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“Probably Your Own Death Will Be Your Last Inflammatory Response”
CONTENTS






1.
2.




INTRODUCTION




INTRODUCTION
 CELSUS,
 VIRCHOW
 JOHN HUNTER
 JULIUS COHNHEIM
 ELIE METCHNIKOFF
PAUL EHRLICH
 SIR THOMAS LEWIS
HISTORICAL HIGHLIGHTS
Inflammation is derived from Latin word “Inflammare” which means “to burn” or “to
set flame”



DEFINITIONS



DEFINITIONS

DEFINITIONS

A.
B.
C.

A.
B.
C.
D.
CAUSES OF INFLAMMATION
CLASSIFICATION
CLASSIFICATION
Boyd’s
Acute
Inflammation
Chronic
Inflammation
Subacute
Inflammation
Granulomatous
Inflammation
CLASSIFICATION
Pathologicalclassificationonthe
basisoftissuerepair
Alternative
Exudative
Proliferative or
productive
1.
2.
3.
4.
5.
SIGNS OF INFLAMMATION
Inflammatory
response
Bacterial infection of 2 week or less in duration
Acute
inflammation
Heat
Redness
Swelling
Pain
Loss of function
Infection of longer than 2 week
Chronic inflammation
No
symptom
No
symptom





ACUTE INFLAMMATION
A.
1.
2.
B.
1.
2.
3.
4.
ACUTE INFLAMMATION




ACUTE INFLAMMATION

A.
B.
C.
D.



E.
F.
G.
H.
ACUTE INFLAMMATION

1.
2.
3.
4.
5.
6.
ACUTE INFLAMMATION
Vascular
Events
Haemodynamic
Changes
Changes in
vascular
permeability
Cellular
Events
Exudation of
leucocytes
Phagocytosis
ACUTE INFLAMMATION

1.
2.
3.
4.
5.
VASCULAR EVENTS

•
•
•
VASCULAR EVENTS





VASCULAR EVENTS



VASCULAR EVENTS

1.


HISTAMINE, BRADYKININ, LEUKOTRIENES.

VASCULAR EVENTS

2.



VASCULAR EVENTS

3.



VASCULAR EVENTS

4.

VASCULAR EVENTS

5.
•
VASCULAR EVENTS

1.


CELLULAR EVENTS

2.


CELLULAR EVENTS

3.



CELLULAR EVENTS

4.


1.
2.
3.
4.
5.
CELLULAR EVENTS

CELLULAR EVENTS

1.
2.
CELLULAR EVENTS

1.
2.
3.
4.
CELLULAR EVENTS

1.



CELLULAR EVENTS

2.





CELLULAR EVENTS

3.


CELLULAR EVENTS

4.


1.
2.
3.
CELLULAR EVENTS
CELLULAR EVENTS
CELLULAR EVENTS
1.
2.
3.
4.
5.
6.
7.
REFERENCES
Thank you…
1.
2.

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7. inflammation dr ibrahim_shaikh

Editor's Notes

  1. WAR IS THE PERFECT METAPHOR FOR INFLAMMATION Inflammation is the sum of the host’s defenses to infectious or noxious stimuli i.e. the changes that occur in the body to any harmful stimuli. One of the major aim of inflammation is to bring defense cells (immune cells) to the areas of concerns and to inactivate and/or destroy any invaders and also to begin repair. Indeed we can say that the survival of the individual depends upon the ability of his or her normal cells to respond to damage. Inflammation is our principal safe guard against injury. Clinically denoted by the suffix – itis e.g. – dermatitis, arthritis.
  2. Repair begins during the early phases of inflammation but reaches completion usually after the injurious influence has been neutralized. Inflammatory reactions for example underline common chronic diseases such as rheumatoid arthritis, atherosclerosis and lung fibrosis as well as life threatening hypersensitivity reactions to insect bites, drugs and toxins. Repair by fibrosis may lead to disfiguring scars or fibrous bands that cause intestinal obstruction or limit the mobility of joints.
  3. John hunter a Scottish surgeon noted hat inflammation is not a disease but a non specific response that has a valuable effect on its host. Julius Cohnheim – in thin transparent membranes like in mesentery and tongue of frog & wrote the description of inflammation Russian biologist….by observing the ingestion of rose thorns by amebocytes of starfish larvae and of bacteria by mammalian leukocytes. He concluded that the purpose of inflammation was to bring phagocytic cells to injured area to engulf invading bacteria. At that time he contradicted the theory that the purpose of inflammation was to bring factors from the serum to neutralize the infectious agents. It soon became clear that both cells (phagocytes) and serum factors (antibodies) were critical for defense against microorganisms
  4. Inflammation is part of the non-specific immune response that occurs in reaction to any type of bodily injury
  5. Old people, children and the persons with poor resistance of the body are more predisposed to inflammatory changes than healthy young adults
  6. Redness caused due to increased blood flow at the site of injury - On injury to a tissue, chemical mediators are released which act on blood vessels leading to the relaxation of smooth muscles of arterioles. Injury also results in constriction & then dilatation of capillaries leading to increased blood flow; this stage is called an active hyperemia. Due to accumulation of inflammatory exudates in the interstitial tissues. It may also be due to increased amounts of blood present in the congested arterioles; capillaries and venules. The results of tissue pressure due to hyperemia, and edema and the release of inflammatory agents such as Bradykinin.
  7. Acute stage may subside / may proceed to subacute or chronic stage.
  8. Acute inflammation is characterized by congestion, edema and exudate.
  9. Bacterial, viral Blunt & penetrating Thermal injury like burns or frostbite, irradiations From any cause Splinters dirt Hypersensitivity reactions
  10. Red line: capillary dilatation. Flare: arteriolar dilatation. Wheal: exudation, edema
  11. Starlings law
  12. It is thus known as immediate transient response.
  13. This reaction is known as immediate sustained response.
  14. Neutrophils appear in the exudate in the first 24 hrs. Monocytes & macrophages appear in the next 24 – 48 hrs. Simultaneous to emigration of leukocytes, escape of red cells through gaps between the endothelial cells, diapedesis, takes place.
  15. Boyden’s Chamber