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Chapter 2
Case study
1. This item describes two deficiencies. First, the hematology laboratory scientist
should have washed his/her hands after removing the gloves and before leaving the
laboratory. Second, the hematology laboratory scientist should have removed his/her
laboratory coat before going to the meeting.
2. This item describes a deficiency. Storage of food in a specimen refrigerator is
prohibited.
3. This may or may not be a deficiency. The laboratory employees may have had on a
personal laboratory coat. A second laboratory coat could have been obtained by the
employees to wear in public areas. Some laboratories require different colored lab
coats for public areas.
4. No deficiency is indicated. Fire extinguishers should be placed every 75 feet.
5. This item describes a deficiency. Fire extinguishers should be inspected monthly and
maintained annually.
6. This item represents a deficiency. All chemicals should be labeled.
7. This item represents a deficiency. The 1:10 bleach solution should be made fresh
daily.
8. No deficiency is indicated. Gloves should be worn by all personnel handling
specimens.
9. No deficiency is indicated. Safety data sheets can be received by fax.
10. This item describes a deficiency. Chemicals should not be stored alphabetically, but
according to storage requirements specified in the safety data sheets.
Review questions
1. d; 2. b; 3. c; 4. c; 5. a; 6. b; 7. c; 8. b; 9. b; 10. b; 11. d
Chapter 3
Case studies
Case 1
The proper procedure is to ask the patient to state his/her full name and
then confirm by asking his/her birth date and/or address. The phlebotomist
should not prelabel tubes; tubes should be labeled after the blood is drawn
and before leaving the patient.
Case 2
Test results that can be affected by this selection of tubes and order of draw
include the prothrombin time (PT), potassium, and type and screen.
The light blue stopper tube for the PT should not have been collected after the
serum separator tube (which contains an inert gel and clot activator). The clot
activator could contaminate the blue stopper tube, activate coagulation factors, and
cause an error in the PT results.
The green stopper tube for potassium should not have been collected after a
lavender stopper tube (which contains EDTA, usually as a potassium salt). The
potassium-EDTA could be carried over into the green stopper tube and falsely
elevate the potassium level. The potassium could, however, be assayed in the
serum separator tube.
The type and screen cannot be done on blood from the serum separator tube
because the gel interferes with blood bank procedures; the lavender stopper tube,
however, could be used for the type and screen. Box 3-2 contains the correct order
of draw for evacuated tubes.
Review questions
Chapter 4
Case study
Is the slide right side up? This is the most common cause of inability to focus
a slide under oil when it has been focused under 10× and 40× objectives.
Is there sufficient oil on the slide? If not, clean off all the residual oil first and then
apply another drop of oil.
Is the objective screwed in tightly? If not, tighten the objective.
If the slide has a coverslip, is there more than one coverslip on the slide? If so,
gently remove the top coverslip.
Has oil seeped into the seal on the oil objective? Examine by removing the objective
and use an inverted eyepiece as a magnifier to check the seal. If the seal is broken,
the objective must be replaced.
Review questions
1. b; 2. c; 3. a; 4. b; 5. c; 6. c; 7. d; 8. a; 9. c; 10. d; 11. b
Chapter 5
Case study
1. This is a systematic error because the magnitude of error remains constant at three
ranges of test results.
2. It is not acceptable to continue using the instrument or to simply subtract the
systematic error from test sample results. All the samples in a two out-of-control test
run must be re-assayed after the error is corrected.
3. Determine from the quality control charts at what moment the error occurred.
Investigate potential changes in instrument settings, calibration, reagent changes, or
instrument malfunction that may have occurred at the time the error was recorded.
Review questions
Chapter 6
Review questions
Chapter 7
Review questions
Chapter 8
Case study
1. When the blood is not well oxygenated, the bone marrow responds by producing
more red blood cells to carry more oxygen.
2. The hormone that stimulates RBC production is erythropoietin (EPO). The
peritubular cells of the kidney detect hypoxia. A hypoxia-sensitive transcription factor
is produced that moves to the peritubular cell nucleus and upregulates transcription
of the EPO gene. EPO acts by preventing apoptosis of the erythroid colony-forming
unit. In RBC precursors, it also shortens the cell cycle time between mitoses and
reduces the number of mitotic divisions; and it promotes early release of
reticulocytes from the bone marrow.
3. Once the patient was receiving oxygen therapy, hypoxia diminished and EPO
production also declined. Thus, production of new RBCs slowed. At the same time,
RBCs reaching 120 days of age were removed from the circulation. Thus the total
number of circulating RBCs decreased.
Review questions
Chapter 9
Case study
Review questions
Chapter 10
Case study
1. The mother’s and infant’s hemoglobin results were within the reference intervals.
(Reference intervals: adult women, 12.0 to 15.0 g/dL; newborns, 16.5 to 21.5 g/dL.)
2. The major hemoglobin at birth is Hb F. It has a high oxygen affinity because it
weakly binds 2, 3-BPG resulting in decreased delivery of oxygen to the tissues. The
hypoxia triggers an increase in secretion of erythropoietin by the fetal kidney, which
results in an increase in the production and release of red blood cells from the fetal
bone marrow. The resultant increase in red blood cell count, hemoglobin
concentration, and hematocrit compensates for the high Hb F oxygen affinity and
reduced oxygen transfer to tissues. The Hb F concentration gradually decreases to
adult physiologic levels by 1 to 2 years of age as most of the Hb F is replaced by Hb
A.
3. The hemoglobin assay measures concentration; high performance liquid
chromatography (and hemoglobin electrophoresis) identifies and quantifies
hemoglobin types.
4. These are the expected results for hemoglobin fractions for a healthy mother and
infant. In the second and third trimesters of fetal life, the α- and γ-globin genes are
activated producing α and γ globin chains that combine to form Hb F. In late fetal life,
γ-β switching begins in which transcription of the β-globin gene begins to be
activated and the γ-globin gene begins to be repressed. With the activation of the β-
globin gene, the β chains combine with the α chains to form Hb A. The Hb F level
decreases from 60% to 90% at birth to 1% to 2% by 1 to 2 years of age, while the Hb
A increases from 10% to 40% at birth to greater than 95% at 1 to 2 years of age and
throughout life. The synthesis of Hb A2begins shortly before birth and remains at less
than 3.5% throughout life.
Review questions
1. d; 2. a; 3. a; 4. a; 5. a; 6. d; 7. c; 8. b; 9. d; 10. b; 11. c
Chapter 11
Case study
1. Iron loss via blood donations and normal physiologic loss was not compensated by
diet or supplementation.
2. Adaptation to the low iron levels. Iron stores of ferritin were mobilized first. But when
storage iron declined, hepcidin levels declined, and as a result, duodenal iron
absorption increased.
3. Ferritin
4. Transferrin saturation reflects the proportion of transferrin binding sites for iron that
are actually filled with iron during transit in the plasma. Transferrin level is an indirect
indicator of the iron storage compartment while serum iron is the transport
compartment, so transferrin saturation effectively reflects both compartments.
Review questions
Chapter 12
Case study
1. The patient had an asthmatic attack. Eosinophils play an important role in the
initiation and maintenance of symptoms. Eosinophils release basic proteins, lipid
mediators, and reactive oxygen species that cause inflammation and damage to the
mucosal cells lining the airway.
2. Eosinophils are typically elevated in the peripheral blood and also in the sputum of
asthmatic patients. The number of eosinophils in the blood correlates with the
severity of the case.
3. IL-5 plays an important role in the differentiation and proliferation of eosinophils.
Monoclonal antibodies to IL-5 block eosinophil development. Since eosinophils are
reduced, the symptoms of asthma are controlled.
Review questions
1. b; 2. d; 3. a; 4. c; 5. b; 6. c; 7. c; 8. a; 9. b; 10. d
Chapter 13
Case study
Review questions
1. d; 2. d; 3. c; 4. b; 5. d; 6. d; 7. a; 8. a; 9. c; 10. d
Chapter 14
Case studies
Case 1
1. HGB × 3 = HCT ± 3
15 × 3 = 45 ± 3 (42−48)
Case 2
1. MCV = 59 fL; MCH = 18.1 pg; MCHC = 30.7 g/dL.
2. Microcytic, hypochromic red blood cells
3. Examine the patient’s peripheral blood film
Case 3
1. The sodium concentration could affect the hematocrit. The sample electrolyte
concentration is used to correct the measured conductivity prior to reporting
hematocrit results. Factors that affect sodium concentration will therefore also affect
the hematocrit.
2. A high sodium concentration would falsely decrease the hematocrit.
3. Factors that decrease the hematocrit by this method are low total protein, settling of
red blood cells in the collection device, presence of cold agglutinins, and specimen
contamination by intravenous solutions.
Review questions
1. b; 2. c; 3. c; 4. d; 5. d; 6. b; 7. c; 8. c; 9. a; 10. d
Chapter 15
Review questions
Chapter 16
Case study
1. d; 2. c; 3. a; 4. c; 5. b; 6. c; 7. a; 8. b; 9. b; 10. a
Chapter 17
Case study
1. Bone marrow cellularity, estimated from the core biopsy specimen, or the aspirate if
a biopsy specimen is unavailable, provides information on blood cell production.
2. The ratio is 9:1, which indicates myeloid hyperplasia.
3. When a bone marrow aspirate or core biopsy specimen is reviewed, the normal
megakaryocyte distribution is 2 to 10 per low-power field. Counts outside these limits
are characterized as decreased or increased megakaryocytes. Megakaryocyte
morphology is also reviewed for diameter, granularity, and nuclear lobularity.
Review questions
1. c; 2. b; 3. c; 4. a; 5. d; 6. c; 7. d; 8. b; 9. b; 10. b; 11. b
Chapter 18
Case study
Review questions
1. b; 2. a; 3. c; 4. b; 5. a; 6. b; 7. c; 8. d; 9. c; 10. a
Chapter 19
Case study
Review questions
1. c; 2. b; 3. d; 4. c; 5. c; 6. b; 7. c; 8. d; 9. b; 10. c; 11. d
Chapter 20
Case study
Review questions
Chapter 21
Case study
1. The complete blood count findings for this patient (notably macrocytic,
normochromic anemia; pancytopenia; hypersegmentation of neutrophils; and oval
macrocytes) were consistent with the physician’s suspicion of megaloblastic anemia
as suggested by the clinical findings.
2. Although the relative reticulocyte count was within the reference interval of 0.5% to
2.5%, and the calculated absolute reticulocyte count (approximately 40 × 109/L) was
within the reference interval of 20 to 115 × 109/L, the calculated reticulocyte
production index was 0.5, which was clearly inadequate to compensate for a
substantial anemia (Chapter 14).
3. The patient’s vitamin assays point to a deficiency of vitamin B12, substantiated by an
increase in serum methylmalonic acid.
4. Based on these results, a test for intrinsic factor blocking antibodies would be
appropriate. However, the physician also inquired further about the patient’s dietary
habits and learned that he enjoyed dishes of raw fish obtained from the surrounding
lakes. Therefore, the physician ordered a stool analysis for ova and parasites. The
study indicated the presence in the stool of both eggs and proglottids of the fish
tapeworm Diphyllobothrium latum. The patient was treated with a suitable purgative,
and the scolex of the tapeworm was discovered in a stool sample after a single
treatment. The patient was counseled on the proper preparation of fresh fish to avoid
reinfection. He received injections of cyanocobalamin to replenish his vitamin
B12stores. His hemoglobin returned to normal over the next month, and his
neurologic symptoms subsided.
Review questions
1. d; 2. c; 3. c; 4. b; 5. a; 6. b; 7. c; 8. d; 9. a; 10. c
Chapter 22
Case study
Review questions
1. c; 2. d; 3. b; 4. d; 5. b; 6. d; 7. c; 8. d; 9. c; 10. d; 11. a
Chapter 23
Case study
1. Intravascular hemolysis is suspected in the patient because the color of the urine
suggests oxidized hemoglobin.
2. Tests for serum haptoglobin, serum unconjugated (indirect) bilirubin, serum lactate
dehydrogenase, plasma hemoglobin, and urine hemoglobin and examination of a
peripheral blood film can differentiate the mechanism of hemolysis as fragmentation
or macrophage-mediated.
3. Due to the likelihood that the patient had hemoglobinuria, fragmentation hemolysis
was suspected. Therefore, the serum haptoglobin would be markedly decreased,
while the serum lactate dehydrogenase and plasma hemoglobin levels would be
increased, if measured. Routine urinalysis should yield positive results for blood on
the test strip with no intact red blood cells in the urine sediment. The serum indirect
bilirubin does not increase immediately after an episode of intravascular hemolysis,
but should begin to increase within several days. The peripheral blood film may
demonstrate schistocytes immediately, but reticulocytosis several days later.
Review questions
1. a; 2. b; 3. d; 4. b; 5. c; 6. a; 7. d; 8. b; 9. c; 10. c
Chapter 24
Case study
1. On the basis of the patient’s jaundice and splenomegaly, history of gallstones, family
history of anemia, low hemoglobin, increased mean cell hemoglobin concentration
and red cell distribution width, and spherocytes and polychromasia on the peripheral
blood film, hereditary spherocytosis (HS) is suspected.
2. Additional laboratory tests to confirm HS should demonstrate increased hemolysis
(increased serum indirect bilirubin level and lactate dehydrogenase activity,
decreased serum haptoglobin level), increased erythropoiesis to compensate for the
premature hemolysis (increased reticulocyte count), and the nonimmune nature of
the hemolysis (negative result on the direct antiglobulin test). Testing family
members to establish a mode of inheritance is desirable. The osmotic fragility test is
expected to show increased fragility and the eosin-5’-maleimide (EMA) binding test
is expected to show low mean fluorescence intensity of the red blood cells when
measured in a flow cytometer. However, special tests are not required for diagnosis
of HS in a patient with a familial inheritance pattern and the typical clinical and
laboratory findings.
3. HS is an inherited intrinsic hemolytic anemia caused by a mutation that disrupts the
vertical protein interactions in the red blood cell (RBC) membrane. Various mutations
in five known genes can result in the HS phenotype. The defective membrane
protein causes the RBCs to lose unsupported lipid membrane over time due to a
local disconnection between transmembrane proteins and the cytoskeleton. The loss
of membrane with minimal loss of cell volume results in a decreased surface area-to-
volume ratio and the formation of spherocytes. Spherocytes do not have the
deformability of normal biconcave discoid RBCs. As the cells repeatedly go through
the spleen, they lose more membrane due to splenic conditioning and eventually
become trapped in the spleen and removed by the splenic macrophages. The RBC
membrane also has abnormal permeability to cations, particularly sodium and
potassium, likely due to the disruption of the cytoskeleton by the mutated protein.
Review questions
1. b; 2. a; 3. a; 4. b; 5. a; 6. d; 7. a; 8. b; 9. b; 10. a; 11. d
Chapter 25
Case study
1. Many malarial ring forms, with multiple ring forms in individual red blood cells
(RBCs), are present in the thin peripheral blood film. Many ring forms and a
crescent-shaped gametocyte are also present in the thick peripheral blood film.
2. The high parasitemia, the presence of multiple ring forms in individual RBCs, the
crescent-shaped gametocyte on the thick film, and the absence of other parasite
stages in the thin and thick peripheral blood films suggest a diagnosis of malaria due
to Plasmodium falciparum.
3. The patient had typical symptoms of malaria after a recent 3-week trip to Ghana in
West Africa. Malaria is endemic in Ghana, and according to the Centers for Disease
Control and Prevention, 52most of the malaria cases in Ghana are due to P.
falciparum.
4. The only forms of P. falciparumthat are seen on a peripheral blood film are ring
forms and gametocytes, and the latter are characteristically crescent-shaped.
5. Anemia in malaria is due to direct lysis of infected RBCs during schizogony; immune
destruction of infected and noninfected RBCs by macrophages in the spleen; and
inhibition of erythropoiesis and ineffective erythropoiesis.
Review questions
1. c; 2. a; 3. b; 4. b; 5. c; 6. b; 7. c; 8. c; 9. c; 10. d; 11. c
Chapter 26
Case study
Review questions
1. b; 2. a; 3. a; 4. d; 5. d; 6. d; 7. a; 8. c; 9. c; 10. c; 11. c
Chapter 27
Case study
Review questions
Chapter 28
Case study
Review questions
Chapter 29
Case studies
Case 1
Case 2
1. Because of the reactive monocytosis, the blood film should be examined for possible
circulating macrophages.
2. On the edges of the blood film, because macrophages are very large cells.
3. Circulating macrophages indicate sepsis.
4. A buffy coat preparation, which concentrates nucleated cells.
Review questions
1. a; 2. d; 3. c; 4. b; 5. d; 6. c; 7. d; 8. c; 9. b; 10. c
Chapter 30
Case study
Review questions
1. c; 2. d; 3. a; 4. d; 5. a; 6. c; 7. d; 8. c; 9. c; 10. b
Chapter 31
Case study
1. DNA isolation for the detection of inherited mutations requires whole blood collected
in a lavender stopper tube containing EDTA to preserve white blood cells.
2. The correct controls are present and include a positive control (Lane B), a negative
control (Lane D), and a “no-DNA” control (Lane E). The no-DNA control is essential
when any polymerase chain reaction (PCR) test is performed in the clinical
laboratory. This control will demonstrate whether cross-contamination occurred
during the setup of the PCR procedure. The no-DNA control region of the gel should
lack a banding pattern, as seen in Figure 31-1. If a banding pattern is present in the
no-DNA control region or this control is missing, the test must be repeated before
reporting patient results.
3. Bands in the patient’s sample (Lane C) appear at 141, 104, and 82 bp.
4. The following band sizes are expected in factor V Leiden DNA analysis:
Normal: 104 and 82 bp (37 bp is sometimes barely visible, as well)
Heterozygous: 141, 104, and 82 bp (37 bp is sometimes barely visible, as well)
Homozygous: 141 and 82 bp
5. The three bands in the patient sample indicate that this patient is heterozygous for
the factor V Leiden mutation.
Review questions
1. d; 2. b; 3. d; 4. b; 5. b; 6. c; 7. a; 8. a; 9. b; 10. b
Chapter 32
Case studies
Case 1
1. The lymphoid population is the most prominent. Forward scatter demonstrates small
to medium-sized cells. These cells are characterized by low side scatter indicative of
sparse agranular cytoplasm.
2. The majority of cells express CD19, CD10, and κ light chain. There is also a small
population of T cells positive for CD5 and negative for CD19 antigen.
3. Prominent κ light chain expression indicates a monoclonal B-cell population that is
characteristic of lymphoma.
Case 2
1. The low density of CD45 antigen coupled with relatively low side scatter is
characteristic of a blast population. Such a prominent blast population can only be
seen in acute leukemias.
2. The expression of immature markers (CD34 and HLA-DR) coupled with positivity for
myeloid and megakaryoblastic antigens (CD33, CD41, and CD61) is seen in acute
megakaryoblastic leukemias.
Review questions
1. c; 2. b; 3. a; 4. d; 5. b; 6. a; 7. a; 8. a; 9. c; 10. a; 11. b
Chapter 33
Case study
1. An elevated white blood cell (WBC) count with a left shift suggests a
myeloproliferative neoplasm or a leukemoid reaction (reactive neutrophilia).
However, in this patient the WBC count was extremely elevated, the left shift was
rather deep (presence of promyelocytes and blasts), and basophilia was present,
which suggests that a myeloproliferative neoplasm is likely present. Chronic
myelogenous leukemia (CML) is the most likely cause of these laboratory findings.
2. The leukocyte alkaline phosphatase (LAP) score is low in CML due to inappropriate
LAP synthesis in the secondary granules, whereas LAP is elevated in bacterial
infections due to activation of enzyme synthesis.
3. The BCR/ABL1fusion gene must be identified to confirm the diagnosis of
CML. BCR/ABL1can be demonstrated from a karyotype analysis showing the t(9;22)
reciprocal translocation known as the Philadelphia chromosome (Chapter 30), by
demonstration of the BCR/ABL1 fusion gene using fluorescence in situ hybridization
(Chapter 30), or by demonstration of the BCR/ABL1 fusion mRNA by qualitative
reverse transcriptase polymerase chain reaction (Chapter 31). Patients who have
complete blood count and differential results that resemble those in CML but test
negative for BCR/ABL1 are considered to have atypical CML, and the disorder is
classified as myelodysplastic syndrome/myeloproliferative neoplasm (Chapter 34).
4. Cytogenetic studies are likely to show the t(9;22) mutation.
5. The t(9;22) translocation produces the BCR/ABL1chimeric gene, which is observed
in four primary molecular forms that produce three versions of the BCR/ABL chimeric
protein: p190, p210, and p230.
6. First-line therapy for CML is the tyrosine kinase inhibitor imatinib mesylate
(Gleevec). Allogeneic stem cell transplantation should be considered for all CML
patients, because it is the only potentially curative treatment for CML. However, few
CML patients qualify for allogeneic stem cell transplantation, because most do not
meet the criteria for low risk: age younger than 40 years, disease in the chronic
phase, transplantation within 1 year of diagnosis, and availability of an HLA-matched
donor. For those patients who qualify for allogeneic stem cell transplantation,
imatinib is used to induce remission prior to transplant, to treat minimum residual
disease, and to provide rescue therapy if the transplant fails. Imatinib is continued as
lifelong therapy until drug resistance is detected.
7. The majority of cases of imatinib resistance result from two primary causes:
acquisition of additional BCR/ABL1mutations and expression of point mutations in
the adenosine triphosphate (ATP) binding site. Additional BCR/ABL1mutations can
occur through the usual translocation of the remaining unaffected chromosomes 9
and 22, which converts the hematopoietic stem cell from heterozygous to
homozygous for the BCR/ABL1 mutation. A double dose of BCR/ABL1 can also be
acquired from gene duplication during mitosis and accounts for 10% of secondary
mutations. An additional BCR/ABL1 mutation will double the tyrosine kinase activity,
which makes the imatinib dosage inadequate. In these cases higher dosages of
imatinib will restore remission in most patients. Over 60 mutations have been
identified in the ATP binding site, and these account for the remaining 50% to 90%
of secondary mutations. Mutations in the ATP binding site reduce the binding affinity
of imatinib, producing some level of resistance.
Review questions
1. b; 2. c; 3. d; 4. c; 5. c; 6. c; 7. b; 8. d; 9. a; 10. c
Chapter 34
Case study
Review questions
1. d; 2. a; 3. b; 4. b; 5. c; 6. c; 7. a; 8. d; 9. c; 10. c
Chapter 35
Case study
1. Due to the presence of blasts on the peripheral blood film, the most likely diagnosis
is acute leukemia. The thrombocytopenia and anemia support that diagnosis.
According to the WHO classification, ≥ 20% blasts in the bone marrow is required for
diagnosis of acute leukemia; an exception to this criterion are those cases that have
specific genetic abnormalities (delineated in the WHO classification) that are
diagnostic, regardless of blast count. Acute lymphoblastic leukemia (ALL) is more
common in children. Immunophenotyping by flow cytometry determines the lineage
and maturation stage of the blasts. Testing for genetic abnormalities is required for
diagnosis and prognosis.
2. This child has clinical and laboratory features indicative of a favorable prognosis:
young age, a white blood cell count less than 20 x 109/L (i.e., low tumor burden), and
hyperdiploidy. The strongest predictor of patient outcome is the presence of certain
genetic abnormalities; the immunophenotype also contributes to the prognosis.
3. Hyperdiploidy carries a favorable prognosis in B-cell ALL in children.
Review questions
Chapter 36
Case study
Review questions
1. d; 2. c; 3. d; 4. d; 5. b; 6. b; 7. b; 8. a; 9. c; 10. a
Chapter 37
Case study
1. Given the family history, this may be an inherited condition, although pregnancy is
an independent risk factor for thrombosis.
2. Thrombosis is probably caused by the deficiency of a coagulation inhibitor such as
protein C, protein S, or antithrombin. It may be caused by a procoagulant gain-of-
function mutation such as the factor V Leiden mutation or the prothrombin G20210A
mutation.
Review questions
1. b; 2. c; 3. b; 4. d; 5. b; 6. d; 7. b; 8. c; 9. a; 10. a
Chapter 38
Case study
In advanced liver disease, poor liver circulation causes pressure in the portal
circulation. This enlarges the spleen (splenomegaly). The enlarged spleen
sequesters and clears platelets more rapidly than normal, a condition
called hypersplenism, which causes thrombocytopenia. In most cases,
platelet function is reduced. This reduced platelet function can be
demonstrated in the laboratory using platelet aggregometry and is the
reason for the patient’s epistaxis.
2. In early liver disease the vitamin K–dependent factors II (prothrombin), VII, IX, and X
are produced with diminished function. This can be corrected with a trial dose of oral
or intravenous vitamin K. In people with true vitamin K deficiency secondary to an
altered diet, the vitamin K therapy corrects bleeding and normalizes the PT and PTT,
but in liver disease vitamin K may not have a lasting effect. This is because the liver
cannot process the vitamin K normally.
Review questions
1. c; 2. d; 3. b; 4. c; 5. b; 6. b; 7. d; 8. a; 9. a; 10. c; 11. c
Chapter 39
Case study
1. The following tests for congenital and acquired risk factors are included in a
thrombophilia profile. Results for the items with asterisks are valid only when the test
is performed 10 to 14 days after termination of antithrombotic therapy or resolution of
a thrombotic event.
Homocysteine
Lupus anticoagulant profile*
Prothrombin G20210A mutation
Activated protein C resistance*
Factor V Leiden mutation (confirmatory for activated protein C resistance)
Anticardiolipin antibodies by immunoassay
Protein C functional assay and follow-up immunoassay*
Protein S functional assay and follow-up immunoassay*
Antithrombin functional assay and follow-up immunoassay*
2. The most common acquired thrombotic risk factors are antiphospholipid antibodies
and lupus anticoagulant, and these are most often implicated in a thrombotic event.
3. Patients with thrombotic risk factors may be instructed to avoid situations and
practices that may trigger thrombosis, such as immobilization, smoking, and use of
oral contraceptives or hormone replacement therapy. They may be provided with
prophylactic antithrombotic therapy at times when circumstances increasing
thrombotic risk cannot be avoided, such as when undergoing orthopedic surgery.
Review questions
Chapter 40
Case study
Review questions
1. b; 2. d; 3. b; 4. c; 5. b; 6. b; 7. b; 8. c; 9. d; 10. a
Chapter 41
Case study
1. Storage pool disease, aspirin-like defects, and use of antiplatelet agents such as
aspirin are possibilities.
2. Storage pool disease or aspirin-like defects seem most likely.
3. Based on the results of the quantitative test for adenosine triphosphate release, the
likely cause is dense granule storage pool disease.
Review questions
1. d; 2. a; 3. a; 4. b; 5. c; 6. c; 7. d; 8. b; 9. d; 10. a
Chapter 42
Case study
1. The laboratory director questioned the phlebotomist about the problem. The
phlebotomist admitted that he had erroneously collected blood in a red- and gray-
stoppered “tiger-top” tube and, responding to the patient’s remark, had immediately
poured the blood into a blue-stoppered tube for analysis. He thought the specimen
would be okay because it had not clotted yet.
2. The red and gray marbleized stopper designates a serum separator tube. The
phlebotomist poured the blood into the blue-stoppered tube before it had begun to
clot; however, the activator from the tiger-top tube shortened the clotting time on the
prothrombin time (PT) test, thus causing an erroneously short PT and low
international normalized ratio (INR).
3. Unexpectedly short PTs during oral anticoagulant therapy are generally indicators of
patient non-compliance to the drug regimen. The second most common
circumstance that affects the PT is dietary changes, most often an increased intake
of vitamin K–rich foods such as green leafy vegetables, liver, or avocado. In this
instance the patient had been fully compliant, carefully following the prescribed
dosage and timing, and her diet had not changed. These facts led the laboratory
director to consider a specimen collection error.
Review questions
Chapter 43
Case study
Review questions
Chapter 44
Case study
1. No. The description of the sample and the instrument flags indicating lipemia should
alert the operator to a potentially invalid test result because lipemia is known to
cause erroneous results on some photo-optical coagulation analyzers.
2. Two options are available to negate the effect of the lipemia and obtain valid test
results:
3. Remove the lipids from the plasma by high-speed centrifugation or
ultracentrifugation.
4. Perform testing using an endpoint detection method that is not susceptible to lipemia
in the sample, such as mechanical clot detection.
5. Because the patient history includes previous surgical procedures without bleeding
symptoms and there is no other indication of abnormal bleeding tendencies for this
patient, it is probably safe to consider that the prolonged prothrombin time and
activated partial thromboplastin time results are due to the lipemic nature of the
sample. The patient would most likely not be at risk for bleeding during the surgery,
and it would be anticipated that repeat testing using one of the options listed
previously would yield test results within the reference interval.
Review questions
1. b; 2. d; 3. a; 4. c; 5. b; 6. c; 7. c; 8. a; 9. d; 10. a
Chapter 45
Case study
1. Yes, the newborn reference interval for hemoglobin is 16.5 to 21.5 g/dL and for the
hematocrit is 48% to 68%.
2. These values are normal for newborns. Erythrocytes of a newborn are markedly
macrocytic. There may be 2 to 24 nucleated red blood cells on the first postnatal
day, but they are not present by day 5. The polychromasia reflects the reticulocytosis
that persists for about 4 days.
3. These values are within the reference intervals for newborns. The white blood cell
count of a newborn fluctuates a great deal with a reference interval of 9.0 to 37.0 ×
109/L, and leukocytosis without evidence of infection is common. The differential may
show an increase in neutrophils rather than the lymphocyte predominance seen after
2 weeks. In this case the neutrophils and lymphocytes were present in equal
amounts, but no immature neutrophils were seen.