Lecture 10.1: Common Gastrointestinal Malignancies Flashcards

1
Q

How to Approach Tumours at any Site?

A
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2
Q

What is Barrett’s Oesophagus?

A
  • Dysplasia of cells in oesophagus (can be seen via
    hyperchromatic nuclei)
  • Columnar lined oesophagus instead of squamous
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3
Q

Why does Barrett’s Oesophagus occur?

A

As a result of Gastro-oesophageal reflux disease(GORD)

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4
Q

What is the complication associated with Barrett’s Oesophagus?

A

Increased incidence of adenocarcinoma compared to general populus

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5
Q

What is the common type of malignancy in the oesophagus? (1 overall, 2 subtypes)

A

Oesophageal Carcinoma:
* Adenocarcinoma
* Squamous Cell Carcinoma

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6
Q

What the other type of malignant tumours can be found in the oesophagus? (3)

A
  • Lymphomas
  • Melanomas
  • Sarcomas
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7
Q

Where is Squamous Cell Carcinoma Oesophageal Cancer more commonly found?

A

Highest incidence seen in Asian oesophageal cancer belt (Turkey to Iran, Iraq and Khazakhistan to northern China)

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8
Q

Where is Adenocarcinoma Oesophageal Cancer more commonly found?

A

Increasing incidence in USA, UK and Europe

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9
Q

What Risk Factors of Squamous Cell Carcinoma Oesophageal Cancer? (8)

A
  • Alcohol
  • Tobacco
  • Hot Drinks (tea)
  • Less intake of fruits and vegetables
  • Infections/Viruses (HPV)
  • Genetic Factors
  • Plummer Vinson Syndrome
  • Associated with other head and neck malignancies
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10
Q

What Risk Factors of Adenocarcinoma Oesophageal Cancer? (7)

A
  • GORD
  • Obesity
  • Smoking/Alcohol (lesser degree)
  • Genetic Factors
  • Zollinger Ellison Syndrome (too much gastric acid)
  • Achalasia
  • Scleroderma
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11
Q

What part of the Oesophagus is Adenocarcinoma found?

A

Distal Third

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12
Q

What part of the Oesophagus is Squamous Cell Carcinoma found?

A
  • Rare in upper third
  • Most common in the middle third
  • Less frequent in lower third
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13
Q

Gross Appearance of Squamous Cell Carcinoma Oesophageal Cancer? (3)

A
  • Exophytic
  • Ulcerating Infiltrating
  • Stricture
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14
Q

Gross Appearance of Adenocarcinoma Oesophageal Cancer? (3)

A
  • Mostly ulcerating
  • Stricturing
  • Less likely to exophytic
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15
Q

How does a patient with Squamous Cell Carcinoma Oesophageal Cancer present? (2)

A
  • Dysphagia
  • Weight Loss
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16
Q

How does a patient with Adenocarcinoma Oesophageal Cancer present? (6)

A
  • Long history of Dyspepsia
  • Dysphagia
  • Weight Loss
  • Vomiting
  • Anaemia
  • Bleeding
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17
Q

Investigations for Oesophageal Cancers?

A
  • Barium swallow
  • Endoscopy
  • Endoscopic Ultrasound (EUS)
  • Staging purposes- CT, PET CT
  • Biopsy
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18
Q

What is the 5 yr survival rate of early mucosa confined oesophageal tumours?

A

SCC: 70%
Adeno Ca: 80 -100%

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19
Q

Survival rates of oesophageal tumours when they invades the muscularis propria?

A

SCC: 50%
Adeno Ca: 10-20%

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20
Q

Treatments for Oesophageal Cancer (7)

A
  • Oesophagectomy
  • Endoscopic mucosal resection (EMR) and radioablation
    for mucosa confined tumours
  • Neoadjuvant chemoradiotherapy
  • Adjuvant chemotherapy for metastatic disease –
    targeted treatments (trials), Her2 guiding treatment in
    adenocarcinomas
  • Stenting to enable swallowing
  • Palliative brachytherapy and radiotherapy
  • Radiotherapy
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21
Q

What percentage of cancers worldwide does Gastric Cancer account for?

A

10%

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22
Q

What percentage of gastric cancers occur in patients before 45 years? Why?

A
  • <10%
  • Germline mutations of e-cadherin and also associated
    with Helicobacter pylori infection
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23
Q

What part of stomach does cancer most commonly occur in?

A
  • Most common site in the cardia
  • Much smaller proportions in the pyloric antrum and
    body of the stomach
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24
Q

Risk Factors for Gastric Cancer (8)

A
  • Infection (H.pylori, EBV)
  • Pernicious Anaemia
  • Autoimmune Gastritis
  • Gastric Ulcers
  • Previous Gastric Surgery
  • Low intake of fresh fruit and vegetables and high
    intake of salt preserved foods or smoked foods (N-
    nitroso compounds and benzopyrene)
  • Smoking
  • Genetic factors
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25
Q

How can H.pylori can lead to development of gastric
carcinoma?

A
  • Produces urease which converts urea into ammonia
    which neutralises stomach acid
  • Allow bacteria to proliferate
  • Adheres to gastric mucosa epithelial cells via the outer
    membrane protein and injects CagA into host cells
  • This causes Chronic Inflammation
  • Leads to gastritis
  • Leads to dysplasia
  • Leads to neoplasia
  • Carcinoma
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26
Q

What are Macroscopic Features of Gastric Cancer? (3)

A
  • Fungating
  • Ulcerating
  • Infiltrative (linitis plastica)
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27
Q

What are Microscopic Features of Gastric Cancer? (2)

A
  • Intestinal variable degree of gland formation
    (commonly associated with H pylori)
  • Diffuse single cells and small groups, signet ring cells
    (common in younger age group and EBV infection)
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28
Q

Symptoms of Gastric Cancer (4)

A
  • Symptoms often Vague
  • Epigastric Pain
  • Vomiting
  • Weight Loss
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29
Q

Investigations for Gastric Cancer (3)

A
  • Endoscopy
  • Biopsy
  • Barium Studies
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30
Q

What is the 5-year survival rate for Gastric Cancer that is confined to mucosa/sub-mucosa?

A

65%

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31
Q

What is the 5-year survival rate for late Gastric Cancer?

A
  • 10%
  • But with curative surgery 50%
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32
Q

Where does Gastric Cancer commonly spread? (4)

A
  • Adjacent Organs (pancreas, liver, spleen, transverse
    colon, greater omentum)
  • Lymphatic Spread (supraclavicular lymph node
    involvement- Virchow’s node)
  • Haematogenous Spread (liver, lung, peritoneum,
    adrenals, ovary)
  • Transcoelomic (peritoneum, ovaries [Krukenberg
    tumours])
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33
Q

Treatment of Gastric Cancer (3)

A
  • Surgery
  • Chemotherapy
  • Herceptin
34
Q

What infection is Gastric Lymphoma (MALT Lymphoma) strongly associated with?

A
  • Strong association with H. pylori
  • Eradication of H. pylori may lead to regression of
    tumour
35
Q

Where are Gastrointestinal Stromal Tumours derived from?

A

Interstitial Cells of Cajal

36
Q

Gastrointestinal Stromal Tumours are uncommon, but where are they most commonly found (percentages)? (3)

A
  • 60% Stomach
  • 30% Small Intestine
  • 10% Other
37
Q

How are Gastrointestinal Stromal Tumours Treated?

A

Specific Targeted Treatment: Imatinib

38
Q

What protien/oncogene is found on the surface of Gastrointestinal Stromal Tumours?

A
  • C-KIT
  • CD117
39
Q

Gastrointestinal Stromal Tumours are unpredictable, what factors can be used to predict the Behaviour of these lesions? (4)

A
  • Site
  • Size
  • Mitoses
  • Necrosis
40
Q

What Type of Malignancies are found in the Small Intestine?

A
  • Lymphomas
  • Neuroendocrine Tumours
  • GIST are tumours that are encountered in this site and
    have a higher risk of malignancy
41
Q

Where in the Body do Neuroendocrine Tumours occur?

A

70% in GI Tract

42
Q

Where in the GI Tract do Neuroendocrine Tumours occur? (5)

A
  • Small Intestine(38%)
  • Rectum (34%)
  • Colon (16%)
  • Stomach (10%)
  • Rare in the Oesophagus and Anus
43
Q

Clinical Presentation of Small Intestine Cancers (6)

A
  • Incidental finding during evaluation of non specific
    symptoms
  • Symptoms due to local mass effect
  • Symptoms due to substances secreted by tumour
  • Symptoms as a result of tumour fibrosis
  • Primary tumour can be silent and present later with
    metastasis
  • Carcinoid Syndrome
44
Q

What is Carcinoid Syndrome?

A
  • Occurs when a carcinoid tumour secretes certain
    chemicals into your bloodstream
  • Cutaneous Flushing
  • Diarrhoea
  • Restrictive Cardiomyopathy
45
Q

3 Stages of Evolving Cancer

A

1) Initiation
2) Promotion
3) Progression

46
Q

What Cancers are found in the Large Intestine? (2)

A
  • Adenomas
  • Adenocarcinoma
47
Q

What is Familial Adenomatous Polyposis? (4)

A
  • Autosomal Dominant
  • Chromosome 5
  • Thousands of adenomas by 20 yrs
  • High risk of cancer
48
Q

What is Lynch Syndrome?

A
  • Also known as hereditary non-polyposis colorectal
    cancer (HNPCC)
  • Is the most common cause of hereditary colorectal
    (colon) cancer
  • R-sided colonic tumours
49
Q

What is Gardner’s Syndrome?

A
  • Phenotypic variant of familial adenomatous polyposis.
  • Autosomal Dominant
  • Characterised by numerous adenomatous polyps
    lining the intestinal mucosal surface with a high
    potential for malignancy
  • Bone and Soft Tissue Tumours
50
Q

Are Adenomas Cancerous?

A

No they are Premalignant

51
Q

What are the Types of Adenomas? (3)

A
  • Tubular adenoma
  • Tubulovillous adenoma (>20% villous)
  • Villous adenoma (> 80% villous)- high risk of
    malignancy
52
Q

What is Risk of Malignancy (carcinoma arising within a polyp) based on? (4)

A
  • Type
  • Dysplasia (Malignancy rate increases to 27% if high
    grade dysplasia)
  • Polyp size (Polyps>20mm higher incidence of invasive
    carcinomas 35% to 53%)
  • Number of polyps
53
Q

Who is the Bowel Cancer Screening (2006) aimed at?

A
  • 60-69 year old men and women
  • Phased out to 70-75 (2010)
  • From April 2021 start rolling out to >50 years
54
Q

What test is used in Bowel Cancer Screening?

A
  • Faecal Occult Blood
  • FIT(Faecal Immunochemical Testing)
55
Q

Who is the Bowel Scope Screening Programme aimed at?

A

Men and Women aged 55
BUT THIS IS DISCONTINUED FROM APRIL 2020

56
Q

What test is used in the Bowel Scope Screening Programme?

A

Flexible Sigmoidoscopy
BUT THIS IS DISCONTINUED FROM APRIL 2020

57
Q

How common are Colorectal Adenocarcinomas?

A

Fourth most common cancer with respect to incidence in developed countries (2018)

58
Q

Is Rectal Cancer more common in men or women?

A

Men

59
Q

What percentage of of colon cancers are hereditary?

A

5-10%

60
Q

How aggressive is Colorectal Adenocarcinoma?

A
  • Disease has slow progression
  • 20% present at A&E
  • 55% not diagnosed until disease has spread to lymph
    nodes or elsewhere
61
Q

Risk Factors for Colorectal Adenocarcinoma (4)

A
  • Low residue diet
  • Slow transit time
  • High fat intake
  • Genetic predisposition
62
Q

Investigations for Colorectal Adenocarcinoma (6)

A
  • Blood Tests (CEA marker, FBC, LTFs)
  • Colonic Examination
  • Colonoscopy with Biopsy
  • CT Colonography
  • Barium Enema
  • Radiology
63
Q

What parts of the Large Intestine does Colorectal Adenocarcinoma occur (percentages)?

A
  • About 50% occur in rectum
  • 30% in sigmoid colon
  • Rest are equally distributed in other parts of colon
64
Q

How do Rectal Lesions in Colorectal Carcinoma present?

A

Ulceration present as rectal bleeding

65
Q

How do Left Sided Lesions in Colorectal Carcinoma present?

A

Stenosing lesions and as such present with obstruction (alteration of bowel habit colicky abdominal pain)
relatively early

66
Q

How do Right Sided Tumours in Colorectal Carcinoma present?

A
  • Polypoidal and fungating
  • Present as anaemia due to recurrent occult bleeding
  • Often late presentation (due to more distensibility of
    the right side and the fluid nature of the faeces)
67
Q

Macroscopic Characteristics of Colorectal Adenocarcinoma (3)

A
  • 60-70% rectosigmoid
  • Fungating (esp right side)
  • Stenotic (esp left side)
68
Q

Microscopic Characteristics of Colorectal Adenocarcinoma (3)

A
  • Adenocarcinoma
  • Mucinous (often right sided tumours and associated
    with microsastellite instability)
  • Signet Ring Cell Type
69
Q

How can Colorectal Adenocarcinomas spread? (3 routes)

A
  • Direct through bowel wall to adjacent organs
  • Via lymphatics to mesenteric lymph nodes
  • Via blood stream – liver, lung
70
Q

What used to be used instead of TNM to Stage Colorectal Adenocarcinoma?

A

Dukes’ Staging

71
Q

Colorectal Cancer Staging (T1-T4)

A

T1: Cancer is no deeper than submucosa
T2: Cancer is no deeper than muscularis propria
T3: Cancer is no deeper than subserosa
T4: Cancer has spread outside of the serosa

72
Q

Involvement of muscularis propria in Colorectal Cancer increases risk of metastasis by …?

A

12%

73
Q

Percentage of 5-year survival if 1 lymph node invaded in Colorectal Cancer?

A

63.6%

74
Q

Percentage of 5-year survival if 2-5 lymph nodes invaded in Colorectal Cancer?

A

36.1%

75
Q

Percentage of 5-year survival if 6-10 lymph nodes invaded in Colorectal Cancer?

A

21.9%

76
Q

Percentage of 5-year survival if >10 lymph nodes invaded in Colorectal Cancer?

A

2.1%

77
Q

Management of Colorectal Cancer (7)

A
  • Surgical resection with curative intent
  • +/- Neoadjuvanttherapy in rectal tumours
  • Stenting in obstructive tumours in a palliative setting
  • Palliative chemotherapy and surgery
  • Metatstectomy-liver and lung resections
  • Post operative chemoradiotherapy
  • Targeted therapy
78
Q

Targeted Therapy/Personalised Medicine for Colorectal Adenocarcinoma

A
  • Kras
  • Mismatch Repair Genes
79
Q

Why Kras relevant?

A
  • When there is metastatic colorectal disease, if
    the patient has a mutated form of Kras the patient
    does NOT respond to EGFR inhibitors such as
    cetuximab, and other forms of treatment are
    required
  • However, if the patient has the “wild type Kras” EGFR
    treatment is an option
80
Q

Why are Mismatch Repair Protein’s (MRRP’s) relevant?

A
  • Because in MSI (Microsatellite Instability) CRC there is
    a loss of MMR proteins
  • This means MSI CRC do not respond to 5FU based
    chemotherapy
  • But responds to specific forms of immunotherapy
  • This knowledge can help improve prognosis/outcomes