1. Why is transfusing Rh negative blood usually safe for Rh positive persons?

A. Rh positive persons lack the D antigen B. Rh positive persons do not develop anti-D antibodies against Rh negative blood C. Rh negative blood contains anti-D antibodies that neutralize Rh antigen D. Rh factor is not antigenic in Rh positive persons

2. What is the mode of action of anti-D antibody given to Rh-negative mothers?

A. It destroys fetal RBCs in utero B. It neutralizes fetal Rh antigen before the mother's immune system can react C. It builds passive immunity and prevents formation of Rh antibodies in mother D. It stimulates fetal RBC production

3. What happens when Rh positive blood is transfused to an Rh negative person for the first time?

A. Immediate severe transfusion reaction B. No reaction; however anti-D antibodies develop within one month causing later delayed reaction C. The donor RBCs are immediately destroyed D. Permanent immunity is established

4. What is the prophylactic measure to prevent hemolytic disease in Rh-negative mothers?

A. Iron therapy B. Administration of anti-D antibody at 28th and 34th weeks of gestation and within 48 hours after delivery if baby is Rh positive C. Blood transfusion during pregnancy D. Antibiotic prophylaxis

5. Which parts of the brain are most commonly affected by kernicterus?

A. Frontal cortex and occipital lobe B. Basal ganglia, hippocampus, geniculate bodies, cerebellum, and cranial nerve nuclei C. Medulla oblongata only D. Spinal cord

6. Why is the Rh system different from the ABO system?

A. Because Rh antigens are sugar molecules and ABO antigens are proteins B. Because Rh factor does not have corresponding natural antibodies in serum C. Because Rh antibodies are naturally present in all blood types D. Because Rh antigens are always absent in blood

7. What triggers jaundice in the fetus/newborn during erythroblastosis fetalis?

A. Liver failure B. Excess bilirubin from hemolysis of RBCs C. Infection causing bile duct obstruction D. Deficiency of bile acids

8. Which blood group is called universal recipient and why?

A. O group because it has no antibodies B. AB group because their plasma has no antibodies causing agglutination C. A group because they have anti-B antibodies D. B group because they have anti-A antibodies

9. Why can people with blood group O donate blood to all other groups?

A. Because their plasma contains no antibodies B. Because their RBCs have no A or B antigens C. Because they have all antigens D. Because they have high antibody levels

10. What are the three severe complications of erythroblastosis fetalis?

A. Liver failure, brain damage, anemia B. Severe anemia, hydrops fetalis, kernicterus C. Kidney failure, jaundice, infections D. Cardiac arrest, pneumonia, hematoma

11. According to Landsteiner's law, what is true about agglutinogens and agglutinins in blood?

A. Both agglutinogen and corresponding agglutinin are always present together B. If an antigen is present on RBCs, the corresponding antibody is absent in serum C. Agglutinins are always absent from plasma D. The law does not apply to ABO blood groups

12. During cross-matching for blood transfusion, what is mixed together?

A. Donor’s serum and recipient’s serum B. Donor’s RBCs and recipient’s RBCs C. Recipient’s serum and donor’s RBCs D. Recipient’s RBCs and donor’s serum

13. What clinical complications can result from hemolytic transfusion reactions?

A. Jaundice, cardiac shock, renal shutdown B. Diabetes, hypertension, renal stones C. Hemophilia, thrombocytopenia, anemia D. Asthma, bronchitis, pneumonia

14. What causes erythroblastosis fetalis in a fetus?

A. ABO blood group incompatibility B. Rh incompatibility between mother and fetus C. Deficiency of vitamin K in the fetus D. Infection during pregnancy

15. What is the role of Rh antibodies developed in an Rh-negative mother after delivery?

A. They have no effect on future pregnancies B. They can cross the placenta and destroy fetal RBCs if the next fetus is Rh positive C. They protect the fetus in subsequent pregnancies D. They cause infections in the mother

16. What is the most severe outcome of hydrops fetalis in a fetus caused by severe hemolysis?

A. Spontaneous abortion in the first trimester B. Renal failure in the fetus C. Intrauterine death due to edema, cardiac failure, and organ enlargement D. Development of cerebellar ataxia

17. What is the primary mechanism causing kernicterus in infants with erythroblastosis fetalis?

A. Excessive RBC production in bone marrow B. Bilirubin crossing the immature blood-brain barrier causing brain damage C. Failure of kidney to excrete bilirubin D. Direct infection of brain by Rh antibodies

18. Why can Rh antibodies cause a delayed transfusion reaction in Rh negative individuals receiving Rh positive blood for the first time?

A. Because the antibodies appear only within a month after exposure B. Because the blood cells instantly agglutinate and lyse C. Because Rh antigen is not immunogenic D. Because the transfused blood is always destroyed immediately

19. During ABO incompatibility, why does agglutination usually occur between recipient’s plasma and donor’s RBCs but not vice versa?

A. Because donor plasma antibodies are diluted in recipient plasma and ineffective B. Because donor antibodies are stronger C. Because recipient plasma lacks antibodies D. Because donor RBC antigens are absent

20. What happens to the Rh antigens from fetal blood at the time of delivery in Rh incompatibility?

A. They remain confined in fetal circulation B. They cross into the mother’s blood due to placental detachment C. They are destroyed by maternal enzymes D. They enter amniotic fluid only

21. What is the initial clinical sign indicating brain damage due to kernicterus in infants?

A. Seizures B. High-pitched cry and lethargy C. Hypertonia and opisthotonus D. Inability to suckle milk

22. What happens when Rh antibodies from an Rh negative mother cross the placenta to an Rh positive fetus in subsequent pregnancies?

A. They stimulate production of more RBCs in fetus B. They cause agglutination and hemolysis of fetal RBCs C. They increase oxygen delivery to the fetus D. They protect the fetus from infections

23. Why does renal shutdown occur during a hemolytic transfusion reaction?

A. Due to infection of kidneys B. Due to precipitation of hemoglobin and toxic substances obstructing renal tubules C. Due to high blood flow in kidneys D. Due to excessive urine production

24. Which of the following is NOT a symptom of acute hemolytic transfusion reaction?

A. Fever and chills B. Low blood pressure and tachycardia C. Red urine and back pain D. Weight gain and constipation

25. Why does the first Rh positive baby of an Rh negative mother usually escape complications?

A. Maternal antibodies are not produced before delivery B. Placental barrier prevents fetal Rh antigen from entering mother’s circulation before delivery C. Rh antibodies cannot cross the placental barrier D. The baby has natural resistance to Rh incompatibility

26. Which regions of the brain are most commonly affected by kernicterus?

A. Cerebral cortex and spinal cord B. Basal ganglia, hippocampus, geniculate bodies, cerebellum, cranial nerve nuclei C. Hypothalamus and pituitary gland D. Medulla oblongata and pons

27. What does Landsteiner’s Law state about the presence of antigens and antibodies?

A. If an agglutinogen (antigen) is present, corresponding antibody must be present B. If an agglutinogen is absent, the corresponding antibody must also be absent C. If an agglutinogen is present, the corresponding antibody must be absent in serum D. Agglutinogens and antibodies always coexist

28. What is the clinical significance of hydrops fetalis in erythroblastosis fetalis?

A. It is characterized by high blood pressure in fetus B. It is characterized by fetal edema, organ enlargement, and cardiac failure C. It causes fetal hypoglycemia D. It prevents anemia in the fetus

29. Which blood group is called "universal recipient" and why?

A. Group O, because it has no antigens on RBCs B. Group AB, because its plasma has no antibodies to agglutinogens of other groups C. Group B, because it has anti-A antibodies D. Group A, because it has anti-B antibodies

30. Which blood type individuals are known as universal donors?

A. AB group B. A group C. B group D. O group

31. What is the main cause of hemolytic transfusion reactions?

A. Viral contamination B. Recipient’s antibodies adhere to donor RBCs causing agglutination and lysis C. Inadequate blood volume transfused D. Incompatible electrolyte solution

32. What is the role of cross-matching before transfusion?

A. To determine recipient’s blood group B. To check compatibility of donor RBCs with recipient’s serum to avoid agglutination C. To check donor’s white blood cells D. To determine blood volume required

33. What characteristic distinguishes hemolytic transfusion reactions caused by Rh incompatibility from those caused by ABO incompatibility?

A. Rh incompatibility usually causes immediate reactions on first exposure B. Rh negative persons do not develop anti-D antibodies C. Rh antibodies cause delayed reactions upon first transfusion, but severe immediate reactions upon subsequent exposures D. ABO incompatibility reactions usually do not cause agglutination

34. What is the primary treatment for a baby born with erythroblastosis fetalis?

A. Antibiotics B. Iron supplements C. Exchange transfusion with Rh-negative blood D. Corticosteroids

35. What are the early signs of kernicterus in infants?

A. Hypertonia and seizures B. Lethargy, high-pitched cry, hypotonia, and head arching backwards C. Fever and rash D. Excessive sucking and eating

36. What happens to Rh antibodies developed in the infant’s bloodstream after exchange transfusion?

A. They persist forever B. They are destroyed gradually over six months along with Rh positive blood replacement C. They immediately cause transfusion reactions D. They increase in concentration

37. Which of the following is TRUE about ABO blood groups?

A. Group O blood has both A and B antigens B. Group AB plasma contains both anti-A and anti-B antibodies C. Group O blood cells have no A or B antigens and can be given to all groups D. Group A plasma contains anti-B antibodies only in the serum

38. Which cells increase in the fetal circulation in erythroblastosis fetalis?

A. Mature erythrocytes only B. Lymphocytes C. Large, immature erythroblasts in the proerythroblastic stage D. Platelets

39. How can kernicterus progress if untreated?

A. Infant normalizes with time B. Develop hypertonia, opisthotonus, inability to suckle, seizures, spasticity, fever, and coma C. Develops only mild jaundice D. Causes liver enzyme abnormalities only

40. What inheritance pattern does the Rh factor follow?

A. Autosomal recessive B. X-linked dominant C. Autosomal dominant, with D allele dominant over d allele D. Mitochondrial inheritance

41. What types of antibodies primarily cause transfusion reactions in ABO incompatibility?

A. IgA B. IgE C. IgG and IgM D. IgD

42. Why do transfusion reactions occur immediately during a second transfusion of Rh positive blood to an Rh negative recipient?

A. Because the recipient’s preformed anti-D antibodies agglutinate and lyse donor RBCs immediately B. Because donor blood is always contaminated C. Because of allergic reaction to plasma proteins D. Because of ABO incompatibility

43. What causes hemolytic disease of the fetus and newborn, also known as erythroblastosis fetalis?

A. ABO incompatibility between mother and fetus B. Rh incompatibility between mother and fetus C. Infection during pregnancy D. Vitamin deficiency in fetus

44. Which of the following is NOT a severe complication of erythroblastosis fetalis?

A. Severe anemia B. Hydrops fetalis C. Kernicterus D. Diabetes mellitus

45. Why is exchange transfusion effective in treating erythroblastosis fetalis?

A. It removes maternal Rh antibodies and replaces infant’s Rh positive blood with Rh negative blood B. It provides antibodies to fight infection C. It increases hemoglobin levels rapidly D. It improves liver function

46. Which organ(s) increase production of RBCs to compensate for hemolysis in erythroblastosis fetalis?

A. Bone marrow only B. Bone marrow and lymph nodes C. Bone marrow, spleen, and liver D. Spleen only

47. How is anti-D antibody used to prevent erythroblastosis fetalis in Rh negative mothers?

A. Administered at 28th and 34th weeks of gestation and within 48 hours of delivery if baby is Rh positive B. Given only after the baby is born C. Administered orally throughout pregnancy D. Only given during labor

48. Why does kernicterus develop in infants affected by erythroblastosis fetalis?

A. Because of low bilirubin levels in plasma B. Because the infant’s blood-brain barrier is not fully developed, allowing bilirubin to enter the brain C. Due to infection of the brain tissue D. Because of hypoxia during birth

49. What is the purpose of exchange transfusion in infants born with erythroblastosis fetalis?

A. To provide the infant with more Rh positive blood B. To replace infant’s Rh positive blood with Rh negative blood, eliminating maternal antibodies C. To increase bilirubin levels in infant’s blood D. To boost antibody production in the infant

50. Why does the first child of an Rh-negative mother with an Rh-positive fetus usually escape complications?

A. The Rh antigen cannot pass through the placental barrier during pregnancy B. The mother has pre-existing Rh antibodies C. The fetus produces protective antibodies D. The placenta completely blocks all antibodies