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Clinical Medicine > Heme-Pharm > Flashcards

Heme-Pharm Flashcards

1
Q

Deferoxamine

A

chelating drug used to irrigate the bowel after an iron overdose

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2
Q

dihydrofolate reductase

A

enzyme that switches dietary folate to tetrahydrofolate (middle man) to active folate - once active folate can assist in DNA synthesis

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3
Q

What do these drugs do?

Methotrexate, trimethoprim, pyrimethamine

A

target dihdyrofolate reductase inhibiting the action of the enzyme that converts folic acid to active form

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4
Q

Apoetin alfa (epogen)

A

erythropoietin stimulating agent
3x a week

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5
Q

Darbepoetin alfa (mircera)

A

erythropoietin stimulating agent
1x a week

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6
Q

Epoetin beta (aranesp)

A

erythropoietin stimulating agent
every other week/monthly

don’t use on cancer patients due to increased risk of death

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7
Q

3 iron salts

A

ferrous sulfate, ferrous fumarate, ferrous gluconate

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8
Q

sodium ferric gluconate (ferrlecit)
Iron sucrose (venofer)
Iron dextran (infed)
ferumoxytol (feraheme)

what kind of drugs are these)

A

parenternal iron preparations

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9
Q

Filgrastim (neupogen)

A

myeloid growth factor - granulocyte
administer daily due to 2-7 hr half life

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10
Q

pegfilgrastim (neulasta)

A

myeloid growth factor - granulocyte
administer once per chemo cycle

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11
Q

sagramostim (leukine)

A

myeloid growth factor - granulocyte macrophage
administer daily (1/2/ life 2-7 hrs)

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12
Q

oprelvekin (recombinant IL-11 or Neumega)

A

megakaryocyte growth factor
administer daily half life 7-8 hrs

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13
Q

antidote for nitrogen mustard

A

thiosulfate

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14
Q

antidote for vinca alkaloids

A

hyaluronidase

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15
Q

antidote for anthracyclines

A

dexrazoxane

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16
Q

what is the active and inactive form of folic acid

A

active: folinic acid
inactive: folic acid

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17
Q

folic acid
- mechanism of action
- pharmacokinetics

A

synthesis of purines/pyrimidines
oral, absorbed in jejunum

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18
Q

B12
- mechanism of action
- pharmacokinetics

A

cofactor required for enzymatic rxns (succinyl co-A)
IM/SubQ or oral for maintenance

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19
Q

iron salts (3)
- MOA
- Pharmacokinetics

A

attached “salt” helps iron absorption
- Ferrous sulfate, ferrous fumarate, ferrous gluconate
oral, absorbed in duodenum

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20
Q

what do Erythropoietin stimulating agents do?

A

Raise erythroid proliferation/differentiation
Release of reticulocytes from bone marrow

Indications:
- Anemia secondary to chronic kidney dz
- Myeloid- suppressive cancer chemo (only give to improve QOL)
- Hgb below 10 mg (12 for those w/ kidney dz)

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21
Q

Erythropoietin stimulating agents pharmacokinetics

A

IV/SC administration

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22
Q

Granulocyte colony stimulating factor (G-CSF)- myeloid
- MOA
- pharmacokinetics

A

Pharmacokinetics: IV of SC administration
Mech of Action:
- Increase proliferation/differentiation of neutrophil progenitors
- Increase phagocytic activity of neutrophils
- Increase hematopoietic stem cell mobilization (make more myeloid)

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23
Q

Granulocyte-macrophage colony stimulating factor (GM-CSF)- myeloid
- MOA
- pharmacokinetics
- why take it?

A

Pharmacokinetics: IV/SC (SC more common)
Mech of Action:
- Increase proliferation/differentiation of early/late granulocytic progenators
- Increase erythroid/megakaryocyte progenators
- Increase phagocytic activity of mature neutrophils
- Increase hematopoietic stem cell mobilization (less than G-CSF)

neutropenia, chemo induced myelosuppression

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24
Q

Megakaryocyte growth factor
- pharmacokinetics
-MOA
- why take it?

A

Pharmacokinetics: SC daily

Mech of Action
- Increase growth in multiple myeloid and lymphoid cells
- Increase circulating platelets and neutrophils

Indications:
- Prevention of thrombocytopenia due to cytotoxic chemo for non-myeloid cancers

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25
Q

5-Fu pharmacokinetics

A

IV (adrucil)
topical (fluorplex)

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26
Q

5-fu MoA

A

inhibits thymidylate synthetase which feeds to folic acid cycle = no DNA synthesis

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27
Q

5-FU indications

A

breast tumors
colorectal tumors
non-invasive skin cancers (topical)

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28
Q

5-FU OD treat with?

A

uridine-triacetate (vistogard)

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29
Q

Mercaptopurine(purinethol) pharmacokinetics

A
  • Oral
  • Metabolized by xanthine oxidase
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30
Q

Mercaptopurine(purinethol) MoA

A

converted to ribonuceotide by HGPRT and acts as fake NT putting itself into DNA and making it nonfunctional

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31
Q

Mercaptopurine(purinethol) indications

A
  • Acute lymphocytic leukemia (remission maintenance w/ methotrexate)
  • Chronic myeloid leukemia
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32
Q

Mercaptopurine(purinethol) interacts with?

A

allopurinol - raises serum levels (xanthine oxidase inhibitor

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33
Q

Methotrexate pharmacokinetics

A
  • Oral/parenteral
  • Bioavailability dose dependent
  • Wide distribution EXCEPT CNS
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34
Q

Methotrexate MoA

A
  • Inhibits dihydrofolate reductase which feeds into folic acid cycle
  • No pyrimidine synthesis
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35
Q

Methotrexate indications

A
  • Breast cancer
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36
Q

Methotrexate adverse effects

A
  • MYELOSUPPRESSION – rescue w/ leucovorin
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37
Q

Pemetrexed (alimta) pharmacokinetics

A

IV ONLY

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38
Q

Pemetrexed (alimta) MoA

A

inhibits thymidylate synthetase and dihydrofolate reductase to block DNA synthesis

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39
Q

Pemetrexed (alimta) indications

A

non-small cell lung cancer
- In combination w/ cistplatin (alkalating agent)

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40
Q

Pemetrexed (alimta) adverse effects

A
  • MYELOSUPPRESSION
  • ORAL ULCERATION
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41
Q

Vincristine (cincasar, marquibo) pharmacokinetics

A

IV administration (no CNS penetration)
- Vincasar: conventional
- Marquibo: liposomal
–encapsulated in liposomes which slows down the release and decreasing side effects/toxicity

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42
Q

Vincristine (cincasar, marquibo) MoA

A
  • MT built and disassembled
  • Blocks assembly of MT to cell division
  • Disassembly process continues as normal but MT nonfucnitonal to divide into two cells
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43
Q

Vincristine (cincasar, marquibo) indications

A
  • Acute lymphoblastic leukemia
  • Non-hodgkin lymphoma
  • Hodgkin lymphoma
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44
Q

Vincristine (cincasar, marquibo) adverse effects

A

neurotoxicity

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45
Q

Docetaxel (taxotere) pharmacokinetics

A

V administration
- Give dexamethasone as pre-treatment to avoid fluid retention and hypersensitivity rxns

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46
Q

Docetaxel (taxotere) MoA

A

MT block and unable to divide into 2 cells, decreases tumor

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47
Q

Docetaxel (taxotere) indication

A

metastatic prostate and breast cancer

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48
Q

Docetaxel (taxotere) adverse effects

A
  • MYELOSUPPRESSION (neutropenia)
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49
Q

Cyclophosphamide (Cytoxan)- pharmacokinetics

A
  • Oral and IV administration (90-95% bioavailability)
  • Prodrug converted to phosphoramide (active)
  • Acrolein formed as a byproduct (no therapeutic value, can cause side effects)
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50
Q

Cyclophosphamide (Cytoxan)- MoA

A
  • Active metabolites form covalent bonds w/ N7 nitrogen of guanine
  • Cross linking of DNA strands = no DNA replication/transcription
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51
Q

Cyclophosphamide (Cytoxan)- indication

A
  • Non-hodgkin lymphoma
  • Breast cancer
  • Neuroblastoma (tumor on immature nerve cells)
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52
Q

Cyclophosphamide (Cytoxan)- adverse effects

A
  • MYELOSUPPRESSION
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53
Q

Busulfan (myleran) pharmacokinetics

A

oral (low half life 2-2.5 hrs)

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54
Q

Busulfan (myleran) MoA

A
  • Active metabolites form covalent bonds w/ N7 nitrogen of guanine
  • Cross linking of DNA strands = no DNA replication/transcription
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55
Q

Busulfan (myleran) indications

A

acute myeloid leukemia, chronic myeloid leukemia

56
Q

Busulfan (myleran) adverse effects

A

myelosuppression and pulmonary fibrosis (fatal)
Hyperpigmentation of skin creases

57
Q

Cisplatin (platinol-aq) pharmacokinetics

A

: IV administration

58
Q

Cisplatin (platinol-aq) MoA

A

INTRAstrand cross link
- Same strand of DNA becomes stuck together distorting/bending the shape and making it unfit to be unzipped

59
Q

Cisplatin (platinol-aq) indications

A

ovarian cancer and lung cancer

60
Q

Cisplatin (platinol-aq) adverse effects

A

severe n/v

61
Q

temozolomide (temodar) pharmacokinetics

A

oral/IV

62
Q

temozolomide (temodar) MoA

A
  • alkylating agent adds a methyl group to guanine residues
  • DNA damage and tumor cell death
63
Q

temozolomide (temodar) indications

A

astrocytoma or glioblastoma – cross BBB

64
Q

Doxorubicin (Adriamycin)- pharmacokinetics

A

IV (widely distributed to tissues except CNS)

65
Q

Doxorubicin (Adriamycin)- MoA

A
  • Inhibition of topoisomerase II (uncoiler)
  • Formation of free radicals
  • Drug jams itself between DNA leading to distortion and generation of hydroxyl radicals causing strands to break
66
Q

Doxorubicin (Adriamycin)-indications

A
  • Breast, lung, thyroid cancer
  • Hodgkin and non-hodgkin lymphoma
67
Q

Bleomycin (blenoxane) pharmacokinetics

A

IV
- Widely distributed to tissues except CNS
- Inactivated by aminohydrolase

68
Q

Bleomycin (blenoxane) MoA

A
  • Inhibition of topoisomerase II (uncoiler)
  • Formation of free radicals
  • Drug jams itself between DNA leading to distortion and generation of hydroxyl radicals causing strands to break
69
Q

Bleomycin (blenoxane) indications

A
  • Testicular cancer, head/neck cancer
70
Q

Irinoteca (camptosar) – topoisomerase I inhibitor pharmacokinetics

A

IV administration
- Metabolite has greater antitumor activity than parent compound

71
Q

Irinoteca (camptosar) – topoisomerase I inhibitor MoA

A
  • Permanent single strand break due to blockage of topoisomerase I nick does not get sealed back
72
Q

Irinoteca (camptosar) – topoisomerase I inhibitor indicators

A

colon cancer, solid tumors of cervix/lung

73
Q

Irinoteca (camptosar) – topoisomerase I inhibitor adverse affects

A

diarrhea

74
Q

Etoposide (toposar) – topoisomerase II inhibitor pharmacokinetics

A

oral or IV (oral 50% bioavailability)

75
Q

Etoposide (toposar) – topoisomerase II inhibitor MoA

A

irreversible double stranded break

76
Q

Etoposide (toposar) – topoisomerase II inhibitor indications

A

testicular cancer and small cell lung cancer

77
Q

Etoposide (toposar) – topoisomerase II inhibitor adverse effects

A
  • MYELOSUPPRESSION
78
Q

Dasatinib (vuman) BCR-ABL inhibitors pharmacoknetics

A

oral

79
Q

Dasatinib (vuman) BCR-ABL inhibitors MoA

A
  • Acts on BCR/ABL kinase expressed on Philadelphia chromosome for chronic myeloid leukemia
  • Oncoprotein results in transition swap in chromosomes leading to abnormal TK expression and hematopoietic stem cells
  • See malignant cell proliferation and kinase is not able to inhibit nfkb so you dis-inhibited the apoptotic pathway
80
Q

Dasatinib (vuman) BCR-ABL inhibitors indicators

A

chronic myeloid leukemia

81
Q

Erlotinib (tarceva) pharmacokinetics

A

oral
- Need to test tumor cells whether they have the EGFR mutation before you can use the drug

82
Q

Erlotinib (tarceva) moA

A
  • Specific inhibition of epidermal growth factor receptor tyrosine kinase
    –prevents GTPase activation of DNA synthesis and cell proliferation
83
Q

Erlotinib (tarceva) indications

A

metastatic non-small cell lung cancer (second line)

84
Q

Sunitinib (sutent) pharmacokinetics

A

oral

85
Q

Sunitinib (sutent) indications

A
  • Advanced renal cell carcinoma
  • Gastrointestinal stromal tumor resistant to imatinib
86
Q

Sunitinib (sutent) MoA

A

blocks angiogenesis
- Vascular endothelial growth factor binds to receptor
- When activated it increases vascular permeability promoting cell proliferation and migratin
- Angiogenesis forms new blood vessels – how tumors survive
- Blocking vascularization helps kill the tumor

87
Q

Debrafinib (tafinlar) + trametinib (mekenist) pharmacodynamics

A

oral

88
Q

Debrafinib (tafinlar) + trametinib (mekenist) MoA

A
  • Dabrafenib Drug targets gene mutation braf and trametinib blocks signaling downstream of gene mutation mek
  • Synergistically work together to inhibit cell proliferation
  • Ras gene
89
Q

Debrafinib (tafinlar) + trametinib (mekenist) indicators

A

inoperable and metastatic melanoma

90
Q

Bortezomib (velcade) pharmacokinetics

A

subQ or IV

91
Q

Bortezomib (velcade) MoA

A
  • Inhibition of catalytic site of 26S protease prevents degradation of ubiquitinated proteins (protease is trash that disposes tagged things)
  • Drug inhibits proteasome to save proteins that shouldn’t be killed
92
Q

Bortezomib (velcade) indications

A
  • Multiple myeloma
93
Q

Alemtuzumab (lemtrada)pharmacokinetics

A

SC or IV

94
Q

Alemtuzumab (lemtrada) MoA

A
  • IgG w/ kappa chain binds CD52 on B/T cell (normal and malignant)
  • Lymphocyte targets cell for lysis/apoptosis
  • Recommended to people who don’t respond to at least 2 other MS medications
95
Q

Alemtuzumab (lemtrada) indications

A
  • B-cell chronic lymphocytic leukemia
  • Relapsing MS
96
Q

Bevacizumab(avastatin) pharmacokinetics

A

IV

97
Q

Bevacizumab(avastatin) MoA

A
  • IgG binds to VEGF (vascularized endothelial growth factor) in membrane
  • Binds and signaling cascades are activated angiogenesis
  • Tumor grows w/ blood supply
  • W/ drug it binds to ligand circulating VEGF via lock and key mechanism
  • VEGF receptor won’t be able to fit it and activate the pathway
  • Angiogenesis is decreased
98
Q

Bevacizumab(avastatin) indications

A

colorectal cancer and lung cancer

99
Q

Cetuximab (erbutix) pharmacokinetics

A

IV

100
Q

Cetuximab (erbutix) MoA

A
  • Epidermal growth factor receptor (tyrosine kinase)
  • EGF ligand binds to receptor and activate signal transduction
  • MAPK activated increased proliferation, decreased apoptosis, promotion of invasion/metastasis/angiongenesis
  • W/ drug ligand is prevented from interacting w. receptor so as a result you get opposite – no proliferation, apoptosis promoted, decrease in metastasis and angiogenesis
101
Q

Cetuximab (erbutix) indications

A

metastatic colorectal cancer

102
Q

Ipilimumab (yervoy) pharmacodynamics

A

IV

103
Q

Ipilimumab (yervoy) MoA

A
  • MCH presents peptide to TCR for activation
  • Costimulator interacts and T cell is activated
  • CTLA-4 functions to prevent autoimmune dz by suppressing T-cell activation (interacts w. second signal)
  • Drug can bind to CTLA4 so it can’t interact w. costimulatory and T-cell can activate
104
Q

Ipilimumab (yervoy) indications

A

metastatic melanoma and unresectable melanoma

105
Q

Ipilimumab (yervoy) adverse effect

A

Colitis, neuropathy, hepatitis, pneumonitis, progressive multifocal leukoencephalopathy – severe/possibly fatal

106
Q

Pembrolizumab (keytruda) pharmacokinetics

A

IV

107
Q

Pembrolizumab (keytruda) MoA

A
  • Tumor cell interacts w/ T-cell ag and is presented to T-cell receptor
  • Costimulatory PD1 interacts with PDL1 (programmed death)
  • Interaction causes inhibition of T-cell from killing tumor
  • Drug interacting with PD1 on T-cell blocks it and ligand can’t interact/block T-cell from activating so now the T-cell can promote death
108
Q

Pembrolizumab (keytruda) Indications

A

non-small cell lung cancer

109
Q

Rituximab (rituxan)pharmacokinetics

A

IV administration

110
Q

Rituximab (rituxan) MoA

A
  • Malignant cancerous B-cell w/ CD20 leads to increase in cell death, drug binds to cd20 ag found on non-hodgkin lymphoma
  • Started for apoptosis
111
Q

Rituximab (rituxan) Indications

A
  • Relapsed or refractory B-cell non Hodgkin lymphoma
  • Chronic lymphoid leukemia
112
Q

Trastuzumab (Herceptin) pharmacokinetics

A

IV

113
Q

Trastuzumab (Herceptin) MoA

A
  • Directed against human epidermal receptor 2 HER2 that dimerizes with a partner
  • Activates signaling cascade leading to transcription/dysregulation of cell cycle
  • Drug binds to HER2 and inhibits cellular pathways normally activated and pro-apoptotic pathways are instead stimulated
114
Q

Trastuzumab (Herceptin) indications

A

metastatic breast cancer

115
Q

Mycophenolate Mofetil (cellcerpt) pharmacokinetics

A

oral or IV
- Oral gets meatabolized to mycophenolic acid

116
Q

Mycophenolate Mofetil (cellcerpt) MoA

A
  • inhibition of ionsine monophosphate dehydrogenase to decrease synthesis of nucleic acids and suppress immune system
117
Q

Mycophenolate Mofetil (cellcerpt) indications

A
  • prevention of solid organ transplant rejection
  • alternative to cyclosporine or tacrolimus
  • graft vs host dz (prophylaxis and ex in hematopoietic stem cell transplant recipients)
  • long term administration bc immunosuppressants for rest of life
118
Q

Azathioprine pharmacokinetics

A

oral or IV
- prodrug converted to 6-mercaptopurine

119
Q

Azathioprine MoA

A
  • converted to NT by addition of a ribose phosphate
  • inhibits DNA synthesis required for B/T cell proliferation
  • trying to suppress immune system
120
Q

Azathioprine indications

A

prevention of renal transplant rejection

121
Q

Basiliximab (simulect) pharmacokinetics

A

IV administration

122
Q

Basiliximab (simulect) MOA

A
  • drug binds to and blocks IL-2 receptor
  • CD25 on surface of T-lymphocyte acts as a receptor that it binds to
  • When IL-2 is activated a cascade causes proliferation of T-cells and decreases apoptosis
  • When inhibited proliferation is lowed and apoptosis is slowed suppressing the immune system – T-cells decrease
123
Q

Basiliximab (simulect) indication

A

prevention of renal transplant rejection

124
Q

Belatacept (nulojix) pharmacokinetics

A

IV administration

125
Q

Belatacept (nulojix) MoA

A
  • Recombinant fusion protein made in lab CTLA4 is fused to IgG
  • MHC interacts w/ TCR and second stimulation CD80/86 interacts w/ CD28
  • Drug blocks activation of T-cell by binding to CD80 on APC preventing the second signaling co-stimulation.
  • Second signal is not received and T-cell does not activate
126
Q

Belatacept (nulojix) indications

A

prevention of renal transplant rejection
- In combination w/ basiliximab and mycophenolate mofetil

127
Q

Cyclosporine pharmacokinetics

A

oral, iv, or topical ocular administration (oral 20-50%)

128
Q

Cyclosporine MoA

A
  • CSA = cyclosporine
  • CSA crosses onto T-cell and interacts with CpN
  • When they bind inhibits CaN (calcinurin)
  • Inhibition will block singanling that would lead to increased production of IL-2 (pro-inflammatory)
  • IL-2 shut down and suppresses immune system
129
Q

Cyclosporine indications

A
  • Prevention of organ transplant rejection
  • Idiopathic urticaria
  • Psoriasis
130
Q

Tacrolimus (profraf) pharmacokinetics

A

oral/IV or topical

131
Q

Tacrolimus (profraf) MoA

A
  • Fk506 is tacrolimus
  • Leads to decrase in IL-2 like cyclosporine by inhibiting calcinurin
  • Interacts with FKBP to inhibit CaN which inhibits IL-2 cascade
132
Q

Tacrolimus (profraf) indications

A
  • prevention of organ transplant rejection
  • Atopic dermatitis
133
Q

Sirolimus(rapamune) pharmacokinetics

A

ORAL ONLY half life of 60 hrs

134
Q

Sirolimus(rapamune) MoA

A
  • Proliferation signal inhibitor
  • Activation of IL-2 normally leads to activation of MTOR to increase proliferation and division
  • SRL crosses T-cell and interacts with FKBP like tacrolimus
  • This inhibits MTOR
  • Decrease in normal IL-2 driven process
135
Q

Sirolimus(rapamune) indications

A
  • Prevention of organ transplant rejection
  • Graft vs host dz
136
Q

Sirolimus(rapamune) adverse rxn

A
  • Profound myelosuppression thrombocytopenia
  • Hepatotoxicity
  • Hypertriglyceridemia
    Pneumonitis

Clinical Medicine (3 decks)

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