This document outlines the key topics and contents covered in a lecture on inflammation. The lecture objectives are to describe the signs of inflammation, differentiate between acute and chronic inflammation, explain the morphological types of inflammation, and describe the mechanisms of healing and repair. The contents include definitions of inflammation, the stages and mediators of inflammation, morphological patterns of acute and chronic inflammation, and the process of repair and healing.
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.
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.
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
“Inflame” redirects here. For the 2017 Turkish film, see
Inflame (film).
Toes inflamed by chilblains
Inflammation (from Latin inflammatio) is part of the
complex biological response of body tissues to harmful
stimuli, such as pathogens, damaged cells, or irritants,[1]
and is a protective response involving immune cells,
blood vessels, and molecular mediators. The function of
inflammation is to eliminate the initial cause of cell injury,
clear out necrotic cells and tissues damaged from
the original insult and the inflammatory process, and to
initiate tissue repair.
The classical signs of inflammation are heat, pain, redness,
swelling, and loss of function. Inflammation is a
generic response, and therefore it is considered as a mechanism
of innate immunity, as compared to adaptive immunity,
which is specific for each pathogen.[2] Too little
inflammation could lead to progressive tissue destruction
by the harmful stimulus (e.g. bacteria) and compromise
the survival of the organism. In contrast, chronic
inflammation may lead to a host of diseases, such as hay
fever, periodontitis, atherosclerosis, rheumatoid arthritis,
and even cancer (e.g., gallbladder carcinoma). Inflammation
is therefore normally closely regulated by the body.
Inflammation can be classified as either acute or chronic.
Acute inflammation is the initial response of the body to
harmful stimuli and is achieved by the increased movement
of plasma and leukocytes (especially granulocytes)
from the blood into the injured tissues. A series of biochemical
events propagates and matures the inflammatory
response, involving the local vascular system, the
immune system, and various cells within the injured tissue.
Prolonged inflammation, known as chronic inflammation,
leads to a progressive shift in the type of cells
present at the site of inflammation, such as mononuclear
cells, and is characterized by simultaneous destruction
and healing of the tissue from the inflammatory process.
Inflammation is not a synonym for infection. Infection
describes the interaction between the action of microbial
invasion and the reaction of the body’s inflammatory response
— the two components are considered together
when discussing an infection, and the word is used to imply
a microbial invasive cause for the observed inflammatory
reaction. Inflammation on the other hand describes
purely the body’s immunovascular response, whatever the
cause may be. But because of how often the two are
correlated, words ending in the suffix -itis (which refers
to inflammation) are sometimes informally described as
referring to infection. For example, the word urethritis
strictly means only “urethral inflammation”, but clinical
health care providers usually
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
“Inflame” redirects here. For the 2017 Turkish film, see
Inflame (film).
Toes inflamed by chilblains
Inflammation (from Latin inflammatio) is part of the
complex biological response of body tissues to harmful
stimuli, such as pathogens, damaged cells, or irritants,[1]
and is a protective response involving immune cells,
blood vessels, and molecular mediators. The function of
inflammation is to eliminate the initial cause of cell injury,
clear out necrotic cells and tissues damaged from
the original insult and the inflammatory process, and to
initiate tissue repair.
The classical signs of inflammation are heat, pain, redness,
swelling, and loss of function. Inflammation is a
generic response, and therefore it is considered as a mechanism
of innate immunity, as compared to adaptive immunity,
which is specific for each pathogen.[2] Too little
inflammation could lead to progressive tissue destruction
by the harmful stimulus (e.g. bacteria) and compromise
the survival of the organism. In contrast, chronic
inflammation may lead to a host of diseases, such as hay
fever, periodontitis, atherosclerosis, rheumatoid arthritis,
and even cancer (e.g., gallbladder carcinoma). Inflammation
is therefore normally closely regulated by the body.
Inflammation can be classified as either acute or chronic.
Acute inflammation is the initial response of the body to
harmful stimuli and is achieved by the increased movement
of plasma and leukocytes (especially granulocytes)
from the blood into the injured tissues. A series of biochemical
events propagates and matures the inflammatory
response, involving the local vascular system, the
immune system, and various cells within the injured tissue.
Prolonged inflammation, known as chronic inflammation,
leads to a progressive shift in the type of cells
present at the site of inflammation, such as mononuclear
cells, and is characterized by simultaneous destruction
and healing of the tissue from the inflammatory process.
Inflammation is not a synonym for infection. Infection
describes the interaction between the action of microbial
invasion and the reaction of the body’s inflammatory response
— the two components are considered together
when discussing an infection, and the word is used to imply
a microbial invasive cause for the observed inflammatory
reaction. Inflammation on the other hand describes
purely the body’s immunovascular response, whatever the
cause may be. But because of how often the two are
correlated, words ending in the suffix -itis (which refers
to inflammation) are sometimes informally described as
referring to infection. For example, the word urethritis
strictly means only “urethral inflammation”, but clinical
health care providers usually
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
Inflammation is the body's mechanism for coping with agents that could damage it.
In other words, inflammation is a protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces.
Although the processes of acute and chronic inflammation are an important protective mechanism used by the body to deal with potentially damaging agents, they are potentially damaging to the body and must be closely regulated.
Inflammation is a fundamental process for human survival, this lecture covers the basics of the process, its components and affects. Developing an understanding of this process will enable the student to comprehend this omnipresent process and how it is directly linked to our survival.
Normal Labour/ Stages of Labour/ Mechanism of LabourWasim Ak
Normal labor is also termed spontaneous labor, defined as the natural physiological process through which the fetus, placenta, and membranes are expelled from the uterus through the birth canal at term (37 to 42 weeks
Model Attribute Check Company Auto PropertyCeline George
In Odoo, the multi-company feature allows you to manage multiple companies within a single Odoo database instance. Each company can have its own configurations while still sharing common resources such as products, customers, and suppliers.
Francesca Gottschalk - How can education support child empowerment.pptxEduSkills OECD
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A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
Read| The latest issue of The Challenger is here! We are thrilled to announce that our school paper has qualified for the NATIONAL SCHOOLS PRESS CONFERENCE (NSPC) 2024. Thank you for your unwavering support and trust. Dive into the stories that made us stand out!
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2. Topic Outcomes
At the end of this lecture, students are able to :
1.Describe orally the signs of inflammation
2.Describe and differentiate in written between
acute and chronic inflammation
3.Explain the morphological of types of
inflammation
4.Describe in written the mechanism of healing
and repairing
3. CONTENTS
2.1: Definitions & Concepts Of Inflammation
2.2: Stages Of Inflammation
2.3: Mediators Of Inflammation
2.4: Morphologic Pattern Of Acute & Chronic
Inflammation
2.5: Repair Or Healing
3
4. 2.1: Definitions & Concepts Of
Inflammation
• The local response of living mammalian
tissues to injury due to any agent.
• Body defense reaction in order to eliminate or
limit the spread of injurious agent as well as to
remove the consequent necrosed cells and
tissues.
4
5. • Causes of inflammation;
i. Physical agent e.g. mechanical trauma, radiation
etc.
ii. Chemical agent e.g. simple chemical poisons,
organic poisons
iii. Infective agents e.g. bacteria, viruses, parasites,
their toxins
iv. Immunological agents e.g. Ag-Ab reaction, cell
mediated
5
6. • Involves 2 basic
processes (overlapping):
Inflammatory • Have protective role
response against injurious agents
• Cause considerable
harm to the body
healing eg; anaphylaxis,
atherosclerosis etc
6
7. Signs of Inflammation
• The famous 4 cardinal signs of inflammation:
(i) rubor (redness)
(ii) tumor (swelling)
(iii) calor (heat)
(iv) dolor (pain)
Added latest – functio laesa (loss of function)
7
10. • Acute inflammation
– Short duration & represents the early body
reaction and usually followed by repair
– The main features :
(a) Accumulation of fluid & plasma at the
affected site
(b) Intravascular activation of platelets
(c) Polymorphonuclear neutrophils as
inflammatory cells
10
11. • Chronic Inflammation
- longer duration and occurs either :
(a) after the causative agent of acute
inflammation persists for a long
time
(b) Stimulus that induces chronic
inflammation from the beginning
- main features :
presence of chronic inflammatory cells
(lymphocytes, plasma cells and
macrophages)
12. I) ACUTE INFLAMMATION
• The changes can be conveniently described
under:
(i) Vascular events
(ii) Cellular events
Infected toenail showing the characteristic redness and
swelling associated with acute inflammation
13
13. (i) VASCULAR EVENTS
• Alteration in the microvasculature
(arterioles, capillaries & venules)
• Earliest response to tissue injury
• Alterations includes:
(a) haemodynamic changes
(b) changes in vascular permeability
14
14. (a) Haemodynamic Changes
• Earliest features of inflammatory response
result from changes in the vascular flow and
calibre of small blood vessels in the injured
tissue
15
15. The sequence of these changes:
Transient vasoconstriction
Persistent progressive vasodilatation
Local hydrostatic pressure
Slowing or stasis
Leucocytic margination
16
16. • Lewis Triple Response/ red line response;
(Eg: form stroking with a blunt point)
i. Red line : Appears a few second;
Capillary & venules dilatation
ii. Flare : Bright reddish
appearance/flush surrounding
the red line; Anteriolar dilation
iii. Wheal : Swelling or oedema of the
surrounding skin occurring due
to transudation of fluid into the
extravascular space 17
18. (b) Altered vascular permeability
• Vascular changes begin quickly after the injury
but may develop at variables rates, depending on
the nature & severity of the original injury.
• The interchange of fluid between the vascular &
extra vascular space results from balance of fluid
into the vascular space or out into the tissues;
i. Hydrostatic pressure
ii. Oncotic pressure - protein
iii. Osmotic pressure
iv. Lymph flow
19
19. Fluid interchange between blood and
extracellular fluid (ECF). (HP = Hydrostatic
pressure, OP = Osmotic pressure)
NO
OEDEMA OEDEMA
20
27. e) Neovascularisation
• Microvasculature : All levels
• Response type :
Any type
• Pathogenesis :
Angiogenesis, vascular endothelial growth
factor (VEGF)
• Examples : Healing, tumors
29
28. ii) CELLULAR EVENTS
• Cellular events; cells of the acute inflammatory
response are the neutrophils, monocytes &
macrophages.
Polymorphonuclear neutrophils (PMNs)
(within 24 hrs; Life long 24-48 hrs)
Monocytes
Macrophages
(24-48 hrs; Survive much longer) 30
29. • The movements of neutrophils out of the vessels
& their role in combat can be divided into 5
steps;
i. Margination = ?
ii. Adhesion = ?
iii. Emigration/ diapedesis=?
iv. Chemotaxis = ?
v. Phagocytosis & degranulation=?
31
30. • Concentrates the leucocytes adjacent to endothelial
wall- Margination
• Adherence of inflammatory cell to the endothelium/
vascular basement membrane- Adhesion
• Neutrophil lodged between endothelial cell and
basement membrane and escape out into the
extravascular space- Diapedesis
• Chemotactic factor mediated transmigration of
leucocytes to reach the interstitial tissue- Chemotaxis
• The process of engulfment of solid particulate material
bt the cell (cell eating)- Phagocytosis
32
34. FATE OF ACUTE INFLAMMATION
• Acute inflammation generally has one of FOUR
(4) outcomes;
i. Resolution – complete return to normal/ tissue
changes are slight and cellular changes are
reversible eg; resolution in lobar pneumonia
ii. Healing by scarrimg– tissue destruction is
extensive, no tissue regeneration; healing by
fibrosis
36
35. iii) Suppuration – the progression process of
severe necrosis cause by pyogenic bacteria;
neutrophilic infiltration; form an abcess;
abcess – organised by dense fibrous tissue
and get calcified
iv) Progression to chronic inflammation may
follow acute inflammation, although signs
of chronic inflammation may be present at
the onset of injury; healing proceed side by
side.
37
36. An abscess on the skin, showing the redness and swelling characteristic of inflammation. Black rings of
necrotic tissue surround central areas of pus
38
37. II) CHRONIC INFLAMMATION
• Chronic inflammation;
prolonged process in which tissue
destruction and inflammation occur
at the same time.
39
38. • Caused one of the following 3 ways:
i) Chronic inflammation following acute
inflammation – the tissue destruction is
extensive, or bacteria survive & persist in
small numbers at the site of acute
inflammation
ii) Recurrent attacks of acute inflammation –
repeated bouts of acute inflammation eg;
repeated acute infection of gallbladder
chronic cholecystitis
iii) Starting de novo – infection with organisms
of low pathogenecity (chronic from the
beginning) 40
39. • General features of Chronic inflammation:
i. Infiltration with mononuclear cells
Infiltrated by mononuclear inflammatory cells :
phagocytes & lymphoid cells
phagocytes : circulating monocytes, tissue
macrophages, epithelioid cells, multinucleated
giants cells
ii. Tissue destruction
Central feature of lesions
iii. Proliferative changes
Result of necrosis, proliferation of small vessels
and fibroblasts; healing by fibrosis and collagen
41
40. Systemic effects of chronic
inflammation
Associated with following systemic features:
1. Fever – mild fever, loss of weight and
weakness
2. Anemia – varying degree of anemia
3. Leucocytosis - general
4. ESR – elevated in all cases
5. Amyloidosis – long term cases of chronic
suppurative inflammation (secondary
systemic (AA) amyloidosis 42
41. Types of chronic inflammation
NON-SPECIFIC SPECIFIC
• Formation of granulation • Injurious agent causes a
tissue and healing by characteristic histologic
fibrosis tissue response
• Eg; Chronic osteomyelitis, • Eg;
Chronic ulcer tuberculosis, leprosy, syphili
s
43
42. Types of chronic inflammation (based
on histological classification)
CHRONIC NON-SPECIFIC CHRONIC GRANULOMATOUS
INFLAMMATION INFLAMMATION
• Characterised by: • Formation of granulomas
(a) non-specific • Eg;
inflammatory cell tuberculosis, leprosy, syphili
infiltration eg; chronic s, sarcoidosis
osteomyelitis, lung abcess
(b) Infiltration by
polymorphs and abcess
formation Eg; Actinomycosis
44
43. Granulomatous Inflammation
• Granulomatous inflammation; mechanism whereby the
body deals with certain “indigestible” bacteria, fungi, or
foreign particles.
• Examples;
i. Bacteria e.g. Tuberculosis, Leprosy
ii. Parasitic e.g. Schistosomiasis
iii. Fungal e.g. Blastomycosis, Histoplasma capsulatum
iv. Inorganic metals or dusts e.g. Silicosis
v. Foreign body e.g. Vascular graft
vi. Unknown e.g. Sarcoidosis
45
44. INJURY
(e.g; by M. tuberculosis, talc
Failure to digest agent
Weak acute inflammatory response
Persistence of injurious agent
T cell-mediated immune response Poorly digestible agent
•Activation of CD+4 T cells (release of
lymphokines IL-1, IL-2. growth factors
IFN-ˠ and IFN-ɑ)
•Monocyte chemotactic factor
46
45. Accumulation of tissue macrophages
(Increased recruitment from circulation, local proliferation)
Macrophages activated by IFN-ˠ
Transformed to epithelioid cells, giant cells
GRANULOMA
47
47. • Examples of disorders associated with inflammation
include;
i. Asthma
ii. Autoimmune diseases
iii. Hypersensitivities
iv. Pelvic inflammatory disease
v. Rheumatoid arthritis
vi. Transplant rejection
49
48. 2.3: Mediators Of Inflammation
• What are mediators?
i. May be circulating in the plasma or may be produced
locally by cells at the site of inflammation.
ii. Induce their effects by binding to specific reactors on
target cells.
iii. May stimulate target cells to release secondary effector
molecules.
iv. May act on only one or a very few targets.
v. Function is generally tightly regulated.
50
49. • 2 types of chemical mediators of Acute inflammation;
i. Plasma-derived mediators e.g. kinin system,
coagulation & fibrinolytic system, complement
system.
ii. Cell-derived mediators e.g. vasoactive amines,
cytokines, platelet activating factor, growth factor.
51
50. • Chronic inflammatory cells & mediators;
i. Macrophages
ii. T & B-lymphocytes
iii. Eosinophils
iv. Mast cells
52
51. • Inflammatory cells release mediators such as;
i. Cytokines-
(IL-8, interferon-neutrophil)
ii. Vasoactive amines-
(histamine, serotinin- mast cell, basophil, platelet)
iii. Prostanoids-
(arachidonic acid metabolics)
iv. Reactive oxygen intermediates-
(released from activated neutrophil)
53
52. • If the mediators in the inflammatory response are
successful;
i. Invading & infectious agents will be removed.
ii. Damaged tissues will be disposed of.
iii. New tissue will be induced to form.
iv. New blood supply to the area will be established.
54
55. 2.4: Morphologic Patterns Of Acute & Chronic
Inflammation
• Serous inflammation; excessive clear watery
fluid with a variable protein content but no
fibrin e.g. pleural effusion associated with
tuberculosis.
57
67. 2.5: Repair Or Healing
• The processes that take place during & after
the injury are;
i. Removal of dead & foreign material.
ii. Regeneration of injured tissue from cells
of the same type.
iii. Replacement of damage tissue by new
connective tissue.
69
68. • Cells can be divided into 3 major groups;
i. Labile (continuous dividing) e.g. epithelial &
blood cells.
ii. Stable (low level of replication; decrease or lose
their ability to proliferate after adolescence) e.g.
fibroblast, smooth muscle cells, bone & cartilage
cells
iii. Permanent (never divide) e.g. nerve cells, cardiac
myocytes.
70
70. (i) Granulation tissue formation
• 3 phases :
(a) PHASE OF INFLAMMATION
trauma, blood clots (site of injury)
acute response :exudation of plasma,
neutrophils, monocytes (24 hours)
72
71. (b) PHASE OF CLEARANCE
- proteolytic enzymes from neutrophils
- Autolytic enzymes from dead tissue
cells
- Phagocytic activity : macrophages
(function : clear of the necrotic tissue,
debris & RBCs)
73
72. (c) PHASE OF INGROWTH OF GRANULATION
2 main processes:
i. Angiogenesis (neovascularisation)
formation of new blood vessels
ii. Fibrogenesis
formation of fibrocytes and mitotic
division by fibroblasts; myofibroblasts
In 6th days, more collagen is formed
74
73. ii) Contraction of wounds
• Start after 2 -3 days; completed: 14th day
• Wound reduced 80% of its original size
• Contraction occur: rapid healing process
• Factors under mechanism of wound
contraction:
(a) dehydration
(b) contraction of collagen
(c) myofibroblasts
75
74. WOUND HEALING
1. Healing by first intention (Primary union)
characteristics:
- clean & uninfected
- surgical incised
- without much loss of cells & tissue
- edges of wound – surgical sutures
76
75. 2. Healing by second intention (Secondary
union)
Characteristics:
- Large tissue defect
- extensive loss of cells & tissues
- not approximated by surgical sutures but
left open
77
76. • 5 stages of healing (primary Union);
i. Initial Haemorrhage
ii. Acute Inflammation response
iii. Epithelial changes
iv. Organization
v. Suture tracks
78
77. • 6 stages of healing (secondary Union);
i. Initial Hemorrhage
ii. Inflammation phase
iii. Epithelial changes
iv. Granulation tissue
v. Wound contraction
vi. Presence of infection
79
78. • Repair; regeneration of injured tissue by
parenchymal cells of the same type.
• Replacement by connective tissue occur when
repair by parenchymal regeneration alone cannot
be accomplished.
• Involves production of Granulation tissue.
• Replacement of parenchymal cells with
proliferating fibroblasts & vascular endothelial
cells.
80
79. Scars present on the skin, evidence of fibrosis &
healing of a wound
81
83. • Factors affecting healing;
i. Systemic e.g. age, nutrition, immune
status.
ii. Local e.g. infection, blood supply,
mobility, foreign body.
85
84. "Each time you are honest and conduct
yourself with honesty, a success force will
drive you toward greater success. Each
time you lie, even with a little white
lie, there are strong forces pushing you
toward failure."
86