Week 5 - Oesophagus, Gastric Disorders & Acute Abdomen

Question 1

Outline dysphagia:
• Sites.
• Symptoms.
• Causes.

Answer 1

• Normally, food - deagglutination, peristaltic movements, food enters stomach (back flow prevented by lower oesophageal sphincter - important anatomic landmark/structure).
• Disorders of the oesophagus - commonest clinical presentation is dysphagia - can be functional or mechanical.
• Dysphagia - difficulty swallowing
- Odynophagia - painful swallowing - inflammation, ulcer.

Sites (3 normal narrowings - strictures common at these sites):
• Oropharyngeal.
• Oesophageal.
• Oesophagogastric.

Symptoms:
• Difficulty with solids - mechanical obstruction - tumours/strictures.
• Solids & liquids - motility disorders - achalasia (increased tone of lower sphincter).
• Liquids - pharyngeal disorders.

Causes:
• Local, systemic, central.
• Mechanical, neural, functional.
• Ulcers, tears, webs, rings, tumours, strictures, neural.

Question 2

Identify oesophageal disorders.

Answer 2

• Reflux oesophagitis.
- Commonest clinically - due to reflux of acid coming up from stomach AKA GORD. Barrett's and cancer are complications of GORD.
• Barrett’s oesophagus.
• Cancer.
• Achalasia.
• Fistula.
• Hernia.
• Stricture (Plummer Vinson syndrome).
• Varices - dilation of the veins.
• Mallory-Weiss - rupture.

Question 3

Outline oesophageal varices.

Answer 3

• Dilated veins - lower part.
• Dilation of porta systemic collateral circulation - common whenever there is obstruction to portal circulation in liver e.g. cirrhosis → bleeding more common (dilation → bleeding).
• Pathogenesis - portal hypertension (cirrhosis) → dilation of porta-systemic shunts rupture → massive bleeding.

• Extremely dilated sub-mucosal veins in the lower oesophagus.
Aetiology/Pathogenesis:
1. Portal hypertension (due cirrhosis, hepatic schistosomiasis etc.) results in the development of collateral channels at sites where portal and caval systems communicate in an attempt to allow some drainage of venous blood to occur.
2. Collateral veins develop into congested subepithelial and submucosal venous plexus within the distal oesophagus → varices.

Morphology:
• Tortuous, dilated veins lying within submucosa of distal oesophagus & proximal stomach.
• Haemorrhage in lumen/oesophageal wall → ulcerated and necrotic mucosa.
• Venous thrombosis.
• Evidence of chronic inflammation (in the event of past variceal rupture).

Clinical features:
• Usually asymptomatic.
• Haematemesis due to variceal rupture.
• Haemorrhage due to variceal rupture (medical emergency).

Question 4

Describe Mallory-Weiss tears (syndrome). What is Boerhaave syndrome?

Answer 4

• Severe/forced vomiting.
• Longitudinal mucosal tear (rupture of mucosa causing acute bleeding following severe dilation. Usually longitudinal mucosal tear).
• Alcohol intoxication, over eating (usually at gastroesophageal junction following severe vomiting e.g. binge drinking, alcoholic intoxication, over eating)
• Hiatal hernia in 75%.
• Spontaneous healing (supportive therapy only).
• Boerhaave syndrome - same but severe with rupture & mediastinitis (Pacific Islands). Total rupture of oesophagus releasing contents into the mediastinum is known as Boerhaave syndrome - seen in Pacific Islands usually following festival/heavy meal.

• Longitudinal tear in the oesophagus near the gastoesophageal junction.
Aetiology/Pathogenesis:
Trauma due to:
• Severe retching or forced vomiting.
- Gastroesophageal musculature fails to relax in prolonged vomiting so the oesophageal wall stretches and tears.
• Vomiting secondary to acute alcohol intoxification
• Hiatus hernia.

Clinical features:
• Vomiting up blood (haematemesis) after violent retching or vomiting.
• Melaena (blood in stool).
• Contributes to about 10% of upper GIT bleeding.

Investigation:
• Endoscopy.

Management:
• Supportive therapy.
• Spontaneous healing.

Question 5

Outline congenital oesophageal disorders.

Answer 5

• Congenital atresia - total obstruction of oesophagus with just a fibrous thread.
• Fistula - one of the ends communicating with the trachea.
*See diagrams.

Question 6

Outline motility disorders of the oesophagus.

Answer 6

• More common clinically - disorders of oesophageal motility.
• Achalasia most common - narrowing of LOS due to lack of dilation (of LOS)
• Sliding hernia - when a portion of the stomach gets pulled up following strictures or congenital. Produces hyperacidity and gastric heartburn. Commonest (95%).
• Rolling hernia - herniation of stomach wall. Rare (5%).

Question 7

Outline oesophagitis.

Answer 7

• Inflammation due to erosions by toxins, alcohol, infections, acids, poisons.
• Acute: erosive, alcohol, infection (in immunocompromised e.g. Candida).
• Chronic: acid reflux (GORD), chemical, alcohol, smoking, candida, radiation, idiopathic (eosinophilic).

Microscopy:
• Acute inflammation.
• Eosinophils - few (reflux) more in eosinophilic.

• Commonest clinically - reflux oesophagitis - inflammation of lower end of oesophagus due to gastric acid escaping into the oesophagus.

• Inflammation of the oesophageal mucosa.
Aetiology/Pathogenesis:
• Irritation/damage to oesophageal mucosa results in inflammation
• Causes include:
- Acute oesophagitis - erosive, alcohol, infection
- Chronic oesophagitis - acid reflux (GORD), chemical, alcohol, smoking, candida, radiation.

Morphology:
• Ranges from mild redness to severe, bleeding ulceration with stricture formation.
• Varies with aetiology.
• Irradiation causes luminal narrowing.
• Candida is characterised by grey-white pseudomembrane (fungal hyphae/inflammation).
• Herpes virus causes punched out ulcers.

Clinical features:
• Poor correlation between symptoms and histological/endoscopic findings.
• Dysphagia (difficulty swallowing).
• Pain.

Question 8

Outline acid reflux disorders.

Answer 8

• Escape of acid into the oesophagus.
• Gastric acid pH - 1 (million times more acidic than blood).
• Protected by LOS (although it is resistant to mechanical damage by food and very sensitive to acid damage).
• Cause - decreased LOS tone or increased abdominal pressure → GORD.
- Either loss of LOS tone or increased abdominal pressure → escape of acid into oesophagus → results in sudden severe burning pain in epigastrium (typical heartburn AKA GORD).
• Risk factors - alcohol, tobacco, obesity, CNS depressants, pregnancy, hiatal hernia, delayed gastric emptying, increased gastric volume. In many cases, no definitive cause is identified. (Many causes but in most cases clinically may not be able to identify some of these causes. Labelled idiopathic).

Question 9

Identify the classification of GORD.

Answer 9

Clinical stages:

1. Functional heartburn.
2. NERD - non erosive reflux disease.
3. MERD - minimal erosive reflux disease.
4. GORD - erosion, inflammation.
5. Barrett’s - metaplasia.
6. Adenocarcinoma (rare).

• Clinically, GORD is not one disease. Although patient just presents with heartburn. Typically 75% of patients will have no pathology (oesophageal biopsy is normal - non-erosive or very mild inflammation) - nothing will be seen clinically in 3/4 of patients.
• Significant inflammation is seen in approx. 24%.
• Metaplasia/cancer seen in <1%.
• AET (acid exposure index) and SI (symptoms index) are measured to know the different types of clinical GORD.
• Heartburn - NERD (normal endoscopy 75%), oesophagitis (24%), Barrett’s (1%).

Question 10

Outline the aetiology of GORD.

Answer 10

• Reflux of gastric juices causes mucosal injury.
• Risk factors include:
- Defective lower sphincter (reduced tone, inappropriate clearance).
- Delayed oesophageal clearance.
- Gastric regurgitation (e.g. hiatus hernia, varicies).
- Defective gastric emptying.
- Obesity and motility disorders (e.g. defective perastalsis).
- Increased intra-abdominal pressure (e.g. pregnancy).
- Inflammatory bowel syndromes.
- Hyperacidity of gastric contents.
- Fat, alcohol, coffee.
- N.B. Smoking, NSAIDS not risk factors.

Question 11

Describe the pathogenesis of GORD.

Answer 11

1. Prolonged reflux of gastric juices causes damage to the oesophageal mucosa → inflammation.
2. Basal cell hyperplasia occurs in response to damage.
3. Intestinal metaplasia within oesophageal squamous mucosa → Barret’s Oesophagus (change of epithelium from stratified squamous to glandular epithelium. Clear border = Barrett’s).
4. Dysplasia of oesophageal mucosa may eventually lead to adenocarcinoma.

Normal → inflammation → hyperplasia → metaplasia (transformation from squamous cell to glandular epithelium known as glandular metaplasia). When further damage occurs → nuclei become irregular, mutations start occurring (dysplasia) → cancer.

• Hyperplastic epithelium due to loss of cells due to acid (damage due to acid).
• Become glandular because producing mucus - more resistant to mucus. Acid digestion.
• Metaplastic cells gradually become more crowded and glandular/irregular → start infiltrating as the cancer.
• When there is metaplasia and cancer - the inflammation becomes well demarcated - clear border.

Question 12

Describe the morphology of GORD.

Answer 12

• Normal oesophagus - white stratified squamous epithelium.
• Normal gastric - reddish columnar epithelium.
• In the case of reflux oesophagitis and Barrett’s - oesophageal epithelium becomes inflamed → then transforms to columnar epithelium.

Oesophagitis:
• Gross - inflammation/redness. May have bleeding and ulceration.
• Microscopy - mucosa histology often unremarkable, eosinophils, basal zone hyperplasia, elongation lamina propria papillae.

Barrett’s:
• Gross - tongues or patches of red velvety mucosa extending upwards.
• Microscopy - intestinal metaplasia, squamous cells replaced by columnar mucosa, goblet cells with distinct mucous vacuoles that stain blue.

Dysplasia:
• Gross - abnormal mucosa, possible gross tumour mass.
• Microscopy - increased epithelial proliferation, atypical mitosis, immature cells and abnormal glands, invasion of neoplastic cells to lamina propria.

Question 13

Identify the clinical features of GORD.

Answer 13

• Heartburn and regurgitation (provoke bending, straining, lying down).
- Burning retrosternal discomfort after meals, lying, stooping or straining, relieved by antacids.
• Belching.
• Salivation due to reflex salivary gland stimulation (waterbrash - “my mouth fills with saliva”).
• Dysphagia/odynophagia.
• Cough as reflex fluid irritates larynx.
• Atypical chest pain.

Question 14

What are the complications of GORD?

Answer 14

• Oesophagitis - inflammation/ulcer (possible bleeding and perforation).
• Benign oesophageal stricture - fibrosis due to long-standing oesophagitis.
• Barrett’s oesophagus - pre-malignant condition characterised by metaplasia.
• Oesophageal tumour
- Adenocarcinoma - Affects lower 1/3 of oesophagus. Causes include acid reflux, GORD & Barret’s oesophagus. More common.
- Squamous carcinoma - Affects upper 1/3 of oesophagus. Environmental causes: Diet, smoking, alcohol, toxins. Less common.

• Ulcers.
• IDA.

Question 15

Identify differential diagnoses for GORD.

Answer 15

• Oesophagitis (from corrosives, NSAIDs, herpes, Candida).
• Duodenal/gastric ulcers or cancers.
• Non-ulcer dyspepsia.
• Sphincter of Oddi malfunction.
• Cardiac disease.

Question 16

Outline investigations and management of GORD.

Answer 16

Investigations:
• Endoscopy - generally if patient presents with atypical symptoms. Endoscopy of symptoms >4 weeks, persistent vomiting, GI bleeding/iron deficiency, palpable mass, age >55y, dysphagia, symptoms despite treatment, relapsing symptoms, weight loss.
• Barium swallow may show hiatus hernia.
• 24h oesophageal pH monitoring +/- manometry help diagnose GORD when endoscopy is normal.

Management:
• Lifestyle advice - weight loss, elevation of bed head, smoking caessation, small regular meals. Avoid hot drinks, alcohol, citrus fruits, tomatoes, onions, fizzy drinks, spicy foods, coffee, tea, chocolate and eating <3h before bed (late meals).
• Drugs - antacids relieve symptoms. For oesophagitis,, try a PPI (better than H2 blockers). If unresponsive, try twice daily PPI.
• Surgery - e.g. laparoscopic, aims to increase resting oesophageal sphincter pressure. Consider in severe GORD (confirm by pH monitoring/manometry) if drugs are not working. Atypical symptoms (cough, laryngitis) are less likely to improve with surgery compared to patients with typical symptoms.

Question 17

Outline the 2 types of oesophageal cancer.

Answer 17

• 2 common types of cancer in the oesophagus - squamous cell carcinoma and adenocarcinoma.
• Squamous carcinoma:
• Upper end and middle 1/3 of oesophagus.
• Common in Asian countries.
• Due to tobacco, diet, toxins.
• Keratin, hard tumour (usually hard due to keratin production).
• Microscopy - keratin pearls.

• Adenocarcinoma:

• Lower end.
• Western countries.
• Reflux disease (due to acid).
• Glands, mucous.
• Glandular cancer, soft and mucous producing adenocarcinoma (multiple glands that produce mucin).

Question 18

Oesophageal disorders summary.

Answer 18

• Numerous disorders - commonest is reflux disease → transforms to Barrett’s oesophagus → transforms to cancer in rare cases.
• Obstructions - 2 types
- Functional - achalasia and aperistalsis.
- Mechanical - strictures and tumors.
• Oesophagitis - common, infections - immunocompromised. Due to diet/alcohol.
• Chronic oesophagitis commonest - GORD.
• Barrett’s - glandular metaplasia (1% of patients) → dysplasia → adenocarcinoma (precursor for dysplasia and adenocarcinoma).
• Squamous carcinoma - Asian, alcohol, tobacco, toxins, upper end/middle 1/3 of oesophagus.

Question 19

Outline gastric defences.

Answer 19

NORMAL
Defensive forces:
• Surface mucus secretion.
• Bicarbonate secretion into mucus.
• Mucosal blood flow.
• Apical surface membrane transport. 
• Epithelial regenerative capacity.
• Elaboration of prostaglandins.

Mucus markedly thick and sticky → protects the epithelium/epithelial stem cells. Prostaglandins also important.

Damaging forces:
• Gastric acidity.
• Peptic enzymes (can digest any tissue).

INJURY → ULCER
• H. pylori infection.
• NSAIDs.
• Aspirin.
• Cigarettes.
• Alcohol.
• Gastric hyperacidity.
• Duodenal-gastric reflux.

Injurious exposures or impaired defences (ischaemia, shock, delayed gastric emptying, host factors) → ulcer.

*See diagram.

Question 20

Outline acute peptic ulcers.

Answer 20

• Acute ischaemic ulcers, secondary to systemic dysfunction.
• 3 types of ulcers important in stomach (occur in severely diseased patients):
- Stress ulcers - shock, sepsis, trauma (more common in stomach. Multiple dark black small shallow ulcers - black in colour due to digested Hb because patient is bleeding).
- Curling ulcers - burns, usually in proximal duodenum only.
- Cushing ulcers - gastric, duodenal and oesophageal ulcers in intracranial disease. High incidence of perforation (all over upper GIT in intracranial disease, more prone to perforation).

Pathogenesis:
• Ischaemia? Hypoxia?
• Cyclooxygenase inhibition.
- Ischaemia, hypoxia and inhibition of cyclooxygenase (inhibit production of prostaglandins) - commonest aetiologies.

Complications (heal in days):
• Bleeding - 20%.
• Perforation - 5%.
- May bleed or may perforate but if primary condition improves e.g. sepsis, trauma - then will heal quickly in days (because it is a mucosa).

Question 21

Differentiate between acute and chronic gastritis.

Answer 21

Acute (with or without ulcer):
• Generalised inflammation with or without ulcer.
• Inflammation due to drugs, NSAIDs, toxins, alcohol, infections.
• Usually produces discomfort, nausea, vomiting, haematemesis.

Chronic:
• Helicobacter pylori - 90%.
• Autoimmune - pernicious anaemia, atrophic - 10%.
• Radiation, bile reflux etc. - rare.
• Systemic diseases - Crohn’s, amyloidosis.
- Typically due to H. pylori. Inflammation is chronic - there is more atrophy and healing. Mucosa becomes so thin that submucosa vessels appear more prominently and loss of folds. Can also occur with autoimmune disorders, radiation, bile - not so common.

Question 22

Describe the morphology of acute and chronic gastritis.

Answer 22

Acute:
• Microscopy - vasodilation and acute inflammatory cells.

Chronic:
• More important because precursor for peptic ulcer and cancer.
• Gross - atrophy of mucosal folds, loss of rugae.
• Microscopy - plenty of inflammatory cells with atrophy of glands.
- Abnormal atrophic glands without lack of function. Plenty of inflammatory cells. Not malignant, still round, nucleus still at base, some still functioning (more atrophy than malignant).

Question 23

Outline the aetiology and risk factors of peptic ulcer disease.

Answer 23

• PUD refers to a gastric ulcer in the lower oesophagus, stomach, duodenum or jejunum
• Ulcers may be acute or chronic.

Aetiology:
• H. pylori - nearly 100% of patients with PUD and chronic gastritis have H. pylori.
• Due to infection by H. pylori - bacteria that remains in the mucus of stomach (spirochete group). Bacteria typically reside in mucus layer not the cells.
• H pylori is a gram negative spirochete that colonises gastric mucosa.
• Is a common infection (overall prevalence in Australia of 76%)
• More commonly infects males than females.

Risk factors:
• NSAIDs.
- Inhibit COX-1 therefore decreased prostaglandin synthesis.
- Decreased production of mucus and bicarbonate.
- Gastric epithelial cells more vulnerable to damage by HCl and pepsin → Decreased defences.
• Smoking.
• Alcohol.
• Hyperacidity.
• Steroids.
• Rapid gastric emptying.
• Duodenal reflux.
• Personality, stress, genetic.

Question 24

What is Zollinger Ellison Syndrome?

Answer 24

• Hyperacidity, multiple ulcers.
• Gastrinoma of pancreas, MEN1 syndrome.
• Hyperacidity causing multiple ulcers due to gastrinoma - adenoma of pancreas that produces gastrin that produces gastric hormone → stimulates too much acid production. Part of multiple endocrine neoplasia type 1 syndrome.

Triad - severe peptic ulceration, gastric acid hypersecretion, pancreatic tumour (non-beta cell islet tumour known as gastrinoma).

Question 25

Outline H. pylori and its role in the pathogenesis of peptic ulcer disease.

Answer 25

• Commonest in population (10-80%), hygiene* - from 10-80% of population based on their hygiene (more hygiene → less incidence and vice versa).
• Positive in ~100% of chronic gastritis and PUD patients.
• Gram negative, spirochete, does not invade tissue.
• Colonise mucous layer of acidic gastric mucosa only*
• Duodenal ulcers precedes gastric metaplasia* (ulcers common in duodenum).
• H. pylori infection produces antral gastritis (gastric inflammation - bacteria typically located/inhabit antrum), hyperacidity and hypogastrinemia (decreased gastrin because too much acid in the stomach).

Pathogenesis (imbalance between mucosal defences and damaging forces):
• Protease → break down mucous barrier → release urea.
• Urease → urea → ammonia → neutralise acid → reflex hyperacidity.
Protease - breaks down mucus barrier and releases urea from the mucus protein.
Urease - breaks down urea to produce ammonia which is highly alkaline substance and neutralises the acid. Through neural reflex (vagus nerve) - causes reflex hyperacidity - inhibits gastrin secretion because there is too much acidity.

1. H. pylori secretes urease → breakdown urea → increased release of ammonia → alkaline pH → reflex acid production → hyperacidity → mucosal damage → Increased damaging forces.
2. H. pylori secretes protease → breakdown mucosa → expose epithelium for digestion.
3. Results in chronic inflammation leading to gastric metaplasia and ulcer formation.

Question 26

Identify H. pylori related disorders.

Answer 26

• Chronic gastritis - 90% (commonest).
• Peptic ulcer disease - 95-100%.
• Gastric carcinoma - 70%.
• Gastric lymphoma.
• Reflux oesophagitis.
• Non ulcer dyspepsia.

Question 27

Outline the diagnosis of H. pylori.

Answer 27

• Fecal antigen test.
• C13 urea breath test (radioactive carbon urea breath test).
• H. pylori serology IgG - new (blood test).

Question 28

Describe the morphology of peptic ulcer disease.

Answer 28

• More common in proximal duodenum than stomach (4:1).

• Bacteria remains in antrum mostly, gastric mucosa → causes ulcer in duodenum through hyperacidity (so much excess acid - stomach is capable of handling due to its defence mechanisms but the duodenum is not - ulcers common in the first half of the duodenum before opening of common bile duct - excess acid damages the delicate duodenal mucosa).
• Before the duodenal ulcers, there is gastric metaplasia of the epithelium → ulceration occurs because bacteria enters there - makes its place and then starts ulceration).
• Round, small, punched out, <2cm.
• > 80% single ulcer, radiating mucosal folds due to scarring.
• Single ulcer most common - unknown why.
• Radiating folds - ulcers go for many years - continuous damage and scarring occurring - ulcer is damaging and scarring continuously being produced. There is fibrosis at the base of the ulcer → wound scar contraction - contraction of scar at base of ulcer which pulls the mucosal folds together → radiating mucosal folds (used in radiology to differentiate between benign and malignant ulcers).
• Duodenal ulcer clinical - hunger pain.
• 1-3 hours after meal during the day, > at night.

• Gastric ulcer - pain with food (because it is in the stomach).
- Duodenal ulcers - contraction of stomach prevents acid into the ulcer - relieved by food as pylorus contracts (stomach starts mixing). Patients start eating food frequently.

• Relieved by antacids/food.
• Microscopy:

1. Necrotic layer (top - thin).
2. Inflammatory cells (thin).
3. Granulation tissue (zone - thin).
4. Collagenous scar (dense area of collagen).

Question 29

Identify the clinical features of peptic ulcer disease.

Answer 29

• Chronic condition with natural history of relapse and remission.
• Recurrent epigastric abdominal pain with episodic occurrence and relationship with food (often related to hunger, specific foods or time of day +/- bloatness).
• Occasional vomiting in ~40% of patients.
• Other symptoms - weight loss, loss of appetite, foul-smelling breath (halitosis), fatigue (anaemia).

Question 30

What are the complications of peptic ulcer disease?

Answer 30

• Chronic bleeding - anaemia (IDA)*
- Commonest.

• Acute bleeding - massive, shock.
- Can occur when it invades and ruptures a major blood vessel → shock.

• Perforation, peritonitis, pancreatitis.

• Stricture (pyloric stenosis).
- Patients take prescribed antacids for many years without knowing the antacids were causing more damage - neutralises acid leading to increased acid production (vagus nerve). Antacids provide temporary relief but cause more damage due to stomach physiology. Constant PUD - causes narrowing due to scar contraction. First part of duodenal ulcer contraction causes pyloric stenosis. Patients get severe projectile vomiting and severe GI disturbance - pain, vomiting, cannot digest - undergo surgery (gastroduostomy - making a hole connecting duodenum so food bypasses duodenum. Food enters directly). Pyloric stenosis and gastroduostomy now rare - different treatment available.

• Gastric carcinoma (not duodenal cancer).

Question 31

Outline gastric cancer (tumours).

Answer 31

• Benign tumours - polyps (associated with chronic gastritis), adenoma - rare.
• Adenocarcinoma (90%) - most important.

• Japan, Chile - 20x high incidence. Chronic gastritis.
- Common in certain countries because of incidence of chronic gastritis.

• Adenocarcinoma intestinal and diffuse types.

• Intestinal type - common, associated with chronic gastritis, early diagnosis, better prognosis.
• Diffuse type - rare, genetic, late diagnosis, poor prognosis. Diffuse infiltrating.

• Other tumours:

• Gastric lymphoma (MALT tumours) - B cell, some are H. pylori related - 4%.
• Carcinoid tumour - endocrine tumour.
• Gastrointestinal stromal tumour* (GIST) - sarcoma.

Question 32

Describe the morphology of gastric adenocarcinoma (intestinal type).

Answer 32

Gross:
• Large, tumour, central ulcerations and haemorrhage.

Microscopy:
• Pleomorphic, hyperchromatic cells forming irregular glands.

• Large projectile exophytic tumors - tumors come out of tissue layer producing a solid growth. Large tumor with ulceration and haemorrhage. The rest of the gastric mucosa may show features of chronic gastritis.
• Microscopically, very irregular cells forming irregular glands. Cells are much more dark blue compared to surrounding tissue because too much nuclear material - malignant cells.

Question 33

Describe the morphology of gastric adenocarcinoma (diffuse type).

Answer 33

Gross:
• Diffuse, thickened wall. Atrophic mucosa (no folds).

Microscopy:
• Signet cells. No glands.

• Less common, the tumor infiltrates the whole stomach making it very thick walled - tinctus plastica or leather bottled stomach.
• Microscopically, do not see glands (no gland formation) but malignant mucus cells produce a signet wedding ring appearance - each cell like a ring with a diamond.
• Endoscopically, just produces some depressions. Actual tumor will be inside under the mucosa (infiltrating).

Question 34

Differentiate between intestinal and diffuse gastric adenocarcinoma.

Answer 34

Intestinal type:
• Intestinal metaplasia, common.
• Chronic gastritis/atrophy, H. pylori.
• APC mutation (patients with FAP).
• Well differentiated.
• Better prognosis.
• Gland formation.
• No Signet ring cells.

Diffuse type:
• Idiopathic/familial, less common.
• No precursor lesion (no H. pylori).
• E-Cadherin mutations (loss).
• Poorly differentiated.
• Poor prognosis.
• No gland formation.
• Signet ring cells.

• Intestinal - most common, better prognosis. Associated with chronic gastritis/atrophy. Solid tumors that project out (exophytic), irregular glands.
• Diffuse - diffusely infiltrating and producing depressions only. Loss of mucosal folds. Signet ring cells.

Question 35

Summary peptic ulcer disease/gastric tumours.

Answer 35

Peptic ulcer - duodenum (most common)/gastric - acid and pepsin induced digestion
• Aetiology: H. pylori, gram -ve, spirochete, does not invade tissue. Produces protease and urease causing reflex hyperacidity.
• Mucosal damage - inflammation - ulcer - cancer.
• Single ulcers, punched out, clean, radiating folds (not in cancer - radiating folds not seen in carcinoma).
• Complications - bleeding, IDA (due to chronic bleeding), perforation, stenosis, cancer (carcinoma not seen in duodenal).
• Atrophic gastritis: autoimmune, pernicious anaemia.

Gastric tumors
• Polyps, adenoma, carcinoid, GIST: rare.
• MALT B cell lymphoma 4%.
• Adenocarcinoma 90%, intestinal (H. pylori) and diffuse (genetic) types.

Question 36

Identify the differential diagnoses of an acute abdomen.

Answer 36

1. Cholecystitis (lithiasis).
2. Peptic ulcer.
3. Appendicitis.
4. Diverticulitis.
5. Bowel obstruction.
6. Bowel ischaemia.
7. Pancreatitis.
8. Biliary colic.
9. Oesophagitis, GORD.
10. Gastroenteritis, IBD.
11. Peritonitis.
12. Abdominal aortic aneurysm.
13. Pelvic inflammatory disease.
14. Non specific.

Right hypochondriac:
• Gallstones*
• Cholangitis.
• Hepatitis.
• Liver abscess.
• Cardiac causes.
• Lung causes.

Epigastric:
• Oesophagitis.
• Peptic ulcer.
• Perforated ulcer.
• Pancreatitis*

Left hypochondriac:
• Spleen abscess.
• Acute splenomegaly.
• Spleen rupture.

Lumbar:
• Ureteric colic.
• Pyelonephritis.

Umbilical:
• Appendicitis (early).
• Mesenteric adenititis.
• Meckel's diverticulitis.
• Lymphomas.

Right iliac:
• Appendicitis*
• Crohn's disease.
• Caecum obstruction.
• Ovarian cyst.
• Ectopic pregnancy.
• Hernias.

Hypogastric (urinary/genital):
• Testicular torsion.
• Urinary retention.
• Cystitis.
• Placental abruption.

Left iliac:
• Diverticulitis*
• Ulcerative colitis.
• Constipation.
• Ovarian cyst.
• Hernias.

Question 37

Outline acute appendicitis.

• Aetiology/Pathogenesis.
• Clinical features.
• DDx.
• Morphology.
• Complications.

Answer 37

• Young adults, luminal obstruction by stool/fecalith/tumour (carcinoid).
- More common younger age, luminal obstruction by stool/fecalith (concentrated hard stool) - obstructing opening/mouth of appendix or can be due to obstruction from tumour - carcinoid (endocrine) tumour only common tumour.
• Increased luminal pressure, infection, acute inflammation (increased luminal pressure leading to secondary infection and acute inflammation).
• Periumbilical pain → RLQ, nausea, vomiting (typically presents with periumbilical pain that gradually migrates to RLQ, nausea and vomiting. McBurney’s point).
• DDx:
- Mesenteric lymphadenitis* - often missed, common bacterial/viral gastroenteritis - can give rise to lymphadenitis.
- Diverticulitis - pain typically on left side.
- Salpingitis - fallopian tube inflammation.
- Ovulation pain (mittelschmerz).
• Gross and microscopy - acute inflammation, oedema, swelling, pain, haemorrhage. Plenty of neutrophils, normal lymphocytes.
• Complications - abscess, rupture, peritonitis.

Question 38

Outline diverticulosis/itis.

Answer 38

• Diverticula are blind pouches. Multiple, usually in sigmoid colon. Usually known as false diverticula as do not have all the layers (do not have muscular layer). Acquired most common.
• Later age >30 years.
• Sigmoid colon, false, acquired, common, no muscular layer. (True - all layers e.g. Meckles - congenital diverticulitis - has all the layers).
• Constipation (low motility)/low fibre diet - hard stools - increased pressure → herniation of mucosa through muscle layer.
- Usually due to constant constipation for a long time (low motility). Low fibre in diet - hard stool - increased pressure (intestinal peristalsis cannot push the hard stool for long time) - increased pressure results in herniation of the mucosa through the muscle layer.
• Pellet or sheep stools alternating with diarrhoea (infection).

• Mucosa pushes in through the muscular wall to form diverticula. Multiple diverticula occur whenever there is deficiencies in the muscle layer - appears as multiple blind pouches. If stool gets stuck there and secondary inflammation - known as diverticulitis. Without inflammation - diverticulosis.

Question 39

What are the complications of acquired diverticulosis?

Answer 39

• Rupture - peritonitis.
• Bleeding (common).
• Diverticulitis - inflammation.
• Inflammation forming an abscess.
• Left sided - diverticulitis.
• Right sided - appendicitis.

Question 40

Outline intestinal obstructions.

Answer 40

• Clinical - abdominal pain, distension, vomiting (constipated - no further movement - has to get out somehow) and constipation.
• Mechanical:
• Hernia (defects/weak).
• Adhesions (surgery, inflammation).
• Intussusception (children, idiopathic - telescoping of the intestinal wall).
• Volvulus (rare, sigmoid - twisting of the intestinal loops - volvulus inflammation e.g. IBD (Crohns)/TB - can give rise to narrowing of the intestine due to stricture).
• Tumours, strictures.

• Functional:

• Ischaemia/infarction.
• Inflammation (toxic megacolon).
• Commonest is herniations - intestines projecting out through a defect in the abdominal wall (inguinal, femoral, umbilical).
• Adhesions very common following past surgery (any abdo surgery) or past inflammation (e.g. gastroenteritis/scar tissue within abdomen obstructs/strangulates intestinal loops → gives rise to obstruction).
• Functional (no mechanical obstruction) - ischaemia or infarction of segment of the intestine - dead portion is an obstruction as there is no movement. Severe inflammation (toxic megacolon) - common in ulcerative colitis - inflammation so severe that it blocks peristaltic waves → results in marked dilation.

Question 41

Describe hernias.

Answer 41

• Commonest is inguinal hernia through inguinal canal (either direct or indirect).
• Weak areas in abdominal wall → results in projection/herniation of intestinal loops.
• Femoral, umbilical hernia.
• Incisional hernia - past surgeries.
• Epigastric hernia.
• Incarcerated/strangulated hernia - when the hernia strangulates obstructing the blood flow - resulting in gangrene. Congenital inguinal hernia in young children.

Question 42

Describe intussusception.

Answer 42

• Commonest in children (<2y). Idiopathic or inflammation.
• Adults - secondary to tumour/polyp.
• Usually idiopathic or may have some inflammation (gastroenteritis).
• One segment of the tube gets into the distal portion resulting in obstruction and telescoping.
• Telescoping - internal portion is known as intussusceptum - is narrow - causes obstruction/ischaemia and there is dilation/retention of the proximal portion known as intussuscipens.

Question 43

Outline ischaemic bowel disease:
• Clinical.
• Types.
• Pathogenesis.
• Morphology.
• Aetiology.

Answer 43

• Ischaemia and infarction of the bowel. Bowel segments become gangrenous due to blood vessel obstruction (segments of intestine becomes gangrenous).
• Clinical: late age, >70y, colon/any segment (commonest in colon but can effect any part of GI tract).
• Types:
• Chronic mucosal - intermittent bloody diarrhoea (usually causes mucosal gangrene only. Present with intermittent attacks of bloody diarrhoea followed by recovery). Results in just mucosal gangrene and the wall still intact → bloody diarrhoea.
• Acute transmural - sudden cramping, LLQ pain, desire to defecate, blood or bloody diarrhoea. (Major blood vessel obstruction - gives rise to transmural infarction - the whole thickness of intestinal wall - not just mucosa - results in sudden cramping, LLQ pain, desire to defecate, wholly blood or bloody diarrhoea).

• Pathogenesis: reperfusion injury - bacterial products, inflammatory mediators.
- Reperfusion injury - initial blood vessel obstruction → death of tissue → reperfusion results in release of bacterial products, inflammatory mediators into the general circulation causing systemic shock and organ failure.

• Gross: dark, inflammation, ranges from oedematous → black (depending on gangrene development).
• Aetiology: multiple but atherosclerosis most common.
• Atherosclerosis (mesenteric artery).
• Aortic aneurysm, cocaine abuse.
• Hypercoagulable states: OCD use.
• Cardiac failure, shock, dehydration.
• Vasculitis: PAN, Wegener’s.

Question 44

Outline Meckel’s diverticulum.

Answer 44

• Vitello-intestinal duct remnant (congenital remnant of vitello-intestinal duct which connect terminal ileum to umbilicus.
• 2% population.
• 2 feet from IC (ileocolic) junction.
• 2cm in size.
• Presents at 2 years.
• True diverticulum - all layers.
• 50% of cases have ectopic gastric/pancreatic rests.
• Bleeding, ulcer, infection, torsion, hernia, obstruction (just like appendix - can give rise to bleeding, ulcer, infections).
• DDx appendicitis (right).
• Congenital abnormality - can have ectopic gastric and pancreatic tissue inside the diverticulum - can give rise to PUD - 74% just diverticulum.

Question 45

Outline Hirschsprung/congenital megacolon.

Answer 45

• Congenital absence of ganglions. Absence of ganglion in the terminal rectum results in total narrowing (because not responding to peristalsis) and the normal part dilates. Presents with marked intestinal obstruction - vomiting, constipation, diarrhoea.
• Lack of ganglions → loss of motility narrowing → dilation of proximal segment.
• Males 4:1.
• Mild (infancy) or severe (at birth) - when severe can present at birth.
• Constipation, vomiting and diarrhoea.
• Complications: enterocolitis (secondary infections), fluid and electrolyte disturbances - due to total obstruction.

Question 46

Outline acquired megacolon.

Answer 46

• Inflammation, strictures, toxic in ulcerative colitis - ganglia normal.
- The same loss of ganglion can occur in rare conditions due to inflammation, strictures, toxic in UC (ganglia normal).

• Chaga’s disease: Trypansoma cruzi (South America) loss of ganglia.
- Parasitic disease, common in Latin American countries, protozoa literally damages the ganglia. Common in iso veins but can also occur in colon. Parasite in blood.