Blood Transfusion Medicine Flashcards | Flashcards | OmpathStudy Kenya

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Flashcards

  1. Q1. List the ABO blood group system — antigens, antibodies, can donate to, can receive from

    Answer: Group A → A antigen, Anti-B → donate to A, AB → receive from A, O Group B → B antigen, Anti-A → donate to B, AB → receive from B, O Group AB → A and B antigens, no antibodies → donate to AB only → Universal Recipient → receive from all Group O → no antigens, Anti-A and Anti-B → Universal Donor → receive from O only Universal RBC donor = O negative Universal plasma donor = AB positive

  2. Q2. Explain the Rh blood group system and the pathogenesis of HDN

    Answer: Most important antigen = D antigen Rh negative = no D antigen; antibodies NOT naturally present → develop only after exposure ( sensitisation ) HDN pathogenesis: 1st pregnancy → Rh-negative mother carries Rh-positive fetus → uneventful At delivery → fetal RBCs enter maternal circulation → mother forms anti-D IgG 2nd Rh-positive pregnancy → maternal anti-D IgG crosses placenta → attacks fetal RBCs → haemolysis Consequences → mild jaundice → severe anaemia → hydrops fetalis → intrauterine death Prevention → anti-D immunoglobulin (Rhogam) within 72 hours of delivery/sensitising event + at 28 weeks

  3. Q3. List the clinically important blood group systems after ABO and Rh with key associations

    Answer: Kell (3rd) → strong immunogen; causes HDN and haemolytic transfusion reactions Duffy (4th) → Duffy-null individuals resistant to Plasmodium vivax malaria Kidd (5th) → notorious for causing delayed haemolytic transfusion reactions MNS (6th) → variable clinical significance

  4. Q4. List the 3 steps of pre-transfusion compatibility testing

    Answer: Step 1 — ABO and Rh typing → determine patient's blood group and Rh status Step 2 — Antibody screen → patient's serum tested against panel of reagent RBCs to detect unexpected/irregular antibodies Step 3 — Crossmatch → patient's serum mixed directly with donor RBCs → agglutination or haemolysis = incompatible → do not transfuse Crossmatch primarily detects irregular antibodies in patient serum reacting against donor RBC antigens

  5. Q5. Distinguish DAT from IAT — what each detects and clinical uses

    Answer: DAT (Direct Antiglobulin Test) Detects antibodies already bound to patient's own RBCs in vivo Uses → haemolytic transfusion reactions, autoimmune haemolytic anaemia, HDN Positive DAT = antibodies actively coating patient's RBCs inside the body IAT (Indirect Antiglobulin Test) Detects free antibodies in patient's serum in vitro Uses → pre-transfusion antibody screening, crossmatching Crossmatch = essentially a form of IAT

  6. Q6. What is the metabisulfite test? What does it detect and what is its limitation?

    Answer: Sodium metabisulfite added to blood → creates deoxygenating environment HbS becomes insoluble → RBCs sickle → positive result confirms presence of HbS Detects both sickle cell trait (HbAS) and sickle cell disease (HbSS) Limitation → does NOT distinguish trait from disease Haemoglobin electrophoresis needed to distinguish

  7. Q7. List the blood products, their contents, storage conditions, and indications

    Answer: pRBCs → red cells, minimal plasma → 1–6°C, 35–42 days → symptomatic anaemia, haemorrhage FFP → all coagulation factors, fibrinogen, albumin, immunoglobulins; NO platelets → −18°C, 12 months → coagulopathy, liver disease, warfarin reversal, DIC, TTP Platelets → platelets in plasma → 20–24°C with agitation, 5 days → shortest shelf life; highest bacterial contamination risk Cryoprecipitate → fibrinogen, Factor VIII, Factor XIII, vWF, fibronectin; NO Factor IX, VII → −18°C, 12 months → haemophilia A, vWD, hypofibrinogenaemia, DIC Albumin → heat-treated, virus-safe → hypoalbuminaemia, burns, cirrhosis, nephrotic syndrome

  8. Q8. Describe acute haemolytic transfusion reaction — cause, mechanism, features, management

    Answer: Most serious immediate reaction Cause → ABO incompatibility; most common cause = clerical error (wrong blood, wrong patient) Mechanism → recipient preformed IgM antibodies bind donor ABO antigens → complement activation → rapid intravascular haemolysis Features → fever, rigors, back/flank pain, haemoglobinuria (red/brown urine), haemoglobinaemia, hypotension, tachycardia, DIC, acute renal failure Management: Stop transfusion immediately — most important first step Keep IV line open with normal saline Check patient identity against blood product label Send samples → repeat crossmatch, DAT, FBC, renal function, urine for Hb Monitor urine output; treat DIC and renal failure Notify blood bank

  9. Q9. Describe febrile non-haemolytic transfusion reaction — cause, features, management, prevention

    Answer: Most common transfusion reaction overall Cause → recipient antibodies react against donor leukocyte HLA antigens OR cytokines accumulate in stored blood Features → fever (≥1°C rise), chills, malaise — no haemolysis Management → slow or stop transfusion; give paracetamol Prevention → leukoreduction (filtration removes white cells before storage)

  10. Q10. Describe allergic/urticarial reaction and anaphylactic transfusion reaction

    Answer: Allergic/Urticarial: Cause → recipient IgE antibodies react against donor plasma proteins Features → urticaria, pruritus, flushing; no fever, no haemolysis Management → slow transfusion; antihistamines (chlorpheniramine) Anaphylaxis: Most commonly in IgA-deficient patients with anti-IgA antibodies Even trace IgA in donor plasma triggers severe anaphylaxis Management → stop transfusion immediately; adrenaline, corticosteroids, IV fluids Future transfusions → washed RBCs or IgA-deficient products

  11. Q11. Distinguish TACO from TRALI — mechanism, BP, JVP, diuretics, CXR

    Answer: TACO → volume overload BP → elevated JVP → raised Responds to diuretics → YES CXR → bilateral infiltrates + cardiomegaly TRALI → donor antibodies (anti-HLA/anti-neutrophil) attack recipient leukocytes in lungs → non-cardiogenic pulmonary oedema Onset within 6 hours BP → normal or low JVP → normal Responds to diuretics → NO CXR → bilateral infiltrates, normal heart size Management → supportive; high-flow O2, mechanical ventilation

  12. Q12. Describe bacterial contamination as a transfusion reaction — which product, organisms, features, management

    Answer: Most commonly affects platelet concentrates → stored at room temperature → allows bacterial growth Common organisms → Staphylococcus epidermidis, Staphylococcus aureus, gram-negative bacteria Features → high fever, rigors, severe hypotension, septic shock during or immediately after transfusion Management: Stop transfusion immediately Blood cultures from patient AND blood bag Broad-spectrum antibiotics Resuscitate

  13. Q13. Describe delayed haemolytic transfusion reaction — timing, cause, features, management

    Answer: Timing → 3–10 days after transfusion Cause → low-level alloantibodies from previous transfusion/pregnancy not detected on antibody screen → after transfusion, anamnestic (memory) immune response → antibody levels rise → attack transfused RBCs Kidd system antibodies → notorious for causing this Features → unexpected fall in Hb, mild jaundice, positive DAT Management → usually mild and self-limiting; monitor renal function

  14. Q14. Describe post-transfusion purpura — timing, mechanism, features, management

    Answer: Timing → 5–10 days after transfusion Mechanism → patient develops antibodies against platelet-specific antigen ( HPA-1a ) on donor platelets → antibodies cross-react with and destroy patient's own platelets Features → sudden severe thrombocytopenia → widespread purpura and bleeding Predominantly affects women sensitised through previous pregnancies Management → high-dose IVIG

  15. Q15. Describe TA-GvHD — timing, mechanism, features, mortality, prevention, who needs irradiated blood

    Answer: Timing → 1–6 weeks after transfusion Mechanism → viable donor T-lymphocytes engraft in immunocompromised host → attack host tissues (skin, liver, GI tract, bone marrow) Features → rash, diarrhoea, liver dysfunction, pancytopenia Mortality → exceeds 90% — no effective treatment once established Prevention → irradiation of blood products with gamma radiation (25–50 Gy) → inactivates donor T-lymphocytes Who needs irradiated blood: Immunocompromised patients Intrauterine transfusion recipients Directed donations from blood relatives HSCT recipients Hodgkin lymphoma patients

  16. Q16. List special blood product modifications, what they prevent, and when they are used

    Answer: Leukoreduced → WBCs removed by filtration → prevents FNHTR, CMV transmission, HLA alloimmunisation, platelet refractoriness → standard for most transfusions Irradiated → gamma radiation inactivates donor T-lymphocytes → prevents TA-GvHD → for immunocompromised, HSCT, intrauterine transfusions, directed donations from relatives Washed RBCs → plasma proteins, IgA, cytokines removed by saline washing → for IgA-deficient patients with anti-IgA antibodies; severe/recurrent allergic reactions CMV-negative → from CMV-seronegative donors → for CMV-seronegative immunocompromised patients, pregnant women, premature neonates; leukoreduced blood is acceptable alternative

  17. Q17. Define massive transfusion. List its complications

    Answer: Definition → replacement of 100% blood volume in 24 hours OR 10 units pRBCs in 24 hours OR 4 units pRBCs in 1 hour Complications: Hypothermia → cold stored blood lowers core temperature; worsens coagulopathy Hypocalcaemia → citrate in stored blood chelates circulating calcium Hyperkalaemia → K+ leaks from stored RBCs during storage Dilutional coagulopathy → clotting factors and platelets diluted Metabolic acidosis → stored blood has low pH

  18. Q18. Describe the massive transfusion protocol (MTP) and additional management

    Answer: Ratio → 1:1:1 (FFP : Platelets : pRBCs) → mimics whole blood, prevents dilutional coagulopathy Additional management: Tranexamic acid given early → inhibits fibrinolysis → reduces blood loss in trauma Calcium supplementation → counteracts citrate chelation Warm all blood products → prevents hypothermia Correct acidosis

  19. Q19. How do you manage an unknown blood group in an emergency? Suspected acute haemolytic reaction?

    Answer: Unknown blood group emergency: Give O negative pRBCs immediately If plasma needed → give AB positive FFP Switch to type-specific blood once blood group identified Suspected acute haemolytic reaction: Stop transfusion immediately Keep IV line open with normal saline Check patient identity against blood label Send → repeat crossmatch, DAT, FBC, renal function, urine Hb Monitor urine output; manage DIC and renal failure Notify blood bank; complete incident report

  20. Q20. List the complications of repeated transfusions and their management

    Answer: Iron overload → each unit pRBCs = ~250 mg iron; no mechanism to excrete excess → treat with desferrioxamine or deferasirox Alloimmunisation → repeated exposure to foreign RBC antigens → multiple alloantibodies → crossmatching increasingly difficult Delayed haemolytic reactions → from previously formed alloantibodies CMV infection → use leukoreduced or CMV-negative blood Hypersplenism → from chronic haemolysis and repeated transfusions

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