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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
What are the etiologies of non-megaloblastic anemia?
Hemolysis, hemmorhage, alcoholism, liver disease
26
What is the cause of spurious macrocytosis?
Cold agglutinins
27
What is the pathogenesis of megaloblastic anemia?
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
28
What is the morphology of megaloblastic anemia?
RBCs- macro-ovalcytes; WBCs- hypersegmented neutrophils; thrombocytopenia
29
What is the morphology of the bone marrow during megaloblastic anemia?
Erythroid hyperplasia with megaloblatic change characterized by nuclear/cytoplasmic dysynchrony; Giant band cells and metamyelocytes, and maybe hypersegmented neutrophils
30
What CBC results are indicative of megaloblastic anemia?
Pancytopenia (decreased Hb, WBC, and platelets); Macrocytosis (increased MCV); Decreased corrected reticulocyte count
31
What blood chemistry panel results are indicative of megaloblastic anemia?
Increased levels of circulating LDH or indirect bilirubin
32
True or False: A low RBC folate result is specific to a folate deficiency.
False- can also be decreased in B12 deficiency
33
What is the primary cause of megaloblastic anemia? What is the mechanism?
B12 deficiency;
34
What are the major dietary sources of folate?
Meat, liver, fish, dairy
35
How long do the normal body stores of B12 last?
3-4 years
36
What is the most common mechanism of B12 deficiency?
Malabsorption
37
What is pernicious anemia?
An autoimmune chronic atrophic gastritis-- megaloblastic anemia due to B12 deficiency that results from a lack of intrinsic factor
38
Why does a B12 deficiency cause neurological symptoms but not a folate deficiency?
Only B12 is necessary for nerve myelination
39
What metabolite builds up with a B12 deficiency?
Methylmalonic acid
40
How can a B12 deficiency lead to a decrease in folate?
With B12 deficiency , CH3-folate can acumulate in the RBC and then diffuse out into the plasma
41
What is the etiology of Pernicious anemia?
Anti-parietal cell and anti-intrinsic factor Abs which destroy parietal cells and intrinsic factor production
42
What tests are specific for pernicious anemia?
Anti-parietal cell Abs or Anti-intrinsic factor Abs
43
What are the symptoms of B12 deficiency?
Weakness and sore tongue, glossitis
44
How will a B12 deficiency present during the physical exam?
Pallor with mild jaundice, neurological impairment
45
What specific neurological symptoms and signs manifest due to B12 deficiency?
Demyelination of dorsal and lateral columns of the spinal cord; Peripheral neuropathy; Uncoordinated gait
46
What is the dietary sources of folate?
Leafy green veggies, fruits, cereals, dairy, liver
47
True or False: Folate is heat labile and destroyed by cooking
True
48
Where are B12 and folate absorbed in the GI tract?
B12 in the ileum and folate in the jejunum
49
Where does the body store folate? How long can this store last?
Stores in the liver and only lasts 3-4 months
50
What are the causes of folate deficiency?
Inadequate diet (malnutrition. alcoholism); Increased folate requirements (pregnancy, infancy, tumors, hemolytic anemia with compensatory myeloproliferative syndromes; Malabsorption; Drugs
51
How are B12 and folate deficiencies treated?
Replacement therapy with parenteral B12 or folate
52
What are non-megaloblastic macrocytic anemias?
Increased MCV NOT due to impaired DNA synthesis
53
What are the etiologies of non-megaloblastic, microcytic anemia?
Hemolysis, hemorrhage, alcohol, chronic liver disease
54
What etiologies of non-megaloblastic microcytic anemia can result in the presence of target cells in a PBS
Alcohol or liver disease
55
What is the relative amount of cytoplasmic Hb in microcytic anemias compared to healthy patients?
Hypochromia- decreased Hb
56
What is the major cause of microcytic anemia?
Disorders of iron metabolism and utilization (Fe deficiency or anemia of chronic disease)
57
What anemia results from disorders of heme synthesis?
Sideroblastic anemia
58
What results from disorders of globin synthesis?
Thalassemia
59
Where is iron stored (cells and organs)?
Within macrophages- primarily in bone marrow and liver, but some in splenic macrophages
60
What are the forms that Fe can be stored as?
Ferritin and hemosiderin
61
What are the normal amounts of Fe stored in the adult male and female body?
Male~ 1000 mg; Females~400 mg
62
Why do females require a daily Fe requirement 1 mg higher than men?
They lose 20 mg Fe every menstrual cycle
63
How much Fe is contained in 1 mL RBCs?
1 mg
64
What are the general categories of Iron Deficiency Anemia etiologies? What is the most common cause?
Chronic blood loss, increased requirement, decreased iron absorption, and inadequate dietary intake
65
What is achlorhydria?
An upset in the acid balance of the stomach
66
What is koiloncychia?
Spooning of the nails (substantial indentation in surface of fingernails)
67
What epithelial abnormalities are associated with Fe deficiency?
Koilonychia, Glossitis +/- tongue atrophy, angular cheilitis , esophageal webs with dysphagia
68
What is Plummer-Vinson Syndrome?
Occurs in people with long-term IDA resulting in the combination of esophageal web with dysphagia and glossitis/ angular cheilitis
69
What is measured as serum iron?
The amount of iron bound to transferritin
70
What is the total iron binding capacity?
The max concentration of Fe that existing transferrin within the body can bind
71
How is the total iron binding capacity affected by Iron-deficiency anemia?
Increases
72
What is serum ferritin an estimate of? How is it affected by IDA?
Body storage iron- decreased in IDA
73
What is free erythrocyte protoporphyrin (FEP)? What is indicated by an increased FEP?
Heme minus Fe= FEP; Increased FEP indicates not enough Fe is available to form heme or failure of iron incorporation into heme
74
What specific conditions would lead to an increase in FEP?
IDA, anemia of chronic disease, sideroblastic anemia, or lead toxicity
75
How does Fe deficiency affect serum soluble transferrin receptor?
Increased in IDA
76
What is the peripheral blood morphology of IDA?
Hypochromic, microcytic RBCs, +/- thrombocytosis
77
What is the bone marrow morphology in IDA?
Absent iron within macrophages
78
What are the stages of IDA?
1- Fe depletion; 2- Fe-deficient erythropoiesis occurs once Fe stores are depleted; 3- IDA
79
How is IDA treated?
Iron replacement- oral or parenteral
80
What is the pathophysiology of Sideroblastic anemia?
Impaired incorporation of Fe into protoporphyrin ring resulting in accumulation of excess Fe in perinuclear mitochondria
81
What are the causes of sideroblastic anemia?
Hereditary (rare) or Acquired through myelodysplastic syndrome or drug usage
82
What is the peripheral blood morphology of sideroblastic anemia?
Dimorphic RBC population (hypochromic/microcytic or normochromic/cytic) and Pappenheimer bodies
83
What are Pappenheimer bodies?
Iron-containing intracellular inclusions in RBCs
84
What is the bone marrow morphology in sideroblatic anemia?
Increased storage iron in macrophages and ring sideroblasts
85
How does lead toxicity lead to anemia?
Lead interferes with enzymatic processes involved in heme synthesis- blocks Fe incorporation into protoporphyrin
86
What molecules increase in circulation due to lead toxicity?
FEP and delta-aminolevulinic acid
87
What kind(s) of anemia can be caused by lead toxicity?
Normochromic/ normocytic OR hypochromic/microcytic
88
What are the signs and symptoms of lead toxicity?
Abdominal pain, peripheral neuropathy, renal dysfunction, encephalopathy, and gingival lead line
89
What is the differential diagnosis for normochromic, normocytic anemias?
Anemia of chronic disease, chronic kidney disease, endocrinopathy, myelophthisic anemia, aplastic anemia, or acute blood loss
90
What is anemia of chronic disease?
Mild-moderate anemia, usually of at least several months' duration associated with inflammatory, infectious, or neoplastic processes
91
What is the second most common type of anemia?
Anemia of chronic disease
92
What are the 2 mechanisms of pathogenesis of anemia of chronic disease?
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
How does anemia of chronic disease affect iron studies?
Decreased serum Fe, Decreased or normal TIBC, decreased % transferrin saturation, and increased ferritin
94
What abnormal PBS findings may be observed in anemia of chronic kidney disease?
There may or may not be burr cells/ echinocytes
95
What is the pathophysiology of anemia of chronic kidney disease?
Decreased erythropoietin secretion, bone marrow suppression by retained uremic substances, and effects of dialysis
96
What is myelophthisic anemia?
Anemia caused by extensive infiltration of bone marrow by neoplastic or non-neoplastic process (fibrosis) resulting in decreased hematopoiesis and peripheral cytopenia
97
What is the peripheral blood morphology of myelophthisic anemia?
Normochromic, normocytic anemia; Leukoerythroblastic appearance (nRBCs, immature myeloid cells, +/- teardrop RBCs
98
True or False: Diagnosis of myelophthisic anemia can be based on peripheral blood smear findings.
False- a bone marrow biopsy is necessary for diagnosis
99
What is aplastic anemia
Pancytopenia due to failure of bone marrow hematopoiesis
100
What are the symptoms of aplastic anemia?
Anemia, infections secondary to leukopenia, and bleeding secondary to thrombocytopenia
101
What are the causes of aplastic anemia?
Primary- Inherited, idiopathic; Secondary- drugs, viral infections, radiation, toxic exposure to benzene, solvents, insecticides, paroxysmal nocturnal hemoglobinuria
102
How can the corrected reticulocyte count be calculated?
Corrected RC (%) = Reported RC (%) x (Patients HCT / 45 (nl HCT)

01 Hematology (16 decks)

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