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Y2 BRS (Haroop) > Gastrointestinal Cancers > Flashcards

Gastrointestinal Cancers Flashcards

1
Q

What is a primary tumour?

A

Arising directly from a cell in an organ

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2
Q

What is a secondary organ?

A

Spread from another organ, directly, or by other means

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3
Q

What are 6 hallmarks of cancer?

A 
Sustaining proliferative signalling 
Evading growth suppressors
Activating invasion and metastasis 
Enabling replicative immortality 
Inducing angiogenesis 
Resisting cell death
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4
Q

What is sustaining proliferative signalling

A

Ability to sustain chronic proliferation, fundamental trait of cancer cells. 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

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5
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.
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6
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.

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7
Q

Which is a common tumour suppressor gene?

A

tp53

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8
Q

What are tumour suppressor genes?

A

Limit cell growth and proliferation.

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9
Q

Which proteases are involved in apoptosis?

A

Capsases

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10
Q

How do tumour cell circumvent apoptosis?

A

Loss of tp53 tumour suppressor gene

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11
Q

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

A

Telomerase

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12
Q

Which cancer is associated with squamous epithelial cells?

A

Squamous cell carcinoma (SCC)

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13
Q

Which cancer is associated with glandular epithelium?

A

Adenocarcinoma

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14
Q

Which cancer is associated with enteroendocrine cells?

A

Neuroendocrine tumours (NETs)

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15
Q

Which cancer is associated with intestinal cells of Cajal?

A

Gastrointestinal stromal tumours (GISTs)

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16
Q

Which cancer is associated with smooth muscle?

A

Leiomyoma/meiomyosarcoma

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17
Q

Which cancer is associated with adipose tissue?

A

Liposarcoma

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18
Q

Which organs are typically concerned in GI tumours?

A 
Oesophagus
Liver
Pancreas
Colon 
Gastric cancer stomach
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19
Q

Which cancer is the most common, in terms of incidence within the UK?

A

Breast cancer, followed by prostate and lung cancer

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20
Q

What is the fourth most prevalent diagnosed cancer in the UK?

A

Bowel cancer

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21
Q

Which cancers have the highest mortality?

A 
Liver
Pancreatic
Oesophageal 
Stomach
Gallbladder
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22
Q

Which criteria is employed for testing asymptomatic individuals for cancer?

A

Wilson & Jugner Criteria

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23
Q

Which cancer has the lowest survival rate?

A

Pacreatic cancer

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24
Q

Which surgical intervention helps to improve 5-year survival diagnoses?

A

Resectable intervention for cancer

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25
Q

Why is colorectal associated with a higher 5-year survival rate?

A

• The large bowel (colorectal) is mobile with a mesentery, these structures are thus isolated from other peritoneal organs, thus metastasises to other organs is less likely when compared peritoneal organs of the small bowel.

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26
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.
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27
Q

What is the screening tool for colorectal cancer?

A
  • Faecal Immunochemical Test (FIT) - Detects haemoglobin in faeces, every 2 years for everyone aged 60-74.
  • One-off sigmoidoscopy – Individuals aged >55 to remove polyps (reduces future risk of cancer).
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28
Q

What is the screening tool for oesophageal cancer?

A

Regular endoscopy

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29
Q

What screening tool is used in pancreatic and gastric cancer?

A

No tests are available that satisfy the W&J

Depends on the incidence -Japan screens for gastric cancer

30
Q

What screening tool is used for hepatocellular cancer?

A

Regular ultrasound & AFP for high-risk individuals with cirrhosis

Alpha-fetoprotein - elevated levels are a marker of cirrhosis or HPCC

  • Viral hepatitis
  • Alcoholic hepatitis
31
Q

What is familial adenomatous polyposis (FAP)?

A

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

32
Q

Which genes are linked with hereditary pancreatitis?

A

SPINK1 (panc secretory trypsin inhibitor)

CFTR

33
Q

What three stages are involved in the patient cancer journey?

A

Diagnosis
Staging
Treatment

34
Q

What blood test is a screening programme for colon cancer?

A

Faecal occult blood

35
Q

How is cancer diagnosed?

A

using a biopsy

36
Q

Which tumours are most commonly associated with the pancreas?

A

Neuroendocrine tumours

37
Q

Which tumours are most commonly associated with the stomach?

38
Q

What is molecular typing?

A

Molecular typing:
Identify type of mutations present in the cancer, alongside histological type this can determine the most appropriate treatment that is available – targeted chemotherapy.

39
Q

What is the TNM cancer classification?

A

TNM Cancer Classification is conducted
• T – Size of Tumour
• N – Lymph node involvement
• M – Presence of distant metastases

40
Q

What is interventional radiology?

A

Percutaneous biopsies of the liver and retroperitoneal cancers (CT-guided needle aspirates).

41
Q

What is neo-adjuvant chemotherapy?

A

• Pre-surgical intervention to reduce the size of the tumour, in order to increase the efficacy of surgery.

42
Q

What is adjuvant chemotherapy?

A

• Post-operative intervention to ensure that the cancer has effectively been suppressed and removed.

43
Q

What are the main causes of gastric adenocarcinomas?

A

Chronic gastritis is the major driver.

H. Pylori Infection -Due chronic acid overproduction

Pernicious anaemia
• Autoantibodies targeted against parietal cells and intrinsic factor.

Partial gastrectomy
• Leading to bile reflux
• Gastrectomy for peptic ulcers

Epstein-Barr Virus Infection

44
Q

What is 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
45
Q

What is diagnostic laparoscopy?

A

Peritoneal & liver metastases disease prior to full operation.

46
Q

What is endoscopic ultrasound?

A

Will give most detail about local invasion & node involvement.

47
Q

What is a NET?

A

Arise from the gastroenteropancreatic (GEP) tract (or bronchopulmonary system).
• Regarded as common entity as arise from secretory cells of the neuroendocrine system.

48
Q

Where are NETs typically found?

A

Gastroenteropancreatic tract

Bronchopulmonary system

49
Q

What is VIPoma?

A

Tumours arising from the pancreatic neuroendocrine cells that reside within the islet of Langerhans.

50
Q

Which gastric peptides are released from VIPomas?

A

Vasoactive intestinal peptide (VIP)

51
Q

What effect does an increase in VIP have?

A

Causes overstimulation of the gastrointestinal tract leading to profuse watery diarrhoea

Resultant intestinal losses lead to dehydrations, hypokalaemia, hypochlorhydria and metabolic acidosis (loss of bicarbonate)

VIP directly stimulates bon e resorption and vasodilation

52
Q

Which genetic syndrome is predominantly associated with NETs?

A

Multiple endocrine neoplasias type 1 (MEN1)

53
Q

Which hormones are elevated in NETs?

A

Serotonin, tachykinins, substance p, and vasoactive peptides

54
Q

What happens to serotonin 5HT in portal circulation?

A

Metabolised int he liver

55
Q

Why do bronco-pulmonary NETs lead to carcinoid syndrome?

A

Directly secretes serotonin into systemic circulation, bypassing hepatic metabolism

56
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.

57
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.

58
Q

What are the main symptoms of carcinoid syndrome?

A
  • Bronchoconstriction
  • Increased intestinal motility
  • Endocardial fibrosis (Tricuspid incompetence and right-sided valvular regions).

Flushing

59
Q

What are the clinical features of an insulinoma?

A

Hypoglycaemia and Whipple’s Triad

60
Q

What are the clinical features of glucagonoma?

A

Diabetes mellitus, necrolytic migrator erythema

61
Q

Which cells are affected in insulinoma?

A

Pancreatic beta-cells

62
Q

Which cells are affected in a glucagonoma?

A

Pancreatic alpha-cells

63
Q

What are the clinical features of a gastronoma?

A

Zollinger-Ellison syndrome (Gastrin secretion is elevated - potentiates development of peptic ulcers

64
Q

Which cells are concerned with a gastroma?

65
Q

What are the clinical features of a VIPoma?

A

Verner-Morrison Syndrome, Watery Diarrhoea

66
Q

What are the clinical features of a somatostatinoma?

A

Gallstones, diabetes mellitus, steatorrhea

67
Q

Which cells are concerned with somatostatinoma?

A

Pancreatic delta cells

68
Q

What is Whipple’s Triad?

A

Whipple’s triad (Insulinoma)

  1. Low plasma glucose
  2. Symptoms are relieved upon glucose administration
  3. Hypoglycaemic associated symptoms: Epilepsy, syncope and seizures
69
Q

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

A

Chromagranin A

Gut hormone: INsulin, gastrin, somatostatin, peptide YY

70
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)

71
Q

Which imaging is used GI cancers?

A
  • Cross-sectional imaging (CT and/or MRI)
  • Bowel imaging (endoscopy, barium follow through, capsule endoscopy (swallowed)).
  • Endoscopic ultrasound
  • Somatostatin receptor scintigraphy – Pancreatic neuroendocrine tumours express somatostatin receptors that have the ability to bind to radioactively labelled markers (intravenously administered) – 68Ga-DOTATATE PET/CT most sensitive.
72
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

Y2 BRS (Haroop) (62 decks)

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