Acute inflammation involves vascular and cellular events. Vascular events include hemodynamic changes like vasoconstriction and vasodilation, and permeability changes in endothelial cells. Cellular events involve the exudation of white blood cells through processes like rolling, adhesion, and chemotaxis. White blood cells then phagocytose pathogens and produce inflammatory mediators. Healing occurs through regeneration of original cells and repair by proliferation of connective tissue, forming granulation tissue through angiogenesis and fibrogenesis.
Definition of inflammation, Causes, Signs of inflammation, Types of inflammation, Triple response, Phagocytosis, Transudate or Exudate, Difference between transudate and exudate, Granuloma and Granulomatous inflammation
Inflammation- General Pathology seminar PG 1st yearDr. Ritu Gupta
this seminar includes general inflammation, its etiology, acute inflammation, features, events, fate, chronic inflammation, causes, features, types, granulomatous inflammation, acute v/s chronic inflammation, inflammatory disorders of pulp and periradicular tissues
Definition of inflammation, Causes, Signs of inflammation, Types of inflammation, Triple response, Phagocytosis, Transudate or Exudate, Difference between transudate and exudate, Granuloma and Granulomatous inflammation
Inflammation- General Pathology seminar PG 1st yearDr. Ritu Gupta
this seminar includes general inflammation, its etiology, acute inflammation, features, events, fate, chronic inflammation, causes, features, types, granulomatous inflammation, acute v/s chronic inflammation, inflammatory disorders of pulp and periradicular tissues
This is a presentation on the topic of Adaptations, Cell injury and cell death, 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
aetiology of inflammation; types of inflammation; how inflammation occur; cells involve in inflammation; role of wbc in inflammation; outcome of inflammation; how inflammation associated with immunity, clotting system, complementary system kinin system, how inflammation is associated with oral cavity; disease associated with inflammatory system
This is a presentation on the topic of Inflammation and repair, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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This is a presentation on the topic of Adaptations, Cell injury and cell death, 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
aetiology of inflammation; types of inflammation; how inflammation occur; cells involve in inflammation; role of wbc in inflammation; outcome of inflammation; how inflammation associated with immunity, clotting system, complementary system kinin system, how inflammation is associated with oral cavity; disease associated with inflammatory system
This is a presentation on the topic of Inflammation and repair, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
1. List the main components of acute inflammation. 2. Describe t.pdfarihantcomp1008
1. List the main components of acute inflammation.
2. Describe the vascular and cellular changes in acute inflammation.
3. Define the following terms pertaining to leukocyte involved in an inflammatory response:
margination, diapedesis, emigration, exudation, chenotaxis, phagocytosis, and microbicidal
substances.
4. Define the following pathologic terms: serous inflammation, fibrinous inflammation, purulent
inflammation, abscess ulcer, wound, scar, and keloid.
5. Describe the typical local and systemic symptoms of inflammation.
6. List the principal cells of acute and chronic inflammation.
1. List the main components of acute inflammation.
2. Describe the vascular and cellular changes in acute inflammation.
3. Define the following terms pertaining to leukocyte involved in an inflammatory response:
margination, diapedesis, emigration, exudation, chenotaxis, phagocytosis, and microbicidal
substances.
4. Define the following pathologic terms: serous inflammation, fibrinous inflammation, purulent
inflammation, abscess ulcer, wound, scar, and keloid.
5. Describe the typical local and systemic symptoms of inflammation.
6. List the principal cells of acute and chronic inflammation.
2. Describe the vascular and cellular changes in acute inflammation.
3. Define the following terms pertaining to leukocyte involved in an inflammatory response:
margination, diapedesis, emigration, exudation, chenotaxis, phagocytosis, and microbicidal
substances.
4. Define the following pathologic terms: serous inflammation, fibrinous inflammation, purulent
inflammation, abscess ulcer, wound, scar, and keloid.
5. Describe the typical local and systemic symptoms of inflammation.
6. List the principal cells of acute and chronic inflammation.
Solution
1. Acute inflammation is the rapid response given to injury consisting of 3 components i.e. Any
changes in veins caliber which may lead to increase of obstruction in blood flow, anatomical
changes which lead plasma protein and WBC to leave, accumulation of leucocyte at the site of
injury.
2.v vascular changes- due to injury vasodilation of superior veins mainly occur which result in
increased vascular permeability
Cellular changes- it include accumulation of WBC and plasma protein at the site of injury which
result in pus formation
3.emigration- movement from capillary and post capillary venules, exedution- transfer of blood
cells, fluid and protein from vascular system to body cavities, chemotaxis- it is the movement of
neutrophils as per concentration gradient towards chemical substance, phagocytosis- it is the
process by which cell engulf external molecule , bacteria and later on kill them, dia, pedesis-
movement of leucocyte out of circulation, margination-5 it is the process by which free flow of
leucocyte exit the blood system, microbial substances is regarded as antimicrobial agent which
is.produced by microbes and responsible to kill other microbes in dilute form.
4. Serous inflammation-it is the type of acute inflammat.
Inflammation_ Lecture material for beginners as PPT.pdfBerhanu Mekale
Organized and illustrated lecture material for better understanding of inflammation for undergraduate students. Enjoy reading and let me know if you have any questions or additional information and materials.
series of events which takes place at the time of acute inflammation includes two different kinds of, one at the vascular level and other one is at the cellular level. which works as the primary level of immunity protection and leads to the phagocytosis of the pathogenic microbes. The presence of foreign bodies such as bacteria within the bodies provokes a protective inflammatory response...characterized by redness, swelling, warmth and the pain at the site of infection. These signs are due to increased blood flow, increased capillary permeability and the escape of fluid and cells into the tissue spaces. The increased permeability is due to several chemical mediators of which histamines, prostaglandins and leukotriens are the most important ones.
Mistry Shivangi,M.Pharm Pharmacology, Assistant Professor, Bhagwan Mahavir College of Pharmacy, clinical sign of inflammation, type, chemical mediator of inflammation, wound healing
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
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It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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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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4. Hemodynamic changesHemodynamic changes
1.1. Transient vasoconstriction of ArteriolesTransient vasoconstriction of Arterioles
2.2. Persistant progressive vasodilatationPersistant progressive vasodilatation
3.3. Elevated local Hydrostatic pressureElevated local Hydrostatic pressure
4.4. Stasis of microcirculationStasis of microcirculation
5.5. WBC migrationWBC migration
5. Lewis experimentLewis experiment
1.1. Red lineRed line vasodilatationvasodilatation
2.2. FlareFlare vasodilatation of surroundingvasodilatation of surrounding
vesselsvessels
3.3. WhealWheal traqnsudation of fluid into thetraqnsudation of fluid into the
extra vascular space..extra vascular space..
6. Vascular permeability changeVascular permeability change
1.1. Endothelial contractionEndothelial contraction immediateimmediate
transienttransient
2.2. Endothelial retractionEndothelial retraction delayed anddelayed and
prolongedprolonged
3.3. Direct endothelial injuryDirect endothelial injury immediate andimmediate and
prolonged / delayed and prolongedprolonged / delayed and prolonged
4.4. Injury by WBCInjury by WBC
5.5. NeovascularisationNeovascularisation
8. Exudation of WBCExudation of WBC
1.1. Margination( formed elements widen ) andMargination( formed elements widen ) and
pavementing( PMN comes in contact wothpavementing( PMN comes in contact woth
vessel wall )vessel wall )
2.2. Rolling and adhesionRolling and adhesion
3.3. EmigrationEmigration
4.4. ChemotaxisChemotaxis
9. RollingRolling
SelectinsSelectins
Three typesThree types
1.1. E selectinE selectin in Endotheliumin Endothelium
2.2. P selectinP selectin Endo + PlatletsEndo + Platlets
3.3. L selectinL selectin WBCWBC
13. ChemotaxisChemotaxis
1.1. Bacterial ProductsBacterial Products esp. with N formylesp. with N formyl
methionine terminalsmethionine terminals
2.2. Cytokines of Chemokine family IL 8Cytokines of Chemokine family IL 8
3.3. Complements –C 3a ,C5aComplements –C 3a ,C5a
4.4. LT B4LT B4
14. Leukocyte activationLeukocyte activation
PhagocytosisPhagocytosis
Production of substances that destroysProduction of substances that destroys
phagocytosed microbesphagocytosed microbes lysosomallysosomal
enzynes , reactive oxygen and nitrogen speciesenzynes , reactive oxygen and nitrogen species
Production of mediaters that amplifyProduction of mediaters that amplify
inflemmatory reactioninflemmatory reaction AA metabolites andAA metabolites and
cytokinescytokines
15. PhagocytosisPhagocytosis
1.1. Recognition and attachment of particles toRecognition and attachment of particles to
WBCWBC
2.2. Formation of phagocytic vacouleFormation of phagocytic vacoule
3.3. Killing and degradation of ingestedKilling and degradation of ingested
substancesubstance
16.
17. HealingHealing
RegenerationRegeneration proliferation of parenchymalproliferation of parenchymal
cellscells
RepairRepair proliferation of connective tissueproliferation of connective tissue
results in fibrosis and scarringresults in fibrosis and scarring
18. RegenerationRegeneration
Proliferation of the original cells from theProliferation of the original cells from the
margin of the injurymargin of the injury
Migrated cells will differentiates and maturatesMigrated cells will differentiates and maturates
20. Granulation tissueGranulation tissue
Slightly granular and pink appearance of theSlightly granular and pink appearance of the
tissuetissue
Each granule is a new small blood vesselEach granule is a new small blood vessel
there is thin covering of fibroblasts and youngthere is thin covering of fibroblasts and young
collagencollagen
21. Granulation tissue formationGranulation tissue formation
1.1. Phase of inflammationPhase of inflammation
2.2. Phase of clearancePhase of clearance
3.3. Phase of in growth of granulation tissuePhase of in growth of granulation tissue
23. HealingHealing
Healing by First intention / Primary UnionHealing by First intention / Primary Union
Healing by second intention / secondary unionHealing by second intention / secondary union