Histopath 2 Flashcards
Oesophagitis
The redness is a cardinal sign of inflammation
Histology: neutrophils, which is the hallmark of acute inflammation
Aet: usually caused by GORD
Produces:
- Firbosis & Ulceration, which produces a necrotic slough, inflammatory exudate and granulation tissue
LA Classficiation
Mx: lifestyle changes (stop smoking, weight loss), PPI/H2 receptor antagonists
Cx:
• Haemorrhage
• Perforation
• Stricture
• BARRETT’s OESOPHAGUS
Barret’s
- 10% of those presenting with GORD have Barret’s
- Squamous tissue -> Columnar -> Columnar + IM (goblet cells -> Dysplasia -> Adenocarcinoma
- Upwards migration in Z line
Oesophageal Adenocarcinoma
- Associated with Barret’s so distal 1/3
- Caucasian, M»F
- Other Rf: Previous radiation therapy, smoking obesity
Squamous cell oesophageal carcinoma
- PC: Progressive dysphagia, pain on swallowing, anorexia,
- African population (6x more common)
- Rf: Alcohol & smoking, achalasia, plummer vinson syndrome, nutritional deficiencies, nitrosamines, HPV
- Histopath: Usually found in middle third of oesophagus > lower third > upper third. Cells produce KERATIN and INTERCELLULAR BRIDGES (SCC sx)
- Cx: Rapid growth and early spread (to LNs, liver and directly to proximal structures)
- Mx: Palliative care
How does the gastric mucosa change?
Body and Fundus - Gastric columnar mucosa > Specialised cells in Lamina propria -> Muscularis Mucosa.
Pyloric Canal and Antrum- Gastric columna mucosa> Non-specialised cells in Lamina propria (gastric pits) -> Muscular Mucosa
GOBLET CELLS SHOULD NTO BE PRESENT!
Gastritis types
Acute gastritis is characterised by neutrophils and is caused by NSAIDs, Aspirin, Alcohol, Corrosive and infection (H Pylori)
Chronic gastritis is characterised by lymphocytes* and is caused by ABC (autoimmune, bacterial and chemical)
A- Crohn’s Disease, anti-parietal antibodies
B- H Pylori (antral) Other: HSV, CMV, Strongyloides
C- Chronic NSAID/aspirin usage/ bile acid reflux (foveolar hyperplasia)
Cx: Ulceration
*Neutrophils can be present from coexisting acute inflammation
Chronic H Pylori infection
• Induces lymphoid tissue in the stomach: lymphoid follicles in germinal centres (i.e. the presence of lymphoid follicles/plasma cells is NOT part of the normal stomach mucosa)
• The fact that H. pylori induces MALT formation is important because it is associated with an increased risk of lymphoma
CLO –> IM* –> Dysplasia
Adenocarcinoma (8 x increased risk)
Lymphoma (MALToma)
Mx: Eradicate H. pylori using triple therapy – PPI, Clarithromycin + Amox or Metro
* GOBLET CELLS SHOULDN’T BE PRESENT IN STOMACH
Cag-A H Pylori
Cag-A positive H. pylori have a needle like appendage that injects toxins into intercellular junctions allowing the bacteria to attach more easily
Cag-A is a toxin
This strain is associated with more chronic inflammation
Stomach Ulcers
Technical Definition of Ulcer: the depth of the loss of tissue goes beyond the muscularis mucosa (into the submucosa) I.e. if you only get loss of the epithelium +/- lamina propria, then it is an erosion, not an ulcer
Difference between acute and chronic ulceration:
Chronic ulcers are accompanied by scarring and fibrosis
IMPORTANT: ALL ULCERS SHOULD BE BIOPSIED TO EXCLUDE MALIGNANCY
Complications of Ulcers
o Bleeding –> anaemia, shock (massive haemorrhage)
o Perforation –> peritonitis
Stomach Cancer
High incidence in Japan, Chile, Italy, China, Portugal and Russia
More common in MALES
>95% of all malignant tumours in the stomach are ADENOCARCINOMAS, can be split morphologically into:
1. Intestinal
• Well-differentiated
• Presence of big glands containing mucin
2. Diffuse (poorly differentiated, composed of single cells with no attempt at gland formation)
Poorly differentiated, Composed of single cells with no attempt at gland formation
Types of Diffuse Adenocarcinoma:
• Linitis plastica
• Signet ring cell carcinoma
Remaining 5%: SCC, MALToma, Stromal Tumour, Neuroendocrine tumour
Duodenal Ulcer
- 4 times more common than GU
- Epigastric pain, worse at night
- Relieved by food and milk
- Occurs in younger adults
- RFs: H. pylori, drugs, aspirin, NSAIDs, steroids, smoking, ↑ drugs, acid secretion
- Complications: anaemia (IDA) and perforation (erect CXR)
- Aet: Excess acid from stomach spills over into duodenum, it can also occur due to chronic inflammation and gastric metaplasia with H. pylori infection
Duodenitis
Excess acid from stomach spills over into duodenum.
The intestinal epithelium will change to look more like gastric epithelium because the gastric epithelium is well designed to deal with acid
Chronic inflammation can also lead to duodenal ulceration
Other pathogens:
o CMV
o Cryptosporidium
o Giardiasis
o Whipple’s disease (Tropheryma whippelii)
Coeliac disease
Malabsorption resulting in partial villous atrophy
Histological features:
1. Villous atrophy
2. Crypt hyperplasia (normal of V to C is 2:1)
3. AND ARCHITECTURAL CHANGE -> Increased intraepithelial lymphocytes (> 20/100 enterocytes)
Ix:
Antibodies:
• Endomysial Antibodies (best sen and spec)
• Tissue Transglutaminase Antibodies (IgA)
Duodenal Biopsies:
• ON gluten rich diet showing villous atrophy (gold standard)
• OFF gluten rich diet showing normal villi
DDx: Tropical sprue is another cause of malabsorption with very similar histology to coeliac disease
Cx: Increased risk of GIT cancers. MALTomas associated with coeliac disease are found in the duodenum. They are T cell lymphomas (NOTE: lymphomas in the stomach due to H. pylori are B cell lymphomas).
NOTE: the T cell response to gliadin in Coeliac disease is responsible for the damage to the villi. Crypt hyperplasia occurs in an attempt to regenerate the damaged villi so as a result the crypts take up a bigger proportion
Lymphocytic Duodenitis
This occurs when you have inflammatory changes (increased intraepithelial lymphocytes) without architectural changes
Many people with this condition either have coeliac disease or are going to develop coeliac disease
Coeliac presentation
T cell mediated autoimmune disease ( DQ2, DQ8 HLA status)
Gluten intolerance results in villous atrophy and malabsorption Presentation: young children (paeds) and Irish women (EMQs)
Symptoms (of malabsorption): steatorrhoea, abdo pain, bloating, n&v, ↓wt, fatigue, IDA, failure to thrive, rash (dermatitis herpetiformis)
