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1B GI cancers Flashcards

1
Q

What are GI tract squamous cell cancers called?

A

Squamous cell carcinoma (SCC)

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2
Q

What are GI tract glandular epithelium cell cancers called?

A

Adenocarcinoma

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3
Q

What are GI tract enteroendocrine cell cancers called?

A

Neuroendocrine tumours (NETs)

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4
Q

What are GI tract interstitial cells of Cajal cancers called?

A

Gastrointestinal stromal tumours (GISTs)

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5
Q

What are GI tract smooth muscle cell cancers called?

A

Leiomyoma/leiomyosarcoma

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6
Q

What are GI tract adipose tissue cell cancers called?

A

Liposarcoma

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7
Q

Which age group does colorectal cancer affect most?

A

> 50 years (more than 90% of cases)

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8
Q

What is lifetime risk for colorectal cancer in men and women?

A
  • 1 in 10 for men
  • 1 in 14 for women
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9
Q

What are the three forms of colorectal cancer?

A
  • Sporadic
  • Familial
  • Hereditary
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10
Q

What are the criteria of sporadic colorectal cancer?

A
  • Absence of family history
  • Older pop
  • Isolated lesion
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11
Q

What are the criteria for familial colorectal cancer?

A
  • Family history
  • Higher risk if index case is young (<50 years) and the relative is close (1st degree)
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12
Q

What are the criteria for hereditary colorectal cancer?

A
  • Family history
  • Younger age of onset
  • Specific gene defects
  • e.g. Familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome)
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13
Q

What is the histopathology (type of cancer) for all colorectalcancers?

A

Adenocarcinoma

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14
Q

Describe the progression of colorectal cancer

A
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15
Q

What does the progression of colorectal cancer mean for people who have 1 polyp?

A
  • They get repeat colonoscopies to check for new polyps developing
  • It’s straightforward to endoscopically take polyps away before they become cancer- prophylactic endoscopic polyp/adenoma resections
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16
Q

What does aspirin do?

A

Protects against the development of the progression of polyps in colorectal cancer

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17
Q

What are the three types of risk factors for colorectal cancer?

A
  • Past history
  • Family history
  • Diet/environmental
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18
Q

What should past history look like for patients with colorectal cancer?

A
  • Colorectal cancer
  • Adenoma (polyps), ulcerative colitis, radiotherapy-treated patients
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19
Q

What should family history include for patients with colorectal cancer?

A
  • 1st degree relative <55 years
  • Relatives with identified genetic predisposition e.g.
    • FAP
    • HNPCC
    • Peutz-Jegher’s syndrome (increases risk of polyp development and cancer)
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20
Q

What are dietary/environmental risk factors for patients with colorectal cancer?

A
  • Smoking
  • Obesity
  • Socioeconomic status
  • Carcinogenic foods
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21
Q

What are the locations of colorectal cancer?

A
  • 2/3 in descending colon (left colon) and rectum
  • 1/2 in sigmoid colon and rectum (i.e. within reach of flexible sigmoidoscopy)
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22
Q

How do caecal and right sided colorectal cancer patients present?

A
  • Iron deficiency anaemia (most common)
  • Change of bowel habit (diarrhoea)
  • Distal ileum obstruction (late sign)
  • Palpable mass (late sign)
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23
Q

How do left sided and sigmoid carcinoma colorectal cancer patients present?

A
  • PR (rectal) bleeding, mucus
  • Thin stool (late sign)
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24
Q

How do rectal carcinoma colorectal cancer patients present?

A
  • PR bleeding, mucus
  • Tenesmus- the feeling of needing to open bowels but nothing comes out when you try
  • Anal, perineal, sacral pain (late sign)
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25
Q

What is a late sign of bowel cancer?

A

Bowel obstruction

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26
Q

What kind of signs show local invasion of colorectal cancer?

A

These are late signs

  • Bladder symptoms
  • Female genital tract symptoms
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27
Q

Where can colorectal cancer metastasise to (late sign) and how can these present?

A
  • Liver (hepatic pain, jaundice)
  • Lung (cough)
  • Regional lymph nodes
  • Peritoneum (Sister Mary Joseph nodule is metastasis in umbilicus- image below)
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28
Q

What are the signs of primary colorectal cancer and how do we find these signs?

A
  • Abdominal mass
  • Abdominal tenderness and distension- large bowel obstruction
  • DRE: most <12cm from dentate line and reached by examining finger
  • Rigid sigmoidoscopy
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29
Q

What are the signs of metastasis and complications?

A
  • Hepatomegaly
  • Monophonic wheeze
  • Bone pain
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30
Q

What investigations are done for colorectal cancer?

A
  • Faecal occult blood
  • Blood tests
  • Colonoscopy
  • CT colonoscopy/colonography
  • MRI pelvis
  • CT chest/abdo/pelvis
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31
Q

What are the two types of faecal occult blood?

A
  • Guaiac test (Haemoccult)- based on pseudoperoxidase activity of haematin
    • 40-80% sensitivity and 98% specificity
    • Dietary restrictions- avoid red meat, melons, horse-radish, vitamin C and NSAIDs for 3 days before test
  • FIT (faecal immunochemical test)- detects minute amounts of blood in faeces (faeces occult blood)
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32
Q

What blood tests are done for colorectal cancer?

A
  • FBC: anaemia, haematinics- low ferritin
  • Tumour markers: CEA (carcinoembryonic antigen) which is useful for monitoring evidence of recurrence but not as a diagnostic tool
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33
Q

What does a colonoscopy do?

A
  • Visualise lesions <5mm
  • Small polyps can be removed- reduced cancer incidence
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34
Q

How can small polyps be removed using colonoscopy?

A

Pedunculated polyp (with a stalk) → we put wire around it and use heat to cut it and to close wound to prevent bleeding

Usually performed under sedation

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35
Q

How does a CT colonoscopy compare with normal colonoscopy?

A
  • Can visualise lesions >5mm
  • No need for sedation
  • Less invasive, better tolerated
  • If lesions identified then patient needs colonoscopy for diagnosis
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36
Q

When is MRI pelvis performed?

A

If you have a tumour that you think is relatively advanced

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37
Q

What is looked at in MRI pelvis?

A
  • Depth of invasion, mesorectal lymph node involvement- to see whether we can do an R0 resection (take all of cancer out with good margin)
  • No bowel prep or sedation required
  • Help choose between preop chemoradiotherapy to reduce tumour size or go straight to surgery
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38
Q

Why is CT chest/abdo/pelvis done for colorectal cancer?

A

Staging prior to treatment to exclude liver or lung metastases

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39
Q

What is the primary management for colorectal cancer?

A

Surgery

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40
Q

What can you do to give yourself time to plan surgery for colorectal cancer?

A

Put a stent in or use radio or chemo

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41
Q

What do you do with a right and transverse colon obstructing carcinoma?

A
  • Usually they don’t obstruct because there’s more leeway for carcinoma to expand
  • If it is obstructing, we can resect and join up straight away with primary anastomosis because blood supply is good so it won’t leak
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42
Q

Why do you have to be more careful with a left sided obstruction?

A

The blood supply on left colon isn’t as good

We can put in a palliative stent

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43
Q

What is a Hartmann’s procedure?

A

Remove the tumour but then instead of joining proximal bowel and rectum, we bring proximal bowel up to skin and do a colostomy (leaving a stoma)- called a proximal end colostomy (LIF)

We can reverse in 6 months if patient is fine

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44
Q

What’s the difference between a stoma on the left or right side of a patient?

A
  • left side means colostomy (large bowel)
  • right side means ileostomy (small bowel)
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45
Q

If patient has left sided obstruction, we can do a primary anastomosis (joining up proximal bowel and rectum). Why is this not the safest?

A
  • We would do an intraoperative bowel lavage with primary anastomosis
  • However there’s a 10% chance of leak because the blood supply isn’t the best
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46
Q

What are the important right sided arteries?

A
  • Ileocolic
  • Right colic
  • Middle colic
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47
Q

What are the important left sided arteries?

A
  • Left colic
  • When we get to pelvis, sigmoid arteries are important
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48
Q

What is a right hemicolectomy?

A

Remove right colon then anastomose terminal ileum to transverse colon

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49
Q

What is an extended right hemicolectomy?

A

Take around 2/3 of large bowel out- right colon and part of transverse

Then do ileocolic anastomosis

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50
Q

What is a left hemicolectomy?

A

Resect left colon then anastomose remaining colon parts

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51
Q

Why is a rectal cancer resection difficult?

A
  • Blood supply around rectum/anus is poor
  • We can do the resection and join up the other parts but then do an ileostomy (bring up loop of small bowel to skin to divert faeces going through delicate anastomosis)
52
Q

How common/lethal is pancreatic cancer?

A
  • Relatively common and highly lethal
  • 4th commonest cause of cancer death
  • UK and USA annual incidence is 100 per mil
53
Q

Who is pancreatic cancer more common in?

A
  • Rare before 45 years, 80% occur between 60-80 years of age
  • Men > women (1.5-2.1)
54
Q

Where in the world is pancreatic cancer more common?

A

Incidence is higher in Western/industrialised countries

55
Q

How is incidence relative to mortality for pancreatic cancer?

A

Incidence and mortality are basically the same

56
Q

What is the commonest form of pancreatic cancer?

A

Pancreatic ductal adenocarcinoma (PDA)

57
Q

When does pancreatic cancer present and how does that affect survival?

A
  • 80-85% have late presentation
  • Overall median survival is <6 months- by the time it starts causing symptoms it’s usually too late
  • 5 year survival is 0.4-5%
58
Q

How resectable is pancreatic cancer?

A
  • 15-20% have resectable disease
  • 5 year survival is 20-25%
  • Virtually all patients dead within 7 years of surgery
59
Q

What are the risk factors for developing pancreatic cancer?

A
  • Chronic pancreatitis (inflammation followed by healing inflammation) → 18 fold increase in risk
  • Cigarette smoking → causes 25-30% PDAs
  • T2DM → relative risk is 1.8
  • Occupation (insecticides, aluminium, nickel and acrylamide)
  • Cholelithiasis, previous gastric surgery and pernicious anaemia- Weak link
  • Diet (increased fat and protein, less fruit and veg, coffee and EtOH)- weak link
  • 7-10% have a family history
    • Relative risk of PDA is increased by 2x if one 1st degree fam member had it, 6x if two had it and 30x if three had it
60
Q

Describe the commonest pathogenesis of pancreatic cancer

A
  • PDAs evolve through non-invasive neoplastic precursor lesions (similar to polyps in colorectal cancer)
  • The PanINs (intraepithelial neoplasms) acquire clonally selected genetic and epigenetic alterations along the way
  • PanINs are microscopic (<5mm diameter) and not visible by pancreatic imaging- usually only see them when examining cut up specimens of someone’s cancer
61
Q

Mutations in which genes are PanIN1 associated with?

A
  • ERBB2
  • KRAS
62
Q

Mutations in which gene is PanIN2 associated with?

A

CDKN2A

63
Q

Mutations in which genes is PanIN3 associated with?

A
  • TP53
  • SMAD4
  • BRCA2
64
Q

Complete the labels

A
65
Q

How does carcinoma of the head of the pancreas present?

A

At least 2/3 of PDAs arise in the head

  • Jaundice
  • Weight loss
  • Pain
  • Acute pancreatitis
  • Persistent vomiting ( in advanced cases, duodenal obstruction)
  • GI bleeding (duodenal invasion or varices secondary to portal or splenic vein occlusion)
66
Q

Why and how does jaundice occur with carcinoma of the head of the pancreas?

A
  • > 90% due to either invasion or compression of CBD
  • Often painless
  • Palpable gallbladder (Courvoisier’s sign)

If the cancer is away from CBD, then the cancer metastasises before going yellow so it’s harder to spot/people present late

67
Q

Why does weight loss occur with carcinoma of the head of the pancreas?

A
  • Anorexia
  • Malabsorption- secondary to exocrine insufficiency
  • Diabetes- some get diagnosed 2 years before pancreatic cancer so it’s a big association
68
Q

Where is the pain in carcinoma of the head of the pancreas?

A
  • 70% at time of diagnosis
  • Happens in epigastrium
  • Radiates to back in 25%
69
Q

What is pain in pancreatic cancer usually a sign of?

A

That the cancer is locally invasive or locally advanced

70
Q

What does back pain usually indicate?

A

Posterior capsule invasion and irresectability

71
Q

How does carcinoma of the body and tail of pancreas present?

A
  • Develop insidiously and are asymptomatic in early stages
  • At diagnosis they’re often more advanced than lesions in head because there’s nothing really to block to show signs
  • Marked weight loss with back pain in 60% of patients
  • Jaundice is uncommon because it’s on the left side away from bile duct
  • Vomiting sometimes occurs at a late stage from invasion of the DJ flexure
  • Most unresectable at time of diagnosis
72
Q

What investigations are done for pancreatic cancer?

A
  • Tumour marker CA19-9
  • Ultrasonography
  • Dual-phase CT
  • MRI
  • MRCP
  • ERCP
  • EUS
73
Q

What concs of tumour marker CA19-9 confer with pancreatic cancer?

A
  • Concs >200 U/ml confer 90% sensitivity
  • Concs in 1000s associated with high specificity
74
Q

What is CA19-9 falsely elevated in ?

A
  • Pancreatitis
  • Hepatic dysfunction
  • Obstructive jaundice
75
Q

What can ultrasonography identify in pancreatic cancer?

A
  • Pancreatic tumours
  • Dilated bile ducts
  • Liver metastases
76
Q

What does dual-phase CT show in pancreatic cancer?

A

Done commonly

  • Accurately predicts resectability in 80-90% of cases
  • Contiguous organ invasion
  • Vascular invasion (coeliac axis and SMA)
  • Distant metastases
77
Q

What does MRI do in pancreatic cancer?

A

Not as useful as CT but detects and predicts resectability with accuracies similar to CT

78
Q

What does MRCP show in pancreatic cancer?

A

Provides ductal images without complications of ERCP

79
Q

What does ERCP show in pancreatic cancer?

A

Most useful

  • Confirms the typical ‘double duct’ sign
  • Aspiration/brushing of the bile-duct system
  • Therapeutic modality → biliary stenting to relieve jaundice
80
Q

Why is EUS used for pancreatic cancer?

A
  • Used when we can’t resect it but want to prove there’s cancer before chemo
  • Highly sensitive in the detection of small tumours- do aspiration of single cells or biopsy
  • Assessing vascular invasion
  • FNA (fine needle aspiration)
81
Q

How do we do HOP resection?

A

Do a Whipple’s resection- remove HOP, distal bile duct and gallbladder, distal stomach and all of duodenum

82
Q

What three things need to be sorted after Whipple’s resection?

A
  • Pancreatic juice has to go somewhere
  • Bile has to go somewhere
  • Stomach has to empty contents somewhere
83
Q

How do we do TOP resection?

A

TOP can just be removed along with spleen because if preserved it’s very likely to have some cancer cells on it

84
Q

What is primary liver cancer- hepatocellular carcinoma (HCC)?

A

Cancer of liver hepatocytes

85
Q

What are two causes of primary liver cancer?

A
  • Cirrhosis due to Hep B, C or alcoholic liver disease
  • Aflatoxin- toxin made by certain fungi
86
Q

What happens to patients if we do nothing about HCC?

A

4-6 months of living

87
Q

What is 5 year survival rate of HCC?

A

<5%

88
Q

What is systemic chemo response rate for HCC?

A

<20% so it’s ineffective

89
Q

What is the optimal Rx (intervention) for HCC?

A
  • Surgical excision with curative intent (5 year survival is >30%)
  • Only 5-15% suitable for surgery
90
Q

What effective options for HCC other than surgical excision are there?

A
  • OLTx- liver transplant- if you have <3 hepatocellular cancers in liver and they’re <3cm you can do this
  • TACE- transarterial chemo embolisation- put small catheters inside blood supply of tumour, giving high chemo dose then embolising (blocking) the blood supply
  • RFA- radiofrequency ablation- stick a needle into tumour and burn it
91
Q

Where does cholangiocarcinoma (ChCA) most often occur?

A

Bifurcation where common hepatic duct goes right and left- are small tumours but big operation to take it away

92
Q

Other than CHD bifurcation, where else can you find ChCA?

A
  • You get distal ChCA through HOP for which you need Whipple’s resection
  • You can get it them at periphery for which you need to take away that bit of liver
93
Q

What is the aetiology of ChCA?

A
  • Primary Sclerosing Cholangitis & UC
  • Choledochal cyst
  • Associated with liver fluke (clonorchis sinesis) in Asia- comes from uncooked fish- worms inhabit bile ducts, cause irritation and cancer
94
Q

What is the median survival of ChCA without Rx?

A

<6 months

95
Q

What is 5 year survival rate of ChCA?

A

<5%

96
Q

How effective is systemic chemo for ChCA?

A

Ineffective although it’s improving- currently median survival is 11.7 months

97
Q

What is effective treatment for ChCA?

A
  • Optimal Rx is surgical excision with curative intent
  • 5 year survival is 20-40%
  • Only 20-30% suitable for surgery
98
Q

How does gallbladder cancer (GB CA) usually show itself?

A

GB CA spreads very quickly everywhere but doesn’t cause problems

99
Q

What is the aetiology of GB CA?

A

Unknown

  • It’s associated with gallstones
  • Porcelain GB occurs- chronic inflammation in gall bladder causes calcification so it looks like porcelain
  • Associated also with chronic typhoid infection
  • All 3 of the above are long term inflammation
100
Q

What is the median survival of GB CA without Rx?

A

5-8 months

101
Q

Is systemic chemo effective for GB CA?

A

No

102
Q

What are effective Rx options for GB CA?

A
  • Only surgical excision with curative intent
  • 5 year survival at:
    • Stage II: 64%
    • Stage III: 44%
    • Stage IV: 8%

Only <15% suitable for surgery

103
Q

What happens in stage II GB CA?

A
  • Transmural invasion of cancer- going through mucosa to muscle
  • We can take away a bit of the liver and lymph nodes
  • If we do nothing, 64% die
104
Q

What happens at Stage III GB CA?

A

Beginning to invade liver

105
Q

What happens at stage IV GB CA?

A

Invading liver >2cm and there’s distal metastases

106
Q

How does colorectal cancer (CRC) affect liver?

A

Through metastases

107
Q

What is the median survival of CRC without Rx?

A

Less than a year

108
Q

What is 5 year survival of CRC?

A

0%

109
Q

What are effective Rx of CRC?

A
  • Systemic chemo is improving
  • Other effective Rx options (RFA and SIRT)
  • Most effective is surgical excision with curative intent
    • 5 year survival raves of 25-50%
    • Only 25% is suitable for surgery
110
Q

How is HCC resection done?

A

Take away that bit of liver and try not to take much else

111
Q

How is ChCA resection done?

A

Take away a whole half of the liver for something only 1cm

112
Q

How is GB CA resection done?

A

Take away GB, bit of liver and lymph nodes

113
Q

What are NETs?

A

Neuroendocrine Tumours

  • Arise from the gastroenteropancreatic (GEP) tract (or bronchopulmonary system)
    • Diverse group of tumours
    • Regarded as common entity as arise from secretory cells of the neuroendocrine system
114
Q

What type of tumours are seen in NETs?

A

Sporadic tumours in 75%

115
Q

What are NETs associated with?

A

Associated with a genetic syndrome in 25%, in particularly Multiple Endocrine Neoplasia Type 1 (MEN1)

  • Parathyroid tumours
  • Pancreatic tumours
  • Pituitary tumours
116
Q

Describe the presentation of NETs

A
  • Most NETs are asymptomatic & incidental findings
  • Secretion of hormones & their metabolites in 40%
    serotonin, tachykinins (substance P) & other vasoactive peptides
  • < 10% of NETs produce symptoms
  • Can result in a variety of debilitating effects (Carcinoid syndrome)
117
Q

What is carcinoid syndrome?

A
  • Vasodilatation
  • Bronchoconstriction
  • ↑ed intestinal motility
  • Endocardial fibrosis (PR & TR)
118
Q

What are the clinical features of pancreatic NETs and what cell type does it affect?

A

Insulinoma
- Hypoglycaemia
- Whipple’s triad
- beta cells

Glucagonoma
- Diabetes mellitus
- Necrolytic migratory erythema
- alpha cells

119
Q

What are the clinical features of pancreatic, duodenal NETs and what cell types do they effect?

A

Gastrinoma
- Zollingere-Ellison syndrome
- G cells

120
Q

What are the clinical features of NETs affecting the entire GIT and what cell types do they effect?

A

VIPoma
- Verner-Morrison syndrome
- Watery diarrhoea
- VIP cells

Somatostatinoma
- Gallstones
- DM
- Steatorrhoea
- D cells

121
Q

What are the clinical features of midgut NETs?

A

Most are non-functioning, 40% develop carcinoid syndrome

122
Q

What are the clinical features of hindgut NETs?

A

Usually non-functioning

123
Q

What investigations are done to diagnose NETs?

A

When suspected, investigations are done to localise the tumour and histology is done to confirm the diagnosis

There is a biochemical assessment and imaging

124
Q

What biochemical assessments are done to diagnose NETs?

A
  • Chromogranin A is a secretory product of NETs
  • Other gut hormones: insulin, gastrin, somatostatin, PPY
    • Measured in fasting state
  • Other screening: Calcium, PTH, prolactin, GH
  • 24 hr urinary 5-HIAA (serotonin metabolite)
125
Q

What imaging is done to diagnose NETs?

A
  • Cross-sectional imaging (CT and/or MRI)
  • Bowel imaging (endoscopy, barium follow through, capsule endoscopy)
  • Endoscopic ultrasound
  • Somatostatin receptor scintigraphy
    • 68Ga-DOTATATE PET/CT most sensitive
126
Q

What is the grading system for GEP-NETs?

A
127
Q

What are treatment modalities for NETs?

A

gastro (7 decks)

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