Anemias of Blood Loss & Decreased Production Flashcards

1
Q

What is the unifying feature of hypoproliferative anemias? Classify them by pathophysiology.

A

low reticulocyte

  • Extrinsic cause
    • nutritional deficiencies
    • renal failure
    • chronic disease
  • Intrinsic cause (bone marrow failure)
    • infiltrative processes
    • aplastic anemia
    • hematopoietic neoplasms
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2
Q

What diseases are associated with microcytic anemia?

A

iron deficiency

chronic disease

sidroblastic anemia

thalassemia

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3
Q

What diseases are associated with Normochromic normocytic anemia?

A

chronic disease

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4
Q

What diseases are associated with macrocytic anemia?

A

Vitamin B12 or folate deficiency

medication/toxin effect

infections

neoplasms

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5
Q

What are the defects seen in microcytic hypochromic anemias?

A

decreased RBC hemoglobin production

cytoplasmic maturation defect

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6
Q

What is the most common cause of anemia world-wide?

A

iron deficiency

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7
Q

What are the common causes of iron deficiency anemia?

A

dietary deficiency

impaired absorption

increased requirement

chronic blood loss

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8
Q

What is the cause of iron deficiency in post-menopausal women & adults without uteruses?

A

chronic blood loss (cancer, etc.) until proven otherwise

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9
Q

Where is iron absorbed & in what form?

A

duodenum

most in the form of heme iron

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10
Q

How are we able to control the amount of iron stores in the body?

A

by controlling the absorption

we do not have good ways of getting rid of iron once it is absorbed

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11
Q

Free iron is bound to what carrier protein? Why?

A

transferrin

because free iron is toxic to cells

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12
Q

Iron is transferred from the duodenum to what main locations?

A
  • bone marrow
    • production of erythroid precursors
  • liver
    • storage
    • production of some enzymes
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13
Q

The storage of iron in the liver triggers the production/secretion of what protein? What does it do?

A

Hephaestin

induce the degradation of ferroportin (iron membrane transporter), therefore decreasing the amount of iron absorbed

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14
Q

What are the general physical signs of anemia?

A
  • Pale nail beds
  • Pallor
  • tachycardia (palpitations)
  • fatigue
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15
Q

What is koilonychia & what pathology does it indicate?

A

“spooning” of the fingernails

long-standing severe iron deficiency anemia

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16
Q

Glossitis is a sign indicative of what types of anemia?

A

inflammation of the tongue

iron or B12/folate deficiency

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17
Q

What are the features of Plummer-Vinson syndrome?

A

iron-deficiency anemia,

postcricoid dysphagia,

upper esophageal webs.

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18
Q

What are the classic findings in peripheral blood associated with iron deficiency?

A
  • Microcytic hypochromic cells
    • small cells w/ large area of central pallor
  • anisocytosis
  • poikilocytosis (elliptocytes, mainly with “pencil cells”
  • decreased reticulocyte count
  • mild thrombocytosis
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19
Q

A trick for estimating red blood cell size: a normal red blood cell should be about the same size as what other cell?

A

lymphocyte

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20
Q

Why do you commonly see mild thrombocytosis with iron deficiency anemia?

A

because have erythropoietin stimulating erythroid precursors in the bone marrow to start proliferating & maturing into RBC

it also stimulates the megakaryocytes

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21
Q

What type of bone marrow biopsy is shown in the provided image?

A

normal

iron is stained blue- the high power image is an example of an iron granule in a normal erythroid-precursor

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22
Q

What type of bone marrow biopsy is shown in the provided image?

A

iron deficiency anemia

(negative iron stain) – looking for blue

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23
Q

What tests should be performed to diagnose iron deficiency?

A

serum iron (measuring bound iron)

total iron-binding (equivalent to plasma transferrin)

serum ferritin quantitation (estimation of bone marrow iron store)

serum soluble transferrin receptor (soluble protein in the plasma that helps RBC accept iron form transferrin, gives good estimation of what is going on with transferrin receptors on RBC)

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24
Q

What condition could cause elevated levels of serum ferritin quantitation?

A

chronic inflammatory states - it is an acute phase reactant

(serum soluble transferrin receptor measure developed to assess individuals with severe chronic inflammatory diseases)

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25
Q

What is the relationship between iron stores and serum soluble transferrin receptor levels?

A

inversely proportional

-don’t memorize, but check out these relationships if it helps you-

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26
Q

Fill out the provided table

A
27
Q

What is the second most common cause of microcytic hypochromic anemia world-wide?

A

Anemia of chronic disease

28
Q

Anemia of chronic disease is general what type?

A

microcytic hypochromic

normocytic normochromic

29
Q

How quickly after onset of chronic disease is anemia usually detcted?

A

1-2 months

29
Q

How quickly after onset of chronic disease is anemia usually detcted?

A

1-2 months

30
Q

What are the 3 effects of chronic disease that lead to anemia?

A

failure of erythropoiesis

lack of iron for hemoglobin synthesis

decreased RBC survival

all cytokine mediated

31
Q

What are the characteristic morphologic features of a peripheral blood smear from a patient with anemia of chronic disease?

A

NO characteristic morphologic feature

32
Q

What would you expect from the RDW & reticulocyte count in patients with anemia of chronic disease?

A

normal RDW

low reticulocyte count

33
Q

Fill out the provided table

A
34
Q

Why do you see an increase in bone marrow iron with anemia caused by chronic disease?

A

reticularendothelial cells are not releasing the iron, leading to a buildup of iron in the marrow

35
Q

What happens in sideroblastic anemias?

A

abnormal iron metabolism within the RBC itself

iron is sequestered in the developing erythroblast mitochondria & is unavailable for heme synthesis

36
Q

What are the characteristic morphological findings seen in a peripheral blood smear from a patient with sideroblastic anemia?

A

blood appearance varies with cause

37
Q

What type of anemia is shown in the provided bone marrow stains?

A

Sideroblastic anemia

the stain on the right had a counterstain performed to make the nuclei more visible, which helps to identify the ringed sideroblasts (arrows)

left hand side shows an increase in iron stores (blue)

38
Q

Fill out the provided table

A
39
Q

What is the most common cause of megaloblastic anemia?

A

Vitamin B12 deficiency or folate deficiency

40
Q

What are the most common

A

reduced intake

impaired absorption

increased requirement

drug effect

41
Q

What cofactor is necessary for absorption of Vitamin B12?

A

intrinsic factor

(produced by parietal cells in gastric mucosa)

42
Q

Describe the pathophysiology associated with how the disease depicted in the slides causes anemia?

A

autoimmune destruction of gastric mucosa – destruction of the parietal cells

parietal cells are unable to produce intrinsic factor

the body is unable to absorb vitamin B12

43
Q

What is a unique feature of megaloblastic anemia?

A

jaundice

44
Q

What features of the provided peripheral blood smear are indicative of megaloblastic anemia?

A

jaundice

45
Q

Describe the pathophysiology associated with Vitamin B12 and Folate Deficiency megaloblastic anemia.

A

Vitamin B12 7 folate are required for DNA synthesis - Cells divide more slowly in deficiency

However, RNA synthesis continues normally, which leads to enlarged precursor cells with immature nuclei as compared to the cytoplasm

46
Q

How would you describe the bone marrow in the provided image?

A

normal erythroblasts

47
Q

How would you describe the bone marrow in the provided image?

A

Megaloblastic Anemia

large erythroid precursors

large bands

nucleus is larger & less mature for the amount of cytoplasm

48
Q

Severe megaloblastic anemia bone marrow biopsy can mimic what other condition?

A

leukemia

immature nuclei causes cells to be mistaken for blasts

49
Q

Why do you see hypercellular marrow in severe megaloblastic anemia?

A

erythroid & granulocytic hyperplasia because of ineffective hematopoiesis

50
Q

Fill out the provided table

A
51
Q

Are folate or Vitamin B12 deficiencies more common?

A

folate – can become deficient within months

Vitamin B12 will take about 5 years to develop symptoms of deficiency

52
Q

What are the clinical features seen in apalstic anemia?

A

any age / sex

insidious onset

  • Pancytopenia
    • anemia: weakness, pallor, dyspnea, tachycardia
    • thrombocytopenia: ecchymoses, petechiae
    • neutropenia
      • frequent persistent minor infections
      • acute serous infections with fever, chills, etc.
      • risk for disseminated fungal infections
53
Q

What type of anemia is Fanconi Anemia?

What is its cause?

Clinical features?

A

Constitutional Aplastic Anemia

defect in DNA repair - autosomal recessive

usually die of marrow failure - risk of leukemia / malignancies

54
Q

What features of the provided slides are consistent with Fanconi Anemia?

A
54
Q

What features of the provided slides are consistent with Fanconi Anemia?

A
55
Q

What is the cause of pure red cell aplasia?

A

only erythroid progenitors are suppressed

56
Q

Thymomas as associatd with what type of anemia?

A

pure red cell aplasia

& Myasthenia Gravis

57
Q

Large glandular lymphocytic leukemia is associated with what type of anemia?

A

pure red cell aplasia

58
Q

The provided condition shown in the slide is associated with what condition?

A

giant erythroblasts - nuclear inclusions composed of viruses

Pure Red Cell Aplasia Associated with Parvovirus B19

59
Q

What types of hematopoiesis is affected in Parvo B19 virus?

A

erythropoiesis is messed up

granulopoiesis & megakaryopoiesis is normal

60
Q

What is the cause of Blackfan-Diamond Anemia?

It is what type of condition?

Clinical associations?

A

Defect in generation of ribosome in RBC precursors (pure red cell aplasia)

Autosomal dominant

short stature, craniofacia, thumb, skeletal

61
Q

How can you differentiate Inherited Red Cell Aplasia from Parvo B19 associated Red Cell Aplasia?

A

No giant erythroblasts in inherited Red Cell Aplasia?

62
Q

What is the cause of Myelophthisic Anemia?

A

Metastatic Carcinoma