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?
What cells have longest life among cells of inflammation?
Among cells of inflammation, which cells have similar function?
neutrophils and macrophages
Which cells create fever in acute I inflammation?
Among cells of inflammation, which cells are response to allergy?
What cells contain histamine among cells of inflammation?
List the cells of inflammation
neutrophils, eosinphils, basophils, macrophages, other cells (lymphocytes, plasma cells, platelets)
Among cells of inflammation, which can release histamine?
basophils, and platelets
What is the main function of platelets?
hemostasis (vascular spasm, platelet plug formation, blood coagulation)
What does histamine do during inflammation?
promoting formation of connective tissue
What are the 4 ways to classify inflammation?
How long does Acute I inflammation last?
few hours to few days (or kill you)
examples of Chronic I inflammation
What are the infectious agents for inflammation?
bacterial, viral, protozoal, fungal, helmintic
What are the chemical causes of inflammation?
acids, alkaline substances
What are the physical causes of inflammation?
heat, radiation, etc.
What are the immune causes of inflammation?
Which of the following is localized inflammation?
Which of the following is widespread inflammation?
Which of the following is systemic inflammation?
What is the mildest form of inflammation?
Serous inflammation is the ___ stages of most inflammation?
Examples of serous inflammation
1) viral infection
2) autoimmune diseases (pericarditis, pleuritis, peritonitis, rheumatoid arthritis)
3) blisters caused by 2nd-3rd burn
Feature of fibrinous inflammation
transudate rich in fibrin (large protein molecules)
What's the major difference between transudation and exudation?
Transudation leaks clear fluid without cells.
Exudation leaks cells.
Example of fibrinous inflammation
bacterial infections: strep throat, bacterial pneumonia, fibrinous pericarditis
What causes purulent inflammation?
pus-forming bacteria (streptococci, staphylococci)
What is absecess?
localized collection of pus within an organ or tissue
What is empyema?
accumulation of pus in preformed cavity (gallbladder, thoracic cavity)
What are the locations for ulcerative inflammation?
body surface or mucosa of hollow organs
What is ulcer?
Defect involving epithelium, may extend into deeper connective tissue.
Examples of ulcerative inflammation
What is pseudo-membranous inflammation?
fibrino and purulent exudation.
It has fibrin, pus, cellular debris, mucus form pseudo-membrane on the surface of ulcers.
Example of pseudo-membranous inflammation
What's the feature of chronic inflammation?
more extensive tissue destruction
What does chronic inflammation's exudate contain?
lymphocytes, macrophages, plasma cells
Chronic inflammation of kidney will cause kidney to ___.
Examples of chronic inflammation
obliteration of fallopian tubes
Healing of chronic inflammation
scars, fibrosis, adnesions
What is granulomatous inflammation?
A special form of chronic inflammation.
macrophages and T-lymphocytes accumulate at the site of injury and form nodules = granulomas
Features of granulomatous inflammation
persist for a long time
undergo central necrosis
microorganisms can survive in fibrotic lesions
Tuberculosis is __________ inflammation.
a) pseudo-membranous I.
b) granulomatous I.
c) ulcerative I.
d) purulent I.
b) granulomatous I.
Clinicopathologic correlations of inflammation
-local findings (5 signs & symptoms of inflammation)
-constitutional (nonspecific) symptoms: fatigue, weakness, depression, lack of appetite, generalized pain, exhaustion
What are the constitutional symptoms for inflammation?
fatigue, weakness, depression, lack of appetite, generalized pain, exhaustion
What are the consequences of healing of acute inflammation?
or progression to chronic inflammation
Example of mitotic cells
basal layer of skin or mucosa
bone marrow cells (precursors of blood cells)
What are the mitotic cells?
never stop dividing (unstable cells)
What are the facultative mitotic cells?
They are stable cells.
Do not divide regularly, can be stimulated to divide.
Where can you find facultative mitotic cells?
What are the postmitotic cells?
Examples of postmitotic cells
neurons, myocardial cells
Postmitotic cells can only be repaired by _____.
List of all cells related to healing
neutrophils, macrophages, myofibroblasts, angioblasts, fibroblasts
What does neutrophils do during inflammation?
scavenging the site of injury.
What does macrophages do during wound healing?
produce growth factors
produce chemicals (mediators) that act on other cells (fibroblasts, angioblasts, myofibroblasts)
What does myofibroblasts do during wound healing?
secrete substances like fibroblasts (collagen)
contract like muscle cells => reduction of defect, holding margins in close approximation
What does angioblasts do during wound healing?
(precusors of blood vessels)
sprout from small blood vessels around the wound
What does fibroblasts do during wound healing?
produce extracellular matrix of connective tissue
collagen fibers need to mature, cross-link => full strength of scar tissue (several weeks after injury)
What are the substances needed for collagen formation?
Vitamin C, zinc, protein
Describe the healing by First intention
(sterile surgical wounds)
1. blood clot -> scab
2. invasion of neutrophils and macrophages
3. ingrowth of myofibroblasts, angioblasts, fibroblasts
4. granulation tissue formation (=vascularized CT) - temporary structure, undergoes changes
5. collagenous scar (3-6 weeks)
6. proliferation of epithelial cells from margins of the wound (3-7 days)
Describe the healing by Second intention
(large, infected wounds)
wound contraction cannot be accomplished by myofibroblasts
granulation tissue remains exposed (more abundant)
epithelial cells take longer to cover the defect
more excessive scarring
What are the factors for wound healing?
1. site of the wound (skin, brain)
2. mechanical factors: approximation of margins, tension, movement, foreign particles
3. size of the wound
4. infection (prevention, treatment）
5. circulatory status: ischemic tissues heal poorly (diabetes mellitus, smoking)
6. nutritional and metabolic factors: protein, zinc, vitamin C
What are keloids?
hypertrophic scars composed of immature collagen.
What can cause excess scar formation?
contractures due to large scars, esp. after burns -> immobilization or lower ROM