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!!!!! BRS YR2 !!!!! > Gastro - GI Cancers > Flashcards

Gastro - GI Cancers Flashcards

1
Q

What is a cancer?

A

disease caused by an uncontrolled division of abnormal cells in a part of the body

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2
Q

What is a primary cancer?

A

arises directly from the cells of an organ

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3
Q

What is a secondary / metastasis cancer?

A

spread to another organ, directly or by other means (lymph, blood)

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4
Q

What are 6 biological capabilities acquired by tumours?

A

→ resisting cell death
→ sustaining proliferative signalling
→ evading growth supression
→ inducing angiogensis
→ enabling replicative immortality
→ activating invasion + metastasis

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5
Q

What are emerging hallmarks of cancer?

A

→ deregulating cellular energetics
→ avoiding immune destruction

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6
Q

What are the enabling characteristics of cancer?

A

→ genome instability
→ tumour-promoting inflammation

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7
Q

What are the epithelial cells of the GI tract?

A

squamous “glandular” epithelium

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8
Q

What are the epithelial cell cancers of the GI tract?

A

→ SCC (squamous cell carcinoma)
→ Adenocarcinoma

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9
Q

What are the neuroendocrine cells of the GI tract?

A

→ enteroendocrine cells
→ interstitial cells of Cajal

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10
Q

What are the neuroendocrine cancers of the GI tract?

A

→ NETs (neuroendocrine tumours)
→ GISTs (Gastrointestinal Stromal Tumours)

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11
Q

What are some of the connective tissues of the GI tract?

A

→ smooth muscle
→ adipose tissue

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12
Q

What are the connective tissue cancers of the GI tract?

A

→ leiomyoma / leiomyosarcomas
→ liposarcomas

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13
Q

What are the 2 main types of oesophageal cancers?

A

→ SCCs
→ Adenocarcinomas

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14
Q

What do SCCs in the oesophagus develop from?

A

from normal oesophageal squamous epithelium

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15
Q

Where in the oesophagus do SCCs occur?

A

upper 2/3

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16
Q

What GI pathways are oesophageal SCCs related to?

A

acetaldehyde pathway :
→ when alcohol is metabolised, acetaldehyde is produced
→ acetaldehyde = carcinogen

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17
Q

Where are SCCs of the oesophagus more common?

A

in the less developed world

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18
Q

What do oesophageal adenocarcinomas develop from?

A

metaplastic columnar epithelium

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19
Q

What part of the oesophagus does adenocarcinoma affect?

A

lower 1/3

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20
Q

What GI process or pathways are oesophageal adenocarcinomas related to?

A

related to acid reflux, GORD, etc.

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21
Q

Where are adenocarcinomas of the oesophagus more common?

A

more developed world

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22
Q

What is the progression pathway from acid reflux to cancer?

A

→ oesophagitis, GORD
→ Barret’s Oesophagus
→ low grade dysplasia
→ high grade dysplasia
→ adenocarcinoma

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23
Q

What is oesophagitis? What percentage of UK population have it?

A

→ inflammation of the oesophagus
→ 30% of UK population

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24
Q

What is Barret’s oesophagus? What percentage of the GORD population progress to Barret’s?

A

→ metaplasia of the oesophagus
→ 5% of GORD population

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25
Q

What percentage of Barret’s population have a lifetime risk of cancer?

A

0.5%-1% a year

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26
Q

What is the Barret’s surveillance guideline for no dysplasia?

A

survey every 2-3 years

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27
Q

What is the Barret’s surveillance guideline for low grade dysplasia?

A

survey every 6 months

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28
Q

What is the Barret’s surveillance guideline for high grade dysplasia?

A

intervention is necessary

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29
Q

How common are oesophageal cancers?

A

9th most common

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30
Q

What demographic of people do oesophageal cancers mainly affect?

A

→ affects the elderly
→ M : F, 10 : 1

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31
Q

What are the main presenting factors for oesophageal cancers?

A

dysphagia + weight loss

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32
Q

When do symptoms for oesophageal cancer mainly present?

A

late presentation

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33
Q

What is the prognosis of oesophageal cancers?

A

→ 65% palliative care
→ high morbidity
→ complex surgery
→ poor 5-year survival <20%
→ palliation - difficult

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34
Q

What is involved in diagnosis of oesophageal cancer?

A

→ endoscopy (biopsy)
→ staging
→ CT scan
→ laparoscopy
→ endoscopy ultrasound scan (looks outside the lumen)
→ PET scan (important for adenocarcinomas)

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35
Q

What is the treatment plan for SCCs?

A

→ radiotherapy
→ usually very effective
→ not many need surgery after radiotherapy

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36
Q

What is the treatment plan for Adenocarcinomas?

A

→ Neo-adjuvant chemotherapy for all
→ then restaging, then consideration of radical surgery with curative intent

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37
Q

What is the treatment plan for palliative oesophageal cancers?

A

→ palliative
→ chemotherapy
→ DXT = radiotherapy
→ stent to keep oesophagus patent

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38
Q

*What is the process of an oesophagectomy?

A

2-stage Ivor Lewis approach:
→ open abdomen to remove upper part of stomach
→ open chest to remove lower part of oesophagus contains the cancer
→ rejoin the two parts

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39
Q

How common is colorectal cancer? What is the lifetime risk?

A

→ most common GI cancer in the Western Societies
→ 3rd most common cancer death in men + women
→ 1 in 10 for men
→ 1 in 14 for women

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40
Q

What age group does colorectal cancer mainly affect?

A

patients over 50 years of age in 90% of cases

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41
Q

What are the different forms of colorectal cancer?

A

→ sporadic
→ familial
→ hereditary syndrome

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42
Q

What is sporadic colorectal cancer?

A

cancer that emerges with:
→ an absence of family history
→ in older population
→ tends to be an isolated lesion

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43
Q

What is familial colorectal cancer?

A

cancer that emerges with:
→ family history
→ higher risk of index case is young (under 50 years) and relative is close (1st degree)

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44
Q

What is hereditary syndrome cancer?

A

cancer that emerges with:
→ family history
→ younger age of onset
→ specific gene defects

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45
Q

What are some examples of hereditary syndrome colorectal cancer?

A

→ familial adenomatous polyposis (FAP) : present young with many polyps, tend to have their large bowel removed at a young age to treat or prevent cancers
→ hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome) :

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46
Q

What does the histopathology of most colorectal cancer show up as?

A

adenocarcinomas

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47
Q

What is the general pathogenesis of colorectal cancer?

A
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48
Q

What can be done to prevent progression of polyps into cancers?

A

resection of polyps before they can progress to adenocarcinomas

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49
Q

What are the past history risk factors of colorectal cancer?

A

→ colorectal cancer
→ adenomas (polyps)
→ ulcerative colitis
→ radiotherapy

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50
Q

What is the family history risk factors for colorectal cancer?

A

→ 1st degree relative < 55 years
→ relatives with identified genetic predisposition (e.g. FAP, HNPCC, Peutz-Jegher’s syndrome)

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51
Q

What are the diet or environmental factors for colorectal cancer?

A

→ carcinogenic foods
→ smoking
→ obesity
→ socioeconomic status

52
Q

What does clinical presentation of colorectal cancer depend on?

A

location of cancer

53
Q

What proportion of colorectal cancers occur where in the colon?

A

→ 2/3 in descending colon + rectum
→ 1/2 in sigmoid colon + rectum (i.e. within reach of flexible sigmoidoscopy)

54
Q

How do caecal + right-sided colon cancers present?

A

→ iron-deficiency anaemia (most common)
→ change of bowel habit (diarrhoea)
late presentations:
→ distal ileum obstruction
→ palpable mass

55
Q

How do left-sided + sigmoid cancers present?

A

→ PR bleeding, mucus
→ thin stool (late)

56
Q

How do rectal carcinomas present?

A

→ PR bleeding, mucus
→ Tenesmus (sensation of wanting to open your bowels, but nothing comes out)
→ Anal, perineal + sacral pain (late)

57
Q

How does local invasion colorectal invasion clinically present?

A

→ presents late
→ bladder symptoms
→ female genital tract symptoms

58
Q

How do colorectal metastasis clinical present?

A

→ presents late
→ liver (hepatic pain, jaundice) (rarely causes pain)
→ lung (cough)
→ regional lymph nodes
→ peritoneum
→ Sister Mary Joseph nodule (nodule in the umbilical region)

59
Q

What are the signs of primary colorectal cancer?

A

→ abdominal mass
→ DRE : most <12cm dentate + reached by examining finger
→ rigid sigmoidoscopy
→ abdominal tenderness + distention = large bowel obstruction

60
Q

What are signs of metastasis + complications of colorectal cancer?

A

→ hepatomegaly (mets)
→ monophonic wheeze (a small number of notes starting and ending at different times)
→ bone pain

61
Q

What investigations can be done to diagnose colorectal cancer?

A

→ blood tests
→ faecal occult blood
→ colonoscopy
→ CT colonoscopy / colonography
→ pelvic MRI
→ chest, abdo + pelvic CT

62
Q

What faecal blood occults can be done for colorectal cancer?

A

→ Guaiac test (Hemoccult)
→ FIT (Faecal Immunochemical Test)

63
Q

What is the Guaiac test (Haemoccult)?

A

→ based on pseudoperoxidase activity of haematin
→ Sensitivity of 40-80%;
→ Specificity of 98%
→ Dietary restrictions – avoid red meat, melons, horse-radish, vitamin C & NSAIDs for 3 days before test

64
Q

What is the FIT test?

A

→ faecal immunochemical test
→ detects minute amounts of blood in faeces (faecal occult blood).

65
Q

What blood tests are done for colorectal cancers? What are the markers to look for?

A

→ do an FBC : anaemia, haematinics, low ferritin
→ look for tumour markers : CEA (isn’t very specific but is useful for monitoring)

66
Q

How does colonoscopy help diagnose colorectal cancer?

A

→ can visualise lesions <5mm
→ small polyps can be removed to reduce cancer incidence
→ usually performed under sedation

67
Q

How does a CT colonoscopy or colonography help diagnose colorectal cancer?

A

→ can visualise lesion > 5mm
→ no need for sedation
→ bowel prep is still necessary
→ less invasive, better tolerated
→ if lesions are identifies, patient needs colonoscopy for diagnosis

68
Q

How does a pelvic MRI help diagnose colorectal cancer?

A

→ good for rectal cancer detection
→ Depth of invasion, mesorectal lymph node involvement
→ No bowel prep or sedation required
→ Help choose between preoperative chemoradiotherapy or straight to surgery

69
Q

Why are chest, abdomen and pelvic CTs done for colorectal cancer?

A

check for metastases
help with staging prior to treatment

70
Q

How is colorectal cancer primarily managed?

A

→ primarily managed by surgery
→ stent, radiotherapy or chemotherapy can be used to give time instead of doing an emergency surgery

71
Q

*What surgeries can be done for right or transverse obstructing colon carcinomas?

A

resection + primary anastomosis

72
Q

What surgeries can be done for left sided obstructing colon carcinomas?

A

→ Hartmann’s procedure : proximal end colostomy, reversal in 6 months?
→ primary anastomosis : intraoperative bowel lavage with primary anastomosis (10% chance of leak), defunctioning ileostomy
→ palliative stent

73
Q

What surgeries can be done for rectal cancers?

A
74
Q

Why is it more difficult to operate on the left-side of the colon?

A

→ right side of the colon has better blood supply
→ left side has worse blood supply

75
Q

What is the commonest form of pancreatic cancer?

A

pancreatic ductal adenocarcinomas

76
Q

How many PDAs have late presentation?

A

80-85%

77
Q

What is the prognosis like for late presentation PDAs?

A

→ overall median survival <6 months
→ 5 year survival 10-15%

78
Q

How many PDAs present when they are still resectable?

A

15-20%

79
Q

What is the prognosis like for resectable PDAs?

A

→ median survival 11-20 months
→ 5 year survival = 20-25%

80
Q

What is the overall prognosis for PDA like?

A

virtually most patients dead within 7 years of surgery

81
Q

What is the incidence of PDA?

A

→ Incidence ↑er in Western/industrialised countries
→ Rare before 45 years, 80% occur between 60 & 80 years of age
→ Men > women (1.5 - 2:1)
→ UK & USA annual incidence panc CA 100 per million popn
→ 4th commonest cause of cancer death
→ Incidence & mortality roughly equivalent – UK in 2015
9,921 new cases of PDA
9263 deaths from PDA
→ 2nd commonest cause of cancer death – in USA 2030
- 48,000 deaths

82
Q

What are the risk factors for pancreatic cancer?

A

→ Chronic pancreatitis → 18-fold ↑er risk
→ Type II diabetes mellitus → relative risk 1.8
→ Cholelithiasis, previous gastric surgery & pernicious anaemia – WEAK
→ Diet (↑fat & protein, ↓fruit & veg, coffee & EtOH) - WEAK
→ Occupation (insecticides, aluminium, nickel & acrylamide)
→ Cigarette smoking → causes 25-30% PDAs
→ 7-10% have a family history,
Relative risk of PDA increased by: 2, 6 & 30-fold with:
1, 2 & 3 affected first degree relatives

83
Q

*What other inherited genetics syndromes increase the chances of getting PDA?

A

v

84
Q

*What is the pathogenesis of PDAs?

A

Pancreatic Intraepithelial Neoplasias (PanIN) :
→ PDAs evolve through non-invasive neoplastic precursor lesions
→ PanINs are microscopic (<5 mm diameter) & not visible by pancreatic imaging
→ Acquire clonally selected genetic & epigenetic alterations along the way

85
Q

Where can PDAs present in the pancreas?

A

→ head of the pancreas
→ body + tail of pancreas

86
Q

How do PDAs in the head of the pancreas clinically present?

A

→ 2/3 arise in head
→ Jaundice >90% due to either invasion or compression of CBD
- often painless
- palpable gallbladder (Courvoisier’s sign)
→ Weight loss
- anorexia
- malabsorption (secondary to exocrine insufficiency)
- diabetes.
→ Pain 70% at the time of diagnosis
- epigastrium
- radiates to back in 25%
- back pain usually indicates posterior capsule invasion and irresectability.
→ 5% atypical attack of acute pancreatitis.
→ In advanced cases, duodenal obstruction results in persistent vomiting.
→ Gastrointestinal bleeding
- duodenal invasion or varices secondary to portal or splenic vein occlusion.

87
Q

How do PDAs in the body + tail of the pancreas clinically present?

A

→ Develop insidiously and are asymptomatic in early stages
→ At diagnosis they are often more advanced than lesions located in the head
→ There is marked weight loss with back pain in 60% of patients.
→ Jaundice is uncommon
→ Vomiting sometimes occurs at a late stage from invasion of the DJ flexure
→ Most unresectable at the time of diagnosis

88
Q

What investigations can be done for PDAs?

A

→ tumour marker CA19-9
→ ultrasonography
→ dual-phase CT
→ MRI imaging
→ MRCP
→ ERCP
→ EUS
→ Laparoscopy + laparoscopy ultrasound
→ PET scan

89
Q

How useful is tumour marker CA19-9 at identifying PDAs?

A

→ falsely elevated in pancreatitis, hepatic dysfunction & obstructive jaundice.
→ concentrations > 200 U/ml confer 90% sensitivity
→ concentrations in the thousands associated with high specificity

90
Q

How useful is ultrasonography at identifying PDAs?

A

→ can identify pancreatic tumours
→ dilated bile ducts
→ liver metastases

91
Q

How useful is a dual phase CT when investigating PDAs?

A

→ accurately predicts resectability in 80–90% of cases
→ contiguous organ invasion
→ vascular invasion (coeliac axis & SMA)
→ distant metastases

92
Q

How useful is MRI imaging in PDAs?

A

→ imaging detects and predicts resectability with accuracies similar to CT
→ but not as useful at CT

93
Q

How useful is MRCP in PDAs?

A

provides ductal images without complications of ERCP

94
Q

How useful is ERCP in PDAs?

A

→ confirms the typical ‘double duct’ sign
→ aspiration/brushing of the bile-duct system
→ therapeutic modality → biliary stenting to relieve jaundice

95
Q

How useful is a EUS at investigating PDAs?

A

→ highly sensitive in the detection of small tumours
→ assessing vascular invasion
→ FNA

96
Q

How useful is laparoscopy + laparoscopic ultrasound in PDAs?

A

detect radiologically occult metastatic lesions of liver & peritoneal cavity

97
Q

How useful are PET scans in investigating PDAs?

A

mainly used for demonstrating occult metastases

98
Q

What is the surgical treatment of the cancer in the head of the pancreas?

A

→ head of pancreas resection
→ Whipple procedure
→ pancreaticoduodectomy

99
Q

What is the process of HOP resection?

A

→ removal of the head of pancreas, bile duct, gall bladder, duodenum, and sometimes the distal part of the stomach
→ bile duct, rest of pancreas and stomach is attached to the small intestine

100
Q

What is the surgical treatment for pancreatic cancer in the tail of pancreas?

A

TOP resection

101
Q

What is the process of TOP resection?

A

tail + body o pancreas and spleen + splenic artery are removed

102
Q

Why is the spleen removed in TOP resection?

A

→ splenic artery dips in and out of the tail of pancreas
→ attempts to preserve spleen could lead to cancer cells being left behind

103
Q

What are the 4 main types of pancreatic cancer?

A

→ Hepato cellular cancer
→ Colorectal Cancer w Liver metastases
→ Cholangiocarcinoma
→ Gall Bladder Cancer

104
Q

What is a HCC? What is its prevalence + location?

A

→ hepato cellular cancer
→ most common
→ affects hepatocytes of liver

105
Q

What are some of the underlying aetiologies of HCC?

A

→ 70-90% of HCCs have underlying cirrhosis
→ also occurs those with Hepatitis B or C + alcohol liver disease
→ aflatoxins (produced by certain fungi)

106
Q

What is the prognosis like for HCCs?

A

→ Median survival without Rx 4-6 m
→ 5yr survival <5% without Rx
→ 5yr survival >30% with Rx

107
Q

What are optimal treatment for HCCs?

A

resection surgical excision w curative intent
→ however only 5-15% of HCCs are suitable for surgery

108
Q

What are some other treatment options for HCCs? What treatments are not used and why?

A

→ liver transplant (can cure both HCC and any underlying cirrhosis)
→ TACE (trans arterial chemo embolism)
→ RFA (radio frequency ablation)
→ Systemic chemotherapy ineffective (RR <20%)

109
Q

What is the aetiology of GB cancers?

A

→ gall stones
→ porcelain GB (chronic inflammation of GB that leads to calcification)
→ chronic typhoid infection

110
Q

What is the main issue with GB cancers?

A

doesn’t cause a lot of harm at first but spreads very quickly

111
Q

What is the prognosis like with GB cancers?

A

→ Median survival without Rx = 5-8 m
→ 5yr survival without Rx = <5%
→ 5 yr survival with surgery = stage II 64%; stage III 44%; stage IV 8%

112
Q

What are the treatment options for GB cancers? What is not used?

A

→ Systemic chemotherapy ineffective
→ No other effective Rx options
→ Optimal Rx surgical excision with curative intent but <15% suitable

113
Q

What is ChCA?

A

→ cholangiocarcinoma
→ cancer of the bile ducts
→ happens most commonly at the bifurcation of common bile duct
→ usually very small tumours

114
Q

What is the aetiology of ChCA?

A

→ primary sclerosing cholangitis
→ ulcerative colitis
→ liver fluke
→ choledochal cyst

115
Q

What is primary sclerosing cholangitis?

A

scarring of the bile ducts that leads to their narrowing

116
Q

What is liver fluke?

A

→ clonorchis sineses
→ parasite that infects the liver + bile ducts

117
Q

What is choledochal cyst?

A

→ dilatation of the bile ducts
→ has 10-15% chance of becoming cancerous

118
Q

What is prognosis + survival chances of ChCA?

A

→ Median survival (depends on site) without Rx <6 m
→ 5yr survival without Rx <5%
→ 5yr survival with Rx = 20-40%

119
Q

What are the treatment options for ChCA?

A

→ Systemic chemotherapy ineffective
→ No other effective Rx options other than liver transplant
→ Optimal Rx surgical excision with curative intent but only 20-30% suitable for surgery

120
Q

What proportion of secondary metastases are synchronous?

A

15-20% synchronous

121
Q

What proportion of secondary liver metastases are metachronous?

A

25% metachronous

122
Q

*What is the prognosis like for secondary liver metastases?

A

→ median survival without Rx = <1yr
→ 5yr survival without Rx = 0%
→ 5yr survival rates with Rx = 25-50%

123
Q

What are the treatment options for secondary liver metastases?

A

→ Systemic chemotherapy improving
→ Other effective Rx options (RFA & SIRT)
→ Optimal Rx surgical excision with curative intent

124
Q

What is the surgical resection process for HCCs?

A

v

125
Q

What is the surgical resection process for GB cancers?

A

v

126
Q

What is the surgical resection process for ChCA?

A

v

!!!!! BRS YR2 !!!!! (72 decks)

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