AUTOIMMUNE DISEASE AUTOANTIBODY TIME OF PREDOMINANT

TYPE CAUSE
1. SLE Anti- DNA DAMAGE MECHANISM
Anti- Nuclear Hyperacute Within minutes Humoral Preformed
Anti- Ribosome Antibodies of
Anti- DNP recipient against
2. Primary Biliary Cirrhosis Anti- mitochondrial donor’s blood
3. Chronic Active Hepatitis Anti- Smooth Muscle Accelerated 2-5 days Cell-mediated Previous
4. Hypothyroidism Anti- TPO sensitization (HDFN)
Anti- Microsomal Acute 7-21 days Cell-mediated Allogeneic Reaction
Anti- TGB (ADCC); to donor
5. Hyperthyroidism Anti- TSH receptor Chronic >3 months Cell-mediated Disturbance of
Anti- TGB Host-graft tolerance
6. Goodpasture Syndrome Anti- glomerular basement membrane (GvHD)
7. Wegener’s Dx p-ANCA Immunopathologic >3 months Immune complex
8. Churg-Strauss Syndrome c-ANCA damage to the disorder; Complex
9. DM Type 1 (IDDM) Anti- Insulin new organ formation with
Anti- Beta Cells soluble antigens
10. Addison’s Dx Antibodies against Adrenal glands
11. Multiple Sclerosis Anti- Myelin Sheath
GRADE CELLS SUPERNATANT
12. Myasthenia Gravis Anti- Acetylcholine receptor
0 No agglutinates Dark, turbid, homogenous
13. Pernicious Anemia Anti- Parietal Cells
Tiny Agglutinates Dark, turbid
14. RA Rheumatoid Factor
W+ Many free cells
15. ITP Anti- Platelets Visible under microscope
16. Pemphigus Vulgaris Anti- desmoglein (anti-desmosome) Small agglutinates Turbid
17. Bullous Pemphigoid Anti- hemidesmosome 1+ (25%)
Many free cells
Medium agglutinates Clear
2+ (50%)
Moderate free cells
PATTERN AUTOANTIBODY DISEASE ASSOCIATED
Large agglutinates Clear
Homogenous/ Anti- dsDNA SLE 3+ (75%)
Few free cells
Diffused Anti- Histones
4+ (100%) One solid agglutinate Clear
Nucleolar Anti- RNP Scleroderma
Sjogren’s Syndrome
Speckled Anti- RNP Sjogren’s Syndrome
Anti- Smith SLE
MCTD Scleroderma
Peripheral Anti- DNA SLE
Anti- Lamins
Centromere Anti- Centromere CREST
(No fluorescence)
 AGGLUTINATION REACTIONS Viral
Direct Agglutination Natural Carrier of Antigen Hemagglutination
Detects Antibodies
Examples:
- Febrile Agglutination Tests (WIDAL, WEIL-FELIX)
- ABO Forward Typing Hemagglutination
Indirect Artificial Carrier of Antigen Inhibition
Agglutination - Carriers: Polystyrene Latex, Bentonite, Beads, Charcoal
Detects Antibodies
Example:
- ASO Latex Agglutination Test (Detects Anti-Streptolysin
O)
GENE PRODUCT
Reverse Passive Artificial Carrier of Antibodies via Fc Region Gag (Group Antigen Gene) p25
Agglutination - Carriers: Polystyrene Latex, Bentonite, Beads, Charcoal - precursor protein which form core proteins:
Detects Antigens p6,p9,p17,p24
Example: Pol (Polymerase) Reverse Transcriptase
- CRP Latex Agglutination Test (Detects CRP by using - p66/ p51
Anti-CRP antibodies) Note: - RNA to DNA
Agglutination 2 stages: Target of treatment are Integrase
Inhibition 1. Add soluble reagent antibodies + antigen (of patient) = Integrase, Protease, and RNAse - p31
Neutralized - insert viral DNA to host
2. Add antigen-coated latex particle (indicator phase) = Protease
No agglutination - p10
Remember: - cleaves protein precursor
- If inhibited/neutralized = + - matures the virion
- If agglutination occur = - RNAse
AHG Mediated DAT (VIVO) Env (Envelope) gp160
- Specimen: RBCs (Antigen) - cleaved to form gp120 and gp41
- Rgt: AHG (Antibody) gp120
- Positive in: AHH! [AIHA, HDFN, HTR] - binds to CD4 on Tcell
gp41
IAT (VITRO) - transmembrane protein
- Specimen: Serum (Antibody)
- Use in: Crossmatching, Ab Screening, Ab Panel
 A SUBGROUPS ABO Antigen and Antibody Detection
A1 Reacts with Anti-A1 and Anti A Appear as early as Peak at Decline
A2 Reacts with Anti-A only ABO Antigens 37th day of fetal life 2-4 y/o Remain constant
Ax Reacts with Anti-AB only throughout life
A3 MF reaction Examine microscopically ABO Antibodies BIRTH but detected 3-6 5-10 y/o After 10 y/o
Aend MF reaction with few agglutinates months after birth
Am Weak/No reaction Adsorption/Elution of anti-A to (4-6 months: Harmening)
Ael No reaction confirm the presence of these A
Ay No reaction Subgroups
BLOOD GROUP Can receive blood from Can donate blood to
(Consider antigens) (Consider antibodies)
B SUBGROUPS A A, O A, AB
B Reacts with Anti-B and Anti-AB B B, O B, AB
B3 MF reaction [Most frequent] AB A,B,AB,O AB
Bx Weak reaction O O only A,B,AB,O
Bm No/Weak reaction Adsorption/Elution of anti-B to Universal RBC Donor O (No Antigens)
Converted to B if incubated with confirm the presence of these B Universal Plasma Donor AB (No Antibodies)
UDP (Uracil Diphosphate) Subgroups Universal RBC Recipient AB (No Antibodies)
Bel No reaction [Extremely rare] Universal Plasma O (No Antigens)
Recipient

LECTINS
Anti-A1 Dolichos biflorus
Anti-B Bandeiraea simplicifolia/ Griffonia simplicifolia
Anti-H Ulex europaeus
Anti-N Vicia graminea
Anti-M Iberis amara
Anti-T, Th Arachis hypogea
Anti-Tn Salvia sclarea
 DISCREPANCIES G4 (Forward Cold reactive autoantibodies (use 0.01 DTT, or cold autoadsorption)
G1 (Reverse) Newborns and Reverse) Unexpected ABO isoagglutinin (ex. A2B)
Elderly Unexpected non-ABO alloantibodies (run Antibody screen)
Hypogammaglobulinemia Miscellaneous More than one ABO group RBCs
- CLL Problems - By transfusion or bone marrow transplant
- Malignant lymphoma Polyagglutination
- Immunosuppressive drugs usage Antibody to acriflavine (Reacts with Anti-B antisera)
- Bone marrow or stem cell transplantations Cis-AB phenotype
Agammaglobulinemia - Offspring inherit A,B, and O gene (3 genes)
- Congenital or acquired
- Immunodeficiency disease
Patients undergone plasma transfusion or exchange transfusion IgM IgG
ABO subgroups Le, I, P1, M, ABH, N Rh, MNSs, Duffy, Kell, Kidd, Lutheran
G2 (Forward) ABO subgroups MIXED FIELD REACTION
Weakened/depression of A or B antigens Sid, Lutheran
- Leukemia ABSENT IN PNH III
- Hodgkin’s disease JMH, Cartwright, Colton, Dombrock
Pseudo antigens CARBOHYDRATE and NO HDN
- Acquired A Le, I, P
- Acquired B POORLY DEVELOPED
Blood group-specific soluble substances (neutralize antisera) Le, Lu, P1
Antibodies to low-incidence antigens in reagent Anti-A or Anti-B WELL DEVELOPED
Chimerism MNSs, Duffy, Kell, Kid
- True: Twins INVITRO HEMOLYSIS
- Artificial: Blood transfusions, bone marrow or stem cells Anti-Lea/ Anti-Leb , Anti-Tja, Anti-Vel
transplantation, Exchange transfusions, Feta-maternal DOSAGE
bleeding Rh, MNSs, Duffy, Kell, Kidd
G3 (Forward Elevated Globulin Levels HTLA Antibodies
and Reverse) - Multiple myeloma Chido/Rodgers, Kn, JMH, York, Cost, McCoy
- Waldenstrom macroglobulinemia DECREASED IN PREGNANCY
Plasma/protein - Plasma cell dyscrasia Lewis
abnormalities - Advanced cases of Hodgkin’s Lymphomas ENHANCED BY ENZYMES
Elevated fibrinogen levels Kidd, ABH, Lewis, I, P1, Rh [KALIPERh]
Rouleaux Plasma expanders DESTROYED BY ENZYMES
- Dextran MNSs, Duffy, Xga, JMH, Ch/Rg, Pr (Under P Blood Group)
- Polyvinylpyrrolidone (PVP) UNAFFECTED BY ENZYMES
Wharton’s jelly in cord blood samples
U, Kell, Lutheran, Scianna
 ALLOGENEIC DONATION AUTOLOGOUS DONATION DEFERRALS
Age: Age: - Parenteral drug use
- 18 y.o. above; - No requirement - M2M Sexual contact (1977- 2015)
- 16-17 y.o. with written consent Hgb: - Prostitution (since 1977)
- 60 and up with physician approval - 11 g/dL - + Viral Hepatitis since 11 yo
Weight: Hct: - + HCV, HTLV, HIV Infection
- 50kg and more (110 lbs) - 33% or more - + HBsAg
- If <50 = adjustment General condition: - + anti-HBc (more than one)
Hct: - No predisposition to Bacteremia or - 3 months in UK (1980-1996)
- 38% or more any form of severe CV/ Pulmonary - 5 years in Europe (1980-p)
Hgb: condition Permanent - Babesiosis/Chagas Dx
- 12.5 g/dL Last donation: - Leukemia/Lymphoma
Temperature: - At least 72 hours (3 days) before - Cancer
- < 37.5 C or 99.5 F surgery - Risk factors for CJD (Prions)
BP: Prescribed by Physician - Immediate family with CJD
- <180/<100 - Received Human-derived Growth Hormone (grafts)/ corneal/ dura
Pulse Rate: mater
- 50-100; <50 (Athlete with - Received Clotting factor concentrates (for Hemophiliac Px)
increased exercise tolerance) - Received Bovine Insulin (Mad cow dx)
- Tegison (for psoriasis)
- Mucous membrane exposed to blood
- Nonsterile/ Needle penetration
TYPES OF AUTOLOGOUS DONATION
- Received Blood transfusion
Preoperative • Done prior surgery
- Dental operations
Collection/ • Reinfused during/after surgery - Tattoo & Skin Piercing
Predeposit
- History of Syphilis/ Gonorrhea
Acute • Done after anesthesia and before surgery
- Sexual contact with +HBsAg/ Viral Hepatitis/ +HIV Infection/ High-
Normovolemic • Replaced with Colloids (simultaneously) risk for HIV
Hemodilution/ • Saved and reinfused as WB 1 YEAR (12
- Incarceration/Imprisonment >3 Days (72 hours)
Intraoperative months)
- Rape victims
Intraoperative • Collection and reinfusion of blood lost during surgery
Collection/ • Utilized Vacuum Vaccination:
Salvage • Blood is washed with Saline and concentrated to Hct 50-60% - Rabies Vaccine
• Blood is collected via Drainage Tube at surgical site - Hepatitis B Ig
Postoperative
• Reinfused with/without processing via Microaggregate filter - Gamma globulin
Collection
(screen debris) - RhoGam

`
 Blood donation Soriatane (Psoriasis) 3 years
AABB 8 weeks/ 2 months Avodart (Benign Prostatic Hyperplasia) 6 months
PH Accutane/Isotretinoin
- 450mL 12 weeks/ 3 months Propecia (baldness) 1 month
MEDICINE
- 200mL 6-8 weeks Proscar/ Finasteride (BPH)
Apheresis Donation (WBC, PLT) 48 hours/ 2 days Aspirin WB = No Deferral
Aspirin-derived products Platelets = 3 days
OTHER Infrequent Plasma pheresis 4 weeks German Measles (Rubella)
4 weeks/ 1 month
Deferrals Double RBC- eryhtrocytapheresis 16 weeks Chicken Pox
Childbirth Measles (Rubeola)
AABB 6 weeks after delivery Oral Polio (Sabin)
VACCINES
PH 9 months after delivery or Mumps
2 weeks
3 months after weaning (start Oral Typhoid
solid food) Yellow Fever
Tooth Extraction 3 days Small Pox (Henry’s)
Fever 2-3 weeks Toxoids/killed/ synthetic viral, bacterial, rickettsia vaccines (especially if
Alcohol Intake 12-24 hours asymptomatic)
Visit countries with SARS Infected = 28 days
Not infected = 14 days Injection Polio (Salk)
NO
Malaria diagnosed DEFERRALS
Resident in malaria endemic for 5 COVID Vaccines
years However, if symptomatic:
3 years after symptomatic stage - WHO/DOH = 28 days
Travel to endemic area (prior resident - AABB/USFDA = 14 days
<3 years after leaving)
Travel to endemic area; >24 hours; < 5
years of stay ANTICOAGULANTS
TRAVEL 1 year after symptomatic stage Citrate Chelate Calcium
Travel to endemic area (prior resident Glucose/ Dextrose Energy source of cells; Substrate for ATP Production
>3 years after leaving) Phosphate Maintains pH during storage
Maintains proper level of 2,3-DPG
Travel to endemic country but not Citric Acid Prevents caramelization of glucose
endemic area Adenine Increase ADP levels, reason why shelf-life is increased to 35 days

History of TB (fully treated)

NO DEFERRALS
Received recombinant-type growth
hormone
 GLYCEROLIZATION TRANSFUSION REACTION WORK-UP
- RBCs to be frozen should be <6 days old 1. STOP Transfusion, but continue NSS
- Glycerol is added thru vigorous shaking 2. CLERICAL error check
- Lifespan: 10 years 3. HEMOLYSIS check
- After thawing: 24 hours - Visual inspection of Px’s pre and post transfusion specimen
High 40% w/v Low 20% w/v - Pink plasma = 20 mg/dL free Hgb
Initial Temp. -80 -196 - Red plasma = >100 mg/dL free Hgb
Control freezing rate NO YES - >25 mg/dL = Observable by naked Eye
Freezer Mechanical Liquid Nitrogen 4. ABO testing
Shipping Dry Ice Liquid Nitrogen 5. DAT Testing
Max. Storage temp -65 (can be thawed and -120 6. Compatibility Testing (Ab Screen & Panel)
frozen) 7. Crossmatching
DEGLYCEROLIZATION 8. Bilirubin Test
- Done before infusion to prevent cell lysis - Max. evident 3-6 hours after transfusion
- Replace glycerol with decreasing amounts of saline 9. Urine
Saline Concentration (HIGH) Saline Concentration (LOW) - First voided urine checked for free Hgb and Urine Urobilinogen
10. Hemosiderin
1. 12% Saline 1. 45% Saline in 15%
- Found weeks after transfusion
2. 1.6% Saline Mannitol
11. Hemoglobin & Hematocrit
3. 0.2% Dextrose with 2. 0.2% Dextrose with
NSS NSS