clinical pathology(BB)

B. 16 years old.
The minimum age for whole blood donation is 16 or 17 years old, depending on the state.

C. 12.5/38.
Most allogeneic donors must have a minimum hemoglobin concentration of 12.5 g/dL and/or a minimum hematocrit of 38%. The regulations for donation of autologous
blood are less stringent with a minimum hemoglobin of 11 g/dL and a hematocrit of 33%

E. amount of anticoagulant must be proportionally decreased.
While many of the choices seem plausible, only choice E is correct. The volume of the average whole blood unit should be 450 +/- 50 mL. Anything less than that but
more than 300 mL should be labeled as low-volume and cannot be used for component therapy. Volume less than 300 mL requires that the amount of anticoagulant be
proportionally decreased.

D. pulse.
The manifestations of both of the reactions are overlapping - hypotension, nausea, and syncope. However, a vasovagal reaction characteristically manifests with
bradycardia while hypovolemia usually has tachycardia. The treatment differs primarily in the fact that the hypovolemic patients need volume replacement, while
vasovagal reactions are treated with supportive therapy.

A. viral hepatitis after 11th birthday.
While all the other choices do have stipulated deferral lengths, any viral hepatitis after the 11th birthday is the only permanent deferral choice. A positive syphilis
screening test is a 12-month post-treatment deferral. The interval between whole blood donations should be at least one red blood cell life (8 weeks, 56 days). Being
incarcerated for more than 72 hours and paying for sex have a 1-year deferral, presumably for the same reasons.

A. viral hepatitis after 11th birthday.
While all the other choices do have stipulated deferral lengths, any viral hepatitis after the 11th birthday is the only permanent deferral choice. A positive syphilis
screening test is a 12-month post-treatment deferral. The interval between whole blood donations should be at least one

C. a 42-year-old man who spent 2 days in jail last month after getting drunk, fighting, and getting a tattoo in Mexico.
There is a “must know” list of deferrals that can be divided into three broad categories: permanent or indefinite deferral, 12-month deferral, and miscellaneous deferrals.
In addition, a donor center may adopt more strict criteria than those required. For the most part, permanent deferrals are for someone with a history of viral hepatitis
after the 11th birthday or other indications of current viral hepatitis (positive anti-HBc, etc), anyone with Creutzfeldt-Jakob risk (travel to endemic area, family relative
with CJD, bovine insulin in the UK, or a dura mater graft) or very high risk of HIV (money for sex or IV drug use).

D. test for weak D.
Weak D refers to D+ donors who do not react at immediate spin or even after incubation at 37°C. Only after addition of AHG is there a reaction. There are several
causes of weak D- either due to low amounts of the D antigen or poorly-reactive antigen variants. It is important to label weak D as D (+) because previously sensitized
D (-) patients can experience a potential hemolytic transfusion reaction when given weak D cells.

A. A positive.
Forward typing tests the patient's red cells for the presence of an antigen (A and Rh in this case). Reverse typing confirms it by testing the patient's serum for the
presence of antibodies. In a type A patient, there is an expected naturally-occurring anti-B antibody.

D. serological testing for babesiosis.
A panel of serological and nucleic acid tests is required to screen donor blood. Among the serological are HBsAg, anti-HBc, anti-HCV, anti-HTLV-I, anti-HTLV-II, anti-HIV1
and 2, RPR, and West Nile virus. Nucleic acid testing for HCV and HIV is also performed. There is no good serological test for babesiosis at this time and screening
history questions are used.

B. clerical errors.
Of the choices presented, clerical errors account for the largest number of fatal transfusion reactions. For that reason, there must be very strict rules for the labeling of
specimens and specimen identification. In 2004, however, the FDA reported that the most common cause of fatal hemolytic transfusion reactions was TRALI (transfusionrelated
acute lung injury), perhaps due to better controls of clerical issues and increased awareness of TRALI

B. patient's stated blood type.
The most common patient identifiers are the patient's name and social security number or hospital medical record number. There must also be a way to identify who the
phlebotomist is and when the specimen was collected. Samples that are not clearly labeled with this information should not be accepted by the blood bank. Many blood
banks will take the sample from the submitter, so that it cannot be relabeled and resubmitted.

E. previous transfusion or pregnancy.
Patients that may have been exposed to foreign blood, such as those previously transfused and pregnant, are the most likely to develop alloantibodies. For this reason,
patients with a previous transfusion or pregnancy history must have a sample drawn within three days of testing.

E. addition of high ionic strength buffer.
The indirect antiglobulin test (IAT) is used for the identification of antibodies in the patient's serum. Typically, an antibody screen utilizes patient serum incubated at
37°C. For control purposes, an additional tube utilizing patient blood cells instead of test cells is included.

D. look for previously documented alloantibodies.
While it could be important to review the record for a past history of transfusion reactions, the most important reason to review the previous records is to identify an
alloantibody. Several antibodies are known for their evanescent nature, virtually disappearing but then reappearing with an antigen-positive transfusion and causing a
hemolytic transfusion reaction.

D. antibody panel.
Only in case of a positive antibody screen is a panel indicated. All the other choices are required for each and every transfusion. In addition, a visual inspection of the
unit and a review of the transfusion history should be performed.

E. none of the above.
Because patients with the Bombay phenotype do not make H antigen, they are unable to make ABO antigen. As a result, they have the potential to make an anti-H
antibody that could react with any ABO blood type other than Bombay. Also, as H antigen is converted to A or B antigen, less H antigen is present. As a result, type O
blood has the most H antigen and would therefore be the worst choice for a Bombay phenotype patient

D. O.
In all Americans, white and black, O type blood is the most common, followed by A, B, and AB, respectively.

C. R°.
The Weiner classification system (R, r, etc) and the Fisher-Race system (DCE) are both often used. When discussing blood cell phenotypes, the Weiner system is often
used, while the Fisher-Race classification is most commonly used for discussing patient phenotypes. It is very easy to convert from one system to the other if one
remembers a few principles:
1. Organize the Fisher-Race in order of D, C, E. I know that it's not alphabetical, but it makes it easier later.
2. In Fisher-Race, capital “D” means the presence of the D antigen, while “d” means the absence of D. Sometimes “d” is omitted. For C and E, the capital and lower
case representations are of different alleles.
3. In the Weiner system, a capital “R” implies the presence of D (Rh positive), while a lower case “r” implies the absence of D (Rh negative).
4. The numbers in the Weiner system after the “R” or “r” represent the position of capitalized antigen after the “D” - for example - R2 is DcE and R1 is DCe. Don't be
fooled - after “r,” hash marks (' or “) are used instead of numbers.
5. A naught after the “R” or “r” means that neither of the following antigens are capitalized, eg, R° is Dce.
6. Finally, a letter after “R” or “r” means that both of the following antigens are capitalized, eg, ry is dCE.
Now to answer the question, the R° (quick, what's the Fisher-Race nomenclature?) phenotype is the most common in African-Americans, while R1 is the most common in
whites.

E. A, B, C.
The weak D phenotype is of particular concern with donor blood. The possibility exists that the blood could be labeled as Rh negative and transfused to Rh-negative
patients who may have been previously sensitized to D antigen. In that case, the transfusion may trigger a hemolytic transfusion reaction. For that reason, all donor
blood that tests on forward typing as negative (choice A) must undergo the next two tests to either prove or disprove the presence of weak D.

A. R°/r',
or Dce/Ce, is a common phenotype in the African-American population and results in quantitatively decreased D expression due to the trans effect of the C antigen on
the other chromosome, the so-called Cepelli effect. The other means of expressing the weak D phenotype is partial D, where certain epitopes of the D antigen are
absent. The most significant issue for partial D is in a pregnant woman who could produce anti-D antibodies if exposed to a D+ fetus.

C. Lw.
Certain epitopes are most affected by the Rhnull phenotype, where individuals lack the Rh antigens. These include Fy5, Lw, S, s, and U. Rhnull individuals have structural
red blood cell abnormalities that result in stomatocytosis and mild chronic anemia.

D. 80%.
Estimates range from 75% to 80% of D-negative individuals exposed to a unit of D positive red cells that subsequently develop anti-D. The antibodies are clinically
significant, warm-reactive, non-natural IgG.

D. anti-c.
The setup is an individual with R1R1 phenotype (DCe/DCe) being transfused with R2 (DcE) blood. There is a high likelihood that the patient will develop a detectable
anti-E. However, in addition to the anti-E, patients often develop a very weak anti-c - a frequent cause of delayed hemolytic transfusion reactions. For this reason,
patients with an anti-E should be given E-negative, c-negative red blood cells.

C. Lw.
Certain epitopes are most affected by the Rhnull phenotype, where individuals lack the Rh antigens. These include Fy5, Lw, S, s, and U. Rhnull individuals have structural
red blood cell abnormalities that result in stomatocytosis and mild chronic anemia.

C. Duffy.
Treatment of red blood cells with enzymes such as papain or ficin leads to predictable changes in the reactivity of the red cells to specific antibodies. Some antigens are
enhanced, some destroyed, some unchanged. It's useful to remember them, as they are easily testable. Those that are enhanced include Lewis, I/i, ABO, Rh, P, and
Kidd. I use the mnemonic “Lewis Is A Rhotten Peeing Kidd”. Among the ones that are destroyed are Duffy, Lutheran, MNS, and Chido. I use the mnemonic “Daffy MeNS
Lutheran Choir” and I imagine the church crumbling down on top of them to signify that they are destroyed.

D. 80%.
Estimates range from 75% to 80% of D-negative individuals exposed to a unit of D positive red cells that subsequently develop anti-D. The antibodies are clinically
significant, warm-reactive, non-natural IgG.

A. Jk (a+b-).
For the most part, the most common phenotype among both whites and blacks is Jk (a+). The major difference phenotypically comes with Jkb, which is more often
positive in whites and negative in blacks.

D. anti-c.
The setup is an individual with R1R1 phenotype (DCe/DCe) being transfused with R2 (DcE) blood. There is a high likelihood that the patient will develop a detectable
anti-E. However, in addition to the anti-E, patients often develop a very weak anti-c - a frequent cause of delayed hemolytic transfusion reactions. For this reason,
patients with an anti-E should be given E-negative, c-negative red blood cells.

C. Duffy.
Treatment of red blood cells with enzymes such as papain or ficin leads to predictable changes in the reactivity of the red cells to specific antibodies. Some antigens are
enhanced, some destroyed, some unchanged. It's useful to remember them, as they are easily testable. Those that are enhanced include Lewis, I/i, ABO, Rh, P, and
Kidd. I use the mnemonic “Lewis Is A Rhotten Peeing Kidd”. Among the ones that are destroyed are Duffy, Lutheran, MNS, and Chido. I use the mnemonic “Daffy MeNS
Lutheran Choir” and I imagine the church crumbling down on top of them to signify that they are destroyed.

A. Jk (a+b-).
For the most part, the most common phenotype among both whites and blacks is Jk (a+). The major difference phenotypically comes with Jkb, which is more often
positive in whites and negative in blacks.

B. dosage.
Antibodies against Kidd exhibit dosage - that is, homozygotes for Kidd antigens express more antigen than heterozygotes. In antibody panels, there may be red blood
cells that are heterozygous or homozygous for the Kidd antigens. Since Kidd antibodies are usually weak, it would not be unusual to get a positive reaction from a
homozygous panel red blood cell, but negative from a heterozygote. Also remember that Kidd can be enhanced by enzyme treatment.

D. 2-month-old Caucasian boy.
More important than race or gender for the levels of i antigen is age. The little i antigen is made up of the unbranched type 1 and type 2 precursor oligosaccharide
molecules. Branching increases with age, leading to the conversion of i antigen to I antigen.

A. fucosyltransferase that adds fucose to type 1 oligosaccharides.
Similar to the H (whose function is described in choice B), the Le gene product catalyzes the addition of fucosyl groups to the secretory type 1 oligosaccharides to make
Lea antigen. This antigen is then passively absorbed onto the surface of red blood cells (remember that type 1 precursors are secreted).

C. Le (a-b+).
Irrespective of race, the most common phenotype is a-b+. Leb is made from Lea precursor by the action of the Secretor gene product. This means that the levels of each
are inversely proportional. If an individual has just the Le gene, he or she will be Le (a+b-); if the individual expresses both Le and Se, he or she will be Le (a-b+).
Lacking both Le and Se leads to the phenotype Le (a-b-). Note that the phenotype Le (a+b+) cannot exist except transiently.

D. Fy (a-b-).
The absence of Duffy a and b confers resistance to P vivax malaria. The Fy (a-b-) phenotype is found in more than 2/3 of people of African descent, while it is rare
otherwise.

A. anti-M.
Of all the MNS antibodies, only anti-M and anti-N are naturally occurring and clinically insignificant IgM antibodies. Anti-S, anti-s, and anti-U are all acquired IgG
antibodies and can pose a threat of hemolytic transfusion reactions.

C. Kell.
McLeod phenotype is a chronic hemolytic anemia due to RBC structural abnormalities. The Kx gene on the X chromosome encodes a support protein that stabilizes Kell
expression. Without Kx protein, the expression of Kell proteins is greatly diminished. In addition to decreased Kell expression and reduced RBC survival, there is an
association with X-linked chronic granulomatous disease.