1) Asthma is an inflammatory disease, so effective treatments should reduce inflammation. Glucocorticoids are potent anti-inflammatory drugs that are widely used to treat asthma.
2) Glucocorticoids reduce inflammation by repressing genes for inflammatory molecules. However, they can cause side effects due to systemic exposure.
3) Newer glucocorticoids are delivered directly to the lungs via inhalers to minimize systemic exposure and side effects while still reducing airway inflammation.
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
It is a anti- hypertensive drug. It is non-selective beta blocker drug. Hence it is beta blocker drug so it has many side effect.Not only Propranolol but also Timolol,Atenolol are beta blocker drugs.
Anti anginal drugs, uses, mechanism of action, adverse effectsKarun Kumar
A presentation outlining the causes of angina, mechanism of action of various anti-anginal drugs, their uses and side effects alongwith contraindications
Proton pump inhibitors (PPIs) block the gastric H,K-ATPase, inhibiting gastric acid secretion. This effect enables healing of peptic ulcers, gastroesophageal reflux disease (GERD), Barrett's esophagus, and Zollinger-Ellison syndrome, as well as the eradication of Helicobacter pylori as part of combination regimens.Proton-pump inhibitors (PPIs) are a class of medications that cause a profound and prolonged reduction of stomach acid production. They do so by irreversibly inhibiting the stomach's H+/K+ ATPase proton pump.[1]
They are the most potent inhibitors of acid secretion available.[2] Proton-pump inhibitors have largely superseded the H2-receptor antagonists, a group of medications with similar effects but a different mode of action, and antacids.[3]
PPIs are among the most widely sold medications in the world. The class of proton-pump inhibitor medications is on the World Health Organization's List of Essential Medicines.[4][5] Omeprazole is the specific listed example.[4][5]
Mechanism of action
The activation of PPIs
Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or, more commonly, the gastric proton pump) of the gastric parietal cells.[71] The proton pump is the terminal stage in gastric acid secretion, being directly responsible for secreting H+ ions into the gastric lumen, making it an ideal target for inhibiting acid secretion.[citation needed]Because the H,K-ATPase is the final step of acid secretion, an inhibitor of this enzyme is more effective than receptor antagonists in suppressing gastric acid secretion.[72] All of these drugs inhibit the gastric H,K-ATPase by covalent binding, so the duration of their effect is longer than expected from their levels in the blood.[73]
Targeting the terminal step in acid production, as well as the irreversible nature of the inhibition, results in a class of medications that are significantly more effective than H2 antagonists and reduce gastric acid secretion by up to 99%.[2
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
It is a anti- hypertensive drug. It is non-selective beta blocker drug. Hence it is beta blocker drug so it has many side effect.Not only Propranolol but also Timolol,Atenolol are beta blocker drugs.
Anti anginal drugs, uses, mechanism of action, adverse effectsKarun Kumar
A presentation outlining the causes of angina, mechanism of action of various anti-anginal drugs, their uses and side effects alongwith contraindications
Proton pump inhibitors (PPIs) block the gastric H,K-ATPase, inhibiting gastric acid secretion. This effect enables healing of peptic ulcers, gastroesophageal reflux disease (GERD), Barrett's esophagus, and Zollinger-Ellison syndrome, as well as the eradication of Helicobacter pylori as part of combination regimens.Proton-pump inhibitors (PPIs) are a class of medications that cause a profound and prolonged reduction of stomach acid production. They do so by irreversibly inhibiting the stomach's H+/K+ ATPase proton pump.[1]
They are the most potent inhibitors of acid secretion available.[2] Proton-pump inhibitors have largely superseded the H2-receptor antagonists, a group of medications with similar effects but a different mode of action, and antacids.[3]
PPIs are among the most widely sold medications in the world. The class of proton-pump inhibitor medications is on the World Health Organization's List of Essential Medicines.[4][5] Omeprazole is the specific listed example.[4][5]
Mechanism of action
The activation of PPIs
Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or, more commonly, the gastric proton pump) of the gastric parietal cells.[71] The proton pump is the terminal stage in gastric acid secretion, being directly responsible for secreting H+ ions into the gastric lumen, making it an ideal target for inhibiting acid secretion.[citation needed]Because the H,K-ATPase is the final step of acid secretion, an inhibitor of this enzyme is more effective than receptor antagonists in suppressing gastric acid secretion.[72] All of these drugs inhibit the gastric H,K-ATPase by covalent binding, so the duration of their effect is longer than expected from their levels in the blood.[73]
Targeting the terminal step in acid production, as well as the irreversible nature of the inhibition, results in a class of medications that are significantly more effective than H2 antagonists and reduce gastric acid secretion by up to 99%.[2
The presentation include basics like adrenal gland and functions. Synthesis of glucocorticoids, details of glucocorticoid receptor, Human Glucocorticoid Receptor ultra structure, and domains. The presentation give special preference to its receptor signaling and and biological effects,
4. IMPORTANT CONCEPT 1: Asthma is an inflammatory disease and thus effective treatments for the chronic management of asthma should be directed to reduce the inflammatory response www.freelivedoctor.com
5.
6. Steroid Hormones: Derived from Cholesterol Lipid Soluble: Able to cross plasma membrane by passive diffusion www.freelivedoctor.com
9. CELL TYPE FACTOR COMMENTS Macrophages Prostaglandins, Inhibition of COX-2, Monocytes Leukotrienes Phospholipase A2 IL-1, IL-6. TNF Inhib. Transcript., Release Endothelial Cells ICAM-1. ELAM-1 Inhib. Transcript., Release IL-1, Prostagl., Leuko. As above Basophils Histamine, Leukotriene Inhib. IgE Release Lymphocytes IL-1, IL-2, IL-3, etc As above Effects of Glucocorticoids on Components of Inflammatory/Immune Responses www.freelivedoctor.com
10. IMPORTANT CONCEPT 2: The anti-inflammatory and immunosuppressive actions of glucocorticoids play an important role in preventing potential damaging effects of an unopposed inflammatory response and can be exploited therapeutically www.freelivedoctor.com
12. IMPORTANT CONCEPT 3: The beneficial effects of systemic glucocorticoids to limit inflammation is counter-balanced by its many adverse side effects www.freelivedoctor.com
16. Glucocorticoid Response Unit of the PEPCK Gene CEBP/ß TBP -27 -90 -325 COUP GR GR -380 HNF3 HNF4 -410 -445 +1 Accessory DNA-binding Factors Required!! ( Can impart tissue-specificity) NOTE: Phosphoenolpyruvate carboxykinase (PEPCK) gene is glucocorticoid regulated in liver only www.freelivedoctor.com
17. IMPORTANT CONCEPT 4: Tissue- and cell type-specific effects of glucocorticoids are likely to be driven by many factors that influence the gene regulatory activity of the glucocorticoid receptor www.freelivedoctor.com
18. +1 GRE Transcriptional Activation Transcriptional Repression I ( Direct DNA-binding ) H H +1 nGRE GR H +1 cGRE GR H Transcriptional Repression II ( Co-occupancy ) +1 GR H NF B Transcriptional Repression III ( Tethering ) AP1 Basic Mechanisms of Transcriptional Activation/Repression by the Glucocorticoid Receptor www.freelivedoctor.com GR GR
20. IMPORTANT CONCEPT 5: The broad anti-inflammatory actions of glucocorticoids are due primarily to transcriptional repression of many pro-inflammatory genes in multiple cell types by the glucocorticoid receptor. www.freelivedoctor.com
24. IMPORTANT CONCEPT 6: The glucocorticoid receptor regulates gene transcription (either positively or negatively) through the gene-selective recruitment of histone modifying enzymes www.freelivedoctor.com
27. IMPORTANT CONCEPT 7: Structural modifications of the natural glucocorticoid cortisol generate hormones with enhanced half-life and more potent and efficacious glucocorticoid activity www.freelivedoctor.com
28. Lung Topical effect ~2-10% Liver First pass Metabolism (inactivation) GI Tract Mouth Deposition ~90% swallowed Lung Pulmonary absorption BLOOD STREAM Drug systemic effect + inactive metabolite Schematic representation of the disposition of inhaled drugs www.freelivedoctor.com
29. IMPORTANT CONCEPT 8: The aerosol delivery of glucocorticoids to the lungs limits systemic exposure to the hormone and greatly reduces side effects www.freelivedoctor.com
30.
31. New Approaches for Glucocorticoid Treatment of Asthma fluticasone propionate (FP) FP-17ß-carboxylic acid derivative cytochrome P450 3A4 (Liver) 1/2000 affinity for GR than FP!! www.freelivedoctor.com
32. IMPORTANT CONCEPT 9: New generation synthetic glucocorticoids with more rapid metabolism in the liver overcome potential side effects due to ingested hormone upon aerosol delivery www.freelivedoctor.com
34. IMPORTANT CONCEPT 10: New generation synthetic glucocorticoids that maintain gene repression but limit gene activation by the glucocorticoid receptor (i.e. dissociated glucocorticoids) may hold promise as anti-inflammatory drugs with reduced side effects www.freelivedoctor.com
36. Increased GRß Expression in Airway T cells of Patients with Glucocorticoid-Insensitive Asthma From: Hamid QA et al., (1999) Am J Respir Crit Care Med 159 , pp. 1600-1604 Bronchoalveolar lavage (BAL) cells and peripheral blood mononuclear cells (PBMC) www.freelivedoctor.com
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38. IMPORTANT CONCEPT 11: Disruptions in GR expression and signal transduction can contribute to corticosteroid-resistant asthma and underlie the worsening effects of stressful events on asthma symptoms. www.freelivedoctor.com
43. Leukotriene-Modifying Drugs for the Treatment of Asthma ZYFLO : 5-Lox Inhibitor SINGULAIR : Leukotriene-receptor antagonist www.freelivedoctor.com
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45. Mechanism of Action of Omalizumab (XOLAIR) Omalizumab www.freelivedoctor.com
46. Novel Therapy: Nasal Delivery of an Anti-inflammatory Peptide Omalizumab Intranasal delivery of the cytoplasmic domain of CTLA-4 using a novel protein transduction domain prevents allergic inflammation Je-Min Choi et al. (2006) Nature Medicine Vol. 12, pp 574-579 www.freelivedoctor.com
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48.
49. Novel Therapy: Nasal Delivery of an Anti-inflammatory Peptide Omalizumab Goblet cell staining Ovalbumin-induced asthma in mice PTD-linked peptide www.freelivedoctor.com
50. IMPORTANT CONCEPT 12: Anti-inflammatory drugs that act on selective targets may be effective for the treatment of asthma and are likely to have fewer side effects than glucocorticoids www.freelivedoctor.com
Editor's Notes
Glucocorticoids: Simple, derivatives of cholesterol Regulate nearly every organ system in the body Maintain homeostasis; e.g. dampen immunoresponses, regulate glucose metabolism Most prescribed class of drugs world wide (treatment of varioue inflammatory diseases)