The Oesophagus and Its Disorders Flashcards
Describe the basic anatomy of the oesophagus
- Fibromuscular 25cm tube composed of striated squamous epithelium
- Posterior to trachea
- Begins at end of laryngopharynx, joins stomach a few cm from diaphragm (at cardiac orifice of stomach)
Describe the muscular structure of the oesophagus
- Skeletal muscles surround upper third oesophagus, below pharynx
- Smooth muscle surround lower two thirds
Oesophagus has 2 sphincters:
- Upper oesophageal sphincter (UOS): striated muscle;
- Musculo-cartilaginous structure
- Constricted to void air entering oesophagus
- Lower oesophageal sphincter (LOS) smooth muscle; acts as flap valve:
- Area of high pressure
- Intrinsic and extrinsic components
- Intrinsic - Oesophageal muscles; under neurohormonal influence (CCK, secretin, glucagon, these relax this, but gastrin motillin etc contract the LOS)
- Extrinsic - Diaphragm muscle (Adjunctive external sphincter)
- Extrinsic and intrinsic sphincters work together, food pushe dintmo stomach
- Malfunction of these sphincters’ components leads to GORD
Describe the components of LOS
Intrinsic components:
- Thick circular smooth muscle layers and longitudinal muscles
- Clasp-like semi-circular smooth muscle fibres on right side - Have myoenic activity (some resting tone initiated by cells within), but less Ach responsive
- Sling-like olblique gastric (angle of His- angle create b/w entrance of stomach (cardiac orifice) and oesophagus) muscle fibres on left side - Work in convert with clasp-like semicircular smooth muscle fibres, help prevent regurgitation, responsive to cholinergic innervation
- Angle of His poorly developed in infants, makes vertical junction with stomach, hence why reflux common in infants
Extrinsic components:
- Crural diaphragm encircles LOS - Forms channel through which oesophagus enters abdomen
- FIbres of crural portion of diaphragm possess a “pinchcock-like” actions (extrinsic sphincter; diaphragmatic sphincter) - Myogenic tone
Describe the innervation of the oesophagus
- Upper part - Striated muscle; Supplied by somatic motor neurones of vagus nerve w/o interruption
- Splanchnic nerves (thoracic sympathetic trunks)
- Lower part - Smooth muscles;
- Innervated by visceral motor neurones of vagus nerve with inerruptions (synapse with postganglionic neurones; cell bodies in oesophagus and splanchnic plexus)
Involvment of cholinergic and non-cholingeric, NANC interaction in control of tone of LOS
Neural control of oesophageal sphincters:
- Oesophagus encircled by nerves of oesophageal plexus
- Ach and SP contract intrinsic sphincters
- NO and VIP relax intrinsic sphincters
- Gastrin contracts the intrinsic sphincters)
Describe the motor innervation of the oesophagus
- Striated muscle of upper oesophagus is innervated by somatic efferent cholinergic fibres of the vagus nerve originating from nucleus ambiguus
- Smooth muscle of distal oesophagus innervated by preganglionic vagus nerve fibres from dorsal motor nucleus
- Ach affect 2 types of post-ganglionic neurones in the myenteric plexus: excitatory cholinergic neurones and inhibitory nitrergic neurones via NO, VIP
What are the functions of the oesophagus?
- Swallowing (deglutition); secreted mucus eases swallowing
- Conveys food and fluids from pharynx to stomach
- Afferent impulse in glossopharyngeal nerve - vagal reflex
- Integration of impulse in nucleus of tractus solitarius (NTS), nucleus ambiguus (NA) and dorsal vagal nucleus
- Efferent impulses/motor pathways pass to pharyngeal musculature, tongue, along oesophagus, LOS opens
- Coordinated opening and closing of UOS and LOS permits food mass to reach stomach
Describe how swallowing is initiated and the reflex responses
Initiation:
- Voluntary action of collecting material on the tongue and pushing it backwards into the pharynx (skeletal muscle, mucus membrane)
- Food moves from mouth → oropharynx → laryngopharynx → oesophagus → stomach
- Swallowing centre = brain stem; sensory and cortical input with respect to swallowing are integrated in NTS, NA and DVN
Reflex responses:
- Inhibition of respiration - Nasopharynx close doff
- Closure of flottis (around vocal cords) by epiglottis
- Prevents food entering trachea
- Ring of peristaltic waves behind food mass moves it towards stomach. The LOS opens and stays open throughout swallowing. Progressive muscular contractions and relaxation move food towards stomach and along whole length of GI tract
- Second wave peristalsis moves any food remnants along oesophagus
Describe the secondary peristalsis
Upon relaxation of UOS, food mass passes:
- UOS closes as soon as food passes
- Glottis opens
- Breathing resumes
- Coordinated peristalsis moves food towards LOS
LOS closes after food mass passed
Large food material doesn’t often reach stomach after 1st peristaltic wave
Distension of lumen of oesophageal body by food remnants stimualtes receptors, leading to repeated waves of peristalsis (this is secondary peristalsis)
Secondary peristalsis makes sure all ingested food reaches the stomach
Describe why oesophageal monometry is needed
- To determine cause of non-cardiac chest pain
- Evaluate cause of reflux of stomach acid and other contents back up into oesophagus
- Determine cause of swallowing difficult
- Allows evaluation of strength of coordination of muscle contractions
- Functional relaxation of LOS
- Overall tests if oesophagus contracting + relaxing properly
- Results may be as follow
- Pressure of LOS <26mm Hg is normal; >100 mm Hg is considered achalasia; > 200 mm Hg is nut cracker achalasia
- Low LOS pressure suggests GORD, but GORD can occur in individuals with normal LOS pressure
What would normal results of oesophageal manometry look like? What are the characteristics of abonormal results and achalasia?
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- Normal LOS pressure and normal muscle contractions upon swallowing
- Muscle contractions follow normal pattern down oesophageal body
- Normal pressure LOS approx 15mmHg but:
- When relaxed, pressure less than 10mmHg
- If LOS is less 10mmHg in absence of allowing food mass to pass into stomach, GORD can be suspected
- Presence of muscle spasms in oesophageal body
- Presence of weak contractions along length of oesophagus
- Lack of coordinated LOS relaxation in response to swallowing
Describe the procedure of an oesophageal manometry
- Spray local anaesthetic/numbing gel
- Lubricated pressure-sensitive tube (catheter) inserted into nostril → throat → oesophagus → stomach;
- Deep breath and swallow water
- Measure strength and coordination of contractions
- Also evaluates strength and relaxation function of LOS
- Slowly remove catheter at end
- Data may also help determine where in oesophagus to place pH probe
Describe the mechanisms that prevent gastro-oesophageal reflux
There’s an anti-reflux barrier in the region of the gastro-oesophageal junction:
- LOS closs after food mass passes
- “Pinchcock” effect of diaphragmatic sphincter on lower oesophagus
- Plug-like action of mucosal folds in cardia - occludes lumen of gastro-oesophageal junction:
- Intrabdominal pressure compresses intra-abdominal parts of oesophagus
- Valve-like effect of oblique entry of oesophagus into stomach
- Sphincter muscles of UOS and LOS = Strong circular muscles
- Act as valves; law of gut promotes and controls movement of food mass aborally (movement towards anus)
- Prevent reflux by forming and opening when relaxed AND closing completely when contracted
Describe oropharyngeal dysphagia/aphagia
Swallowing difficulty caused by inability of UOS to open or discoordination of timing b/w opening of UOS an the pharyngeal push behind ingested mass of food
Describe oesophageal spasms
Abnormal oesophageal contractions so food doesn’t reach stomach effectively
Diffuse oesophageal spasm - Chest pain coming from oesophagus (angina-like pain)
Describe achalasia and its pathology
Disorders of motility or peristalsis of oesophagus )asses motor function of UOS, LOS and oesophageal body)
- Impaired LOS relaxation (spasms)
- Can be accompanied by impaired peristalsis (sphincter spasms)
- Food and liquids fail to reach stomach - delayed opening of LOS
- Dilation of oesophageal body with distal narrowing (bird beak appearance) of the barium-filled oesophaus on oesophagram
- Long period of sporadic dysphagia (difficulty swallowing)
- Regurgitation of food
Describe the aetiology of achalasia
Initiating factor unkown, but thought to be autoimmune or triggered by infection
What are the symptoms of achalasia?
- Dysphagia - Difficult and/or painful swallowing
- Vomiting/regurgitation
- Heartburn
- Retrosternal burning sensation due to oesophageal dysmotility
- Retention of ingested (acidic) food
- Generation of lactic acid in process of decomposition of retained food
- Can be caused by retention of small quantitie of gastric acid refluxed in oesophagus due to poor emptying and incomplete relaxation of LOS
How is achalasia diagnosed?
Patient’s history/symptoms, examination of patient, elderly may have abnormalities in swallowing
- Barium radiography (swallow) - Dilation of oesophagus with beak deformity at lower end, evaluates entire swallowing channel (mouth, pharyx and oesophagus)
- Oesophageal manometry: absent peristalsis
How can achalasia be treated?
Achalasia is a risk factor for squamous carcinoma
Determine surgery risk:
If low:
- Laparascopic Heller’s myotomy (<40y/o, men) if this fails then do redo myotomy, pneumatic dilation, if this fails, oesphagectomy
- Pneumatic dilation (>40y/o, women), if fails then laparoscopic, Heller’s myotomy, if that fails then oesphagectomy
High surgical risk:
- Botulinum toxin injection, if that fails CCBs/nitrates
Describe regurgitation
Reflux of stomach acids into oesophagus; weak LOS (GORD); assess causes of regurgitation
It’s normal to experience some regurgitation after meals, reflux usually stimulates salivation. Saliva is an effective natural antacid that dilutes and neutralises refluxed gastric acid
Low rates of salivation or the lack of ability to swallow own saliva ca cause prolongation of contact of refluxed gastric juice with oesophagus
Malfunction of extrinsic and intrinsic components of LOS → GORD
Describe GORD and its symptoms
Retrograde movemnt of gastric content into oesophagus, due to prolonged relaxation of LOS
GORD is when reflux more frequent and troubling
Causes oesophageal irritation and damage
Chronic oesophagitis (erosive or non-erosive) has 30% prevalance
Symptoms:
- Heartburn - retrosternal (angina-like pain) often after eating
- Coughs as reflux can irritate larynx, may also cause interrupted sleep
- Belching
- Regurgitation
- Dysphagia
What causes reflux in GORD?
- Transient spontaneous LOS relaxation
- Resting LOS pressure too weak to resist pressure within stomach
- Sudden (+ sustained) relaxation of LOs NOT induced by swallowing
Describe the factors that contribute to the severity of GORD
- Weak or uncoordinated oesphageal contractions/poor oesophageal motor activity - poor oesophageal peristalsis → decreased clearance of gastric acid
- Duration of contact of gastric acid with oesophagus
- Impaired gastric emptying alone an cause severe GORD
- Increased Gastric acid secretion as well as presence of bile in gastric contents → severe oesophageal damage
- Amount of pressure placed on anti-reflux barrier and less functional LOS; low or absent resting LOS tone
- LOS tone fails to increase when lying flat or during pregnancy
- Some foods, heavier meals
- Some drugs
- Pregnancy or obesity
How is GORD investigated?
- Low dose PPI (proton pump inhibitor) challenge is 1st line
- Upper GI endoscopy
- Monometry
- 24hr ambulatory pH monitoring
FIndings from 24hr pH:
- 24 hr pH monitoring shows that most normal indivuals reflux on a daily basis
- GORD implies not just the presence of reflu but reflux in excess of what would be normally
Describe GORD in pregnancy
- Last trimester associated with increased abdominal pressure which forces gastric contents into oesophagus
- Foetus increases pressure on abdominal contents
- Pushes terminal segments of oesophagus into thoracic cavity
- Heartburn subsides in the last month of pregnancy as uterus descends into pelvis
Describe the pharmacological treatment methods for GORD
Rationale:
- Neutralise secreted acid with antacids (alkali substances e.g. Mg(OH)2, Al(OH)3; Increases pH of gastric lumen and inhibits peptic activity
- Reduce acid secretion with H2 receptor antagonists, these block the binding of histamine to parietal cells, inhibiting the production of HCl
- Attempt to eradicate H.pylori - This is a gram-negative bacillus, can lead to chronic gastritis which can lead to dudoenal ulcers, it’s a risk factor for gastric ulcers
Inhibition of acid secretion removes constant irritation, allows ulcers to heal
Drugs can be used to inhibit or neutralise gastric acid secretion for the following conditions:
- Peptic ulcer
- Reflux oesophagitis: gastric acid secretion can damage oesophagus
- Zollinger-Ellision syndrome: gastrin-producing tumour
Describe the general mechanism of action of antacids
- Neutralise stomach acid
- Increase pH of gastric activity (peptic acivity stops at pH 5)
- Prolong dosing can lead to healing of duodenal ulcers; less effective for gastric ulcers
Alginic acid and saliva form a raft which floats on the content of the gastric lumen and protects the oesophageal mucosa from the refluxed gastric acid
Bismuth chelate:
- Protects gastric mucosa
- Forms base over crater of ulcer
- Absorbs pepsin
- Increases HCO2- and prostaglandin secretion
- Toxic against H.pylori - Used as part of triple therapy to eradicate it
- Blackens stool and tongue
- Not for use in children with chicken-pox or flu-like symptoms as can cause Reye’s syndrome and contains aspirin
What are some examples of H2 receptor antagonists and PPIs and explain their rationale
Rationale - Neutralsie secreted acid or inhibit the ability of mediators of acid secretion (gastrin, histamine, Ach) to elicit secretion of gastric acid
H2 receptor antagonists include cimetidine, famotidine
PPIs include omeprazole, lansoprazole
All of the above agents decrease acid secretion and help heal ulcers, but removal of H pylori is needed to prevent recurrence, hence combination therapy with the use of antibiotics must be used
Describe the pharmacological management of gastric ulcers
Use of H2 receptor antagonists - Cimetidine, famotidine, nizatidine
- Inhibit histamine, Ach, gastrin stimulated acid secretion
- Reduce gastric acid secretion and as a result reduce pepsin secretion
- Can decrease basal and food stimulated acid secretion by 90%
- Promote healing of duodenal ulcers
- Peptic ulcer
- Reflex oesophagitis
Describe non-pharmacological treatment of GORD
Rationale - Reduce/remove aggravators of acid secretion
- Life-style modifications - Raise head of bed at night, lose weight
- Avoid large meals or meals at bedtime
- Modify food - eat healthier, decrease intake of food + drink which cause symptoms (e.g. acidic foods, fatty foods that increase emptying time)
- Avoid lying down after meals, raise head of bed
- Avoid some drugs and smoking
- GORD can be stressed-induced, so exercise, mindfulness, yoga can help
Anti-reflux surgery (fundoplication - wrap fundus around LOS) - This can cause dysphagia as it can reduce the distensibility of the LOS
Describe the complications associated with GORD
Oesophagus has squamous mucosa:
- Acid reflux can lead to desquamation of oesophageal cells (injury of squamous mucosa)
- Increased cell loss leads to basal cell hyperplasia
- Excessive desquamation can leads to ulceration
- Ulcers can haemorrhage, perforate or heal by fibros with strictures
This leads to Barrett’s oesophagus (tissue appears similiar to that in stomach lining) and oesophageal cancer
Describe the long term effects of GORD
- Oesophagitis (erosive oesophagitis causes gastrointestinal bleeding), oesophageal strictures
- Oesophageal ulcer
- Barrett’s syndrome - may predispose an individual to oesophageal adenocarcinoma
- Squamous cell carcinoma
How do prostaglandins protect the stomach?
They increase secretion of mucus, bicarbonate and inhibit the secretion of HCl by parietal cells
