Pathogenesis of bronchial asthma
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Bronchial asthma is a chronic inflammatory airway disease typically caused by an immunologic reaction. Key cells involved include eosinophils, mast cells, T-lymphocytes, neutrophils and basophils which release mediators that cause bronchoconstriction, mucus production and other symptoms. Asthma is classified based on frequency and severity from mild intermittent to severe persistent. The pathogenesis includes atopic asthma triggered by allergens as well as non-atopic asthma triggered by respiratory infections, stress or other environmental factors. Histopathology findings include thickening of the airway walls and remodeling of the airways.
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This document provides an overview of COPD (chronic obstructive pulmonary disease). It defines COPD and discusses its burden, risk factors, pathology, and history. It notes that COPD is characterized by airflow limitation caused by an inflammatory response in the lungs to noxious particles. The document outlines the learning objectives which are to understand COPD definition, burden, risk factors, and pathogenesis. It also discusses the prevalence of COPD internationally, underdiagnosis in the US, and the economic and social burden of the disease.
01_IJPBA_2029_23.pdf
This document summarizes recent research on using phytochemicals (phytoleads) to treat respiratory disorders. It discusses how abnormal angiogenesis contributes to diseases like lung cancer and COPD. Phytochemicals have anti-inflammatory and antioxidant properties and have shown efficacy in treating respiratory inflammation. Conditions like asthma involve inflammation in the respiratory tract while COPD involves inflammation from smoke exposure. Oxidative stress and inflammation activate pathways that promote angiogenesis. Phytochemicals may target these pathways and related mediators like VEGF to help treat respiratory diseases.
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Asthma is characterized by airway inflammation and constriction leading to reversible airflow obstruction. Most asthma begins in childhood due to sensitization to common inhaled allergens like dust mites, cockroaches, animal dander, fungi and pollen. These allergens stimulate immune cells that cause inflammation and excess mucus in the lungs. The inflammation results in thickened airway walls, increased mucus production, and smooth muscle constriction causing breathing difficulties. Long term inflammation can damage the airway walls over time.
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Corticosteroids are the most effective treatment for asthma. They work by suppressing the chronic inflammation in the airways that is characteristic of asthma. This inflammation is mediated by increased expression of inflammatory genes regulated by transcription factors like NF-κB. Corticosteroids suppress these inflammatory genes by reversing the histone acetylation that activates them. This involves binding of glucocorticoid receptors to coactivators and recruitment of histone deacetylases, switching off the inflammatory gene expression. Understanding this molecular mechanism of corticosteroid action may help develop new anti-inflammatory therapies for asthma.
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The document provides an overview of the immune system and inflammation. It discusses the inflammatory response process, including the vascular and cellular stages. It describes the signs of inflammation (rubor, tumor, calor, dolor, functio laesa) and cells involved in inflammation like neutrophils, eosinophils, basophils, and monocytes. It also discusses mediators of inflammation like kinins, complement system, histamine, serotonin, arachidonic acid metabolites, platelet activating factor, cytokines, and nitric oxide. Finally, it covers acute phase response, types of inflammation (acute vs chronic), and factors that influence wound healing.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Physiology of Chemical Sensation of smell.pdf
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
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Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
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Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Pathogenesis of bronchial asthma
- 1. PATHOGENESIS OF BRONCHIAL ASTHMA Presenter: Gopal Kr. Yadav Group E 02/17/18
- 2. OBJECTIVES: DEFINITION CELLS AND CELLULAR MEDIATORS CLASSIFICATION PATHOGENESIS HISTOPATHOLOGY 02/17/18
- 3. Definition: Asthma is a chronic inflammatory disorder of the conducting airways, usually caused by an immunologic reaction, which is marked by episodic bronchoconstriction due to increased airways sensitivity to a various stimuli ; and increased mucous production. 02/17/18
- 4. Cells involved in chronic allergic inflammation 1. Eosinophils 2. Mast cells 3. T-lymphocytes 4. Neutrophils 5. Basophils 6. APC
- 5. CELLULAR MEDIATORS a) 1st Group Of Mediators LTC4 , LTD4, LTE4: Vasoconstriction, inc. Vascular permeability. Ach: smooth muscle contraction. b) 2nd Group Histamine : bronchoconstriction PGD2: bronchoconstriction, vasodialation PAF: Platelet aggregation and release of serotonin. 02/17/18
- 6. Cont… c) 3rd Group IL-13: mucus production IL-1, TNF, IL-4, eotaxin, Nitric Oxide, bradykinin. 02/17/18
- 7. Classification based on frequency and severity: Mild intermittent Mild Moderate Severe persistent 02/17/18
- 8. 02/17/18
- 9. Asthma Pathogenetic Types: 1. Extrinsic (Atopic/Allergic/Immune) 2. Intrinsic (Idiosyncratic/Non Atopic) Others: Seasonal Exercise – induced Drug – induced Occupational Asthmatic bronchitis in smokers02/17/18
- 10. Atopic asthma
- 11. 02/17/18
- 12. Non atopic asthma (Unknown mechanism) Respiratory infection Stress Exercise Cold temperature Drug induced (aspirin)
- 13. 02/17/18
- 14. 02/17/18 Asthma- Histopathology Airway remodeling: thickening of basement membrane of bronchial epithelium. edema and inflammatory infiltrate. Hypertrophy of sub mucosal glands and bronchial wall muscle.
- 15. 02/17/18
- 17. Important fact: IL-13 gene polymorphism is strongly associated with Bronchial asthma. ADAM-33 is another gene causing proliferation of smooth muscles and fibroblasts in bronchi resulting in bronchial and sub epithelial fibrosis. 02/17/18
- 18. REFERENCES: Robbin’s Pathology, 9th Edition Harrison’s Principles of Internal Medicine, 18th Edition Harsh Mohan’s textbook of Pathology, 6th Edition. 02/17/18
- 19. 02/17/18