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SBL Ex 1 Path > Pharm: Anemia and Hematopoietic GF's > Flashcards

Pharm: Anemia and Hematopoietic GF's Flashcards

1
Q

Which type of iron is used for therapy for iron malabsorption, intolerance of oral therapy, or non compliance?

A

Parenteral (colloidal) iron —> iron dextran, sodium ferric gluconate complex and iron-sucrose complex

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2
Q

What is the urgent treatment for iron poisoning?

A

Parenteral deferoxamine (potent iron-chelating compound)

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3
Q

When would oral vs. parenteral therapy for Vit B12 supplementation be indicated to tx deficiency?

A
  • Oral: generally effective, EVEN in pt’s w/ pernicious anemia
  • Parenteral therapy: used if neurological sx’s are present
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4
Q

What are 3 types of iron supplements that can be taken orally; what should they be taken with?

A
  • Ferrous sulfate, gluconate, or fumarate that is ideally NOT enteric-coated and NOT-sustained release
  • Pt should take with ONLY water/juice, not with food
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5
Q

Nitrous oxide inhaled for analgesia during surgey can have what effect on B12?

A

Inactivates cyanocobalamin (common form of B12)

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6
Q

What is the MOA of epoetin alfa?

A
  • Stimulates erythropoiesis
  • ↑ reticulocyte count ≤10 days
  • ↑ RBC count, hemoglobin, and hematocrit in 2-6 weeks
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7
Q

What are the clinical uses of epoetin alfa?

A
  • Anemia due to: CKD; cancer chemotherapy; and zidovudine tx for HIV
  • ↓ allogenic RBC transfusions in pt’s undergoing elective surgery
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8
Q

There is an increased risk for what serious AE’s associated with epoetin alfa?

A
  • MI
  • Stroke
  • Venous thrombo-embolism
  • Thrombosis of vascular access and tumor progression or recurrence
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9
Q

How does darbepoetin alfa differ from epoetin alfa?

A

Has 3x longer half-life

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10
Q

What are the 2 MOA of Hydroxyurea?

A
  • Targets ribonucleotide reductase, results in S-phase cell cycle arrest
  • Somehow boosts levels of fetal hemoglobin (HbF, α2γ2)
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11
Q

What is the only disease modifying therapy for sickle cell anemia?

A

Hydroxyurea

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12
Q

List 4 AE’s associated with hydroxyurea used for sickle cell anemia.

A
  • Cough or hoarseness
  • Fever or chills
  • Lower back or side pain
  • Painful or difficult urination
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13
Q

What is the MOA of eculizumab?

A
  • Monoclonal Ab that binds complement protein C5 and inhibits cleavage to C5a and C5b
  • Prevents generation of the MAC (C5b-9)
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14
Q

What are the 2 effects of using eculizumab for paroxysmal nocturnal hemoglobinuria and atypical HUS?

A
  • Inhibits terminal complement-mediated intravascular hemolysis in PNH
  • Inhibits complement-mediated thrombotic micorangiopathy in pt’s w/ atypical HUS
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15
Q

What must be given 2-weeks prior to using eculizumab?

A

Meningococcal vaccine

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16
Q

List some common presenting sx’s of neutropenia?

A
  • Low-grade fever
  • Sore mouth
  • Odynophagia
  • Gingival pain and swelling
  • Perirectal pain and irritation
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17
Q

What is filgrastim and pegfilgrastin; how do they differ?

A
  • Both are G-CSF
  • Pegfilgrastim is longer lasting (PEGylated = conjugated to polyethylene glycol)
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18
Q

What are some of the serious AE’s associated with Filgrastim (G-CSF)?

A
  • Splenic rupture, sometimes fatal
  • ARDS
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19
Q

What is sargramostim?

A

GM-CSF

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20
Q

What are some of the serious AE’s associated with the GM-CSF, Sargramostim?

A
  • Contains benzyl alcohol, can cause fatal “grasping syndrome” in prematue infants
  • Fluid retention —> edema; also pleural effusion and pericardial effusion
  • Dyspnea from sequestration of granulocytes in pulmonary circulation
  • Occsaional transient SVT
  • May worse pre-existing renal and hepatic dysfunction
How well did you know this?
1
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21
Q

Between Filgrastim and Sargramostim which has fewer AE’s and should be used?

A

Filgrastim (G-CSF)

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22
Q

What is the MOA of Plerixafor?

A

Partial agonist at CXCR4 receptor, important for homing of hematopoietic stem cells to BM

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23
Q

What is Plerixafor used for?

A

In patient who do not mobilize sufficient stem cells for autologous transplant with just G-CSF

How well did you know this?
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24
Q

What is the main AE associated with Plerixafor?

A

Hypersensitivity rxn

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25
Q

What is the MOA of Romiplostim?

A
  • A “peptibody” of human IgG1 kappa heavy chain constant regions (an Fc fragment)
  • Binds TPO receptor
  • Must be given SQ because it’s a peptide!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the effect and clinical use of Romiplstim?

A
  • ↑ the platelet count in: healthy pt’s, pt’s with ITP and pt’s with myelodysplastic C syndrome
  • Use for excess platelet destruction due to idiopathic thrombocytopenia purpura (ITP)
27
Q

What is the MOA of Eltrombopag; effects in pt’s?

A
  • Potent, orally available NON-peptide TPO receptor agonist
  • ↑ platelet count in: healthy pt’s, those with ITP, and thromobocytopenia due to hepatitis C
28
Q

What are the 2 clinical uses for Eltrombopag?

A
  • Excess platelet destruction due to idiopathic thrombocytopenic purpura
  • Cirrhosis due to hepatitis C
29
Q

What is an AE associated with Eltrombopag?

A

Hepatotoxicity when used in combo w/ interferon and ribavirin in pt’s with hepatitis C

30
Q

What is the most common drug class which causes hemolytic anemia; what is another common class?

A
  • Cephalosporins, especially ceftriaxone and cefotetan = most common
  • Penicillin and its derivative, especially piperacillin
31
Q

Which drugs are the most common immune and non-immune causes of drug-induced thrombocytopenia?

A
  • Immune = heparin
  • Non-immune = quinidine and quinine
32
Q

What are 3 major drugs/classes that may cause aplastic anemia?

A
  • Cancer chemotherapeutics, especially alkylating agents, antimetabolites, and cytotoxic antibiotics
  • Chloramphenicol, an Abx that is no longer used
  • Benzene
33
Q

Parenteral (colloidal) iron —> iron dextran, sodium ferric gluconate complex and iron-sucrose complex

A

Which type of iron is used for therapy for iron malabsorption, intolerance of oral therapy, or non compliance?

34
Q

Parenteral deferoxamine (potent iron-chelating compound)

A

What is the urgent treatment for iron poisoning?

35
Q
  • Oral: generally effective, EVEN in pt’s w/ pernicious anemia
  • Parenteral therapy: used if neurological sx’s are present
A

When would oral vs. parenteral therapy for Vit B12 supplementation be indicated to tx deficiency?

36
Q
  • Ferrous sulfate, gluconate, or fumarate that is ideally NOT enteric-coated and NOT-sustained release
  • Pt should take with ONLY water/juice, not with food
A

What are 3 types of iron supplements that can be taken orally; what should they be taken with?

37
Q

Inactivates cyanocobalamin (common form of B12)

A

Nitrous oxide inhaled for analgesia during surgey can have what effect on B12?

38
Q
  • Stimulates erythropoiesis
  • ↑ reticulocyte count ≤10 days
  • ↑ RBC count, hemoglobin, and hematocrit in 2-6 weeks
A

What is the MOA of epoetin alfa?

39
Q
  • Anemia due to: CKD; cancer chemotherapy; and zidovudine tx for HIV
  • ↓ allogenic RBC transfusions in pt’s undergoing elective surgery
A

What are the clinical uses of epoetin alfa?

40
Q
  • MI
  • Stroke
  • Venous thrombo-embolism
  • Thrombosis of vascular access and tumor progression or recurrence
A

There is an increased risk for what serious AE’s associated with epoetin alfa?

41
Q

Has 3x longer half-life

A

How does darbepoetin alfa differ from epoetin alfa?

42
Q
  • Targets ribonucleotide reductase, results in S-phase cell cycle arrest
  • Somehow boosts levels of fetal hemoglobin (HbF, α2γ2)
A

What are the 2 MOA of Hydroxyurea?

43
Q

Hydroxyurea

A

What is the only disease modifying therapy for sickle cell anemia?

44
Q
  • Cough or hoarseness
  • Fever or chills
  • Lower back or side pain
  • Painful or difficult urination
A

List 4 AE’s associated with hydroxyurea used for sickle cell anemia.

45
Q
  • Monoclonal Ab that binds complement protein C5 and inhibits cleavage to C5a and C5b
  • Prevents generation of the MAC (C5b-9)
A

What is the MOA of eculizumab?

46
Q
  • Inhibits terminal complement-mediated intravascular hemolysis in PNH
  • Inhibits complement-mediated thrombotic micorangiopathy in pt’s w/ atypical HUS
A

What are the 2 effects of using eculizumab for paroxysmal nocturnal hemoglobinuria and atypical HUS?

47
Q

Meningococcal vaccine

A

What must be given 2-weeks prior to using eculizumab?

48
Q
  • Low-grade fever
  • Sore mouth
  • Odynophagia
  • Gingival pain and swelling
  • Perirectal pain and irritation
A

List some common presenting sx’s of neutropenia?

49
Q
  • Both are G-CSF
  • Pegfilgrastim is longer lasting (PEGylated = conjugated to polyethylene glycol)
A

What is filgrastim and pegfilgrastin; how do they differ?

50
Q
  • Splenic rupture, sometimes fatal
  • ARDS
A

What are some of the serious AE’s associated with Filgrastim (G-CSF)?

51
Q

GM-CSF

A

What is sargramostim?

52
Q
  • Contains benzyl alcohol, can cause fatal “grasping syndrome” in prematue infants
  • Fluid retention —> edema; also pleural effusion and pericardial effusion
  • Dyspnea from sequestration of granulocytes in pulmonary circulation
  • Occsaional transient SVT
  • May worse pre-existing renal and hepatic dysfunction
A

What are some of the serious AE’s associated with the GM-CSF, Sargramostim?

53
Q

Filgrastim (G-CSF)

A

Between Filgrastim and Sargramostim which has fewer AE’s and should be used?

54
Q

Partial agonist at CXCR4 receptor, important for homing of hematopoietic stem cells to BM

A

What is the MOA of Plerixafor?

55
Q

In patient who do not mobilize sufficient stem cells for autologous transplant with just G-CSF

A

What is Plerixafor used for?

56
Q

Hypersensitivity rxn

A

What is the main AE associated with Plerixafor?

57
Q
  • A “peptibody” of human IgG1 kappa heavy chain constant regions (an Fc fragment)
  • Binds TPO receptor
  • Must be given SQ because it’s a peptide!
A

What is the MOA of Romiplostim?

58
Q
  • ↑ the platelet count in: healthy pt’s, pt’s with ITP and pt’s with myelodysplastic C syndrome
  • Use for excess platelet destruction due to idiopathic thrombocytopenia purpura (ITP)
A

What is the effect and clinical use of Romiplstim?

59
Q
  • Potent, orally available NON-peptide TPO receptor agonist
  • ↑ platelet count in: healthy pt’s, those with ITP, and thromobocytopenia due to hepatitis C
A

What is the MOA of Eltrombopag; effects in pt’s?

60
Q
  • Excess platelet destruction due to idiopathic thrombocytopenic purpura
  • Cirrhosis due to hepatitis C
A

What are the 2 clinical uses for Eltrombopag?

61
Q

Hepatotoxicity when used in combo w/ interferon and ribavirin in pt’s with hepatitis C

A

What is an AE associated with Eltrombopag?

62
Q
  • Cephalosporins, especially ceftriaxone and cefotetan = most common
  • Penicillin and its derivative, especially piperacillin
A

What is the most common drug class which causes hemolytic anemia; what is another common class?

63
Q
  • Immune = heparin
  • Non-immune = quinidine and quinine
A

Which drugs are the most common immune and non-immune causes of drug-induced thrombocytopenia?

64
Q
  • Cancer chemotherapeutics, especially alkylating agents, antimetabolites, and cytotoxic antibiotics
  • Chloramphenicol, an Abx that is no longer used
  • Benzene
A

What are 3 major drugs/classes that may cause aplastic anemia?

SBL Ex 1 Path (13 decks)

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