WV$OM -- Anticoagz and Anemia
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| What are the 2 major type of Thrombi? | White and red
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| What causes red thrombi? | hemostasis problems (DVT, PE, Atrial)
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| What is the difference between UA, NsTEMI and sTEMI? | UA has no cardiac enzymes, NsTEMI has + Cardiac Enzymes,sTEMI has a full occlusion.
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| How do you monitor Heparin? | aPTT
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| What is tx for PE/DVT? | Fibrinolyisis, immediate anticoagulation and long term anticoagulation
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| What is tx for atrial fib coagulation? | immediate anticoagulation and long term anticoagulation
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| Why do you not use fibrinolysis for atrial fib? | Risk of bleeding is too high.
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| What Is tx for sTEMI? | Fibrinolysis, immediate anticoag and antiplatelet
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| What is tx for NsTEMI, Unstable angina and PCI? | immediate anticoagulation and antiplatelet therapy
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| What causes white Thrombus? Damaged vessel wall |
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| What is the main difference between the pharmacological tx of sTEMI and NsTEMI? | fibrinolysis
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| Classes of anticoag | Heparin, Direct thrombin inhibitor and warfarin
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| Route of Heparin | parenteral
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| Route of direct thrombin inhibitor | parenteral
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| Route of warfarin? | oral
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| Heparin agents | UFH and LMWH
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| Name of LMWH end in…. | -parin
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| UFH MoA | accelerates reaction between antithrombin and thrombin and antithrombin and Factor Xa
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| LMWH MoA | accelerate reaction between antithrobin and factor Xa
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| What is a ternary complex? | Thrombin and antithrombin wrapped up with UFH
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| Route of UFH | IV or subQ… usually IV
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| Pharmacokinetic of UFH | IV or subQ, unpredictable anticoag effect, monitor aPTT
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| Pharmoacokinetic of LMWH | subQ (usually) or IV, predictable, no monitoring needed. Can be used at home
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| Why I LMWH better than Heparin? | predicable. Can be used at home. No monitoring needed. Lower chance of HIT.
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| Where is heparin metabolized? | liver and reticuloendothelial system
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| Rate of clearance of UFH | dose dependant
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| How I LMWH eliminated? | renal elimination
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| Rate of clearance of LMWH? | independent clearance
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| Which has a longer half life between UFH and LMWH? | LMWH (4.5 h)
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| Heparin clinical use | PE, DVT, postop venous thrombosis, arterial embolism, sTEMI, UA, NsTEMI, PCI
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| What anti coag used in sTEMI? | heparin
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| Heparin Adverse reactions | HIT and bleeding
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| Why does HIT occur? | Heparin binds to PF4 and cause Thrombocytopenia
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| What happens to platelet count with HIT type 2? | Decreased (used up platelets)
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| What is the predominant clinical presentation with HIT type 2? | Clots
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| HIT tx | Heparin must be stopped. Put on Direct Thrombin inhibitors
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| should you give enoxaparin to a patient who has HIT? | NO
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| Heparin antidote | protamine sulfate
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| What I MOA of fondaparinux? | Synthetic pentasaccharide that I selective factor Xa. Binds to antithrobin binding region of Heparin. Accelerate AT and Xa
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| How is fondapariuz administered? | subQ
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| Does fondapariunx require monitoring? | no
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| Clincial use of Fondapariux? | prophylaxis of DVT in patients undergoing orthopedic or ABD surgery, PE and DVT, UA/NsTEMI and sTEMI
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| Fondaparinux adverse effects | bleeding, thrombocytopenia and renal impairment
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| Thrombin Inhibitors | -irudin
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| Thrombin Inhibitor MoA | directly bind to and inhibit thrombin. Independent of anti-thrombin. Inhibits free and fibrin bound
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| What is the difference between lepirudin and heparin? | Lepirudin I direct thrombin inhibitor and inhibits soluble and clot bound thrombin. Heparin requires anti-thrombin and only inhibitssoluble thrombin
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| How I rudins administered?: | IV
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| Clinical use of thrombin inhibitors | HIT and HIT undergoing PCI
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| Drug of choice for PCI | Bivalirudin
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| Adverse reaction Thrombin Inhibitors | bleeding and allergic reaction (Lepirudin)
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| Oral Anticoagulant | warfarin
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| Warfarin MoA | Vitamin K antagonist. Inhibits synthesis of vit K dependent clotting factor in liver (II, VII, IX and X) and synthesis of protein C and s.
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| How does warfarin inhibit vit K? | Reduces KO to KH2 by KO reductase. Warfarin inhibits vit KO reductase. Prevents carboxylation of vit K dependant coagulation factors.
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| When do you start warfarin? | in conjunction with heparin
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| How do you monitor warfarin? | PT time (INR)
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| Where is warfarin metabolized? | metabolized in liver and most I bound to albumin
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| Clinical use of warfarin | chronic a fib prosthetic heart valve, people at risk following surgery, trauma or cancer. DVT or PE. sTEMI
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| How would you use heparin and warfarin to anticoag a person who develops a DVT? | same time
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| A patient is scheduled for an angioplasty. What anticoagulant may be administered just prior to the procedure? | heparin and thrombin inhibitor
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| Warfarin adverse effects | bleeding and skin necrosis
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| What causes skin necrosis with Warfarin? | reduced activity of protein C causing hyper coaguable state
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| What is protein C? | endogenous anti coagulant.
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| When is warfarin the most teratogenic? | first trimester. syndrome characterized by nasal hypoplasia and stippled epiphyseal calcifications that resemble chondrodysplasia punctata
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| What happens with warfarin in 2nd and 3rd trimester? | CNs abnormalities and fetal or neonatal hemorrhage. Much less common than first trimester exposure
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| What drugs are used in HIT? | Thrombin inhibitor
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| What determines the response to heparin dosages? | diet, compliance, liver function, thyroid function, genetics, drugs and herbals
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| What is narrow therapeutic index of warfarin? | narrow
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| Antidote for warfarin | vitamin K1 and fresh frozen plasma or prothrombin complex concentrate
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| What are the antiplatelet agents? | cyclooxygenase inhibitors, ADP receptor antagonist, glycoprotein IIb/IIIa receptor antagonists and PDE inhibitors
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| What is a cyclooxygenase inhibitor? | AsA
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| Aspirin MoA | irreversibly inhibits cyclooxygenase. COX-1 more than COX-2. Block production of TxA2 (platelet)
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| COX-1 convert prostaglandin H2 to? | TxA2 (vasoconstrictor. Promotes platelet aggregation
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| Do you want to inhibit the production of PGI2 or TxA? | TxA2 becuae PGI2 inhibits platelet aggregation
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| Why I cyclooxygenase inhibited for only a short time in endothelial cells and forever in the platelet? | endothelial cells make new enzyme while platelets can’t make any more
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| Why do other NsAIDs not work in platelet inhibition? | reversibly inhibits PGI2 AND TxA2
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| Clinical use of Aspirin | sTEMI and NsTEMI and UA. PCI. Embolic stroke
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| What is dose of aspirin? | 81 mg
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| Aspirin adverse effect | GI irritation and bleeding becaue it inhibit the synthesis of prostaglandins that promote secretion of bicarb and mucous
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| ADP receptor antagonist | clopidogrel (Plavix)
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| GP IIb/IIIa receptor antagonist | Abciximab (antibody)
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| Route of clopidogrel | oral. Use similar to Aspirin
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| Route of Abciximab | IV
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| Use of abciximab | PCI, UA or NsTEMI
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| Which agents may be used for the secondary prevention of an acute MI? | clopinadril, aspirin and warfarin
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| Which agents may be used to prevent thrombosis during PCI? | heparin, abciximab and rudin
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| Thrombolytic agents | alteplase, reteplase, tenecteplase, streptokinase, anistreplase
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| Which thrombolytic agents are recombinant t-pa? | alteplase, reteplase and tenecteplase
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| Which thrombolytics are isolated from Hemolytic strep? | streptokinase
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| What is t-pa? | breaks down fibrin
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| Thrombolytics MoA | catalyze formation of plasmin from plasminogen
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| Thrombolytic Clincal use | sTEMI, DVT, PE, CVA
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| Why give tenecteplase over streptokinase? | Lots more nursing time with streptokinase due to short half life and allergic anaphylactic reactions that are possible
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| Administration of streptokinase compaired to other thrombolytics | constant infusion
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| What are causes of IDA? | blood loss, inc requirement (Pregnancy) and inadequate iron intake
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| Clincal use or iron | IDA (microcytic, hypochromatic anemia)
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| Dose for Iron and why | 200mg because 50-100mg can be incorporated into Hb a day and 25% of oral iron a ferrous alt can be absorbed.
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| Parenteral Preparation of iron | iron dextran, iron sucrose and sodium ferric glucaonate complex in sucrose
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| Why would you give parenteral form of iron? | GI problems, malabsorption, intolerance, chronic blood loss, noncompliance, anemia of chronic renal failure
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| Why do you need parenteral production of iron with anemia of chronic renal failure? | inc production of Hb and there I not enough hb
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| IM adverse effect of iron | skin di#coloration , local inflammation and pain. Hypersensitivity and delayed hypersensitivity
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| Acute Iron Toxicity | occurs in children due to corrosive effects on GI mucosa
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| stage 1 Acute Iron Toxicity | GI irritation, nausea, vomiting, diarrhea, lassitude, drowsiness, pallor, cyansis, seizures, shock and coma
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| stage 2 Acute Iron Toxicity | Apparent recovery
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| stage 3 Acute Iron Toxicity | Multiorgan Failure – CNs, Metabolic acidosis, hepatotoxicity, renal failure, bleeding, cardiovascular collapse
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| stage 4 Acute iron toxicity | delayed effect – intestinal obstruction, pyloric stenosis, hepatic cirrosis, severe gastric scarring
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| Treatment Acute Iron Toxicity | induce vomiting, gastric lavage, iron chelator (deferoxamine), supportive therapy
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| Chronic Iron Toxicity | excess deposits in hheart, liver, pancreas#, pituitary and synovia. Organ failure and death
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| Causes of chronic iron toxicity | hereditary hemochromatosis, red cell transfusions and excess ingestion
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| What I hereditary hemochromatosis? | more Fe absorbed than normal
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| Chronic Iron toxicity tx | phlebotomy, deferoxamine or deferasirox
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| Oral Fe chelator | deferasirox
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| IM/IV Fe Iron Chelator | deferoxamine
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| What causes B12 deficiency? | antacid, vegan, PPI, perniciouss anemia, bariatric surgery, small bowel disease, pancreatitiss
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| If your intake of B12 stops, how long will ti be before you have a B12 deficiency? | years
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| Where is folic acid absorbed? | proximal small intestine
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| Where is B12 absorbed? | duodenum
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| What are causes of folic acid deficiency? | nutritional deficiency, malaborption, drugs and pregnancy (inc requirement), chronic EtOH
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| What are some things that cause folic acid malabsorption? | sprue and Inflammatory Bowel Disease
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| What I folate needed for? | H4-folate needed for DNA synthesis
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| DNA synthesis I affected by what deficiency | Folic acid and B12
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| Myelin sheath of neuron I affected by what deficiency? | B12
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| Why are RBC very large with a B12 deficiency? | no DNA synthesis
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| B12 deficiency Tx | cyanocobalamin or hydroxocoboalmin IM, deep ubQ or intranasal
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| What happen if you treat a B12 deficiency with large dose of folic acid | correct anemia but will not prevent neurological damage
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| Will you see nerve demylenation with folic acid deficiency? | no
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| Folic acid deficiency tx | folic acid orally
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| What agents are for increasing RBC? | EPOetin
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| What agent I used for increasing neutrophils? | -stims (sargramostrim)
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| What agents are used for increasing platelets? | oprelvekin
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| Why do you get anemia with chronic renal failure? | no erythropoietin
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