Gastrointestinal Pathology

Question 1

What is hiatus hernia

Answer 1

• Upper part of stomach pushes through diaphragm
• Heartburn due to reflux of gastric acid
• Shortness of breath, palpitation
• Discomfort swallowing

Question 2

What is GERD (gastro-oesophageal reflux disease)

Answer 2

• Common, can occur with hiatus hernia
• Increased gastric volume, leads to inflammation of lower oesophagus due to acid reflux damage from stomach
• Early detection prevents complications of ulceration, stricture, barrett’s metaplasia and adenocarcinoma

Question 3

What is oesophageal dysplasia / cancer

Answer 3

• Barrett’s oesophagus predisposes to adenocarcinomas (glandular origin)
• Oesophageal squamous cell carcinomas
• Junction between oesophagus and stomach

Question 4

Describe the histology of the stomach

Answer 4

• Mucosa, submucosa, muscularis and serosa
• Protective mechanisms include mucous layer, bicarbonate secretion, epithelial tight junctions, mucosal blood flow and prostaglandins

Question 5

What is acute vs chronic gastritis

Answer 5

• Acute: Chemical injury, exfoliation / erosion / effacement of surface epithelial cells and diminished secretion of mucous leading to reduction protection against acid attack
• Chronic: H. pylori / chronic bile reflux and autoimmune disorders

Question 6

What are peptic ulcers

Answer 6

• Sores that develop in the lining in the stomach
• Inflammation / erosion
• Complications of haemorrhage, penetration of organs, perforation, anaemia, obstruction (fibrous strictures) and malignancy
• Types: gastric and duodenal

Question 7

What are gastric peptic ulcers

Answer 7

• Epithelial lining of stomach
• Follow destruction / removal of mucous barrier or loss of integrity of surface epithelium
• Excess acid, bacterial infection / certain medications
• Males : females (2:1)
• Failure of mucous defence (mucous-bicarbonate barrier and surface of epithelium)

Question 8

What are duodenal peptic ulcers

Answer 8

• Epithelial lining of duodenum
• Elevated maximal acid secretion
• Ulceration follows gastric metaplasia in response to excess acid
• Males : females (4:1)
• Non-steroidal anti-inflammatory drug induced ulcers arise, with / without pre-existing duodenitis

Question 9

What are polyps and malignant lesions

Answer 9

• Polyps: Benign lesions / masses of the stomach epithelium
• Causes: Chronic stomach inflammation or from certain medications
• Types: Hyperplastic polyps, fund gland polyps or adenomas
• Malignant Lesions: Carcinoid, early / advanced gastric cancer

Question 10

What is appendicitis

Answer 10

• Obstruction of appendix leads to swelling of lumen with secretion causing ischaemia allowing bacteria to invade

Question 11

What is colonic diverticulum

Answer 11

• Bowel obstruction, thickening of propria and prominence of mucosal folds (lumen occlusion)
• Raised intra-luminal colonic pressure (forceful contractions)
• Can become inflamed (diverticulitis)
• Common in older people
• Risk factors include constipation, high meat low fibre diet, genetic wall weaknesses
• Most are asymptomatic and remain uncomplicated

Question 12

What is volvulus

Answer 12

• Abnormal twisting of bowel
• Bowel obstruction (abdominal distension / vomiting)
• Ischaemia (venous obstruction, haemorrhage infarction, surgical intervention)
• Sigmoid (most common)

Question 13

What are haemorrhoids

Answer 13

• Dilation of venous complexes, straining during bowel movements
• Obesity or pregnancy
• Enlarged veins (internal / external), bleeding with bowel movement

Question 14

List 5 types of congenital abnormalities

Answer 14

• Pyloric stenosis
• Duodenal atresia
• Hirschsprung disease
• Intussusception
• Meckel diverticulum

Question 15

What is pyloric stenosis

congenital abnormalities

Answer 15

• Hyperplasia of the pyloric muscle blocks food from entering the small intestine
• Persistent regurgitation + projectile vomit (non-bile)
• Signs of pyloric stenosis usually appear within 3-5 five weeks after birth

Question 16

What is duodenal atresia (congenital abnormalities)

Answer 16

• Congenital absence or complete closure of duodenal lumen
• Failure of recanalisation of duodenal lumen, bilious vomiting in first 24 h of life
• Type 1 (membrane, obstructing septum formed by mucosa / submucosa, 92%)
• Type 2 (fibrous cord)
• Type 3 (complete interruption)

Question 17

What is Hirschsprung disease (congenital abnormalities)

Answer 17

• Most common cause of neonatal colonic obstruction, failed neuronal plexus development
• Can involve entire colon or just rectum / sigmoid colon
• Peristaltic contractions are uncoordinated and weak
• Dilation of proximal segments (mega-colon)
• May present as constipation or diarrhoea
• Commonly associated with down syndrome

Question 18

What is intussusception (congenital abnormalities)

Answer 18

• Collapse of proximal portion of bowel into a distal portion causing bowel obstruction
• Most frequent occurs in ileum and enters cecum
• ‘Red currant jelly’ stool in children (mixture of sloughed mucosa, blood and mucous)

Question 19

What is meckel diverticulum (congenital abnormalities)

Answer 19

• Light bulge in small intestine present at birth
• Congenital abnormality that results from failure of vitelline duct to obliterate during 5th week
• Vestigial remnant of the vitelline duct (yolk stalk), 2% of population
• True diverticulum containing all 3 layers of bowel wall with normal intestinal lining
• Most are asymptomatic but present with obstruction, melena and volvulus

Question 20

What are malabsorption syndromes (acquired diseases)

Answer 20

• Caused by anything that interferes with delivery of bile or pancreatic juice, damaged intestinal mucosa, weight loss, bloating and sometimes diarrhoea
• Celiac or lactose intolerance

Question 21

What is celiac disease (acquired diseases)

Answer 21

• Gluten intolerance (found in endosperm of grains)
• Autoimmune disease, genetic component (HLA-DQ2 / HLA-DQ8)
• Increased intestinal permeability (leaky tight junctions)
• Leads to villus atrophy (inflamed / flattened), interferes with nutrient absorption
• Histology of normal vs damaged / celiac disease

Question 22

What is lactose intolerance (acquired diseases)

Answer 22

• Deficient amounts of lactase
• > 70% of population, unable to digest lactose
• Osmotic gradient created in intestine prevents absorption of water (diarrhoea)
• Undigested lactose gets fermented by bacteria in LI (bloating, flatulence and cramping)
• Treated by avoiding lactose or adding lactase enzymes to lactose products before consuming

Question 23

What is Crohn’s disease (acquired diseases)

Answer 23

• Chronic inflammation of the entire wall of the bowel
• Genetic and environmental factors, most commonly involves ileum and colon
• Local destruction of bowel, non-caseating granulomas, transmural inflammation and fissures
• Transmural inflammation, submucosa granulomas and mural thickening, cobble-stoning appearance
• Poor absorption, diarrhoea, weight loss)
• Stenosis / intestinal stricture (bowel obstruction) and penetrating disease (fistulae between bowel / skin)
• Treatments control inflammation

Question 24

What is ulcerative colitis (acquired diseases)

Answer 24

• Inflammation of superficial layers of bowel wall
• Abdominal pain / diarrhoea mixed with blood, affects colon and rectum
• May be limited to rectum, extending variable distances to sigmoid, descending, transverse, and ascending
• Sporadic and erratic symptoms (ulcers of colon),
• Genetic component in 75% cases (P-ANCA)
• Shallow inflammation confined to mucosa and crypt abscesses (filled with neutrophils)