Upper Gi Tract Flashcards
Landmarks of oesophagus trachea and aorta
Oesophagus approximately 25cm long - C5/6 to T10, where it enters the diaphragm, progressing from skeletal to smooth muscle
Upper Oesophageal sphincter approx 15cm lower approx 40cm
Trachea lies anterior to oesophagus
Aorta lies on left hand side of oesophagus
Perfusion of thoracic and abdominal part as well as drainage
- Thoracic part supplied by branches of aorta, superior supplied by branches of the thyroid artery (from the thyrocervical trunk)
- Abdominal part supplied by left gastric artery and inferior phrenic artery
- Drainage from thoracic part is the azygous vein (systemic), but also has portal vein
Anatomy of lower oesophagus
Phrenoesophageal ligament upper and lower limbs anchor oesophagus to the diaphragm
The Lower Oesophageal sphincter is surrounded by the diaphragm
The angle of His is the angle between the peritoneum of the stomach and the oesophagus (surrounded by subhiatal fat ring)
3-4 cm distal within abdomen
Swallowing phases
- Stage 0 - Oral phaseChewing and Saliva prepare the bolusBoth oesophageal sphincters are constricted
- Stage 1 - Pharyngeal phaseBolus guided to upper sphincter by pharyngeal musculatureUpper oesophageal sphincter opens reflexivelyLOS opened by vasovagal reflex
- Stage 2 - Upper oesophageal phaseUpper sphincter closesSuperior circular muscle rings contract, inferior rings dilateSequential contractions of longitudinal muscle
- Stage 3 - Lower oesophageal phaseLower oesophageal sphincter closes as food passes
Motility
- Determined by pressure managements (manometry)
- Peristaltic waves ~40mmHG
- Resting pressure of lower sphincter ~ 20mmHg
This goes down by less than 5mmHg during receptive relaxation
This is mediated by inhibitory noncholinergic nonadrenergic neurones (NCNA) of the myenteric plexus
Functional disorders of oesophagus
- Absence of a stricture
Caused by abnormal oesophageal contraction, as a result of disordered coordination, hyper OR hypomotility - Failure of protective mechanisms for reflux
Gastrooesophageal Reflux Disorder (GORD)
Dysphagia
Difficulty swallowing
Localisation is important - upper (cricopharyngeal) or lower (distal) sphincter
Types:
- For fluids or solids
- Intermittent or progressive
- Precise or vague in appreciation
Odynophagia
Pain when swallowing
Regurgitation
Return of oesophageal contents from above an obstruction
May be functional or mechanical
Reflux
Passive return of gastroduodenal contents to mouth
Hypermotility achalasia
Achalasia - a condition in which the muscles of the lower part of theoesophagus fail to relax, preventing food from passing into the stomach.
Occurs as a result of loss of ganglion cells in Auerbach’s myenteric plexus in the LOS wall causing decreased activity of inhibitory NCNA neurones
- Primary - cause unknown
- Secondary - known disease with similar oesophageal motor abnormalities, e.g.:
- Chagas’ disease
- Protozoa infection
- Amyloid / sarcoma / eosinophilic oesophagitis
Pathophysiology of achalasia
Increased resting pressure of LOS
Receptive relaxation is late and too weak
During reflex phase pressure in LOS is much higher than in stomach
Swallowed food collects in oesophagus causing increased pressure throughout with dilation of oesophagus
Propagation of peristaltic waves
Get weight loss pain and trouble swallowing
Progression of achalasia
- Insidious onset, people have symptoms for years before seeking help
- Without treatment, there is a progressive dilation of the oesophagus
- Risk of oesophageal cancer increased 28 fold, but incidence rate is only 0.34%
Treatment of achalasia
- Pneumatic dilation (PD)
Weakens the LOS by circumferential stretching, and sometimes tearing of its muscle fibres
71-90% of patients initially respond, but many subsequently relapse - Surgery
- Heller’s Myotomy: a continuous myotomy performed for 6cm on oesophagus and 3cm onto stomach
- Dor Fundoplication - anterior fundus folded over oesophagus and sutured to right side of myotomy
Risks:
-Oesophageal & gastric perforation (10-16%)
-Division of vagus nerve (rare)
-Splenic injury (1-5%)
Hypomobility scleroderma
Scleroderma - autoimmune disease
- Hypomotility in its early stages as a result of neuronal defects causes atrophy of the oesophageal smooth muscle
- Ultimately peristalsis in the distal oesophagus stops entirely, which causes:
- Decreased resting pressure of LOS
- GORD develops (this is often associated with CREST syndrome, a less severe form of scleroderma) (Calcinosis,raynauds,esophageal,sclerodactyly,tengeictasia)
Treatment of hypomobility scleroderma
- Exclude organic obstruction
- Improve force of peristalsis with prokinetics (cisapride)
- When peristaltic failure occurs this is usually irreversible
Disordered coordination -corkscrew oesophagus
Diffuse oesophageal spasms:
- Incoordinate contractions causing dysphagia and chest pain
- Pressures reaching 400-500mmHg
- Marked hypertrophy of circular muscle
- Will appear as a corkscrew oesophagus in a Barium study
Treatment of corkscrew oesophagus
May respond to forceful PD of cardia, but results are less predictable than achalasia
Oesophageal perforation
Anatomy: 3 areas of oesophageal perforations
Pathological narrowing, could be due to cancer, foreign bodies, physiological dysfunction
Can have cricopharyngeal constriction,aortic and bronchial,diaphragmatic
##
Aetiology of Oesophageal perforation
- Iatrogenic (OGD) >50%
- Spontaneous (Boerhaave’s) - 15%
- Foreign body - 12%
- Trauma - 9%
- Intraoperative - 2%
- Malignant - 1%
Iatrogenic
Usually at OGD, more common in the presence of diverticula or cancer
Incidence:
- OesophagoGastroDuodenoscopy (OGD) = 0.03%
- Stricture dilation = 0.1-2%
- Sclerotherapy = 1-5%
- Achalasia dilation = 2-6%
Boerhaave’s
- Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
- Vomiting against a closed glottis
- Incidence rate = 3.1 per 1,000,000
- Transmural laceration, most frequently at left posterolateral aspect of the distal oesophagus
Foreign Body
Common problems:
- Disc batteries - can cause electrical burns if embedded in mucosa (growing problem)
- Magnets
- Sharp objects
- Dishwasher tablets
- Acid / alkali
Trauma
Locations:
- Neck - penetration injury
- Thorax - blunt force
Difficult to diagnose, some symptoms are:
- Dysphagia
- Blood in saliva
- Haematemesis
- Surgical emphysema
Primary Management of an Oesophageal Perforation
Surgical EMERGENCY - mortality rate double if there is a 24 hour delay in diagnosis
Presentation of eosphgeal perforation
- Pain - 95%
- Fever - 80%
- Dysphagia - 75%
- Emphysema - 35%
Investigations of oesophagus perforation
- Chest X-ray
- CT (with gastrogaffin)
- OGD (Oesophagogastroduodenoscopy)
Management for oesophageal perforation
- Initial
- Nil by mouth
- IV fluids
- Broad spectrum antibiotics and antifungals
- After
- ITU/HDU care
- Bloods including G&S (group and save)
- Tertiary referral centre
- Definitive management
- Conservative management - cover with metal stent
- Operative management should be default, ideally primary repair
Oesophagectomy is also a definitive solution
Stomach function
Functions:
- Breaks food into smaller particles (via acid and pepsin)
- Holds food, releasing it in a controlled steady rate into the duodenum
- Kills parasites and certain bacteria
Location of secretion glands in stomach:
- Cardia & Pyloric regions - Mucous only
- Body and Fundus - Mucous, HCl, pepsinogen
- Antrum - Gastrin
Protective mechanisms against reflux
LOS is usually closed to prevent reflux of gastric juice (pepsin and HCl)
What impacts pressure of LOS
Increases:
- Acetylcholine
- Alpha-adrenergic agonists
- Hormones
- Protein-rich food
- Histamine
- High intra-abdominal pressure
- PGF2a
These may inhibit reflux
Decreases:
- VIP
- Beta-adrenergic agonists
- Hormones
- Dopamine
- Nitric Oxide
- PGI2
- PGE2
- Chocolate
- Acidic gastric juice
- Fat
- Smoking
These may promote reflux
Sporadic reflux
entirely normal and can be result of:
- Pressure on a full stomach
- Swallowing
- Transient sphincter opening
protective mechanisms following reflux:
Volume clearance (oesophageal peristalsis reflex)
- pH clearance via saliva
- Epithelial barrier properties (mucus,bicarbonate,tight junctions)
Failure of protective mechanisms - GORD
- Reduced volume clearance
- caused by abnormal peristalsis
- Reduced pH clearance
- caused by reduced saliva production, e.g. xerostomia or sleeping
- also caused by reduced buffering capacity of saliva, e.g. as a result of smoking
- Others:
- Decreased sphincter pressure
- Increased transient sphincter opening
- Hiatus hernia
- Defective Mucosal protective mechanism (e.g. from drinking alcohol)
ALL of the above result in reflux esophagitis, which can lead to epithelial metaplasia (Barrett’s oesophagus) and potentially carcinoma
Investigations for gord
- Oesophagogastroduodenoscopy
Helps to exclude cancer, and confirm oesophagitis, peptic stricture or Barrett’s oesophagus - Oesophageal manometry
- 24 hour oesophageal pH recording
Prescription for GORD
Medical:
- Lifestyle changes ( weight loss, smoking, reduce alcohol intake)
- Proton Pump Inhibitors
Surgical
- Dilatation peptic strictures
- Laparoscopic Nissen’s fundoplication
Gastritis types
Types:
- Erosive & haemorrhagic
- Numerous causes such as NSAIDs alcohol multi organ failure burns trauma ischemia
- Acute ulcers - cause gastric bleeding and perforation
- Nonerosive, chronic activeOccurs in the antrumMay be with H pylori, in which case prescribe amoxicillin, clarithromycin, pantoprazole for 7-14 / 7
- Atrophic (fundal gland)Occurs in the fundusAutoantibodies against parts and products of parietal cells, results in parietal cell atrophyDecreased acid and IF secretion
- Reactive
Stomach and ulcers
Mucosal protection of Basal membrane
- Mucus film - prevents pepsin and H+ reaching surface epithelium
- HCO3- Secretion - neutralises H+, acts as a buffer
pH of gastric juice = 1
pH near the surface epithelium of the stomach = 7 - Epithelial barrier - permeability and barrier integrity regulated by epidermal growth factor in saliva
- Mucosal blood perfusion allows H+ to enter the blood supply
Epithelial repair & wound healing
Wound healing involves:
- Granulation
- Angiogenesis
- Restitution of basal membrane
Mechanisms repairing epithelial defects:
- MigrationAdjacent epithelial cells flatten to close gap via sideward migration along basal membrane
- Gap closed by cell growthThis is stimulated by EGF, TGF-a, IGF-1, GRP, Gastrin
- Acute wound healingBasal membrane destroyed - attracts leukocytes & macrophages; necrotic cells phagocytosed, angiogenesis occurs, regeneration of extracellular matric after BM repairEpithelium closed by restitution and cell division
Regulation of gastric secretion
- Stimulation
- Neural
- ACh - postganglionic transmitter of vagal parasympathetic fibres
- Endocrine
- Gastrin - G cells of antrum
- Paracrine
- Histamine (Enterochromaffin-like cells & Mast cells of gastric wall)
- Inhibition
- Endocrine
- Secretin (small intestine)
- Paracrine
- Somatostatin (SIH)
- Paracrine & Autocrine
- Prostaglandins (E2 & I2), TGF-a, adenosine
Ulcer formation
Presence of H pylori near the wound may result in an ulcer
This is increased in likelihood by:
- Increased secretion of gastric juice
- Decreased HCO3- secretion
- Reduced cell formation
- Reduced blood perfusion
Outcomes of H pylori infections:
- Asymptomatic or chronic gastritis - >80%
- Chronic atrophic gastritis, intestinal metaplasia, gastric or duodenal ulcer - 15-20%
- Gastric cancer, MALT lymphoma <1%
Ulcer treatment
Mainly medical:
- PPI or H2 blocker
- Amoxicillin, clarithromycin & pantoprazole for 7-14 days
Elective surgery:
Rare, as most uncomplicated ulcers heal within 12 weeks, but if this doesn’t occur, change the medication and observe for 12 more weeks.
Check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison] syndrome)
OGD: biopsy all 4 quadrants of the ulcer if refractory to rule out malignancy
Surgical indications for ulcer treatment and complications
- Intractability (after medical therapy)
- Relative: continuous requirement of steroid therapy / NSAIDSs
- Haemorrhage
- Obstruction
- Perforation
Erosive and haemorraguc ulcer
NSAIDS,alcohol,trauma,ischaemia,multi organ failure
Causes erosive and haemorrhagic ulcer
Causes acute ulcer
Bleeding or perforation can occur
Autoantibodies
Causes atrophic findal gland gastritis
Causes decreased pepsinogen,IF secretion decreases thus less cobalamine (b12) this deficiency,acid secretion decreases thus increased Gastrin this ECL cell hyperplasia thus carcinoid
Sliding and rolling (para Oesophageal) hiatus hernia
Sliding hernia where portion of stomach and LOS slip into diaphragm due to wearing on diaphragm hiatus
Rolling hernia is wherestomahc rolls up besides the oesophagus through the diaphragm
