- Asthma is associated with chronic inflammation of the lower airways, characterized by infiltration of eosinophils, mast cells, and T lymphocytes. There is thickening of the basement membrane and mucus plug formation.
- The specific pattern of airway inflammation involves mast cells, macrophages, dendritic cells, eosinophils, neutrophils, and T lymphocytes and their release of inflammatory mediators like chemokines, cytokines, leukotrienes, and prostanoids.
- Chronic inflammation leads to structural changes in the airways called airway remodeling, involving thickening of the subepithelial basement membrane, smooth muscle hypertrophy, goblet cell hyperplasia, subepithelial fibrosis,
This is a presentation on the topic of hemodynamic disorders, thromboembolic diseases and shock, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
This is a presentation on the topic of hemodynamic disorders, thromboembolic diseases and shock, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
Localised protective response elicited by injury or destruction of tissues which serves to destroy , dilute or wall off (sequester) both injurious agent and the injured tissues (Dorlands medical dictionary). Cardinal signs of inflammation
Celsus 1st century AD
Rubor – redness
Tumor -swelling
Calor -heat
Dolor -pain
Virchow
“function laesa”- loss of function
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
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:
Rapid adaptation within the first second, with further slow adaptation.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. Asthma is associated with a
specific chronic inflammation of
the mucosa of the lower
airways.
3. PATHOLOGY
• The airway mucosa is infiltrated with
activated eosinophils and T lymphocytes,
and there is activation of mucosal mast cells.
• A characteristic finding is thickening of the
basement membrane due to subepithelial
collagen deposition.
• In fatal asthma there will be thickened and
edematous wall along with occlusion of
lumen by mucus plug
4. • Mucous plug is formed by glycoproteins
secreted from goblet cells and plasma
proteins from leaky bronchial vessels.
• There is also vasodilation and angiogenesis.
• Pathologic changes are found in all
airways,but do not extend to lung
parenchyma.
5.
6. INFLAMMATION
• There is inflammation in the respiratory
mucosa from the trachea to terminal
bronchioles, but with a predominance in
bronchi.
• The specific pattern of airway inflammation
is assosciated with airway
hyperresponsiveness(AHR)
• This physiological abnormality is assosciated
with variable airflow obstruction.
• Many inflammatory cells are know to be
involved in asthma with no key cell that is
predominant.
8. MAST CELLS: Are activated by allergens through an
IgE-dependent mechanism.
• Mast cells release several bronchoconstrictor
mediators like histamine,prostaglandin D2,and
cysteinyl leukotrienses, but also several cytokines,
chemokines,growth factors and neurotrophins.
NEUTROPHILS:Increased in airways and sputum during
acute exacerbations and in the presence of smoking
• Determinant of lack of response to CS treatment
9. Macrophages and dendritic cells:
• Macrophages initiate a type of inflammatory
response via the release of certain
cytokines.
• Dendritic cells are the major antigen
presenting cells.
• Migrate to regional lymphnodes,interact with
regulatory cells to stimulate TH₂ production.
10. Eosinophils: These infiltration is a characteristic feature
of asthmatic airways.
• These are linked to the development of AHR
through the release of basic protiens and oxygen
derived free radicals.
11. T-LYMPHOCYTES
• Prominent source of cytokines
• Increased no of activated T cells(CD₄) in
airway
• TH₁ - IL-12,IFN-ɣ
• TH₂ - IL-4,IL-5,IL-9,IL-13
• TH₂ predominant in asthma
• IgE production (IL-4,IL-13)
• Eosinophilia (IL-5)
• Mucus secretion(IL-13)
• Airway hyper responsiveness (IL-13)
13. CHEMOKINES:
• Recruitment or chemotaxis of inflammatory cells
• Additional signalling function
• Attractive target for therapy
CYTOKINES:
• Multiple cytokines regulate chronic inflammation of
asthma
• The TH2 cytokines IL-4,IL-5 and IL-13 mediate allergic
reaction
• TNF-α and IL-1β, amplify the inflammatory response
• Thymic stromal lymphopoietin causes release of
chemokines that attract TH2 cells.
14. Leukotrienes
• Arachidonic acid metabolites
• Rapidly synthesised within minutes,following
activation
• LT C4,D4,E4 potent bronchoconstrictors
• Produced by several cell types including
eosinophils,mast cells
• Also increase mucus secretion
• Facilitate plasma leak,generating airway
edema
15. PROSTANOIDS:
• Arachidonic acid metabolites via COX pathway
• PGD₂,PGF₂,TXA₂ potent bronchoconstrictors
• Produced by eosinophils,mast cells
• PGD₂ predominant prostanoid involved.
16.
17. NITRIC OXIDE:
• Role unclear
• Low levels,a bronchodilator & vasodilator
• Higher levels of NO in asthma
• NO react with superoxide anion in inflamed
tissue to produce biologic oxidants
• Level of severity of airway inflammation
• Exhaled NO tool to reflect airway
inflammation
18. AIRWAY EPITHELIUM is central to
pathogenesis of ASTHMA
• Epithelial stimulation to epithelial
shedding,even extensive areas of
denudation
• Injured & stimulated epithelial cells secrete
GM-CSF,IL-1,IL-8,RANTES.
• Significant denudation of epithelium itself
result in variety of secondary effects
19. • Loss of barrier function permit direct access
of allergens on tissue cells (eg; mast cells)
• Loss of epithelial cells reduces ability to
degrade peptide and kinin mediators and to
secrete EDRF(which maintain dilatation)
• Sensory nerve exposure promote
inflammation and bronchoconstriction
• Provoke proliferation of
myofibroblasts,secretion of extracellular
matrix protein(collagen) leading to thickened
basement membrane
20.
21. EXTRACELLULAR MATRIX
• Prominent structural feature in Asthma
• Thickening of lamina reticularis
• Denuded epithelium expose BM to airspace
• Subepithelium is enlarged and dense by
deposition of collagen,fibronectin,laminin….
• Epithelial cells and myofibroblasts contribute
to thickening
• GF:TGF B,PDGF,FGF,endothelin
22. FIBROBLASTS AND
MYOFIBROBLASTS
• Abnormal mesenchymal cell proliferation &
no of Fibroblasts,Myofibroblasts ↑ed.
• MFB- tissue remodelling by releasing ECM
components elastin,fibronectin,laminin.
• Allergen challenge ↑no of MFB
• Role : contractile
response,mitogenesis,synthetic and
secretory.
• Release RANTES
23. SMOOTH MUSCLE CELLS
• Excess accumulation of bronchial smooth muscle
cells prominent feature of airway wall remodeling
• pro-activating signals for converting airway smooth
muscle cells into a proliferative and secretory cell in
asthma are unknown, but may include viruses and
IgE
• Another mechanism regulating smooth muscle
proliferation is through production of
metalloproteinase (MMP)-2
• Nonspecific BHR is a basic mechanism underlying
the excessive smooth muscle contraction and
airway narrowing
24. NERVES
• Dysfunction of the airway innervation in asthma contributes
to its pathophysiology.
• β-Adrenergic blockers and cholinergic agonists are known
to induce bronchoconstriction and produce symptoms of
asthma.
• Nonadrenergic noncholinergic (NANC) neural pathways
involving new neuromediators, such as bradykinin,
neurokinin, vasoactive intestinal peptide (VIP), and
substance P.
• These neuromediators produce in vitro and in vivo features
of clinical asthma involving bronchoconstriction,
vasodilation, and inflammation.
• The NANC system has been proposed as an explanation
for bronchial hyperreactivity .
25. BLOOD VESSELS
• Airway wall remodeling in asthma involves a number
of changes including increased vascularity,
vasodilation, and microvascular leakage.
• number and size of bronchial vessels is moderately
increased.
• neovascularization or angiogenesis is still unclear.
• Vascular endothelial growth factor (VEGF) levels
are variable in asthmatic airways suggesting a low
degree of angiogenesis in patients with controlled
asthma.
26. GLANDS
• Bronchial hypersecretion is the consequence of
hypertrophy and hyperplasia of submucosal glands
and epithelial goblet cells.
• Increased mucus will certainly result in sputum
production and contribute to excessive airway
narrowing.
• The replacement of ciliated cells by goblet cells
contributes to airway remodeling in asthma.
• Impaired clearance of mucus is present during
exacerbations and is a potential important
contributor to fatal asthma.
27. AIRWAY HYPERRESPONSIVENESS
• Increased smooth muscle sensitivity and contracture
• Dysfunctional neuroregulation
• Increased maximal contraction of bronchial muscle
as consequence of reduction/uncoupling of
opposing forces (elastic recoil)
• Airway wall edema result in functional detachment
of alveolar walls
• Thickening of airway wall due to chronic
inflammation ,result in increased resistance to
airflow