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Cancer - Vicki > Colorectal Cancer > Flashcards

Colorectal Cancer Flashcards

1
Q

3rd most common uk cancer

A

Colorectal.

More common in males > females.

> 60 years old.

Incidence varies worldwide: more meat in west = more cancer, more veg in east = less cancer.

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2
Q

What are the risk factors for colorectal cancer?

A

Familial: Familial adenomatous polyposis [FAP] (APC mutation).
HNPCC - hereditary non-polyposis colorectal cancer.

Dietary/lifestyle (low fibre, smoking, inactivity, obesity, alcohol)
Other colorectal conditions (UC, Crohns (less than UC tho))

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3
Q

How does colorectal cancer develop?

A

Polyp –> benign adenoma –> malignant tumour.

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4
Q

Where does colorectal cancer metastasise?

A

Liver (good blood supply)
Lungs
Brain

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5
Q

What is the clinical presentation of colorectal cancer?

A

Changes in bowel habit, abdo pain, rectal bleeding/mucus, weight loss + Anorexia (advanced tumours).

Signs: Anaemia from chronic bleeding from tumour site.

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6
Q

What are the differential diagnoses of colorectal cancer?

A

IBS

IBD

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7
Q

What is FOB screening?

A

Everyone aged 60-74 in UK.

The faecal occult blood (FOB) test and faecal immunochemical test (FIT) can detect tiny amounts of hidden blood in your poo. The FIT test is being introduced in Scotland, and is sometimes used in Wales and Northern Ireland.

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8
Q

What are the diagnositic investigations used in colorectal cancer?

A

Colonoscopy - tube up the bum, laxatives for days before.

Flexible sigmoidoscopy - for people who cannot tolerate colonscopy. (60% detection).

Barium enema, visualise bowel via X-ray. Less specificity than either of the above.

CT scan of chest/abdo/pelvis

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9
Q

Colorectal cancer treatment depends on

A

Site and extent of tumour.

Most patients will have surgery as 1st line for 80% of patients. A segment of large bowel is resected = hemicolectomy/sigmoid colectomy/hartmann’s procedure.

> 50% of patients suffer recurrent disease.

Radiotherapy only in RECTAL cancers.

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10
Q

Radiotherapy is used for

A

RECTAL cancers.

Pre-op mostly to reduce tumour size (with chemo for 5 weeks, mon-fri)

Post-op to reduce the risk of local recurrence or if not all the tumour could be removed during surgery.

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11
Q

What is the aim of using adjuvant chemotherapy?

A

Aimed at eradicating micrometastases which have been shed from tumour prior to or during resection.

7% absolute increase in survival. Duke C.
Not Duke A.
Not sure about Duke B.

Fluorouracil (5-FU) has been mainstay of treatment for 50years.

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12
Q

What is the MOA of 5FU?

A

Converted intracellularly to metabolites that bind the enzyme thymidylate sunthase, inhibiting the synthesis of thymidine, DNA and RNA.

To increase the efficacy of 5-FU, folinic acid given as this increases and prolongs the inhibition of TS.

Side effects: 
Diarrhoea
Stomatitis (sore mouth)
N+V
BM suppression. 
Hand-foot syndrome 
Excessive tear shedding.
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13
Q

What are the side effects of 5FU?

A

Converted intracellularly to metabolites that bind the enzyme thymidylate sunthase, inhibiting the synthesis of thymidine, DNA and RNA.

To increase the efficacy of 5-FU, folinic acid given as this increases and prolongs the inhibition of TS.

Side effects: 
Diarrhoea
Stomatitis (sore mouth)
N+V
BM suppression. 
Hand-foot syndrome 
Excessive tear shedding.
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14
Q

What is FOLFOX?

A

NICE guidance 2006 – oxaliplatin + 5-FU + folinic acid (e.g. oxaliplatin de Gramont) or capecitabine are options for Duke’s C colorectal cancer

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15
Q

What is oxaliplatin?

A

3rd generation platinum derivative

Cross-links DNA, prevents replication & cell division

Less nephrotoxicity than other platinums (e.g. cisplatin) but 95% of patients suffer neurological side effects

Side effects: 
Peripheral neuropathy 
Acute pharyngolaryngeal dyasthesia (1-2%, Vicki says higher). 
BM suppression 
Mild alopecia
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16
Q

What are the side effects of oxaliplatin?

A

3rd generation platinum derivative

Cross-links DNA, prevents replication & cell division

Less nephrotoxicity than other platinums (e.g. cisplatin) but 95% of patients suffer neurological side effects

Side effects: 
Peripheral neuropathy 
Acute pharyngolaryngeal dyasthesia (1-2%, Vicki says higher). 
BM suppression 
Mild alopecia
17
Q

What is the FOLFOX regime?

A

Chemo given every 2 weeks for 12 cycles as outpatient
Oxaliplatin 85mg/m2 over 2hrs IV infusion
Folinic acid 350mg over 2hrs IV infusion
Fluorouracil 400mg/m2 IV stat
Fluorouracil 2400mg/m2 IV infusion over 46hrs in portable infusion device
Need Hickman (central) line or PICC line

DONT NEED TO REMEMBER DOSES?

18
Q

What is a Hickman line?

A

Line into heart.

19
Q

Why is the infusion aspect of colorectal cancer treatment important?

A

Colorectal cancer tumour cells have low growth fraction.

5FU is S-phase specific and has a short half-life of 10 minutes.

Increased risk of hand-foot syndrome.

20
Q

What are the problems with infusion devices for colorectal cancer?

A

Anxiety for patients
Disposal of cytotoxic waste in the patients own homes is an issue.
Can be time-consuming to fill them.

21
Q

What is capecitabine?

A

Oral chemo pro-drug of 5FU, often used in combination with oxaliplatin (=XELOX regimen) instead of the “de Gramont” component.

Advantages of oral chemotherapy wth Capecitabine:

  • less invasive and distressing for the patient to take oral medication.
  • no issues with sterility/short expiry date from being made up in hospital pharmacy.
  • reduces pharmacy costs
  • patients can administer at home, problems with correct adherence.

Capecitabine has a 3 step activation process, 2 of which occur preferentially in tumour cells.

22
Q

What are the advantages of oral capecitabine therapy?

A

Oral chemo pro-drug of 5FU, often used in combination with oxaliplatin (=XELOX regimen) instead of the “de Gramont” component.

Advantages of oral chemotherapy wth Capecitabine:

  • less invasive and distressing for the patient to take oral medication.
  • no issues with sterility/short expiry date from being made up in hospital pharmacy.
  • reduces pharmacy costs
  • patients can administer at home, problems with correct adherence.

Capecitabine has a 3 step activation process, 2 of which occur preferentially in tumour cells.

23
Q

How often is Capecitabine given?

A

Orally,
bd for 14 days out of 21.

Side effects:
Diarrhoea 
Hand-foot syndrome
N+V
Stomatitis
24
Q

What are the treatment options of advance (metastatic) disease?

A

Surgery still used to relieve obstruction/symptoms.

Resection of liver metastases (11% of patients)

5-FU based regimens e.g. oxaliplatin de Gramont, capecitabine.

25
Q

How is Duke A treated?

A

Surgery only.

26
Q

How is Duke B treated?

A

Surgery + adjuvant chemotherapy in some cases (patients with risk factors such as vascular invasion of tumour, poorly differentiated tumour).

27
Q

How is Duke C treated?

A

Surgery + adjuvant chemotherapy.

28
Q

How is Duke D treated?

A

This is metastatic disease.
Surgery is used to relieve the obstruction if needed, palliative chemotherapy +/- monoclonal antibodies are given to relieve symptoms and prolong survival.

29
Q

What is Lonsurf?

A

Oral agent: Trifluridine + Tipiracil.

Trifluridine - thymidine analogue, which is phosphorylated by thymidine kinase, further metabolised in cells to a DNA substrate and incorporated into DNA, therefore preventing cell proliferation.

Trifluridine is rapidly degraded by thymidine phosphorylase enzyme (TPase) - that is where tipiracil comes in, tipiracil is a TPase inhibitor.

30
Q

How do the two components of Lonsurf complement each other?

A

Oral agent: Trifluridine + Tipiracil.

Trifluridine - thymidine analogue, which is phosphorylated by thymidine kinase, further metabolised in cells to a DNA substrate and incorporated into DNA, therefore preventing cell proliferation.

Trifluridine is rapidly degraded by thymidine phosphorylase enzyme (TPase) - that is where tipiracil comes in, tipiracil is a TPase inhibitor.

31
Q

When is Lonsurf used?

A

For metastatic colorectal cancer, usually after other therapies.

Oral agent: Trifluridine + Tipiracil.

Trifluridine - thymidine analogue, which is phosphorylated by thymidine kinase, further metabolised in cells to a DNA substrate and incorporated into DNA, therefore preventing cell proliferation.

Trifluridine is rapidly degraded by thymidine phosphorylase enzyme (TPase) - that is where tipiracil comes in, tipiracil is a TPase inhibitor.

32
Q

What are the side effects of Lonsurf?

A 
N+V
D/C
Sore mouth, 
Taste changes, 
Bone marrow suppresion --?> low WBCs, RBCs, platelets and risk of infection etc.
33
Q

What is Bevacizumab?

A

1 +2. Monoclonal antibody for VEGF which binds to VEGF therefore inhibiting angiogenesis.

  1. Used in Colorectal, metastatic breast, renal cell carcinoma, NSCLC and glioblastoma.

4.Bone marrow suppression, bleeding, VTE, stroke, TIA, MI, angina, CHF (esp. in those prev. treated with anthracyclines)
Hypertension, proteinuria, asthenia, Abdo pain, Mucosal inflammation, diabetes, anaemia.

  1. Re-establishing neovascularisation through other means.
    Altering their behaviour to metastasize without the need to angiogenesis.
  2. CR – with 5FU or campecitibine
    NSCLC – Pt based chemotherapy
  3. Make sure patient monitored for bone marrow suppression, that they get BP check, ECGs frequently,and blood glucose levels.
34
Q

What is Cetuximab?

A

Chimeric monoclonal antibody targeting EGFR (no Ras mutations pls).

Signal transducton via EGFR causes the activation of Ras. Which, in turn, activates Raf via phosphorylation. Activated Raf then phosphorylates MAPK and MEK.

MAPK and MEK then act as transcription factors for a number of genes (CREB, c-myc, BRAF, PTEN, KRAS, PIK3CA), the end result of which is cell growth, proliferation, survival etc.

No point using Cetixumab in people with Ras activating mutations as Cetixumab only works via overexpression of EGFR.

Cetixumab can be used to treat Squamous cell cancer of the head and neck and their are CT into NSCLC.

SE: Skin dryness and fissures, hyperpigmentation, photosensitivity and radiosensitising effects. SJS. Mucositis, disruption of normal hair growth, nail changes, headache, GI, LFT disturbances and fatigue. Hypocalcamia and hypomagnesia

Can be used with:
FOLFOX and FOLFIRI regimes.

Cancer - Vicki (12 decks)

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