thrombosis Flashcards
abnormalities that lead to thrombus formation (called Virchow’s triad)
- endothelial injury
- alteration in blood flow
- hypercoagulability
____ induces endothelial dysfunction and activation- contributes to ____ and ____ thrombosis
turbulence; arterial; cardiac
____ disrupts laminar flow, displacing ____ to periphery of vessel; allows concentration of ____ and activates endothelial cells
stasis; platelets; clotting factors
stasis is a major factor in ____ and some ____
venous thrombi; intra-cardiac thrombi
____ create local stasis and _____ expose subendothelial ECM and cause turbulence
aneurysms; atherosclerotic plaques
inherited conditions associated with hypercoagulability
- factor V Leiden mutation (Va cannot be cleaved; anti-thrombotic mechanism lost)
- prothrombin mutation (increased prothrombin transcription)
- deficiencies of anticoagulent proteins (such as AT III)
acquired conditions for hypercoagulability
- prolonged bed rest
- extensive tissue injury
- cancer
- pregnancy
- antiphospholipid antibody syndrome (lupus anticoagulent)
arterial thrombi tend to occur at sites of ____ or _____
turbulence; endothelial injury and loss
arterial thrombi have a ____ appearance with distinct ____; may be ___ or ____
pale (white); lines of zahn (seen grossly and microscopically); occlusive; mural
sterile (non-infectious) thrombi on heart valves called _____
nonbacterial thrombotic endocarditis (NBTE)
venous thrombi have a ____ color and indistinct _____; often form in ____
dark maroon (red); lines of zahn; deep veins of the leg
4 fates of thrombi
- propagation
- embolization
- dissolution
- organization
in propagation, thrombi ___ by additional ____ deposition
enlarge; fibrin/platelet
dissolution involves ____ by _____ activity
lysis; fibrinolytic
organization involves ingrowth of ____ and ____; leads to deposition of _____ (replacing the fibrin) and _____, which may re-establish some flow through the thrombus
fibroblasts; smooth m. cells
collagen; recanalization
disseminated intravascular coagulation (DIC) occurs through widespread act. of the ____ and ____ leading to depletion of ____ and _____ and accumulation of ____
coagulation cascade; fibrinolytic system; coagulation factors; platelets; fibrin split products
DIC can be assoc with widespread formation of ____ and risk of _____
microthrombi; hemorrhage
etiologies of DIC
- infection (gram neg bacteria)
- obstetric complications (placental abruption, retained dead fetus)
- neoplasm
- shock
- massive tissue injury
consequences of pulmonary thromboemboli (mostly from deep veins of the legs)
- no clinical manifestations
- pulmonary hemorrhage and hematemesis (due to ischemic injury without infarction)
- pulmonary infarction
- sudden death (saddle embolus)
- gradual obstruction of many small pulmonary aas. (can result in pulmonary hypertension)
origin of systemic embolization
left atrium, left ventricle (including heart valve vegetation), or ulcerated atherosclerotic plaque
embolus that arises in a systemic vein and crosses a communication from the venous side to the arterial side of the circulation
paradoxical embolus
paradoxical embolus communication is usually in the ____ through ____, ____, or other anomalous communication
heart; patent foramen ovale; atrial septal defect
types of emboli
thrombus fat air amniotic fluid atherosclerotic plaque material
conditions leading to red (hemorrhagic) infarcts
- venous occlusion
- loose tissue (lung)
- dual circulation/extensive overlap of arterial supply (lung, small intestine)
- previous congestion
- infarction followed by reflow of blood into area (reperfusion injury)
causes of white (pale) infarcts
- occur with arterial occlusions in solid organs
2. where tissue density limits blood seepage from adjacent vascular beds
infarcts tend to be ____ with the point of the ____ at the site of _____
wedge-shaped; wedge; arterial obstruction
infarction is followed by an _____ that begins within several hours and peaks at ____; healing occurs by _____, starting at the edge of the infarct, followed by _____
acute inflammatory response; 2 to 3 days
granulation tissue ingrowth; scar formation
infarcts in the brain result in _____ and heal with formation of a _____
liquefactive (not coagulative) necrosis; cystic space
factors that influence infarct development
- nature of the vascular supply (dual supply vs. single artery)
- rate of development of occlusion
- vulnerability to hypoxia
- oxygen carrying capacity of the blood
categories of shock
- cardiogenic
- hypovolemic
- septic
- anaphylactic
- neurogenic
in septic shock, ____ bind to ____ on ____ and ____, mediating the release of ___ and ____
pathogen-assoc molecular patterns (PAMPS, including LPS); toll-like receptors (TLRs) on monocytes; neutrophils
release of IL-1 and TNF
____ occurs in half of septic shock patients
DIC
factors assoc with pathogenesis of septic shock
- vasodilation
- hypotension
- endothelial cell activation and injury
- reduced myocardial contractility
stages of shock
nonprogressive, progressive, and irreversible
in the nonprogressive stage, compensatory mechanisms maintain tissue perfusion by:
- tachycardia
- renal conservation of water
- redist of blood away from vital organs and away from skin through peripheral vasoconstriction
in the progressive stage of shock, there is inadequate perfusion with metabolic imbalances such as ____ and _____
acidosis; increased lactic acid
acidosis reduces vasomotor response to ____ leading to ____ and ____
sympathetic stimulation; pooling of blood; reduced perfusion
____ to endothelium leads to ____ in the progressive stage
hypoxic injury; DIC
in the irreversible stage, tissue injury cannot be reversed by _____
reperfusion
pathologic changes in shock in the
-brain, heart, kidney, lungs, intestinal tract, and liver
- ischemic necrosis of neurons (hippocampus and cerebellum)
- contraction band necrosis
- necrosis of tubular epithelial cells (acute tubular necrosis)
- diffuse alveolar damage due to endothelial injury (adult respiratory distress syndrome/ ARDS)
- mucosal hemorrhage and necrosis
- centrizonal necrosis
