Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Yr 2 - Clinical Pathology > Upper GI Pathology > Flashcards

Upper GI Pathology Flashcards

1
Q

What type of epithelium is the oesophagus mostly lined by?

A
  • Squamous epithelium (majority)
  • Distal 1.5/2cm are below the diaphragm and lined by glandular (columnar) mucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 2 sphincters present in the oesophagus?

A
  1. Cricopharyngeal (upper)
  2. Gastro-oesophageal (lower)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the oesophagus join together?

A

The pharynx & stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Roughly how far is the squamo-columnar junction located from the incisor teeth?

A

40cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is oesophagitis?

A
  • Inflammation of the oesophagus
  • Can be acute or chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the most common cause of oesophagitis in Western countries?

A

Due to reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Oesophagitis can also be cause by infections such as…

A

Bacterial, viral (HSV1, CMV), fungal (candida)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What 2 types of reflux is reflux oesophagitis due to?

A
  1. Gastric acid: gastro-oesophageal reflux
  2. Bile: duodeno-gastric reflux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors for reflux oesophagitis?

A
  • Defective lower oesophageal sphincter
  • Increased intra-abdominal pressure
  • Increased gastric fluid volume due to gastric outflow stenosis
  • Hiatus hernia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a hiatus hernia?

A
  • Abnormal bulging of a portion of the stomach through the diaphragm
  • Sliding hiatus hernia leads to reflux symptoms, whereas para-oesophageal hernia leads to strangulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 2 types of hiatus hernias?

A
  1. Sliding hiatus hernia –> most likely to lead to reflux
  2. Paraesophageal hiatus hernia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Symptoms of reflux oesophagitis?

A

Heartburn (upper abdomen, lower thorax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Histological changes in reflux oesophagitis?

A

Normal squamous epithelium undergoes:

  • Basal cell hyperplasia
  • Elongation of papillae
  • Increased cell desquamation
  • Inflammation
  • Ulceration if severe
  • Lamina propria experiences inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Potential complications of oesophagitis?

A
  • Ulceration
  • Haemorrhage
  • Perforations; especially into trachea
  • Benign stricture due to repair through fibrosis (segmental narrowing)
  • Barrett’s oesophagus (metaplastic process)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the cause of Barrett’s oesophagitis?

A

Longstanding gastro-oesophageal reflux (risk factors are same for reflux)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is the squamo-columnar junction affected in Barrett’s oesophagus?

A

Proximal extension of the squamo-columnar junction (this can be identified endoscopically)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which histological change occurs in Barrett’s oesophagus?

A

Squamous mucosa replaced by columnar mucosa –> ‘glandular metaplasia’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Is Barrett’s oesophagus malignant? What can it predispose to?

A

Premalignant condition with an increased risk of developing adenocarcinoma:

  • Screening with regular endoscopic surveillance
  • Disease progression: Barrett’s oesophagus –> low-grade dysplasia –> high-grade dysplasia –> adenocarcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 2 main histological types of oesophageal carcinomas?

A
  • Squamous cell carcinoma (arising from original squamous lining)
  • Adenocarcinoma (arising from epithelium that has changed from sqaumous to glandular)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does distribution of different histological types of oesophageal carcinomas vary around the world?

A
  • UK = 30% squamous
  • China/Japan = >95% squamous (as not as obese as Westerners)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How has the incidence of oesophageal adenocarcinoma changed?

A
  • Incidence has risen dramatically in industrialised countries
  • Higher incidence in men
  • Higher incidence among Caucasians
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the underlying aetiology of nearly all oesophageal adenocarcinomas?

A

Barrett’s oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Risk factors for oesophageal squamous carcinoma?

A
  • Tobacco and alcohol
  • Nutrition (potential sources of nitrosamines)
  • Thermal injury (hot beverages)
  • Human Papilloma Virus
  • Male
  • Ethnicity (black)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Location of oesophageal squamous carcinoma?

A

Middle and lower third (<15% in upper third of oesophagus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which viral infection is linked to oesophageal squamous carcinoma?

A

HPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What histological changes occur in oesophageal SCC?

A

Normal squamous epithelium –> high grade squamous dysplasia –> invasive squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Macroscopic appearances of oesophageal carcinomas:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Major symptom of oesophageal carcinoma?

A
  • Dysphagia
    • Starts with solid food, moving on to liquids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What system is used to stage oesophageal carcinomas?

A

TNM system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does the TNM staging system consist of?

A
  • T = primary tumour
    • T1 to T4 (based on depth of invasion)
  • N = regional lymph nodes
    • N0 (no lymph node metastasis)
    • N1 to N3 (depending on number of lymph node metastases)
  • M = distant metastasis
    • M0 (no distant metastasis)
    • M1 (distant metastasis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the commonest cause of oesophagitis?

  1. Bacterial infection
  2. Reflux of gastric contents
  3. Viral infection

Smoking

A

Reflux of gastric contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is Barrett’s oesophagus?

  1. Development of oesophagitis due to gastric reflux
  2. Change in the lining of the oesophagus from columnar to squamous
  3. Change in the lining of the oesophagus from squamous to columnar
  4. Development of adenocarcinoma in the oesophagus
A

Change in the lining of the oesophagus from squamous to columnar

33
Q

What is a well recognised aetiology for squamous cell carcinoma of the oesophagus?

  1. Barrett’s oesophagus
  2. Human papilloma virus infection
  3. Gastro-oesophageal reflux
  4. Lynch syndrome
A

Human papilloma virus infection

34
Q

Normally in the stomach there is a balance of aggressive (acid) and defensive forces. Examples of these defensive forces?

A
  • Surface mucous
  • Bicarbonate secretion
  • Mucosal blood flow
  • Regenerative capacity
  • Prostaglandins
35
Q

Risk factors for increased aggression of stomach acid?

A
  • Excessive alcohol
  • Drugs
  • Heavy smoking
  • Corrosive
  • Radiation
  • Chemotherapy
  • Infection
36
Q

Risk factors for impaired defences of stomach against acid?

A
  • Ischaemia
  • Shock
  • Delayed emptying
  • Duodenal reflux
  • Impaired regulation of pepsin secretion
37
Q

What are the 2 major causes of acute gastritis in the UK?

A
  1. Chemical injury
  2. Initial response to Helicobacter pylori infection
38
Q

What are the 2 most common agents causing chemical injury in acute gastritis?

A
  1. NSAIDs
  2. Alcohol
39
Q

Severity of gastritis?

A
  • Effects depend on severity of the injury –> Can get erosions and haemorrhage
  • Generally heal quickly
40
Q

What are 3 aetiologies of chronic gastritis?

A
  1. Autoimmune
  2. Bacterial infection
  3. Chronic chemical injury; NSAIDs, bile reflux, alcohol etc
41
Q

How can autoimmunity lead to chronic gastritis?

A

Anti-parietal and anti-intrinsic factor antibodies

42
Q

Which bacterial infection can lead to chronic gastritis?

A

Helicobacter pylori

43
Q

What can chronic infection with H. pylori predispose you to?

A
  • 2-5% have gastric ulcers, 10-15% have duodenal ulcers
  • Increased risk of gastric cancer and MALT lymphoma
44
Q

Classification of H. pylori?

A

Gram negative spiral shaped bacterium

45
Q

How does H. pylori affect stomach?

A

Damages the epithelium leading to chronic inflammation –> can result in glandular atrophy and intestinal metaplasia

46
Q

Which part of the stomach is H. pylori more common in?

A

More common in antrum than body

47
Q

Major sites of peptic ulcer disease?

A

–First part of duodenum

–Junction of antral and body mucosa

–Distal oesophagus (GOJ)

48
Q

Main aetiologies of peptic ulcer disease?

A

–Hyperacidity

–H. pylori infection

–Duodeno-gastric reflux

–Drugs (NSAIDs)

–Smoking

49
Q

Gastric vs duodenal ulcer;

  • Relative incidence?
  • Age distribution?
  • Acid levels?
  • H. pylori gastritis?
  • Localisation?
  • Blood group?
A
50
Q

Potential complications of gastric/duodenal ulcers?

A
  • Haemorrhage (acute and/or chronic –> anaemia)
  • Perforation –> peritonitis
  • Penetration into an adjacent organ (liver, pancreas)
  • Stricturing –> hour-glass deformity (can cause contents to reflux back up)
51
Q

What is the most common type of gastric cancer?

A

Adenocarcinoma

52
Q

There are slight differences in aetiologies behind adenocarcinomas at the gastro-oesophageal junction (GOJ) vs in body/antrum of stomach.

Which is associated with H. pylori?

A

Adenocarcinoma of body/antrum

53
Q

Aetiology of GOJ adenocarcinomas?

A
  • White males
  • Association with GO reflux
  • No association with H. pylori/diet
  • Increased incidence in recent years (increase in obesity)
54
Q

Aetiology of adenocarcinomas located in body/antrum?

A
  • Association with H. pylori
  • Association with diet (salt, low fruit & vegetables)
  • No association with GO reflux
  • Decreased incidence in recent years (eradication of H. pylori)
55
Q

What is hypochlorhydria?

A

Low stomach acid levels

56
Q

How can hypochlorhydria predispose to gastric adenocarcinoma?

A

Allows bacterial growth

57
Q

2 major causes behind gastric adenocarcinoma?

A
  1. Diet (smoked/cured meat or fish, pickled vegetables)
  2. H. pylori infection
58
Q

What are the 2 microscopic types of gastric adenocarcinomas?

A
  1. Intestinal type (most common)
  2. Diffuse type
59
Q

What defines ‘intestinal type’ gastric adenocarcinoma?

A

– Well or moderately differentiated

– May undergo intestinal metaplasia and adenoma steps

60
Q

What defines ‘diffuse type’ gastric adenocarcinoma?

A

– Poorly differentiated

– Scattered growth

– Cadherin loss/mutation

61
Q

How is gastric adenocarcinoma staged?

A

TNM staging system

62
Q

What is Helicobacter pylori associated with?

  1. Gastritis
  2. Peptic ulcer disease
  3. Gastric cancer
  4. All of the above
A

All of the above

63
Q

Which of the following statements is correct?

  1. Helicobacter pylori are most commonly seen in the gastric cardia
  2. NSAIDs commonly cause duodenal ulcers
  3. Gastric ulcers may harbour adenocarcinoma
  4. Haemorrhage within an ulcer may lead to stricturing
A

Gastric ulcers may harbour adenocarcinoma –> ALWAYS biopsy an ulcer

  • H. pylori are most commonly seen at gastric antrum
  • NSAIDs commonly cause gastric NOT duodenal ulcers
  • Haemorrhage within an ulcer does NOT cause stricturing (is the healing fibrosis that does)
64
Q

Which of the following statements is correct?

  1. Gastric cancers are staged according to the Dukes’ classification
  2. Around half of all gastric adenocarcinomas are caused by a germline mutation in E-cadherin
  3. Diffuse-type tumours are more common than intestinal-type tumours
  4. Stomach cancer is the 17th most common cancer in the UK, accounting for 2% of all new cancer cases
A

Stomach cancer is the 17th most common cancer in the UK, accounting for 2% of all new cancer cases.

  • Gastric cancers staged according to TNM
  • Germline mutation in E-cadherin only accounts for around 1% of gastric adenocarcinomas
  • Intestinal-type are more common than diffuse-type tumours
65
Q

What is Coeliac disease also known as?

A

Also known as Coeliac sprue or gluten sensitive enteropathy

66
Q

Which foods are involved in Coeliac disease?

A

Ingestion of gluten containing cereals by genetically predisposed individuals; wheat, rye, or barley

67
Q

Prevalence of Coeliac disease?

A

Estimated prevalence of 0.5% to 1% (fairly common)

68
Q

Typical age of onset of Coeliac?

A

Commonly affects adults between 30 and 60 years

69
Q

Pathogenesis of coeliac disease?

A

Immune mediated enteropathy:

  • Reaction to gliadin (the alcohol soluble component of gluten)
  • Induces epithelial cells to express IL-15
  • IL-15 causes activation and proliferation of CD8+ IELs (intra-epithelial lymphocytes)
  • These are cytotoxic and kill enterocytes

Mechanism –> gliadin-induced IL-15 secretion by epithelium

70
Q

Which cytokine is involved in Coeliac disease?

A

IL-15

71
Q

Do CD8+ IELs recognise gliadin directly in Coeliac disease?

A

No - via gliadin-induced IL-15 secretion by epithelium

72
Q

Diagnosis of Coeliac disease?

A
  • Non-invasive serologic tests usually performed before biopsy
  • The most sensitive tests
    • IgA antibodies to tissue transglutaminase (TTG)
    • IgA or IgG antibodies to deamidated gliadin
    • Anti-endomysial antibodies - highly specific but less sensitive
  • Tissue biopsy is diagnostic (2nd biopsy after gluten free diet)
73
Q

Treatment of Coeliac disease?

A

Gluten free diet –> symptomatic improvement for most patients

74
Q

Potential long-term complications of Coeliac disease?

A

Anaemia, female infertility, osteoporosis, and cancer

75
Q

Other disease associations with Coeliac disease?

A
  • Dermatitis herpetiformis - 10% of patients
  • Lymphocytic gastritis and lymphocytic colitis
  • Cancer:
    • Enteropathy-associated T-cell lymphoma
    • Small intestinal adenocarcinoma (due to chronic inflammation)
    • BEWARE!!!! Symptoms despite gluten free diet
76
Q

What are the 4 histological criteria for Coeliac disease?

A
  1. Loss of finger-like villous projections (villous atrophy)
  2. Crypt elongation
  3. Increased IELs
  4. Increased lamina propria inflammation
77
Q

Coeliac disease is associated with which histopathological features?

  1. Villous atrophy
  2. Crypt elongation
  3. Increased intraepithelial lymphocytes
  4. All of the above
A

All of the above

78
Q

What are IELs?

A
  • Intraepithelial lymphocytes (form of T cells) are found in the epithelial layer of mucosal linings, such as the GI tract
  • However, IELs do not need priming; upon encountering antigens, they immediately release cytokines
  • In the GI tract, they are components of gut-associated lymphoid tissue (GALT).
  • IELs significantly increase in coeliac disease.

Yr 2 - Clinical Pathology (80 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions