Kruse - Anemia and Hematopoietic Growth Factors Flashcards Preview

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Flashcards in Kruse - Anemia and Hematopoietic Growth Factors Deck (42)
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1
Q

Iron is absorbed as Fe__ state.

Iron is transported and stored in Fe___ state

A
  • Absorbed: Fe2+ (ferrous) – ORAL

- Transported/Stored: Fe3+ (ferric); with transferrin – PARENTERAL

2
Q

Increased erythropoiesis is associated with an increase in number of ___-receptors on developing erythroid cells.

A

Transferrin

3
Q

Iron store depletion and iron deficiency anemia are associated with an increased concentration of serum ___.

A

Transferrin

4
Q

Iron is stored as ___.

A

ferritin

5
Q

In what states can iron be administered orally?

A

Administer as FERROUS salt (Fe2+): ferrous sulfate, ferrous gluconate, ferrous fumarate

6
Q

How should oral iron be administered (taken with…?)

A

water or juice on an empty stomach; may be admin with food to prevent irritation.

7
Q

Adverse effects of oral iron therapy.

A

N, epigastric pain, black stools, abdominal cramps, constipation, diarrhea (dose related; reduced if taken with or immediately after meals).

8
Q

Parenteral iron therapy is reserved for what type of pateints?

A

People unable to tolerate/absorb oral iron or with chronic anemia that can’t be maintained with oral iron (CRD, IBD, SI resection)

9
Q

Parenteral iron administration bypasses what regulatory mechanisms - beneficial why?

A

Bypasses iron storage regulatory mechanisms of the intestine – can deliver more iron than can can safely be stored.

10
Q

Name the three forms of parenteral iron is USA.

A
  1. Iron dextran - (IV>IM), adverse effects - HA/fever/arthralgia/ N/V/back pain, flushing BRONCHOSPASM, ANAPHYLAXIS
  2. Sodium ferric gluconate complex
  3. Iron-Sucrose Complex
11
Q

What age is acute iron toxicity seen in? Symptoms?

A

Young children - see vomiting, abdominal pain, bloody diarrhea –> shock, lethargy, dyspnea –> metabolic acidosis, coma, death

12
Q

Treatment of acute iron toxicity.

A

Whole bowel irrigation and parenteral deferoxamine.

13
Q

Signs and symptoms of Chronic Iron Toxicity.

A

Deposits onto heart, liver, pancreas, etc = organ death.

14
Q

Treatment for Chronic Iron Toxicity.

A

Intermittent phlebotomy.

Oral iron chelator deferasirox.

15
Q

Two forms of active Vitamin B12 in humans + form of administration.

A

Cyanocobalamin and hydroxocobalamin - parenteral

16
Q

Most common clinical manifestation of B12 deficiency

A

Megaloblastic, macrocytic anemia.

17
Q

Describe the neurologic syndrome associated with B12.

A

Begins with paresthesias in peripheral nerves/weakness –> COT to spasticity, ataxia.

-homocysteine

18
Q

Richest dietary sources of folic acid.

A

Yeast, kidney, liver, green veggies.

19
Q

What is the clinical manifestation of folic acid deficiency?

A

Megaloblastic anemia.

20
Q

How does presentation of folic acid deficiency v. B12 deficency differ.

A

Both have megaloblastic anemia, but B12 has neuro syndrome and Folic Acid deficiency does not.

21
Q

Name four drugs that can cause folic acid deficiency.

A
  • Inhibitors of DHFR: MTX, Trimethoprim, Pyrimethamine

- Phenytoin (long term)

22
Q

In what scenarios does EPO rise to induce erythropoiesis?

A

Anemia, hypoxemia, (kidney disease, marrow damage, iron deficiency, vitamin deficiency).

23
Q

Two erythrocyte-stimulating agents

A

Epoetin alpha and darbepoetin alpha

24
Q

Results of inducing erythropoiesis -

A

inc reticulocyte count (10 days), rise in Hct/Hb (2-6 weeks)

25
Q

Clincal scenarios when Erythropoiesis-Stimulating Agents are used.

A

Anemia (secondary to CKD or due to primary bone marrow disorders), AIDS, MM, MDS, MPD, etc).
Banned in professional athletes.

26
Q

Toxicity of ESAs

A

HTN, thrombotic complications (due to increase in blood)

27
Q

Function of myeloid growth factors

A

Enhance function of mature granulocytes and monocytes.

28
Q

Name two Granulocyte Colony-Stimulating Factors (G-CSF)

A

Filgrastim (recombinant human G-CSF) and pegfilgrastin (longer 1/2 life, administer less frequent)

(plerixafor)

29
Q

When is plerixafor used?

A

when patients respond suboptimally to G-CSF alone.
Use: filgrastim + plerixafor = inc. CD34+
Function - to increase HSC from marrow to PB

30
Q

Function of G-CSF

A

Stimulates proliferation and differentiation of progenitors already committed to the neutrophil lineage - activates phagocytic activity of mature neutrophils.

31
Q

Name a Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)

A

Sargramostim

32
Q

How does GM-CSF differ from G-CSF.

A

GM-CSF’s primary effect is to stimulate myelopoiesis (broader then G-CSF) - erythroid/megakaryocyte progenitors, mature neutrophil function, T-cell proliferation with IL-2

33
Q

Tx for cancer chemo-induced ***neutropenia

A

G-CSF accelerates neutrophil recovery

34
Q

Toxicity of Filgrastim and pegfilgrastim

A

bone pain

35
Q

Toxicity of GM-CSF

A

fever, malaise, arthralgia, myalgia, capillary leak syndrome (would see peripheral edema and pleural/pericardial effusion)

36
Q

What class of growth factor should be given for patients with thrombocytopenia?

A

Megakaryocyte growth factor.

37
Q

Name the two megakaryocyte growth factors.

A

Oprelvekin (IL-11) and Romiplostim (recombinant thrombopoietin)

38
Q

Clinical use for oprelvekin

A

Secondary prevention of thrombocytopenia in people receiving cytotoxic/myelosuppressive chemotherapy for NONmyeloid cancers - reduced # of platelet transfusions.

39
Q

Clinical use for romiplostim

A

Used to treat thrombocytopenia in people with chronic immune (idiopathic) thrombocytopenia purpura.
(ITP)

40
Q

AE of oprelvekin v. romplostim

A
  • Oprelvekin - HA, dizziness, fatigue, CV, hypOk (all reversible)
  • Romiplostim - mild HA
41
Q

MOA of oprelvekin

A

Activates surface cytokine receptors to stimulate growth of lymphoid/myeloid cells. Stimulate primitive megakaryocyte progenitors = inc. peripheral platelet and neutrophils.

42
Q

MOA of romiplostim

A

activates Mpl TPO receptor to cause dose dependent increase in platelet count.