Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SBL > Pharmacology of Anemia and Hematopoietic Growth Factors > Flashcards

Pharmacology of Anemia and Hematopoietic Growth Factors Flashcards

1
Q

Example of a drug used to treat hypochromic microcytic anemia?

A

iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

example of 2 drugs used to treat megaloblastic (macrocytic) anemia?

A

vitamin B12 and folate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

example of 3 drugs used to treat anemia of chronic renal disease?

A

epoetin alfa, hydroxyurea, and eculizumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

4 drugs used to treat neutropenia?

A

filgrastim, pegfilgrastim, sargramostim, and plerixafor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3 drugs used to treat thrombocytopenia?

A

oprelvekin, romiplastin, eltrombopag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the most common nutritional cause of anemia?

A

iron deficiency anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how do you treat iron deficiency anemia if it is severe?

A

with RBC transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

more hepcidin leads to what?

A

block of iron uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are 2 examples of things that decrease hepcidin and therefore cause an increase in more iron uptake?

A

increased need for RBCs and hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are two examples of things that increase hepcidin and therefore cause a decrease in iron uptake?

A

iron and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

absorption of iron is regulated by what?

A

hepcidin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 4 broad causes of microcytic anemia?

A
  1. reduced iron availability 2. reduced heme synthesis 3. reduced globin production 4. rare disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what could lead to reduced heme synthesis?

A

lead poisoning or congenital or acquired sideroblastic anemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What could cause reduced globin production?

A

thalassemic disorders or other hemoglobinopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

iron through the diet is best absorbed from what 3 things?

A

meat, poultry, and fish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the recommended iron therapy?

A

oral iron 200-400 mg of elemental ferrous iron/ day in a single dose with only water/juice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are some of the side effects of oral iron?

A

nausea, constipation, anorexia, heartburn, vomiting, and diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the least expensive option for parenteral (colloidal) iron IV?

A

LMW dextran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is an iron medication that can be given quickly (e.g 5 min)?

A

ferumoxytol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When does iron therapy begin to work?

A

expect reticulocytosis in a few days and an increase in Hb in 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the symptoms of acute iron toxicity?

A

necrotizing gastroenteritis with vomiting, abdominal pain and bloody diarrhea–> shock, lethargy, and dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

suggestion of improvement from acute iron toxicity may be noted and then followed by what?

A

severe metabolic acidosis, coma, and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what does treatment for acute iron toxicity include?

A

urgent!! includes whole bowel irrigation and parenteral deferoxamine (which is a potent iron-chelating compound)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is activated charcoal’s role in acute iron toxicity?

A

it does not bind to iron and it is ineffective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is chronic iron toxicity?

A

when iron deposits in the heart, liver, and pancreas leading to organ failure and death; seen in patients with hereditary hemochromatosis and patients who receive many red cell transfusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

the interaction with vitamin B12 in the folic acid cycle is crucial for what?

A

the synthesis for methionine, which is needed for methylation reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

a bone marrow aspirate from someone with megaloblastic anemia shows what?

A

erythroid hyperplasia with cells messed up at every stage of the maturation process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is vitamin b12 important for?

A

for RBCs and CNS function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

where is vitamin b12 found?

A

in animal products and fortified breakfast cereals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how much vitamin b12 do we need daily? and how much does the body store?

A

need ~2micrograms/daily; body stores 2-5 mg; because the normal body stores greatly exceed the daily requirement, it takes years to develop a vitamin b12 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the effect of nitrous oxide on vitamin b12?

A

it inactivates cyanocobalamin (a common form of b12); if body stores are depleted, there is a rapid onset of neurological dysfunction that may not fully reverse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

the IF-Cbl complex binds where before being basorbed?

A

binds to a specific receptor- cubulin- in the ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are four causes of pernicious anemia?

A

autoantibodies are formed blocking the IF-cbl interction or blocking the IF-cbl receptors in the ileum; chronic atrophic gastritis; gastrectomy; H. pylori infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how would you treat vitamin b12 deficiency?

A

oral vitamin b12 supplementation- x500 daily need or if there are neurological symptoms present parenteral therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the best dietary sources for folate?

A

yeast, liver, kidney, and green leafy vegetables

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the estimated daily requirement for folate? and what is the recommended daily allowance for folate?

A

5-50 micro grams a day; recommended 400 micrograms a day for adults and 800 micrograms a day for pregnant or lactating females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

where is folate absorbed?

A

in the jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

when do plasma levels of folate begin to fall following inadequate intake?

A

within three weeks due to metabolism and urinary excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are 2 usual causes of folate deficiency?

A

inadequate dietary intake or alcoholism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

which causes neuropsychiatric symptoms: B12 or folate deficiency?

A

B12; FOLATE DEFICIENCY DOES NOT CAUSE NEUROPSYCHIATRIC SYMPTOMS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how do you treat folate deficiency?

A

typically 1 mg/day for 4 months; if folate malabsorption then dose of 1-5 mg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

folate is generally well-tolerated at recommended doses; higher doses can cause what?

A

hypotension and hypoglycemia

43
Q

hypoxia is sensed by what organ?

A

the kidneys

44
Q

in response to hypoxia, what does the kidney do?

A

EPO is made by the renal cortical fibroblasts and with hypoxia the number of fibroblasts that are making EPO increases

45
Q

What is the mechanism of action of epoetin alfa?

A

it is an erythropoiesis-stimulating glycoprotein

46
Q

how is epoetin alfa manufactured?

A

recombinant DNA technology

47
Q

what are the effects of epoetin alfa?

A

stimulates erythropoiesis; increases the reticulocyte count in less than 10 days; increased the RBC count, hemoglobin, and hematocrit in 2-6 weeks

48
Q

what is also included in epoetin alfa treatment?

A

iron and folate

49
Q

what are the clinical applications for epoetin alfa treatment?

A

anemia due to: chronic kidney disease, cancer chemotherapy, when using zidovudine tx for HIV;

50
Q

how is epoetin alfa administered?

A

via IV or subcutaneously

51
Q

what are some of the toxicities of epoetin alfa?

A

20-50% have increased diastolic BP; there is an increased risk of death, myocardial infarction, stroke, embolism, and tumor progression or recurrence

52
Q

what is the half life of epoetin alfa? and what is an example of a similar drug with 3x a longer half life?

A

half life= 4-13 hours; darbepoetin alfa (half life is 21 hours)

53
Q

what is the mechanism of action for hydroxyurea?

A

it targets ribonucleotide reductase, resulting in s-phase cell cycle arrest; it also somehow boosts the levels of fetal hemoglobin

54
Q

what are the effects of hydroxyurea?

A

lowers the concentration of Hb S within a cell–> less polymerization of the abnormal hemoglobin

55
Q

what are the clinical applications for hydroxyurea?

A

it is the only disease modifying therapy approved for sickle cell anemia

56
Q

how is hydroxyurea administered?

A

orally–> it is readily absorbed

57
Q

what are the toxicities associated with hydroxyurea?

A

neutropenia anemia, oral ulcers, mild GI upset, hyperpigmentation, rash, nail changes

58
Q

what is the mechanism of action for eculizumab?

A

it is a monoclonal antibody that specifically binds to the complement protein C5 with high affinity; it inhibits its cleavage to C5a and C5b; prevents generation of terminal complement complex C5b-9

59
Q

what are the effects of eculizumab?

A

inhibits terminal complement mediated intravascular hemolysis in paroxysmal nocturnal hemoglobinuria; inhibits complement-mediated thrombotic microangiopathy in patients with atypical hemolytic uremia syndrome

60
Q

what are the clinical applications of eculizumab?

A

PNH, atypical hemolytic uremic syndrome; it is only available under a risk evaluation and mitigation strategy (REMS) to which prescribers must enroll

61
Q

how is eculizumad administered?

A

given IV over 35 minutes once per week for 1st 4 weeks; maintenance doses then given IV every 2 weeks

62
Q

what are the toxicities associated with eculizumab?

A

viral infections, life-threatening meningococcal infections (must give meningococcal vaccine 2 weeks before using); immunogenic

63
Q

what are some common presenting symptoms of neutropenia?

A

low-grade fever, sore mouth, severe pain when swallowing, gingival pain, symptoms of PNA

64
Q

What is filgrastim?

A

a human granulocyte colony-stimulating factor (G-CSF) produced by recombinant DNA technology

65
Q

what is G-CSF produced by endogenously?

A

monocytes, fibroblasts, and endothelial cells

66
Q

what are the effects of filgrastim?

A

it regulates the production of neutrophils within the bone marrow–> affects neutrophil progenitor proliferation and differentiation

67
Q

what are the clinical applications of filgrastim?

A

indicated to decreased the incidence of infection as manifested by febrile neutropenia in patients with nonmyeloid malignancies receiving myelosuppressive anticancer drugs or in those receiving a bone marrow transplant; used to mobilize hematopoietic progenitor cells into the peripheral blood; used for those with severe chronic neutropenia

68
Q

how is filgrastim administered?

A

as 4 or 24 hour IV infusion; wait 24 hours after chemotherapy and stop 24 hours before chemotherapy

69
Q

what is the half life of filgrastim? and what similar medication has a longer half life?

A

3.5 hours; pegfilgrastim- due to conjugation with monomethoxypolyethylene glycol

70
Q

what are the toxicities associated with filgrastim?

A

allergic reaction and bone pain sometimes

71
Q

what is sargramostim?

A

a recombinant form of granulocyte-macrophage colony stimulating factor (GM-CSF) made in yeast

72
Q

what are the effects of sargramostim?

A

acts in the bone marrow to increase production of neutrophils, eosinophils, and monocytes/macrophages

73
Q

what are the clinical applications of sargramostim?

A

used to accelerate recovery of myeloid cells after autologous bone marrow transplantation; can be used to mobilize hematopoietic stem cells into peripheral blood; indicated for use following induction chemotherapy in patients> 55 years with AML to shorten time to neutrophil recovery

74
Q

how is sargramostim administered?

A

given IV or subcutaneously

75
Q

what is the half life of sargramostim?

A

60 minutes

76
Q

what are the toxicities associated with sargramostim?

A

edema, sequestration of granulocytes in pulmonary circulation–> causing dyspnea; has worsened preexisiting renal and hepatic dysfunction

77
Q

when comparing filgrastim versus sargramostim, which one wins?

A

filgrastim has fewer adverse effects, so filgrastim wins

78
Q

what are the UpToDate recommendations on CSF use in cancer?

A

no role for CSF in afebrile patients with neutropenia; primary prophylaxis: use only if incidence of febrile neutropenia is estimated at >20%; secondary prophylaxis: only use if delay or reduction of chemotherapy dose would prevent full doses of potentially curative chemotherapy

79
Q

what is plerixafor?

A

a partial agonist of the CXCR4 receptor

80
Q

what is the CXCR4 receptor important for?

A

the homing of hematopoietic stem cells to the bone marrow

81
Q

what are the effects of plerixafor?

A

it mobilizes hematopoietic stem cells from the bone marrow to the plasma

82
Q

what are the clinical applications for plerixafor?

A

patients who do not mobilize sufficient stem cells

83
Q

what is plerixafor known to be?

A

an orphan drug (it is expensive)

84
Q

how is plerixafor administered?

A

subcutaneous injection

85
Q

what is the metabolism like of plerixafor/ half life?

A

half life is 3-5 hours; it is not metabolized- it’s eliminated by the kidneys

86
Q

both thrombopoietin and its PEG-derivatized variant have been withdrawn from the market- why?

A

due to autoantibodies that caused severe thrombocytopenia

87
Q

stem cell factor has potent synergistic actions on early progenitor cells, so why can’t it be used clinically?

A

it is also found on mast cells, and administration causes severe allergic reactions

88
Q

what is oprelvekin?

A

a recombinant form of IL-11

89
Q

what is the effect of oprelvekin?

A

it increases platelet levels by promoting the formation and maturation of megakaryocytes

90
Q

what are the clinical applications for oprelvekin?

A

does not have a major clinical use

91
Q

what other interleukins increase platelet levels, but are too toxic to use?

A

IL-3 and IL-6

92
Q

what is romiplostim?

A

a peptibody which binds to the TPO receptor but has no TPO homology

93
Q

what are the effects or romiplostim?

A

increases the platelet count in: healthy individuals, patients with ITP, and patients with MDS

94
Q

what are the clinical applications of romiplostim?

A

excess platelet destruction due to ITP; used after failure of glucocorticoids and immune globin, and splenectomy

95
Q

how is romiplostim administered?

A

weekly as subcutaneous injection

96
Q

what are the toxicities associated with romiplostim?

A

generally well-tolerated, but could have allergic reaction

97
Q

what is eltrombopag?

A

a potent orally available non-peptide TPO receptor agonist

98
Q

what are the effects of eltrombopag?

A

it increases the platelet count in healthy individuals, patients with ITP, and thrombocytopenia due to hepatitis C

99
Q

what are the clinical applications for eltrombopag?

A

excess platelet destruction due to ITP or cirrhosis due to hepatitis C

100
Q

how is eltrombopag administered?

A

orally given once per day

101
Q

what are the toxicities associated with eltrombopag?

A

may cause hepatotoxicity when used in combination with interferon and ribavirin in patients with chronic hepatitis C

102
Q

what are the first options used when treating ITP?

A

glucocorticoids and immune globin

103
Q

what are the second options of treating ITP?

A

rituximab + splenectomy

104
Q

what are the third options for treating ITP?

A

romiplostim and eltrombopag

SBL (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions