GI cancers Flashcards
What is meant by primary and secondary cancers?
Primary-arising directly from cells within the organ
Secondary/Metastis- spread from another organs(
e.g from lymph into blood where it can then spread)
What are some of the cells of the GI Tract and what cancers can they give rise to?
EPITHELIAL CELLS:
Squamous -squamous cell carcinoma
Glandualar epithelium-Adenocarcinoma
NEUROENDOCRINE CELLS:
Enteroendocrine cells- Neuroendocrine tumours
Interstitual cells of Cajal- Gastrointestinal stromal tumours (GISTS)
CONNECTIVE TISSUE:
smooth muscle-Leiomyoma /leiomyosarcomas
Adipose tissues-liposarcomas
What are the 3 sections of the oesophagus and waht happens to the muscle as you go down the oesophagus?
Cervical Oesophagus
Middle Oesophagus
Lower oesophagus
As you go down the smooth muscle increases and skeletal muscle decreases
What are the 2 main types of cancer in the oesophagus
SQUAMOS CELL CARCINOMA:
- from normal oesphageal squamous epithelium
- upper 2/3 of oesophagus
- strongly related to alcohol as this gets oxidised via the acetaldehyde pathway
- More common in the less developed world
ADENOCARCINOMA:
- from metaplastic columnar epithelium
- lower 1/3 of the epithelium
- relted to acid reflux
- more common in the developed world
Describe how Adenocsarcinoma develops briefly?
1) 30% of the population has GORD(Gastro-oesophageal reflux disease) which causes OESOPHAGITIS(inflammation)
2) 5% of the GORD population get BARRETS where metaplasia of squamos cells to columnar epithelial cells occurs
3) This can develop into low grade dysplasia and then into high grade dysplasia and then into Adenocarcinoma(0.5-1% risk per year)
What are the guidelines of dealing with patients with Baretts?
No dysplasia-do OGD(where you view oesophagus through camera) every 2-3 years
Low grade dysplasia-every 6 months
High grade dysplasia-intervention so it doesnt turn into cancer
Which people are mostly effected by oesophageal cancer and what does this mean for survival?
-Elderly people, particularly men -means Survival rate is low (less than 20% survive 5 years) also complex surgery is involved which is more risky to the elderly
What are the symptoms of Oesophageal cancer?
can swallow-not even saliva
-this causes weight loss
What is the management pathway for Oesophageal cancer?
1) DIAGNOSIS- look down via endoscopy, take a biopsy and then look at the cells histalogically to identify cancer
2) STAGING- CT scan to see if the cancer has spread, LAPAROSCOPY-cut a hole underneath the belly button, blow it up with CO2 and put a camera in and look around peritoneum and liver to spot small things that the CT scan can’t, PET scan-give patient radioactive glucose as cancers absorb more glucose and then this shows u as light on the scan
3) TREATMENT PLAN-If you think its curable give NEO-ADJUVANT CHEMO(chemo before surgury) and then aim for radical surgery. PALLITVE TREATMENT-chemo, stent(opens up oesophagus), DXT
What surgey do you os on oesophageal cancer?
Oesophagectomy-via the IVOR LEWIS approach where you make an incosion in the uppe abdomen and remove the cncerous part of the oesophagus through this .
What is the most common GI cancer in western society?
What is the lifetime risk for men and women?
Who is effected by it?
Colorectal cancer
Men-1 in 10
Women-1 in 14
90% of causes affect people pver 50
In what froms do you get colorectal cancer?
SPORADIC-no fam history just a genetic mistake, isolated lesion
FAMILIAL- famiy history, effects <50, has to be a close 1st degree relative
HEREDITORY SYNDROME-family history, younger age of onset, multiple polips, specific gene defects
What are examples of hereditory syndrome colorectal cancers?
Familial adenomatous polyposis(FAP)
Hereditory nonpolyposis colorectal cancer(lynch syndrome)
Describe briefly the development of colorectal cancer?
Normal epithelium-> mutation occurs causing polip to develop which enetually turns into cancer
What are the rick factors of colorectal cancer?
Past history
Fmaily History (1st degree relative)
Diet/ environment- low fibre diet, smoking, obesity, carcinogenic foods
What are the comoon locations of colorectal cancer?
2/3 are in the descending xolon and rectum
1/2 are in the sigmoid colon and rectum
What are the ways you can look for colorectal cancer?
SIGMOIDOSCOPY- thinner tube but you only see as far as the spleenic flexture(most cancer picked up by this but should still do colonoscopy)
COLONOSCOPY-look at whole of large bowel
What are the clinical presentations of Caecal and right sided colorectal cancer?
- iron defficiency (anaemia)
- change of bowel habit(diarrhoea)
- Distal ilieum obstruction(late)
- palpabel mass(late)
What are the clincial presentations of left sided and sigmoid carcinoma ?(colorectal)
- PR bleeding
- mucus
- Thin stool (late)
What investigations for colorectal cancer can you do?
FAECAL OCCULT BLOOD(Guaic test):
- checks for blood in stool based on pseudoperoxidase activity of haematin(component of haemoglobin)
- avoid red meat, melons, horse radish, vitamin C and NSAIDS for 3 days before the test
BLOOD TESTS:
FBC- anaemia, haematinics-low ferritin
Tumour markers- Monitor CEA (measure CEA before and after tumour is removed-it should go down significantly- monitor CEA every 6months and if it goes up something ain’t right)
DOUBLE CONTRAST BARIUM ENEMA:
- put barium up someones bum and dye in the small bowel and you will see aplly core type lesions in the GI Tract
- does not require sedation
- not as good at detecting smal, lesions
- all lesions to be confirmed with colonscopy and biopsy
- done in the past
COLONSCOPY:
-can visulaise lesion less than 5mm
- small polyps can then be removed(reduce cancer incidence)
- performed under sedation
CT COLONOSCOPY/CONOGRAPHY:
- can visualise lesions more than 5mm
- bowel has to be completely emptied first
- no need for sedation
- less invasive and better tolerated than colonoscopy
- if lesion identified then patinet needs colonscopy for diagnosis
What are the risk factors of pancreatic cancer?
CHRONIC PANCREATITIS- 18 fold increased risk
Type 2 diabetes mellitus
- cholelithiasis, previous gastric surgery and pernicious anaemia(weak correlation)
- Diet(high fat and protein, low friut and veg)(weak correlation
-CIGARETTE SMOKING-causes 25-30%
-FAMILY HISTORY-in 7-10% of cases (relative risk increase 2fold if you have one effected relative, 6 fold if you have 2 relatives effected, 30 fold if you have 3 relatives effected)
INHERITED SYNDROMES -assosiated with increased risk e.g. Lynch syndrome, hereditory pancreatitus, FAP
How does pancreatic cancer develop?
Start with non-invasive neoplastic lesion- Pancreatic intraepithelial Neoplasias (panIN)
these are less than 5mm and not visible from pancreatic imaging
They aquire clonally selected GENETIC and EPIGENETIC mutations along the way
Takes years to develop and often only detected when it metastisises
How do you get rid of pancreatic cancer in the head of the pancrease?
remove head of pancreas, bile duct, Duodenum round to the DJ flexure, bottom end of the stomach
Then you have to join 3 things up: stomach, pancreas as pancrease juice has to go somewhere, and liver as bile juice has to go somewhere
What are the types of iver cancer?
Hepatocellular Carcinomas (HCC)-most common, primary liver cancer
cholangiocarcinoma(ChCA)- cancer in bile duct
Gallbladder Cancers-grow directly into the liver
Colorectal ccaner-most common cause of operation on the liver
