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197 Cards in this Set
- Front
- Back
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What occurs in Stage 1 of Hemostasis?
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In this stage Prostacyclin is released from the vessel endothelium to relax endothelium and inhibit platelet aggregation. The Injury initials this transient vessel spasm. Platelets release Thromboxane A2 and promotes vasoconstriction and spasm.
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What is stage 2 of Hemostasis?
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This stage is the formation of the plug and platelet adhesion. Thromboxane A2 promotes platelet adhesion. It is then inhibited by Prostacyclin I2. Platelets fill endothelial gaps. Adhesion between platelet and collagen is promoted by the plasma proteins, von willebrand factor (factor Vlll) and ADP.
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What three factors promote platelet adhesion in stage 2 of Hemostasis?
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Von willebrand (factor Vlll), Plasma proteins, and ADP promote adhesion in this phase.
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In stage two platelet activation entails what?
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Change in the platelet shape, formation of pseudopods, activation of arachidonic acid pathway. Platelets release TXA2 And ADP
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In stage two Aggregation of platelets occurs by what means?
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Induced by TXA2 platelets release more TXA2 and ADP. Stabilization of the platelet plug. Blood clot occurs by activation of the coagulation factors thrombin, and fibrin.
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Stage 3 is known by what name?
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The Coagulation Cascade.
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What two pathways are there in the Coagulation pathway
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Intrinsic pathway- triggered in the blood. And the Extrinsic pathway- this starts with trauma to the tissue or vessels and the release of a tissue factor.
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The steps of the extrinsic and intrinsic pathway are the same once initiated. True or False
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True
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What are the 3 terminal steps of the coagulation cascade?
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1. Activation of factor X. 2.Conversion of Prothrombin to Thrombin. 3. Thrombin acts as an enzyme to convert fibrinogen to fibrin. Fibrin stabilizes the clot.
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What is the enzyme that converts fibrinogen to fibrin?
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Thrombin.
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What is involved in stage 4 of Clot Retraction?
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Large number of platelets join the edges of the vessel. Platelets contract and squeeze the serum from the clot. edges of the broken vessels are then joined. dries the clot making it acellular.
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What is stage 5 of clot dissolution?
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Regulated by thrombin and plasminogen activators. Plasminogen activators activate plasmin. Plasmin digest fibrin. Macrophages clean up. Plasmin is rapidly inactivated to keep the effect local.
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What is the name of the enzyme that digest Fibrin?
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Plasmin.
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What are the two types of Hypercoagulability States?
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Increased Platelet function and Accelerated Activity of coagulation.
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What are some situations/ disease that cause platelet increase function which leads to hypercoagulability?
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Artherosclerosis, Diabetes Mellitus, Smoking (Increased Lipids/Cholesterol, Increased Lipids)
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What are some factors for accelerated activity of coagulations?
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Pregnancy, Oral birth control, (both having due to hormonal balance) Postoperative (Tissue Injury) Immobility (stasis of blood) Congestive Heart Failure, Malignant Dx.
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Immobility causes the stasis of blood, which doesn't allow for movement of vascular system, and in turn a lack of this is produced?
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Prostaglandins.
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What is thrombophlebitis?
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Presence of a thrombus in a vein and accompanying inflammatory response. Venous thrombosis.
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What causes the venous return of blood?
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The muscle pump.
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Venous thrombosis can be both deep or ________.
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Superficial
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DVT common occurs where? And what is its major complications.
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It commonly occurs in the extremities and its major complication is a pulmonary embolism.
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What is the Virchow Triad, which leads to great increase in Thrombosis?
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1.Stasis of Blood (bed rest, immobility, MI, CHF) 2.Increased blood Coagulability (stress, trauma, pregnancy, childbirth, birth control pills, dehydration) 3. Vessel wall injury (catherets, surgery, trauma, infection.
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What percentage of individuals with venous thrombosis are asymptomatic?
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50%
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What are the manifestation of venous thrombosis?
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Inflammatory process, Redness, pain, swelling, deep muscle tenderness and fever
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What is the most common site of a venous thrombosis?
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Posterior tibial vein in the calf.
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What is the test for DVT?
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Homan's sign. calf pain with dorsiflexion of the foot.
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What are the treatment steps for venous thrombosis?
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Prevention is key, early ambulation after surgery, leg exercise, support stockings, pneumatic compression devices, anticoagulate therapy for treatment and or prevention.
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Anticoagulation Drugs should be used for DVT when....
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patients have a history of DVT or as prophylaxis in post-surgical patients.
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Anticoagulation drugs should be used in patients with a likelihood or history of thrombotic stroke....
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patients have a transient ischemic attack (stroke prodrome). Spasm of vessel. Patient with a previous thrombotic stroke. Patients who are likely to have clot formation in their heart (atrial fibrilation or artificial valves)
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For what reason might artificial valves or atrial fibrillation lead to the need for anticoagulation therapy?
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There is no proper filling or delivery of the blood. No endothelium lining to keep platelets from sticking.
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Individuals with Hypercoagulability syndrome should be treated with what?
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Anticoagulation therapy.
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This is a polysaccharide made in our bodies that bind and activates antithrombin lll?
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Heparin.
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Heparin binds actively to Antithrombin lll which prevents the activation of what factor
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Factor X.
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Heparin directly prevents the conversion of prothrombine to what?
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Thrombine, with less thrombine clotting is inhibited.
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Heparin is a physiological check on the coagulation cascade, and is made where?
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In the tissues at the lower levels.
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By what method is Heparin administered and why?
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Administered by IV via continuous fusion. Not PO stomach acid would destroy it. Takes effect 20-60 minutes. May or may not give a loading dose.
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Rate of Heparin Infusion is adjusted based upon what test?
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Adjusted based on the Activated Partial Thromboplastin Time aPTT.
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This is the clotting time from the activation of factor VII through the formation of fibrin clot, Indicates factor deficiencies?
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aPTT, Activated Partial thromboplastin time.
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How many areas after the IV administration of Heparin, should an aPTT test be taken?
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6-8 hrs. Heparin has a long 1/2 life.
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Is heparin safe in pregnancy?
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Yes
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What is the INR?
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The international normalized ratio used in prothrombine time test. It takes into account the different reagents used at different labs. INR compared across labs. Target INR rate is 2 and 3.
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What should the INR be for Prothrombin time test in patients who are being treated for high risk of clot formation?
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It should be 2-3 on average, those with very high risk should have an INR of 2.5-3.5
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What effect dose Heparin have on a clot that has already been formed?
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None. That is why post surgical patients who have been stabilized with no post surgical bleeding can be given heparin to prevent DVT and other clotting problems.
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Enozaparin (Lovanox), ardeprin (Normiflo), dalteparin (Fragmin), tinzaparin (Innohep) are all types of what anticoagulate?
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Low Molecular Weight Heparin.
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These preparation are heparin molecules with a lower molecular weight than what type of heparin?
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Unfractionated Heparin
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How is Low Heparin given?
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Subcutaneous injection in a fixed dose.
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What are some of the benefits of Low Heparin?
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It does not create antibodies to platelets and thus does not cause thrombocytopenia, and constant lab testing is not necessary so, it can be given at home.
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What is the method of action for Low Heparin?
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Inhibit the factor X but not that of thrombin. Same contraindication as heparin.
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Thrombocytopenia is what?
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It is a lack of platelet. Patients on IV heparin can develop this adverse effect.
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What drugs might be contraindicated for patients receiving heparin?
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Aspirin and NSAIDS, they increase bleeding. If they are taking this heparin should be adjusted.
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What is aPTT?
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Test conducted for patients on heparin. Clotting time is tested. the factor Vll to time it takes for the fibrin clot to form. Should be taken 6-8hrs after dose given. want a aPTT time that is 1.5 to 2 times the normal value.
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What is the average Activated Partial Thromboplastin Time?
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Average aPTT is 35 seconds.
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Heparin is or is not safe to be used during pregnancy.
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It is safe for pregnancy.
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Prothrombin time is another type of test given to check coagulation factors. What is the INR?
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This is the international Normalized Ratio which is chart of values used to compare PT values across labs by taking into effect the various reagents used in different labs. The desired value is usually 2-3.
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Patients with a high risk for clots should have an INR of what?
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2.5-3.5
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Heparin has no effect on a clot that has already formed therefore it can be used in after surgery...
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Once the surgical site has been stabilized with no post operative bleeding. Used to prevent DVT and other post-surgical clotting problems.
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What is done for a heparin overdose? what is the first line of treatments?
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Often just to stop the heparin. Once the aPTT reaches the desired levels. It then can be restarted at the therapeutic dose needed to maintain that aPTT.
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What are the formed elements of the blood?
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The cellular components the buffy coat and the erythrocytes.
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Heparin by nature is a small or large molecule?
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Large
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This anticoagulant inhibits the synthesis of particular clotting factors and the binding ability of Vitamin K...
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This is warfarin. Trade name is Coumadin.
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What clotting factors does warfarin affect?
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Factor ll (prothrombin), Facto Vll, lX, X. An individual will have some working factors and some that do not. It doesn't prevent clotting altogether.
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What is a risk of warfarin OD?
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Internal Bleeding
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What is the method of warfarin administration? what do you do when the patient is already on IV heparin?
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It is given PO. Must continue to give heparin a few days with it, until therapeutic levels are stable.
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Warfarin has what effect on clotting factors that were synthesized before its administration was started?
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No effect.
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What vitamin will warfarin compete with for binding sites?
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Vitamin K, so the patient should not eat foods rich in Vitamin K.
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Vitamin K is considered a coagulant or clotting factor?
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Clotting factor.
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What consideration should be made when giving warfarin to the elderly?
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They do not have a lot of fat, muscle mass is declined. not usually well hydrated (low plasma levels).
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Name two platelet drugs...
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Clopidogrel (Plavix) and ticlodipine (Ticlid).
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Platelet drugs have what MOA?
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The inhibit platelet aggregation differently than aspirin. Irreversibly activation of platelet aggregation.
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Clopidrogrel is a prodrug which means what?
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It is activated on 1st pass by the liver.
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What are the indications for Platelet drugs?
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Prophylaxis for patients with artherosclerotic events in patients who have had on MI or stroke. Patients at high risk for these. Patients who have had CABG or angioplasty.
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Can aspirin be used with plavix and what are the surgical considerations that must be taken into account?
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May be used with aspirin for prophylaxis, must be discontinued 7 days before surgery to prevent excessive bleeding.
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What are the adverse effects of Ticlid?
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Neutropenia, agranulocytosis, and thrombocytopenia, thrombolytic purpura, GI distress, Must take with food. Can contribute to hemorrhage if the person bleeds for some reason.
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What should be monitored when administering Plavix or Ticlid?
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Measure bleeding time and platelet function. CBC with differential for neutrophil count. Look for Aplastic anemia or agranulycytosis- no granulocytes.
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This is a fragment of an antibody that blocks the glycoprotein receptor?
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Abciximab (Reo PRo) used short term to prevent ischemic events in patients with acute coronary syndromes.
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Eptifibatide (integrillin) is a small peptide that blocks the receptor what type of drug is this?
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It is a glycoprotein receptor and is used in patients with acute coronary syndromes. Stop clots from growing
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What is the method of action for glycoprotein receptor antagonist?
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Platelet drugs that reversibly block platelet GP llb/llla. It prevents coagulation by all other factors, given IV as a protein.
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Glycoproteins have what type of lifespan are they reversible?
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Short acting half life. They are reversible.
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Thrombolytic Drugs are tissue plasminogen activators which do what?
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tPA, and others work by activating plasminogens to plasmin.
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Plasmin degrades what to dissipate clots?
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Fibrin.
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Tenecteplase and reteplase are mutant tpa.
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These mutant tpa are shorter and have longer duration of action.
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tPa is a natural protein produced as a drug by what?
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Recombinant DNA technology.
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Why must tPA drugs be given shortly after the onset of symptoms?
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Because if you wait too long Post Ischemia Reprofusion Injury will occur. because the dead tissues will erupt and start to release all their toxins.
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What should be done for a person in a mid- to late- ischemic event?
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Must stabilize them and ride the event through
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tPA should never be administered for this type of stroke?
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Hemorrhagic
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What is Streptokinase (Streptase) ?
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It is another plasminogen. purified from strept bacteria. Similiar to tPA, much cheaper. May provoke allergic reaction, because it is a foreign protein.
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What method is used to administer Plasminogens?
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They can be given intra-arterially into a clotted blood vessel. or by IV. Intra-arterially is safer, because it is a much smaller dose needed.
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Bleeding disorders involve defects associated with what three factors?
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Platelets, Coagulation Factors, Vascular Integrity.
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What role do platelets play in bleeding disorders?
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decrease in number due to decrease in production, excess platelet destruction, abnormal platelet function. Lack of VW.
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What role does coagulation factors play in bleeding disorders?
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Deficiency of 1 or more clotting factors.
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Vascular Integrity plays what role in bleeding disorders?
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Structurally weak vessels, damage due to inflammation, immune mechanism.
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What is thrombocytopenia?
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decrease in number of platelets. severe is 10,000 -15,000/ml. bleeding small vessels, petechia, purpura.
Normal is 150,000-200,000. Too anticoagulated. Spontaneous bleeds. |
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What are petechia hemmorhages?
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These are spontaneous bleeds which result from an individual being too anticoagulated. happens in thrombocytopenia can also lead to bleeding from GI and nose.
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Platelet defects can also be caused by the bone marrow by what?
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Platelets are made in the bone marrow, Leukemia, HIV, radiation, chemo decrease platelets, decrease production in bone marrow.
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Splenomegaly cause what to happen to platelets?
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Increase in the pooling of platelets in the spleen (normally 30-40%). Platelet pooling can be greater than 80%.
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What disorders cause Splenomegaly?
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Cirrhosis, portal Hypertension, Lymphomas
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What is immune thrombocytopenia?
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Antibodies are produced against plateles. Decreases the survival of the platelets, leads to destruction. Autoimmune Attack.
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What drugs are likely to destroy platelets causing platelet defects and bleeding disorders?
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Quidine, sulfa and heparin. form immune complex with platelets leading to platelet destruction. Low molecular weight heparin does not cause this. If this happens with these other drugs, stop therapy and monitor the PT.
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What is thrombocytopathia?
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Impaired function of the platelets.
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What makes blood come back to the heart?
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The muscle pump. forces blood up the venous system, stopped from going back down due to the valves in the venous system.
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What disease causes impaired function of platelets?
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Von Willebrand Disease , having bleeding problems-- don't work properly.
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Platelet defects can be caused by drugs, what drugs, how, and why?
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Asprin, NSAIDS inhibit TXA2 inhibiting platelet aggregation. They inhibit prostaglandins.
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Where are platelets made?
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The Bone Marrow
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Where do platelets reside?
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1/3rd end up in the spleen and 2/3rd reside through out the circulation.
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What are three types of Coagulation Defects?
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Defect in synthesis of factors. Inherited coagulation defects. Increased consumption of factors.
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Individuals with liver disease are likely to experience defective synthesis of clotting factors, why?
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Because prothrombin, fibrinogen are synthesized in the liver.
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Vitamin K is needed for clotting factors. what is a problem with antibiotics?
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Gut flora is a good source for Vitamin K. Antibiotics can decrease gut flora. Bile salts are needed to absorb Vitamin K.
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What is Hemophilia A?
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Inherited Coagulation defect. . decrease in factor Vlll (8). shows up in childhood with spontaneous bleeding. In adults, severe bleeding with mild trauma.
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What is the treatment for Hemophilia A?
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To give factor Vlll therapeutically.
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What is Von Willebrand's Disease?
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Decrease in VW factor--- decrease in platelet adhesion. Usually diagnosed in adulthood. primarily problem with platelet adhesion, but also can effect the coagulation cascade.
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What is DIC?
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This is Disseminated Intravascular Coagulation. Widespread Coagulation and bleeding in vasculature. Usually secondary disorder. Stroke is secondary. Stroke-like all over
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DIC involves what three factors?
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1.Systemic formation of Fibrin, 2. Excessive clot formation. 3.consumption of clotting factors
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What is the treatment of DIC?
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prevent further clotting and replace clotting components.
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What primary disorders can DIC occur with?
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OB complications, cancer, infections, septic shock, trauma (injury and burns)
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What is the function and shape of RBC?
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Large surface area. bioconcave discs, cells change shape without rupturing. Transport O2 to tissues via hemoglobin.
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Three scenarios for Hemoglobin Oxidation?
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1. Hemoglobin bound to O2
2. Methemoglobin (Bound to chemicals) Nitrates in smokers, this lowers affinity for oxygen. |
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What is carboxyhemoglobin?
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Carbon monoxide. leads to decrease in O2 affinity.
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Iron Availability affects what?
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Rate at which Hb is synthesized. because a decrease in iron leads to a decrease Hb.
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Iron in the body is stored and complexed where?
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20% is stored in BM, liver, spleen. 80% complexed to heme in Hb
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Where is dietary iron absorbed?
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Duodenum
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When iron enters the circulation it binds to protein to form_________, then it goes to the liver where it is stored as ___________.
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Transferrin, ferritin.
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Ferriten can or can not be quickly transferred back to circulation?
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It can be quickly transferred back.
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Iron in the blood is measured as _______.
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Serum ferritin.
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What is the rate of RBC destruction?
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1% per day.
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What is the production rate of RBC in healthy individuals?
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1% per day---- equal to destruction.
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What are RBC's destroyed by?
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They are destroyed by phagocytosis in the spleen, liver, bone marrow, and lymph.
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Amino acids and iron are excreted or recycled?
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Iron is recycled.
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Heme is converted to what and excreted.
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It is converted to bilirubin
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When do you lose iron?
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Only when you bleed.
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What cytokine is released in order to start the production of RBC?
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Erythropoietin, this is excreted by the kidney in response to low O2 levels.
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What is erythropoiesis?
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The production of RBC
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Stem cells in the bone marrow are stimulated to become RBC what are the steps?
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Proliferation- erythroid precursor.
Maturation Extrution of the Nucleus creating a Reticulocyte Released into the blood as RBC. |
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Standard labs for RBCs check for what?
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1)Number of RBCs in the blood. Check 2)Reticulocytes- Rate of RBC production.
3)Hemoglobin- Hb content of the blood. |
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What is a hematocrit?
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Measurement of the percentage of RBCs in 100ml of blood.
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What factors can increase a RBC count in an Hematocrit, What can decrease them?
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Increase may be caused by dehydration. Decreased with overexpansion ECF --- Overhydration
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What is a Mean Corpuscular Volume?
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Size of the red blood vessels.
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What is the significance of an increased Mean Corpuscular Volume?
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MCV increased--- Macrocytic (large cell)
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What is the significance of a decreased Mean Corpuscular Volume?
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MCV decreased---- Microcytic (small cell)
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What is Normocytic anemia?
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Normal Size cells in a mean corpuscular volume.
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What is a mean corpuscular hemoglobin concentration?
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Concentration of Hb in RBC, accounts for "red " color. How much hemoglobin per red blood cell.
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What is normochromic?
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Normal color, Normal MCHC
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What is hypochromic?
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This decrease in color, decrease in MCHC
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What is anemia?
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An Abnormally low number of RBCs or Hemoglobin (or both). This leads to decreased O2 carrying capacity.
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What are the causes of anemia?
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Excessive loss of blood. Destruction of RBCs.(ex. Septcemia) Decreased production of RBCs.(Leukemia).
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What are the manifestations of anemia?
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Fatigue, heart palpitations
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What is Hemolytic anemia?
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This is the destruction of RBCs & Iron retention. (Normocytic and Normochromic cells) Large number of reticulocytes.
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Where does the destruction of RBC, as in hemolytic anemia occur?
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It occurs in the spleen or intravascularly.
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What are the causes of Hemolytic anemia?
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The intrinsic cause would be a defect in the cell membrane, An extrinsic cause would be things that destroy RBC such as trauma, toxins, antibodies.
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What is Sickle Cell Anemia?
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Abnormal Hb structure leading to RBC destruction.
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What is abnormal about the sickle cell hemoglobin?
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Substitution of one amino acid in Hb molecule (Beta chain)
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What percent of African Americans are affected by sickle cell?
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.1%-.2%
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What sets off a sickle cell crisis?
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When the partial pressure of oxygen drops. Protein begins to change. Hemoglobin binds together making its own change. This can occur after an athletic event. causes mini-ischemic strokes Secondarily.
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What is the pathophysiology of Sickle cell?
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Low partial pressure of O2, Low Hb of O2, changed shapes of RBC, they sickle. Sickled cells are hyper adhesive. obstruct flow in microcirculation, hypoxia, cell dies, hemolytic anemia.
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What type of anemia does sickle cell lead to?
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Hemolytic anemia.
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Sickle cell chronically leads to what?
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Splenomegaly, CVA
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What is are some exogenous factors that might cause hemolytic anemia?
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Drugs, chemicals, Toxins, Infections (malaria).
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What are some Mechanical factors that lead to hemolytic anemia?
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Valves or Pumps, (dialysis, CP bypass)
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What is an immune mediated factor leading to hemolytic anemia?
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Antibodies that destroy RBCs
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What is Mycrocytic Anemia?
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This is an anemia of deficient RBC production, It is a nutritional deficiency, Not enough Iron in the diet. Small cells , lack hemoglobin and color.
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What is megaloblastic normochromic anemia?
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This is a nutritional deficiency anemia due to Folic acid deficiency / vitamin B 12 deficiency. Decreased cell division and decreased maturation. Large erythrocytes are formed due to defective DNA synthesis.
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What is another name for large erythrocytes?
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Megablasts
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What is pernicious anemia?
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This is means Highly injurious. Alter absorption of vitamin B12. Usually due to an autoimmune disorder. can be caused by gastric bypass that disturbs parietal cells or iliac resectioning, where it is absorbed.
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Bone marrow depression can lead to what type of anemia?
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A lack of RBC production, a deficient anemia.
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A decrease in the production of all blood cells, No RBCs. Primarily caused by a decrease number or function of bone marrow stem cells.
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Aplastic Anemia
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What are two of the primary causes of Aplastic Anemia?
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Radiation and Chemotherapy
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What is the treatment for Aplastic Anemia?
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Stem Cell transplant.
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How do you treat a deficient anemia?
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You supplement what is missing. i.e. B12, Iron, Folate.
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How do you treat hemolytic anemia?
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If it can not be treated transfusion might be necessary. Erythropoietin might not help because the bone marrow might be at maximal capacity.
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If due to hemorrhage?
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Should replace blood, small hemmorhage transfusion might not be necessary. May give supplemental Iron.
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How can kidney failure cause anemia?
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Since the kidneys make erythropoietin, renal failure produces an anemia. For treatment give supplemental erythropoietin.
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How can bone marrow depression cause anemia?
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Chemo, drugs treat HIV AIDS, sometimes erythropoietin is helpful, sometimes only a transfusion can help.
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Why is erythropoietin not helpful for aplastic anemia or myelodysplastic syndrome?
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There are no cells to make RBCs. Transfusion is necessary.
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This is a recombinant protein marketed under the name epoetin alfa. (Procrit, Epogen)
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Erythropoietin
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What is the advantage of darbepoetin alfa over epoetin alfa?
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Darbepoetin can be distributed less frequently. It is given weekly. Epoetin is usually give 3x a wk.
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Both darbepoetin and epoetin alfa are approved as a treatment for what?
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Both are approved treatments of renal failure anemia
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What is the target hematocrit for individuals being treated with epoetin alfa?
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36% going over this value can adverse effects such as uncontrolled hypertension, thrombolytic events (MI or stroke)
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Does epoetin alfa have an immediate effect?
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No, it may take a few weeks seeing that RBC take many steps to mature.
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How is erythropoetin administered?
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Ususally subcutaneous injection. Can be given by IV.
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Why can erythropoetin not be given PO?
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It is a protein and would be digested.
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What specific procedures must be taken when administering erythropeitin?
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1. Do not shake (it is a protein)
2. Discard any left over 3. Use preservative free in infants |
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Can erythropeitin be self administered?
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Yes once the patient learns to take subcutaneous injections.
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What are Leukocytes and what role do they play in the body?
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These are WBC. Phagocytic cells that protect against invasion by foreign cells.
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Granulocytes and monocytes also mediate what type of immune responses?
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Innate Immune response
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What are Lymphocytic leukocytes?
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T cells and B cells; they are involved in acquired immunity.
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Monocytes are involved in what type of immunity?
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Acquired immunity.
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What is Leukopenia?
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This is a decrease in the absolute number of WBCs.
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What form of WBC does Leukopenia most often affect?
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Most often neutrophils are affected.
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What is neutropenia?
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This is a decrease in the number of neutrophils, decrease caused by bone marrow production decrease. peripheral destruction. shift from circulatory system to peripheral tissue. Disease is often combination of the above.
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What cause acquired neutropenia?
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Complication of procedures (radiation, chemo) Disease that interfere with formation of blood cells (aplastic anemia, lupus, rhem. arthritis.) Infections.
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What are the manifestations of neutropenia?
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Neutrophil is essential to inflammation. If absent unable to fight infection. Infection can occur in any epithelial area.
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What care is indicated for individuals with neutropenia?
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Keep individual very clean, and away from any sick individuals.
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What is a treatment for leukopenia?
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Use G-CSF: granulocyte colony stimulating factor.
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How does G-CSF work?
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Promotes the proliferation and maturation of granulocyte precursors. Stimulates their maturation. Only effective in bone marrow is capable of increasing its function.
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What is Filgrastin?
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This is a recombinant protein which has a short half-life and might have to be administered several times a week. Used to treat Neutropenia. Given IV or SC.
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What is Pegfilgrastin?
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Same drug as Filgrastin, except encapsulated. Can be administered less frequently and a one time dose may be sufficient.
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Filgrastin and Pegfilgrastin can be used to treat febrile neutropenia, which is a serious complication of what?
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Chemotherapy, drug should be given at least 24 hrs after last dose.
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What is a common adverse effect of Filgrastin and Pegfilgrastin?
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Bone pain is common due to the expanding bone marrow. Should treat with opioids or NSAIDS.
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