Upper GI Tract Flashcards
What types of muscles make up the trachea?
- Skeletal muscle
- Skeletal muscle / Smooth muscle
- Smooth muscle
What are the two sphincters that are at the beginning and end of the trachea?
- Upper oesophageal sphincter
- Lower oesophageal sphincter
What are these 3 structures?
- Red: Trachea
- Green: Aorta
- Purple: Diaphragm
Does the oesophagus extend within abdomen?
- Extends 3-4 cm distal oesophagus within abdomen
What structures make up the phrenoesophageal ligament?
- A seal where the esophagus passes from the thorax into the abdomen through the diaphragmatic hiatus
Formed by the right and left crus of the diaphragm
What is the angle formed between the oesophagus and the stomach (red-dotted line)?
- Angle of His
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: Oral phase” of swallowing?
Stage of food and status of oesophageal sphincters
- Chewing & saliva prepare bolus
- Both oesophageal sphincters constricted
What happens during “Stage 1: Pharyngeal phase” of swallowing?
Stage of food and status of oesophageal sphincters
- Pharyngeal musculature guides food bolus towards oesophagus
- UOS opens reflexly
- LOS opened by vasovagal reflex (receptive relaxation reflex)
What happens during “Stage 2: Upper oesophageal phase” of swallowing?
Status of oesophageal muscles and status of oesophageal sphincters
- UOS closes
- Superior circular muscle rings contract & inferior rings dilate
- Sequential contractions of longitudinal muscle
What happens during “Stage 3: Lower oesophageal phase” of swallowing?
Status of oesophageal sphincters
- LOS closes as food passes through
The LOS has a resting pressure ~ 20 mmHg and decreases to ↓< 5 mmHg during receptive relaxation. Which neurones facilitate this change?
- Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus
Define dysphagia.
Difficulty in swallowing
- Localisation is important – cricopharyngeal sphincter or distal
- Type of dysphagia
- For solids or fluids
- Intermittent or progressive
- Precise or vague in appreciation
Define odynophagia.
Pain on swallowing
Define regurgitation.
Return of oesophageal contents from above an obstruction
May be functional or mechanical
Define reflux.
Passive return of gastroduodenal contents to the mouth
What are the causes of absence of a stricture?
-
Abnormal oesophageal contraction
- Hypermotility
- Hypomotility
- Disordered coordination
-
Failure of protective mechanisms for reflux
- GastroOesophageal Reflux Disease (GORD)
Outline the pathophysiology of achalasia (oesophageal hypermobility) (3 steps).
- Loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
- Decreased activity of inhibitory NCNA neurones
- Hypermobility
What is the primary cause of achalasia (oesophageal hypermobility)?
Unkown
What is the secondary cause of achalasia (oesophageal hypermobility) (5)?
- Diseases causing oesophageal motor abnormalities similar to 1o achalasia
- Chagas’ Disease
- Protozoa infection
- Amyloid
- Sarcoma
- Eosinophilic Oesophagitis
What are the pathophysiological effects of acahalasia (oesophageal hypermobility)?
- Increased resting pressure of LOS
- Receptive relaxation sets in late & is too weak
- During reflex phase pressure in LOS is markedly higher than stomach
- Swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus
- Propagation of peristaltic waves ceas
What are the symptoms of achalasia (oesophageal hypermobility) (3)?
- Weight loss
- Trouble swallowing
- Pain
Outline the disease course of achalasia (oesophageal hypermobility).
- Has insidious onset - symptoms for years prior to seeking help
- Without treatment → progressive oesophageal dilatation
What is the risk of oesophageal cancer following achalasia (oesophageal hypermobility)?
- Increased 28-fold
What are the available treatments for achalasia (oesophageal hypermobility) (2)?
- Pneumatic Dilatation (PD)
-
Surgery
- Heller’s Myotomy
- Dor fundoplication
Describe Pneumatic Dilatation (PD) for the treatment of achalasia (oesophageal hypermobility).
- PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres
What is the efficacy of Pneumatic Dilatation (PD) for the treatment of achalasia (oesophageal hypermobility)?
- 71 - 90% of patients respond initially but many patients subsequently relapse
Outline the surgery used to treat achalasia (oesophageal hypermobility).
- Heller’s Myotomy - A continuous myotomy performed for 6 cm on the oesophagus & 3 cm onto the stomach
- Dor fundoplication – anterior fundus folded over oesophagus and sutured to right side of myotomy
What are the risks of the surgery used to treat achalasia (oesophageal hypermobility)?
- Oesophageal & gastric perforation (10 – 16%)
- Splenic injury – 1 – 5%
- Division of vagus nerve – rare
What is the cause of scleroderma (oesophageal hypomobility)?
Autoimmune disease
Outline the pathophysiology of scleroderma (oesophageal hypomobility) (3).
- Hypomotility in its early stages due to neuronal defects → atrophy of smooth muscle of oesophagus
- Peristalsis in the distal portion ultimately ceases altogether
- Decreased resting pressure of LOS
What are the pathophysiological effects of scleroderma (oesophageal hypomobility)?
- Decreased resting pressure of LOS
- → Gastroesophageal reflux disease develops
Often associated with CREST syndrome
What is the treatment available for scleroderma (oesophageal hypomobility)?
- Exclude organic obstruction
- Improve force of peristalsis with prokinetics (cisapride)
- Once peristaltic failure occurs → usually irreversible
Outline the pathophysiology of corkscrew oesophagus (3).
- Diffuse oesophageal spasm
-
Incoordinate contractions
- Pressures of 400-500 mmHg
- Marked hypertrophy of circular muscle
How is corkscrew oesophagus diagnosed?
Barium swallowing
What are the symptoms of corkscrew oesophagus (2)?
- Dysphagia
- Chest pain
What treatment is available for corkscrew oesophagus?
- May respond to forceful pneumatic dilation (PD) of cardia
Results not as predictable as achalasia
What are the 3 areas of anatomical constriction of the oesophagus?
- Cricopharyngeal constriction (larynx)
- Aortic and bronchial constriction
- Diaphragmatic and ‘sphincter’ constriction
What are the causes of oesophageal perforation (6)?
- Iatrogenic (OGD) >50%
- Spontaneous (Boerhaave’s) - 15%
- Foreign body - 12%
- Trauma - 9%
- Intraoperative - 2%
- Malignant - 1%
- Usually at OesophagoGastroDuodenoscopy (OGD)
- More common in presence of diverticula or cancer
Outline the pathophysiology of Boerhaave’s syndrome.
- Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
Vomiting against a closed glottis
How common is Boerhaave’s syndrome?
3.1 per 1,000,000
What are common foreign bodies that cause oesophageal perforation (5)?
-
Disk batteries
- Cause electrical burns if embeds in mucosa
- Magnets
- Sharp objects
- Dishwasher tablets
- Acid/Alkali
What are the symptoms of oesophageal perforation caused by trauma (4)?
Neck = penetrating
Thorax = blunt force
- Dysphagia
- Blood in saliva
- Haematemesis
- Surgical empysema
How does oesophageal perforation present (4)?
- Pain 95 %
- Fever 80 %
- Dysphagia 70 %
- Emphysema 35 %
What investigations are recommended in suspected oesophageal perforation (4)?
- CXR
- CT
- Swallow (gastrograffin)
- OesophagoGastroDuodenoscopy (OGD)
What is the primary managements of oesophageal perforation (6)?
- NBM
- IV fluids
- Broad spectrum ABx & Antifungals
- ITU/HDU level care
- Bloods (including G&S)
- Tertiary referral centre
- Surgical emergency - Oesophagectomy
2x ↑mortality if 24h delay in diagnosis
What are the protective mechanisms against reflux?
- Increased LOS pressure
- Angle of His
- Volume clearance - oesophageal peristalsis reflex
- pH clearance - saliva
- Epithelium - barrier properties
What does the failure of the protective mechanisms against reflux lead to?
Gastro-oesophageal reflux disease (GORD)
What is the diagnosis?
Sliding Hiatus Hernia
What is the diagnosis?
Rolling / Paraoesophageal Hiatus Hernia
What investigations are recommended in suspected gastro-oesophageal reflux disease (GORD) (3)?
-
OesophagoGastroDuodenoscopy (OGD)
- To exclude: Cancer
- To confirm: Oesophagitis / Peptic stricture / Barretts oesophagus
- Oesophageal manometry
- 24-hr oesophageal pH recording
What treatments are available for gastro-oesophageal reflux disease (GORD) (2M / 2S)?
- Medical
- Lifestyle changes (wt loss, smoking, EtOH)
- PPIs
- Surgical
- Dilatation peptic strictures
- Laparoscopic Nissen’s fundoplication
What are the functions of the stomach (3)?
- Breaks food into smaller particles (acid & pepsin)
- Holds food, releasing it in controlled steady rate into duodenum
- Kills parasites & certain bacteria
What is found in the cardia & pyloric region of the stomach to assist with its functions (1)?
Mucus
What is found in the body & fundus of the stomach to assist with its functions (3)?
- Mucus
- HCl
- Pepsinogen
What is found in the antrum of the stomach to assist with its functions (1)?
Gastrin
What are the 4 main forms of gastritis?
- Erosive & haemorrhagic gastritis
- Nonerosive, chronic active gastritis
- Atrophic (fundal gland) gastritis
- Reactive gastritis
What is the main cause (numerous causes) of erosive & haemorrhagic gastritis?
- Acute ulcer - gastric bleeding & perforation
What is the main cause of nonerosive, chronic active gastritis?
- Helicobacter pylori infection in the antrum of the stomach
What is the main cause of atrophic (fundal gland) gastritis?
- Autoantibodies vs parts & products of parietal cells in the fundus of the stomach
- Parietal cells atrophy
- ↓acid & IF secretion
What are the 3 forms of stimulations of gastric secretions?
- Neural
- Endocrine
- Paracrine
Describe the neural stimulation of gastric secretion.
- ACh from postganglionic transmitter of vagal parasympathetic fibres
Describe the endocrine stimulation of gastric secretion.
- Gastrin from G cells of antrum
Describe the paracrine stimulation of gastric secretion.
- Histamine from ECL cells & mast cells of gastric wall
What are the 3 forms of inhibition of gastric secretions?
- Endocrine
- Paracrine
- Paracrine & Autocrine
Describe the endocrine inhibition of gastric secretion.
- Secretin from the small intestine
Describe the paracrine inhibition of gastric secretion.
Somatostatin
Describe the paracrine & autocrine inhibition of gastric secretion (4).
- PGE2
- PGI2
- TGF-α
- Adenosine
How does the stomach protect itself from its acid (4)?
- Mucus film
- HCO3- secretion
- Epithelial barrier
- Mucosal blood perfusion
What mechanisms repairing epithelial defects are in place in the stomach (3)?
- Migration
- Gap closed by cell growth
- Acute wound healing
How is ‘migration’ used as a repairing mechanism in the epithelial defects in the stomach?
- Adjacent epithelial cells flatten to close gap via sideward migration along Basal membrane
What factors stimulate the cell growth that closes the gap in epithelial defects in the stomach (5)?
- EGF
- TGF-α
- IGF-1
- GRP
- Gastrin
How is ‘acute wound healing’ used as a repairing mechanism in the epithelial defects in the stomach (6 steps)?
- Basal membrane (BM) destroyed
- Attraction of leukocytes & macrophages
- Phagocytosis of necrotic cells
- Angiogenesis
- Regeneration of ECM after repair of BM
- Epithelial closure by restitution & cell division
What happens when repairing mechanism in the epithelial defects fail?
Ulcers form
What are the possible outcomes of a Helicobacter pylori infection?
Outline the pathophysiology of a Helicobacter pylori infection leading to an ulcer (5 steps).
What is the primary treatment of an ulcer (2)?
Primarily medical
* PPI or H2 blocker
* Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
What are the surgical indications for the treatment of an ulcer (3)?
- Intractability (after medical therapy)
- Relative: continuous requirement of steroid therapy/NSAIDs
-
Complications:
- Haemorrhage
- Obstruction
- Perforation
