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Gastro > Gastro Cancers > Flashcards

Gastro Cancers Flashcards

1
Q

What is cancer

A

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

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2
Q

What is primary cancer

A

Arising directly from the cells in an organ

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3
Q

What is secondary cancer/metastasis ?

A

Spread from another organ, directly or by other means (blood or lymph)

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4
Q

Epithelial cells - what are the cells of the GI tract and what are the cancerous cells

A

Squamous Squamous Cell Carcinoma (SCC)
“Glandular epithelium” Adenocarcinoma

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5
Q

Neuroendocrine cells - what are the cells of the GI tract and what are the cancerous cells

A

Enteroendocrine/bronchial cells Neuroendocrine Tumours (NETs)
Interstitial cells of Cajal Gastrointestinal Stromal Tumours (GISTs)

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6
Q

Connective tissue - what are the cells of the GI tract and what are the cancerous cells

A

Smooth muscle Leiomyoma/leiomyosarcomas
Adipose tissue Liposarcomas

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7
Q

What age does colorectal cancer affect

A

Lifetime risk
—-1 in 10 for men
—1 in 14 for women
Generally affects patients > 50 years (>90% of cases)

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8
Q

What are the 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 - Adenocarcinoma

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9
Q

What are the risk factors for colorectal cancer

A

Past history
Colorectal cancer
Adenoma, ulcerative colitis, radiotherapy

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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10
Q

Where can cancer present

A

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

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11
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)

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12
Q

What is the clinical presentation of left sided and sigmoid carcinoma

A

PR bleeding, mucus
Thin stool (late)

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13
Q

What is the clinical presentation of rectal carcinoma

A

PR bleeding, mucus
Tenesmus
Anal, perineal, sacral pain (late)

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14
Q

What is the clinical presentation of bowel obstruction (late)

A

Late sign

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15
Q

What is the clinical presentation of local invasion

A

Bladder symptoms
Female genital tract symptoms

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16
Q

What is the clinical presentation of metastasis

A

Liver (hepatic pain, jaundice)
Lung (cough)
Regional lymph nodes
Peritoneum
—>Sister Marie Joseph nodule

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17
Q

On examination, what are the signs of primary cancer

A

Abdominal mass
DRE: most <12cm dentate and reached by examining finger
Rigid sigmoidoscopy
Abdominal tenderness and distension – large bowel obstruction

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18
Q

On examination, what are the signs of metastasis and complications

A

Hepatomegaly (mets)
Monophonic wheeze
Bone pain

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19
Q

What does a Faecal occult blood show

A

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).

20
Q

What do blood tests show

A

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

21
Q

What is the purpose of a colonoscopy

A

Can visualize lesions < 5mm
Small polyps can be removed
—Reduced cancer incidence
Usually performed under sedation

22
Q

What is the purpose of a CT colonoscopy / colonography

A

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

23
Q

What other imaging tests can be done for colorectal cancer

A
24
Q

How does colorectal cancer develop?

A

Normal epithelium
Hyperproliferative epithelium
Small adenoma
Large adenoma
Colon carcinoma

25
Q

What investigations are done colorectal cancel

A

Faecal occult blood
Blood markers

26
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

27
Q

Describe primary cancer (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
- TACE
- RFA
Optimal Rx surgical excision with curative intent
- 5yr survival >30%
5-15% suitable for surgery

28
Q

Describe gallbladder cancer

A

Aetiology unknown
- GS
- porcelain GB - lots of calcium
- 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

29
Q

Describe cholangiocarcinoma

A

Aetiology
- PSC & UC
- liver fluke (clonorchis sinesis)
- choledochal cyst (in 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

30
Q

Describe secondary liver metastases

A

15-20% synchronous, 25% metachronous
median survival without Rx <1yr
5yr survival 0%
Systemic chemotherapy improving
Other effective Rx options (RFA - burning & SIRT - radioactive)
Optimal Rx surgical excision with curative intent
- 5yr survival rates of 25-50%
25% suitable for surgery

31
Q

What does surgical resection in HCC look like

A

Only take away part of liver with cancer

32
Q

What does surgical resection in GB CA look like

A

Disconnect the gallbladder
Take away that part of liver
In hilum, take away from lymph nodes
Remove bile duct if cancer going inside that as well

33
Q

What does surgical resection in ChCA look like

A

Left hepatic duct divided

Distal common bile duct detached

Take portal vein and then whole liver comes out

Join bile duct

34
Q

Describe the epidemiology of pancreatic cancer

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 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

More men than women

35
Q

What are 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

Inherited Syndromes associated with ↑ed Risk

36
Q

What is the pathogenesis behind pancreatic cancer

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

37
Q

What is the clinical presentation of pancreatic cancer

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.

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

38
Q

What are investigations 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

MRI imaging detects and predicts resectability with accuracies similar to CT

MRCP provides ductal images without complications of ERCP

  • ERCP
    - 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

39
Q

What happens in TOP resection

A

Spleen has to be taken away along with tail as the artery is closely

40
Q

What happens in HOP?

A

Take away head; then join bile duct, pancreas and stomach

41
Q

Where do neuroendocrine tumours arise from?

Are they sporadic or genetic

A

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

Sporadic tumours in 75%

Associated with a genetic syndrome in 25%:
Multiple Endocrine NeoplasiaType 1 (MEN1)
Parathyroidtumours
Pancreatic tumours
Pituitarytumours

42
Q

How to NETs present

A

Most NETs are asymptomatic & incidental findings

Secretion of hormones & their metabolites in 40%
serotonin, tachykinins (substance P) & other vasoactive peptides

< 10% of NETs produce symptoms

Liver metastases and bronchial carcinoids - symptoms

Can result in a variety of debilitating effects:
Carcinoid syndrome :
Vasodilatation
Bronchoconstriction
↑ed intestinal motility
Endocardial fibrosis (PR & TR)

43
Q

How to diagnose NETs

A

When suspected, investigations to localise the tumour & confirm the diagnosis with histology

Biochemical Assessment:
Chromogranin A is a secretory product of NETs
Other gut hormones: insulin, gastrin, somatostatin, PPY
–Measured in fasting state
Other screening: Calcium, PTH, prolactin, GH
24 hr urinary 5-HIAA (serotonin metabolite)

Imaging:
Cross-sectional imaging (CT and/or MRI)
Bowel imaging (endoscopy, barium follow through, capsule endoscopy)
Endoscopic ultrasound
Somatostatin receptor scintigraphy
–68Ga-DOTATATE PET/CT most sensitive

44
Q

How do you grade NETs

A

Tumour grade provides valuable prognostic info. & influences management

Grade Mitoses Ki-67 Index
G1 <2/10 H.P.F. </= 2%
G2 2-20/10 H.P.F. 3-20%
G3 >20/10 H.P.F. >20%

> High Grade (Poorly Differentiated) Neuroendocrine Carcinoma

45
Q

Primary GEP-NET Sites & Frequency of Liver Metastases?

A

Mainly pancreas and intestine

46
Q

What are the treatment modalities for NETs

A

Curative resection (R0)
Cytoreductive resection (R1/R2)
Liver transplantation (OLTx)
RFA, microwave ablation
Embolisation (TAE), chemoembolisation (TACE)
Selective Internal RadioTherapy (SIRT)
–90Y-Microspheres
Somatostatin receptor radionucleotide therapy
—90Y-DOTA
—177 Lu-DOTA
Medical therapy, targeted therapy, biotherapy
—Octreotide, Lanreotide, SOM203
—PK-inhibitors, mTOR-inhibitors
—⍺-Interferon

Gastro (6 decks)

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