Inflammation Latest

INFLAMMATION
MRS. LUPIYA
General objective
• At the end of the lecture/ discussion, students

should be able to gain knowledge about
inflammation and its management.
Specific objectives
At the end of the lesson/ discussion,

students should be able to;
Define the term inflammation
List the causes of inflammation
outline the types of inflammation
Describe the basis of cardinal signs
Explain the process of inflammation
Describe the management of
inflammation
INTRODUCTION
• Inflammation is the process by which body tissue

responds or reacts to injury or infection.
• Inflammation can occur in the absence of infection;

but infection cannot occur without inflammation.
INTRODUCTION CONT’
• Inflammation is sometimes called “natural” immunity

which provides immediate protection against the
effects of tissue injury and invading foreign proteins.
• The ability to produce an inflammatory response is

critical to our health and well-being.
INTRODUCTION CONT’
• The inflammatory process is tightly regulated by the

immune system to avoid excessive tissue damage and
spill over to normal tissue.
Figure 1 below shows severe bilateral inflammation and
swelling of the legs.
cardinal signs of inflammation
There are 5 cardinal signs of inflammation. These are:

• 1.Heat (calor)
• 2.Redness (rubor)
• 3.Swelling (tumor)
• 4.Pain (dolor)
• 5.Loss of function(Functio nae lesa)
Types of Inflammation
There are two types of Inflammation and these are:
• 1.Acute Inflammation
• 2. Chronic inflammation
Acute Inflammation
• Acute inflammation is a rapid response to an injurious

agent that serves to deliver mediators of host defence.
• These mediators are known as leucocytes and plasma

proteins.
• They are sent to the site of injury to immediately start the

healing process and/or stop bleeding.
Causes of Acute Inflammation
The causes of acute inflammation include:

• Infection and microbial toxins (bacterial, viral, fungal,
parasitic)
• Trauma which can be blunt or penetrating trauma

• Physical and chemical agents e.g. thermal injuries,
burns, frost bite (extreme coldness)
• Foreign bodies e.g. swelling thorns, needle, pins, etc.
• Immune reactions e.g. swelling due to a bee bite
Components of Acute Inflammation
There are two main components of acute inflammation,

namely:
1. vascular changes and
2. cellular events.
Vascular changes
Vascular changes involve the following:

• Vasodilation: is the widening of blood vessels.
• It results from relaxation of smooth muscle cells within

the vessel walls, in particular in the large veins, large
arteries, and smaller arterioles.
Vascular changes Cont’
• Vascular permeability: Vascular permeability, often in the

form of capillary permeability or microvascular
permeability, characterizes the capacity of a blood vessel
wall to allow for the flow of small molecules (drugs,
nutrients, water, ions) or even whole cells (lymphocytes on
their way to the site of inflammation) in and out of the
vessel.
• Blood vessel walls are lined by a single layer of endothelial

cells.
Vascular changes Cont’
• Increased adhesion of white blood cells: - Leukocyte

extravasation (also commonly known as leukocyte
adhesion cascade or diapedesis – the passage of cells
through the intact vessel wall) is the movement of
leukocytes out of the circulatory system and towards the
site of tissue damage or infection.
Cellular events
• Cellular recruitment and activation of neutrophils

(polymorphonuclear leukocytes)
Chronic Inflammation
• Chronic inflammation is of longer duration and is

associated histologically with the presence of
lymphocytes and macrophages, the proliferation of blood
vessels, fibrosis and tissue death (necrosis).
Causes of chronic inflammation
The causes of chronic inflammation include:

• Persistent infections by certain microorganisms, such
as, mycobacterium tuberculosis and Treponema pallidum,
which cause tuberculosis and syphilis respectively.
Causes of chronic inflammation Cont’
• Prolonged exposure to potentially toxic agents either

exogenous or endogenous, for example, pulmonary
silicosis (Silica in the lungs)
• Autoimmunity where an immune reaction develops against
an individual’s own tissues leading to auto immune disease
or self-perpetuating immune reaction.
• Autoimmunity results in tissue damage and inflammation,
such as, rheumatoid disease, systemic lupus
erythematosus, and multiple sclerosis
• Prolonged exposure to a rough surface causing chronic
friction e.g. a jagged tooth.
Features of chronic inflammation
Chronic inflammation lasts for a long duration. Its main

components are:
• Lymphocyte, plasma cell, macrophage (mononuclear cell)
infiltration
• Tissue destruction by inflammatory cells
• Repair with fibrosis and angiogenesis (new vessel

formation)
Table 1:Comparison between acute and chronic
inflammation
The Process of Inflammation
• The mechanism of inflammation is basically the same

regardless of the causative agent.
• The intensity of the response depends on the extent and

severity of injury and on the reactive capacity of the
injured person.
The Process of Inflammation Cont’
The inflammatory response can be divided into:
• 1.a vascular response

• 2.cellular response
• 3.exudate formation
• 4.cellular healing.
Vascular Response
• After cell injury, arteries in the area briefly undergo

transient vasoconstriction.
• After the release of histamine and other chemicals by the

injured cells, the vessels dilate.
• This vasodilatation results in hyperaemia or redness (due

to increased blood flow into the area) which raises
filtration pressure.
Vascular Response Cont’
• Vasodilatation and chemical mediators cause the

retraction of endothelial cell which increases capillary
permeability.
• This facilitates the movement of fluid from capillaries into

tissue spaces.
• Initially, the inflammatory exudate is composed of serous

fluid, but later it contains plasma proteins, primarily
albumin.
Vascular Response Cont’
• The proteins exert oncotic (tissue) pressure that further

draws fluid from the blood vessels.
• The tissue thus becomes oedematous.
• As the plasma protein fibrinogen leaves the blood, it is

activated to fibrin by the products of injured cells. Fibrin
strengthens a blood clot to trap bacteria, prevents their
spread, and thus serves as a framework for the healing
process.
Cellular Response
• During a cellular response to injury, there is a slowing down of

blood flow through the capillaries to the injured area, as fluid
is lost and the blood viscosity increases.
• Neutrophils and monocytes move to the inner surface of the

capillaries (margination) and then in amoeboid fashion, enter
through the capillary wall (diapedesis) to the site of injury.
• Neutrophils and monocytes accumulate at the focus of injury

by chemotaxis (that is, the directional migration of white
blood cells).
Cellular Respons Cont’
• Neutrophils are the first leucocytes (white blood cells) to

arrive (usually 6 – 12 hours) and have a shorter life span
(24 – 48hours).
• Monocytes usually arrive at the site within 3 – 7 days after

the onset of inflammation.
• In the tissue monocytes transform into macrophages which

have a longer life span as they can multiply in the tissue
and stay for weeks.
Cellular Response Cont’
• They remain to clean the tissues of dirty material before

healing can occur.
• Lymphocytes arrive later at the site of injury.
• They function primarily by producing substances that aid

in attacking foreign material.
• T-lymphocytes kill foreign cells directly or by releasing a

variety of lymphokines which enhance the activity of
phagocytic cells.
• T-lymphocytes are responsible for delayed allergic

reactions, rejection of foreign tissue, or destruction of
tumour cells.
• This is known as cellular immunity. B-lymphocytes are

lymphocytes that are capable of differentiating into plasma
cells.
• Plasma cells in turn produce immunoglobulins or

antibodies.
• These are protein molecules that destroy foreign material

through several mechanisms.
• This is known as humoral immunity.

• Eosinophils and basophils have a more selective role in

inflammation.
• They function in hypersensitivity reactions.
• They work to neutralise histamine while basophils

produce and store histamine and other substances
involved in hypersensitivity reactions.
Exudate Formation
• Exudate consists of fluid and leucocytes that move from

the circulation to the site of injury.
• The nature and quantity of exudate depends on the type

and severity of the injury and the tissues involved.
Cellular Healing
• The reparative process begins at approximately the same

time as the injury and is interwoven with inflammation.
• Healing proceeds after the inflammatory debris is

removed.
• Healing may be by regeneration or replacement.

Cellular Healing Cont’
• In regeneration there is gradual repair of the defect by

proliferation of cells of the same type (hyperplasia) as
those destroyed.
• While in replacement, cells of another type, usually

connective tissue, fill in the tissue defect, resulting in scar
formation.
Signs and Symptoms of Inflammation
The signs and symptoms of inflammation can be divided

into:
• local and
• General.
Local or Cardinal Signs and Symptoms
These include the following:

• Redness: is caused by dilatation of capillaries in the
injured area allowing more blood.
• Warmth/Heat: due to increased blood flow to the area

bringing with it more heat from the central part of the body.
• Swelling: caused by plasma which is poured in the

underlying tissues by extravasation of intravascular fluid.
Local or Cardinal Signs and Symptoms Cont’
• Pain: due to the accumulation of toxins which irritate the

nerve endings; hormones released locally from the nerve
fibres; and stretching caused by excess fluid in the tissue
which increases as the tension grows.
• Loss of Function: occurs as a result of pain, swelling and

the effect of toxin on the tissue itself. The patient’s
natural desire is to rest and avoid using the painful part.
General or Systemic Signs and Symptoms of Inflammation
The general signs and symptoms include:

• General body malaise
• Loss of appetite
• Fatigue
• Fever
• Tachycardia
• Oliguria
• Constipation
Evaluation
 What is inflammation?
 What are the causes of inflammation?
 What are the types of inflammation?
 What are the clinical features of inflammation?
 Describe the management of inflammation
THANK-YOU
•THANK-YOU

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INFLAMMATION

• At the end of the lecture/ discussion, students

At the end of the lesson/ discussion,

• Inﬂammation is the process by which body tissue

• Inﬂammation can occur in the absence of infection;

• Inﬂammation is sometimes called “natural” immunity

• The ability to produce an inﬂammatory response is

• The inﬂammatory process is tightly regulated by the

There are 5 cardinal signs of inﬂammation. These are:

There are two types of Inﬂammation and these are:

• Acute inﬂammation is a rapid response to an injurious

• These mediators are known as leucocytes and plasma

• They are sent to the site of injury to immediately start the

The causes of acute inﬂammation include:

• Trauma which can be blunt or penetrating trauma

There are two main components of acute inﬂammation,

Vascular changes involve the following:

• It results from relaxation of smooth muscle cells within

• Vascular permeability: Vascular permeability, often in the

• Blood vessel walls are lined by a single layer of endothelial

• Increased adhesion of white blood cells: - Leukocyte

• Cellular recruitment and activation of neutrophils

• Chronic inﬂammation is of longer duration and is

The causes of chronic inﬂammation include:

• Prolonged exposure to potentially toxic agents either

Chronic inﬂammation lasts for a long duration. Its main

• Tissue destruction by inﬂammatory cells

• Repair with ﬁbrosis and angiogenesis (new vessel

• The mechanism of inﬂammation is basically the same

• The intensity of the response depends on the extent and

The inﬂammatory response can be divided into:

• 1.a vascular response

• After cell injury, arteries in the area brieﬂy undergo

• After the release of histamine and other chemicals by the

• This vasodilatation results in hyperaemia or redness (due

• Vasodilatation and chemical mediators cause the

• This facilitates the movement of ﬂuid from capillaries into

• Initially, the inﬂammatory exudate is composed of serous

• The proteins exert oncotic (tissue) pressure that further

• The tissue thus becomes oedematous.

• As the plasma protein ﬁbrinogen leaves the blood, it is

• During a cellular response to injury, there is a slowing down of

• Neutrophils and monocytes move to the inner surface of the

• Neutrophils and monocytes accumulate at the focus of injury

• Neutrophils are the ﬁrst leucocytes (white blood cells) to

• Monocytes usually arrive at the site within 3 – 7 days after

• In the tissue monocytes transform into macrophages which

• They remain to clean the tissues of dirty material before

• Lymphocytes arrive later at the site of injury.

• They function primarily by producing substances that aid

• T-lymphocytes kill foreign cells directly or by releasing a

• T-lymphocytes are responsible for delayed allergic

• This is known as cellular immunity. B-lymphocytes are

• Plasma cells in turn produce immunoglobulins or

• These are protein molecules that destroy foreign material

• This is known as humoral immunity.

• Eosinophils and basophils have a more selective role in

• They function in hypersensitivity reactions.