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Heme/Lymph 2 > Kruse - Anemia Drugs > Flashcards

Kruse - Anemia Drugs Flashcards

1
Q

Symptoms of anemia

A

Pallor, fatigue, dizziness, exertional dyspnea, tachycardia, increased blood volume, vasodilation

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2
Q

Iron deficiency = ____ anemia

A

Microcytic, hypochromic

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3
Q

Iron must be in the ___ state to be absorbed

A

Ferrous (2+)

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4
Q

Oral iron is administered in what form? Why?

Drug names?

A

Ferrous (2+) salts - for easiest absorption

Ferrous sulfate, Ferrous gluconate, Ferrous fumarate

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5
Q

Adverse effects of oral iron

A

GI - nausea, epigastric pain, cramps, constipation, black stools, diarrhea

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6
Q

Who receives parenteral iron?

A
  • Iron deficiency who can’t tolerate or absorb oral iron
  • Extensive chronic anemia who need more than oral (advanced renal disease w/ hemodialysis and EPO treatment, small bowel resection, IBD of small bowel, or malabsorption)
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7
Q

How to avoid iron toxicity since it’s infused as ferric form?

A

Colloid containing core of iron oxyhydroxide around carbohydrates, thus released slowly after infusion

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8
Q

Ways to administer iron dextran?

A
  • Deep IM injection

- IV infusion

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9
Q

Adverse effects of iron dextran

A

Headache, light-headed, fever, arthralgias, N/V, back pain, flushing, urticaria, bronchospasm, anaphylaxis

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10
Q

What should always be done first when giving iron dextran?

A

Give a small test dose, to rule out hypersensitivity

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11
Q

3 forms of parenteral iron

A
  • Iron dextran
  • Sodium ferric gluconate
  • Iron-sucrose
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12
Q

Why would you give sodium ferric gluconate or iron-sucrose complexes, instead of iron dextran?

A

Less chance of hypersensitivity

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13
Q

Small child w/ vomiting, abdominal pain, bloody diarrhea, followed by shock and lethargy. Improves for a bit, then declines. Most likely?

A

Acute iron toxicity (accidental tablet ingestion OD)

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14
Q

How to treat acute iron toxicity?

A

Deferoxamine + whole bowel irrigation

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15
Q

Who is most likely to have chronic iron toxicity?

A

Hemochromatosis (excessive absorption), or those who receive many RBC transfusions over time

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16
Q

How to remove iron deposits from liver in chronic toxicity?

A

Deferasirox

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17
Q

Treatment of chronic iron toxicity

A

Intermittent phlebotomy + Deferasirox (liver)

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18
Q

B12 deficiency = ____ anemia

A

Megaloblastic, macrocytic

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19
Q

Most common causes of B12 deficiency

A
  • Lack of intrinsic factor
  • Deficient uptake mechanism in distal ileum
  • Strict vegetarian (many years later)
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20
Q

B12 deficiency causes the accumulation of what 3 things?

A

N5-methyl-THF
Homocysteine
Methylmalonic acid

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21
Q

B12 deficiency causes the depletion of what important chemical?

A

THF

22
Q

Characteristic findings of B12 or folic acid deficiency

A

Megaloblastic, macrocytic anemia w/ leukopenia or thrombocytopenia, and hypercellular BM w/ megaloblastic erythroid precursors

23
Q

Most common symptoms of B12 deficiency

A

Paresthesias, weakness, spasticity, ataxia

24
Q

Almost all cases of B12 deficiency are due to a lack of ___, thus all B12 must be administered via ____

A

Absorption; parenteral injections

25
Q

Folic acid deficiency causes

A
  • Alcoholics w/ poor diet and less hepatic storage
  • Pregnant women w/ increased need
  • Hemolytic anemics w/ increased need
  • Malabsorption syndromes
  • Renal dialysis
26
Q

Drugs causing folic acid deficiency

A
  • MTX
  • TMP
  • Pyrimethamine
  • Phenytoin
27
Q

What does folic acid deficiency NOT have, compared to B12 deficiency?

A

Neural symptoms

28
Q

Epoetin alpha vs. Darbepoetin alpha

A

Darb = more glycosylated, thus much longer half life (less frequent dosing)

29
Q

What to look for following EPO administration?

A

Risk in reticulocyte count, then rise in Hct and Hgb

30
Q

Diseases requiring EPO administration?

A
  • Chronic kidney disease (low endogenous EPO)

- BM disease (aplastic anemia, MPD, MDS, MM, AIDS, myelosuppressive chemo)

31
Q

EPO is almost always coupled w/ administration of ___ in CKD?

A

Iron, and sometimes folate

32
Q

Adverse effects of EPO

A
  • HTN

- Thrombotic complications

33
Q

Filgrastim…what is it?

A

Recombinant human G-CSF

34
Q

How to give G-CSF less frequently than Filgrastim?

A

Pegfilgrastim (polyethylene glycol = longer 1/2 life)

35
Q

Sargramostim…what is it?

A

Recombinant human GM-CSF

36
Q

Plerixafor…what is it?

MoA

A

Mobilizer of hematopoietic stem cells and progenitor cells from BM into peripheral blood

Inhibits SDF-1-alpha (BM stromal cells) from binding CXCR4 (blood cells)

37
Q

When and how is Plerixafor used?

A

When G-CSF alone does not work well

Used w/ Filgrastim

38
Q

G-CSF does what? (2)

A

Stimulates proliferation of NEUTROPHILS, and increases hematopoietic stem cells in peripheral blood for transplantation

39
Q

GM-CSF does what?

A

Stimulates proliferation of granulocytes, erythrocytes, and megakaryocytes

40
Q

When is G-CSF (Filgrastim) used?

A

Chemo-induced neutropenia, other causes of neutropenia, myelodysplasia, and aplastic anemia, autologous stem cell transplantation

41
Q

Side effect of Filgrastim

A

Bone pain

42
Q

Side effects of Sargramostim

A

Fever, malaise, arthralgias, myalgias, peripheral edema, effusions

43
Q

Oprelvekin…what is it?

A

Recombinant IL-11 (megakaryocyte growth factor)

44
Q

Romiplostim…what is it?

MoA

A

Recombinant TPO

Activate Mpl TPO receptor

45
Q

Oprelvekin causes increased _____

A

Platelets and neutrophils

46
Q

After giving Romiplostim, when can the effects be seen?

A

5 days after administration

47
Q

Use of Oprelvekin

A

Thrombocytopenia in non-myeloid cancer chemo

48
Q

Use of Romiplostim

A

Thrombocytopenia in chronic ITP that hasn’t responded to corticosteroids, Ig, or splenectomy

49
Q

IL-11 toxicities

A

Fatigue, headache, dizzy, anemia, dyspnea, transient atrial arrhythmias

50
Q

Romiplostim toxicities

A

Mild headache when administered

Heme/Lymph 2 (16 decks)

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