HEMOSTASIS

Question 0

WHAT ARE TEH 4/5 PROCESSES THAT SLOW DOWN BLEEDING/CAUSES HEMOSTASIS?

Answer 0

1. VASOCONSTRICTION OF VESSEL WALL LOCAL/SYSTEMIC CONTROL
2. PLATELET( THROMBOCYTE) CLUMPING AT THE BLEEDING SITE.
3. CLOTTING FACTORS/PROTEINS FORM FIBRIN CLOT VIA INTRINSIC/EXTRINSIC TO COMMON PATHWAY.
4. FACTOR 13 IS ACTIVATED WHICH CONSOLIDATES CLOT BY CROSSLINKING FIBERS AND TRAPPING RBC.
   5ISH: FIBRINOLYSIS=BREAKDOWN OF FIBRIN (SLOWER THAN CLOTTING CASCADE) AS ENDOTHELIUM REGENERATES.

Question 1

HEMOSTASIS IS DEPENDENT ON WHICH 2 THINGS?

Answer 1

FLOW AND TIME. FOR A CLOT TO FORM YOU NEED LOW FLOWS (HYPOTENSION) AND APPROX 10 MIN.

Question 2

WHAT ARE THE LOCAL VS. SYSTEMIC CONTROLS FOR VASOCONSTRICTION OF VESSEL WALL?

Answer 2

LOCAL: THROMBOXANE, ADP, 5HT……RELEASED AT THE SITE OF INJURY.
SYSTEMIC: EPI RELEASED BY THE ADRENAL GLANDS AND STIMULATES GENERAL VASOCONSTRICTION.

ONCE VASOCONSTRICTORS ARE EXPOSED PLTS CLUMP.

Question 3

WHEN FORMING A PLT PLUG IN STEP 2…WHAT CAUSES PLTS TO BE STICKY?

Answer 3

ADP, THROMBOXANE. AND VON WILLIBRAND FACTOR COMBINED WITH GLYCOPROTEIN 1B ACTS AS GLUE TO HOLD PLT IN PLACE AT THE SITE OF THE DAMAGE TO THE BLOOD VESSEL.

Question 4

WHAT INHIBITS PLT AGGREGATION?

Answer 4

PROSTACYCLINE

Question 5

WHAT ARE THE FUNCTIONS OF THROMBIN ?

Answer 5

CONVERTS FIBRINOGEN TO FIBRIN.
ACTIVATES FACTOR 5, 8, 13
STIMULATES PLT AGGREGATION
ACTS AS ANTICOAGULANT TO PREVENT OUT OF CONTROL CLOTTING BY RELESASE OF TPA.

(ESSENTIALLY IT PROVIDEES POSITIVE FEEDBACK FOR THE ACCELERATION OF CLOTTING.

Question 6

WHAT DOES FACTOR 13 ACT ON AND WHAT DOES IT DO?

Answer 6

ACTS ON FIBRIN. TAKES “LOOSE” FIBRIN POLYMERS AND CROSS LINKS THEM TO MAKE A FIRM INSOLUBLE CLOT THAT ATTRACTS RBC’S.

Question 7

WHAT DOES PT/PTT MEASURE?

Answer 7

THE TIME IT TAKES FOR CLOTTING FACTORS (OF THE INTRINSIC AND EXTRINSIC PATHWAYS) TO DO THIER WORK.

Question 8

WHAT FACTORS ARE INVOLVED IN THE INTRINSIC PATHWAY?

Answer 8

8,9, 11, 12.

TRIGGERED BY ELEMENTS THAT LIE WITHIN THE BLOOD, STIMULATED BY DAMAGE TO VESSEL WALL.

Question 9

WHAT CLOTTING FACTORS ARE INVOLVED IN THE EXTRINSIC PATHWAY?

Answer 9

3 &7. TRIGGERED BY DAMAGE OUTSIDE THE BLOOD VESSEL AND ACTS TO CLOT BLOOD THAT HAS ESCAPED FROM VESSEL INTO TISSUES.

Question 10

WHAT IS THE COMMON PATHWAY?

Answer 10

WHERE EXTRINSIC AND INTRINSIC PATHS CONVERGE ON FACTOR 10, WHICH CONVERTS PROTHROMBIN TO THROMBIN. THIS PATH INVOLVES FACTORS 1,2, 5, 10, 13.

Question 11

WHERE ARE COAGULATION FACTORS/PROTEINS FORMED?

Answer 11

LIVER. EXCEPT VWF AND FACTOR 8 (WHICH FORM A COMPLEX) ARE PRODUCED IN ENDOTHELIAL CELLS.

Question 12

IS CALCIUM IMPORTANT FOR CLOTTING?

Answer 12

YES. ITS OBTAINED FROM THE DIET. IMPORTANT FOR FIBRIN MONOMERS TO BECOME FIBRIN POLYMERS.

Question 13

WHAT ARE THE VIT K DEPENDENT FACTORS?

Answer 13

2, 7, 9, 10. VIT K IS PRODUCED BY INTESTINAL BACTERIA AND BILE SALTS FORMED IN THE LIVER ARE ALSO REQUIRED FOR VIT K ABSORPTION FROM THE GUT.

Question 14

WHAT ARE SOME EXAMPLES OF INITIAL DAMAGE THAT WOULD CAUSE THROMBUS FORMATION?

Answer 14

• ENDOTHELIAL DAMAGE….HTN, TOXINS, IMMUNE INJURY.
• DECREASED BLOOD FLOW VENOUS STASIS OF HYPOTENSION PROMOTE BUILDUP OF THROMBIN IN VESSELS….AS IN PVD, AFIB.
• HYPER COAGULABILITY. IMBALANCE BTW CLOT FORMING/BREAKING PROTEINS….REDUCED ANTITHROMBIN 3, PROTEIN C/S, DECR. FIBROLYTIC ACTIVITY.
• DISEASES THAT CAUSE HEMOSTATIC DISORDER….DEFECT IN PLT, COAG, AND FIBRINOLYTIC SYSTEMS…IE: HEMOPHILIA, VWB DISEASE, LIVER DISEASE, MALNUTRITION.

Question 15

HOW ARE CLOTS CONTROLLED SO THEY DONT GET OUT OF HAND?

Answer 15

• FIBRIN IS BROKEN DOWN. AKA FIBRINOLYSIS.
• ENZYMES (PLASMIN: FORMED BY PLASMINOGEN, ANTITHROMBIN 3, AND UROKINASE COMBINATION) INHIBIT CLOTTING FACTORS AND DISSOLVE THE BLOOD CLOT.

Question 16

WHAT STUDIES EVALUATE COAGULATION?

Answer 16

• BLEEDING TIME AND PLT COUNT LOOK AT PLT QUALITY AND QUANTITY.
• aPTT LOOKS AT INTRINSIC AND COMMON PATHWAYS (HEPARIN THERAPY).
• PT LOOKS AT EXTRINSIC AND COMMON PATHWAYS (COUMADIN).
• TT MEASURES CONVERSION OF FIBRINOGEN TO FIBRIN VIA THROMBIN.
• BLEEDING TIME LOOKS AT THE TIME IT TAKES FOR BLEEDING TO STOP/TIME IT TAKES FOR PLT PLUG TO FORM (ASA THERAPY, VW DISEASE, THROMBOCYTOPENIA.
• ACT LOOKS AT INTRINSIC AND COMMON PATHWAYS (HEPARIN) OPEN HEART.
• TEG LOOKS AT THE WHOLE 4/5 STEPS (INTEGRITY OF ENTIRE COAGULATION CASCADE. CLOT FORMATION AND DISSOLUTION OVER TIME.

Question 17

WHAT TESTS LOOK AT THE BREAKDOWN OF A CLOT?

Answer 17

FIBRINOGEN AND FIBRINOGEN DEGRADATION PRODUCTS.

Question 18

WHAT IS THE BEST METHOD TO IDENTIFY BLEEDING OR THROMBOSING TENDENCIES?

Answer 18

THOROUGH H AND P.

Question 19

WHAT IS VON WILLEBRANDS DISEASE?

Answer 19

INHERITED DISEASE IN MENA ND WOMEN LESS SEVERE THAN HEMOPHILIA A. LOW VWF SO IT CANT BIND WITH FACTOR 8 AND CREATE PLT ADHESION IN STEP 1. S/S VARY. TEST: PT AND HISTORY…MAY HAVE NORM PLT COUNT. TX: FASTEST IS RECOMBINANT FACTOR 8-VWF CONCENTRATE. DDAVP (INCR RELEASE OF VWF). CRYO (PROVIDES FACTOR 8) ESP USEFUL IF UNRESPONSIVE TO DDAVP. FFP(HAS ALL CLOTTING FACTORS)

Question 20

WHAT IS HEMOPHILIA A OR B.?

Answer 20

A: FACTOR 8 DEFICIENCY. OCCURS ONLY IN MALES…X LINKED.
B (CHRISTMAS DISEASE): FACTOR 9 DEFICIENCY.
TEST FOR BOTH: PLT CT, FXN, AND COAG PANNEL.
TX: FACTOR 8 OR CONCENTRATES. CRYO. DDAVP.

Question 21

WHAT MEDICATIONS ARE ASSOCIATED WITH BLEEDING?

Answer 21

AMITRIPTYLIINE, CEPHALOSPORINS, INDOMETHACIN, IMIPRAMINE, PHENYLBUTAZONE. HERBAL SUPPLEMENTS, ASA AND NSAIDS. PLAVIX AND TICLID. HEPARIN. COUMADIN OR DICOUMAROL.

Question 22

WHAT ARE FACTORS THAT INCREASE POSTOP BLEEDING?

Answer 22

ABNORMAL PROP LOTTING, ELEVATED POSTOP BP, USE OF ANTIBIOTICS, DILUTIONAL COAGULOPATHY, BYPASS SURGERY.

Question 23

WHAT DEFICIENCIES WOULD YOU SEE WITH ABNORMAL CLOTTING….CREATING A RISK OF THROMBOEMBOLISM?

Answer 23

ANTITHROMBIN 3 DEFICIENCY, PROTEIN C OR PROTEIN S DEFICIENCY.