Acute/chron Inflamm Flashcards
Acute vs chronic
Short duration : long
Fast onset: slow
Infiltrated w granulocytes(neutrophils): agranulocytes (macrophage, lymphocyte, plasma cells)
Acute onset/fast rising fever: low grade/slow rising fever
Increase WBC count:no change in WBC count
Shows cardinal signs : slow progressive tissue necrosis, fibrosis
Vasodilation, increased permea: new vessel formation (granulation tissue)
Clinical signs of acute inflamm
Calor Rubor Tumor Dolor Functio laesa
systemic manifestations that indicate presence of inflamm
fever (due to vasodilation); increase in peripheral WBCs (WBC emigration to injury site); increase plasma pro levels
exudate
inflamm extravasc fluid containing increased protein, cellular debris and having spec gravity of >1.020
transudate
ultra filtrate of plasma resulting from hydrostatic imbalance across vascular endothelium containing decreased protein (specific gravity <1.012)
edema
excess fluid in interstitial areas/body cavity due to exudate OR transudate
effusion
escape of fluid from anatomical vessels by exudation/rupture
changes in vascular flow that occur in acute inflamm
- initial transient vasoconstriction
- subsequent vasodilation causing increased blood flow, heat, redness
- increased mean capillary pressure, hydrostatic pressure (cap bed now has overflow of fluid), and decreased colloid pressure
- exudates escape into interstitium (to compensate for overload of pressure) resulting in excess of fluid in interstitial tissues
- vascular permeability increasing= edema
emigration of leukocytes to injury site
designed to ingest offending agents, kill bacteria, and degrade necrotic tissues and foreign antigens
cell events resulting in leukocytes to injury site: leukocyte extravasation
- margination
- rolling
- adhesion
- transmigration
cell events resulting in leukocytes to injury site: chemotaxis
occurs after leukocyte extravasation; chem gradients signal leukocytes to move toward injury
cell events resulting in leukocytes to injury site: phagocytosis
once leukocytes have accumulated at inflamm site, neutrophils and macrophages work to eliminate the invading matter:
- recognition and attachment of the particle to be ingested (opsonization)
- engulfment
- killing
chemical mediators: arachadonic acid metabolites
located on lipid membrane:
- leukotrienes (synthesized by lipooxygenases; involved in vasoconstriction, bronchospasm, vascular permeability)
- prostaglandins/thromboxanes (synth by cycooxygenases; cause pain/fever)
chem mediators: vasoactive amines: histamine/seratonin
found in basophils, platelets, mast cells; cause vasodilation and increased vascular permeability
chem mediators: complement system
protein cascade that assists the antibodies destroy bacteria, ends in lysis of bacteria. cascade properties enable massive response/amplification to original signal