GI Pathology Flashcards

1
Q

What is the pathogenesis of Diverticular Disease? (protrusions of mucosa/ submucosa through bowel wall, commonly sigmoid colon)

A
  • Increased intra-luminal pressure
  • Irregular, uncoordinated peristalsis
  • Points of relative weakness in bowel wall
  • Age related changed in connective tissue
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2
Q

Colorectal Polyps…

a) features
b) cause

A

a) -‘mucosal protrusion’, pedunculated, sessile or ‘flat’
- Solitary or multiple (polyposis)
- neoplastic, hamartomatous, inflammatory or reactive
b) Due to mucosal/ submucosal pathology or a lesion deeper in bowel wall

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3
Q

What are 6 types of non-neoplastic polyps in the colo-rectum?

A
  1. Hyperplastic polyps
  2. Hamartomatous polyps (juvenile polyps)
  3. Polyps related to mucosal prolapse
  4. Post-inflammatory polyps (‘pseudopolyps’)
  5. Inflammatory fibroid polyps
  6. Benign lymphoid polyps
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4
Q

What are hyperplastic polyps?

A

Common, 1-5mm, located in rectum & sigmoid colon.
Small, distal HPs have no malignant potential
Some large right sided HPs may give rise to microsatellite unstable carcinoma

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5
Q

What are harmatomatous polyps?

A

(Juvenile polyps- commonest type in children) Spherical and pedunculated, 10-30mm, usually in distal colon & rectum.
No malignant potential but associated with increased risk of colorectal & gastric cancer.

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6
Q

What are adenomas and what relevance do they have to the colon?

A

Adenomas are benign epithelial tumours
Precursor of colorectal cancer (at least 80%)
Histological grade= high vs low grade dysplasia.

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7
Q

What are some risk factors for colorectal cancer?

A
Diet
Obesity/ alcohol
HRT & oral contraceptives
Schistosomiasis
UC & Crohn's
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8
Q

2 types of inheritance of colorectal cancer?

A

-FAP (familial adenomatous polyps) <1%
Autosomal dominant, due to a mutation in the APC tumour suppressor gene
-Lynch Syndrome 1-2%
Direct invasion of adjacent tissue, lymphatic & haematogenous metastasis

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9
Q

What is A-D of Duke’s Staging of Colorectal cancer?

A

Stage A: adenocarcinoma confined to bowel wall, no lymph node metastasis
Stage B: invading bowel wall, no lymph node metastasis
Stage C: adenocarcinoma with regional lymph node metastasis
Stage D: distant metastasis present

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10
Q

What is Angular Cheilitis caused by?

A

Excessive moisture & maceration from saliva, and secondary infection with C albicans or S aureus

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11
Q

What is Hairy Leucoplakia?

A

Seen in HIV patients, caused by Epstein Barr Virus

Well-demarcated white plaques visible on lateral aspects of the tongue.

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12
Q

What are some periodontal infections? (plaque between the gingival margin)

A
  • Gingivitis (presents with red swollen bleeding gums)
  • Periodontitis (progression of gingivitis & inflammation with loss of supportive connective tissues)
  • Periodontal abscess
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13
Q

What is Vincent’s angina, or trench mouth?

A

Acute necrotising ulcerative gingivitis (superficial greyish pseudomembranes. Requires antibiotics)

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14
Q

What is a Peritonsillar abscess (quinsy)?

A

Unilateral swellings of the tonsil
Caused by Streprococcus pyogenes
Painful swallowing, unilateral deviation of uvula towards the unaffected side.

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15
Q

What is Ludwig’s angina?

A

Bilateral infection of the submandibular space.

An aggressive, rapidly spreading cellulitis with potential for airway obstruction.

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16
Q

What does Carotid Sheath involvement mean?

A

The carotid sheath abuts all three layers of the deep cervical fascia. It is a dreaded complication becuase of potential for carotid artery erosion & supportive jugular thrombophlebitis.

17
Q

What are the 2 clinical manifestations of Thrush (oral & oesophageal candidiasis)?

A

1) The pseudomembranous form (most common, white plaques on buccal mucosa, palate, tongue)
2) The atrophic form (denture stomatitis) (more common in older adults, erythema without plaques.

18
Q

What is mucositis? And what induces it?

A

Inflammation of the mucosa linking of the GI tract.
Chemotherapy induced
Increased risk of bacteraemia, principally viridans streptococci.

19
Q

What is Boerhaave syndrome?

A

Oesophageal rupture.- spontaneous perforation of the oesophagus that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure.
Results in contamination of the mediastinal cavity with gastric contents

20
Q

What is H. Pylori Infection, how is it diagnosed and what treats it?

A

Bacterial urease hydrolyses gastric urea to form ammomia that helps neutralise gastric acid- enabling organism to penetrate the gastric mucus layer.
Diagnosis: Urease breath test, faecal antigen test
Treatment: Triple antibiotic therapy plus PPI (for 7-14 days)

21
Q

What is Charcot’s triad and what is it associated with?

A

Fever, abdominal pain & jaundice

Associated with Cholangitis

22
Q

Whipple’s Disease… agent? 4 cardinal manifestations?

A

Agent= Tropheryma whepplei
Multi-systemic process characterised by joint symptoms, chronic diarrhoea, malabsorption and weight loss. (mainly affects white european males)
Should be considered in patients with the 4 cardinal manifestations: arthralgias, diarrhea, abdo pain and weight loss

23
Q

What does Entamoeba histolytica cause?

A

Amebic liver abscesses

the parasite exists in 2 forms: a cyst stage (infective form) and a throphozoite stage (causes invasive disease

24
Q

What bacteraemia is usually associated with colonic malignancy?

A

Streptococcus bovis (nor renamed S. gallolyticus). Also associated with endocarditis.

25
Q

What is the pathology of Gastroenteritis?

A

Preformed toxins eg)Staphylococcal toxin

Toxins eg) Shiga toxin

26
Q

What are the 2 types of Hiatus Hernia?

A

1- Sliding Hiatus Hernia = reflux symptoms

2- Para-oesophageal Hernia = strangulation (part of stomach above diaphragm)

27
Q

What is Barrett’s oesophagus and what causes it?

A

A premalignant condition with increased risk of developing adenocarcinoma
Cause: longstanding gastro-oesophageal reflux
Macroscopy: Proximal extension of the squamo-columnar junction
Histology: Squamous mucosa replaced by columnar mucosa&raquo_space; ‘glandular metaplasia’

28
Q

What are the 2 main types of oesophageal carcinoma?

A

1) Adenocarcinoma (mainly lower oesophagus, higher incidence rate among men & Caucasians.
2) Squamous Cell Carcinoma (Middle & lower 1/3 oesophagus, preceded by squamous dysplasia. Risk factors include tobacco, alcohol, nutrition, HPV, male.

29
Q

How do you stage oesophageal cancer?

A

Use TNM system (with pT = depth of invasion of primary tumour) (N= regional lymph nodes) (M= distant metastasis)

30
Q

What is acute gastritis usually due to?

A

Usually due to chemical injury (Drugs eg. NSAIDS, Alcohol, H Pylori)
Generally heal quickly

31
Q

What is chronic gastritis usually due to?

A
Autoimmune --> anti-parietal &amp; anti-intrinsic factor antibodies.
Bacterial infection (H pylori)
Increased risk of gastric cancer and MALT lymphoma
32
Q

What is H pylori?

A

Gram negative spiral bacterium.
Damaged the epithelium leading to chronic inflammation of the mucosa.
Results in glandular atrophy, replacement fibrosis and intestinal metaplasia

33
Q

What are the main causes of peptic ulceration?

A
Hyperacidity
H pylori infection
Duedeno-gastric reflux
Drugs (NSAIDs)
Smoking
34
Q

What are the features of acute gastric ulceration?

A

Full-thickness coagulative necrosis of mucosa.
Covered with ulcer slough (necrotic debris + fibrin + neutrophils)
Granulation tissue at ulcer floor

35
Q

What are the features of chronic gastric ulceration?

A

Clear-cut edges overhanging the base
Extensive granulation & scar tissue on ulcer floor
Scarring through entire gastric wall with breaching of the muscularis propria?

36
Q

Causes of gastric carcinoma?

A
Diet
H Pylori infection (carcinoma of body/antrum)
Bile reflux
Hypochlorhydria
~1% hereditary
37
Q

What is the pathogenesis behind coeliac disease?

A

Reaction to gliadin (alcohol soluble component of gluten) induces IL15 secretion by epithelium

38
Q

Histology of Coeliac disease?

A

Villous atrophy
Crypt elongation
Increased IELs
Increased lamina propria inflammation