انت هنا الان : شبكة جامعة بابل > موقع الكلية > نظام التعليم الالكتروني > مشاهدة المحاضرة
الكلية كلية طب الاسنان
القسم العلوم الاساسية
المرحلة 3
أستاذ المادة علي زكي ناجي الاسدي
5/31/2011 6:43:02 AM
Inflammation:
Definition: It’s a protective response of living tissue to injury, its intended to localized and to eliminate the initial cause of tissue injury.
Types of inflammation:
Inflammation can be classified according to the time course and type of cells taking part in inflammatory response into two types:
1- Acute inflammation: Its early response to injury and of short duration starting within few minutes and last up to few days, and characterized by fluid and plasma proteins exudates with predominantly neutrophils accumulation.
Causes of acute inflammation:
1- Microbial infections " pyogenic bacteria, viruses".
2- Hypersensitivity reactions " drugs , and allergies".
3- Physical agents " trauma, radiation, heat (burn), cold (frostbite)".
4- Chemical agents " acids, alkali, toxins".
5- Tissue necrosis " ischemic infraction".
Essential appearance (cardinal signs), of acute inflammation:
1- Redness: the acutely inflamed tissue appear red for example the skin affected by sunburn, and in conjunctivitis, this occur due to dilation of small vessels within the damaged area.
2- Heat: Increase in temperature at site of inflammation, its due to increased blood flow (hyperemia).
3- Swelling: Its due to accumulation of fluid in the extravascular apace (edema).
4- Pain: Its partly due to the stretching and distortion of tissues due to inflammatory edema, and also due to chemical mediators of acute inflammation like (bradykinin and serotonin).
5- Lose of function: the movement of inflamed part of the body inhibited by pain, while sever swelling may physically immobilize the tissue.
Mechanism of acute inflammation:
1- vascular (events) changes:
• Transient vasoconstriction of arterioles, mediated by neurogenic mechanism.
• Persistent vasodilatation, this lead to increase blood flow at the site of inflammation and engorgement of downstream capillary beds, this increment in the blood flow responsible for redness and warmth of the site of inflammation. The engorgement of the capillary bed lead to increase in the hydrostatic pressure and lead to ooze of low protein fluid called transudate to the extra vascular compartment.
• Increase permeability of the vessel wall leads to infiltrate of high protein fluid called exudates, to the extra vascular compartment.
Note: accumulation of both exudates and transudate responsible for Oedema at site of inflammation.
Mechanisms of increase vessels permeability:
1- Endothelial cells contraction: reversible process mediated by chemical substances (histamine, bradykinin).
2- Junctional retraction: reversible process mediated by chemical substances (TNF, and IL-1).
3- Direct endothelial cells damage, (burn and infection).
4- Leukocytes dependant endothelial cells injury.
5- Increase transcytosis via an intracellular vesicles pathway.
6- Leakage from newly formed blood vessels (angiogenesis).
• Increase viscosity of blood due to extravasations of blood plasma.
• Slow of blood flow ( Stasis).
2- cellular events:
• (Margination): Accumulation of leukocytes along the endothelial surface and leaving the normal axial stream
• (Pavement): Adhesion of the leukocytes to the endothelial cells.
• After tight adhesion of the leukocytes to the endothelial cells, the leukocytes start (transmigration), by squeezing between endothelial cells at the intercellular junctions.
• Chemotaxis: Its migration of leukocytes toward site of inflammation along a chemical gradient.
Types of chemotactic factors: The chemotactic factors are either endogenous or exogenous, and these are:
1- Bacterial products.
2- Complement component (C5a).
3- Arachidonic acid (A.A.), and leukotriene B4.
4- Cytokines (IL-8).
• Phagocytosis: It’s the process of engulfment and internalization of particular materials include (micro-organisms, damaged cells and tissue debris), by phagocytic cells which are (neutrophils, monocytes and tissue macrophages)
. • Opsonization: Phagocytosis is enhanced if the material to be phagocytosed is coated with certain plasma proteins called (opsonins), this process called Opsonization, so the opsonins promote the adhesion between the particular material and the phagocyte cell membrane.
Types of opsonins:
1- specific antibodies of IgG class.
2- C3b component of complement.
3- Plasma fibronectin.
• Microbial killing: Oxygen independent mechanism by lysosomal enzymes.
Oxygen dependent mechanism, by free radicals like super-oxide anion O2?, and OH?
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
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