HEMATOLOGY - coagulopathy & DIC Flashcards
EXAM 2 content
what is hemostasis?
the process of arresting/stopping bleeding by forming clots at sites of vascular injury
what is the process of hemostasis?
- vascular injury –> transient arteriolar vasoconstriction –> limits blood flow at site
- damage to endothelial lining of vessels –> plate adherence, activation & formation of PLATELET PLUG = primary hemostasis
– > tissue factor works w secreted plate factors + activated platelets –> activate clotting (coagulation) system –> forms fibrin clots = secondary hemostasis
–> fibrin/plate clot contracts –> more permanent plug
–> fibrinolysis = clot retraction & clot dissolution
what is coagulation? what is the coagulation cascade?
- coagulation = presence of all clotting factors + functioning of each component
- component = cascades = a step by step process
- coagulation cascade = presence of clotting factors functioning in a step by step process
what are the two pathways that can stimulate the coagulation cascade? what happens in them?
- intrinsic pathway: activated by collagen exposure from endothelial injury = when blood vessel in damaged (tested by aPTT)
- extrinsic pathway: activated by tissue injury when tissue factor or tissue thromboplastin in released into bloodstream (tested by PR + INR)
when the intrinsic or extrinsic pathway is activated, what is the clotting cascade that happens?
conversion of prothombin to thrombin –> thrombin acts to convert fibrinogen to fibrin –> fibrin mesh forms –> traps platelets & RBCs –> stable fibrin clot
what is disseminated intravascular coagulation (DIC)?
bleeding & thrombotic disorder bc of an underlying disease or disorder – its ALWAYS caused by something else
- infection and sepsis!
- cancer!
- trauma
- shock
- obstetrical complications
- blood transfusion reactions
what is the pathophysiology of DIC?
underlying disorder triggers proinflammatory cytokine release –> activates coagulation cascade –> microclots obstructing capillaries of organs & tissues –> organ failure –> body attempts to break down clots –> fibrin split products that inhibits clotting –> clotting factors are gone –> bleeding & hemorrhage
clot clot clot –> bleed bleed bleed
- clots –> all clotting factors are used –> bleeds
what are the signs of microvascular thrombosis of DIC?
- neurologic: multifocal, delirium & coma
- integumentary: focal ischemia & superficial gangrene
- renal: oliguria, azotemia & cortical necrosis
- pulmonary: acute respiratory distress syndrome
- GI: paralytic ileus
what are the signs of hemorrhage of DIC? (develops later after all clotting factors are consumed)
- neurologic: intracerebral bleeding
- integumentary: petechiae, ecchymoses & venipuncture oozing
- renal: hematuria
- pulmonary: respiratory congestion, dyspnea & hemoptysis
- mucous membranes: epistaxis & gingival oozing
- GI: massive bleeding
what kind of lab findings would we see in someone with DIC? is there a definitive test?
NO DEFINITIVE TEST
prolonged PT & aPTT
- prothrombin time: measures clotting factors of EXTRINSIC & common pathways of coagulation
aPTT: measure clotting factors of INTRINSIC & common pathways of coagulation
- decreased plate count – bc consumed by clotting
- decreased fibrinogen – clotting factors consumed
- increased d-dimer – shows ongoing hemostatic system = coagulation, clumping, fibrinolysis
- detection of fibrin split products – produced when body tries to break down clots
what is the disease track of DIC? what is our goal? what is the treatment?
GOAL: eliminate underlying disorder –> liver can restore norm lvls of clotting factors within 24-48 hrs if eliminated
- maintenance of organ function – fluid & oxygen
- blood products for active bleeding or for invasive procedures
- anticoagulants –> increase risk of bleeding
lets say we give anticoagulants, what if the pt starts bleeding?
replacement of coagulation factors, platelets, & other coagulation elements
- risk of increase thrombosis
controlling ongoing thrombosis is difficult to attain
- earlier recognized & treated –> more likely pt will survive
