Coagulation and Hemostasis Flashcards
edema
abnormal fluid accumulation in tissue or body cavity
-in body cavities, we call it hydrothorax, hydropericardium, hydroperitoneum (ascites)
-can be transudate or exudate
transudate
low-protein content in edematous fluid
-mechanism usually due to increased pressures
exudate
protein-rich edematous fluids
-mechanism usually due to leaky vessels
anasarca
massive edema
hemorrhage
loss of blood from vessels
increased hydrostatic pressure - pathogenesis of edema
can lead to local or systemic edema
etiologies include:
-congestive heart disease
-portal hypertension
-venous obstruction/stasis
reduced plasma osmotic pressure - pathogenesis of edema
usually leads to systemic edema, and often associated with hypoalbuminemia (low albumin)
etiologies include:
-nephrotic syndrome
-cirrhosis/liver failure (ascites)
-protein malnutrition
-gastroenteropathy
lymphatic obstruction - pathogenesis of edema
usually leads to localized edema
etiologies include:
-inflammation
-parasites
-neoplasia
-iatrogenic/post-surgical
inflammation - pathogenesis of edema
usually leads to localized edema
sodium retention - pathogenesis of edema
usually leads to systemic edema
etiologies include:
renal insufficiency
hyperemia
increased blood in an area compared to normal, due to increased blood flow due to ARTERIAL DILATION
-active process
-organ turns red and hot, because this is increased oxygenated blood
congestion
increased blood in area compared to normal, due to impaired OUTFLOW from a tissue (constricted venules)
-passive process
-affected region is cyanotic because of increased deoxygenated blood
examples of congestion
-hepatic chronic passive congestion due to right-sided CHF (blood backup in liver)
-pulmonary chronic passive congestion due to left-sided CHF (blood backup in lungs)
hemorrhage
extravasation of blood because of vessel rupture
etiologies of hemorrhage
TRAUMA (most common), inflammatory, neoplastic
hematoma
trapped hemorrhage
ecchymoses
bruise; > 1-2 cm
-usually from trauma
purpura
> 3 mm hemorrhages
-etiologies include vasculitide, thrombocytopenia, platelet/clotting coag defects, infections
petechia
1-2 mm hemorrhages (tiny)
-etiologies include thrombocytopenia, platelet/clotting coagulation defects, capillary abnormalities
-specific locations include skin, mucous membranes, serosal surfaces
massive hemorrhage filling a body cavity
hemothorax, hemopericardium, etc
hemostasis
well-regulated processes to:
1) maintain blood in fluid, clot-free state AND
2) induce rapid and localized hemostatic plug at site of vascular injury
3 components of hemostasis
- endothelial cells
- platelets
- coagulation cascade
normal function of endothelium during hemostasis
inhibit thrombosis (normal endothelial cells prevent blood clotting)
-inactivates thrombin and factors Xa and IXa
-inhibit platelet aggregation
endothelial cells after cell injury
favor thrombosis (tell the blood to clot)
-exposure of membrane-bound tissue factor initiates extrinsic coagulation sequence
-express vWF, which promotes platelet aggregation
platelets and hemostasis
- adhesion and conformational shape change (exposed vWF interacts with platelet glycoprotein Ib receptor)
- secretion (release of pro-binding chemokines and cofactors like Ca2+; exposure of phospholipid membrane/complex)
- aggregation (fibrinogen links platelets via GpIIb-IIIa; secrete thromboxane, ADP, and aggregating factors)
antithrombin III - coagulation inhibition
inhibits factors XIIa, XIa, Xa, IXa, and thrombin
*heparin stimulates antithrombin III
proteins C and S - coagulation inhibition
proteins C and S inactivate Va and VIIIa (accelerants)
*activated by thrombin and thrombomodulin
plasmin
plasminogen is activated to plasmin, which DEGRADES FIBRIN
-activated by tPA
thrombosis
inappropriate activation of normal hemostasis (formation of blood clots in normal vasculature)
*pathologic opposite to hemostasis
what causes thrombosis
pathologic endothelial injury (ex. atherosclerosis)
stasis
venous thrombosis (ex. DVT)
turbulence
arterial thrombosis
-disruption of laminar flow
*common where there is bifurcation of blood vessels
arterial thrombi
common sites: coronary, cerebral, femoral
-begin at site of endothelial injury
**Lines of Zahn
lines of Zahn
alternating pale layers of platelets with dark layers of trapped RBCs; imply thrombosis at site of blood flow
**characteristic of ARTERIAL thrombosis
venous thrombi
common sites: veins of lower extremities and gonadal veins
-occur at sites of stasis (sluggish blood flow)
-impaired venous outflow increases hydrostatic pressure and can cause edema
sequelae of thrombus - what can happen to a thrombus after it forms
- propagation (obstruction of a blood vessel)
- embolization (thrombi may dislodge and travel to other sites in vasculature)
- dissolution (thrombi may be removed by fibrinolytic activity)
- organization and recanalization (thrombi induce inflammation, fibrosis, and re-endothelialization, ultimately re-establishing vascular flow)
embolization
detached intravascular solid, liquid, or gas carried by blood to distant site from point of origin
*typically caused by dislodged thrombi
pulmonary thromboembolism
-usually originate from deep leg vein thrombi
-passes through the right heart into pulmonary vasculature
systemic thromboembolism
-arise from/traveling within ARTERIAL circulation
-commonly from a cardiac mural thrombi (thrombus in the wall of the heart)
-travels to lower extremities, brain, etc
fat embolism
common following fracture of long bones with fatty marrow
air embolism
most commonly associated with chest wall injury or decompression sickness (the bends)
tumor embolism
tumor enters circulation and acts like a blood clot, then pieces go wherever the blood flow goes
amniotic fluid embolism
amniotic membrane tear and rupture of uterine veins
-rare complication of labor
infarction
ischemic necrosis caused by occlusion of arterial supply or venous drainage
red/hemorrhagic infarct
-VENOUS occlusions
-commonly impacts loose tissues or tissues with dual circulations; blood pools from other blood supplies to re-perfuse the tissue
white/pale infarcts
-ARTERIAL occlusions
-commonly impact solid organs (heart, spleen, kidneys)
-no dual blood supply
-no re-perfusion
