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(gastro) gastrointestinal cancers Flashcards

1
Q

define cancer

A

a disease caused by uncontrollable division of abnormal cells in a specific part of the body

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2
Q

what are the two borad categories of cancer?

A

1) primary cancers

2) secondary cancers

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3
Q

what is primary cancer?

A

when the uncontrollable cell division arises directly from the cells of an organ

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4
Q

what is secondary cancer?

A

spread from a primary cancer from the primary site/organ to another organ either

1) directly
2) indirectly (via blood/lymph)

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5
Q

what is the alternative term for secondary cancers?

A

metastasis/es

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6
Q

differentiate between primary and secondary cancers

A

primary = arise from within the cells of the organ itself

secondary = arise as a result of the spread of primary cancers to another organ directly or indirectly

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7
Q

what are the two ways in which a primary cancer can spread?

A

1) directly to other organs

2) indirectly to other organs VIA blood vessels or lymphatic vessels

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8
Q

name two types of epithelial cells in the GI tract

A

1) squamous epithelium

2) glandular epithelium

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9
Q

name two types of neuroendocrine cells in the GI tract

A

1) enteroendocine cells

2) intestinal cells of Cajal

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10
Q

name two types of connective tissue cells in the GI tract

A

1) smooth muslce

2) adipose tissue

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11
Q

how does cancer of squamous epithelium manifest?

A

squamous cell carcinoma (SCC)

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12
Q

how does cancer of glandular epithelium manifest?

A

adenocarcinoma

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13
Q

how does cancer of enteroendocrine cells manifest?

A

neuroendocrine tumours (NETs)

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14
Q

how does cancer of the intestinal cells of Cajal manifest?

A

gastrointestinal stromal tumours (GISTs)

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15
Q

how does cancer of the smooth muscle manifest?

A

leiomyoma OR leiomyosarcomas

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16
Q

how does cancer of the adipose tissue manifest?

A

liposarcomas

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17
Q

what are GISTs?

A

gastrointestinal stromal tumours = cancers of the intestinal cells of Cajal

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18
Q

what are liposarcomas?

A

cancers of the adipose tissue

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19
Q

what are NETs?

A

neuroendocrine tumours = cancers of the enteroendocrine cells

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20
Q

what are leiomyomas/leiomyosarcomas?

A

cancers of smooth muscle

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21
Q

where do neuroendocrine cells form?

A

developm from the neuroendocrine cells in teh body so can occur anywhere, in any organ as neuroendocrine cells are present everywhere

BUT when the occur in enteroendocrine cells of the GI tract = form NETs

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22
Q

what are the divisions of the oesophagus?

A 
cervical oesophagus
upper thoracic oesophagus
middle thoracic oesophagus
lower thoracic oesophagus
abdominal oesophagus
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23
Q

which muscle types are present as you progress through the thoracic oesophagus?

A

upper thoracic = skeletal
middle thoracic = skeletal/smooth
lower thoracic = smooth

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24
Q

which structure divided the lower thoracic oesophagus and the abdominal oesophagus?

A

oesophagogastric junction

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25
Q

which vertebral levels does the oesophagus run down?

A

from C6 to T10

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26
Q

what are the two main types of oesophageal cancers?

A

squamous cell carcinomas (upper 2/3)

adenocarcinomas (lower 1/3)

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27
Q

where do squamous cell carcinomas develop in the oesophagus?

A

upper 2/3rd of the oesophagus

more common in less developed world

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28
Q

where do adenocarcinomas develop in the oesophagus?

A

lower 1/3rd of the oesophagus

more common in developed world

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29
Q

why do SCCs develop in the oesophagus?

A

alcohol consumed is metabolised via the acetaladehyde pathway

resultant acetaldehyde
= potent carcinogen, highly toxic
= causes development of SCC

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30
Q

why do adenocarcinomas develop in the oesophagus?

A

gastric acid reflux causes (reversible) conversion of normal squamous epithelium into (metaplastic) columnar epithelium
= increases risk of adenocarcinoma formation

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31
Q

what is the acetaldehyde pathway and why is it harmful?

A

alcohol consumed is metabolised into acetaldehyde by alcohol dehydrogenase

resultant acetaldehyde
= potent carcinogen, highly toxic

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32
Q

from which cells do SCCs arise?

A

normal squamous epithelium of upper 2/3rd of the oesophagues

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33
Q

from which cells do adenocarcinomas arise?

A

metaplastic columnar epithelium of the lower 1/3rd of the oesophagus

(formed form gastric acid reflux)

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34
Q

how is the resultant acetaldehyde removed from the body?

A

metabolised to acetate by aldehyde dehydrogenase and then converted into water and carbon dioxide for easy elimination

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35
Q

how can reflux lead to the development of oesophageal cancer?

A 
repetitive gastric acid reflex
= GORD
= oesophagitis
= Barrett's oesophagus (non-dysplastic, low-grade dysplasia, high-grade dysplasia)
= adenocarcinoma
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36
Q

what is oesophagitis?

A

inflammation of the oesophagus

= commonly caused by GORD

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37
Q

what is Barrett’s oesophagus?

A

metaplastic changes in the lower oesophagus where the normal squamous epithelium is replaced by columnar epithelium (due to repeat exposure to gastric acid)

has stages =

1) non-dysplastic
2) low-grade dysplasia
3) high-grade dysplasia

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38
Q

what are the stages/progression of Barrett’s oesophagus?

A

1) non-dysplastic
2) low-grade dysplasia
3) high-grade dysplasia
= ADENOCARCINOMA (either non-invasive or invasive)

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39
Q

define neoplasia

A

uncontrolled, abnormal growth of cells of tissues

= forms a neoplasm

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40
Q

what percentage of the UK population is affected by GORD and Barrett’s oesophagus?

A

approx 30% = affected by GORD

5% of GORD patients = affected by Barrett’s

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41
Q

what is the lifetime risk of cancer for Barrett’s oesophagus patients?

A

approx 0.5-1% of Barrett’s oesophagues patients develop adenocarcinomas

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42
Q

how can Barrett’s oesophagus progress to adenocarcinoma formation?

A

1) non-dysplastic
2) low-grade dysplasia
3) high-grade dysplasia
= ADENOCARCINOMA (either non-invasive or invasive)

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43
Q

what is recommended surveillance for non-dysplastic Barrett’s oesophagus and why?

A

endoscopic exploration every 2-3 years

= to look for any metaplastic changes

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44
Q

what is recommended Barrett’s surveillance for low-grade oesophageal dysplasia and why?

A

endoscopic exploration every 6 months

= to look for any metaplastic changes

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45
Q

what is recommended Barrett’s surveillance for high-grade oesophageal dysplasia and why?

A

INTERVENTION!

= to prevent progression onto adenocarcinoma stage

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46
Q

why is a biopsy of high-grade oesophageal dysplasia not fully reliable?

A

very likely that the area biopsied may not have the carcinoma
= cannot assume (!) that carcinoma is not already present elsewhere in the affected region

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47
Q

how common is oesophageal cancer?

A

the 9th most common cancer

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48
Q

what are the non-modifiable risk factors for oesophageal cancer?

A

affects the elderly (60+)

males > females

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49
Q

how does oesophageal cancer usually present?

A

dysphagia & weight loss

= indicative of advanced, late stage disease

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50
Q

how are most people with oesophageal cancer managed?

A

most people are late stage at diagnosis so = palliative care

(surgery less recommended as the morbidity and mortality rate is very high + surgery is very complex w a low survival rate)

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51
Q

how is oesophageal cancer diagnosed?

A

1) endoscopy

2) biopsy

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52
Q

how is oesophageal cancer staged?

A

1) CT scan
2) laparoscopy (to identify intraperitoneal/liver mtastases)
3) EUS = endoscopic ultrasound (to investigate extraluminal neoplasms)
4) PET scan ( to rule out occult metastases)

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53
Q

why is a laparoscopy does to stage oesophageal cancers?

A

to identify intraperitoneal/liver metastases

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54
Q

why is a EUS (endoscopic ultrasound) does to stage oesophageal cancers?

A

to investigate extraluminal neoplasms

cannot be seen on CT scan

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55
Q

why is a PET scan done to stage oesophageal cancers?

A

to identify any occult metastases (previously undetected but now identified tumours)

(cannot be seen on CT scan)

56
Q

how are SCCs treated most commonly?

A 
radical radiotherapy
(don't usually require surgery)
57
Q

how are adenocarcinomas treated most commonly?

A

neo-adjuvant chemotherapy followed by radical surgery (oesophagectomy)

58
Q

how are late-stage, metastatic oesophageal cancers managed?

A

palliative care

= chemotherapy, radiotherapy (DXT), oesophageal stent

59
Q

when is an oesophagectomy done in oesophageal cancer?

A

usually to remove lower oesophageal adenocarcinomas that are non-invasive

(neo-adjuvant chemotherapy given before the surgery)

60
Q

what is the method of oesophagectomy in treating oesophageal cancers?

A

two-stage Ivor Lewis approach

resent upper stomach and lower oesophagus and rejoin ends together

61
Q

why is surgery not commonly done to treat oesophageal cancer?

A

1) surgery is very complex for a low subsequent survival late
2) associated with high morbidity and mortality

62
Q

who is at greatest risk of colorectal cancer?

A

western societies = third highest reason for cancer deaths

older people (50+)
men > women
63
Q

what are the three forms of colorectal cancer?

A

sporadic
familial
hereditary syndrome

64
Q

what is sporadic colorectal cancer?

A

absence of family history

= isolated lesion usually affects older population

65
Q

what is familial colorectal cancer?

A

family history

= if patient is <50 & has a 1st degree relative w colorectal cancer, significantly increased risk

66
Q

what is hereditary colorectal cancer?

A

family history + specific gene defects (YOUNGER AGE OF ONSET)

e.g FAP, Lynch syndrome (HNPCC)

67
Q

which conditions is hereditary colorectal cancer associated with?

A

FAP (familial adenomatous polyposis)

Lynch syndrome/HNPCC (hereditary nonpolyposis colorectal cancer)

68
Q

what is FAP?

A

familial adenomatous polyposis

= loads of precancerous polyps in the colon that can develop into adenocarcinomas

69
Q

what is Lynch syndrome?

A

hereditary nonpolyposis colorectal cancer

= colorectal cancer caused when there are no/very few polyps

70
Q

what is the most likely histopathology of colorectal cancer?

A

adenocarcinomas

71
Q

what are the stages of development of colorectal cancer?

A 
normal epithelium
hyperproliferative epithelium
small adenoma
large adenoma
colon carcinoma
72
Q

which bowel structure is most likely to lead to colorectal cancer development?

A

polyps

adenomatous

73
Q

what is the main driver of the colorectal cancer development from a polyp?

A

genetic mutations

  • APC mutation = normal to healthy epithelium
  • K-ras mutation = small to large adenoma
  • p53 mutation = large adenoma to colorectal carcinoma
74
Q

why are endoscopic resections of polyps important?

A

polyps need to be removed as soon as possible

= if they are allowed enough time and space to grow, high chance of becoming cancerous (adenocarcinomas)

75
Q

which drug is said to reduce progression of colorectal cancer?

A

aspirin

and other NSAIDs, folate, calcium & oestrogen

76
Q

what in the PMH is a risk factor for colorectal cancer?

A
  • previous colorectal cancer
  • colorectal polyps
  • ulcerative colitis
  • radiotherapy
77
Q

what in the family history is a risk factor for colorectal cancer?

A
  • 1st degree relative w colorectal cancer

- genetic defects i.e. FAP, Lynch syndrome

78
Q

what in the lifestyle history (diet/environment) is a risk factor for colorectal cancer?

A
  • carconigenic foods
  • smoking
  • obesity
  • socioeconomic status
79
Q

what is significant about hereditary colorectal cancer?

A

as there are specific gene defects, age of onset is much younger than usual (50+)

80
Q

do all polyps become cancerous?

A

no!

all colorectal cancers start as polyps BUT only 5-10% of polyps that are allowed to grow/not removed, develop into colon cancer (Adenocarcinomas)

81
Q

what are the most common locations for colorectal cancer development?

A

approx 2/3 in descending colon and rectum (do a colonoscopy)

approx 1/2 in sigmoid colon and rectum (do a flexible sigmoidoscopy)

82
Q

which investigative procedure is carried out for sigmoid/rectal cancers and why?

A

flexible sigmoidoscopy = much quicker and easier

83
Q

which investigative procedure is carried out for general colorectal cancers?

A

colonoscopy (investigates entire colon)

= longer, explores in greater detal

84
Q

how do caecal and right-sided colorectal cancers present clinically?

A

1) iron deficiency anaemia
2) change in bowel habit (usually diarrhoea)

late sign = obstruction of the distal ileum, palpable mass

85
Q

what are the late signs of caecal & right-sided cancers?

A

obstruction of the distal ileum

palpable mass

86
Q

why do caecal & right-sided cancers cause iron deficiency anaemia?

A

increased risk of bleeding with right-sided cancers so

iron deficiency anaemia = increased blood loss

87
Q

how do sigmoid and left sided carcinomas present clinically?

A 
PR bleeding (per rectum)
mucus in stool

thin stools (late sign)

88
Q

how do rectal carcinomas present clinically?

A

PR bleeding (per rectum)
mucus in stool
tenesmus

anal, perineal, sacral pain (late sign)

89
Q

what is a late sign of sigmoid & left-sided cancers?

A

thin stools

90
Q

what is a late sign of rectal cancers?

A

anal, perineal, sacral pain

91
Q

what is a tell-tale sign of rectal cancers?

A

tenesmus

92
Q

what does colorectal cancer that has caused a local invasion present with?

A

bladder symptoms

female genital tract symptoms

93
Q

what does colorectal cancer that has caused extensive metastases present with?

A

1) lung metastases (cough, monophonic wheeze)
2) liver metastases (pain, jaundice, hepatomegaly)
3) regional lymph nodes
4) peritoneum (Sister Mary Joseph nodule)
5) bone pain

94
Q

what do colorectal cancers that spread to the liver present with?

A

pain, jaundice

hepatomegaly

95
Q

what do colorectal cancers that spread to the lung present with?

A

cough

monophonic wheeze

96
Q

what do colorectal cancers that spread to the peritoneum present with?

A

Sister Mary Joseph nodule

97
Q

what are signs of primary colorectal cancer?

A
  • abdominal mass
  • most cancers are <12cm array from dentate in a digital rectal exam and can be palpated by the examining finger
  • abdominal tenderness and distention (bowel obstruction)
98
Q

how do most colorectal cancers present in a digital rectal exam?

A

approx <12cm away most of the time from the dentate line

= can easily be palpated by the examining finger

99
Q

what is a rigid sigmoidoscopy and when is it done?

A

a procedure to examine the insides of the rectum and the anus

= when you suspect rectal carcinomas

100
Q

how does large bowel obstruction present clinically?

A

abdominal distention and tenderness?

101
Q

which investigations are carried out to look for faecal occult blood?

A

1) FIT (faecal immunochemical test)

2) Guaiac test (hemoccult) = not commonly done anymore

102
Q

why is a FIT test carried out for colorectal cancer?

A

detects minute amounts of blood in faeces (faecal occult blood)

103
Q

what is a Guaiac test for colorectal cancer?

A

based on pseudoperoxidase activity of haematin

has dietary restrictions = avoid red meat, melons, horse-radish, vitamin C & NSAIDs for 3 days before test

104
Q

which blood tests are carried out to investigate colorectal cancer?

A

1) FBC (to assess anaemia, haematinics, ferritin)

2) tumour markers (not diagnostic but to monitor recurrence)

105
Q

why is an FBC done for colorectal cancers?

A

to assess anaemia, haematinics (iron, B12, folate), ferritin

106
Q

why is a tumour marker test done for colorectal cancers?

A

e.g. CEA test

not diagnostic but to monitor recurrence of cancers (the CEA level would increase if recurrence occurs)

107
Q

what are haematinics?

A

nutrient required for hematopoiesis (RBC formation) = iron, B12, folate

108
Q

which is the main procedure carried out to visualise colorectal cancer?

A

colonoscopy

usually performed under sedation

109
Q

why are colonoscopies useful?

A

1) can visualise lesions < 5mm

2) small polyps can be removed (reducing cancer incidence)

110
Q

how are polyps removed in colonoscopies?

A

diathermy (using heat)

111
Q

in older patients who cannot have colonoscopies done, what is the most suitable alternative?

A

CT colonoscopy/colonography

112
Q

what is the advantage of CT colonoscopies/colonographies over normal colonoscopies?

A
  • no need for sedation

- better tolerated, less invasive

113
Q

what is the disadvantage of CT colonoscopies/colonographies?

A

1) cannot visualise lesions < 5mm

2) if lesions are identified, patient may need to have a colonscopy anyway

114
Q

which imaging test is done specifically for rectal cancer?

A

MRI pelvis

115
Q

why is an MRI pelvis usually done for rectal cancer?

A

to identify

1) depth of invasion
2) mesorectal lymph node involvement
3) decide between preoperative chemoradiotherapy or straight to surgery

116
Q

how does an MRI pelvis inform the surgical treatment for rectal cancer?

A

results of the MRI pelvis can give two options:

1) if rectal cancer is smaller and can be resected w healthy margins = immediate surgery
2) if rectal cancer too large to be resected w healthy margins = preoperative chemoradiotherapy to shrink tumour size and subsequently enable efficient resection

117
Q

why can preoperative chemoradiotherapy be offered to rectal cancers?

A

if rectal cancer too large to be resected w healthy margins = preoperative chemoradiotherapy to shrink tumour size and subsequently enable efficient resection

118
Q

why is essential to do a CT chest/abdo/pelvis for colorectal cancer?

A

to identify any possible metastases

119
Q

what is the main method of management for colon cancer?

A

surgery

can do radiotherapy, chemotherapy, stent in the meantime while prepping for surgery

120
Q

how is an obstructing colon carcinoma of the ascending/transverse colon treated?

A

resection and primary anastomosis

possible due to good blood supply

121
Q

how is an obstructing colon carcinoma of the descending/sigmoid colon treated?

A

1) if you don’t want to risk impairing already poor blood supply
= Hartmann’s procedure (resection, formation of Hartmann’s pouch, proximal end colostomy)

2) if you can risk burdening the already poor blood supply
= resection + primary anastomosis (approx 10% risk of leakage)
= OR defunctioning ileostomy

122
Q

what is Hartmann’s procedure and when is it done?

A

bowel resection of left-sided affected area

formation of Hartmann’s pouch

proximal colon colostomy

123
Q

what is a colostomy and when is it done?

A

suturing the open proximal end of the colon onto the anterior abdominal wall so it opens + releases colonic contents outwards

= when you resect a left-sided colorectal carcinoma + cannot rejoin ends immediately due to poor blood supply

124
Q

which type of colorectal cancers are easier to treat with bowel resection and why?

A

left-sided (caecal, ascending, proximal transverse) better than right-sided
= much better blood supply here than the distal bowel

125
Q

is the colostomy in Hartmann’s procedure permanent?

A

no - most commonly reversed in approx 6 months

126
Q

summarise the three treatment options available for a left-sided colorectal cancer/obstruction

A

1) Hartmann’s procedure w proximal end colostomy
2) primary anastomosis w ileostomy (+ bowel lavage)
3) palliative STENT

127
Q

which arteries supply the proximal colon?

A

ileocolic artery

right colic artery

middle colic artery

128
Q

which arteries supply the distal colon?

A

left colic artery

sigmoid artery

129
Q

which part of the colon has a better blood supply?

A

right side (ascending + a portion of the transverse colon)

130
Q

which two surgical procedures are carried out for right-sided colorectal cancer?

A

right hemicolectomy

extended right hemicolectomy

131
Q

what are the following and what is the difference between the two?

a) right hemicolectomy
b) extended right hemicolectomy

A

a) when tumour is in the proximal ascending colon, the right, ascending side of your colon is removed
b) when tumour is in the distal ascending colon/trasnverse colon, the ascending AND transverse colon is removed

= both result in a ileocolic anastomosis

132
Q

which surgical procedure is carried out for left-sided colorectal cancer?

A

left-sided hemicolectomy

133
Q

which surgical procedure is carried out for rectal cancer?

A

excision of the rectum

134
Q

what is a stoma?

A

brings the end of the bowel out as an opening on your abdomen

135
Q

what are the two types of stoma?

A

ileostomy – the cut made in the small bowel is put through the lining of the abdomen

colostomy – the cut made in the large bowel is put through the lining of the abdomen

brs (phase 1b) (71 decks)

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