Colorectal Flashcards

1
Q

Aetiology of Colorectal cancer

A

From epithelial cells lining colon/rectum most commony adenocarcinoma. Most develop via progression of normal mucosa to colonic adenoma (colorectal polyps) to invasive adenocarcinoma. Adenomas can be present 10+years before malignant and progression to adenocarcinoma is about 10%.

  • Some genetic mutations implication to predispose: Adenomatous polyposis coli (APC) -leads to Familial adenomatous polyposis and Hereditary nonpolyposis colorectal cancer (HNPCC)-leads to defects in DNA repair such as Lynch syndrome.
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2
Q

RFs of colorectal cancer

A

Approx 75% sporadic but potential RFS are: Increasing age, male, family history, IBD, low fibre diet, high processed meat intake, smoking and excess alcohol intake

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3
Q

Clinical features of colorectal cancer

A

Change in bowel habit, rectal bleeding, weight loss, abdominal pain, symptoms of (iron deficiency) anaemia.

  • Right-sided colon cancers – abdominal pain, iron deficiency anaemia, palpable mass in RIF, often present late.
  • Left sided- Rectal bleeding, change in bowel habit, tenesmus, palpable mass in LIF or PR exam.

Urgent referral (NICE):

>/40 unexplained weight loss and abdo pain

50 unexplained rectal bleeding

>/60 irond ef anaemia or change in bowel habit

Positive occult blood screening test

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4
Q

Invetsiagtions for colorectal cancer

A
  • Lab tests – FBC, CEA tumour marker
  • Imaging – colonoscopy with biopsy then CT (metastasis), MRI rectum (depth invasion and chemo need for rectal), Endo-anal US – to assess suitability for trans-anal resection.
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5
Q

DDx Colorectal cancer

A

IBD (20-40yrs) with diarrhoea with blood and mucus, haemorrhoids with bright red rectal bleeding on pain or surface but not usually abdominal pain, altered bowel or weight loss.

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6
Q

Explain pathological staging systems for colorectal cancer

A
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7
Q

Explain the principles of surgical treatments for colorectal cancer

A

All discussed in the MDT – only definitive curative option is surgery as chemo and radiotherapy are neoadjuvants and adjuvant treatments alongside role in palliation.

General plan is suitable regional colectomy to ensure removal of the primary tumour with adequate margins and lymphatic drainage, followed either by primary anastomosis or formation of a stoma.

  • Right Hemicolectomy or extended right hemicolectomy: for caecal tumours or AC tumour with extended one for transverse colon ones.Ilecolic, Rigth colic and right branch of middle colic vessel divded and removed with mesenteries.
  • Left hemicolectomy – Descending colon timours. Left branch of middle colic vessels divided and removed with mesenteries
  • Sigmoidcolectomy – Sigmoid colon tumours. IMA fulyl dissected out with tumour to ensure adequate margins obtained
  • Anterior resection – High rectal tumours typically if >5cm from anus. Favoured as leaves rectal sphincter intact if anastomosis formed unlike ap. Often a defunctioning loop ileostomy performed to protect anastomosis and reduce complications if there’s a leak which can be reversed.
  • Abdominoperineal resection (AP) – ow rectal tumours typically <5cm from anus. Excision of distal colon, rectum and anal sphincters, resulting in permanent colostomy.

Usually elective colectomies laprascopically.

Hartmann’s Procedure: In emergency bowel surgery, like bowel obstruction or perforation. Involves complete resection of recto-sigmoid colon with formation of an end colostomy and closure of rectal stump.

Colorectal cancer presenting with bowel obstruction can be relieved by decompressing colostomy or endoscopic stenting.

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8
Q

Explain the principles of adjuvant or neoadjuvant treatment of colorectal cancer

A

Neoadjuvant therapy: Delivered before main treatment to help reduce size of a tumour or kill cancer cells that have spread

Adjuvant: Delivered after primary treatment to destroy remaining cancer cells

Adjuvant Stage 2

  • (T3/4, NO MO). Only treat high risk stage 2 (
  • If MSI-instabke/MSI-high/dMMR then no adjuvant chemo
  • 6months oral capecitabine – reducse risk recurrence

Adjuvant Stage 3

  • Any T, N1/2, MO
  • Nosaic trial 2004 – adjuvant benefit to single agent 5-FU was 1-%, improved with adding oxaliplatin by 3-5%/ Now we offer doublet chemo with 15% benefit.
  • Treatment paradigm changed with SCOT trial: now 3m/6m CAPOX (capecitabine + oxaliplatin), based on risk. T4/N2 6m, T1-3,N1 3m
  • Aim to start within 8weeks surgery, definitely before 12 weeks

Chemotherapy:

  • Typically for those with advanced disease. Systemic therapy for metastatic colorectal cancer is tailored with patient-specific and disease-specific predictive markers.
  • Eg,for metastatic colorectal cancer – FOLFOX Folinic acid, Fluorouracil (5-FU), Oxaliplatin which significant imprives 3year disease free survival
  • Newer biologic agents or immunotherapies are being developed

Radiotherapy:

  • Can be used in rectal cancer (not usually colon as risk of damage to small bowel), most often as neo0adjuvant and alongside chemo
  • Can have pre operative long course chemo-radiotherapy t shrink tumour to increase chance of complete resection and cure.
  • Due to some cases getting complete respond with chemo-radiotherapy, some with rectal cancer do a rectal preserving treatment watching and waiting with omission of radical surgery and close surveillance.
    *
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9
Q

Identify the different types of stomas (ileostomy, colostomy) and relate each stoma type to its function and use in clinical practice

A
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10
Q

Identify which populations are offered colorectal screening

A

Every 2 years to men and women 60-75. Mostly Fecal immunochemistry test (FIT) used utilities antibodies against human haemaglobin to detect blood in faeces. If positive then appointment with specialist nurse and colonoscopy

(Expanding to 56year olds in 2021)

Those over 75 can askf or kit every 2 years by phoning free bowel cancer screening hotline.

(Bowel scope screening with flexible sigmoidoscopy for 55+ one off is no longer offered)

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11
Q

Explain the benefits and potential drawbacks of colorectal screening

A
  • Since intro in 2006, Increased detection of colorectal cancer in people 60-69 by 11%
  • Majority of people called back for additional tests will not have cancer
  • Certain cancers may never causes symptoms or affect life expectancy or quality of life (although research shows most are harmful and should be treated early)
  • Risks of colonoscopy like bleeding and bowel perforation
  • Lower number of people who die from CRC
  • Lowe number of people who develop the disease
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12
Q

barium Enema

A

Highlight large bowel so it can be seen on an X-Ray. Barium passed into bowel through bottom.

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13
Q

CT Colonscopy

A

Uses CT scanner to produce detailed images of colon and rectum. Large bowel inflated with CO2 in CT so get details of lining of the bowel.

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14
Q

Red flags: for colorectal cancer

A

Blood in stools (bright re spots or dark tar-like stools), rectal bleeding, abdominal pain, bloating or cramps. A persistent feeling you can’t completely empty your bowels.

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15
Q

Site vs symptoms of colorectal cancer

A

Right sided – Larger volumes stools, larger lumen, narrow walls and ponyl get pain when obstructing bowel so less pain in this type. Bleeding usually so anaemia symptoms (fatigue, pale)

Left sided – narrower lumen and thicker walls as water taken out. Cramping abdominal pain, change in bowel habit, maybe bleeding but if foot up the colon it might just be mixed in with stool and don’t notice bleeding.

Rectum – bright red blood, tenesmus (feel like u need ot go to the toilet, get bit of wind and blood and cant relieve the feeling but don’t go due to tumour sitting in rectum imitating stool). Pain on opening bowels when contracting (v late cancer).

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16
Q

Obstructive symptoms

A

With obstructive problems in the bowel they can vomit faecal contents (Faecular vomiting). Can get distended abdomen, resonant and maybe tinkling bowel sounds.

Borborygmus – bowel sounds bowels contracting. If you are obstructed sometimes before complete obstruction you will hear these bowel sounds really really loud.

Can stent the bowel open to push air in.

17
Q

SPIKEs- bad news

A
  • Setting up and starting
  • Perception
  • Invitation
  • Knowledge
  • Emotions
  • Strategy and summary
18
Q

Red flags symptoms colorectal cancer

A
  • Older people, new rectal bleeding
  • Abdominal pain
  • Rigors old age
  • Change in bowel habit.
19
Q

FAP

A
  • Familial Adenomatous Polyposis
  • FAP occurs in 1 in 10,000 people. It is caused by mutations in the APC gene (autosomal dominant)
  • Familial adenomatous polyposis (FAP) is a rare, hereditary condition in which a person develops numerous precancerous polyps (adenomas) in the colon and rectum.
  • Polyps develop in teen years or early 20s.
  • The number of polyps varies from less than 100 to thousands, and with increasing age the polyps get larger and more problematic.
  • Eventually, one or more of these adenomas will become cancerous.
  • Without treatment, patients with FAP have a nearly 100% lifetime risk of colorectal cancer. The chance of developing colorectal cancer increases with age; the average age at which people are diagnosed with cancer is 39.
20
Q

Lynch syndrome

A

Lynch Syndrome

  • Lynch syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC), is the most common cause of hereditary colorectal (colon) cancer.
  • People with Lynch syndrome are more likely to get colorectal cancer and other cancers, and at a younger age (before 50), including
  • Uterine (endometrial),
  • Stomach,
  • Liver,
  • Kidney,
  • Brain, and
  • Certain types of skin cancers.
21
Q

gradign CRC (microscope)

A

Grading – Under microscope:

Grade 1 (low grade)

Cancer cells look similar to normal cells (well differentiated)

Grade 2 (moderate grade)

Cancer cells look more abnormal (moderately differentiated)

Grade 3 (high grade)

Cancer cells look very abnormal (poorly differentiated)

22
Q

Patho CRC

A

Patho:

  • Most common is adenocarcinoma – well or moderately differentiated
  • Other tyeps are mucinous caricnomas and colloid carcinomas
  • In paho report also get – vascular or lymphatic invasion, R0/1/2, TNM, Mutations, MSI or MMR
  • MMR = mismatch repair proteins (MLH1/MSH2/MSH6/PMS2) which keep microsatellite regions of DNA stable and help prevent carcinogenic mutations. If you are MMR proficient you are MSI stable and MMR deficient is MSI instable. MMR proficient you are MSI-low, MMR deficieny hen MSI-high
23
Q

lYNCH SYNDROME

A

Lynch Syndrome;

  • Hereditary non-polyposis colorectal cancer (HNPCC)
  • Most common cause of hereditary colorectal cancer
  • MSH2 and/or MSH6 loss suspicious for Lynch Syndrome
  • Increased risk of lots of cancers
  • Younger age (before 50)
    • Uterine (endometrial)
    • Stomach
    • Liver
    • Kidney
    • Brain
  • Surveillance?
  • 2 yearly colonoscopies, annual endometrial US +-biopsy, 1-2 yearly OGDs (if +ve family history)
24
Q

FAP

A

Familial Adenomatous Polyposis

FAP occurs in 1 in 10,000 people. It is caused by mutations in the APC gene (autosomal dominant)

Familial adenomatous polyposis (FAP) is a rare, hereditary condition in which a person develops numerous precancerous polyps (adenomas) in the colon and rectum.

Polyps develop in teen years or early 20s.

The number of polyps varies from less than 100 to thousands, and with increasing age the polyps get larger and more problematic.

Eventually, one or more of these adenomas will become cancerous.

Without treatment, patients with FAP have a nearly 100% lifetime risk of colorectal cancer. The chance of developing colorectal cancer increases with age; the average age at which people are diagnosed with cancer is 39.