patho sheet #5

بسم الله الرحمن الرحيم

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On this link :

http://www.mediafire.com/?trx9c67xm926rr5
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Acute inflammation and chronic inflammation:


*Slide 2:
-inflammation :is a protective or a host response to injurious stimuli.
-The purpose of inflammation is to get rid of the injurious stimuli and to get rid of the necrotic tissues, that results from inflammation.
-During the process of inflammation there will be production of certain substances that might destruct the normal tissue; either during the process of inflammation or during the process of repair.
-Vascular reaction: increases vascular permeability
To release the plasma proteins and immigration of leukocyte to the site of the injury.
-Cellular responses: immigration of the leukocyte to the site of injury in order to kill injurious stimulus.

*Slide 3:
-Recruitment of leukocyte: immigration.
-acute inflammation: happens in short duration and rapid onset.
-chronic inflammation: happens in insidious onset and of long duration.

*slide 4:
-immune reaction :rxns that happen due to foreign substances like allergie.(for example in bronchial asthma).


Immune reaction:>>>>>against environmental substances
>>>>>>against cells (self)antigen (autoimmune rxn)

-Usually acute inflammation continues to become chronic due to the persistence of the injurious stimuli.
- The most common is the infection.

*Slide 5:
-changes in the vascular caliber and flow happens in arterioles, capillaries, venoles.
-warmth and redness due to the vasodilation.
-Histamine and nitric oxide: are considered as dilators.
-Vasodilatation: increases blood flow/exit of plasma protein, so RBC’s concentration increase and become packed in the dilated blood vessels, viscosity increases, slowing of circulation.

*Slide 9:
-The arrow shows neutrophils (margination of neutrophils) at the edge of blood vessel in contact with endothelial cells.

*Slide 6:
-increases blood flow increases the hydrostatic pressure in the blood vessels more than the interstitial pressure so fluid start to leak out to the interstitium.
-Protein poor fluid: (transudate) the first fluid that leak out of the blood vessels this transudate is due to the increase in hydrostatic pressure.
-Exudate :after a while the poor fluid (transudate)become rich in protein and it will be named exudate.
-Now the colloidal (osmotic)pressure is high in the interstitium (due to the big amount of proteins in the interstitium) so fluid will move toward the proteins and edema happens in the interstitium.

*Slide 10:
-Exudate: containing: 1.inflammatory cells
2.proteins(the pink color material)
*Slide 11:
-Mechanisms of increased vascular permeability:
1)Endothelial cells contraction :formation of enterendothelial gaps.
the most common mechanism in increase the vascular permeability.
Occurs in the postcapillary venules.

-Immediate transient: release of leukotriens and histamine and bradykinin.

-Mediators that cause prolonged and slower reactions are:tumor necrotic factor and interleukin-1.

2)delayed prolonged leakage :delayed bcs it begins after 2-12 hrs.
Prolonged bcs it continues for several
days.
3) increased transcytosis: fusion of intracellular vesicles that form channels which allows the movement of protein rich fluid.
6) leakage from new blood vessels:
Granulation tissue: formation of new blood vessel happens after the inflammation (repair process).
The new blood vessel is leaky bcs it lack firm intercellular junction so fluid pass through it easily.
-leakage remain till the endothelial cells mature and form strong junctions.

*Slide14:
-Responses of lymphatic vessels
-Exudate (edema fluid)will be removed by lymphatic vessels.

*Slide 15:
2) cellular response
-rolling :transient sticking .

+what are the important molecules that are involved in rolling?
-they are called selectin :E:endothelium
P:platelates
L:leukocyte

TNF:tumor necrotic factor
IL-1:interleukin 1

B.Adhesion and transmigration
Clustering of the integrins from low affinity to high affinity form ia achieved by chemokines.


Done by: Noor Haddadin
Date of lecture:27.9.2010
Pathology lec.#5
Dr.Fatima Obaidat