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M2 Heme/Lymph > Hypoproliferative Anemia Application Exercises - (Harrington) > Flashcards

Hypoproliferative Anemia Application Exercises - (Harrington) Flashcards

1
Q

What is this? What is biochemical abnormality might be associated with this finding?

A

Hypersegmented neutrophil

Due to tetrahydrofolate or vitamin B12 deficiency

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2
Q

Given these CBC results: (WBC 2.5K, platelets 60K, Hb 9 g/dL), which of the following is most compatible?

  1. Paroxysmal nocturnal hemoglobinuria
  2. Anemia of renal disease
  3. Anemia associated with pica
  4. Anemia of chronic disease/inflammation
  5. Anemia of the elderly
A
  1. Paroxysmal nocturnal hemoglobinuria
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3
Q

Name (2) forms of hypoproliferative anemia characterized by impaired proliferation or differentiation of stem cells

A

aplastic anemia

pure red cell aplasia

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4
Q

Name (5) forms of hypoproliferative anemia characterized by impaired proliferation/maturation of erythroid precursors (ineffective erythropoiesis)

A

megaloblastic anemia

anemia of renal failure

anemia of chronic disease

anemia of liver disorders

myelodysplastic syndromes

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5
Q

Name (3) forms of hypoproliferative anemia characterized by defective hemoglobin synthesis

A

iron deficiency anemia

sideroblastic anemia

thalassemias

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6
Q

Name (3) causes of hypoproliferative anemia characterized by marrow replacement or infiltration

A

hemoatopoietic tumors

metastatic tumors

granulomatous inflammation

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7
Q

Give two invariant lab features of all hypoproliferative anemias

A

anemia

low reticulocyte count

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8
Q

Approximately what proportion of platelets are normally stored in the spleen?

A

1/3

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9
Q

Give (5) differential diagnoses for hypersplenism

A

Portal hypertension

Extramedullary hematopoiesis

Leukemias/lymphomas

Myeloproliferative neoplasms

Storage disorders

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10
Q

Methionine sythetase requires what two cofactors?

A

methyl-THF and vitamin B12

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11
Q

Name the enzyme responsible for the conversion of folate to tetrahydrofolate.

Is this a one-step process?

Which drug blocks the action of this enzyme?

A

dihydrofolate reductase

No. Two-steps (both performed by DHFR)

Methotrexate (MTX)

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12
Q

Describe this cell

What caused this?

What disease is this associated with?

A

Bite cell

Mononuclear cell phagocytosis of denatured protein (Heinz bodies) in the RBC cytoplasm

G6PD deficiency

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13
Q

Describe the morphologic changes seen in the peripheral blood and bone marrow in megaloblastic anemia

A

Peripheral blood

  • hypersegmented neutrophils (5 or more nuclear lobes)
  • macrocytic anemia with oval macrocytes
  • anisopoikilocytosis (size and shape variation)

Bone marrow

  • hypercellularity
  • giant bands
  • nuclear to cytoplasmic dyssynchrony
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14
Q

Which type of cell found in the stomach secretes acid? What other important product does it secrete?

Which cell type secretes pepsin?

A

Parietal cells. Also secrete intrinsic factor (IF)

chief cells

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15
Q

In which part of the GI tract is vitamin B12 normally absorbed. What else is required?

A

Vitamin B12 is absorbed chiefly in the ileum, bound to IF.

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16
Q

Name the two deficiencies that cause megaloblastic anemia

A

Vitamin B12, Folate

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17
Q
A
18
Q

Where do we normally get vitamin B12?

What can cause vitamin B12 deficiency?

A

Animal products

Causes:

  • Impaired absorption (IF deficiency, ileal resection, pancreatic insufficiency)
  • Increased requirement (example: pregnancy)
  • Decreased intake (vegans)
  • Tapeworm (diphyllobothrium latum)
19
Q

If dietary B12 is eliminated, how fast does B12 deficiency develop?

What about folate?

A

Very slowly. Stores within the body can last for years

Folate stores deplete faster (months)

20
Q

Which is normally associated with neurological issues - folate deficiency or vitamin B12 deficiency?

A

vitamin B12 deficiency

21
Q

Define pernicious anemia

What are some typical lab findings?

A

Deficiency of vitamin B12 secondary to IF abnormalities (due to Ab against IF)

Labs: low B12, low reticulocyte count, auto-Ab to IF or parietal cells, elevated methylmalonic acid

22
Q

Where do we normally get dietary folate?

What can cause folate deficiency?

In the setting of pregnancy, what does folate deficiency lead to?

A

Green veggies

Causes:

  • Increased requirement (pregnancy, states of high cell turnover)
  • Decreased intake (alcoholism, malnutrition)
  • Defective absorption (jejunal resection)
  • Folic acid antagonists

Pregnancy: neural tube defects, including spina bifida occulta, anencephaly, etc

23
Q

Describe these cells

Name the disease(s) typically associated with these.

A

Schistocytes

Red cell fragmentation disorders: DIC, TTP/HUS, traumatic hemolysis (mechanical heart valve)

24
Q

What hemoglobin concentration is considered severely low?

A

<7 g/dL Hb

25
Q

Name (5) physiologic compensatory mechanisms seen in the setting of anemia

A

Increased 2,3-DPG (increase unloading in tissues)

Shunting

Increased cardiac output

Increased respiratory rate

Increased red cell production

26
Q

Give the differential diagnosis for microcytic, hypochromatic anemia (3 diseases)

A

Iron deficiency anemia (IDA)

thalassemias

Anemia of chronic disease (ACD)

27
Q

Name some causes of iron deficiency

A

Dietary lack (i.e. milk-fed infants)

Impaired absorption

Increased requirement

Chronic blood loss (GI, menstrual bleeding)

28
Q

Describe the process by which heme iron is absorbed into the blood

A
  • heme iron in the intestinal lumen is transported through the cell membrane by the heme transporter
  • heme iron is transferred to mucosal ferritin
  • The ferroportin-1 channel transfers ferritin-bound iron (Fe2+) through the basolateral surface of the cell, where it is converted to Fe3+ by hephaestin
  • Fe3+ is bound and transported by plasma transferrin
29
Q

Describe the process by which non-heme iron is absorbed into the blood

A
  • Non-heme iron (Fe3+) in the intestinal lumen is converted to Fe2+ by duodenal cytochrome C
  • Fe3+ enters the cell via the DMT1 transporter and is bound by mucosal ferritin
  • Fe2+ leaves the basolateral face of the endothelium via Ferroportin 1
  • Fe2+ is converted to Fe3+ via hephaestin (basolateral surface of endothelial cell)
  • Fe3+ is bound by plasma transferrin
30
Q

What enzyme is secreted by the liver in response to elevated iron?

What specifically does it block?

A

Hepcidin

Blocks ferroportin, the Fe2+ transporter located on the basolateral surface of the duodenal epithelial cells

31
Q

What is the most sensitive assay for iron deficiency anemia?

What is a relatively insensitive assay for IDA?

A

Serum ferritin - very high sensitivity and specificity

Serum iron

32
Q

What is total iron binding capacity (TIBC)?

A

Reflects the amount of protein available to bind iron in the blood - essentially equivalent to transferrin concentration

33
Q

How is % iron saturation calculated?

A

% iron saturation = serum iron / TIBC

34
Q

For IDA, describe each of the follow as increased, decreased, or no change:

  • Reticulocytosis
  • Marrow storage iron
  • Sideroblastic iron
  • Serum ferritin
  • Serum iron
  • TIBC
  • % iron saturation
A
  • decreased
  • decreased
  • decreased
  • decreased
  • decreased
  • increased
  • decreased
35
Q

For IDA, describe each of the follow as increased, decreased, or no change:

  • Reticulocytosis
  • Marrow storage iron
  • Sideroblastic iron
  • Serum ferritin
  • Serum iron
  • TIBC
  • % iron saturation
A
  • decreased
  • increased
  • decreased
  • increased
  • decreased
  • no change / decreased
  • no change / increased
36
Q

What is the most common anemia in hospitalized patients?

How severe is the anemia (generally)?

What are its major clinical associations?

What is the general mechanism behind the anemia?

A

Anemia of chronic disease (ACD)

usually mild to moderate

Clinical associations: chronic infections, immune dysfunction disorders, neoplastic disorders

Heptcidin-mediated (acute phase reactant) block in iron transport from macrophages into erythroid precursors.

37
Q

Name (4) major physiologic responses to inflammatory stimulus that leads to ACD

A

All due to activated monocytes and T-cells (INF-gamma, TNF-alpha, IL-1, IL-6)

  • Increased hepatic synthesis of hepcidin
  • inhibited EPO release -> decreased erythropoiesis
  • Direct inhibition of erythroid proliferation
  • Augmented hematophagocytosis
38
Q

Is ACD microcytic, normocytic, or macrocytic?

A

normocytic (80%) or microcytic (20%)

39
Q

What is the treatment for ACD?

A

treatment of underlying disorder

EPO or iron therapy

40
Q

What is anemia or renal failure?

A

Decreased EPO production due to kidney damage

41
Q

Describe pure red cell aplasia

A

selective abscence of erythroid precursors

often associated with thymic hyperplasia, thymomas, autoimmune disorders, drugs, LGLL

42
Q

What is myelophthisic anemia?

A

Anemia secondary to bone marrow infiltration by metastatic carcinoma

Leukoerythroblastic reaction with teardrop cells may be observed

M2 Heme/Lymph (32 decks)

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