Arterial Thrombi Morphology
adherent masses of blood that have areas of pale alternating with areas of red - lines of zahn
4 Arterial Thrombi outcome
3. embolization (arterial)
*all similar to venous thrombi
Disseminated Vascular Coagulation
a sudden onset of fibrin thrombi in the microcirculation with consumption of coagulation factors and formation of fibrin degradation products. Potential complication with widespread of thrombin.
a detached solid, gaseous, or liquid mass that is carried by the blood from site of origin to a distal site. May lodge in pulmonary or systemic circulation.
5 types of embolisms
Thrombi, fat, amniotic fluid, foreign substances, and bone marrow
-20 to 25 per 100,000 PTs have it
-fatal if 60% of circulation is obstructed
Patho of Pulmonary Thromboembolism
deep venous thrombi is usual cause; often following immobilization, i.e. bed rest from hospitalization
sudeen death, clinically silent; resolution, organization, dyspnea, pulmonary infarct
emobilzation to small distal vessels in lung may cause ischemic necrosis of tissue infarct
emboli that travel from venous arterial circulation via a communication between arterial and venous circulation
ischemic necrosis of tissue distal to an area of arterial occulsion or in an area of obstructed venous outflow
hemorrhagic; organs with dual blood supply; soft aerated tissues
white; organs with single blood supply
excess fluid in the interstital spaces of the body
major factors KEEPING fluid in vessel
major factors PUSHING fluid out of vessel
increased inflow into a vessel; i.e. exercise, inflammation
decreased outflow of a vessel; i.e. local obstruction, congestive heart failure
hypoperfusion of tissues; the circulatory system can no longer supply nutrients and oxygen to peripheral tissues.
loss of blood volume; i.e. hemorrhages, water loss from burns, vomitting/diarrhea
pump failure; i.e. secondary to MI, conduction block or arrythmia, myocarditis or valvular heart disease
loss of peripheral vascular tone and pooling of blood in dilated peripheral blood vessels
3 causes of hypotonic shock
Allergen (bee sting), neurogenic (spinal cord, pain from trauma), and bacterial endotoxins (septic shock)
Is shock reversible?
early stages of shock are reversible and treatable. in the early stages, peripheral vasoconstriction helps compensate for hypoperfusion. the central pooling redirects blood to vital organs. if untreated, can cause death.
Pathology of shock
(upon autopsy) interal organs are congested and wet from edema; the lungs are 2-3 times heavier. the liver is congested and blood oozes from it. the intestines are dark from blood pooling and wet. the kidneys are swollen, pale, and congested. and the brain is edematous, flattened gyri.
Why are hemorrhages widespread?
because of DIC
Clinicopatholgic correlations of shock
-early of compensated shock
-decompensated, but reversible shock
a set of adaptations occur to compensate for the circulatory imbalance. i.e. tachycardia, vasoconstriction of peripheral arteries, and reduced urine production
when early shock fails: hypotension occurs, BP and CO fall. Tachypnea and SOB lead to heart failure and pulmonary edema causing anoxia, lead to ARDS.
constriction of the renal cortical vessels reduces GFR. results in renal output.
mixed acidosis occurs. result of renal, anaerobic glycolosis, and respiratory insufficiency.
the end result of decompensated shock. marked by: circulatory collapse, hypoperfusion of vital organs, and loss of vital functions. PTs are in distress and are frantic, DIC is common, and high mortality.