INFLAMMATION

At the end of the period, the students should be able

to:

1. identify the causes of inflammation,

2. Identify the signs of inflammation, and
3. describe the process of inflammations.
INFLAMMATION

olocal response of living mammalian tissue to injury

due to endogenous or exogenous stimuli

obody‘s defense reaction – eliminate or limit the

spread of injurious agent
CAUSES OF
INFLAMMATION
Immunological
Infective agents
agents

Physical agents Chemical agents

Inert materials
How inflammation distinct from infection?
oINFLAMMATION oINFECTION

oprotective response by oinvasion into the body

the body to variety of by harmful microbes
etiologic agents and resultant ill-effects
by toxins
 Events of Acute Inflammation
Vascular response

Immediate vasoconstriction
– due to neurogenic or chemical stimuli

Vasodilation of arterioles and venules

– result of increase blood flow

Stasis (slowing of blood flow)

– due to increased vascular permeability
– oozes protein-rich fluid into extravascular tissues (exudate)
–dilated vessels are packed with RBC – stasis
– swelling
 Events of Acute Inflammation
Cellular response

Migration, rolling, pavementing, & adhesion of leukocytes

– margination (WBCs positioning along endothelial cells)

– leukocytes tumble slowly along endothelium (rolling)
– WBCs lined up along endothelium (pavementing)
– endothelial cells are facilitated by cell adhesion
molecules
 Events of Acute Inflammation
Cellular response

Transmigration of leukocytes

– leukocytes escape venules and

capillaries
– leukocytes extend pseudopodia
(diapedesis)
– widening of inter-endothelial
junctions
– disrupting basement
membrane and resealed after
 Events of Acute Inflammation
Cellular response

Chemotaxis

– leukocytes migrate toward site

of inflammation
– guided by chemotactic factors
(i.e. complement system – C5a
and cytokines)
 Events of Acute Inflammation
Cellular response
Recognition and attachment
Phagocytosis
Engulfment

– engulfment and internalization by

specialized cells
– two types of phagocytic cells:
polymorphonuclear neutrophils
(PMNs): acute inflammatory response
(microphages)
macrophages: circulating monocytes
– release proteolytic enzymes Degradation
 Outcomes of Acute Inflammation

Resolution Healing Progression

–restoration to –tissue destruction
normal, limited –abscess formation into CI
injury (pus) –persistence of
–normalization of –fibrinous inflammatory
vascular inflammation responses
permeability (extensive leakage –beyond
–apoptosis of of fluid from physiological 
inflammatory cells vasculature tissue destruction
 Chemical Mediators of Inflammation
oresponsible for vascular and cellular events

Sources of Mediators

oPlasma- derived chemical mediators

– complement activation
*increases vascular permeability
*activates chemotaxis
* opsonization (bacteria targeted for destruction by phagocytes)

– Factor XII (Hegman factor) activation

*results in recruitment of kinin, clotting, fibrinolytic, and
complement systems
 Chemical Mediators of Inflammation
oresponsible for vascular and cellular events

Sources of Mediators

oCell- derived chemical

mediators
Quiz!

What are the five cardinal signs of inflammation?

Quiz!

What is the first response of arterioles to injury?

Quiz!

What is the name of the phenomenon where WBCs

marginate and become attached to the edge of the
endothelium?
Quiz!

__________ is the active movement of

polymorphonuclear cells a concentration gradient.
Quiz!

The process by which the cytoplasm of the PMN

surrounds the bacteria and encloses it into an
invagination of the cell membrane is known as
what?
Quiz!

Dead and dying PMN's admixed with tissue debris

form a viscous yellow fluid called what?
 Morphology of Acute Inflammation

Serous inflammation

–outpouring of thin fluid from blood serum or

mesothelial cells secretion

–begins with a dilation of blood vessels and

increased blood flow
 Morphology of Acute Inflammation

Fibrous inflammation

–result greater vascular permeability –

exudation of larger molecules

–presence of fibrous exudate in serous body

cavities (pericardium and pleura)
 Morphology of Acute Inflammation

Purulent inflammation

–characterized by pus production

–types:
(a) abscess formation (accumulation of pus)
(b) acute diffuse inflammation (spread of exudate)
 Morphology of Acute Inflammation

Catarrhal inflammation

–mild and superficial inflammation of the

mucous membrane
–commonly seen in the upper respiratory
tract (viral infections, e.g. rhinitis)
 Morphology of Acute Inflammation

Psedomembranous inflammation

–extensive confluent necrosis

–in many cases, it occurs after taking
antibiotics
 Morphology of Acute Inflammation

Hemorrhagic inflammation

–bloody due to a large component of RBCs

released from ruptured blood vessels
http://dmnemonics.blogspot.com/2014/02/types-of-inflammatory-exudate.html
 Effects of Acute Inflammation
oBeneficial Effects

–dilution of toxins: conc. of toxins is reduced

and its removal by exudate flow

–protective antibodies: exudation 

presence of plasma proteins  promotes
microbial destruction
 Effects of Acute Inflammation
oBeneficial Effects

–fibrin formation: prevents bacterial spread

and enhanced phagocytosis

–plasma mediator systems: complement

systems are provided to injury area
 Effects of Acute Inflammation
oBeneficial Effects

–cell nutrition: inflammatory exudates brings

nutrients to meet metabolic requirements 
increasing # of cells

–promotes immunity: stimulation of immune

response
 Effects of Acute Inflammation
oHarmful Effects

–tissue destruction: may lead to tissue

necrosis
–swelling: may cause serious mechanical
effects (Example: epiglotititis interferes
breathing; meningitis increased cranial pressure)
–exaggerated response
 CHRONIC INFLAMMATION
prolonged duration (weeks-months-
years)

–active inflammation
–tissue destruction
–healing (attempts to repair)

https://www.franciscanhealth.org/news-and-events/news/chronic-inflammation-key-driver-disease
 CAUSES OF CHRONIC INFLAMMATION
persistent infections

prolonged exposure to non-degradable but

partially toxic substances

progression from acute inflammation

autoimmunity (rheumatoid arthritis – chronic

from the onset)

https://www.franciscanhealth.org/news-and-events/news/chronic-inflammation-key-driver-disease
 Morphology of Chronic Inflammation
oCells involved

–monocytes and macrophages

–T-lymphocytes – involved in cellular

immunity; regulator and effector cells
 Morphology of Chronic Inflammation
oCells involved

–B-lymphocytes and plasma cells – produce

antibodies (against antigen or altered tissue
components)

–mast cells and eosinophils - in response to

parasitic infestations and allergic reactions
https://www.researchgate.net/figure/Comparison-between-acute-and-chronic-inflammation-from-38_tbl3_292244527