“INFLAMMATION”

Dr.Zulcaif Ahmad

+92 03204998472

INTRODUCTION• It is derived from LATIN word

meaning ignite.

• It literally means flaming, burning

Defination:

“It refers to reaction of living

tissue to all forms of injury, and

involves vascular, neuralgic,

humoral & cellular response at

the site of injury.”

“NOMENCLATURE OF

INFLAMMATION”• The nomenclature used to

describe inflammation in

different tissues employs the

tissue name & suffix “itis”.

• Example:

pancreatitis

nephritis

appendicitis & etc.

Clinical Significance

“It is a protective or defensive

process why?”• it removes or destroys causative agents

• Repairs tissue damage

• Inactivate toxins

• Prepare tissue or organ for healing & repair

WITHOUT INFLAMMATION??

• Infections would go unchecked.

• Wounds would never heal.

• Injured organs may remain permanently

damaged.

“TYPES OF INFLAMMATION”

• On the basis of severity, duration,

onset &other factors it can be

categorized as,

1) Acute inflammation

2) Chronic inflammation

Acute Inflammation

• “The acute inflammatory response rapidly

delivers leukocytes and plasma proteins to

site of injury. once there leukocytes clear

the invaders and begins the process of

digesting and getting rid of necrotic

tissue.”

• Cells of Acute Inflammation:

• Neutrophils (for first 24-48 hours)

• Macrophages (after 48 hours)

ETIOLOGY OF ACUTE

INFLAMMATION

• MECHANICAL TRAUMA: cutting or crushing

• CHEMICAL INJURY: corrosive acids, alkalis,

phenol, general poisons.

• RADIATION INJURY: heat, UV light, all forms of

ionizing radiations.

• INJURY DUE TO COLD AND HEAT

• INJURY BY LIVING ORGANISM: infection by

viruses, bacteria & larger parasites.

• INJURY DUE TO IMMUNOLOGICAL

MECHANISM: diseases mediated by Ag-

AB interactions

• Hypoxia

• BURNS

• TOXINS

• STRESS

• CHEMICAL IRRITANTS etc.

Internal View & External View

Of Rubor.

DOLOR Tumor

FUNCTIO LAESA

.

CELLULAR EVENTS OF

ACUTE INFLAMMATION

• Vascular changes (Vasodilation, inc.

vascular permeability)

• Cellular events takes place such as;

MARGINATION

ADHESION

EMIGRATION

CHEMOTAXIS

PHAGOCYTOSIS

Process of acute inflammation

Initiated by cells already present

Cells present on surface receptor

(PRRs)Pattern recognition

receptor

Distinguish from host cell

(PAMP) Pathogen assosiatedmolecular patterns

Onset of infection burn or

injury

Cell undergo activation and

release mediator

Vasodilation

Increased blood flow

Causes redness & heat

Inc.permeabilityof blood vessels

result

Exudation (leakage) of

plasma protein

And fluid into tissue

Manifests itself as swelling

Some mediator such as

bradykinin

Mediator alter the migration of leukocytes

Mainly neutrophil& macrophages

out side he b.vessels

Neutrophilsmigrate along chemotactic

gradient

Reach the site of injury

Loss of function result of neurological

reflex

Inflammation ceased once

the stimuli has been removed

Triple response

• LEWIS in 1942 noted that firm stroking of a

human skin results in a triple response.

The features of this response are

RED LINE: it is sharply demarcated red

line at the site of stroking due to capillary

dilation.

THE FLARE: after 15-30sec flare appears

surrounding a line due to arteriolar dilatation.

THE WEAL: on the site of red line a wheel

subsequently appears due to exudation of

fluid through vessel wall.

“EXUDATION”• EXUDATION:

“The escape of fluid, cells, and cellular debris

from blood vessels and their deposition in or

on to the tissues as result of inflammation is

known as exudation.”

• Exudate:

“It is an inflammatory extravascular fluid that

has high protein conc., much cellular debris

which leaks from vessels into the interstitial

space due to increased vascular

permeability.”

MEDIATORS OF ACUTE

INFLAMMATION• MEDIATORS:-

These are the chemical substances that

trigger certain process in an inflammation.

TYPES OF MEDIATORS:

1. Histamine

2. Serotonin

3. NEUTROPHILIC PROTEASES

4. ADRENALINE AND NOR ADRENALINE

5. The kinins

6. Plasmin

7)DERRIVATIVES OF ARACHIDONIC ACID(AA)

– THE PROSTAGLANDINS

– LEUKOTRIENES

8) PLATELET ACTIVATING FACTOR (PAF)

9) CYTOKINES

10) LYSOSOMAL CONTENTS OF

NEUTROPHILS

11) COMPLEMENT SYSTEM

12) OTHER MEDIATORS:

NEUROPEPTIDES

NITRIC OXIDE:

OUTCOMES OF ACUTE

INFLAMMATION

• COMPLETE RESOLUTION

• SCARRING OR FIBROSIS

• ABCESS FORMATION

• PROGRESSION TO CHRONIC

INFLAMMATION

• SCARRING

*ABCESS

CHRONIC INFLAMMATION

SPECIAL TYPES OF ACUTE

INFLAMMATIONOn principle components of exudates, acute

inflammation has followimg types:

1. Serous Inflammation

2. Fibrinous Inflammation

3. Suppurative Inflammation

4. Abcess Forming Inflammation

5. HEMORRHAGIC INFLAMMATION

CHRONIC INFLAMMATION

• It is the prolong response of the body to the

persistent injurious stimulus and is characterized

by:

• Infiltration with mononuclear cells.

• Tissue destruction.

• Repair.

• CHRONIC INFLAMMATORY CELLS

• Lymphocytes

• Macrophages

• Plasma cells

ETIOLOGY• Unresolved acute inflammation:

Due to persistence of injurious agent

interference of normal process of healing

• Chronic inflammation without acute

phase:

It may start from the very beginning

Such type of injurious agents are of low

toxicity in comparison of those that lead to

acute inflammation.

CAUSES

1. CHRONIC VIRAL INFECTIONS:

chronic viral hepatitis

2. CHRONIC AUTOIMMUNE DISEASES:

rheumatoid arthritis

3.CHRONIC CHEMICAL INTOXICATION:

chronic alcoholic liver disease

4.ALLERGIC INFLAMMATION:

bronchial asthma

TYPES

1) GRANULOMATOUS CHRONIC

INFLAMMATION

2) NON GRANULOMATOUS CHRONIC

INFLAMMATION

GRANULOMATOUS

• This type of chronic inflammation is

characterized by formation of epithelioid

cells & granuloma

• GRANULOMA:

A collection of modified macrophages

resembling epithelial cells, usually

surrounded by a rim of lymphocytes.

NON GRANULOMATOUS

It is characterised by accumulation of:

• Sensitized lymphocytes

• Plasma cells

• Macrophages in the injured area.

• Cells are scaterred throughtout the tissues

• Do not form granulomas

• Scaterred tissue necrosis and fibrosis are

common.

FEATURES ACUTE CHRONIC

• DURATION Short (days) Long (weeks-

months)

• ONSET Acute Insidious

• INFLAMMATORY

CELLS

Neutrophils,

macrophages

Lymphocytes,plasma

cells,macrophages &

fibroblasts

•VASCULAR

CHANGES

Active vasodilation,

increased

permeability

New vessel formation

“granulation tissue”

•FLUID

EXUDATION

Present Absent

•CARDINAL

CLINICAL SIGNS

Present Absent

REFERENCES• COLOR ATLAS OF PATHOLOGY BY

URUS.

• GROSS PATHOLOGY BY JAWAD

AHMED.

• GENERAL PATHOLOGY BY ROBIN’S

AND CARTON’S.

• GENERAL PATHOLOGY BY WALTER

AND ISRAEL.

• SHORT TEXTBOOK OF PATHOLOGY

BY INAM DANISH.