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