Sem 1 Final Flashcards

1
Q

Ferrous sulfate, ferrous gluconate, ferrous fumarate: SE’s?

A

N/V, *melena

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2
Q

Ferrous sulfate, ferrous gluconate, ferrous fumarate: indications?

A

Inadequate absorption of Fe; blood loss; (increased Fe requirements for pregnant, children, premies)

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3
Q

Ferous sulfate, ferrous gluconate, ferrous fumarate: how long does it take to work?

A

Quick response- anemia reversed in 1-3 months

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4
Q

Ferrous sulfate, ferrous gluconate, ferrous fumarate: MoA?

Route?

A

Fe supplementation

PO

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5
Q

Iron dextran, iron sucrose, iron gluconate: MoA?

Route?

A

Fe supplementation

IV or IM

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6
Q

Iron dextran, iron sucrose, iron gluconate: indications?

A

When the oral form (ferrous __) isn’t tollerated, such as post-GI resection; malabsoprtive syndromes

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7
Q

Iron dextran, iron sucrose, iron gluconate: SE’s?

A

Pain, tissue staining (IM), HA, fever, N/V, back/joint pain, allergic rxns, anaphylaxis (more than oral ferrous forms)

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8
Q

What can acute Fe toxicity cause?

What can chronic Fe toxicity cause?

A
  • Acute Fe toxicity (usually from over-ingestion of tabs) can cause necrotizing gastroenteritis; death in children.
  • Chronic toxicity (hemochromatosis, multiple transfusions) can cause organ failure.
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9
Q

What are some techniques drugs for treating acute Fe toxicity? (3)

A
  • Gastric aspiration
  • Gastric lavage (phosphate or carbonate solns)
  • Deferoxamine
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10
Q

What are some techniques drugs for treating chronic Fe toxicity? (3)

A
  • Deferoxamine
  • Deferasirox
  • Intermittent phlebotomy
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11
Q

What can be given for B12 supplementation? Folate supplementation?

A
  • B12: Cyanocobalamine, hydroxycobalamine

- Folate: folic acid

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12
Q

What route can Cyanocobalamine and hydroxycobalamine be given besides PO?
What is the response time?

A

IM

- Quick response (1-2 months). PO might be even better!

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13
Q

If someone is experiencing B12 or folic acid def., if they are given supplemental folic acid, will the CNS sx be reversed?

A

No

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14
Q

EPO: routes?

A

IV, SubQ

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15
Q

EPO: indications?

A

CKD, aplastic anemia, leukemia, HIV/AIDS-associated anemias, cancers, anemia of prematuraty, post-phlebotomy

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16
Q

EPO: toxicity?

A

HTN, thrombotic complications, allergic rxns, tumor recurrence and progression

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17
Q

Sargamostrim: MoA?

A

Recombinant GM-CSF. Stimulates proliferation and differentiation of erythroid and megakaryocytic cells (less specific than below).

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18
Q

Sargamostrim, filgastrim, pegfilgastrim: indications?

they have different MoA’s and SE’s

A

S/p intesive chemo (particularly for AML), congenital neutropenia, cyclic neutropenia, neutropenia a/w myelodysplasia and aplastic anemia, high-dose chemo w/autologous stem cell rescue, autologous transplant (mobilization of peripheral blood cells)

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19
Q

Sargamostrim: SE’s?

A

Fever, arthralgia, myalgia, peripheral edema, pleural/pericardial effusion, allergic rxns

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20
Q

Filgastrim, pegfilgastrim: MoA?

A

Recombinant G-CSF. Promotes the release of hematopoietic stem cells from the marrow into the peripheral circulation. Increases PMN count.

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21
Q

Filgastrim, pegfilgastrim: SE’s?

A

Bone pain, rarely splenic rupture, allergic rxns.

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22
Q

Which drug is better: sarmostrim or filgastrim?

A

Filgastrim

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23
Q

How does pegfilgastrim differ in T1/2 from filgastrim?

A

Pegfilgastrim (conjugated to polyethylene glycol) has a longer T1/2

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24
Q

Oprelvekin: MoA?

A

Recombinant IL-11. Promotes proliferation of megakaryocyte progenitors. Increases peripheral platelet counts.

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25
Q

Oprelvekin: indications?

A

Chemo pts who become thrombocytopenic

(Platelet transfusions can produce adverse rxns and pts can be refractory to platelet transfusions as well, so use this drug instead to increase platelet counts)

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26
Q

Oprelvekin: SE’s?

A

Fatigue, HA, dizziness, dyspnea, arrhythmia, hypokalemia

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27
Q

Romiplostim: MoA?

A

A novel protein known as a “peptibody” with two domains; a peptide domain that binds the TPO (thrombopoietin) receptor (Mpl), and an antibody Fc domain that increases half-life.

(TPO receptors are also on stem cells, so all stages of hematopoiesis are increased, including RBCs, WBCs, and platelets, making this a promising drug to treat aplastic anemia.)

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28
Q

Romiplostim, eltrombopag: indications?

they have different MoA’s

A

Thrombocytopenia, idiopathic thrombocytopenic purpura (ITP), asplastic anemia, post-chemo

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29
Q

Romiplostim, eltrombopag: SE’s?

They have different MoA’s

A

HA, myalgia, bone marrow fibrosis (reversible)

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30
Q

Eltrombopag: MoA?

A

A thrombopoietin-receptor agonist (small molecule)

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31
Q

Prednisone, prednesilone: MoA?

A

A glucocorticoid; activates the glucocorticoid receptor TS factor; modifies expression of cytokines and other immunomodulatory genes; suppresses active immune response

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32
Q

Prednisone, prednesilone: indications?

A

Immunosuppression; to prevent graft rejection; to prevent GvHD; tx of cytokine release syndrome; tx of a wide variety of autoimmune and inflammatory dz’s (SLE, RA, asthma, etc)

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33
Q

Prednisone, prednesilone: toxicity?

A

Hyperglycemia, HTN, HLD, obesity, diabetes, poor wound healing, increased infection risk, mania & psychosis

*Dose should be gradually reduced and not withdrawn abruptly.

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34
Q

Azathioprine: MoA?

A

Prodrug that’s converted to active 6-mercaptopurine (6-MP) by HGPRT. Inhibits de novo purine synthesis. Incorporated into DNA and causes SSB mispairing –> apoptosis (inhibits lymphocyte proliferation). Inhibits CD28 co-stimulation.

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35
Q

Azathioprine: indications?

A

Immunosuppression; to prevent graft rejection; to prevent GvHD; tx of autoimmune dz’s

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36
Q

Azathioprine: toxicity?

A

Leukopenia/thrombocytopenia, hepatotoxicity, ^ risk infections, ^ risk malignancy

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37
Q

Azathioprine: contraindications?

A

*Interacts w/anti-gout drugs allopurinol and febuxostat –> ^ [azathioprine] –> ^ toxicity.

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38
Q

Mycophenolate mofetil: MoA?

A

Prodrug that’s converted to mycophenolic acid, inhibits IMPDH2 (which is selectively expressed in lymphocytes) –> inhibition of purine NT synthesis (no salvage pw in lymphocytes –> selectively inhibits lymphocyte proliferation)

39
Q

Mycophenolate mofetil: indications?

A

Immunosuppression; to prevent graft rejection; to prevent GvHD; tx of autoimmune dz’s

40
Q

Mycophenolate mofetil: toxicity?

A

Leukopenia/anemia, teratogenic (male + female), ^ risk infections, ^ risk malignancy, *RARE- risk of progressive multifocal leukoencephalopathy (PML) (Fatal dz caused by reactivation of JC virus)

41
Q

Mycophenolate mofetil: contraindications?

A

Pregnancy, women who wish to become pregnant, and men who wish to become fathers

42
Q

Cyclosporin, tacrolimus: MoA?

A

Cyclosporin and tacrolimus bind cyclophilin and FKBP respectively to form inhibitory complexes, which inhibit calcineurin, a Ca-regulated phosphatase, thus inhibiting the NFAT ts factor, which is involved in regulating the expression of IL-2 and multiple other immunoregulatory genes. Potently inhibits the T cell immune response by inhibiting signal 1.

43
Q

Cyclosporin, tacrolimus: indications?

A

Immunosuppression; to prevent graft rejection; to prevent GvHD; tx of autoimmune dz’s

44
Q

Cyclosporin, tacrolimus: toxicity?

A

Nephrotoxicity**, hypertension*, neurotoxicity, tremor, glc intolerance (T>C), HLD (C>T), hypertrochosis (C), alopecia (T), ^ risk infections, ^ risk malignancy

45
Q

Cyclosporin, tacrolimus: contraindications?

A

*Metabolized by CYP3A4, many drug interactions. CYP3A4 inhibitors –> ^ drug level –> ^ toxicity. CYP3A4 inducers –> v drug level –> ^ risk graft rejection.

46
Q

Sirolimus, everolimus: MoA?

A

Drugs form complex w/FKBP, which inhibits IL-2-mediated activation of mTOR kinase (T cell signal 2). Inhibits IL-2-mediated ptn synthesis, cell proliferation and survival.

47
Q

Sirolimus, everolimus: indications?

A

Immunosuppression; to prevent graft rejection (NOT liver, NOT lung); to prevent GvHD; included in arterial stents to inhibit restenosis

48
Q

Sirolimus, everolimus: toxicity?

A

Hypertriglyceridemia, hypercholesterolemia, ^ lung dz, ^ risk diabetes, anemia/cytopenia/leukopenia, v wound healing, teratogenic, ^ risk infections, ^ risk malignancy

49
Q

Sirolimus, everolimus: contraindications?
Why aren’t they recommended for lung xplant?
Why aren’t they recommended for liver xplant?

A

Pregnancy. Metabolized by CYP3A4, many drug interactions.

NOT RECOMMENDED IN: lung xplant (risk anastomatic dehiscence), liver xplant (risk hepatic a. thrombosis)

50
Q

Rabbit anti-thymocyte globulin: MoA?

A

Rabbit polyclonal AB’s specific for human lymphocytes (depletes lymphocytes from the blood).

51
Q

Rabbit anti-thymocyte globulin: indications?

A

Induction immunotherapy

52
Q

Rabbit anti-thymocyte globulin: toxicity?

A

*Cytokine release syndrome, leukopenia.

53
Q

Alemtuzumab: MoA?

A

Binds to CD52 expressed on T cells, B cells, macrophages, NK cells, & granulocytes. Depletes cells from the blood by AB-mediated lysis.

54
Q

Alemtuzumab: indications?

A

Induction immunotherapy

55
Q

Alemtuzumab: toxicity?

How long can it take to recover from this?

A

*Cytokine release syndrome, leukopenia.

Can take > 1 year for immune system to recover from the toxicity.

56
Q

Basaliximab: MoA?

A

Antagonist of the IL-2R (blocks T cell proliferation).

57
Q

Basaliximab: indications?

A

Induction immunotherapy

58
Q

IV IG: MoA?

A

Pooled Ig from healthy individuals; provides pt w/Ig from healthy immunized donors to provide immunity from common pathogens

59
Q

IV IG: indications?

A

Provides short-lived humoral immunity to pts w/deficiency in humoral immune system (e.g. hypogammaglobulinemia)

60
Q

Rho (D): MoA?

When is it given to mothers?

A

Purified AB to Rh(D) ag. Given to Rh- mother at 28 weeks and 72 hrs post-partum to deplete any fetal RBC in maternal blood to prevent the mother from generating an immune response to RBC

61
Q

Rho (D): indications?

A

Prevention of hemolytic disease of the newbown in newborns born to Rh- mothers

62
Q

Hyperimmune Ig: MoA?

A

Purified Ig to specific Ag’s purified from healthy volunteers. Given IV in order to promote clearance of virus/toxin

63
Q

Hyperimmune Ig: indications?

A

To provide rapid, specific AB immunity to specific viruses and/or toxins

64
Q

Ipilimumab: MoA?

A

AB specific for CTLA-4; antagonizes the negative regulatory CTLA-4 ptn responsible for down-regulating activated T cells, thus enhancing T cell response.

65
Q

Ipilimumab: indications?

A

Tx of late stage melanoma and non-small cell lung cancers.

66
Q

Ipilimumab: toxicity?

A

Potential for RARE autoimmune response (can be fatal)

67
Q

Ipilimumab: contraindications?

A

Not recommended in pregnancy

68
Q

Pembrolizumab, nivolumab: MoA?

A

AB specific for PD1 ptn, which is a negative regulatory receptor expressed on activated T cells that is responsible for down-regulating T cell responses. The PD1 ligand PD-L1 is expressed on tumor cells- this is a mech for tumors to avoid the immune response; AB drugs block PD1/PD-L1 interactions, blocking the inhibitory signal and leading to enhanced tumor immune responses.

69
Q

Pembrolizumab, nivolumab: indications?

A

Tx of late stage melanoma and non-small cell lung cancers.

70
Q

Pembrolizumab, nivolumab: toxicity?

A

Potential for RARE autoimmune response (can be fatal)

71
Q

Pembrolizumab, nivolumab: contraindications?

A

Not recommended in pregnancy

72
Q

Name 3 anti-proliferative agents that are less commonly used in transplants (that we skipped over in class but could come up as other options for answer)

A

Methotrexate
Cyclophosphamide
Chlorambucil

73
Q

Toxicity of rifampin?

(the rest is on sketchy)

A

Hepatotoxicity, red discoloration of body fluids, AKI, influenza syndrome (more common w/intermittent dosing), thrombocytopenia, cholestatic jaundice. [activates CYP450]

74
Q

What defines multi-drug resistance TB?

A

Resistance to both INH and rifampin

More common in HIV infected patients

75
Q

What does acquiring rifampin resistance mean, in terms of duration of TB therapy?

A

Rifampin resistance eliminates short-course (6 month) TB therapy- requires therapy for at least 18-24 months.

76
Q

What defines extensively-drug resistance TB?

A

Resistance to all of the following:

  • INH and Rifampin
  • A fluoroquinolone antibiotic
  • 1 of 3 injectable abx (amikacin, kanamycin, capreomycin)
77
Q

What 3 factors indicate that 6-month TB tx will be effective?

A
  • Adherence is high
  • Sputum cultures convert by 2 months
  • There is no major cavitary lung disease
78
Q

What 2 drugs are effective vs TB only?
What 2 drugs are effective vs NTM only?
What 4 drugs are effective vs TB and NTM organisms?

A

Active vs. TB: INH, PZA

Active vs. NTM: Clarithro, azithro (macrolides)

Active vs. Both: Rif, emb, FQ, AG

79
Q

What organisms does amphotericin B cover?
What 2 does it not cover?
What is it TOC for?

A

Broad spectrum: all life-threatening mycotic infections

  • Candida, cryptoccous, histoplasma, blastomyces, coccidiodes, aspergilus, fusarium, mucor
  • not C. lusitaniae, not p. boydii.
  • TOC: Mucormycosis
80
Q

What specific organism does nystatin cover?

What related organisms does it not cover?

A
  • Mucocutaneous candidiasis

* Not dermatophytes

81
Q

What organisms does flucytosine cover?

A

C’s

- Cryptococcus neoformans (esp. cryptoccocal meningitis), candida, chromoblastomycosis

82
Q

What organisms do echinocandins (caspofungin, micafungin, anidulafungin) cover?
What do they not cover?

A
  • Incasive candida (including glabrata and kruseii), invasive aspergillus
  • Not cryptococcus or dimorphic fungi
83
Q

What organisms does griseofulvin cover?

A

Mycotic infection of stain/hair/nails due to dermatophytes

84
Q

What organisms does terbinafine cover?

A
  • Tx of oncomycosis and superficial skin infections
  • Candida albicans, dermatophytes
  • Tx of tinea’s
85
Q

What anti-fungals have good CSF penetration?

A

Flucytosine
Fluconazole
Voriconazole

86
Q

What anti-fungal can be used in pregnancy?

A

Amphotericin B

87
Q

What organisms does ketoconazole cover?

A
Dermatophytes
Candida sp.
Cryptococcus
Coccidiodes
Histoplasma
Blastomyces

(Denise can cram cocks, historically black)

88
Q

What organisms does fluconazole cover?

A
Dermatophytes
Candida sp.
   C. glabrata (+/-), C. krusei (-)
Cryptococcus
Coccidiodes
    Histoplasma (+/-)
    Blastomyces (+/-)

Lowest SOA, but great bioavailability and effective in CNS, bladder)

(Denise can cram cocks, historically black)

89
Q

What organisms does itraconazole cover?

A
Dermatophytes
Candida
   C. glabrata (+/-), C. krusei (+/-)
Cryptococcus
Coccidioides
Histoplasma
Blastomyces
   Pseudoallerischeri
   Boydii/Scedosporium (+/-)
   Aspergillus (+)

(Denise can cram cocks, historically black + some randoms and a little aspergillus)

90
Q

What organisms does voriconazole cover?

A
Dermatophytes
Candida (all)
Cryptococcus
Coccidioides
Histoplasma
Blastomyces
  Pseudoallerischeri
  Boydii/Scedosporium
    Aspergillus (+++)
    Fusarium

(Denise can cram cocks, historically black, but now great aspergillus and new fusarium)

91
Q

What organisms does posaconazole cover?

A
Dermatophytes
Candida (all)
Cryptococcus
Coccidioides
Histoplasma
Blastomycoses
Pseudoallerischeri
Boydii/Scedosporium
Aspergillus (+++)
Fusarium
   Mucor

(Denise can cram cock, historically black. Basically covers all, but also salvage therapy for mucor)

92
Q

Which azole requires a renal dose adjustment?

A

Fluconazole

93
Q

Side effects for itraconazole?

A

HTN, hypokalemia, peripheral edema

94
Q

Side effects for voriconazole?

A

Photosensitivity, rash, periostitis, visual changes, hallucinations, seizures