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GI cancers Flashcards

1
Q

What are the different types of GI cancers and how do you classify them?

A
  1. epithelial cells. Eg. Squamous cell –> squamous cell carcinoma. Glandular epithelium –> adenocarcinoma
  2. neuroendocrine cells: enteroendocrine cells –> neuroendocrine tumours. Intestinal cells of cajal —> gastrointestinal stromal tumours GISTs
  3. connective tissue: smooth muscle –> leiomyoma/leiomyosarcoma. Adipose tissue –> liposarcoma
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2
Q

What are the most common type of GI cancer?

A

adenocarcinoma

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3
Q

In oesophageal cancer, what is a squamous cell carcinoma and what is it related to?

A
  • SCC arises from normal oesophageal squamous epithelium (upper 2/3rds of oesophagus).
  • Related to acetaldehyde pathway (alcohol metabolised by alcohol dehydrogensase to form acetaldehyde).
  • More in less developed world
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4
Q

In oesophageal cancer what is an adenocarcinoma and what is it related to?

A
  • Arises from metaplastic columnar epithelium in lower 1/3rd of oesophagus.
  • Related to acid reflux & more common In developed world
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5
Q

What is the progression of gastric reflux to cancer? What interventions do you do at each stage?

A

Oesophagitis (GORD) –> barret’s oesophagus (metaplasia) –> dysplasia (low or high grade) –> adenocarcinoma.

  • Metaplasia: endoscopy every 2-3 years.
  • Low grade dysplasia: endoscopy every 6 months.
  • High grade dysplasia intervene to prevent it becoming adenocarcinoma
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6
Q

What are the demographics of oesophageal cancer?

A

Affects elderly. More men than women

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7
Q

What is survival in oesophageal cancer like and why?

A
  • Usually present late with dysphagia & weight loss by then too advanced.
  • High morbidity & complex surgery with poor 5-year survival.
  • Palliation hard (rely on oesophageal stents)
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8
Q

How do you diagnose and stage oesogphageal cancer?

A
  • In endoscopy if anything abnormal biopsy it.
  • For staging: CT scan, laparoscopy for metastases, if highly suspicious but submucosal do EUS, PET scan to pick up metastases (occult)
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9
Q

How do you treat oesophageal cancer?

A
  1. squamous cell carcinoma: radiotherapy
  2. adenocarcinoma: neo-adjuvant chemotherapy, re-staging, radical therapy (surgery).
  3. palliative (chemo, DXT radiotherapy, stent)
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10
Q

What is oesophagectomy? Risks?

A
  • Ivor Lewis approach: remove some of oesophagus and join it to stomach.
  • High morbidity & mortality risks
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11
Q

What are the demographics of colorectal cancer?

A

Most common GI cancer in west. Little more in men. Usually >50 years old

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12
Q

What are the forms of colorectal cancer?

A
  1. sporadic: no Fx, older, isolated lesion.
  2. familial: Fx, higher risk if case is under 50 & relative is 1st degree
  3. hereditary syndrome: Fx, younger age onset, gene defects eg. Familial adenomatous polyposis FAP or hereditary non-polyposis colorectal cancer HNPCC or lynch syndrome
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13
Q

How does an adenocarcinoma (colorectal) happen/progress? What can be done to prevent?

A
  • Normal epithelium gets mutated, hyperproliferative epithelium with COX2 expression leads to small adenoma –> large adenoma –> colon carcinoma.
  • If polyp seen in colonoscopy remove them.
  • Aspirin may help progression of polyps to cancer
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14
Q

What are risk factors of colorectal cancer?

A
  • Past history of colorectal cancer, adenoma, ulcerative colitis, radiotherapy.
  • Family history 1st degree <55 years or relatives with genetic predisposition (FAP, HNPCC, peutz-jeghers syndrome), diet/environment, carcinogenic foods, smoking, obesity, socioeconomic status
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15
Q

What does clinical presentation of colorectal cancer depend on?

A

Location of cancer.

  • 2/3rd in descending colon/rectum.
  • 1/2 in sigmoid colon/rectum (within reach of sigmoidoscopy)
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16
Q

What is clinical presentation of colorectal cancer?

A
  1. caecal & R sided cancer: iron deficiency, change bowel habits (diarrhoea), distal ileum obstruction later, palpable mass later. More likely to bleed
  2. L-sided & sigmoid carcinoma: PR bleeding, mucus, thin stool
  3. rectal carcinomas: PR bleeding, mucus, tenesmus (feeling want to open bowels but not - because of sensation of tumour there), anal/perineal/sacral pain (late). 4. bowel obstruction (late)
  4. local invasion (late - bladder, female genital tract symptoms)
  5. metastases (late) - liver causing hepatic pain & jaundice, lung causing cough, regional lymph nodes, peritoneum (sister mary joseph nodule - metastasis in umbilical)
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17
Q

What are examinations for colorectal cancer? For primary cancer & secondary cancer signs?

A
  1. primary cancer: abdominal mass, digital rectal examination DRE most <12cm dentate & by reach of finger, rigid sigmoidoscopy, abdominal tenderness & distension point to large bowel obstruction
  2. metastasis/complications -> hepatomegaly, monophonic wheeze, bone pain
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18
Q

What are investigations used for colorectal cancer?

A
  1. Faecal occult blood FIT test: detect small amounts of blood in stool
  2. Guaiac test (haemoccult - based on pseudoperoxidase activity of haematin - avoid red meat, melons, vitamin C, NSAIDS 3 days before test)
  3. FBC - anaemia, low ferritin
  4. tumour markers: CEA useful in monitoring (if high initially and goes down after treatment)
  5. colonoscopy - visualises lesions <5mm, small polyps removed, usually sedation
  6. CT colonoscopy/colonography: no sedation, better tolerated. Lesions >5mm, if lesions need colonoscopy for diagnosis.
  7. MRI pelvis (rectal cancer –> depth of invasion, mesorectal lymph nodes, no bowel prep needed, helps choose between pre-op chemo or straight to surgery)
  8. CT chest/abdo/pelvis - staging to exclude metastases before treatment
19
Q

How is colorectal cancer managed? what do you do if right/left obstructing cancer?

A
  • Surgery. Resection of bowel depends on blood supply. remove part of bowel + join remaining to the others
    1. right & transverse colon - resection & primary anastamosis if obstructing (usually don’t)
    2. left sided obstruction do hartmann’s procedure (proximal end colostomy LIF +/- reversal in 6 months. Or primary anastomosis but 10% leak, defunctioning ileostomy. Can do palliative stent.
20
Q

What is the most common type of pancreatic cancer and when do they usually present?

A

Pancreatic ductal adenocarcinoma PDA.

-Most present late because causes symptoms late (by then invading or metastases)

21
Q

What is the epidemiology of pancreatic cancer?

A

Higher in wester countries, rare before 45, 4th commonest, 2nd commonest cause of cancer death

22
Q

What are risk factors for pancreatic cancer?

A

Chronic pancreatitis, type II diabetes, cholelithiasis, previous gastric surgery, pernicious anaemia, smoking, family history, occupation (insecticides, aluminium, nickel, acrylamide)

23
Q

What genes are involved in hereditary pancreatitis and what do they cause risk of?

A

PRSS1, SPINK1, CGTR.

Cause 40% lifetime risk of PDA

24
Q

What is the pathogenesis of pancreatic cancer?

A

PanIN progression model.
Normal epithelium –> PanIN1 –> PanIN2 –> PanIN3 –> stage before cancer.
-Each stage associated with different mutation, often takes years to progress but when become cancer metastasize quickly before causing local problems

25
Q

How does carcinoma of the head of the pancreas present?

A
  • Most in head.
  • Jaundice (invasions/compression of CBD), painless, palpable gallbladder (courvoiser’s sign), weight loss (anorexia, malabsorption, diabetes), pain (epigastrium, back radiation in some associated with posterior capsule invasion & irresectability), rarely acute pancreatitis attack or GI bleeding (duodenal invasion or varices secondary to portal or splenic vein occlusion), advanced cases duodenal obstruction causes persistent vomiting
26
Q

How does carcinoma of the body & tail of pancreas present?

A

-More insidious because don’t block things, usually more advanced at diagnosis, marked weight loss with backpain, uncommon jaundice, vomiting sometimes due to DJ flexure, most unresectable.

27
Q

What are investigations used for pancreatic cancer and the purpose of each?

A
  1. tumour marker CA19-9: falsely elevated in pancreatitis, hepatic dysfunction & obstructive jaundice. Concentrations >200 U/ml give 90% sensitivity, thousands concentrations high specificity.
  2. ultasonography - not so useful, can identify tumours, dilated bile ducts & liver metastases
  3. dual-phase CT scan: predicts resectability, organ invasion, vascular invasion, distant metastases
  4. MRI - not useful
  5. MRCP - ductal images without complications of ERCP
  6. ERCP - confirms typical double duct sign, aspiration/brushing of bile duct - therapeutic modality biliary stenting + biopsy.
  7. EUS - very sensitive in detection of small tumours, assessing vascular invasion, FNA
  8. laparoscopy & lap ultrasound - radiologically occult metastatic lesions of liver & peritoneal cavity.
    9: PET scan - for demonstrating occult metastases
28
Q

What treatment for head of pancreas cancer?

A

Whipple resection - head of pancreas, beginning of duodenum, gallbladder & bile duct removed.

29
Q

What treatment for tail of pancreas cancer? What should be done too?

A

Resection. Because of splenic artery take spleen as well.

30
Q

What is an example of a liver cancer?

A

Hepatocellular carcinoma HCC

31
Q

What do most people with liver cancer have underlying?

A

Most have underlying cirrhosis, aflatoxin

32
Q

What is effective and ineffective for liver cancer? What is the optical treatment but problem with it?

A
  • Ineffective: systemic chemo.
  • Effective: transplant, TACE (trans-arterial haemoembolization - small catheters in tumour supply, chemo and embolizing).
  • Optimal is surgical excision with curative intent (but small amount suitable for surgery)
33
Q

potential gallbladder cancer causes?

A

Unknown cause: gallstones, porcelain gallbladder, chronic typhoid infection.

34
Q

What is effective and ineffective for gallbladder cancer?

A
  • Systemic chemo ineffective.
  • Other treatments: optical surgical excision with curative intent.
  • <15% suitable for surgery
35
Q

What are secondary liver metastases like? ( from colorectal cancer) What treatments are effective? What is optimal treatment?

A

15-20% synchronous, 25% metachornous.

  • Systemic chemo improving.
  • Effective treatments RFA & SIRT.
  • Optimal is excision with curative intent.
36
Q

What investigations for staging cancers?

A

Staging CT CAP, PET , staging laparoscopy

37
Q

Causes of microcytic anaemia?

A

iron deficiency, anaemia of chronic disease, thalassaemia, sideroblastic anaemia

38
Q

Causes of normocytic anaemia ABCDE?

A

aplastic anaemia, bleeding, chronic disease, destruction (haemolysis), endocrine disorders (hypothyroidism, hypoadrenalism)

39
Q

Causes of macrocytic anaemia (FAT RBC)?

A

foetus (pregnancy), alcohol excess, thyroid disorders, reticulocytosis, b12/folate deficiency, cirrhosis

40
Q

Causes of iron-deficiency anaemia?

A

Due to blood loss, increased demand or decreased absorption.

  • GI causes - aspirin/NSAID, colonic adenocarcinoma, gastric carcinoma, benign gastric ulcer, angiodysplasia, coeliac disease, gastrectomy, H.pylori.
  • Non- GI causes: menstruation, blood donation, haematuria, epistaxis
41
Q

What are symptoms suggesting colorectal cancer?

A

Change in bowel habit, mucus, blood in stool, faecal incontinence, tenesmus

42
Q

What antibody is for coeliac disease?

A

Anti-TTG

43
Q

What management for adenocarcinoma of descending colon with liver metastases?

A

Primary colonic resection, neoadjuvant chemo, then liver resection

44
Q

causes of cholangiocarcinoma?

treatment?

A
  • primary sclerosing cholangitis PSC, UC
  • liver fluke
  • choledochal cyst
  • systemic chemo ineffective
  • surgical excision with curative intent

BRS (81 decks)

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