Pharmacology of Anemia Flashcards

1
Q

Where is most of the iron in the body found?

A

In hemoglobin

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2
Q

What form of iron is absorbed?

A

Ferrous (Fe2+)

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3
Q

Transferrin

A

Transferrin takes iron to bone marrow

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4
Q

Ferritin

A

Ferritin takes iron to plasma/liver/spleen

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5
Q

Ferroportin

A

Exports iron from the small intestine

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6
Q

What can be used to estimate iron stores in the body?

A

Ferritin in plasma is in equilibrium with body storage and can be used to estimate total body stores

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7
Q

Hepcidin

A

Downregulates ferroportin

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8
Q

How does anemia of chronic disease (ACD) affect hepcidin?

A

It increases hepcidin levels which will decrease ferroportin and decrease iron uptake

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9
Q

What are the transferrin and ferritin levels in iron deficiency?

A

Ferritin is low to store less iron

Transferrin is high

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10
Q

What are the transferrin and ferritin levels in iron overload?

A

Ferritin is high to store more iron

Transferrin is low

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11
Q

What population has increased iron requirements?

A
  • premature infants
  • children
  • pregnant or lactating women
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12
Q

What is used as oral iron therapy?

A

Ferrous sulfate, ferrous gluconate, ferrous fumarate

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13
Q

When is parenteral iron therapy used?

A

Indicated when oral iron is not tolerated, post GI resection, malabsorption syndromes

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14
Q

What is acute iron toxicity?

A

(1) May be fatal in small children
(2) Necrotizing gastroenteritis
(3) After short improvement, metabolic acidosis, coma and death

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15
Q

What is chronic iron toxicity?

A

Seen in hemochromatosis, multiple red cell tranfusions and it leads to organ failure like heart failure

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16
Q

How is acute iron toxicity treated?

A
  • Gastric aspiration
  • Gastric lavage-phosphate or carbonate solutions
  • Iron chelation (deferoxamine)
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17
Q

How is chronic iron toxicity treated?

A
  • Intermittent phlebotomy (if no anemia)

- Iron chelation (deferoxamine, deferasirox)

18
Q

What atom is in all vitamin B12 forms?

A

Cobalt

19
Q

What is required for vitamin B12 absorption?

A

Intrinsic Factor

20
Q

Where is vitamin B12 absorbed?

A

In the distal ileum

21
Q

Where is folic acid stored?

A

In the liver

22
Q

What are the effects of vitamin B12 or folate deficiency?

A
  • Alimentary tract: atrophic glossitis, chronic gastritis
  • Blood and bone marrow: megaloblastic anemia, leukopenia with hypersegmented granulocytes, mild to moderate thrombocytopenia
  • CNS: “subacute combined degeneration”: spastic paraparesis, sensory ataxia, lower limb paresthesias (not seen in folic acid deficiency)
23
Q

What is the treatment for vitamin B12 deficiency?

A

Vitamin B12 deficiency is treated by parenteral injections (IM) of cyanocobalamin or hydroxycobalamin

24
Q

What is the treatment for folic acid deficiency?

A

Oral folic acid

25
Q

Are CNS symptoms of B12 deficiency reversed with folic acid treatment?

A

NO

26
Q

Does treatment of vitamin B12 deficiency with oral vitamin B12 work even if the patient cannot make IF?

A

YES. High doses of oral B12 can bypass IF absence

27
Q

What is erythropoietin?

A
  • Glycoprotein, binds to its receptor and stimulates proliferation, differentiation of erythroid cells
  • Stimulates release of reticulocytes from bone marrow
  • Produced by the kidney
28
Q

What is the usual relationship between the levels of erytrhopoietin and Hb?

A

Inverse.

29
Q

When is erythropoietin therapy necessary?

A
  • Chronic renal failure
  • Aplastic anemia
  • Anemia of prematurity
30
Q

ROA of erythropoietin

A

IV or subcutaneous

31
Q

Erythropoietin SE

A

Hypertension, thrombotic complications , allergic reactions

32
Q

What is a major black box warning of erythropoietin?

A

Erythropoietin not as safe as was thought - increased

risk of tumor progression or recurrence as many tumors have an erythropoietin receptor present on them

33
Q

What are G-CSF and GM-CSF?

A

G-CSF and GM-CSF are growth factors that stimulate proliferation and differentiation of myeloid cells

34
Q

What is a unique function of G-CSF?

A

G-CSF promotes release of hematopoietic stem cells from the bone marrow into the peripheral circulation (much better than GM-CSF)

35
Q

What is a unique function of GM-CSF?

A

GM-CSF also stimulates proliferation and differentiation of erythroid and megakaryocytic cells

36
Q

What are indications for G-CSF and GM-CSF use?

A
  • After intensive chemotherapy
  • Treatment of congenital neutropenia, cyclic neutropenia, neutropenia associated with myelodysplasia and aplastic anemia
  • High dose chemotherapy with autologous stem cell rescue
37
Q

Which of G-CSF or GM-CSF is better tolerated?

A

G-CSF preferred since it is better tolerated in general

38
Q

G-CSF and GM-CSF SE

A
  • G-CSF can cause bone pain, splenic rupture (very rare)

- GM-CSF can cause fever, arthralgia, myalgia, peripheral edema, pleural/pericardial effusion

39
Q

IL-11 Actions

A
  • Promotes proliferation of megakaryocytic progenitors

* Increases peripheral platelet counts

40
Q

IL-11 Indications

A

• Patients with thrombocytopenia after chemotherapy

41
Q

Romiplostim

A

A novel protein known as a “peptibody” with two domains; a peptide domain that binds the thrombopoietin receptor (MPL), and an antibody Fc domain that increases half-life. Romiplostim is FDA approved for the treatment of idiopathic thrombocytopenia purpura (ITP).

42
Q

Eltrombopag

A

A small molecule thrombopoietin receptor agonist of the thrombopoietin receptor, approved for the treatment of ITP and new approval for the treatment of aplastic anemia.