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Phase 1b - Gastroenterology > Gastrointestinal Cancers > Flashcards

Gastrointestinal 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 a primary tumour?

A
  • Tumour arising directly from a cell in an organ
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3
Q

What is a secondary tumour?

A

Tumour spread from another organ, directly, or by other means

Metastasis

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4
Q

Which cancer is associated with squamous epithelial cells?

A

Squamous cell carcinoma (SCC)

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5
Q

Which cancer is associated with glandular epithelium?

A

Adenocarcinoma

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6
Q

Which cancer is associated with enteroendocrine cells?

A

Neuroendocrine tumours (NETs)

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7
Q

Which cancer is associated with intestinal cells of Cajal?

A

Gastrointestinal stromal tumours (GISTs)

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8
Q

Which cancer is associated with smooth muscle?

A

Leiomyoma/meiomyosarcoma

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9
Q

Which cancer is associated with adipose tissue?

A

Liposarcoma

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10
Q

Which organs are typically concerned in GI tumours (5)?

A
  • Oesophagus
  • Liver
  • Pancreas
  • Colon
  • Gastric cancer stomach
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11
Q

Which cancers is the most common, in terms of incidence within the UK (4 in order)?

A
  1. Breast cancer
  2. Prostate cancer
  3. Lung cancer
  4. Bowel cancer
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12
Q

Which cancers have the highest mortality (5 in order)?

A
  1. Liver
  2. Pancreatic
  3. Oesophageal
  4. Stomach
  5. Gallbladder
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13
Q

What is sporadic colorectal cancer?

A

When there is:
* Absence of family history
* Older population
* Isolated lesion

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14
Q

What is familial colorectal cancer?

A

When there is :
* Family history, higher risk if:
* Index case is young (< 50 years)
AND
* The relative is close (1st degree)

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15
Q

What is hereditary syndrome colorectal cancer?

A

When there is:
* Family history
* Younger age of onset
* Specific gene defects

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16
Q

Which cancers are related to hereditary colorectal cancer?

A
  • Familial adenomatous polyposis (FAP)
  • Hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome)

Familial adenomatous polyposis (FAP)
* An autosomal dominant condition caused by germ-line adenomatous polyposis coli gene mutations.
* Patients present with an increased incidence of colorectal adenomas, and at a 100% risk of colorectal cancer by the age of 40 years
* Prophylactic colectomy is performed

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17
Q

What are the past history risk factors of colorectal cancer (4)?

A
  • Colorectal cancer
  • Adenoma
  • Ulcerative colitis
  • Radiotherapy
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18
Q

What are the family history risk factors of colorectal cancer (2)?

A
  • 1st degree relative < 55 yrs
  • Relatives with identified genetic predisposition
    • e.g. FAP, HNPCC, Peutz-Jegher’s syndrome
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19
Q

What are the diet / environmental risk factors of colorectal cancer (4)?

A
  • Carcinogenic foods
  • Smoking
  • Obesity
  • Socioeconomic status
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20
Q

Where does colorectal cancer usually present?

A
  • ⅔ in descending colon and rectum
  • ½ in sigmoid colon and rectum
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21
Q

What is the clinical presentation of caecal & right sided cancer (4)?

Colorectal cancer clinical presentation is location dependent

A
  • Iron deficiency anaemia (most common)
  • Change of bowel habit (diarrhoea)
  • Distal ileum obstruction (late)
  • Palpable mass (late)
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22
Q

What is the clinical presentation of left sided & sigmoid carcinoma (2)?

Colorectal cancer clinical presentation is location dependent

A
  • PR bleeding, mucus
  • Thin stool (late)
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23
Q

What is the clinical presentation of rectal carcinoma (3)?

Colorectal cancer clinical presentation is location dependent

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

Tenesmus is the feeling that you need to pass stools, even though your bowels are already empty.

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24
Q

What is the clinical presentation of coloeractal metastasis to:
* Liver (2)
* Lung (1)
* Regioinal lymph nodes (1)
* Peritoneum (1)

A
  • Liver: hepatic pain, jaundice
  • Lung: cough
  • Palpable regional lymph nodes
  • Peritoneum: Sister Marie Joseph nodule
Sister Marie Joseph Nodule
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25
Q

What are the signs of primary colorectal cancer (4)?

A
  • Abdominal mass
  • Digital Rectal Exam (DRE): most < 12cm dentate and reached by examining finger
  • Rigid sigmoidoscopy
  • Abdominal tenderness and distension – large bowel obstruction
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26
Q

What are the signs of metastasis and complications of colorectal cancer (3)?

A
  • Hepatomegaly (mets) (Liver)
  • Monophonic wheeze (Bronchus / Lungs)
  • Bone pain (Bones)
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27
Q

What non-invasive investigations are recommended in suspected colorectal cancer (4)?

A
  • Faecal occult blood:
    • Guaiac test (Hemoccult)
    • FIT (Faecal Immunochemical Test)
  • Blood tests:
    • FBC
    • Tumour markers

  • Guaiac test (Hemoccult): based on pseudoperoxidase activity of haematin
  • FIT (Faecal Immunochemical Test): detects minute amounts of blood in faeces (faecal occult blood)
  • FBC: anaemia, haematinics – low ferritin
  • Tumour markers: CEA which is useful for monitoring - NOT diagnostic tool
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28
Q

What imaging investigations are recommended in suspected colorectal cancer (4)?

A
  • Colonoscopy
  • CT colonoscopy / colonography
  • MRI pelvis – Rectal Cancer
  • CT Chest / Abdo / Pelvis
Colonoscopy Vs CT colonoscopy / colonography
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29
Q

How is colorectal cancer managed?

A
  • Colon cancer is primarily managed by surgery
    • May require: 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

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30
Q

What is the aetiology of primary liver cancer (Hepatocellular Carcinoma [HCC]) (2)?

A
  • 70-90% have underlying cirrhosis
  • Aflatoxin
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31
Q

What is the median survival without Rx of primary liver cancer (Hepatocellular Carcinoma [HCC])?

A
  • 4-6 / 12
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32
Q

What is the 5yr survival without Rx of primary liver cancer (Hepatocellular Carcinoma [HCC])?

A
  • < 5%
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33
Q

What is the optimal Rx of primary liver cancer (Hepatocellular Carcinoma [HCC])? What is 5yr survival and how many are suitable for it?

A
  • Surgical excision with curative intent
    • 5yr survival >30%
    • Only 5-15% suitable for surgery
Surgical Resection HCC

  • Systemic chemotherapy ineffective (RR < 20%)
  • Other effective Rx options
    • OLTx
    • TACE
    • RFA
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34
Q

What is the aetiology of gallbladder cancer?

A

Unkown

Possible suspects:
* GS
* Porcelain GB
* Chronic typhoid infection

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35
Q

What is the median survival without Rx of gallbladder cancer?

A
  • 5-8 / 12
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36
Q

What is the 5yr survival without Rx of gallbladder cancer?

A
  • < 5%
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37
Q

What is the optimal Rx of gallbladder cancer? What is 5yr survival and how many are suitable for it?

A
  • Surgical excision with curative intent
    • 5yr survival: stage II 64%; stage III 44%; stage IV 8%
    • Only < 15% suitable for surgery
Surgical Resection GB CA

  • Systemic chemotherapy ineffective
  • No other effective Rx options
38
Q

What is the aetiology of cholangiocarcinoma (ChCA) (3)?

A
  • Primary Sclerosis & Ulcerative Colitis
  • Liver fluke (clonorchis sinesis)
  • Choledochal cyst
39
Q

What is the median survival without Rx of cholangiocarcinoma (ChCA)?

A
  • < 6/ 12
40
Q

What is the 5yr survival without Rx of cholangiocarcinoma (ChCA)?

A
  • < 5%
41
Q

What is the optimal Rx of cholangiocarcinoma (ChCA)? What is 5yr survival and how many are suitable for it?

A
  • Surgical excision with curative intent
    • 5yr survival: 20-40%
    • Only 20-30% suitable for surgery
Surgical Resection ChCA

  • Systemic chemotherapy ineffective
  • No other effective Rx options
42
Q

When does secondary liver cancer (CRC) usually occur (synchronous Vs metachronous)?

A
  • 15-20% synchronous
  • 25% metachronous
43
Q

What is the median survival without Rx of secondary liver metastases (CRC)?

A
  • > 12 / 12
44
Q

What is the 5yr survival without Rx of secondary liver metastases (CRC)?

A
  • 0 %
45
Q

What is the optimal Rx of secondary liver metastases (CRC)? What is 5yr survival and how many are suitable for it?

A
  • Surgical excision with curative intent
    • 5yr survival 25-50%
    • Only 25% suitable for surgery
Surgical Resection HCC

  • Systemic chemotherapy improving
  • Other effective Rx options (RFA & SIRT)
46
Q

What is the commonest form of pancreatic cancer?

A
  • Pancreatic ductal adenocarcinoma (PDA)
47
Q

What is the overall median survival of late presentation pancreatic cancer?

80-85% have late presentation

A
  • < 6 / 12
48
Q

What is the 5-year survival of late presentation pancreatic cancer?

80-85% have late presentation

A
  • 0.4 - 5%
49
Q

What is the overall median survival of early presentation pancreatic cancer?

15-20% have resectable disease

A
  • 11-20 / 12
50
Q

What is the 5-year survival of early presentation pancreatic cancer?

15-20% have resectable disease

A
  • 20–25%

Virtually all pts dead within 7 years of surgery

51
Q

Outline the epidemiology of pancreatic cancer:
* Geographical incidence
* Age incidence
* Gender incidence
* Incidence & mortality
* Incidence of death / cancer death

A
  • Incidence higher in Western / industrialised countries
  • Rare before 45 years, 80% occur between 60 & 80 years of age
    • UK & USA annual incidence panc CA 100 per million popn
  • Men > women (1.5 - 2:1)
  • Incidence & mortality roughly equivalent – UK in 2015
    • 9,921 new cases of PDA
    • 9263 deaths from PDA
  • 4th commonest cause of cancer death
  • 2nd commonest cause of cancer death
    • In USA 2030
    • 48,000 deaths
52
Q

What are the risks of pancreatic cancer (7)?

A
  • Chronic pancreatitis → relative risk 18
  • 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
53
Q

Which genes are related to hereditary pancreatitis (3)?

A
  • PRSS1
  • SPINK1
  • CFTR
54
Q

Outline the pathogenesis of pancreatic cancer (2 steps).

A

Pancreatic Intraepithelial Neoplasias (PanIN)
1. PDAs evolve through non-invasive neoplastic precursor lesions
2. Acquire clonally selected genetic & epigenetic alterations along the way

PanIN progression model, showing genetic alterations

  • PanINs are microscopic (< 5 mm diameter) & not visible by pancreatic imaging
55
Q

What is the clinical presentation of pancreatic cancer of the head of the pancreas (6)?

A
  • 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
56
Q

What is the clinical presentation of pancreatic cancer of the body & tail of the pancreas (4)?

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
57
Q

What investigations are recommended in suspected pancreatic cancer (9)?

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
58
Q

How is pancreatic cancer managed?

A
59
Q

What is the aetiology of neuroendocrine tumours (NETs)?

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
60
Q

How do neuroendocrine tumours (NETs) present (5)?

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
    • Carcinoid syndrome
      • Vasodilatation
      • Bronchoconstriction
      • Increased intestinal motility
      • Endocardial fibrosis (PR & TR)
61
Q

What is carcinoid syndrome?

A
  • Occurs due to a release of serotonin (5HT), and other vasoactive peptides into systemic circulation from a carcinoid tumour
62
Q

When does carcinoid syndrome arise in gastroenteropancreatic tumours?

A

Liver metastases – amines drain into the circulation prior to being broken down and metabolised -> Leads to carcinoid syndrome

63
Q

What are the clinical features of pancreatic neuroendocrine tumour (NET) insulinoma (2)?

β Cell type

A
  • Hypoglycaemia
  • Whipple’s triad
64
Q

What is Whipple’s Triad?

A
  1. Low plasma glucose
  2. Symptoms are relieved upon glucose administration
  3. Hypoglycaemic associated symptoms: Epilepsy, syncope and seizures
65
Q

What are the clinical features of pancreatic neuroendocrine tumour (NET) glucagonoma (2)?

α Cell type

A
  • Diabetes mellitus
  • Necrolytic migratory erythema
66
Q

What are the clinical features of pancreatic / duodenal neuroendocrine tumour (NET) gastrinoma (2)?

G Cell type

A
  • Zollingere-Ellison syndrome
67
Q

What is the Zollinger-Ellison syndrome?

A
  • A rare digestive disorder that results in too much gastric acid
68
Q

What are the clinical features of GIT neuroendocrine tumour (NET) VIPoma (2)?

Vasoactive intestinal peptide (VIP) Cell type

A
  • Verner-Morrison syndrome
  • Watery diarrhoea
69
Q

What is the Verner-Morrison syndrome (3)?

A
  • Watery diarrhea
  • Hypokalemia
  • Achlorhydria
70
Q

What are the clinical features of GIT neuroendocrine tumour (NET) somatostatinoma (3)?

D Cell type

A
  • Gallstones
  • Diabetes mellitus
  • Steatorrhoea
71
Q

What are the clinical features of midgut / hindgut neuroendocrine tumour (NET)?

A
  • Most are non-functioning, 40% develop carcinoid syndrome
72
Q

What investigations are recommended in suspected neuroendocrine tumour (NET) (10)?

A
  • 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)
73
Q

What imagings are recommended in suspected neuroendocrine tumour (NET) (10)?

A
  • 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
74
Q

What biochemical assessments are conducted in a patient with a suspected NET?

A

Chromagranin A

Gut hormone: Insulin, gastrin, somatostatin, peptide YY

75
Q

What 24-hour urinary test is done with a patient with a suspected NET, and with potential carcinoid syndrome?

A

Urinary 5-HIAA (a serotonin metabolite)

76
Q

What is the treatment for NETs?

A
  • Curative resection should be performed (R0)
  • Cytoreductive resection (R1/R2)
  • Liver transplantation (OLTx)
  • RFA microwave ablation
  • Embolization (TAE), chemoembolization (TACE)
  • Selective internal radiotherapy (SIRT)
    • 90Y-microspheres
  • Somatostatin receptor radionucleotide therapy
    • 90Y-DOTA
    • 177Lu-DOTA
  • Medical therapy- targeted therapy, biotherapy
    • Octreotide, lanreotide, SOM203
    • PK-Inhibitors, mTOR-inhibitors
    • Alpha interferon
77
Q

What are the 6 hallmarks of cancer?

A
  • Sustaining proliferative signalling
  • Evading growth suppressors
  • Activating invasion and metastasis
  • Enabling replicative immortality
  • Inducing angiogenesis
  • Resisting cell death
78
Q

What is sustaining proliferative signalling?

A
  • Ability to sustain chronic proliferation

Cancer cells reregulate release of growth-promoting signals, enabling signals are conveyed by growth factors that bind cell-surface receptors (intracellular tyrosine kinase domains). The latter proceed to emit signals via branched intracellular signalling pathways that regulate progression through the cell cycle as well as cell growth.

79
Q

How do cancer cells sustain proliferative signalling?

A
  • Self-synthesis of growth factor ligands, respond to via the expression of cognate receptors, resulting in autocrine proliferative stimulation.
  • Alternatively, cancer cells may transmit signals to stimulate normal cells within the supporting tumour-associated stroma, which reciprocate by supplying cancer cells with growth factors.
  • Receptor signalling deregulated by elevating levels of receptor proteins displayed at cancer cell surface; hyperresponsive to growth factor ligand. Structural alterations in the receptor molecules that facilitate ligand-independent firing.
80
Q

How do cancer cells evade growth suppresors?

A
  • Defects in RB pathway permits cell proliferation

RB transduces growth-inhibitory signals, TP53 inputs from stress and abnormality sensors; degree of damage to genome is excessive, TP53 can halt cell-cycle progression. Sensation of irreparable damage can trigger apoptosis.

81
Q

Which is a common tumour suppressor gene?

A

tp53

82
Q

What are tumour suppressor genes?

A
  • Limit cell growth & proliferation
83
Q

Which proteases are involved in apoptosis?

A
  • Capsases
84
Q

How do tumour cell circumvent apoptosis?

A
  • Loss of tp53 tumour suppressor gene
85
Q

Which enzyme is responsible for adding telomere repeat segments to the end of telomeric DNA?

A
  • Telomerase
86
Q

Which criteria is employed for testing asymptomatic individuals for cancer?

A

Wilson & Jugner Criteria

87
Q

What are the 6 Wilson & Jugner criteria for cancer screening tools?

A
  1. The condition sought should be an important health problem
  2. There should be an accepted treatment for patients with recognised disease
  3. Facilities for diagnosis and treatment should be available
  4. There should be a recognisable latent or early symptomatic stage
  5. There should be a suitable test or examination
  6. The natural history of the condition, including development from latent to declared disease, should be adequately understood
88
Q

What three stages are involved in the patient cancer journey?

A

Diagnosis
Staging
Treatment

89
Q

What is molecular typing?

A
  • Identify type of mutations present in the cancer, alongside histological type this can determine the most appropriate treatment that is available – targeted chemotherapy
90
Q

What is the TNM cancer classification?

A
  • T – Size of Tumour
  • N – Lymph node involvement
  • M – Presence of distant metastases
91
Q

What are the red flag symptoms accompanying dyspepsia (ALARMS55)?

A
  • A: Anaemia
  • L: Loss of weight or appetite
  • A: Abdominal mass or examination
  • R: Recent onset of progressive symptoms
  • M: Melaena or haematemesis
  • S: Swallowing difficulty
  • 55: 55 years of age or above

Phase 1b - Gastroenterology (13 decks)

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