HEMOSTASIS COAGULATION Flashcards

(25 cards)

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
ASPIRIN MOA?
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.