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Y2 NnD > GI cancers > Flashcards

GI cancers Flashcards

(54 cards)

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1
Q

What is a neoplasm

A

an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissue, and which persists even after the evoking stimulus (if known) is removed

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2
Q

How do GI cancers cos obstruction of luminca

A

Intussusception , where polyp causes the bowel to telescope and drags the blood vessels in the mesentery along with it causing ischemia

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3
Q

what are the cytological features of malignancy

A
  • High nucleus/cytoplasm ratio ⇒ Suggests proliferation
  • Hyperchromasia ⇒ Production of nuclear material in DNA
  • Pleomorphism ⇒ Irregular appearances of different aspects of cells
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4
Q

How to diff adenocarcinoma with adenoma histologically

A

Abnormal glands invading the wall of the colon with a stromal reaction

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5
Q

Symptoms of GI Neoplasms

A
  • Tiredness (anaemia)
  • Bleeding
  • Anorexia and vomiting
  • Weight loss
  • Pain caused by obstruction
  • Dysphagia
  • Alteration in bowel habit
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6
Q

What genes are involved in the A-C sequence

A

k-ras( activated oncogene), p53(inactivated TSG)

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7
Q

What is the APC protein

A

encoded by APC (TSG), negative regulator that controls beta-catenin concentrations and interacts with E-cadherin, whichareinvolved in cell adhesion → Deletion of the APC gene predisposes to cancer.

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8
Q

what genes cause early adenoma and then intermediate adenoma

A

APC, then KRAS

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9
Q

what does TMN staging show

A

how far the cancer has spread ( extent)

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10
Q

what are T1, 2, 3, and 4 respectively in colon

A

Ti is LP till submucosa, T2 has reached muscularis propria, T3 reaches serosa, T4 reaches nearby organs

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11
Q

Common Lymph node areas for oseophageal cancer

A

Bifrucation of trachea

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12
Q

Most common type of oesophageal cancer in the UK and which part of the oesophagus does it occur in
Common risk?

A

Adenocarcinoma, lower 1/3 oesophagus
Obesity , associated with reflux

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13
Q

Risk factors for squamous cell carcinoma of oesophagus

A
  • Smoking is major factor ⇒Tobacco
  • Alcohol
  • Diet and very hot beverages
  • Infection
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14
Q

What are the main symptoms and presentations for oesophageal cancer

A
  • VERY FEW symptoms until late-difficulty swallowing ⇒ New, progressive dysphagia for solids first then liquids
    • More likely in elderly
  • May present with heartburn and increasing dysphagia
  • May also have regurgitation and weight loss
  • Advanced cancer may present with hoarse voice due to
    • Left recurrent laryngeal nerve infiltrated in advanced tumour
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15
Q

Investigations and diagnosis fo oescophageal cancer

A

Endoscopy, then biopsy for diagnosis
- CT thorax and abdomen ⇒ Check for Metastases and Lymph Nodes around tumour
- May need more specialised testing like PET scanning
Endoscopic ultrasound to stage tumour ⇒ give info about depth of tumour

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16
Q

treatment for oeso cancer

A

If T3N1M0 for example, patient deemed fit for surgery and can have preoperative chemotherapy followed by surgery
Palliation if treatment nor possible
- Improve quality of life ⇒ swallowing ( using stent) and maintaining weight
- Re-establish connection between healthy bit of oesophagus and stomach

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17
Q

Is gastric cancer more common in males or females

A

More common in males

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18
Q

What germline mutations may contribute to gastric cancer

A

TP53, CDH 1 genes

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19
Q

Aetiology of gastric cancer

A

multifactorial: diet, H. pylori, bile reflux ⇒ Anything that causes chronic gastritis

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20
Q

Can gastric cancer cause melena

A

Yes, because of ulceration which can bleed

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21
Q

What are the two main histological patterns of gastric adenocarcinoma

A

Intestinal ( obvious gland formation) and diffuse (signet ring cells)

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22
Q

Which group of patients have higher risk of intestinal type gastric adenocarcinoma

Study These Flashcards
A

Patients with FAP ( cancer predisposition syndrome)

23
Q

Are females or males more likely to get diffuse gastric adenocarcinoma, and are patients likely to be younger or older

Study These Flashcards
A

Younger, females.

24
Q

What genes are more likely to cause diffuse gastric adenocarcinoma, and what appearance is likely on biopsy

Study These Flashcards
A

e cadherin expression is lost in inactivation or mutation of CDH1

leather bottle stomach appearance ⇒ due to diffuse infiltration of gastric wall leading to distended stomach, rather than discrete

25
Where is adenocarcinoma in lower GI least likely?
In the small intestine
26
Where can Nueroendocrine tumours be found and what kind of tumours are they
Epithelial tumours associated with the synthesis of hormones or neurotransmitters
27
What is a high grade, poorly differentiated NET
Small cell carcinoma
28
Is NET submucosa or mucosa based
NET is submucosa based
29
What kind of tumour is GIST, what cell type is it related to
gastrointestinal stromal tumour, soft tissue tumour (sarcoma) that can arise anywhere in the GI tract Pacemaker cells in the muscularis propria
30
What mutation is common in GISTs
75-80% of GISTs have activating mutations in the KIT receptor tyrosine kinase gene
31
most common site of GIST
stomach
32
GIST histology patterns
epitheliod or spindle cell
33
what cancer is related to coeliacs
Enteropathy type T-cell lymphoma (EATL)
34
WHich colorectal cancer is more common in one gender
Rectal, in males
35
What familial syndromes are related with colorectal cancer
FAP, HNPCC
36
risk factors for colorectal cancer
- A diet high in red meats and processed meats - Cooking meats at very high temperatures (frying, broiling, or grilling) creates chemicals that might raise cancer risk - Diet low in fibre - Obesity - Physical inactivity - Smoking - Alcohol excess in rectal carcinomas esp beer - A family history of colorectal polyps or colorectal cancer - History of inflammatory bowel disease ⇒ can create environment suitable for dysplasia - Older age ⇒ More mutations escaping, less ability of TSG to stop suppression - Occupational factors e.g. solvents - Radiation ⇒ Radiotherapy - Schistosomiasis ⇒ Infection - parasitic - Excessive calories relative to requirement - High intake of refined carbohydrates - Low intake of protective micronutrients e.g. vitamins A, C, D and E
37
Which layer must adenocarcinoma of colon invade to be recognised as T1
submucosa
38
What genes are involved in first hit and second hit in adenoma carcinoma sequence, what happens after second hit
APC, then APC and B catenin Second hit, becomes adenoma
39
What gene is involved in higher grade adenomas
Mutation of proto-oncogenes like KRAS
40
What pathways are FAP and HNPCC related to
APC/B catenin vs microsatelite instability
41
Is FAP or HNPCC related colorectal cancer more common
HNPCC more common
42
What genes are related to HNPCC
DNA mismatch repair genese like MSH 2, MLH1
43
Which part of the colon are sessile serrated lesions more common in and what gene is related. Are these more likely or less likely to progress to malignancy.
Right colon BRAF or KRAS More likely Beter prognosis
44
Common presentation of colorectal cancer
May be bleeding from rectum for few weeks but not other symptoms, may have mild IDA
45
red flags for colorectal cancer
- Weight loss ⇒ Latest of the symptoms - Rectal bleeding ⇒ NB: Haemorrhoids and local irritation can also cause bleeding - Anaemia and thrombocytosis ⇒ Sign of inflammation and reactivity of bone marrow due to blood loss - Persistent diarrhoea (lack of day-day variability) in R side colon cancers ( ascending colon and caecal tumours) - Frequent nocturnal symptoms ⇒ eg. diarrhoea in middle of night - New onset over 50 yrs - FHx bowel cancer/ - PMHx IBD
46
Investigation for colon cancer
Colonoscopy to detect polyps of lesions Can stage with CT scan or MRI
47
How to screen for colorectal cancer and who gets it
Routine and regular Quantitative Faecal Immunochemical Test (qFIT) in population over the age of 50 -74
48
Are more or less differentiated tumours more aggressive
less
49
What factors affect prognosis appart from stage and grade
- Presentation with obstruction or perforation (usually indicates advanced disease) - Involvement of surgical resection margins ⇒ Likely to recur if on margin - Extramural vascular invasion ⇒ Main route of metastasis - Pattern of invasion and host response ⇒ Activate immune response- may have better prognosis - ?Genetic markers ⇒ For prognosis and treatment - KRAS- MAB targets receptors that KRAS is part of cascade of. - If KRAS mutation present, drug may not work
50
Where are bowel cancer cases most common
Rectosigmoid area, then right colon
51
Are tubular or villous ademonas of a higher risk
Villous
52
What is the most important prognostic factor for oesophagus cancers
STAGE
53
What gastric cancer is most commonly associated with H pylori infection
Lymphoma
54
what polyps is most commonly assoicated with PPIs
Fundic gland polyps

Y2 NnD (10 decks)

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