Haematology

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What effect could cold agglutinin disease have on a routine full blood count? (1 mark)
, it can cause hemolytic anemia and lead to a low RBC count and hemoglobin.

Cold Agglutinins
Why Get Tested?
To help determine the cause of hemolytic anemia; to help diagnose cold agglutinin disease

When To Get Tested?

When you have symptoms associated with anemia and/or pain, pale skin, and bluing in the fingers,
toes and tips of the ears that occurs after exposure to cold temperatures; when you have been
diagnosed with hemolytic anemia and your healthcare practitioner is investigating the cause

Sample Required?
A blood sample drawn from a vein in your arm

Test Preparation Needed?

None
What is being tested?

Cold agglutinins are autoantibodies produced by a person's immune system that mistakenly target
red blood cells (RBCs). They cause RBCs to clump together when a person is exposed to cold
temperatures and increase the likelihood that the affected RBCs will be destroyed by the body. This
test detects and measures the amount of cold agglutinins in the blood.

When the presence of cold agglutinins in a person's blood leads to significant RBC destruction, it can
cause hemolytic anemia and lead to a low RBC count and hemoglobin. This rare form of autoimmune
hemolytic anemia is known as cold agglutinin disease. Cold agglutinin disease may be primary or
secondary, induced by some other disease or condition.
Primary cold agglutinin disease typically affects those who are middle age to elderly, and it tends
to continue over time (chronic). Secondary cold agglutinin disease may affect anyone and may be
acute or chronic, temporary or persistent. It may cause hemolytic anemia to a greater or lesser
degree and is associated with a variety of conditions. For details see the "What does the test
result mean?" section in Common Questions below.

The cold agglutinin test is not routinely ordered. It is a test that has been available for a long time,
but it has become less commonly used as more specific tests for secondary causes, such as
Mycoplasma pneumoniae infection, have become available.
How is it used?

A cold agglutinin test may be used to help detect cold agglutinin disease and determine the
cause of a person's hemolytic anemia. It may be used as a follow-up test after a complete
blood count (CBC) shows a decrease in a person's red blood cell (RBC) count and
hemoglobin, especially if these findings are linked to an exposure to cold temperatures.

Cold agglutinin disease is a rare autoimmune disorder in which autoantibodies produced by a

person's immune system mistakenly target and destroy RBCs, causing hemolytic anemia.
These autoantibodies are cold-reacting and can cause signs and symptoms related to anemia
after an affected person is exposed to cold temperatures. This disease may be classified as
either primary or secondary, triggered by an infection or other condition.
When is it ordered?
This test may be ordered when a person has reactions to cold temperature
exposures and has signs of hemolytic anemia that may be due to cold agglutinin
disease. Symptoms may include:

•Fatigue, weakness, lack of energy, pale skin (pallor), dizziness and/or headaches
from anemia
•In some cases, painful bluish fingers, toes, ears, and the tip of the nose that
occur with exposure to cold temperatures
What does the test result mean?

The result of a cold agglutinin test is typically reported as a titer, such as 1:64 or 1:512. A
higher number means that there are more autoantibodies present.
A positive titer may mean that the person tested has cold agglutinin disease. Cold agglutinin
disease may be primary or secondary, induced by some other disease or condition such as:
•Mycoplasma pneumoniae infections—up to 75% of those affected will have increased cold
agglutinins.
•Mono (infectious mononucleosis)—more than 60% of those affected will have increased
cold agglutinins, but anemia is rare with this infection.
•Some cancers, including lymphoma, leukemia, and multiple myeloma
•Some other bacterial infections, such as Legionnaires disease and syphilis
•Some parasitic infections, such as malaria
•Some viral infections such as HIV, influenza, CMV, EBV, hepatitis C
Higher titers of autoantibodies and those that react at warmer temperatures are
associated with hemolytic anemia and worse symptoms.
The degree of red blood cell (RBC) hemolysis and hemolytic anemia will vary
from person to person and with each episode of cold exposure. Some conditions,
such as infectious mononucleosis, are frequently associated with elevated cold
agglutinins but rarely associated with anemia.
What does the D-Dimer test indicate? (1 mark)
Intravascular clotting (measures the breakdown products of cross-linked fibrin), but it
can’t pinpoint the location of the cause. D-dimer test is highly elevated in
disseminated intravascular coagulation (DIC).
What does the D-Dimer test indicate?
The level of D-dimer in the blood can significantly rise when there is significant formation and
breakdown of fibrin clots in the body.
help diagnose disseminated intravascular coagulation (DIC)
•Deep vein thrombosis (DVT)
•Pulmonary embolism (PE)
•Stroke
D-dimer
Why Get Tested?
To help rule out clotting (thrombotic) episodes and to help diagnose conditions related to thrombosis
When To Get Tested?
When you have symptoms of a blood clot or a condition that causes
inappropriate blood clots, such as deep vein thrombosis (DVT), pulmonary
embolism (PE), or disseminated intravascular coagulation (DIC), and to
monitor treatment of DIC and excessive clotting conditions
Sample Required?
A blood sample drawn from a vein in your arm
Test Preparation Needed?
None
What is being tested?

D-dimer is one of the protein fragments produced when a blood clot gets dissolved in the body. It is
normally undetectable or detectable at a very low level unless the body is forming and breaking
down blood clots. Then, its level in the blood can significantly rise. This test detects D-dimer in the
blood.

When a blood vessel or tissue is injured and begins to bleed, a process called hemostasis is
initiated by the body to create a blood clot to limit and eventually stop the bleeding. This process
produces threads of a protein called fibrin, which crosslink together to form a fibrin net. That net,
together with platelets, helps hold the forming blood clot in place at the site of the injury until it
heals.
Once the area has had time to heal and the clot is no longer needed, the body uses an enzyme called
plasmin to break the clot (thrombus) into small pieces so that it can be removed. The fragments of the
disintegrating fibrin in the clot are called fibrin degradation products (FDP), which consist of variously
sized pieces of crosslinked fibrin. One of the final fibrin degradation products produced is D-dimer,
which can be measured in a blood sample when present. The level of D-dimer in the blood can
significantly rise when there is significant formation and breakdown of fibrin clots in the body.

For a person who is at low or intermediate risk for blood clotting (thrombosis) and/or
thrombotic embolism, the strength of the D-dimer test is that it can be used in a
hospital emergency room setting to determine the likelihood of a clot's presence. A
negative D-dimer test (D-dimer level is below a predetermined cut-off threshold)
indicates that it is highly unlikely that a thrombus is present. However, a positive D-
dimer test cannot predict whether or not a clot is present. It indicates that further
diagnostic procedures are required (e.g., ultrasound, CT angiography).
There are several factors and conditions associated with inappropriate blood clot formation. One of
the most common is deep vein thrombosis (DVT), which involves clot formation in veins deep within
the body, most frequently in the lower legs. These clots may grow very large and block blood flow in
the legs, causing swelling, pain, and tissue damage. It is possible for a piece of the clot to break off
and travel to other parts of the body. This "embolus" can lodge in the lungs, causing a pulmonary
embolus or embolism (PE). Pulmonary embolisms from DVT affect more than 300,000 people in the
U.S. each year.

While clots most commonly form in the veins of the legs, they may also form in other areas as well.
Measurements of D-dimer can be used to help detect clots in any of these sites. For example, clots
in coronary arteries are the cause of myocardial infarction (heart attacks). Clots may form on the
lining of the heart or its valves, particularly when the heart is beating irregularly (atrial fibrillation) or
when the valves are damaged. Clots can also form in large arteries as a result of narrowing and
damage from atherosclerosis. Pieces of such clots may break off and cause an embolus that blocks
an artery in another organ, such as the brain (causing a stroke) or the kidneys.
Measurements of D-dimer may also be ordered, along with other tests, to help diagnose
disseminated intravascular coagulation (DIC). DIC is a condition in which clotting factors are
activated and then used up throughout the body. This creates numerous tiny blood clots and at
the same time leaves the affected person vulnerable to excessive bleeding. It is a complex,
sometimes life-threatening condition that can arise from a variety of situations, including some
surgical procedures, sepsis, poisonous snake bites, liver disease, and after childbirth. Steps are
taken to support the affected person while the underlying condition resolves. The D-dimer level
will typically be very elevated in DIC.
How is the test used?
D-dimer tests are used to help rule out the presence of an inappropriate blood clot
(thrombus). Some of the conditions that the D-dimer test is used to help rule out
include:
•Deep vein thrombosis (DVT)
•Pulmonary embolism (PE)
•Stroke
This test may be used to determine if further testing is necessary to help diagnose
diseases and conditions that cause hypercoagulability, a tendency to clot
inappropriately.
A D-dimer level may be used to help diagnose disseminated intravascular coagulation
(DIC) and to monitor the effectiveness of DIC treatment.
When is it ordered?
D-dimer testing is often ordered when someone goes to the emergency room with
symptoms of a serious condition (e.g., chest pain and difficulty in breathing).
A D-dimer test may be ordered when someone has symptoms of deep vein
thrombosis, such as:
•Leg pain or tenderness, usually in one leg
•Leg swelling, edema
•Discoloration of the leg
It may be ordered when someone has symptoms of pulmonary embolism such as:
•Sudden shortness of breath, labored breathing
What does the test result mean?

A normal or "negative" D-dimer result (D-dimer level is below a predetermined cut-off threshold) means
that it is most likely that the person tested does not have an acute condition or disease causing abnormal
clot formation and breakdown. Most health practitioners agree that a negative D-dimer is most valid and
useful when the test is done for people who are considered to be at low to moderate risk for thrombosis.
The test is used to help rule out clotting as the cause of symptoms.
A positive D-dimer result may indicate the presence of an abnormally high level of fibrin degradation
products. It indicates that there may be significant blood clot (thrombus) formation and breakdown in the
body, but it does not tell the location or cause. For example, it may be due to a venous thromboembolism
(VTE) or disseminated intravascular coagulation (DIC). Typically, the D-dimer level is very elevated in
DIC.
However, an elevated D-dimer does not always indicate the presence of a clot because a number of
other factors can cause an increased level. Elevated levels may be seen in conditions in which fibrin is
formed and then broken down, such as recent surgery, trauma, infection, heart attack, and some cancers
or conditions in which fibrin is not cleared normally, such as liver disease. Therefore, D-dimer is typically
not used to rule out VTE in hospitalized patients (inpatient setting).
Fibrin is also formed and broken down during pregnancy, so that may result in an elevated D-dimer
level. However, if DIC is suspected in a woman who is pregnant or is in the immediate postpartum
period, then the D-dimer test may be used, along with a PT, PTT, fibrinogen, and platelet count to
help diagnose her condition. If the woman has DIC, her D-dimer level will be very elevated.

D-dimer is recommended as an adjunct test. Since D-dimer is a sensitive test but has a poor
specificity, it should only be used to rule out deep vein thrombosis (DVT), not to confirm a diagnosis.
It should not be used for pulmonary embolism when the clinical probability of that condition is high.
Both increased and normal D-dimer levels may require follow-up and can lead to further diagnostic
testing. People with positive D-dimer tests and those with moderate to high risk for DVT require
further study with diagnostic imaging (e.g., CT angiography).
When used to monitor DIC treatment, decreasing levels indicate that treatment is effective while
increasing levels may indicate that treatment is not working.
What are some common risk factors for inappropriate blood clotting?

Some risk factors include:

•Major surgery or trauma
•Hospitalization or living in a nursing home
•Prolonged immobility—this can include long trips by plane, car, etc. or prolonged bed rest
•Use of birth control or hormone replacement therapy
•Broken bone, cast
•Pregnancy or recent childbirth
•Antiphospholipid syndrome
•Certain cancers
•Inherited clotting disorder such as factor V Leiden mutation
•History of prior venous thromboembolism (VTE)
•Obesity
•Smoking
What test would you use to distinguish Auto-Immune Haemolytic Anaemia from
Hereditary Spherocytosis? (1 mark) Coomb’s test

What laboratory studies should you request to help confirm the diagnosis? How should you interpret
the results?
Initial laboratory studies should include a CBC with attention to red cell morphology, a reticulocyte
count, serum bilirubin, and a direct antiglobulin test (DAT). A mild to moderate anemia with
hemoglobin ranging from 9-12 gm/dl is most commonly encountered. An elevated reticulocyte count
is usual. The DAT is negative in HS, HE and HPP.
Red cell morphology may be strikingly abnormal with numerous spherocytes, elliptocytes, or more
bizarre shaped red cells with fragmentation and budding characteristic of HPP.
While red cell morphology is variable, typically HS patients will have easily identifiable spherocytes
lacking a central pallor, and polychromasia reflecting the reticulocytosis on the blood smear. Mean
corpuscular hemoglobin concentration (MCHC) is increased (35-38%) in approximately 50% of
patients. Mean corpuscular volume (MCV) is usually normal except in cases of severe HS when the
MCV may be mildly decreased.
An incubated Osmotic Fragility test (at 37°C for 24 hours) is considered the standard test in diagnosing
HS. Spherocytes have increased fragility at higher than normal saline concentrations. Limitation of the
osmotic fragility test is poor sensitivity in the mild form of HS. Increased RBC osmotic fragility may also
be seen in other conditions where spherocytes are present. Therefore, it is important that autoimmune
hemolytic anemia caused by warm (IgG) or cold (IgM) autoantibody is excluded. In neonates, ABO
incompatibility must also be considered. The DAT should be positive in autoimmune hemolysis and in
ABO incompatibility.

Diagnosis of HS in the neonate may be difficult for several reasons. Splenomegaly is infrequent,
reticulocytosis is variable, spherocytes are commonly seen on neonatal blood smears without disease,
and neonatal blood cells are more osmotically resistant rendering the Osmotic Fragility Test less
reliable for diagnosis in neonates. Therefore, testing should be postponed until the child is at least 6
months of age or older, unless the need for diagnosis is urgent.

Specialized testing is available for difficult cases but is not routinely performed. Examples include
structural and functional studies of erythrocyte membrane proteins, use of an ektacytometer to study
membrane rigidity and fragility, cDNA and genomic DNA analysis to obtain a molecular diagnosis.
What test would you use to distinguish Auto-Immune Haemolytic Anaemia
from Hereditary Spherocytosis? (1 mark) Direct antiglobulin test (DAT) or
coombs test.
Glucose-6-phosphate dehydrogenase deficiency can lead to which haematological
syndrome ?
Non autoimmun syndrome.
Haemolytic anaemia.
G6PD

Why Get Tested?

To determine whether you have an inherited G6PD deficiency

When To Get Tested?

When a child experienced persistent jaundice as a newborn for unknown reasons; when
you have had one or more intermittent bouts of hemolytic anemia that may be triggered
by an infection or certain medications

Sample Required?
A blood sample drawn from a vein in your arm, by fingerstick, or by heelstick (newborns)

Test Preparation Needed?

Generally, none; however, if symptoms are acute, it is advised that you wait to be tested
for at least several weeks after the episode has resolved.
What is being tested?
Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme involved in energy production. It is
found in all cells, including red blood cells (RBCs) and helps protect them from certain toxic by-
products of cellular metabolism. A deficiency in G6PD causes RBCs to become more vulnerable to
breaking apart (hemolysis) under certain conditions. This test measures the amount of G6PD in
RBCs to help diagnose a deficiency.

G6PD deficiency is a genetic disorder. When individuals who have inherited this condition are
exposed to a trigger such as stress, an infection, certain drugs or other substance(s), significant
changes occur in the structure of the outer layer (cell membrane) of their red blood cells.
Hemoglobin, the life-sustaining, oxygen-transporting protein within RBCs, forms deposits
(precipitates) called Heinz bodies. Some individuals may experience these reactions when exposed
to fava beans, a condition called "favism." With these changes, RBCs can break apart more readily,
causing a decrease in the number of RBCs. When the body cannot produce sufficient RBCs to
replace those destroyed, hemolytic anemia results and the individual may develop jaundice,
weakness, fatigue, and/or shortness of breath.
Since women have two X sex chromosomes, they inherit two copies of the G6PD gene. Women with
only one mutated gene (heterozygous) produce enough G6PD that they usually do not experience
any symptoms (i.e., asymptomatic), but under situations of stress, they may demonstrate a mild form
of the deficiency. In addition, a mother may pass the single mutated gene to any male children.
Rarely do women have two mutated gene copies (homozygous), which could result in G6PD
deficiency.
G6PD deficiency is a common cause of persistent jaundice in newborns. If left untreated, this can
lead to significant brain damage and mental retardation.

G6PD deficiency is the most common enzyme deficiency in the world, affecting more than 400
million people. It may be seen in up to 10% of African-American males and 20% of African males. It
is also commonly found in people from the Mediterranean and Southeast Asia.
G6PD deficiency is inherited, passed from parent to child, due to mutations or changes in the G6PD
gene that cause decreased enzyme activity. There are over 440 variants of G6PD deficiency. The
G6PD gene is located on the sex-linked X chromosome. Since men have one X and one Y sex
chromosome, their single X chromosome carries the G6PD gene. This may result in a G6PD
deficiency if a male inherits the single X chromosome with an altered gene.
Most people with G6PD deficiency can lead fairly normal lives, but there is no specific treatment apart
from prevention. They must be cautious and avoid certain medications such as aspirin,
phenazopyridine and rasburicase, antibiotics with "sulf" in the name and dapsone, anti-malarial drugs
with "quine" in the name, foods such as fava beans, and chemical substances such as naphthalene
(found in moth balls). Note that fava beans, often called broad beans, are commonly grown in the
Mediterranean area. Acute viral and bacterial infections can also initiate episodes of hemolytic anemia
as well as elevated levels of acid in the blood (i.e., acidosis). Individuals should consult with their
healthcare practitioner to get a comprehensive list of these triggers. A good starting point is the list
found on the G6PD Deficiency Favism Association website.

With hemolytic anemia, RBCs are destroyed at an accelerated rate and the person affected becomes
pale and fatigued (anemic) as their capacity for providing oxygen to their body decreases. In severe
cases of RBC destruction, jaundice can also be present. Most of these episodes are self-limiting, but if
a large number of RBCs are destroyed and the body cannot replace them fast enough, then the
affected person may require a blood transfusion. This condition can be fatal if not treated. A small
percentage of those affected with G6PD deficiency may experience chronic anemia.
How is it used?

Glucose-6-phosphate dehydrogenase (G6PD) enzyme testing is used to screen for and

help diagnose G6PD deficiencies. It may be used to screen children who had unexplained
persistent jaundice as a newborn. Currently, newborns are not routinely screened for
G6PD deficiency; however, this is dependent upon the specific state that provides the
testing. According to the National Newborn Screening and Genetics Resource Center, as
of November 2014, two states provide G6PD testing as part of their newborn screening
panel: Pennsylvania and the District of Columbia.

G6PD is an enzyme found in all cells, including red blood cells (RBCs), and helps protect
them from certain toxic by-products of cellular metabolism. A deficiency in G6PD causes
RBCs to become more vulnerable to breaking apart (hemolysis) under certain conditions.
(For more on this, see the "What is being tested?" section.)
G6PD testing may also be used to help establish a diagnosis for people of any age who
have had unexplained episodes of hemolytic
When is it ordered?

G6PD enzyme testing is primarily performed when an individual has signs and symptoms associated
with hemolytic anemia. Testing may be done when someone has had an episode of increased RBC
destruction but after the crisis has resolved. Some signs and symptoms include:
•Fatigue, weakness
•Pale skin (pallor)
•Fainting
•Shortness of breath
•A rapid heart rate
•Jaundice
•Red or brown urine (from the presence of blood/hemoglobin)
•Enlarged spleen
Testing may also be done when other laboratory test results are consistent with a hemolytic anemia.
These may show increased bilirubin concentrations (bulirubinemia), hemoglobin in the urine
(hemoglobinuria), decreased RBC count and haptoglobin levels, increased reticulocyte count and
lactate dehydrogenase levels, presence of bite cells on a blood smear, and sometimes the presence of
Heinz bodies inside the RBCs on a specially stained blood smear.
G6PD activity testing is typically ordered when other causes of anemia and jaundice have been ruled
out and several weeks after an acute incident has been resolved.
If available, screening may be performed on a newborn in the first day or two after birth.
What does the test result mean?

A low level of G6PD enzyme indicates a deficiency. An affected person is more likely to
experience symptoms when exposed to a trigger. The results, however, cannot be used to predict
how an affected person will react in a given set of circumstances. The severity of symptoms will
vary from person to person and from episode to episode.
A normal G6PD enzyme level in a male indicates that it is unlikely he has a deficiency, and if
anemia is present, it is likely due to another cause. However, if the test was performed during an
episode of hemolytic anemia, it should be repeated several weeks later when the RBC population
has had time to replenish and mature.
Women who are carriers, having one mutated and one normal gene copy (heterozygous), will
have some RBCs that are G6PD-deficient and some that are not. These women will usually have
normal or near normal G6PD levels and rarely experience symptoms. A carrier will have a normal
or low normal G6PD level, thus may not be identified through G6PD screening but would be
detected in a G6PD confirmation test that quantitates the overall amount of enzyme present in
the cells. Note that rare female who has two mutated gene copies (homozygous) will likely show
a significant decrease in G6PD level.
The red cell distribution width (RDW) has become a very useful calculated measurement in
haematology. How is it calculated? (1 mark)
standarddeviation of ¿cell volume
¿
mean cell volume(MCV

ed Blood Cell Distribution Width (RDW): Definition and Calculation

The red cell distribution width (RDW) is a measurement derived from the red blood
cell distribution curves generated on automated hematology analyzers and is an
indicator of variation in RBC size within a blood sample. The RDW is used along
with the indices (MCV, MCH, MCHC) to describe a population of RBCs. The RDW
measures the deviation of the RBC width, not the actual width or size of individual
cells.
The two RDW measurements currently in use are the red cell distribution width - coefficient
of variation (RDW-CV) and the red cell distribution width - standard deviation (RDW-SD).
The RDW-CV is a calculation based on both the width of the distribution curve and the mean
cell size. It is calculated by dividing the standard deviation of the mean cell size by the MCV
of the red cells and multiplying by 100 to convert to a percentage. A normal range for the
RDW-CV is approximately 11.0 - 15.0%. Because it is a calculation, the RDW-CV is
dependent not only on the width of the distribution curve but also the MCV of the red cell
population and may not always reflect the actual variation in red cell size. Be aware that:
•A homogenous population of red cells with a narrow distribution curve and low MCV may
have an elevated RDW-CV
•A heterogeneous population of red cells with a broad distribution curve and a high MCV may
have a normal RDW-CV.
The RDW-SD is an actual measurement of the width of the red cell distribution curve in
femtoliters (fL). The width of the distribution curve is measured at the point that is 20% above
the baseline. Since the RDW-SD is an actual measurement, it is not influenced by the MCV
and more accurately reflects the red cell size variance. The normal RDW-SD range for adults
is 40.0 - 55.0 fL.
List two (2) causes of macrocytosis and one test other than the FBC that may be
used to distinguish between these causes. (2 marks)
B12/folate deficiency and hypothyroidism or liver disease. Test for vitamin B12
levels, TSH to screen for
hypothyroidism, and liver function.

Causes of macrocytosis include alcohol intake, vitamin B12 and folate deficiency, chemotherapy and other drugs,
hemolysis or bleeding, liver dysfunction, myelodysplastic syndrome (MDS), and hypothyroidism. Approximately 10% of
patients will have unexplained macrocytosis after laboratory evaluation.
Background Information of Myeloblastic Auer Rods

Auer rods are clumps of azurophilic lysosomal granular

material that form elongated needles seen in
the cytoplasm of leukemic blasts. They can be seen in the
leukemic blasts of acute myeloid leukemia with maturation
and acute promyelocytic leukemia (known as acute
myeloid leukemia M2 and M3, in the FAB classification,
respectively) and in high grade myelodysplastic
syndromes and myeloproliferative syndromes.
Name one condition associated with each of the following morphological abnormalities: (2 marks)

a) Howell-Jolly bodies – haemolytic anaemia or functional hyposplenism

b) Toxic granulation – severe bacterial infection or septicaemia (sepsis)
c) Stomatocytes – Liver disease , Myelodysplastic syndrome , hereditary stomatocytosis
d) Auer rods – acute myeloid leukaemia (AML)
Name one (1) condition associated with each of the following morphological abnormalities: (2
marks)
a. Howell-Jolly bodies
b. toxic granulation
c. Stomatocytes
d. Auer rods
Howell–Jolly bodies are seen with markedly decreased splenic function. Common
causes include asplenia (post-splenectomy) or congenital absence of spleen (heterotaxy
syndrome with asplenia).

Toxic granulation refers to changes in granulocyte cells seen on examination of the peripheral blood film of
patients with inflammatory conditions. They are commonly found in patients with sepsis. Toxic granulations are
dark coarse granules found in granulocytes, particularly neutrophils. Along with Döhle bodies and cytosolic
vacuolation, which are two other findings in the cytoplasm of granulocytes, toxic granulations are a peripheral
blood film finding suggestive of an inflammatory process.[1]
Name one (1) condition associated with each of the following
morphological abnormalities: (2 marks)
a. Howell-Jolly bodies
b. toxic granulation
c. Stomatocytes
d. Auer rods

Acquired Stomatocytosis

Stomatocytes have been noted in diverse acquired conditions, including neoplasms, cardiovascular
and hepatobiliary disease, alcoholism, and therapy with drugs, some of which are known to be
stomatocytogenic in vitro. In some of these conditions, the percentage of stomatocytes on the
peripheral blood smear can approach 100%. However, the clinical significance of this observation is
unclear because stomatocytes are absent in most patients with the conditions listed. Furthermore,
some stomatocytes can be found in normal individuals (3–5%). The most consistent association is that
of stomatocytosis and heavy alcohol consumption.
Name one (1) condition associated with each of the following
morphological abnormalities: (2 marks)
a. Howell-Jolly bodies
b. toxic granulation
c. Stomatocytes
d. Auer rods

Auer rods (or Auer bodies) are large, crystalline cytoplasmic inclusion bodies sometimes
observed in myeloid blast cells during acute myeloid leukemia, acute promyelocytic leukemia,
and high-grade myelodysplastic syndromes and myeloproliferative disorders. Composed of
fused lysosomes and rich in lysosomal enzymes, Auer rods are azurophilic and can resemble
needles, commas, diamonds, rectangles, corkscrews, or rarely granules.[1]
Name the white blood cell which is normally found in greatest numbers in the peripheral
circulation of a four (4) year old child? (1 mark)

Lymphocytes

Compared to adults, a relative lymphocytosis is common in normal children. Lymphocyte counts

up to 11 x 109/L are normal in children under twelve months and elevated counts persist until mid-
adolescence.1 Results that may suggest lymphoproliferative disorders in adult patients, are usually
either normal, or reflect common clinical and sub-clinical viral infections in children. Less
commonly understood is the fact that morphologically normal lymphocytes in young infants often
appear atypical, or even blast-like. Experience with paediatric blood films is required to avoid the
unnecessary suggestion of leukaemia in many children, or the over diagnosis of specific viral
infections associated with atypical lymphocytes.
Why is the haemoglobin of a patient with chronic renal failure usually low?

Due to kidney failure, less EPO is produced and as a result, there will be less RBCs which causes anaemia to
develop and a drop in haemoglobin levels.

Why do people with kidney disease get anemia?

Your kidneys make an important hormone called erythropoietin (EPO). Hormones are chemical messengers that travel to tissues and organs to help
you stay healthy. EPO tells your body to make red blood cells. When you have kidney disease, your kidneys cannot make enough EPO. Low EPO
levels cause your red blood cell count to drop and anemia to develop.
Most people with kidney disease will develop anemia. Anemia can happen early in the course of kidney disease and grow worse as kidneys fail and
can no longer make EPO.
What is meant by the term "left-shift"? is an increase in the number of immature leukocytes
Left shift or blood shift is an increase in the number of immature leukocytes in the peripheral blood,
particularly neutrophil band cells.[1]
Less commonly, left shift may also refer to a similar phenomenon in severe anemia, when reticulocytes and
immature erythrocyte precursors appear in the peripheral circulation.[2]
What is meant by the term "lefte-shifte"? (1 mark) Increased immature cells.
A patient has a prolonged PT, APTT, TCT and marked thrombocytopenia. Give two (2) possible
causes of these results. (2 marks)

Thrombotic thrombocytopenic purpura

Liver cirrhosis
DIC
DIC or severe liver disease
Your routine coagulation QC material suddenly gives abnormal results. What
would you do? Register the results and request a new sample
Explain why EDTA anticoagulated blood CANNOT be used for the measurement of the
Activated Partial Thromboplastin Time?

APTT [and PT] rely on the presence of calcium ions to measure the clotting time of plasma. EDTA irreversibly binds to
and removes the calcium ions which will affect APTT [and PT].
This is known as Pseudo thrombocytopenia which may cause a misleading diagnosis due to the presence of the
anticoagulant.
What are reticulocytes? Why do we count them?

A nucleated immature RBCs – final stage of development before released into

peripheral blood as erythrocytes. We count them to determine how effcient the bone
marrow is at pumping out normal red blood cells.

Reticulocytes are immature red blood cells. ... It's also known as a retic count, corrected reticulocyte
count, or reticulocyte index. A reticulocyte count can help your doctor learn if your bone
marrow is producing enough red blood cells.
What affect does lipaemia have on the measurement of haemoglobin?

Causes a falsely elevated haemoglobin value

Lipemia interferes with hematology tests by the following mechanism by light scattering. This
affects the following results: Hemoglobin and hemoglobin-related indices: Results in falsely
increased absorbance readings of hemoglobin, causing a falsely high measurement.
When a haematology analyser does a delta check, what is it checking? (1 mark)

Delta check compares the current results for specific parameters (such as MCV and
MCHC) to the previous results.
We developed a computerized algorithm for real-time hematology delta checks, comparisons between
current and previous patient automated blood cell counts. Delta checking is restricted to an arbitrarily set
maximum of seven days and uses linear as well as variable-rate nonlinear discriminant functions.Two
delta levels were used–one for intralaboratory use and one requiring interaction with the referring unit or
physician.

The delta checks are useful for (1) random error detection mainly using a combination of two RBC
parameters, mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH), that remain
stable over time;

(2) warning for significant clinical changes in hemoglobin, MCV, WBC, and/or platelets;

and (3) the elimination of manual checks on abnormal RBC morphology, WBC counts, and for platelet
counts in specimens with repeatedly abnormal values.
 http://textbookhaematology4medical-
scientist.blogspot.com/2014/05/erythrocyte-sedimentation-rate-
esr.html
Erythrocyte sedimentation rate (ESR),

ESR is a common hematology tests to determine/measure the rate at which RBCs sediment in a period of
one hour. However it is a non-specific measure of inflammation and other confirmatory tests are required
concurrently to diagnose clinical conditions of abnormal results.
The ESR is governed by the balance between pro-sedimentation factors, mainly fibrinogen, and those
factors resisting sedimentation, namely the negative charge of the erythrocytes (zeta potential). When an
inflammatory process is present, the high concentration of fibrinogen in the blood promotes the adherence
and aggregation of RBCs together leading to a phenomenon called 'rouleaux,' (RBCs stacked up like a
stack of coins). This rouleaux formation of RBCs will lead to an enhanced rate of sedimentation due to the
increased density.

Females tend to have a higher ESR, and menstruation and pregnancy can cause temporary elevations.
Visual presentation/explanation:
http://www.youtube.com/watch?v=wkQFXVp9TU0&feature=youtu.be
Chem
External QC and purpose
Acromegaly
Tests for coeliac disease
Anion gap calculation
Causes of increased potassium preanalytical
Causes of hypercalcemia
Steps or studies taken before a new assay is introduced in the lab - 4 freaking points
Interpretation of swear electrolytes

Hema
Types of hemolytic anemia
Interpretation of indices
Schillings test
Retticulocyte ct and purpose
Erroneous CBC result from analyzer
Conditions seen with burr cells stomatocyte elliptocyte target cells
Micro
Dermatophytes
Hemolysis of bacteria
Color of colony in different media
Causative agents of diseases
Betalactamase meaning and purpose inbacterioa
Mic
Temperature requirements of bacteria

Histopath
Types of connective tissues and epithelial tissues
Stain for myelin melanin iron glycogen
Pas stains
Other cytological stain
Fixatives
Giemsa stain coomponents

Bb
Storage temp of red cells
Selection of donor blood for cross matching - given yung census ng blood na pagpipilian
Factors affecting at ab reaction
Labeling of sample for crossmatch
Explain kung piano magkakaroon ng offspring na o hung parents na a
Computer crossmatch
teps or studies taken before a new assay is introduced in
the lab?

Anybody knows the answer of March examination

question please?

Also in BT, list 4 factors of Ag-Ab reactions?

You answers much appreciated, giving mine this

September.