Pathology of the stomach Flashcards

1
Q

What can cause acute gastritis?

A

Irritant chemical injury - sever burns, shock, severe trauma, head injury

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2
Q

What can cause chronic gastritis?

A

Autoimmune
Bacterial
Chemical

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3
Q

What are rare inflammaotry disorders of the stomach?

A

Lymphocytic
Eosinophilic
Granulomatous

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4
Q

What causes autoimmune chronic gastritis?

A

Anti-parietal and anti-intrinsic factor antibodies which causes atrophy and intestinal metaplaia in the body of the stomach

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5
Q

Why does anaemia occur in autoimmune chronic gastritis?

A

Deficiency of B12 as the parietal cells that produce intrinsic factor strophy so absorbtion of B12 cannot occur. B12 is needed for the production of myelin and red blood cells

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6
Q

What is pernicious anaemia?

A

Pernicious anaemia causes your immune system to attack the cells in your stomach that produce the intrinsic factor, which means your body is unable to absorb vitamin B12

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7
Q

What is macrocytic anaemia?

A

A macrocytic class of anemia is an anemia in which the red blood cells (erythrocytes) are larger than their normal volume.

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8
Q

What are common presentations of autoimmune gastritis?

A

Anaemia
Tired
Staggering gate

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9
Q

What type of bacteria are H. Pylori?

A

Gram negative, curvilnnear rod

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10
Q

How does H. Pylori cause chronic gastritis?

A

Bacteria inhabits a niche between the epithelial cell surface and mucuous barrier causing an acute inflammatory response
IL8 is critical

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11
Q

What does H. Pylori gastritis increased the risk of?

A

Duodenal ulcer
Gastric ulcer
Gastric carcinoma
Gastric lymphoma

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12
Q

What chemicals can cause chemical gastritis?

A

NSAIDs
Alcohol
Bilre reflux

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13
Q

How do chemicals cause gastritis?

A

Direct injury to mucus layer by fat solvents, marked epithelial regenration, hyperplasia, congestion and little inflammation
May produce erosions or ulcers

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14
Q

What is a peptic ulcer?

A

A breach in the GI mucosa as a result of acid and pepsin attack
Complication of gastritis

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15
Q

What are common sites for chronic peptic ulcers?

A

Duodenum
Stomach
Oesophago-gastric junction
Stomal ulcers

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16
Q

What is the pathogenesis of chronic duodenal ulcers?

A

Increased attack and failure of defence
50% of people with duodenal ulcers have increased acid secretion
Many have inappropriate sustained secretion of acid
Excess acid in duodenum produces gastric metaplasia and leads to H. Pylori infection, inflammataion, epithelial damage and ulceration

17
Q

What is the microscopic appearance of peptic ulcers?

A

Layered appearance
Floor of necrotic fibrinopurulent debris
Base of inflamed granulation tissue
Deepest layer is fibrotic scar tissue

18
Q

What are common complications of peptic ulcers?

A
Perforation 
Penetration 
Haemorrhage
Stenosis
Intractable pain
19
Q

What are examples of bengn gastric tumours?

A

Hyperplastic polyps

Cystic fundic gland polyps

20
Q

What are examples of malignant gastric tumours?

A

Carcinomas
Lymphomas
GI stromal tumours

21
Q

What affects rates of gastric cancer?

A

Genetics, diet and prevalance of H. Pylori infection

22
Q

What is the pathogenesis of gastric adenocarcinomas?

A
H. Pylori infection 
Chronic gastritis
Intestinal metaplasia/atrophy
Dysplasia
Carcinoma
23
Q

What are examples of pre-malignant conditions?

A

Pernicious anaemia
Partial gastrectomy
HNPCC/lynch syndrome
Menetrier’s disease

24
Q

What is a signet ring cell?

A

Cell with a large vaculoe, the malignant type is seen in carcinomas

25
Q

What is the prognosis like for intestinal vs diffuse gastric adenocarcinoma?

A

Intestinal type has a slightly better prognosis

26
Q

Where is gastric adenocarcinoma likely to spread localy?

A

Directly onto other organs

27
Q

What lymph nodes is gastric adenocarcinoma likely to spread to?

A

Omental

28
Q

Where is gastric adenocarcinoma likely to spread in the blood?

A

To the liver and beyond

29
Q

What is a gastric lymphoma (maltoma)

A

Derived from mucosa associated lymphoid tissue
Associated with H. Pylori infection
Continous inflammation induces an evolution into a clonal B-cell proliferation