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Neoplasia > Cancer chemotherapy > Flashcards

Cancer chemotherapy Flashcards

1
Q

When are drugs more effective?

A

Drugs are more effective when a large proportion of tumor cell are proliferating.

High growth fraction.

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2
Q

Advantages and Disadvantage of using CCNS drugs

A

ADVANTAGES

They have a broad activity
Effective in slow-growing tumors
- Because they also target non-
specific dividing cells.

DISADVANTAGE

Increased Toxicity
- non-specific nature
- Can cause damage to normal cell
as well
Resistance

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2
Q

Cell Cycle Non-Specific drugs (CCNS)

A

Drugs that act on cancer cell in all phases. Including G0

Can kill both dividing and non-dividing cell.

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2
Q

S-phase Specific drugs

A

Antimetabolites

  1. Methrotrexate
  2. Fluorouracil
  3. Mercaptopurine
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3
Q

Examples of Cell cycle non-specific drugs.

A
  1. Alkalylation Agents
    • Cyclophosphamide
    • Cisplatin
    • Lomustine
    • Carmustine
  2. Antitumor antibiotics.
    • Doxorubicin
    • Bleomycin
    • Mitomycin
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3
Q

General adverse effect of antineoplastic drugs ( Cancer drugs)

A
  1. Nausea/vomiting
  2. Alopecia= loss hair
  3. Myelosuppression= bone marrow loss
  4. Low WBC= Decrease immunity
  5. Ulceration of the mouth and IG
  6. Increase serum uric acid= increase risk of gout
  7. Secondary cancers= many cancer drugs mutate the DNA and can lead to another cancer.
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3
Q

Cell Cycle Specific Drugs (CCS)

A

They act on cancer cell during a specific phase of cell cycle.

S-phase, M-phase, G2 phase

Target in DIVIDING cells

Most effective agains the rapidly growing tumors.

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3
Q

Advantage and Disadvantage of cell cycle specific drug

A

ADVANTAGES

-Target action
-Fewer side effect on non-dividing cell

DISADVANTAGE

-Less effective on slow-growing tumor
-Toxicity on rapidly dividing normal cell. Like hair loss, GI symptoms, Myelosuppression.

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4
Q

M-phase Specific drugs

A

Microtubule inhibitors

Vinca Alkaloids
1. Vincristine
2. Vinblastine

Taxanes
1. Paclitaxel
2. Docetaxel

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4
Q

G2 phase Specific drugs

A

Toposiomerase II inhibitors
1. Etoposide
2. Teniposide
3. Irinotecan
4. Topotecan

Bleomycin

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5
Q

Tumor lysis syndrome

A

The anti cancer drug is causing this.

Occur when a large number of cancer cell die in response to therapy within a short period, releasing their content into the blood.

We can give Allopurinol to inhibit Xanthine Oxidase.

Rasburicase can inhibit Uric acid to Allantoin

Characteristics finding:
- Hyperuricemia
-Hyperkalecemia
-Hyperphosphatemia
- Hypocalcemia

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6
Q

Log-kill hypothesis

A

Chemotherapy drugs kill a constant fraction of tumor cell, rather than a constant number.

Initial treatment may reduce the tumor size but not eliminate it. We need multiple treatment cycles. Each cycle kills a fraction of the remaining cells. But the remain cell may become resistance over time

Role of combination therapy

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7
Q

Combination therapy

A

Optimizing therapeutic efficacy while minimizing toxicity.

Combining Drugs that act on different phases of the cell cycle.

Minimize resistance: Different mechanism of action. If some drugs are resistance to one drug they might be to the other one.

Non- overlapping Toxicities.

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8
Q

Primary induction chemotherapy

A

Primary treatment
Palliation- Relief of symptoms and suffering caused by cancer
extended time of tumor progression.

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9
Q

Neoadjuvant chemotherapy

A

Reduce the tumor size for better surgical outcome

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10
Q

Adjuvant chemotherapy

A

Procedure following after surgical procedure. To reduces risk of local and systemic recurrence.

11
Q

Alkylating Agents

A

Are non-specific drugs

Alkalynation of nucleophilic group on DNA bases especially N-7 position of guanine.

Causes-
1. Cross linking of bases
2. Abnormal base pairing
3. DNA strand breakage.

12
Q

Cyclophosphamide

A

Alkylating agent- non specific drug

  • is a pro drug
  • Hepatic cytochrome P450 enzyme converts it to its active metabolite ( phosphoramide mustard)
  • Metabolite called Acroline that causes Hemorrhagic cystitis*. This can be reduced by Mesna.
  • Also Cause SIADH
13
Q

Mechlorethamine

A

Alkylating agent- non specific drug

Converts in the body to a reactive cytotoxic product.

Toxicity:
1. GI distress
2. Alopecia
3. Myelosupression
4. Sterility
5. Vesicant (blisters)

14
Q

Procarbazine

A

Alkylating agent- non specific drug

Forms hydrogen peroxide, which generates DNA-damaging free radicals

Toxicity
1. GI distress
2. Myelosuppression
3. CNS dysfunction
4. Leukemogenic
5. Disulfiram like reaction ( is like the drug they give to alcoholics to stop drinking)
6. Inhibit monoamine oxidase (MAO)

15
Q

Dacarbazine

A

Alkylating agent- non specific drug

Clinical use for Hodgkins lymphoma
(Epstein-Barr virus)

toxicity
1. GI distress
2. Alopecia

16
Q

Carmustine and Lomustine

A

Alkylating agent- non specific drug

Nitrosoureas

Highly lipid soluble: Can cross BBB

DNA alkylation: cross linking

Useful for treatment of CNS cancer

17
Q

Temozomide

A

Penetrates the CNS

Clinical use for
1. Anaplastic astrocytoma (brain tumor) refractory to nitrosoureas
2. Glioblastoma

18
Q

Busulfan

A

Alkylating agent- non specific drug

Very important one

DNA alkylation: cross-linking

Clinical use:
1. Chronic myelogenous leukemia

Toxicity:
1. Skin pigmentation
2. Adrenal Insufficiency*
3. Pulmonary fibrosis*

19
Q

Cisplatin
Carboplatin
Oxaliplatin

A

Alkylating agent- non specific drug

Platinum Analogs

Platinum atoms binds to DNA bases
Croslinks DNA

Toxicity of Cisplatin and Carboplatin
1. GI distress- Severe nauseas and vomiting*
2. Nephrotoxicity* ( can be reduced by using mannitol with severe hydration)

Toxicity of Oxaliplatin
Neurotoxicity*
But do NOT give nephrotoxicity

20
Q

Antimetabolites

A

Cell specific drugs acting on S-phase

They have immunosuppressant action

Folic acid blocker- Methotrexate
Purine- Mercaptopurine and Thioguanine
Pyrimidines- Fluorouracil, Cytarabine and Gemcitabine

21
Q

Methrotrexate (MTX)

A

Antimetabolite- S phase

Binds with high affinity to active catalytic site of Dihydrofolate Reductase and inhibits it *.
- Decrease the synthesis of
thymidylate (dTMP), purine,
pyrimidine and amino acids

  • Interfere with protein metabolism

Resistance
1. Reduced drug accumulation
2. Changes in enzyme sensitivity/activity
3. Reduced formation of polyglutamate

Clinical uses:
1. Choriocarcinoma
2. acute leukemias
3. solid tumor
4. ectopic pregnancy
5. Rheumatoid arthritis
6. psoriasis

Toxicity-
1. Bone marrow suppression*
2. mucositis
3. Hepatotoxicity

  • Leucovorin reduces the toxic effect of methotrexate on normal cell.
22
Q

Mercaptopurine (6-MP) and Thioguanine (6-TG)

A

Purine Antimetabolites

Activation by HGPRTases*
inhibition of enzymes in purine metabolism.

Metabolism of 6-MP by xanthine oxidase is inhibit by Allopurinol and Febuxostat **

Clinical use: Acute leukemia, chronic myelocytic leukemia

Toxicity: bone suppression and hepatic dysfunction.

23
Q

Cladribine

A

Purine antimetabolites

Converted to Cladribine triphosphate
Incorporated into the DNA and causes strands breakage and kills T cell.

24
Q

Fluorouracil (5-FU)

A

Pyrimidine Antimetabolites

5-FU is converted into 5-FdUMP

5-FdUMP inhibits Thymidylate synthase* and inhibit DNA synthesis

Another metabolite called FUTP Interferes with RNA function.

Clinical uses:
1. Bladder, breast, colon and ovarian cancer
2. Topically for Keratoses and basal cell carcinoma.

Resistance:
Increased Thymidylate synthase activity ( basically is more than the drug)

Toxicity: Neurotoxicity (hand-foot syndrome)

Give them a dose of thymidine*

25
Q

Cytarabine

A

Pyrimidine Antimetabolites

Convert to AraCTP- inhibits DNA polymerases*

26
Q

Gemcitabine

A

Deoxycitytidine analog

Metabolite Gemcitabine diphosphate- inhibits ribonucleotide reductase - inhibit DNA synthase.

27
Q

Vinca Alkaloids

A

Plant-base drug Works on M phase

  1. Vinblastine
  2. Vincristine
  3. Vinorelbine

Prevents assembly of tubulin dimers into microtubules. Block mitotic formation. *

Toxicity:
Neurotoxic * “glove and stocking” neuropathy

Clinical
Vinblastine and Vincristine- acute leukemias lymphomas

Vinorelbine- nonsmall cell lung cancer and breast cancer.

28
Q

Taxanes

A

Pland-based drug - M phase cannot progress to Anaphase.

  1. Paclitaxel
  2. Docetaxel

Prevent the microtubule from disassembly into tubulin monomers. Interfere with mitotic spindle.

Hyperstabilize microtubules in M phase.

Toxicity:
Paclitaxel- Peripheral neuropathy “glove and stocking”* (same as Vinca)

Docetaxel- Neurotoxicity*

29
Q

SLIDE 35

A

Neoplasia (7 decks)

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