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Year 2 Pharmacology > Anti-Neoplastics > Flashcards

Anti-Neoplastics Flashcards

1
Q

When is medical therapy needed for cancer?

A

Neoadjuvant therapy
Eradication of micro-metastasis
Medical treatment of sensitive tumour
Palliatation

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2
Q

When are chemotherapies most effective?

A

When tumours/metastasis are small

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3
Q

What considerations are there affecting medical therapies for cancer treatment?

A

Naturally resistant populations (tumour heterogeneity)
Tumour growth kinetics
Factors influencing drug penetration of tumour
Patient factors

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4
Q

How can cancer resistances be overcome?

A

Reduce tumour burden before medical therapy- surgery
Multi-drug chemotherapy
High dose intensity

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5
Q

Why is the frequency of treatment important?

A

If too far apart the tumour tissue has the time to regenerate
If too close together it is cumulative toxic to normal tissue

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6
Q

What factors affect response and side effects?

A 
ADME
A- Administration- dose/administration
D- Distribution- target site
M- Metabolism- activation, deactivation
E- Excretion- clearance
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7
Q

What factors of response and side effects can be detected?

A

Pharmacogenetics- mutations in PgP
Co-morbidities
Poly-pharmacy

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8
Q

What are the two categories of chemotherapy and what are their mechanisms of action?

A

Damage DNA- cell cycle non-specific

Inhibits DNA replication- cell cycle specific

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9
Q

What is the problem with un-targeted therapy?

A

Well affect all rapidly dividing tissues

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10
Q

Where are the main side effects of un-targeted therapy?

A

Bone marrow- Low white count
Alopecia- uncommon in fods/cats
Gastrointestinal

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11
Q

What is the mechanism of action of the drug Alkylators?

A

Bind to DNA, insert on alkyl group leading to a change in structure- transcription and replication are inhibits
Cell cycle non-specific

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12
Q

What are the main mechanisms of actions of resistance of alkylators, where is is metabolised and excreted?

A

Resistance- DNA repair from MGMT/ Exclusion from cell
Metabolised to active by liver
Excreted by kidneys

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13
Q

What are the commonly used agents of alkylators and what are the side effects?

A

Chlormabucil, cyclophosphamide, lomustine, melphalan

Side effects- myelosupression, sterile haemoorhagic cystitis (cyclophospamide), Lomustine- hepatic toxicity

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14
Q

What is the mechanism of action of vinca-alkaloids?

A

Either binds to or inhibits formation of microtubules preventing the formation of mitotic spindle
Cell cycle specific

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15
Q

Where is vinca-alkaloids metabolised to active form and excreted?

A

Metabolised in liver

Excreted in the bile

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16
Q

What are the common used agents of vinca-alakloids and what are their possible side effects?

A 
Vincristine, vinblastine, Vinorelbine 
GI
Mylosupression 
Perivsascular irritation
Mutations on PgP can lead to severe side effects
TEST PATIENT
17
Q

What is the mechanism of action of anti-tumour antibiotics and what are the main resistance mechanisms?

A

MOA-
Topoisimerase inhibtion- DNA strand breaks
Intercalation with DNA- prevents transcription
Free radical formation- DNA damage
Cycle non-specific
Resistance- upregulation of ABC-B1, topoisomerase II activity

18
Q

Where are anti-tumour antibiotics metabolised and excreted?

A

Metabolised in liver

Excreted through bile

19
Q

What drugs are used and what are the side effects of anti-tumour antibiotics?

A

Drugs- doxorubicin, epirubicin
Side effects- GI, Mylosupression, cumulative cardio toxicity, arrhythmia (admin too quickly), severe perivascular irritation

20
Q

What is the mechanism of action of platinating agents and what are the mechanisms of resistance?

A

MOA- platinum binds both within and between strands

Resistance- decreased uptake, increased DNA repair, increases detoxifying enzymes

21
Q

Where is platinizing agents metabolised and secreted?

A

Metabolised- isn’t

Excreted- kidney

22
Q

What platiniating agents are used and what are the side effects?

A

Drug- carboplatin

Side effects- myelosuppression, GI toxicity, kidney toxicity

23
Q

What is the mechanism of action, resistance mechanisms, normal metabolisation/excretion, drugs and side effects of anti-metabolites?

A

Interact with DNA production pathways, but differing mechanisms- cell cycle specific
Resistance- reduced uptake, reduction in pathway enzymes
Metabolised- liver, plasma
Excretion- kidneys
Drugs- cytosine arabinoside, fluorouracil
Side effects- mylosupression, GI, transient hepatic dysfunction

24
Q

What is the mechanism of action of l’asparaginase, side effects, main use?

A

MOA- l’asparaginase metabolises asparagine to aspartic acid, malignant lymphocytes dependent on asparagine therefore lymphocyte death
Side effects- anaphylaxis (rare), pancreatic inflammation, transient alterations in liver function
Use- lymphoma, leukaemia

25
Q

What glucocorticoids are commonly used, what is their MOA and the possible side effects?

A

Commonly used- prednisolone, dextamethasone
MOA- bind to cytosolic receptors, transport to the nucleus, acts as transcription factor, stays in cytosol reducing inflammatory protein production
Side effects- increased appetite/thirst, Lethargy, GI bleeding and ulcers

26
Q

What are NSAIDs used for?

A

Biotherapy

27
Q

What are receptor tyrosine kinases functions?

A

Proliferation and cell growth
Cell survival
Chemotherapy and radiation resistance

28
Q

What causes tyrosine kinase overactivity?

A

Excessive growth factor or receptor
Mutations
Leads to excess growth and tumours
Therefore needs to be inhibited

29
Q

What are examples of receptor tyrosine kinase inhibitors?

A

Toceranib
Mastinib
Side effects not predictable- some GI, some bone marrow suppression

30
Q

What is the mechanism of action of metronomic chemotherapy?

A

Kills chemotherapy sensitive cells, reduces cancer supporting new blood vessels, improves anti-cancer immune response

31
Q

What is used for metronomic chemotherapy?

A

Low doses of cyclophosphamide with piroxicam

32
Q

What are the two approaches of immunotherapy?

A

Active immunotherapy- aim is to stimulate the immune system against tumour
Passive- use monoclonal antibodies to target tumour

33
Q

What is imiquimod used for and what is its MOA?

A

Non-specific immune stimulator

Action- activates TLR7 encourages langerhans cell maturation and transit lymph nodes

34
Q

What can be vaccinated for?

A

Melanoma

Year 2 Pharmacology (11 decks)

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