groups-pptx/274453021 yisihakchalachew@slideshare.net(yisihakchalachew) drug therapy in specific patient groups.pptx yisihakchalachew Osteoporosis is a bone disorder characterized by low bone density, impaired bone architecture, and compromised bone strength predisposing to fracture. PATHOPHYSIOLOGY Bone loss occurs when resorption exceeds formation, usually from a high bone turnover when the number or depth of bone resorption sites greatly exceeds the ability of osteoblasts to form new bone. Accelerated bone turnover can increase the amount of immature bone that is not adequately mineralized. Men and women begin to lose bone mass starting in the third or fourth decade because of reduced bone formation. Estrogen deficiency during menopause increases osteoclast activity, increasing bone resorption more than formation. Men are at a lower risk for developing osteoporosis and osteoporotic fractures because of larger bone size, greater peak bone mass, increase in bone width with aging, fewer falls, and shorter life expectancy. Male osteoporosis results from aging or secondary causes. Age-related osteoporosis results from hormone, calcium, and vitamin D deficiencies; decreased production or function of cytokines; decreased body water; less exercise; and other factors that result in accelerated bone turnover and reduced osteoblast formation. Drug-induced osteoporosis may result from systemic corticosteroids, excessive thyroid hormone replacement, antiepileptic drugs (eg, phenytoin, phenobarbital), depot medroxyprogesterone acetate, and other agents. CLINICAL PRESENTATION Many patients are unaware that they have osteoporosis and only present after fracture. Fractures can occur after bending, lifting, or falling or independent of any activity. The most common fractures involve vertebrae, proximal femur, and distal radius (wrist or Colles fracture). Vertebral fractures may be asymptomatic or present with moderate to severe back pain that radiates down a leg. The pain usually subsides after 24 weeks, but residual back pain may persist. Multiple vertebral fractures decrease height and sometimes curve the spine (kyphosis or lordosis). Patients with a nonvertebral fracture frequently present with severe pain, swelling, and reduced function and mobility at the fracture site. DIAGNOSIS The World Health Organization (WHO) Fracture Risk Assessment Tool (FRAX tool) uses the following risk factors to predict the percent probability of fracture in the next 10 years: age, race/ethnicity, sex, previous fragility fracture, parent history of hip fracture, body mass index, glucocorticoid use, current smoking, alcohol (3 drinks per day), rheumatoid arthritis, and select secondary causes with femoral neck or total hip bone mineral density (BMD) data optional. The Garvan calculator uses four risk factors (age, sex, low-trauma fracture, and falls) with the option to also use BMD. It calculates 5- and 10-year risk estimates of any osteoporotic/fragility fracture and hip fracture. This tool corrects some disadvantages of FRAX because it includes falls and the numb <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/drugtherapyinspecificpatientgroups-241228055241-5053d7ab-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Osteoporosis is a bone disorder characterized by low bone density, impaired bone architecture, and compromised bone strength predisposing to fracture. PATHOPHYSIOLOGY Bone loss occurs when resorption exceeds formation, usually from a high bone turnover when the number or depth of bone resorption sites greatly exceeds the ability of osteoblasts to form new bone. Accelerated bone turnover can increase the amount of immature bone that is not adequately mineralized. Men and women begin to lose bone mass starting in the third or fourth decade because of reduced bone formation. Estrogen deficiency during menopause increases osteoclast activity, increasing bone resorption more than formation. Men are at a lower risk for developing osteoporosis and osteoporotic fractures because of larger bone size, greater peak bone mass, increase in bone width with aging, fewer falls, and shorter life expectancy. Male osteoporosis results from aging or secondary causes. Age-related osteoporosis results from hormone, calcium, and vitamin D deficiencies; decreased production or function of cytokines; decreased body water; less exercise; and other factors that result in accelerated bone turnover and reduced osteoblast formation. Drug-induced osteoporosis may result from systemic corticosteroids, excessive thyroid hormone replacement, antiepileptic drugs (eg, phenytoin, phenobarbital), depot medroxyprogesterone acetate, and other agents. CLINICAL PRESENTATION Many patients are unaware that they have osteoporosis and only present after fracture. Fractures can occur after bending, lifting, or falling or independent of any activity. The most common fractures involve vertebrae, proximal femur, and distal radius (wrist or Colles fracture). Vertebral fractures may be asymptomatic or present with moderate to severe back pain that radiates down a leg. The pain usually subsides after 24 weeks, but residual back pain may persist. Multiple vertebral fractures decrease height and sometimes curve the spine (kyphosis or lordosis). Patients with a nonvertebral fracture frequently present with severe pain, swelling, and reduced function and mobility at the fracture site. DIAGNOSIS The World Health Organization (WHO) Fracture Risk Assessment Tool (FRAX tool) uses the following risk factors to predict the percent probability of fracture in the next 10 years: age, race/ethnicity, sex, previous fragility fracture, parent history of hip fracture, body mass index, glucocorticoid use, current smoking, alcohol (3 drinks per day), rheumatoid arthritis, and select secondary causes with femoral neck or total hip bone mineral density (BMD) data optional. The Garvan calculator uses four risk factors (age, sex, low-trauma fracture, and falls) with the option to also use BMD. It calculates 5- and 10-year risk estimates of any osteoporotic/fragility fracture and hip fracture. This tool corrects some disadvantages of FRAX because it includes falls and the numb
drug therapy in specific patient groups.pptx from yisihakchalachew
]]> 7 0 https://cdn.slidesharecdn.com/ss_thumbnails/drugtherapyinspecificpatientgroups-241228055241-5053d7ab-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Chapter 1 Introduction to Pharmaceutical Analysis - 1.1-1.3.pdf /slideshow/chapter-1-introduction-to-pharmaceutical-analysis-1-1-1-3-pdf/273093425 chapter1introductiontopharmaceuticalanalysis-1-241107101218-bd544553
Analysis ]]>
Analysis ]]> Thu, 07 Nov 2024 10:12:18 GMT /slideshow/chapter-1-introduction-to-pharmaceutical-analysis-1-1-1-3-pdf/273093425 yisihakchalachew@slideshare.net(yisihakchalachew) Chapter 1 Introduction to Pharmaceutical Analysis - 1.1-1.3.pdf yisihakchalachew Analysis <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/chapter1introductiontopharmaceuticalanalysis-1-241107101218-bd544553-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Analysis
Chapter 1 Introduction to Pharmaceutical Analysis - 1.1-1.3.pdf from yisihakchalachew
]]> 39 0 https://cdn.slidesharecdn.com/ss_thumbnails/chapter1introductiontopharmaceuticalanalysis-1-241107101218-bd544553-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 chapt -1-Basic.pptx what is analysis do us? /slideshow/chapt-1-basic-pptx-what-is-analysis-do-us/272129848 chapt-1-basic-241001154050-3b80958b
particular rhythmic abnormalities. These vital information(s) could help a physician in the correct diagnosis vis-a-vis right choice of medicaments. In short, any disturbance to the conductance of the electrical impulses in a perfect sequential and orderly manner ultimately forms the basis of an arrythmia. Fig. 11.1(b) shows the schematic diagram of the cardiac electrical activity. It is, however, pertinent to state here that the electrophysiology of the heart is overwhelmingly governed by the prevailing transmembrane resting potential. Hence, the existing potential inside a Purkinje fibre cell at rest, with regard to the outside, is found to be almost equal to 90 mV. Interestingly, the potential difference is maintained by an active transport system (i.e., a pumping device) which essentially sustains a higher extracellular Na+ concentration in comparison to the intracellular K+ level. It has been observed that upon excitation, the prevailing voltage quite rapidly gets reversed to a positive voltage, most probably spiking around + 30 mV. This situation gives rise to an extremely rapid spontaneous and simultaneous movement of Na+ into the cell, just like a gate had all-of-a-sudden opened a channel (usually known as a gating mechanism). Therefore, the recovery from excitation status gives rise to the gradual restoration of the ensuing resting potential in various phases from 1 through 4. Phase-4 : the resting potential is followed by the rapid depolarization and its reversal. Phase-0 : gets started with a series of three repolarization phases, namely : Phase-1, 2 and 3. Importantly, depending on the areas measured*, the distinct separation of phases are not quite feasible ; and the prevailing voltages invariably alter amongst the major cell types of the heart, viz., Purkinje fibres**, AV-node, atrial cells, and the SA-node. There are two types of influx, namely : (a) rapid influx ; (b) slow influx. A. Rapid Influx. The rapid influx of Na+ through the channels (or gates) during phase 0 results in the cell a rapid depolarization, which in turn closes the gate behind them to enable further influx to occur. B. Slow Influx. The slow influx of Ca2+ gets triggered off to equalize (balance) the K+ loss besides maintaining a proper relative voltage plateau as shown in Fig. 11.1(b). In fact, as the Ca2+ entry slows down, the membrane potential becomes low very swiftly to the predepolarization levels (i.e., phase 4). Thus, in the heart muscle the elcetrical activity is coupled to a mechanical activity by Ca2+ as the potential trigger. An effective refractory period (ERP) [See Fig. 11.1(b)]. Comprising of several hundred milliseconds follows during which no further stimulus may propagate an impulse effectively. However, the impulse initiation happens to be an inherent characteristic features of the cardiac fibres which evidently enables them to modulate action potentials almost spontaneously, and hence, the corresponding impulses. Anti-arrhythmic a]]>
particular rhythmic abnormalities. These vital information(s) could help a physician in the correct diagnosis vis-a-vis right choice of medicaments. In short, any disturbance to the conductance of the electrical impulses in a perfect sequential and orderly manner ultimately forms the basis of an arrythmia. Fig. 11.1(b) shows the schematic diagram of the cardiac electrical activity. It is, however, pertinent to state here that the electrophysiology of the heart is overwhelmingly governed by the prevailing transmembrane resting potential. Hence, the existing potential inside a Purkinje fibre cell at rest, with regard to the outside, is found to be almost equal to 90 mV. Interestingly, the potential difference is maintained by an active transport system (i.e., a pumping device) which essentially sustains a higher extracellular Na+ concentration in comparison to the intracellular K+ level. It has been observed that upon excitation, the prevailing voltage quite rapidly gets reversed to a positive voltage, most probably spiking around + 30 mV. This situation gives rise to an extremely rapid spontaneous and simultaneous movement of Na+ into the cell, just like a gate had all-of-a-sudden opened a channel (usually known as a gating mechanism). Therefore, the recovery from excitation status gives rise to the gradual restoration of the ensuing resting potential in various phases from 1 through 4. Phase-4 : the resting potential is followed by the rapid depolarization and its reversal. Phase-0 : gets started with a series of three repolarization phases, namely : Phase-1, 2 and 3. Importantly, depending on the areas measured*, the distinct separation of phases are not quite feasible ; and the prevailing voltages invariably alter amongst the major cell types of the heart, viz., Purkinje fibres**, AV-node, atrial cells, and the SA-node. There are two types of influx, namely : (a) rapid influx ; (b) slow influx. A. Rapid Influx. The rapid influx of Na+ through the channels (or gates) during phase 0 results in the cell a rapid depolarization, which in turn closes the gate behind them to enable further influx to occur. B. Slow Influx. The slow influx of Ca2+ gets triggered off to equalize (balance) the K+ loss besides maintaining a proper relative voltage plateau as shown in Fig. 11.1(b). In fact, as the Ca2+ entry slows down, the membrane potential becomes low very swiftly to the predepolarization levels (i.e., phase 4). Thus, in the heart muscle the elcetrical activity is coupled to a mechanical activity by Ca2+ as the potential trigger. An effective refractory period (ERP) [See Fig. 11.1(b)]. Comprising of several hundred milliseconds follows during which no further stimulus may propagate an impulse effectively. However, the impulse initiation happens to be an inherent characteristic features of the cardiac fibres which evidently enables them to modulate action potentials almost spontaneously, and hence, the corresponding impulses. Anti-arrhythmic a]]> Tue, 01 Oct 2024 15:40:50 GMT /slideshow/chapt-1-basic-pptx-what-is-analysis-do-us/272129848 yisihakchalachew@slideshare.net(yisihakchalachew) chapt -1-Basic.pptx what is analysis do us? yisihakchalachew particular rhythmic abnormalities. These vital information(s) could help a physician in the correct diagnosis vis-a-vis right choice of medicaments. In short, any disturbance to the conductance of the electrical impulses in a perfect sequential and orderly manner ultimately forms the basis of an arrythmia. Fig. 11.1(b) shows the schematic diagram of the cardiac electrical activity. It is, however, pertinent to state here that the electrophysiology of the heart is overwhelmingly governed by the prevailing transmembrane resting potential. Hence, the existing potential inside a Purkinje fibre cell at rest, with regard to the outside, is found to be almost equal to 90 mV. Interestingly, the potential difference is maintained by an active transport system (i.e., a pumping device) which essentially sustains a higher extracellular Na+ concentration in comparison to the intracellular K+ level. It has been observed that upon excitation, the prevailing voltage quite rapidly gets reversed to a positive voltage, most probably spiking around + 30 mV. This situation gives rise to an extremely rapid spontaneous and simultaneous movement of Na+ into the cell, just like a gate had all-of-a-sudden opened a channel (usually known as a gating mechanism). Therefore, the recovery from excitation status gives rise to the gradual restoration of the ensuing resting potential in various phases from 1 through 4. Phase-4 : the resting potential is followed by the rapid depolarization and its reversal. Phase-0 : gets started with a series of three repolarization phases, namely : Phase-1, 2 and 3. Importantly, depending on the areas measured*, the distinct separation of phases are not quite feasible ; and the prevailing voltages invariably alter amongst the major cell types of the heart, viz., Purkinje fibres**, AV-node, atrial cells, and the SA-node. There are two types of influx, namely : (a) rapid influx ; (b) slow influx. A. Rapid Influx. The rapid influx of Na+ through the channels (or gates) during phase 0 results in the cell a rapid depolarization, which in turn closes the gate behind them to enable further influx to occur. B. Slow Influx. The slow influx of Ca2+ gets triggered off to equalize (balance) the K+ loss besides maintaining a proper relative voltage plateau as shown in Fig. 11.1(b). In fact, as the Ca2+ entry slows down, the membrane potential becomes low very swiftly to the predepolarization levels (i.e., phase 4). Thus, in the heart muscle the elcetrical activity is coupled to a mechanical activity by Ca2+ as the potential trigger. An effective refractory period (ERP) [See Fig. 11.1(b)]. Comprising of several hundred milliseconds follows during which no further stimulus may propagate an impulse effectively. However, the impulse initiation happens to be an inherent characteristic features of the cardiac fibres which evidently enables them to modulate action potentials almost spontaneously, and hence, the corresponding impulses. Anti-arrhythmic a <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/chapt-1-basic-241001154050-3b80958b-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> particular rhythmic abnormalities. These vital information(s) could help a physician in the correct diagnosis vis-a-vis right choice of medicaments. In short, any disturbance to the conductance of the electrical impulses in a perfect sequential and orderly manner ultimately forms the basis of an arrythmia. Fig. 11.1(b) shows the schematic diagram of the cardiac electrical activity. It is, however, pertinent to state here that the electrophysiology of the heart is overwhelmingly governed by the prevailing transmembrane resting potential. Hence, the existing potential inside a Purkinje fibre cell at rest, with regard to the outside, is found to be almost equal to 90 mV. Interestingly, the potential difference is maintained by an active transport system (i.e., a pumping device) which essentially sustains a higher extracellular Na+ concentration in comparison to the intracellular K+ level. It has been observed that upon excitation, the prevailing voltage quite rapidly gets reversed to a positive voltage, most probably spiking around + 30 mV. This situation gives rise to an extremely rapid spontaneous and simultaneous movement of Na+ into the cell, just like a gate had all-of-a-sudden opened a channel (usually known as a gating mechanism). Therefore, the recovery from excitation status gives rise to the gradual restoration of the ensuing resting potential in various phases from 1 through 4. Phase-4 : the resting potential is followed by the rapid depolarization and its reversal. Phase-0 : gets started with a series of three repolarization phases, namely : Phase-1, 2 and 3. Importantly, depending on the areas measured*, the distinct separation of phases are not quite feasible ; and the prevailing voltages invariably alter amongst the major cell types of the heart, viz., Purkinje fibres**, AV-node, atrial cells, and the SA-node. There are two types of influx, namely : (a) rapid influx ; (b) slow influx. A. Rapid Influx. The rapid influx of Na+ through the channels (or gates) during phase 0 results in the cell a rapid depolarization, which in turn closes the gate behind them to enable further influx to occur. B. Slow Influx. The slow influx of Ca2+ gets triggered off to equalize (balance) the K+ loss besides maintaining a proper relative voltage plateau as shown in Fig. 11.1(b). In fact, as the Ca2+ entry slows down, the membrane potential becomes low very swiftly to the predepolarization levels (i.e., phase 4). Thus, in the heart muscle the elcetrical activity is coupled to a mechanical activity by Ca2+ as the potential trigger. An effective refractory period (ERP) [See Fig. 11.1(b)]. Comprising of several hundred milliseconds follows during which no further stimulus may propagate an impulse effectively. However, the impulse initiation happens to be an inherent characteristic features of the cardiac fibres which evidently enables them to modulate action potentials almost spontaneously, and hence, the corresponding impulses. Anti-arrhythmic a
chapt -1-Basic.pptx what is analysis do us? from yisihakchalachew
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5 THE MEVALONATE AND METHYLERYTHRITOL PHOSPHATE PATHWAYS: TERPENOIDS AND STEROIDS Terpenoids form a large and structurally diverse family of natural products derived from C5 isoprene units (Figure 5.1) joined in a head-to-tail fashion. Typical structures contain carbon skeletons represented by (C5)n, and are classified as hemiterpenes (C5), monoterpenes (C10), sesquiterpenes (C15), diterpenes (C20), sesterterpenes (C25), triterpenes (C30), and tetraterpenes (C40) (Figure 5.2). Higher polymers are encountered in materials such as rubber. Isoprene itself (Figure 5.1) was known as a decomposition product from various natural cyclic hydrocarbons, and had been suggested as the fundamental building block for these compounds, also referred to as isoprenoids. Isoprene is produced naturally but is not involved in the formation of these compounds; the biochemically active isoprene units were subsequently identified as the diphosphate (pyrophosphate) esters dimethylallyl diphosphate (DMAPP) and isopentenyl diphosphate (IPP) (Figure 5.2). Relatively few of the natural terpenoids conform exactly to the simple concept of a linear head-to-tail combination of isoprene units as seen with geraniol (C10), farnesol (C15), and geranylgeraniol (C20) (Figure 5.3). Squalene (C30) and phytoene (C40), although formed entirely of isoprene units, display a tail-to-tail linkage at the centre of the molecules. Most terpenoids are modified further by cyclization reactions, though the head-to-tail arrangement of the units can usually still be recognized, e.g. menthol, bisabolene, and taxadiene. The linear arrangement of isoprene units can be much more difficult to appreciate in many other structures when rearrangement reactions have taken place, e.g. steroids, where, in addition, several carbon atoms have been lost. Nevertheless, such compounds are formed by way of regular terpenoid precursors. Terpenoids comprise the largest group of natural products, with over 35 000 known members. Many other natural products contain terpenoid elements in their molecules, in combination with carbon skeletons derived from other sources, such as the acetate and shikimate pathways. Many alkaloids, phenolics, and vitamins discussed in other chapters are examples of this. A particularly common terpenoid fragment in such cases is a single C5 unit, usually a dimethylallyl substituent, and molecules containing these isolated isoprene units are sometimes referred to as meroterpenoids. Some examples include furocoumarins (see page 162), rotenoids (see page 175), and ergot alkaloids (see page 387). One should also note that the term prenyl is in general use to indicate the dimethylallyl substituent. Even macromolecules like proteins can be modified by attaching terpenoid chains. Cysteine residues in proteins are alkylated with farnesyl (C15) or geranylgeranyl (C20) groups, thereby increasing the lipophilicity of the protein and its ability to associate with mem]]>
5 THE MEVALONATE AND METHYLERYTHRITOL PHOSPHATE PATHWAYS: TERPENOIDS AND STEROIDS Terpenoids form a large and structurally diverse family of natural products derived from C5 isoprene units (Figure 5.1) joined in a head-to-tail fashion. Typical structures contain carbon skeletons represented by (C5)n, and are classified as hemiterpenes (C5), monoterpenes (C10), sesquiterpenes (C15), diterpenes (C20), sesterterpenes (C25), triterpenes (C30), and tetraterpenes (C40) (Figure 5.2). Higher polymers are encountered in materials such as rubber. Isoprene itself (Figure 5.1) was known as a decomposition product from various natural cyclic hydrocarbons, and had been suggested as the fundamental building block for these compounds, also referred to as isoprenoids. Isoprene is produced naturally but is not involved in the formation of these compounds; the biochemically active isoprene units were subsequently identified as the diphosphate (pyrophosphate) esters dimethylallyl diphosphate (DMAPP) and isopentenyl diphosphate (IPP) (Figure 5.2). Relatively few of the natural terpenoids conform exactly to the simple concept of a linear head-to-tail combination of isoprene units as seen with geraniol (C10), farnesol (C15), and geranylgeraniol (C20) (Figure 5.3). Squalene (C30) and phytoene (C40), although formed entirely of isoprene units, display a tail-to-tail linkage at the centre of the molecules. Most terpenoids are modified further by cyclization reactions, though the head-to-tail arrangement of the units can usually still be recognized, e.g. menthol, bisabolene, and taxadiene. The linear arrangement of isoprene units can be much more difficult to appreciate in many other structures when rearrangement reactions have taken place, e.g. steroids, where, in addition, several carbon atoms have been lost. Nevertheless, such compounds are formed by way of regular terpenoid precursors. Terpenoids comprise the largest group of natural products, with over 35 000 known members. Many other natural products contain terpenoid elements in their molecules, in combination with carbon skeletons derived from other sources, such as the acetate and shikimate pathways. Many alkaloids, phenolics, and vitamins discussed in other chapters are examples of this. A particularly common terpenoid fragment in such cases is a single C5 unit, usually a dimethylallyl substituent, and molecules containing these isolated isoprene units are sometimes referred to as meroterpenoids. Some examples include furocoumarins (see page 162), rotenoids (see page 175), and ergot alkaloids (see page 387). One should also note that the term prenyl is in general use to indicate the dimethylallyl substituent. Even macromolecules like proteins can be modified by attaching terpenoid chains. Cysteine residues in proteins are alkylated with farnesyl (C15) or geranylgeranyl (C20) groups, thereby increasing the lipophilicity of the protein and its ability to associate with mem]]> Sun, 07 Jul 2024 19:23:39 GMT /slideshow/alkaloids-1-pdf-for-pharmacognosy-student/270109093 yisihakchalachew@slideshare.net(yisihakchalachew) alkaloids (1).pdf for pharmacognosy student yisihakchalachew 5 THE MEVALONATE AND METHYLERYTHRITOL PHOSPHATE PATHWAYS: TERPENOIDS AND STEROIDS Terpenoids form a large and structurally diverse family of natural products derived from C5 isoprene units (Figure 5.1) joined in a head-to-tail fashion. Typical structures contain carbon skeletons represented by (C5)n, and are classified as hemiterpenes (C5), monoterpenes (C10), sesquiterpenes (C15), diterpenes (C20), sesterterpenes (C25), triterpenes (C30), and tetraterpenes (C40) (Figure 5.2). Higher polymers are encountered in materials such as rubber. Isoprene itself (Figure 5.1) was known as a decomposition product from various natural cyclic hydrocarbons, and had been suggested as the fundamental building block for these compounds, also referred to as isoprenoids. Isoprene is produced naturally but is not involved in the formation of these compounds; the biochemically active isoprene units were subsequently identified as the diphosphate (pyrophosphate) esters dimethylallyl diphosphate (DMAPP) and isopentenyl diphosphate (IPP) (Figure 5.2). Relatively few of the natural terpenoids conform exactly to the simple concept of a linear head-to-tail combination of isoprene units as seen with geraniol (C10), farnesol (C15), and geranylgeraniol (C20) (Figure 5.3). Squalene (C30) and phytoene (C40), although formed entirely of isoprene units, display a tail-to-tail linkage at the centre of the molecules. Most terpenoids are modified further by cyclization reactions, though the head-to-tail arrangement of the units can usually still be recognized, e.g. menthol, bisabolene, and taxadiene. The linear arrangement of isoprene units can be much more difficult to appreciate in many other structures when rearrangement reactions have taken place, e.g. steroids, where, in addition, several carbon atoms have been lost. Nevertheless, such compounds are formed by way of regular terpenoid precursors. Terpenoids comprise the largest group of natural products, with over 35 000 known members. Many other natural products contain terpenoid elements in their molecules, in combination with carbon skeletons derived from other sources, such as the acetate and shikimate pathways. Many alkaloids, phenolics, and vitamins discussed in other chapters are examples of this. A particularly common terpenoid fragment in such cases is a single C5 unit, usually a dimethylallyl substituent, and molecules containing these isolated isoprene units are sometimes referred to as meroterpenoids. Some examples include furocoumarins (see page 162), rotenoids (see page 175), and ergot alkaloids (see page 387). One should also note that the term prenyl is in general use to indicate the dimethylallyl substituent. Even macromolecules like proteins can be modified by attaching terpenoid chains. Cysteine residues in proteins are alkylated with farnesyl (C15) or geranylgeranyl (C20) groups, thereby increasing the lipophilicity of the protein and its ability to associate with mem <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/alkaloids1-240707192339-2e2d5851-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> 5 THE MEVALONATE AND METHYLERYTHRITOL PHOSPHATE PATHWAYS: TERPENOIDS AND STEROIDS Terpenoids form a large and structurally diverse family of natural products derived from C5 isoprene units (Figure 5.1) joined in a head-to-tail fashion. Typical structures contain carbon skeletons represented by (C5)n, and are classified as hemiterpenes (C5), monoterpenes (C10), sesquiterpenes (C15), diterpenes (C20), sesterterpenes (C25), triterpenes (C30), and tetraterpenes (C40) (Figure 5.2). Higher polymers are encountered in materials such as rubber. Isoprene itself (Figure 5.1) was known as a decomposition product from various natural cyclic hydrocarbons, and had been suggested as the fundamental building block for these compounds, also referred to as isoprenoids. Isoprene is produced naturally but is not involved in the formation of these compounds; the biochemically active isoprene units were subsequently identified as the diphosphate (pyrophosphate) esters dimethylallyl diphosphate (DMAPP) and isopentenyl diphosphate (IPP) (Figure 5.2). Relatively few of the natural terpenoids conform exactly to the simple concept of a linear head-to-tail combination of isoprene units as seen with geraniol (C10), farnesol (C15), and geranylgeraniol (C20) (Figure 5.3). Squalene (C30) and phytoene (C40), although formed entirely of isoprene units, display a tail-to-tail linkage at the centre of the molecules. Most terpenoids are modified further by cyclization reactions, though the head-to-tail arrangement of the units can usually still be recognized, e.g. menthol, bisabolene, and taxadiene. The linear arrangement of isoprene units can be much more difficult to appreciate in many other structures when rearrangement reactions have taken place, e.g. steroids, where, in addition, several carbon atoms have been lost. Nevertheless, such compounds are formed by way of regular terpenoid precursors. Terpenoids comprise the largest group of natural products, with over 35 000 known members. Many other natural products contain terpenoid elements in their molecules, in combination with carbon skeletons derived from other sources, such as the acetate and shikimate pathways. Many alkaloids, phenolics, and vitamins discussed in other chapters are examples of this. A particularly common terpenoid fragment in such cases is a single C5 unit, usually a dimethylallyl substituent, and molecules containing these isolated isoprene units are sometimes referred to as meroterpenoids. Some examples include furocoumarins (see page 162), rotenoids (see page 175), and ergot alkaloids (see page 387). One should also note that the term prenyl is in general use to indicate the dimethylallyl substituent. Even macromolecules like proteins can be modified by attaching terpenoid chains. Cysteine residues in proteins are alkylated with farnesyl (C15) or geranylgeranyl (C20) groups, thereby increasing the lipophilicity of the protein and its ability to associate with mem
alkaloids (1).pdf for pharmacognosy student from yisihakchalachew
]]> 82 0 https://cdn.slidesharecdn.com/ss_thumbnails/alkaloids1-240707192339-2e2d5851-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 4. Autacoids and therapy of Inflammation(0).pdf /slideshow/4-autacoids-and-therapy-of-inflammation-0-pdf/270048104 4-240703194049-29551338
signifi cantly. Th is implies that these receptors have evolved over millions of years from an ancient common ancestral protein. Comparing the amino acid sequences of the receptors allows us to construct an evolutionary tree and to group the receptors of this superfamily into various sub-families, which are defi ned as class A (rhodopsin-like receptors), class B (secretin-like receptors), and class C (metabotropic glutamate-like and pheromone receptors). Th e most important of these, as far as medicinal chemistry is concerned, is the rhodopsin-like familyso called because the fi rst receptor of this family to be studied in detail was the rhodopsin receptor itself, a receptor involved in the visual process. A study of the evolutionary tree of rhodopsin-like receptors throws up some interesting observations ( Fig. 4.16 ). First of all, the evolutionary tree illustrates the similarity between diff erent kinds of receptors based on their relative positions on the tree. Th us, the muscarinic, 留-adrenergic, 硫-adrenergic, histamine, and dopamine receptors have evolved from a common branch of the evolutionary tree and have greater similarity to each other than to any receptors arising from an earlier evolutionary branch (e.g. the angiotensin receptor ). Such receptor similarity may prove a problem in medicinal chemistry. Although the receptors are distinguished by diff erent neurotransmitters or hormones in the body, a drug may not manage to make that distinction. Th erefore, it is important to ensure that any new drug aimed at one kind of receptor (e.g. the dopamine receptor) does not interact with a similar kind of receptor (e.g. the muscarinic receptor). Receptors have further evolved to give receptor types and subtypes which recognize the same chemical messenger, but are structurally diff erent. For example, there are two types of adrenergic receptor (留 and 硫), each of which has various subtypes (留1 , 留2A , 留2B , 留2C , 硫1 , 硫2 , 硫3 ). Th ere are two types of cholinergic receptornicotinic (an ion channel receptor) and muscarinic (a 7-TM receptor). Five subtypes of the muscarinic cholinergic receptor have been identifi ed. Th e existence of receptor subtypes allows the possibility of designing drugs that are selective for one receptor subtype over another. Th is is important, because one receptor subtype may be prevalent in one part of the body (e.g. the gut), while a diff erent receptor subtype is prevalent in another part (e.g. the heart). Th erefore, a drug that is designed to interact selectively with the receptor subtype in the gut is less likely to have side eff ects on the heart. Even if the diff erent receptor subtypes are present in the same part of the body, it is still important to make drugs as selective as possible because diff erent receptor subtypes frequently activate diff erent signalling systems, leading to diff erent biological results. A closer study of the evolutionary tree reveals ]]>
signifi cantly. Th is implies that these receptors have evolved over millions of years from an ancient common ancestral protein. Comparing the amino acid sequences of the receptors allows us to construct an evolutionary tree and to group the receptors of this superfamily into various sub-families, which are defi ned as class A (rhodopsin-like receptors), class B (secretin-like receptors), and class C (metabotropic glutamate-like and pheromone receptors). Th e most important of these, as far as medicinal chemistry is concerned, is the rhodopsin-like familyso called because the fi rst receptor of this family to be studied in detail was the rhodopsin receptor itself, a receptor involved in the visual process. A study of the evolutionary tree of rhodopsin-like receptors throws up some interesting observations ( Fig. 4.16 ). First of all, the evolutionary tree illustrates the similarity between diff erent kinds of receptors based on their relative positions on the tree. Th us, the muscarinic, 留-adrenergic, 硫-adrenergic, histamine, and dopamine receptors have evolved from a common branch of the evolutionary tree and have greater similarity to each other than to any receptors arising from an earlier evolutionary branch (e.g. the angiotensin receptor ). Such receptor similarity may prove a problem in medicinal chemistry. Although the receptors are distinguished by diff erent neurotransmitters or hormones in the body, a drug may not manage to make that distinction. Th erefore, it is important to ensure that any new drug aimed at one kind of receptor (e.g. the dopamine receptor) does not interact with a similar kind of receptor (e.g. the muscarinic receptor). Receptors have further evolved to give receptor types and subtypes which recognize the same chemical messenger, but are structurally diff erent. For example, there are two types of adrenergic receptor (留 and 硫), each of which has various subtypes (留1 , 留2A , 留2B , 留2C , 硫1 , 硫2 , 硫3 ). Th ere are two types of cholinergic receptornicotinic (an ion channel receptor) and muscarinic (a 7-TM receptor). Five subtypes of the muscarinic cholinergic receptor have been identifi ed. Th e existence of receptor subtypes allows the possibility of designing drugs that are selective for one receptor subtype over another. Th is is important, because one receptor subtype may be prevalent in one part of the body (e.g. the gut), while a diff erent receptor subtype is prevalent in another part (e.g. the heart). Th erefore, a drug that is designed to interact selectively with the receptor subtype in the gut is less likely to have side eff ects on the heart. Even if the diff erent receptor subtypes are present in the same part of the body, it is still important to make drugs as selective as possible because diff erent receptor subtypes frequently activate diff erent signalling systems, leading to diff erent biological results. A closer study of the evolutionary tree reveals ]]> Wed, 03 Jul 2024 19:40:49 GMT /slideshow/4-autacoids-and-therapy-of-inflammation-0-pdf/270048104 yisihakchalachew@slideshare.net(yisihakchalachew) 4. Autacoids and therapy of Inflammation(0).pdf yisihakchalachew signifi cantly. Th is implies that these receptors have evolved over millions of years from an ancient common ancestral protein. Comparing the amino acid sequences of the receptors allows us to construct an evolutionary tree and to group the receptors of this superfamily into various sub-families, which are defi ned as class A (rhodopsin-like receptors), class B (secretin-like receptors), and class C (metabotropic glutamate-like and pheromone receptors). Th e most important of these, as far as medicinal chemistry is concerned, is the rhodopsin-like familyso called because the fi rst receptor of this family to be studied in detail was the rhodopsin receptor itself, a receptor involved in the visual process. A study of the evolutionary tree of rhodopsin-like receptors throws up some interesting observations ( Fig. 4.16 ). First of all, the evolutionary tree illustrates the similarity between diff erent kinds of receptors based on their relative positions on the tree. Th us, the muscarinic, 留-adrenergic, 硫-adrenergic, histamine, and dopamine receptors have evolved from a common branch of the evolutionary tree and have greater similarity to each other than to any receptors arising from an earlier evolutionary branch (e.g. the angiotensin receptor ). Such receptor similarity may prove a problem in medicinal chemistry. Although the receptors are distinguished by diff erent neurotransmitters or hormones in the body, a drug may not manage to make that distinction. Th erefore, it is important to ensure that any new drug aimed at one kind of receptor (e.g. the dopamine receptor) does not interact with a similar kind of receptor (e.g. the muscarinic receptor). Receptors have further evolved to give receptor types and subtypes which recognize the same chemical messenger, but are structurally diff erent. For example, there are two types of adrenergic receptor (留 and 硫), each of which has various subtypes (留1 , 留2A , 留2B , 留2C , 硫1 , 硫2 , 硫3 ). Th ere are two types of cholinergic receptornicotinic (an ion channel receptor) and muscarinic (a 7-TM receptor). Five subtypes of the muscarinic cholinergic receptor have been identifi ed. Th e existence of receptor subtypes allows the possibility of designing drugs that are selective for one receptor subtype over another. Th is is important, because one receptor subtype may be prevalent in one part of the body (e.g. the gut), while a diff erent receptor subtype is prevalent in another part (e.g. the heart). Th erefore, a drug that is designed to interact selectively with the receptor subtype in the gut is less likely to have side eff ects on the heart. Even if the diff erent receptor subtypes are present in the same part of the body, it is still important to make drugs as selective as possible because diff erent receptor subtypes frequently activate diff erent signalling systems, leading to diff erent biological results. A closer study of the evolutionary tree reveals <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/4-240703194049-29551338-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> signifi cantly. Th is implies that these receptors have evolved over millions of years from an ancient common ancestral protein. Comparing the amino acid sequences of the receptors allows us to construct an evolutionary tree and to group the receptors of this superfamily into various sub-families, which are defi ned as class A (rhodopsin-like receptors), class B (secretin-like receptors), and class C (metabotropic glutamate-like and pheromone receptors). Th e most important of these, as far as medicinal chemistry is concerned, is the rhodopsin-like familyso called because the fi rst receptor of this family to be studied in detail was the rhodopsin receptor itself, a receptor involved in the visual process. A study of the evolutionary tree of rhodopsin-like receptors throws up some interesting observations ( Fig. 4.16 ). First of all, the evolutionary tree illustrates the similarity between diff erent kinds of receptors based on their relative positions on the tree. Th us, the muscarinic, 留-adrenergic, 硫-adrenergic, histamine, and dopamine receptors have evolved from a common branch of the evolutionary tree and have greater similarity to each other than to any receptors arising from an earlier evolutionary branch (e.g. the angiotensin receptor ). Such receptor similarity may prove a problem in medicinal chemistry. Although the receptors are distinguished by diff erent neurotransmitters or hormones in the body, a drug may not manage to make that distinction. Th erefore, it is important to ensure that any new drug aimed at one kind of receptor (e.g. the dopamine receptor) does not interact with a similar kind of receptor (e.g. the muscarinic receptor). Receptors have further evolved to give receptor types and subtypes which recognize the same chemical messenger, but are structurally diff erent. For example, there are two types of adrenergic receptor (留 and 硫), each of which has various subtypes (留1 , 留2A , 留2B , 留2C , 硫1 , 硫2 , 硫3 ). Th ere are two types of cholinergic receptornicotinic (an ion channel receptor) and muscarinic (a 7-TM receptor). Five subtypes of the muscarinic cholinergic receptor have been identifi ed. Th e existence of receptor subtypes allows the possibility of designing drugs that are selective for one receptor subtype over another. Th is is important, because one receptor subtype may be prevalent in one part of the body (e.g. the gut), while a diff erent receptor subtype is prevalent in another part (e.g. the heart). Th erefore, a drug that is designed to interact selectively with the receptor subtype in the gut is less likely to have side eff ects on the heart. Even if the diff erent receptor subtypes are present in the same part of the body, it is still important to make drugs as selective as possible because diff erent receptor subtypes frequently activate diff erent signalling systems, leading to diff erent biological results. A closer study of the evolutionary tree reveals
4. Autacoids and therapy of Inflammation(0).pdf from yisihakchalachew
]]> 39 0 https://cdn.slidesharecdn.com/ss_thumbnails/4-240703194049-29551338-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 b.pharma introduction to pathology.ppttx /slideshow/b-pharma-introduction-to-pathology-ppttx/269974898 b-240630114109-edb115ea
D The figure shows a dark red hemorrhagic infarction extending to the pleura, a typical finding when a medium-sized thromboembolus lodges in a peripheral pulmonary artery branch. The infarct is hemorrhagic because the bronchial arterial circulation in the lung (derived from the systemic arterial circulation and separate from the pulmonary arterial circulation) continues to supply a small amount of blood to the interstitium in the affected area of infarction. Persons with underlying heart or lung disease are at greater risk for pulmonary infarction. Passive congestion, whether acute or chronic, is a diffuse process, as is edema, which does not impart a red color. Pulmonary venous thrombosis is rare. PBD9 129130 BP9 9293 PBD8 128 BP8 101 33 B The figure shows a pale ischemic infarction of the renal cortex extending nearly to the renal capsule, a typical finding when a medium-sized arterial thromboembolus lodges in a peripheral renal artery branch. The infarct is wedge-shaped, typical for many parenchymal organs, because there is minimal collateral circulation. An abscess is a form of liquefactive necrosis from a localized collection of neutrophils in association with infection, and though it could be yellowish, it is likely to be round. Liquefactive necrosis from arterial occlusion and infarction occurs in the brain. Multiorgan failure occurs with shock, and whole organs are affected by ischemia. Venous thrombosis tends to produce hemorrhagic lesions. PBD9 129130 BP9 9293 PBD8 128 BP8 101 34 D The liver has a dual blood supply, with a hepatic arterial circulation and a portal venous circulation. Infarction of the liver caused by occlusion of hepatic artery is uncommon. Cerebral infarction typically produces liquefactive necrosis. Infarcts of most solid parenchymal organs such as the kidney, heart, and spleen exhibit coagulative necrosis, and emboli from the left heart often go to these organs. PBD9 130 BP9 93 PBD8 129 BP8 101 35 B The patient has septic shock from infection with gram-negative organisms that have lipopolysaccharide, which binds along with other microbe-derived substances containing pathogen-associated molecular patterns (PAMPs) to cells via Toll-like receptors (TLRs). Binding initiates release of various cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1) that produce fever. Macrophages are stimulated to destroy the organisms. Nitric oxide is released, promoting vasodilation and circulatory collapse. Complement C3b generated by bacteria via the alternative pathway acts as an opsonin. Plateletactivating factor mediates many features of acute inflammation and in large quantities can cause vasoconstriction and bronchoconstriction. Toxic shock syndrome toxin-1 is a superantigen released by staphylococcal organisms that is a potent activator of T lymphocytes, inducing cytokine evidenced by the high lactate level. Vasodilation is a feature of septic shock, typically as a result of ]]>
D The figure shows a dark red hemorrhagic infarction extending to the pleura, a typical finding when a medium-sized thromboembolus lodges in a peripheral pulmonary artery branch. The infarct is hemorrhagic because the bronchial arterial circulation in the lung (derived from the systemic arterial circulation and separate from the pulmonary arterial circulation) continues to supply a small amount of blood to the interstitium in the affected area of infarction. Persons with underlying heart or lung disease are at greater risk for pulmonary infarction. Passive congestion, whether acute or chronic, is a diffuse process, as is edema, which does not impart a red color. Pulmonary venous thrombosis is rare. PBD9 129130 BP9 9293 PBD8 128 BP8 101 33 B The figure shows a pale ischemic infarction of the renal cortex extending nearly to the renal capsule, a typical finding when a medium-sized arterial thromboembolus lodges in a peripheral renal artery branch. The infarct is wedge-shaped, typical for many parenchymal organs, because there is minimal collateral circulation. An abscess is a form of liquefactive necrosis from a localized collection of neutrophils in association with infection, and though it could be yellowish, it is likely to be round. Liquefactive necrosis from arterial occlusion and infarction occurs in the brain. Multiorgan failure occurs with shock, and whole organs are affected by ischemia. Venous thrombosis tends to produce hemorrhagic lesions. PBD9 129130 BP9 9293 PBD8 128 BP8 101 34 D The liver has a dual blood supply, with a hepatic arterial circulation and a portal venous circulation. Infarction of the liver caused by occlusion of hepatic artery is uncommon. Cerebral infarction typically produces liquefactive necrosis. Infarcts of most solid parenchymal organs such as the kidney, heart, and spleen exhibit coagulative necrosis, and emboli from the left heart often go to these organs. PBD9 130 BP9 93 PBD8 129 BP8 101 35 B The patient has septic shock from infection with gram-negative organisms that have lipopolysaccharide, which binds along with other microbe-derived substances containing pathogen-associated molecular patterns (PAMPs) to cells via Toll-like receptors (TLRs). Binding initiates release of various cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1) that produce fever. Macrophages are stimulated to destroy the organisms. Nitric oxide is released, promoting vasodilation and circulatory collapse. Complement C3b generated by bacteria via the alternative pathway acts as an opsonin. Plateletactivating factor mediates many features of acute inflammation and in large quantities can cause vasoconstriction and bronchoconstriction. Toxic shock syndrome toxin-1 is a superantigen released by staphylococcal organisms that is a potent activator of T lymphocytes, inducing cytokine evidenced by the high lactate level. Vasodilation is a feature of septic shock, typically as a result of ]]> Sun, 30 Jun 2024 11:41:09 GMT /slideshow/b-pharma-introduction-to-pathology-ppttx/269974898 yisihakchalachew@slideshare.net(yisihakchalachew) b.pharma introduction to pathology.ppttx yisihakchalachew D The figure shows a dark red hemorrhagic infarction extending to the pleura, a typical finding when a medium-sized thromboembolus lodges in a peripheral pulmonary artery branch. The infarct is hemorrhagic because the bronchial arterial circulation in the lung (derived from the systemic arterial circulation and separate from the pulmonary arterial circulation) continues to supply a small amount of blood to the interstitium in the affected area of infarction. Persons with underlying heart or lung disease are at greater risk for pulmonary infarction. Passive congestion, whether acute or chronic, is a diffuse process, as is edema, which does not impart a red color. Pulmonary venous thrombosis is rare. PBD9 129130 BP9 9293 PBD8 128 BP8 101 33 B The figure shows a pale ischemic infarction of the renal cortex extending nearly to the renal capsule, a typical finding when a medium-sized arterial thromboembolus lodges in a peripheral renal artery branch. The infarct is wedge-shaped, typical for many parenchymal organs, because there is minimal collateral circulation. An abscess is a form of liquefactive necrosis from a localized collection of neutrophils in association with infection, and though it could be yellowish, it is likely to be round. Liquefactive necrosis from arterial occlusion and infarction occurs in the brain. Multiorgan failure occurs with shock, and whole organs are affected by ischemia. Venous thrombosis tends to produce hemorrhagic lesions. PBD9 129130 BP9 9293 PBD8 128 BP8 101 34 D The liver has a dual blood supply, with a hepatic arterial circulation and a portal venous circulation. Infarction of the liver caused by occlusion of hepatic artery is uncommon. Cerebral infarction typically produces liquefactive necrosis. Infarcts of most solid parenchymal organs such as the kidney, heart, and spleen exhibit coagulative necrosis, and emboli from the left heart often go to these organs. PBD9 130 BP9 93 PBD8 129 BP8 101 35 B The patient has septic shock from infection with gram-negative organisms that have lipopolysaccharide, which binds along with other microbe-derived substances containing pathogen-associated molecular patterns (PAMPs) to cells via Toll-like receptors (TLRs). Binding initiates release of various cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1) that produce fever. Macrophages are stimulated to destroy the organisms. Nitric oxide is released, promoting vasodilation and circulatory collapse. Complement C3b generated by bacteria via the alternative pathway acts as an opsonin. Plateletactivating factor mediates many features of acute inflammation and in large quantities can cause vasoconstriction and bronchoconstriction. Toxic shock syndrome toxin-1 is a superantigen released by staphylococcal organisms that is a potent activator of T lymphocytes, inducing cytokine evidenced by the high lactate level. Vasodilation is a feature of septic shock, typically as a result of <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/b-240630114109-edb115ea-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> D The figure shows a dark red hemorrhagic infarction extending to the pleura, a typical finding when a medium-sized thromboembolus lodges in a peripheral pulmonary artery branch. The infarct is hemorrhagic because the bronchial arterial circulation in the lung (derived from the systemic arterial circulation and separate from the pulmonary arterial circulation) continues to supply a small amount of blood to the interstitium in the affected area of infarction. Persons with underlying heart or lung disease are at greater risk for pulmonary infarction. Passive congestion, whether acute or chronic, is a diffuse process, as is edema, which does not impart a red color. Pulmonary venous thrombosis is rare. PBD9 129130 BP9 9293 PBD8 128 BP8 101 33 B The figure shows a pale ischemic infarction of the renal cortex extending nearly to the renal capsule, a typical finding when a medium-sized arterial thromboembolus lodges in a peripheral renal artery branch. The infarct is wedge-shaped, typical for many parenchymal organs, because there is minimal collateral circulation. An abscess is a form of liquefactive necrosis from a localized collection of neutrophils in association with infection, and though it could be yellowish, it is likely to be round. Liquefactive necrosis from arterial occlusion and infarction occurs in the brain. Multiorgan failure occurs with shock, and whole organs are affected by ischemia. Venous thrombosis tends to produce hemorrhagic lesions. PBD9 129130 BP9 9293 PBD8 128 BP8 101 34 D The liver has a dual blood supply, with a hepatic arterial circulation and a portal venous circulation. Infarction of the liver caused by occlusion of hepatic artery is uncommon. Cerebral infarction typically produces liquefactive necrosis. Infarcts of most solid parenchymal organs such as the kidney, heart, and spleen exhibit coagulative necrosis, and emboli from the left heart often go to these organs. PBD9 130 BP9 93 PBD8 129 BP8 101 35 B The patient has septic shock from infection with gram-negative organisms that have lipopolysaccharide, which binds along with other microbe-derived substances containing pathogen-associated molecular patterns (PAMPs) to cells via Toll-like receptors (TLRs). Binding initiates release of various cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1) that produce fever. Macrophages are stimulated to destroy the organisms. Nitric oxide is released, promoting vasodilation and circulatory collapse. Complement C3b generated by bacteria via the alternative pathway acts as an opsonin. Plateletactivating factor mediates many features of acute inflammation and in large quantities can cause vasoconstriction and bronchoconstriction. Toxic shock syndrome toxin-1 is a superantigen released by staphylococcal organisms that is a potent activator of T lymphocytes, inducing cytokine evidenced by the high lactate level. Vasodilation is a feature of septic shock, typically as a result of
b.pharma introduction to pathology.ppttx from yisihakchalachew
]]> 11 0 https://cdn.slidesharecdn.com/ss_thumbnails/b-240630114109-edb115ea-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Non steroidal anti inflamatoryNSAIDs 2016 (1).pdf /slideshow/non-steroidal-anti-inflamatorynsaids-2016-1-pdf/269576877 nsaids20161-240608175217-b972df6d
cific in its activity upon those innervations which categorically activate both functionalities, namely : (a) GI-motility ; and (b) gastric secretion. Interestingly, based on the extremely specific nature of its pharmacological activity on the gastric functions actually renders diphemanil particularly beneficial in the control, management and treatment of peptic ulcer. Besides, its inherent lack of atropine-like effects makes this specific usage relatively less painful in comparison to several other antispasmodic drugs. Note. The methylsulphate salt is considered to be the best in terms of its stability in comparison to its corresponding halides e.g., Cl (hygroscopic) ; Br and I (toxic reactions). 7.8.7.2. Methixene Hydrochloride The drug essentially exhibits both antihistaminic and direct antispasmodic activities. It has been duly observed that the drug is invariably absorbed from the GI-tract. It subsequently gets excreted through the urine, partly as its corresponding isomeric sulphoxides or their metabolites ; and a reasonable quantum as unchanged product. Methixene hydrochloride has been profusely indicated in such preparations that may ultimately relieve gastro-intestinal spasms. 7.8.7.3. Glycopyrronium Bromide It is a quaternary ammonium antimuscarinic agent having marked and pronounced peripheral effects that are quite akin to those of atropine. It has been found that approximately 1025% of the drug gets absorbed from the GI-tract when administered orally. It penetrates the blood brain barrier (BBB) rather very poorly. It gets ultimately excreted in bile and urine. 7.8.7.4. Diphemanil Methylsulphate The drug is quite active for the symptomatic management and subsequent control of visceral spasms. It may also cause enough relief from the ensuing painful and distressing spasms of the biliary and the genitro-urinary systems. Importantly, it also finds its adequate usage for the treatment of symptomatic bradycardia. 8. GANGLIONIC BLOCKING AGENTS Langley first studied the action of drugs on the autonomic ganglia with the alkaloid nictoine obtained from Nicotiana tabacum. Subsequently, some other alkaloids were also found to possess similar effects, namely ; coniine from the poison Hemlock obtained from Conicum maculatum, gelsemine from the yellow jasmine and lobeline from the lobelia, a native of America. Generally, ganglionic blocking agents normally exert their action by competing with acetylcholine from the cholinergic receptors present in the autonomic postganglionic neurons. In fact, the ganglia of either of the sympathetic and parasympathetic nervous systems are cholinergic in character, these therapeutic agents interrupt the outflow through both these systems. Therefore, it is not practically possible to accomplish a complete therapeutic block of the autonomic outflow to a specific locus without encountering a few undesirable but unavoidable side effects that may arise as a consequence from the blockade of other ensuing a]]>
cific in its activity upon those innervations which categorically activate both functionalities, namely : (a) GI-motility ; and (b) gastric secretion. Interestingly, based on the extremely specific nature of its pharmacological activity on the gastric functions actually renders diphemanil particularly beneficial in the control, management and treatment of peptic ulcer. Besides, its inherent lack of atropine-like effects makes this specific usage relatively less painful in comparison to several other antispasmodic drugs. Note. The methylsulphate salt is considered to be the best in terms of its stability in comparison to its corresponding halides e.g., Cl (hygroscopic) ; Br and I (toxic reactions). 7.8.7.2. Methixene Hydrochloride The drug essentially exhibits both antihistaminic and direct antispasmodic activities. It has been duly observed that the drug is invariably absorbed from the GI-tract. It subsequently gets excreted through the urine, partly as its corresponding isomeric sulphoxides or their metabolites ; and a reasonable quantum as unchanged product. Methixene hydrochloride has been profusely indicated in such preparations that may ultimately relieve gastro-intestinal spasms. 7.8.7.3. Glycopyrronium Bromide It is a quaternary ammonium antimuscarinic agent having marked and pronounced peripheral effects that are quite akin to those of atropine. It has been found that approximately 1025% of the drug gets absorbed from the GI-tract when administered orally. It penetrates the blood brain barrier (BBB) rather very poorly. It gets ultimately excreted in bile and urine. 7.8.7.4. Diphemanil Methylsulphate The drug is quite active for the symptomatic management and subsequent control of visceral spasms. It may also cause enough relief from the ensuing painful and distressing spasms of the biliary and the genitro-urinary systems. Importantly, it also finds its adequate usage for the treatment of symptomatic bradycardia. 8. GANGLIONIC BLOCKING AGENTS Langley first studied the action of drugs on the autonomic ganglia with the alkaloid nictoine obtained from Nicotiana tabacum. Subsequently, some other alkaloids were also found to possess similar effects, namely ; coniine from the poison Hemlock obtained from Conicum maculatum, gelsemine from the yellow jasmine and lobeline from the lobelia, a native of America. Generally, ganglionic blocking agents normally exert their action by competing with acetylcholine from the cholinergic receptors present in the autonomic postganglionic neurons. In fact, the ganglia of either of the sympathetic and parasympathetic nervous systems are cholinergic in character, these therapeutic agents interrupt the outflow through both these systems. Therefore, it is not practically possible to accomplish a complete therapeutic block of the autonomic outflow to a specific locus without encountering a few undesirable but unavoidable side effects that may arise as a consequence from the blockade of other ensuing a]]> Sat, 08 Jun 2024 17:52:17 GMT /slideshow/non-steroidal-anti-inflamatorynsaids-2016-1-pdf/269576877 yisihakchalachew@slideshare.net(yisihakchalachew) Non steroidal anti inflamatoryNSAIDs 2016 (1).pdf yisihakchalachew cific in its activity upon those innervations which categorically activate both functionalities, namely : (a) GI-motility ; and (b) gastric secretion. Interestingly, based on the extremely specific nature of its pharmacological activity on the gastric functions actually renders diphemanil particularly beneficial in the control, management and treatment of peptic ulcer. Besides, its inherent lack of atropine-like effects makes this specific usage relatively less painful in comparison to several other antispasmodic drugs. Note. The methylsulphate salt is considered to be the best in terms of its stability in comparison to its corresponding halides e.g., Cl (hygroscopic) ; Br and I (toxic reactions). 7.8.7.2. Methixene Hydrochloride The drug essentially exhibits both antihistaminic and direct antispasmodic activities. It has been duly observed that the drug is invariably absorbed from the GI-tract. It subsequently gets excreted through the urine, partly as its corresponding isomeric sulphoxides or their metabolites ; and a reasonable quantum as unchanged product. Methixene hydrochloride has been profusely indicated in such preparations that may ultimately relieve gastro-intestinal spasms. 7.8.7.3. Glycopyrronium Bromide It is a quaternary ammonium antimuscarinic agent having marked and pronounced peripheral effects that are quite akin to those of atropine. It has been found that approximately 1025% of the drug gets absorbed from the GI-tract when administered orally. It penetrates the blood brain barrier (BBB) rather very poorly. It gets ultimately excreted in bile and urine. 7.8.7.4. Diphemanil Methylsulphate The drug is quite active for the symptomatic management and subsequent control of visceral spasms. It may also cause enough relief from the ensuing painful and distressing spasms of the biliary and the genitro-urinary systems. Importantly, it also finds its adequate usage for the treatment of symptomatic bradycardia. 8. GANGLIONIC BLOCKING AGENTS Langley first studied the action of drugs on the autonomic ganglia with the alkaloid nictoine obtained from Nicotiana tabacum. Subsequently, some other alkaloids were also found to possess similar effects, namely ; coniine from the poison Hemlock obtained from Conicum maculatum, gelsemine from the yellow jasmine and lobeline from the lobelia, a native of America. Generally, ganglionic blocking agents normally exert their action by competing with acetylcholine from the cholinergic receptors present in the autonomic postganglionic neurons. In fact, the ganglia of either of the sympathetic and parasympathetic nervous systems are cholinergic in character, these therapeutic agents interrupt the outflow through both these systems. Therefore, it is not practically possible to accomplish a complete therapeutic block of the autonomic outflow to a specific locus without encountering a few undesirable but unavoidable side effects that may arise as a consequence from the blockade of other ensuing a <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/nsaids20161-240608175217-b972df6d-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> cific in its activity upon those innervations which categorically activate both functionalities, namely : (a) GI-motility ; and (b) gastric secretion. Interestingly, based on the extremely specific nature of its pharmacological activity on the gastric functions actually renders diphemanil particularly beneficial in the control, management and treatment of peptic ulcer. Besides, its inherent lack of atropine-like effects makes this specific usage relatively less painful in comparison to several other antispasmodic drugs. Note. The methylsulphate salt is considered to be the best in terms of its stability in comparison to its corresponding halides e.g., Cl (hygroscopic) ; Br and I (toxic reactions). 7.8.7.2. Methixene Hydrochloride The drug essentially exhibits both antihistaminic and direct antispasmodic activities. It has been duly observed that the drug is invariably absorbed from the GI-tract. It subsequently gets excreted through the urine, partly as its corresponding isomeric sulphoxides or their metabolites ; and a reasonable quantum as unchanged product. Methixene hydrochloride has been profusely indicated in such preparations that may ultimately relieve gastro-intestinal spasms. 7.8.7.3. Glycopyrronium Bromide It is a quaternary ammonium antimuscarinic agent having marked and pronounced peripheral effects that are quite akin to those of atropine. It has been found that approximately 1025% of the drug gets absorbed from the GI-tract when administered orally. It penetrates the blood brain barrier (BBB) rather very poorly. It gets ultimately excreted in bile and urine. 7.8.7.4. Diphemanil Methylsulphate The drug is quite active for the symptomatic management and subsequent control of visceral spasms. It may also cause enough relief from the ensuing painful and distressing spasms of the biliary and the genitro-urinary systems. Importantly, it also finds its adequate usage for the treatment of symptomatic bradycardia. 8. GANGLIONIC BLOCKING AGENTS Langley first studied the action of drugs on the autonomic ganglia with the alkaloid nictoine obtained from Nicotiana tabacum. Subsequently, some other alkaloids were also found to possess similar effects, namely ; coniine from the poison Hemlock obtained from Conicum maculatum, gelsemine from the yellow jasmine and lobeline from the lobelia, a native of America. Generally, ganglionic blocking agents normally exert their action by competing with acetylcholine from the cholinergic receptors present in the autonomic postganglionic neurons. In fact, the ganglia of either of the sympathetic and parasympathetic nervous systems are cholinergic in character, these therapeutic agents interrupt the outflow through both these systems. Therefore, it is not practically possible to accomplish a complete therapeutic block of the autonomic outflow to a specific locus without encountering a few undesirable but unavoidable side effects that may arise as a consequence from the blockade of other ensuing a
Non steroidal anti inflamatoryNSAIDs 2016 (1).pdf from yisihakchalachew
]]> 5 0 https://cdn.slidesharecdn.com/ss_thumbnails/nsaids20161-240608175217-b972df6d-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 6 Epidemiologic Study Designs feke.ppptx /slideshow/6-epidemiologic-study-designs-feke-ppptx/269576622 6epidemiologicstudydesignsfeke-240608172313-7c84cba4
may be reproduced or distributed in any form or by any means, or stored in a data base or retrieval system, without the prior written permission of the publisher. Previous editions copyright 息 2015, 2012, 2010, 2009, 2007, 2004, 2001 by McGraw-Hill Companies, Inc.; copyright 息 1998, 1995, 1992, 1989, 1987 by Appleton & Lange; copyright 息 1984, 1982 by Lange Medical Publications. 1 2 3 4 5 6 7 8 9 LWI 22 21 20 19 18 17 ISBN 978-1-259-64115-2 MHID 1-259-64115-5 ISSN 0891-2033 Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. This book was set in Adobe Garamond by Cenveo速 Publisher Services. The editors were Michael Weitz and Peter Boyle. The copyeditors were Caroline Define and Greg Feldman. The production supervisor was Richard Ruzycka. Project management provided by Neha Bhargava, Cenveo Publisher Services. Cover photo: Tumor necrosis factor alpha (TNF-a) cytokine protein molecule, 3D rendering. Clinically used inhibitors include infliximab, adalimumab, certolizumab and etanercept. Photo credit: Shutterstock. This book is printed on acid-free paper. McGraw-Hill Education books are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs. To contact a representative please visit the Contact Us pages at www.mhprofessional.com. International Edition ISBN 978-1-260-28817-9; MHID 1-260-28817-X. Copyright 息 2018. Exclusive rights by McGraw-Hill Education for manufacture and export. This book cannot be re-exported from the countryand also survilance data must be dent it how it is thbt monmt to over ride to bedone on them about of corundum taper roundtable action on it them it that about on holder them thi]]>
may be reproduced or distributed in any form or by any means, or stored in a data base or retrieval system, without the prior written permission of the publisher. Previous editions copyright 息 2015, 2012, 2010, 2009, 2007, 2004, 2001 by McGraw-Hill Companies, Inc.; copyright 息 1998, 1995, 1992, 1989, 1987 by Appleton & Lange; copyright 息 1984, 1982 by Lange Medical Publications. 1 2 3 4 5 6 7 8 9 LWI 22 21 20 19 18 17 ISBN 978-1-259-64115-2 MHID 1-259-64115-5 ISSN 0891-2033 Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. This book was set in Adobe Garamond by Cenveo速 Publisher Services. The editors were Michael Weitz and Peter Boyle. The copyeditors were Caroline Define and Greg Feldman. The production supervisor was Richard Ruzycka. Project management provided by Neha Bhargava, Cenveo Publisher Services. Cover photo: Tumor necrosis factor alpha (TNF-a) cytokine protein molecule, 3D rendering. Clinically used inhibitors include infliximab, adalimumab, certolizumab and etanercept. Photo credit: Shutterstock. This book is printed on acid-free paper. McGraw-Hill Education books are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs. To contact a representative please visit the Contact Us pages at www.mhprofessional.com. International Edition ISBN 978-1-260-28817-9; MHID 1-260-28817-X. Copyright 息 2018. Exclusive rights by McGraw-Hill Education for manufacture and export. This book cannot be re-exported from the countryand also survilance data must be dent it how it is thbt monmt to over ride to bedone on them about of corundum taper roundtable action on it them it that about on holder them thi]]> Sat, 08 Jun 2024 17:23:13 GMT /slideshow/6-epidemiologic-study-designs-feke-ppptx/269576622 yisihakchalachew@slideshare.net(yisihakchalachew) 6 Epidemiologic Study Designs feke.ppptx yisihakchalachew may be reproduced or distributed in any form or by any means, or stored in a data base or retrieval system, without the prior written permission of the publisher. Previous editions copyright 息 2015, 2012, 2010, 2009, 2007, 2004, 2001 by McGraw-Hill Companies, Inc.; copyright 息 1998, 1995, 1992, 1989, 1987 by Appleton & Lange; copyright 息 1984, 1982 by Lange Medical Publications. 1 2 3 4 5 6 7 8 9 LWI 22 21 20 19 18 17 ISBN 978-1-259-64115-2 MHID 1-259-64115-5 ISSN 0891-2033 Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. This book was set in Adobe Garamond by Cenveo速 Publisher Services. The editors were Michael Weitz and Peter Boyle. The copyeditors were Caroline Define and Greg Feldman. The production supervisor was Richard Ruzycka. Project management provided by Neha Bhargava, Cenveo Publisher Services. Cover photo: Tumor necrosis factor alpha (TNF-a) cytokine protein molecule, 3D rendering. Clinically used inhibitors include infliximab, adalimumab, certolizumab and etanercept. Photo credit: Shutterstock. This book is printed on acid-free paper. McGraw-Hill Education books are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs. To contact a representative please visit the Contact Us pages at www.mhprofessional.com. International Edition ISBN 978-1-260-28817-9; MHID 1-260-28817-X. Copyright 息 2018. Exclusive rights by McGraw-Hill Education for manufacture and export. This book cannot be re-exported from the countryand also survilance data must be dent it how it is thbt monmt to over ride to bedone on them about of corundum taper roundtable action on it them it that about on holder them thi <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/6epidemiologicstudydesignsfeke-240608172313-7c84cba4-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> may be reproduced or distributed in any form or by any means, or stored in a data base or retrieval system, without the prior written permission of the publisher. Previous editions copyright 息 2015, 2012, 2010, 2009, 2007, 2004, 2001 by McGraw-Hill Companies, Inc.; copyright 息 1998, 1995, 1992, 1989, 1987 by Appleton &amp; Lange; copyright 息 1984, 1982 by Lange Medical Publications. 1 2 3 4 5 6 7 8 9 LWI 22 21 20 19 18 17 ISBN 978-1-259-64115-2 MHID 1-259-64115-5 ISSN 0891-2033 Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. This book was set in Adobe Garamond by Cenveo速 Publisher Services. The editors were Michael Weitz and Peter Boyle. The copyeditors were Caroline Define and Greg Feldman. The production supervisor was Richard Ruzycka. Project management provided by Neha Bhargava, Cenveo Publisher Services. Cover photo: Tumor necrosis factor alpha (TNF-a) cytokine protein molecule, 3D rendering. Clinically used inhibitors include infliximab, adalimumab, certolizumab and etanercept. Photo credit: Shutterstock. This book is printed on acid-free paper. McGraw-Hill Education books are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs. To contact a representative please visit the Contact Us pages at www.mhprofessional.com. International Edition ISBN 978-1-260-28817-9; MHID 1-260-28817-X. Copyright 息 2018. Exclusive rights by McGraw-Hill Education for manufacture and export. This book cannot be re-exported from the countryand also survilance data must be dent it how it is thbt monmt to over ride to bedone on them about of corundum taper roundtable action on it them it that about on holder them thi
6 Epidemiologic Study Designs feke.ppptx from yisihakchalachew
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pharmacopeia, with numerous new monoclonal antibodies and other biologic agents. Case studies accompany most chapters, and answers to questions posed in the case studies appear at the end of each chapter. The book is designed to provide a comprehensive, authoritative, and readable pharmacology textbook for students in the health sciences. Frequent revision is necessary to keep pace with the rapid changes in pharmacology and therapeutics; the 23 year revision cycle of this text is among the shortest in the field, and the availability of an online version provides even greater currency. The book also offers special features that make it a useful reference for house officers and practicing clinicians. This edition continues the sequence used in many pharmacology courses and in integrated curricula: basic principles of drug discovery, pharmacodynamics, pharmacokinetics, and pharmacogenomics; autonomic drugs; cardiovascular-renal drugs; drugs with important actions on smooth muscle; central nervous system drugs; drugs used to treat inflammation, gout, and diseases of the blood; endocrine drugs; chemotherapeutic drugs; toxicology; and special topics. This sequence builds new information on a foundation of information already assimilated. For example, early presentation of autonomic nervous system pharmacology allows students to integrate the physiology and neuroscience they have learned elsewhere with the pharmacology they are learning and prepares them to understand the autonomic effects of other drugs. This is especially important for the cardiovascular and central nervous system drug groups. However, chapters can be used equally well in courses and curricula that present these topics in a different sequence. Within each chapter, emphasis is placed on discussion of drug groups and prototypes rather than offering repetitive detail about individual drugs. Selection of the subject matter and the order of its presentation are based on the accumulated experience of teaching this material to thousands of medical, pharmacy, dental, podiatry, nursing, and other health science students. Major features that make this book particularly useful in integrated curricula include sections that specifically address the clinical choice and use of drugs in patients and the monitoring of their effectsin other words, clinical pharmacology is an integral part of this text. Lists of the trade and generic names of commercial preparations available are provided at the end of each chapter for easy reference by the house officer or practitioner evaluating a patients drug list or writing a prescription. Significant revisions in this edition include: Major revisions of the chapters on immunopharmacology, antiseizure, antipsychotic, antidepressant, antidiabetic, antiinflammatory, and antiviral drugs, prostaglandins, and central nervous system neurotransmitters. Continued expansion of the coverage of general concepts relating to newly dis]]>
pharmacopeia, with numerous new monoclonal antibodies and other biologic agents. Case studies accompany most chapters, and answers to questions posed in the case studies appear at the end of each chapter. The book is designed to provide a comprehensive, authoritative, and readable pharmacology textbook for students in the health sciences. Frequent revision is necessary to keep pace with the rapid changes in pharmacology and therapeutics; the 23 year revision cycle of this text is among the shortest in the field, and the availability of an online version provides even greater currency. The book also offers special features that make it a useful reference for house officers and practicing clinicians. This edition continues the sequence used in many pharmacology courses and in integrated curricula: basic principles of drug discovery, pharmacodynamics, pharmacokinetics, and pharmacogenomics; autonomic drugs; cardiovascular-renal drugs; drugs with important actions on smooth muscle; central nervous system drugs; drugs used to treat inflammation, gout, and diseases of the blood; endocrine drugs; chemotherapeutic drugs; toxicology; and special topics. This sequence builds new information on a foundation of information already assimilated. For example, early presentation of autonomic nervous system pharmacology allows students to integrate the physiology and neuroscience they have learned elsewhere with the pharmacology they are learning and prepares them to understand the autonomic effects of other drugs. This is especially important for the cardiovascular and central nervous system drug groups. However, chapters can be used equally well in courses and curricula that present these topics in a different sequence. Within each chapter, emphasis is placed on discussion of drug groups and prototypes rather than offering repetitive detail about individual drugs. Selection of the subject matter and the order of its presentation are based on the accumulated experience of teaching this material to thousands of medical, pharmacy, dental, podiatry, nursing, and other health science students. Major features that make this book particularly useful in integrated curricula include sections that specifically address the clinical choice and use of drugs in patients and the monitoring of their effectsin other words, clinical pharmacology is an integral part of this text. Lists of the trade and generic names of commercial preparations available are provided at the end of each chapter for easy reference by the house officer or practitioner evaluating a patients drug list or writing a prescription. Significant revisions in this edition include: Major revisions of the chapters on immunopharmacology, antiseizure, antipsychotic, antidepressant, antidiabetic, antiinflammatory, and antiviral drugs, prostaglandins, and central nervous system neurotransmitters. Continued expansion of the coverage of general concepts relating to newly dis]]> Sat, 08 Jun 2024 16:54:49 GMT /slideshow/pharmacology-autonomous-nervous-system-s-pptx/269576320 yisihakchalachew@slideshare.net(yisihakchalachew) pharmacology autonomous nervous system s.pptx yisihakchalachew pharmacopeia, with numerous new monoclonal antibodies and other biologic agents. Case studies accompany most chapters, and answers to questions posed in the case studies appear at the end of each chapter. The book is designed to provide a comprehensive, authoritative, and readable pharmacology textbook for students in the health sciences. Frequent revision is necessary to keep pace with the rapid changes in pharmacology and therapeutics; the 23 year revision cycle of this text is among the shortest in the field, and the availability of an online version provides even greater currency. The book also offers special features that make it a useful reference for house officers and practicing clinicians. This edition continues the sequence used in many pharmacology courses and in integrated curricula: basic principles of drug discovery, pharmacodynamics, pharmacokinetics, and pharmacogenomics; autonomic drugs; cardiovascular-renal drugs; drugs with important actions on smooth muscle; central nervous system drugs; drugs used to treat inflammation, gout, and diseases of the blood; endocrine drugs; chemotherapeutic drugs; toxicology; and special topics. This sequence builds new information on a foundation of information already assimilated. For example, early presentation of autonomic nervous system pharmacology allows students to integrate the physiology and neuroscience they have learned elsewhere with the pharmacology they are learning and prepares them to understand the autonomic effects of other drugs. This is especially important for the cardiovascular and central nervous system drug groups. However, chapters can be used equally well in courses and curricula that present these topics in a different sequence. Within each chapter, emphasis is placed on discussion of drug groups and prototypes rather than offering repetitive detail about individual drugs. Selection of the subject matter and the order of its presentation are based on the accumulated experience of teaching this material to thousands of medical, pharmacy, dental, podiatry, nursing, and other health science students. Major features that make this book particularly useful in integrated curricula include sections that specifically address the clinical choice and use of drugs in patients and the monitoring of their effectsin other words, clinical pharmacology is an integral part of this text. Lists of the trade and generic names of commercial preparations available are provided at the end of each chapter for easy reference by the house officer or practitioner evaluating a patients drug list or writing a prescription. Significant revisions in this edition include: Major revisions of the chapters on immunopharmacology, antiseizure, antipsychotic, antidepressant, antidiabetic, antiinflammatory, and antiviral drugs, prostaglandins, and central nervous system neurotransmitters. Continued expansion of the coverage of general concepts relating to newly dis <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/pharmaans-240608165449-a7025945-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> pharmacopeia, with numerous new monoclonal antibodies and other biologic agents. Case studies accompany most chapters, and answers to questions posed in the case studies appear at the end of each chapter. The book is designed to provide a comprehensive, authoritative, and readable pharmacology textbook for students in the health sciences. Frequent revision is necessary to keep pace with the rapid changes in pharmacology and therapeutics; the 23 year revision cycle of this text is among the shortest in the field, and the availability of an online version provides even greater currency. The book also offers special features that make it a useful reference for house officers and practicing clinicians. This edition continues the sequence used in many pharmacology courses and in integrated curricula: basic principles of drug discovery, pharmacodynamics, pharmacokinetics, and pharmacogenomics; autonomic drugs; cardiovascular-renal drugs; drugs with important actions on smooth muscle; central nervous system drugs; drugs used to treat inflammation, gout, and diseases of the blood; endocrine drugs; chemotherapeutic drugs; toxicology; and special topics. This sequence builds new information on a foundation of information already assimilated. For example, early presentation of autonomic nervous system pharmacology allows students to integrate the physiology and neuroscience they have learned elsewhere with the pharmacology they are learning and prepares them to understand the autonomic effects of other drugs. This is especially important for the cardiovascular and central nervous system drug groups. However, chapters can be used equally well in courses and curricula that present these topics in a different sequence. Within each chapter, emphasis is placed on discussion of drug groups and prototypes rather than offering repetitive detail about individual drugs. Selection of the subject matter and the order of its presentation are based on the accumulated experience of teaching this material to thousands of medical, pharmacy, dental, podiatry, nursing, and other health science students. Major features that make this book particularly useful in integrated curricula include sections that specifically address the clinical choice and use of drugs in patients and the monitoring of their effectsin other words, clinical pharmacology is an integral part of this text. Lists of the trade and generic names of commercial preparations available are provided at the end of each chapter for easy reference by the house officer or practitioner evaluating a patients drug list or writing a prescription. Significant revisions in this edition include: Major revisions of the chapters on immunopharmacology, antiseizure, antipsychotic, antidepressant, antidiabetic, antiinflammatory, and antiviral drugs, prostaglandins, and central nervous system neurotransmitters. Continued expansion of the coverage of general concepts relating to newly dis
pharmacology autonomous nervous system s.pptx from yisihakchalachew
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https://vm.tiktok.com/ZMrRSCt74/]]>
https://vm.tiktok.com/ZMrRSCt74/]]> Sat, 08 Jun 2024 16:48:19 GMT /slideshow/cvs-pharmacology-pharma-pptx-pharmacology/269576258 yisihakchalachew@slideshare.net(yisihakchalachew) CVS Pharmacology - Pharma.pptx pharmacology yisihakchalachew https://vm.tiktok.com/ZMrRSCt74/ <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/cvspharmacology-pharma-240608164819-388c1875-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> https://vm.tiktok.com/ZMrRSCt74/
CVS Pharmacology - Pharma.pptx pharmacology from yisihakchalachew
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Ipp chap 5]]>
Ipp chap 5]]> Sat, 08 Jun 2024 16:40:42 GMT /slideshow/ipp-chapt-5-pptx-pack-and-packagings-material/269576152 yisihakchalachew@slideshare.net(yisihakchalachew) IPP chapt-5.pptx pack and packagings material yisihakchalachew Ipp chap 5 <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/ippchapt-5-240608164042-4895c26e-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Ipp chap 5
IPP chapt-5.pptx pack and packagings material from yisihakchalachew
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Ipp unit 10]]>
Ipp unit 10]]> Sat, 08 Jun 2024 16:36:36 GMT /slideshow/ipp-chapt-10-pdfsuspension-for-regular-class/269576108 yisihakchalachew@slideshare.net(yisihakchalachew) IPP chapt-10.pdfsuspension for regular class yisihakchalachew Ipp unit 10 <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/ippchapt-10-240608163637-4279ceff-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Ipp unit 10
IPP chapt-10.pdfsuspension for regular class from yisihakchalachew
]]> 30 0 https://cdn.slidesharecdn.com/ss_thumbnails/ippchapt-10-240608163637-4279ceff-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Diureticsmedicenal chapter 7 about drug that.pptx /slideshow/diureticsmedicenal-chapter-7-about-drug-that-pptx/269427793 diuretics-240530185321-a5ebac5e
Medicinal chemistry abranch of integrated catagory]]>
Medicinal chemistry abranch of integrated catagory]]> Thu, 30 May 2024 18:53:21 GMT /slideshow/diureticsmedicenal-chapter-7-about-drug-that-pptx/269427793 yisihakchalachew@slideshare.net(yisihakchalachew) Diureticsmedicenal chapter 7 about drug that.pptx yisihakchalachew Medicinal chemistry abranch of integrated catagory <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/diuretics-240530185321-a5ebac5e-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Medicinal chemistry abranch of integrated catagory
Diureticsmedicenal chapter 7 about drug that.pptx from yisihakchalachew
]]> 21 0 https://cdn.slidesharecdn.com/ss_thumbnails/diuretics-240530185321-a5ebac5e-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 https://public.slidesharecdn.com/v2/images/profile-picture.png https://cdn.slidesharecdn.com/ss_thumbnails/physicalandchemicalpropertiesofdrugmolecules1-250105183748-94d0104f-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/physical-and-chemical-properties-of-drug-molecules-1-pdf/274652772 Physical and Chemical ... https://cdn.slidesharecdn.com/ss_thumbnails/pharmacotherapeuticsidiagnostictest1-250102194019-ca6fdf98-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/pharmacotherapeutics-i-diagnostic-test-1-pptx/274594377 Pharmacotherapeutics I... https://cdn.slidesharecdn.com/ss_thumbnails/drugtherapyinspecificpatientgroups-241228055241-5053d7ab-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/drug-therapy-in-specific-patient-groups-pptx/274453021 drug therapy in specif...