ON4 Pharmacology of Anti-Cancer Drugs

Beschreibung

PHCY320 (Oncology) Quiz am ON4 Pharmacology of Anti-Cancer Drugs , erstellt von Mer Scott am 05/10/2019.
Mer Scott
Quiz von Mer Scott, aktualisiert more than 1 year ago
Mer Scott
Erstellt von Mer Scott vor etwa 5 Jahre
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Zusammenfassung der Ressource

Frage 1

Frage
Cytotoxic drugs damage the reproductive potential of cells by acting on DNA [blank_start]synthesis[blank_end]. Selectivity depends on [blank_start]rate[blank_end] of synthesis/division: • [blank_start]Rapidly[blank_end] dividing cells more likely to respond to Tx • [blank_start]Resting[blank_end] cancer cells resistant Cell-cycle phase[blank_start]-specific[blank_end] drugs: schedule dependent (time dependent) Cell-cycle phase-[blank_start]nonspecific[blank_end] drugs: dose dependent
Antworten
  • synthesis
  • rate
  • Rapidly
  • Resting
  • -specific
  • nonspecific

Frage 2

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Growth fraction is number of cells in [blank_start]cell cycle[blank_end] over the total number of cells. This is normally [blank_start]20[blank_end]%. It changes in cancers eg Burkitt’s lymphoma: 100% GF, Colon carcinoma: <5%. Greater growth fraction means a [blank_start]better[blank_end] chance of cell death. The [blank_start]proportional cell kill[blank_end] is the proportion of cells a cytotoxic dose kills. Note that drugs kill a proportion of cells, not a given number of cells. Intermittent therapy [blank_start]maximizes[blank_end] tumour cell killing and allows [blank_start]recovery[blank_end] of healthy cells.
Antworten
  • cell cycle
  • 20
  • better
  • proportional cell kill
  • maximizes
  • recovery

Frage 3

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Toxicity related to cytotoxic drugs: The therapeutic index is a measurement of the relative [blank_start]safety[blank_end] of a drug, usually around 1(below one is less safe). It is a comparison of the amount of a therapeutic agent that causes the therapeutic [blank_start]effect[blank_end], to the amount that causes [blank_start]toxicity[blank_end]. In cancer a therapeutic dose is a [blank_start]toxic[blank_end] dose. The drug action is [blank_start]proportional[blank_end] to the growth rate; meaning a greater effect in [blank_start]high[blank_end] growth fraction & vice versa. The drug with affect [blank_start]rapidly[blank_end] dividing (cancerous AND non-malignant) tissue.
Antworten
  • safety
  • effect
  • toxicity
  • toxic
  • proportional
  • high
  • rapidly

Frage 4

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Match the tissues to their types of proliferation. Continuous rapid proliferation - [blank_start]Bone[blank_end] marrow, [blank_start]Gastrointestinal[blank_end] mucosa, [blank_start]Hair[blank_end] follicles, [blank_start]Testicular[blank_end] germ cells Continuous slow proliferation - [blank_start]Tracheobronchial[blank_end] epithelium, [blank_start]Vascular[blank_end] endothelium Cyclical proliferation - Glandular female [blank_start]breast[blank_end] tissue, [blank_start]Endometrial[blank_end] lining of uterus Capacity to proliferate after injury - [blank_start]Liver, Bone[blank_end] Non proliferating - [blank_start]Skeletal muscle, Cardiac muscle,[blank_end] Cartilage
Antworten
  • Bone
  • Gastrointestinal
  • Hair
  • Testicular
  • Tracheobronchial
  • Vascular
  • breast
  • Endometrial
  • Liver, Bone
  • Skeletal muscle, Cardiac muscle,

Frage 5

Frage
Hematopoietic system toxicity: Bone marrow suppression occurs when [blank_start]stem[blank_end] cell pool is damaged by chemotherapy. Clinically we see a [blank_start]fall[blank_end] in circulating cells. Platelets gone within [blank_start]1-2[blank_end] weeks. Granulocytes within 14 days. Fall in white cell count by [blank_start]3-7[blank_end] days. No change in RBCs for [blank_start]6-8[blank_end] weeks. Then, bone marrow [blank_start]recovery[blank_end] occurs. (Erythrocyte life span: [blank_start]120[blank_end] days. Platelet: [blank_start]9-10[blank_end] days. WBCs: [blank_start]4-5[blank_end] days.)
Antworten
  • stem
  • fall
  • 1-2
  • 3-7
  • 6-8
  • recovery
  • 120
  • 9-10
  • 4-5

Frage 6

Frage
Infection, bruising and anaemia are signs of hematopoietic system toxicity.
Antworten
  • True
  • False

Frage 7

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Nearly all cytotoxics cause BM suppression at therapeutic doses but severity and duration [blank_start]varies[blank_end]. Why? 1. Different effects on [blank_start]precursor[blank_end] stem cells (pluripotent vs unipotent) 2. Kinetics of cell types in peripheral blood ([blank_start]life span and turnover[blank_end] of cells) 3. Cycle nonspecific drugs: greater [blank_start]duration of BMS[blank_end] than phase specific Low BMS with [blank_start]bleomycin[blank_end]. Cancer cells have [blank_start]low[blank_end] [hydrolase], BM cells have [blank_start]high[blank_end] [hydrolase].
Antworten
  • varies
  • precursor
  • life span and turnover
  • duration of BMS
  • bleomycin
  • low
  • high

Frage 8

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Nausea and vomiting as a SE has a complex mechanism, only partly due to [blank_start]direct[blank_end] action of drugs on GIT. It can affect the [blank_start]vagus[blank_end] nerve which affects the [blank_start]emetic[blank_end] centre. Anticipatory nausea is common and the pathway uses [blank_start]catecholamines/DA[blank_end].
Antworten
  • direct
  • vagus
  • emetic
  • catecholamines/DA

Frage 9

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GI Tract toxicity: Observed as oesophagitis, diffuse ileitis, colitis, oral [blank_start]mucositis[blank_end]. • Mucosal cells have [blank_start]high[blank_end] turnover (4-7 days) • [blank_start]3-4 days[blank_end] after cytotoxic administration: Pain, tingling, dryness, loss of taste - - - [blank_start]ulceration[blank_end] • Consider the combo of [blank_start]local[blank_end] trauma/low [blank_start]WBC[blank_end] count/pathogen [blank_start]rich[blank_end] environment • Severity: dose related, schedule of administration • Worse in [blank_start]younger[blank_end] people.
Antworten
  • mucositis
  • high
  • 3-4 days
  • ulceration
  • local
  • WBC
  • rich
  • younger

Frage 10

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Dermatological toxicity: 1. Alopecia • [blank_start]60-90%[blank_end] hair follicles actively dividing, 24h doubling time • [blank_start]Reversible[blank_end] 2. Specific skin toxicity (uncommon) • [blank_start]Capecitabine[blank_end]: Palmar-plantar syndrome (redness, swelling, and [blank_start]pain[blank_end] on palms and soles). Affects growth of skin cells, capillaries 3. Extravasation
Antworten
  • 60-90%
  • Reversible
  • Capecitabine
  • pain

Frage 11

Frage
Match the cytotoxics to the cell phase they act in. G1 - [blank_start]Steroids, asparaginase[blank_end] S phase - [blank_start]Antimetabolites[blank_end] G2 - [blank_start]Bleomycin[blank_end] Mitosis - [blank_start]Vinca alkaloids, taxanes[blank_end] Phase non-specific - [blank_start]Alkylating[blank_end] agents, Cytotoxic [blank_start]antibiotics[blank_end], [blank_start]Platinum[blank_end]-based drugs
Antworten
  • Steroids, asparaginase
  • Antimetabolites
  • Bleomycin
  • Vinca alkaloids, taxanes
  • Alkylating
  • antibiotics
  • Platinum

Frage 12

Frage
Alkylating agents: [blank_start]Covalent[blank_end] binding to 1) DNA - blocks DNA/RNA [blank_start]synthesis[blank_end] and 2) proteins - blocks DNA [blank_start]repair[blank_end]. Cell-cycle [blank_start]nonspecific[blank_end]. Causes [blank_start]BM[blank_end] suppression, hair loss, GI disturbances. PK depends on structure. e.g. [blank_start]Cyclophosphamide[blank_end] for breast and bronchi cancer. Hydroxylation in liver makes the active [blank_start]metabolites[blank_end]. Risks: Haemorrhagic cystitis (stay [blank_start]hydrated[blank_end]), [blank_start]Cardiac[blank_end] damage (with high dose).
Antworten
  • Covalent
  • synthesis
  • repair
  • nonspecific
  • BM
  • Cyclophosphamide
  • metabolites
  • hydrated
  • Cardiac

Frage 13

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Cytotoxic antibiotics: Anthracyclines (Streptomyces): e.g. Daunorubicin, [blank_start]doxorubicin[blank_end], epirubicin In general - cell cycle [blank_start]non[blank_end] specific. • DNA intercalation • Inhibits [blank_start]topoisomerase II[blank_end] • Blocks [blank_start]transcription[blank_end], disrupt normal replication = cell death Poor gut absorbtion so given [blank_start]IV[blank_end]. Toxicitity: [blank_start]Cardiotoxicity[blank_end] – dose dependent and cumulative Maximum [blank_start]cumulative[blank_end] dose recommended to prevent heart failure. Special case: Bleomycin. Non-anthracycline cytotoxic AB for [blank_start]germ cell[blank_end] tumours, Hodgkin’s [blank_start]Lymphoma[blank_end]. Mode: DNA intercalation, free radical-induced [blank_start]strand breaks[blank_end] (cell cycle [blank_start]specific[blank_end]). Pulmonary and dermatological toxicity, low BM suppression: pulmonary [blank_start]fibrosis[blank_end] (partially reversible), [blank_start]erythema, hyperkeratosis, pigmentation[blank_end](50% of patients).
Antworten
  • doxorubicin
  • non
  • topoisomerase II
  • transcription
  • IV
  • Cardiotoxicity
  • cumulative
  • germ cell
  • Lymphoma
  • strand breaks
  • specific
  • fibrosis
  • erythema, hyperkeratosis, pigmentation

Frage 14

Frage
Platinum compounds e.g. cisplatin, carboplatin, oxaliplatin. AKA ‘Non-classical alkylating agents’. MoA: [blank_start]Clions[blank_end] interact with [blank_start]N-7 of guanine[blank_end] - INTRA strand [blank_start]X[blank_end]-linking. [blank_start]IV[blank_end] infusion, excreted by [blank_start]kidney[blank_end]. Long t1/2: [blank_start]24-60[blank_end]h, due to protein binding. ◦ BM suppression and GI toxiciity - requires [blank_start]anti-emetic[blank_end] support ◦ Renal toxicity ([blank_start]reversible[blank_end]) ◦ [blank_start]Ototoxicity[blank_end], tinnitus, hearing loss ◦ Peripheral neuropathy
Antworten
  • Clions
  • N-7 of guanine
  • cross
  • IV
  • kidney
  • 24-60
  • anti-emetic
  • reversible
  • Ototoxicity

Frage 15

Frage
Antimetabolites: • Structural similarity to [blank_start]intermediates[blank_end] of normal metabolism • Incorporation into nucleic acids e.g. [blank_start]5-FU, capecitabine[blank_end] (prodrug) • Enzyme substrates that inhibit RNA and DNA [blank_start]synthesis[blank_end] • Good [blank_start]gut[blank_end] absorption, also IV, intrathecal • [blank_start]Renal[blank_end] excretion e.g. Methotrexate (MTX) for leukaemias (breast, head, lung and neck). • [blank_start]Folate[blank_end] analogue, stops [blank_start]purine[blank_end] synthesis Toxicity: BM (leukocytes) – infection, GI (mucosa)
Antworten
  • intermediates
  • 5-FU, capecitabine
  • synthesis
  • gut
  • Renal
  • Folate
  • purine

Frage 16

Frage
Mitotic inhibitors which are [blank_start]plant[blank_end] derivatives are cell cycle-specific. 1. Vinca alkaloids e.g. Vincristine, vinblastine, vindesine, vinorelbine Bind to [blank_start]tubulin[blank_end], inhibits polymerisation (mitosis). Eliminated via metabolism. Given [blank_start]IV[blank_end] usually. Toxicity: constipation, BMS usually dose limiting (absent for [blank_start]vincristine[blank_end]), dose-limiting [blank_start]neurotoxicity[blank_end] for vincristine, neuropathy (mixed motor/sensory), paraesthesia, loss of deep reflexes (axonal transport). 2. Taxanes e.g. Docetaxel, paclitaxel Stabilise [blank_start]microtubule[blank_end] structure, prevent cell division. Poor [blank_start]oral[blank_end] absorbtion. Hepatic metabolism. Toxicity: Dose-limiting [blank_start]neutropaenia[blank_end], arthralgia/myalgia syndrome (mechanism unknown) Paclitaxel: [blank_start]sensory[blank_end] neuropathy (motor at higher dose) Docetaxel: leg [blank_start]oedema[blank_end] (fluid retention – peripheral effect)
Antworten
  • plant
  • tubulin
  • IV
  • vincristine
  • neurotoxicity
  • microtubule
  • oral
  • neutropaenia
  • sensory
  • oedema
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