Blood Bank Flashcards

Question

What is the receptor for P. falciparum?

Answer 1

MNS System: Glycophorin A carries *M or N* antigens Glycophorin B carries *S or s* and *U* antigens **Glycophorin A AND Glycophorin B are both receptors for P. falciparum!**

Answer 2

Fy(a-b-) are resistant to P. vivax 68% of blacks have this phenotype due to inheritance of two copies of the *Fy* gene which gives no functioning DARC glycoprotein (which carries the Duffy antigens) P. vivax merozoites attach to RBCs via this DARC glycoprotein so if you don't make it, organism can't attach Because of differing mechanisms of Duffy negativity in whites and blacks, most Fy(a-b-) blacks do not form anti-Fy Abs but Fy(a-b-) whites do

Answer 3

Acanthocytic Anemia Neuro/Muscular Disorders Psych Disorders X-linked CGD association

Answer 4

Both are caused by sex-linked deletion of portion of X chromosome where Xk gene for Kx Ag resides. Kx antigen is a non-Kell system antigen that is adjacent to Kell structure on RBC membrane and is required for Kell antigen expression \*If transfused, either syndrome or phenotype patients can form anti-Kx and anti-Km; only McLeod RBCs compatible McLeod Phenotype: Kx and Km are absent, all other Kell antigens markedly decreased but not absent like K₀ McLeod Syndrome: Hemolytic anemia with acanthocytes, neuromuscular disorders, psych disorders, X-linked CGD association

Answer 5

**_Infectious Risks_** -High-risk behavior for AIDS (IVDA, male-male sexual contact since 1977) -Receiving money or drugs for sex -Serologic positive for HIV, HBV, HCV, HTLV -Viral hepatitis after 11th birthday -Transfusion of clotting factor concentrates (in hemophilia) -History of Babesiosis or Chagas’ disease -Growth hormone from human sources (pre-1985) -Insulin from bovine sources -Dura mater graft **_Malignancies_** -Leukemia or lymphoma **_Teratogens_** -Tegison (Psoriasis med that hangs around a long time)

Answer 6

**_Infectious Risks_** -Recovered from malaria -Immigrants from malaria-endemic countries (after 5 consecutive years of living there) **_Teratogens_** -Soriatane (Psoriasis med that doesn't hang around as long as Tegison)

Answer 7

**_Infectious Risks_** -Needle sticks or other contact with blood -Sex contact with person with HIV or hepatitis -Sex contact with person who used needles for drugs -Rape victims -Incarcerated \> 72 consecutive hours -Paying money/drugs for sex -Blood transfusion (Allogeneic); including plasma/clotting factors in nonhemophiliacs -Allogeneic transplant of organ/skin/bone -Living with person with active hepatitis (exception: Asymptomatic Hepatitis C) -Receiving HBIG -Tattoos/piercings (unless by regulated entity) -Travel to malaria-endemic areas for residents of non-endemic countries (\>24 hrs, \< 5 years) -Syphilis or gonorrhea -Non-prophylactic rabies vaccination -“Travel” to Iraq

Answer 8

Rubella and Varicella

Answer 9

**Measles Mumps** Oral polio Yellow fever Oral typhoid

Answer 10

Anthrax Cholera **DPT Hepatitis A Hepatitis B Influenza** Lyme disease Meningococcus **Pneumococcus** Polio (injection) RMSF Typhoid (injection)

Answer 11

Autologous: \>11 or 33% Allogeneic: \>12.5 or 38% Other allogeneic parameters: temp _\<_ 37.5C (99.5F), HR 50-100, BP no higher than 180/100

Answer 12

21 days for all ACD is used for apheresis platelets and formerly for RBCs CPD and CP2D are for RBCs

Answer 13

1) 35 days 2) 42 days more adenine=more ATP for cells

Answer 14

``` 21 days (CPD/2D) 35 days (CPDA-1) 42 days (AS) All @ 1-6 C ```

Answer 15

10 years @ –65 C 24 hours @ 1-6 C after thaw

Answer 16

24 hours @ 1-6 C

Answer 17

5 days @ 20-24 C (gentle agitation); 4 hours if pooled in open system

Answer 18

24 hrs @ 20-24 C | (no agitation)

Answer 19

1 year @ –18 C 7 years @ –65 C; 24 hours at 1-6 C after thawing at 30-37C \*must be separated and placed in -18C within 8 hours of collection

Answer 20

1 year @ –18 C 6 hours @ 20-24 C after thaw (4 hrs if pooled in open system)

Answer 21

HCT \< 80% (all); \> 50 g HGB in 95% (apheresis RBCs)

Answer 22

≤ 5 x 10⁶ WBCs in 95%, retain 85% of RBCs

Answer 23

≥ 5.5 x 10¹⁰ and pH ≥ 6.2 in 90%

Answer 24

≥ 5.5 x 10¹⁰in 75%, pH ≥ 6.2 in 90%, AND \<8.3 x 10⁵WBCs in 95%

Answer 25

≥ 3.0 x 10¹¹and pH ≥ 6.2 in 90%

Answer 26

≥ 3.0 x 10¹¹and pH ≥ 6.2 in 90% AND \< 5.0 x 10⁶residual WBCs in 95%

Answer 27

Factor VIII ≥ 80 IU (all) Fibrinogen ≥ 150 mg (all)

Answer 28

≥ 1.0 x 10¹⁰in 75%

Answer 29

15mL **\>150mg fibrinogen** **\>80 IU Factor VIII** **80-120 IU vWF** **40-60 IU Factor XIII** **Fibronectin**

Answer 30

Prevention of febrile nonhemolytic transfusion reactions, prevention of HLA immunization, prevention of CMV transmission (both CMV neg and safe have 1-4% chance of transmission), reduction of reperfusion injury post cardiac bypass

Answer 31

Storage of rare, autologous or O negative units, plasma hypersensitivities (as with washed) and repeated febrile reactions (as with washed) _Red cell_: 10 years at -65C (40% glycerol), 24 hours at 1-6C after thawing/deglycerolizing _Platelets_: At least two years at -80C after thawing/deglycerolizing

Answer 32

_"Rules"_ “R” = D, “r” = d “1” or “prime” = C “2” or “double prime” = E “0” or “blank” = ce Any sub- or superscript letter = CE **R₁: DCe r’ : dCe R₂: DcE r”: dcE R₀: Dce r : dce R_z: DCE r^y : dCE**

Answer 33

To prevent transfusion associated graft vs host disease 2500 cGy dose required targeted to center of bag, with at least 1500 cGy in all parts of the bag Maximum storage: 28 days after irradiation or regular expiration date, whichever comes first

Answer 34

1) Begins at time of treatment and ends when full engraftment has occurred. In ABO-incompatible transplants, phase II ends when recipient’s blood type has converted to donor’s type. 2) Transfusion in different phases: * Phase I--it's pre transplant so give patient usual compatible products * Phase II--tricky stage * In **_major mismatch**_ (NON-O donor to O recipient or AB donor to A or B recipient), _**transfuse the recipient’s red cell type and donor’s FFP/platelet type_** (of course, you can always use AB FFP). * In **_minor mismatch_** (O donor to NON-O recipient or A or B donor to AB recipient), **_transfuse the donor’s red cell type and recipient’s FFP/platelet type_**. c) **_For both major and minor mismatches_** (giving A to B or B to A), give O red cells and AB plasma. * Phase III--post transplant so they have converted to donor's blood type so use the transplant DONORs type to make decisions

Answer 35

--R₀ most common in blacks, least common in whites. --r is always second in frequency. --R₁ always comes before R₂. **“The Big Four” Whites: R₁ \> r \> R₂ \> R₀ Blacks: R₀ \> r \> R₁ \> R₂** --Asians usually D+; order is R₁ \> R₂ \> r = R₀.

Answer 36

**_KB% x 5/3 = number of vials_** In above example, (2 x 5)/3 = 3.33 Remember, the 5 is if you are assuming a BV of 5000mL because the test did not give you amount. Otherwise, if they tell you the weight of the mother, then you can calculate actual BV by using 70mL/kg conversion. If it is 6 liters, you would multiply by 6 in the above example. _Rounding rules_: If number after decimal is \< 5, round up once. If \> 5, round up twice. So, “3.4” would mean give 4 vials, while “3.5” would mean to give 5 vials

Answer 37

Calculate the % compatible units by using frequency like usual. Then you divide the number of units the stem wants by the %. For example, how many units would you have to test to find 2 compatible units with someone who has anti-K1 and anti-Jka? Frequency is 21% compatible so 2/.21 = 9.5 or 10 units

Answer 38

Body Surface Area (Plt_post- Plt_pre) x 10¹¹/ Number of platelets transfused x 10¹¹ \*The 10¹¹is irrelevant and you can ignore it because it is on top and bottom so they cancel out. The stem should give you the amount of platelets transfused because each apheresis bag gets an exact number. 7500 or above defines "adequate" response and two consecutive counts below 5000 defines refractoriness

Answer 39

Critical Data Needed: **Weight in Kg, Hct, and current fibrinogen level**, **target fibrinogen level** If they do not give target level, 100mg/dL is "adequate" and 150 mg/dL is "optimal". **_STEPS:_** 1. **Calculate Blood Volume** Body weight x 70 ml/Kg 2. **Calculate Plasma Volume (PV)** Blood volume x (1 - hematocrit) Divide by 100 to convert to dL 3. **Calculate mg fibrinogen needed** Plasma volume x concentration change desired \*Subtract desired level from current (ie, 150 mg/dl – 50 mg/dl) \*Multiply level change by PV (ie, 100 mg/dl x 36 ml) 4. **Calculate bags of cryo needed** Fibrinogen needed / 250 mg per bag

Answer 40

Almost identical to fibrinogen cryo calculation Critical data: **body weight in Kg, Hct, current and target VIII level** If not given a target level, use 50% (remember FVIII is measured in percent present) for hemarthrosis, minor bleed or minor surgery and use 100% for major surgery or life threatening hemorrhage. **_STEPS_**: 1. **Calculate Blood Volume** Body weight x 70 ml/Kg 2. **Calculate Plasma Volume (PV)** Blood volume x (1 - hematocrit) **DO NOT HAVE TO DIVIDE BY 100 TO CONVERT!** 3. **Calculate FVIII units needed** Plasma volume x increase desired = FVIII units needed 4. **Only if asked, ca****lculate bags of CRYO needed** FVIII units needed / 80 units per bag **IF ASKED TO CALCULATE FOR FACTOR IX, IT IS THE SAME CALCULATION EXCEPT MULTIPLE BY 2 AT THE END** and CRYO amount isn't issue

Answer 41

Anti A Anti KELL Anti Jk^a Anti Fy^a

Answer 42

Anti Jk^a Anti E Anti D Anti C

Answer 43

Anti A,B Anti D Anti KELL Anti C

Answer 44

ABO Kidd P (Paroxysmal Cold Hemoglobinuria)

Answer 45

1) RBCs collected in CPD or CPDA-1 may be rejuvenated up to 3 days after expiration and then frozen for 10 years 2) RBCs stored in AS-1 may be rejuvenated up to the original 42 day expiration date and then frozen for up to 3 years

Answer 46

Sulfhydryl reagents reduce disulfide bonds to produce free sulfhydryl groups. There are multiple disulfide bonds between **cysteine residues** in the extracellular domains of the Kell antigen.

Answer 47

Desmopressin acetate (DDAVP)

Answer 48

Patients who are HPA-1a negative and who have the HLADRB\*0101 are more likely to develop HPA-1a antibodies following exposure to the antigen. ## Footnote Although 98% of the population is HPA-1a positive, not all of the remaining 2% of HPA-1a negative population will make antibody when exposed to the antigen. This is due to genetic restriction associated with HLA type DRw52a (DRB3\* 0101). HPA-5b is the second most common cause of NAIT (10%) after HPA -1a. HPA-1a is found on glycoprotein IIIa.

Answer 49

H amount: O\>A₂\>B\>A₂B\>A₁\>A₁B \*A₁ antigen has 5x more antigen than A₂ which makes sense based on A₁ having the least amount of H present

Answer 50

_Group A and B_: Anti-A or Anti-B is predominately IgM but each reacts strongly at body temp _Group O_: Anti-A and B are predominately IgG and react best at body temp. Anti A,B is IgG

Answer 51

Reagent Anti-A = BLUE Reagent Anti-B = YELLOW so if you see a test tube with clumping with blue fluid, it's Type A blood group This is backwards of what you would think but they love to ask this on boards for some reason!

Answer 52

Type I chains only, one gene: Le **(FUT3)** FUT enzyme adds fucose to subterminal GlcNAc. This makes Le^a (Lewis A) antigen. In a non-secretor, Le^a is the only Lewis antigen possible. Le^aantigens cannot be further modified to make Le^b . In secretors, Se product adds fucose, then Le product adds fucose; this makes Le^b (Lewis B). In secretors, this interaction occurs preferentially over Le^aformation. As a result, the vast majority the chains of secretors who carry Le are Le^b rather than Le^a. In non-secretors, the Le^a is the only possible Lewis antigen. Le(a-b+) HAVE Lewis A; just undectable routinely.

Answer 53

* 22% of blacks are Le(a-b-) vs ony 6% of whites * 10-40% of Asians are Le(a+b+) due to "weak secretor" gene so Se and Le compete equally * Lewis antigens decrease during pregnancy (increased plasma volume dilutes antigens and increased plasma lipoproteins bind the antigens) so they may appear Le(a-b-) and have transient insignificant Lewis Abs * Le(a-b+) don't make anti-Le^a * H. pylori attaches to gastric mucosa via Le^b antigen * Norwalk virus also attaches via Le^b * Le(a-b-) are at risk for Candida and E.coli infection

Answer 54

_Low frequency_: C_w, Kp^a, Js^a, Lu^a _High frequency_: Kp^b, Js^b

Answer 55

This is a VERY rare antibody that can be seen in people that are P1-P^k-P- It causes SEVERE HTRs with P₁ or P₂ phenotype blood and patients can have spontaneous abortions from **placental P/P^k attack**

Answer 56

Fy⁵, Lw, S, s, and U

Answer 57

A *quantitative* defect in the D antigen (less D than normal) _Possible reasons_: mutated form of RHD (most common by far)--point mutations cause altered amino acids in membrane or inner part of RHD. Another reason is RHCe on opposite chromosome to RHD inhibits D expression (C in trans) _Testing requirements_: weak D test for all D neg DONORS but not required for D neg recipients **Only non-donors who definitely need weak D testing: D neg babies born to D neg moms** Weak D moms do NOT need RhIg

Answer 58

A *qualitiative* defect (abnormal forms, missing part of the antigen) Some also have a *quantitative* defect (so called partial weak D) _Cause_: RHD gene mutations leading to alteration of the EXTERIOR part of the RHD antigen Antibodies form against absent parts of RHD and this Ab appears to be Anti-D at first glance **Classic scenario is Anti-D in a D positive person** Most common: DVI (D six) in whites, DIIIa in blacks

Answer 59

* Partial D moms need RhIg while weak D's do not * Partial D recipients may make Anti-D when receiving D+ RBCs, weak D recipients generally do not * Partial D OR weak D donor RBCs may induct anti-D in a D neg recipient * The distinction may be impossible without molecular testing so when in doubt, just give D neg blood

Answer 60

An Rh antigen that is present when EITHER C or D is present Anti-G reacts against (D+C-), (D-C+), or (D+C+) RBCs (rarely against (D-C-G+) Common presentation: D neg person forms Anti-D and anti-C despite no exposure to D Important because if D neg mom has anti-G, she DOES still need RhIg to prevent anti-D

Answer 61

An Rh antigen that is present when RHce is inherited (r and R₀) Anti-f is often seen with anti-e or anti-c Can cause mild HDFN and HTR Most common alloAb directed against compoud Rh antigens It is found primarily in persons with DCe/DcE (R1R2)

Answer 62

**Delayed HTRs, anamnestic response, intravascular and often severe** Jk^a, Jk^b, Jk3 (VERY high frequency) Antigens reside on urea transport protein--**Jk(a-b-) RBCs are RESISTANT to hemolysis in high conc 2M urea because there is no urea transport so no resultant osmotic lysis)** Abs require exposure, are warm reacting IgG (many with IgM component as well) Can fix complement (with IgM component, 50%) **Marked dosage effect**, variable antibody expression (Ab often dissapears with time, \>3 months)--"kids like to play hide and seek"

Answer 63

**Kidd negative phenotype** Jk(a-b-) RBCs are RESISTANT to hemolysis in high conc 2M urea because there is no urea transport so no resultant osmotic lysis) Kidd antigens reside on urea transport protein so if no Kidd antigens, no urea transport

Answer 64

Auto-anti-N

Answer 65

Blacks ## Footnote Glycophorin B always has terminal amino acid sequence that matches the N version of glycophorin A Not really a TRUE N antigen but close enough that most M+N- people won't form Anti-N Present in all cases except those lacking glycophorn B ( **Anti-N almost exclusive to blacks and presence suggest possibility of patient lacking glycophorin B and at risk for anti-U**

Answer 66

Probably not Fy (no a or b) is a Fy^b variant that doesn't make Fy^b on RBCs but it DOES make it on non-RBC tissues so they won't make antibody. Usually from mutation in the GATA box

Answer 67

Thiol reagents (2-ME, DTT, ZZAP) but are unaffected by enzymes alone ## Footnote Kell antigens are carried on a large glycoprotein held together by disulfide bonds and thiol reagents break those bonds, enzymes do not

Answer 68

Damages early RBC _precursors_ so may be suppressive as well as hemolytic Lower bilirubin and fewer reticulocytes compared to anti-D HDFN (early precursors = less hemoglobin for bilirubin formation) Significant at lower titers (1:8 is critical)

Answer 69

1) history of malaria = **3 years (if asymptomatic)** 2) living in endemic country for more than 5 consecutive years = **3 years (if asymptomatic)** 3) resident of non-endemic country travels to endemic AREA for more than 24 hours and less than 5 years = **1 year (if asymptomatic)** 4) resident of non-endemic country travels to endemic COUNTRY but not endemic AREA for more than 24 hours = **no deferral** 5) previous resident of endemic country travel to endemic area less than 3 years after leaving endemic country = **3 years (if asymptomatic)** 6) previous resident of endemic country travel to endemic area more than 3 years after leaving endemic country = **1 year (if asymptomatic)**

Answer 70

10-15 mL/kg

Answer 71

~4 hours Most FFP transfusions are given for elevated INR/PT (factor VII most responsible) but this is not really good practice because the INR of a unit of FFP is 1.2-1.5!

Answer 72

Potassium triples and free hemoglobin increases in plasma indicative of mild RBC membrane damage ## Footnote _Storage lesion_: * **Glucose decreased** * **2,3 DPG decreased** * **ATP decreased** * **pH decreased (acidosis)** * **Lactate increased** * **Potassium increased**

Answer 73

The neutrophil is the villiain! Good PMNs behaving badly (they are doing normal functions but in the wrong time and place). About 30% of PMNs are in the lungs at all times Anti-HLA or HNA from DONOR bind to recipient PMNs and the Ab-Ag complexes deposit in pulmonary vasculature and activate PMN bactericidal response Damage to pulmonary endothelial cells lining capillaries with resultant leakage of fluids into the alveolar spaces (pulm edema) _Another theory_: because this doesn't explain all TRALI reactions or why TRALI doesn't occur in some situations where it should, there is the two event pathway. 1) pre-existing condition activates lung endothelial cells and primes PMNs (sepsis, major surgery, massive transfusion) and then 2) transfusion of stored products prime the PMNs to secrete toxic substances

Answer 74

IgE anti-IgA Usually in IgA deficient patients, can also be seen in Asians with _haptoglobin deficiency_ WASH products

Answer 75

Definition: hemolysis occuring at least 24 hours but less than 28 days after transfusion **Kidd, Duffy and Kell** Anamnestic rapid production of IgG antibody Classically leads to extravascular hemolysis **NOTE due to Kidd antibodies may be intravascular and severe** DAT usually shows MIXED FIELD

Answer 76

This is usually due to getting product from relative or similiar HLA type The recipient is heterozygous for HLA type and donor is homozygous. The donor WBCs attack the recipient because it recognizes the heterozygous part that it DOESN'T have whereas the donor doesn't mount a counterattack because it recognizes the HLA type as "self" since it has one copy too

Answer 77

A transfusion reaction that is rare and caused marked thrombocytopenia and increased risk of bleeding about 10 days after transfusion Multiparous females at risk (5:1 female to male ratio) Caused by antibody vs common PLT antigen Anti-HPA-1A 70-80% HPA1A POSITIVE transfused plts and HPA1A NEGATIVE platelets are BOTH destroyed IVIG normalizes plt count in about 3-5 days Mortality about 10% without tx and 0% with tx

Answer 78

1) _single unit whole blood_: _\>_ 8 weeks 2) _2 unit red cell donation by apheresis_: _\>_16 weeks 3) _Plasma by apheresis_: "frequent" donor programs: _2 donations/week at least 2 days apart_ others: 4 weeks apart 4) _Platelets by apheresis_: _2 donations/week at least 2 days apart and 24 in a 12 month period_ plt count _\>_ 150,000 is required \*if there is whole blood donation or if red cells cannot be returned to a donor during apheresis then 8 weeks must elapse before repeat apheresis

Answer 79

Type O RBCs Type AB plts and plasma Match Rh if possible \*not necessary to cross match products for pts less than 4 months if there are no significant materal allantibodies

Answer 80

170 um filter (standard blood infusion) ## Footnote \*RBCs, platelets, FFP ALL must be ran through a 170 filter 40 um (microaggregate filter)--not required The same filter can be reused for multiple transfusions for up to 4 hours Neonatal transfusions may be filtered by the blood bank staff prior to release

Answer 81

2mL/min for 15 minutes ## Footnote \*do not transfuse with other fluids other than normal saline and certain FDA approved crystalloids (LRs have a lot of calcium and bind all citrate so blood clots, half normal saline or other hypotonic solns may cause hemolysis) All units released at one time must be transfused in 4 hours!

Answer 82

Adult plasma contains naturally occuring IgM Abs to T, Tn, Tk and Cad These are normally cryptic antigens that are expressed only when bacterial neuraminidase enzymatically alter red cell antigens (T activation) In adults, this phenomenon is primarily a factor in pretransfusion testing In infants, it can be clinically significant in two instances: **1. Necrotizing enterocolitis (NEC)--T activation occurs in up to 25% caused be neuraminidase of Clostridia** **2. Atypical HUS--neuraminidase of Strep pneumoniae** Testing: The lectin *Arachis hypogaea* can detect T activation. Polyagglutinable red cells are agglutinated by adult, not cord, serum. Adult plasma contains naturally occuring anti-T Abs and therefore infants with T activation can develop intravascular hemolysis when transfused and such infants should receive RBCs with minimal plasma or washed RBCs The effect is transient and abates following resolution of the infection

Answer 83

K = 10% k = 98% Kpa = 2%

Answer 84

Both 75% \*Jk(a-b-) rare except in Pacific Islanders

Answer 85

Fy^a = 65% in whites, 10% in blacks Fy^b = 83% in whites, 20% in blacks Fy(a-b-) rare in whites, 68% in blacks

Answer 86

M = 80% N = 72% S = 55% s = 90% U = 99.9% whites, 99% blacks

Answer 87

Hematolymphoid neoplasms

Answer 88

Gastric adenoCA

Answer 89

With nonphenotypically matched blood, rate of alloimmunization per transfusion is 3%, overall rate is between 19-47% The most common alloAbs are anti K, C, E, Fy^a, Jk^b With blood matched for Cc, Ee, D and Kell, rate of alloimmunization rate per transfusion is 0.5%

Answer 90

2% of individuals are HPA1A neg It can affect the first pregnancy There is a 20% incidence of intracranial hemorrhage overall; about half of hemorrhages occur in utero Tx should begin as soon as diagnosis is suspected (high dose IVIG and/or steroids) Intrauterine platelet transfusion may begin at 18-20 weeks with antigen negative platelets (maternal platelets may be used if washed and irradiated) Deliver by C section if possible; after birth the risk of hemorrhage is **greatest during the first 24-36 hours** so expedient plt transfusion is desirable

Answer 91

15% The incidence is **LOWER** if the mom and fetus are also ABO incompatible

Answer 92

Plasma not frozen within 8 hours may be frozen within 24 hours and labeled "plasma frozen within 24 hours after phlebotomy" or FP24 \*relatively deplete of Factors V and VIII Useful for all indications for FFP **EXCEPT DIC**

Answer 93

1) Congenital dyserythropoietic anemia (CDA) type II 2) Blackfan-Diamond syndrome

Answer 94

A₂ = 5% A₂B = 35% Usually clinically insignificant

Answer 95

They will form an anti total Rh antibody (anti Rh29)

Answer 96

Results from homozygous inheritance of the amorph K0 such that red cells have no Kell antigen but an abundance of Kx ## Footnote Different from McLeod which is from mutations in Kx gene so no Kx with depressed Kell antigens

Answer 97

1) Diego negative 2) Gerbich negative (Leach phenotype)

Answer 98

1) _4 MC Abs in immediated HTR_: anti A, anti Kell, anti Jk^a, anti Fy^a 2) _4 MC Abs in delayed HTR_: anti Jk^a, anti E, anti D, anti C 3) _4 MC Abs in HDN_: anti AB, anti D, anti Kell, anti C 4) _Abs causing mixed field rxn_: Lutheran, Sid, A3 (and post bone marrow transplant) * Kidd, Duffy and Kell cause a mixed field **DAT** due to delayed hemolytic transfusion reaction* 5) _Abs commonly produce intravascular hemolysis_: ABO, Kidd, P (PCH)

Answer 99

*Clostridium*

Answer 100

10.5 mL/kg

Answer 101

120 days (4 months) from onset of symptoms or diagnosis, whichever is more recent

Answer 102

**d) cold autoantibody** ## Footnote A number of drugs are associated with each mechanism and it's helpful to remember 1 or 2 for each. _Immune complex mediated_: quinidine, cephalosporins _Nonimmune protein adsorption_: cephalothin (a first gen cephalosporin) _True autoimmune hemolytic anemia_: procainamide and aldomet (methyldopa) _Hapten associated_: penicillin

Answer 103

a) _Immune complex mediated_: quinidine, cephalosporins b) _Nonimmune protein adsorption_: cephalothin (a first gen cephalosporin) c) _True autoimmune hemolytic anemia_: procainamide and aldomet (methyldopa) d) _Hapten associated_: penicillin

Answer 104

**b) IgG2** ## Footnote In addition to dimeric IgA and pentameric IgM, IgG2 is unable to cause HDN. Like IgA and IgM, IgG2 is unable to cross the placental membrane and therefore unable to initiate hemolysis

Answer 105

200mg Each red cell unit contains ~200mL of RBCs with each mL of red blood cells containing 1mg of iron. This means that each RBC unit has 200mg iron

Answer 106

First it goes through a soft slow spin to separate into red blood cells and platelet rich plasma Then the PRP undergoes a hard fast spin to separate into platelets and plasma

Answer 107

* DIC (loss of multiple coagulation factors) * TTP to replace ADAMTS13 * Hereditary angioedema to replace C1q * Antithrombin deficiency * Massive transfusion * Reversal of warfarin therapy

Answer 108

**d) RBCs leukoreduced to 8 WBCs** ## Footnote Leukoreduced red cells: ≤ 5 x 10⁶ WBCs in 95%, retain 85% of RBCs CMV negative = CMV "safe" which is leukoreduced Washed RBCs are considered leukoreduced

Answer 109

**c) PKHD1** While this is located on Chr 6, it is not within the MHC like the rest are

Answer 110

**b) megakaryocytes** Class I HLA antigens are expressed on virtually all nucleated cells while Class II is much more restricted and facilitates humoral and cell mediated immunity

Answer 111

12.5 g/dL \* 4.5 dL (450 ml) = **56.25g Hb** ## Footnote \*minimal allowable Hgb for donating is 12.5

Answer 112

Undercentrifugation, delay in adding antiglobulin agent, failure to adequately wash cells

Answer 113

Rh Null **LACK Lw antigen!!** \*they could phrase it like this on exam (instead of saying Rh null, say lack Lw antigen--this is actually a Rh LIKE antigen but Rh null pts lack this)

Answer 114

The storage lesion refers to changes in red cells during storage. Over time, glucose in stored blood is consumed, levels of 2,3-diphosphoglycerate (DPG) and ATP decrease, while potassium levels increase. * **Glucose decreased** * **2,3 DPG decreased** * **ATP decreased** * **pH decreased (acidosis)** * **Lactate increased** * **Potassium increased**

Blood Bank Flashcards

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