Posttransfusion purpura (PTP) is a rare but serious condition that typically occurs in people who lack the common HPA-1a platelet antigen. After a blood transfusion, they develop an alloantibody against this antigen, which then destroys both the transfused platelets and their own platelets, leading to severe thrombocytopenia and purpura.

The first and most critical action for any suspected transfusion reaction is to stop the transfusion immediately to prevent further administration of the potentially harmful product. Keeping the IV line open with normal saline ensures venous access for administering emergency medications or fluids if needed. All other investigative and therapeutic steps follow this initial action.

Why others are incorrect:

• (a) Slow the infusion and monitor the patient: ❌ Dangerous — if the reaction is hemolytic or anaphylactic, continuing the transfusion can worsen the condition.

• (c) Administer epinephrine and call the physician: Used only if an anaphylactic reaction is evident, not as the universal first step.

• (d) Send a post-transfusion sample to the lab immediately: Important, but comes after stopping the transfusion and maintaining IV access.

• HDN due to ABO incompatibility occurs when a mother has antibodies against the infant’s ABO blood group antigens.

• Group O mothers naturally produce anti-A and anti-B antibodies (IgG type in addition to IgM), which can cross the placenta.

• In contrast, group A mothers have anti-B (mostly IgM, which doesn’t cross placenta well), group B mothers have anti-A (mostly IgM), and group AB mothers have neither anti-A nor anti-B.

• Therefore, ABO HDN is most common in type O mothers with a type A or B baby.

Among all transfusion-transmitted infections, hepatitis (especially hepatitis B and hepatitis C) remains the most frequent complication worldwide — even though screening has greatly reduced its incidence in developed countries.

TA-GVHD occurs when donor T lymphocytes are not recognized as foreign by the recipient’s immune system and can therefore engraft and attack. This risk is highest when the donor is homozygous for an HLA haplotype that the recipient is heterozygous for, a scenario that is much more likely when the donor is a first-degree relative (e.g., parent, sibling).

Why the others are incorrect:

• (a) A full-term infant: Risk is low unless the baby is immunodeficient or receives blood from a relative.

• (c) A patient with a positive DAT: Indicates immune hemolysis, not GVHD risk.

• (d) A patient with a history of febrile reactions: At risk for FNHTR, not GVHD.

Hives (urticaria) and itching (pruritus) are the classic signs of a mild to moderate allergic transfusion reaction. This is caused by a hypersensitivity reaction to a protein or other soluble substance in the donor plasma. It is distinct from a febrile reaction (fever/chills), a hemolytic reaction (pain, dark urine), or TRALI (respiratory distress).

Why others are incorrect:

• (a) Febrile non-hemolytic: Causes fever and chills, not hives or itching.

• (c) Hemolytic: Causes fever, chills, back pain, dark urine, hypotension — not just hives.

• (d) TRALI (Transfusion-Related Acute Lung Injury): Causes acute respiratory distress, hypoxemia, and non-cardiogenic pulmonary edema, not isolated skin symptoms.

The clerical check is the most critical first step in a transfusion reaction investigation. It involves re-verifying that the patient’s identity (on their wristband and all records) matches the information on the blood unit label and compatibility tag. This is done to rule out a misidentification error, which is the most common cause of life-threatening acute hemolytic reactions.

Why the others are incorrect:

• (b) Bacterial contamination:  Checked through culture or Gram stain, not clerical review.

• (c) Plasma protein content:  Not relevant to reaction investigation.

• (d) Temperature control:  Related to storage/transport, not clerical verification.

Post-transfusion purpura (PTP) is a rare but severe condition characterized by sudden thrombocytopenia about 5-10 days after transfusion. It is most frequently caused by an antibody (often in an HPA-1a-negative patient) directed against the human platelet antigen HPA-1a (formerly Pl^A1) on transfused platelets. Paradoxically, this antibody also attacks the patient’s own HPA-1a-negative platelets.

Why the others are incorrect:

• (b) Leukocytes:  Associated with febrile non-hemolytic reactions, not PTP.

• (c) Plasma proteins:  Cause allergic reactions, not thrombocytopenia.

• (d) Hemoglobin:  Hemolytic reactions involve red cells, not platelets.

• Anti-K is the most important non-RhD antibody causing severe HDFN after anti-RhD.

• It can cause severe anemia not only by hemolysis but also by suppressing fetal erythropoiesis.

• Anti-K HDFN may lead to hydrops fetalis at lower antibody titers compared to anti-RhD.

Other options:

• a) Anti-Leᵃ → Lewis antigens are poorly developed in fetal RBCs; not a cause of significant HDFN.

• b) Anti-P1 → typically IgM, does not cross placenta; not a cause of HDFN.

• d) Anti-M → often IgM, can sometimes be IgG but rarely causes severe HDFN.

A transfusion reaction is broadly defined as any adverse event that occurs during or after the transfusion of blood or blood components. This definition includes both immune-mediated (e.g., hemolytic, febrile, allergic) and non-immune (e.g., circulatory overload, TRALI, bacterial contamination) events. It is not limited to hemolytic reactions (b) or allergic responses (d).

Why others are incorrect:

• (b) Only includes one specific type (ABO hemolytic) →  Too narrow

• (c) Fever after surgery →  Not necessarily related to transfusion

• (d) Allergic response unrelated to transfusion →  Not a transfusion reaction

A delayed hemolytic transfusion reaction is caused by a secondary (anamnestic) immune response. The recipient has been previously sensitized to a red cell antigen, but the antibody is undetectable before transfusion. After exposure to the antigen during transfusion, the antibody production rapidly increases, leading to hemolysis 2 to 14 days later.

Why the others are incorrect:

• (a) Within 24 hours:  Too soon — suggests acute hemolytic reaction.

• (c) 3–4 weeks:  Possible but rare; most occur within 2 weeks.

• (d) Immediately after completion:  Typical of acute hemolytic or allergic reactions.

The danger in HDN is unconjugated bilirubin, which is lipid-soluble and can cross the blood-brain barrier, causing kernicterus. Phototherapy uses light to convert unconjugated bilirubin in the skin into water-soluble isomers (lumirubin) that can be excreted in the bile and urine without needing liver conjugation.

Why the others are incorrect:

• (a) Break down conjugated bilirubin:  Phototherapy acts on unconjugated bilirubin, not conjugated.

• (b) Prevent further hemolysis:  Phototherapy does not affect red cell destruction.

• (d) Stimulate liver enzyme production:  It acts physically on bilirubin, not through hepatic metabolism.

An anaphylactic reaction is an acute, severe allergic (IgE-mediated) response. Its hallmark symptoms are hypotension (low blood pressure), bronchospasm (wheezing, respiratory distress), and often cutaneous signs like urination. A key feature that distinguishes it from a febrile or septic reaction is the absence of fever.

Why the others are incorrect:

• (a) Fever and chills: → Seen in febrile non-hemolytic or acute hemolytic reactions.

• (c) Hypertension and tachycardia: → More typical of transfusion-associated circulatory overload (TACO).

• (d) Generalized edema and dark urine: → Seen in acute hemolytic transfusion reaction (due to hemoglobinuria and renal injury).

Rh immune globulin (RhIG) is given to an Rh-negative mother to neutralize Rh-positive fetal red cells that may have entered her circulation, thereby preventing Rh sensitization.

Transfusion-associated graft-versus-host disease (TA-GVHD) is caused by donor lymphocytes that engraft and attack the recipient’s tissues. Irradiation of cellular blood components (RBCs, platelets) damages the DNA of these lymphocytes, preventing them from proliferating and causing GVHD. Leukocyte reduction (a) reduces the number of white cells but is not sufficient to prevent GVHD.

Why the others are incorrect:

• (a) Leukocyte reduction: Removes most white cells to reduce febrile reactions, CMV transmission, and HLA alloimmunization, but does not inactivate lymphocytes — GVHD can still occur.

• (c) Washing of blood components: Removes plasma proteins to prevent severe allergic/anaphylactic reactions, not GVHD.

• (d) Using CMV-safe blood products: Prevents CMV infection, not GVHD.

An acute hemolytic transfusion reaction (AHTR) is a medical emergency caused most often by ABO incompatibility.
Hemolysis releases free hemoglobin, which can cause hypotension, shock, and acute renal failure.

Other options:

• a) Antihistamines → for allergic reactions, not the main issue here.

• c) Antipyretics → fever is a symptom, but not the primary threat.

• d) Exchange transfusion → may be used in some severe hemolytic cases, but it’s not the primary initial goal; first stabilize BP and renal perfusion.

The hallmark of TRALI is the sudden onset of acute respiratory distress (severe hypoxia, dyspnea) and bilateral pulmonary edema, typically within 6 hours of transfusion. The edema is non-cardiogenic, meaning it is not due to heart failure, but rather to increased capillary permeability in the lungs.

Why the others are incorrect:

• (b) High fever:  Can occur in TRALI, but not characteristic; fever is more prominent in bacterial contamination or febrile reactions.

• (c) Rash and hives:  Typical of allergic or anaphylactic reactions, not TRALI.

• (d) Hemoglobinuria:  Characteristic of acute hemolytic reactions, not TRALI.

Hemoglobinuria (hemoglobin in the urine) occurs when free hemoglobin in the plasma (hemoglobinemia) exceeds the binding capacity of the haptoglobin protein and is filtered by the kidneys. This is a classic sign of intravascular hemolysis, where red blood cells are destroyed within the bloodstream, as seen in severe acute hemolytic transfusion reactions.

Why the others are incorrect:

• (b) Extrinsic anemia:  Refers to anemia due to blood loss or destruction by external factors, not intravascular hemolysis.

• (c) Platelet destruction:  Causes thrombocytopenia, not hemoglobinuria.

• (d) Plasma protein deficiency:  Does not cause hemoglobinuria.

The most common and severe form is due to ABO incompatibility from an error in blood typing or patient identification, leading to immediate intravascular hemolysis (hence elevated plasma hemoglobin).

Other options:

• a) Rh typing error → Usually causes delayed hemolytic reactions, not immediate intravascular hemolysis with hemoglobinemia.

• c) Anti-Fyᵃ → Can cause delayed hemolytic reaction, not typically this acute presentation with hemoglobinemia during transfusion.

• d) Gram-negative bacteria in blood bag → Causes septic shock, not specifically elevated plasma hemoglobin.

The administration of Rh immune globulin (RhIG) to Rh(D)-negative mothers during pregnancy and after delivery is a highly effective prophylactic treatment. It works by clearing fetal Rh(D)-positive red cells from the maternal circulation before they can sensitize the mother, thereby preventing the formation of anti-D antibodies and protecting future pregnancies.

Why the others are incorrect:

• (b) Transfusing O-positive blood during pregnancy:  Would increase risk of sensitization

• (c) Giving corticosteroids after delivery:  Does not prevent antibody formation

• (d) Delaying labor:  No effect on maternal sensitization

A positive Direct Antiglobulin Test (DAT) on a post-transfusion sample is a key laboratory finding in an acute hemolytic reaction. It indicates that antibody and/or complement is coating the transfused red cells, causing their destruction. While hemoglobinemia/uria (not listed) are also classic, a positive DAT provides direct immunologic evidence of incompatibility.

Why the others are incorrect:

• (b) Negative antibody screen:  In AHTR, the antibody screen may detect anti-A or anti-B if tested beforehand.

• (c) Normal plasma color:  Plasma often turns pink or red due to hemoglobinemia.

• (d) Elevated platelet count:  Platelets are not directly affected; may even decrease due to DIC.

The Kidd (Jk) system antibodies, particularly anti-Jkᵃ and anti-Jkᵇ, are among the most common causes of delayed hemolytic transfusion reactions. These antibodies are notorious for falling to undetectable levels in the plasma between exposures, making pre-transfusion screening difficult, but they rapidly reappear (anamnestic response) after a transfusion, causing delayed hemolysis.

Why the others are incorrect:

• (a) Lewis: Usually IgM, naturally occurring, and clinically insignificant.

• (c) P: Rarely causes transfusion reactions (mainly involved in paroxysmal cold hemoglobinuria).

• (d) I: Associated with cold agglutinins in Mycoplasma infections, not DHTRs.

An allergic transfusion reaction is characterized by symptoms of histamine release, most commonly urticaria (hives) and pruritus (itching). These are caused by a hypersensitivity reaction to an allergen in the donor plasma, such as a medication, food, or other soluble substance.

Why the others are incorrect:

• (a) Acute hemolytic:  Causes fever, chills, hypotension, hemoglobinuria — not urticaria.

• (c) Septic reaction:  Causes high fever, rigors, hypotension, often due to bacterial contamination.

• (d) Delayed hemolytic:  Occurs days to weeks later, with mild jaundice or anemia — not allergic symptoms.

• In ABO Hemolytic Disease of the Newborn (HDN), maternal IgG anti-A or anti-B antibodies cross the placenta and bind to fetal red cells.

• However, ABO antigens are poorly developed at birth, and most anti-A and anti-B antibodies are IgM (which don’t cross the placenta).

• As a result, only small amounts of IgG antibodies attach to fetal RBCs.

• Therefore, the Direct Antiglobulin Test (DAT) is typically weakly positive or even negative, unlike Rh HDN, where the DAT is strongly positive (3+ to 4+).

When a transfusion reaction is suspected, the very first and most critical step is to stop the transfusion immediately to prevent further infusion of potentially incompatible blood.

Why others are incorrect:

• (b) Increase transfusion rate:  Worsens the reaction.

• (c) Discard the blood bag:  Never discard—it must be sent for investigation.

• (d) Add saline to the IV line:  Correct after stopping the transfusion, not before.

The triad of fever, skin rash, and diarrhea occurring 1-2 weeks post-transfusion, along with liver involvement (elevated enzymes) and pancytopenia, is the classic presentation for Transfusion-Associated Graft-Versus-Host Disease (TA-GVHD). This is caused by donor lymphocytes engrafting in an immunocompromised (or HLA-similar) recipient and attacking the host’s tissues. It is a fatal complication that is prevented by irradiating cellular blood products.

Why the others are incorrect:

• (a) Transfusion-associated hepatitis: Causes elevated liver enzymes, but no rash, diarrhea, or cytopenia.

• (c) Anaphylactic reaction: Occurs immediately during transfusion, with hypotension and bronchospasm, not days later.

• (d) Sepsis from bacterial contamination: Occurs during or shortly after transfusion, with high fever, chills, and shock, not delayed systemic symptoms.

Rh immune globulin (RhIG), also known as Rho(D) immune globulin, is given to prevent Rh sensitization in an Rh-negative mother who is carrying or delivering an Rh-positive fetus.

Why other options are incorrect:

• (a) Delivery of an Rh-negative infant: ❌ No risk of sensitization — baby and mother are both Rh-negative.

• (c) A positive antibody screen for anti-D: ❌ Too late — the mother is already sensitized; RhIG will not help once anti-D is formed.

• (d) A positive direct antiglobulin test on the mother: ❌ DAT is performed on RBCs, and a positive maternal DAT suggests immune coating of her own cells, not an indication for RhIG.

Rh immune globulin (RhIG) is used for prophylaxis to prevent the formation of anti-D. A patient with a high anti-D titer of 1:4096 is already actively immunized to the D antigen. Administering RhIG would be ineffective and is not indicated.

Why the others are incorrect:

• (a) First trimester abortion:  RhIG is indicated, as fetomaternal hemorrhage may occur even early in pregnancy.

• (b) Husband who is Rh-positive: RhIG is indicated because the fetus may be Rh-positive.

• (d) Positive direct antiglobulin test (DAT):  The DAT is performed on red cells (usually newborn or transfused cells), not on the mother; it does not determine maternal sensitization status.

The Kleihauer-Betke test is an acid elution technique that takes advantage of the different hemoglobin types in fetal and adult red cells. Fetal red cells (containing HbF) are resistant to acid and remain stained, while adult red cells (containing HbA) are lysed and appear as “ghost cells.”

Why others are incorrect:

• (b) Determine the blood type of a fetus:  Requires DNA testing or amniocentesis, not Kleihauer–Betke.

• (c) Detect maternal antibodies in cord blood:  Done by indirect antiglobulin test (IAT) or antibody screen.

• (d) Diagnose Hemolytic Disease of the Newborn (HDN):  Diagnosed by DAT on cord blood and bilirubin/hemoglobin levels, not this test.

This history describes the classic worsening of hemolytic disease of the fetus and newborn (HDFN) with each subsequent pregnancy in an Rh-negative mother.

• First pregnancy: Sensitizes the mother (often at delivery), so the first baby is unaffected.

• Second pregnancy: The now-sensitized mother produces anti-D antibodies that cross the placenta, causing significant jaundice requiring exchange transfusion.

• Third pregnancy: The antibody titer is even higher, leading to severe anemia, hydrops fetalis, and stillbirth.

Transfusion-associated graft-versus-host disease (TA-GVHD) occurs when viable donor T lymphocytes engraft in the recipient and attack host tissues.

Why the others are incorrect:

• (b) Freezing red cells:  Used for storage, does not inactivate lymphocytes

• (c) Leukoreduction: Reduces WBCs but may not remove all T cells, so it’s not sufficient to prevent TA-GVHD

• (d) Washing plasma:  Removes plasma proteins, not lymphocytes; not preventive

The primary purpose of an antibody titer in a sensitized pregnant woman is to assess the risk to the fetus. A rising or high titer (e.g., ≥ 16) indicates a greater likelihood of significant Hemolytic Disease of the Fetus and Newborn (HDFN) and identifies pregnancies that require additional fetal monitoring, such as middle cerebral artery (MCA) Doppler ultrasound to check for anemia.

Why the others are incorrect:

• (a) Identify the antibody specificity:  That’s done by an antibody identification panel, not a titer.

• (c) Decide if the baby needs an intrauterine transfusion:  That decision is based on fetal monitoring results (e.g., Doppler studies, amniotic fluid bilirubin), not on the titer alone.

• (d) Determine if early induction of labor is indicated:  Induction decisions depend on fetal condition and maturity, not directly on the titer.

Platelet concentrates are stored at room temperature (20-24°C) to maintain viability, which is an ideal environment for bacterial growth. In contrast, red blood cells and frozen components like plasma and cryoprecipitate are stored at cold or freezing temperatures that inhibit bacterial proliferation. This makes platelets the most common blood product associated with bacterial contamination.

Why the others are incorrect:

• (a) RBC units:  Stored at 1–6°C → inhibits bacterial growth.

• (c) Cryoprecipitate:  Frozen until use → bacteria cannot multiply.

• (d) Plasma:  Frozen storage prevents contamination growth.

Febrile nonhemolytic transfusion reactions (FNHTRs) are most commonly caused by recipient antibodies reacting against donor white blood cells (WBCs). This immune reaction triggers the release of pyrogenic cytokines. They can also be caused by cytokines that have accumulated in the blood product during storage. This is why leukoreduction (removing WBCs) significantly reduces the incidence of these reactions.

Why the others are incorrect:

• (b) ABO incompatibility:  Causes acute hemolytic reactions, not FNHTR.

• (c) Bacterial toxins:  Cause septic reactions, which are more severe (high fever, hypotension).

• (d) Platelet alloimmunization:  Leads to platelet refractoriness, not FNHTR.

The most well-defined cause of a true anaphylactic transfusion reaction is the presence of anti-IgA antibodies in an IgA-deficient recipient. When such a recipient receives blood components containing IgA, a severe, life-threatening anaphylactic reaction can occur.

Why others are incorrect:

• (b) High bilirubin levels:  Seen in hemolysis, not anaphylaxis.

• (c) Iron overload:  Caused by repeated transfusions, not anaphylactic reactions.

• (d) Cold agglutinins:  Associated with hemolytic anemia, not allergic responses.

Transfusion-Related Acute Lung Injury (TRALI) is a serious, non-cardiogenic pulmonary edema that occurs within 6 hours of a blood transfusion.
It is typically caused by donor anti-HLA or anti-neutrophil antibodies reacting with recipient leukocytes.

Other options:

• a) Hypertension and bradycardia → Not typical of TRALI; more likely in other conditions.

• b) Hives and itching → These are signs of an allergic reaction, not TRALI.

• d) Generalized edema and headache → Not characteristic of TRALI; could be seen in other conditions like transfusion-associated circulatory overload (TACO) or hypertensive crisis.

Acute Hemolytic Transfusion Reaction (AHTR) occurs within minutes to hours after transfusion of incompatible red cells, most commonly due to ABO incompatibility.
It leads to intravascular hemolysis, releasing free hemoglobin into the plasma and urine.

Why others are incorrect:

• (a) Positive DAT: Can be seen in many immune hemolytic conditions — supportive but not diagnostic of acute reaction.

• (c) Positive antibody screen: Indicates presence of antibodies, but not proof of active hemolysis.

• (d) Elevated bilirubin 24 hours post-transfusion: Seen in delayed hemolytic reactions, not acute.

The most frequent nonhemolytic transfusion reaction is the febrile nonhemolytic transfusion reaction (FNHTR).
It is common, usually benign, and caused by cytokines or antibodies reacting with donor leukocytes or platelets.

Why the others are incorrect:

• (b) Hemolytic reaction: Less common but more severe; often due to ABO incompatibility.

• (c) Anaphylactic reaction: Rare; typically in IgA-deficient patients.

• (d) Delayed hemolytic reaction: Occurs days to weeks later; much less frequent.

The most common cause of fatal transfusion reactions is human clerical error, such as misidentifying the patient or the blood unit, which results in the transfusion of ABO-incompatible blood. This causes a severe, acute hemolytic reaction. While bacterial contamination (c) is also a significant cause of fatality, error leading to ABO incompatibility has historically been the most frequent cause of death from transfusion.

Why the others are incorrect:

• (b) Contaminated anticoagulant → Rare, not a common cause.

• (c) Bacterial contamination → Can be fatal (especially with platelets), but less frequent than ABO mismatch.

• (d) Wrong storage temperature → Causes decreased product quality, not usually fatal.

In an acute hemolytic reaction, intravascular hemolysis releases hemoglobin into the plasma. A centrifuge or spun hematocrit tube will show a pink or red-tinged plasma (hemoglobinemia), which is a key immediate visual clue. Elevated bilirubin (b) is a later finding as the hemoglobin is metabolized.

Why the others are incorrect:

• (b) Elevated bilirubin only: ❌ Bilirubin rises later, not immediate; early plasma inspection shows hemoglobin.

• (c) Increased viscosity: ❌ Not a feature of hemolysis.

• (d) Coagulation factors: ❌ Not directly relevant for detection of hemolysis; DIC may occur secondarily.

The Direct Antiglobulin Test (DAT) is the most critical and rapid initial test in a transfusion reaction workup. A positive DAT on the post-transfusion sample provides the first objective evidence of an immune-mediated hemolytic reaction by demonstrating antibody or complement coating the patient’s red cells. All other investigations, like re-crossmatching or antibody identification, follow this key finding.

Why the others are incorrect:

• (b) Antibody identification panel:  Performed after DAT, not first

• (c) Crossmatch:  Done before transfusion, not during reaction workup

• (d) Urinalysis:  Helpful for hemoglobinuria, but not the first test

Transfusion-associated sepsis is a serious, potentially fatal complication caused by the introduction of bacteria into the recipient during transfusion.

Why the others are incorrect:

• (b) ABO incompatibility:  Causes acute hemolytic reactions, not sepsis

• (c) Allergic reaction:  Causes urticaria and itching, not bacterial sepsis

• (d) Cold autoantibody:  Associated with cold agglutinin hemolysis, not sepsis

TRALI (Transfusion-Related Acute Lung Injury) is often caused by antibodies in donor plasma (especially from multiparous women) that react with recipient leukocytes. Using plasma from male donors, who are less likely to have these antibodies, has been a highly effective strategy in reducing the incidence of TRALI.

Why other options are incorrect:

• (b) Pre-medicating with acetaminophen: Helps reduce febrile reactions (FNHTR), not TRALI.

• (c) Using leukoreduced blood products: Reduces FNHTR and CMV transmission, not TRALI (since TRALI is antibody-mediated).

• (d) Slowing the infusion rate: May help prevent circulatory overload (TACO), not TRALI.

Massive transfusion involves infusing large volumes of blood products anticoagulated with citrate. Citrate binds to calcium in the recipient’s blood, leading to hypocalcemia. While hyperkalemia (c) can occur from stored red cells, it is less consistently a major complication compared to the predictable effect of citrate.

Why the others are incorrect:

• (a) Hypercalcemia: Opposite effect — calcium levels fall, not rise.

• (c) Hyperkalemia from stored platelets:  Hyperkalemia comes from stored RBCs, not platelets.

• (d) Iron deficiency:  Occurs after chronic transfusions, not massive acute transfusion.

TRALI is a serious complication characterized by acute respiratory distress. It is most often caused by donor antibodies (from multiparous women or previously transfused donors) that react with the recipient’s HLA or neutrophil antigens. This activates neutrophils in the pulmonary vasculature, leading to capillary leak and non-cardiogenic pulmonary edema.

Why the others are incorrect:

• (b) ABO mismatch:  Causes acute hemolytic reaction, not TRALI.

• (c) Platelet transfusion only:  TRALI can occur with any plasma-containing product, not platelets alone.

• (d) Plasma protein deficiency:  Not related to TRALI mechanism.

Hemolytic disease of the newborn (HDN) occurs when maternal IgG antibodies cross the placenta and destroy fetal red blood cells.

Why the others are less common:

• (b) ABO antigen: Usually mild; many babies are unaffected

• (c) Kell antigen:  Less frequent cause

• (d) Duffy antigen:  Rare cause

An acute hemolytic transfusion reaction, most often due to ABO incompatibility, is an immediate, catastrophic event. Signs and symptoms (e.g., fever, chills, pain, hypotension, hemoglobinuria) typically begin within minutes to a few hours of starting the transfusion.

Why others are incorrect:

• (b) 24 hours after transfusion: Too late — that timing fits some delayed febrile or mild hemolytic reactions.

• (c) 7 days or (d) 2 weeks: Those indicate delayed hemolytic transfusion reactions (secondary immune responses involving IgG antibodies, like Kidd or Duffy).

In Hemolytic Disease of the Newborn (HDN), the blood smear can provide key diagnostic clues. The presence of spherocytes (small, dense red cells without central pallor) is a classic finding, especially in ABO incompatibility, where antibody-coated red cells are partially phagocytosed in the spleen, leading to their spherical shape.

Why the others are incorrect:

• (a) Estimation of WBC and platelet counts: Done by a CBC, not primarily diagnostic for HDN.

• (c) Absolute lymphocyte count: Relates to immune status, not hemolysis.

• (d) Immature neutrophil count: Reflects infection or stress, not HDN.

A severe, acute reaction with high fever, shock, hemoglobinuria, DIC, and renal failure is the classic presentation of a transfusion reaction due to bacterial contamination of the blood product (most often platelets). This causes an overwhelming septic shock and endotoxemia, leading to this dramatic and life-threatening syndrome.

Why the others are incorrect:

• (b) Circulatory overload (TACO): Causes dyspnea, hypertension, pulmonary edema, but no fever or DIC.

• (c) Febrile non-hemolytic: Causes mild fever and chills only, no shock, DIC, or hemoglobinuria.

• (d) Allergic: Causes urticaria and itching, occasionally mild hypotension — not high fever or DIC.

• Timing (5 days post-transfusion) fits a delayed hemolytic transfusion reaction, which typically occurs 3–10 days after transfusion due to an anamnestic antibody response to foreign RBC antigens.

• Clinical signs include mild jaundice and a falling hemoglobin, reflecting extravascular hemolysis.

• Other options:

  • a) Febrile non-hemolytic reaction → occurs during or shortly after transfusion, causes fever but not jaundice or hemoglobin drop.

  • c) TACO → causes respiratory distress due to volume overload, not jaundice or hemolysis.

  • d) Allergic reaction → usually urticaria, itching, or anaphylaxis during transfusion, not delayed jaundice.

A transfusion reaction due to bacterial contamination often presents as the sudden onset of high fever, rigors (severe chills), and hypotension (shock), mimicking severe sepsis or septic shock. This is caused by endotoxins or the bacteria themselves in the contaminated unit.

Why the others are incorrect:

• (b) Mild itching:  Typical of allergic reactions.

• (c) Delayed hemolysis:  Caused by IgG antibodies (e.g., Kidd system), not bacteria.

• (d) Elevated bilirubin:  Seen in hemolytic reactions, not bacterial sepsis.

Transfusion-associated graft-versus-host disease (TA-GVHD) occurs when donor T lymphocytes engraft in an immunocompromised recipient and attack host tissues.

Why the others are incorrect:

• (b) High fever only:  Nonspecific; fever alone is not diagnostic

• (c) Hemoglobinuria:  Seen in acute hemolytic transfusion reactions, not TA-GVHD

• (d) Cold agglutination:  Related to cold antibody hemolysis, not GVHD

A febrile non-hemolytic transfusion reaction (FNHTR) is defined by a fever (typically a rise of ≥1°C from baseline) that occurs during or shortly after a transfusion, with no other explanation. It is most commonly caused by cytokines in the blood product or recipient antibodies reacting against donor white blood cells.

Other options explained:

• (b) Hemoglobinuria and renal failure → Seen in acute hemolytic transfusion reaction.

• (c) Hypotension and wheezing → Suggests anaphylactic reaction.

• (d) Generalized bleeding and shock → Seen in disseminated intravascular coagulation (DIC) due to severe hemolytic reaction or sepsis.

TA-GVHD is caused by viable donor T lymphocytes engrafting and proliferating in a susceptible recipient. The most common scenario is the transfusion of non-irradiated cellular blood products (RBCs, platelets) to immunocompromised patients (e.g., those with hematologic malignancies, stem cell transplants, or congenital immunodeficiencies) who cannot reject the donor cells.

Why the others are incorrect:

• (b) Transfusion of plasma only:  Plasma has no viable T cells, so TA-GVHD does not occur

• (c) Platelet transfusion:  Only dangerous if non-irradiated and containing donor lymphocytes

• (d) ABO mismatch:  Causes hemolytic reactions, not TA-GVHD

A delayed hemolytic transfusion reaction occurs due to a secondary (anamnestic) immune response. The recipient has been previously sensitized to a red cell antigen, but the pre-transfusion antibody screen is negative or too weak to detect. After transfusion, the antigen stimulates a rapid antibody production, which becomes detectable in the plasma 2 days to 2 weeks later and leads to the destruction of the transfused red cells.

Why others are incorrect:

• (a) 3–6 hours after transfusion: Too early — typical of acute hemolytic transfusion reaction.

• (c) 60–90 days after transfusion: Too late — antibodies would already be detectable.

• (d) Immediately after transfusion: Suggests preexisting antibodies, again seen in acute reactions.

Transfusion-associated circulatory overload (TACO) is a mechanical complication caused by the rapid or large-volume infusion of blood products, which exceeds the circulatory system’s capacity. This leads to increased hydrostatic pressure, pulmonary edema, and signs of heart failure (e.g., dyspnea, tachycardia, hypertension).

Why the others are incorrect:

• (b) ABO incompatibility:  Causes acute hemolytic reaction, not TACO.

• (c) Iron deficiency:  Result of chronic blood loss, not transfusion overload.

• (d) Leukocyte antibodies:  Cause TRALI, not TACO.

Iron overload (transfusional hemosiderosis) is a long-term complication for patients who receive multiple chronic transfusions (e.g., those with thalassemia, sickle cell disease, or myelodysplastic syndromes). Each unit of red blood cells contains about 200-250 mg of iron, and the body has no active mechanism to excrete this excess iron, which accumulates in and damages organs like the liver, heart, and endocrine glands.

Why the others are incorrect:

• (b) Single transfusion:  Insufficient iron load to cause overload.

• (c) Platelet transfusion:  Platelets contain minimal iron.

• (d) Plasma donation:  Plasma has no red cells, so no iron is transferred.