Gastrointestinal Pathology Flashcards
1
Q
What is hiatus hernia
A
- Upper part of stomach pushes through diaphragm
- Heartburn due to reflux of gastric acid
- Shortness of breath, palpitation
- Discomfort swallowing
2
Q
What is GERD (gastro-oesophageal reflux disease)
A
- 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
3
Q
What is oesophageal dysplasia / cancer
A
- Barrett’s oesophagus predisposes to adenocarcinomas (glandular origin)
- Oesophageal squamous cell carcinomas
- Junction between oesophagus and stomach
4
Q
Describe the histology of the stomach
A
- Mucosa, submucosa, muscularis and serosa
- Protective mechanisms include mucous layer, bicarbonate secretion, epithelial tight junctions, mucosal blood flow and prostaglandins
5
Q
What is acute vs chronic gastritis
A
- 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
6
Q
What are peptic ulcers
A
- 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
7
Q
What are gastric peptic ulcers
A
- 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)
8
Q
What are duodenal peptic ulcers
A
- 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
9
Q
What are polyps and malignant lesions
A
- 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
10
Q
What is appendicitis
A
- Obstruction of appendix leads to swelling of lumen with secretion causing ischaemia allowing bacteria to invade
11
Q
What is colonic diverticulum
A
- 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
12
Q
What is volvulus
A
- Abnormal twisting of bowel
- Bowel obstruction (abdominal distension / vomiting)
- Ischaemia (venous obstruction, haemorrhage infarction, surgical intervention)
- Sigmoid (most common)
13
Q
What are haemorrhoids
A
- Dilation of venous complexes, straining during bowel movements
- Obesity or pregnancy
- Enlarged veins (internal / external), bleeding with bowel movement
14
Q
List 5 types of congenital abnormalities
A
- Pyloric stenosis
- Duodenal atresia
- Hirschsprung disease
- Intussusception
- Meckel diverticulum
15
Q
What is pyloric stenosis
congenital abnormalities
A
- 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
16
Q
What is duodenal atresia (congenital abnormalities)
A
- 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)
17
Q
What is Hirschsprung disease (congenital abnormalities)
A
- 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
18
Q
What is intussusception (congenital abnormalities)
A
- 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)
19
Q
What is meckel diverticulum (congenital abnormalities)
A
- 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
20
Q
What are malabsorption syndromes (acquired diseases)
A
- 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
21
Q
What is celiac disease (acquired diseases)
A
- 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
22
Q
What is lactose intolerance (acquired diseases)
A
- 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
23
Q
What is Crohn’s disease (acquired diseases)
A
- 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
24
Q
What is ulcerative colitis (acquired diseases)
A
- 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)
