Download week 4-5 inflammation

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Dr. Saleem Shaikh
Inflammation is defined as local response of living tissues to
injury by any agent
It is a body defense reaction in order to eliminate or limit the
spread of injurious agent.
Inflammation can be caused by
◦ Infectious agents
◦ Immunologic agents
◦ Physical agents
◦ Chemical agents
◦ Inert materials
Inflammation is different from infection
Though it is protective in nature it may cause considerable
harm to the body as well
Signs of Inflammation
4 cardinal signs - Celsus
 Rubor – redness
 Tumor – swelling
 Calor – heat
 Dolor – pain
Functio lessa – loss of function (virchow)
Acute inflammation – early body reaction, lasts for less than 2
 The main features of acute inflammation are –
◦ Accumulation of fluid and plasma at the affected site
◦ Intravascular activation of platelets
◦ Neutophils as inflammatory cells
Chronic inflammation is of longer duration and occurs either
after the causative agent of acute infection persists for a long
time, or the stimulus is such that it induces chronic
inflammation from the beginning.
presence of chronic inflammatory cells – lymphocytes, plasma
cells etc.
Granulomatous inflammation – variant of chronic inflammation
Acute inflammation
The events happening during inflammation can be divided into
Vascular events
Cellular events
Vascular events – alteration in the vasculature is the earliest
change to tissue injury
1. Hemodynamic changes – the first vascular response is
transient vasoconstriction; the blood flow is re-established
very quickly.
next follows is progressive vasodilation. This results in
increased blood volume in the capillaries.
vasodilation increases the local hydrostatic pressure; this
causes fluid to come out of cappilaries (transudate). This is
responsible for swelling at the location.
Stasis or slowing of circulation – this facilitates the
movement of leucocytes from inside to outside of
the blood vessel.
Lewis experiment – ‘triple response’ or ‘red line
 Firm stroking of inners aspect of the forearm with a
blunt point shows the following changes
◦ Redline – after few seconds; due to local
◦ Flare – spreading of the white line; due to
vasodilation of adjacent arterioles
◦ Wheal – swelling or odema of the surrounding
2. Altered Vascular permeability- initial swelling produced in
inflammation is because of elevated hydrostatic pressure
(transudate) in later stages there is migration of cells and
fluid into the extracellular spaces (exudate). This is due to
increased vascular permeability.
Contraction of endothelial cells- most common (venules);
immediate, transient
Retraction of endothelial cells – delayed and prolonged
Direct injury to endothelial cells – immediate, prolonged
Endothelial cell injury caused by leucocytes - delayed,
Cellular events:
◦ Exudation of leucocytes
◦ Phagocytosis
Exudation of leucocytes: escape of neutrophils from the
lumen of vessels to the tissue.
Mechanism – In normal pattern of blood flow, the cells of the
blood will be in the center and the cell free plasma will
be at the periphery (near the vessel wall).
due the vascular events (stasis), the cells come closer to
the vessel wall. (margination & pavementing)
As the neutrophils come close to the vessel wall, they start
rolling over the endothelial cells (rolling phase). This is
followed by bonding between the neutrophils and
endothelial cells (adhesion phase).
Next the neutrophils move along the endothelial cells till they
come to a suitable site where they can move out (Emigration).
Once the neutrophils are out of the vessel, they move towards
the site of injury. This movement is guided by chemical
messengers (Chemotaxsis)
2. Phagocytosis – it is the process of engulfing solid material by
cell (cell eating).
The neutrophils once they reach the site of injury produce many
enzymes which kill the bacteria and also degrades some of the
The phagocytic cells develop receptors for the bacteria, the
bacteria are also coated by certain chemicals (opsonins)
which makes them more recognisable by the bacteria.
(recognition and attachment)
Once the bacteria is attached, the cell develops cytoplasmic
extensions around the particle. This bacteria is then taken
inside as a phagocytic vacuole. Inside the cell the vacuole
fuses with a lysosome. (Engulfment)
Killing and Degradation of the bacteria can occour by many
different mechanisms.
◦ Oxidative mechanism by oxygen free radicals
◦ Oxidative mechanism by Lysosomal granules
◦ Nonoxidative bacterial mechanism
Extracellular mechanisms