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BRS YEAR 2 > GI Cancers > Flashcards

GI Cancers Flashcards

1
Q

Cancer

A

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

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2
Q

Primary vs secondary cancers

A

Primary arisss from cells in an organ

Secondary is spread to another organ directly or by other means

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3
Q

What are GI tract squamous cell cancers called?

A

Squamous cell carcinoma (SCC)

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4
Q

What are GI tract glandular epithelium cell cancers called

A

Adenocarcinoma

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5
Q

What are GI tract enteroendocrine cell cancers called?

A

Neuroendocrine tumours

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6
Q

What are GI tract interstitial cells of Cajal cancers called?

A

Gastrointestinal stromal tumours (GISTs)

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7
Q

What are GI tract smooth muscle cell cancers called

A

Leiomyoma/leiomyosarcoma

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8
Q

What are GI tract adipose tissue cell cancers called?

A

Liposarcoma

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9
Q

Colorectal cancer prevalence

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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10
Q

Forms of colorectal cancer

A

Forms
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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11
Q

How does colorectal cancer

A

Normal epithelium becomes hyperproliferative epithelium, aberrant cryptic foci.

Hyperproliferatife epithelium and abherrant cryptic foci become small adenoma (cox over expression)

Small adenoma becomes a larger adenoma

Large adenoma becomes colon carcinoma

NSAIDS ,ASPIRIN,FOLATE,CALCIUM have protective affects

Normal epithelium-hyperproliferative epithelium and aberrant cryptic foci-small adenoma-large adenoma-colon carcinoma

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12
Q

What mutations occur in colorectal cancer

A

APC mutation between normal epithelium and hyperproliferative epithelium

COX2 overexpression at hyperproliferative epithelium stage

K ras mutation from small to large adenoma

P53 mutation from large adenoma to colon carcinoma

Loss of 18q in between large and colon carcinoma

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13
Q

Colorectal cancer risk factors

A

Risk factors
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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14
Q

Colorectal cancer presentation for caecal and right sided cancer

A

Depends on location of cancer

Iron deficiency anaemia (most common)
Change of bowel habit (diarrhoea)
Distal ileum obstruction (late)
Palpable mass (late)

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15
Q

Common locations for colorectal cancer

A

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

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16
Q

Presentation for left sided sigmoid carcinoma

A

PR bleeding,mucus
Thin stool (late)

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17
Q

Presentation for rectal carcinoma

A

PR bleeding mucus
Tenesmus (feeling like you need to open bowel)
Anal Perineural and sacral pain

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18
Q

What are late presentations for colorectal cancer

A

Bowel obstruction

Local invasion:bladder symptoms,female genital tract symptoms

Metastasis’s:
Liver (hepatic pain jaundice)
Lung (cough)
Regional lymph nodes
Peritoneum
Sister Marie joesph nodule

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19
Q

Signs of primary cancer (colorectal)

A

Abdominal mass
DRE (digital rectum exam) <12cm dentate and reached by examining finger
Abdominal tenderness and distension (large bowel obstruction)

20
Q

Signs of mestasis and complications for colorectal cancerous

A

Hepatomegaly
Monophonic wheeze
Bone pain

21
Q

Colorectal cancer investigations

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

22
Q

Colonoscopy

A

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

23
Q

Colonography

A

Used for elderly or more frail patients as colonoscopy can dehydrate the pt
CT colonoscopy/colonography
Can visualize lesions > 5mm
No need for sedation
Less invasive, better tolerated
If lesions identified patient needs colonoscopy for diagnosis

24
Q

Other imaging done for colorectal

A

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
Is the CRM threatened?

CT Chest/Abdo/Pelvis
Staging prior to treatment

25
Q

Colorectal cancer management

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

26
Q

Primary liver cancer;hepatocellular carcinoma aetiology and survival rate and optimal treatment

A

Aetiology
- 70-90% have underlying cirrhosis
- Aflatoxin (toxin made by certain fungi)
Median survival without Rx 4-6 m
5yr survival <5%
Systemic chemotherapy ineffective (RR <20%)
Other effective Rx options
- OLTx:liver transplant if you have less than 3 cancers in liver and they’re <3cm
- TACE:transarterial chemo embolisation (put small catheter in blood dull,T of tumour then embolism blood supply
- RFA:radio frequency ablation, stick a needle into tumour and burn it
Optimal Rx surgical excision with curative intent
- 5yr survival >30%
5-15% suitable for surgery

27
Q

Gallbladder cancer aetiology survival and treatment

A

Aetiology unknown
- GS
- porcelain GB
- 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%
Stage II-transmural invasion of cancer going through mucosa to muscle we can remove some liver and lymph nodes
Stage III-begins to invade liver
Stage IV-invaded liver >2cm and distal metastasis
<15% suitable for surgery

28
Q

Cholangiocarcinoma aetiology survival and treatment

A

Aetiology
- Primary sclerosing cholangitis& Ulcerative colitis
- liver fluke (clonorchis sinesis)
- choledochal cyst
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

29
Q

Secondary liver metastases aetiology survival treatment

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

30
Q

Secondary liver metastases

A

Best supportive care 4-6 months

5-FU/LV 12-14 months

IFL OR FOLFIRI 15-16 months

5 FU/LV and bevacuzimab 18.3 months

FOLFOX4 or CAPEOX 19-20 months

IFL AND BEVACIZUMAB 20.3 months

FOLFOX6 20.6

IFL+BV to OX 25.1 months

31
Q

Pancreatic cancer epidemiology

A

IRelatively 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%
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

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

32
Q

Pancreatic cancer risk factors

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

33
Q

What inherited syndrome cause an increased risk of pancreatic cancer

A

Heridatery pancreatitis (genes PRSS1,SPINK1,CFTR) genes cause cationic trypsinogen,panc secretory trypsin inhibitors,CFTR prtone

Familial atypical mutltiple mole melanoma (gene CDKN2A) which is a tumour suppressor

Familial breast ovarian syndrome (BRAC1,BRACW,PALB2) are tumiur suppressors

Peutz jeghers syndrome (STK11) tumiur suppressor

HNPCC (lynch syndrome) and FAP mismatch repair and tumour support (MLH1,MSH2,MSH6,PMS2)APC

34
Q

Pancreatic cancer Pathogenesis

A

Pancreatic Intraepithelial Neoplasias (PanIN) are precancerous lesions found in pancreatic ducts
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

35
Q

What is the Pathogenesis of pancreatic cancer (stages) PanIn progression model

A

Normal
PANIN-1A
(ERBB2 KRAS MUTATION)
PANIN-1B
PANIN-2
(CDKN2A)
OANIN-3
(TP53,SMAD4,BRCA2)

Minimal changes in 1 to moderate dysplasia

36
Q

Pancreatic cancer presentation

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.

37
Q

Carcinoma of body and tail of pancreas

A

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

Pancreatic cancer investigations

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

39
Q

Other investigations for pancreatic cancer

A

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

40
Q

Neuroendocrine tumiurs

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

41
Q

NETS presentation

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

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

42
Q

Nets clinical features

A

Pancreatic:
Insulinoma-hypoglycaemua,whipples triad
Glucagonoma-diabetes mellitus,necrolytic migratory erythema

Pancreatic/duodenal:
Gastrinoma-zollinger ellison syndrome

Entire GIT
VIPoma-vernor morrison syndrome,watery diarrhea
Somatostatinima-gallstones,diabetes,steatorrhea

Midgut-most are non functioning some may develop carcinoid syndrome

Hindgut-usually non functioning

43
Q

NET diagnosis

A

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

Grading of GEP-NETS

A

G1-mitosis <2-10 HPF, ki67 <=2

G2-mitosis 2-20 HPF,ki67 3-20%

G3->20/10 HPF ki67 >20%

High grade (poorly differentiated)Neuroendocrine carcinoma

45
Q

Treatment 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

BRS YEAR 2 (56 decks)

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