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Flashcards in HEMA LEC - Anemia Deck (134):
1

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.

Anemia

2

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.

Anemia

3

The anemias can be classified morphologically using

RBC indices (MCV, MCH, and MCHC).

4

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

5

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.

Relative (pseudo) anemia

6

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

Relative (pseudo) anemia

7

causes of relative pseudo anemia include conditions ___

conditions which result in hemodilution

8

RBC mass is decreased, but plasma volume is normal.

Absolute anemia

9

indicative of a true decrease in erythrocytes and hemoglobin.

Absolute anemia

10

mechanisms involved in absolute anema

Decreased delivery of red cells into circulation
Increased loss of red cells from the circulation

11


a. Most common form of anemia in the United States

Iron-deficiency anemia

12

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

Iron-deficiency anemia

13

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.

Iron-deficiency anemia

14

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

Iron-deficiency anemia

15

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

ACD
Anemia of Chronic Disease

16

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

ACD
Anemia of Chronic Disease

17

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

Hepcidin

18

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

Hepcidin

19

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

increase

20

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)

ACD

21

second only to iron deficiency as a common cause of anemia

ACD

22

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


Sideroblastic anemia

23

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

Sideroblastic anemia

24

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)

Sideroblastic anemia

25

Siderocytes are best demonstrated using ___

Perl’s Prussian blue stain.

26

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

Sideroblastic anemia

27

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

PRIMARY
SECONDARY

28

type of sideroblastic anemia
irreversible; cause of the blocks unknown

Primary

29

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

primary sideroblastic anemia

30

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

primary sideroblastic anemia

31

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

secondary sideroblastic anemia

32

Multiple blocks in the protoporphyrin pathway affect heme synthesis.

Lead poisoning

33

Seen mostly in children exposed to lead-based paint

Lead poisoning

34

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

Lead poisoning

35

Laboratory: Normocytic/ normochromic anemia with characteristic coarse basophilic stippling

Lead poisoning

36

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.

Porphyrias

37

Clinical Symptoms: Photosensitivity, abdominal pain, CNS disorders

Porphyrias

38

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

Megaloblastic anemias

39

Caused by either a vitamin B12 or folic acid deficiency.

Megaloblastic anemias

40

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

Megaloblastic anemias

41

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

Vitamin B12 deficiency (cobalamin)

42

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

INTRINSIC FACTOR

43

Prevalent in older adults of English, Irish and Scandinavian descent

Pernicious anemia–

44

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

Pernicious anemia–

45

Characterized by achlorhydria and atrophy of gastric parietal cells

Pernicious anemia–

46

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

Vit B12 deficiency

47

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

Vitamin B12 deficiency

48

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

folic acid deficiency

49

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

folic acid deficiency

50

low body stores

folic acid

51

anti-folic acid drugs

methotrexate

52

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

Non-megaloblastic macrocytic anemias

53

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

Non-megaloblastic macrocytic anemias

54

Bone marrow failure causes pancytopenia

Aplastic Anemia

55

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

Aplastic Anemia

56

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

Aplastic Anemia

57

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

Aplastic Anemia

58

Can be genetic, acquired or idiopathic.

aplastic anemia

59

a.) Autosomal recessive trait
b.) Dwarfism, renal disease, mental retardation

Genetic aplastic anemia (Fanconi anemia)

60

antibiotics that cause AA

Chloramphenicol and sulphonamides

61

Chemicals that cause AAA

Benzene and herbicides

62

About 30% of acquired aplastic anemias are due to

drug exposure

63

viruses that cause AAA

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

64

50-70% of aplastic anemias are

idiopathic

65

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

Diamond-Blackfan anemia

66

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

Myelophthisic (marrow replacement) anemia

67

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

Myelophthisic (marrow replacement) anemia

68

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

Myelophthisic (marrow replacement) anemia

69

The anemias can be classified morphologically using

RBC indices (MCV, MCH, and MCHC).

70

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

71

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.

Relative (pseudo) anemia

72

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

Relative (pseudo) anemia

73

causes of relative pseudo anemia include conditions ___

conditions which result in hemodilution

74

RBC mass is decreased, but plasma volume is normal.

Absolute anemia

75

indicative of a true decrease in erythrocytes and hemoglobin.

Absolute anemia

76

mechanisms involved in absolute anema

Decreased delivery of red cells into circulation
Increased loss of red cells from the circulation

77


a. Most common form of anemia in the United States

Iron-deficiency anemia

78

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

Iron-deficiency anemia

79

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.

Iron-deficiency anemia

80

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

Iron-deficiency anemia

81

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

ACD
Anemia of Chronic Disease

82

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

ACD
Anemia of Chronic Disease

83

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

Hepcidin

84

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

Hepcidin

85

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

increase

86

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)

ACD

87

second only to iron deficiency as a common cause of anemia

ACD

88

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


Sideroblastic anemia

89

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

Sideroblastic anemia

90

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)

Sideroblastic anemia

91

Siderocytes are best demonstrated using ___

Perl’s Prussian blue stain.

92

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

Sideroblastic anemia

93

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

PRIMARY
SECONDARY

94

type of sideroblastic anemia
irreversible; cause of the blocks unknown

Primary

95

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

primary sideroblastic anemia

96

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

primary sideroblastic anemia

97

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

secondary sideroblastic anemia

98

Multiple blocks in the protoporphyrin pathway affect heme synthesis.

Lead poisoning

99

Seen mostly in children exposed to lead-based paint

Lead poisoning

100

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

Lead poisoning

101

Laboratory: Normocytic/ normochromic anemia with characteristic coarse basophilic stippling

Lead poisoning

102

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.

Porphyrias

103

Clinical Symptoms: Photosensitivity, abdominal pain, CNS disorders

Porphyrias

104

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

Megaloblastic anemias

105

Caused by either a vitamin B12 or folic acid deficiency.

Megaloblastic anemias

106

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

Megaloblastic anemias

107

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

Vitamin B12 deficiency (cobalamin)

108

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

INTRINSIC FACTOR

109

Prevalent in older adults of English, Irish and Scandinavian descent

Pernicious anemia–

110

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

Pernicious anemia–

111

Characterized by achlorhydria and atrophy of gastric parietal cells

Pernicious anemia–

112

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

Vit B12 deficiency

113

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

Vitamin B12 deficiency

114

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

folic acid deficiency

115

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

folic acid deficiency

116

low body stores

folic acid

117

anti-folic acid drugs

methotrexate

118

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

Non-megaloblastic macrocytic anemias

119

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

Non-megaloblastic macrocytic anemias

120

Bone marrow failure causes pancytopenia

Aplastic Anemia

121

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

Aplastic Anemia

122

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

Aplastic Anemia

123

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

Aplastic Anemia

124

Can be genetic, acquired or idiopathic.

aplastic anemia

125

a.) Autosomal recessive trait
b.) Dwarfism, renal disease, mental retardation

Genetic aplastic anemia (Fanconi anemia)

126

antibiotics that cause AA

Chloramphenicol and sulphonamides

127

Chemicals that cause AAA

Benzene and herbicides

128

About 30% of acquired aplastic anemias are due to

drug exposure

129

viruses that cause AAA

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

130

50-70% of aplastic anemias are

idiopathic

131

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

Diamond-Blackfan anemia

132

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

Myelophthisic (marrow replacement) anemia

133

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

Myelophthisic (marrow replacement) anemia

134

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

Myelophthisic (marrow replacement) anemia

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