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GI Pathology > 16. Colorectal Cancer, Screening and Surgery > Flashcards

16. Colorectal Cancer, Screening and Surgery Flashcards

1
Q

Colorectal cancer:

  1. T/F: 95% are adenocarcinomas.
  2. Which part of the bowel does it affect the most?
A
  1. True

2. Two thirds = colonic. 1/3 = rectal.

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2
Q

What are the risk factors for colorectal cancer?

A
  • Most (85%) are sporadic with no familial/genetic influence
  • 10% have a familial risk
  • Inheritable conditions: HNPCC (5%), FAP (<1%), other CRC syndromes
  • 1% associated with underlying Inflammatory Bowel Disease (IBD)
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3
Q

What are the risk factors for sporadic causes of colorectal cancer?

A
  • Age
  • Male gender
  • Previous adenoma/CRC
  • Environmental influences: Diet ( less fibre, fruit & veg, calcium. Increased intakes of red meat and alcohol)
    > Obesity
    > Lack of exercise
    > Smoking
    > Diabetes Mellitus
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4
Q

What do majority of colorectal cancers arise from?

A

The majority of colorectal cancers arise from pre-existing polyps. These are protuberant growths, variety of histological types, epithelial or mesenchymal, benign or malignant.

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5
Q

Adenomas:

  1. Are these benign or malignant?
  2. Where do they originate from?
  3. What are the main histological types?
  4. What are the morphological types?
  5. Which factors determine whether lesions are high risk or not?
A
  1. Benign, pre-malignant
  2. Epithelial in origin (abnormal growth of tissue projecting from the colonic mucosa)
  3. Main histological types: tubular (75%), villous (10%), indeterminate tubulovillous (15%).
  4. Single or multiple, pedunculated, sessile or ‘flat’
  5. size (>1.5cm), number (multiple polyps), degree of dysplasia, villous architecture
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6
Q

How does adenoma transforms into carcinoma?

A

Cell growth, proliferation and apoptosis due to:

  • Activation of oncogene – k-ras, c-myc
  • Loss of tumour suppressor gene – APC, p53, DCC
  • Defective DNA repair pathway genes – microsatellite instability
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7
Q

How does colorectal cancer present?

A
  • Rectal bleeding: especially if mixed in with stool, colour? anorectal pain?
  • Altered bowel opening to loose stools >4 weeks
  • Iron Deficiency Anaemia men of any age and non-menstruating women (more likely to have right sided colonic malignancy)
  • Palpable rectal or right lower abdominal mass
  • Acute colonic obstruction if stenosing tumour
  • Systemic symptoms of malignancy: Weight loss, Anorexia
  • Tenesmus (a continual or recurrent inclination to evacuate the bowels)
  • Fatigue
  • Vomiting
  • Abdominal pain - colicky
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8
Q

What is the protocol for managing patients with rectal bleeding and associated symptoms?

A

Patient presents with low risk features e.g. Transient symptoms (<6 weeks) - Rectal bleeding with anal symptoms. Patient less than 40 years.

Then watch and wait. Review the patient in 6 weeks.

After 6 weeks: if no further symptoms then discharge the patient. However, if symptoms persist or recur or
deteriorate or patient will not agree to “watch and wait” then perform further investigations.

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9
Q

What investigations would you perform in suspected colorectal cancer patient?

A
  1. Colonoscopy +/- biopsies (gold standard)
  2. Radiological imaging: barium enema
    > CT colonography (3D virtual colonoscopy)
    > Plain CT abdo/pelvis with contrast
  3. Staging: CT if confirmed CRC (CT chest/abdo/pelvis)
    - PET scan / rectal endoscopic ultrasound in selected cases
  4. Pre-op MRI in confirmed rectal cancer
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10
Q

What are advantages and disadvantages of colonoscopy?

A

Advantages:

  • Allows tissue biopsies to be taken
  • Therapeutic as well as diagnostic (polypectomy)

Disadvantages:

  • Sedation
  • Bowel preparation
  • Risks (perforation, bleeding)
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11
Q

What are disadvantages of radiological imaging?

A

Ionising radiation
Bowel preparation
No histology
No therapeutic intervention

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12
Q

Why perform pre-operative MRI for rectal cancer?

A
  • Best imaging modality for looking at CRM
  • could dictate if neoadjuvant chemotherapy, radiotherapy or both required followed by surgery
  • Neoadjuvant treatment for circumferential resection margin (CRM) threatened disease, Extramural venous invasion (EMVI), nodal disease, Very low rectal cancer
  • Restaging 6-8 weeks later following neoadjuvant treatment
  • Surgery 8-10 weeks after treatment (Total Mesorectal Excision)
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13
Q

Outline criteria used for colorectal staging.

A

Dukes’ Criteria:
- Dukes’ A: confined to mucosa
- Dukes’ B: invasion through muscularis but no lymph node involvement
- Dukes’ C: invasion through muscularis with lymph node involvement (C1: LN 1-4), C2: >4 LNs involved). Confined to serosa
- Dukes’ D: breached serosa: distant metastasis.
TNM staging

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14
Q

What does mesorectum include? Why is it important during surgery in rectal cancer?

A

Rectum surrounded by fatty envelope called the mesorectum. This contains all the draining lymph nodes of the rectum.

To reduce local recurrence rate, the rectum and it’s surrounding mesorectum has to be excised en bloc. i.e. perform total mesorectal excision (TME).

If mesorectal fascia involved, surgery will be pointless unless we can downstage tumour and get clear circumferential resection margins (CRM).

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15
Q
  1. What is the treatment for colorectal cancer?
  2. Operative procedure is based on what?
  3. What would you do for Dukes A and ‘cancer polyps’?
A
  1. Surgery is basis for therapy: Colon cancer almost always straight to surgery if no metastatic disease & patient fit: Laparotomy or Laparoscopic . Removal of lymph nodes for histological analysis. Partial hepatectomy for metastases. Stoma formation - colostomy (permanent/temporary).
  2. Depends on site, size, stage of tumour, pathology and vascular anatomy.
  3. Dukes A and ‘cancer polyps’: endoscopic or local resection
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16
Q

What needs to be considered while deciding on treatment?

A

Resection
Restoration intestinal continuity
Faecal diversion: Stoma
Preservation of function

17
Q

What is performed for rectal cancer before surgery?

A

Radiotherapy: ‘neoadjuvant’ +/- chemotherapy to control primary tumour prior to surgery.

18
Q

What is the post-op management?

A
  • Dependent on pathological staging. Presence of high risk pathological features.
  • Adjuvant chemotherapy may be required (FOLFOX): especially for Dukes C, ?Dukes B or if positive lymph node histology. It mops up micrometastases, Agents used - 5-FU (fluorouracil) +/- other agents
  • Post-operative complications might hinder or delay adjuvant treatment
  • Surveillance CT CAP, colonoscopy.
  • In NHSG alternate USS liver + CT CAP every 6 months
19
Q

How is advanced disease treated?

A

Palliative care for advanced disease: chemotherapy, colonic stenting to prevent colonic obstruction.

20
Q

Bowel anastomosis:

  1. When is it performed?
  2. What are the most important factors in the creation of a successful bowel anastomosis?
  3. What are the complications of the procedure?
A
  1. A surgical procedure performed to establish communication between 2 formerly distant portions of the intestine. This procedure restores intestinal continuity after removal of a pathologic condition affecting the bowel.
  2. Bowel ends must have no tension, Well perfused, Well oxygenated, Clean surgical site, Acceptable systemic state.
  3. Anastomotic leak. Bleeding. Infection (superficial & deep).
21
Q
  1. Compare site, contents and appearance of ileostomy and colostomy.
  2. What are the complications of stoma procedure?
A
  1. Ileostomy:
    - Site = usually RIF
    - Contents = liquid, looser stools
    - Appearance = spouted

Colostomy:

  • Site = usually LIF
  • Contents = solid stools
  • Appearance = no spout, flush with skin
  1. Stoma problems (ischaemia, retraction, prolapse, hernia, high output).
22
Q

What are the complications in low anterior resections?

A

Damage to pelvic nerves – bowel, urinary, sexual dysfunction

Possible impaired fecundity in younger women

23
Q

Define screening?

A

Screeningis defined as the presumptive identification of unrecognized disease in an apparently healthy, asymptomatic population by means of tests, examinations or other procedures that can be applied rapidly and easily to the target population.

24
Q

How do we screen patients for CRC?

A
  • Quantitative faecal immunochemical test (qFIT):
  • Faecal occult blood test (FOBT) every 2 years: If FOBT positive then do colonoscopy.
  • Once off flexible sigmoidoscopy (In certain areas in England only >age 55)
  • Colonoscopy
  • CT Colonography
25
Q

List advantages and disadvantages of FOBT.

A

Advantages:

  • Specific for human haemoglobin
  • Automated
  • Quantitative
  • User friendly format that increases uptake
  • Provides flexibility to alter the cut-off to accommodate risk factors including age and gender which could reduce the interval cancer rate

Disadvantages: FOBT has lower positivity in women

26
Q

Which high-risk groups are screened for CRC?

A
  • Heritable conditions: FAP (familial adenomatous polyposis), HNPCC (hereditary non-polyposis colorectal cancer)
  • Inflammatory bowel disease
  • Familial risk
  • Previous adenomas/Colorectal cancer
27
Q

Familial adenomatous polyposis (FAP):

  1. T/F: Autosomal recessive condition.
  2. Which genes are mutated?
  3. How is it screened?
  4. How is it treated?
A
  1. False. Autosomal dominant condition.
  2. Mutation of the APC gene on chromosome 5 (~25% of all cases are due to new mutations).
  3. Screening – annual colonoscopy from age 10-12 yrs.
  4. Prophylactic proctocolectomy (surgical removal of the rectum and all or part of the colon) usually age 16 - 25 yrs. NSAIDs chemoprevention: Sulindac reduces polyp number and prevents recurrence of higher-grade adenomas in the retained rectal segment.
28
Q

What are the extracolonic manifestations of FAP?

A
  • benign gastric fundic cystic hyperplastic
  • duodenal adenomas in 90% with periampullary cancer ~5% (surveillance endoscopy)
  • Desmoid tumours (10-20%)
  • CHRPE – congenital retinal hypertrophy of the pigment epithelia
29
Q

Hereditary non-polyposis colorectal cancer (HNPCC):

  1. T/F: Autosomal recessive condition.
  2. Which genes are mutated?
  3. What molecular characteristic do the tumours have?
  4. What cancers is it associated with?
  5. How is it diagnosed?
  6. How is it screened?
A
  1. False. Autosomal dominant condition.
  2. Mutation in DNA mismatch repair (MMR) genes: e.g. MLH1 and MSH2.
  3. Tumours typically have a molecular characteristic called microsatellite instability (MSI) - frequent mutations in short repeated DNA sequences (microsatellites).
  4. Early onset colorectal cancer (40’s) right sided. Associated with cancers at other sites – endometrial, genitourinary, stomach, pancreas.
  5. Diagnosis – clinical criteria (Amsterdam / Bethesda), genetic testing
  6. Screening from age 25: 2 yearly colonoscopy
30
Q

When to perform colonoscopy in high risk groups for CRC?

A
  1. If familial history of CRC: 5 yearly colonoscopy from age 50 yrs in high-moderate risk group.
    - Low Moderate Risk: once-only colonoscopy at age 55 yrs
  2. IBD – Index surveillance colonoscopy 10 years post diagnosis, then dependant on duration, extent and activity of inflammation and presence of dysplasia
  3. Previous CRC – 5 yearly colonoscopy
  4. Previous adenomas – dependant on number of polyps, size, degree of dysplasia.
31
Q

Case: 65yr male fit and healthy. Presented with 1 week history of abdominal pain and vomiting. Bowels not opened for 5 days.
O/E: acutely distended abdomen, generalised tenderness but not guarding. Tympanic on percussion. No obvious groin hernias. PR exam reveals empty rectum. In reasonable physiological state. Not haemodynamically compromised. What’s the diagnosis?
1. Small bowel obstruction
2. Bowel perforation
3. Sigmoid volvulus
4. Large bowel obstruction
5. Toxic megacolon

A
  1. Small bowel obstruction
32
Q

What are the cardinal signs of bowel obstruction?

A 
Abdominal pain
Vomiting
Absolute constipation (flatus and solids)
Abdominal distension
33
Q

What is the aetiology of small bowel obstruction?

A

Adhesions

Hernias

34
Q

What is the aetiology of large bowel obstruction?

A
  • Malignant (60%)
  • Benign:
    > Strictures (diverticular, ischaemic)
    > Volvulus
    > Faecal impaction
    > Intussusception
    > Pseudo-obstuction
35
Q

How is the bowel obstruction managed?

A
  • ABC
  • Fluid resuscitation: frequently underestimate amount required
  • NBM and consider nasogastric tube if vomiting
  • Analgesia (pain out of proportion suggests ischaemia or perforation) and antiemetics
  • Consider IV antibiotics
  • Bloods (FBC, U&Es, G&S, Coagulation screen)
  • Blood gas (Lactate, pH, BE): Normal lactate doesn’t exclude bowel ischaemia.
  • CT abdo/pelvis
  • If closed loop obstruction, needs urgent surgical review

GI Pathology (20 decks)

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