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(J2) RBCs and Bleeding Disorders > Anemias of Diminished Erythropoiesis > Flashcards

Anemias of Diminished Erythropoiesis Flashcards

1
Q

What is iron deficiency anemia?

A

anemia due to insufficient iron for one of many reasons

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2
Q

What morphologic changes occur in iron deficiency anemia?

A
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3
Q

What are the common mechanisms of iron deficiency anemia?

What are examples of each?

A
  • dietary insufficiency
    • breast fed babies
    • impoverished
  • malabsorption
    • gastrectomy (acid favors Fe2+ which is more readily absorbed)
      • increased requirement
    • growing children
    • pregnancy
  • blood loss
    • menorrhagia
    • GI bleed
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4
Q

What would expected lab changes be in iron deficiency anemia?

A
  • decreased HGB
  • decreased ferretin (don’t have it)
  • increased TIBC
  • decreased serum iron (don’t have it)
  • decreased saturation
  • increased free erythrocyte protoporphyrin (FEP) (have but can’t use)
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5
Q

How do the lab changes of iron deficiency anemia present as it is developing?

A
  1. depletion of stores ( decreased ferritin, increased TIBC)
  2. depletion of serum (add decreased serum iron, decreased transferrin saturation)
  3. normocytic anemia (BM just makes less cells but keeps them normal)
  4. microcytic, hypochromic anemia (fewer cells as well)
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6
Q

What treatment is used in iron deficiency anemia?

A
  • ferrous sulfate
  • address source of blood loss (if present)
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7
Q

What clinical feature can be found in iron deficiency anemia?

A

Nonspecific symptoms

  • koilnychia (spooned nails)
  • pica (eat non-food stuffs)
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8
Q

What is Plummer-Vinson syndrome?

A

disease characterized by iron deficiency anemia, atrophic glossitis (beefy red tongue), and esophageal webbing (dysphagia)

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9
Q

What is anemia of chronic disease?

A

anemia due to decreased availability of iron in the setting of chronic inflammation or cancer

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10
Q

What morphologic changes occur in anemia of chronic disease?

A

normocytic anemia progressing to microcytic, hypochromic anemia

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11
Q

What is the mechanism of anemia of chronic disease?

A

increases hepcidin as part of inflammation

  • decreased release of iron from MΦ -> increased sequesteration of iron
  • decreased EPO production

the body interprets inflammation as infection so it tries to take iron away from the blood because come bacteria need iron to grow

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12
Q

What would expected lab changes be in anemia of chronic disease?

A
  • increased ferretin (it is all being stored)
  • decreased TIBC
  • decreased serum iron
  • decreased saturation
  • increased free erythrocyte protoporphyrin (FEP) (have but can’t use)
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13
Q

What treatment is used in anemia of chronic disease?

A
  • treat underlying cause
  • EPO can be used in cancers
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14
Q

What is sideroblastic anemia?

A

anemia due to decreased protoporphyrin production

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15
Q

What morphologic changes occur in sideroblastic anemia?

A

Ring sideroblasts:

-iron-laden mitochondria form ring around nucleus of erythroid precursors

micro

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16
Q

What are the common mechanisms of sideroblastic anemia?

A

Iron is available and in excess, however, there is not enough protoprophyrin to produce hemoglobin

Congenital:

  • mutation of ALAS (rate limiting, protoporphyrin production)

Aquired:

  • alcoholism (mitochondiral toxin; inhibit ferrochelatase)
  • lead poisoing (inhibit ALAD and ferrochelatase)
  • vitamin B6 deficiency (cofactor for ALAS)
17
Q

What would expected lab changes be in sideroblastic anemia?

A
  • increased ferretin (have but can’t use
  • decreased TIBC
  • increased serum iron (have but can’t use)
  • increased transferrin saturation
  • decreased free erythrocyte protoporphyrin (FEP) (don’t have)
18
Q

What is aplastic anemia?

A

Primary hematopoietic failure resulting in pancytopenia

(anemia, low reticulocyte count leukopenia, and thrombocytopenia)

fatty marrow

-normally no

19
Q

What would expected lab changes be in aplastic anemia?

A
  • all ages, both genders
  • pancytopenia (anemia, low reticulocyte count, neutropenia, and -thrombocytopenia)
  • hypocellular, fatty marrow
20
Q

What is the common presentation of aplastic anemia?

A
  • weakness, pallor, dyspnea (anemia)
  • hemorrhage, petechiae, ecchymosis (thrombocytopenia)
  • infections (neutropenia)
  • NO SPLENOMEGALY
21
Q

What are common causes of aplastic anemia?

A
  • idopathic
  • drugs (many chemotherapeutics)
  • whole body irradiation
  • certain viral infections
  • genetic (fanconi anemia)
22
Q

What is pure red cell aplasia?

A

disorder where only erythroid progenitors are suppressed

-results in anemia with no change to WBCs

23
Q

What are common causes of pure red cell aplasia?

A
  • thymoma
  • autoimmune disorder (particularly targeting EPO)
  • parvovirus B19
24
Q

How does parvovirus B19 relate to anemia?

A

Infects RBC progenitors and halts hematopoiesis

  • typcially asymptomatic in healthy individuals
  • can result in aplastic anemia in those who already have anemia
25
Q

What groups are particularly at risk for developing aplastic crisis from parvovirus B19 infection?

A

Severe hemolytic anemias

  • hereditary spherocytosis
  • sickle cell anemia
26
Q

How does chronic renal failure related to anemia?

A

decreased EPO

(J2) RBCs and Bleeding Disorders (10 decks)

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