gastrointestinal cancers Flashcards

1
Q

what type of cancers are most commonly found in the GI tract?

A

adenocarcinoma - cancers of the glandular epithelium

but there are also:
squamous cell carcinoma
neuroendocrine tumours
gastrointestinal stromal tumours
leiomyoma/leiomyosarcomas
liposarcomas
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2
Q

what are the two types of oesophageal cancers?

A

Squamous Cell Carcinoma:
From normal oesophageal squamous epithelium
Upper 2/3
Acetaldehyde pathway (related to alcohol)
more common in the Less developed world

Adenocarcinoma:
From metaplastic columnar epithelium
Lower 1/3 of oesophagus
Related to acid reflux
More developed world
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3
Q

what is the progression from reflux to cancer like?

A

Oesophagitis (Inflammation) - 30% of UK population has GORD

->

Barrett’s (metaplasia) - 5% of GORD populn → Barrett’s

->

Adenocarcinoma (neoplasia) - Barrett’s lifetime risk of cancer - 0.5-1%/ year.

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4
Q

what is the progression of barrett’s oesophagus like and how is each stage surveyed?

A
barrets oesophagus 
->
dysplasia (low grade)
->
dysplasia (high grade)
->
adenocarcinoma
Barrett’s surveillance
BSG guidelines:
No dysplasia → Every 2-3 years
LGD → every 6 months
HGD → intervention
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5
Q

what is the epidemiology of oesophageal cancer?

A

squamous and adenocarcinoma combined

9th most common cancer

affects the elderly

more common in men than women (10:1)

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6
Q

what are some facts about presentation and prognosis of oesophageal cancer?

A

Late presentation
- dysphagia & wt loss

65% palliative

High morbidity & complex surgery

Poor 5-year survival <20%

Palliation- difficult

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7
Q

what is the management pathway of oesophageal cancer?

A

diagnosis:
endoscopy -> biopsy

staging:
CT
laparoscopy
EUS (endoscopic ultrasound) for some
PET scan for some

treatment plan:
curative - (for adenocarcinoma) neoadjuvant chemo -> radical surgery
(squamous cell carcinoma is pretty effectively treated with radiotherapy)
also two stage ivor lewis approach surgery (oesophagectomy around the cancer)

palliative - chemo, DXT (radiotherapy), stent

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8
Q

what is the epidemiology of colorectal cancer?

A

Most common GI cancer in Western Societies

Third most common cancer death in men & women

Lifetime risk:
1 in 10 for men
1 in 14 for women

Generally affects patients > 50 years (>90% of cases)

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9
Q

what are the different forms of colorectal cancer?

A

Sporadic:
Absence of family history, older population, isolated lesion

Familial:
Family history, higher risk if index case is young (<50years) and the relative is close (1st degree)

Hereditary syndrome:
Family history, younger age of onset, specific gene defects
e.g. Familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome)

Histopathology - pretty much all Adenocarcinoma

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10
Q

how does colorectal cancer develop?

A

normal epithelium - cause APC mutation

->

hyperproliferative epithelium

->

small adenoma

->

large adenoma (K-ras mutation)

->

colon carcinoma (p53 mutation) this one can metastasise)

aspirin and NSAIDs may stop this progression

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11
Q

what are the risk factors for colorectal cancer?

A

Past history:
Colorectal cancer
Adenoma, ulcerative colitis, past radiotherapy has a big effect on the bowels

Family history:
1st degree relative < 55 yrs
Relatives with identified genetic predisposition
(e.g. FAP, HNPCC, Peutz-Jegher’s syndrome)

Diet/Environmental:
?carcinogenic foods 
Smoking
Obesity
Socioeconomic status
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12
Q

what is the clinical presentation of colorectal cancer?

A

Depends on location of cancer

Locations:
⅔ occur in descending colon and rectum
½ in sigmoid colon and rectum (i.e. within reach of flexible sigmoidoscopy)

Caecal & right sided: cancer 
Iron deficiency anaemia (most common)
Change of bowel habit (diarrhoea)
Distal ileum obstruction (late)
Palpable mass (late)

Left sided & sigmoid carcinoma:
PR bleeding, mucus
Thin stool (late)

Rectal carcinoma:
PR bleeding, mucus
Tenesmus (cant get poo out)
Anal, perineal, sacral pain (late)

Bowel obstruction (late)

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13
Q

how do local invasion and metastasis of colorectal cancer present clinically?

A

Local invasion (late):
Bladder symptoms
Female genital tract symptoms

Metastasis (late):
Liver (hepatic pain (rare), jaundice (also rare))
Lung (cough)
Regional lymph nodes
Peritoneum
Sister Mary Joseph nodule (belly button bump)

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14
Q

what are the signs of colorectal cancer on examination?

A

Signs of primary cancer:
Abdominal mass
DRE (digital rectal examination): most <12cm dentate and reached by examining finger
Rigid sigmoidoscopy
Abdominal tenderness and distension – large bowel obstruction

Signs of metastasis and complications:
Hepatomegaly (mets)
Monophonic wheeze
Bone pain

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15
Q

what investigations are done for colorectal cancer?

A

Faecal occult blood:
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).

Blood tests:
FBC: anaemia, haematinics – low ferritin
Tumour markers: CEA which is useful for monitoring (NOT diagnostic tool)

Colonoscopy:
Can visualize lesions < 5mm
Small polyps can be removed
Reduced cancer incidence 
Usually performed under sedation
CT colonoscopy/colonography:
Can visualize lesions > 5mm
No need for sedation
Less invasive, better tolerated
If lesions identified patient needs colonoscopy for diagnosis
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16
Q

what are imaging tests used in colorectal cancer?

A
CT colonoscopy/colonography:
Can visualize lesions > 5mm
No need for sedation
Less invasive, better tolerated
If lesions identified patient needs colonoscopy for diagnosis

MRI pelvis – Rectal Cancer:
Depth of invasion, mesorectal lymph node involvement
No bowel prep or sedation required
Help choose between preoperative chemoradiotherapy or straight to surgery

CT Chest/Abdo/Pelvis:
Staging prior to treatment

17
Q

how is colorectal cancer managed?

A

Colon cancer is primarily managed by surgery

? Stent/Radiotherapy/Chemotherapy

Obstructing colon carcinoma:
Right & transverse colon – resection and primary anastomosis
Left sided obstruction - 
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
18
Q

how common is pancreatic cancer and what is the prognosis like?

A

Relatively common & highly lethal:

Commonest form of panc CA is pancreatic ductal adenocarcinoma (PDA)

80-85% have late presentation
Overall median survival <6 months
5-year survival 10-15%

15-20% have resectable disease
Median survival 11-20 months
5-year survival 20–25%
Virtually all pts dead within 7 years of surgery

19
Q

what is the epidemiology of pancreatic cancer?

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

20
Q

what are the risk factors for pancreatic cancer?

A

Chronic pancreatitis → 18-fold increased 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

21
Q

what inherited syndromes are associated with an increased risk of pancreatic cancer?

A

hereditary pancreatitis (40% lifetime risk of PDA)

familial atypical multiple mole melanoma (10-17%)

familial breast-ovarian cancer syndrome (5%)

peutz-jeghers syndrome (11-36%)

HNPCC (lynch syndrome) (3.7%)

all involve mutations in tumour supressor genes

22
Q

what is the pathogenesis of pancreatic cancer?

A

commonest
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

progression from PanIN-1 to PanIN-3
this is the stage before pancreatic cancer

they are similar to polyps

23
Q

what is the clinical presentation of pancreatic cancer - head of pancreas?

A

Carcinoma of the head of the pancreas:
At least two-thirds of PDAs arise in the 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.

24
Q

what is the clinical presentation of pancreatic cancer - body and tail?

A

Carcinoma of the body & tail of pancreas:
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

25
Q

what investigations are done for pancreatic cancer?

A

Tumour marker CA19-9:

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

Ultrasonography:

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

Dual-phase CT accurately predicts resectability in 80–90% of cases:

  • contiguous organ invasion
  • vascular invasion (coeliac axis & SMA)
  • distant metastases

dual phase CT is main choice

26
Q

what imaging is done for pancreatic cancer?

A

CT is good

MRI :
imaging detects and predicts resectability with accuracies similar to CT

MRCP:
provides ductal images without complications of ERCP

ERCP (most useful)

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

EUS:

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

Laparoscopy & laparoscopic ultrasound:
- detect radiologically occult metastatic lesions of liver & peritoneal cavity

PET:
mainly used for demonstrating occult metastases

27
Q

how do you resect a pancreatic tumour?

A

head of pancreas:
whipples
take out a ton, gall bladder, HOP, end of stomach and proximal duodenum
reconnect bile duct, stomach and body of pancreas to the next bit of small bowel

tail of pancreas:
just take distal part of pancreas
spleen has to go to

28
Q

what are the different t types of liver cancer?

A

HCC:
hepato cellular carcinoma
most cancer
happens in patients with cirrhosis (for whaever reason)

ChCA:
cholangiocarcinoma
commonest at the bifurcation between the right and left hepatic ducts

GB CA:
gall bladder cancer
doesnt cause problems but spreads very easily

CRC:
colorectal cancer liver metastases

29
Q

what is hepatocellular carcinoma?

A

Aetiology:

  • 70-90% have underlying cirrhosis
  • Aflatoxin

Median survival without Rx 4-6 m

5yr survival <5%

Systemic chemotherapy ineffective (RR <20%)

Other effective Rx options:

  • OLTx (liver transplant)
  • TACE
  • RFA

Optimal Rx surgical excision with curative intent:
- 5yr survival >30%

5-15% suitable for surgery

30
Q

what is gall bladder cancer?

A

Aetiology unknown:

  • gall stones
  • porcelain GB (recurrent inflammation causing calcification)
  • chronic typhoid infection

Median survival without Rx 5-8 m

5yr survival <5%

Systemic chemotherapy ineffective

No other effective Rx options

Optimal Rx surgical excision with curative intent:
- 5yr survival: stage
II 64%; stage III 44%; stage IV 8%

<15% suitable for surgery

31
Q

what is cholangiocarcinoma?

A

Aetiology:

  • PSC & UC
  • liver fluke (clonorchis sinesis)
  • choledochal cyst (dilatation of bile duct)

Median survival (depends on site) without Rx <6 m

5yr survival <5%

Systemic chemotherapy ineffective
GEMCIS - median overall survival 11.7 months*

No other effective Rx options (OLTx)

Optimal Rx surgical excision with curative intent:
- 5yr survival 20-40%

20-30% suitable for surgery

32
Q

what are secondary liver metastases (CRC)?

A

15-20% synchronous, 25% metachronous

median survival without Rx <1yr

5yr survival 0%

Systemic chemotherapy improving

Other effective Rx options (RFA & SIRT)

Optimal Rx surgical excision with curative intent:
- 5yr survival rates of 25-50%

25% suitable for surgery