Blood and blood products
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| Transfusion transmitted disease tests performed on each blood donation | HIV: ab and NAT, HCV: ab and NAT, HBV: ab-HBCAg, HBSag, NAT, Syphilis, HTLVI/II-abs, WNV NAT, Chagas ab- once for life of donor (Babaesia is regional NAT;14states and DC)
Malaria update 2025
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| Transfusion transmitted disease tested for once in a donor's lifetime | Chagas ab
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| When is testing is required for autologous units? | If collected in same facility: no required testing.
If collected in another facility: first unit and same testing every 30 days.
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| If a blood product does not have an expiry on the label, when does it expire? | midnight
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| When does a platelet product expire AFTER being washed? | 4 hours
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| When does a RBC expire AFTER being washed? | 24 hours
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| Please list all medications approved for administration in the same line with blood products. | none
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| List IV fluids compatible with blood products. | normal saline
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| First step in managing a transfusion reaction. | stop the transfusion
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| A transfusion must be completed within this timeframe | 4 hours
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| Definition of febrile non-hemolytic reaction (FNHTR) | temperature rise of >1 degree C during or within 4 hours of transfusion with no other symptoms
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| This blood product modification reduces the incidence of FNHTRs. | leukoreduction
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| Most common cause of an anaphylactic transfusion reaction. | unknown
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| Blood product modification that can help prevent anaphylactic transfusion reactions in patients with a h/o that reaction. | washing cellular products
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| Definition of TRALI. | non-cardiogenic pulmonary edema within 6 hours of transfusion with hypoxemia without underlying lung disease or heart failure
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| Pathogenesis of TRALI. | predominantly, HLA-abs in donor plasma opsonize WBCs in recipient. The WBCs get stuck in pulmonary capillaries and release their contents causing damage.
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| How is the risk of TRALI mitigated? | 1. prefer male donors for high plasma content products
2. test female donors who report a h/o pregnancy for HLA antibodies
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| How is TRALI treated? | supportive care including mechanical ventilation and oxygen. Steroids are not evidenced based.
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| Why are TRALI reactions reported to the blood bank? | So co-components can be quarantined.
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| What is post-transfusion purpura (PTP)? | thrombocytopenia 7 to 10 days after transfusion. Most cases are self limited.
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| What is the treatment of PTP? | IVIG
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| What is TA-GVHD? | Transfusion associated graft versus host disease.
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| Explain pathogenesis of TA-GVHD. | T-cells in transfused cellular products attack and engraft in host tissues.
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| What is the blood product modification which can help prevent TA-GVHD? | irradiation
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| What patient groups are at greater risk for TA-GVHD? One specific group that is not at risk. | patients with defective cell mediated immunity are at risk (Digeorge's, fludarabine, SCID, BMT, hematologic malignancies).
HIV patients are not at risk.
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| What is the dose of gamma irradiation delivered to the central portion of a blood product bag? | 2500cGy
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| What is the dose of gamma irradiation delivered to the corner portions of a blood product bag? | 1500cGy
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| What % of blood donors are CMV positive? | up to 70%
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| Describe 3 methods to reduce risk of transfusion transmitted CMV. | leukoreduction, pathogen reduction, CMV seronegative products
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| Blood product most frequently implicated in a septic transfusion reaction. | platelets
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| List organisms causing septic transfusion reactions by blood product. | platelets: skin contaminants (staph, strep)
RBCs: Yersinia enterocolytica
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| Why is it very important to report any febrile reaction to the blood bank? | If it is a septic transfusion reaction, co-components need to be quarantined
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| Describe TACO including pathogenesis and treatment. | fluid overload in transfusion setting. Diuretics
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| Describe “citrate toxicity” including metabolism, electrolytes | citrate is the anticoagulant in blood units. In high doses it can cause hypocalcemia. Perioral and distal extremity numbness and tingling are reported
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| How are fatal transfusion reactions reported? Who? What? When? How? | ASAP by fax or phone to CBER at FDA.
Written report within 7 days.
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| Qualifying hematocrit for an autologous blood donor. | 33%
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| Shelf life of RBCs by anticoagulant: ACD-A? AS-5? CPD? CPDA-1? CP2D? | ACD-A = 21
AS-5 - 42
CPD =21
CPDA-1= 35
CP2D =21
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| Hematocrit of an RBC unit stored in AS-1. | 55% to 65%
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| Amount of residual plasma in a RBC unit | 20 to 100 ml
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| Indications for RBC transfusion | symptomatic anemia, RBC exchange
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| Contraindications to RBC transfusion | don't treat iron deficiency, B12 or folate deficiency with RBCs.
don't use RBCs for volume expansion
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| Average bump in hemoglobin after a one unit RBC transfusion | 1 gm/dL
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| Compatibility requirements for: Whole Blood? RBC units? | whole blood: exact
RBCs: cells compatible with patient serum; so O is universal donor
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| 45. What RBC units may be used emergently (prior to complete crossmatch)? | uncrossmatched group O RBCs
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| 46. Most common cause of severe hemolytic transfusion reactions. . | clerical errors; misidentification of patient
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| 47. Describe the workup of a hemolytic transfusion reaction | 1. stop the transfusion
2. clerical check
3. post transfusion sample for testing
4. return remainder of unit to blood bank
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| 48. List signs and symptoms of an acute hemolytic transfusion reaction | FEVER
tachycardia, blood pressure changes, shock, pain, bleeding
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| 49. What is a delayed hemolytic transfusion reaction? | evanescent antibody has an amamnestic response on re-exposure. 2 to 14 days after transfusion. hemolysis with +DAT. Most have a benign course.
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| 50. Describe the hyperhemolysis syndrome. | in sickle cell patients, sometimes hemolysis occurs without an antibody. Even autologous RBCs are lysed. Rx: IVIG
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| 51. Briefly outline all of the human body’s physiologic pathways for eliminating excess iron. Stop at the molecular level listing genes, but do not iterate all nucleotide base pairs. | none
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| 52. List non-immune causes of hemolysis | mechanical valves, small bore IV for blood transfusion, hypotonic fluids, medications, bacterial toxins, thermal injury
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