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01 Hematology > Nutritional and Normocytic Anemias > Flashcards

Nutritional and Normocytic Anemias Flashcards

1
Q

What is the general definition of anemia?

A

Decreased RBC, HGB, HCT or Decreased oxygen carrying capacity

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2
Q

What is spurious anemia? What are the potential causes?

A

Dilutional anemia due to the expansion of plasma volume; Hydremia of pregnancy, congestive heart failure, iatrogenic

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3
Q

What are the physiologic adaptations to anemia?

A

Tachycardia, increased SV, increased 2,3-BPG (decreasing HGB affinity for O2 allowing more delivery), and erythroid hyperplasia with reticulocytosis

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4
Q

What is reticulocytosis?

A

Proliferation of nucleated/immature RBCs or erythroblasts

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5
Q

At what point in the course of anemia will reticulocytosis begin?

A

Only after the first 2 compensatory mechanisms become inadequate

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6
Q

What stain is necessary to visualize reticulocytes? What does it stain?

A

Supravital stain that precipitates ribosomal RNA as a reticulin network

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7
Q

What is the reticulocyte count a measure of?

A

THe ability of the marrow to produce and deliver RBCs to the periphery (effective erthyropoiesis

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8
Q

Approximately what percentage of circulating RBCs are reticulocytes under normal circumstances?

A

~1%

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9
Q

What does a decreased reticulocyte count associated with anemia indicate?

A

Lack of an appropriate marrow response

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10
Q

What is a corrected reticulocyte count?

A

The count is adjusted for the degree of anemia and allows us to see what the RC would be if the pt had a normal HCT of 45

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11
Q

What are the non-specific symptoms of anemia?

A

SOB, fatigue, weakness, palpitations, dizziness, syncope

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12
Q

What are the clinical signs of anemia?

A

Pallor of mucocutaneous membranes; Hyderdynamic circulation (tachycardia, bounding pulse, and systolic flow murmur

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13
Q

What are the pathophysiologic classifications of anemia? What lab test is this classification based on?

A

Hypoproliferative anemia, Maturation defect, or Hyperproliferative anemia; based on corrected RC

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14
Q

What are the specific types of hypoproliferative anemia?

A

Aplastic anemia and myelophthisic anemia

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15
Q

What is aplastic anemia?

A

Bone marrow is replaced with fat, so you have a lower number of hematopoietic cells for hematopoiesis

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16
Q

What is myelophthisic anemia?

A

Replacement of marrow by fibrosis, tumor, etc.

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17
Q

How do maturation defect anemias come about?

A

RBC’s are produced but many are destroyed in the marrow and not peripheral circulation

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18
Q

What are the two sub types of anemia due to maturation defect?

A

Megaloblastic anemias and myelodysplastic syndromes

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19
Q

What is the pathophysiology of hyperproliferative anemias?

A

Marrow effectively produces and releases RBCs to peripheral circulation =, but are then destroyed in the periphery by hemolysis or hemorrhage

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20
Q

What are the two ways anemias are generally classified? Which system is used for often

A

Based on functionality or based on morphology (more common)

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21
Q

What lab value/result is used as the basis of the morphological classification of anemias?

A

MCV

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22
Q

What are the three types of morphologic classifications of anemia?

A

Normocytic, microcytic, and macrocytic

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23
Q

What are the two major types of macrocytic anemias?

A

Megaloblastic anemia and Non-megaloblastic anemia

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24
Q

What is the pathophysiology/ etiologies of megaloblastic anemia?

A

Decreased corrected RC due to ineffective hematopoiesis- can be due to B12 or folate deficiencies, folate antagonsits, chemotherapies, or antiretrovirals, Myelodysplastic syndromes, and Maturation deficiency

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25
Q

What are the etiologies of non-megaloblastic anemia?

A

Hemolysis, hemmorhage, alcoholism, liver disease

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26
Q

What is the cause of spurious macrocytosis?

A

Cold agglutinins

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27
Q

What is the pathogenesis of megaloblastic anemia?

A

Defective nuclear maturation caused by impaired DNA synthesis causes nuclear maturation to lag behind unaffected cytoplasmic maturation resulting in nuclear-cytoplasmic dysynchrony/ asynchrony and impaired cell division and fewer cell multiplications

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28
Q

What is the morphology of megaloblastic anemia?

A

RBCs- macro-ovalcytes; WBCs- hypersegmented neutrophils; thrombocytopenia

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29
Q

What is the morphology of the bone marrow during megaloblastic anemia?

A

Erythroid hyperplasia with megaloblatic change characterized by nuclear/cytoplasmic dysynchrony; Giant band cells and metamyelocytes, and maybe hypersegmented neutrophils

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30
Q

What CBC results are indicative of megaloblastic anemia?

A

Pancytopenia (decreased Hb, WBC, and platelets); Macrocytosis (increased MCV); Decreased corrected reticulocyte count

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31
Q

What blood chemistry panel results are indicative of megaloblastic anemia?

A

Increased levels of circulating LDH or indirect bilirubin

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32
Q

True or False: A low RBC folate result is specific to a folate deficiency.

A

False- can also be decreased in B12 deficiency

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33
Q

What is the primary cause of megaloblastic anemia? What is the mechanism?

A

B12 deficiency;

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34
Q

What are the major dietary sources of folate?

A

Meat, liver, fish, dairy

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35
Q

How long do the normal body stores of B12 last?

A

3-4 years

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36
Q

What is the most common mechanism of B12 deficiency?

A

Malabsorption

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37
Q

What is pernicious anemia?

A

An autoimmune chronic atrophic gastritis– megaloblastic anemia due to B12 deficiency that results from a lack of intrinsic factor

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38
Q

Why does a B12 deficiency cause neurological symptoms but not a folate deficiency?

A

Only B12 is necessary for nerve myelination

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39
Q

What metabolite builds up with a B12 deficiency?

A

Methylmalonic acid

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40
Q

How can a B12 deficiency lead to a decrease in folate?

A

With B12 deficiency , CH3-folate can acumulate in the RBC and then diffuse out into the plasma

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41
Q

What is the etiology of Pernicious anemia?

A

Anti-parietal cell and anti-intrinsic factor Abs which destroy parietal cells and intrinsic factor production

42
Q

What tests are specific for pernicious anemia?

A

Anti-parietal cell Abs or Anti-intrinsic factor Abs

43
Q

What are the symptoms of B12 deficiency?

A

Weakness and sore tongue, glossitis

44
Q

How will a B12 deficiency present during the physical exam?

A

Pallor with mild jaundice, neurological impairment

45
Q

What specific neurological symptoms and signs manifest due to B12 deficiency?

A

Demyelination of dorsal and lateral columns of the spinal cord; Peripheral neuropathy; Uncoordinated gait

46
Q

What is the dietary sources of folate?

A

Leafy green veggies, fruits, cereals, dairy, liver

47
Q

True or False: Folate is heat labile and destroyed by cooking

A

True

48
Q

Where are B12 and folate absorbed in the GI tract?

A

B12 in the ileum and folate in the jejunum

49
Q

Where does the body store folate? How long can this store last?

A

Stores in the liver and only lasts 3-4 months

50
Q

What are the causes of folate deficiency?

A

Inadequate diet (malnutrition. alcoholism); Increased folate requirements (pregnancy, infancy, tumors, hemolytic anemia with compensatory myeloproliferative syndromes; Malabsorption; Drugs

51
Q

How are B12 and folate deficiencies treated?

A

Replacement therapy with parenteral B12 or folate

52
Q

What are non-megaloblastic macrocytic anemias?

A

Increased MCV NOT due to impaired DNA synthesis

53
Q

What are the etiologies of non-megaloblastic, microcytic anemia?

A

Hemolysis, hemorrhage, alcohol, chronic liver disease

54
Q

What etiologies of non-megaloblastic microcytic anemia can result in the presence of target cells in a PBS

A

Alcohol or liver disease

55
Q

What is the relative amount of cytoplasmic Hb in microcytic anemias compared to healthy patients?

A

Hypochromia- decreased Hb

56
Q

What is the major cause of microcytic anemia?

A

Disorders of iron metabolism and utilization (Fe deficiency or anemia of chronic disease)

57
Q

What anemia results from disorders of heme synthesis?

A

Sideroblastic anemia

58
Q

What results from disorders of globin synthesis?

A

Thalassemia

59
Q

Where is iron stored (cells and organs)?

A

Within macrophages- primarily in bone marrow and liver, but some in splenic macrophages

60
Q

What are the forms that Fe can be stored as?

A

Ferritin and hemosiderin

61
Q

What are the normal amounts of Fe stored in the adult male and female body?

A

Male~ 1000 mg; Females~400 mg

62
Q

Why do females require a daily Fe requirement 1 mg higher than men?

A

They lose 20 mg Fe every menstrual cycle

63
Q

How much Fe is contained in 1 mL RBCs?

A

1 mg

64
Q

What are the general categories of Iron Deficiency Anemia etiologies? What is the most common cause?

A

Chronic blood loss, increased requirement, decreased iron absorption, and inadequate dietary intake

65
Q

What is achlorhydria?

A

An upset in the acid balance of the stomach

66
Q

What is koiloncychia?

A

Spooning of the nails (substantial indentation in surface of fingernails)

67
Q

What epithelial abnormalities are associated with Fe deficiency?

A

Koilonychia, Glossitis +/- tongue atrophy, angular cheilitis , esophageal webs with dysphagia

68
Q

What is Plummer-Vinson Syndrome?

A

Occurs in people with long-term IDA resulting in the combination of esophageal web with dysphagia and glossitis/ angular cheilitis

69
Q

What is measured as serum iron?

A

The amount of iron bound to transferritin

70
Q

What is the total iron binding capacity?

A

The max concentration of Fe that existing transferrin within the body can bind

71
Q

How is the total iron binding capacity affected by Iron-deficiency anemia?

A

Increases

72
Q

What is serum ferritin an estimate of? How is it affected by IDA?

A

Body storage iron- decreased in IDA

73
Q

What is free erythrocyte protoporphyrin (FEP)? What is indicated by an increased FEP?

A

Heme minus Fe= FEP; Increased FEP indicates not enough Fe is available to form heme or failure of iron incorporation into heme

74
Q

What specific conditions would lead to an increase in FEP?

A

IDA, anemia of chronic disease, sideroblastic anemia, or lead toxicity

75
Q

How does Fe deficiency affect serum soluble transferrin receptor?

A

Increased in IDA

76
Q

What is the peripheral blood morphology of IDA?

A

Hypochromic, microcytic RBCs, +/- thrombocytosis

77
Q

What is the bone marrow morphology in IDA?

A

Absent iron within macrophages

78
Q

What are the stages of IDA?

A

1- Fe depletion; 2- Fe-deficient erythropoiesis occurs once Fe stores are depleted; 3- IDA

79
Q

How is IDA treated?

A

Iron replacement- oral or parenteral

80
Q

What is the pathophysiology of Sideroblastic anemia?

A

Impaired incorporation of Fe into protoporphyrin ring resulting in accumulation of excess Fe in perinuclear mitochondria

81
Q

What are the causes of sideroblastic anemia?

A

Hereditary (rare) or Acquired through myelodysplastic syndrome or drug usage

82
Q

What is the peripheral blood morphology of sideroblastic anemia?

A

Dimorphic RBC population (hypochromic/microcytic or normochromic/cytic) and Pappenheimer bodies

83
Q

What are Pappenheimer bodies?

A

Iron-containing intracellular inclusions in RBCs

84
Q

What is the bone marrow morphology in sideroblatic anemia?

A

Increased storage iron in macrophages and ring sideroblasts

85
Q

How does lead toxicity lead to anemia?

A

Lead interferes with enzymatic processes involved in heme synthesis- blocks Fe incorporation into protoporphyrin

86
Q

What molecules increase in circulation due to lead toxicity?

A

FEP and delta-aminolevulinic acid

87
Q

What kind(s) of anemia can be caused by lead toxicity?

A

Normochromic/ normocytic OR hypochromic/microcytic

88
Q

What are the signs and symptoms of lead toxicity?

A

Abdominal pain, peripheral neuropathy, renal dysfunction, encephalopathy, and gingival lead line

89
Q

What is the differential diagnosis for normochromic, normocytic anemias?

A

Anemia of chronic disease, chronic kidney disease, endocrinopathy, myelophthisic anemia, aplastic anemia, or acute blood loss

90
Q

What is anemia of chronic disease?

A

Mild-moderate anemia, usually of at least several months’ duration associated with inflammatory, infectious, or neoplastic processes

91
Q

What is the second most common type of anemia?

A

Anemia of chronic disease

92
Q

What are the 2 mechanisms of pathogenesis of anemia of chronic disease?

A

1) Direct inhibition of erythropoiesis by cytokines that are being chronically produced by underlying disease 2) Block of Fe transfer from marrow macrophages to erythroid cells

93
Q

How does anemia of chronic disease affect iron studies?

A

Decreased serum Fe, Decreased or normal TIBC, decreased % transferrin saturation, and increased ferritin

94
Q

What abnormal PBS findings may be observed in anemia of chronic kidney disease?

A

There may or may not be burr cells/ echinocytes

95
Q

What is the pathophysiology of anemia of chronic kidney disease?

A

Decreased erythropoietin secretion, bone marrow suppression by retained uremic substances, and effects of dialysis

96
Q

What is myelophthisic anemia?

A

Anemia caused by extensive infiltration of bone marrow by neoplastic or non-neoplastic process (fibrosis) resulting in decreased hematopoiesis and peripheral cytopenia

97
Q

What is the peripheral blood morphology of myelophthisic anemia?

A

Normochromic, normocytic anemia; Leukoerythroblastic appearance (nRBCs, immature myeloid cells, +/- teardrop RBCs

98
Q

True or False: Diagnosis of myelophthisic anemia can be based on peripheral blood smear findings.

A

False- a bone marrow biopsy is necessary for diagnosis

99
Q

What is aplastic anemia

A

Pancytopenia due to failure of bone marrow hematopoiesis

100
Q

What are the symptoms of aplastic anemia?

A

Anemia, infections secondary to leukopenia, and bleeding secondary to thrombocytopenia

101
Q

What are the causes of aplastic anemia?

A

Primary- Inherited, idiopathic; Secondary- drugs, viral infections, radiation, toxic exposure to benzene, solvents, insecticides, paroxysmal nocturnal hemoglobinuria

102
Q

How can the corrected reticulocyte count be calculated?

A

Corrected RC (%) = Reported RC (%) x (Patients HCT / 45 (nl HCT)

01 Hematology (16 decks)

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