Acute inflammation is characterized by rapid onset, short duration, and neutrophil infiltration. It serves to destroy, dilute, or wall off injurious agents. The key steps are vascular changes that increase blood flow and permeability, allowing plasma proteins and leukocytes to exit circulation and reach injured tissues. Leukocytes are recruited through chemotaxis and remove pathogens via phagocytosis. Mediators like histamine and prostaglandins regulate vascular changes and leukocyte behavior. Common patterns include purulent inflammation seen in abscesses and serous inflammation seen in effusions. Acute inflammation typically resolves completely or leads to scarring, and can progress to chronic inflammation if the cause persists.
Introduction, History , Types of inflammation, Cellular events, Vascular events, Morphology of inflammation, Systemic effects of inflammation, Fate of inflammation
Introduction, History , Types of inflammation, Cellular events, Vascular events, Morphology of inflammation, Systemic effects of inflammation, Fate of inflammation
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
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
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
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
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
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
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
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
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
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.
1. Item-05 and 06
Inflammation
Acute Inflammation
Dr. A K M Maruf Raza
Associate Professor of Pathology
Based on Robbins and Cotran
9th edition
2. Inflammation
Inflammation is a protective response essential
for survival.
It serves to protect the host from both the
initial cause of cell injury (microbes, toxins)
and the consequences of such injury.
The mediators of defense against infection
include phagocytic leukocytes (nutrophils,
macrophages), antibodies and complement
proteins.
2
3. Inflammation
The process of inflammation delivers these
cells and proteins to damaged or necrotic
tissues and microbes.
Activates them to get rid of the harmful or
unwanted substances.
Without inflammation, infections would go
unchecked, wounds would never heal, and
injured tissues might remain permanent
festering sores. 3
4. Sequential steps of inflammatory
reaction
The steps of the inflammatory response can be
remembered as the five R:
(1) recognition of the injurious agent
(2) recruitment of leukocytes
(3) removal of the injurious agent
(4) regulation (control) of the response
(5) resolution (repair)
4
5. Inflammation; Definition:
Inflammation is a response of:
i. vascularized tissues to infections and
damaged tissues
ii. that brings cells and molecules of host
defense from the circulation to the sites
where they are needed
iii. in order to eliminate the offending agents.
5
7. Types of inflammation
Acute inflammation:
The initial, rapid response to infections and tissue
damage is called acute inflammation.
i. rapid in onset (seconds or minutes)
ii. short duration, lasting for minutes to
several hours or a few days.
iii. predominant cell is neutrophil.
iv. characteristic features are exudation of
fluid and plasma protein and
emigration of neutrophils.
7
8. Types of inflammation
Chronic inflammation:
If acute inflammation fails to clear the offending
agent, it may progress to a long period phase
is called chronic inflammation.
i. is of longer duration.
ii. associated with presence of lymphocyte
and macrophages.
iii. and proliferation of blood vessels and
deposition of connective tissue (fibrosis)
8
9. Acute inflammation VS Chronic inflammation
Feature Acute Chronic
Onset Fast: minutes to
hours
Slow: weeks to
days
Cellular
infiltrate
Mainly
neutrophils
Lymphocytes,
Monocytes/
macrophages
Tissue injury
and fibrosis
Usually mild and
self-limited
Often severe and
progressive
Local and
systemic signs
Prominent Less 9
10. Advantage of inflammation
Inflammation usually functions in a beneficial
manner.
It serves to destroy, dilute or wall off the
injurious agent.
Remove necrotic debris and other exudates.
Prepare the remaining tissue framework for
tissue repair.
10
11. Disadvantage of inflammation
Often accompanied by local tissue damage.
May underlie some life threatening
hypersensitivity reactions to insect bites,
drugs and toxins.
Sometimes associated with common
chronic diseases such as rheumatoid
arthritis, atherosclerosis, crohn disease.
11
12. Cardinal signs of inflammation
Celsus, first listed the four cardinal signs:
1. Rubor- redness
2.Tumor- swelling
3. Calor- heat
4. Dolor- pain
Rudolf Virchow in the 19th century added:
5. loss of function (Functio laesa).
So there are five cardinal signs of inflammation.
12
13. Causes of Inflammation
Inflammatory reactions may be triggered by a variety
of stimuli:
i. Infections (bacterial, viral, fungal,
parasitic) and microbial toxins are the
most common and medically important
causes of inflammation.
ii. Tissue necrosis elicits inflammation in
myocardial infarction, trauma, physical
and chemical injury.
13
14. Causes of Inflammation
iii. Foreign bodies (splinters, sutures).
Even endogenous substances in excess
amount such as urate crystals (gout).
iv. Immune reactions (hypersensitivity):
are reactions in which the protective immune
system damages own tissues.
Immune responses may be directed against
self antigens, causing autoimmune diseases,
or may be against environmental substances,
as in allergies. 14
16. Acute Inflammation
Acute inflammation is the inflammation of
rapid in onset, has relatively short duration
characterized by exudation of fluid and
plasma protein and emigration of
leukocytes predominantly neutrophils.
Example: Acute tonsillitis, Acute appendicitis,
Acute cholecystitis, Abscess, Boil.
16
17. Acute inflammation: Terminology
Exudate: An exudate is an inflammatory
extravascular fluid that has high protein
concentration, cellular debris, and a specific
gravity above 1.020.
Transudate: Is a fluid with low protein
content, and a specific gravity below 1.020
caused by increased hydrostatic pressure
or reduced plasma osmotic pressure.
17
18. Exudate VS Transudate
Exudate
Inflammatory fluid
Total protein more than 30gm/L
Protein as plasma
Fibrinogen present so clot is formed
Plenty of inflammatory cells,
neutrophils or lymphocytes
Specific gravity more than 1.020
Transudate
Non inflammatory fluid
Less than 10gm/L
Practically all albumin
Not present, no clot
A few cells may be present
Specific gravity less than 1.012
19. Three components of the acute
inflammation
1. Dilation of the vessels leading to an increase
in blood flow,
2. Increased permeability of the
microvasculature causing plasma proteins and
leukocytes to leave the circulation,
3. Emigration of the leukocytes from the
microcirculation, accumulation and activation
to eliminate the offending agent. 19
20. Reactions of Blood Vessels in Acute
Inflammation
The vascular reactions of acute inflammation
consist of:
i. changes in the flow of blood and the
permeability of vessels
ii. Maximize the movement of plasma
proteins and leukocytes out of the
circulation and into the site of
infection or injury.
20
21. Vescular reaction in Acute
Inflammation
1. Changes in Vascular Flow and Caliber.
2. Increased Vascular Permeability.
(Vascular Leakage)
21
22. Changes in Vascular Flow and Caliber
Vasodilation is induced by histamine on
vascular smooth muscle causing increased
blood flow, causing heat and redness at the
site of inflammation.
Vasodilation is quickly followed by increased
permeability of the microvasculature with the
outpouring of protein-rich fluid into the
extravascular tissues.
22
24. Increased Vascular Permeability
(Vascular Leakage)
Mechanisms for increased vascular permeability:
i. Contraction of endothelial cells resulting in
increased interendothelial spaces (most common
mechanism).
ii. Endothelial injury, resulting in endothelial cell
necrosis and detachment.
iii. Transcytosis, transport of fluids and proteins
through the endothelial cell involving intracellular
channels.
24
26. Leukocyte Recruitment to Sites of
Inflammation
The changes in blood flow and vascular
permeability are quickly followed by an influx
of leukocytes into the tissue.
These leukocytes (neutrophils, macrophages)
ingest and destroy bacteria and other
microbes, as well as necrotic tissue and
foreign substances.
26
27. Leukocyte recruitment to sites of
inflammation
The journey of leukocytes from the vessel lumen to the
tissue is a multistep process:
1. In the lumen of blood vessel: margination,
rolling, and adhesion to endothelium.
2. Migration across the endothelium and vessel
wall.
3. Exiting from the vessel migration in the
tissues towards injurious agent (chemotaxis).27
28. margination, rolling, and adhesion to
endothelium
Vascular endothelium in normal state does not
bind circulating cells. In inflammation, the
endothelium is activated and can bind
leukocytes.
In inflammation hemodynamic conditions
changes and white cells comes along the
endothelial surface.
This process of leukocyte redistribution is
called margination.
28
29. In the lumen: margination, rolling, and
adhesion to endothelium
The leukocytes adhere transiently to the
endothelium, detach and bind again which is
called rolling.
This rolling is mediated by a family of proteins
called selectins and intigrins.
The next step is migration of the leukocytes
through the endothelium called transmigration
or diapedesis.
29
31. Chemotaxis of Leukocytes
After exiting the circulation, leukocytes move
in the tissues toward the site of injury by a
process called chemotaxis.
Chemotaxis is defined as locomotion along a
chemical gradient.
The chemical gradient (chemoattractants) can
be both exogenous and endogenous
substances.
31
32. Chemotaxis
The Chemoattractants causing chemotaxis are:
i. Exogenous: bacterial protein, bacterial
cell membrane lipids.
ii. Endogenous: Cytokines IL8, complement
system C5a, Leukotriene-B4.
32
33. Phagocytosis and Clearance
of the Offending Agent
Phagocytosis, or “cell eating” is the process
by which a cell engulfs a particle and digests it.
Destruction of microbes is caused by free
radicals (ROS, NO) generated in activated
leukocytes and lysosomal enzymes.
There are three steps of phagocytosis.
33
34. Phagocytosis
i. Recognition and attachment of the particle to
be ingested by the leukocytes.
ii. Engulfment of the particle with subsequent
formation of a phagocytic vacuole
(phagosome).
iii. Killing or Degradation of the ingested
material by free radicals (ROS, NO) generated
in activated leukocytes and lysosomal
enzymes (Phagolysosome).
34
36. Mediators of inflammation
The mediators are the substances that
initiate and regulate inflammatory reactions.
Active mediators are produced only in
response to various stimuli.
Most of the mediators are short-lived.
One mediator can stimulate the release of
other mediators. 36
37. Mediators of inflammation
Mediators are either secreted by cells or generated
from plasma proteins.
1. Cellular/ Cell derived mediators :
a) Preformed mediators: Histamine,
Serotonin, lysosomal enzymes.
b) Newly synthesized: Prostaglandins,
Leukotrienes, Cytokines.
2. Plasma derived mediators:
Complement: C3a, C5a, C3b, C5b-9.
37
38. Role of Mediators in different Reactions of
inflammation
Reaction of inflammation Principal Mediators
Vasodilation Histamin, Prostaglandins
Increased vascular
permiability
Histamin, Serotinin
Leukotriens C4,D4,E4
Chemotaxis, leukocyte
recruitment and activation
TNF, IL-1
Leukotriene B4
Fever IL-1,TNF
Prostaglandins
Pain Prostaglandin
Bradykinin
40. Morphologic Pattern of Acute
Inflammation
The morphologic hallmarks of acute
inflammatory reactions are dilation of small
blood vessels and accumulation of leukocytes
and fluid in the extravascular tissue.
Special morphologic patterns are often provide
valuable clues about the underlying cause.
40
41. Morphologic Pattern of Acute
Inflammation
1. Purulent (Suppurative) Inflammation
(Abscess):
It is characterized by production of large
amount of pus consisting of dead or dying
neutrophils, necrotic cells and tissue debris.
It usually caused by pyogenic bacteria.
Abscess is the localized collection of purulent
inflammatory tissue (Pus).
41
42. Morphologic Patterns of Acute
Inflammation
2. Serous inflammation: Characterized by
accumulation of serous fluid. Skin blister,
Pleural and pericardial effusion.
3. Fibrinous inflammation: Accumulation of fibrin
rich fluid in the extracellular space. Inflammation
in the lining of body cavities (meninges,
pericardium and pleura).
4. Ulcer: An ulcer is a local defect or excavation of
the surface of an organ or tissue produced by
the shedding of inflamed necrotic tissue.
42
43. Outcome of acute Inflammation
1. Complete resolution.
2. Healing by connective tissue replacement
(scarring or fibrosis).
3. Progression to chronic inflammation
43