Upper GI tract Flashcards
What spinal level does the oesophagus a) originate b) pass through oesophageal hiatus of diaphragm
C5
T10
What are 2 ways of dividing the oesophagus?
- Proximal (upper) 1/3, middle 1/3, distal (lower) 1/3
- Cervical (0-18), upper thoracic (18-24), mid thoracic (24-32), lower thoracic oesophagus (32-40)- 0 is level of incisors
What types of epithelium is found in upper oesophagus, then lower oesophagus?
Non-keratinising squamous in upper, columnar lower
What types of muscle tissue is found in upper, middle, lower third of oesophagus?
Skeletal, skeletal and smooth, smooth
What are the 2 sphincters of the oesophagus?
Upper oesophageal sphincter, lower oesophageal sphincter
What muscles are involved in the formation of the upper oesophageal sphincter?
Thyropharyngeus, cricopharyngeus
What are the anatomical contributions to the lower oesophageal sphincter?
3-4cm of distal oesophagus within the abdomen
Diaphragm surrounds LOS (right and left crus)
Intact phrenoesophageal ligament
Angle of His
((also intraabdominal pressure?))
What are the 4 stages of swallowing?
Stage 0 (oral phase)
Stage 1 (pharyngeal phase)
Stage 2 (upper oesophageal phase)
Stage 3 (lower oesophageal phase)
What happens during stage 0 of swallowing?
Chewing and saliva prepares bolus
Both oesophageal sphincters are closed
What happens during stage 1 of swallowing?
Pharyngeal muscle guides food bolus towards oesophagus
UOS opens reflexively
LOS opens by vasovagal reflex (receptive relaxation reflex)
What happens during stage 2 of swallowing?
UOS closes
Superior rings of smooth muscle constrict while inferior rings dilate
Sequential contraction of longitudinal muscle
What happens during stage 3 of swallowing?
LOS closes as food passes through
How do we determine oesophageal motility?
Manometry (pressure measurement)
Oesophageal pressure during peristaltic contractions?
40mmHg
a)LOS resting pressure? b)What happens to this during receptive relaxation?
a)20mmHg
b) drops below 5mmHg
What neurons mediate receptive relaxations?
Non-cholinergic noradrenergic (NCNA) neurons of the myenteric plexus
Name 2 causes of functional disorders of the oesophagus
Abnormal oesophageal contractions (hyper motility, hypomotility, disordered co-ordination)
Failure of protective mechanisms for reflux (GORD)
a)What is dysphagia?
b)Name 3 types of dysphagia.
a)Difficulty swallowing (localisation is important- cricopharyngeus/ distal oesophagus)
b)solids or fluids, intermittent or progressive, precise or vague in appreciation
What is odynophagia?
Pain on swallowing
Difference between regurgitation and reflux?
Regurgitation is the return of oesophageal contents from above a mechanical/ functional obstruction, while reflux is passive return of gastroduodenal contents to the mouth
Loss of what type of cells causes achalasia?
Ganglion cells in myenteric (Auerbach’s) plexus in LOS wall- this leads to decreased inhibitory NCNA neuronal activity
What are the causes of achalasia?
Primary- aetiology unknown
Secondary- Chagas disease, protozoan infection, amyloid/ sarcoid/ eosinophilic oesophagitis
What is seen on barium swallow in achalasia?
Bird’s beak
Describe the pathophysiology of achalasia
Increased resting pressure of LOS
Receptive relaxation sets in late and is too weak- during reflex phase LOS pressure is markedly higher than in the stomach
Swallowed food accumulates in oesophagus eating to increased pressure throughout and dilatation through oesophagus
Propogation of peristaltic waves cease
Describe the ONSET and disease course of achalasia
insidious onset and progressive course- symptoms for years prior to seeking help
without treatment there is progressive dilation of the oesophagus
What does achalasia increase the risk of?
Oesophageal cancer
How is achalasia treated non-surgically and how effective is this?
Pneumatic dilatation- weakens LOS by circumferential stretching and in some cases tearing of its muscle fibres
71-90% of patients respond initially but then relapse
What surgical treatments are available for achalasia?
Heller’s myectomy (continuous myectomy for 6cm on oesophagus and 3cm on abdomen) and dor fundoplication (anterior fundus is folded over oesophagus and sutured to right side of myectomy)
What are some risks of surgical treatments for achalasia?
oesophageal and gastric perforation
splenic injury
division of the vagus nerve (rare)
What type of disease is scleroderma?
autoimmune
Describe the pathophysiology of scleroderma
Initial hypomotility is caused by neuronal defects–> atrophy of smooth muscle of oesophagus
Peristalsis in distal portion eventually ceases altogether
Resting pressure of LOS decreases
GORD develops, often associated with crest syndrome
How is scleroderma treated?
First exclude organic obstruction
Increase force of peristalsis with prokinetics (cisapride)
Once peristaltic failure occurs- usually irreversible
What happens in disordered co-ordication of oesophageal contraction?
Diffuse oesophageal spasm
Causes dysphagia and chest pain
Pressures of 400-500mmg
Marked hypertrophy of circular muscle
corkscrew oesophagus on Barium swallow
How is corkscrew oesophagus treated?
May respond to forced PD of cardia (results less predictable than in achalasia)
What is the anatomy of oesophageal perforation?
Three areas of anatomical constriction (aortic and bronchial, cricopharyngeal, diaphragmatic and sphincter)-ABCD
Pathological narrowing- cancer, foreign body, physiological dysfunction
What is the aetiology of oesophageal perforation?
ISFTIM
Iatrogenic (OGD)
Spontaneous (Boerhaave’s)
Foreign body
Trauma
Intraoperative
Malignant
What are iatrogenic causes of oesophageal perforation?
OGD (more common in the presence of diverticula/ cancer)
Stricture dilatation
Sclerotherapy
Achalasia dilatation
What is Boerhaave’s syndrome?
Sudden increase in oesophageal pressure with negative intrathoracic pressure (e.g. vomiting against a closed glottis)
What is the most common oesophageal rupture point in Boerhaave’s syndrome?
left posterolateral aspect of distal oesophagus
What foreign bodies are commonly implicated in oesophageal rupture?
Disk batteries
Magnets
Sharp objects
Dishwasher tablets
Acids/alkali
What types of trauma can cause oesophageal rupture?
Neck (penetrating)
Thorax (blunt force)
What are some indications of oesophageal rupture?
Dysphagia
Blood in saliva
Haematemesis
Surgical emphysema
How does oesophageal rupture usually present?
Pain
Fever
Dyphagia
Surgical emphysema
What investigations are carried out for oesophageal rupture?
Chest Xray
CT
OGD
Swallow (gastrografin)
How is oesophageal perforation treatment managed
It’s a surgical emergency (*2 increased risk of mortality if treatment is delayed 24hrs
initial management- NBM, IV fluids, broad spectrum antibiotics, antifungals, treatment on ICU/HDU in tertiary referral centre, bloods (including group and save)
conservative management with metal stent
operative management- primary management is first line, oesophagectomy is definitive solution
What can cause increased LOS pressure and what does this lead to?
Anticholinergics, alpha adrenergic agonists, hormones, histamine, high intra-abdominal pressure, protein rich food, PGF 2α
Inhibits reflux
What can cause decreased LOS pressure and what does this lead to?
VIP, beta adrenergic agonists, hormones, dopamine, PGI2, PGE2, chocolate, fat, smoking, NO, gastric acid juice
Promotes reflux
What can cause sporadic reflux?
Pressure on a full stomach
Swallowing
Transient LOS opening
What are the 3 protective mechanisms against reflux
- volume clearance- oesophageal peristalsis reflex
- pH clearance-saliva
- epithelial barrier function
Give examples of how protective mechanisms against reflux can fail
Decreased sphincter pressure
Increased transient sphincter opening (Air, CO2)
Decreased saliva production (sleep, xerostomia) or decreased buffering capacity of saliva (smoking)
Abnormal peristalsis (decreased volume clearance)
Defective mucosal protective mechanism (alcohol)
Hiatus hernia
What is a sliding hiatus hernia?
In a sliding hiatus hernia, the stomach distends superiorly through the diaphragm, increasing gastric acid reflux into the distal oesophagus and gastroesophageal junction
What is a rolling/paraoesphageal hiatus hernia?
In a rolling hiatus hernia the gastroesophageal junction is intact, and the herniated portion of the stomach lies alongside the oesophagus
surgical emergency due to risk of hernia strangulation
In barium swallow can see fundus containing barium alongside oesophagus
What are the investigations for GORD?
OGD (To exclude oesophageal cancer. Oesophagitis, Barrett’s oesophagus and peptic stricure confirm)
Oesophageal manometry
24 hour oesophageal pH recording
How is GORD treated?
Medical- lifestyle changes (weight loss, smoking, EtOH), PPIs
Surgical- Dilatation peptic stricure, laparoscopic nissen’s fundoplication
What are the basic functions of the stomach?
Breaks food down into smaller particles (pepsin, stomach acid)
Holds food and releases in a steady, controlled stream into the duodenum
Kills parasites and some bacteria
What substances are secreted by different regions of the stomach
Cardia and pyloric region- mucus only
Body and fundus- mucus, pepsinogen, HCl
Antrum- gastrin
What are the 4 types of gastritis?
Erosive and haemorrhage gastritis
Non-erosive, chronic active gastritis
Reactive gastritis
Atrophic (fundal gland) gastritis
What causes erosive and haemorrhage gastritis and what can it lead to?
Numerous causes
Leads to formation of acute ulcer- perforation and bleeding
What causes non-erosive, chronic active gastritis?
H. pylori infection
What region of the stomach does non-erosive, chronic active gastritis occur in?
Antrum
How is non-erosive, chronic active gastritis treated?
Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
What region of the stomach does atrophic gastritis occur in?
fundus
Explain the pathophysiology of atrophic gastritis
Autoantibodies form and attack parietal cell parts and products
Parietal cells atrophy
Decrease in HCl and IF
What factors stimulate gastric secretion?
Neural- ACh (vagal postganglionic fibres)
Endocrine- gastrin (G cells of antrum)
Paracrine- histamine (ECL cells and mast cells of gastric wall)
What factors inhibit gastric secretion?
Endocrine- secretin (small intestine)
Paracrine- somatostatin (SIH)
Paracrine and autocrine- PGs (E2 and I2), TGF-α, adenosine
What factors contribute to mucosal protection against ulcers?
Mucus film
Mucosal blood perfusion
HCO3- secretion
Epithelial barrier
What mechanisms are involved in gastric ulcer healing?
Migration- adjacent cells flatten and migrate sideways along BM to close gap
Gap closed by cell growth- stimulated by EGF, TGF-α, IGF-1, GRP and gastrin
Acute wound healing- BM destroyed, attraction of leukocytes and neutrophils, phacytosis of necrotic cells, angiogenesis, BM repaired, ECM regenerated
What factors contribute towards gastric ulcer formation?
Helicobacter pylori
Increased gastric acid secretion
Decreased HCO3- secretion
Decreased blood perfusion
Decreased cell formation
What are the possible clinical outcomes of an H. pylori infection?
- Asymptomatic or chronic gastritis
- Atrophic gastritis and intestinal metaplasia
- Gastric/ duodenal ulcer
- Gastric cancer/ MALT lymphoma
What is the primary medical treatment for H. pylori infections?
PPI or H2 blocker
Triple Rx (amoxicillin, clarythromycin, pantoprazole for 7-14 days)
What are the indications for surgical treatment for peptic ulcers?
Intractability (after medical treatment)
Relative- requiring continuous treatment with steroid therapy/ NSAIDs
Complications- haemorrhage, obstructions, perforations
When would you carry out elective surgery for peptic ulcers?
Rare - most uncomplicated ulcers heal within 12 weeks
If don’t, change medication, observe additional 12 weeks
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
