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Heme and Lymph Midterm > Kruse: Pharmacology of anemia; hematopoietic growth factors > Flashcards

Kruse: Pharmacology of anemia; hematopoietic growth factors Flashcards

1
Q

Where is iron aborbed?

A

the duodenum

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2
Q

What form of iron can be absorbed?

A

the Fe2+ kind

-ferrous

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3
Q

What transfers iron in the blood?

A

transferrin

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4
Q

What protein lets ferrous iron intot he cell?

A

DMT1

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5
Q

What is Iron stored as?

A

ferritin

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6
Q

What do we do with someone who has an iron deficiency anemia?

A

give them iron preparations

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7
Q

What kind of iron should be in oral preparations?

A

the ferrous form, that is what gets absorbed!

-ferous sulfate, gluconate, or fumarate will do

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8
Q

When would use parenteral iron therapy?

A

when the patient cant tolerate or absorpb the oral kind

  • be careful, it bypasses the regulatory mechanisms and deliver more iron than can be stored
  • gotta watch iron levels for toxicity
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9
Q

What are the 3 forms of parenteral iron in the US?

A

Iron dextran: small test first because of hypersensitivity risk
Sodium ferric gluconate complex
Iron-sucrose complex
-the last 2 are less likely to cause hypersensitivity rxns

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10
Q

Acute Iron toxicity

A
  • exclusively in young children who accidentally ingest iron tablets
  • vomiting, bloody poo, shock, lethargy
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11
Q

What do we treat iron toxicity with?

A

Deferoxamine

-potent iron-chelating compound

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12
Q

Chronic Iron toxicity

A
  • deposits in heart, liver, pancreas, and other organs.. can lead to organ failure and death
  • common in patients with inherited hemochromatosis
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13
Q

What do we treat chronic iron toxicity with?

A

deferasirox

-reduces liver iron concentrations buyt data in removing iron form heart is lacking

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14
Q

What does B12 deficiency give us?

A

megaloblastic anemia

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15
Q

What needs to bind to B12 before we can absorb it?

A

intrinsic factor

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16
Q

Where is B12 absorbed in the GI tract?

A

the distal ileum

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17
Q

What 2 things does B12 do?

A
  • takes a Methyl group from THF and gives it to homocystein to make METHIONINE
  • helps methylmalonic acid turn into Succinyl CoA
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18
Q

What is a common cause of B12 deficiency?

A

pernicious anemia

-antibodies against Intrinsic factor

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19
Q

What neuro effects happen in B12 deficiency?

A

parasthesias int he peripheral nerves

-progresses to spasticity, ataxia, and other CNS dysfunctions

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20
Q

What are almost all B12 deficiencies due to?

A

malabsorption

-so, we need to give parenteral B12 injections (cyanocobalamin and hydroxocobalamin)

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21
Q

What is Folic Acid required for?

A

the synthesis or amino acids, purines, and DNA (dTMP)

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22
Q

What are the richest sources of folic acid?

A

yeast, liver, kidney, and green veggies

23
Q

what enzyme lets folic acid reenter the cycle as dihydrofolate?

A

Folate reductase

24
Q

How does folic acid deficiency look clinically?

A

a lot like B12 defiency, but there’s no neuro symptoms because methylmalonic acid is just fine

25
Q

What are some drugs that can cause folic acid deficiency

A

methotrexate, trimethoprim, and pyrimethamine (all inhibit dihydrofolate reductase)

26
Q

What is sufficient to reverse the megaloblastic anemia caused by folic acid deficiency?

A

1 mg/day PO folic acid

27
Q

Erythropoietin

A
  • JAK/STAT signaling
  • rises in hypoxemia
  • inflammatory cytokines suppress its secretion
28
Q

What is Darbepoetin alpha?

A

a modified form or EPO that is more glycosylated and has a half-life of 24-26 hours

29
Q

What gets released fromt he bone marrow into the blood stream as a result of EPO?

A

reticulocytes

30
Q

When are ESAs used (erythropoiesis-stimulating agents)

A

pts with anemia secondary to chronic kidney disease

31
Q

When else can ESAs be used?

A

for the treatment of anemia due to primary bone marrow disorders and secondary anemias

32
Q

When can ESAs NOT be used?

A

in the Olympics

33
Q

What is EPO always couple with?

A

parenteral iron supplementation

-in patients with chronic kidney disease

34
Q

What are the most common adverse effects of EPO?

A

htn

thrombotic complications

35
Q

What does EPO bind onto?

A

receptor on the surface of COMMITTED ERYTHROID PROGENITORS in the marrow after secretion
-initiate JAK/STAT signal transduction pathway

36
Q

Name the Myeloid growth factors

A
  • Fligrastim
  • Pegfilgrastim
  • Sargramostim
  • Plerixafor
37
Q

Filgrastim

A

recombinant human G-CSF produced in a

-IV or subcue administration

38
Q

Pegfilgrastim

A
  • covalent conjugation product of filgrastim and polyethylene glycol (PEG)
  • longer serum half-life than filgrastim
  • can be injected once per myelosuppressive chemotherapy cyle instead of daily for several days
39
Q

What do myeloid growth factors do?

A

enhance the function of mature granulocytes and monocytes

40
Q

Sargramostim

A
  • recombinant human GM-CSF produced in a yeast expression system
  • Iv or sub cue administration
41
Q

Plerixafor

A

MOA: reversibly inhibits binding of stromal cell-derived factor-1-alpha (SDF-1a, this is on the bone marrow stromal cells) to the CXCR4

  • results in moblization of hematopoietic stem and progenitor cells from the bone marrow into peripheral blood
  • used in combo with filgrastim results in synergistic increase in CD34+ cell mobilization prior to autologous transplantation
  • used in patients who respond suboptimally to G-CSF alone
42
Q

G-CSF

A

nuetrophils

-increases the concentration of hematopoietic stem cells in the peripheral blood

43
Q

GM-CSF

A

broader biologic actions than G-CSF

  • primary therapeutic effect is to stimulate myelopoiesis
  • increases HSC’s in peripheral blood to a lesser extent than G-CSF
44
Q

What is a super common use of G-CSF?

A

accelerate neutrophil recovery after myelosuppressive chemotherapy
-reduce duration of neutropenia

45
Q

Which is better tolerated? Filgrastim and pegfilgrastim or GM-CSF?

A

filgrastim and pegfligrastim

46
Q

what toxicity can filgrastim and pegfilgrastim cause?

A

bone pain

-clears when discontinuied

47
Q

What toxicity does GM-CSF cause?

A

-fever, malaise, arthralgias, myalgias, and a capillary leak syndrome characterized by peripheral edema and pleural or pericardial effusions

48
Q

What do patients with thrombocytopenia has a high risk of?

A

hemorrhage

49
Q

What 2 drugs are endogenous regulators of platelet production?

A

Thrombopoietin and IL-11

50
Q

IL-11

A
  • Oprelvekin
  • MOA: activates cell surface cytokine receptors, makes more myeloid and lymphoid cells, eventually makes more peripheral platelets and neutrophils
51
Q

Romiplostim

A
  • it’s just recombinant thrombopoietin
  • -peptibodies
  • MOA: activates Mpl thrombopoietin receptor to cause a dose dependent increase in platelet count
  • Increase in platelet count begins 5 days after SubQ injection and peaks at 12-15 days
52
Q

What is IL-11 used for?

A

secondary prevention of thrombocytopenia in patients with chronic ITP who have had insufficient response to corticosteroids, immune globulin, or splenectomy

53
Q

Toxicity of IL-11

A
  • fatigue, headache, dizziness, and CV effects
  • Hypokalemia
  • all adverse effects are reversible
54
Q

Toxicity of Romiplotim

A

well tolerated except for a mild headache on the day of administration

Heme and Lymph Midterm (11 decks)

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