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STEP Pharm I > Agents Used in Anemias > Flashcards

Agents Used in Anemias Flashcards

1
Q

What are the symptoms of iron deficiency?

A

pallor, fatigue, dizziness, exertional dyspnea, tissue hypoxia

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2
Q

How does the cardiovascular system adapt to chronic anemia?

A

-tachycardia-increased cardiac output-vasodilation

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3
Q

What happens to hemoglobin when iron is deficient?

A

small hemoglobin-deficient erythrocytes are formed, giving rise to microcytic hypochromic anemia

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4
Q

T or F. Nearly all of the iron used to support hematopoiesis is reclaimed from catalysis of the hemoglobin in senescent or damaged erythrocytes

A

T. Normally, only a small amount of iron is lost from the body each day

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5
Q

When are iron requirements higher in people?

A

-pregnancy-small children-menstruating women

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6
Q

In men and postmenopausal women, where is the most common site of blood loss?

A

GI tract. Diagnosed via occult blood

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7
Q

How should iron be given as a supplement?

A

Ferrous iron is most efficiently absorbed, only ferrous salts should be usedFerrous sulfate and ferrous gluconate are both effective and inexpensive and are recommended for the treatment of most patients

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8
Q

How much iron should be given to correct iron deficiency most rapidly?

A

200-400mg of elemental iron About 50–100 mg of iron can be incorporated into hemoglobin daily, and about 25% of oral iron given as ferrous salt can be absorbed

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9
Q

How long after correction of the cause of the iron loss should treatment with oral iron continue?

A

Treatment with oral iron should be continued for 3–6 months after correction of the cause of the iron loss. This corrects the anemia and replenishes iron stores

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10
Q

Side effects of oral therapy? How can this be avoided (assuming you continue to take the drug)?

A

-nausea-epigastric discomfort-abdominal cramps-diarrhea or constipation-black stoolusually can be avoided by taking smaller doses or with meals

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11
Q

Is parenteral iron therapy an option?

A

Yes, for those unable to tolerate oral dosing

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12
Q

Who else might require parenteral iron therapy?

A

-Patients with chronic anemia not maintained with oral iron alone-Advanced chronic renal disease requiring hemodialysis and treatment with erythropoietin-Various postgastrectomy conditions-Anything messing the small bowel

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13
Q

What are the challenges of parenteral iron administration?

A

Parenteral administration of inorganic free ferric iron produces serious dose-dependent toxicitySeverely limits the dose of that can be administered

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14
Q

What is the name of parenteral iron therapy?

A

Iron dextran (IV/IM)- sodium ferric gluconate complex

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15
Q

Side effects of iron dextran? 13 things

A

-headache, light-headedness-fever, flushing-back pain-urticaria-nausea, vomiting, coughing -palpations -CV problems, hard to breatheRare: anaphylaxis (due to release of histamine) and death- test with a small dose

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16
Q

What is transferrin saturation?

A

Ratio of total serum iron concentration to total iron-binding capacity (TIBC)

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17
Q

What does acute iron toxicity cause?

A

-vomiting, GI pain-blood in stool-shock, lethargy, and dyspnea-possible coma and death

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18
Q

How can acute iron toxicity be corrected?

A

-whole bowel irrigation (activated charcoal not effective)-Deferoxamine

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19
Q

How does Deferoxamine work?

A

It is a potent iron-chelating compound given IVo Does not effectively chelate other important trace metals

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20
Q

Side effects of Deferoxamine? How is it excreted?

A

o Excreted in urine and bile; gives urine red discolorationo Tachycardia, hypotension, and shocko Could add to the cardiovascular collapse caused by iron toxicityo Abdominal discomfort, N/V, and diarrhea, which may add to symptoms of acute iron toxicity

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21
Q

What does chronic iron toxicity lead to?

A

hemochromatosis- excess iron despots in the heart, liver, pancreas, etc. which can lead to organ failure

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22
Q

Chronic iron overload in the absence of anemia is most efficiently treated by _____.

A

intermittent phlebotomy - One unit of blood removed about every week

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23
Q

What does deficiency of B12 lead to? Symptoms?

A

megaloblastic/macrocytic anemia GI symptoms, glossitis, and neurologic abnormalities

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24
Q

What kinds of neurologic symptoms does B12 deficiency cause? Does fixing the deficiency fix/reverse these symptoms?

A

-Paresthesias in peripheral nerves and weakness and progresses to spasticity, ataxia, and other central nervous system dysfunctionsCorrection of vitamin B12 deficiency arrests the progression of neurologic disease, but it may not fully reverse neurologic symptoms that have been present for several months

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25
Q

What are common causes of B12 deficiency?

A

-Pernicious anemia-gastrectomy (anything that affects the distal ileum- IBS, etc.)- acid blocking drugs like Omeprazole (protein pump inhibitor) and Tagamet-histamine 2 receptor antagonist (both OTC)

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26
Q

Rare causes of B12 deficiency?

A

-Bacterial overgrowth of small bowel-Chronic pancreatitis-Thyroid disease-In children: secondary to congenital deficiency of IF or to defects of the receptor sites for vitamin B12-intrinsic factor complex in the distal ileum

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27
Q

Why are almost all B12 therapies parenteral?

A

Almost all cases of vitamin B12 deficiency are caused by malabsorption of the vitamin

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28
Q

How is B12 available as a vitamin?

A

cyanocobalamin or hydroxocobalamin (preferred)

29
Q

Why is hydroxocobalamin preferred?

A

more highly protein-bound and remains longer in circulation

30
Q

Does folic acid need to be oxidized or reduced for biochemical reactions?

A

reduced

31
Q

T or F. Folic acid deficiency is easily corrected.

A

T, via administration of folic acid

32
Q

Folic acid deficiency is common in which people?

A

Those with liver disease or chronic alcoholism pregnant women and patients with hemolytic anemia that have increased requirements (no folic acid=spina bifida)

33
Q

T or F. Oral absorption of folic acid is high, even in patients with malabsorption syndrome

A

T.

34
Q

How much folic acid should be given typically?

A

1 mg folic acid orally daily is sufficient to reverse megaloblastic anemia, restore normal serum folate levels, and replenish body stores of folates in almost all patientsContinue therapy until the underlying cause of the deficiency is removed or corrected (i.e. forever if malabsorption is the cause)

35
Q

What drugs can cause folic acid deficiency?

A

-methotrexate-trimethoprim- rare-pyrimethamine (antimalaria)-rare-phenytoin (antiepileptic agent)

36
Q

How does phenytoin cause folate deficiency?

A

inhibiting intestinal uptake processes

37
Q

What drug can be used as a folate rescue?

A

leocovorin

38
Q

What are some recombinant mammalian human erythropoietin (rHuEPO) used?

A

-epotein alfa-darbepoetin alfa-methoxy polyethylene glycol (PEG) -epoetin beta

39
Q

How does epoetin alfa work?

A

agonist of EPO receptors expressed by red cell progenitors that stimulates erythroid proliferation ad differentiation and induces reticulocyte release from bone marrow

40
Q

What is epoetin alfa used to treat?

A

anemia, especially assoicated with chronic renal failure, HIV, cancer, and prematurity

41
Q

Side effects of epoetin alfa? How could these be avoided?

A

-hypertension-thrombus formation -pure red cell aplasia maintain hemoglobin at less than 12 g/dl to avoid

42
Q

Darbepoetin alfa and methoxy PEG-epoetin beta are long lasting from of epoetin alfa. How often are they given?

A

darbe- weeklymethoxy- 1-2x per month

43
Q

How do erythropoietin receptors work?

A

JAX/STAT family that use phosphorylation and transcription factors to regulate cellular function

44
Q

How cell differentiation works.

A

A self- sustaining pool of marrow stem cells differentiates under the influence of specific hematopoietic growth factors to form a variety of hematopoietic and lymphopoietic cells. Stem cell factor (SCF), ligand (FL), IL-3, and GM-CSF, together with cell–cell interactions in the marrow, stimulate stem cells to form a series of burst-forming units (BFU) and colony-forming units (CFU): CFU-GEMM (granulocyte, erythrocyte, monocyte and megakaryocyte), CFU-GM (granulocyte and macrophage), CFU-Meg (megakaryocyte), BFU-E (erythrocyte), and CFU-E (erythrocyte). After considerable proliferation, further differentiation is stimulated by synergistic interactions with growth factors for each of the major cell lines—granulocyte colony–stimulating factor (G-CSF), monocyte/macrophage-stimulating factor (M-CSF), TPO, and EPO. Each of these factors also influences the proliferation, maturation, and in some cases the function of the derivative cell line.

45
Q

Where is endogenous erythropoietin made?

A

mostly in kidneys- gene transcription is inversely related to tissue oxygenation levels thus, renal failure= low EPO

46
Q

What are normal and abnormal serum erythropoietin levels?

A

• Non-anemic individuals: less than 20 IU/L• Moderately severe anemia: 100–500 IU/L range• Severe anemia: thousands of IU/L

47
Q

Are renal deficient patients likely to respond to exogenous EPO?

A

Yes

48
Q

Are patients with primary bone marrow disorders (aplastic anemia, leukemias, myeloproliferative disorder, etc.) and most nutritional and secondary anemias likely to respond to exogenous erythropoietin?

A

No- endogenous levels are usually high here

49
Q

BBW of recombinant EPOs?

A

1) chronic kidney disease exacerbation that can lead to death, stroke, CV risk when hemoglobin is above 11 g/dL2) Cancer progression3) Increased thromboembolic events in surgery patients

50
Q

How can recombinant EPOs cause cancer? Which cancers?

A

• ESAs shortened overall survival and/or increased the risk of tumor progression in some clinical studies in patients with breast, head, and neck; lymphoid; non-small cell lung; and cervical cancers• Prescribers and hospitals must enroll in and comply with the ESA APPRISE Oncology Program to prescribe and/or dispense ESAs to patients with cancer

51
Q

Rules of the ESA APPRISE Oncology Program?

A

• Use the lowest dose to avoid RBC transfusions• Use ESAs only for anemia from myelosuppressive chemotherapy• ESAs are not indicated for patients receiving myelosuppressive chemotherapy when the anticipated outcome is cure• Discontinue following the completion of a chemotherapy course

52
Q

Other risk of recombinant EPOs?

A
  • Due to increased risk of deep venous thrombosis (DVT), DVT prophylaxis is recommended- hypertension (24%), headache (16%), arthralgias, nausea (11%)Rare: edema, fatigue, GI distress, chest pain
53
Q

Erythropoietin has been used successfully to:o Offset the anemia (23% of children) produced by zidovudine [Retrovir;ZDV] treatment in patients with HIV infection o In the treatment of the anemia of prematurity

A

Erythropoietin has been used successfully to:o Offset the anemia (23% of children) produced by zidovudine [Retrovir; ZDV] treatment in patients with HIV infection o In the treatment of the anemia of prematurity

54
Q

What are Filgrastim (or Pegfilgrastim)? What do they do?

A

G-CSF drugs used to stimulate proliferation and differentiation of progenitors already committed to the neutrophil lineage activates the phagocytic activity of mature neutrophils and prolongs their survivalMobilizes hematopoietic stem cells, i.e., to increase their concentration in peripheral blood.

55
Q

T or F. Filgrastim permits use of peripheral blood stem cells (PBSCs) rather than bone marrow stem cells for autologous and allogeneic hematopoietic stem cell transplantation

A

T

56
Q

What is Sarogastrim? What does it do? 5 main things

A

GM-CSF (Sarograstim) that has broader biologic actions than G-CSF1) multipotential hematopoietic growth factor --Stimulates proliferation and differentiation of early and late granulocytic progenitor cells –Erythroid and megakaryocyte progenitors2) GM-CSF also stimulates the function of mature neutrophils3) Acts together with interleukin 2 (IL-2) to stimulate T-cell proliferation4) Appears to be a locally active factor at the site of inflammation 5) GM-CSF mobilizes peripheral blood stem cells, but less effectively than G-CSF

57
Q

How can G-CSF be used in chemotherapy?

A

G-CSF accelerates the rate of neutrophil recovery after dose-intensive myelosuppressive chemotherapy by reducing episodes of febrile neutropenia, requirements for broad-spectrum antibiotics, infections, and days of hospitalization BUT has no effect upon patient survivalPegfilgrastim can be administered less frequently, and it may shorten the period of severe neutropenia slightly more than G-CSF

58
Q

What else can neutrophil stimulating drugs be used for?

A

• Neutropenia associated with congenital neutropenia, cyclic neutropenia, myelodysplasia, and aplastic anemia• In autologous stem cell transplantation for patients undergoing high-dose chemotherapyo High doses of chemotherapy are necessitated by the resistance of the tumor cell populationo Myelosuppression is then counteracted by reinfusion of the patient’s own hematopoietic stem cells (which are collected prior to chemotherapy)• Mobilization of PBSCso PBSCs have largely replaced bone marrow as the hematopoietic preparation used for autologous transplantation

59
Q

Toxicities of neutrophil stimulators?

A

All 3 factors (G-CSF, pegfilgrastim & GM-CSF) have similar effects on neutrophil countso G-CSF and pegfigrastim are better tolerated and used more• Bone pain upon discontinuation

60
Q

Side effects specific to GM-CSF?

A

More severe side effects with GM-CSF, particularly at higher doseso Fever, malaise, arthralgias, myalgias, and a capillary leak syndrome characterized by peripheral edema and pleural or pericardial effusionso Allergic reactions may occur but are infrequent

61
Q

Splenic rupture is a rare but serious complication of the use of G-CSF for PBSC

A

Splenic rupture is a rare but serious complication of the use of G-CSF for PBSC

62
Q

What is oprelvekin?

A

rh-IL-11 which stimulates megakaryotcytopoiesis and thrombopoiesis

63
Q

Toxicities of oprelvekin?

A

fatigue, headache, dizziness, CV effects, hypokalemiaall reversible

64
Q

What kinds of CV effects are common with oprelvekin?

A

o Anemia (due to hemodilution)o Dyspnea (due to fluid accumulation in the lungs) o Transient atrial arrhythmias

65
Q

What is Romiplostin?

A

• Thrombopoietin-mimetic Fc-peptide fusion protein (peptibody)• Contains two identical single-chain subunits, each consisting of human immunoglobulin IgG1 Fc domain (constant region), covalently linked at the C- terminus to two identical peptide sequences that each bind and activate the TPO receptor• Fc component of the romiplostim peptibody extends the half-lifeo Remains active in the circulation much longer than endogenous TPO o Eventually removed by the reticuloendothelial system

66
Q

Red cell lysis in G6-PD deficient patients can be brought about by what?

A

I. Acute bacterial or viral infectionII. Acidosis (e.g., diabetic ketoacidosis; DKA)III. Fava beans (historically called favism)IV. DRUGS

67
Q

Drugs used for G6-PD deficiency?

A

– SULFONAMIDES (Trimethoprim/sulfamethoxazole (Bactrim) – DAPSONE – PRIMAQUINE – CHLOROQUINE.

68
Q

Upon “challenge”, patient with G6PD deficiency experience symptoms of anemia, including decreased hemoglobin and hematocrit with normal mean corpuscular volume (MCV).

A

Upon “challenge”, patient with G6PD deficiency experience symptoms of anemia, including decreased hemoglobin and hematocrit with normal mean corpuscular volume (MCV).

STEP Pharm I (36 decks)

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