ABO and Rh blood type incompatibilities between mother and fetus can result in hemolytic disease of the newborn. ABO incompatibility is more common but less severe, as the mother's naturally occurring antibodies can cross the placenta and destroy fetal RBCs starting from the first pregnancy. Rh incompatibility is less common but more severe, as sensitization only occurs after the first Rh-positive pregnancy, allowing subsequent pregnancies to be affected. Clinical management includes phototherapy, exchange transfusions, and Rh immune globulin shots to prevent sensitization. Understanding the biochemical basis of blood group antigens and maternal-fetal immune response is important for managing these conditions.

1. ABO Blood Type
Incompatibility09/19/2020

2. Dr. Agnas, Jennifer Jane L.
Dr. Aragon, Earl Jason N.
Dr. Cortez, Ylanie Scheherezade
Dr. Daza, Djev David
Dr. Loreno, Madonna E.
Dr. Pastrana, Jose Ranelle
Dr. Songcuya, Melissa
Presented By
Medicine-1st Year

3. 1.Composition and importance of RBC membrane;
2. Comparison of direct and indirect blood typing; major and minor cross-matching;
3. Biochemical basis of ABO and Rh incompatibility;
4. Role of genetics and sugar in determining blood type;
5. Clinical management of Hemolytic disease of the newborn

4. Terminologies…
• Antigen – determine blood type and can either be protein or complexes of sugar molecules.
• Allele – is one of two or more version of gene, meaning it is one of two more versions of mutation at the same place
on a chromosomes. It can be dominant or recessive.
• Fucose - is an unusual sugar that is present in a variety of glycolipids and glycoproteins produced by mammalian cells
• Locus - is a specific, fixed position on a chromosome where a particular gene or genetic marker is located
• Homozygous - s a word that refers to a particular gene that has identical alleles on both homologous chromosomes. It
is referred to by two capital letters (XX) for a dominant trait, and two lowercase letters (xx) for a recessive trait.
• Heterozygous - refers to having inherited different forms of a particular gene from each parent. A heterozygous
genotype stands in contrast to a homozygous genotype, where an individual inherits identical forms of a particular
gene from each parent.

5. Terminologies…
• Fucosyl Transferase - is an enzyme that transfers an L-fucose sugar from a GDP-fucose (guanosine diphosphate-fucose)
donor substrate to an acceptor substrate.
• Galactose Transferase - catalyzes the galactosylation of the H antigen and is responsible for the formation of the blood
group antigen of phenotype B.
• N- Acetylgalactose Transferase - which catalyzes the transfer of GalNAc residues from the UDP-GalNAc donor nucleotide
to the Gal residues of the acceptor H antigen, converting the H antigen into A antigen in A and AB individuals.
• RBC (Red Blood Cell) – also known as erythrocyte, these are the cellular component of blood
• Oligosaccharides – is made up of group or chain of monosaccharide that can be attached to the RBC.

7. 50% proteins
40% lipids
10% carbohydrates
The membrane has vertical and horizontal interaction.
Vertical interaction -stabilizes the lipid bilayer
Horizontal interaction - supports the structural Integrity of the RBC, It
also maintains biconcave shape of the RBC.
RBC Membrane

8. 1. Lipid Bilayer
2. Membrane Skeleton
3. Glycocalyx

9. Horizontal Interaction
Source: https://www.researchgate.net/figure/A-schematic-representation-of-red-blood-cell-
RBC-membrane-structure-with-major_fig1_318273023

10. The lipid bilayer is semipermeable Contains:
30% Unesterified cholesterol
10% Glycerides
60% Phospholipids
➔ Phosphatidylcholine (30%)
➔ Sphingomyelin (25%)
➔ Phosphatidylethanolamine (28%)
➔ Phosphatidylserine (14%)

11. -Responsible for the elasticity and stability of the red cell membrane
A. Integral proteins
▰ Glycophorin (A, B, C) - imparts negative charge to the cell,
reducing interaction with other cells
▰ Band 3 - maintain red blood cell hydration anion exchanger protein
- Provides channel for exchange of bicarbonate and chloride (chloride shift)
▰ Aquaporins - water channel proteins

12. B. Peripheral Proteins
❖ Spectrin - major constituent, maintains cell shape and resists swelling
due to osmotic pressure
- Responsible for the biconcave shape of RBC
❖ Ankyrin - serves as anchor of the assembled spectrin molecules to the lipid bilayer
❖ Protein 4.1 - binds to spectrin close to actin binding site thereby strengthening and stabilizing the
cytoskeletal lattice
❖ Actin - globular protein composed of filaments that bind weakly to tail end of both α and β
spectrin

14. -The exterior part rich in carbohydrates. Glycophorins contributes
to the major portion of glycosylation at this extracellular layer
★ Glycophorins - have a single spanning alpha helix and are a
general class of proteins. These are glycoproteins which bear the
antigenic determinants of the blood groups.
Glycocalyx

15. ★ For regulation of surface deformability, flexibility, cell adhesion, and
immune recognition

16. 2. Discuss the biochemical basis of blood
typing and of blood type determination

17. • What is ABO blood group System?
• ABO blood group system used to denote the presence of one, both, or
neither of the A and B antigens of erythrocytes.
• The ABO blood types were discovered by Karl Landsteiner in 1901.
• Determination of blood type is essential to human blood transfusion,
mismatch can cause fatal adverse reaction that’s why this discovery played an
important role in medical practices.

18. Blood types are determined by the presence or absence of certain antigens – substances
that can trigger an immune response if they are foreign to the body. Since some antigens
can trigger a patient's immune system to attack the transfused blood, safe blood
transfusions depend on careful blood typing and cross-matching.
Typically, blood type tests are performed through addition of a blood sample to a solution
containing antibodies corresponding to each antigen. The presence of an antigen on the
surface of the blood cells is indicated by agglutination.
How Blood Type Is Determined And Why You Need To
Know?

19. Matching compatible blood types is important for blood transfusions.
Knowing your type and compatibility is crucial if you ever need a
transfusion. For those with rare blood types the supply can be limited. It is
important to know your blood type, especially if you have a rare type.
Don't wait until an emergency to find out your blood type.
The importance of knowing the blood type

20. All about blood typing…
A blood type (also known as a blood group) is a classification of blood, based on the
presence and absence of antibodies and inherited antigenic substances on the surface
of red blood cells (RBCs).
There are four major blood groups determined by the presence or absence of two antigens – A and B – on
the surface of red blood cells. In addition to the A and B antigens, there is a protein called the Rh factor, which
can be either present (+) or absent (–), creating the 8 most common blood types (A+, A-, B+, B-, O+, O-
, AB+, AB-).

21. Blood Type Determination
A B AB O
A AB B AB AB A AB B O
- - +
-+ + not
RH (+ or -)

22. Blood Typing
Blood Type: A-
Donate: A+, A-, AB+, AB-
Receive: A-, O-
Blood Type: A+
Donate: A+, AB+
Receive: A-, O-, A+, O+

23. Blood Typing
Blood Type: B+
Donate: B+, AB+,
Receive: B-, B+, O+, O-
Blood Type: B-
Donate: B+, B-, AB+, AB-
Receive: B-, O-

24. Blood Typing
Blood Type: AB-
Donate: AB+, AB-
Receive: A-,B-, AB-, O-
Blood Type: AB+
Donate: AB+
Receive: A-,A+, B-, B+, AB-,
AB+, O-, O+
Blood type AB+ is
universal recipient.

25. Blood Typing
Blood Type: O-
Donate: A+, A-, B+, B-, AB+,
AB-, O+, O-
Receive: O-
Blood type O- is the
universal donor
Blood Type: O+
Donate: A+, B+, AB+, O+,
Receive: O-, O+

26. Blood Type Chart

27. 3. Explain the importance of the oligosaccharide sequence in the RBC
membrane in blood determination

28. How does the antigens form…
oligossacharide
RBC
NOTE: Surface antigens determines blood group
oligossacharide
oligossacharide

29. H-Antigen
H - antigen is form when chromosome no. 9 found in the precursor cell of the
RBC cannot produce any enzyme but the gene found in chromosome no. 19
expresses Fucose transferase (the enzyme that catalyze FUCOSE) attaching it
to the OLIGOSSACHARIDE found in the surface of our red blood cells thereby
producing H substance or H antigen. H antigen acts as precursor of both A
and B antigen that’s why this process is always present in all ABO system.
Note: H antigen has no antibodies.

30. A-Antigen
A–antigen is form when the gene in chromosome no. 19 found in the precursor
cell expresses Fucose transferase which catalyze the FUCOSE and when the gene
in Chromosome no.9 expresses N-Acetyl Galactosamine Transferase which
catalyze the NAGA (N-Acetyl Galactosamine) thereby attaching it to the
OLIGOSSACHARIDE of the Red blood cell.
Note: A-antigen has B antibodies.

31. B-Antigen
B–Antigen – is form when the gene in chromosome no. 19 found in the
precursor cell expresses fucose transferase that catalyze FUCOS and the gene
in chromosome no. 9 expresses the enzyme galactose transferase which
catalyze galactose. When galactose and fucose attached to the
OLIGOSSACHARIDE found in the surface of the red blood cell it is know called
as B antigen.
Note: B-antigens has A antibodies.

32. AB - Antigens
AB-antigens has both the A antigen and B antigens attached to the surface of the
RBC but no A and B antibodies . Chromosome no. 9 in either maternal or paternal
sides produces both A transferase and B transferase which are both active.
Note: AB antigens has no A or B antibodies.

34. 4. Explain the role of genetics in
determining the blood type, especially in
the oligosaccharides content of membrane
lipoproteins

35. OLIGOSACCHARIDES
• ABO Antigens are complex oligosaccharides
present in most cell of the body and in certain
secretions.
• These oligosaccharides are bound to membrane
proteins or lipids and are referred to as: ABO
SUBSTANCES.

36. A Blood Group = A Antigen
B Blood Group = B Antigen
AB Blood Group = A and B Antigen
O Blood Group = H Antigen

37. HOW DOES
ABO ALLELES
WORK?
Chromosome
no. 09
Chromosome
no. 19
Precursor
Cell

38. 1. Individuals expressing A – Allele
2. Individuals expressing B - Allele
3. Individuals expressing O - Allele
4. Individuals expressing AB - Allele

39. H ANTIGEN

40. BLOOD TYPE A
•- A gene and H gene
•- Sugar: N-acetylgalactosamine
•- Enzyme: Glycosyltransferase
•- A antigens are present on the RBC
membrane
•- Have antibodies for B antigens
(Anti-B)

41. BLOOD TYPE B
•B gene and H gene
•- Sugar: D-galactose
•- Enzyme: Glycosyltransferase
•- B antigens are present on the RBC
membrane
•- Have antibodies for A antigens
(Anti-A)

42. BLOOD TYPE AB
•A gene, B gene and H gene
•- Sugar: N-acetylgalactosamine and
D-galactose
•- Enzyme: Glycosyltransferase
•- A and B antigens are present on
the RBC membrane
•- No antibodies against A and B
antigens

43. BLOOD TYPE O
•H gene only
•- Enzyme: Fucosyltransferase
•- No A and B antigens are present on
the RBC membrane
•- Have antibodies against both A and
B
•(Anti-A and Anti-B)

44. Blood Type Genes Enzyme Sugars
A H gene;
A gene
Fucosyl Transferase;
A transferase
N-acetylgalactosamine
B H gene;
B gene
Fucosyl Transferase;
B transferase
D-galactose
AB H gene;
AB gene
Fucosyl Transferase;
AB transferase
N-acetylgalactosamine
D-galactose
O H gene Fucosyl Transferase None

45. Blood group Antigen and Antibodies

46. 5. Discuss the biochemical basis of ABO incompatibility and Rh
incompatibility and correlate clinically with hemolytic disease of the
newborn

47. • also called Erythroblastosis fetalis
• A blood disorder in a fetus or newborn infant.
• caused by the destruction of the RBCs of the neonate by maternal
immunoglobulin G antibodies.
▻ during pregnancy, mother’s antibodies are transported to the placenta
towards the fetal circulation for protection
▻ due to the incompatibility, antibodies of the mother detect antigens
absent in its system therefore destroying these antigen-containing RBCs.
Hemolytic Disease of the Newborn

48. RH
INCOMPATIBILITYDETERMINE THE RH TYPE AND DIRECT THE PRODUCTION OF A NUMBER
OF BLOOD GROUP FACTORS
▻ OCCURS WHEN FATHER IS RH(+) OR D(+) AND MOTHER IS RH(-) OR
D(-)
▻ MOTHER BECOMES PREGNANT WITH RH(+) OR D(+) FETUS
▻ MOTHER'S IMMUNE RESPONSE TO THE FETAL D ANTIGEN IS TO
FORM ANTIBODIES AGAINST IT (ANTI-D).
• LESS COMMON, MORE SEVERE
• DOES NOT OCCUR ON 1ST PREGNANCY BUT WITH SUBSEQUENT
ONES.

49. During 1st pregnancy,
SENSITIZATION occurs.
How does sensitization happen?
▻ Occurs during Fetomaternal Hemorrhage
▻ Labor & delivery
▻ Ruptured ectopic pregnancies
▻ Placental abruption
▻ Abortion

52. ▻ Severe Anemia
▻ High bilirubin released
▻ Immediate jaundice
S Y M P T O M S

53. • Occurs when mother is Type O becomes pregnant
with a Type A/B/AB fetus
• Mother's serum contains naturally occurring
anti-A and anti-B
▻ Antibodies are of IgG type and can
therefore cross the placenta and
hemolyse fetal RBCs.
• May occur on 1st pregnancy and subsequent
pregnancies
• More common, less severe
ABO
INCOMPATIBILITY

55. INCOMPATIBILITY SUMMARY
RH
INCOMPATIBILTYLess common, more severe
Mother: Rh(-) Fetus: Rh(+)
SENSITIZATION OCCURS
1st pregnancy safe;
subsequent
pregnancies are affected
Symptoms:
▻ Severe anemia
▻ High bilirubin released
▻ Immediate jaundice
ABO INCOMPATIBILTY
More common, less severe
Mother: Type O Fetus: Type
A/B/AB
NO SENSITIZATION
Can be affected at 1st
pregnancy and subsequent
pregnancies
Symptoms:
▻ Mild anemia
▻Low bilirubin released
▻Delayed jaundice

56. CLINICAL
MANAGEMENT

57. conversion of unconjugated
bilirubin into a water soluble form
for more rapid excretion through
the bile or urine without involving
any process of conjugation
Wavelength of 420-475 nm
TREATMENT/PREVENTIO
N
• Plasma Exchange
performed in pregnant
women with the goal of
removing the all of
antibody
• Phototherapy

58. • Exchange
Transfusion▻ replacing
infant’sblood with
compatible RBCs and
plasma
• Rh Immune Globulin
(RhIg) or RhoGAM shot
(IM)
▻ contains antibodies to Rh-positive
blood, but not enough of them to
cause harm to the fetal
bloodstream.
▻ Administered to women (Rh
negative) at 28 weeks of pregnancy
(2nd Trimester) and 72 hours after
birth (1st Pregnancy)

60. 5. Discuss the biochemical basis of ABO incompatibility and Rh
incompatibility and correlate clinically with hemolytic disease of the newborn

61. • also called Erythroblastosis fetalis
• A blood disorder in a fetus or newborn infant.
• caused by the destruction of the RBCs of the neonate by maternal
immunoglobulin G antibodies.
▻ during pregnancy, mother’s antibodies are transported to the
placenta towards the fetal circulation for protection
▻ due to the incompatibility, antibodies of the mother detect
antigens absent in its system therefore destroying these antigen-
containing RBCs.
Hemolytic Disease of the Newborn

62. INCOMPATIBILITYRH
DETERMINE THE RH TYPE AND DIRECT THE PRODUCTION OF A NUMBER
OF BLOOD GROUP FACTORS
▻ IN RH FACTORS, THE MOST COMMON ANTIGEN OF THIS GROUPIS
ANTIGEN D.
▻RH(+) WILL HAVE THE GENE TO CREATE THE ANTIGEN D PROTEIN
UNLIKE THE RH(-)
▻ OCCURS WHEN FATHER IS RH(+) OR D(+) AND MOTHER IS RH(-) OR
D(-)

63. RH INCOMPATIBILITY
• Mother becomes pregnant with Rh(+) or D(+) fetus
• Mother's immune response to the fetal D antigen is to form antibodies against it (anti-
D).
• Less common, more severe
• Does not occur on 1st pregnancy but with subsequent ones.

64. During 1st pregnancy,
SENSITIZATION occurs.
How does sensitization happen?
▻ Occurs during Fetomaternal Hemorrhage
▻ Labor & delivery
▻ Ruptured ectopic pregnancies
▻ Placental abruption
▻ Abortion

67. ▻ Severe Anemia
▻ High bilirubin released
▻ Immediate jaundice
S Y M P T O M S

68. • Occurs when mother is Type O becomes pregnant
with a Type A/B/AB fetus
• Mother's serum contains naturally occurring
anti-A and anti-B
▻ Antibodies are of IgG type and can
therefore cross the placenta and hemolyse fetal
RBCs.
• May occur on 1st pregnancy and subsequent
pregnancies
• More common, less severe
INCOMPATIBILITYABO

70. INCOMPATIBILITY SUMMARY
RH
INCOMPATIBILITY
Less common, more severe
Mother: Rh(-) Fetus: Rh(+)
SENSITIZATION OCCURS
1st pregnancy safe;
subsequent
pregnancies are affected
Symptoms:
▻ Severe anemia
▻ High bilirubin
released
▻ Immediate jaundice
ABO INCOMPATIBILTY
More common, less severe
Mother: Type O Fetus: Type
A/B/AB
NO SENSITIZATION
Can be affected at 1st
pregnancy and subsequent
pregnancies
Symptoms:
▻ Mild anemia
▻Low bilirubin released
▻Delayed jaundice

71. CLINICAL
MANAGEMENT

72. conversion of unconjugated
bilirubin into a water soluble
form for more rapid excretion
through the bile or urine
without involving any process of
conjugation
Wavelength of 420-475 nm
TREATMENT/PREVENTION
• Plasma Exchange
performed in pregnant
women with the goal
of removing the all
of antibody
• Phototherapy

73. • Exchange
Transfusion▻ replacing
infant’sblood with
compatible RBCs and
plasma• Rh Immune Globulin
(RhIg) or RhoGAM shot
(IM)
▻ contains antibodies to Rh-positive
blood, but not enough of them to
cause harm to the fetal
bloodstream.
▻ Administered to women (Rh
negative) at 28 weeks of pregnancy
(2nd Trimester) and 72 hours after
birth (1st Pregnancy)

75. • Introduction and Summary - Dr. Cortez, Ylanie Scheherezade Z.
• Reporter on No. 1 question- Dr. Aragon, Earl Jason N.
• Reporter on No. 2 question- Dr. Loreno, Madonna E.
• Reporter on no. 3 question - Dr. Pastrana, Jose Ranelle T.
• Reporter on No. 4 question- Dr. Daza, Djev David
• Reporter on No. 4 question- Dr. Agnas, Jennifer Jane L.
• Reporter on no. 5 question - Dr. Songcuya, Melissa R.

76. • Hemolytic disease of the Newborn. (2018). Retrieved from Stanford Children's Health:
https://www.stanfordchildrens.org/en/topic/default?id=hemolytic-disease-of-the-newborn-90-P02368
• Dean L. Blood Groups and Red Cell Antigens [Internet]. Bethesda (MD): National Center for
Biotechnology Information (US); 2005. Chapter 4, Hemolytic disease of the newborn. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK2266/
• Rodwell, V., Bender, D., Botham, K., Kennelly, P., & Weil., P. (2015). Harper’s illustrated biochemistry
(30th ed.). New York, NY: Mcgraw-Hill Education.
• Dr. Najeeb Lectures https://www.drnajeeblectures.com/

77. End of Slide Presentation