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Heme/Lymph Exam I > Drugs for the treatment of anemia > Flashcards

Drugs for the treatment of anemia Flashcards

1
Q

oprelvekin, IL-11

A

megakaryocyte growth factor

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2
Q

romiplostim

A

megakaryocyte growth factor

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3
Q

Sargramostim

A

granulocyte-macrophage colony stimulating factor (GM-CSF)

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4
Q

pegfilgrastim

A

granulocyte colony stimulating factor (G-CSF)

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5
Q

filgrastim (neupogen)

A

granulocyte colony stimulating factor (G-CSF)

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6
Q

epoeitin alpha (Epogen, Procrit)

A

Erythrocyte stimulating agent

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7
Q

Darbepoietin alpha

A

Erythrocyte stimulating agent

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8
Q

cyanocobalamin

hydroxocobalamin

A

Vitamin B12 prep

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9
Q

deferoxamine

A

iron chelator

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10
Q

deferasirox

A

iron chelator

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11
Q

iron dextran

A

parenteral iron

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12
Q

iron sucrose complex

A

parenteral iron

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13
Q

sodium ferric gluconate complex

A

perenteral iron

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14
Q

ferrous sulfate
ferrous gluconate
ferrous fumarate

A

oral iron

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15
Q

what re the causes of iron deficiency

A

nutrition
iron malabsorption- after gastrectomy, severe small bowel disease

blood loss

increased iron requirement –> pregnant, lactating, growing children, infants, premature infants, pt’ with chronic kidney disease

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16
Q

what are the common signs of anemia

A

pallor, fatigue, dizziness
exertional dyspnea

tachycardia
increased CO

vasodilation

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17
Q

what happens to erythrocytes in the absence of iron

A

small erythrocytes form with insufficient hemoglobin

microcytic hypochromic anemia

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18
Q

where does iron absorption occur

when does iron absorption increase

A

duodenum and proximal jejunum

increases –> low iron stores or increased iron requirements

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19
Q

non heme iron vs heme iron and absorption?

A

(4) Heme iron in hemoglobin and myoglobin can be absorbed intact without first having to be dissociated into elemental iron (e.g., iron in meat protein)
(5) Nonheme iron must be reduced by ferroreductase to ferrous iron (Fe2+) before absorption can occur

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20
Q

what happens when iron stores are high/ or iron requirements are low

what happens when iron stores are low/ or iron requirements are high

A

(6) When iron stores are high and/or iron requirements are low, absorbed iron is diverted into ferritin in the intestinal epithelial mucosal cells for storage
(7) When iron stores are low and/or iron requirements are high, absorbed iron is immediately transported from the mucosal cells to the bone marrow to support hemoglobin production

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21
Q

how is inorganic (non heme iron) absorbed by intestinal epithelial cells

A

via the divalent metal transporter (DMT1)

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22
Q

how is (heme iron) absorbed by intestinal epithelial cells

A

HCP1

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23
Q

what transport iron that is absorbed into the blood

A

ferroportin or complexes with apoferritin and stored as ferritin

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24
Q

in the blood how is iron transported and where does it go

A

transferrin

goes to erythroid precursors in the bone marrow for synthesis of hemoglobin

or to the hepatocytes for storage as ferritin

The transferrin-iron complex binds to transferrin receptors (TfR) in erythroid precursors and hepatocytes and is internalized.

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25
Q

transferrin

A

a β-globulin that binds two molecules of ferric iron (Fe3+) and transports iron in the plasma

increased concentration when there is iron store depletion and iron deficiency anemia

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26
Q

where is iron stored

A

(2) Iron is stored in intestinal mucosal cells, in macrophages in the liver, spleen, and bone, and in parenchymal liver cells

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27
Q

what is the only clinical indication for the use of iron preparations

A

treatment or prevention of iron deficiency anemia

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28
Q

what are the adverse effects of oral iron supplements

A 
nausea
epigastric discomfort
abdominal cramps
constipation **
black stools
diarrhea

can be reduced if taken with or immediately after food

switching to a different ferrous salt prep may reduce GI problems

be careful of poisoning!!! make sure its in a childproof container

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29
Q

what type of patients shoulder be given parenteral iron

A

(a) Reserved for patients with documented iron deficiency who are unable to tolerate or absorb oral iron and for patients with extensive chronic anemia who cannot be maintained with oral iron alone
(e. g., patients with advanced chronic renal disease requiring hemodialysis and treatment with erythropoietin, small bowel resection, inflammatory bowel disease involving the proximal small bowel, or malabsorption syndromes)

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30
Q

how are parenteral iron therapies made so that the iron is released slowly

A

(b) All parenteral forms of iron are formulated as colloid containing particles with a core of iron oxyhydroxide surrounded by a core of carbohydrate so that iron is released slowly from the stable colloid particle after infusion (avoids the severe toxicity of free ferric iron upon administration)

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31
Q

why should monitoring of iron storage levels be done with parenteral iron supplements

A

(c) Parenteral administration bypasses iron storage regulatory mechanisms of the intestine and can deliver more iron than can safely be stored; monitoring iron storage levels helps to avoid serious toxicity of iron overload

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32
Q

what are the adverse effects of iron dextran

A 
headache
light-headed
fever
arthralgias
nausea/vomiting
back pain
flushing
urticaria
bronchospasm
anaphylaxis -- death (rare)

give IM-local pain and tissue staining

most given IV

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33
Q

what should usually be done before giving iron dextran

A

a small test dose to test for hypersensitivity rx

34
Q

how do you administer sodium ferric gluconate

A

IV only

and it is less likely to cause hypersensitivity

35
Q

how do you administer iron sucrose complex

A

IV

less likely to cause hypersensitivity

36
Q

when is acute iron toxicity most often seen

A

(1) Seen almost exclusively in young children who accidentally ingest iron tablets (as few as 10 tablets of common iron preparations can be lethal)

37
Q

what are the symptoms of acute iron toxicity

A

necrotizing gastroenteritis, accompanied by vomiting and abdominal pain, and bloody diarrhea followed by shock, lethargy, and dyspnea

improvement may be noted and followed by severe metabolic acidosis, coma and death

38
Q

what is the treatment for acute iron toxicity

A

whole bowel irrigation

parenteral deferoxamine (iron chelator that promotes excretion in the feces and urine)

39
Q

chronic iron toxicity is common in what pt’s

A

(2) Toxicity is most common in patients with inherited hemochromatosis, a disorder characterized by excessive iron absorption, and in patients who receive many red cell transfusions over a long period of time
(1) Excess iron deposits in the heart, liver, pancreas, and other organs can lead to organ failure and death

40
Q

how do you treat chronic iron toxicity

A

(3) Efficiently treated with intermittent phlebotomy (deferoxamine is less efficient and potentially hazardous but may be only option for iron overload unsuccessfully managed by phlebotomy)

oral iron deferasirox reduces liver iron concentrations but is not sure about how well it removes iron from the heart

41
Q

what can a vitamin B12 deficiency lead to

A

deficiency can lead to megaloblastic anemia, gastrointestinal symptoms, and neurologic abnormalities

42
Q

what are the 2 Vitamin B12 preps available for clinical use

A

cyanocobalamin and hydroxocobalamin

43
Q

what is the ultimate source of vit b12

A

microbial synthesis

chief dietary source is derived from B12 in meats, eggs, dairy products

44
Q

where is vit b12 stored

A

liver

45
Q

how long would it take for effects of b12 deficiency to occur if a patient stopped taking in vit B12 completelet

A

5 years to develop megaloblastic anemia

46
Q

how is B12 absorbed

A

only absorbed after complexing with intrinsic factor –> a glycoprotein secreted by the parietal cells of the gastric mucosa

47
Q

where does vitamin b12 absorption occur

A

distal ileum by highly selective receptor mediated transport system

48
Q

how does B12 deficiency occur

A

most often from malabsorption due to lack of IF or to loss or malfunction of the absorptive mechanism in the distal ileum
(IBS)

vegans- diet

pernicocious anemia

partial or total gastrectomy

49
Q

what 2 enzymatic rxns in humans require B12

A

synthesis of amino acid methionine

synthesis of succinyl-CoA

50
Q

explain the synthesis of methionine

job of:
methylcobalamin
N5-methyltetrahydrofolate
homocysteine
tetrahydrofolate ***

how can a B12 deficiency be partially corrected

what is a diagnostic marker for Viramin B12 deficiency

A

(1) Methylcobalamin serves as an intermediate in the transfer of a methyl group from N5-methyltetrahydrofolate to homocysteine, forming methionine
(2) During the methyl transfer, N5-methyltetrahydrofolate is converted to tetrahydrofolate, the precursor of folate cofactors that leads to the synthesis of deoxythymidylate and purines required for DNA synthesis
(3) B12 deficiency causes the accumulation of N5-methyltetrahydrofolate and depletion of tetrahydrofolate (link between B12 and folic acid metabolism; B12 deficiency can be partially corrected by ingestion of large amounts of folic acid, which largely corrects the anemia caused by B12 deficiency; folic acid does not prevent neurologic manifestations of B12 deficiency, which are thought to be caused by loss of methionine synthesis; see Figure 33-3 below)
(4) B12 deficiency causes the accumulation of homocysteine due to the reduced formation of methylcobalamin; increased serum levels are diagnostic of B12 deficiency

51
Q

what is the role of Vitamin B12 in the synthesis of succinyl -CoA

what is a diagnostic marker that can accumulate from this rxn that helps diagnose Vit B12 deficiency

A

iii) Synthesis of succinyl-CoA
(1) Deoxyadenosylcobalamin is required for the isomerization of methylmalonyl-CoA to succinyl-CoA by the enzyme methylmalonyl-CoA mutase
(2) In patients deficient in B12, methylmalonic acid and methylmalonyl-CoA accumulate (serum and urine levels of methylmalonic acid are diagnostic for B12 deficiency)

52
Q

what are some common clinical characteristics of Vitamin B12 deficiency

A

megaloblastic macrocytic anemia

mild or moderate leukopenia or thrombocytopenia

hypercellular bone marrow

iv) Neurologic syndrome associated with B12 deficiency usually begins with paresthesias in peripheral nerves and weakness and progresses to spasticity, ataxia, and other CNS dysfunctions (B12 treatment stops the progression of neurologic disease but may not fully reverse neurologic symptoms)

53
Q

what is the treatment of vit B12 deficiency

A

v) Almost all cases of B12 deficiency are due to malabsorption; therefore parenteral injections are required for therapy (often lifelong if syndrome causing deficiency is incurable)
vi) Parenteral injections are available as cyanocobalamin and hydroxocobalamin forms of B12
vii) Initial therapy: 100-1000 mcg B12 IM daily or every other day for 1-2 weeks to replenish body stores
viii) Maintenance therapy: 100-1000 mcg B12 IM once a month for life

54
Q

if neuro symptoms are present,, how should vitamin b12 deficiency treatment be adjusted

A

maintenance therapy should be given every 1-2 weeks for 6 months before switching to monthly injections

55
Q

what is folic acid required for

A

synthesis of amino acids, purines and DNA

56
Q

what are the richest dietary sources of folic acid

A

yeast
liver
kidney
green vegetables

57
Q

how long does it take for folate levels to fall after you stop taking it

A

few days

due to low body stores and high daily requirements, folic acid deficiency and megaloblastic anemia may develop within 1-6 months after the inatke of folic acid stops

58
Q

where is folic acid absorbed

A

proximal jejunum

59
Q

once inside the cell, folate (N5-methyltetrahydrofolate) is converted what? what does this require

A

converted to tetrahydrofolate requiring vitamin B12

60
Q

does folate deficiency result in neuro symptoms like vitamin b12 deficiency?

A

no

61
Q

in what patients is risk for folate deficiency high

A 
alocholics
pregnant women
pt's with hemolytic anemia 
pt's with malabsorption syndromes
pt's undergoing renal dialysis
62
Q

what drugs can cause folic acid deficiency

A

methotrexate
trimethoprim
pyrimethamine

phenytoin

63
Q

WHERE IS erythropoietin normally expressed

what triggers its production

A

peritubular interstitial cells of the kidney

production is triggered by anemia or hypoxemia

64
Q

what suppresses erythropoietin

A

inflammatory cytokines

65
Q

what is the MOA of erythrocyte stimulating drugs:
epoetin alpha
darbepoitein alpha

and what is the result after administration of these drugs

A

i) MOA: induces erythropoiesis by stimulating the division and differentiation of committed erythroid progenitor cells; induces the release of reticulocytes from the bone marrow into the bloodstream, where they mature to erythrocytes (agonist at erythropoietin receptors on red cell progenitors)
ii) Results in an increase in reticulocyte counts (10 days) followed by a rise in hematocrit and hemoglobin levels (2-6 weeks)

66
Q

what are the clinical uses of erythropoiesis stimulating agents

A

-used to decrease the need for RBC transfusions in pt’s with anemia secondary to chronic kidney disease
(usually always couple with oral or parenteral iron supplementation)

  • anemia due to myelosuppressive chemotherapy in pt’s with cancer of nonmyeloid malignancy for palliative care
  • treat anemia associated with HIV therapy (zidovudine)
    (3) Reduction of allogenic RBC transfusion for elective, noncardiac, nonvascular surgery when perioperative Hgb is 10-13 g/dL and there is a high risk for blood loss
67
Q

in what pt’s are erythropoiesis stimulating drugs NOT indicated

A

(1) Cancer patients receiving hormonal therapy, therapeutic biologic products, or radiation therapy unless also receiving concurrent myelosuppressive chemotherapy
(2) Cancer patients receiving myelosuppressive chemotherapy when the expected outcome is curative***

(3) Surgery patients who are willing to donate autologous blood
(4) Surgery patients undergoing cardiac or vascular surgery

(5) As a substitute for RBC transfusion in patients requiring immediate correction of anemia

68
Q

what are the adverse effects of erythropoietin stimulating drugs

A

HTN
thrombotic complications

aggressive used in chemotherapy pt’s or those with chronic renal failure has been linked to increased mortality and CV events

69
Q

what do myeloid growth factors do?

A

i) Myeloid growth factors stimulate proliferation and differentiation of one or more myeloid cell lines and enhance the function of mature granulocytes and monocytes

70
Q

what are the specific functions of G-CSF

A

(1) Stimulates proliferation and differentiation of progenitors already committed to the neutrophil lineage
(2) Activates the phagocytic activity of mature neutrophils and prolongs survival
(3) Increases concentration of hematopoietic stem cells in peripheral blood (major advance in transplantation because peripheral blood stem cells (PBSCs) may be used rather than bone marrow stem cells)

71
Q

what are the specific actions of GM-CSF

effect on myeloid cells
effect on T cells?

A

(1) Broader biologic actions than G-CSF
(2) Primary therapeutic effect is to stimulate myelopoiesis ***

(a) Stimulates the proliferation and differentiation of early and late granulocytic progenitor cells as well as erythroid and megakaryocyte progenitors
(b) Stimulates the function of mature neutrophils
(c) Stimulates T-cell proliferation together with interleukin-2
(3) Increases concentration of peripheral blood stem cells to a lesser extent than G-CSF

72
Q

what are the clnical uses of GM-CSF and G-CSF

A

cancer chemotherapy induce neutropenia

-G-CSF–> accelerate neutrophil recovery after chemo, reduce requirements for broad-spectrum antibiotics, infections and days of hospitalizations

doesn’t improve survival in cancer pt’s

treat neutropenia associated with congenital neutropenia, myelodysplasia and aplastic anemia

combine with other growth factors to treat pancytopenia

autologous stem cell transplants in pt’s undergoing high dose chemo

73
Q

filgrastim and pegfilgrastim are used more frequently than GM-CSF b/c they are better tolerated

but what are the adverse effects of these drugs…

A

bone pain

74
Q

what are the adverse effects of GM-CSF

A 
fever
malaise
arthralgias
myalgias
capillary leak syndrome- peripheral edema, pleural or pericardial effusions
75
Q

what are the endogenous regulators of platelet production

A

thrombopoietin and IL-11

c) Recombinant thrombopoietin cannot be used clinically due to production of autoantibodies that result in development of thrombocytopenia

76
Q

what is the mOA of oprelvekin (IL-11)

A

activates specific cell surface cytokine receptors to stimulate the growth of multiple lymphoid and myeloid cells; acts synergistically with other growth factors to stimulate the growth of primitive megakaryocytic progenitors; increases the number of peripheral platelets and neutrophils

77
Q

what is romiplostim

MOA

when do its actions start to take place

A

peptide agonist of the thrombopoietin receptor MpI

it is a megakaryocyte growth factor

(1) Member of a new class of therapeutics called peptibodies, which are peptides with key biologic activities covalently linked to antibody fragments that serve to extend the peptide’s half-life

activates Mpl thrombopoietin receptor to cause a dose-dependent increase in platelet count that begins 5 days after SubQ injection and peaks at 12-15 days

78
Q

what is the clinical use of oprelvekin (IL-11)

A

prevention of thrombocytopenia in pt’s receiving cytotoxic chemo for nonmyeloid cancer

reduces the number of platelet transfusions

79
Q

what is the clinical use of romipolstim

A

treatment of thrombocytopenia in patients with chronic immune (idiopathic) thrombocytopenia purpura (ITP) who have had insufficient response to corticosteroids, immune globulin, or splenectomy

80
Q

what is the toxicity effects of IL-11

A

fatigue
headache
dizziness
CV–> anemia, dyspnea, atrial arrythmias

hypokalemia

all adverse effects are reversible

81
Q

what are the adverse effects of romiplostim

A

(1) Well tolerated except for a mild headache on the day of administration

Heme/Lymph Exam I (4 decks)

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