Dunedin-Gastro Flashcards
Which high resolution manometry shows features consistent with achalasia?
A
What is achalasia?
Impaired lower oesophageal sphincter relaxation and peristalsis in distal oesophagus.
Due to myenteric plexus inflammation
Experience dysphasia for solids and liquids
Barium swallow- birds beak
What is the proposed model for the development of achalasia?
1) Viral trigger/ HLA Class II/ Mutations and SNPs
2) extracellular matrix turnover and wound repair, inflammatory infiltrate, humeral response (myenteric antibodies)
3) myenteric plexitis, ganglion cell loss, fibrosis, impaired LES
What is the treatment options for achalasia?
Surgical: Pneumatic dilation (recommended initial therapy) , Peroral endoscopic myotomy (POEM), Heller myotomy (HM) with Dor fundoplication. Complication: GERD. Esophagectomy
Medical: botulinic toxin injection, CCB, isosorbide dinitrate
Botulinum injection causes sub-mucosal fibrosis which can interfere with future surgical therapies
What is the clinical presentation of eosinophilic oesophagitis?
younger patient M>F
food bolus obstruction
chronić dysphagia solids >liquids
refractory GORD
chronic immune mediated condition related to food
infiltration of eosinophils into oesophageal mucosa >15/hpf
chronic inflammation leads to deposition of sub epithelial fibrous tissue
What is the management of eosinophilic oeseophagitis?
Double dose PPI for 8 weeks.
if not resolved:
*topical steroids 6-12 weeks (swallowed fluticasone propionate, swallowed viscous budesonide)
*dietary therapy: targeted diet, six-food elimination diet, elemental diet
Alternative therapies: endoscopic dilation in case of stenosis, prednisone, some role of immunomodulators (dupulimab) or antiallergic agents
What is included in the 6-food elimination diet?
Milk, soy, wheat, egg, nut and fish/seafood
What is the histology of Barrett’s oesophagus?
Stratified squamous epithelium replaced by cardiac type mucus secreting columnar epithelium +/- intestinal metaplasia
What is the rate of Barrett’s oesophagus progression to oesophageal adenocarcioma? and is there anything to slow/slow progression?
No dysplasia –> 0.12%
Low grade dysplasia –> 1.8%
high grade dysplasia –> 10%
if have GORD symptoms at least once a week, the risk of oesophageal adenocarcinoma is markedly increased 7.7 vs 1
Stop/slow progression:
- PPI, PPI + aspirin (less evidence)
- surgical therapy not more effective than PPI
- low grade dysplasia confirmed on 2 occasional 6 months apart by two pathologist- can trial endoscopic radiofrequency ablation.
- high grade dysplasia: oesophagectomy vs endoscopic resection
Describe the pattern of development of oesophageal adenocarcinoma compared to CRC?
oesophageal adenocarcinoma: develops in non-linear pattern over 4 years
CRC: develops in linear pattern over 10 years
Discuss screening programs for Barrett oesophagus
1) Not recommended in general population
2) consider in those with chronic reflux and multiple risk factors (Age >50 years, male sex, white race, central obesity, smoking use, first-degree relative with BE or oesophageal adenocarcinoma and presence of hiatal hernia)
3) not usually in men/women <50 with chronic GORD
Evidence for Barrett’s surveillance is weak However post-ablation should do annual gastroscopy for 5 years
What is the role of PPI initiation prior to endoscopic diagnosis in upper GI bleeding?
does NOT reduce mortality, the need for surgery, or the proportion of patients with high risk stigmata
DOES reduce need for endoscopic intervention
What is the relationship between H.Pylori and ITP?
H.Pylori can cause ITP as anti-cage antibodies cross-react with platelet antigens
Is there a good use of tranxemic acid in GI bleeding?
not really
Describe the classification of peptic ulcers
Forest 1 and 2A, collective risk of bleeding is 50%
