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Inflammation

Inflammation is a protective response involving host cells, blood vessels and proteins. It aims to eliminate the initial cause of cell injury, remove necrotic cells and tissue, and initiate the repair process. Inflammation is divided into acute and chronic types. Acute inflammation is characterized by edema and neutrophils in tissue and arises in response to infection or necrosis. It involves hemodynamic changes, neutrophil arrival and function, and can resolve or transition to chronic inflammation. Chronic inflammation is caused by persistent injury, infection, or exposure and involves granulomatous inflammation, which forms collections of immune cells known as granulomas.

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0% found this document useful (0 votes)
46 views35 pages

Inflammation

Inflammation is a protective response involving host cells, blood vessels and proteins. It aims to eliminate the initial cause of cell injury, remove necrotic cells and tissue, and initiate the repair process. Inflammation is divided into acute and chronic types. Acute inflammation is characterized by edema and neutrophils in tissue and arises in response to infection or necrosis. It involves hemodynamic changes, neutrophil arrival and function, and can resolve or transition to chronic inflammation. Chronic inflammation is caused by persistent injury, infection, or exposure and involves granulomatous inflammation, which forms collections of immune cells known as granulomas.

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Sajjad Ali
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Basic Pathology

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INFLAMMATI
ON
LEARNING OBJECTIVES:
 What is inflammation
 How is it divided

 Acute inflammation and its types

 Chronic inflammation and its types

 Hemodynamic changes
A protective response involving host cells,
blood vessels and proteins
– Goals are: • eliminate the initial cause of
cell injury • Remove necrotic cells and
tissue • Initiate the process of repair
Types of Inflammation
 Divided into acute and chronic
inflammation
ACUTE INFLAMMATION

BASIC PRINCIPLES
 A. Characterized by the presence of

edema and neutrophils in tissue


 B. Arises in response to infection (to

eliminate pathogen) or tissue necrosis (to


clear necrotic debris)
 C. Immediate response
Important components of acute
inflammation

 • Hemodynamic changes
 • Neutrophils

 • Chemical mediators (histamine,

bradykinin, etc.)
Hemodynamic changes

 a. Initial vasoconstriction
 b. Massive vasodilatation

 c. Increased vascular permeability


Hemodynamic changes
 > The mechanism of increased vascular
permeability involves endothelial cell
contraction; direct endothelial cell injury
 d. Blood flow slows (stasis) due to

increased viscosity, allows neutrophils to


marginate
NEUTROPHIL ARRIVAL AND FUNCTION

 A. Step 1-Margination
l. Vasodilation slows blood flow.

2. Cells marginate from center of flow to


the periphery.
B. Step 2-Rolling

l. Selectins

2. Interaction results in rolling of


leukocytes along vessel wall.
Step 3-Adhesion

1.Cellular adhesion molecules are upregulated


on Endothelium.
2. Integrins are upregulated on leukocytes.
3. Interaction between CAMs and integrins
results in firm adhesion of leukocytes to the
vessel wall.
 4. Leukocyte adhesion deficiency is most
commonly due to a defect of integrins.
 delayed separation of the umbilical cord

recurrent bacterial infections that lack


pus formation
Step 4-Transmigration and
Chemotaxis
l. Leukocytes transmigrate across the
endothelium
Step 5-Phagocytosis

l. Consumption of pathogens or
necrotic tissue
Step 6-Destruction of
phagocytosed material

 0 2-dependent killing is the most


effective mechanism
Step 7-Resolution

1. Neutrophils undergo apoptosis and


disappear within 24 hours after resolution
of
the inflammatory stimulus.
MACROPHAGES

 Macrophages predominate after neutrophils


and peak 2-3 days after inflammation begins.
 Arrive in tissue via the margination, rolling,

adhesion, and transmigration sequence


 Ingest organisms via phagocytosis and destroy

phagocytosed material using enzymes (02-


independent killing)
FOUR OUTCOMES OF ACUTE INFLAMMATION

 1 . Complete resolution with


regeneration
 2. Complete resolution with scarring

 3. Abscess formation

 4. Transition to chronic inflammation


CARDINAL SIGNS OF INFLAMMATION

 Dolor (pain)
 Calor (heat)

 Rubor (redness)

 Tumor (swelling)

 Functio laesa (loss of function)


CHRONIC
INFLAMMATI
ON
CAUSES OF CHRONIC INFLAMMATION

 • Persistent injury or infection – Ulcer,


tuberculosis
• Prolonged exposure to a toxic agent –
Pulmonary silicosis (silica in the lung)
• Autoimmune disease—self-perpetuating
immune reaction that results in tissue
damage and inflammation
– Rheumatoid arthritis
GRANULOMATOUS
INFLAMMTION
 It is found in many diseases. It is a
collection of immune cells known as
histiocytes.
Granulomas form when the immune
system attempts to wall off substances it
perceives as foreign but is unable to
eliminate.
Divided into noncaseating and caseating subtypes

 Noncaseating granulomas lack


central necrosis
*Common etiologies include reaction
to foreign material, beryllium
exposure.
 Caseating granulomas exhibit central
necrosis
*Characteristic of tuberculosis and fungal
infections.
LEARNING OUTCOMES:
 What is inflammation
 How is it divided

 Acute inflammation and its types

 Chronic inflammation and its types

 Hemodynamic changes
REFERENCES
Robbins Basic Pathology - 10th Edition – Elsevier
Short Textbook of Pathology by Inam
Danish - 2nd Edition
Caseating granuloma T.B.

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