Love medical

1. INFLAMMATION
Response of vascularized tissues to injury intended to resolve injury and to
eradicate and destroy the causative agent and to prepare the tissues for
healing and repair.
REPRESENTED AS: Inflammation is usually represented by the suffix of itis
added to the name of tissue or organ etc. Examples are gastritis, pancreatitis,
tonsillitis.
TYPES: Inflammation may be acute or chronic.
ACUTE INFLAMMATION:It is the immediate and early response of tissues
1.
to any injury.
DURATION:
Quick onset
•
Short duration
•
If not resolved , changes to chronic inflammation.
•
PREPARED By
Mr. Javid Khan
Lecturer SUIT

2. CAUSES: Causes of acute inflammation include
Mechanical Trauma: Cut , crushing
•
Chemical Injury: Acids , base
•
Radiations : Heat , uv radiations, ionizing radiations
•
Temperature: cold or frost bite, heat or burn
•
Infections : Bacterial, viral, fungal, parasitic
•
Immune reactions
•
CARDINAL SIGNS OF ACUTE INFLAMMATION:
Following are the cardinal signs or features of acute inflammation
RUBOR: Redness/ erythema, it is due vascular dilation and congestion
•
Histamine released by mast cells → vasodilation → hyperaemia ,congestion → redness
CALOR: Heat/ warmth/ ↑ temperature , it is due to hyperaemia and IL-1, IL-6 and
•
TNF-α
Histamine release → vasodilation → hyperaemia → ↑ temperature
IL-1 and IL-6 → elevation of set point of temperature in hypothalamus → ↑body
temperature → fever
PREPARED By
Mr. Javid Khan
Lecturer SUIT

3. DOLOR: Pain, it is due to prostaglandin and bradykinin release and pressure on
•
nerve endings due to edema
TUMOR: Edema, it is due to increased vascular permeability
•
Histamine release → vasodilation → ↑ vascular permeability → release of plasma
fluid (exudate) → edema
FUNCTIO LAESA: Loss of function, due to pain and edema.
•
MAJOR COMPONENTS OF ACUTE INFLAMMATION OR
RESPONSES IN ACUTE INFLAMMATION:
Acute inflammation has three basic components or there are three basic responses in
acute inflammation.
VASCULAR RESPONSE: In acute inflammation the vascular response is in the
A.
form of change in vascular caliber and change in blood flow.
1. Change in Vascular Caliber
Vasoconstriction : Initially there is vasoconstriction for a few seconds. This is due
•
to thromboxane A2 (TXA2) released as a result of endothelial cell injury .
Vasodilation: After a few seconds there is persistent vasodilation → increased
•
blood flow into the area of injury → increased hydrostatic pressure → leakage of
fluid from circulation.

4. 2. Change in Blood Flow : Vasodilation and fluidloss → increased blood viscosity
and increased RBCs concentration → congestion/stasis → erythema.
B. INCREASED VASCULAR PERMEABILITY:
In acute inflammation chemical mediators like histamine, bradykinin, and leukotriene
cause ↑ vascular permeability → leakage of fluid and proteins ( exudate ).
C. RESPONSE OF LEUKOCYTES: In acute inflammation leukocytes usually
neutrophils and macrophages are delivered to the site of injury, this is called
extravasation which consists of the following steps
Margination: movement of leukocytes towards the endothelium and their adhesion
•
to it.
Transmigration / Diapedesis: Movement of leukocytes through the endothelium
•
into the tissues.
Migration: movement of leukocytes in the tissues towards the chemotactic
•
stimulus.
The offending agent is recognized , engulfed and destroyed by the leukocytes.
PREPARED By
Mr. Javid Khan
Lecturer SUIT

5. SEQUELS / FATE OF ACUTE INFLAMMATION:
In general acute inflammation is affected by the nature and intensity of the injury and
may have one of the following three outcomes .
Complete Resolution: The inflammed area may be recovered and restored to
•
normalcy by healing and regeneration.
Healing by connective tissues replacement (fibrosis) after tissue destruction or
•
when inflammation occurs in non regenerating tissues or when there is abundant
fibrin exudate.
Progression to chronic inflammation, if not resolved.
•
PREPARED By
Mr. Javid Khan
Lecturer SUIT

6. MORPHALOGICAL PATTRENS IN ACUTEINFLAMMATION:
Following morphological patterns may occur in acute inflammation depending upon
the type of injury or cause.
SEROUS INFLAMMATION:
•
It is characterized by the fluid transudate which is due to moderately increased vascular
permeability .Such accumulations in peritoneal ,pleural and pericardial cavities are
called effusions. Burn and blister are examples in skin.
FIBINOUS INFLAMMATION:
•
Marked increase in the vascular permeability → formation of fibrin rich exudate which
is converted to fibrous scar ( organization ) by the ingrowth of vessels and fibroblasts.
SUPPURATIVE / PURULENT INFLAMMATION (ABSCESS):
•
In this type there is purulent exudate (pus) consisting of neutrophils ,necrotic cells and
edematous fluid.
ULCER:
It is a local breech / break in the epithelial surface , produced by sloughing of
inflammed necrotic tissues, examples are peptic ulcer, diabetic foot ulcer .
PREPARED By
Mr. Javid Khan
Lecturer SUIT

7. INFLAMMATORY MEDIATORS:
These are the molecules derived either from cells or plasma, which mediate vascular
and cellular events of inflammation.
PRODUCTION AND RELEASE:
Mediators are produced and released by the damaged tissue, other cells or plasma in
response to either microbial products or factors released by necrotic tissues.
ACTION:
Mediators can act by binding to specific receptors or as by direct enzymatic activity or
by activating oxidative damage (ROS).
Mediators can act in regulatory cascades to produce effects or to stimulate secretion or
formation of the others.
DURATION: Mediators are usually short lived degraded by enzymes etc.
PREPARED By
Mr. Javid Khan
Lecturer SUIT

8. MEDIATORS ALONG WITH THEIR SOURCES AND ACTIONS
CELL DERIVED MEDIATORS:
1.
These are preformed vasoactive amines and are among the first mediators of
inflammation which cause vascular dilation and increased permeability.
MEDIATOR SOURCE ACTIONS
Histamine Mast cells, basophils, platelets Vasodilation, ↑vascular permeability,
endothelial activation
Serotonin Platelets Vasodilation, ↑vascular permeability
Prostaglandins Mast cells , leukocytes Vasodilation, pain , fever
Leukotrienes Mast cells , leukocytes Vasodilation, ↑vascular permeability,leukocytes
activation, adhesion and chemotaxis
Platelets activating
factors
Mast cells , leukocytes
Damaged endothelium
Vasodilation, ↑vascular permeability,leukocytes
adhesion, chemotaxis, degranulation , oxidative
burst
ROS (nitric oxide) leukocytes Killing of microbes , tissue damage
PREPARED By
Mr. Javid Khan
Lecturer SUIT

9. CYTOKINES: Proteins produced by activated lymphocytes , macrophages, epithelial
cells and connective tissue cells.
PLASMA DERIVED MEDIATORS :Synthesized in the liver and circulate in inactive
form, activated by enzymatic activity, play important role in inflammation.
CYTOKINE SOURCE ACTIONS
TNF, lymphphokines
( IL-1, IL-6, IL-17)
Macrophages, mast cells,
lymphocytes ,
endothelium
Local endothelial
activation, fever, pain
,anorexia, hypotension, ↓
vascular resistance, shock
Chemokines (CC and
CXC Chemokines)
Leukocytes , macrophages Leukocytes activation,
chemotaxis
PLASMA DERIVED
MEDIATORS
SOURCE ACTION
Complements (C1-C9 ) Plasma, produced in
liver
Leukocytes
activation,chemotaxis,
mast cells stimulation,
cell lysis

10. KININS: Plasma derived mediators ,examples are bradykinin and kallikrein and
cause vasodilation, pain, increase vascular permeability.
KININS SOURCE ACTIONS
Bradykinin,
Kallikrein
plasma Vasodilation,
hypotension, pain,
↓vascular
permeability,
smooth muscles
contraction
PREPARED By
Mr. Javid Khan
Lecturer SUIT