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Pharmacology SNQ > cancer pharmacology > Flashcards

cancer pharmacology Flashcards

1
Q

What are the anti-tumour antibiotics produced from streptomyces bacteria ?

A

Belyomycin, anthracyclines, Dactinomycin or actinomycin D the later two are cell cycle non-specific.

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2
Q

What happens in G1 phase of the cell cycle ( interphase) ?

A

cell grows and performs its function.

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3
Q

What happens in G1 check point ?

A

Screening for potential DNA damage and protein synthesis abnormalities. The cell will either progress to S phase or go to G0 phase where DNA repair or progression to apoptosis will happen.

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4
Q

What is the action of DNA helicase in S phase ?

A

It unwindes the DNA strands create replication fork.

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5
Q

What is the action of topoisomerase enzyme ?

A

In the S phase it helps to loosen up the DNA helix during the unwinding process mediated by the DNA helicase.

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6
Q

What is the action of RNA primase and DNA polymarase ?

A

they together create the new RNA template by adding base pairs to the unwound DNA strand.

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7
Q

What are the events in G2 phase and G2 check point ?

A

In G2 phase the cell grows again before entering mitosis and the G2 chekpoint does the final screening before mitosis for DNA damage.

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8
Q

Why are cytotoxic medications toxic to cancer cells and rapidly dividing normal cells?

A

These cells divide more rapidly and therefore they are more sensitive to DNA damage and errors in checkpoint functions. This makes them susceptible to cytotoxic drug mediated destruction.

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9
Q

What is the structure and action of Belomycin ?

A

It is a G2 phase of the cell cycle specific medication with an iron binding and DNA binding sites. In the presence of O2 it acts as an oxidase and generate ROS which oxidise DNA bases causing breaks in DNA strands.

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10
Q

What are the cancers treated using Belomycin ?

A

Hodgkin’s lymphoma, tetsticular cancer, and squamous cell carcinoma of the skin.

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11
Q

What is the mechanism of Belomycin toxicity ?

A

The enzyme hydrolase is essential for the inactivation of bleomycin. The lungs and skin lacks it. Therefore, Bleomycin causes pulmonary toxicity in the form of pneuomitis and fibrosis as well as skin rashes, exfoliation and hyper-pigmentation. It can also cause stomatitis and mucocytis in the mouth.

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12
Q

What is the unique feature of Bleomycin ?

A

Minimal myelosupression.

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13
Q

What is the action of Dactinomycin or actinomycin D ?

A

It is a peptide that intercalates into the DNA molecule. Which prevents the binding of RNA and DNA polymarase to the DNA leading to RNA and DNA synthesis inhibition. It also cause breaks in DNA strands through ROS generation in a cell cycle non-specific manner.

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14
Q

What is the indication for Dactinomycin ?

A

It is used to treat Wilm’s tumour, rhabdomyosarcoma and Ewing’s sarcoma. The main side effects are significant mylosupression and alopecia.

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15
Q

What are the drugs in the anthracyclin category ?

A

Doxorubcin, Daunorubicin, Idarubicin and Epirubicin.

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16
Q

What are the 3 MOAs of anthracyclins ?

A
  • Inhibits RNA and DNA synthesis through intercalation into the DNA strand.
  • Inhibits topoisomerase II.
  • Damage DNA base pairs through ROS mediated oxidation.
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17
Q

What are the indications for Anthracyclins ?

A

treatment of solid tumours of the , thyroid, lungs, ovary, Lukemias and lymphomas.

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18
Q

What is the main side effect of anthracyclins ?

A

Dose dependent irreversible dilated cardiomyopathy.

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19
Q

What is the prophylaxis for Anthracyclins cardio toxicity ?

A

Iron chelating agent Dexrazoxane.

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20
Q

What is the general action of DNA alkylating medications?

A

They are anti-cancer agents which act all stages of cell cycle by adding an alkyl group at the number 7 nitrogen atom of the guanine leading to abnormal base pairing in the form of the T-G instead of T- cytosine leading to cell death.

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21
Q

What is the second MOA of DNA alkylating medications?

A

inter- and intra-strand cross linking which prevents DNA unwinding and replication.

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22
Q

What are the medications in the nitrogen mustard category ?

A

The nitrogen mustards comprise mechlorethamine, chlorambucil, melphalan, and the oxazaphosphorines cyclophosphamide, ifosfamide, and trofosfamide.

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23
Q

What are nitrogen Mustards ?

A

These are related to the mustard gas phosgene and are the first IV chemotherapy agents. these are pro-drugs which are converted to their active from by the CYP450 enzymes in the liver.

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24
Q

What are the cancers treated using cyclophosphamide and ifosfamide ?

A

leukemias, lymphomas, and solid ovarian and breast cancers.

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25
Q

What are the main non-oncological uses of cyclophosphamide ?

A

*Small vessel vascultiies such as granulomatosis with polyangitis ( Wegner’s ), microscopic polyangitis.
* Medium vessel vasculitis such as polyarteritis nodosa.
* refractory SLE and MS

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26
Q

What are the side effects of nitrogen mustards ?

A
  • Aplastic anaemia
  • Lukemia and other malignancies due to long term use.
  • GI disturbance and infertility.
  • Hair loss
  • Teratogenicity.
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27
Q

What is the specific side effect of nitrogen mustards ?

A

SIADH

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28
Q

What are the common side effects of cyclophosphamide ?

A

Transitional cell carcinoma of the bladder and hemorrhagic cystitis.

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29
Q

What are the prophylactic measures for cyclophosphamide induced hemorrhagic cystitis ?

A

High Fluid intake + Mensa or sodium 2 mercaptoethane sulfonate.

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30
Q

What is the action and indication, and side effects of Busalfan ?

A

It is a drug that is highly myelotoxic and is a drug of choice for myeloablative Tx of CML before transplant. It decreases the formation of ganulocytes and platelets at low dosage and RBC at high dosage. The main side effects are pancytopenia and less commonly pulmonary fibrosis.

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31
Q

What are the drugs in the alkylating drug category nitrosoureas ?

A

Carmustine and Lomustine.

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32
Q

What is the MOA and side effects of nitrosoureas ?

A

They are lipid soluble drugs that can cross the blood brain barrier and are primarly used to treat CNS tumours. The side effects are neutroxicity induced convulsions and ataxia

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33
Q

Carmustine is an alkylating chemotherapy agent that ———– which prevents gene expression.

A

crosslinks DNA

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34
Q

What type of alkylating antineoplastic agent is Streptozocin?

A

Nitrosourea

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35
Q

The mechanism of action of cyclophosphamide is?

A

formation of carbonium ions with guanine-N7 which inhibit the duplication of DNA and the creation of RNA.

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36
Q

What are the major teratogenic effect of alkylating agents?

A

Skeletal abnormalities including syndactyly, digital aplasia.

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37
Q

What is the MOA of platins ?

A

Platins are cell cycle non-specific agents which act by attaching to the number 7 nitrogen atom of the two adjacent guanines and creates intra- strand cross-bridges. This leads to inhibition of DNA repair and replication leading to cell death.

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38
Q

What are the commonly used platinum containing agents ?

A

Cisplatin, carboplatin, and oxaloplatin. which are administered IV and renaly eliminated.

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39
Q

What are the indications for cisplatin and carboplatin ?

A

For the treatment of solid tumours and osteosarcoma.

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40
Q

What are the indications for oxaloplatin?

A

It is indicated for the Tx of advanced colon cancer, hepato-billiary, pancreatic, ovarian cancer, and lymphomas.

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41
Q

What are the side effects of platins ?

A

*GI disturbances
* Nephrotoxicity
* Neuotoxic peripheral neuropathy
* Ototoxicity causing tinitus.
* Allergic reactions and mild bone marrow suppression.

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42
Q

what is the prophylaxis for Platin induced nausea and emesis ?

A

5-HT3R antagonist Odansterone.

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43
Q

What is the prophylaxis for platin induced nephrotoxicity ?

A
  • Hydration and osmotic diuresis using manitol.
  • ROS scavenger Amifostin can also be used to prevent renal damage.
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44
Q

Which is the platin that causes most severe nephrotoxic and neurotoxic side effects ?

A

Cisplatin

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45
Q

What is the main side effect of Carboplatin ?

A

Bone marrow suppression.

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46
Q

Which is the platin with minimal side effects ?

A

Oxaloplatin.

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47
Q

What are the classes of drugs in the Microtubule inhibitors category ?

A

Vinka alkaloids and taxens which inhibit mitosis.

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48
Q

What is the structure and function of the cytoskeleton of the cell ?

A

It is a network consisting of actin filaments, intermediate filaments, and microtubules. It gives the cells their shape and anchors organells in place and responsible for conformational changes.

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49
Q

What is the structure of microtubules ?

A

It is a cluster of 13 protofilaments each containing alternating chain of alpha and beta tubulin.

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50
Q

what are the steps of mitosis ?

A
  • Prophase- nuclear membrane disintegration and chromosome condensation occurs.
  • Metaphase- Formation of metaphase plate.
  • Anaphase- centrosome mediated separation of cistocromatides occurs resulting in the formation of mitotic spindle.
  • Telophase- Formation of new nuclear membrane around the each pairs of 46 chromosomes. leading to cytokinesis.
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51
Q

All Microtubule inhibitors are given ______

A

IV

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52
Q

What are the drugs in the vinka alkaloid class of medications ?

A

vinCRIStine, vinBLAStine, vindesine, vinORELBbine and vinflunine

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53
Q

What is the MOA of vinka alkaloids ?

A

They are metaphase specific drugs that bind to beta tubulin and block its polymarization into proto- filaments leading to mitotic arrest at metaphase.

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54
Q

What are the indications for vinka alkaloids ?

A

They are indicated for the Tx of breast cancer, rhabdomyosarcoma, nephroblastoma and leukaemias.

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55
Q

Vincristine and Vinblastine are both indicated for the treatment of both ——– and ————lymphoma.

A

Hodgkins and non-hodgkins.

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56
Q

What are the side effects of vinka alkaloids ?

A

Alopecia, GI symptoms and bone marrow supression. Vincrestine is myelotoxic whereas vinblastine is more neurotoxic.

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57
Q

What are the neurotoxic effects of vinblastine ?

A
  • peripheral neuropathy.
  • Dysautonomia
  • Urinary retention
  • Constipation
58
Q

What are the drugs belonging to the class of Taxanes?

A

Pacletaxel and Docetaxel.

59
Q

What is the MOA of Taxanes ?

A

They act by directly hyper-stabilising cistochromatids leading to inhibition of the progression of mitosis from metaphase to anaphase.

60
Q

What is the indication of Taxanes ?

A

Tx of solid tumours.

61
Q

What are the side effects of Taxanes ?

A
  • Alopacia
  • Myelosuppression
  • Neurotoxicity.
  • Infusion HSR.
62
Q

Topoisomerase inhibitors inhibits both ______ and ____.

A

Topoisomerase I and II

63
Q

What is the functional difference b/w Topoisomerase I and II?

A

Topoisomerase I cuts only one strand of DNA. Whereas the Topoisomerase II cuts both.

64
Q

What is the key MOA of Topoisomerase inhibitors?

A

Inhibition of Topoisomerase enzymes leads to DNA over-winding triggering cell death cascades.

65
Q

What are the phases of cell cycle in which Topoisomerase inhibitors are most effective ?

A

Late S and early G2 phase.

66
Q

What are the common drugs in Camptothecine class of Topoisomerase inhibitors?

A

irenotecan and topotecan which are derived from the stumps of Camptotheca tree.

67
Q

What is the MOA of Camptothecine’s ?

A

Inhibition of Topoisomerase I leading to cell death.

68
Q

What is the pharmacology of Irenotecan ?

A

It is a prodrug and is eliminated through the bile and feces.

69
Q

In who should the dose of Topotecan be reduced ?

A

As it is eliminated by the kidenye’s, its dose should be reduced in patients with renal impairment.

70
Q

What are the indications of Camptotechan’s ?

A

Irenotecan- Metastatic colon cancer
Topotecan- Advanced ovarian cancer and small cell lung cancer.

71
Q

What are the common side effects of Camptotecans ?

A

Myelosuppression and GI problems. In general these drugs have fewer toxicity than most other anti-cancer agents.

72
Q

What are the medications in the class of podophyllotoxins ?

A

Etoposide and teniposide they are derived from the roots of podophylum peltatum also known as Madrake root.

73
Q

What is the MOA of podophyllotoxins ?

A

They act by inhibiting the enzyme Topoisomerase II leading to DNA breakage. They are mainly renally excreted.

74
Q

What are the indications for podophyllotoxins?

A
  • Solid tumours such as testicular and SCLC
  • Leukaemia and Lymphomas.
75
Q

What are the main side effects of podophyllotoxins?

A

GI disturbances, alopecia and Myelosuppression.

76
Q

What are the indications for antimetabolites in medicine ?

A

To treat cancer, infections, and autoimmune diseases.

77
Q

What are the pyramidine bases of DNA ?

A

Cytosine and Thymine

78
Q

What are the purine bases of DNA ?

A

Adenine and Guanine

79
Q

What are the antimetabolites that mimic purine ?

A

Azathioprine and Cladribine

80
Q

What are the antimetabolites that mimic pyramidine?

A

Cytarabine and 5-FU

81
Q

What is the MOA of Azathioprine ?

A

It is a purine analogue pro-drug that gets converted to 6 Mercapto-purine and 6-Thioguanine by the enzyme Thyopurine S methyletransferease. Both 6-MP and 6-TG get conjugated to ribonucelotides and can mimic neucleotides base pairs of DNA. Incorporation of these neucelotide analogues leads DNA replication arrest.
In addition, the active metabolites of 6MP also inhibits the enzyme PRPP synthatse and AMP deaminase preventing the conversion of PRPP to IMP and AMP to IMP respectively leading to impaired nucleotide synthesis.

82
Q

What are the indications for azathioprine ?

A

For the Tx of ALL and CML.

83
Q

What are the common side effects of antimetabolites ?

A
  • Pancytopenia and megaloblastic anaemia.
84
Q

What are the specific side effects of azathioprine ?

A

Hepatotoxicity causing cholistasis and acute pancreatitis. Teratogenicity and GI disturbances.

85
Q

What is the MOA of Cladribine ?

A

Phosphorelated tri-phosphate form of Cladribine gets inserted into the newly formed DNA strand leading to the arrest of DNA synthesis. It also inhibits DNA polymarase. It is also resistant to adenosine deaminase leading to increased accumulation of the drug intracellularly which reduces the de novo purine synthesis.

86
Q

What is the indication for Cladribine ?

A
  • Hairy cell leukaemia and other forms of leukaemia.
87
Q

What is the MOA of pyrimidine analogue Cytarabine ?

A

Cytarabine gets phosphorylated to Ara-CTP: a tri-phosphate metabolite that binds and competitively inhibits DNA polymarase arresting DNA synthesis.

88
Q

What is the indication for Cytarabine ?

A

It is indicated for the Tx of haematological malignancies such as Leukaemia and Lymphoma.

89
Q

What is the MOA of pyrimidine analogue 5-FU?

A

5-FU interferes with folic acid cycle as it is metabolised to its active form 5-FdUMP which forms a complex with THF. The 5-FdUMP- THF complex inhibits the enzyme thymidylate synthatase which decreases the synthesis of thymidine essential for DNA synthesis. Besides, other active metabolites intercalates into DNA and RNA impairing their synthesis.

90
Q

What is the indication of 5-FU?

A

For the Tx of all forms of solid tumours and as a topical agent for the Tx of basal cell carcinoma.

91
Q

What is the drug that enhances the effect of 5-FU

A

Leucovorin also known as Folinic acid which gets converted to folic acid.

92
Q

What are the side effects of 5-FU ?

A

Side effects include gastrointestinal disturbances like severe diarrhea, mucositis, alopecia, CNS toxicity, cutaneous reactions such as photosensitivity, and palmar-plantar erythrodysesthesia, or hand-foot syndrome.

93
Q

What is the anti-dot for 5-FU overdose ?

A

Uridine.

94
Q

What is the MOA of Methotrexate ?

A

It inhibits the DHFR enzyme reducing the levels of THF essential for purine synthesis which leads to inhibition of cell division by decreasing the synthesis of DNA, RNA and proteins.

95
Q

what are the indications of MTX ?

A

Tx of ALL, Primary CNS and Non-Hodgkins lymphoma, solid tumours of the breast, head and neck , bladder, and Choriocarcinoma.

96
Q

what are the other clinical uses of MTX?

A
  • Abnormal proliferation of the trophoblastic tissue.
  • Unruptured ectopic pregnancy and autoimmune diseases.
97
Q

What are the side effects of MTX ?

A
  • Bone marrow suppression which can be reduced by using Lucovorin.
  • Megaloblastic anaemia.
  • Macro-vascular hepatosteatosis.
    *Pulmonary fibrosis
  • teratogenicity, alopecia and mucocitis.
98
Q

How does monoclonal antibodies work in general ?

A

They target specific antigens that are over expressed on the tumour cell surface and create MAC complexes which cause complement mediated cell lysis or the monoclonal anti-bodies trigger immune mediated destruction. All monoclonal antibodies are administered IV.

99
Q

what is the speciality of human cell derived monoclonal antibodies which ends with ‘ umab’ ?

A

They are less likely to cause HSR.

100
Q

What is the speciality of chimeric antibodies ends with ‘ Ximab’ ?

A

They have both human and non-human components. They are more likely to be recognized as foreign leading to HSR.

101
Q

what is the speciality of humanised monoclonal antibodies ends in ‘Zumab’ ?

A

These are drugs derived from non human species and are less likely to cause HSR as compared to chimeric antibodies.

102
Q

What is the MOA of Cetuximab ?

A

It inhibits the activation of K-RAS pathway by binding to the tyrosine kinase receptor EGFR resulting in inhibition of cell proliferation, migration , and angiogenesis.

103
Q

What are the indications for Cetuximab ?

A

They are indicated for the Tx of metastatic colorectal cancer as well as Head and neck cancers.

104
Q

What are the side effects of chimeric antibody Cetuximab?

A
  • infusion HSR
  • GI and hepatic toxicity.
  • Acniform skin rashes with pruritus.
105
Q

What is the MOA and indication of Trastuzumab ( Herceptin) ?

A

It is a HER2 receptor antagonist which act by inhibiting HER2 mediated tumorogenesis by inhibiting the signaling through PI3K AKt mTOR pathway, and MAPK pathway. It is mainly used to treat HER2 positive breast cancer. It is also used to treat gastric, ovarian, and lung cancers caused by HER2 mutation.

106
Q

What is the main side effect of Trastuzumab ?

A

Inhibition of HER2 receptors on the normal cardiomyocytes leads to cardiotoxic heart failure. Other side effects are GI disturbances, fever, chills, and headaches.

107
Q

What is the MOA and indication of Bevacizumab?

A

It inhibits VEGF and prevent angiogenesis of the solid tumours leading to the apoptosis of the tumour cells. It is used to treat colorectal cancer, renal cell carcinoma, breast cancer and non-small cell lung cancer.

108
Q

What are the side effects of Bevacizumab ?

A
  • Impaired angiogenesis of normal tissue.
  • Impaired wound healing.
  • Epistaxis and hemoptysis.
  • GI and intracerebral haemorrhage.
109
Q

What is the MOA and indication of Rituximab ?

A

It binds to the CD20 receptor of the B cell and drives cmplement mediated MAC formation which causes pores on the cell leading to cell lysis. In addition, it also enhance apoptosis signaling and anti-body dependent cell mediated cytotoxicity.
It is indicated for the Tx of non-hodgkins B cell lymphoma, CLL, Ideopathic thormbocytopaenic purpura and RA.

110
Q

What are the side effects of Rituximab ?

A
  • HSR and immune supression.
  • Activation of latent viral infections.
  • JC virus activation leading to progressive multifocal leukoencephalopathy.
111
Q

What is the MOA and indication of Alemtuzumab ?

A

It acts by binding to CD52 receptors of all lymphocytes and destroy them through complement mediated lysis, apoptosis, and phagocytosis by NK cells. It is indicated to treat CLL and MS.

112
Q

What is the MOA and indication of Imatinibe ?

A

It inhibits the signaling mediated by the BCR-ABL gene formed by the 9 , 22 chromosomal translocation. It is indicated to treat the Philadelphia chromosome positive CML.

113
Q

What is the MOA of dual pan PI3K and mTOR inhibitors ?

A

They target P85 subunit and mTOR simultaneously. improved therapeutic effect due to the more efficient inhibition of the PI3K- Akt- mTOR pathway, but greater toxicities and side effects.

114
Q

What is the target of pan PI3K inhibitors ?

A

The p110 subunit of PI3K.
they have greater anticancer activity.Less toxicity and dual inhibitory effect.

115
Q

What is the target of Isoform-selective PI3K inhibitors?

A

catalytic isoforms of P110 (alpha,beta ,delta). They are less toxic hence can be administered at higher doses.

116
Q

What are the cancers in which PI3K-AKT-mTOR pathway is implicated ?

A

Breast and liver cancer.

117
Q

What is the action and indication of Alpelisib ?

A

It is a P110 alpha isoform specific oral agent. which can be given orally at a maximum dose of 300 mg/day for the treatment of PICK3CA positive breast cancer.

118
Q

What are the drugs used to treat EGFR positive non-small cell lung cancers?

A

Lapatinib, Erlotinib and Gefitinib all inhibit the kinase activity of EGFR by competing for ATP binding.

119
Q

What is the MOA of BRAF inhibitor Vemurafenib?

A

It is a oral selective inhibitor of BRAF kinase used to treat V600 E positive cancers such as melanoma. Inhibition of BRAF kinase stops ERK signalling cascade. However, resistance occurs in 2-18 months. If there are downstream target mutations combining it with MEK inhibitor Trametinib can help.

120
Q

What are the most basic structures of nucleotide ?

A
  • A 5 carbon sugar ( ribose in RNA) and Deoxyribose in DNA).
  • Phosphate group
  • A nitrogenous base.
121
Q

What are the pyramidine bases of DNA / RNA ?

A

Cytosine , DNA specific Thymine, and RNA specific uracil.

122
Q

What are the purine bases of DNA/ RNA ?

A

Adenine and guanine.

123
Q

What is the difference b/w nucleotide and nucleoside ?

A

Nucleotide composed of nitrogenous base+ ribose + phosphate group. Where as Nucleoside composed of only nitrogenous base and ribose.

124
Q

What is the action of the enzyme ribonucleotide diphosphate reducatase ?

A

It is responsible for converting the RNA nucelotide which is in the monophosphate form to DNA nucleotide which is in the diphosphate form.

125
Q

What phase of the cell cycle ribonucleotide reductase inhibitors act ?

A

S phase.

126
Q

What are the commonly used riboneucleotide reductase inhibitors ?

A

Hydroxyurea, Fludarabine phosphate, and Gemcitabine.

127
Q

What is the MOA and indication of hydroxyurea?

A

It is an oral drug which binds to the iron molecules of the ribo-neucleotide reductase and prevent them from functioning.
It is indicated to treat myeloproliferative disorders such as CML and polycythemia vera. It is also used to treat sickle cell disease as it stimulates the production of foetal haemoglobin.

128
Q

What are the main side effects of hydroxyurea ?

A

Severe myelosuppression, thrombocytopaenia, Leukopaenia, and macrocytic anaemia. In addition they may cause GI disturbance, and pneumonitis.

129
Q

What is the MOA of Fludarabine phosphate ?

A

It is the flurinated and phosphorylated analogue of the anti-viral agent vidarabine. It can be given PO or IV. In the body it gets converted to fludarabine triphosphate which directly inhibits riboneucleotide reductase. It also intercalates into the DNA and prevents the action of DNA polymarase. These two actions together leads to impaired DNA synthesis and cell death.

130
Q

What are the indications and side effects of Fludarabine phosphate ?

A

To treat CLL and low grade lymphomas. The main side effects are myelosuppression, fever, and GI disturbances.

131
Q

What is the MOA of Gemcitabine ?

A

It is an IV drug which gets converted to gemcitabine diphosphate and directly inhibit ribonucelotide reductase enzyme. It’s tri-phosphate form blocks the DNA polymarase together leading to impaired DNA synthesis and cell death.

132
Q

What are the indications and side effects of gemcitabine ?

A

It is indicated for the Tx of several carcinomas and non-hodgkin’s lymphoma. The side effects are pulmonary toxicity and myelosuppression.

133
Q

Why is Chemo usually given every 3-4 weeks ?

A

Bone marrow recovery requires at least 20 days.

134
Q

What is the maximum number of chemo cycles ?

A

6

135
Q

What are the chemotheraputic agents with high emetic risk?

A

Carmustine, cisplatin, high dose cyclophosphamide, dacarbazine

136
Q

What are the chemotheraputic agents with moderate emetic risk?

A

Carboplatin, Daunorubicin, Doxorubicin

137
Q

What are the chemotheraputic agents with low emetic risk?

A

5-Fluororuacil, Bortezomib, Etoposide, Methotrexate, Paclitaxel

138
Q

What is the hemotheraputic agents withminimal emetic risk?

A

Vincristine

139
Q

What is the management of tumour lysis syndrome ?

A

*Treating any electrolyte abnormalities and/oracute kidney injury.
*Administration ofrasburicase.
*Administration of loop diuretic and intravenous fluids.
*Appropriate use of renal replacement therapy (dialysis)

140
Q

What is the MOA of Selective estrogen receptor modulator Tamoxifan?

A

In the breast it binds to the estrogen receptor and antagonises it. In the bone and endometrium it acts as a partial agonist. It is taken daily for 5 to 10 years to post surgery.

141
Q

What are the advantages and disadvantages of small molecule inhibitors ?

A
  • They can cross blood brain barrier and work on a wide varity of targets.
  • Can be administered orally or as combination therapy.
    *Low and short duration of response and resistance are a problem.
  • Toxic effects.
142
Q

What are the limitations of targeted therapy ?

A

*Tumour heterogeneity and molecular evolution
*Acquired resistance
*Lack of biomarkers
*High toxicity
*Financial toxicity

Pharmacology SNQ (16 decks)

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