Gastro - GI Cancers Flashcards
(126 cards)
1
Q
What is a cancer?
A
disease caused by an uncontrolled division of abnormal cells in a part of the body
2
Q
What is a primary cancer?
A
arises directly from the cells of an organ
3
Q
What is a secondary / metastasis cancer?
A
spread to another organ, directly or by other means (lymph, blood)
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
5
Q
What are emerging hallmarks of cancer?
A
→ deregulating cellular energetics
→ avoiding immune destruction
6
Q
What are the enabling characteristics of cancer?
A
→ genome instability
→ tumour-promoting inflammation
7
Q
What are the epithelial cells of the GI tract?
A
squamous “glandular” epithelium
8
Q
What are the epithelial cell cancers of the GI tract?
A
→ SCC (squamous cell carcinoma)
→ Adenocarcinoma
9
Q
What are the neuroendocrine cells of the GI tract?
A
→ enteroendocrine cells
→ interstitial cells of Cajal
10
Q
What are the neuroendocrine cancers of the GI tract?
A
→ NETs (neuroendocrine tumours)
→ GISTs (Gastrointestinal Stromal Tumours)
11
Q
What are some of the connective tissues of the GI tract?
A
→ smooth muscle
→ adipose tissue
12
Q
What are the connective tissue cancers of the GI tract?
A
→ leiomyoma / leiomyosarcomas
→ liposarcomas
13
Q
What are the 2 main types of oesophageal cancers?
A
→ SCCs
→ Adenocarcinomas
14
Q
What do SCCs in the oesophagus develop from?
A
from normal oesophageal squamous epithelium
15
Q
Where in the oesophagus do SCCs occur?
A
upper 2/3
16
Q
What GI pathways are oesophageal SCCs related to?
A
acetaldehyde pathway :
→ when alcohol is metabolised, acetaldehyde is produced
→ acetaldehyde = carcinogen
17
Q
Where are SCCs of the oesophagus more common?
A
in the less developed world
18
Q
What do oesophageal adenocarcinomas develop from?
A
metaplastic columnar epithelium
19
Q
What part of the oesophagus does adenocarcinoma affect?
A
lower 1/3
20
Q
What GI process or pathways are oesophageal adenocarcinomas related to?
A
related to acid reflux, GORD, etc.
21
Q
Where are adenocarcinomas of the oesophagus more common?
A
more developed world
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
23
Q
What is oesophagitis? What percentage of UK population have it?
A
→ inflammation of the oesophagus
→ 30% of UK population
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
25
What percentage of Barret's population have a lifetime risk of cancer?
0.5%-1% a year
26
What is the Barret's surveillance guideline for no dysplasia?
survey every 2-3 years
27
What is the Barret's surveillance guideline for low grade dysplasia?
survey every 6 months
28
What is the Barret's surveillance guideline for high grade dysplasia?
intervention is necessary
29
How common are oesophageal cancers?
9th most common
30
What demographic of people do oesophageal cancers mainly affect?
→ affects the elderly
→ M : F, 10 : 1
31
What are the main presenting factors for oesophageal cancers?
dysphagia + weight loss
32
When do symptoms for oesophageal cancer mainly present?
late presentation
33
What is the prognosis of oesophageal cancers?
→ 65% palliative care
→ high morbidity
→ complex surgery
→ poor 5-year survival \<20%
→ palliation - difficult
34
What is involved in diagnosis of oesophageal cancer?
→ endoscopy (biopsy)
→ staging
→ CT scan
→ laparoscopy
→ endoscopy ultrasound scan (looks outside the lumen)
→ PET scan (important for adenocarcinomas)
35
What is the treatment plan for SCCs?
→ radiotherapy
→ usually very effective
→ not many need surgery after radiotherapy
36
What is the treatment plan for Adenocarcinomas?
→ Neo-adjuvant chemotherapy for all
→ then restaging, then consideration of radical surgery with curative intent
37
What is the treatment plan for palliative oesophageal cancers?
→ palliative
→ chemotherapy
→ DXT = radiotherapy
→ stent to keep oesophagus patent
38
\*What is the process of an oesophagectomy?
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
39
How common is colorectal cancer? What is the lifetime risk?
→ 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
40
What age group does colorectal cancer mainly affect?
patients over 50 years of age in 90% of cases
41
What are the different forms of colorectal cancer?
→ sporadic
→ familial
→ hereditary syndrome
42
What is sporadic colorectal cancer?
cancer that emerges with:
→ an absence of family history
→ in older population
→ tends to be an isolated lesion
43
What is familial colorectal cancer?
cancer that emerges with:
→ family history
→ higher risk of index case is young (under 50 years) and relative is close (1st degree)
44
What is hereditary syndrome cancer?
cancer that emerges with:
→ family history
→ younger age of onset
→ specific gene defects
45
What are some examples of hereditary syndrome colorectal cancer?
→ 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) :
46
What does the histopathology of most colorectal cancer show up as?
adenocarcinomas
47
What is the general pathogenesis of colorectal cancer?
48
What can be done to prevent progression of polyps into cancers?
resection of polyps before they can progress to adenocarcinomas
49
What are the past history risk factors of colorectal cancer?
→ colorectal cancer
→ adenomas (polyps)
→ ulcerative colitis
→ radiotherapy
50
What is the family history risk factors for colorectal cancer?
→ 1st degree relative \< 55 years
→ relatives with identified genetic predisposition (e.g. FAP, HNPCC, Peutz-Jegher's syndrome)
51
What are the diet or environmental factors for colorectal cancer?
→ carcinogenic foods
→ smoking
→ obesity
→ socioeconomic status
52
What does clinical presentation of colorectal cancer depend on?
location of cancer
53
What proportion of colorectal cancers occur where in the colon?
→ 2/3 in descending colon + rectum
→ 1/2 in sigmoid colon + rectum (i.e. within reach of flexible sigmoidoscopy)
54
How do caecal + right-sided colon cancers present?
→ iron-deficiency anaemia (most common)
→ change of bowel habit (diarrhoea)
late presentations:
→ distal ileum obstruction
→ palpable mass
55
How do left-sided + sigmoid cancers present?
→ PR bleeding, mucus
→ thin stool (late)
56
How do rectal carcinomas present?
→ PR bleeding, mucus
→ Tenesmus (sensation of wanting to open your bowels, but nothing comes out)
→ Anal, perineal + sacral pain (late)
57
How does local invasion colorectal invasion clinically present?
→ presents late
→ bladder symptoms
→ female genital tract symptoms
58
How do colorectal metastasis clinical present?
→ 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
What are the signs of primary colorectal cancer?
→ abdominal mass
→ DRE : most \<12cm dentate + reached by examining finger
→ rigid sigmoidoscopy
→ abdominal tenderness + distention = large bowel obstruction
60
What are signs of metastasis + complications of colorectal cancer?
→ hepatomegaly (mets)
→ monophonic wheeze (a small number of notes starting and ending at different times)
→ bone pain
61
What investigations can be done to diagnose colorectal cancer?
→ blood tests
→ faecal occult blood
→ colonoscopy
→ CT colonoscopy / colonography
→ pelvic MRI
→ chest, abdo + pelvic CT
62
What faecal blood occults can be done for colorectal cancer?
→ Guaiac test (Hemoccult)
→ FIT (Faecal Immunochemical Test)
63
What is the Guaiac test (Haemoccult)?
→ 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
What is the FIT test?
→ faecal immunochemical test
→ detects minute amounts of blood in faeces (faecal occult blood).
65
What blood tests are done for colorectal cancers? What are the markers to look for?
→ do an FBC : anaemia, haematinics, low ferritin
→ look for tumour markers : CEA (isn't very specific but is useful for monitoring)
66
How does colonoscopy help diagnose colorectal cancer?
→ can visualise lesions \<5mm
→ small polyps can be removed to reduce cancer incidence
→ usually performed under sedation
67
How does a CT colonoscopy or colonography help diagnose colorectal cancer?
→ 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
How does a pelvic MRI help diagnose colorectal cancer?
→ 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
Why are chest, abdomen and pelvic CTs done for colorectal cancer?
check for metastases
help with staging prior to treatment
70
How is colorectal cancer primarily managed?
→ primarily managed by surgery
→ stent, radiotherapy or chemotherapy can be used to give time instead of doing an emergency surgery
71
\*What surgeries can be done for right or transverse obstructing colon carcinomas?
resection + primary anastomosis
72
What surgeries can be done for left sided obstructing colon carcinomas?
→ 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
What surgeries can be done for rectal cancers?
74
Why is it more difficult to operate on the left-side of the colon?
→ right side of the colon has better blood supply
→ left side has worse blood supply
75
What is the commonest form of pancreatic cancer?
pancreatic ductal adenocarcinomas
76
How many PDAs have late presentation?
80-85%
77
What is the prognosis like for late presentation PDAs?
→ overall median survival \<6 months
→ 5 year survival 10-15%
78
How many PDAs present when they are still resectable?
15-20%
79
What is the prognosis like for resectable PDAs?
→ median survival 11-20 months
→ 5 year survival = 20-25%
80
What is the overall prognosis for PDA like?
virtually most patients dead within 7 years of surgery
81
What is the incidence of PDA?
→ 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
What are the risk factors for pancreatic cancer?
→ 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
\*What other inherited genetics syndromes increase the chances of getting PDA?
v
84
\*What is the pathogenesis of PDAs?
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
Where can PDAs present in the pancreas?
→ head of the pancreas
→ body + tail of pancreas
86
How do PDAs in the head of the pancreas clinically present?
→ 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
How do PDAs in the body + tail of the pancreas clinically present?
→ 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
What investigations can be done for PDAs?
→ tumour marker CA19-9
→ ultrasonography
→ dual-phase CT
→ MRI imaging
→ MRCP
→ ERCP
→ EUS
→ Laparoscopy + laparoscopy ultrasound
→ PET scan
89
How useful is tumour marker CA19-9 at identifying PDAs?
→ falsely elevated in pancreatitis, hepatic dysfunction & obstructive jaundice.
→ concentrations \> 200 U/ml confer 90% sensitivity
→ concentrations in the thousands associated with high specificity
90
How useful is ultrasonography at identifying PDAs?
→ can identify pancreatic tumours
→ dilated bile ducts
→ liver metastases
91
How useful is a dual phase CT when investigating PDAs?
→ accurately predicts resectability in 80–90% of cases
→ contiguous organ invasion
→ vascular invasion (coeliac axis & SMA)
→ distant metastases
92
How useful is MRI imaging in PDAs?
→ imaging detects and predicts resectability with accuracies similar to CT
→ but not as useful at CT
93
How useful is MRCP in PDAs?
provides ductal images without complications of ERCP
94
How useful is ERCP in PDAs?
→ confirms the typical ‘double duct’ sign
→ aspiration/brushing of the bile-duct system
→ therapeutic modality → biliary stenting to relieve jaundice
95
How useful is a EUS at investigating PDAs?
→ highly sensitive in the detection of small tumours
→ assessing vascular invasion
→ FNA
96
How useful is laparoscopy + laparoscopic ultrasound in PDAs?
detect radiologically occult metastatic lesions of liver & peritoneal cavity
97
How useful are PET scans in investigating PDAs?
mainly used for demonstrating occult metastases
98
What is the surgical treatment of the cancer in the head of the pancreas?
→ head of pancreas resection
→ Whipple procedure
→ pancreaticoduodectomy
99
What is the process of HOP resection?
→ 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
What is the surgical treatment for pancreatic cancer in the tail of pancreas?
TOP resection
101
What is the process of TOP resection?
tail + body o pancreas and spleen + splenic artery are removed
102
Why is the spleen removed in TOP resection?
→ splenic artery dips in and out of the tail of pancreas
→ attempts to preserve spleen could lead to cancer cells being left behind
103
What are the 4 main types of pancreatic cancer?
→ Hepato cellular cancer
→ Colorectal Cancer w Liver metastases
→ Cholangiocarcinoma
→ Gall Bladder Cancer
104
What is a HCC? What is its prevalence + location?
→ hepato cellular cancer
→ most common
→ affects hepatocytes of liver
105
What are some of the underlying aetiologies of HCC?
→ 70-90% of HCCs have underlying cirrhosis
→ also occurs those with Hepatitis B or C + alcohol liver disease
→ aflatoxins (produced by certain fungi)
106
What is the prognosis like for HCCs?
→ Median survival without Rx 4-6 m
→ 5yr survival \<5% without Rx
→ 5yr survival \>30% with Rx
107
What are optimal treatment for HCCs?
resection surgical excision w curative intent
→ however only 5-15% of HCCs are suitable for surgery
108
What are some other treatment options for HCCs? What treatments are not used and why?
→ 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
What is the aetiology of GB cancers?
→ gall stones
→ porcelain GB (chronic inflammation of GB that leads to calcification)
→ chronic typhoid infection
110
What is the main issue with GB cancers?
doesn't cause a lot of harm at first but spreads very quickly
111
What is the prognosis like with GB cancers?
→ 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
What are the treatment options for GB cancers? What is not used?
→ Systemic chemotherapy ineffective
→ No other effective Rx options
→ Optimal Rx surgical excision with curative intent but \<15% suitable
113
What is ChCA?
→ cholangiocarcinoma
→ cancer of the bile ducts
→ happens most commonly at the bifurcation of common bile duct
→ usually very small tumours
114
What is the aetiology of ChCA?
→ primary sclerosing cholangitis
→ ulcerative colitis
→ liver fluke
→ choledochal cyst
115
What is primary sclerosing cholangitis?
scarring of the bile ducts that leads to their narrowing
116
What is liver fluke?
→ clonorchis sineses
→ parasite that infects the liver + bile ducts
117
What is choledochal cyst?
→ dilatation of the bile ducts
→ has 10-15% chance of becoming cancerous
118
What is prognosis + survival chances of ChCA?
→ Median survival (depends on site) without Rx \<6 m
→ 5yr survival without Rx \<5%
→ 5yr survival with Rx = 20-40%
119
What are the treatment options for ChCA?
→ 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
What proportion of secondary metastases are synchronous?
15-20% synchronous
121
What proportion of secondary liver metastases are metachronous?
25% metachronous
122
\*What is the prognosis like for secondary liver metastases?
→ median survival without Rx = \<1yr
→ 5yr survival without Rx = 0%
→ 5yr survival rates with Rx = 25-50%
123
What are the treatment options for secondary liver metastases?
→ Systemic chemotherapy improving
→ Other effective Rx options (RFA & SIRT)
→ Optimal Rx surgical excision with curative intent
124
What is the surgical resection process for HCCs?
v
125
What is the surgical resection process for GB cancers?
v
126
What is the surgical resection process for ChCA?
v
