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G2MD2 (mechanics of diseases 2) > LT16+17 - Pharmacology, core medication list > Flashcards

LT16+17 - Pharmacology, core medication list Flashcards

1
Q

3 forms of cancer treatment

A

surgery, radiotherapy, pharmacological therapy

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2
Q

4 options of pharmacological therapy

A
  • cytostatics
  • hormones
  • immunumodulators
  • target therapy
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3
Q

Cell cycle

A

G1 phase –> S-phase –> G2 phase –> M-phase

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4
Q

G1 phase

A

SNA systhesis

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5
Q

S-phase

A

DNA replication

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6
Q

G2 phase

A

cell prepares for mitosis

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7
Q

M-phase

A

DNA split in daughter cells

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8
Q

Different cytostatic drugs + functions

A
  • Alkylating drugs: interfere in all 4 phases
  • Antimetabolites: interfere in the S-phase
  • Intimitotics: interfere in mitosis
  • Topo-isomerase inhibitors: interfere in G2-phase
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9
Q

Different cytostatic drugs + function

A
  • Alkylating cytostatics
  • Antimetabolites
  • Intimitotics
  • Topo-isomerase inhibitors

Functions: induce damage to DNA and initiate apoptosis

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10
Q

Alkylating cytostatics mechsanism

A
  • Interfere in all 4 phases

- Prevent unwinding by helicases –> apoptosis

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11
Q

Alkylating cytostatics examples

A

Cyclophosphamide

  • Indication: solid tumors
  • Oral or IV
  • Side effects: nausea, vomiting, myelosuppresion

Cisplatin

  • Indication: solid tumors
  • Side effects: neusea, vomiting, neurotoxicity, acute nephrotoxicity, (myelosuppression is relatively low)
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12
Q

Antimetabolites mechanism

A
  • interfere in the S-phase

- Inhibit enzymes that cause synthesis from thymide to uracil

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13
Q

Antimetabolites examples

A

Methotrexate

  • inhibits dihydrofolate reductase
  • IV preferred

5-Fluorouracil (5-FU)
- prodrug that becomes active by enzymes in the liver

Cytorabine
- Blocks DNA polymerase function –> inhibit DNA replication

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14
Q

Antimetabolites side effects

A

Mucositis, myelosuppression, diarrhea

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15
Q

Antimitotics (mitose inhibitors) mechanism

A
  • interfere in mitosis
  • Antimitotics can block microtubule formatioin, which is important for division of chromosomes into 2 daughter cells –> no cell division
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16
Q

Antimitotics (mitose inhibitors) examples

A
  • paclitaxel
  • vinblastine
  • vincristine
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17
Q

Antimitotics (mitose inhibitors) side effects

A

preipheral oedema, alopecia, bone marrow suppression, hypersensitivity reactions, cardiac disturbances

18
Q

Topo isomerase inhibitors mechanism

A
  • interfere in G2-phase

- inhibition of topoisomerases –> no unwinding and mitosis

19
Q

Topo isomerase inhibitors example

A
  • Doxorubicine

- Etoposide

20
Q

Topo isomerase inhibitor side effects

A

Myelosuppression, vomiting, nausea, alopecia, cardiotoxicity

21
Q

limitation of cytostatics

A

Emesis (=nausea & vomiting)

22
Q

how is vomiting induced by cytostatics?

A

Cytostatics –> trigger via chemo trigger zone (CTZ) –> stimulation of the vomiting centre –> vomiting

23
Q

Anti-emetics mechanism

A

They block receptors in the CTZ

24
Q

Enti-emetics examples

A

5-HT3 receptor antagonists

  • odansetron
  • granisetron

D2 receptor antagonist
- metoclopramide

25
Q

Why can patients develop resistance against anti-emetics?

A
  • Decreased amount of drug taken up by the tumor cell: transmembrane proteins may be changed (e.g. methotrexate)
  • Insufficient activation of the prodrug in the liver (e.g. fluorouracil to FDUMP)
  • Increased inactivation of a drug in the liver (increased elimination)
  • Increased concentration of the target enzyme (e.g. methotrexate)
  • Rapid repair of drug-induced lesions (e.g. alkylating agents)
  • Altered activity of target enzyme such as topoisomerase II (e.g. doxorubicin)
  • Mutation of various genes
26
Q

Limitations of cytostatic drugs?

A
  • Dose limitation because of organ toxocity
  • Some tumors are insensitive/ have resistance
  • Systemic toxicity
  • Cytostatics are not specific for cancer celsl
27
Q

Solution to the limitation that cytostatics are not specific for cancer cells:

A

adding target therapy

28
Q

Soorten target therapy

A
  • Monoclonal antibodies

- Proteine kinase inhibitors

29
Q

Monoclonal antibodies mechanism

A

bind to receptors of immune cells –> immune system can recognize them

30
Q

Monoclonal antibodies examples

A
  • Tratuzumab
  • Ceruximab
  • Bevacizumab
31
Q

Tratuzumab mechanism

A
  • antibody against HER2
  • HER2 is a growth factor in mamma carcinoma’s
  • inhibition of tumor cell proliferation by NK-cells and macrophages
32
Q

Tratuzumab side effects

A

Cardiomyopathy

33
Q

Cetuximab mechanism

A
  • Antibody against EGF
  • EGF is a growth factor in epithelial cancer
  • inhibition of tumor cell proliferation by cytotoxic T-cells
34
Q

Cetuximab side effects

A
  • allergic reactions, acne, dry skin
35
Q

Bevacizumab mechanism

A
  • Antibody against VEGF factor

- anti-angeogenesis drug

36
Q

Bevacizumab side effects

A
  • hypertension, proteinuria, bleeding
37
Q

Proteine kinase inhibitors mechanism

A

target intracellulary, decrease the expression of growth factors

38
Q

Proteine kinase inhibitor example

A

Imatinib

39
Q

Imatinib mechanism

A

inhibition of cell proliferation, induces apoptosis

40
Q

Imatinib side effects

A

headache, nausea, vomiting, diarrhea, dyspepsia

G2MD2 (mechanics of diseases 2) (16 decks)

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