Upper GI tract Flashcards
At what vertebrae does the trachea start and end?
C5 to T4
Where does the diaphragm sit?
T10
What is Stage 0 of swallowing?
Oral Phase
- chewing and saliva prepare bolus
- both oesophageal sphincters constricted
What is Stage 1 of swallowing?
Pharyngeal Phase
- pharyngeal musculature guides bolus towards the oesophagus
- upper oesophageal sphincter opens reflexively
- lower oesophageal sphincter opens due to vasovagal reflex (receptive relaxation reflex)
What is Stage 2 of swallowing?
Upper Oesophageal Phase
- upper sphincter closes
- superior circular muscles contract while inferior rings dilate
- sequential contractions of longitudinal muscle
What is Stage 3 of swallowing?
Lower Oesophageal Phase
- lower sphincter closes as food passes through
How is oesophageal motility measured?
pressure measurements (manometry)
What is the approximate pressure measurement of peristaltic waves?
around 40mmHg
What is the lower oesophageal sphincter’s resting pressure?
around 20 mmHg
What is the approximate change in the oesophageal sphincter’s pressure during receptive relaxation?
decreases to <5mmHg
What is the lower oesophageal sphincter mediated by?
inhibitory noncholinergic nonadrenergic (NCNA) neurons of the myenteric plexus
What are functional disorders of the oesophagus in the absence of a stricture caused by?
- abnormal oesophageal contraction (hyper-motility, hypo-motility, disordered co-ordination)
- failure of protective mechanisms for reflux (GORD)
What are the different types of dysphagia?
- solids or fluids
- intermittent or progressive
- precise or vague
What is important when someone is complaining of dysphagia?
localisation
- cricopharyngeal sphincter or distal
What is odynophagia?
pain on swallowing
What is regurgitation?
return of oesophageal contents from above an obstruction (functional or mechanical)
What may cause mechanical regurgitation?
obstructions eg: tumours
What is reflux?
passive return of gastroduodenal contents to the mouth
What is the biological characteristics of Achalasia?
- loss of ganglion cells in myenteric plexus in the lower oesophageal sphincter wall
- leads to decreased activity of inhibitory NCNA neurones
What is Achalasia?
- the absence of peristalsis, and impaired relaxation of the lower oesophageal sphincter
- progressive cause of dysphagia
- hyper-motility disorder
What causes primary achalasia?
unknown aetiology
What causes secondary achalasia?
diseases that cause similar oesophageal motor abnormalities
- Chagas’ Disease
- Protozoa Infection
- Anyloid/Sarcoma/Eosinophilic Oesophagitis
What happens in the development of Achalasia?
- increased resting pressure of the lower oesophageal sphincter
- receptive relaxation is inadequate in the LOS
- pressure in LOS is much higher than the stomach, so food does not pass through
- swallowed food contents collects in the oesophagus
- causes increased pressure and dilation of the oesophagus
- peristalsis stops
What are the symptoms of Achalasia?
- weight loss
- dysphagia
- regurgitation
- oesophagitis
- pneumonia due to aspiration
Is Achalasia a disorder of hyper or hypomotility?
hypermotility
What is the course of Achalasia?
- insidious onset (symptoms for years before help)
- without treatment leads to progressive oesophageal dilation
What does Achalasia predispose you to?
oesophageal cancer
What are the possible treatment options for Achalasia?
- Pneumatic Dilation
- Heller’s Myotomy + Dor fundoplication
What is pneumatic dilation?
- weakening of the LOS by circumferential stretching with an inflated balloon
- in some cases it tears muscle fibres
What is the efficacy of pneumatic dilation?
71-90% respond initially, many subsequently relapse
What is Heller’s Myotomy?
- a continuous myotomy of the LOS
- 6cm of the oesophagus and 3cm of the stomach is removed
What is Dor Fundoplication?
anterior fundus of stomach is folded over the oesophagus and sutured to the right side of myotomy
What are the risks associated with Heller’s Myotomy and Dor Fundoplication?
- oesophageal and gastric perforation (10-16%)
- splenic injury (1-5%)
- division of the vagus nerve (rare)
What is Scleroderma?
autoimmune disease that is usually irreversible
What are the biological effects of Scleroderma?
- hypo-motility in it’s early stages due to neuronal defects leading to atrophy of the smooth muscle of the oesophagus
- peristalsis in the distal portion ultimately ceases
- decreased resting pressure on the LOS
- GORD develops
What is Scleroderma associated with?
CREST syndrome
What is CREST syndrome?
- Calcinosis
- Reynauds phenomenon
- Esophageal Dysmotility
- Sclerodactyly
- Telangiectasia
How do you treat Scleroderma?
- exclude organic obstruction (no malignancy)
- improve force of peristalsis with prokinetics (cisapride) - low efficacy
- once peristaltic failure occurs, usually irreversible
What is corkscrew oesophagus?
diffuse oesophageal spasm
- uncoordinated contractions
- marked hypertrophy of circular muscle
- pressures of 400-500mmHg (very high)
What symptoms can corkscrew oesophagus present with?
- dysphagia
- chest pain
What is the treatment of corkscrew oesophagus?
may respond to forceful pneumatic dilation - results are not as predictable
Where do oesophageal perforations tend to occur?
- Cricopharyngeal constriction
- Aortic and bronchial constriction
- Diaphragmatic and ‘sphincter’ constriction
What can cause oesophageal perforations?
- Iatrogenic (investigation caused) >50%
- Spontaneous/Boerhaave’s 15%
- Foreign body 12%
- Trauma 9%
- Intraoperative 2%
- Malignant 1%
When do Iatrogenic oesophageal perforations tend to occur?
- usually during OGD
- more common in presence of diverticula or cancer
What can cause an Iatrogenic Oesophageal perforations?
- OGD 0.03%
- Stricture dilation 0.1-2%
- Slcerotherapy 1-5%
- Achlasia dilation 2-6%
What happens in a spontanous (Boerhaave’s) oesophageal perforation?
- sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
- e.g from vomiting against a closed glottis
- causes oesophagus to burst
- tends to happen at the left posterolateral aspect of the distal oesophagus
What common foreign bodies tend to cause a oesophageal perforation?
- disk batteries (electrical burns if impacts in the mucosa)
- magnets
- sharp objects
- dishwasher tablets
- acid/alkali
What can cause a trauma induced oesophageal perforation?
- Neck penetrating trauma
- Thorax blunt force (very rare)
How do trauma induced oesophageal perforations present?
- Dysphagia
- Blood in saliva
- Haematemesis
- Surgical empysema
How do oesophageal perforations present?
- pain (95%)
- fever (80%)
- dysphagia (70%)
- emphysema (35%)
What investigations would you run on a suspected oesophageal perforation?
- chest x-ray
- CT
- swallow test (gastrograffin)
- OGD
What is the initial management plan for a oesophageal perforation?
- IV fluids
- broadspectrum ABx and antifungals
- ITU/HDU care
- Bloods (incl. G+S)
- tertiary referral centre
Why are oesophageal perforations considered a surgical emergency?
2 x increase in mortality if 24hr delay in diagnosis
What should be the default management for oesophageal perforations?
operative management
What is the conservative management option for those where operative solutions CANNOT be used?
covered metal stent
What is the optimal surgical management of a oesophageal perforation?
primary repair
What is the definitive surgical option to treat an oesophageal perforation?
Oesophagectomy
What structural part of the body acts as a barrier against reflux?
Lower oesophageal sphincter
What causes normal sporadic reflux?
- pressure on a full stomach
- swallowing
- transient sphincter opening
What are the mechanisms used to protect from reflux?
- volume clearance (oesophageal peristalsis reflex)
- pH clearance (saliva)
- Epithelium (barrier properties)
What can prevent/inhibit reflux?
increased pressure in the LOS
- protein
- histamine
- high intra-abdominal pressure
What can promote reflux?
decreased pressure in the LOS
- chocolate
- gastric acid
- fat
- smoking
What are examples of the protective measures failing and causing GORD?
- reduced LOS pressure
- increased transient sphincter opening (carbonated drinks)
- reduced saliva production
- reduced buffering capacity of saliva (smoking)
- abnormal peristalsis
- hiatus hernia
- defective mucosal protective mechanism (alcohol)
How can GORD lead to malignancy?
- increased reflux
- reflux esophagitis
- epithelial metaplasia
- carcinoma
What is a sliding hiatus hernia?
- distal oesophagus ligament snaps
- stomach moves into the thorax, through the diaphragm
What is a rolling/paraoesophageal hiatus hernia?
- fundus of stomach moves through the diaphragm into the thorax
- blood flow compromised, ischaemia
What investigations should be done when GORD is suspected?
- OGD
exclude cancer, oesophagitis, peptic stricture and Barretts oesophagus confirmed - oesophageal manometry
- 24-hour oesophageal pH recording
What medical options are there to treat GORD?
lifestyle changes
- weight loss
- no smoking
PPIs
What are the surgical options available to treat GORD?
- dilation of peptic strictures
- laparoscopic Nissen’s fundoplication
What are the functions of the stomach?
- break down food
- release food at a steady rate into the duodenum
- kill parasites and certain bacteria
What is produced in the Cardia and Pyloric regions?
mucus only
What is produced in the body and fundus of the stomach?
- mucus
- HCl
- Pesinogen
What is produced in the antrum of the stomach?
Gastrin
What can cause erosive and hemorrhagic gastritis?
- NSAIDs
- Alcohol
- Trauma
- Ischaemia
- Multi-organ failure
- burns
How does erosive and haemorrhagic gastritis present?
- acute ulcer
- gastric bleeding and perforation of the stomach wall
What causes nonerosive, chronic active gastritis?
H. pylori infections
Where does nonerosive, chronic active gastritis occur?
limited to the antrum
How you manage nonerosive, chronic active gastritis?
triple Rx: amoxicillin, clarithromycin, pantoprazole for 7-14 days
Where does atrophic (fundal gland) gastritis occur?
the fundus of the stomach
What causes atrophic (fundal gland) gastritis?
- autoantibodies that attack the parietal cells in the stomach (eg: gastrin receptor, carbonic anhydrase…)
- parietal cell atrophy
What can atrophic (fundal gland) gastritis cause?
- decreased IF secretion
- reduced cobalamine absorption
- cobalamine deficiency
- pernicious anaemia
What can cause reactive gastritis?
- acute ulcers
What can reactive gastritis cause?
- epithelial metaplasia
- eventually: carcinoma
What stimulates gastric secretion?
- ACh
- Gastrin
- Histamine
What produces gastrin?
G cells of the antrum
What produces histamine?
ECL cells and mast cells of the gastric wall
What releases ACh?
post ganglionic receptor of vagal parasympathetic fibres
What inhibits gastric secretion?
- secretin
- somatostatin
- PGs (E2 and I2), TGF-alpha, adenosine
What produces secretin?
released from the small intestine
What is somatostatin?
somatotropin release-inhibiting hormone
What are the forms of mucosal protection?
- mucus film
- carbonate secretion
- epithelial barrier
- mucosal blood perfusion
How does carbonate secretion protect the gastric wall?
- buffers H+
- propogated by prostaglandins
How does the epithelial barrier protect the gastric wall?
tight junctions prevent H+ penetration.
What is the danger of epithelial wall ischaemia?
increased penetration of H+
What are the 3 mechanisms of epithelial repair?
- migration
- gap closed by cell growth
- acute wound healing
How does migration repair the epithelium?
adjacent epithelial cells flatten to close the gap via sideward migration along the basement membrane
What stimulates epithelial repair via cell growth?
- EGF
- TGF-alpha
- IGF-1
- GRP
- gastrin
When does acute wound healing of the epithelium occur?
when the basement membrane is destroyed
What happens during acute wound healing when the basement membrane is destroyed?
- attraction of leukocytes and macrophages
- phagocytosis of necrotic cells
- angiogenesis
- regeneration of ECM after BM repair
- epithelial closure by restitution and cell division
What factors aid ulcer formation?
- H pylori
- increased gastric juice secretion
- reduced carbonate secretion
- reduced cell formation
- reduced blood perfusion
What symptoms do 80% of the population with H pylori experience?
asymptomatic or chronic gastritis
What symptoms do 15-20% of the population with H pylori experience?
- chronic atrophic gastritis
- intestinal metaplasia
- gastric or duodenal ulcer
What symptoms do <1% of the population with H pylori experience?
- gastric cancer
- MALT lymphoma
What are the medical treatments available for ulcers?
- PPI or H2 blocker
- Triple Rx (amoxicillin, clarithromycin and pantoprazol) for 7-14 days
When is surgery required?
rarely
- most uncomplicated resolve in 12 weeks
- if not, change meds and observe for an additional 12 weeks
- check serum gastrin
- OGD (biopsy)
Why is an OGD done if an ulcer has not healed in 24 weeks?
- to biopsy all 4 quadrants of the ulcer
- rule out malignant ulcer if refractory
What are the surgical indications for ulcer treatment?
- intractability (after medical therapy)
- haemorrhage
- obstruction
- perforation
- relative: continuous requirement of steroid therapy/NSAIDS
What is dysphagia?
Difficulty swallowing
