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HEMA LEC - Anemia Flashcards

1
Q

defined as a decrease in erythrocytes and hemoglobin, resulting in decreased oxygen delivery to the tissues.They can also be classified based on etiology/cause.

A

Anemia

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2
Q

defined as a decrease in erythrocytes and hemoglobin, resulting in decreased oxygen delivery to the tissues.They can also be classified based on etiology/cause.

A

Anemia

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3
Q

The anemias can be classified morphologically using

A

RBC indices (MCV, MCH, and MCHC).

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4
Q

Anemia is suspected when the hemoglobin is [male and female]

A
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5
Q

RBC mass is normal, but plasma volume is increased.
Secondary to an unrelated condition and can be transient in nature.
Reticulocyte count normal; normocytic/normochromic anemia.

A

Relative (pseudo) anemia

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6
Q

Causes include conditions that result in hemodilution, such as pregnancy and volume overload.

A

Relative (pseudo) anemia

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7
Q

causes of relative pseudo anemia include conditions ___

A

conditions which result in hemodilution

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8
Q

RBC mass is decreased, but plasma volume is normal.

A

Absolute anemia

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9
Q

indicative of a true decrease in erythrocytes and hemoglobin.

A

Absolute anemia

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10
Q

mechanisms involved in absolute anema

A

Decreased delivery of red cells into circulation

Increased loss of red cells from the circulation

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11
Q

a. Most common form of anemia in the United States

A

Iron-deficiency anemia

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12
Q

Prevalent in infants and children, pregnancy, excessive menstrual flow, elderly with poor diets, malabsorption syndromes, chronic blood loss (GI blood loss, hookworm infection)

A

Iron-deficiency anemia

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13
Q

Laboratory: Microcytic/hypochromic anemia; serum iron, ferritin, hemoglobin/hematocrit, RBC indices, and reticulocyte count low; RDW and total iron-binding capacity (TIBC) high; smear shows ovalocytes/ pencil forms.

A

Iron-deficiency anemia

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14
Q

Clinical Symptoms: Fatigue, dizziness, pica, stomatisis (cracks in the corners of the mouth), glossitis (sore tongue), and koilonychias (spooning of the nails).

A

Iron-deficiency anemia

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15
Q

Due to an inability to use available iron for hemoglobin production.

A

ACD

Anemia of Chronic Disease

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16
Q

b. Impaired release of storage iron associated with increased hepcidin levels

A

ACD

Anemia of Chronic Disease

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17
Q

is a liver hormone and a positive acute-phase reactant. It

A

Hepcidin

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18
Q

plays a major role in body iron regulation by influencing intestinal iron absorption and release of storage iron from macrophages.

A

Hepcidin

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19
Q

Inflammation and infection cause hepcidin levels to ___; this decreases release of iron from stores.

A

increase

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20
Q

Laboratory: Normocytic/normochromic anemia, or slightly microcytic/hypochromic anemia; increased ESR; normal to increased ferritin; low serum iron and TIBC
a. Associated with persistent infections, chronic inflammatory disorders (SLE, rheumatoid arthritis, Hodgkin lymphoma, cancer)

A

ACD

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21
Q

second only to iron deficiency as a common cause of anemia

A

ACD

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22
Q

Caused by blocks in the protoporphyrin pathway resulting in defective hemoglobin synthesis and iron overload

A

Sideroblastic anemia

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23
Q

Excess iron accumulates in the mitochondrial region of the immature erythrocyte in the bone marrow and encircles the nucleus; cells are called ringed sideroblasts.

A

Sideroblastic anemia

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24
Q

Excess iron accumulates in the mitochondrial region of the mature erythrocyte in circulation; cells are called siderocytes; inclusions are siderotic granules (Pappenheimer bodies on Wright’s stained smears)

A

Sideroblastic anemia

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25
Q

Siderocytes are best demonstrated using ___

A

Perl’s Prussian blue stain.

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26
Q

Laboratory: Microcytic/hypochromic anemia with increased ferritin and serum iron; TIBC is decreased

A

Sideroblastic anemia

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27
Q

Two Types of sideroblastic anemia:

  1. ) Primary – irreversible; cause of the blocks unknown
    a. ) Two RBC populations (dimorphic) are seen.
    b. ) This is one of the myelodysplastic syndromes – refractory anemia with ringed sideroblasts (RARS)
  2. ) Secondary – reversible; causes include alcohol, anti-tuberculosis drugs, chloramphenicol
A

PRIMARY

SECONDARY

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28
Q

type of sideroblastic anemia

irreversible; cause of the blocks unknown

A

Primary

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29
Q

This is one of the myelodysplastic syndromes – refractory anemia with ringed sideroblasts (RARS)

A

primary sideroblastic anemia

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30
Q

Two RBC populations (dimorphic) are seen. [type of sideroblastic anemia

A

primary sideroblastic anemia

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31
Q

reversible; causes include alcohol, anti-tuberculosis drugs, chloramphenicol

A

secondary sideroblastic anemia

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32
Q

Multiple blocks in the protoporphyrin pathway affect heme synthesis.

A

Lead poisoning

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33
Q

Seen mostly in children exposed to lead-based paint

A

Lead poisoning

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34
Q

Clinical Symptoms: Abdominal pain, muscle weakness, and a gum lead line that forms from blue/black deposits of lead sulfate

A

Lead poisoning

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35
Q

Laboratory: Normocytic/ normochromic anemia with characteristic coarse basophilic stippling

A

Lead poisoning

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36
Q

These are a group of inherited disorders characterized by a block in the protoporphyrin pathway of heme synthesis. Heme precursors before the block accumulate in the tissues, and large amounts are excreted in urine and/ or feces.

A

Porphyrias

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37
Q

Clinical Symptoms: Photosensitivity, abdominal pain, CNS disorders

A

Porphyrias

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38
Q

Defective DNA Synthesis causes abnormal nuclear maturation; RNA synthesis is normal, so the cytoplasm is not affected. The nucleus matures slower than the cytoplasm (asynchronism). Megaloblastic maturation is see n

A

Megaloblastic anemias

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39
Q

Caused by either a vitamin B12 or folic acid deficiency.

A

Megaloblastic anemias

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40
Q

Laboratory: Pancytopenia, macrocytic/normochromic anemia with oval macrocytes and teardrops, hypersegmented neutrophils; inclusions include Howell-Jolly bodies, nucleated RBCs, basophilic stippling, Pappenheimer bodies and Cabot rings; elevated LD, bilirubin, and iron levels due to destruction of fragile, megaloblastic cells in the blood and bone narrow

A

Megaloblastic anemias

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41
Q

2.) Other causes of ___ deficiency include malabsorption syndromes, Diphyllobothrium latum tapeworm, total gastrectomy, intestinal blind loops, and a total vegetarian diet.

A

Vitamin B12 deficiency (cobalamin)

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42
Q

secreted by parietal cells and is needed to bind vitamin B12 for absorption into the intestine.

A

INTRINSIC FACTOR

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43
Q

Prevalent in older adults of English, Irish and Scandinavian descent

A

Pernicious anemia–

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44
Q

Caused by deficiency of intrinsic factor, antibodies to intrinsic factor, or antibodies to parietal cells

A

Pernicious anemia–

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45
Q

Characterized by achlorhydria and atrophy of gastric parietal cells

A

Pernicious anemia–

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46
Q

Clinical Symptoms: Jaundice, weakness, sore tongue (glossitis), and gastrointestinal (GI) disorder, numbness and other CNS problems

A

Vit B12 deficiency

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47
Q

takes 3-6 years to develop because of high body stores.

A

Vitamin B12 deficiency

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48
Q

causes a megaloblastic anemia with a blood picture and clinical symptoms similar to vitamin B12deficiency, except there is no CNS involvement.

A

folic acid deficiency

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49
Q

associated with poor diet, pregnancy, or chemotherapeutic anti-folic acid drugs such as methotrexate.

A

folic acid deficiency

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50
Q

low body stores

A

folic acid

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51
Q

anti-folic acid drugs

A

methotrexate

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52
Q

include alcoholism, liver disease, and conditions that cause accelerated erythropoiesis.

A

Non-megaloblastic macrocytic anemias

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53
Q

The erythrocrytes are round, not oval as is seen in the megaloblastic anemias

A

Non-megaloblastic macrocytic anemias

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54
Q

Bone marrow failure causes pancytopenia

A

Aplastic Anemia

55
Q

Laboratory: Decrease in hemoglobin/ haematocrit and reticulocytes; normocytic/normochromic anemia; no response to erythropoietin

A

Aplastic Anemia

56
Q

most commonly affects people around the age of 50 and above. It can occur in children.

A

Aplastic Anemia

57
Q

Patients have poor prognosis with complications that include bleeding.
Treatment includes bone marrow or stem cell transplant and immunosuppression.

A

Aplastic Anemia

58
Q

Can be genetic, acquired or idiopathic.

A

aplastic anemia

59
Q

a. ) Autosomal recessive trait

b. ) Dwarfism, renal disease, mental retardation

A

Genetic aplastic anemia (Fanconi anemia)

60
Q

antibiotics that cause AA

A

Chloramphenicol and sulphonamides

61
Q

Chemicals that cause AAA

A

Benzene and herbicides

62
Q

About 30% of acquired aplastic anemias are due to

A

drug exposure

63
Q

viruses that cause AAA

A

B19 parvovirus secondary to be hepatitis, measles, CMV, and Epstein-Barr Virus

64
Q

50-70% of aplastic anemias are

A

idiopathic

65
Q
  1. ) True red cell aplasia (leukocytes and platelets normal in number)
  2. ) Autosomal inheritance
A

Diamond-Blackfan anemia

66
Q

Hypoproliferative anemia caused by replacement of bone marrow hematopoietic cells by malignant cells or fibrotic tissue

A

Myelophthisic (marrow replacement) anemia

67
Q

c. Laboratory: Normocytic/normochromic anemia; leukoerythroblastic blood picture.

A

Myelophthisic (marrow replacement) anemia

68
Q

b. Associated with cancers (breast, prostate, lung, melanoma) with bone metastasis

A

Myelophthisic (marrow replacement) anemia

69
Q

The anemias can be classified morphologically using

A

RBC indices (MCV, MCH, and MCHC).

70
Q

Anemia is suspected when the hemoglobin is [male and female]

A
71
Q

RBC mass is normal, but plasma volume is increased.
Secondary to an unrelated condition and can be transient in nature.
Reticulocyte count normal; normocytic/normochromic anemia.

A

Relative (pseudo) anemia

72
Q

Causes include conditions that result in hemodilution, such as pregnancy and volume overload.

A

Relative (pseudo) anemia

73
Q

causes of relative pseudo anemia include conditions ___

A

conditions which result in hemodilution

74
Q

RBC mass is decreased, but plasma volume is normal.

A

Absolute anemia

75
Q

indicative of a true decrease in erythrocytes and hemoglobin.

A

Absolute anemia

76
Q

mechanisms involved in absolute anema

A

Decreased delivery of red cells into circulation

Increased loss of red cells from the circulation

77
Q

a. Most common form of anemia in the United States

A

Iron-deficiency anemia

78
Q

Prevalent in infants and children, pregnancy, excessive menstrual flow, elderly with poor diets, malabsorption syndromes, chronic blood loss (GI blood loss, hookworm infection)

A

Iron-deficiency anemia

79
Q

Laboratory: Microcytic/hypochromic anemia; serum iron, ferritin, hemoglobin/hematocrit, RBC indices, and reticulocyte count low; RDW and total iron-binding capacity (TIBC) high; smear shows ovalocytes/ pencil forms.

A

Iron-deficiency anemia

80
Q

Clinical Symptoms: Fatigue, dizziness, pica, stomatisis (cracks in the corners of the mouth), glossitis (sore tongue), and koilonychias (spooning of the nails).

A

Iron-deficiency anemia

81
Q

Due to an inability to use available iron for hemoglobin production.

A

ACD

Anemia of Chronic Disease

82
Q

b. Impaired release of storage iron associated with increased hepcidin levels

A

ACD

Anemia of Chronic Disease

83
Q

is a liver hormone and a positive acute-phase reactant. It

A

Hepcidin

84
Q

plays a major role in body iron regulation by influencing intestinal iron absorption and release of storage iron from macrophages.

A

Hepcidin

85
Q

Inflammation and infection cause hepcidin levels to ___; this decreases release of iron from stores.

A

increase

86
Q

Laboratory: Normocytic/normochromic anemia, or slightly microcytic/hypochromic anemia; increased ESR; normal to increased ferritin; low serum iron and TIBC
a. Associated with persistent infections, chronic inflammatory disorders (SLE, rheumatoid arthritis, Hodgkin lymphoma, cancer)

A

ACD

87
Q

second only to iron deficiency as a common cause of anemia

A

ACD

88
Q

Caused by blocks in the protoporphyrin pathway resulting in defective hemoglobin synthesis and iron overload

A

Sideroblastic anemia

89
Q

Excess iron accumulates in the mitochondrial region of the immature erythrocyte in the bone marrow and encircles the nucleus; cells are called ringed sideroblasts.

A

Sideroblastic anemia

90
Q

Excess iron accumulates in the mitochondrial region of the mature erythrocyte in circulation; cells are called siderocytes; inclusions are siderotic granules (Pappenheimer bodies on Wright’s stained smears)

A

Sideroblastic anemia

91
Q

Siderocytes are best demonstrated using ___

A

Perl’s Prussian blue stain.

92
Q

Laboratory: Microcytic/hypochromic anemia with increased ferritin and serum iron; TIBC is decreased

A

Sideroblastic anemia

93
Q

Two Types of sideroblastic anemia:

  1. ) Primary – irreversible; cause of the blocks unknown
    a. ) Two RBC populations (dimorphic) are seen.
    b. ) This is one of the myelodysplastic syndromes – refractory anemia with ringed sideroblasts (RARS)
  2. ) Secondary – reversible; causes include alcohol, anti-tuberculosis drugs, chloramphenicol
A

PRIMARY

SECONDARY

94
Q

type of sideroblastic anemia

irreversible; cause of the blocks unknown

A

Primary

95
Q

This is one of the myelodysplastic syndromes – refractory anemia with ringed sideroblasts (RARS)

A

primary sideroblastic anemia

96
Q

Two RBC populations (dimorphic) are seen. [type of sideroblastic anemia

A

primary sideroblastic anemia

97
Q

reversible; causes include alcohol, anti-tuberculosis drugs, chloramphenicol

A

secondary sideroblastic anemia

98
Q

Multiple blocks in the protoporphyrin pathway affect heme synthesis.

A

Lead poisoning

99
Q

Seen mostly in children exposed to lead-based paint

A

Lead poisoning

100
Q

Clinical Symptoms: Abdominal pain, muscle weakness, and a gum lead line that forms from blue/black deposits of lead sulfate

A

Lead poisoning

101
Q

Laboratory: Normocytic/ normochromic anemia with characteristic coarse basophilic stippling

A

Lead poisoning

102
Q

These are a group of inherited disorders characterized by a block in the protoporphyrin pathway of heme synthesis. Heme precursors before the block accumulate in the tissues, and large amounts are excreted in urine and/ or feces.

A

Porphyrias

103
Q

Clinical Symptoms: Photosensitivity, abdominal pain, CNS disorders

A

Porphyrias

104
Q

Defective DNA Synthesis causes abnormal nuclear maturation; RNA synthesis is normal, so the cytoplasm is not affected. The nucleus matures slower than the cytoplasm (asynchronism). Megaloblastic maturation is see n

A

Megaloblastic anemias

105
Q

Caused by either a vitamin B12 or folic acid deficiency.

A

Megaloblastic anemias

106
Q

Laboratory: Pancytopenia, macrocytic/normochromic anemia with oval macrocytes and teardrops, hypersegmented neutrophils; inclusions include Howell-Jolly bodies, nucleated RBCs, basophilic stippling, Pappenheimer bodies and Cabot rings; elevated LD, bilirubin, and iron levels due to destruction of fragile, megaloblastic cells in the blood and bone narrow

A

Megaloblastic anemias

107
Q

2.) Other causes of ___ deficiency include malabsorption syndromes, Diphyllobothrium latum tapeworm, total gastrectomy, intestinal blind loops, and a total vegetarian diet.

A

Vitamin B12 deficiency (cobalamin)

108
Q

secreted by parietal cells and is needed to bind vitamin B12 for absorption into the intestine.

A

INTRINSIC FACTOR

109
Q

Prevalent in older adults of English, Irish and Scandinavian descent

A

Pernicious anemia–

110
Q

Caused by deficiency of intrinsic factor, antibodies to intrinsic factor, or antibodies to parietal cells

A

Pernicious anemia–

111
Q

Characterized by achlorhydria and atrophy of gastric parietal cells

A

Pernicious anemia–

112
Q

Clinical Symptoms: Jaundice, weakness, sore tongue (glossitis), and gastrointestinal (GI) disorder, numbness and other CNS problems

A

Vit B12 deficiency

113
Q

takes 3-6 years to develop because of high body stores.

A

Vitamin B12 deficiency

114
Q

causes a megaloblastic anemia with a blood picture and clinical symptoms similar to vitamin B12deficiency, except there is no CNS involvement.

A

folic acid deficiency

115
Q

associated with poor diet, pregnancy, or chemotherapeutic anti-folic acid drugs such as methotrexate.

A

folic acid deficiency

116
Q

low body stores

A

folic acid

117
Q

anti-folic acid drugs

A

methotrexate

118
Q

include alcoholism, liver disease, and conditions that cause accelerated erythropoiesis.

A

Non-megaloblastic macrocytic anemias

119
Q

The erythrocrytes are round, not oval as is seen in the megaloblastic anemias

A

Non-megaloblastic macrocytic anemias

120
Q

Bone marrow failure causes pancytopenia

A

Aplastic Anemia

121
Q

Laboratory: Decrease in hemoglobin/ haematocrit and reticulocytes; normocytic/normochromic anemia; no response to erythropoietin

A

Aplastic Anemia

122
Q

most commonly affects people around the age of 50 and above. It can occur in children.

A

Aplastic Anemia

123
Q

Patients have poor prognosis with complications that include bleeding.
Treatment includes bone marrow or stem cell transplant and immunosuppression.

A

Aplastic Anemia

124
Q

Can be genetic, acquired or idiopathic.

A

aplastic anemia

125
Q

a. ) Autosomal recessive trait

b. ) Dwarfism, renal disease, mental retardation

A

Genetic aplastic anemia (Fanconi anemia)

126
Q

antibiotics that cause AA

A

Chloramphenicol and sulphonamides

127
Q

Chemicals that cause AAA

A

Benzene and herbicides

128
Q

About 30% of acquired aplastic anemias are due to

A

drug exposure

129
Q

viruses that cause AAA

A

B19 parvovirus secondary to be hepatitis, measles, CMV, and Epstein-Barr Virus

130
Q

50-70% of aplastic anemias are

A

idiopathic

131
Q
  1. ) True red cell aplasia (leukocytes and platelets normal in number)
  2. ) Autosomal inheritance
A

Diamond-Blackfan anemia

132
Q

Hypoproliferative anemia caused by replacement of bone marrow hematopoietic cells by malignant cells or fibrotic tissue

A

Myelophthisic (marrow replacement) anemia

133
Q

c. Laboratory: Normocytic/normochromic anemia; leukoerythroblastic blood picture.

A

Myelophthisic (marrow replacement) anemia

134
Q

b. Associated with cancers (breast, prostate, lung, melanoma) with bone metastasis

A

Myelophthisic (marrow replacement) anemia

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