-
5 signs of inflammation
- pain
- redness
- swelling
- heat
- loss of function
-
circulatory changes during inflammation (6)
- vasodilation
- constriction of arteriolar smooth muscles
- active hyperemia
- increased hydrostatic pressure
- congestion
- hemodynamic changes: RBC rouleux formation and margination of WBC
-
Hemodynamic Changes (3) during inflammation
- 1. margination of neutrophil
- 2. adhesion of platelets releasing mediators of coagulation
- 3. pavementing of leukocytes to endothelium
-
cytokines
adhesion molecules that facilitate leukocytes to adhere to endothelium during inflammation
-
4 vessel wall changes
- 1. increased hydrostatic pressure inside congested blood vessels
- 2. slow circulation reducing oxygen and nutrients to endothelial cells
- 3. adhesion of leukocytes and platelets to endothelial cells
- 4. release of soluble mediators
-
types of mediators and inflammation
- plasma derived: circulate inactively in blood, activated during inflammation
- cell derived: stored in granules of platelets and leukocytes
-
steps of inflammatory response
- mast cells and platelets release histamine
- capillary leaks causing increase in vascular permeability
- phagocytes engulf bacteria
- platelets move out of capillary to seal wounded area
-
histamine
- quick reaction/ short action mediator (amine)
- from platelets and mast cells
- increases vascular permeability
- vasodilation
- increase phagocytosis
- pain
- inactivated by histaminase
-
what is bradykinin
- from plasma through Hageman factor (coagulation factor)
- similar to histamine function
- incrs. vascular permeability
- pain
- longer lasting
-
Hageman factor
- AKA coagulation factor
- produces: bradykinin, plasmin, fibrin
-
complement system
group of plasma proteins produced in liver that enhances antibodies and phagocytosis to clear damaged cells and promote inflammation. Circulates in inactive form
-
end product of complement system
produce MAC to cause cell lysis
-
complement proteins C3a and C5a produce
- C3a: anaphylatoxins + opsonin
- C5a: anaphylatoxin + chemotaxis
-
opsonin
signaling chemicals that facilitate phagocytosis
-
anaphylatoxins
- chemicals that release histamine, vasodilation, vascular permeability
- released by C3a and C5a
-
complement fragments promote?
chemotaxis
-
chemotaxis
attraction of white cells to area of inflammation
-
Arachidonic acid is derived from and metabolized thru
derived from membrane phospholipids and metabolized through lipoxygenenase pathway and cyclooxygenase pathway
-
lipoxygenase pathway products
- leukotrienes: promote chemotaxis and vascular permeability. present in anaphylactic shock, bronchospasm
- lipoxins: inhibit chemotaxis, negative regulator of leukotriene, vasodilation
-
cyclooxygenase pathway products
- prostaglandins: smooth muscle contraction, pain and fever, vascular permeability
- thromboxane: platelet aggregation (clots), vasoconstriction
- prostacyclin: counteracts thromboxane
-
transudate
leakage of plasma fluid into interstitial vessel. result of increased permeability
-
exudate
transudate + proteins + inflammatory cells (WBC)
-
extravasation of fluids leads to
- inc vascular permeability
- inc hydrostatic pressure, (edema)
- emigration of leukocytes, releasing exudate
- chemotaxis
-
how leukocytes migrate from vessels, emigration of leukocytes (4)
- 1. adhesion of leukocytes
- 2. insertion of pseudopods between endothelial cells
- 3. passage through basement membrane
- 4. ameboid movement toward chemotactic stimuli
-
phagocytosis process (4)
- 1. bacterium opsonized (coated with phagocytic chemicals)
- 2. bacteria is engulfed by PMN
- 3. Degranulation: phagocytic vacuoles and lysosomes digest bacterium
-
pus
dead leukocytes mixed with tissue debris and lytic enzymes
-
types of inflammation cells (5)
- polymorphonuclear neutrophils
- eosinophils
- basophils
- macrophages
- platelets
- lymphocytes
- plasma cells
-
polymorphonuclear neutrophil
- first responders to acute inflammation
- cytokine production: interleukin -1 --> hypothalamus --> fever
-
eosinophils
- 2-3% of WBC
- appears 2-3 days after PMN
- allergy, parasites
- chronic
-
basophils
- <1% of WBC
- allergy
- from mast cells
-
macrophages
- derived from blood monocytes
- appears 3 - 4 days after onset
- chronic inflammation
- involved in phagocytosis
-
platelets
fragments of megakaryocytes
-
7 types pathological forms of inflammation
- serous inflammation
- fibrinous inflammation
- purulent inflammation
- ulcerative inflammation
- pseudomembranous
- chronic
- granulomatous
-
serous inflammation
- early stage of most inflammation
- joint swelling in rheumatoid arthritis, herpes, pneumonia
- exudation of serum
- mild
-
fibrinous inflammation
- exudate rich in fibrin
- severe
- strep throat (bacterial infection)
-
purulent inflammation
- exudate with pus
- contains dead PMN and necrotic tissue remnants
-
three types of purulent inflammation
- abscess: localized collection of pus enclosed in capsule
- sinus: rupture abscess containing a cavity that drains puss
- fistula: a channel connecting two hollow cavities/organs or to the surface of the body
-
ulcerative inflammation
ulcer: loss of epithelial lining in hollow organs
-
pseudomembranous inflammation
- ulcerative inflammation + fibropurulent
- contain exudate composed of pus, fibrin, cellular debris and mucus
-
chronic inflammation
- fibroblast proliferation
- scarring by deposit of collagen
- fibrosis: hardening of tissue, usually associated with lung disease
- occurs after acute
-
granulomatous inflammation
- granulomas
- consists of lymphocytes, macrophages, and multinucleated giant cells
- common in TB
-
granuloma
- a type of chronic inflammation with many lymphocyte, macrophages (epithelioid cells), and multinucleated giant cells
- not preceded by acute inflammation
- present in TB patients
-
what are the cytokines/pyrogenes released from leukocytes/macrophages during inflammation (2)
- IL-1
- tumor necrosis factor
-
describe the pathogenesis of fever
- 1. leukocytes + macrophages release IL - 1 and tumor necrosis factor
- 2. IL-1 and TMF enter hypothalamus releasing prostaglandins which cause fever.
- can be inhibited by aspirin
-
mitotic cell cycle
- Go: resting phase
- G1: growth
- S: DNA synthesis
- G2: growth and preparations for division
-
quiescent facultative mitotic cells
- cells that do not divide regularly but can be stimulated to proliferate
- ex. parenchymal cells of liver
- stops at G0 phase
-
nondividing postmitotic cells
- cells that cannot divide
- ex. neurons, myocardial cells
-
cells participating in wound healing
- macrophages
- myofibroblasts
- fibroblasts
- angioblasts
-
what cells are involved in wound healing
- myofibroblasts: contract, secret matrix substances
- macrophages: contract, secret matrix
- fibroblasts: extracellular matrix including fibronectin and collagens (III,II,I)
- angioblasts: blood vessel precursors
-
what is granulation tissue
connective tissue rich in macrophages,
-
types of wound healing
- first intention
- secondary intention
-
first intention
- healing for small wounds
- scar --> leukocytes --> granulation tissue (fibroblast, macrophage) --> small scar
-
secondary intention
- prolonged wound healing
- exposed granulation tissue delays healing tremendously
-
what happens when there's healing complications
- deficient scar formation: slow scar formation usually seen in diabetic pts as a result of ischemia
- wound dehiscence: separation of tissue margins
- excess scar formation
- keloids leftover type III collagen
-
cyclooxygenase pathway inhibited by
aspirin
-
most abundant WBC
PMN polymorphonuclear neutrophil
-
Platelets release
- histamine
- coagulation proteins
- cytokines
- growth factors
-
what is platelet-derived growth factor (PDGF)
factor that promotes proliferation of connective tissue
-
opsonization
facilitated phagocytosis of bacteria
-
angiogenesis
formation of new blood vessels
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