6.1 - Upper GI tract Flashcards
At what vertebral level does the oesophagus start and end?
Starts at C5, ends at T10 (where it pierces the diaphragm) - approx 25cm tube
Where are the trachea and aorta found in comparison to the oesophagus?
- trachea anterior
- aorta to the left
What are the two sphincters of the oesophagus?
- upper oesophageal sphincter (UOS)
- lower oesophageal sphincter (LOS)
What are the three muscle types found along the oesophagus?
- upper 1/3 - skeletal
- middle 1/3 - skeletal/smooth
- bottom 1/3 - smooth
What is the arterial supply to the thoracic and abdominal oesophagus?
- thoracic - branches of aorta
- superior aspect also supplied by inferior thyroid artery (branches of thyrocervical trunk)
- abdominal - left gastric artery and inferior phrenic artery
What is the venous drainage of the thoracic and abdominal oesophagus?
- thoracic - drained by azygous vein (systemic circulation)
- abdominal - drained by portal vein (portal circulation)
What are the four anatomical contributions to the effectiveness of the lower oesophageal sphincter?
- 3-4cm distal oesophagus within abdomen (so if increase in intra-abdominal pressure = increase in LOS pressure)
- diaphragm surrounds LOS (left and right crux) - contracts like a pair of scissors around LOS when diaphragm contracts
- an intact phrenoesophageal ligament
- angle of His
What is the phrenoesophageal ligament?
- fibrous band connecting oesophagus to diaphragm (extension of inferior diaphragmatic fascia)
- two limbs:
- superior attaches to lower part of oesophagus
- inferior attaches to cardia of stomach
What is the Angle of His?
Normally there is an acute angle between the abdominal oesophagus and fundus of stomach at oesophageal junction that prevents reflux disease
What are the four stages of swallowing?
- stage 0 - oral phase
- stage 1 - pharyngeal phase
- stage 2 - upper oesophageal phase
- stage 3 - lower oesophageal phase
What happens in stage 0 - oral phase?
- chewing and saliva prepare bolus
- both oesophageal sphincters constricted
What happens in stage 1 - pharyngeal phase?
- pharyngeal musculature guides food bolus towards oesophagus
- upper oesophageal sphincter opens reflexly
- LOS opened by vasovagal reflex (receptive relaxation reflex)
- circular muscles dilate (allow bolus down), longitudinal muscles propel bolus down
What happens in stage 2 - upper oesophageal phase?
- upper sphincter closes
- superior circular muscle rings contract and inferior rings dilate (LOS dilates)
- sequential contractions of longitudinal muscle
What happens in stage 3 - lower oesophageal phase?
Lower sphincter closes as food passes through
How is motility of the oesophagus determined?
- oesophageal motility determined by pressure measurements (manometry)
- peristaltic waves are around 40 mmHg
What is the LOS resting pressure and how does this change during receptive relaxation?
- resting pressure is 20 mmHg
- decreases to <5 mmHg during receptive relaxation (when it opens during pharyngeal phase)
- mediated by inhibitory noncholinergic noradrenergic (NCNA) neurones of myenteric plexus (between circular and longitudinal muscles in distal oesophagus)
What is a functional disorder of the oesophagus?
Absence (?? should be presence) of an oesophageal stricture (abnormal narrowing of oesophagus)
What can (oesophageal strictures) be caused by?
- abnormal oesophageal contraction
- hypermotility
- hypomotility
- disordered coordination
- failure of protective mechanisms for reflux
- gastro-oesophageal reflux disease (GORD)
What is dysphagia?
Difficulty in swallowing
What is important when describing dysphagia?
Localisation is important to describe - cricopharyngeal sphincter or distal
What types of dysphagia are there? (3)
- for solids or fluids
- intermittent or progressive
- precise or vague in appreciation
What is odynophagia?
Pain on swallowing
What is regurgitation (GIT)?
- return of oesophageal contents from above an obstruction
- may be functional or mechanical
What is reflux?
Passive return of gastroduodenal contents to the mouth
What is achalasia?
- hypermotility of oesophagus due to loss of ganglion cells in Auerbach’s myenteric plexus in LOS wall
- leads to decreased activity of inhibitory NCNA neurones (so LOS cannot relax/open)
What is the pathophysiology of achalasia? (What does it lead to?)
- loss of NCNA = loss of inhibitory effects = increased resting pressure of LOS
- receptive relaxation sets in late and is too weak - so during reflex phase pressure in LOS is markedly higher than stomach (LOS cannot open properly)
- swallowed food collects in oesophagus causing increased pressure throughout with dilation of oesophagus
- propagation of peristaltic waves cease
- leads to bird beak appearance + oesophageal dilation on barium swallow
Can be associated with weight loss, trouble swallowing, pain –> eosphagitis and aspiration pneumonia
What is primary achalasia?
Majority of achalasia is primary, aetiology is unknown
What is secondary achalasia?
- diseases causing oesophageal motor abnormalities similar to primary achalasia:
- Chagas’ Disease
- protozoa infection
- amyloid/sarcoma/eosinophilic oesophagitis
What is the disease course of achalasia?
- insidious onset - symptoms for years prior to seeking help
- without treatment: progressive oesophageal dilation of oesophagus
What does achalasia increase the risk of?
- increases risk of oesophageal cancer by 28-fold
- annual incidence only 0.34%
What are the two main treatments for achalasia?
- pneumatic dilatation (PD)
- surgery
What happens in pneumatic dilatation (PD)?
- PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres
- done by inserting balloon and expanding it in LOS
- efficacy: 71-90% of patients respond initially but many patients subsequently relapse
What happens in surgery for achalasia?
Done when PD fails/recurrence
- Heller’s myotomy - a continuous myotomy (cutting of musculature and exposing mucosa - disrupt longitudinal muscle, keep circular intact) performed for 6cm on oesophagus and 3cm onto the stomach
- Dor fundoplication (done after) - anterior fundus folded over oesophagus and sutured to right side of myotomy
What are the risks of surgery for achalasia? (3)
- oesophageal and gastric perforation (10-16%)
- division of vagus nerve - rare
- splenic injury (1-5%)
What is scleroderma (in context of oesophageal motility)?
Autoimmune disease where hypomotility happens in its early stages due to neuronal defects leading to atrophy of smooth muscle of oesophagus (LOS too relaxed)
What does scleroderma lead to/cause (GIT)? (3)
- peristalsis in the distal portion (of oesophagus) ultimately ceases altogether
- decreased resting pressure of LOS
- GORD develops - reflux through open LOS
What is scleroderma often associated with?
CREST syndrome
What is the treatment for scleroderma?
- exclude organic obstruction (and make sure no malignancy)
- improve force of peristalsis with prokinetics (cisapride)
- does not work too well as once peristaltic failure occurs, it is usually irreversible
What is corkscrew oesophagus (diffuse oesophageal spasm)?
- disordered coordination of contraction of oesophagus
- leads to dysphagia and chest pain
- pressures of 400-500 mmHg (compared to normal pressures ~20 mmHg)
What can we see on endoscopy when investigating corkscrew oesophagus/diffuse oesophageal spasm?
- marked hypertrophy of circular muscle
- corkscrew-shaped oesophagus on barium swallow
What is the treatment for corkscrew oesophagus?
- may respond to forceful PD (pneumatic dilatation) of cardia
- results not as predictable as achalasia
What are the three areas of anatomical constriction of the oesophagus?
Prone to perforations
- cricopharyngeal constriction
- aortic and bronchial constriction
- diaphragmatic and ‘sphincter’ constriction
- (pathological narrowing can occur e.g. cancer, foreign body, physiological dysfunction = prone to perforation)
What are the causes of oesophageal perforations? (6)
- iatrogenic (OGD) >50%
- spontaneous (Boerhaave’s) - 15%
- foreign body - 12%
- trauma - 9%
- intraoperative - 2%
- malignant - 1%
I Smell Fruit To Ingest, Mother
When does iatrogenic oesophageal perforation occur?
- usually at OGD
- more common in presence of diverticula or cancer
Usually at Killian’s triangle (oblique inferior constrictor + cricopharyngeus muscle junction)
What is the incidence of iatrogenic oesophageal perforation?
- OGD = 0.03%
- stricture dilatation = 0.1-2%
- sclerotherapy = 1-5%
- achalasia dilatation = 2-6%
How does spontaneous oesophageal perforation (Boerhaave’s) happen?
- sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure
- vomiting against closed glottis occurs
- 3.1 per 1,000,000
Usully secondary to alcohol intake
Where does spontaneous (Boerhaave’s) oesophageal perforation usually occur?
Usually in left posterolateral aspect of distal oesophagus
2cm above gastro-oesophageal junction
What foreign bodies can cause oesophageal perforation? (5)
- disk batteries - growing problem, causes electrical burns if it embeds in the mucosa
- magnets
- sharp objects
- dishwasher tablets
- acid/alkali (can cause burning, stricture, perforation)
What two types of trauma can cause oesophageal perforation?
- neck - penetrating force needed
- thorax - blunt force needed
What do we look for to diagnose trauma-induced oesophageal perforation? (4)
- dysphagia
- blood in saliva
- haematemesis
- surgical emphysema
How do oesophageal perforations present? (4)
- pain 95%
- fever 80%
- dysphagia 70%
- emphysema 35%
What investigations are done for oesophageal perforations? (4)
- CXR
- CT
- swallow (gastrograffin contrast given)
- OGD (only do if necessary as it can make it worse)
What is the primary management of oesophageal perforation?
Surgery - surgical emergency, mortality increased by 2x if 24h delay in diagnosis
Describe the initial management of oesophageal perforation? (6)
- nil by mouth (NBM)
- IV fluids (rehydrate)
- broad spectrum antibiotics and antifungals
- bloods (include G&S)
- ITU/HDU level care
- refer to tertiary referral centre
Usually done for iatrogenic causes as tend not to be full-thickness perforations, unlike Boerhaave’s
What definitive management is there for oesophageal perforation? (2)
- conservative management (with a metal stent covering oesophagus) - only if small, contained perforation that has not leaked - covered metal stent
- operative management should be default as primary repair is optimal
- oesophagectomy is the definitive solution
Sponges can be used to block off hole and drain fluid
What is a protective mechanism against reflux?
LOS usually closed as barrier against reflux of harmful gastric juice (pepsin and HCl)
What is LOS pressure increased by? (7)
- acetylcholine
- alpha adrenergic agonists
- hormones
- protein-rich food
- histamine
- high intra-abdominal pressure
- PGF2alpha etc
- (inhibits reflux)
What is LOS pressure decreased by? (11)
- VIP (vasoactive intestinal polypeptide)
- beta adrenergic agonists
- hormones
- dopamine
- NO
- PGI2
- PGE2
- chocolate
- acid gastric juice
- fat
- smoking etc
- (promotes reflux)
When does sporadic reflux occur (normal)? (3)
- pressure on full stomach
- swallowing
- transient sphincter opening
What three mechanisms protect following reflux?
- volume clearance - oesophageal peristalsis reflex
- pH clearance - saliva (neutralises acid)
- epithelium - barrier properties
What different ways can protective mechanisms fail in GORD? (7)
- decrease in sphincter pressure
- increased transient sphincter opening
- hiatus hernia
- abnormal peristalsis leading to decreased volume clearance
- decreased saliva production (in sleep, xerostomia) leading to decreased pH clearance
- decreased buffering capacity of saliva (e.g. through smoking) = decreased pH clearance
- defective mucosal protective mechanism e.g. alcohol
What happens when the GORD protective mechanisms fail?
Reflux oesophagitis –> potential epithelial metaplasia –> potential carcinoma
What are the two types of hiatus hernia?
- sliding hiatus hernia - ligament holding distal oesophagus down gives way so whole stomach slides up into oesophagus/chest
- rolling/paraoesophageal hiatus hernia - portion of stomach sticks up side = emergency
What happens if a hernia gets strangulated?
The blood supply to it is cut off and then the stomach/oesophagus can become ischaemic
What investigations are done for GORD? (3)
- OGD - to exclude cancer and to look for oesophagitis, peptic stricture and Barrett’s oesophagus
- oesophageal manometry
- 24-hr oesophageal pH recording
What is the medical treatment for GORD? (2)
- lifestyle changes (weight loss, smoking cessation, no alcohol)
- PPIs
What is the surgical treatment for GORD? (2)
- dilatation of peptic strictures
- laparoscopic Nissen’s fundoplication - stitch up perforation, wrap fundus around oesophagus, put stitches (not too tight or cannot swallow)
What are the functions of the stomach? (3)
- breaks food into smaller particles (acid and pepsin)
- holds food, releasing it in controlled steady rate into duodenum
- kills parasites and certain bacteria
What parts of the stomach produce what?
- cardia and pyloric region - mucus only
- body and fundus - mucus, HCl, pepsinogen
- antrum - gastrin
Closest to oesophagus (proximal) = cardia
Main bit: fundus –> body –> antrum
Distal end: pyloric region
What are the four types of gastritis?
- erosive and haemorrhagic gastritis (ischaemia –> acute ulcer)
- nonerosive, chronic, active gastritis (H. pylori)
- atrophic (fundal gland) gastritis (autoimmune)
- reactive gastritis (meds and external factors etc)
What are the causes of erosive and haemorrhagic gastritis? (4)
- NSAIDs, alcohol
- multi-organ failure, burns
- trauma
- ischaemia
What does erosive and haemorrhagic gastritis cause?
Acute ulcer - massive gastric bleeding and perforation, anywhere in stomach
What can cause nonerosive, chronic, active gastritis?
Helicobacter pylori infection –> increased gastrin, acid secretion normal/increased –> chronic gastric and duodenal ulcer –> reactive gastritis –> epithelial metaplasia –> carcinoma
Where does nonerosive, chronic, active gastritis occur?
Antrum
How can we treat nonerosive, chronic, active gastritis?
Triple antibiotics (amoxicillin, clarithromycin and pantoprazole) for 2 weeks
What can cause atrophic (fundal gland) gastritis?
- autoantibodies against parts and products of parietal cells
- decreased acid secretion –> G cell hyperplasia (gastrin secretion) –> epithelial metaplasia –> carcinoma
- decreased acid secretion –> increased gastrin to counteract this –> ECL cell hyperplasia (histamine secretion) –> carcinoid (neuroendocrine tumour)
- decreased IF secretion –> decreased cobalamine absorption –> long term leads to cobalamine (B12) deficiency –> pernicious anaemia
- parietal cell atrophy
Where does atrophic (fundal gland) gastritis occur?
Fundus
What are three ways of stimulating gastric secretion?
- neural - ACh (acts on M1 receptors through postganglionic transmitter of vagal parasympathetic fibres)
- endocrine - gastrin (produced by G cells of antrum)
- paracrine - histamine (made by ECL cells and mast cells of gastric wall on H2 receptors)
What are three ways of inhibiting gastric secretion?
- endocrine - secretin (produced by small intestine)
- paracrine - somatostatin (SIH)
- paracrine & autocrine - PGs (E2 and I2), TGFalpha, adenosine
What are four ways in which the mucosa is protected from H+?
- mucus film - epithelial cells make mucus, protects against pepsin and H+
- HCO3- secretion - HCO3- buffers against acids, needs prostaglandins (NSAIDs decrease production)
- epithelial barrier - apical membrane and tight junctions prevent penetration of H+
- mucosal blood perfusion - good perfusion means any H+ quickly taken away by blood (ischaemia causes issue in ulcers)
What are the three mechanisms/steps of epithelial repair and wound healing?
- migration - adjacent epithelial cells flatten to close gap via sideward migration along BM
- gap closed by cell growth - EGF, TGF-a, IGF-1, GRP, gastrin
- acute wound healing - BM destroyed and repaired, leukocytes/macrophages and phagocytosis, angiogenesis, ECM regeneration, epithelial closure
What happens in migration (mechanisms repairing epithelial defects)?
Adjacent epithelial cells flatten to close gap via sideward migration along BM
What stimulates the gap to close by cell growth (mechanisms repairing epithelial defects)? (5)
- EGF
- TGF-alpha
- IGF-1
- GRP
- gastrin
When and how does acute wound healing occur (mechanisms repairing epithelial defects)?
- BM destroyed:
- attraction of leukocytes and macrophages
- phagocytosis of necrotic cells
- angiogenesis
- regeneration of ECM after repair of BM
- epithelial closure by restitution and cell division
What are the causes of ulcer formation? (5)
- Helicobacter pylori
- secretion of gastric juice
- less HCO3- secretion
- less cell formation
- less blood perfusion
How do the causes of ulcer formation lead to ulcers?
- chemical aggression and barrier function being disturbed –> epithelial damage
- epithelial damage –> wound –> can lead to ulcer if not healed
What are the different clinical outcomes of H. pylori infections?
- 80% asymptomatic or chronic gastritis
- 15-20% chronic atrophic gastritis/intestinal metaplasia/gastric or duodenal ulcer
- <1% gastric cancer/MALT lymphoma
What are the medical treatments (primarily done) for ulcers? (2)
- PPI or H2 blocker
- triple antibiotic therapy (amoxicillin, clarithromycin, pantoprazole) for 7-14 days (if H. pylori proven)
What are the elective surgery procedures for ulcers (and why are they rarely done)?
- check serum gastrin (antral G-cell hyperplasia or gastrinoma - Zollinger-Ellison syndrome)
- OGD - biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory
- rarely done as most uncomplicated ulcers heal within 12 weeks, and if not you change medication and observe for another 12 weeks
What are the surgical indications for ulcer treatment? (3)
- intractability (after medical therapy) - still have symptoms so might consider fundoplication
- relative - continuous requirement of steroid therapy/NSAIDs (impair HCO3- secretion = ulcers)
- complications from ulcer (haemorrhage, obstruction, perforation)
