Kruse - Anemia and Hematopoietic Growth Factors Flashcards Preview

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

Iron is absorbed as Fe__ state.
Iron is transported and stored in Fe___ state

- Absorbed: Fe2+ (ferrous) -- ORAL
- Transported/Stored: Fe3+ (ferric); with transferrin -- PARENTERAL

2

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

Transferrin

3

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

Transferrin

4

Iron is stored as ___.

ferritin

5

In what states can iron be administered orally?

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

6

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

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

7

Adverse effects of oral iron therapy.

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

8

Parenteral iron therapy is reserved for what type of pateints?

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

9

Parenteral iron administration bypasses what regulatory mechanisms - beneficial why?

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

10

Name the three forms of parenteral iron is USA.

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

What age is acute iron toxicity seen in? Symptoms?

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

12

Treatment of acute iron toxicity.

Whole bowel irrigation and parenteral **deferoxamine**.

13

Signs and symptoms of Chronic Iron Toxicity.

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

14

Treatment for Chronic Iron Toxicity.

Intermittent phlebotomy.
Oral iron chelator **deferasirox**.

15

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

Cyanocobalamin and hydroxocobalamin - parenteral

16

Most common clinical manifestation of B12 deficiency

Megaloblastic, macrocytic anemia.

17

Describe the neurologic syndrome associated with B12.

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

-homocysteine

18

Richest dietary sources of folic acid.

Yeast, kidney, liver, green veggies.

19

What is the clinical manifestation of folic acid deficiency?

Megaloblastic anemia.

20

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

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

21

Name four drugs that can cause folic acid deficiency.

- Inhibitors of DHFR: MTX, Trimethoprim, Pyrimethamine
- Phenytoin (long term)

22

In what scenarios does EPO rise to induce erythropoiesis?

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

23

Two erythrocyte-stimulating agents

Epoetin alpha and darbepoetin alpha

24

Results of inducing erythropoiesis -

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

25

Clincal scenarios when Erythropoiesis-Stimulating Agents are used.

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

26

Toxicity of ESAs

HTN, thrombotic complications (due to increase in blood)

27

Function of myeloid growth factors

Enhance function of mature granulocytes and monocytes.

28

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

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

(plerixafor)

29

When is plerixafor used?

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

30

Function of G-CSF

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

31

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

Sargramostim

32

How does GM-CSF differ from G-CSF.

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

Tx for cancer chemo-induced ***neutropenia

G-CSF accelerates neutrophil recovery

34

Toxicity of Filgrastim and pegfilgrastim

bone pain

35

Toxicity of GM-CSF

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

36

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

Megakaryocyte growth factor.

37

Name the two megakaryocyte growth factors.

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

38

Clinical use for oprelvekin

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

39

Clinical use for romiplostim

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

40

AE of oprelvekin v. romplostim

- Oprelvekin - HA, dizziness, fatigue, CV, hypOk (all reversible)
-Romiplostim - mild HA

41

MOA of oprelvekin

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

42

MOA of romiplostim

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