1b// GI Cancers Flashcards
1
Q
What is the definition of cancer?
A
A disease caused by an uncontrolled division of abnormal cells in a part of the body
2
Q
What does it mean a primary cancer?
A
Arising directly from the cells in an organ
3
Q
What does it mean a secondary/ metastasis cancer?
A
Spread from another organ, directly or by other means (blood or lymph)
4
Q
What are the three types of tissues/ cells that can be affected in the GI tract by cancer?
A
epithelial cells
neuroendocrine cells
connective tissue
5
Q
Which epithelial cells in the GI tract become cancer and what type of cancer do they become?
A
6
Q
Which neuroendocrine cells in the GI tract become cancer and what type of cancer do they become?
A
7
Q
Which connective tissues in the GI tract become cancer and what type of cancer do they become?
A
8
Q
What are the most common cancers of the GI tract?
A
adenocarcinoma
neuroendocrine tumours (NETs)
9
Q
Where can GI cancers form/ NETs?
A
liver
oesophagus
gastric
pancreas
colon
NETs can be formed anywhere in the GI tract
10
Q
Who does colorectal cancer generally affect?
A
patients older than 50 y/o
11
Q
What are the forms of colorectal cancer?
A
sporadic
familial
hereditary syndrome
12
Q
What is sporadic colorectal cancer?
A
Absence of family history, older population, isolated lesion
13
Q
What is familial colorectal cancer?
A
Family history, higher risk if index case is young (<50years) and the relative
is close (1st degree)
14
Q
What is hereditary syndrome 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)
15
Q
What is the histopathology of colorectal cancer?
A
adenocarcinoma
16
Q
Describe the mutation of colorectal cancer.
A
17
Q
What are the risk factors for colorectal cancer?
A
18
Q
What does the presentation of colorectal cancer depend on?
A
location of cancer
19
Q
Where can colorectal cancers appear?
A
2⁄3 in descending colon and rectum
1⁄2 in sigmoid colon and rectum (i.e. within reach of flexible
sigmoidoscopy)
- caecal and right sided cancer
- left sided and sigmoid carcinoma
- rectal carcinoma
- bowel obstruction (late)
20
Q
What is the clinical presentation of caecal and right sided cancer?
A
Iron deficiency anaemia (most common)
Change of bowel habit (diarrhoea)
Distal ileum obstruction (late)
Palpable mass (late)
21
Q
What is the clinical presentation of left sided and sigmoid carcinoma?
A
PR bleeding, mucus
Thin stool (late)
22
Q
What is the clinical presentation of rectal carcinoma?
A
PR bleeding, mucus
Tenesmus
Anal, perineal, sacral pain (late)
23
Q
What is the clinical presentation of local invasion (late) colorectal cancer?
A
Bladder symptoms
Female genital tract symptoms
24
Q
What is the clinical presentation of metastasis colorectal cancer (late)?
A
Liver (hepatic pain, jaundice)
Lung (cough)
Regional lymph nodes
Peritoneum
- Sister Marie Joseph nodule
25
What are the signs of primary colorectal cancer?
Abdominal mass
DRE: most <12cm dentate and reached by examining finger
Rigid sigmoidoscopy
Abdominal tenderness and distension – large bowel obstruction
26
What are the signs of metastasis and complications of colorectal cancer?
Hepatomegaly (mets)
Monophonic wheeze
Bone pain
27
What are the type of investigations for colorectal cancer?
Faecal occult blood
Blood Tests
Colonoscopy
CT colonoscopy/ colonography
MRI pelvis
CT chest/ abdo/ pelvis
28
What is tenesmus?
Want to go to loo, but can't
29
What foecal occult blood investigations would be done for colorectal cancer?
Guaiac test (Hemoccult) – 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
FIT (Faecal Immunochemical Test) - detects minute amounts of blood in faeces (faecal occult blood).
30
What blood tests would be done for colorectal cancer investigations?
FBC: anaemia, haematinics – low ferritin
Tumour markers: CEA which is useful for monitoring
* NOT diagnostic tool
31
What are colonoscopies useful for in colorectal cancer?
Can visualize lesions < 5mm
Small polyps can be removed
- Reduced cancer incidence
32
Are colonoscopies sedated?
yes usually
33
Why are CT colonoscopies/ colonography useful for colorectal cancer?
Can visualize lesions > 5mm
No need for sedation
Less invasive, better tolerated
34
If a lesion is identified with a colonography, what do you do for a diagnosis?
If lesions identified patient needs colonoscopy for diagnosis
35
Why do you perform a MRI pelvis for colorectal cancer, and what are the benefits of MRI pelvis?
For rectal cancer
Depth of invasion, mesorectal lymph node involvement
No bowel prep or sedation required
Help choose between preoperative chemoradiotherapy or straight to
surgery
36
Why is there CT of chest/ abdo/ pelvis in colorectal cancer?
staging prior to treatment
37
How is colon cancer primarily managed?
by surgery
38
How do you manage colorectal cancer?
stent (if not fit for surgery)/ radiotherapy/ chemotherapy/ surgery
39
What is the difference between right and left handed obstructing colon carcinoma?
right and transverse colon is safer because it has a good blood supply so good healing
left sided obstruction is more complicated
40
How do you treat a right and transverse colon obstructing colon carcinoma?
resection and primary anastomosis
41
How do you manage a left sided obstructing colon carcinoma?
Hartmann’s procedure
- Proximal end colostomy (LIF)
- +/- Reversal in 6 months
Primary anastomosis
- Intraoperative bowel lavage with primary anastomosis (10% leak)
- Defunctioning ileostomy
Palliative stent (if not fit for surgery e.g., too old)
42
Describe the colonic arterial supply and resection.
43
Does this make sense for right and left sided cancer?
44
Does this make sense for rectal cancer resection?
45
What are the 4 types of liver cancers?
HCC=> Hepatocellular carcinoma
CRC=> secondary liver metastases
GB CA=> gallbladder cancer
ChCA=> Cholangiocarcinoma
*HCC is hepatocytes
*ChCA is branches
46
What is the aetiology of hepatocellular carcinoma?
- 70-90% have underlying cirrhosis
- Aflatoxin
- NASH=> non-alcoholic steatohepatitis due to fatty liver causing inflammation= cancer
47
What is the median survival rate of hepatocellular carcinoma without prescription (Rx)?
4-6m
48
Is systemic chemotherapy effective for hepatocellular carcinoma?
NO
49
What are effecting prescription options for hepatocellular carcinoma?
Liver transplant
TACE (Chemoembolisation)
RFA (Radiofrequency ablation)
optimal prescription excision with curative intent (5yr survival is more than 30%)
50
Can everyone have a liver transplant?
only if they have 3 or less, because you have to suppress the patient meaning cancers will pop up in other places
51
What is TACE?
Chemoembolisation is a treatment directly into the liver. You have chemotherapy into the blood vessel that feeds the tumour. Then you have small particles injected into the blood vessel to block off the blood supply. It's also called trans arterial chemoembolisation (TACE).
52
What is RFA?
Radiofrequency ablation, or RFA, is a minimally invasive technique that shrinks the size of tumors, nodules or other growths in the body
53
What is the aetiology of gallbladder cancer?
Aetiology unknown
- GS
- porcelain GB
- chronic typhoid infection
54
What is the median survival of gallbladder cancer without prescription?
5-8m
55
Is systemic chemotherapy effective for gallbladder cancer?
NO
56
What are the effective prescription options for gallbladder cancer?
there are none
57
What is the optimal treatment for gallbladder cancer?
58
How do you measure the different stages of gallbladder cancer?
III= invading liver but less than 2cm
IV= invading liver and >2cm or metastisised somewhere else
59
What is the aetiology of cholangiocarcinoma?
- PSC & Ulcerative Cholitis
- liver fluke (clonorchis sinensis)
- choledochal cyst
60
What is PSC?
Primary sclerosing cholangitis (PSC) is a chronic liver disease in which the bile ducts inside and outside the liver become inflamed and scarred, and eventually narrowed or blocked.
61
What is the survival with and without prescription and what is ineffective as treatment?
62
What is the survival rate of secondary liver metastasis without prescription and what is effective?
63
What are the types of secondary liver metastases?
64
What do remove when you remove the gallbladder for surgical resection GB CA?
GB
part of liver GB was attached to
high lymphadenectomy (remove lymph nodes)
65
Does this make sense.
66
What is the epidemiology of pancreatic cancer?
relatively common and highly lethal
80-85% have late presentation
- Overall median survival <6 months
- 5-year survival 0.4 - 5%
15-20% have resectable disease
- Median survival 11-20 months
- 5-year survival 20–25%
- Virtually all pts dead within 7 years of surgery
67
What is the commonest form of pancreatic cancer?
pancreatic ductal adenocarcinoma (PDA)
68
Does pancreatic cancer affect women or men more?
men (1.5-2:1)
69
What is dangerous about pancreatic cancer?
the number of cases is v close to number of deaths
so v small ratio
70
What are the risk factors for pancreatic cancer? (6)
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
71
Does family history matter for pancreatic cancer?
72
What are the inherited syndromes that have an associated increased risk of pancreatic cancer and what are the genes involved?
hereditary pancreatitis= gene CFTR
73
What is the pathogenesis of pancreatic cancer?
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
74
Describe (ish) the PanIN progression model, showing genetic alterations.
75
What are the types of pancreatic carcinoma?
carcinoma of the head of the pancreas
carcinoma of the body and tail of pancreas
76
What are the clinical presentations of carcinoma of the head of the pancreas?
77
What are the clinical presentation of carcinoma of the body and tail of pancreas?
78
What are the investigations for pancreatic cancer?
tumour marker CA19-9
ultrasonography
dual phase CT
MRI
MRCP
ERCP
EUS
Laparoscopy and laparoscopic US
PET
79
What is this?
CT scan for pancreatic cancer
80
Why is tumour marker CA19-9 useful for pancreatitis?
- falsely elevated in pancreatitis, hepatic dysfunction & obstructive jaundice.
- concentrations > 200 U/ml confer 90% sensitivity
- concentrations in the thousands associated with high specificity
81
Why is ultrasonography useful for pancreatitis?
- can identify pancreatic tumours
- dilated bile ducts
- liver metastases
82
Why is dual-phase CT useful for pancreatitis?
accurately predicts resectability in 80–90% of cases
- contiguous organ invasion
- vascular invasion (coeliac axis & SMA)
- distant metastases
83
Why is MRI important for pancreatic cancer?
imaging detects and predicts resectability with accuracies similar to CT
84
Why is MRCP important for pancreatic cancer?
provides ductal images without complications of ERCP
85
Why is ERCP important for pancreatic cancer?
- confirms the typical ‘double duct’ sign
- aspiration/brushing of the bile-duct system
- therapeutic modality → biliary stenting to relieve jaundice
86
What is EUS?
- highly sensitive in the detection of small tumours
- assessing vascular invasion
- FNA
87
What is
Laparoscopy and laparoscopic US?
- detect radiologically occult metastatic lesions of liver & peritoneal cavity
88
What is PET?
PET mainly used for demonstrating occult metastases
89
What are the types of resection for pancreatic cancer?
90
What is the presentation of NETs?
Most NETs are asymptomatic & incidental findings
less than 10% of NETs produce symptoms
91
What happens in 40% of NETs?
Secretion of hormones & their metabolites in 40%
- serotonin, tachykinins (substance P) & other vasoactive peptides
92
What can NETs result in?
Carcinoid syndrome:
* Vasodilatation
* Bronchoconstriction
* ↑ed intestinal motility
* Endocardial fibrosis (PR & TR)
93
Where do NETs arise from?
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
94
What are the possible site for NETs?
pancreatic
pancreatic/ duodenal
Entire GIT
Midgut
Hindgut
95
What are the names and clinical features of pancreatic NETs?
96
What are the names and clinical features of pancreatic/ duodenal NETs?
97
What are the names and clinical features of entire GIT NETs?
98
What are the names and clinical features of midgut and foregut NETs?
99
What should you do when a NET is suspected?
When suspected, investigations to localise the tumour & confirm the diagnosis with histology
100
What is the biochemical assessment for NETs?
101
What is the imaging for NETs?
102
What does an insulinoma look like with a CT scan a 68Ga-DOTATATE PET/CT?
103
What does a NET look like in midgut?
104
What is the grading like for GEP-NETs?
Gastroenteropancreatic neuroendocrine tumors (GEP-NETs)
105
Do these make sense?
106
What are the treatments for NETs?
107
Did you check the tutorial notes?
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