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Y2 NnD > GI cancers > Flashcards

GI cancers Flashcards

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

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

A

Younger, females.

24
Q

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

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
Q

Where is adenocarcinoma in lower GI least likely?

A

In the small intestine

26
Q

Where can Nueroendocrine tumours be found and what kind of tumours are they

A

Epithelial tumours associated with the synthesis of hormones or neurotransmitters

27
Q

What is a high grade, poorly differentiated NET

A

Small cell carcinoma

28
Q

Is NET submucosa or mucosa based

A

NET is submucosa based

29
Q

What kind of tumour is GIST, what cell type is it related to

A

gastrointestinal stromal tumour, soft tissue tumour (sarcoma) that can arise anywhere in the GI tract
Pacemaker cells in the muscularis propria

30
Q

What mutation is common in GISTs

A

75-80% of GISTs have activating mutations in the KIT receptor tyrosine kinase gene

31
Q

most common site of GIST

A

stomach

32
Q

GIST histology patterns

A

epitheliod or spindle cell

33
Q

what cancer is related to coeliacs

A

Enteropathy type T-cell lymphoma (EATL)

34
Q

WHich colorectal cancer is more common in one gender

A

Rectal, in males

35
Q

What familial syndromes are related with colorectal cancer

A

FAP, HNPCC

36
Q

risk factors for colorectal cancer

A
  • A diet high in redmeatsand processedmeats
  • Cookingmeatsat 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 colorectalpolypsor colorectal cancer
  • History ofinflammatory 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
Q

Which layer must adenocarcinoma of colon invade to be recognised as T1

A

submucosa

38
Q

What genes are involved in first hit and second hit in adenoma carcinoma sequence, what happens after second hit

A

APC, then APC and B catenin
Second hit, becomes adenoma

39
Q

What gene is involved in higher grade adenomas

A

Mutation of proto-oncogenes like KRAS

40
Q

What pathways are FAP and HNPCC related to

A

APC/B catenin vs microsatelite instability

41
Q

Is FAP or HNPCC related colorectal cancer more common

A

HNPCC more common

42
Q

What genes are related to HNPCC

A

DNA mismatch repair genese like MSH 2, MLH1

43
Q

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.

A

Right colon
BRAF or KRAS
More likely
Beter prognosis

44
Q

Common presentation of colorectal cancer

A

May be bleeding from rectum for few weeks but not other symptoms, may have mild IDA

45
Q

red flags for colorectal cancer

A
  • 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
Q

Investigation for colon cancer

A

Colonoscopy to detect polyps of lesions
Can stage with CT scan or MRI

47
Q

How to screen for colorectal cancer and who gets it

A

Routine and regular Quantitative Faecal Immunochemical Test (qFIT) in population over the age of 50 -74

48
Q

Are more or less differentiated tumours more aggressive

A

less

49
Q

What factors affect prognosis appart from stage and grade

A
  • 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
Q

Where are bowel cancer cases most common

A

Rectosigmoid area, then right colon

51
Q

Are tubular or villous ademonas of a higher risk

A

Villous

52
Q

What is the most important prognostic factor for oesophagus cancers

A

STAGE

53
Q

What gastric cancer is most commonly associated with H pylori infection

A

Lymphoma

54
Q

what polyps is most commonly assoicated with PPIs

A

Fundic gland polyps

Y2 NnD (10 decks)

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