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AAPathology (Robbins) > GI tract > Flashcards

GI tract Flashcards

1
Q

Congenital abnormalities of the GIT include…

oesophagus, hernias, ectopia, small bowel

A

Atresia, commonly near tracheal bifurcation, sometimes with fistula to bronchi. Stenosis can also occur.
Diaphragmatic hernia, omphalocele and gastroschisis.
Ectopic gastric tissue most commonly occurs in the oesophagus. Ectopic pancreatic tissue occurs more rarely.
Pyloric stenosis.
Meckel’s diverticulum.

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2
Q

The rule of 2s for Meckel’s diverticulum.

A

2% of population, within 2 ft of ileocaecal valve, 2” long, twice as common in males, and if symptomatic, are symptomatic by age 2. Only 4% (2 squared) are ever symptomatic.

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3
Q

Cause of Meckel’s diverticulum

A

Failed involution of the vitelline duct.

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4
Q

Varieties of Meckel’s diverticulum

A

Normal, or with ectopic pancreatic or gastric tissue, the latter of which can cause ulceration.
All forms are a true diverticulum, involving all 3 layers of the bowel wall.

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5
Q

Frequency of congenital hypertrophic pyloric stenosis.

A

1 in 300-900 live births. 3-5 times more common in males.

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6
Q

Factors associated with increased risk of pyloric stenosis at birth

A

Erythromycin exposure in first two weeks of life

Turner’s syndrome, trisomy 18.

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7
Q

Presentation of congenital hypertrophic pyloric stenosis

A

3-6 weeks, projectile non-bilious vomiting and demands for refeeding.

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8
Q

Congenital hypertrophic pyloric stenosis on examination

A

Firm ovoid 1-2 cm abdo mass.

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9
Q

What can increase narrowing of congenital hypertrophic pyloric stenosis?

A

Edema and inflammatory changes.

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10
Q

What causes acquired pyloric stenosis?

A

Antral gastritis, peptic ulcers in pyloric region, carcinoma of stomach or pancreas.

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11
Q

Epidemiology of Hirschsprung disease.

A

1/5000 live births, 10% occur in Down’s syndrome and 5% with other neurological deficits.

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12
Q

What is Hirschsprung disease?

A

Problem with neural crest migration from caecum to rectum, or with death of ganglion cells; distal intestinal segment has aganglionosis.
Lacks peristalsis; functional obstruction occurs; congenital aganglionic megacolon.

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13
Q

Mechanism causing loss of neural crest migration in Hirschsprung disease.

A

Not fully understood. Most familial cases involve receptor tyrosine kinase RET. Penetrance is incomplete, and other genes are also thought to contribute.

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14
Q

Clinical features of Hirschsprung disease.

A

Failure to pass meconium.

Obstruction and constipation; occasional passage of stool may occur if only a few cm are involved.

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15
Q

Threats to life of Hirschsprung disease.

A

Enterocolites
Fluid and electrolyte imbalances
Perforation
Peritonitis.

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16
Q

Causes of acquired megacolon disease

A

Chagas’ disease, obstruction due to neoplasm or inflammatory stricture, UC causing toxic megacolon, visceral myopathy or functional psychosomatic disorders.

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17
Q

What are the three forms of oesophageal dysmotility?

A

Nutcracker oesophagus, diffuse oesophageal spasm, lower oesophageal sphincter dysfunction.

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18
Q

What is nutcracker oesophagus?

A

High amplitude contractions of the distal oesophagus due to loss of normal coordination between muscle layers.

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19
Q

Main effect of oesophageal dysmotility.

A

Formation of small diverticulae.

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20
Q

What types of oesophageal obstruction are there?

A

Functional and mechanical

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21
Q

Common causes of mechanical oesophageal dysfunction.

A

Strictures or cancer.

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22
Q

How does mechanical oesophageal obstruction classically present?

A

With progressive dysphagia, starting with solids and moving to liquids.

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23
Q

Common cause of benign oesophageal stenosis

A

GORD, irradiation or caustic injury.

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24
Q

What is the triad associated characterising achalasia?

A

Incomplete lower oesophageal sphincter (LES) relaxation,

increased LES tone and aperistalsis of the oesophagus.

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25
Q

Symptoms of achalasia.

A

Dysphagia, difficulty belching, chest pain.

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26
Q

Cause of primary achalasia.

A

Distal oesophageal inhibitory neuronal degeneration (increases tone).

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27
Q

Secondary causes of achalasia (1 true, 5 achalasia-like)

A

Chagas disease (trypanosoma cruzi infection).
Achalasia-like disease can occur in
DM autonomic neuropathy,
infiltrative diseases (malig., amyloidosis,etc),
lesions of dorsal nuclei (polio, surgery),
with Down syndrome,
in Allgrove syndrome.

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28
Q

Treatments for achalasia

A

Laparoscopic myotomy, pneumatic balloon dilatation, botox.

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29
Q

Types of oesophageal laceration.

A

Mallory-Weiss tears, Boerhaave syndrome

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30
Q

Which type of oesophageal tear is transmural, and involve rupture of the distal oesophagus?

A

Boerhaave syndrome.

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31
Q

Inflammation of the oesophagus can be caused by what?

A

Alcohol, corrosive acids or alkalis, very hot fluids, heavy smoking. Some pills.

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32
Q

Symptoms of oesophagitis.

A

Odynophagia, haemorrhage, stricture or perforation.

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33
Q

How do you confirm a diagnosis of Hirschsprungs disease?

A

Using intraoperative frozen section analysis of presence of ganglion cells at the anastomotic margin.

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34
Q

Iatrogenic causes of oesophagitis.

A

Cytotoxic chemotherapy, radiation therapy, graft vs host disease.

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35
Q

Causes of oesophageal infections.

A

Usually in immunosuppressed. HSV (most common), CMV or candidiasis.

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36
Q

Morphology of oesophagitis.

A

Dense neutrophilic infiltrate, or necrosis.

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37
Q

Morphology of eosophageal irradiation.

A

Intimal proliferation and luminal narrowing of blood vessels.

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38
Q

Advanced candidiasis morphology

A

Adherent grey-white pseudomembrane across oesophageal mucosa.

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39
Q

Morphology of HSV oesophagitis.

A

Punched out ulcers.

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40
Q

Morphology of graft-vs-host disease in oesophagus.

A

Basal epithelial cell apoptosis, mucosal atrophy and submucosal fibrosis without acut inflammatory infiltrates.

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41
Q

Most frequent cause of oesophagitis.

A

GORD

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42
Q

Cause of GORD.

A

Transient lower oesophageal spincter relaxation, mediated via vagal pathways.

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43
Q

Triggers of LES relaxation causing GORD.

A

Gastric distension, moild pharyngeal stimulation, abrupt increase in intra-abdominal pressure.

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44
Q

Conditions that contribute to GORD.

A

Alcohol and tobacco use, obesity, CNS depressants, pregnancy, and hiatus hernia.

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45
Q

Morphology of GORD

A

Simple hyperaemia. In more significant disease there may be eosinophilia and basal zone hyperplasia.

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46
Q

What is eosinophilic oesophagitis?

A

A condition like GORD in children, but with food impaction and dysphagia in adults, which can occur in atopic individuals.

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47
Q

What proportion of patients with cirrhosis get varices? And variceal bleeding?

A

Half have varices, and about a quarter get variceal bleeding.

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48
Q

What is Barrett’s oesphagus?

A

A complication of chronic GORD characterised by intestinal metaplasia within the eosophageal squamous mucosa.

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49
Q

How often is Barrett’s oesophagus thought to occur in patients with symptomatic GORD?

A

10%. Presents most commonly in white males between 40 and 60.

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50
Q

What is the greatest concern in Barrett’s oesophagus?

A

An increased risk of oesophageal carcinoma. It shares mutations with this, and is considered a precursor lesion to cancer. Most people with Barrett’s oesophagus do not develop oesophageal adenocarcinoma, however.

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51
Q

Morphology of Barrett oesophagus.

A

Tongues of velvety red metaplastic mucosa extend up from the gastroesophageal junction. Long segment is greater than 3 cm.

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52
Q

Morphology in diagnosis of Barrett oesophagus.

A

Can only be identified by endoscopy and biopsy. Endoscopic evidence of metaplastic columnar mucosa above gastro-oesophageal junction. Intestinal-type metaplasia is seen as replacem ent of the squamous eosophageal epithelium with goblet cells.

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53
Q

What are the 2 main types of eosophageal cancers?

A

Adenocarcinoma (esp in west) and squamous cell carcinoma (more common worldwide).

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54
Q

Risk factors for oesophageal adenocarcinoma.

A

Barrett oesophagus. Tobacco. Radiation.

Negative risk factors include diet high in veg and fruit, and some types of H. pylori (due to gastric atrophy).

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55
Q

Mutations in oesophageal adenocarcinoma.

A

Early stages: TP53, down regulation of CDKN2A (p16/INK4a).

Late stages: amplification of EGFR, ERBB2, MET, cyclins D and E.

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56
Q

Morphology of eosophageal adenocarcinoma.

A

Distal 1/3 of oesophagus. Initially flat, may form large masses of 5cm diameter, or ulcerate and invade deeply. Often produce mucin and form glands.

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57
Q

Key risk factors for eosophageal squamous cell carcinomas.

A

Alcohol and tobacco. Nutritional deficiencies. Mutagenic compounds in food.

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58
Q

Molecular pathogenesis of squamous cell oesophageal carcinoma.

A

Amplification of SOX2. Overexpression of cyclin D1. LOF of TP53, E-cadherin and NOTCH1.

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59
Q

Morphology of squamous cell carcinoma.

A

Half occur in middle 1/3 of the oesophagus, starting with squamous dysplasia. Can be ulcerative or diffusely infiltrative.

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60
Q

Which lymph nodes do squamous cell oesophageal carcinomas invade to?

A

In upper third, cervical lymph nodes. In middle third, mediastinal, paratracheal and tracheobronchial lymph nodes. In lower third, gastric and coeliac lymph nodes.

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61
Q

Parts of the stomach

A

Cardia, fundus, body and antrum

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62
Q

What is the difference between gastropathy and gastritis?

A

Both are mucosal inflammatory processes, but in gastritis neutrophils are present, and in gastropathy they are rare or absent entirely.

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63
Q

Key agents causing gastropathy

A

NSAIDs, alcohol, bile and stress induced injury.
Acute mucosal erosion or haemorrhage.
Hypertrophic gastropathies.

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64
Q

Normal damaging factors to the gastric mucosa.

A

Gastric acidity, peptic enzymes.

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65
Q

Damaging factors causing injury to gastric mucosa.

A

H. pylori infection, NSAIDs, Tobacco, alcohol, gastric hyperacidity, duodenal-gastric reflux.

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66
Q

Normal protective factors to the gastric mucosa.

A 
Surface mucus secretion, bicarbonate secretion into mucus,
mucosal blood flow
epithelial barrier function,
epithelial regenerative capacity, 
elaboration of the prostaglandins.
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67
Q

Things damaging normal protective factors to the gastric mucosa.

A

Ischaemia, shock, NSAIDs.

Some cancer chemotherapies.

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68
Q

How do NSAIDs damage the gastric mucosa?

A

By preventing prostaglandin synthesis, which stimulates nearly all the defence mechanisms. Although COX-1 plays larger role than COX-2, the latter does have some role.

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69
Q

What are the ulcers caused by stress related mucosal injury (physiological stress) called?

A

In proximal duodenum, associated with sever burns or trauma, they are called Curling ulcers.
Gastric, duodenal and oesophageal ulcers associated with patients with intracranial disease are called Cushing ulcers.

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70
Q

What is the risk with Cushing ulcers?

A

Perforation.

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71
Q

What is the pathogenesis of Cushing ulcers?

A

Systemic hypotension or stress induced splanchnic vasoconstriction cause local ischaemia.
Upregulation of inducible NO synthase and release of vasoconstrictor endothelin 1 also contribute to ischaemia.

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72
Q

What is the pathogenesis of Curling ulcers?

A

Direct stimulation of vagal nuclei, and possibly systemic acidosis.

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73
Q

What is a Dieulafoy lesion?

A

An extra large submucosal artery due to failure to branch properly, which with erosion of the epithelium, can bleed copiously.

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74
Q

What is gastric antral vascular ectasia?

A

Erythematous stripes caused by ectatic mucosal vessels. Usually idiopathic.

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75
Q

Endoscopic appearance of gastric antral vascular ectasia.

A

Longitudinal strips of edematous erythematous mucosa alternating with pale strips of less injured mucosa.

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76
Q

What is the most common cause of chronic gastritis?

A

H. pylori infection.

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77
Q

What is the most common cause of diffuse atrophic gastritis?

A

Autoimmune gastritis.

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78
Q

How does H. pylori infection usually present?

A

Antral gastritis with normal or increased acid production.

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79
Q

Which pattern of H. pylori infection is associated with increased risk of gastric adenocarcinoma?

A

Multifocal atrophic gastritis.

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80
Q

Which H. pylori gene is particularly associated with gastric cancer risk?

A

CagA.

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81
Q

Morphology of H. pylori gastritis.

A

Neutrophils in lamina propria, and some in gastric pits. Superficial lamina propria contains plasma cells. Lymphoid aggregates are common.

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82
Q

Site of autoimmune gastritis.

A

Usually spares the anturm; is associated with hypergastrinaemia.

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83
Q

5 characteristics of autoimmune gastritis.

A 
Abs to parietal cells and intrinsic.
Reduced serum pepsinogen I conc.
Endocrine cell hyperplasia.
Vit B12 deficiency. 
Defective gastric acid secretion.
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84
Q

What is the inflammatory infiltrate in autoimmune gastritis?

A

Lymphocytes and macrophages.

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85
Q

Principle agents of damage in autoimmune gastritis.

A

CD4+ T cells directed against parietal cell components including H+,K+ ATPase.
Autoantibodies to parietal cell components and intrinsic factor are present 80% of patients.

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86
Q

Morphology of autoimmune gastritis.

A

Diffuse mucoase damage of oxyntic mucosa within the body and fundus.

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87
Q

Associations of autoimmune gastritis with other diseases.

A

Pernicious anemia, Hashimoto thyroiditis, T1DM, Addison’s and other autoimmune diseases.

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88
Q

Uncommon forms of gastritis

A

Eosinophilic gastritis, usually caused by an allergic reaction.
Lymphocytic gastritis usually affects women, and is associated with celiac disease.
Granulomatous gastritis, caused by Crohn disease, sarcoidosis and infections.

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89
Q

Complications of chronic gastritis.

A

PUD
Mucosal atrophy and intestinal metaplasia.
Dysplasia
Gastritis cystica.

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90
Q

Peptic ulcer disease associations

A

H pylori infections, NSAID use, cigarette smoking.

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91
Q

Site of gastritis caused by H pylori

A

Antrum.

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92
Q

What is a gastric lesion with a sharply punched out lesion likely to be?

A

A peptic ulcer

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93
Q

What is a gastric lesion with a heaped up margin likely to be?

A

A cancer.

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94
Q

Presenting features of peptic ulcers.

A

Epigastric burning or aching pain.

Iron deficiency anaemia, haemorrhage or perforation.

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95
Q

What is hypertrophic gastropathy?

A

A group of uncommon diseases characterised by giant cerebriform enlargement of the rugal folds due to epithelial hyperplasia without inflammation.

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96
Q

Name the rare hypertrophic gastropathies.

A 
Menetrier disease (associated with TGF-a hypersecretion)
Zollinger-Ellison syndrome (caused by gastrin secreting tumours in small intestine or pancreas)
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97
Q

Inflammatory and hyperplastic polyps. Cause and treatment

A

Caused by chronic inflammation; may regress with H pylori eradication. If larger than 1.5 cm, resect.

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98
Q

Fundic gland polyps: population affected

A

Familial adenomatous polyposis sufferers, especially those on PPIs. Does not involve inflammation.

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99
Q

Gastric adenomas: people affected.

A

Almost always on background of chronic gastritis with atrophy and intestinal metaplasia. Increased incidence in people with FAP.

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100
Q

Gastric adenocarcinoma: types

A

Intestinal type (bulky masses) and diffuse type (diffusely thickens wall, composed of signet ring cells)

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101
Q

Gastric adenocarcinoma: epidemiology.

A

Common in Japan, Chile, Costa Rica and Eastern Europe. Associated with poverty. Environmental factors are important. Generally falling in the West, except for those associated with GORD - cancers of the gastric cardia.

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102
Q

Key genetic changes in pathogenesis of gastric adenocarcinoma diffuse type.

A

Loss of E-cadherin.

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103
Q

Key genetic changes in pathogenesis of gastric adenocarcinoma intestinal type.

A

Increased signalling in Wnt pathway including loss of APC adn gain in B-catenins. FAP patients at risk.

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104
Q

Morphology of intestinal type gastric adenocarcinomas.

A

Exophytic mass or ulcerated tumour. Neoplastic cells contain apical mucin vacuoles

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105
Q

Morphology of diffuse type of gastric adenocarcinomas.

A

Composed of discohesive cells with large mucin vacuoles causing signet cell morphology.
Desmoplastic reaction may stiffen gastric wall. If there is a large area of infiltration, may cause linitis plastica.

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106
Q

Pathogenesis of MALT lymphoma

A

Chronic gastritis induces MALT lymphoma; H. pylori eradication usually is followed by durable remission.

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107
Q

Morphology of MALT lymphoma

A

Neoplastic lymphocytes infiltrate gastric glands to create diagnostic lymphoepithelial lesions. Express B cell markers CD19 and CD20.

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108
Q

Well differentiated neuroendocrine tumours - common sites

A

Most common is the intestine, followed by tracheobronchial tree and lungs.

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109
Q

Diseases associated with gastric well differentiated neuroendocrine tumours.

A

Endocrine cell hyperplasia, autoimmune chronic atrophic gastritis, MEN-1 and Zollinger-Ellison syndrome.

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110
Q

Gross morphology of well differentiated neuroendocrine tumours (carcinoid tumours)

A

Intramural or submucosal masses that ccreate small polypoid lesion. May involve mesentary. Yellow or tan in colour and are very firm.

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111
Q

Histological morphology of well differentiated neuroendocrine tumours (carcinoid tumours)

A

Composed of islands, trabeculae, strands, gland or sheets of uniform cells.
Positive for synaptophysin and chromogranin A (endogrine granule markers).

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112
Q

Characteristics of carcinoid syndrome associated with ileal carcinoid tumours.

A

Cutaneous flushing, sweating, bronchospasm, colicky abdo pain, diarrhoea, right sided cardiac valvular fibrosis.

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113
Q

Prognosis for foregut carcinoid tumours

A

Usually cured by resection, esp if associated with atrophic gastritis.

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114
Q

Prognosis for midgut carcinoid tumours.

A

Usually multiple and aggressive. Poor prognostic factors include deep local invasion, large size, necrosis and mitoses.

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115
Q

Prognosis for hindgut carcinoid tumours.

A

Almost always benign.

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116
Q

How common are GI stromal tumours?

A

Very rare, but the most common mesenchymal tumour of the abdomen.

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117
Q

Key mutations in GI stromal tumours?

A

Tyrosine kinase KIT gain of function.
Or
PDGF receptor alpha gain of function.
Mutations of the mitochondiral succinate dehydrogenase complex.

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118
Q

Causes of mechanical obstruction of the small intestine.

A

Hernias, intestinal adhesions, intussusception, volvulus, tumours, infarction, Crohn disease.

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119
Q

Most common type of hernia to cause intestinal obstruction.

A

Inguinal hernias.

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120
Q

Pathogenesis of entrapment of intestine in hernia.

A

Pressure at neck causes impaired venous drainage of entrapped viscus. Stasis and edema in crease bulk of herniated loop, inding to incarceration, strangulation and infarction.

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121
Q

Causes of bowel adhesions

A

Surgery, infection, endometriosis (e.g. causes of peritoneal inflammation).
Rarely, congenital.

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122
Q

Complications of adhesions

A

Internal herniations through the closed loops formed by adhesions, with sequelae including obstruction and strangulation.

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123
Q

Order of frequency of bowel likely to form volvulus.

A

Sigmoid colon, caecum, small bowel, stomach, or rarely, transverse colon.

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124
Q

What can you do for an idiopathic intussusception in infants and children?

A

A contrast enema, which is both diagnostic and therapeutic. Not if there is a mass!

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125
Q

What causes a transmural infarction of the intestine?

A

Acute arterial obstruction - severe atherosclerosis, aortic aneurysm, hypercoag states and etc.
Systemic vasculitides

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126
Q

Systemic vasculitides causing intestinal damage.

A

Polyarteritis nodosa
Henoch-Schonlein purpura
Granulomatosis with polyangiitis.

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127
Q

What are the stages of ischaemic injury to the intestine?

A

Hypoxic injury - limited damage.

Reperfusion injury - severe damage. Mechanisms unknown, but include leakage of gut bacterial products.

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128
Q

Watershed zones in blood supply to the intestines.

A 
Splenic flexure (superior and inferior mesenteric)
Rectum (inferior mesenteric, pudendal and iliac)
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129
Q

Gross appearance of mucosal or mural infarction of the bowel.

A

Patchy infarction, haemorrhagic and possibly ulcerated.

Bowel wall thickened by edema.

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130
Q

Gross appearance of transmural infarction of the bowel

A

Sharply defined: infarcted bowel is congested and dusky. Later, blood tinged mucus or frank blood in lumen.
Wall becomes edematous.
Coagulative necrosis of muscularis propria in 1-4 days.
Perforation may occure.

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131
Q

Microscopic appearance of ischaemic intestine.

A

Atrophy of surface epithelium.
Hyperproliferative crypts.
Neutrophils present hours after reperfusion.
Chronic may lead to fibrous scarring of lamina propria.
Bacterial superinfection may lead to pseudomembrane formation.

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132
Q

Ischaemic disease of the colon. Associations and precipitating factors.

A

Associations: cardiovascular disease.

Precipitating factors: therapeutic vasoconstrictors, cocaine, endothelial damage, CMV, E coli.

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133
Q

Presentation of acute colonic ischaemia

A

Sudden onset cramping, left lower abdo pain, desire to defecate, passage of blood.

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134
Q

In colonic ischaemia, when should you consider surgical intervention?

A

Peristaltic sounds diminish, guarding or rebound tenderness develop.

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135
Q

What might right sided colonic ischaemia herald?

A

More severe disease of the superior mesenteric artery; the small intestine may be involved.

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136
Q

What can chronic ischaemia of the bowel masquerade as?

A

Inflammatory bowel disease.

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137
Q

How can you differentiate ischaemia of the bowel from radiation enterocolitis?

A

History of radiation. Presence of ‘radiation fibroblasts’.

138
Q

Pathogenesis of angiodysplasia

A

Mechanical and congenital.
Intermittent occlusion of submucosal veins by normal distension and contraction leads to dilatation and tortuosity of overlying submucosal and mucosal vessels.

139
Q

Why might the caecum be particularly prone to angiodysplasia?

A

Its large diameter leads to greatest wall tension.

140
Q

Why might angiodysplasia have a developmental aspect?

A

It is associated with Meckel’s diverticulum.

141
Q

Which four phases of nutrient absorption can result in malabsorption if disrupted?

A

Intraluminal digestion, terminal digestion on the mucosa, transepithelial transport and lymphatic transport.

142
Q

General symptoms of malabsorption

A

Diarrhoea, flatus, abdominal pain and weight loss.

143
Q

What is dysentery?

A

Painful, bloody, small volume diarrhoea.

144
Q

What is secretory diarrhoea like?

A

Isotonic stool which persists during fasting.

145
Q

What is osmotic diarrhoea like?

A

More concentrated than plasma and abates with fasting.

146
Q

What kind of diarrhoea is caused by lactase deficiency?

A

Osmotic diarrhoea?

147
Q

What are key features of exudative diarrhoea?

A

Purulent bloody stools which continue during fasting.

148
Q

What are the GI complications of cystic fibrosis?

A

Pancreatic intraductal concretions, can begin in utero. Leads to exocrine pancreatic insufficiency.
Occasional intestinal obstruction.

149
Q

What is coeliac disease?

A

An immune mediated enteropathy triggered by ingestion of gluten-containing foods in genetically predisposed individuals.

150
Q

What part of gluten contains diseases producing components?

A

Gliadin, the alcohol soluble fraction.

151
Q

How is gliadin involved in the pathogenesis of coeliac disease?

A

It is resistant to degradation by proteases. Some by induce IL-15, triggering activation of CD8+ lymphocytes have NK cell markers that are receptors for MIC-A, an enterocyte marker for stress.
Gliadin molecules deaminated by tissue transglutaminase interact with APCs to stimulate CD4+ cells.

152
Q

To what degree does the HLA locus determine coeliac disease?

A

It appears to contribute half the genetic component.

153
Q

Where should you biopsy for suspected coeliac disease?

A

The second part of the duodenum or the proximal jejunum.

154
Q

What is the histopathology for a coeliac biopsy?

A

Increased intraepithelial CD8 T cells, crypt hyperplasia and villous atrophy.

155
Q

What causes malabsorption in coeliac disease?

A

The loss of mucosal and brush border epithelium.

Increased epithelial turnover may limit differentiation of absorptive enterocytes.

156
Q

How might a coeliac sufferer without GI symptoms present?

A

Anaemia due to chronic iron and vit malabsorption.

157
Q

Symptoms of paediatric coeliac disease.

A

6-24 months.

Irritability, abdo distention, anorexia, chronic diarrhoea, failure to thrive, weight loss and muscle wasting.

158
Q

What dermatological condition is associated with coeliac’s disease.

A

Dermatitis herpetiformis.

159
Q

Sensitive serological tests for coeliac disease.

A

IgA against tissue transglutaminase.

Anti-endomysial antibodies can also be present. Absence of HLA-DQ2 and DQ8 are useful for negative predictive value.

160
Q

What malignancies are associated with coeliac disease?

A

Enteropathy associated T cell lymphoma.

Small intestinal adenocarcinoma.

161
Q

What are other names for environmental enteropathy?

A

Tropical sprue or tropical enteropathy.

162
Q

What is autoimmune enteropathy?

A

An X-linked disorder characterised by severe persistent diarrhoea and autoimmune disease, most often occuring in young children.

163
Q

What does IPEX stand for?

A

Immune dysregulation, polyendocrinopathy, enteropathy and X-linkage: it is a familial enteropathy caused by a germline mutation in FOXP3

164
Q

What aspects of the immune system are commonly affected in autoimmune enteropathies?

A

Treg cells.
Abs to enterocytes and goblet cells.
Sometimes increase in intraepithelial lymphocytes.

165
Q

What are the 2 types of lactase deficiency?

A

Congenital and acquired.

166
Q

Genetic inheritance of congenital lactase deficiency.

A

Autosomal recessive disorder.

167
Q

Symptoms of congenital lactase deficiency

A

Explosive diarrhoea with watery, frothy stools and abdo distension on milk ingestion.

168
Q

What causes acquired lactase deficiency?

A

Downregulation of lactase gene expression following a bacterial or viral infection.

169
Q

Symptoms of acquired lactase deficiency

A

Abdo fullness, diarrhoea and flatulence.

170
Q

What is abetalipoproteinaemia?

A

A rare autosomal recessive disease characterised by an inability to secrete triglyceride-rich lipoproteins.

171
Q

What causes abetalipoproteinaemia?

A

A mutation in MTP.

172
Q

What is the clinical picture of abetalipoproteinaemia?

A

Presents in infancy with failure to thrive, diarrhoea and steatorrhoea.
Complete absence of all plasma lipoproteins containing apolipoprotein B (not mutated).
Acanthocytic red cells.

173
Q

Vibrio cholerae bacteria

A

Comma shaped gram -ive.

174
Q

How does cholera toxin have its effect?

A

B subunit binds GM1 ganglioside. Retrograde transport. Delivery of A subunit by host machinery to cytosol, where it refolds. Interacts with ADP ribosylation factors to activate GsAlpha, stimulating adenylate cyclase. Increase in cAMP opens CFTR, releasing Cl- into lumen.

175
Q

Clinical features of severe cholera.

A

Abrupt onset of wather diarrhoea and vomiting following incubation period of 1-5 days.

176
Q

What is the most common bacterial enteric pathogen in developed countries?

A

Campylobacter jejuni.

177
Q

Virulence factors for Campylobacter.

A

Motility, adherence, toxin production (epithelial damage and cholera toxin like) and invasion (minority; associated with dysentery).

178
Q

Extraintestinal complications of Campylobacter infection

A

Reactive arthritis in patients with HLA B27.

Erythema nodosum and Guillain Barre syndrome (molecular mimicry, rare).

179
Q

Morphology of Campylobacter infection.

A

Comma shaped, flagellated gram negative bacteria.
Mucosal and intraepithelial neutrophil infiltrates.
Crypt architecture preserved.

180
Q

Shigella organism.

A

Gram -ive unencapsulated non-motile facultative anaerobes of the enterobacteriaceae family.

181
Q

What kind of disease does Shigella infection cause?

A

Bloody diarrhoea, esp in children.

182
Q

Pathogenesis of Shigella infection.

A

Resistant to acid. Taken up by M cells. Phagocytosed by macrophages, induce apoptosis, causes inflammation and damages surface epithelium. Allows access to basolateral membranes of colonic epithelial cells. Type III secretion system allows injection of proteins into cytosol.

183
Q

Morphology of Shigella infection

A

Haemorrhagic and ulcerated mucosa esp in left colon.

184
Q

Clinical course of Shigella infection.

A

1 week incubation period followed by 1 week diarrhoea, fever and abdo pain. Dysentery occurs in 50% of pts.
Subacute form can mimic UC.

185
Q

Complications of Shigella infection.

A

Rare: include reactive arthritis, urethritis and conjunctivitis. Hemolyic-uremic syndrome can also follow if Shiga toxin is produced.

186
Q

What can Salmonella infection cause?

A

Typhoid fever (Salmonella typhi), or salmonellosis (S. enteritidis).

187
Q

Pathogenesis of salmonellosis.

A

Proteins transferred by type III secretion systems. Activate host RhoGTPases, bacteria grow in endosomes.
Flagellin stimulates inflammatory response via TLR5.

188
Q

Who is likely to be susceptible to salmonella infection?

A

Those with atrophic gastritis, acid suppressive therapy or genetic defects in Th17.

189
Q

Symptoms of Salmonella infection.

A

Diarrhoea; ranges from profuse and watery to dysentery. Fever for a couple of days. Antibiotics not recommended.

190
Q

What can S. typhi do that S. enteritidis cannot?

A

Disseminate viat hte lymphatic and blood vessels.

191
Q

Key morphological features of typhoid fever.

A

Peyer’s patches in terminal ileum enlarge to plateau-like elevations up to 8 cm.
Typhoid nodules form in liver, bone and lymph.

192
Q

Clinical features of typhoid fever.

A

Anorexia, abdo pain, bloating, nausea, vomitin and bloody diarrhoea.
SHORT BREAK
Bacteraemia and fever with flu-like symptoms. Rose spots.

193
Q

Blood cultures in typhoid fever.

A

Positive in 90% of patients during febrile phase.

194
Q

Who gets Salmonella osteomyelitis?

A

Pts with sickle cell disease.

195
Q

Which Yersinia cause GI disease?

A

Enterocolitica and pseudotuberculosis.

196
Q

Pathogenesis of Yersinia GI disease.

A

Invade M cells, use adhesins to bind B1 integrins. Iron enhances virulence and systemic dissemination.

197
Q

Where do GI Yersinia infections localise to?

A

ileum, appendix and right colon.

198
Q

Effect of Yersinia on regional lymph nodes and Peyer patches.

A

Hyperplasia.

199
Q

Effect of Yersinia on mucosa overlying lymphoid tissue.

A

Haemorrhage and ulcers. Neutrophil infiltrates.

200
Q

Clinical features of Yersinia GI infection.

A

Mostly abdo pain, also fever and diarrhoea. Can mimic acute appendicitis.

201
Q

Extraenteric features of Yersinia infection.

A

Common: pharyngitis, arthralgia and erythema nodosum.

202
Q

What does ETEC cause?

A

Traveller’s diarrhoea

203
Q

What toxins does ETEC use and what are they like?

A

Labile toxin, like cholera toxin and Stable toxin which activates adenylate cyclase increasing cAMP

204
Q

Where is EPEC a problem?

A

It is endemic in developing countries.

205
Q

What characterises EPEC?

A

The ability to cause attaching and effacing lesions encoded by LEE. Proteins include Tir and a type III secretion system.

206
Q

What does EPEC stand for?

A

Enteropathogenic E. coli.

207
Q

What does EHEC stand for?

A

Enterohaemorrhagic E coli.

208
Q

What is a common cause of EHEC outbreaks?

A

Inadequately cooked beef or contaminated milk: cows are a reservoir.

209
Q

What infection is EHEC infection like?

A

Shigella dysenteriae - it encodes Shiga-like toxins, and also produces bloody diarrhoea and haemolytic uraemic syndrome, though more commonly in the O157:H7 strain.

210
Q

What does EIEC stand for and cause?

A

Enteroinvasive E. coli, causing acute self limited colitis.

211
Q

What does EAEC stand for?

A

Enteroaggregative E. coli.

212
Q

What does EAEC cause?

A

Non-bloody diarrhoea in children and adults.

213
Q

What are other names for pseudomembranous colitis?

A

Antibiotic associated colitis/diarrhoea.

214
Q

What causes pseudomembranous colitis?

A

C. difficile after disruption of normal microbiota allows overgrowth.

215
Q

How does C. difficile cause a pseudomembrane in antibiotic associated diarrhoea?

A

Incompletely understood, probably involving the effects of its toxins with ribosylated small GTPases.

216
Q

What is the histopathology of pseudomembranous colitis?

A

Surface epithelium denuded, superficial lamina propria has a dense infiltrated of neutrophils.
Crypts distended by mucopurulent exudate.

217
Q

Presentation of pseudomembranous colitis.

A

In an old person in hospital treated with antibiotics. Causes fever, leukocytosis, abdo pain, cramps, watery pain, diarrhoea and dehydration.

218
Q

Treatment for pseudomembranous colitis.

A

Usually metronidazole or vancomycine are effective, but there can be resistance.

219
Q

Features of Whipple’s disease

A

Malabsorption, lymphadenopathy and arthritis.

220
Q

Microbe causing Whipple’s disease.

A

A gram positive actinomycete called tropheryma whippelii.

221
Q

How does Tropheryma whippelii cause diarrhoea?

A

It obstructs lymphatic transport.

222
Q

What is the morphological hallmark of Whipple disease?

A

Dense accumulation of distended foamy macrophages in the small intestinal lamina propria.
Villous expansion caused by dense macrophage infiltrate.
Bacteria accumulate in mesenteric lymph nodes, synovial membranes of affected joints, cardiac valves and the brain.

223
Q

Presentation of Whipple disease.

A

Diarrhoea, weight loss and arthralgia in people with occupational exposure to soil or animals.

224
Q

How common is norovirus infection?

A

It causes half of all gastroenteritis outbreaks worldwide.

225
Q

Symptoms of norovirus infection.

A

Nausea, vomiting, watery diarrhoea and abdo pain.

226
Q

When is norovirus chronic?

A

In the immunosuppressed.

227
Q

What does rotavirus cause?

A

Severe childhood diarrhoea; a common cause of diarrhoeal mortality worldwide.

228
Q

What ages are particularly susceptible to rotavirus?

A

6-24 months, except in Asia and Africa, where under 6 month infection is common.

229
Q

What causes enterocyte damage in diarrhoea?

A

NSP4 which induces epithelial cell death.

230
Q

What population does adenovirus cause diarrhoea in?

A

Children and the immunosuppressed.

231
Q

Names of intestinal parasites.

A 
Ascaris 
Strongyloides 
Necator
Enterobius vermicularis
Trichuris trichiura
Intestinal cestodes
232
Q

Ascaris

A

Nematode. Ingested eggs hatch in intestine, migrate via lungs.

233
Q

Strongyloides

A

Larvae live in soil, penetrate skin, migrate through lungs. Does not need stage outside body; can autoinfect.

234
Q

Necator (hookworm)

A

Larval penetration of skin. suck blood.

235
Q

Enterobius vermicularis

A

Pinworm. Intraluminal. Eggs cause irritation to perianal area.

236
Q

Trichuris trichiura

A

Whipworms. Do not penetrate mucosa, but heavy infection can cause bloody diarrhoea and rectal prolapse.

237
Q

Intestinal cestodes

A

Tapeworms. Can grow very large.

238
Q

Giardia lambia

A

Flagellated protozoa present in contaminated water (resistant to chlorine).

239
Q

Effects of Giardia infection (microscopic)

A

Decreased expression of brush border enzymes including lactase.

240
Q

Clinical effects of Giardia infection.

A

Acute or chronic diarrhoea, malabsorption and weight loss.

241
Q

Disease caused by cryptosporidium.

A

Chronic diarrhoea in AIDS patients, and acute self limited disease in immunologically normal cases.

242
Q

What kills cryptosporidium oocysts?

A

Not chlorine.

Freezing (not present in Antarctica).

243
Q

Where is the cryptosporidium parasite in the intestine?

A

In the endocytic vacuole in enterocytes in the microvilli.

244
Q

Characteristics of IBS

A

Chronic relapsing abdo pain, bloating and changes to bowel habits.

245
Q

Morphology of IBS

A

Gross and microscopic evaluation is normal.

246
Q

Pathogenesis of IBS

A

Poorly defined interplay between psychological stressors, diet, microbiome disruption, abnormal motility and increased enteric responses to GI stimuli.
Possible defective brain-gut axis signalling.

247
Q

Genes that may be linked to IBS

A

Serotonin reuptake transporters
Cannaboid receptors
TNF related inflammatory mediators.

248
Q

Treatment of diarrhoea-predominant IBS

A

Opioid and psychoactive anti-cholinergic effects.

249
Q

Criteria for diagnosis of IBS

A

Abdo pain or discomfort for at least 3 days/month for 3 months, improvement after defecation.
Change in stool frequency.

250
Q

What is IBD?

A

A chronic condition resulting from inappropriate mucosal immune activation. Comprised of UC and Crohn disease.

251
Q

Where is UC?

A

Limited to the colon and rectum and extends only into mucosa and submucosa.

252
Q

Where is Crohn disease?

A

Typically transmural, anywhere in GI tract.

253
Q

Epidemiology of IBD

A

Usually presents in young adults. Common in caucasians, but on the rise worldwide.

254
Q

Pathogenesis of IBD

A

Alterations in host interactions with microbiota, altered composition of microbiome, epithelial dysfunction and aberrant mucosal responses.

255
Q

Genetic contribution to IBD

A

More dominant in Crohn disease. Several involve genes which are involved in the response to mycobacteria. Each gene only has a small effect, but key genes includ NOD2, ATG16L1 and IRGM.

256
Q

Arms of the mucosal immune response involved in IBD

A

T helper cells in Crohn
Th17 cells - certian polymophisms in IL23 which is involved in their development are protective.
Proinflammatory cytokines.

257
Q

Epithelial defects described in Crohn and UC.

A

Defects in intestinal tight junction barriers in Crohn. Associated with NOD2 polymorphisms.
Some matrix metalloproteinase polymorphisms are associated with UC, not Crohn.

258
Q

Involvement of the microbiota in IBD

A

Abs against flagellin common in Crohn disease, not UC.

Microbial transfer studies induce and reduce IBD in animals, and fecal transplanst may benefit IBD patients.

259
Q

Good model for IBD pathogenesis.

A

Transepithelial flux of luminal bacterial components activate immune responses. Subsequent release of cytokines leads to increase in tight junction permeability so cycle escalates.

260
Q

Gross morphology of Crohn disease - key features.

A

Skip lesions. The earlies is the aphthous ulcer, which can progress and spread leading to a cobblestone appearance. Development of fissures through a thickened rubbery intestinal wall. Mesenteric fat extends around the serosal surface.

261
Q

Microscopic morphology of Crohn disease.

A

Abundant neutrophilia. Crypts filled with neutrophils, distortion of mucosal architecture (crypts not parallel).
Epithelial metaplasia may occure, and paneth cell metaplasia can occur in left colon.
Noncaseating granulomas are a hallmark and cutaneous granulomas form called ‘metastatic’ Crohn disease.

262
Q

Clinical features of Crohn disease

A

Intermittent attacks of mild diarrhoea, fever and abdo pain. 20% may present acutely with RLQ, fever and bloody diarrhoea.

263
Q

Gi complications of Crohn disease

A

Iron def anaemia (colonic)
Serum protein loss and hypoalbuminaemia or malabsorption of vit B12 (small intestine)
Fibrosing strictures may need resection.
Fistulae and perforations common.

264
Q

Extraintestinal manifestations of Crohn disease.

A

Uveitis, polyarthritis, sacroiliitis, ankylosing spondylitis, erythema nodosum and clubbing.
Colonic adenocarcinoma.

265
Q

Extraintestinal manifestations of UC

A

Polyarthritis, sacroiliitis, ankylosing spondylitis, uveitis, skin lesions. Primary sclerosis cholangitis.

266
Q

Gross morphology of UC

A

Always involves rectum, extending proximally.
Extensive broad based ulcers, with abrupt transition between diseased and uninvolved colon. Regenerating mucoas may form pseudopolyps, which fuse to form mucosal bridges.
Mucosal atrophy may occur in chronic disease.
NO mural thickening, strictures or changes to serosal surface.

267
Q

Histological morphology of UC

A

Inflammatory infiltrates, crypt distortion and abscesses. Inflammation diffuse and limited to mucosa and superficial submucosa. NO granulomas.

268
Q

Clinical features of UC

A

Attacks of bloody diarrhoea with mucus, lower abdo pain, and cramps relieved by defecation

269
Q

Risk factors for dysplasia following colitis.

A

Duration of disease
Extent of disease
Nature of inflammatory response.
Cancers include carcinomas and adenomas.

270
Q

What is the precursor to colitis-associated carcinoma?

A

Dysplastic epithelium.

271
Q

What is high-grade IBD associated dysplasia associated with?

A

Invasive carcinoma at the same site or elsewhere in colon. Prompts colectomy.

272
Q

Non-IBD causes of chronic colitis

A 
Diversion colitis post surgery.
Microscopic colitis (collagenous and lymphocytic)
273
Q

Key features of diversion colitis

A

Mucosal erythema and friability.

Numerous mucosal lymphoid follicles.

274
Q

Key feature of collagenous colitis

A

Dense subepithelial collagen layer, increased subepithelial lymphocytes

275
Q

Key feature of lymphocytic colitis.

A

Normal subepithelial collagen layer, increase in intraepithelial lymphocytes, especially T lymphocytes. Strong association with coeliac and autoimmune diseases.

276
Q

What is sigmoid diverticular disease?

A

Acquired pseudodiverticular outpouching of the colonic mucosa and submucosa.

277
Q

Epidemiology of sigmoid diverticular disease.

A

Rare in young, very common in over 60s.

278
Q

Pathogenesis of colonic diverticula

A

Focal discontinuities of the muscle wall are formed where nerves and vasa recta penetrate the inner muscle coat. This is not reinforced by longitudinal muscle as that is gathered into the taeniae coli.
Exaggerated peristaltic contractions (prob due to low fibre) leads to high intraluminal pressure.

279
Q

Morphology of colonic diverticula

A

Outpouchings 0.5-1.0 cm in diameter. Thin walled, with flattened or atrophic mucosa, compressed submucosa and absent muscularis propria.

280
Q

Proportion of people with diverticular disease who get symptoms

A

20%

281
Q

Symptoms of diverticular disease.

A

Intermittent cramping, lower abdo discomfort, constipation, distention or sensation of never being able to empty rectum.

282
Q

Ways to define polyps

A

Sessile or pedunculated.

Non-neoplastic (inflammatory, hamartomatous or hyperplastic) or neoplastic.

283
Q

Key point abut colonic hyperplastic polyps

A

Need to be differentiated from sessile serrated adenomas (malignant potential)

284
Q

Pathogenesis of hyperplastic polyps

A

Decreased epithelial cell turnover and delayed shedding leads to piling up of goblet cells and absorptive cells.

285
Q

Morphology of hyperplastic polyps

A

Smooth nodular protrusions of mucosa, composed of goblet and absorptive cells. Commonly found in left colon.

286
Q

Solitary rectal ulcer syndrome triad

A

Rectal bleeding, mucus discharge and inflammatory lesion of anterior rectal wall.

287
Q

Cause of solitary rectal ulcer syndrome.

A

Impaired relaxation of anorectal sphincter creates sharp angle of anterior rectal shelf which is recurrently abraded. This causes a polyp to form, which can become entrapped.

288
Q

Causes of hamartomous polyps.

A

Sporadic, or due to various genetically determined or acquired syndromes. Can be considered as premalignant in many cases.

289
Q

How do juvenile polyps present?

A

Usually with rectal bleeding.

290
Q

What is Peutz-Jeghers Syndrome?

A

A rare autosomal dominant syndrome presenting at a median age of 11 with multiple GI hamartomatous pollyps and mucocutaneous hyperpigmentation.

291
Q

Importance of Peutz-Jeghers syndrome.

A

Associated with marked increased risk of several malignancies, requiring surveillance from birth.

292
Q

Pathogenesis of Peutz-Jeghers syndrome

A

Germline heterozygous loss of function of the tumour suppressor gene STK11.

293
Q

Adenomas in GI tract - appearance

A

Intraepithelial neoplasms that range from small often pedunculated polyps to large sessile lesions.

294
Q

What is a colonic adenoma a precursor to?

A

Colonic adenocarcinoma.

295
Q

What characterises colorectal adenomas?

A

Epithelial dysplasia; they are precursor lesions, but not all progress.

296
Q

Histological hallmarks of epithelial dysplasia

A

Nuclear hyperchromasia

elongation and stratification. Can be seen on adenomas.

297
Q

Classifications of adenomas

A

Tubular, tubulovillous or villous.

298
Q

Sessile serrated adenomas histology

A

Overlaps with hyperplastic polyps, but more common in right colon.
Malignant potential, but frequently lack cytological features of dysplasia.

299
Q

Definition of intramucosal carcinoma

A

When dysplastic epithelial cells invade lamina propria or muscularis mucosa.

300
Q

Prognosis for intramucosal carcinoma.

A

Little risk of metastasis: polypectomy is usually curative.

301
Q

What is the most important factor that suggests an adenoma may harbor an invasive cancer?

A

Size.

Also high grade dysplasia.

302
Q

How many untreated FAP patients get colorectal adeoncarcionoma?

A

100%

303
Q

What is the standard prophylactic therapy for FAP patients?

A

Prophylactic colectomy. However, risk from neoplasm at other sites remains.

304
Q

Extraintestinal manifestations of FAP

A

Congenital hypertrophy of the the retinal pigment epithelium.

305
Q

What is the mutation, other than APC loss, that can give polyposis.

A

Bi-allelic mutation of the base-excision repair gene MYH. It is autosomal recessive, unlike APC loss.

306
Q

What is the phenotype of MYH associated polyposis?

A

Similar to attenuated FAP, with fewer polyps (fewer than 100), and delayed onset of colon cancer.

307
Q

What is Lynch syndrome?

A

Hereditary nonpolyposis colorectal cancer.

308
Q

How common is HNPCC

A

The most common syndromic form of colon cancer; it accounts for 2-4% of all colorectal cancers.

309
Q

Phenotype of HNPCC

A

Colon cancers occur in younger patients than sporadic cancers, and are often in the right colon.

310
Q

What are the genes involved in HNPCC

A

Genes for proteins responsible for detection, excision and repair of errors in DNA replication.

311
Q

Epidemiology of adenocarcinoma of the colon.

A

1.2 million and 600, 000 associated deaths worldwide; 10% of cancer deaths. More common in Western lifestyles and Japan.

312
Q

Risk factors for adenocarcinoma of the colon.

A

Dietary factors: low intake of vegetable fibre, high in refined carbs and fat.

313
Q

How low fibre diet causes adenocarcinoma of the colon.

A

Theory:
Decreased stool bulk + changed microbiota results in potentially toxic oxidative by-products of bacterial metabolism.
High fat increases hepatic synthesis of cholesterol and bile salts, which are converted to carcinogens by bacteria.

314
Q

Pharmacological chemoprevention of colonic adenocarcinoma.

A

NSAIDS and aspirin may have a protective effect. Also cause polyp regression in FAP patients. Probably mediated by COX2 inhibition which is highly expressed in colorectal carcinomas and promotes epithelial proliferation.

315
Q

Two genetic pathways involved in colorectal carcinogenesis.

A

APC and B-catenin pathway.

Microsatelite instability pathway.

316
Q

Earliest mutationin sporadic colon tumours.

A

80% have mutation of APC gene early.

317
Q

Earliest mutationin sporadic colon tumours.

A

Typically have mutation of APC gene early. Both copies have to be functionally inactive. If not, usually have B-catenin mutation allowing avoidance of APC function.

318
Q

APC function

A

Binds to and increases degradation of B-catenin.

319
Q

B-catenin function

A

Accumulates - translocates to nucleus - binds transcripion factor TCF - activates transcription of MYC and cylin D1 - proliferation.

320
Q

Late genetic events in colonic carcinoma development.

A

KRAS - promotes growth, prevents apoptosis. Mostly present in large adenomas and carcinomas.
Loss of SMAD2 and 4 which effect TGF-B signalling for inhibition of cell cycle.
TP53 - common in cancers, rare in adenomas.

321
Q

Which genes are commonly affected in people with DNA mismatch repair deficiency?

A

Mutations occur in microsatellite repeats leading to microsatellite repair instability. Affects TGF-B receptor (inhibition cell cycle) and BAX (apoptosis)

322
Q

Colon cancers that don’t show either APC or DNA mismatch repair mutation genotypes

A

Often have CG island hypermethylation. MLH1 promoter region often hypermethylated if this is with microsatellite instability, and KRAS mutations if no MSI.

323
Q

Gross morphology of tumours in proximal colon.

A

Tend to be polypoid exophytic masses.

324
Q

Gross morphology of carcinomas of the distal colon

A

Annular lesions.

325
Q

Microscopic morphology of carcinomas

A

Tend to be composed of tall columnar cells resembling dysplastic epithelium. Strong stromal response due to invasiveness. Some have glands.

326
Q

Presentation of right sided colon cancers

A

Fatigue and weakness due to iron deficiency anaemia.

327
Q

Presentation of left sided colon cancers

A

Change in bowel habit, cramping, left lower quadrant pain and occult bleeding.

328
Q

How is the anal canal divided?

A

Into thirds - the upper zone is columnar rectal epithelium, the middle third is transitional epithelium and the lower third is stratified columnar epithelium.

329
Q

What are tumours like in the rectal canal?

A

Upper third; glandular
Lower third; squamous.
Also; basaloid if tumour populated by immature cells derived from the basal layer of transitional epithelium. Hyperchromatic.

330
Q

Association of pure squamous cell carcinoma of the anal canal

A

HPV.

331
Q

Physiological cause of haemorrhoids

A

Persistently elevated venous pressure within haemorrhoidal plexus.

332
Q

Predisposing influences on development of haemorrhoids.

A

Constipation causing straining at defecation, venous stasis at pregnancy, portal hypertension.

333
Q

Presentation of haemorroids

A

Pain and rectal bleeding in people over 30 ad pregnant women.

334
Q

Where do external haemorroids come form?

A

The inferior haemorrhoidal plexus below the anorectal line.

335
Q

Where do internal haemorroids come form?

A

dilation of the superior haemorrhoidal plexus in the distal rectum.

336
Q

Pathogenesis of appendicitis.

A

Progressive increases in intraluminal pressure compromise venous outflow. Associated with overt luminal obstruction e.g. by stool, gallstone, tumour or mass of worms. Stasis promotes bacterial proliferation, triggers ischaemia and inflammatory responses. Tissue necrosis and neutrophilic infiltration of lumen, muscular wall and periappendiceal soft tissues.

337
Q

Commonest tumour of the appendix

A

Well-differentiated neuroendocrine tumour.

338
Q

What causes sterile peritonitis?

A

Leakage of bile or pancreatic enzymes

339
Q

What causes a highly irritating peritonitis with bacterial superinfection.

A

Perforation or rupture of biliary system.

340
Q

What is the result of acute haemorrhagic pancreatitis?

A

Peritonitis with fat necrosis, and bacterial spread if there is damage to the bowel wall.

341
Q

Common bacteria in bacterial peritonitis

A

E. coli, streptococci, S. aureus, enterococci and C. perfringens.

AAPathology (Robbins) (2 decks)

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