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Clin Path > Macrocytic Anemia > Flashcards

Macrocytic Anemia Flashcards

1
Q

Anemia is defined as?

A

dec RBC count, HGB, HCT or O2 carrying capacity of blood

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2
Q

Anemia is NOT what?

A

specific diagnosis - purely abnormal lab test result that signifies and underlying cause

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3
Q

An expansion of plasma volume that results in dilutional anemia is called?

A

spurious anemia

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4
Q

What are some causes of spurious anemia?

A
  1. hydremia of pregnancy (physiologic)
  2. congestive heart failure
  3. overhydration (excessive IV fluids)
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5
Q

Shortness of breath (esp with exertion), fatigue, weakness, palpitations, dizziness, syncope are all symptoms of?

A

anemia

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6
Q

What happens to the mucocutaneous membranes of anemic patients?

A

pallor

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7
Q

What happens cardiovascularly in anemic patients?

A

hyperdynamic circulation: tachy, bounding pulse, systolic flow murmur

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8
Q

What is kolionychia? Which anemia is it associated with?

A

concave (“spoon-shaped”) brittle nails

iron deficienc anemia

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9
Q

Which anemias are leg ulcers indicative of?

A

sickle cell anemia, hemoglobinopathies

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10
Q

What causes bone deformities in some anemic patients?

A

expansions of medularry cavity due to erythroid hyperplasia

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11
Q

How do the bone deformities look on x-ray?

A

“hair-on-end” appearance

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12
Q

What types of anemias will result in bone deformities?

A

thalassemia, sickle cell anemia

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13
Q

Loss of vibratory and position sense in associated with?

A

B12 megaloblastic anemia

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14
Q

What are some initial major adaptations to anemia?

A
  1. cardio: tachy and inc stroke volume
  2. HGB-O2 dissociation curve: right shift due to inc 2,3-DPG - O2 loses affinity
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15
Q

What are some following marrow responses to anemia?

A

erythroid hyperplasia with reticulocytosis (erythroid production can increase 8-fold)

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16
Q

____ reflects ability of the marrow to produce and deliveer RBCs to the peripheral blood (aka?)

is it a part of the routine CBC?

A

reticulocyte count; effective erythropoiesis

NO

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17
Q

What stain is needed to see reticulocytes and how does it work?

A

supravital stain - precipitates ribosomal RNA as a reticulin network

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18
Q

Polychromatic erythrocytes are visible with what smear? What does an increase indicative of?

A

Wright-Stained smear; polychromasia

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19
Q

Reticulocytes are the same cells as?

A

polychromatic RBCs

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20
Q

What does a decrease/normal reticulocyte count with anemia implies?

A

lack of appropriate marrow response - determine cause

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21
Q

What value is normal reticulocytes?

A

0.5-1.5% (percent of circulating RBCs) or

50-165 x 103 cells/microliter

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22
Q

An inc in retic count implies what?

A

increase production and delivery of RBCs in response to anemia

may be adequate OR insufficient depending on degree of anemia

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23
Q

How do we correct reticulocyte count?

A
24
Q

Decrease in RBC production resuts in?

A

hypoproliferative anemia

25
Q

A decrease or “normal” corrected RC is indicative of? (in relation to hypoproliferative anemia)

A
  1. aplastic anemia
  2. myelophthisic anemia
26
Q

Define myelophthisic anemia.

A

replacement of marrow by fibrosis, tumor, etc

27
Q

What’s maturation defect?

A

RBCs produced by die in the marrow - aka ineffective erythropoiesis

28
Q

A decrease or “normal” corrected RC is indicative of? (in relation to maturation defect)

A
  1. megaloblastic anemia
  2. myelodysplastic syndromes
29
Q

What results when the bone marrow effectively produce and deliver RBCs to peripheral blood?

A

hyperproliferative anemia

30
Q

What kinds of peripheral destruction can occur in hyperproliferative anemia?

A

hemolysis or hemorrhage

31
Q

Increased corrected retic count can be indicative of?

A

hyperproliferative anemia

treated nutritional anemia

32
Q

MCV 80 – 100 fL

*MCV being an average*

A

normocytic

33
Q

MCV <80 fL

A

microcytic

34
Q

MCV >100 fL

A

macrocytic

35
Q

What are the 2 major types of macrocytic anemias?

A

megaloblastic vs non-megaloblastic anemia

36
Q

What are some causes for megaloblastic anemia?

A
  1. B12, folate deficiency
  2. drugs - folate antagonists (methotrexate), chemotherapeutic agents, antiretroviral drugs
37
Q

What are some causes of non-megaloblastic anemias?

A
  1. hemolysis, hemorrhage (reticulocytosis)
  2. alcoholism, liver disease
38
Q

What’s the pathogenesis of megaloblastic anemia?

A
39
Q

What’s the source of B12?

A

foods of animal origin: meat, liver, fish, dairy (NOT found in veg, frits, cereals)

normal body stores last 3-4 years

40
Q

How is B12 absorbed in the body?

A
41
Q

What are the causes of B12 deficiency?

A
  1. malabsorption
  2. dietary deficiency (rare in U.S.) - strict vegans and their breast-fed infants
  3. drugs- nitrous oxide exposure
42
Q

What can lead to malabsorption of B12?

A
  1. pernicious anemia - lack of intrinsic factor
  2. surgical: gastrectomy (total or partial), resection of terminal ileum
  3. inflammatory bowel disease
  4. tropical sprue and gluten - sensitive enteropathy
  5. blind loop syndrome - bacterial overgrowth competing for B12
  6. fish tapeworm (diphyllobothrium latum)
43
Q
  • an autoimmune chronic atrophic gastritis
  • results in hypo-/achlorhydria
  • average age = 60 years
  • most common in persons of N. european descent
  • increased risk of gastric carcinoma
  • significant assocation with other autoimmune diseases (grave”s, hashimoto’s)
A

pernicious anemia (PA)

44
Q

Define autoimmune chronic atrophic gastritis.

A

anti-parietal and anti-intrinsic factor antibodes destroy gastric parietal cells and intrinsic factor production

45
Q
  • found in leafy greeen veg, fruits, cereals, dairy products, and liver
  • heat labile and destroyed by cooking (unlike what?)
  • where absorbed?
A

folate

B12

in upper SI (duodenum and jejunum)

46
Q

What’s the most common cause of folate deficiency?

A

inadequate dietary intake since body stores in liver only lasts 3-4 months

47
Q

What are some clinical signs and symptoms of folate deficiency?

A

similar to those in B12 deficiency except lack of neurological features typically seen in B12 deficiency

48
Q
  • symptoms: weakness and sore tongue; glossitis may be painful, smooth, and atrophic or beefy red; angular cheilosis
  • physical exam: pallor with mild jaundice (“lemon-yellow” skin)
  • neurological impairment: may present with this with no anemia or macrocytosis
A

megaloblastic anemia

49
Q

What causes the neurological impairments sometimes seen in megalobastic anemia? reversible or irreversible?

A

B12 deficiency! (unreleated to degree of anemia)

irreversible

50
Q

What are the neuropathologic changes that can occur in B12 deficiency?

A
  • demyelination of dorsal and lateral columns of spinal cord - affecting both sensory and motor pathways - subacute combined degeneration
  • peripheral neuropathy: parethesias (“pins and needles”) in LE; reduced vibration and position sense in extremities
  • uncoordinated gait: difficulty walkng and loss of balance
51
Q

What’s the B12/Folate pathophysiology?

A
52
Q

What are the 3 key reactins B12 is essential for?

A
53
Q

What’s the peripheral blood morphology in megaloblastic anemia?

A
  • RBC: macro-ovalocytes
  • WBC: hypersegmented neutrophils- one of first to appear and among last to disappear after therapy
  • platelets: decreased - thrombocytopenia
54
Q

What’s the bone marrow morphology in megaloblastic anemia?

A
  • erythroid hyperplasia with megalobastic change (nuclear/cytoplasmic dysynchrony)
  • giant bands and metamyelocytes
55
Q
A

Clin Path (3 decks)

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