Upper GI Tract Flashcards
What vertebral level does the oesophagus start and end at?
Starts at C5 ends at T10
What are some anatomical advantages the LOS has
Distal 3-4cm is in the abdomen
Diaphragm surrounds it
Angle of His allows expansion after a heavy meal
What are the 4 phases of swallowing? Describe them briefly
Oral phase: chewing and saliva prepare bolus, both sphincters are constricted
Pharyngeal phase: musculature guides bolus to oesophagus, upper sphincter opens reflexly, LOS opened by vasovagal reflex (receptive relaxation reflex)
Upper oesophageal phase: upper sphincter closes, superior muscle rings contract, inferior rings dilate
Lower oesophageal phase: LOS closes as food passes through
What reflex opens the LOS? What is its name?
The vasovagal reflex aka receptive relaxation reflex
How is the motility of the oesophagus measures?
Manometry
What is the pressure of normal peristaltic waves?
40 mmHg
What is the resting pressure of the LOS?
20 mmHg
What is the pressure of the LOS when it relaxes?
5 mmHg
What mediates the relaxation of the LOS?
Inhibitory noncholinergic noradrenergic neurons of the myenteric plexus
Define dysphagia?
Difficulty swallowing
How do we describe dysphagia?
Is it during solid or fluid intake
Is it intermittent or progressive
Is it precise or vague
What are the 2 localisations for dysphagia?
Cricopharyngeal sphincter
Distal
Define odynphagia
Pain on swallowing
Define regurgitation and what are the 2 types
Return of oesophageal contents from above an obstruction
Can be functional or mechanical
Define reflux
Passive return of gastroduodenal contents to the mouth
What is the other name for hypermotility in the oesophagus?
Achalasia
Why does achalasia arise?
Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall leading to reduced activity of inhibitory NCNA neurones
What are secondary causes of achalasia?
Diseases causing oesophageal motor abnormalities eg
Chagas’ Disease
Protozoa infection
Amyloid/Sarcoma/Eosinophilic Oesophagitis
Describe what happens in achalasia?
Theres increased resting pressure of the LOS
Receptive relaxation is too weak
In reflex LOS pressure is higher then in the stomach
Swallowed food collects in the oesophagus and there is increased pressure and dilation
Peristaltic waves decrease
What type of onset does achalasia have?
Insidious
What happens if achalasia isnt treated?
Progressive oesophageal dilation
What does achalasia increase risk of?
Oesophageal cancer
What is the main non surgical treatment for achalasia?
Pneumatic dilation. it weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres
What are the surgical treatments for achalasia?
Heller’s myotomy= myotomy for 6 cm of oesophagus and 3cm of stomach
Dor fundoplication= the anterior fundus is folded over the oesophagus and sutured to the right side of the myotomy
What type of disease is sclerodoma?
Autoimmune
Why does hypomotility arise and what does it lead to?
Its due to neuronal defects and leads to atrophy of smooth muscle
What condition develops if there is hypomotility?
GORD
How is hypomotility treated?
Exclude organic obstruction
Improve force of peristalsis with prokinetics (cisapride)
Once peristaltic failure occurs its usually irreversible
What is corkscrew oesophagus?
Diffuse oesophageal spasm and incoordinate contractions leading to dysphagia and chest pain
What is the pressure in corkscrew oesophagus?
400-500 mmHg
Where is hypertrophy in corkscrew oesophagus?
In the circular muscle
How is corkscrew oesophagus treated?
It may be responsive to forceful pneumatic dilation of the cardia
What is dysphagia lusoria?
Vascular compression of the oesophagus from an aberrant right subclavian artery
Describe the path of the right subclavian artery from where it arises to where it goes
Arises from the thoracic aorta and goes posterior to the oesophagus
How is dysphoria lusoria treated?
Surgically
What are the 3 areas of constriction in the upper GI tract?
Cricopharyngeal constriction
Aortic and bronchial constriction
Diaphragmatic and sphincter constriction
What might cause pathological constriction in the upper GI tract?
Cancer, foreign body and physiological dysfunction
What is the most common cause of oesophageal perforation?
Latrogenic from OGD (over 50% of perforation is due to this)
What are some other causes of oesophageal perforation?
Spontaneous (boerhaave's) Foreign bodies Trauma Intraoperative Malignant
What is Boerhaave’s?
A cause of oesophageal perforation:
Sudden increase in in intra-oesophageal pressure with negative intra thoracic pressure
Results in vomiting against a closed glottis
How does oesophageal perforation present?
Pain
Fever
Dysphagia
Emphysema
How is oesophageal perforation diagnosed?
CXR
CT
Swallow
OGD
How is oesophageal perforation managed?
Operative management is default unless there is minimal contamination
Primary management is NDM, IV fluids, broad spectrum antibiotics/antifungals, bloods
How is oesophageal perforation managed conservatively?
Via covered metal stent
How is surgical management of oesophageal perforation done?
Primary repair with a vascularised pedicle flap is optimal
Oesophagectomy is a definitive solution with reconstruction
How does LOS act as a barrier against reflex?
it is closed to prevent contents from the stomach coming back up
When does sporadic reflux occur?
When theres pressure on full stomach
When swallowing
When the transient sphincter is opening
What are the protective mechanisms after reflux?
Volume clearance= oesophageal peristalsis reflux pH clearance (saliva) Epithelium, it has barrier properties
What does failure of protective mechanisms cause?
GORD
Sliding or rolling hiatus hernia
What does non surgical management of GORD involve?
OGD to exclude cancer Oesophageal manometry 24 hr oesophageal pH recording Lifestyle changes eg weight loss, smoking etc PPIs
What does surgical management of GORD involve?
Dilation peptic strictures
Laparoscopic Nissen’s fundoplication
What are the functions of the stomach?
Breaks food into smaller particles (acid & pepsin)
Holds food, releasing it in controlled steady rate into duodenum
Kills parasites & certain bacteria
What does the cardia and pylorus of the stomach produce?
Mucus only
What does the body and fundus of the stomach produce?
Mucus, Hcl, pepsinogen
What does the antrum of the stomach produce?
Gastrin
How much acid does the stomach produce everyday?
2L
What is the pH of the stomach at the epithelial and lumen?
Epithelium= 6-7 Lumen= 1-2
What is erosive and haemorrhagic gastritis?
When an acute ulcer causes gastric bleeding and perforation
What is nonerosive, chronic gastritis? What stomach region is it associated with?
Associated with the antrum
Due to helicobacter pylori
What is atrophic gastritis? What stomach region is it associated with?
Associated with the fundus
Autoantibodies attack parts and products of parietal cells causing parietal atrophy leading to reduced acid and IF secretion
What are the 4 types of gastritis?
Erosive and haemorrhagic
Nonerosive, chronic
Atrophic
Reactive
Where does stimulation come from when regulating gastric secretion?
Neural cells: Ach postganglionic transmitter of vagal parasympathetic fibres
Endocrine: Gastrin (G cells of antrum)
Paracrine: Histamine (ECL cells & mast cells of gastric wall)
Where does inhibition come from when regulating gastric secretion?
Endocrine: Secretin (small intestine)
Paracrine: Somatostatin (SIH)
Paracrine & autocrine: PGs (E2 & I2), TGF-α & adenosine
What are the 3 mechanisms that repair epithelial defects from ulcers?
Migration
Gap closed by cell growth
Acute wound healing
What is migration in relation to repairing epithelial defects?
Adjacent epithelial cells flatten to close gap via sideward migration along the basement membrane
What is gap closed cell growth in relation to repairing epithelial defects stimulated by?
EGF, TGF-α, IGF-1, GRP & gastrin
What is acute wound healing in relation to repairing epithelial defects?
BM destroyed and epithelial closure by restitution & cell division
What are some mechanisms by which the basement membrane may be destroyed?
Leukocytes & macrophages; phagocytosis of necrotic cells; angiogenesis; regeneration of ECM after repair of BM
What are some reasons ulcers form?
Infection by helicobacter pylori Increased secretion of gastric juice Reduced HCO3- secretion Reduced cell formation Reduced blood perfusion
What are some of the clinical outcomes of infection by h pylori? How common are they?
Asymptomatic or chronic gastritis (80%)
Chronic atrophic gastritis intestinal metaplasia (15-20%)
Gastric or duodenal ulcer (15-20%)
Gastric cancer/MALT lymphoma (< 1%)
How are ulcers treated?
Primarily via PPI or H2 blocker and triple antibiotics for 7-14 days
They are rarely managed surgically as they usually heal by themselves in 12 weeks
