SEMIO CH11 TRIGGER

HEMOSTASIS DEF

MECHANISM THAT STOPS BLEEDING AFTER VESSEL INJURY

4 PHASES OF PHYSIOLOGICAL HEMOSTASIS

VASOCONSTRICTION → PRIMARY HEMOSTASIS → SECONDARY HEMOSTASIS → FIBRINOLYSIS

VASOCONSTRICTION = DOES WHAT ? DURATION ?

VESSELS CONTRACTS : BLOOD FLOW ↓ → BLOOD LOSS ↓

→ RAPID AND TEMPORARY

PRIMARY HEMOSTASIS GOAL ?

FORM A PLATELET PLUG

THE 3 STEPS OF PRIMARY HEMOSTASIS ?

ADHESION → ACTIVATION → AGGREGATION

ADHESION =

PLATELETS STICK TO EXPOSED COLLAGEN

ADHESION REQUIRES ?

VON WILLEBRAND FACTOR → BIOLOGICAL GLUE

PLATELETS ACTIVATION →

ACTIVATED PLATELETS RELEASE TXA2

TXA2 =

MEDIATORS THAT ATTRACTS MORE PLATELETS

AGGREGATION

PLATELETS BINDS TO EACH OTHER → FORM PRIMARY PLATELET PLUG

PLATELETS NORMAL VALUE

150-450K

3 MAIN FUNCTIONS PLATELETS

PRIMARY HEMOSTASIS

INFLAMMATROY MEDIATORS

TISSUE REPAIR

SECONDARY HEMOSTASIS

FIBRIN USED TO MAKE A STABLE CLOT

COAGULATION FACTORS I–XIII SYNTHESIZED WHERE ?

LIVER

VITAMIN REQUIRED FOR SYNTHESIS OF COAGULATION FACTORS

VITAMINE K

TRIGGER VITAMINE K DEFICIENCY

CLOTTING FACTORS - / BLEEDING RISK +

2 COAGULATION PATHWAYS

EXTRINSIC AND INTRINSIC

BOTH PATHWAYS CONVERGE INTO

COMMON PATHWAY

TRIGGER EXTRINSIC PATHWAY

TISSUE DAMAGE → RELEASE OF FACTOR III

TRIGGER INTRINSIC PATHWAY

EXPOSED COLLAGEN + DAMAGED SURFACES

TRIGGER FACTOR COMMON PATHWAY

FACTOR X

FACTOR II

PROTHROMBIN

FACTOR I

FIBRINOGEN

MOST IMPORTANT FACTOR IN COAGULATION

THROMBIN

4 MAIN F° THROMBIN

CONVERTS FIBRINOGEN → FIBRIN

ACTIVATES PLATELETS

ACTIVATES OTHER COAGULATION FACTOR

AMPLIFIES COAGULATION

FIBRINLOLYSIS DEF

CLOT REMOVAL AFTER TISSUE REPAIR

WHAT USES FIBRINOLYSIS TO DEGRADE FIBRIN ?

PLASMINOGEN

HEMORRHAGIC DIATHESIS

HEMOSTATIC DISORDER → TENDANCE AU SAIGNEMENT

THROMBOTIC DIATHESIS ?

HEMOSTATIC DISORDER → TENDANCE A FORMER DES CAILLOTS → INTRAVASCULAR THROMBOSIS

SKIN + MUCOSAL BLEEDING <2 MM

PETECHIAE

SKIN + MUCOSAL BLEEDING 2MM–1CM

PURPURA

SKIN + MUCOSAL BLEEDING >1CM

ECHYMOSIS / HEMATOMA

MOST COMMON INHERITED BLEEDING DISORDER

VON WILLEBRAND DISEASE

TRIGGER VON WILLEBRAND DISEASE

INHERITED + DEFECTIVE PLATELETS ADHESION

TRIGGER ASPIRIN EFFECTS

TXA2 ↓ + PLATELET AGGREGATION ↓ + BLEEDING RISK ↑

SECONDARY HEMOSTASIS DISORDERS ARE MAINLY

COAGULATION FACTOR DEFICIENCY

HEMOPHILIA A →

FACTOR VIII DEFICIENCY

HEMOPHILIA B →

FACTOR IX DEFICIENCY

HEMOPHILIA DEF

X LINKED COAGULATION DISORDER

<50,000 PLATELETS RISK ?

HIGH BLEEDING RISK

PT TEST SERT A ÉVALUER ?

EXTRINSIC PATHWAY CLOTTING TIME

NORMAL VALUE PT

12 SECONDES

PT PROLONGED =

SANG MET TROP DE TEMPS À COAGULER → PROBLEM EXTRINSIC PATHWAY

APTT SERT A ÉVALUER

INTRINSIC PATHWAY CLOTTING TIME

NORMAL VALUE APTT

34-38S

PROLONGE APTT

PROBLEM W/ INTRINSIC PATHWAY

SI PT ↑ + APTT ↑

COMMON PATHWAY PROBLEM

INR SERT À

DONNER LA MEME INFO QUE PT MAIS DE MANIERE STANDARDISÉE

NORMAL VALULE INR

INR = 1 → COAGULATION NORMALE

HEPARIN ENTRAINE ↑ ?

APTT ↑

WARFARIN ENTRAINE ↑ ?

PT ↑ INR ↑

MAIN CLAUSE DE INR ↑ ?

ANTICOAGULANT DRUG (HEPARIN / WARFARIN)

TRIGGER INR ↑ SANS ANTICOAGULANTS ?

→ PROBLEME DE PRODUCTION DES COAGULATION FACTORS

→ LIVER FAILURE

DIFFERENCE CLAIRE PRIMARY / SECONDARY HEMOSTASIS

PRIMARY → PLATELETS / CLOT FORMATION / BLEEDING TIME

SECONDARY → COAGULATION FACTORS / CLOTTING TIME

ASPIRIN → AGIT SUR QUELLE HEMOSTASIS ?

AGIT SUR PRIMARY HEMOSTASIS → ANTIPLATELETS DRUGS → BLEEDING TIME ↑

HEMOPHILIA = ENDOMMAGE QUEL PATHWAY ? DONC AUGMENTATION DE ↑ ?

ENDOMMAGE INTRINSIC PATHWAY

→ ENTRAINE DONC APTT ↑

TEST POUR PRIMARY HEMOSTASIS

PLATELET COUNT

TEST POUR SECONDARY HEMOSTASIS ?

APTT

PT / INR

TEST POUR INTRINSIC PATHWAY ?

APTT

TEST POUR EXTRINSIC PATHWAY ?

PT / INR