GI Pathology Flashcards
How to differentiate between mechanical & functional oesophageal obstruction clinically?
Onset, difficulty initiating, type of food easier to swallow, associated symptoms
Intramural mechanical oesophageal obstruction (3)
atresia, stricture, webs / rings
Where does oesophageal atresia most likely occur?
near tracheal bifurcation
Which is the most common type of tracheoesophageal fistula?
type III
Presentations of oesophageal atresia
regurgitation, severe fluid / electrolyte imbalance, aspiration pneumonia
Causes of oesophageal stricture (4)
Benign: GERD, injury, idiopathic
Malignant: CA oesophagus
Histology of benign oesophageal stricture
fibrosis, atrophy of muscularis propria
Histology of oesophageal webs / rings
fibrovascular connective tissue covered by epithelium
Plummer-Vinson syndrome (epidemiology, presentations, complication)
female >40y
Presentations: IDA + dysphagia + oesophageal web
Complication: OA oesophagus (SCC)
Oesophageal motility disorders & their barium swallow signs (3)
achalasia (bird’s beak), diffuse oesophageal spasm (corkscrew), hypercontractile oesophagus (nutcracker)
Triad of achalasia
aperistalsis + ↑ resting LES tone + poor relaxation of LES during swallowing
Aetiology (1+2) & pathogenesis of achalasia
Primary or Secondary (Chagas disease, Allgrove syndrome)
Pathogenesis: destruction of inhibitory neurons in myenteric plexus
Complications of achalasia (4)
infection, lower oesophageal diverticulum, aspiration pneumonia, OA oesophagus (SCC)
Types of functional oesophageal obstruction (3)
oesophageal motility disorders (EDM), neurological disorders, connective tissue diseases
Pathogenesis of oesophageal variceal bleeding
portal hypertension –> backflow of portal blood –> dilation of submucosal venous plexus in distal oesophagus –> esophageal varices rupture –> massive haematemesis
Oesophageal lacerations (2) & pathogenesis
Mallory-Weiss syndrome (excessive alcohol intake –> retching), Boerhaave syndrome (failed relaxation of glottis while vomiting –> ↑ intraluminal pressure –> perforation)
MC infectious oesophagitis
Candida oesophagitis
MC oesophagitis
Reflux oesophagitis
Normal protective mechanisms of oesophagus against reflux (7)
oesophageal peristalsis, LES, angle of his, diaphragm, pressure difference, gastric rugae, gastric emptying
Presentations of GERD
heart burn, regurgitation, dysphagia
Histology of reflux oesophagitis
eosinophilic infiltration, intercellular oedema, elongation of stromal papillae
Complications of GERD (3)
minor UGIB, stricture, Barrett oesophagus
Diagnosis of eosinophilic oesophagitis (2)
OGD: feline oesophagus
Histology: large amount of eosinophils
What is Barrett oesophagus?
metaplastic change of distal squamous epithelium into columnar epithelium
Diagnosis of Barrett oesophagus
OGD: proximal migration of squamocolumnar junction, salmon-coloured mucosa [1cm above OGJ]
Histology: goblet cells, columnar cells
CA oesophagus epidemiology
60~70y male
Presentations of CA oesophagus (10)
- painless progressive dysphagia
- odynophagia
- regurgitation
- ## UGIB
- hoarseness of voice
- Horner’s syndrome
- ## respiratory symptoms
- metastasis (e.g. Virchow’s node)
- HHM (hypercalcemia)
- constitutional symptoms
Is prognosis of CA oesophagus good?
poor
OA oesophagus: compare SCC & ADC
SCC (90%) [middle 1/3] associated with intake
ADC (10%) [distal 1/3] associated with reflux
Risk factors for oesophageal SCC
Lifestyle: smoking, alcohol, hot drink
Oesophageal disorders: achalasia, Plummer-Vinson syndrome
Genetic: tylosis
Erosion vs ulcer
Erosion = loss of epithelium
Ulcer = loss of mucosa +/- deeper tissues
Pathogenesis of peptic ulcer disease
imbalance of mucosal defence and attack –> (chronic) gastritis –> PUD
Risk factors for peptic ulcer disease
Infection: H. pylori
Drugs: NSAIDs, steroid, chemotherapy
Lifestyle: smoking, alcohol, caffeine, stress
Severe stress: Curling ulcer, Cushing ulcer
Iatrogenic: NG tube, OGD
Others: Zollinger Ellison syndrome, pernicious anaemia
Where is PUD caused by pernicious anaemia most commonly found in?
gastric body
Pathogenesis of gastritis from pernicious anaemia
antibodies to parietal cells –> loss of H/K ATPase –> loss of gastric acid –> ↑ gastrin
Curling ulcer (most common location & pathogenesis)
[proximal duodenum] burn –> ↓ plasma vol. –> ischaemia & necrosis of gastric mucosa
Cushing ulcer (most common location & pathogenesis)
[stomach, duodenum, oesophagus] intracranial disease –> direct stimulation of vagal nerve –> ↑ gastric acid secretion
MC location for duodenal ulcer
D1
MC location for gastric ulcer
lesser curvature
Differentiate presentations between duodenal and gastric ulcers
DU: pain relieved after eating
GU: pain exacerbated after eating
Differentiate biopsy needs between duodenal and gastric ulcers
DU: antrum only
GU: antrum and ulcer edge, need rescope
Gross morphology of PUD
- sharply punched out, slightly elevated around edges
- clean base
Histology of PUD
necrotic debris, inflammation, granulation tissue, fibrosis
Histology of pernicious anaemia
G cell hyperplasia, mucosal atrophy
Which is the most common gastric polyp?
hyperplastic polyps
Which gastric polyp is associated with PPI use?
Fundic gland polyps
Types of gastric polyps (4)
hyperplastic, fundic gland, inflammatory, adenomatous
Types of gastric neoplasm and percentages
adenocarcinoma (90%), lymphoma (5%), GIST (2%), carcinoid tumour, metastasis
Risk factors for gastric adenocarcinoma
Lifestyle: smoking, alcohol, smoked food, nitrosamines
Pre-existing conditions: adenoma, H. pylori infection, pernicious anaemia
Genetics: hereditary diffuse gastric cancer, HNPCC, FAP, P-J syndrome
Gene mutation for hereditary diffuse gastric cancer
E-cadherin
Classification of gastric adenocarcionoma
Borrmann (endoscopic), Lauren (histologic)
Borrmann classification (4 types)
Type 1 (polypoid), Type 2 (fungating / ulcerative), Type 3 (ulcerative infiltrative), Type 4 (diffuse infiltrative)
Which is the most common gastric adenocarcinoma according to Borrmann classification?
Type 3
Lauren classification (types)
intestinal type, diffuse type, mixed type
Gastric adenocarcinoma: intestinal type vs diffuse type (prevalence, HER2, prognosis, risk factors, histology)
- intestinal type is more common, more HER2 amplification, better prognosis
- risk factors: intestinal type (all except FHx), diffuse type (HDGC)
- histology: intestinal type (well-differentiated, cohesive cells), diffuse type (poorly-differentiated, discohesive cells, Signet ring cells)
Signet ring cells
Diffuse type gastric adenocarcinoma
Transcoelomic metastasis to ovaries from stomach
Krukenberg tumour
Early vs Advanced gastric cancer
EGC: limited to mucosa / submucosa (T1) (95% 5-year OS)
AGC: infiltrative into muscularis propria (>= T2) (50% 5-year OS)
Treatment for gastric lymphoma
H. pylori eradication therapy
Classification of gastric lymphoma (2)
Low grade: MALToma
High grade: Diffuse large B cell lymphoma
GIST location
stomach (50%) > small bowel > large bowel
Origin cells of GIST
intestinal cell of Cajal
Genetic mutations for GIST
c-KIT (95%), PDGFRA
Gross morphology of GIST
dumbbell shaped mass with homogenous pink surface
Histology for GIST
spindle cells with elongated nuclei, c-KIT mutation on IHC
Prognosis model for GIST (parameters, levels)
AFIP model
Parameters: location, size, mitotic index
Levels: low, moderate, high
Management for GIST
surgical resection, TKI: imatinib
Types of non-neoplastic intestinal polyps (3)
hyperplastic, inflammatory, hamartomatous
Most common intestinal polyps
hyperplastic polyps
MC site for hyperplastic polyps
sigmoid colon
What are inflammatory polyps and the association?
mucosal overgrowth secondary to chronic recurrent mucosal injury & regeneration
(Association: IBD, solitary rectal ulcer)
What is hamartomatous polyps?
disorganised overgrowth of tissue indigenous to the site
Types of hamartomatous polyps (4)
- Juvenile polyps
- Peutz-Jeghers syndrome
- Cowden syndrome
- Cronkhite-Canada syndrome
Where is juvenile polyps mostly found?
rectum
Genes for juvenile polyposis syndrome (2)
SMAD4, DPC4 (AD)
Histology for juvenile polyps
cystically dilated glands, inflamed oedematous stroma
Gene for Peutz-Jeghers syndrome
STK11 (AD)
Sites for Peutz-Jeghers syndrome
small intestine > colon > stomach
Presentations of Peutz-Jeghers syndrome
hamartomatous polyps, mucocutaneous hyperpigentation
Histology of Peutz-Jeghers syndrome
Christmas tree appearance / smooth muscle cores
Gene for Cowden syndrome
PTEN (AD)
Which cancers are associated with Cowden syndrome? (4)
Thyroid cancer, Skin lesions, Breast cancer, CRC