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Hematology Lecture > RBC Disorders (Part 2) > Flashcards

RBC Disorders (Part 2) Flashcards

1
Q

This is a macrocytic anemia in which DNA synthesis is unimpaired.

A

Macrocytic nonmegaloblastic anemia

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2
Q

Macrocytosis tends to be mild; the MCV usually ranges from100 to 110 fL and rarely exceeds 120 fL

A

Macrocytic nonmegaloblastic anemia

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3
Q

This macrocytic anemia lacks hypersegmented neutrophils and oval macrocytes in the peripheral blood and megaloblasts in the bone marrow

A

Macrocytic nonmegaloblastic anemia

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4
Q

Pathologic result of nonmegaloblastic macocytic anemia

A

liver disease, chronic alcoholism, or bone marrow failure

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5
Q

What are the characteristics of a macrocytic anemia? Cite atleast three. (HIPA)

A
  • Hypercellular Bone Marrow
  • Presence of megaloblast
  • Ineffective erythropoiesis
  • Active intramedullary hemolysis
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6
Q

It is where there is an impaired DNA synthesis and many of the cells never undergo mitosis & rather they breakdown and
die in the bone marrow

A

Ineffective erythropoiesis

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7
Q

Cite at least three consequences of ineffective erythropoiesis.

A
  • Bone marrow destructions of erythroid presursors
  • Lack of regeneration of bone marrow elements during anemic stress
    -Lack of nucleated red blood cells in peripheral smear
    -Lack of polychromasia in peripheral smear
  • Reticulocytopenia
  • Intramedullary hemolysis
  • Increased bilirubin and LDH
  • Decreased haptoglobin
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8
Q

What are the two major divisions of megaloblastic anemia?

A

Vitamin b12 (cobalamin, Cbl) deficiency
Folic acid deficiency

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9
Q

It manifests macro-ovalocytes and giant hypersegmented neutrophils

A

Megaloblastic anemia

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10
Q

What causes an impaired DNA synthesis?

A

Vitamin B12 or folate deficiency

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11
Q

If DNA synthesis is impaired what happens?

A

Nuclear replication slows down and each step of maturation will be delayed

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12
Q

If this is prolonged it would results in a large nucleus. Resulting to a megaloblast, large nucleus, increase cytoplasmic RNA, and early synthesis of hemoglobin

A

premitotic interval

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13
Q

Cite the megalocyte maturation sequence

A

Promegaloblast (Megaloblastic rubriblast) >
Basophilic megaloblast (Megaloblastic prorubricyte) >
Polychromatophilic megaloblast (Megaloblastic rubricyte) >
Orthochromic megaloblast (Megaloblastic metarubricyte) >
Polychromatophilic megalocyte (Megaloblastic reticulocyte) >
Megalocyte (Oval macrocyte)

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14
Q

A decrease amount of cells in all cell lines
(WBC, RBC, platelets)

A

Pancytopenia

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15
Q

Megaloblastic macrocytic anemia results to?

A
  • Pancytopenia
  • Increased MCV and MCHC
  • Hypersegmented neutrophils (five lobes or
    more in segmented neutrophils)
  • Increased bilirubin
  • Increased LDH
  • Hyperplasia in the bone marrow
  • Decreased M:E ratio (usually 10:1)
  • Reticulocytopenia
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16
Q

These are cells found in the bone marrow of a patient
with megaloblastic anemia

A

Megaloblasts

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17
Q

It is characterized by a more open chromatin
pattern, karyorrhexis, & multiple Howell Jolly
bodies

A

Megaloblasts

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18
Q

It is a product of maturation arrest or nuclear cytoplasmic asynchrony

A

Megaloblast

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19
Q

This causes the nucleus
and then cytoplasm to not mature together

A

nuclear-cytoplasmic asynchrony

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20
Q

Where does cobalamin absorption takes place?

A

Ileum of the small intestine

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21
Q

It is the only vitamin exclusively synthesized by microorganisms

A

Cobalamin

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22
Q

Form of stored cobalamin in the liver

A

adenosylcobalamin

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23
Q

In order to absorb cobalamin, it requires?

A

Castle’s factor or Intrinsic factor

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24
Q

Cobalamin is transported in the plasma in the form of?

A

methylcobalamin

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25
Q

Transporter of methylcobalamin

A

transcobalamin

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26
Q

Vitamin B12 is otherwise known as?

A

cyanocobalamin

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27
Q

What are the causes of Vitamin B12 deficiency?

A
  • Fish tapeworm Diphyllobothrium latum infection
  • Pernicious anemia
  • Malabsorption syndrome caused by gastric resection, gastric carcinoma, and some forms of celiac disease or screw
  • Nutritional deficiency
  • Hypochlorhydria
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28
Q

It refers to the decrease production of hydrochloric acid in the stomach

A

hypochlorhydria

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29
Q

Hypochlorhydria is associated with?

A

pernicious anemia

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30
Q

It is caused by failure of the gastric mucosa to secrete intrinsic factor

A

Pernicious Anemia

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31
Q

Other term for Pernicious Anemia

A

Addison’s anemia or Atrophy gastritis

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32
Q

Pernicious anemia is an autoimmune disease caused by two antibodies called?

A

Anti-parietal cell antibodies and Anti-intrinsic factor antibodies.

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33
Q

It produces a yellow lemon color of the skin

A

Pernicious anemia

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34
Q

Because pernicious anemia has neurologic symptoms, it has been called as?

A

Megaloblastic madness

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35
Q

It is an autosomally recessive inherited defect in the
intestinal absorption of cobalamin

A

Imerslund-Grasbeck Syndrome

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36
Q

There is a problem in the absorption of cobalamin but the intrinsic factor is normal

A

Imerslund-Grasbeck Syndrome

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37
Q

What are the diagnosis used for cobalamin deficiency?

A

Schilling test
Serum Cobalamin Assay
Methylmalonic Acid and Homocysteine
Assays
Deoxyuridine Suppression Test

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38
Q

It tests the ability of the patient to absorb an oral dose of
radioactive cobalamin

A

Schilling test

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39
Q

It is a microbiological assay which utilizes the organism
called Euglena gracilis

A

Serum Cobalamin Assay

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40
Q

It measures the ability of the marrow cells in vitro

A

Deoxyuridine Suppression Test

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41
Q

These both increase in megaloblastic anemia

A

Methylmalonic Acid and Homocysteine
Assays

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42
Q

It is considered as the reference procedure for
the determination of pernicious anemia

A

Schilling test

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43
Q

In Schilling test, If the abnormal result of stage 1 improves with administration of intrinsic factor, it means that a patient has?

A

Intrinsic factor
deficiency

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44
Q

Folate is absorbed where?

A

Jejunum

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45
Q

It cannot be
corrected by having vitamin b12 supplementation

A

folate deficiency

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46
Q

This can be partially corrected by folate even in the absence
of cobalamin supplementation

A

Anemia of cobalamin
deficiency

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47
Q

What are the causes of folate/folate acid deficiency? (CPPS)

A
  • Chronic alcoholics
  • Poor dietary habits
  • Pregnancy
  • Steatorrhea - tropical sprue, nontropical sprue, celiac disease
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48
Q

Diagnosis of folate deficiency

A
  • Microbiological assay (definitive)
  • Serum folate (<3 ug/L)
  • Red cell folate
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49
Q

This test for folate deficiency utilizes the organism Lactobacillus casei

A

Microbiological assay

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50
Q

If the patients has low Vit. B12, normal or high serum folate and low red cell folate the patient has?

A

Vitamin B12 deficiency

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51
Q

If the patient has normal Vit. B12, but low serum folate and red cell folate, the patient has?

A

Folic Acid deficiency

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52
Q

If the patient has low Vit. B12, low serum folate, and low red cell folate, the patient has?

A

Both Vitamin B12 and Folate acid deficiency

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53
Q

How can you spot a megaloblastic anemia?

A

By looking at the MCV. One of the signs of a megaloblastic anemia is the presence of a high MCV .

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54
Q

Aside from a high MCV result what are the other indicators that would confirm that a patient has megaloblastic anemia?

A

hypersegmented neutrophil plus the presence of macroovalocytes in the peripheral blood smear

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55
Q

Termed as “shift reticulocytes”, especially in response to acute blood loss, hemolysis, and bone marrow infiltration

A

Non-megaloblastic anemia

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56
Q

Results in high levels of EPO

A

Non-megaloblastic anemia

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57
Q

Seen in a plastic anemia, refractory anemia, and Diamond-Blackfan anemia

A

High levels of EPO

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58
Q

This macrocyte is seen in folic acid deficiency, vitamin b12 deficiency, and pernicious anemia

A

Oval macrocyte

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59
Q

This macrocyte is seen in alcoholism, hypothyroidism, and liver disease

A

Round hypochromic macrocyte

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60
Q

This macrocyte is seen in neonate response to anemic stress and response to anemic stress

A

Blue- tinged macrocyte

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61
Q

This macrocyte is seen in non-megaloblastic anemia

A

Round hypochromic
macrocyte

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62
Q

Reticulocyte stain with
supravital stain

A

Blue-tinged macrocyte

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63
Q

This macrocyte is seen in megaloblastic anemia

A

Oval macrocyte

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64
Q

Characterized by
Normochromic and normocytic

A

Myelophthisic anemia

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65
Q

Associated with marrow replacement by involvement with abnormal cells or tissue

A

Myelophthisic anemia

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66
Q

Characterized by increased NRBC

A

Myelophthisic anemia

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67
Q

A condition in which bone marrow is replaced by abnormal cells but still the peripheral smear would present a normochromic and normocytic RBCs but there is an increase in the presence of
your nucleated RBC

A

Myelophthisic anemia

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68
Q

A condition in which bone marrow does not produce any blood
cells

A

Aplastic anemia

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69
Q

Seen in pancytopenia, macrocytosis, increase RDW, and chloramphenicol

A

Aplastic anemia

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70
Q

It is a medication that can commonly cause aplastic anemia

A

Chloramphenicol

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71
Q

An inherited Aplastic Anemia

A

Fanconi’s Anemia

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72
Q

Presence of scattered giant pronormoblasts in the bone marrow

A

Transient Aplastic Crises

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73
Q

Caused by increased levels of Hb F and i antigen

A

Fanconi’s Anemia

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74
Q

Caused by parvovirus B19 infection

A

Transient Aplastic Crises

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75
Q

It is often preceeded by an infection.

A

Transient Aplastic Crises

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76
Q

Not an aplastic anemia but just pure red cell aplasia

A

Transient Aplastic Crises

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77
Q

A condition where there is pancytopenia. Wherein all of the cell lines are affected.

A

Fanconi anemia

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78
Q

An anemia wherein only the red cells are affected

A

Diamond Blackfan anemia

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79
Q

Characterized by congenital Red Cell Aplasia, Macrocytic, low reticulocyte level, elevated Hb F, and the frequent presence of antigen i

A

Diamond Blackfan Anemia

80
Q

Blood is lost in small amounts over an
extended period

A

Chronic Posthemorrhagic Anemia

81
Q

Transient fall in the platelet count which made
the platelet count may rise to elevated levels
within 1 hour

A

Acute Posthemorrhagic Anemia

82
Q

Blood is lost over a short time in amounts
sufficient to cause anemia. Reticulocyte increases 3-5 days after blood loss

A

Acute Posthemorrhagic Anemia

83
Q

Increase red blood cell destruction

A

Hemolytic anemia
(Membrane disorders)

84
Q

The lifespan of normal RBC would decrease if they were transfused into the patient but patient’s red cells survive normally if given to a
normal patient

A

Extrinsic hemolytic anemia

85
Q

Increased hemolysis also results in?

A

increased LDH

86
Q

This test is to determine whether it (anemia) is immune- mediated or not

A

Antiglobulin test

87
Q

Patient’s RBC would not survive when
transfused to a normal recipient. Defect of RBC itself, and membrane, metabolic, and hemoglobin
defects

A

Intrinsic hemolytic anemia

88
Q

IDENTIFY: hemoglobinemia, hemoglobinuria, or hemosideriuria is absent. Increase in urine or fecal urobilinogen, increase blood carboxyhemoglobin level, and increase indirect- reacting serum bilirubin

A

Extravascular or Extrinsic hemolytic anemia

89
Q

IDENTIFY: hemoglobinemia, methemalbuminemia, hemoglobinuria, or hemosideriuria is present, there is also an increase in LDH

A

Intravascular or Intrinsic hemolytic anemia

90
Q

Reversal of the LD isoenzyme pattern is seen with LD1 exceeding LD2

A

Intravascular or Intrinsic hemolytic anemia

91
Q

Most red cell destruction about 80-90%is presumed to be
________ within macrophages of the mononuclear phagocytic system of the liver and the spleen.

A

extravascular

92
Q

Identify: MCHC > 36%, decreased surface-area-to-volume ratio, hyperpermeable to sodium thus increase osmotic fragility

A

Spherocytes

93
Q

IDENTIFY: hemoglobinemia, methemalbuminemia, hemoglobinuria, or hemosideriuria is present. Increase in LDH is also observed

A

Intravascular or Intrinsic hemolytic anemia

94
Q

IDENTIFY: MCHC > 36%, decreased surface-area-to-volume ratio, hyperpermeable to sodium thus increase osmotic fragility

A

Spherocytes

95
Q

Most common prevalent hereditary hemolytic anemia among people of Northern European descent

A

Hereditary Spherocytosis

96
Q

Hereditary Spherocytosis is caused by deficiency of the key membrane protein called?

A

spectrin

97
Q

Characterized by increase osmotic fragility. An extravascular hemolysis within creased pigment catabolism, erythroid hyperplasia, and reticulocytosis but is DAT (Direct Anti-Globulin Test) negative because its not immune-mediated–it’s a membrane defect

A

Hereditary Spherocytosis

98
Q

Refers to the weakening of the membrane skeleton and defective association of proteins that hold the skeleton together.

A

Hereditary Elliptocytosis

99
Q

Deficiency of spectrin is again present but there is also a
deficiency in the proteins commonly associated with the
ALPHA & BETA-spectrin regions.

A

Hereditary Elliptocytosis

100
Q

RBCs may
even fragment at 37°C, body
temperature with prolonged heating

A

Hereditary pyropoikilocytosis

101
Q

In normal RBC budding and fragmentation show when heated at?

A

49°C

102
Q

Red cell fragments at 45°C to 46 °C

A

Hereditary pyropoikilocytosis

103
Q

Characterized by a well-defined band 3 molecular deletion and increased resistance to malaria

A

Southeast Asian Ovalocytes

104
Q

It is a severe congenital hemolytic anemia, which is
characterized by microcytosis, striking micropoikilocytosis
and fragmentatin

A

Hereditary pyropoikilocytosis

105
Q

Appears to have two bars across the center

A

Stomatocytic Ovalocyte

106
Q

A thinner variant of elliptocytes or ovalocytes

A

Pencil cells/oat cells

107
Q

Where the red cell is dehydrated due to loss of
cations, predominantly K+ and water

A

Hereditary stomatocytosis

108
Q

MCV is normal or slightly increased and increased MCHC

A

Hereditary stomatocytosis

109
Q

Opposite of hereditary spherocytosis because there is a decrease in osmotic fragility. MCHC is high

A

Hereditary xerocytosis

110
Q

Stomatocytes seen on blood smears

A

Hereditary stomatocytosis

111
Q

Increased surface-to-volume ratio leading to moderate to severe anemia

A

Hereditary xerocytosis

112
Q

Gene suppression or the present of a silent Rh gene

A

Rh null Disease

113
Q

This form of acanthocyte-associated hemolytic anemia is seen in patients with established alcoholic cirrhosis

A

Spur Cell Hemolytic Anemia

114
Q

Increase OFT and autohemolysis

A

Rh null Disease

115
Q

Marked dehydration and irreversible potassium
loss, peculiar red cell morphology where the hemoglobin of
red cells seem paddled at one end of the red cell

A

Hereditary xerocytosis

116
Q

In a peripheral smear you can see stomatocytes and spherocytes

A

Rh null Disease

117
Q

Caused by autoantibodies that are usually directed at Rh antigens

A

Warm Autoimmune Hemolytic Anemia

118
Q

Can also be anti-U, anti-LW, and anti-Kell, and JKa or Fya

A

Warm Autoimmune Hemolytic Anemia

119
Q

Usually anti-I. Complement factors occurs frequently due to M. pneumonia, respiratory infarctions, IMDAT+

A

Cold Autoimmune Hemolytic Anemia

120
Q

It is the more common autoimmune hemolytic anemia

A

Warm Autoimmune Hemolytic Anemia

121
Q

Exhibits spherocytosis, schistocytes, polychromasia, and nucleated erythrocytes

A

Warm Autoimmune Hemolytic Anemia

122
Q

Involves coating of IgG of erythrocytes with or without complement taxation

A

Warm Autoimmune Hemolytic Anemia

123
Q

Presence agglutination of the patient’s RBC in the capillaries

A

Cold Autoimmune Hemolytic Anemia

124
Q

Most common medication associated with Cold Autoimmune Hemolytic Anemia

A

Aldomet

125
Q

Optimal temperature of reactivity of Warm AIHM

A

37°C

126
Q

Immunoglobulin class of cold AIHM

A

IgM

127
Q

Site of hemolysis of cold AIHA

A

Intravascular

128
Q

Optimal temperature of reactivity of Cold AIHM

A

4°C

129
Q

Immunoglobulin class of warm AIHM

A

IgG

130
Q

Site of hemolysis of warm AIHA

A

Extravascular

131
Q

Complement activation of cold AIHA

A

+ (positive)

132
Q

Complement activation of warm AIHA

A

positive (+) & negative (-)

133
Q

In Cold Hemagglutinin Disease, Complement is fixed on the red cells during cold temperatures ________ and then red cells agglutinate and hemolyze as body temperature rises, ________

A

0 to 5 °C and 20 to 25 °C, respectively

134
Q

Decay Accelerating Factor deficiency

A

Paroxysmal Nocturnal Hemoglobinuria

135
Q

Intermittent (paroxysmal) sleep associated
(nocturnal) blood in the urine (hemoglobinuria)

A

Paroxysmal Nocturnal Hemoglobinuria

136
Q

Also called Donath Landsteiner antibody with anti-P specificity

A

Paroxysmal Cold Hemoglobinuria

137
Q

A rare hemolytic anemia caused by anti-P

A

Paroxysmal Cold Hemoglobinuria

138
Q

Positive sucrose hemolysis and Ham’s tests

A

Paroxysmal Nocturnal Hemoglobinuria

139
Q

Screening test for Paroxysmal Cold Hemoglobinuria

A

Donath- Landsteiner test

140
Q

It attaches to the RBC at lower temperature, it
activates complement at a warmer temperature. It’s a cold reacting IgG autoantibody termed as auto hemolysin

A

Anti-P

141
Q

It attaches to the RBC at lower temperature, it
activates complement at a warmer temperature. It’s a cold reacting IgG autoantibody termed as auto hemolysin

A

Anti-P

142
Q

This usually
happens in soldiers after intense marches

A

March Anemia

143
Q

These are consumptive coagulopatis that involves deposition of microthrombi and conditions in the blood vessels

A

Microangiopathic Red Cell Destruction/ Disseminated Intravascular Coagulation

144
Q

Most common human enzyme deficiency in
the world; sex linked; highest in young RBCs

A

G6PD-Dehydrogenase Deficiency

145
Q

Presents with lots of Heinz bodies inclusions

A

G6PD-Dehydrogenase Deficiency

146
Q

For blacks, G6PD-Dehydrogenase Deficiency is triggered by?

A

primaquine

147
Q

For non blacks, G6PD-Dehydrogenase Deficiency is triggered by?

A

ingestion of chloramphenicol, quinine, and
quinidine and the legume fava beans (Favism)

148
Q

In G6PD-Dehydrogenase Deficiency, ingestion of this will cause hemolytic crisis

A

Legume fava beans (Favism)

149
Q

Characterized by increase serum bilirubin and reticulocytes count

A

G6PD-Dehydrogenase Deficiency

150
Q

In this condition, mature erythrocytes lack mitochondria and are exclusively dependent on anaerobic glycolysis for generation of ATP

A

Pyruvate Kinase Deficiency

151
Q

Result is a rigid inflexible cells that are sequestered by the spleen

A

Pyruvate Kinase Deficiency

152
Q

Shown to be resistant to malaria

A

Pyruvate Kinase Deficiency

153
Q

Auto hemolysis is normal in this condition

A

Pyruvate Kinase Deficiency

154
Q

In this condition, ferrous iron is converted into ferric iron instead of a normal hemoglobin, methemoglobin is present

A

Methemoglobin Reductase Deficiency

155
Q

Methemoglobin Reductase Deficiency is also known as?

A

Hemoglobin M disease

156
Q

A deficiency in this enzyme can result from the inheritance of an autosomal recessive traitor in conjunction with hemoglobin M disease, or as a result of exposure to toxic substances or various drugs

A

NADH diaphorase or Methemoglobin Reductase Deficiency

157
Q

There is an impaired nucleotide metabolism, accumulation of
pyridmidine; impairs degradation of RNA;

A

Pyrimidine 5 nucleotide deficiency

158
Q

Third most common enzyme deficiency

A

Glucose phosphate isomerase deficiency

159
Q

In this deficiency, auto hemolysis is increased and is poorly corrected by glucose

A

Pyrimidine 5 nucleotide deficiency

160
Q

In this deficiency, Auto hemolysis is increase and is partially corrected by glucose

A

Glucose phosphate isomerase deficiency

161
Q

Heterozygous state for Hb S

A

Sickle Cell Trait (Hb AS)

162
Q

This is the most common hemoglobinopathy in the United States

A

Sickle Cell Trait (Hb AS)

163
Q

A benign condition without clinical symptoms or hematologic abnormalities

A

Sickle Cell Trait (Hb AS)

164
Q

Glutamic acid in the sixth position on the β- chain is replaced by valine

A

Sickle Cell Disease

165
Q

Confers protection against P. falcifarum

A

Sickle Cell Trait (Hb AS)

166
Q

Infectious crisis is commonly due to?

A

streptococcus
pneumonia

167
Q

It is freely soluble when fully oxygenated; when O2 is
removed, this polymerizes, with formation of tactoids (fluid
crystals) that are rigid and deforms the cell into the shape
that gave the disease its name

A

Hb S or Sickle Cell Disease

168
Q

Primary cause of death of sickle cell disease

A

Infectious crisis

169
Q

The complications involve in infectious crisis are?

A
  • Vaso-occlusive crises
  • Bone and joint crises
  • Aplastic crises
  • No Hb A
170
Q

Common in African Americans

A

Hemoglobin SC Disease

171
Q

In this disease, Patients have only Hb S and C with an
absence of Hb A and normal increased levels
of Hb F

A

Hemoglobin SC Disease

172
Q

Anicytosis and poikilocytosis are mild to severe in?

A

Hemoglobin SC Disease

173
Q

IDENTIFY: No Hemoglobin A present, microcytic hypochromic and splenomegaly is usually present

A

Hemoglobin S-Beta Thalassemia

174
Q

Substitution of lysine for glutamic acid (a2 β2- glu –> lys) in the sixth position of the N- terminal end of the beta chain

A

Hemoglobin C

175
Q

There is a presence of crystalline structures in the red cells
that appears as blocks or bars of gold

A

Hemoglobin C

176
Q

Second most common Hemoglobin variant
worldwide

A

Hemoglobin E

177
Q

Extremely high occurrence in individuals from
Southeast Asian countries. It resembles a thalassemia trait; there’s microcytosis, erythrocytosis but normal MCHC
& only a slight anemia

A

Hemoglobin E

178
Q

This constitutes the most common D variant in African Americans

A

Hb D Los Angeles (Punjab) (B121 glu–> gln)

179
Q

Most common alpha chain variant in black
people

A

Hb G Philadelphia ( a 68asn–> lys)

180
Q

Two major types of Hereditary Persistence of Fetal Hemoglobin

A

(1) Pancellular and (2) heterocellular (or Swiss) HPFH

181
Q

A hemoglobin analogous to the Lepore hemoglobin, which is associated with HPFH phenotype

A

Hb Kenya

182
Q

Has less Hb F ranging from 2% to 5%

A

Heterocellular or Swiss Type HPFH

183
Q

The Hb F is homogeneously or evenly distributed among the red cells

A

Pancellular HPFH

184
Q

The distribution of HbF is uneven: Both F cells and erythrocytes lacking Hb F are present

A

Heterocellular or Swiss Type HPFH

185
Q

Diagnosed based on elevated hematocrit level above the normal range

A

Polycythemia (Erythrocytosis)

186
Q

According to WHO, what is the male and female Hgb range for polycythemia?

A

> 18.5 g/dL for men
16.5g/dL for women

187
Q

Increase in the total red cell mass in the body

A

Absolute Polycythemia

188
Q

The total red cell mass is normal, but the Hct is elevated because the plasma volume is decreased (usually seen in dehydration)

A

Relative Polycythemia

189
Q

Known as apparent polycythemia or Gaisbock syndrome.

A

Spurious Polycythemia

190
Q

The red cell mass is often high normal and the plasma volume is low normal

A

Spurious Polycythemia

191
Q

Characterized by an increase panmyelosis, erythrocytosis, leukocytosis, and
thrombocytosis of varing degrees

A

Polycythemia Vera

192
Q

Where all cell lines are increased

A

panmyelosis

193
Q

A condition where there is an excessive proliferation of erythrocytes as well as other
cells lines

A

Polycythemia Vera

194
Q

Cite the polycythemias classified under absolute polycythemia

A
  1. Secondary polycythemia with appropriately increased EPO production
  2. Secondary polycythemia with inappropriately increased EPO production
  3. Genetic polycythemia
  4. Primary marrow disorders (Polycythemia vera)
195
Q

Cite the polycythemias classified under relative polycythemia

A
  1. Diminished plasma volume: dehydration; shock
  2. Spurious polycythemia (stress polycythemia; Gaisbock syndrome)

Hematology Lecture (2 decks)

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