Inflammation
This presentation is the property of its rightful owner.
Sponsored Links
1 / 28

Inflammation PowerPoint PPT Presentation


  • 144 Views
  • Uploaded on
  • Presentation posted in: General

Inflammation. Dr. Raid Jastania. Cell Injury. Stress. Response. Cell Death. Adaptation. Injury. Acute Inflammation Chronic Inflammation Chemical Mediators of Inflammation. Intended Learning Outcomes:

Download Presentation

Inflammation

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript


Inflammation

Inflammation

Dr. Raid Jastania


Inflammation

Cell Injury

Stress

Response

Cell Death

Adaptation

Injury


Acute inflammation chronic inflammation chemical mediators of inflammation

Acute InflammationChronic InflammationChemical Mediators of Inflammation


Inflammation

  • Intended Learning Outcomes:

  • Students should be able to define inflammation and understand clinical features of inflammation and its systemic effect.

  • Students should know the vascular and cellular events in acute inflammation and understand its morphology.

  • Students should know the cellular events in chronic inflammation.

  • Students should be able to define granulomatous inflammation and know its causes.

  • Students should be able to apply the rules of acute and chronic inflammation to predict and feature of inflammation in the different organs of the body.


Inflammation1

Inflammation

  • Inflammation is a protective response of connective tissue to injury.

  • Aim: to eliminate the injury and start the process of repair.

  • Inflammation starts with activation of endothelial cells and white blood cells.

    • Changes in vessels

    • Cellular events.

    • Chemical mediators


Inflammation2

Inflammation

  • Inflammation is divided into acute and chronic type.

  • Acute inflammation is the immediate response to injury, and neutrophils are the main cell type.

  • Chronic inflammation is mediated by mononuclear cells (macrophages, lymphocytes, plasma cell…)


Clinical features

Clinical Features:

  • Localized or systemic.

    • The localized features are: Redness, Swelling, Heat, Pain and Loss of function.

    • The systemic features include: Fever, elevated WBC, malaise, anorexia, and hypotension.


Acute inflammation

Acute Inflammation


Acute inflammation1

Acute Inflammation:

  • It is the immediate early response to injury. It is characterized by neutorphil infiltrate and fluid exudates.

  • The changes in acute inflammation may be divided to: vascular changes and cellular events.


Vascular changes

Vascular changes:

  • Change in the vascular caliber and flow

  • initial transient vasoconstriction of the arterioles followed by vasodilatation. The end result is blood stasis.

  • Increase in vascular permeability

  • increase in the hydrostatic pressure and leakage of fluid to the extravascualr space (Transudate).

  • increase in the osmotic pressure of the interstitium leading to leakage of protein-rich fluid (Exudate).

  • The end result is Edema.


Mechanisms of increased vascular permeability

Mechanisms of increased vascular permeability:

  • Endothelial contraction: histamine, PG, Immediate transient response

  • Endothelial retraction: 4-6 hours after injury

  • Direct endothelial damage: Immediate sustained Response

  • Delayed prolonged leakage:


Mechanisms of increased vascular permeability1

Mechanisms of increased vascular permeability:

5. Leukocyte-dependent endothelial injury

6. Increased Transcytosis: Through intracellular vesicular pathway, and occurs after exposure to VEGF.

7. Leakage from new blood vessels (angiogenesis)


Cellular events

Cellular Events


Cellular events1

Cellular Events:

  • Margination and Rolling:

  • WBC slow down and are pushed to the side of the vessel near endothelial cells. This process is “Margination”

  • WBC’s transiently stick to endothelial cells. This process is “Rolling”

  • The adhesion is facilitated by the action of adhesion molecules called “Selectins”.


Cellular events2

Cellular Events:

  • Margination and Rolling:

  • Selections are present on WBC, endothelial cells and platelets.

  • E-Selectin: on endothelial cell

  • P-Selectin: on Platelets and endothelial cells

  • L-Selectin: on WBC’s

  • Selectins are up regulated by IL-1, and TNF.

  • Selectins bind to sugar molecules. Example: Sialyl-Lewis X


Cellular events3

Cellular Events:

2. Adhesion and Transmigration:

Firm adhesion of WBC’s to endothelial cells. Integrins on WBC’s and Immunoglobulins on endothelial cells.

Example of immunoglobulins: ICAM (intercellular adhesion molecule), VCAM (vascular adhesion molecule)

ICAM binds to LFA-1 (integrin)

VCAM binds to VLA-4 (integrin)


Cellular events4

Cellular Events:

2. Adhesion and Transmigration:

IL-1 and TNF induce the expression of ICAM and VCAM

Integrins bind only when WBC’s are activated.

Transmigration occurs as the WBC’s pass through intercellular junction. This process is facilitated by PECAM (platelet endothelial cell adhesion molecule, CD31).


Cellular events5

Cellular Events:

3. Migration in interstitium: Chemotaxis

Migration of WBC’s is facilitated by chemotactic agents. These are molecules that attract WBC’s. They include:

  • Bacterial products

  • Complement system, C5a

  • Leukotriene B4 (LTB4)

  • Cytokines (IL-8)


Leukocyte activation

Leukocyte Activation:

  • by G-protein activation

  • WBC activation is characterized by:

    • Degranulation of WBC granules and formation of oxidative burst

    • Secretion of arachidonic acid metabolites (Leukotrienes and prostaglandins)

    • Expression of adhesion molecules.


Phagocytosis

Phagocytosis

  • 1. Recognition and attachment:

    “opsonins”:

    immunoglobulins IgG

    C3b molecule of the complement system

    Collectins

  • WBC’s have specific receptors to these opsonins.


Phagocytosis1

Phagocytosis

  • 2. Engulfment in phagocytic vacuole:

    phagosome.

  • 3. Killing and degradation:

    Phagosome fuses to lysosome to form phagolysosome.

    Killing is facilitated by:

  • a.       Oxygen free radicals (oxidative burst)

  • b.      Lysosomal enzymes (myeloperoxidase)


Outcome of acute inflammation

Outcome of Acute Inflammation:

  • Resolution

    2. Scarring and Fibrosis

    organization and fibrosis

    3. Progression to chronic inflammation


Inflammation induced tissue injury

Inflammation-Induced Tissue Injury


  • Login