Gastric tumours Flashcards

1
Q

what is gastric cancer?

A

uncontrollable growth of cells that start in the stomach

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2
Q

What are the different types of gastric cancers?

A
  1. Adenocarcinoma (from columnar glandular epithelium):
    2 subtypes:
    a. intestinal
    b. diffuse

less common:
2. lymphoma (from lymphocytes)
3. carcinoid tumour (from G-cells in stomach)
4. Leiomyosarcoma (from stomach muscle cells)

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3
Q

What are the different regions of the stomach?

A
  1. Cardia (entrance of stomach below the esophagus)
  2. Fundus (top of the stomach)
  3. Body
  4. Pyloric antrum (lower or distal portion above the duodenum)
  5. Pyloric sphincter (muscular valve -closes while eating)
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4
Q

What are the layers of the gastric wall?

A

outer-> inner
1. Adventitia (serosa)
2. Muscular
3. Submucosa
4. Mucosa [direct contact w/ food]

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5
Q

What are the 3 layers of the mucosa lining the gastric wall?

A

innermost-> outer
1. Epithelial (absorbs/ secretes mucus + digestive enzymes)
2. Lamina propria (blood, lymph vessels, MALT (lymphocytes)
3. Muscularis mucosa (smooth muscle layer- helps break down food)

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6
Q

What cells make up the epithelial layer of the gastric wall?

A
  1. Foveolar cells:
    - secretes mucus
    - coats and protects epithelial cells
  2. Parietal cells:
    - secrete HCL
    - Maintains acid pH
  3. Chief cells:
    - secrete pepsinogen
  4. G cells:
    - Secrete gastrin
    - stimulate parietal cells
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7
Q

What are the 2 types of adenocarcinomas you can get with gastric cancer?

A
  1. Intestinal (well-differentiated)
  2. Diffuse (undifferentiated- much more aggressive)
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8
Q

What causes intestinal adenocarcinomas to develop?

A
  • Caused by H. pylori infection
  • H. Pylori releases virulence factors (cagA) which causes damage
  • Immune system causes inflammatory response to this damage= gastritis (inflammation of gastric lining)
  • chronic gastritis (lining is continuously damaged and repaired)
  • Overtime stomach cells under change- begin to resemble intestinal epithelium (this is known as metaplasia)
  • Metaplastic cells divide uncontrollably + accumulate mutations in tumour suppressor and proto-oncogenes
  • Cells become malignant (invade & spread)
  • This type of carcinoma typically appears on the lesser curvature of the antrum as large, irregular ulcers w/ heaped edges
  • well- differentiated (resemble normal intestinal cells)
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9
Q

Describe lymphomas (gastric cancer)

A
  • Lymphocytes in MALT are affected: role is recognising & responding to any pathogens that cross the peithelial layer
    -appear as diffuse lymphocytes
  • chronic H. pylori infection can lead to excessive B cells proliferation
  • accumulating mutations
  • leading to lymphoma
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9
Q

What causes diffuse adenocarcinomas to develop?

A
  • This type of adenocarcinoma can affect any part of the stomach
  • Caused by mutations in CDH1 (a tumour suppressor gene that codes for a membrane adhesion molecule cells E-cadherin)
  • E- cadherin normally helps cells stick together and controls cell cycle
  • When mutated, cells begin to detach from one another and divide uncontrollably
    = increased ability to spread & invade
  • results in thickening and increased rigidity of the stomach (gastric linitis)
  • histologically: more signet ring cells (cells with large vacuoles that push the nucleus to the edge of the cell)
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9
Q

Describe carcinoid tumours (gastric cancer)

A
  • Cancer of the neuroendocrine cells: G cells
  • well-differentiated
  • Change from mucosa to polyp
  • polyps also found in intestine and pancreas
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10
Q

Describe leiomyosarcomas (gastric cancer)

A
  • Cancer of the smooth muscle cells
  • Extremely rare
  • Look like spindle, epithelial or undifferentiated cells
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11
Q

What are some of the risk factors of gastric cancer?

A
  • Smoked and processed foods, foods high in nitrosamines, high nitrates, high salt, pickling, low vitamin C
  • Smoking
  • Alcohol
  • Helicobacter pylori infection
  • Atrophic gastritis
  • Pernicious anaemia
  • Partial gastrectomy
  • Gastric polyps
  • Blood group A
  • Obesity
  • age
  • male
  • autoimmune gastritis
  • achlorhydria
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12
Q

What are some protective factors against gastric cancer?

A
  • fruits/ veg
  • fiber
  • folate
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13
Q

Summarise the epidemiology of gastric cancer

A
  • COMMON cause of cancer death worldwide
  • Highest incidence in JAPAN (and Asia in general)
  • 6th most common cancer in the UK
  • Usual age of presentation: > 50 yrs
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14
Q

What symptoms of gastric cancer can be found in the history?

A
  • Often asymptomatic early
  • malaise
  • Early satiety (feeling full after eating small amount)
  • Epigastric discomfort
  • Haematemesis, melaena, symptoms of anaemia (Anaemia can be due to blood loss from ulcer or of chronic disease)
  • Systemic symptoms: weight loss, anorexia, nausea/vomiting
  • Dysphagia (in tumours of the gastric cardia)
  • Dyspepsia/ indigestion
  • Symptoms of metastases (e.g. ascites, jaundice)
15
Q

What signs of gastric cancer can be found on physical examination?

A
  • May be normal
  • Epigastric mass
  • Abdominal tenderness
  • Ascites
  • Signs of anaemia
  • Virchow’s Node (aka Troisier’s sign) – lymphadenopathy in left supraclavicular fossa
  • Sister Mary Joseph’s Nodule (metastatic node on the umbilicus)
  • Krukenberg’s Tumour (ovarian metastases)
  • Acanthosis nigricans
  • leser trelat sign (brown spots on skin)
16
Q

What investigations are used to monitor and diagnose gastric cancer?

A
  1. Upper GI endoscopy – with biopsy of all gastric ulcers
  2. X-ray w/ barium contrast
  3. Bloods - FBC (check for anaemia), LFTs
  4. Abdominopelvic CT/MRI - for staging
  5. Endoscopic USS - assess depth of gastric invasion and lymph node involvement
  6. Liver ultrasound and bone scan – for tumour staging
  7. Laparoscopy may be needed to determine if tumour resectable
  8. Oesophago-gastro-duodenoscopy OGD and biopsy for advanced cancer
17
Q

How are gastric cancers treated?

A
  1. Surgery: Surgical resection as the sole treatment modality is recommended in early-localised disease (T1b-T2, N0). However, in more advanced disease (T2 or higher, and any N), preoperative treatment or adjuvant treatment in addition to gastrectomy is advised. 
  2. Chemoradiation: Patients with pathological stage II-IIIC or any T, N+ disease or R1 resection should receive postoperative radiation with adjuvant fluorouracil chemotherapy, as this regimen has been shown to improve overall survival 
    - Preoperative chemoradiation may be offered as it potentially downstages the cancer and increases resect ability 
    - Perioperative chemotherapy with ECF (epirubicin, cisplatin, and fluorouracil) has been shown to improve overall survival in patients with stage II or higher disease compared with surgery alone 
    - Metastatic disease : Chemotherapy and/or immunotherapy with or without radiation 
  3. Palliative gastrectomy : May improve symptoms such as bleeding and obstruction. 
18
Q

What are possible complications that can be caused by surgical treatment of gastric cancer?

A
  • Gastroparesis, dumping syndrome, anastomotic leak, wound infection, postoperative cardiopulmonary complications, and malnutrition 
  • Postoperative cardiac and pulmonary complications, such as myocardial infarction and pneumonia. 
  • Osteopenia
  • Diarrhoea
  • Nutritional deficiency
  • Indigestion
  • Gastric obstruction 
  • Gastrointestinal bleeding 
  • Gastric perforation 
  • Small bowel obstruction 
  • Postoperative dumping syndrome 
19
Q

What are possible complications that can be caused by chemotherapy of gastric cancer?

A
  • Febrile neutropenia, thrombocytopenia, nausea, and fatigue. 
  • Radiation 
  • Anorexia, thrombocytopenia, and nausea 
  • A feeding tube in patients receiving upper abdominal radiation for nutrition may be considered. 
20
Q

Describe the prognosis of gastric cancer

A
  • POOR: v. low survival (usually diagnosed at later stage)
21
Q

Describe the pathophysiology of gastric cancer

A

Several events at the molecular level have been implicated in the development and progression of gastric cancers. Gastric cancer can involve loss of the tumour suppression gene, p53 

Several proto-oncogenes, such as ras, c-myc, and erbB2 (HER2/neu), have been shown to be over-expressed in gastric cancers. Helicobacter pylori has been associated with molecular events that could lead to gastric cancer, such as an increase in p53 mutations. Causes inflammatory response = damage mucosa = chronic gastritis. Epithelium undergo metaplasia.