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Year 2 - BRS > 6.11 - Gastrointestinal cancers > Flashcards

6.11 - Gastrointestinal cancers Flashcards

1
Q

What is a cancer?

A

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

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2
Q

What is a primary cancer?

A

Arising directly from the cells in an organ

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3
Q

What is a secondary cancer/metastasis?

A

Spread from another organ, directly or by other means (blood or lymph)

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4
Q

What are GI tract squamous cell (epithelial) cancers called?

A

Squamous cell carcinoma (SCC)

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5
Q

What are GI tract glandular epithelium cell (epithelial) cancers called?

A

Adenocarcinoma

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6
Q

What are GI tract enteroendocrine cell (neuroendocrine) cancers called?

A

Neuroendocrine tumours (NETs)

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7
Q

What are GI tract interstitial cells of Cajal (neuroendocrine) cancers called?

A

Gastrointestinal stromal tumours (GISTs)

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8
Q

What are GI tract smooth muscle cell (connective tissue) cancers called?

A

Leiomyoma / leiomyosarcoma

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9
Q

What are GI tract adipose tissue cell (connective tissue) cancers called?

A

Liposarcoma

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10
Q

Where can GI neuroendocrine tumours occur?

A

Throughout the whole GI tract

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11
Q

How common is colorectal cancer?

A
  • most common GI cancer in Western societies
  • third most common cancer death in men and women
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12
Q

What is the lifetime risk of colorectal cancer in men and women?

A
  • 1 in 10 for men
  • 1 in 14 for women
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13
Q

Which age group does colorectal cancer affect the most?

A

Generally affects patients >50 years (>90% of cases)

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14
Q

What are the three forms of colorectal cancer?

A
  • sporadic
  • familial
  • hereditary syndrome
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15
Q

What are the criteria for sporadic colorectal cancer? (3)

A
  • absence of family history
  • older population
  • isolated lesion
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16
Q

What are the criteria for familial colorectal cancer? (2)

A
  • family history
  • higher risk if index case is young (<50 years) and the relative is close (1st degree)
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17
Q

What are the criteria for hereditary colorectal cancer? (3 + examples)

A
  • family history
  • younger age of onset
  • specific gene defects
  • e.g. familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome)
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18
Q

What is the histopathology (type of cancer) for all three types of colorectal cancer?

A

Adenocarcinoma

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19
Q

Describe the progression of colorectal cancer.

A

Normal epithelium –> (APC mutation) –> hyperproliferative epithelium, aberrant cryptic foci, polyp (COX-2 overexpression) –> small adenoma –> (K-ras mutation) –> large adenoma –> (p53 mutation) –> (loss of 18q) –> colon carcinoma

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20
Q

What do we do for people with a polyp / 50+ years old (colorectal cancer)?

A
  • routine colonoscopies to screen for new polyp development
  • straightforward to endoscopically remove polyps before they become colorectal cancer - prophylactic endoscopic polyp/adenoma resections
  • this is because over years a small polyp can become a large cancer
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21
Q

What does aspirin/NSAIDs do in colorectal cancer development?

A

Protects against the development of colorectal cancer

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22
Q

What are the risk factors for developing colorectal cancer?

A
  • past history
    • colorectal cancer
    • adenoma, ulcerative colitis, radiotherapy
  • family history
    • 1st degree relative <55 years
    • 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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23
Q

What are the locations that colorectal cancers are found in?

A
  • 2/3 in descending colon (left colon) and rectum
  • 1/3 in sigmoid colon and rectum (i.e. within reach of flexible sigmoidoscopy)
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24
Q

How do caecal and right-sided colorectal cancer patients present?

A
  • iron deficiency anaemia (most common)
  • change of bowel habits (diarrhoea)
  • distal ileum obstruction (late)
  • palpable mass (late)
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25
Q

How do left-sided and sigmoid carcinoma colorectal cancer patients present?

A
  • PR (rectal) bleeding (fresh red blood), mucus
  • thin stool (pencil-type stools = late)
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26
Q

How do rectal carcinoma colorectal cancer patients present?

A
  • PR (rectal) bleeding, mucus
  • tenesmus - the feeling of needing to open bowels but nothing comes out when you try
  • anal, perianal, sacral pain (late)
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27
Q

What kind of sign of colorectal cancer is bowel obstruction?

A

Late sign

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28
Q

What are some signs of local invasion (late) of colorectal cancer? (2)

A
  • bladder symptoms
  • female genital tract symptoms
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29
Q

Where can colorectal cancer metastasise to (late sign) and how can these present? (5)

A
  • liver (hepatic pain, jaundice, hepatomegaly)
  • lung (cough, monophonic wheeze)
  • bone (bone pain)
  • regional lymph nodes (e.g. inguinal)
  • peritoneum (Sister Marie Joseph nodule is metastasis in umbilicus)
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30
Q

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

A
  • abdominal mass
  • digital rectal examination (DRE): most <12cm from dentate line and reached by examining finger
  • rigid sigmoidoscopy (bedside/outpatient test)
  • abdominal tenderness and distension - large bowel obstruction
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31
Q

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

A
  • hepatomegaly (liver)
  • monophonic wheeze (lung)
  • bone pain (bones)
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32
Q

What investigations can we do for colorectal cancer? (6)

A
  • faecal occult blood
  • blood tests
  • colonoscopy
  • CT colonoscopy/colonography
  • MRI pelvis
  • CT chest/abdo/pelvis
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33
Q

What two types of faecal occult blood tests for colorectal cancer are there?

A
  • Guaiac test (Hemoccult) - based on pseudoperoxidase activity of haematin
    • 40-80% sensitivity and 98% specificity
    • dietary restrictions - avoid red meat, melons, horseradish, vitamin C and NSAIDs for 3 days before test
  • FIT (faecal immunochemical test) - detects minute amounts of blood in faeces (faecal occult blood)
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34
Q

What two types of blood tests are there for colorectal cancer?

A
  • FBC - anaemia, haematinics (low ferritin)
  • tumour markers - CEA (carcinoembryonic antigen) which is useful for monitoring evidence of recurrence but NOT as a diagnostic tool
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35
Q

What does colonoscopy do for colorectal cancer?

A
  • can visualise lesions <5mm
  • small polyps can be removed = reduced cancer incidence
    • pedunculated polyp (with stalk) –> wire around it + heat to cut and close wound to prevent bleeding
  • usually performed under sedation
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36
Q

How does CT colonoscopy/colonography compare with normal colonoscopy (colorectal cancer)?

A
  • can visualise lesions >5mm (not under)
  • no need for sedation
  • less invasive, better tolerated
  • if lesions identified then patient needs colonoscopy for diagnosis
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37
Q

When do we do MRI pelvis for (colo)rectal cancer?

A
  • if you have a tumour you think is relatively advanced
  • look at: depth of invasion, mesorectal lymph node involvement - to see whether we can do R0 resection (take all cancer out with good margin)
  • no bowel prep or sedation required
  • help choose between preoperative chemotherapy (to reduce tumour size) or straight to surgery
  • is the CRM (circumferential resection margin - prognostic predictor) threatened?
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38
Q

Why is CT chest/abdo/pelvis done for colorectal cancer?

A

Staging prior to treatment to exclude liver or lung metastases

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39
Q

What is the primary management for colorectal cancer?

A

Surgery

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40
Q

What can you do to give yourself time to plan colorectal cancer surgrey?

A

Put in a stent, or use radiotherapy / chemotherapy

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41
Q

What do you do with a right and transverse colon obstructing carcinoma?

A
  • resection and primary anastomosis - resect and join up straight away with primary anastomosis as blood supply is good so will not leak
  • usually do not obstruct as more leeway for carcinoma to expand

Right / extended right hemicolectomy

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42
Q

Why do you have to be more careful with a left colon obstruction?

A

Blood supply to left colon is not as good as to right colon

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43
Q

What can you do with a left colon obstructing carcinoma? (3)

A
  • Hartmann’s procedure
    • proximal end colostomy (LIF) - remove tumour, instead of joining proximal bowel and rectum, bring proximal bowel up to skin and do a colostomy (staple distal end)
    • reversal in 6 months if patient is okay
  • primary anastomosis (join up proximal bowel and rectum) but not safest:
    • intraoperative bowel lavage with primary anastomosis but 10% chance of leak due to poor blood supply
    • defunctioning ileostomy
  • palliative stent
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44
Q

What is the difference between a stoma on the left or right side of a patient?

A
  • left side = colostomy (large bowel)
  • right side = ileostomy (small bowel)
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45
Q

What are the most important right-sided colonic arteries? (3)

A
  • ileocolic
  • right colic
  • middle colic
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46
Q

What are the most important left-sided colonic arteries? (2)

A
  • left colic
  • when we get to the pelvis, sigmoid arteries are important
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47
Q

What is resection of the bowel dependent on?

A

Blood supply to that region

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48
Q

What is a right hemicolectomy?

A

Remove right colon, then anastomose terminal ileum to transverse colon

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49
Q

What is an extended right hemicolectomy?

A
  • take around 2/3 of large bowel out - right colon and part of transverse
  • then do ileocolic anastomosis (ileum to remaining colon)
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50
Q

What is a left hemicolectomy?

A

Resect left colon then anastomose remaining colon parts

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51
Q

Why is a rectal cancer resection difficult and what can we do?

A
  • blood supply around rectum/anus is poor
  • we can do the resection and join up the other parts (e.g. colon to anus), and then do an ileostomy (bring up loop of small bowel to skin to divert faeces going through delicate anastomosis)
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52
Q

What are some different types of liver cancer? (3 + 1)

A
  • primary liver cancer - hepatocellular carcinoma (HCC)
  • gallbladder cancer (GB CA)
  • cholangiocarcinoma (ChCA)
  • (colorectal cancer CRC can also affect the liver)
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53
Q

What is hepatocellular carcinoma?

A

Cancer of liver hepatocytes, usually in cirrhotic livers

54
Q

What are the two causes of hepatocellular carcinoma?

A
  • 70-90% have underlying cirrhosis due to Hep B, C or alcoholic liver disease
  • aflatoxin (toxin made by certain fungi)
55
Q

What is the median survival and 5y survival of hepatocellular carcinoma without treatment?

A
  • median survival: 4-6 months of living
  • 5 year survival rate <5%
56
Q

How effective is systemic chemotherapy for hepatocellular carcinoma?

A

Ineffective - response rate <20%

57
Q

What is the optimal Rx (intervention) for hepatocellular carcinoma?

A
  • surgical excision with curative intent (5y survival >30%)
  • only 5-15% suitable for surgery
58
Q

What are some alternative treatment options for hepatocellular carcinoma? (3)

Apart from surgical excision (optimal)

A
  • OLTx - liver transplant (if you have <3 hepatocellular tumours in liver and they are <3 cm)
  • TACE - transarterial chemo embolisation (small catheters inside blood supply of tumour, giving high chemo dose then embolising/blocking blood supply)
  • RFA - radiofrequency ablation (stick needle into tumour and burn it)
59
Q

What is the aetiology/causes of gallbladder cancer? (3)

A

Unknown - chronic cholecystitis

  • associated with gallstones
  • porcelain gallbladder occurs - chronic inflammation causes calcification so it looks like porcelain
  • associated with chronic typhoid infection
60
Q

What is the median survival and 5y survival of gallbladder cancer without treatment?

A
  • median survival: 5-8 months
  • 5yr survival <5%
61
Q

Is systemic chemotherapy effective for gallbladder cancer?

62
Q

What is the only effective treatment option for gallbladder cancer?

A
  • surgical excision with curative intent
  • 5yr survival at:
    • stage II (transmural invasion through mucosa into muscle) = 64%
    • stage III (beginning to invade liver <2cm) = 44%
    • stage IV (invading liver >2cm and distal metastases) = 8%
  • only <15% suitable for surgery
63
Q

Where do cholangiocarcinomas often occur?

A
  • bifurcation where the common hepatic duct –> right and left (small tumours but large operation to remove)
  • distal ChCA through HOP - need Whipple’s resection
  • periphery - need to take away that bit of liver
64
Q

What is the aetiology of cholangiocarcinoma?

A
  • associated with primary sclerosing cholangitis (PSC) and ulcerative colitis (UC)
  • associated with liver fluke (clonorchis sinesis) in SE Asia - from uncooked fish, worms inhabit bile ducts causing irritation and cancer
  • choledochal cyst - dilatation of bile duct with 10-15% risk of becoming cancer
65
Q

What is the median survival and 5y survival of cholangiocarcinoma without treatment?

A
  • median survival (depends on the site): <6 months
  • 5yr survival <5%
66
Q

How effective is systemic chemotherapy for cholangiocarcinoma?

A

Ineffective but improving - currently median survival is 11.7 months

67
Q

What is the only effective treatment for cholangiocarcinoma?

A
  • surgical excision with curative content
  • 5yr survival 20-40%
  • 20-30% suitable for surgery
68
Q

How does colorectal cancer affect the liver?

A
  • through secondary liver metastases
  • 15-20% synchronous (appear at same time as CRC)
  • 25% metachronous (liver metastases appear after CRC)
69
Q

What is the median survival and 5y survival of secondary liver metastases from colorectal cancer without treatment?

A
  • median survival: <1yr
  • 5yr survival: 0%
70
Q

What are effective treatments for secondary liver metastases?

A
  • systemic chemotherapy is improving
  • other effective Rx options (RFA and SIRT)
  • optimal Rx is surgical excision with curative intent
    • 5yr survival rates of 25-50%
    • only 25% suitable for surgery
  • rapid advancement in treatments e.g. cases where tumour cannot be removed but treated with chemo etc –> 25.1 months medial overall survival
71
Q

How is surgical resection of hepatocellular carcinoma done?

A

Take away that bit of liver and not much else

72
Q

How is surgical resection of gallbladder cancer done?

A

Remove GB, part of liver it is stuck to, and hilum lymphadenectomy (lymph nodes)

73
Q

How is surgical resection of cholangiocarcinoma done?

A

Remove bile duct and any part of liver stuck to it (remove whole half of the liver for something only 1cm)

74
Q

How common / lethal is pancreatic cancer?

A

Relatively common & highly lethal

75
Q

Describe the epidemiology of pancreatic cancer.

A
  • 4th commonest cause of cancer death
  • UK and USA annual incidence is 100 per million
  • rare before 45yrs, 80% occur between 60-80 years of age
  • men > women (1.5-2 : 1)
  • incidence higher in Western/industrialised countries
  • incidence and mortality are roughly equivalent
76
Q

What is the commonest form of pancreatic cancer?

A

Pancreatic ductal adenocarcinoma (PDA)

77
Q

When does pancreatic cancer present and how does this affect survival?

A
  • 80-85% have late presentation
  • overall median survival is <6 months (by the time it causes symptoms it is usually too late)
  • 5yr survival is 0.4-5%
78
Q

How resectable is pancreatic cancer and how does this affect survival?

A
  • only 15-20% have resectable disease
  • median survival 11-20 months
  • 5yr survival 20-25%
  • virtually all patients dead within 7 years of surgery
79
Q

What are the risk factors for developing pancreatic cancer? (7)

A
  • chronic pancreatitis (inflammation followed by healing inflammation) = 18-fold increased risk
  • T2DM = relative risk 1.8
  • cigarette smoking = causes 25-30% PDAs
  • occupation (insecticides, aluminium, nickel and acrylamide)
  • cholelithiasis, previous gastric surgery & pernicious anaemia = weak link
  • diet (increased fat and protein, less fruit and veg, coffee and alcohol) = weak link
  • 7-10% have family history (relative risk of PDA increased by 2x if one 1st degree relative, 6x if two 1st degree relatives, 30x if three 1st degree relatives)
80
Q

What inherited syndromes are associated with increased risk of pancreatic ductal adenocarcinoma? (6)

A
  • hereditary pancreatitis
  • familial atypical multiple mole melanoma
  • familial breast-ovarian cancer syndrome
  • Peutz-Jegher’s syndrome
  • HNPCC (Lynch syndrome)
  • FAP
81
Q

Describe the pathogenesis of pancreatic ductal adenocarcinomas (PDAs).

A
  • PDAs evolve through non-invasive neoplastic precursor lesions - PanINs (similar to polyps in colorectal cancers, but cannot be seen by imaging)
  • pancreatic intraepithelial neoplasias (PanIN) are microscopic (<5mm in diameter) and not visible by pancreatic imaging
  • the PanINs acquire clonally selected genetic and epigenetic alterations along the way

Similar to colonic progression where polyp–>cancer, but unlike colon you cannot see it

82
Q

Why is it thought that the death rate of pancreatic cancer is so high?

A

Mutations develop slowly but as soon as it becomes cancerous it starts metastasising quickly before causing local problems

83
Q

Describe the PanIN progression model of pancreatic cancer pathogenesis.

A

Normal –> PanIN-1A –> PanIN-1B –> PanIN-2 –> PanIN-3

84
Q

Mutations in which genes is PanIN1 associated with?

A
  • ERBB2
  • KRAS
85
Q

Mutations in which gene is PanIN2 associated with?

86
Q

Mutations in which genes is PanIN3 associated with?

A
  • TP53
  • SMAD4
  • BRCA2
87
Q

What proportion of pancreatic ductal adenocarcinomas arise in the head of the pancreas?

A

At least two thirds of PDAs arise in HoP (RHS)

88
Q

How does carcinoma of the head of the pancreas present? (6)

A
  • jaundice
  • weight loss
  • pain
  • acute pancreatitis - 5% atypical attack
  • persistent vomiting - in advanced cases, duodenal obstruction can result in this
  • GI bleeding - duodenal invasion or varices secondary to portal/splenic vein occlusion
89
Q

Why and how does carcinoma of the head of the pancreas cause jaundice?

A
  • > 90% due to either invasion or compression of CBD
  • often painless
  • palpable gallbladder (Courvoisier’s sign)
  • if cancer is away from CBD, it metastasises before patient goes yellow so harder to spot/presents late
90
Q

Why does carcinoma of the head of the pancreas cause weight loss? (3)

A
  • anorexia
  • malabsorption (secondary to exocrine insufficiency)
  • diabetes
91
Q

Describe the pain felt in carcinoma of the head of the pancreas.

A
  • 70% have pain at the time of diagnosis
  • epigastrium
  • radiates to back in 25%
  • back pain usually indicates posterior capsule invasion and irresectability
  • pain usually a sign that the cancer is locally invasive/advanced
92
Q

How does carcinoma of the body & tail of the pancreas present? (6)

A
  • develop insidiously and are asymptomatic in early stages
  • at diagnosis they are often more advanced than lesions located in the HoP
  • marked weight loss with back pain in 60% of patients
  • jaundice is uncommon (LHS away from bile duct)
  • vomiting sometimes occurs at a late stage from invasion of the duodenojejunal flexure
  • most unresectable at time of diagnosis
93
Q

What investigations do we do for pancreatic cancer? (9)

A
  • tumour marker CA19-9
  • ultrasonography
  • dual-phase CT
  • MRI
  • MRCP
  • ERCP
  • EUS (endoscopic ultrasound)
  • laparoscopy & laparoscopic ultrasound
  • PET
94
Q

How is tumour marker CA19-9 used in pancreatic cancer investigation?

A
  • concentrations >200 U/ml confer 90% sensitivity
  • concentrations in the thousands associated with high specificity
  • monitoring purposes, not diagnostic
  • falsely elevated in pancreatitis, hepatic dysfunction and obstructive jaundice
95
Q

What can ultrasonography identify in pancreatic cancer investigation? (3)

A
  • pancreatic tumours
  • dilated bile ducts
  • liver metastases
96
Q

How is dual-phase CT used in pancreatic cancer investigation?

A
  • accurately predicts resectability in 80-90% of cases
  • contiguous organ invasion
  • vascular invasion (coeliac axis and SMA)
  • distant metastases
97
Q

How is MRI used in pancreatic cancer investigation?

A

Imaging detects and predicts resectability with accuracies similar to CT (but not as useful as CT)

98
Q

How is MRCP used in pancreatic cancer investigation?

A

Provides ductal images without complications of ERCP

99
Q

How is ERCP used in pancreatic cancer investigation?

A
  • confirms the typical ‘double duct’ sign (combined dilation of CBD and pancreatic duct)
  • aspiration/brushing of the bile-duct system
  • therapeutic modality –> biliary stenting to relieve jaundice
  • most useful
100
Q

How is EUS (endoscopic ultrasound) used in pancreatic cancer investigation?

A
  • highly sensitive in the detection of small tumours (aspiration of single cells/biopsy)
  • assessing vascular invasion
  • FNA (fine needle aspiration)
  • useful when cannot resect but want to confirm cancer before chemo
101
Q

How is laparoscopy & laparoscopic ultrasound used in pancreatic cancer investigation?

A

Detect radiologically occult metastatic lesions of liver and peritoneal cavity

102
Q

How is PET scan used in pancreatic cancer investigation?

A

Mainly used for demonstrating occult metastases

103
Q

How do we do a head of pancreas resection?

A
  • Whipple’s resection - remove HoP, distal bile duct and gallbladder, distal stomach and all of duodenum + join up
  • but:
    • pancreatic juice has to go somewhere
    • bile has to go somewhere
    • stomach has to empty contents somewhere
104
Q

How do we do a tail of pancreas resection?

A

ToP can be removed along with spleen because if preserved it is very likely to have some cancer cells on it

105
Q

Where do neuroendocrine tumours arise from and what are they?

A
  • arise from gastroenteropancreatic (GEP) tract (or bronchopulmonary system)
  • diverse group of tumours
  • regarded as common entity as arise from secretory cells of the neuroendocrine system
106
Q

What % of neuroendocrine tumours are sporadic and what % are genetic?

A
  • 75% sporadic
  • 25% associated with a genetic syndrome
107
Q

What is an example of a gene mutation leading to neuroendocrine tumours?

A

MEN1 - multiple endocrine neoplasia type 1

  • parathyroid tumours
  • pancreatic tumours
  • pituitary tumours
108
Q

What symptoms are associated with neuroendocrine tumours?

A
  • patients are asymptomatic and incidental findings
  • <10% produce symptoms
109
Q

What do neuroendocrine tumours secrete?

A
  • secretion of hormones and their metabolites in 40%:
  • serotonin, tachykinins (substance P) and other vasoactive peptides
110
Q

What effects can neuroendocrine tumours lead to?

A

Carcinoid syndrome:

  • vasodilatation
  • increased intestinal motility
  • bronchoconstriction
  • endocardial fibrosis (PR & TR)

Acronym: VIBE

111
Q

What are some examples of neuroendocrine tumours and their clinical features?

A

Pancreatic:

  • insulinoma –> hypoglycaemia, Whipple’s triad (beta cells)
  • glucagonoma –> DM, necrolytic migratory erythema (alpha cells)

Pancreatic, duodenal:

  • gastrinoma –> Zollinger-Ellison syndrome (G cells)

Entire GIT:

  • VIPoma –> Verner-Morrison syndrome, watery diarrhoea (VIP cells)
  • somatostatinoma –> gallstones, DM, steatorrheoa (D cells)

Midgut: most are non-functioning, 40% –> carcinoid syndrome
Hindgut: usually non-functioning

112
Q

What biochemical assessments are done to diagnose neuroendocrine tumours? (4)

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
  • 24hr urinary 5-HIAA (serotonin metabolite)
113
Q

What imaging is done to diagnose neuroendocrine tumours? (4)

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)
114
Q

How are GEP-NETs graded?

A
  • tumour grade provides valuable prognostic information and influences management
  • grade : mitoses : Ki-67 index:
    • GI : <2/10 H.P.F : </=2%
    • G2 : 2-20/10 H.P.F : 3-20%
    • G3 : >20/10 H.P.F : >20%
  • G3 = high grade (poorly differentiated) neuroendocrine carcinoma
115
Q

Proportions of GEP-NET sites and frequency of liver metastases?

A
  • small intestine 28% –> 45% mets
  • appendix 20% –> 3% mets
  • pancreas 16% –> 42% mets
  • rectum 15% –> 6% mets
  • colon 13% –> 40% mets
  • stomach 9% –> 15% mets
116
Q

What are treatment modalities for NETs? (Many since they are like cancer but not exactly cancer)

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, 177Lu-DOTA)
  • medical therapy, targeted therapy, biotherapy
    • octreotide, lanreotide, SOM203
    • PK-inhibitors, mTOR-inhibitors
    • alpha-interferon
117
Q

What are the causes of upper dysphagia?

A
  • structural causes - pharyngeal cancer, pharyngeal pouch
  • neurological causes - Parkinson’s, stroke, motor neuron disease
118
Q

What are the causes of lower dysphagia?

A
  • structural causes:
    • inside (mural and luminal) - oesophageal or gastric cancer, stricture, Schatzki ring
    • outside (extrinsic compression) - lung cancer
  • neurological causes - achalasia, diffuse oesophageal spasm
119
Q

How can we differentiate between cardiac pain and dysphagia?

A
  • angina can occur after meals (blood shifts to bowel for digestion, limiting blood supply through narrowed coronaries)
  • however, history of discomfort seconds after swallowing is inconsistent with angina
  • unusual for angina to occur only after eating - ask about exertional chest pain
120
Q

How can we tell if pain is of oesophageal origin, and differentiate between upper and lower?

A
  • is food painful on swallowing? (upper)
  • is food easy to swallow but feels stuck seconds later? (lower)
121
Q

How can we differentiate between mechanical and neurological causes of dysphagia?

A

Are both solids and liquids hard to swallow? (Likely neurological)

122
Q

What, in the patient’s history, can increase their risk of strictures due to a mechanical cause of dysphagia?

A

History of reflux

123
Q

What can blood in stool suggest, and what should be done to investigate this?

A

Could suggest a GI malignancy - perform a digital rectal examination

124
Q

What are some causes of microcytic (MCV<80) anaemia? (4)

A
  • iron deficiency anaemia
  • anaemia of chronic disease
  • thalassaemia
  • sideroblastic anaemia
125
Q

What are some causes of normocytic (MCV 80-96) anaemia? - ABCDE

A
  • Aplastic anaemia
  • Bleeding
  • Chronic disease
  • Destruction (haemolysis)
  • Endocrine disorders - hyperthyroidism, hypoadrenalism
126
Q

What are some causes of macrocytic (MCV>96) anaemia? FAT RBC

A
  • Foetus (pregnancy)
  • Alcohol excess
  • Thyroid disorders
  • Reticulocytes
  • B12/folate deficiency
  • Cirrhosis
127
Q

What can lead to iron deficiency anaemia caused by blood loss? (2)

A
  • increased demand (growth, pregnancy)
  • decreased absorption
128
Q

What are some GI causes of iron deficiency anaemia in order of frequency? (8)

A
  • aspirin/NSAID use
  • colonic adenocarcinoma
  • gastric carcinoma
  • benign gastric ulcer
  • angiodysplasia
  • coeliac disease
  • gastrectomy (decreased absorption)
  • H. pylori
129
Q

What are some non-GI causes of iron deficiency anaemia in order of frequency? (4)

A
  • menstruation
  • blood donation
  • haematuria (1% of iron deficiency anaemia)
  • epistaxis
130
Q

What symptoms may suggest an upper GI cancer? (2)

A
  • dysphagia
  • dyspepsia
131
Q

What symptoms may suggest colorectal cancer? (4)

A
  • change in bowel habit
  • blood or mucus in stool
  • faecal incontinence
  • feeling of incomplete emptying of bowels (tenesmus)

Year 2 - BRS (84 decks)

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