inflammation and repair

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inflammation and repair
2011-01-24 15:23:04
inflammation repair pathology

inflammation and repair, Dr. Said, pathology
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  1. What is the job of acute inflammation?
    • clean up dead tissue
    • protect the injured area against infection
    • enable elemtns of the immune system tto eneter the injured area
  2. Describe the difference between acute inflammation v. chronic inflammation.
    • acute inflammation: short duration - minutes to few days. immediate and early response
    • chronic inflammation - longer duration
  3. What is the four classic signs of acute inflammation (and one additional one)?
    • 1. rubor (redness)
    • 2. calor (heat)
    • 3. dolor (pain)
    • 4. Tumor (swelling)
    • 5. temporary loss of function
  4. what is an exudation?
    the escape of fluid, proteins, and blood cells from the vascular system into the intersitital tissue or body cavity
  5. what is exudate?
    inflammatory extravascular fluid that has a high protein ceontent (specific gravity above 1020), water, salt, and cellular debris
  6. what is transudate?
    • a fluid with low protein content (specific gravity below 1020)
    • ultrafiltrate of the plasma that results from hydrystatic imbalance across the vascular endothelium when the endothelial permeability is normal
  7. what is endema?
    excess fluid in the intersititial or serous cavities (exudates or transudate)
  8. What is pus?
    a purulent exudates, rich in leukocytes (mostly neutrophils) and parynchymal cell debris
  9. What is fibrionous exudate?
    an exudate rich in fibrin
  10. in response to substances released at the sight of injury, what 2 main critical vascular changes occur?
    • 1. Changes in vascular flow and caliber. seconds of vasoconstriction and dilation in response to histamine and bradykinin. Then blood flow slows. This causes the redness and heat. Bradykinin causes pain.
    • 2. increased vascular pearmeability: endothelial cells lining vessels swell and contract with junctional retraction resulting in leaky vessels that allow passage of the exudates => swelling-tumor
  11. in the cellular event, neutrophils join the exudate by adhering to endothelial cells (_______) and then migrating through the basement membrane of the vessel into the area of damage (__________). a small # of _______ and _______ are also present in the area of damage to _______.
    • a. margination
    • b. emigration
    • c. monocytes
    • d. lymphocytes
    • e. phagocytize
  12. what are the components of the acute inflammatory exudate?
    • 1. water, salt, glucose, and oxygen (to sustain inflammatory cells)
    • 2. Proteins. Ig opsonizes for neutrophil phagocytosis. Fibrinogen => fibrin through protease that forms meshwork that facilitate the migration of neutrophils and inhibit invasion by microorganisms
    • 3. neutrophils = primary cells
    • 4. specific gravity more than 1020
  13. what are the 2 events of acute inflammation?
    • vascular changes
    • cellular events
  14. What are the details of vascular permeabiilty changes in acute inflammation?
    • immediate transient (reversible) response lasts 30-60 minutes and is caused mainly by endothelial cell contraction elicited by histamine, bradykinin, nitric acid and...
    • endothelial cells junctional retraction 4-6 hour after stimulus can persist for 24 hours and causes increase vascular permeability with cytokines involved such as TNF (tumor necrosis factor) and interleuken (IL1)
    • an immediate sustained response: result from direct injury to endothelial cels with necresosis and detachment causing increased permeability and begins immediatey after the injury and lasts for hours or days until damaged vessel is repaired
    • a delayed prolonged leakage: (2-12 hour delay and lasts for several hours or even days). mechanism is not fully understood. delayed cell damage attribute to apoptosis and actions of cytokines
  15. describe the details of cellular events in acute inflammation.
    • 1. several cytokines activate the endothelium
    • 2. activated endothelium expresses adhesion molecules (ELAM-1 endothelial leukocyte adhesion molecules -1, ICAM-1 intercellular adhesion molecules -1, CD34, and P-selectin) that allows neutrophils to adhere. This adhesion + aggregation = margination
    • 3. neutrophils emigrate through the wall into damage area due to chemotactic factors (complement fragment like C5a, bacterial component).
    • 4. Neutrophil's main job is to phagocytose foreign/noxious agents. Neutrophils have membrane receptors for the Fc portion of Ab