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GI > Pathology: Stomach & Duodenum > Flashcards

Pathology: Stomach & Duodenum Flashcards

1
Q

What are potential causes of acute gastritis?

A
  • irritant chemical injury
  • severe burns
  • severe trauma
  • shock
  • head injury
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2
Q

What are potential causes of chronic gastritis?

A
  • autoimmune
  • bacterial e.g. H.Pylori
  • chemical
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3
Q

What cell types are rarely associated with gastritis?

A
  • eosinophilic
  • lymphocytic
  • granulomatous
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4
Q

What is rarest cause of gastritis?

A

autoimmune

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5
Q

What is most common cause of gastritis?

A

H.pylori infection

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6
Q

How does autoimmune gastritis affect the stomach?

A
  • atrophic gastritis
  • intestinal metaplasia (dysplasia of stomach cells)
  • loss of parietal cells, achlorhydria and intrinsic factor deficiency
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7
Q

What is achlorhydria?

A

Loss of hydrochloric acid in gastric secretions

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8
Q

What clinical syndrome is often associated with autoimmune gastritis?

A

Pernicious anaemia

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9
Q

What causes loss of parietal cells and intrinsic factor deficiency in autoimmune gastritis?

A

Anti-parietal and anti-intrinsic factor antibodies

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10
Q

What risk is increased with autoimmune gastritis?

A

Malignancy (due to metaplasia)

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11
Q

What is SACDC and what is it often associated with?

A
  • Sub acute combined degeneration of the spinal cord

- often associated with pernicious aneamia

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12
Q

What causes pernicious anaemia?

A

Autoimmune disorder due to atrophic gastritis with loss of parietal cells with consequent failure of intrinsic factor production meaning malabsorption of vitamin B12 (Gastric intrinsic factor is associated with B12 absorption)

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13
Q

What type of anaemia is pernicious anaemia?

A

macrocytic

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14
Q

Describe H.pylori as a bacteria?

A
  • Gram negative

- curvilinear rod

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15
Q

Where does H.pylori bacteria inhabit?

A

-niche between epithelial cell surface and mucous barrier

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16
Q

What is the inflammation process of H.pylori infections?

A

Excites early acute inflammatory response and if not cleared then chronic inflammatory response follows

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17
Q

What cytokine is important in H.pylori response?

A

IL8

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18
Q

What cells produce H.pylori antibodies and where are these cells located?

A
  • Plasma cells

- Lamina propria

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19
Q

What do H.pylori infections lead to an increased risk in?

A

Increased risk in:

  • gastric ulcer
  • duodenal ulcer
  • gastric carcinoma
  • gastric lymphoma
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20
Q

How do H.pylori infections look histopathologically?

A

Lots of little/big circles like blobs of infection throughout edge of stomach.

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21
Q

What can cause chemical gastritis?

A
  • NSAIDs
  • alcohol
  • bile reflux
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22
Q

What can cause direct injury to mucous layer?

A

fat solvents

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23
Q

What are histopathological signs of chemical gastritis?

A
  • epithelial regeneration
  • hyperplasia
  • congestion
  • little inflammation
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24
Q

What can chemical gastritis cause?

A
  • erosions

- ulcers

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25
Q

How can chemical gastritis present endoscopically?

A

Black dots along lining

26
Q

What is the difference between peptic ulcer and erosions?

A

Both are superficial breaks in the mucosa however peptic ulcers can penetrate down to muscularis mucosa.

27
Q

What is a peptic ulcer?

A

Breach in the gastriointestinal mucosa due to acid and pepsin attack

28
Q

Where do chronic peptic ulcers usually present?

A
  • duodenum (1st part)
  • stomach (junction of body and antrum)
  • gastro-oesophageal junction
  • stomal ulcers
29
Q

What size do peptic ulcers range from?

A

2-10cm

30
Q

How do peptic ulcers appear through endoscope?

A

edges are clear cut and looks punched out

31
Q

What are the two factors of pathogenesis of peptic ulcers?

A
  • increased acid + pepsin production (due to hypersecretory state)
  • defect in mucosal defence mechanisms (e.g. due to gastric hyperacidity, NSAIDs, alcohol)
32
Q

Outline the concept of synergism in relation to peptic ulcers.

A

Synergism is where sum of effects is greater than individual effects by themselves. In this case its combination of increased acidity combined with defect in mucosal defence mechanisms (increased attack and failure of defence)

33
Q

What does excess acid in duodenum cause?

A

Gastric metaplasia and consequent H.pylori infection, inflammation, epithelial damage and ulceration

34
Q

What do many duodenal peptic ulcer patients have?

A

Inappropriately sustained acid secretion

35
Q

How do peptic ulcers present microscopically and what is each layer?

A
  • layered appearance:
  • floor of fibrinopurulent debris
  • base of inflamed granulation tissue
  • deepest layer is fibrotic scar tissue
36
Q

What is fibrinopurulent debris?

A

Pus or suppurative exudate containing relatively large amount of fibrin

37
Q

What is granulation tissue and what does it contain?

A
  • Tissue that grows during repair of soft tissue wounds

- connective tissue cells and young blood vessels

38
Q

What are 5 complications of peptic ulcers?

A
  • perforation
  • penetration
  • haemorrhage
  • stenosis
  • intractable pain
39
Q

What are two benign gastric polyps?

A
  • hyperplastic polyps

- cystic fundic gland polyps

40
Q

What are three types of malignant gastric tumours?

A
  • carcinoma (adenocarcinomas)
  • lymphoma
  • gastrointestinal stromal tumours (GISTs)
41
Q

What is the stroma?

A

The connective tissue cells that form the framework of an organ as opposed to parenchyma (functioning part)

42
Q

What type of gastric adenocarcinomas are increasing in incidence in UK and which are decreasing?

A
  • Proximal tumours of cardia/GOJ increasing

- distal tumours decreasing

43
Q

What is often prevalent in patients with gastric adenocarcinomas?

A

H.pylori infections

44
Q

What is the pathogenesis of gastric adenocarcinomas?

A

H.pylori infection -> chronic gastritis -> intestinal metaplasia/atrophy -> dysplasia -> carcinoma

45
Q

What is intestinal metaplasia?

A

The transformation of mucosa (particularly stomach) into glandular mucosa that resembles intestinal mucosa, increase in goblet cells

46
Q

What are 5 potential causes of gastric adenocarcinoma?

A
  1. H.pylori infections
  2. pernicious anaemia
  3. partial gastrectomy
  4. HNPCC/Lynch Syndrome
  5. Menetrier Disease
47
Q

What is HNPCC and what is another name for it?

A
  • Hereditary nonpolyposis colorectal cancer

- AKA Lynch Syndrome

48
Q

What is Menetrier disease?

A

Characterised by massive overgrowth of mucosal cells in stomach resulting in large gastric folds

49
Q

What are the two types of gastric adenocarcinoma and explain the types?

A
  • intestinal type i.e. polypoid mass, exophytic

- diffuse type i.e. expands and infiltrates stomach wall

50
Q

How can you tell the difference between malignant gastric adenocarcinoma and peptic ulcer?

A

Peptic ulcer don’t have raised rolled edge and is more punched out

51
Q

What is linitis plastica?

A

Type of stomach adenocarcinoma that causes stomach tissue to be thicker and “leather-like”

52
Q

What type of cancer is signet ring cell adenocarcinoma in stomach?

A

-Diffuse type

53
Q

How does signet ring cell adenocarcinoma look histopathologically?

A

Like little rings or white blobs of cells

54
Q

What are 3 types of diffuse gastric adenocarcinoma?

A
  • signet ring cell
  • linitis plastica
  • sclerosis
55
Q

Which of intestinal or diffuse carcinoma has better prognosis?

A

Intestinal

56
Q

Where do gastric adenocarcinomas spread?

A
  • locally e.g. organs, peritoneal cavity, ovaries
  • lymph nodes
  • haematogenous (to liver)
57
Q

What is a kruckenberg tumour?

A

Malignancy in the ovary that metastasised from a primary site usually gastric adenocarcinoma

58
Q

What structures form in intestinal gastric adenocarcinoma?

A

glandular structures

59
Q

What is another name for gastric lymphoma?

A

Maltoma - mucosa associated lymphoid tumour

60
Q

What stomach infection is gastric lymphoma/maltoma associated with?

A

H.pylori infection

61
Q

What is the pathogenesis of gastric lymphoma?

A

Chronic inflammation -> evolution into a clonal B-cell proliferation (low-grade)

62
Q

What happens if low-grade gastric lymphoma is untreated?

A

Evolves into high-grade B cell lymphoma

GI (29 decks)

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