![Topics ,[object Object],[object Object],[object Object],[object Object],[object Object]](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
Recomendados
Más contenido relacionado
La actualidad más candente
La actualidad más candente (20)
Destacado
Destacado (20)
Similar a Gi drugs outline
Similar a Gi drugs outline (20)
Más de raj kumar
Más de raj kumar (20)
Gi drugs outline
- 1. Pharmacology Drugs that Affect the Gastrointestinal System
- 3. Peptic Ulcer Disease Factors that Increase Acidity Factors that Protect Against Acidity
- 5. Regulation of Gastric Acid Secretion
- 32. Mucosa protective factors www.freelivedoctor.com
- 33. Parietal cell and acid regulation www.freelivedoctor.com
- 80. Navarro, V. J. et al. N Engl J Med 2006;354:731-739 Liver Injury and Its Patterns www.freelivedoctor.com
- 81. Navarro, V. J. et al. N Engl J Med 2006;354:731-739 Key Guidelines in the Recognition and Prevention of Hepatotoxicity in Clinical Practice www.freelivedoctor.com
- 82. Navarro, V. J. et al. N Engl J Med 2006;354:731-739 Diagnosis of Drug-Related Hepatotoxicity www.freelivedoctor.com
- 83. Navarro, V. J. et al. N Engl J Med 2006;354:731-739 Key Elements of and Caveats in Assessing Cause in the Diagnosis of Drug-Related Hepatotoxicity www.freelivedoctor.com
- 84. Hoofnagle, J. H. et al. N Engl J Med 1997;336:347-356 Factors Predictive of a Sustained Beneficial Response to Interferon Alfa in Patients with Chronic Hepatitis www.freelivedoctor.com
- 86. Test for H. pylori 2 H. pylori negative Gastric ulcer Full-dose PPI for 1 or 2 months Periodic review 6 Return to self care Stop NSAIDs , if used 1 Endoscopy 4 Healed Not healed Refer to specialist secondary care Low-dose treatment as required 5 Full-dose PPI for 2 months H. pylori positive, ulcer associated with NSAID use H. pylori positive, ulcer not associated with NSAID use Eradication therapy 3 Ulcer not healed, H. pylori negative Ulcer healed, H. pylori negative H. pylori positive Endoscopy and H. pylori test 4 Refer to specialist secondary care Flow chart for Mx of GU www.freelivedoctor.com Entry or final state Action Action and outcome
- 87. Test for H. pylori 2 Test negative Eradication therapy 3 Test positive, ulcer not associated with NSAID use Duodenal ulcer Full-dose PPI for 1 or 2 months Re-test for H. pylori 4 No response or relapse Negative Positive Low-dose treatment as required 6 Review 8 Response No response Eradication therapy 5 Response No response or relapse No response Exclude other causes of DU 7 Response Response Return to self care Stop NSAIDs , if used 1 Full-dose PPI for 2 months Test positive, ulcer associated with NSAID use Flow chart for Mx of DU www.freelivedoctor.com Entry or final state Action Action and outcome
- 88. Lauer, G. M. et al. N Engl J Med 2001;345:41-52 Characteristics of Hepatitis A Virus, Hepatitis B Virus, and Hepatitis C Virus www.freelivedoctor.com
- 89. Ganem, D. et al. N Engl J Med 2004;350:1118-1129 The Replication Cycle of HBV www.freelivedoctor.com
- 90. The Natural History of HCV Infection and Its Variability from Person to Person www.freelivedoctor.com
- 91. Lauer, G. M. et al. N Engl J Med 2001;345:41-52 Side Effects of Treatment with Interferon Alfa and Ribavirin www.freelivedoctor.com
- 92. Pathogen-Host Interactions in the Pathogenesis of Helicobacter pylori Infection www.freelivedoctor.com
Notas del editor
- Table 3. Factors Predictive of a Sustained Beneficial Response to Interferon Alfa in Patients with Chronic Hepatitis.
- Table 3. Characteristics of Hepatitis A Virus, Hepatitis B Virus, and Hepatitis C Virus.
- Figure 2. The Replication Cycle of HBV. HBV virions bind to surface receptors and are internalized. Viral core particles migrate to the hepatocyte nucleus, where their genomes are repaired to form a covalently closed circular DNA (cccDNA) that is the template for viral messenger RNA (mRNA) transcription. The viral mRNA that results is translated in the cytoplasm to produce the viral surface, core, polymerase, and X proteins. There, progeny viral capsids assemble, incorporating genomic viral RNA (RNA packaging). This RNA is reverse-transcribed into viral DNA. The resulting cores can either bud into the endoplasmic reticulum to be enveloped and exported from the cell or recycle their genomes into the nucleus for conversion to cccDNA. The small, peach-colored sphere inside the core particle is the viral DNA polymerase.
- Figure 2. The Natural History of HCV Infection and Its Variability from Person to Person. The course of infection varies widely among persons. Factors that decrease the risk of progression include female sex and a younger age at infection; factors that increase the risk include alcohol intake, an older age at infection, male sex, and coinfection with other viruses. Persons with a favorable risk profile often do not have progressive liver disease until 30 or more years after infection. In contrast, 20 percent of persons with chronic hepatitis C will eventually have cirrhosis, and this can occur 20 years or less after infection, especially in those with alcohol abuse or coinfection with human immunodeficiency virus type 1 or hepatitis B virus. Once cirrhosis is established, the risk of hepatocellular carcinoma is 1 to 4 percent per year.
- Table 2. Side Effects of Treatment with Interferon Alfa and Ribavirin.
- Figure 2. Pathogen-Host Interactions in the Pathogenesis of Helicobacter pylori Infection. The host response to H. pylori participates in the induction of damage to the gastric epithelium and therefore has an integral role in H. pylori pathogenesis. During the early phase of the infection, binding of H. pylori to gastric epithelial cells, in particular through BabA and by strains harboring the cag pathogenicity island, results in the production of interleukin-8 and other chemokines, such as epithelial-cell-derived neutrophil-activating peptide 78 (ENA-78) and growth-related oncogene {alpha} (GRO-{alpha}), by epithelial cells. Nuclear factor-{kappa}B (NF-{kappa}B) and the early-response transcription-factor activator protein 1 (AP-1) are the intracellular messengers involved in this process. The chemokines secreted by epithelial cells bind to the proteoglycan scaffolding, generating a gradient along which polymorphonuclear cells (PMN) are recruited. The chronic phase of H. pylori gastritis associates an adaptive lymphocyte response with the initial innate response. Lymphocyte recruitment is facilitated by chemokine-mediated expression of vascular addressins such as vascular-cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) that are required for lymphocyte extravasation. Macrophages that participate in interleukin-8 production produce proinflammatory cytokines involved in the activation of the recruited cells, in particular T helper cells (Th0, Th1, Th2), that respond with a biased Th1 response to H. pylori. In turn, Th1-type cytokines such as interferon-{gamma} (INF-{gamma}) induce the expression of class II major histocompatibility complexes (MHC) and accessory molecules B7-1 and B7-2 by epithelial cells, making them competent for antigen presentation. The cytotoxin VacA- and Fas-mediated apoptosis induced by tumor necrosis factor {alpha} (TNF-{alpha}) leads to disruption of the epithelial barrier, facilitating translocation of bacterial antigens and leading to further activation of macrophages. Cytokines produced by macrophages can also alter the secretion of mucus, contributing to H. pylori-mediated disruption of the mucous layer. Cytokines produced in the gastric mucosa induce changes in gastric-acid secretion and homeostasis (dashed lines). TNF-{alpha}, interleukin-1{beta}, and interferon-{gamma} increase gastrin release, stimulating parietal and enterochromaffin cells and thus acid secretion. TNF-{alpha} also induces a decrease in the number of antral D cells, leading to decreased somatostatin production and indirectly enhancing acid production. LPS denotes lipopolysaccharide.