Circulation 2 Flashcards
hemostasis
the blood is maintained in normal vessels and hemorrhage is stopped by sealing blood vessels after rupture
thrombosis
inappropriate clotting in uninjured endothelium or after minor injury
thrombi
inside blood vessels and heart tissues
clots
outside blood vesses or in blood vessels after flow has ceased
causes of thrombosis
virchows triad
endothelial injury- most important factor
abnormal blood flow
hypercoagulability
causes of loss of endothelial cells
myocradial infarction
hypertension
inflammation
trauma
anatomic alterations
endothelial activation
response to stimuli by adjusting steady-state functions and expressing new properties
show:
adhesion molecules
produce cytokines, vasoactive molecules
endothelial dysfunction
shifting of the pattern of gene expression in endotheloium to one that is prothrombotic and proinflammatory
causes of endothelial activation
inflammatory cytokines
hemodynamic stress/lipid products (atherosclerosis)
advanced glycation end products (diabetes)
viruses
complement
hypoxia
end results of endothelial activation and dysfunction
procoagulant changes and antifibrinolytic effects that cause thrombosis
why is aspirin used for CAD?
inhibits platelet activation in the heart, where the circulation is rich in platlets
types of abnormal flow
decreased blood flow
turbulence
types of hypercoagulability
primary- genetic
secondary- acquired
heperain induced thrombocytopenia
unfractionated heparin induces Abs which activate and aggregate platelets causing a procoagulant state
anti phospholipid antibody syndrome
effects caused by the binding of Abs to plasma proteins causing damage, and platelet and complement activation
ventricular mural thrombosis
caused by injury to endocardium by decreased flow following an MI
thrombosis of heart valve
caused by bacteria, immune complexes, or trauma
phlebothrombosis
d/t stasis in uninflammed veins
sites: deep veins in calf, popliteal fossa, IVC tributaries
appears w/ anchor and loose tail
can result in pulmonary embolism
thrombophlebitis
thrombosis in inflammed veins
sterile: trauma, radiation, chemicals
septic: d/t bacteria
thrombosis in microcirculation
disseminated intravasular coagulation
apparent only by microscope
widespread thrombi in microcirulatoin consumes platelets and coagulatoin and manifests itself as bleeding
outcomes of thrombosis
lysis = resolution
organization into connective tissue
propogation towards heart
embolization to lungs
embolism
intravascular mass that is detached from the vascular wall and carried by the blood to a distant site from its origin
pulmonary thromboembolism
most frequent emboli- 95% originate in deep veins of the legs and pass into pulmonary circulation
small artery (60-80%) are silent
large artery- sudden death, right heart failure, shock
medium arteries- hemorrhage d/t infarct/brohial arterys
end artery branches- infarct/hemorrhage
multiple emboli over time- pulmonary hypertensoin w/ right heart failure
systemic thromboembolism
origin- 80% in heart
location- can lend in any vascular bed, usually lower extremities
effect- infarction
fat embolism
microscopic fat glubles enter circulation and block artery
sources: fractures of long bones w/ bone marrow
burns
trauma
usually silent
cause blockage and endothelial activation
fat embolism syndrome
pulmonary insufficiency, neurologic symptoms, anemia
air embolism
gas bubbles within the circulatoin cause physical obstruction by themselves or coalesce forming frothy masses that occlude large arteries
occurs: decompression sickness
decompression sickness
sudden transition from high to low pressure
breathed gas bubbles come out of solution in the blood to form gas emboli
“the bends”- pain d/t rapid formation of air
amniotic fluid embolism
infusion of amniotic fluid or fetal mass pass into maternal circulation
occurs during labor or immediately postpartum
very rare, but high mortality
site lung
shock
decreased systemic perfusion of tissues
d/t decreased CO or BV
causes- hypotension, impaired perfusion, hypoxia
three phases of shock
nonprogressive-compensated
- compensatory mechanisms maintain CO and BV enabling brain and heart perfusion
progressive-reversible
- generalized tissue hypoperfusion and worsening of circulatory and metabolic imbalances
irreversible- severe tissue and cellular injury that results in multiple organs that is irreversible even if hemodynamic defects are corrected
