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Gastrointestinal pathophysiology > Cancer of the GI tract > Flashcards

Cancer of the GI tract Flashcards

1
Q

Which staging system is used for bowel cancer?

A

Dukes’ staging

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2
Q

Where are the main areas of interest in the GI tract for cancer?

A
  1. Oesophagus
  2. Stomach
  3. Pancreas
  4. Colon and rectum
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3
Q

Symptoms of GI tract cancer

A
  1. Insidious onset - Often discovered at advanced stage
  2. Bleeding - Overt, occult (–> anaemia)
  3. Pain - Tubular blockage, tumour invasion
  4. Alteration of flow - Constipation, diarrhoea, dysphagia
  5. Weight loss - At advanced stages
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4
Q

Most tumours of the GI tract are adenocarcinomas, true or false?

A

True

- This means they are glandular

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5
Q

How do cancers of the GI tract spread?

A
  1. Local spread
  2. Intramural
  3. Nodal
  4. Blood born (usually to liver or lungs)
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6
Q

Aetiology of GI tract cancer

A
  • Usually multi-factoral
  • Genetic
  • Dietary
  • Environmental
  • Chemical (smoking, alcohol)
  • Inflammation - Oesophagus (Barrett oesophagus), stomach (H. pylori)
  • Usually middle/older age
  • Slight male predominance (except familial conditions like APC and HNPCC)
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7
Q

Aetiology of oesophageal cancer: squamous cell carcinomas

A
  • Alcohol and tobacco
  • Poverty
  • Caustic injury, very hot beverages, radiation to mediastinum
  • Diet deficient in fruit and vegetables
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8
Q

Prevalence of oesophageal cancer: squamous cell carcinomas

A

Higher rates in: Iran, China, Brazil and South Africa

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9
Q

Aetiology of oesophageal cancer: adenocarcinomas

A

 - Less frequent (but on the rise), higher rates in Western countries
 - Most arise from Barrett oesophagus

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10
Q

Clinical features of oesophageal cancer

A
  • Usually elderly patients (70+)
  • Insidious onset with dysphagia, odynophagia
  • Progressive weight loss
  • Haematemesis (-> anaemia)
  • Usually already spread (loco-regional) when symptomatic
  • Requires major surgery (high risks)
  • RT and CT widely used
  • Very poor 5-year survival (20% or less)
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11
Q

Clinical features of oesophageal cancer

A
  • Usually elderly patients (70+)
  • Insidious onset with dysphagia, odynophagia
  • Progressive weight loss
  • Haematemesis (-> anaemia)
  • Usually already spread (loco-regional) when symptomatic
  • Requires major surgery (high risks)
  • RT and CT widely used
  • Very poor 5-year survival (20% or less)
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12
Q

What is Barrett’s oesophagus?

A

Barrett’s oesophagus is a condition in which the stratified squamous epithelium of oesophagus becomes damaged by acid reflux, which causes the lining to be replaced by the columnar epithelium type of the stomach (metaplasia), it also thickens and become red

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13
Q

Causes of chronic GERD?

A 
Obesity
Alcohol
Tobacco
Hiatal hernia
- Some medicines can cause GERD or make it worse: benzodiazepines, calcium channel blockers, NSAIDs
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14
Q

Symptoms of GERD

A
  1. A burning sensation in your chest (heartburn), usually after eating, which might be worse at night.
  2. Chest pain.
  3. Difficulty swallowing.
  4. Regurgitation of food or sour liquid.
  5. Sensation of a lump in your throat.
  6. Nausea
  7. Chronic cough or hoarseness
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15
Q

What is the main cause of Barrett’s oesophagus?

A

Chronic GERD

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16
Q

How does Barrett’s oesophagus become an adenocarcinoma?

A
  • It already has metaplasia due to displacement of the stratified squamous epithelium by the columnar epithelium due to GERD
  • Then there is further dysplasia from this which leads to the development of an adenocarcinoma
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17
Q

What are the different types of gastric cancer?

A
  1. Intestinal type - Bulky or ulcerative with glandular structure
    - Precursor lesions (adenoma)
    - Pathogenesis - Increased Wnt signalling (decrease APC, increase beta-
    catenin)
  2. Diffuse infiltrative type - Permeates stomach wall, causes desmoplastic reactions (linitis plastica - leather bottle)
    - No precursor lesions
    - Pathogenesis - Key step is loss of E-cadherin (CDH1)
18
Q

Epidemiology of gastric cancer

A
  • Marked variation of incidence (Eastern Europe>north Europe), high frequency in Japan
  • More common in lower socioeconomic groups
  • Bonaparte (familial gastric cancer)
19
Q

Why is gastric cancer becoming less common in western countries?

A
  1. Decreased H. pylori prevalence

2. Decreased salt and smoking for food conservation

20
Q

Clinical features of gastric cancer

- Incl. where it spreads to

A
  1. Patients usually in their 50-60s
  2. Early - Resemble chronic gastritis and peptic ulcer (dyspepsia, dysphagia, nausea)
  3. Advanced - Weight loss, anorexia, early satiety, haemorrhage (-> anaemia)
  4. Often discovered at advanced stage
  5. Spreads locally - Duodenum, pancreas, retroperitoneum
  6. Requires resection when possible
  7. RT/CT also used
  8. Poor 5-year survival (30% or less)
21
Q

What are the 4 leading causes of cancer deaths?

A
  1. Lung
  2. Colon
  3. Breast
  4. Pancreatic
22
Q

What is the strongest risk factor for pancreatic cancer?

A

Smoking

23
Q

Pathogenesis of pancreatic cancer

A
  • Arises from precursor lesions (intraepithelial neoplasia)
  • Oncogene KRAS altered in 90-95% cases
  • Tumour suppressor CDKN2A inactivated in 95% of cases
24
Q

Clinical features of pancreatic cancer

A
  1. Silent until it invades adjacent structures
  2. Highly invasive
  3. Brief progressive clinic course
  4. Pain usually the first symptom
  5. Obstructive jaundice (courvoisier’s sign) - Painless jaundice is always pancreatic cancer until proved otherwise
  6. Weight loss, anorexia (when advanced)
  7. Migratory thrombophlebitis (Trousseau’s sign of malignancy)
  8. Surgery (whipples) is the only option but only possible in <10% cases
25
Q

Survival rates for pancreatic cancer

A

<5%

26
Q

Where does colorectal cancer have the highest incidence and why?

A

Western countries

  • Lifestyle
  • Diet poor in vegetable fibre
  • Diet high in refined carbs and fat
27
Q

What does colorectal cancer usually begin as?

A

Usually stars as a benign polyp 3-5 years earlier (suitable for screening, polyp-cancer sequence is well characterised)

28
Q

What does colorectal cancer usually begin as?

A

Usually stars as a benign polyp 3-5 years earlier (suitable for screening, polyp-cancer sequence is well characterised)

29
Q

Clinical features of colonic adenomas (neoplastic polyps)?

A
  • Sporadic
  • Familial - FAP (familial adenomatous polyposis): Associated to APC gene, less frequently DNA mismatch repair genes
  • Most clinically silent (unless large)
  • Majority do not progress into adenocarcinoma
  • Size correlates with risk of malignancy
  • Surveillance (colonoscopy) recommended >50 years, especially if there is a family history
30
Q

Prevalence of colonic adenomas

A

Present in 30% western adults >60 years

31
Q

Pathogenesis of adenocarcinomas

A
  1. Sporadic - 80% Wnt pathway, 20% DNA mismatch repair genes
  2. Familial - HNPC (hereditary non-polyposis colorectal cancer, Lynch syndrome):
    - Associated to DNA mismatch repair genes
32
Q

What are Familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC)?

A

Familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC) are two syndromes of colorectal cancer predisposition, inherited in an autosomal dominant fashion. They account for about 1% and 5-7% of all colorectal cancer cases, respectively.

33
Q

Clinical manifestation of colorectal cancer

A
  1. 20% present as emergency intestinal obstruction - Colicky abdominal pain, abdominal distension, vomiting, absolute constipation
  2. Commonest with solid faeces passing through narrow bore lumen - Sigmoid colon, ileocaecal valve
    - Less common with liquid faeces or side lumen (unless advanced) - Ascending colon and rectum
  3. Alteration in bowel habits - More frequent that usual, sometimes constipation, feeling of incomplete evacuation (tenesmus), main point is a change that persists, may have associated abdominal cramps
  4. Bleeding - Dark red, mixed with stool, persists over weeks/months, may not be all the time, may present as silent anaemia (classically from right sided cancer)
34
Q

What are the genes associated with FAP and HNPCC?

A

FAP = APC gene

HNPCC AKA Lynch syndrome = MMR gene

35
Q

The underlying cause of iron deficiency in older men or postmenopausal females is what until proven otherwise?

A

GI cancer

36
Q

Clinical presentation of rectal cancer

A
  1. Usually produces visible bleeding or mucous
  2. Often palpable on digital rectal examination
  3. Tenesmus is a classic symptom
  4. Pain -> poor prognosis
  5. Reasons for no PR - No anus or no finger
37
Q

Treatment of colorectal cancer

A
  • Surgery is the only curative option
  • Adjucant RT and CT widely used - RT common in treating rectal cancer
  • Antibody therapy now used
38
Q

Prognosis of colorectal cancer

A

Outcome is totally stage dependent

  1. Stage A - >95% cure
  2. Stage D - <5% alive at 5 years
  3. Overall 50% 5 year survival rate
39
Q

Main cause of death of colorectal death is tumour spread, to which organ does this most commonly spread to?

A

The liver

40
Q

Explain the Dukes’ staging for colorectal cancer, with survival rates

A

A: Tumour confined to the mucosa = 90-95% survival

B1: Tumour growth into muscularis propria = 75-80%

B2: Tumour growth through muscularis propria and serosa (full thickness) = 60% survival

C1: Tumour spread to 1-4 regional lymph nodes = 25-30% survival

C2: Tumour spread to more than 4 regional lymph nodes = 25-30% survival

D: Distant metastases (liver, lung, bones) = <1% survival

Gastrointestinal pathophysiology (22 decks)

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