One question at a time. Build your MLT understanding.
First 50 of 200 questions. Each one lists the choices, the correct answer, and an explanation. The checker at the top of this page saves progress in this browser when it is available.
Continue in the practice tool above to load more questions, 50 at a time.
Group A red cells carry the A antigen, so the individual is tolerant to A and forms antibody only to the missing B antigen. Group A plasma therefore contains anti-B, which is IgM and reacts at room temperature. This is the basis of the reverse (serum) grouping used to confirm the forward type.
The D antigen of the Rh system elicits an immune response in a large proportion of D-negative recipients exposed to D-positive red cells. This high immunogenicity is why D typing and Rh immune globulin prophylaxis are central to transfusion and obstetric practice. Other antigens such as K, Jka and Fya are immunogenic but considerably less so.
Bombay individuals lack the H antigen that is the precursor for A and B antigens, so they do not express A or B on red cells. Because H, A and B are all foreign to them, they produce anti-H along with anti-A and anti-B. They must receive only Bombay-compatible (Oh) units.
Polyspecific AHG contains anti-IgG and anti-C3d, allowing detection of red cells coated with IgG antibody, complement, or both. Monospecific reagents are used when the coating protein must be identified. Anti-IgM and anti-IgA are not components of routine AHG reagent.
Red cells are refrigerated at 1 to 6 °C to slow glycolysis and inhibit bacterial growth while preserving viability. Storage at 1 to 6 °C allows units to remain usable for 21 to 42 days depending on the preservative solution. Warmer or frozen temperatures would either promote proliferation or damage the cells.
Platelets require room temperature storage with continuous gentle agitation to maintain viability and to allow gas exchange. They are typically usable for up to 5 days. Refrigeration causes platelet shape change and loss of function.
Thawed plasma is stored at 1 to 6 °C and must be used within 24 hours because labile coagulation factors, especially factor VIII and factor V, progressively degrade. After the 24-hour window the unit is no longer labeled as plasma. Frozen plasma itself may be kept for up to 1 year at −18 °C or colder.
Dolichos biflorus lectin agglutinates A1 cells and is used to resolve A1 versus A2 subgroups. Ulex europaeus anti-H is used to demonstrate H antigen. Correct identification of subgroups matters in donor-recipient selection and in ABO discrepancy workups.
The immediate-spin phase detects IgM antibodies that bind at room temperature, and the ABO system is the clinically critical example. If the recipient has been screened for unexpected antibodies, the immediate-spin crossmatch serves as a final ABO check. IgG antibodies such as anti-Jka or anti-K are detected only in the antihuman globulin phase.
In gel testing, unagglutinated cells pass through the gel and form a pellet at the bottom, which is negative. Agglutinated cells are too large to migrate and remain within or on top of the gel, with the height of the agglutinate reflecting reaction strength. Colour change is not the endpoint of this method.
Lowering the ionic strength of the medium reduces the zeta potential around red cells, so antibody molecules can approach the membrane more closely and bind faster. This shortens incubation to about 10 to 15 minutes. It does not act by increasing surface charge or by inactivating cold antibodies.
PEG is a water-excluding polymer that increases the effective concentration of antibody in the fluid surrounding red cells, promoting uptake. It shortens incubation and boosts detection of weak IgG antibodies. Its main drawback is a greater tendency toward nonspecific reactions.
Cold hemagglutinin disease is mediated by IgM anti-I that binds red cells at cool temperatures in the extremities and fixes complement. Warm autoimmune hemolytic anemia is usually caused by IgG with specificity within the Rh system. HDN and delayed transfusion reactions are typically caused by alloimmune IgG.
Lewis antibodies are IgM that react best at room temperature, and they are neutralized when donor units contain plasma with soluble Lewis substance. Lewis antigens are not present on fetal red cells, so these antibodies do not cause hemolytic disease of the newborn. They are naturally occurring rather than the result of immune exposure.
Jka and Jkb antibodies are IgG that react by the indirect antiglobulin test, show dosage, and decline to undetectable levels over time. Because they fall below detection yet reappear rapidly after transfusion, they are a classic cause of delayed hemolytic transfusion reactions. They are not IgM-complement binders.
The Duffy antigen is the receptor used by Plasmodium vivax to invade red cells, so Fy(a−b−) individuals are resistant to vivax malaria. This phenotype is common in populations of West African descent. It also matters in transfusion because anti-Fya is a clinically significant antibody.
Delayed hemolytic transfusion reactions occur about 5 to 10 days after transfusion when an anamnestic alloantibody response destroys the transfused cells. The antibody is often undetectable before transfusion but reappears and coats circulating red cells, producing a positive DAT. Kidd antibodies are a frequent cause.
Febrile non-hemolytic reactions are the most frequently reported adverse transfusion event, characterized by a temperature rise without hemolysis. They are attributed to cytokines accumulated during storage and to recipient antibodies against donor leukocytes. Universal leukoreduction reduces their frequency.
TRALI presents within 6 hours of transfusion with acute hypoxemia and bilateral infiltrates in the absence of volume overload, often linked to donor HLA or neutrophil antibodies in plasma-rich components. Management is supportive and the pulmonary edema resolves as the antibody clears. Diuretic therapy is not the primary treatment.
A standard antenatal dose of Rh immune globulin is given at about 28 weeks' gestation, with a second dose within 72 hours after delivery of a D-positive infant. Some protocols add a dose earlier in pregnancy after events such as amniocentesis or bleeding. The goal is to clear fetal D-positive cells before the mother mounts an immune response.
Fetal hemoglobin resists acid elution and stains dark, while adult hemoglobin is eluted from maternal cells, allowing the proportion of fetal cells to be estimated. That percentage is converted into an estimated volume of fetal-maternal hemorrhage so the Rh immune globulin dose can be adjusted. The test does not measure antibodies or red cell survival.
The prewarm technique keeps reactants at 37 °C so cold autoantibodies do not bind, while warm-reacting IgG alloantibodies remain able to attach. Warm saline washes prevent cooling during the procedure. Prolonged room temperature incubation or extra LISS would only strengthen the cold reactivity.
Autologous adsorption removes warm autoantibody from the serum while leaving alloantibodies, which can then be detected in the adsorbed serum. It is valid only when the patient has not been transfused in the preceding 3 months, because transfused donor cells could adsorb alloantibodies. Allogeneic adsorption is used when recent transfusion makes autoadsorption unsuitable.
Anti-K is an immune IgG antibody detected in the indirect antiglobulin phase and is clinically significant for both hemolytic transfusion reactions and hemolytic disease of the newborn. Kell antigens are well developed on fetal red cells, so anti-K can cause severe fetal anemia. Enzyme treatment may weaken or destroy some Kell antigens, so enzyme-only testing is not appropriate.
Weak A subgroups carry few A antigen sites, so adsorption of anti-A onto the cells followed by elution demonstrates antigen that direct agglutination may miss. The eluate's reactivity confirms the presence of A antigen. Crossmatching or anti-B titration does not characterize the red cell antigen status.
Reverse grouping tests the patient's serum for anti-A and anti-B using reagent A1 and B cells. Agglutination with A1 cells indicates anti-A, and agglutination with B cells indicates anti-B. Group O cells are not used because they lack A and B antigens.
Red cells are stored refrigerated at 1 to 6 °C to limit bacterial growth and preserve red cell viability. Frozen storage at −18 °C or colder is used for plasma or rare red cell units with cryoprotectant, not routine red cell storage. Room temperature and 37 °C are not acceptable for red cell storage.
The DAT detects antibody and/or complement already bound to the patient's red cells in vivo. Washed red cells are reacted with antihuman globulin, and agglutination indicates sensitization. Serum antibody is detected by the indirect antiglobulin test, not the DAT.
IgM is a pentamer and is the most efficient activator of the classical complement pathway per molecule. IgG can activate complement, but usually requires two adjacent IgG molecules on the red cell surface. IgA and IgE do not efficiently activate classical complement.
The weak D test uses antihuman globulin after incubation with anti-D to detect D antigen that is present but expressed at reduced levels. It is used to classify donors and patients whose direct agglutination with anti-D is negative. It does not type for Kell or assess the DAT.
IgG antibodies typically react at 37 °C and are detected at the antihuman globulin phase. IgM antibodies usually agglutinate at room temperature or immediate spin. IgA and IgE are not typical red cell antibodies detected in routine screening.
Acid elution disrupts the bond between antibody and red cell antigen, releasing antibody into the eluate for testing. The eluate can be tested against panel cells to identify the specificity of the bound antibody. It is not used to remove complement, enhance antigens, or fractionate blood.
Proteolytic enzymes such as ficin and papain enhance many Rh system antibodies by increasing antigen accessibility. The same treatment destroys Duffy antigens and some MNS antigens, so enzyme-treated cells are not used alone for antibody detection. Kell antigens are generally resistant to enzymes.
Anti-A1 in A2 or A2B individuals is usually a cold-reacting IgM antibody that is clinically insignificant. It may cause a discrepancy between forward and reverse ABO grouping but rarely causes hemolysis. It does not typically cause hemolytic disease of the newborn.
Rh immune globulin should be administered within 72 hours of delivery of a D-positive infant to a D-negative, unsensitized mother. Administration within this window prevents active immunization to the D antigen. Giving it later is less reliable, although some sources allow dosing up to 28 days if the 72-hour window was missed.
Allogeneic adsorption uses selected donor red cells to adsorb warm autoantibody from the patient's serum. Testing the adsorbed serum against panel cells can then reveal underlying alloantibodies that were masked by the autoantibody. It is not a method for measuring autoantibody titer or enhancing complement.
DTT reduces disulfide bonds and denatures Kell system antigens, which are highly sensitive to this treatment. Many other blood group antigens remain intact, so DTT-treated cells can help distinguish anti-K from other antibodies. It does not enhance Kell reactivity or complement binding.
A delayed serologic transfusion reaction occurs when an antibody becomes detectable days after transfusion and the DAT turns positive, but red cell survival remains normal. If hemolysis also occurs, it is classified as a delayed hemolytic transfusion reaction. The antibody screen may become positive, not negative.
TACO is transfusion-associated circulatory overload and is supported by hypertension, elevated BNP, jugular venous distension, and improvement with diuresis. TRALI also causes bilateral infiltrates and hypoxemia, but it is more often associated with fever and hypotension and lacks volume overload. Both can occur within 6 hours.
Mixed-field agglutination describes clumps of agglutinated cells among unagglutinated cells, which occurs when two red cell populations coexist, such as after transfusion or in a chimera. The patient's own cells and donor cells may differ in antigen expression. Autoantibodies usually produce uniform reactivity rather than a mixed field.
Sodium fluoride inhibits enolase, a glycolytic enzyme, slowing the fall in glucose concentration after collection. EDTA, heparin, and citrate are anticoagulants but do not effectively block glycolysis.
Transferrin binds ferric iron and delivers it to erythroid precursors and other tissues. Ferritin stores iron, ceruloplasmin transports copper, and haptoglobin binds free hemoglobin.
Alkaline phosphatase (ALP) rises with impaired bile flow because it is concentrated in bile canaliculi and biliary epithelium. AST and ALT are more associated with hepatocellular injury, and CK with muscle injury.
The hexokinase method measures true glucose with high specificity and is widely used as a reference procedure. Glucose oxidase is specific but can be affected by interferences, while o-toluidine and Folin-Wu are older, less specific methods.
Absorbance increases with the concentration of the absorbing species and with the light path length through the cuvette. Molar absorptivity at a given wavelength is also part of the relationship, but wavelength and temperature are not the paired variables stated in the law.
Arterial blood pH is normally maintained between about 7.35 and 7.45. Values below 7.35 indicate acidemia, and values above 7.45 indicate alkalemia.
Hemoglobin A1c reflects glucose exposure over the lifespan of red cells, roughly 2 to 3 months. Fructosamine and glycated albumin reflect shorter-term control, and 1,5-anhydroglucitol reflects recent hyperglycemia over days.
Potassium is the predominant intracellular cation, with high intracellular concentration maintained by the sodium-potassium pump. Sodium is the major extracellular cation, and calcium and magnesium are mostly extracellular or stored in bone.
The anion gap is calculated as sodium minus the sum of chloride and bicarbonate. Here, 140 minus (104 + 22) equals 14 mmol/L, which is within the usual reference interval.
An osmolal gap above about 10 mOsm/kg suggests an unmeasured osmotically active substance such as methanol, ethylene glycol, or isopropanol. Hypernatremia and uremia raise both measured and calculated osmolality, so the gap remains normal.