Basic Pathology
Slpbpa-203
Bsott-124
Bsabpa-203
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
[Link] 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.