Blood Groups Major and Minor Systems Quiz

The Lewis blood group system is the only blood group system where antigens are not manufactured by red blood cells (RBCs).

Helicobacter pylori bacteria use Lewis blood group system antigens as receptors to bind to and infect the stomach lining.

The Secretor gene controls the expression of Lewis antigens on RBCs and in body secretions like saliva.

The Lewis antigen expression follows a specific developmental pattern: Le(a-b-) is the initial stage, followed by Le(a+b-), then Le(a+b+), and finally Le(a-b+).

The Lewis System includes three primary phenotypes: Le(a+b-), Le(a-b+), Le(a-b-).

The Le b antigen is present in an individual only if they inherit both the Lewis gene (Le) and the Secretor gene (Se).

Anti-I is an autoantibody that is commonly associated with cold agglutinin syndrome, particularly in cases of primary atypical pneumonia caused by Mycoplasma pneumoniae.

Anti-i is an autoantibody frequently found in individuals with infectious mononucleosis, caused by the Epstein-Barr virus (EBV).

Anti-P1 antibody can be neutralized by components found in hydatid cyst fluid from Echinococcus granulosus infection, pigeon droppings, or turtle dove eggwhite.

Anti-Tja (Anti-PP1Pk) is an autoantibody first described in a patient with adenocarcinoma of the stomach.

Autoanti-P autoantibody is predominantly found in patients with paroxysmal cold hemoglobinuria (PCH), a rare autoimmune hemolytic disorder.

The P antigen acts as a receptor for Parvovirus B19, known to cause erythema infectiosum (Fifth Disease).

Conditions such as pregnancy, cancer, viral and parasitic infections, and alcoholic cirrhosis can influence changes in the Lewis phenotype.

Lewis antibodies are naturally occurring IgM antibodies, characterized as cold reactive. Their non-clinical significance is due to their ability to be neutralized by Lewis substances present in secretions such as plasma or saliva.

MN antigens are found on the surface of red blood cells, specifically located on a protein called glycophorin A. The difference between M and N antigens lies in their amino acid sequence at positions 1 and 5.

Enzyme treatments, like those used in blood typing, can destroy MN antigens. Anti-M antibodies are naturally occurring, saline agglutinins, cold reactive, and of the IgM type.

Ss antigens reside on glycophorin B, another protein found on red blood cells. Anti-N antibodies are generally cold reactive, often IgM, and can be found in renal patients undergoing dialysis with formaldehyde-containing equipment.

The U phenotype represents a universal blood type within the MNSs blood group system. Individuals lacking both S and s antigens are considered U phenotype and are typically of Black African origin. They often produce anti-U antibodies.

The McLeod phenotype in the Kell blood group system is inherited in an X-linked manner. This means that the gene responsible for this phenotype is located on the X chromosome.

The Duffy null (Fy(a-b-)) phenotype, a lack of both Duffy antigens, is more prevalent in the African-American population. This phenotype is linked to resistance to malaria caused by Plasmodium vivax.

Patients with the McLeod phenotype exhibit a deficiency in the NADH-oxidase enzyme. This enzyme plays a crucial role in cellular metabolism.

The Duffy null phenotype (Fy(a-b-)) provides resistance against Plasmodium vivax infection because the parasite requires Duffy antigens to enter red blood cells.

Kidd antibodies are known for their rapid disappearance both in vivo (within the body) and in vitro (in laboratory tests). This property makes them challenging to detect, often leading to Delayed Hemolytic Transfusion Reactions (DHTR).

The Jk(a-b-) or Jk null phenotype in the Kidd blood group system exhibits resistance to lysis in 2M urea solution. This unique characteristic helps distinguish this phenotype.

The Lutheran blood group system was named after a blood donor named Luteran, whose name was misinterpreted during the discovery of this system.

Diego blood group system antigens are located on the anion exchange protein (AE-1), also known as the erythrocyte band 3. This protein facilitates the transport of anions across the red blood cell membrane.

Mutations in the AE-1 protein can result in various red blood cell abnormalities, including hereditary spherocytosis, congenital acanthocytosis, and Southeast Asian ovalocytosis.

The Scianna blood group system antigens are expressed by the RBC adhesion protein ERMAP in humans. This protein plays a role in cell-cell interactions.

Anti-Lua antibody has an optimal temperature range for binding to its target antigens, which is between 12°C and 23°C (54°F and 73°F), making it a cold-reactive antibody.

The Lu(a-b-) phenotype can arise from either an amorphic gene (Lu, which is recessive) or an inhibitor gene (InLu, which is dominant).