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BRS2 Term 2 > GI cancers > Flashcards

GI cancers Flashcards

1
Q

What is cancer?

A
  • when abnormal cells divide without control and can invade nearby tissues
  • cancer cells can also spread to other parts of the body through blood and lymph systems–> secondary/metastases
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2
Q

What is an adenocarcinoma?

A

type of cancer that starts in mucus-producing glandular cells e.g. in colon, lungs, breast

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3
Q

What is cancer screening and what are the Wilson&Jungner criteria?

A

testing asymptomatic individuals to identify cancer at an early stage

  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 test should be acceptable to the population
  7. the natural history of the condition, inc. development from latent to declared disease, should be adequately understood
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4
Q

What is the current screening program for colorectal cancer?

A
  • offered to healthy individuals
  • faecal immunochemical test (FIT): detects Hb in faeces- every 2 years for everyone aged 60-74
  • one-off sigmoidoscopy for everyone aged >55–> if polyps present, they are removed (reduces risk of cancer)
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5
Q

What is the current screening program for oesophageal cancer?

A

regular endoscopy for patients with Barrett’s oesophagus or low - high grade dysplasia

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6
Q

What is the current screening program for pancreatic and gastric cancer?

A
  • no test that meets W&J criteria
  • depends on incidence- Japan screens for gastric cancer w/endoscopies
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7
Q

What is the current screening program for hepatocellular cancer?

A

regular ultrasound and AFP (alpha-fetoprotein) for high-risk individuals w/ cirrhosis: either due to viral hepatitis or alcoholic hepatitis (or NASH)

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8
Q

What is the 2-week wait cancer pathway?

A

within 2 weeks of presenting with worrying symptoms to GP or other, patient must have had diagnostic tests and been discussed in MDT meeting- and then offered treatment

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9
Q

What is molecular typing in pathology?

A

determines what mutatino the cancer has- can help to determine type of treatment

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10
Q

What is the difference between neoadjuvant and adjuvant chemotherapy?

A

neoadjuvant= chemo before surgery (to make tumour smaller and operable)

adjuvant= chemo after surgery (‘mopping up’)

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11
Q

What is the major driver of gastric adenocarcinoma?

A

chronic gastritis= major driver

  • H. pylori infection–> causes inflammation of gastric mucosa–> gastritis, esp. in antrum of stomach–> duodenal ulcers–> inc. acid prod.–> metaplasia–> cancer
  • pernicious anaemia–> autoantibodies against parts/products of parietal cells
  • partial gastrectomy (e.g. for ulcer, before PPIs)–> bile reflux
  • epstein-barr infection
  • family history, inc. heritable diffuse-type gastric cancer due to E-cadherin mutations
  • high salt diet and smoking
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12
Q

How do people with gastric cancer present and what are the red flags?

A

dyspepsia= commonest symptom (upper abdo discomfort after eating or drinking)

red flags- ALARMS55:

  • Anaemia
  • Loss of weight or appetite
  • Abdominal mass on examination
  • Recent onset of progressive symptoms
  • Melaena (black, tarry stool) or haematemesis (vomiting blood)
  • Swallowing difficulty
  • 55 years or older
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13
Q

How do you diagnose gastric cancer?

A

endoscopy + biopsy

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14
Q

How do you stage gastric cancer?

A
  • CT of chest, abdomen and pelvis - provides info on metastases
  • PET-CT to pick up lesions you miss on CT scan
  • diagnostic laparoscopy- to pick up peritoneal+ liver metastases before full op
  • endoscopic US (backup) will give most detail about local invasion and node involvement
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15
Q

What are the treatment options for gastric cancer?

A
  • neoadjuvant chemotherapy: to reduce tumour size before surgery
  • for tumour at oesophago-gastric junction–> oesophago-gastrectomy- then join what’s left of stomach and oesophagus
  • for tumour <5cm away from OG junction–> total gastrectomy, as you can’t save sphincter mechanism *
  • for tumour >5cm away from OG junction–> subtotal gastrectomy, usual distal gastrectomy
  • after successful gastric surgery- consider adjuvant chemotherapy in advanced tumours to reduce risk of relapse
  • N.B. palliative approches: stenting or gastro-jejunal anastomosis if not possible to resect something
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16
Q

What are neuroendocrine tumours (NETs)?

A
  • arise from gastroenteropancreatic (GEP) tract- GEP-NETs (or bronchopulmonary system)
  • arise from secretory cells of neuroendocrine system
  • sporadic tumours in 75% of cases
  • but 25% associated w/ genetic syndrome e.g. Multiple Endocrine Neoplasia type 1 (MEN1)- parathyroid, pancreatic and pituitary tumours
17
Q

How do patients with NETs present?

A
  • most NETs= asymptomatic and incidental findings
  • 40% of NETs secrete hormones and their metabolites e.g. serotonin, tachykinins (e.g. substance P), and other vasoactive peptides
  • but <10% of NETs produce symptoms
  • can result in a variety of debilitating effects- carcinoid syndrome: flushing due to vasodilatation (bc of serotonin), bronchoconstriction, inc. intestinal motility/diarrhoea, endocardial fibrosis (pulmonary and tricuspid regurgitation)
  • N.B. if no liver metastases, GEP-NETs = no carcinoid syndrome, as hormones are metabolised, but bronchiopulmonary NETs release serotonin directly into systemic circulation, so symptomatic (even if no liver metastases)
18
Q

What are the clinical features of pancreatic NETs?

A
  • beta cells- insulinoma–> hypoglycaemia (may present with epilepsy), Whipple’s triad: (1) symptoms of hypoglycemia, (2) hypoglycemia (blood glucose level <50 mg/dL), and (3) relief of symptoms following ingestion of glucose
  • alpha cells- glucagonoma–> diabetes mellitus, necrolytic migratory erythema (rash)
19
Q

What is a gastrinoma?

A
  • NET in pancreas or duodenum
  • produces excessive levels of gastrin–> stimulates stomach to secrete acid and enzymes, causing peptic ulcers- lots of abdominal pain and diarrhoea (Zollinger–Ellison syndrome)
20
Q

What is Verner-Morrison syndrome?

A
  • results from a VIPoma- type of NET
  • characterised by watery diarrhoea (results in massive intestinal loss of water, potassium, sodium and bicarbonate)
  • can arise from entire GIT
  • N.B. VIP= vasoactive intestinal peptide
21
Q

What is a somatostatinoma?

A
  • NET that arises from delta cells- producing excess somatostatin
  • can result in gallstones, diabetes mellitus and steatorrhoea
  • can arise from entire GIT
22
Q

What are the clinical features of NETs in the midgut and hindgut?

A
  • midgut- most are non-functioning, but 40% develop carcinoid syndrome
  • hindgut- usually non-functioning
23
Q

What biochemical tests do you carry out in a suspected NET case?

A
  • chromogranin A- secretory product of NETs
  • other gut hormones- measured in fasting state: insulin, gastrin, glucagon, somatostatin, PPY
  • other screening: calcium, PTH, prolactin, GH
  • 24h urinary 5-HIAA (serotonin metabolite)
24
Q

What imaging do you carry out in a suspected NET?

A
  • cross sectional CT and/or MRI
  • bowel imaging (endoscopy, barium follow through- rare, or capsule endoscopy)
  • endoscopic US- invaluable in finding pancreatic NETs
  • somatostatin receptor scintigraphy- 68Ga-DOTATATE PET/CT most sensitive
25
Q

How are GEP-NETs staged?

A

G1, G2 and G3- high grade (poorly differentiated- don’t look like normal cells) neuroendocrine carcinoma

26
Q

What are the treatment options for NETs?

A
  • if possible, curative resection- aim for R0
  • cytoreductive resection (leaving some of tumour)- R1/R2
  • liver transplantation (OLTx)
  • RFA, microwave ablation
  • embolisation (TAE), chemoembolisation (TACE)
  • selective internal radiotherapy (SIRT)
  • somatostatin receptor radionucleotide therapy
  • medical therapy, targeted therapy, biotherapy

BRS2 Term 2 (14 decks)

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