edema/congestion,hemostasis Flashcards
(26 cards)
edema
increased fluid within interstitial tissues
edema pathophysiology
increased hydrostatic pressure&decreased venous return, reduced plasma osmotic pressure(kidney disease), lymphatic obstruction, sodium&water retention, inflammation
generalized edema also called
anasarca, hydrops
effusion
collection of fluid in body cavity or space
examples of effusion
pleural, pericardial, peritoneal(ascites), joint space(synovial) —- transudate or exudate
hyperemia
increased tissue blood volume secondary to neurogenic mechanisms or inflammation (active
congestion
increased tissue blood volume secondary to impaired venous return (passive) –things are slowing down,can’t get blood out
hemorrhage
loss of blood secondary to vessel injury or physical disruption
external hemorrhage aka
bleeding
internal hemorrhage
hematoma- large mass (tumor) of blood
ecchymosis- >1cm (bruise)
purpura- .3-.9cm
petechia(e)- 1-2mm (pinpoint) often multiple
examples of hemorrhage in body spaces
hemothorax, hemopericardium, hemarthrosis, hemoperitoneum
acute hemorrhage
shock, >20% blood volume
chronic hemorrhage
anemia
hemostasis
rapid arrest of blood loss at site of injury
the 3 major components of hemostasis are
- endothelium-both anticoagulant and procoagulant
- platelets - fill in area of injury, adhesion, secretion, aggregation
- coagulation cascade- glue things down
platelet adhesion
von Willebrand factor- link on connective tissue
GP 1b on platelets
platelet secretion
release ADP and Ca, surface phospholipid (PL) complex
platelet aggregation
mediated by ADP, TXA2, and thrombin
fibrinogen binds to GP IIb-IIIa
coagulation cascade is a
series of proteolytic conversions
more stuff about coagulation cascade
Ca active enzyme-cofactor-substrate, enzyme activity occurs at PL complex on platelet surface, extrinsic system-tissue factor, intrinsic system-factor XII(Hageman),
final products: thrombin and fibrin
final products of coagulation cascade
thrombin and fibrin
endothelin release causes vasocontriction– good because?
injured area diminishes in size, helps platelets fill in
counter-regulation of hemostasis– why?
bleeding has stopped, don’t want to continue to grow a big clot– trim clot to just fit area of injury– stable area of hemostasis while still allowing blood flow
platelets in counter-regulation
PGI2, NO, ADPase
ADPase cleaves ADP-shuts stuff down