HEMOSTASIS COAGULATION Flashcards

0
Q

WHAT DOES ANTITHROMBIN DO?

A

ITS A NATURAL ANTICOAG. THAT INACTIVATES CLOTTING FACTORS 2,10.

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1
Q

WHAT DOES HEPARIN DO TO ANTITHROMBIN?

A

HEPARIN MAKES ANTITHROMBIN ( A NATURAL ANTICOAGULANT PROTEIN IN YOUR BODY) WORK FASTER.

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2
Q

DOES UNFRACTIONATED HEPARIN WORK EQUALLY WELL ON FACTOR 2 (THROMBIN) AND FACTOR 10?

A

YES. THE LONGER UNFRACT. HEPARIN CHAIN MAKES IT POSSIBLE TO CATALYZE THE INACTIVATION OF FACTOR 2 AND 10 IN A 1:1 RATIO.

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3
Q

WHAT PREFERENCE OF CLOTTING FACTOR DOES LMWH HAVE AND WHY?

A

LMWH CATALYZES THE INACTIVATION OF FACTOR 10 MORE EFFICIENTLY THAN FACTOR 2 BECAUSE LMWH HAS A SHORTER TAIL THAN UNFRACT. HEPARIN.

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4
Q

WHICH IS MONITORED WITH PTT?

A

UNFRACTIONATED HAPARIN.

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5
Q

WHY ISNT LMWH MONITORED WITH A PTT?

A

PTT IS MORE SENSITIVE TO CHANGES IN FACTOR 2 LEVEL AND LMWH AFFECTS FACTOR 10 MUCH MORE THAN 2.

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6
Q

WHAT ARE SOME OF THE MAJOR RESULTS OF THE SHORTER CHAIN ON LMWH?

A

MOSTLY RENAL EXCRETION AND METABOLISM, 90-100% ABSORBED SYSTEMICALLY FROM SUBQ (OPPOSED TO 20%) , IT IS ONLY PARTIALLY REVERSED BY PROTAMINE.

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7
Q

IS LMWH USED FOR BRIDGING?

A

YES

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8
Q

WHAT DO YOU USE TO MONITOR VERY HIGH LEVELS OF HEPARIN (UFH)?

A

ACT, ACTIVATED CLOTTING TIME

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9
Q

WHAT ARE ADVERSE EFFECTS OF EITHER TYPE OF HEPARIN?

A

BLEEDING, HIT, RARE-OSTEOPOROSIS, HYPERKALEMIA, INCREASED AST AND ALT.

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10
Q

WHAT ARE SIDE EFFECTS AND THINGS TO THINK ABOUT WHEN GIVING PROTAMINE?

A

COMMON SIDE EFFECTS: BRADYCARDIA, HYPOTENSION, FLUSHING, N/V.
PRIOR EXPOSURE TO NPH INSULIN IS THE MOST COMMON FACTOR FOR PREDISPOSING TO AN ANAPHYLACTIC RXN WITH PROTAMINE. OTHER REASONS: FISH ALLERGY, MEN WITH VASECTOMY HAVE ANTIPORTAMINE IgG.

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11
Q

WHICH HAS A LONGER HALF LIFE, HEPARIN OR PROTAMINE?

A

HEPARIN SO REPEAT PROTAMINE DOSING MAY BE REQUIRED.

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12
Q

WHAT IS MOA OF DIRECT THROMBIN INHIBITORS (DTI)?

A

DONT NEED ANTITHROMBIN (LIKE UFH AND LMWH DO), IT DIRECTLY INHIBITS ALL ACTIONS OF THROMBIN. WORKS ONLY ON FACTOR 2.

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13
Q

WHY IS ARGATROBAN AN OUTLIER OF THE DTI’S?

A

ITS METABOLIZED IN THE LIVER INSTEAD OF THE KIDNEYS LIKE OTHER DTI’S.

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14
Q

WHAT IS A MAJOR DRAWBACK TO DABIGATRAN? A DIRECT THROMBIN INHIBITOR.

A

NO REVERSAL AGENT IS AVAILABLE!

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15
Q

IS PTT A USEFUL TEST FOR DABIGATRAN?

A

LIMITED USEFULNESS. THERE IS NOT A LINEAR RELATIONSHIP BTW DABIGATRAN AND PTT BUT IF PTT IS AT BASELINE, SURGERY CAN PROCEED.

16
Q

WHAT IS THE MOA OF FACTOR 10 INHIBITORS?

A

INHIBIT FACTOR 10 ONLY (NOT 2) EITHER INDIRECTLY USING ANTI THROMBIN OR DIRECTLY BY ACTING DIRECTLY ON FACTOR 10

17
Q

WHAT IS A GOOD RULE OF THUMB FOR ALL DRUGS TO FIGURE OUT IF DRUG IS CLEARED FROM SYSTEM?

A

5X (1/2 LIFE) OF DRUG

18
Q

WHAT IS THE MOA OF WARFARIN?

A

ITS A VIT K ANTAGONIST (VIT K PRODUCES CLOTTING FACTORS). CLOTTING FACTOR 2 7 9 10 PRODUCTION IS INHIBITED. VIT K ALSO INHIBITS SYNTHESIS OF NATURAL ANTICOAGULANTS POTEIN C AND C.

19
Q

HOW DO YOU MONITOR WARFARIN?

A

INR. DESIRED THERAPUTIC INR IS 2-3.

20
Q

DIETARY CONSIDERATIONS WITH COUMADIN?

A

CONSISTANT INTAKE OF VIT K FOODS. SEPARATE SOY AND FIBER FOODS BY A MINIMUM OF 4 HRS BECAUSE IT BINDS TO COUMADIN IN THE GUT AND PREVENTS ITS ABSORPTION.

21
Q

WHO SHOLD RECEIVE BRIDGE THERAPY?

A

ONLY PTS WITH SIGNIFICANT RISK FOR THROMBOSIS, AVOID IT IF YOU CAN. MECHANICAL HEART VALVE, STROKE OR TIA IN PAST 3 MO. VTE IN KPAST 3 MO.

22
Q

HOW IS COUMADIN REVERSED?

A

IMMEDIATE REVERSAL: FFP OR PROTHROMBIN COMPLEX CONCENTRATE PCC.
REVERSAL IN 8 HRS: VIT. K WILL TAKE EFFECT IN 8 HRS. SO TAKE AN INR 8 HRS LATER….NOT SOONER.

23
Q

WHAT IS THE ONLY CLASS OF DRUGS THAT DISSOLVES THE CLOT?

A

FIBRINOLYTICS OR THROMBOLYTICS.

24
Q

ASPIRIN MOA?

A

IRREVERSIBLE INHIBITION OF PLATELET COX ENZYME. UNLIKE OTHER NSAIDS ASA ACETYLATES COX1 AND 2. THIS INHIBITS PLATELET AGGREGATION FOR THE LIFE SPAN OF THE PLT (7-10 DAYS) SO NEED TO HOLD ASA 7-10 DAYS PRIOR TO SURGERY.