Upper GI Tract Flashcards
Oesophagus anatomical landmark
Start - C5
End - T10
Oesophageal motility determined by
Pressure measurements
Manometry
Peristaltic waves
~40 mmHg
LOS resting pressure
~20 mmHg
Decreases by more then 5 mmHg during receptive relaxation
Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus
Disorders of oesophagus
Absence of stricture
Caused by
- abnormal oesophageal contraction - hypermotility, hypomotility, disordered coordination
- failure of protective mechanism for reflux - gastroesophageal reflux disease (GORD)
Dysphagia
Difficulty in swallowing
-localisation is important - cricopharyngeal sphincter or distal
Types of dysphagia
For solids or fluids
Intermittent or progressive
Precise or vague in appreciation
Odynophagia
Pain on swallowing
Regurgitation
Return of oesophageal contents from above an obstruction - may be functional or mechanical
Reflux
Passive return of gastroduodenal contents to mouth
Achalasia pathophysiology
Hypermotility
Loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
Decreased activity of inhibitory NCNA neurones
Primary and secondary achalasia
-Aetiology unknown
-diseases causing oesophageal motor abnormalities similar to primary achalasia
—Chagas’ disease
—Protozoa infection
—amyloid/sarcoma/eosinophilic oesophagitis
Achalasia effects
Increased resting pressure of LOS
Receptive relaxation sets in late and is too weak
-during reflex phase pressure in LOS is markedly higher than stomach
Swallowed food collects in oesophagus causing increased pressure throughout with dilation of oesophagus
Propagation of peristaltic waves cease
Achalasia disease course
Insidious onset - symptoms for years prior to seeking help
Without treatment - progressive oesophageal dilation of oesophagus
Achalasia risk of oesophageal cancer
Increased 28 fold
Achalasia treatment
Pneumatic dilation
Weakens LOS by circumferential stretching and in some cases, tearing of its muscle fibres
Efficacy - 71-90% but many relapse
Surgery
Heller’s myotomy - continuous myotomy for 6cm on oesophagus and 3cm onto stomach
Dor fundoplication - anterior Fundus folded over oesophagus and sutured to right side of myotomy
Treatment risks
Surgery
- oesophageal and gastric perforation 10-16%
- division of vagus nerve - rare
- splenic injury - 1-5%
Scleroderma
Hypomotility
Autoimmune
Neuronal defects - atrophy of smooth muscle of oesophagus
Peristalsis in the distal portion ultimately ceases altogether
Decreased resting pressure of LOS
Gastroesophageal reflux disease develops - often associated with CREST syndrome
Scleroderma treatment
Exclude organic obstruction
Improve force of peristalsis with prokinetics (cisapride)
Once peristalsis failure occurs - usually irreversible
Corkscrew oesophagus
Disordered coordination Diffuse oesophageal spams Incoordinate contractions - dysphagia and chest pain Pressures of 400-500 mmHg Marked hypertrophy of circular muscle Corkscrew oesophagus on Barium
Corkscrew oesophagus treatment
May respond to forceful PD of cardia
Results not as predictable as achalasia
Anatomy of oesophageal perforation
3x areas of anatomical construction - cricopharyngeal, aortic and bronchial, diaphragmatic and ‘sphincter’ Pathological narrowing (cancer, foreign body, physiological dysfunction)
Iatrogenic oesophageal perforation
Usually at OGD - more common in presence of diverticula or cancer
Boerhaave’s oesophageal perforation
Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
-vomiting against closed glottis
Usually at left posterolateral aspect of distal oesophagus
Foreign body oesophageal perforation
Disk batteries growing problem - cause electrical burns if embeds in mucosa Magnets Sharp objects Dishwater tablets Acid/alkali
Trauma oesophageal perforation
Neck - penetrating
Thorax - blunt force
Can be difficult to diagnose
- dysphagia
- blood in saliva
- haematemesis
- surgical emphysema
Oesophageal perforation presentation
Pain 95%
Fever 80%
Dysphagia 70%
Emphysema 35%
Oesophageal perforation investigations
Chest x ray
CT
Swallowing gastrograffin
OGD
Oesophageal perforation initial management
Surgical emergency - 2x mortality if 24h delay in diagnosis
Initial management -Nil by mouth -IV fluids -broad spectrum antibiotic and antifungal ITU/HDU level care Bloods (including G&S) Tertiary referral centre
Oesophageal perforation conservative management
Covered metal stent
Oesophageal perforation definitive management
Operative management is default
Primary repair is optimal
Oesophagectomy - definitive solution
Stomach mechanism against reflux
LOS closed as barrier against reflux of harmful gastric juice (pepsin and HCl)
Sporadic reflux is normal
- pressure on full stomach
- swallowing
- transient sphincter opening
Mechanisms protect following reflux
- volume clearance - oesophageal peristalsis reflex
- pH clearance - saliva
- epithelium - barrier properties
LOS pressure increased by
Acetylcholine
Hormones
Prostaglandin
Inhibits reflux
LOS pressure decreased by
Eating fat
Smoking
Nitrous oxide
Promotes reflux
Failure of protective mechanism against reflux
GORD
Decreased sphincter pressure
Increased sphincter opening
Decreased volume clearance - from abnormal peristalsis
Slowed pH clearance - from decreased saliva production or decreased buffering capacity of saliva
Hiatus hernia
Defective mucosal protective mechanism
Could lead to epithelial metaplasia and then carcinoma
Sliding hiatus hernia
Peritoneal reflection
Ligament holding stomach gives way
Stomach slides up to chest
Rolling hiatus hernia
Portion of stomach slips up the side
Can be strangulated - blood flow compromised
Surgical emergency
GORD investigation
OGD to exclude cancer. Oesophagitis, peptic stricture and Barretts oesophagus confirm
Oesophageal manometry
24 hour oesophageal pH recording
GORD treatment
Medical
- lifestyle changes
- PPIs
Surgical
- dilation peptic stricture
- laparoscopic Nissen’s fundoplication (definitive)
Stomach functions
Break food into smaller particles (acids and pepsin)
Holds food, releasing it in controlled steady rate into duodenum
Kills parasites and certain bacteria
Stomach productions
Cardia and pyloric region - mucus only
Body and Fundus - mucus, HCl, pepsinogen
Antrum - gastrin
Erosive and haemorrhagic gastritis
Numerous causes (NSAIDs, stress, alcohol) Commonest cause of acute ulcer - gastric bleeding and perforation
Nonerosive chronic active gastritis
Antrum
Helicobacter pylori - triple treatment with amoxicillin, clarithromycin, pantoprazole for one to two weeks
Increased gastrin - increased acid secretion
Can lead to reactive gastritis
Atrophic (fundal gland) gastritis
Fundus
Autoantibodies vs parts and products of parietal cells like gastrin receptor, carbonic anhydrase intrinsic factor
Decreased acid secretion lead to G cell hyperplasia and epithelial metaplasia - carcinoma, and also increased gastrin and ECL cell hyperplasia - carcinoid
Decreased intrinsic factor leads to decreased cobalamine absorption and deficiency
Parietal cell secretion
Hydrogen ions
Chief cells secretion
Pepsinogen
Gastric secretion stimulation
Neural
-acetylcholine - postganglionic transmitter of a gal parasympathetic fibres
Endocrine
-gastrin - G cells of antrum
Paracrine
-histamine - ECL cells and mast cells of gastric wall
Gastric secretion inhibition
Endocrine
-secretin - small intestine
Paracrine
-somatostatin - SIH
Paracrine and aurocrine
- Prostaglandins - PGE2, PGI2
- adenosine
- TGF-alpha
Mucosal protection
Mucus film protects against pepsin and hydrogen ion
Epithelial cell produce bicarbonates (propagated by prostaglandins) which buffers hydrogen ions
Epithelial barrier and tight junction prevent penetration of hydrogen ions
Good mucosal blood perfusion so that hydrogen ions get taken away if they do get through
Mechanisms repairing epithelial defects
Migration
-adjacent epithelial cells flatten to close gap via sideward migration along basement membrane
Gap closed by cell growth
-stimulated by EGF, TGF-alpha, IGF-1, GRP and gastrin
Acute wound healing
- basement membrane destroyed - attraction of leukocytes and macrophages, phagocytosis of necrotic cells, angiogenesis, regeneration of ECM after repair of basement membrane
- epithelial closure by restitution and cell division
Ulcer formation
Due to increased chemical aggression or barrier function disturbed
Helicobacter pylori - gastritis - barrier function disturbed Increased secretion of gastric juice Decreased bicarbonate secretion Decreased cell formation Decreased blood perfusion
NSAIDs and smoking - decreased prostaglandin synthesis - decreased mucosal protection - barrier function disturbed
Psychogenic components and gastrinoma - increased hydrogen and pepsinogen secretion - chemical aggression
Outcomes of Helicobacter pylori
> 80% asymptomatic or chronic gastritis
15-20% chronic atrophic gastritis or intestinal metaplasia and gastric or duodenal ulcers
<1% gastric cancer or MALT lymphoma
Ulcer treatment
Primarily medical
- PPI or H2 blocker
- amoxicillin, clarithromycin, pantaprazole for one to two weeks
Elective surgery
- rare - most heal within 12 weeks
- if not, change medication, observe additional 12 weeks
- check serum gastrin (natural G cell hyperplasia or gastrinoma -Zollinger-Ellison syndrome)
- OGD - biopsy all 4 quadrants of ulcer (rule out malignant)
Ulcer surgery indications
Intractability after medical therapy Relative - continuous requirement of steroid therapy/NSAIDs Complications -haemorrhage -obstruction -perforation
