Term
| HOW DOES INDIRECT THROMBIN INHIBITORS WORK? |
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Definition
| BIND TO AND ENHANCE ANTITHROMBIN TO PRODUCE ANTITHROMBOTIC EFFECTS. INCLUDES THE HEPARINS: UNFRACTIONATED (STANDARD) AND LOW-MOLECULAR WEIGHT) |
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Term
| IN THE BEGINING OF HEPARIN ACTIVATION WHAT DOES HEPARIN FORM A BOND WITH? |
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Definition
| ANTITHROMBIN AND CAUSES A CONFORMATIONAL CHANGE. THE HEPARIN ACCELERATES THE ACTIONS OF THE ANTITHROMBIN TO 1000 TIMES FASTER THAN NORMAL. |
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Term
| WHAT FACTORS DOES ANTITHROMBIN INHIBIT? |
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Definition
| IIA, IXA, XA, XIA, XIIA. IIA AND XA ARE BIGGEST. |
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Term
| WHAT PATHWAY DOES HEPARIN WORK ON? |
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Definition
| INTRINSIC AND COMMON PATHWAY. ONCE THE HEPARIN CAUSES THE CONFORMATIONAL CHANGE AND THE ANTITHROMBIN HAS INTERACTED WITH THE PROTEASES AND CLOTTING FACTORS, THE HEPARIN CAN DISSOCIATE FROM THE ANTITHROMBIN AND BE RELEASED INTACT TO BIND TO NEW ANTITHROMBIN. |
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Term
| EXOGENOUS HEPARIN IS FOUND IN WHAT TYPE OF CELLS (X2) AND IN WHAT ORGAN? |
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Definition
| BASOPHILS, MAST CELLS, AND THE LIVER |
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Term
| ONLY ABOUT __ OF THE HEPARIN IN COMMERCIAL PREPARATIONS BIND TO ANTITHROMBIN. |
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Definition
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Term
| WHERE DOES EXOGENOUS HEPARIN TYPICALLY COME FROM? |
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Definition
| BOVINE LUNG, OR BOVINE OR PORCINE GI MUCOSA (INCREASED R/O ALLERGENIC POTENTIAL). |
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Term
| IS HEPARIN LIPID OR FAT SOLUBLE? + OR - CHARGE? |
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Definition
| POORLY LIPID SOLUBLE. HEPARIN IS HIGH MOLECULAR WEIGHT. HIGHLY NEGATIVELY CHARGED PARTICLES. THESE 3 RELATE IN POOR DISTRIBUTION. |
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Term
| ELIMINATION OF HEPARIN IS BY WHAT? EXCRETION IS THROUGH WHAT ORGAN? |
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Definition
| RETICULOENDOTHELIAL SYSTEM AND SOME HEPATIC. EXCRETION IS RENAL (ABOUT 50% UNCHANGED) |
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Term
| WHAT 3 THINGS CAN GREATLY PROLONG ELIMINATION? |
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Definition
| HYPOTHERMIA, HEPATIC, AND RENAL DYSFUNCTION |
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Term
| WHAT IS THE DOSE OF HEPARIN FOR DVT PROPHYLAXIS? |
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Definition
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Term
| WHAT IS THE DOSE OF HEPARIN FOR VASCULAR SURGERY? |
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Definition
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Term
| WHAT IS THE DOSE OF HEPARIN FOR CARDIOPULMONARY BYPASS? |
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Definition
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Term
| WHAT IS THE ONSET OF HEPARIN IV AND SQ? |
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Definition
| IMMEDIATE FOR IV (GIVE AND WAIT 3 MINUTES FOR CIRCULATION). SQ USUALLY 1-2 HRS |
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Term
| WHAT IS THE HALF-LIFE OF HEPARIN? |
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Definition
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Term
| WHEN SHOULD HEPARIN BE DISCONTINUED PRIOR TO SX? |
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Definition
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Term
| WHAT 4 SIDE EFFECTS ARE ASSOCIATED WITH HEPARIN? |
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Definition
| BLEEDING, HYPOTENSION, ALLERGIC REACTIONS, AND HEPARIN-INDUCED THROMBOCYTOPENIA (HIT) |
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Term
| WHAT IS THE HYPOTENSION R/T WITH HEPARIN? |
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Definition
| RAPID IV ADMINISTRATION OF LARGE DOSES, AS USED IN CPB CAN CAUSE A DECREASE IN MAP AND PAP (R/T SOME HISTAMIN RELEASE). |
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Term
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Definition
| ANTIBODIES DEVELOP THAT TARGET PLTS AND REMOVE THEM FROM CIRCULATION. PLT COUNT DECREASES BY 50-75% BY 5 DAYS INTO HEPARIN THERAPY. PLTS ARE ALSO ACTIVATED, LEADING TO AGGREGATION AND THROMBOSIS (BECOMES HITT AT THIS POINT). NEARLY ALWAYS REQUIRES PREVIOUS EXPOSURE TO HEPARIN. |
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Term
| DESCRIBE WHAT ESTROGEN DOES TO HEPARIN? |
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Definition
| ESTOGEN CONTAINING CONTRACEPTIVES DECREASE CIRCULATING ANTITHROMBIN. LESS EFFECT FROM HEPARIN D/T LESS TARGET SITES FOR IT TO WORK ON. |
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Term
| DESCRIBE THE INTERACTION WITH NTG AND HEPARIN. |
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Definition
| NTG MAY INCREASE THE DOSE OF HEPARIN REQUIRED. |
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Term
| WHAT 5 THINGS CAUSES HEPARIN RESISTANCE? |
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Definition
| ANTITHROMBIN DEFICIENCY, LIVER DISEASE, HEMODILUTION, CPB, PRIOR HEPARIN THERAPY (RECENT). |
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Term
| WHAT IS THE TREATMENT OF HEPARIN RESISTANCE? |
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Definition
| FFP TO ALLOW MORE SITES FOR HEPARIN TO WORK. |
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Term
| WHAT LAB DOES SHOULD BE MONITORED FOR HEPARIN? |
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Definition
| APTT, ACT, H&H, AND PLTS. PT/INR MEASURE EXTRINSIC AND COMMON PATHWAY. PTT AND ACT MEASURE INTRINSIC AND COMMON PATHWAY |
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