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41 Cards in this Set
- Front
- Back
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using virchow's triangle what are the ways thrombosis occurs?
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- endothelial injury => abnormal blood flow => hypercoagulability
OR - endothelial injury => hypercoagulability OR - etc... |
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how is endothial injury able to lead to thrombosis?
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- exposes a very thrombogenic surface
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what ex of endothelial injury?
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- MI
- atherosclerotic aa. - vascular injuries |
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turbulent blood flow leads to?
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- endothelial cell injury
- hypercoagulability/stasis |
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how does turbulent blood flow lead to hypercoagulability?
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- since blood is not flowing laminarly, platelets bump up against walls giving them opportunity to stick
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what are genetic ways of getting hypercoagulability?
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- mutation in clotting factor 5=leiden mutation where it becomes resistant to anti-coags
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signs of both genetic and acquired hypercoagulability?
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- DVT in addition for genetic could be pulmonary thromboembolic disease
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what are causes of acquiring hypercoagulability?
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- hyperestrogenemia
- increased production of procoags & decreased production of antithrombin III by liver - CA which changes blood chem |
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what are the types of thrombi?
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- cardiac thrombi
- venous thrombi - arterial thrombi |
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cause of cardiac thrombi?
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- MI where myocytes replaced by fibroblasts
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venous thrombi aka?
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- phlebothrombi
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where are poss. venous thrombi?
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- DVT(larger vv at or above knee)
- SVT(saphenous vv.) |
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what are clinical findings of venous thrombi?
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- coldness, swelling lower legs
- stasis dermititis where skin falls off due to lack of O2 blood |
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how do arterial thrombi occur?
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- due to atherosclerosis(in tunica intima) or when the plaque breaks off taking endothelial cell monolayer w/it
- this type of thrombi always form secondary to some other cause |
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what are poss outcomes of thrombi?
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- resolution by fibrinolytic system
- embolize to lungs - become organized into the wall where smooth m. cells and fibroblasts join the clot make it more stronger - organize and recanalized by macs |
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what is dissemination intravascular coagulation(DIC)?
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- when clotting pathways are activated system wide and not enough clotting factors are present so instead several small micro fibrin clusters form leaving no clotting mechanisms causing bleed diathesis
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what is DIC caused by ?
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gram neg sepsis/septicemia
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dic aka?
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- consumption coagulopathy
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what is an embolism?
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- solid, liquid, gas that travels w/in vasculature
- naming occurs w/adding embolism at the end ie thromboembolism |
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what are diff types of embolisms?
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- air
- fat - amniotic fluid |
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what is cause of fat emboli?
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- long bone fracs esp in elder
- soft tissue trauma, - burns |
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describe fat embolism syndrome?
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- happens 1-3 days after injury
- pulmonary capillary occulsion - neurologic symptoms like microstrokes in brain - anemia - thrombocytopenia bc fat just absorbs them - petcheial rash - fatal in 10% pts |
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pathogenesis of fat emboli?
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- occulsion leading to chemical injury
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what does air emboli do overall?
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- bubbles obstruct pathway in vessels leading to ischemia
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what is cause of air emboli?
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- obstetric procedure
- chest injury - decompression sickness seen in divers |
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what happens when air emboli in lungs?
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called "chokes"
- edema - hemorrhage - respiratory distress |
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what happens when have gas/air embolis in skeletal m.?
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- very painful cond called "bends"
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tx for air emboli?
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- compression chamber
- more gradual decompression so gases can go back into soln |
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describe amniotic fluid emboli syndrome?
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- complication of labor where uterus is traumatized and vessel is torn to which amniotic fluid enters
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S/S of amniotic fluid emboli syndrome?
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- acute severe dyspnea(shortness of breath or cant breathe)
- cyanosis - hypotensive shock - seizures - coma pt rarely survives, if does will endup w/ -pulmonary edema -DIC in 50% cases |
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what is a infarction?
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- occulsion of a or v. leading to ischemic necrosis
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what is majority reason for infarct?
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- embolic event
MINOR: - vasospasm - extrinsic compression of vessel - twisting of vessels ie testicular a. twisted by twisted testicle |
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what are factors that influence development of infarction?
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- vascular supply and if there is collateral supply
- occulsion rate - tissue susceptibility - blood O2 content |
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describe shock
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- aka "cardiovascular collapse"
- occurs due to systemic hypoperfusion where not enough oxygenated blood to supply end organs - 3 types: cardiogenic, hypovolemic, septic |
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S/S of shock?
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- drop in bp (hypotension)
-reduction in Cardiac Output, drop in blood volume - pooling of blood |
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overall clinical course of shock?
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drop in absolute blood vol
hypotension impaired perfusion cellular hypoxia shock death if not resolved |
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describe cause of septic shock?
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- gram neg bacilli that produce endotoxin
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describe low quantities of endotoxin fm LPS
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- infxn will be localized
- macs, endothial cells, complement will be activated and lead to local inflammation which will improve chances of clearing infxn |
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describe moderate quantities of endotoxin fm LPS
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- infxn will cause fever
- acute phase reactants - circulating neutrophils & lead to system wide effects |
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describe high quantities of endotoxin fm LPS
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- immune system over-reacts: hypotension due to systemic vasodilation w/low cardiac output, DIC, ARDS
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examples of cardiogenic shock?
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- MI
- ventricular rupture - arrhythmia - cardiac tamponade (pericardium has fluid which prevent ventricles fm filling properly) - pulmonary embolism |
