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Transes-IHBB Final

BS Medical Laboratory Science (University of Baguio)

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LECTURE / SECOND SEMESTER

LESSON 1: INTRODUCTION TO IMMUNOHEMATO/BLOOD BANKING

OUTLINE
I. Immunohematology/ Blood Banking Collection of Donors Blood
a. Donor Selection and Blood Collection ➢ Follows registration, medical history, and physical
b. Collection of Donors Blood examination.
c. Donor Deferral ➢ Preparation of venipuncture site will minimize risk of
d. General Requirement for Autologous Donation
e. Donor Identification and Phlebotomy bacterial contamination; drawing will be with aseptic
f. Blood Component Preparation technique.
g. Blood and Anticoagulant Preservation ➢ Scrub site for minimum 30 seconds
h. Storage Lesions Donor Deferral (Permanent/Definite)
➢ Viral hepatitis after age 11
IMMUNOHEMATOLOGY ➢ POSITIVE Confirmatory test /or HBsAg (Hepatitis B
Immunohematology is the study of: surface antigen)
➢ Blood group antigens and antibodies, ➢ Repeatedly reactive test for anti-HBc (Hepatitis B core
➢ HLA antigens and antibodies, Antigen)
➢ Pre transfusion (BEFORE) testing, Identification of ➢ Present or past Infection of HCV (Hepatitis C virus), HTLV
unexpected alloantibodies, (Human T-Lymphotropic virus), or HIV (Human Immuno-
➢ Immune hemolysis, deficiency)
➢ Autoantibodies, ➢ Evidence of parenteral drug use
➢ Drugs ➢ Received dura mater or pituitary growth hormone of
➢ Blood collection, blood components, cryopreservation of human origin.
blood ➢ History of Chagas disease or babesiosis
➢ Transfusion-transmitted viruses, ➢ History of Creutzfeld -Jakob diseases
➢ Tissue banking and organ transplantation, ➢ AIDS <200 cells (CD4) or HIV Positive
➢ Blood transfusion practice Donor Deferral (3 Years)
o Safety, quality assessments, records, blood ➢ Possible exposure to Malaria
inventory management and blood usage review ➢ Asymptomatic during the time
Donor Selection and Blood Collection • Visitor/immigrant from area endemic for
Gen. Requirements for Allogeneic Donation malaria
Age 17-66 years old • Previously diagnosed with malaria
Temperature 37.5OC or ≤99.5OF Donor Deferral (1 Year)
Pulse 60-100 bpm ➢ Mucous membrane exposure to blood; nonsterile skin or needle
Blood pressure ≤ 180 mmHg systolic/s100 penetration
mmHg diastolic pressure ● Sexual contact with an individual with a confirmed positive
Hemoglobin ≥ 12.0 g/dL test for HbsAg.
Hematocrit ≥ 38% or ≥ 0.38 L/L ● Sexual contact with an individual with viral hepatitis
Weight 50 kg or 110 lbs ● Sexual contact with an individual with HIV or higher risk
General appearance Appears Healthy for HIV infection
● Incarceration in a correctional institution for longer than
72 consecutive hours

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● History of Syphilis (Trypanosoma Pallidum) or Gonorrhea Apheresis Donation

(Neisseria Gonorrhea) ➢ To remove/separate
● Tattoo/piercing Apheresis Instrument
● Post blood transfusion ➢ An electronic Instrument that takes blood from a
● Rape victim donor, separates the desired component, and
Donor Deferral returns the remaining components to the donor
Whole blood donation 8 weeks (International) (process takes from 20 minutes to 2 hours)
3 Months/ 12 weeks (PHIL) Plateletpheresis
Pregnancy 6 weeks post-partum but not o Donor should have at a platelet count of at least
recommended 150,000/uL
Rubella, chicken pox vaccine 4 weeks o Interval donation is at least 2 days.
o Donation should not exceed more than twice a week
Measles, mumps, polio, typhoid, 2 weeks or 24 times a year.
yellow fever vaccines Plasmapheresis
Aspirin 2 days ● At least 48hrs should elapse before subsequent donation
Autologous Donation ● Maximum of 2 donations in a 7-day period
➢ Autologous donation is a donation of blood given by a person to ● Serum/plasma should be tested for total protein and
be used for transfusion on themselves later. There are 4 types: serum electrophoresis or quantitative Ig.
o Preoperative collection Leukapheresis
o Intraoperative (Acute Nonmonomeric) hemodilution o special agents Include: Hydroxyethyl starch (HES)
o Intraoperative collection Sediment Antigen, corticosteroid
o Postoperative collection (prednisone/dexamethasone), G-CSF.
➢ Advantages: Erythrocytapheresis/ Red Cell Pheresis
➢ No disease transmitted o 2 standard units of RBCs can be collected, or one unit of
➢ No alloantibodies formed RBCs collected concurrently with plasma and/or
➢ No transfusion reaction possible platelets.
➢ Disadvantages: Therapeutic Cytapheresis and Therapeutic Plasmapheresis
➢ High waste amount (unused if surgery postponed) o Removal of pathogenic substance (Platelets, WBC, Plasma
➢ Increased cost Substance)
General Requirement for Autologous Donation Donor Identification and Phlebotomy
Age No age requirement 1. Use aseptic technique: Iodine compound or chlorhexidine
gluconate and Isopropyl alcohol
Hemoglobin At least 11 g/dL
2. Apply tourniquet or blood pressure cuffs:40-60 mmHg
Hematocrit At least 33%
3. Gauge number 16 is often used for blood donation.
General condition Patient should have no condition
4. Position the blood-drawing unit at 20 degrees
predisposing to BACTEREMIA or any form
5. Instruct the donor to open and close his or her hand every
of severe cardiovascular/pulmonary
10-12 seconds
condition, thus tolerates blood loss
6. Mix the unit of bag periodically 1-2 times per minute
poorly.
7. Amount of Blood collected: 450 mL ‡ 10% (405-495 mL)

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8. Process of collection should be finished within: 7-10 ➢ Serologic test for Syphilis
minutes. ➢ HbsAg
9. Components must be prepared 6-8 hours after collection ➢ Anti-HIV 12 and NAT
Low Volume Collection ➢ Malaria
● Standard volume: 63 mL of anticoagulant for 450 mL When to Transfuse the Blood?
collections ➢ After pretransfusion compatibility testing
● If an autologous unit is drawn on a patient weighing less ➢ Goal: ensure that donor's blood will be acceptable by
than 100 lbs, the anticoagulant must be reduced. recipient
o Reduced volume factor (A) = Weight of ptx ÷ 110lb ➢ Pretransfusion compatibility testing:
o Amt. of anticoagulant needed (B) = A x 63mL • Abo typing
o Amt. of anticoagulant to remove = 63 – B • Rh typing
o Amt. of bld to collect = A x 450mL • Antibody screen
Republic Act of 1517 o Additional: antibody identification, enzyme
BLOOD TYPE COLOR LABEL treatment, elution, adsorption,
A BLUE inhibition/neutralization, and antibody titer
B YELLOW determination.
AB PINK • Crossmatching
O WHITE o Major Crossmatching = Donor Red Cell Mix w/
Mnemonics: “BABY” Patient Serum/Plasma
Post Donation Care o Minor Crossmatching = Donor Serum/Plasma
➢ Raise arm and apply pressure Mix w/ Patient Red cell
➢ Rest after blood collection, reclining for a few minutes, o Auto Control Crossmatching = Patient Red
then sit upright and allow to walk. Cell Mix with Patient Serum
➢ Drink lots of water, refrain from smoking and avoid Blood Component Preparation
strenuous works. ➢ Whole blood is centrifuged and can be separated into
Adverse Reactions RBCs, platelets, fresh frozen plasma (FFP), and
➢ Syncope (Fainting) cryoprecipitate antihemophilic factor
➢ Hyperventilation o Process: Whole blood bag is centrifuged; plasma
➢ Decrease BP, pulse rate. is separated into a satellite bag. If platelets are
➢ Convulsions, marked hyperventilation, epilepsy. to be prepared from whole blood, 'soft spin,
➢ Arterial puncture during whole blood donation leaving platelets suspended two spins are
➢ Nausea, or vomiting. required. The first centrifugation will be a in the
➢ Twitching or muscle spasms plasma layer. If platelets will not be produced, a
➢ Hematoma single "hard" spin (increased time and rotations
Tests Performed on Donor’s Blood per minute) will be performed
➢ ABO Rh ➢ RBC bag is sealed and remove from system
➢ Antibody Screen ➢ Plasma bag is centrifuged to sediment platelets (hard
➢ Anti-HBC' spin)
➢ Anti HTLV WI ➢ Plasma is separated into FFP bag, leaving platelets with
➢ Anti-HCV and NAT 40-70ml of plasma in platelet bag

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LECTURE / SECOND SEMESTER

➢ Platelet bag is sealed off and cut

➢ Plasma is either frozen to make FFP within 8hrs of
collection or frozen and later thawed in refrigerated
conditions to make cryoprecipitate and cryo-poor plasma

BLOOD COMPONENT FUNCTION

Random Donor Platelets Bleeding due to quantitative or
qualitative platelet defect 1
unit increases platelet by
5,000 – 10,000/uL
Who Should Receive Blood? Single Donor Platelets Bleeding due to quantitative or
BLOOD COMPONENT FUNCTION qualitative platelet defect,
Whole blood (450 ml) ● Symptomatic anemia with prevention of HLA
large volume deficit alloimmunization 1 unit
Packed RBC (250ml) ● Symptomatic anemia increases platelet count by
● 1 unit increases hemoglobin 30,000 – 60, 000/uL
by 1 g/dL and hematocrit by Fresh Frozen Plasma Multiple coagulation factor
3% deficiency
Washed RBC ● Symptomatic Anemia on Cryoprecipitate Hypofibrinogenemia, factor
patients with severe allergic XIII deficiency, VWD, DIC,
(caused by allergen) or Hemophilia A
anaphylactic conditions Granulocyte Concentrate Neutropenia with infection
(caused by anti-(gA unresponsive to antibiotics
antibodies) Factors Concentrate Specific coagulation factor
Leuko-reduced/leuk- ● Prevents febrile transfusion deficiencies
poor components Reactions and TRALI caused Immune Serum Globulins Patients with congenital
by antibodies against WBCs hypogammaglobulinemia
● To reduce CMV transmission (given monthly)
Irradiated blood ● To prevent graft-vs-host Volume Expander Patients with hemorrhagic
components disease shock and bum patients
● For newborns with marrow
transplants Blood Preservation
Neocyte ● To prolong time between Blood Bag Contains:
transfusion in chronically ✓ Citrate: binds ionized calcium.
transfusion-dependent ✓ Phosphate: source of 2,3 diphosphoglycerate (2,3 DG)
patients (e.g., sickle cell ✓ Glucose: serves a food for the cells.
anemia) ✓ Adenine: increases ADP levels.

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LECTURE / SECOND SEMESTER

Anticoagulant Preservatives Storage Lesions

ANTICOAGULANT STORAGE TIME DECREASED INCREASED
HEPARIN 2 days pH Plasma hemoglobin
ACD (Acid-Citrate- 21 Days Glucose Plasma potassium
Dextrose) ATP Plasma ammonium
CPD (Citrate-phosphate- 21 Days 2,3 DPG = affinity Lactic acid
Dextrose Decrease plasma sodium Inorganic Phosphates
CP2D (Citrate- 21 Days
Phosphate-Double
Dextrose)

CPDA-1 (Citrate- 35 Days

Phosphate-Dextrose-
Adenine)
** most common
➢ Additive solutions are preserving solutions that are added to
RBCs after removal of plasma with or without platelets. Units
with additive solution are stored with additional 7 days
➢ They contain CPDA-1 + ADDITONAL SOLUTION
ADDITIONAL SOL’N such as: “SAD Man”
o Saline
o Adenine
o Dextrose
o Mannitol = stabilizer
➢ Rejuvenating solutions are used to restore "ATP and 2,3 DPG
levels. They often contain “PIGPA”
o Pyruvate
o Inosine
o Glucose
o Phosphate
o Adenosine
➢ Post storage viability: 70% viable at end of storage
➢ Post transfusion viability: 75% viable 24 hours after post
transfusion
➢ Shipment of blood is maintained at a temperature of not
more than 10oC

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LECTURE / SECOND SEMESTER

Blood Component Standard & Quality Control Storage & Shell Life
Whole Blood Hct approximately 40% 1-6oC
ACD, CPD OR CP2D = 21 DAYS
CPAD1 = 35 DAYS
Packed RBC Hct ≤ 80% 1-6oC
ACD, CPD, OR CP2D = 21 DAYS
CPDA1 = 35 DAYS
Open System = 24 hours
Random Donor Platelet (RDP) pH ≥ 6.2 20-24oC
≥ 5.5 x 1010 5 DAYS
Pooled: 4 hours
Single Donor Platelet pH ≥ 6.2 20-24oC
≥ 3.0 x 1011 5 DAYS
Freshn Froze Plasma Should be prepared within: -18oC = 1 year
6hrs after collect for ACD -65oC = 7 years
6hrs after collect for CPD, CPD2, CP2DA1
Cryoprecipitate FVIII:C=80 IU Frozen:
Fibrinogen of at least 150 mg/unit -18oC= 1 year
Thawed: 20-24oC = 6 hours
Pooled: 20-24oC = 4 hours
Granulocytes ≥ 1.0 x 1010 PMNs/unit 20-24oC = 24 hours
Frozen Red Blood Cell 80% RBC Recovery ≤ 65oC
1% glycerol 10 years
<300mg Hgb
Irradiated Components 25 Gy to the center of the canister 1-6oC
Original outdate or 28 days from irradiations
Leuko-reduced Components WBS should be <5 x 106 RBCs:
≥ 85% RBC Recovery Closed = Same
Platelets (pH ≥6.2) Open = 24 hours
Platelets:
In SDP, WBC should be <5 x 106
20 – 24oC
In RDP, WBC should be <8.3 x 105 5 days

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LECTURE / SECOND SEMESTER

LESSON 2: BASIC IMMUNOLOGIC CONCEPTS IN BLOOD BANKING

OUTLINE
II. Basic Immunologic Concepts in Blood Banking ABO Blood Group System
a. Basic Genetics ➢ The most important of all the blood groups in transfusion
b. ABO Blood Group System practice; ISBT # 1
c. Characteristics of ABO Antigens
d. Characteristics of ABO Antibodies ➢ The only blood group system with naturally occurring
e. Bombay Phenotype antibodies in serum against the antigens that are absent from
f. H Gene their RBCs
g. Secretor Gene (Se Gene) ➢ Incompatibility to the ABO blood group system can cause the
III. Procedure: ABO Typing
i. Forward Typing most severe hemolytic transfusion reactions
ii. Reverse Typing ➢ Frequency of Blood types:
IV. Discrepancies on Forward and Reverse Typing o O > A > B > AB
Basic Immunologic Concept in Blood Banking ➢ Blood groups are characterized based on the antigens present
➢ Red blood cells have Antigen in the RBCs
➢ Plasma/Serum have Antibodies Blood Type Genotype Antigens Antibodies
➢ Antigen “Antibody Generator” (Phenotype)
o Proteins, glycoproteins or glycolipids found in the A AA, AO A Anti-B
serum, plasma, RBCs or other cells that can induce B BB, BO B Anti-A
antibody production AB AB A, B ----
➢ Antibodies O OO ----- Anti-A, B, AB
o Gamma globulins that act against the antigen or bind Characteristics of ABO Antigens
the antigen ➢ Develop as early as the 37th day of fetal life
o They may be naturally occurring or may be ➢ Are formed upon the coding of the ABO genes found on
immunogenic chromosome 9
o Antibodies to the blood group antigens may be IgM, ➢ The ABH genes produce specific glycosyl transferase that add
IgG, or IgA in nature sugar to the type 2 precursor substance of RBC
o May be warm reactive or cold reactive antibodies ➢ A gene codes for the production of N- acetylgalactosaminyl
o Some can activate/fix the complement, some cannot transferase
Basic Genetics ➢ B genes code for the production of galactosyl transferase
➢ Phenotype: refers to the physical manifestation/products of ➢ Immunodominant sugar in group A: N-acetylgalactosamine
the genes ➢ Immunodominant sugar in group B: D- galactose
➢ Genotype: refers to the genes; they usually come in pairs ➢ Immunodominant sugar in group O: L-fucose
➢ Homozygous: occurs when genes assume a single form; two Characteristics of ABO Antibodies
copies of same allele ➢ Develop around 3 to 6 months of Age
➢ Heterozygous: occur when inherited genes have different ➢ Predominantly IgM in nature, but some cue IgG
forms; different allele Bombay Phenotype (Oh phenotype; hh gene)
➢ Amorph: genes with no visible products or physical ➢ Rare phenotype in which patients lacks H antigen
manifestation ➢ Lacks expression of ABO antigens both in RBCs and secretions
➢ Codominant: genes that are both expressed simultaneously; ➢ Bombay red cells do not react with anti-H lectin (Ulex
both genes have products or physical manifestation Europaeus)

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LECTURE / SECOND SEMESTER

➢ Bombay serum contains anti-A, anti-B, anti-AB, and anti-H ➢ Specimen: Serum
H Gene ➢ Reagents: A1 cells and B cells
➢ Codes for the production of the enzyme L-fucosyl
transferase
➢ Responsible for the expression of H antigen in the surface of
the RBCs
➢ Prerequisite for A and B antigens to attach to the type 2
precursor substance
➢ Present in more than 99.99% of the population
Secretor Gene (Se Gene)
➢ Gene responsible for the secretion of A, B, and H antigens in Discrepancies on Forward and Reverse Typing
the body fluids ➢ Type I – Caused by weak or missing antibodies, unexpected
➢ Two alleles: Se and se antibodies
Procedure: ABO Typing Forward Typing Reverse Typing
Detecting ABO Antigens: Forward Typing Anti-A Anti-B A1 Cells B cells
➢ Also known as the direct typing or front typing or cell typing 0 0 0 0
➢ Detects: A & B antigen on patient RBCs BT: “O” “AB”
➢ Specimen: Whole blood or 2-5% Red Cell Suspension Causes:
➢ Reagents: Anti-A sera, anti-B sera Newborns Patient with Leukemia Patients on
Immunosuppressive
drugs
Elderly Aggamaglobulinemia Bone marrow
patient transplants
ABO Plasma Transfusion
subgroup
➢ Type II – Caused by weak or missing antigens, extra antigens
present
Forward Typing Reverse Typing
Anti-A Anti-B A1 Cells B cells
4+ 2+ 0 4+
Detecting ABO Antibodies: Reverse Typing BT: “AB” “A”
➢ Also known as the indirect typing or back typing or serum Causes:
typing Acquired B phenomenon Subgroups of A or B
➢ Detects: anti-A and anti-B in patients’ serum Leukemia Hodgkin’s Disease

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LECTURE / SECOND SEMESTER

ADDITIONAL NOTES

Type A: Anti-B Platelets: 150,000 – 450,000 /uL

Type B: Anti-A Blood Volume:
Type AB: No Ab o Female: 4 – 6 L
Type O: Anti A, B, and AB o Male: 5 – 7
Age Limit Whole blood: 450 ml
18 years old (start) – 65 years old (cut off) PRBC: 280 ml
17 years old – Parents’ Consent Graft vs Host
> 65 years old – Doctors approval Immunocompromised
Screening Hemoglobin o Graft → attack → Host
Hemoglobin: carries oxygen Immunocompetent
Copper Sulfate: Gravimetric Method o Host → reject → Graft
: Specific Gravity: 1.053 2,3 – diphosphoglycerate (2,3 DPG)
Increase specific gravity: sink (applicable) Increase: facilitate the release of oxygen into the tissue
Decrease specific gravity: float (not applicable) Temperature
Normal Values Blood Bank Ref: 1 – 6oC
Hemoglobin: 12.0 g/dL Shipment: not more than 10oC
AIDS = 0.81 x 63 = 51.03 → anticoagulant
< 200 cells/ uL(CD4) – vulnerable . = 63 mL – 51mL = 12 mL → reduce anticoagulant
Electrolytes = 0.81 x 450 = 364.5 mL → blood needs to be collected
Ca, Mg, K+: affects heart Example: (Kilogram)
Citrate: binds calcium Formula:
Increase Citrate = Decrease Calcium = affects heart Reduce Volume Factor (A) = weight of px / 50kg
Acronym Solution:
HBsAg – Hepatitis B Surface Antigen A = 45 kg / 50 kg = 0.9
Anti-HBc – Anti-Hepatitis B core = 0.9 x 63 mL = 56.7 mL → anticoagulant
HCV – Hepatitis C Virus = 63 mL – 56.7 mL = 6.3 mL → reduce anticoagulant
HIV – Human Immunodeficiency Virus = 0.9 x 450 mL = 405 mL → blood needs to be collected
AIDS – Acquired Immunodeficiency Syndrome Example: (Quiz)
Indicator for Platelet Transfusion Solution:
< 50,000/ uL: A = 38 kg / 50 kg = 0.76
Low Volume Collection = 0.76 x 450 mL = 342 mL → amount of blood to collect
Pounds – 110 lbs = 0.76 x 63 = 47.88
Kilogram – 50 kg = 47.88 – 63 = 15.12 mL → anticoagulant to be removed
Example: (Pounds)
Formula:
Reduce Volume Factor (A) = weight of px /110lbs
Solution:
A = 90 lbs / 110 lbs = 0.81

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LECTURE / SECOND SEMESTER

LESSON 3: RH BLOOD GROUP SYSTEM (ISBT 004)

OUTLINE GENE FREQUENCY

I – Rh Blood Group System (ISBT 004) D 85%
i. Rh Terminology d 15%
ii. Rules for converting Wiener to Fisher-Race C 70%
iii. Gene Frequency of Rh Antigen c 80%
II – Rh System Antigens E 30%
III – Rh Null Phenotype
e 98%
IV – Rh Antibodies
i. Clinical Significance of Rh Blood Group Rh SYSTEM ANTIGENS
V – Other Blood Group System WEAK D
i. Kell Blood Group ➢ Formerly known as Du
ii. Duffy Blood Group System ➢ Occurs when D is weakly expressed
iii. Lutheran Blood Group System ➢ Most common in blacks
iv. I Blood Group System o Partial D
v. P Blood Group System ▪ Qualitative Problem
vi. MNS Blood Group System ▪ Cause: One or more parts of D antigens is
VI – Other Minor Blood Group Systems missing
Rh BLOOD GROUP SYSTEM (ISBT 004) Rh NULL PHENOTYPE
Rh ANTIGENS ➢ This appears to have no Rh antigens. The membranes of their
➢ Production is coded by RHD and RHCE genes found in RBCs are abnormal and the RBCs have shortened lifespan
chromosome 1 ➢ This can result from inheriting two non-functional RHCE alleles
➢ Antigens are protein and polypeptide in nature along with the dual deletion of the RHD alleles
Rh TERMINOLOGY ➢ Weakly reactive D means a person is D-positive
➢ Fisher-Race ➢ AABB standards state that all Rh-negative donor units must be
o Five antigens: D, C, E, c, e tested for weak D, and those units that test positive must be
o “Rh +” means “D+” identified as D-positive. However, weak-D recipients are
o Rh – described as “d” transfused with D-negative blood
➢ Weiner (Rh-Hr) Rh ANTIBODIES
Weiner Fisher-Race ➢ Produced in humans through pregnancy or transfusions
R0 Dce ➢ IgG antibody; Rh antibodies generally do not activate
R1 DCe complement
R2 DcE ➢ Optimal reaction temperature: 37oC
RZ DCE ➢ Reaction Phase: AHG (Antihuman globulin)
r dce ➢ Agglutination enhancement occurs with LISS, Enzymes, PEG
r’ dCe CLINICAL SIGNIFICANCE OF Rh BLOOD GROUP
r’’ dcE ➢ Rh antibodies produce hemolytic transfusion reaction and
ry dCE hemolytic disease of the newborn
RULES FOR CONVERTING WEINER TO FISHER-RACE ➢ Antibodies may not be currently detectable, but the person
R=D should always receive antigen negative blood if they have a
r=d history of Rh antibodies
1 or ‘ = C + e ➢ Rules of HDN:
2 or ‘’ = c + E o Mother must be negative
0 or (NO PRIME) = c + e o Baby must be positive
Z or y = C + E o Antibody must be capable of crossing the placenta
GENE FREQUENCY OF Rh ANTIGEN

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➢ Rh antibodies can cause hemolytic disease of the newborn V- I BLOOD GROUP SYSTEM
(HDN), because they can cross the placenta. ➢ Abbreviation: I
➢ Rh immune globulin (RhIg) administered after delivery (within ➢ Antibody class: IgM
72 hours) can protect a woman from making anti-D ➢ Optimal reaction temperature: 4 degC
OTHER BLOOD GROUP SYSTEM ➢ Reaction phase: Intermediate spin (IS) and occasionally
I - KELL BLOOD GROUP 37 degC
➢ Abbreviation: K ➢ Enzyme treatment: Enhanced agglutination
➢ Clinically significant: No
➢ Originated from Mrs. Kellaher, from whom anti-k was first
➢ Strong anti-I is associated with Mycoplasma pneumoniae
identified
infection
➢ Second rated to D in terms of immunogenicity. Although ➢ I antigen is found adults; infants are rich in i antigen
the K antigen is found in only about 9% of the population, ➢ Anti-i= associated with Infectious mononucleosis (EBV)
anti-k is encountered quite frequently and can cause HTR ➢ Pathogenic autoanti-I
and HDN o Associated with cold agglutinin syndrome in
➢ Antigens: K (kell), k (cellano), Kpa, Kpb, Kpc, Jsa, Jsb and Ku cases of Primary Atypical Pneumonia
o Can be neutralized by human milk
➢ Antibody class: IgG
VI-P BLOOD GROUP SYSTEM
➢ Reaction Phase: AHG
➢ Abbreviation: P₁
➢ Enzyme treatment: No effect ➢ Antibody Class: IgM (anti-P₁)
➢ McLeod phenotype: X-linked inheritance, males are ➢ Optimal reaction temperature: 4 deg C Reaction Phase: IS,
affected; RBCs are acanthocytic. Associated with Chronic 37 degC and AHG
Granulomatous Disease ➢ Enzyme treatment: Enhanced Agglutination
II - DUFFY BLOOD GROUP SYSTEM ➢ Clinically significant: Anti-P₁ is not clinically significant
➢ Abbreviation: Fy o Anti-P1+P+Pk is an IgG clinically significant
➢ Antibody Class: IgG antibody
➢ Optimal reaction temperature: 37 degC ➢ Phenotypes: P₁, P2, P. P1k, P2k and luke
➢ Reaction Phase: AHG ➢ Anti-P₁ = can be neutralized using hydatid cyst fluid
➢ Enzyme treatment: Destroys Fya and Fyb from Echinococcus granulosus infection, pigeon
➢ Clinically significant: anti- Fya and anti-Fyb can cause droppings or turtle dove eggwhite
HTR and HDN ➢ Autoanti-P is Donath-Landsteiner antibody, naturally
o The Fy(a-b-) phenotype is more resistant to occurring biphasic antibody associated with Paroxymal
malarial infection by Plasmodium vivax Cold Hemoglobinuria. It binds to the antigen on the
➢ Antigens: Fya and Fyb patient's RBCs in the cold and fixes complement. The RBCs
➢ 4 phenotypes: Fy (a+b-); Fy(a-b+); Fy(a+b+); Fy(a-b-) are hemolyzed when the temperature reaches 37oC
IV-LUTHERAN BLOOD GROUP SYSTEM VII-MNS BLOOD GROUP SYSTEM
➢ Abbreviation: Lu ➢ M&N antigens
➢ Antibody Class: Lua IgM; Lub IgG ➢ Abbreviation: MN
➢ Optimal reaction temperature: Lua 4degC; Lub 37 degC ➢ Antibody class: IgM
➢ Reaction phase: Lua room temp; Lub AHG ➢ Optimal reaction temperature: 4oC or 37oC
➢ Clinically significant: no clinical significance. Anti-Lua can ➢ Reaction phase: IS, 37oC or AHG
be present w/o prior transfusion or pregnancy ➢ Enzyme treatment: Destroys antigens
o Anti-Lub is rare and associated with HTR and ➢ Clinically significant: No
HDN ➢ Antigens: Found in GLYCOPHORIN A
➢ Antigens:18 total, including Au and Aub

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VII-MNS BLOOD GROUP SYSTEM

• S and s antigens
o Abbreviation: Ss
o Antibody class: IgG
o Optimal reaction temperature: 37 degC
o Reaction phase: AHG
o Enzyme treatment: variable effect
o Clinically significant: Yes
o Antigens: S, s, and U associated with
GLYCOPHORIN B
• Anti-M
o Saline agglutinins, cold reactive, IgM in nature;
reacts best at pH: 6.5
• Anti-N- very rare (found in renal patient who dialyzed in
equipment sterilized with formaldehyde
• Anti-S, anti-s and Anti-U
o Clinically significant, causing HTR and HDN
o Anti-U is formed by S-s- individuals, usually of
Blacks (S-s-)
OTHER MINOR BLOOD GROUP SYSTEMS
• Diego- marker of Mongolian Ancestry; Southeast
Asian ovalocytosis
• Cartwright
• Xg
• Scianna Dombrock
• Colton
• Chido/Rogers- C4 Complement component
• Gerbich- LEACH PHENOTYPE presents with
elliptocytosis
• Cromer
• Knops
• Indian- 4% Indians, 11% Iranians, 12% Arabs
• Jhon Milton Hagen
• Bennet- Goodspeed antigens- Associated with HLA
• Sid
ADDITIONAL NOTES:
• Paroxysmal Cold Hemoglobinuria (Clear red)
• Hematuria (Cloudy red)
• MN= Glycophorin A
• Ss= Glycophorin B
• Bga= HLA B7
• Bgb= HLA B17
• Bgc= HLA A28

Downloaded by Shinah Danica Alonzagay ([email protected])