Oesophagus Flashcards
What is the structure of the oesophagus?
- Muscosa- non ketratinising stratified squamous epithelium
- Submucosa - glands are connected to lumen by squamous lined ducts
- Muscularis propria - inner circular muscle, outer longitudinal muscle (smooth), myenteric plexus
- Adventitia
- Squamocolumnar junction/Z-line
- Gastrooesophageal junction - marked by rugal folds.
Name some benign incidental findings of the oesophagus
- Gastric inlet patch - heterotopic gastric mucosa (fundic/oxyntic type admixed with mucous glands) in upper 1/3 of oesophagus. Can resemble malignancy radiologically.
- Pancreatic metaplasia/heterotopia- benign pancreatic acini and ducts
- Heterotopic sebaceous gland.
- Glycogenic acanthosis- epithelial hyperplasia, abundent glycogen accumulation in superficial squamous cells. endoscopic appearance: white plaques
extensive glycogenic acanthosis - could be linked to Cowden Syndrome.
Describe Achalasia
- Functional disorder
- Lack of progressive peristalsis, partial/incomplete relaxation of LES
- Issue is with circular layer of muscularis propria
- T Cell mediated destruction, or complete absence of myenteric ganglion cells in lower third of oesophagus
- Myenteric plexus inflammation/damage -> loss of inhibitory ganglion cells -> neurotransmitter inhibition is decreased (nitric oxide), imbalance of acetylcholine and nitric oxide -> Achalasia
- bird beak on barium swallow
Risk of:
* Barrett’s
* Candida infection
* GERD
* Lower Oesophageal diverticula
* Pepic ulceration
* Stricture
What are the causes of Achalasia?
Primary - idiopathic
Secondary
Diabetes
Malignancy
Chagas Disease
Amyloidosis
Sarcoidosis
Neurofibromatosis
Eosinophilic Gastroenteritis
MEN 2B
Anderson-Fabry Disease
Juvenile Sjogren’s syndrome
What is the treatment of Achalasia?
- Laparoscopic myotomy
- Pneumatic balloon dilation
- Botulinum neurotoxin (BOTOX) injection - inhibits contraction promotic cholinergic neurons
Describe Oesophageal Rings
- AKA Schatzki rings
- Circumferential, thicker
- Include mucosa, submucosa, occasionally hypertrophic muscularis propria
A RING: distal oesophagus - above GOJ, covered in squamous mucosa
B RING: at squamocolumnar junction of lower oesophagus, may have gastric cardia-type mucosa on under-surface
Describe Oesophageal Webs
- Semi-Circumferential lesions
- Fibrovascular connective tissue and overlying epithelium
Seen in women >40
May be associated with GERD, graft vs host, blistering skin diseases
Forms part of Plummer-Vinson Syndrome
* Iron deficient anaemia
* Glossitis
* Cheilosis
Plummer-Vinson Syndrome
- AKA Paterson-Brown-Kelly syndrome
TRIAD:
* IDA
* Dysphagia
* Cervical oesophageal web
Premalignant disease
Describe GERD
- Gastro-oesophageal reflux disease
- Endoscopy: varies - normal to erythema/hyperemia to erosion/ulceration
- Micro: spongiosis, basal cell hyperplasia, elongation of vascular papilla, scattered inflammatory cells (eosinophils, lymphocytes, neutrophils
- Usually more prominent in distal aspect near GEJ
Describe Candida Oeophagitis
- Endoscopy: white plaques, scraped off to reveal erythematous/ulcerated underlying mucosa
- Micro: fungal pseudohyphae and budding yeast, squamous debris, active oesophagitis
- Stains: GMS (Grocotts), PAS
- Treat with Fluconazole
Describe HSV Oesophagitis
- Endoscopy: shallow, punched out ulcers, necrotic exudate
Biopsy taken from ulcer edge:
* Acantholysis
* Multinucleated squamous cells - steel blue nuclei, Cowdry type A inclusions (dense, eosinophillic, intranuclear).
- viral cytopathic effects in epithelial cells - ground glass nuclei
*** the 3 Ms **- margination of chromatin, multinucleation, and nuclear molding
Tests:
HSV1 and HSV2 IHC stain
PCR for HSV DNA
ISH
Treatment:
Acyclovir in immunosuppressed
Self-limited in immunocompetent individuals
Describe CMV Oesophagitis
- Common in patients with AIDS
- Endoscopy: erythema, erosions, ulceration - non specific ulcers
- Viral cytopathic effects in mesenchymal cells - enlarged cells with nucleomegaly and inclusions
- Owls -eye intranuclear inclusions and granular intracytoplasmic inclusions
Test:
CMV immunostain
ISH
Describe pill/medicine-induced Oesophagitis
- Endoscopy: ulceration
- Inflammatory exudate (neutrophils), polarisable foreign material/pill filler
- Microcrystalline cellulose - refractile, transparent
- Crospovidone - pink/purple
Describe eosinophilic oesophagitis
- Endoscopy: concentric rings/linear furrows - trachealisation/felinization
- white plaques/exudates
- micro: intraepithelial eosimophils (>15 per hpf), eosinophilic microabscesses, superficial concentrations of eosinophils with degranulation and surface desquamation
- basal cell hyperplasia, oedema. elongated papillae, lamina propria fibrosis.
immune/antigen driven - type 2 helper t-cell mediated (Th2)
clinicopathlogical diagnosis:
* clinical features - dysphagia, food impaction, feeding intolerance
* endoscopic appearance
* >15 intraepithelial cells per hpf
* exclusion of other causes of eosinophilia
Association with ectopic triad - allergies, asthma, eczema
Often worse proximally
Treat with PPI for symptoms and corticosteroids
Describe Oesophagitis Dessicans Superficialis
- Sloughing Oesophagitis
- Endoscopy: white plaques of peeling and sloughing epithelium
- two tone appearence - superficial hypereosinophilic/necrotic epithelium with parakeratosis and underlying viable uninflamed/minimally inflamed deeper layers
oedema and vacuolisation of interface will eventually cause splitting of squamous epithelium
associated with medications, autoimmune bullous dermatoses, thermal/chemical injury, heavy smoking, alcohol and having multiple comorbidities.
Describe Lymphocytic Oesophagitis
- Endoscopy: may mimic oesinophilic esophagitis - rings/furrows/white plaques
- increased intraepithelial lymphocytes - concentrated around dermal papillae
- intracellular oedema, dyskeratotic epithelial vells
associated with:
* GERD
* Crohn’s
* Coeliac
* achalasia and dysmotility
* lichen planus (of oesophagus)
* graft vs host
* common variable immunodeficiency
Describe Barrett’s Oesophagus
- extension of salmon-coloured mucosa into the oesophagus extending >1cm prox to the GEJ.
- Intestinal metaplasia (goblet cells, ACID MUCIN) - seen with Alcian-Blue/PAS
- True goblet cells - rounded/ovoid, blue tinged cytoplasmic mucin, eccentric nucleus
- Incomplete IM: only goblet cells with mucin are present
- Complete IM: goblet cells and brush border present, paneth cells can be seen
British definition doesnt rely on IM, unlike American.
But needs both endoscopic and histological correlation
- SHORT segment: <3cm
- LONG segment: >3cm
SEATTLE protocol for biopsies:
* four quadrant biopsies
* taken every 2cm through Barrett’s segment
Dysplasia needs to be double reported
What are the risk factors for BE?
- Chronic GERD
- Male
- Caucasian
- Central obesity
- Smoking
- Age >50
- Lack of nonsteroidal anti inflammatory agent use
- Lack of PPI use
- Lack of statin use
Describe the pathgenesis of BE
- Chronic GERD induces tissue damage
- Upregulation of columnar transcription factors (SOX9)
- Induces columnar differentiation
- Upregulation of intestinal differentiation factors (CDX2)
- Intestinal metplasia
- Molecular alterations
- Low-grade dysplasia
- TP53, DNA aneuploidy
- High-grade dysplasia and carcinoma
Negative for dysplasia
Polarity seen in 4 lines:
* apical neutral mucin cap
* base of mucin cap
* eosinophilic cytoplasm below the mucin
* row of nuclei
Endoscopic surveillance interval:** 3-5 years**
Indefinite for dysplasia
Used if unsure if reactive vs neoplastic
ie - inflammation/ulceration/technical artifacts/diathermy
Treat for GERD and repeat biopsy in 3-6 months
Low grade dysplasia
- Adenoma-like or intestinal type
- Cytological abnormality, little/no architectural complexity
- Nuclear enlargement
- Hyperchromasia
- Retained nuclear polarity
- Both strong or absent (null phenotype) p53 staining considered significant
- AMACR and **IMP3 **sometimes useful
Findings extend to surface and often show abrupt transition point from non-dyplastic to dysplastic area
- Manage with endoscopic mucosal ablation
- endoscopic surveillance every 12 months an acceptable alternative
High grade dysplasia
- greater degree of cytological atypia
- Often with architectural abnormalities
- No surface maturation
- Crowded crypts with variable size and shape
What are endoscopy timelines in Barretts?
- Just Squamous epithelium - ?sampling error - Repeat
Barretts
* <3cm, gastric metaplasia –> repeat –> if same, consider discharge
* <3cm, IM –> repeat OGD every 3 to 5 years
* >3cm –> repeat OGD every 2 to 3 years
Dysplasia
* Indefinite –> repeat OGD in 6 months with max acide suppression
* Low grade –> OGD every 6 months until 2 consecutive non-dysplastic –> follow Barratts flowchart
* High grade –> MDT discussion –> Therapeutic intervention