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Pathology > RBC Pathology 1 > Flashcards

RBC Pathology 1 Flashcards

1
Q

In RBC development, the ______ is the first source of red cell elements. What week of fetus development?

A

Yolk sac. 3rd week

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2
Q

At what month does the liver become the chief site of red cell formation?

A

3rd month

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3
Q

What does it mean when the baby has a hematopoetic liver at birth? Is this pathologic?

A

Baby had anemia in utero; Yes it is pathologic

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4
Q

Sole source of all blood cells and lymphocyte precursors at birth

A

Bone marrow

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5
Q

In utero, when does hematopoesis switch to the bone marrow?

A

4th month

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6
Q

Which bones are the most hematopoetically active in an 18 year old?

A

Central bones (vertebrae, ribs, sternum, skull, pelvis)

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7
Q

In adults, _______ marrow can be reactivated to red marrow with increased demand for blood cells

A

Yellow / Fat

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8
Q

Fetal hemoglobin diminishes after ______ of age

A

5-6 months

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9
Q

Beta Hemoglobin occurs only after _______ postnatally

A

6 months

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10
Q

Hemoglobin with 4 beta chains

A

Hgb H (nonfunctional)

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11
Q

Hgb with 4 gamma chains

A

Hemoglobin barts (nonfunctional)

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12
Q

Fetal hemoglobin has 2 ____ chains and 2 _____ chians

A

alpha; gamma

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13
Q

Hemoglobin ___ has 2 alpha and 2 beta chains and in normal adults constitutes ___% of Hgb

A

A; 95%

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14
Q

Hemoglobin A2 has 2 ____ chains and 2 ____ chains

A

alpha; delta

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15
Q

_____ is the youngest and largest of all cell types with prominent nucleoli

A

Blast

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16
Q

Progression of red blood cell maturation

A

Myeloid stem cell –> Pronormoblast –> Basophilic Normoblast –> Polychromatic Normoblast –> Orthochromatic Normoblast –> Polychromatic erythrocyte (reticulocyte) –> Eryrthrocyte

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17
Q

In RBC maturation, what is the first cell apparent in the PBS?

A

reticulocyte (polychromatic erythrocyte)

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18
Q

General S/S of anemia

A

weakness, malaise, easy fatigability, dyspnea on mild exertion

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19
Q

PE findings in anemia

A

Pallor, dizziness & headache, angina, anemic murmur (hemic murmur), koilonychias & brittle nails, oliguria, anuria

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20
Q

Normal Hgb levels

A

12-14 g/dl (F); 13-16 g/dL (M)

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21
Q

Normal Hct levels

A

33-42% (F); 39-48% (M)

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22
Q

Normal reticulocyte count

A

0.5 - 1.5%

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23
Q

What the the reticulocyte count measure?

A

Bone marrow activity

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24
Q

Normally, reticulocyte count is (elevated / depressed) in anemia

A

Elevated

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25
Q

Normal MCV; formula for MCV; measure of?

A

80-94 fl; Hct/RBC count x 10; average volume of RBCs

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26
Q

Normal MCHC; formula for MCHC; measure of?

A

32-36 gm/dL; Hb/Hct x 100; Average concentration of Hgb in a given volume of packed RBCs

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27
Q

Normal size of central pallor of RBC

A

1/3 of the diameter

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28
Q

Central pallor >1/3 of the diameter

A

hypochromic

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29
Q

Central pallor <1/3 of the diameter

A

hyperchromic

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30
Q

Change in size of RBC

A

Anisocytosis

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31
Q

Change in shape of RBC

A

Poikilocytosis

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32
Q

Normal MCH; formula of MCH; Measure of?

A

25-34 pg; Hb/RBC count x 10; average content of Hb per RBC

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33
Q

Anemias that are hypochromic, microcytic

A

IDA, Thalassemia, Sideroblastic

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34
Q

Macrocytic anemias

A

Vitamin B12 and Folic Acid deficiency anemias

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35
Q

What is the first response to acute blood loss?

A

leukocytosis and thrombocytosis

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36
Q

Type of anemia in acute blood loss

A

normocytic, normchromic

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37
Q

Type of anemia in chronic blood loss; what does it manifest as?

A

hypochromic, microcytic; IDA

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38
Q

Intrinsic hemolytic anemias

A

G6PD deficiency, sickle cell, pyruvate kinase deficiency, spherocytosis, thalassemia

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39
Q

Extrinsic hemolytic anemias

A

Malaria, Ab-mediated, lead poisoning, SLE

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40
Q

Give the 3 characteristics of hemolytic anemia

A

1) Accumulation of Hb catabolism
2) Increased erythropoesis
3) Premature destruction of RBCs

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41
Q

Anemias of defective DNA synthesis

A

B12 and Folic acid deficiency

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42
Q

Anemias of defective Hb synthesis

A

IDA, thalassemia

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43
Q

Anemias d/t disturbance of proliferation of stem cells

A

Aplastic anemia, Anemia of renal failure

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44
Q

Normal Erythroid:Myeloid ratio in BM

A

1:4

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45
Q

In erythroid hyperplasia, myeloid cells are replaced by?

A

red cell progenitors

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46
Q

3 changes in intravascular hemolytic anemia not found in extravascular hemolytic anemia

A

Hemoglobinuria, Hemoglobinemia, Decrease in hepatoglobin

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47
Q

Why is there a decrease in hepatoglobin in intravascular hemolytic anemia?

A

Free Hb in blood combine with hepatoglobin, get transported to the RES system in the spleen

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48
Q

Causes on intravascular hemolytic anemia

A

Mechanical injury, infection (malaria), complement fixation, exogenous toxic factors

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49
Q

Splenomegaly is not seen in intravascular hemolysis (T / F)

A

True

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50
Q

Type of bilirubin in ALL types of hemolytic anemia

A

Unconjugated

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51
Q

Main characteristics of Extravascular hemolytic anemia

A

Anemia, Jaundice, Splenomegaly

52
Q

Cause of splenomegaly in extravascular hemolytic anemia

A

splenic trapping of RBCs, usually caused by alterations that render the red cell less deformable
Splenomegaly does not occur in all cases

53
Q

Defective membrane proteins in spherocytosis:

A

Spectrin
Actin
Ankyrin

54
Q

PBS of spherocytosis

A

Small, dark-staining spheroidal RBCs with loss of central pallor

55
Q

Main sign in spherocytosis

A

Splenomegaly and Jaundice

56
Q

How is spherocytosis diagnosed?

A

Family history, hematologic findings, laboratory evidence

57
Q

The course of spherocytosis is stable unless the following happens

A

1) Aplastic crisis

2) Hemolytic crisis

58
Q

The ONLY red cell disorder that is HYPERCHROMIC and MICROCYTIC

A

Spherocytosis

59
Q

In spherocytosis, chronic hemolytic anemia happens when…

A

the bone marrow cannot compensate

60
Q

What can be done in chronic hemolytic anemia d/t spherocytosis?

A

exchange transfusion

61
Q

Pathogenesis of G6PD deficiency

A

Abnormalities in HMP shunt or glutathione metabolism –> reduced ability of cells to protect against oxidative injuries –> hemolysis

62
Q

In G6PD deficiency, increasing amounts of Hb+3 causes production of?

A

Heinz bodies (denatured globin chains)

63
Q

How are bite cells produced?

A

Macrophages plucking out the Heinz bodies

64
Q

PBS: normocytic, normochromic, with increased reticulocytes, Heinz bodies and bite cells

A

G6PD deficiency anemia

65
Q

Precipiating factors for G6PD deficiency anemia

A

Infections (most common), Oxidant drugs (anitmalarials, sulfonamides, nitrofurantoins), Flava beans, Stress

66
Q

G6PD deficiency variant wherein only mature RBC are lacking the enzyme

A

G6PD -

67
Q

G6PD deficiency variant wherein all RBCs are lacking the enzyme

A

G6PD Mediterranean

68
Q

During the recovery phase of G6PD deficiency there is…

A

Reticulocytosis

69
Q

S/S of G6PD deficiency

A

1) Primarily intravascular hemolysis 2-3 days after exposure to oxidative stress
2) Self-limited
3) Increased reticulocyte count during recovery
4) Mild extravascular hemolysis
5) NO signs of chronic hemolysis

70
Q

HbS formation is from the substitution of _______ for valine at the ____ position of the beta chain

A

glutamine; 6th

71
Q

Pathogenesis of sickle cell anemia

A

HbS aggregation in presence of deoxygenation –> distortion –> sickling of RBC (Holly leaf appearance) –> (1) Chronic hemolysis in the spleen (2) Small vessel occlusion (3) Tissue damage

72
Q

Presence of ____ and ____ in liquid chromatography is indicative of sickle cell trait

A

HbA and HbS

73
Q

Presence of HbA and HbS in liquid chromatography is indicative of sickle cell Anemia (T/F)

A

False (only HbS)

74
Q

The PBS in sickle cell anemia shows

A

1) normocytic, normochromic RBCs
2) (+) sickle cells
3) (+) normoblasts

75
Q

In infants with sickle cell anemia, the spleen is _______

A

Enlarged

76
Q

In adults with sickle cell anemia, the spleen is _______ and this is d/t _________

A

Small; Autosplenectomy

77
Q

Lab abnormalities in sickle cell anemia

A

Decreased Osmotic fragility and ESR

78
Q

Lab abnormalities in sickle cell trait

A

None

79
Q

Pain and infarction in different organs cause by plugging up of capillaries is seen in sickle cell (Anemia / Trait)

A

Anemia

80
Q

4 Factors that affect sickling

A

1) Amount of interaction of HbS
2) Increase in MCHC & intracellular dehydration
3) Decrease in pH
4) Length of exposure to decreased O2

81
Q

Sickle cell anemia cannot be seen until the infant is at least _______ of age d/t the increased presence of ______

A

6 months; HbF

82
Q

Evidence of chronic hemolysis in sickle cell anemia

A

1) Increased RBC destruction

2) Increased erythropoesis (extramedullary hematopoesis, hyperplastic bone marrow, increased retic and normoblasts)

83
Q

In sickle cell anemia, the skull x-ray show…

A

“Crew haircut” appearance of the skull

84
Q

Critical episodes that can complicate sickle cell anemia

A

1) Vaso-occlusive crisis
2) Aplastic crisis
3) Sequestration crisis

85
Q

Sickle cell anemia: Sequestration crisis pathogenesis

A

Massive RBC destruction –> sudden splenomegaly –> hypovolemia –> shock

86
Q

In children, vaso-occlusive crisis of sickle cell anemia typically affects:

A

Bone

87
Q

Triggers of vaso-occlusive crisis

A

Infection, dehydration, acidosis

88
Q

Most common sites of vaso-occlusive crisis

A

bone, lungs, liver, brain, spleen, penis

89
Q

What is the pathology of Thalassemias?

A

Defective globin synthesis

90
Q

Type of thalssemia with defective beta globin chain

A

Beta thalassemia

91
Q

Beta thalassemia minor is also known as

A

Cooley’s trait

92
Q

Critical episodes that can complicate sickle cell anemia

A

1) Vaso-occlusive crisis
2) Aplastic crisis
3) Sequestration crisis

93
Q

3 types of beta thalassemia

A

minor, intermedia, major

94
Q

Sickle cell anemia: Sequestration crisis pathogenesis

A

Massive RBC destruction –> sudden splenomegaly –> hypovolemia –> shock

95
Q

Beta thalassemia major is also known as

A

Cooley’s anemia

96
Q

In sickle cell anemia, what is a vaso-occlusive crisis?

A

Multiple simultaneous painful thrombosis in different organs, most commonly in bone (in children)

97
Q

Necessary for survival in beta thalassemia major:

A

Blood transfusion

98
Q

Triggers of vaso-occlusive crisis

A

Infection, dehydration, acidosis

99
Q

Type of thalassemia with defective alpha chain

A

alpha thalassemia

100
Q

Most common sites of vaso-occlusive crisis

A

bone, lungs, liver, brain, spleen, penis

101
Q

Type of Hb found in hydrops fetalis

A

Hb Barts (4 gamma)

102
Q

Most common cause of mutation in beta thalassemia

A

Splicing mutations

103
Q

4 classifications of alpha thalassemia and their cause:

A

1) Silent carrier state (single gene deletion)
2) Alpha thalassemia trait (deletion of 2 genes from a single chromosome)
3) Hemoglobin H disease (Deletion of 3 genes)
4) Hydrops fetalis (deletion of all 4 alpha globin genes)

104
Q

S/Sx of Thalassemia:

A 
Massive erythroid hyperplasia
Skull X-ray "crewcut" appearance
Facial alteration
Hemosiderosis
Massive hepatosplenomegaly
Jaundice
105
Q

PBS of Thalassemia

A

Hypochromic, microcytic anemia
Marked anisocytosis
Target cells
Basophilic stippling

106
Q

Laboratory diagnosis of thalassemia

A

1) Hb electrophoesis
2) PBS
3) Evidences of BM hyperplasia (inc retic)
4) Iron overload (increased siderocytes, sideroblasts)

107
Q

Iron administration is therapeutic in ___ but fatal in ___:

A

IDA; Thalassemia

108
Q

______ provides a sensitive means for detecting red cells that are deficient in GPI-linked proteins

A

flow cytometry

109
Q

What is the only hemolytic anemia that is caused by an ACQUIRED gene defect?

A

Paroxysmal nocturnal hemoglobinuria

110
Q

In PNH, why is there a tendency for RBCs to lyse at night?

A

d/t decreased pH durin sleep = increased complement activity

111
Q

Other S/S of thalassemia (aside from facial and skull)

A

Expansion of red marrow, hemosiderosis / hemochromatosis, Massive splenomegaly, Jaundice

112
Q

How is PNH diagnosed? What is the only cure?

A

Flow cytometry; BM transplant

113
Q

Benefit and drawback of C5a monoclonal Ab infusion in PNH patients

A

Reduces hemolysis BUT increased risk for fatal meningococcal infections

114
Q

3 classifications of Immuno-hemolytic anemias

A

1) Warm Ab IHA
2) Cold agglutin IHA
3) Cold hemolysis IHA

115
Q

Warm Ab IHA is Ig_ that is active at __ C and __ fix complement:

A

IgG; 37 degrees; does not fix complement

116
Q

Secondary causes of warm Ab IHA

A

drugs, lymphomas & leukemias, autoimmune disorders

117
Q

Cold agglutin IHA is Ig_ active from ___ C and ___ fix complement:

A

IgM; 0-30 degrees; does fix complement

118
Q

Most common causes of cold agglutin IHA

A

Mycoplasma pneumonia

Infectious mononucleosis

119
Q

Cold hemolysin IHA is Ig_ active at ___ C and ___ fix complement:

A

IgG; low temperature; does fix complement

120
Q

Common causes of cold hemolysin IHA

A

mycoplasma pneumonia, measles, mumps, other viral flu-like syndromes

121
Q

Many ___ cells are present in microangiopathic hemolytic anemia with vessel narrowing due to ___:

A

Schistocytes; fibrin deposition

122
Q

Common pathogenic feature in mircoangiopathic hemolytic anemia

A

microvascular lesion

123
Q

Common pathogenic feature in mircoangiopathic hemolytic anemia

A

microvascular lesion

124
Q

Major diagnostic criterion for immuno-hemolytic anemias:

A

Coomb’s antiglobin test

125
Q

In PNH, abnormal __ gene leads to defects in these proteins __:

A

PIGA; CD 59, CD 55, C8 protein

126
Q

S/Sx of PNH:

A

Intravascular hemolysis
Episodic venous thrombosis
Acute myeloid leukemia

127
Q

A hemolytic anemia resulting from trauma to RBC d/t narrowing or ostruction in microvaculature

A

mircoangiopathic hemolytic anemia

Pathology (7 decks)

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