Flashcards in Inflammation - Pathology Deck (93)
What are the sings & symptoms of inflammation? (5)
Pathology of inflammation (4)
vessel wall changes
mediators of inflammation (M of I)
cellular events of inflammation
What are the circulatory changes?
1) hyperemia (redness, swelling, warmth): increased intracapillary pressure
2) edema: (in capillaries and venules) filtration of plasma through vessel wall
3) congestion: blood flow in dilated capillaries and venules is slow
--> WBCs attach to endothelium (wall of blood vessel)--> release of mediators of inflammation (derived from WBC and platelets)--> platelets initiate clotting
Vessel wall changes
changes in permeability of capillary walls in response to inflammation
Reasons for vessel wall changes during inflammation
1) increased intravascular pressure (congestion)
2) slowing of the circulation => less oxygen and nutrients to endothelial cells
3) adhesion of WBC and platelets to endothelial cells
4) release of mediator of inflammation (from WBC, platelets, endothelial cells, plasma)
What are the mediators of inflammation? (2)
Plasma derived inflammatory mediator
circulate in inactive form -> transformed into active form by ACTIVATOR
Cell derived inflammatory mediator
1) preformed and stored in WBC, platelets ... or synthesized on demand.
2) preformed mediators - quick release (histamine)
3) synthesized mediators - released later
Sample of preformed cell derived inflammatory mediator
Chemistry of mediators of inflammation
- biogenic amines (histamine)
- peptides (bradykinin)
- arachidonic acid derivatives (prostaglandins)
Effects of meditoary of inflammation
- vasodilation or vasoconstriction
- alternation of vascular permeability
- activation of inflammation cells
- degradation of tissues
Which cells release histamine during inflammation? (3)
Effects of histamine
- increased blood vessel permeability => fluids and cells can exit into intersititial spaces
- effects are quick but last less than 30 min. (histamine inactivated by enzyme histaminase)
Effects of bradykinin
- similar to histamine but slower
- amplifies and sustains response to injury
Which chemical causes pain during inflammation?
What can activate the complement system of inflammation?
antigen-antibody complexes, bacterial toxins, fungi, snake venom, etc.
All components of complement system promote ____.
Where does arachidonic acid derived from?
phospholipids of cell membrane
Arachidonic acid synthesis blocks by _______.
Prostaglandin synthesis blocks by _______.
emigration of leukocytes (WBC)
diapedesis = active movement of WBCs through capillary wall into tissues
leakage of fluid rich in proteins
transudate from capillaries (more permeable) into interstitial space
emigration (diapedesis) of cells and fluid through capillary wall
What's the difference between transudation and exudation?
exudation contains inflammatory cells (WBCs) and much more protein than transudation
active movement of WBCs towrads certain chemicals;
movement along concentration gradient of those chemicals.
It's chemotactic agent.
It derived from bacteria damaged tissues, activated complement, etc.
What cells arrive first in acute I inflammation?