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YR5 Histopathology > Upper Gastrointestinal Disease > Flashcards

Upper Gastrointestinal Disease Flashcards

1
Q

What are the different parts of the stomach?

A

Cardia

Fundus

Body

Pyloric antrum

Pylorus

Duodenum

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2
Q

What are normal features of a histology slide for the body of a stomach from top to bottom?

A

Lined by gastric mucosa columnar epithelium (foveolar, mucin secreting)

Specialised glands in lamina propria

Muscularis mucosa

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3
Q

What are normal features of a histology slide of the antrum of a stomach from top to bottom?

A

Lined by gastric mucosa columnar epithelium (fovelolar, mucin secreting)

Non-specialised glands in lamina propria (gastric pits)

Mucularis mucosa

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4
Q

What are normal features of a histology slide of the duodenum?

A

Glandular epithelium with goblet cells: Intestinal type epithelium.

Villous architecture- villous:crypt ratio >2:1

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5
Q

What is this?

A

Acute oesophagitis

Inflamed: red, swollen

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6
Q

What is this?

A

Acute oesophagitis

Neutrophils in epithelium

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7
Q

What is reflux oesophagitis?

A

Gastro-oesophageal reflux disease

Commonest cause of oesophagitis

Reflux of acidic gastric contents

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8
Q

What are complications associated with reflux oesophagitis?

A

Ulceration

Haemorrhage

Perforation

Stricture

Barrett’s oesophagus: Reversible.

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9
Q

What is Barrett’s oesophagus?

A

Replacement of squamous epithelium by metaplastic columnar epithelium

AKA columnar lined oesophagus (CLO).

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10
Q

What is this?

A

Barrett’s oesophagus

Islands of columnar epithelium- look like gastric epithelium

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11
Q

What is this?

A

Normal

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12
Q

What is this?

A

Barrett’s oesophagus

Simple columnar epithelium

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13
Q

What is this?

A

Barrett’s oesophagus

with goblet cells: intestinal metaplasia

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14
Q

What is the sequelae of disease progression to neoplasia?

A

“Flat pathway”

Squamous

Metaplastic glandular epithelium- Intestinal type

Dysplasia: Changes showing some cytological + histological features of malignancy but no invasion through BM

Adenocarcinoma: Invasion through BM

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15
Q

Give 4 features of squamous cell carcinoma of the oesophagus?

A

A/W: alcohol + smoking.

Mid/ lower oesophagus.

Commonest oesophageal cancer in developing countries

Invasion into the submucosa.

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16
Q

What is this?

A

Squamous cell carcinoma of the oesophagus

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17
Q

What is this?

A

Squamous cell carcinoma of the oesophagus

Produces keratin (pink)

Strong intracellular bridges

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18
Q

What is the prognosis of oesophageal carcinoma?

A

Prognosis poor

Dx of pre-invasive stage important

Early dx is important

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19
Q

What is gastritis?

A

Inflammation of the gastric mucosa

Acute: Acute insult

Chronic: Chronic/ persistent insult

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20
Q

What is this?

A

Gastritis

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21
Q

What are causes of acute gastritis?

A

Chemical:

  • Aspirin/ NSAIDs
  • Alcohol
  • Corrosives

Infection: Helicobacter pylori

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22
Q

What is this?

A

Acute gastritis

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23
Q

What are causes of chronic gastritis?

A

AI (antiparietal antibodies: to parietal cells in Body)

B: H. pylori: Antrum

Chemical (NSAIDs, bile reflux; antrum)

(ABC: AI, Bacterial, Chemical)

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24
Q

What is Helicobacter associated gastritis?

A

Caused by H. pylori.

Pattern: Chronic gastritis +/- activity spikes

Outcome:

  • CLO-IM-Dysplasia,
  • Adenocarcinoma
  • Lymphoma (MALToma)
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25
Q

What is this?

A

Helicobacter associated gastritis

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26
Q

How is Helicobacter associated with cancer?

A

Helicobacter infection A/w 8x increased risk of (non-cardia) gastric cancer.

cag-A-positive H.pylori have a needle like appendage that injects toxin into intercellular junctions allowing bacteria to attach more easily.

This strain is A/w more chronic inflammation.

Tx with abx drastically reduces risk of cancer.

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27
Q

What are other causes of gastritis?

A

Infection e.g. CMV, strongyloides (immunosuppression)

Inflammatory bowel disease: Crohn’s Disease

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28
Q

Why worry about gastritis?

A
  1. Chronic gastritis
  2. Intestinal metaplasia
  3. Dysplasia
  4. Cancer

“Flat pathway”

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29
Q

What is this?

A

Gastric ulcer

30
Q

Why should all ulcers be biopsied?

A

To exclude malignancy.

31
Q

What are complications associated with ulcers?

A

Bleeding:

  • Anaemia
  • Shock (massive haemorrhage)

Perforation:

  • Peritonitis
32
Q

What is intestinal metaplasia?

A

Intestinal metaplasia (goblet cells) in gastric mucosa in response to long term damage (As in oesophagus)

Increased cancer risk.

33
Q

What is this?

A

Intestinal metaplasia

34
Q

What is gastric epithelial dysplasia?

A

Abnormal epithelial pattern of growth.

Some cytological + histological features of malignancy are present, but no invasion through BM.

35
Q

What is this?

A

Gastric epithelial dysplasia

High nuclear: cytoplasmic ratio

Lots of mitosis

Abnormal mitosis

36
Q

What is the epidemiology of gastric cancer?

A

High incidence in Japan, Chile, Italy, China, Portugal, Russia.

M > F

>95% of all malignant tumors in stomach are adenocarcinomas.

37
Q

What is this?

A

Gastric cancer

38
Q

What is this?

A

Gastric cancer

39
Q

What is gastric cancer and how can it be split?

A

95% of stomach cancers are adenocarcinoma.

Split morphologically into:

  • Intestinal: Well differentiated.
  • Diffuse: Poorly differentiated (Linitis plastica), inc. signet ring cell carcinoma
40
Q

What is this? Give 3 features of this.

A

Intestinal gastric cancer

Well differentiated

Form glands

Secrete mucin

41
Q

What is this? Give 5 features of this

A

Diffuse gastric cancer

Poorly differentiated

No architecture

Single cells, lost cohesion

Don’t form glands

White dots= signet ring cells- make mucin which stays in cell

42
Q

What are less common types of gastric cancer?

A

Remaining 5% is made up of:

  • Squamous cell carcinoma (col to squa)
  • Lymphoma (MALToma)
  • Gastrointestinal stromal tumour (GIST)
  • Neuroendocrine tumours
43
Q

What is the overall survival of gastric cancer?

A

15%

44
Q

What is Gastric MALToma/Lymphoma and the treatment?

A

Chronic inflammation causes chronic immune stimulation

Development of single clone that proliferates: B cell (marginal zone) lymphocytes.

Tx: If limited to stomach + H.pylori is present= H.pylori eradication.

45
Q

What is this?

A

Gastric MALToma/Lymphoma

46
Q

What is this?

A

Gastric MALToma/Lymphoma

47
Q

What are the associations between duodenitis, duodenal ulcers and H. Pylori?

A

H pylori A/w increased acid secretion driven by increased gastrin secretion

Increased acid in stomach spills over into duodenum.

Chronic inflammation + gastric metaplasia

Normal goblet cell containing small intestine replaced by gastric mucosa

H pylori grow wherever there is gastric mucosa

H pylori duodenitis + ulcer

48
Q

What is this?

A

Duodenal ulcer

49
Q

Which pathogens are responsible for duodenal ulcers?

A

Immunosuppressed: CMV, Cryptosporidiosis

Giardia lamblia infection

Whipple’s disease -Tropheryma whippelii.

50
Q

What is seen on a histology slide for malabsorption?

A

Partial villous atrophy

Crypt hyperplasia

Increased Intraepithelial lymphocytes: Normal: < 20 lymphocytes /100 enterocytes

51
Q

Describe the histology of the gastro-oesophageal junction

A

Stratified squamous (same as oesophageal folds superiorly)

Z line: abrupt non linear change

Columnar (same as gastric rugae inferiorly)

52
Q

What is secreted in the body of the stomach?

A

Acid

Intrinsic Factor

53
Q

What type of malignancy occurs in the body of the stomach?

A

Adenocarcinoma

(Columnar mucus secreting epithelium)

54
Q

What are the 2 types of Barrett’s Oesophagus?

A

Without goblet cells: gastric metaplasia

With goblet cells: intestinal type metaplasia, greater risk of progression to cancer

55
Q

What is the most important risk factor for carcinoma in the colon?

A

Polyps

56
Q

Give 3 features of adenocarcinoma of the oesophagus

A

Commonest oesophageal carcinoma in Developed countries

A/w reflux

Lower oesophagus (where most reflux affects)

57
Q

What 2 features are common to all adenocarcinomas?

A

Make glands

Secrete mucin

58
Q

What is shown here?

A
  1. Barrett’s oesophagus
  2. Adenocarcinoma
59
Q

What is the commonest cause of oesophageal varices?

A

Cirrhosis

Blood can’t get through liver, diverts through vessels via systemic circulation

Gives rise to varices, haemorrhoids, around umbilicus

60
Q

What is this?

A

Gastric ulcer

61
Q

Name 2 defects in lining of stomach wall

A

Ulcer: through muscular mucosa into submucosa

Erosion: more superficial

62
Q

Describe the villi in a normal duodenum

A

Villi twice as high as crypts

Crypts: stem cell, cell proliferation, cells migrate up

If something wrong with villi: villi shorten, crypts become thicker, cells proliferate more rapidly to try to regenerate villi

63
Q

Describe the correlation between duodenitis and duodenal ulcers

A

Good correlation between endoscopy + biopsy pathology

If “itis” on endoscopy: 74% progress to ulcer

64
Q

What is seen here?

A

LHS: normal villi

RHS: flattening of villi (partial villous atrophy)

65
Q

Which antibodies are required for diagnosis of coeliac disease?

A

Endomysial

Tissue transglutimase

66
Q

What will be seen on duodenal biopsy in coeliac disease?

A

Gluten rich diet: villous atrophy

GF: Normal villi

67
Q

Give a cause of malabsorption that shows similar histology to coeliac

A

Tropical sprue

68
Q

In coeliac disease which cancer is there higher risk of?

A

Duodenal MALToma/ lymphoma

T cell origin (Enteropathy associated T cell lymphoma)

69
Q

True or false: most oesophageal and gastric cancers arise from pre-existing adenomas

A

False

Most arise from the flat pathway

70
Q

In a patient with coeliac disease on a diet containing gluten, the most likely histological change in the duodenum is…

A

Villous atrophy

(can have normal architecture with increased intra-epithelial lymphocytes in v early stages)

71
Q

Which of the following is not a cause of chronic gastritis?

Auto-immunity

Infection

Drugs

Metabolic disease

A

Metabolic disease is NOT

YR5 Histopathology (27 decks)

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