UPPER GI TRACT Flashcards
What anatomical structures contribute to the effectiveness of the lower oesophageal sphincter (LOS)?
- 3-4 cm oesophagus within abdomen
- Diaphragm surrounds LOS and contracts around sphincter
- Phrenoesophageal ligament
- Angle of His
What is the phrenoeophageal ligament?
Extension of inferior diaphragmatic fascia
Has superior and inferior limbs:
- Superior attaches lower oesophagus
- Inferior attaches cardia of stomach
Allows for individual movement of diaphragm for respiration and oesophagus for swallowing
What is the angle of His?
Acute angle between abdominal oesophagus and fundus of stomach at oesophageal junction
What are the stages of swallowing?
Oral phase:
- Chewing and saliva prepare bolus
- Both sphincters closed
Pharyngeal phase:
- UOS open, LOS opens by receptive relaxation reflex (vasovagal reflex)
Upper oesophageal phase:
- UOS closes
- Superior circular muscle rings contract and inferior rings dilate
- Sequential contractions of longitudinal muscle
Lower oesophageal phase:
- LOS closes as food passes through
How is oesophageal motility determined?
By measuring pressure at different points via manometry
Tube passed through nose to oesophagus
What pressure are peristaltic waves?
~ 40 mmHg
What is the resting pressure of the LOS?
~ 20 mmHg
What happens to pressure in LOS during receptive relaxation?
Decrease < 5 mmHg
What mediates receptive relaxation?
Inhibitory noncholinergic nonadrenergic (NCNA) neurone of myenteric plexus
What is an absence of stricture caused by?
Abnormal oesophageal contraction:
- Hypermotility - achalasia
- Hyopmotility - scleroderma
- Disordered coordination - corkscrew oesophagus
Failure of protective mechanisms for reflux:
- Gastro oesophageal reflux disease (GORD)
What is dysphagia?
Difficulty swallowing
Different types e.g. for solids/fluids, intermittent/progressive, precise/vague in appreciation
Localisation is important
What is odynophagia?
Pain on swallowing
What is regurgitation?
Return of oesophageal contents from above an obstruction
Can be functional or mechanical
What is reflux?
Passive return of gastroduodenal contents to the mouth
What is hypermotility also know as?
Achalasia
How does achalasia occur?
Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall. Causes decreased activity of inhibitory NCNA neurones
Describe the 2 types of achalasia
Primary - unknown aetiology
Secondary - diseases which cause oesophageal motor abnormalities similar to primary achalasia
What are some examples of secondary achalasia?
Chagas’ disease
Protozoa infection
Amyloid/Sarcoma/Eosinophilic oesophagitis
What is the proposed model of achalasia pathophysiology?
Environmental trigger Genetic predisposition Causing Non autoimmune inflammatory infiltrates Extracellular turnover/wound repair/fibrosis And Loss of immunological tolerance Apoptosis of neurones Humoral response
What occurs in achalasia?
Increased resting LOS pressure than normal because receptive relaxation sets in late and is too weak.
During the reflex phase pressure in the LOS is much higher than stomach so food can’t get through it
Swallowed food collects in oesophagus causing increased pressure and dilation.
Overtime the propagation of peristaltic waves cease
What are the symptoms of achalasia?
Weight loss
Dysphagia
Regurgitation
Pain
Could lead to oesophagitis, pneumonia and increases risk of oesophageal cancer
Why can achalasia lead to pneumonia?
Aspiration of stomach contents into lungs which can contain bacteria
By how much does the risk of oesophageal cancer increase in a patient with achalasia and why?
28 fold
Aspiration of stomach acid which can cause oesophageal metaplasia
Describe the onset of achalasia
Insidious onset with symptoms for years prior to seeking help
What are the treatments for achalasia?
Pneumatic dilation
Surgery: Heller’s myotomy, dor fundoplication
Describe how pneumatic dilation is carried out
Guide wire inserted and balloon put into LOS.
Balloon then inflated to expand the LOS and then removed. Can tear muscle fibres in some cases
What is the efficacy of pneumatic dilation?
71-90% of patients respond initially but many subsequently relapse
Describe a Heller’s myotomy
Continuous myotomy (muscle cut) of 6cm oesophagus and 3cm of stomach Vertical cut
Describe dor fundoplication
Anterior fundus folded over oesophagus and sutured to right side of myotomy
Surgical treatment for achalasia
What are the risks of surgery to treat achalasia
Oesophageal and gastric perforation
Division of splenic nerve
Splenic injury
What is scleroderma and what occurs?
Autoimmune disease causing hypomotility in early stages due to neuronal defects causing atrophy of oesophageal smooth muscle
Peristalsis in the distal portion ultimately ceases together
LOS resting pressure decreases
Gastroesophageal reflux disease develops
- Often associated with CREST syndrome
What is the treatment for scleroderma?
Exclude organic obstruction e.g. tumour
Improve force of peristalsis with prokinetics
If peristaltic failure occurs, usually irreversible
What is corkscrew oesophagus?
Diffuse oesophageal spasm with uncoordinated contractions
How can you identify corkscrew oesophagus?
Dysphagia and chest pain
Pressures around 400-500 mmHg
Marker hypertrophy of circular muscle
Barium dye shows corkscrew oesophagus
What is the treatment for corkscrew oesophagus?
May respond to forceful pneumatic dilation of cardia
Results not as predictable
Where are oesophageal perforations likely to occur?
Cricopharyngeal constriction
Aortic and bronchial constriction
Diaphragmatic/sphincter constriction
Places with pathological narrowing e.g. cancers, foreign bodies, physiological dysfunction
What are the aetiology (causes) of oesophageal perforation?
Iatrogenic (OGD) > 50% Spontaneous (Boerhaave's) - 15% Foreign body - 12% Trauma - 9% Intraoperative - 2% Malignant - 1%
When are iatrogenic oesophageal perforations more common?
In presence of diverticula or cancer
What is Boerhaave’s and what does it cause to occur?
Spontaneous sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure - rupture of oesophagus
Vomiting against a closed glottis
Left posterolateral aspect of distal oesophagus usually gives way
What is the incidence of Boerhaave’s?
3.1 per 1000000
What are some common foreign bodies which cause oesophageal perforation?
Disk batteries (electrical burns if embeds in mucosa) Magnets Sharp objects Dishwasher tablets Acid/Alkali
How does oesophageal perforation by trauma usually present?
Neck: usually penetrating
Thorax: usually blunt force
Dysphagia
Blood in saliva
Haematemesis
Surgical emphysema (air trapped under skin - crackling when you touch it)
What are some investigations that can be done for a patient suspected with oesophageal perforation?
Chest X ray
CT scan
Swallow (gastrograffin contrast)
OGD (Oesophago-Gastro-Duodenoscopy)
OGD should only be done when absolutely needed due to risk of perforation
What is the primary management of oesophageal perforation?
Surgical emergency (2x mortality if 24 hr delay diagnosis)
IV fluids Broad spectrum antibiotics/antifungals ITU/HDU level care Bloods Tertiary referral centre
What definitive managements of oesophageal perforation should be done?
Operative management should be default:
- Primary repair is optimal
- Oesophagectomy
Conservative management with covered metal stent only when very small perforation that hasn’t leaked
What are bodies protective mechanisms against reflux?
LOS usually closed as a barrier
Following reflux:
- Volume clearance (oesophageal peristalsis reflex)
- pH clearance (saliva buffers low pH)
- Epithelium (barrier)
What is LOS pressure increased by?
Acetylcholine Alpha-adrenergic agonists Hormones Protein-rich food Histamine High intra-abdominal pressure
What is LOS pressure decreased by?
Beta-adrenergic agonists Hormones Dopamine Nitric oxide PGI2 PGE2 Chocolate Acid gastric juice Fat Smoking
When might normal sporadic reflux occur?
Pressure on full stomach
Swallowing
Transient sphincter opening throughout day
What causes GORD?
Volume clearance - abnormal peristalsis
pH clearance - decreased saliva/buffering capability (smoking)
Decreased sphincter pressure
Increased transient sphincter opening (air/CO2 from fizzy drinks)
Hiatus hernia
Defective mucosal protective mechanism
What can GORD lead to?
- reflux oesophagitis
- epithelial metaplasia
- carcinoma
What is a sliding hiatus hernia?
Phrenoesophageal ligament gives way and part of stomach slides up past diaphragm where the LOS usually is
What is a rolling/paraoesophageal hiatus hernia?
Defect in diaphragm and portion of stomach slips up past the diaphragm via defect
What are some investigations that can be undertaken in a patient with GORD
OGD (exclude cancer, confirm oesophagitis/Barrett’s)
Oesophageal manometry
24hr oesophageal pH recording (frequency of reflux)
What are the treatments for GORD?
Lifestyle changes (smoking, weight loss...) PPIs
Surgical:
- Dilation peptic strictures
- Laparoscopic Nissen’s fundoplication
How does laparoscopic Nissen’s fundoplication work?
Hiatus is closed
Fundus wrapped around oesophagus to provide further reinforcement
What do the cardia and pyloric region of the stomach produce?
Mucus only
What do the body and fundus of the stomach produce?
Mucus, HCl, pepsinogen
What does the antrum of the stomach produce?
Gastrin
Name the different types of gastritis
Erosive and haemorrhagic gastritis
Nonerosive chronic gastritis
Atrophic gastritis
Reactive gastritis
What is the cause of erosive and haemorrhagic gastritis and what does it cause?
Numerous causes
Forms acute ulcers which can lead to reactive gastritis
What is nonerosive chronic gastritis?
Occurs in the antrum
Caused by Helicobacter pylori
Treat with antibiotics
What is atrophic gastritis and what does it lead to?
Occurs in fundus
Autoantibodies attacks parts/products of parietal cell
Parietal cell atrophy
Decreased acid secretion potentially causing cancer
Decreased IF secretion causing pernicious anemia
Name the causes of erosive and haemorrhagic gastritis
NSAIDs Alcohol Multi-organ failure Burns Trauma Ischaemia
Why might patients with nonerosive chronic gastritis also develop reactive gastritis?
Helicobacter pylori infection causes gastric and duodenal ulcers which in turn can cause this
Which 2 types of gastritis can cause epithelial metaplasia and thus carcinoma?
Reactive gastritis
Atrophic gastritis
What stimulates the release of gastric secretion?
Ach of vagal PNS fibres
Endocrine gastrin
Paracrine histamine
What inhibits the release of gastric secretion?
Endocrine secretin
Paracrine somatostatin
Paracrine/autocrine PGs, TGF-alpha, adenosine
How is the stomach mucosal adapted to protect against the acidic environment and thus gastric ulcer formation?
Mucus film
HCO3- secretion to buffer (prostaglandins propagate this)
Epithelial barrier
Mucosal blood perfusion (takes away any H+ that does make it through)
What mechanisms are in place to repair epithelial damage/wound healing due to ulcer?
Migration - adjacent epithelial cells flatten to close gap via sideward migration along BM
Cell growth - stimulated by EGF, TGF-alpha, IGF-1, GRP and gastrin
Acute wound healing:
- BM destroyed - leukocytes/macrophages attracted and phagocytose necrotic cells, angiogenesis…
- Epithelial closure by restitution and cell division
What are the gastric outcomes of a H. Pylori infection?
Asymptomatic/chronic gastritis > 80%
Chronic atrophic gastritis/intestinal metaplasia 15-20%
Gastric/duodenal ulcer 15-20%
Gastric cancer/MALT lymphoma < 1%
What are the treatments for ulcers?
Medical:
- PPI/H2 blocker
- Antibiotics for 7-14 days
Elective surgery (rare - most heal in 12 weeks)
What do you do if ulcer hasn’t healed after 12 weeks?
Change medication and observe for another 12 weeks
Check serum gastrin
OGD for biopsy of all 4 quadrants of ulcer if still refractory to rule out malignancy
List negatives for surgery to treat an ulcer
Complications:
- Haemorrhage
- Obstruction
- Perforation
Intractability
Continuous requirement of steroid/NSAID therapy
