Disorders of Upper GI Tract Flashcards
What type of muscle is found in the oesophagus
cervical oesophagus → skeletal
upper and middle thoracic oesophagus → mix of skeletal and smooth
lower thoracic oesophagus → smooth
at lower end towards the lower esophageal sphincter is where the majority of pathology is
at what level does oesophagus start and end
C5 - upper esophageal sphincter
T10 - diaphragm/LOS
explain the structure of the LOS
physiological sphincter - does not have specific sphincteric muscle, sphincteric control is maintained by these factors
number of anatomical contributions to sphincter (things can go wrong with each):
3-4cm distal oesophagus are within abdomen → therefore when diaphragm contracts → increase in intra abdominal pressure → compresses distal oesophagus in abdomen → increases the LOS pressure
left and right crus of diaphragm surround the LOS → diaphragm contracts → contraction of the crura against the sphincter → very important for effective sphincter
intact phrenoesophageal ligament (extension of inferior diaphragmatic fascia) - 2 limbs of the ligament, upper limb attaches esophagus and superior diaphragm surface and lower limb attaches inferior diaphragm surface to cardia of stomach → ligament allows the diaphragm and esophagus to move independently of each other during respiration and swallowing respectively
angle of His - the acute angle between the abdominal oesophagus and fundus of stomach at esophagogastric junction → prevents reflux disease → when you eat, fundus expands → pushes structures from left to right → compressing distal oesophagus
when are the upper and lower esophageal sphincters open and closed
oral phase of swallowing - both closed (only phase under conscious control)
pharyngeal phase - upper opens, then lower opens via receptive relaxation through vasovagal reflex
upper esophageal phase - upper closes. lower still open
lower esophageal phase - lower closes
at rest both sphincters are normally closed
how is normal swallowing measured
manometry - tube passed through nose and down oesophagus → records the pressure of contractions at different points of the oesophagus → used to determine esophageal motility
normal peristaltic waves are around 40mmHg → would see the propagation of this size of wave down oesophagus in normal swallowing
explain the manometry of normal swallowing
swallowing induces peristaltic wave of around 40mmHg
migration of 40mmHg wave down oesophagus as peristalsis occurs
baseline pressure of LOS is around 20mmHg
due to the receptive relaxation caused by swallowing there is a decrease in the pressure by 5mmHg as it opens
(opening is controlled by noncholinergic nonadrenergic neurons of myenteric plexus)
when the peristaltic waves reach the LES the pressures increase to around 40mmHg then returns to 20mmHg once passed
explain how the lower oesophageal sphincter opens
receptive relaxation reflex
vagal efferent fibres synapse onto inhibitory noncholinergic, non-adrenergic neurons in the myenteric plexus which then inhibit the tonic contraction of the LOS → opening of sphincter (as it relaxes)
what is dysphagia
difficulty swallowing
need to localise where the difficulty is - cricopharyngeal (UES) or more distal
type of dysphagia:
for solid or fluids
intermittent or progressive
precise or vague in appreciation (how aware are they of what the swallowing problem is)
what is odynophagia
pain on swallowing
what is regurgitation
return of oesophageal contents from above an obstruction
can be functional (no physical blockage) or mechanical (physical blockage)
what is reflux
passive return of gastroduodenal contents to mouth
what is the difference between reflux and regurgitation
reflux - return of gastroduodenal contents into mouth (passive)
regurgitation - return of oesophageal contents from above an obstruction
summarise pathological problems of oesophagus
stricture is most common (narrowing) → due to cancer → can be benign or malignant
absence of stricture (sphincter does not work properly) can be caused by:
disordered esophageal contraction:
hypermotility
hypomotility
disordered coordination of swallowing
failure of protective reflux mechanisms leads to GORD
what is oesophageal hypermotility
achalasia:
loss of ganglion cells in aurebach’s myenteric plexus in the wall of LOS → decreased inhibitory activity of the noncholinergic non-adrenergic (NCNA) neurones
NCNA neurons are responsible of the receptive relaxation of the LOS → without them the LOS remains in a tonically constricted state
what causes achalasia
cause of primary achalasia is unknown, suggested mechanism:
environmental trigger e.g. chronic infection + genetic predisposition → non autoimmune inflammatory infiltrate e.g. TH1 → extracellular turnover + wound repair → eventually fibrosis → loss of immunological tolerance → apoptosis of neurons → humoral autoimmune response → antimyenteric antibodies → loss of myenteric neurons + impaired LES relaxation
secondary achalasia:
diseases which cause esophageal motor abnormalities which are very similar to primary achalasia and have the same symptoms
Chagas’ disease - south american parasitic infection
Protozoa infection
amyloid, sarcoma, eosinophilic oesophagitis
what are the physiological effects of achalasia
increased resting pressure of LOS
baseline resting pressure in healthy individual is normally around 20mmHg, then when swallowing occurs there is receptive relaxation and pressure of LOS decreases to less than 5mmHg
in achalasia, receptive relaxation sets in late and is too weak, as baseline/resting pressure is much higher than normal
therefore during reflex relaxation pressure in LOS is markedly higher than in stomach → swallowed food collects in oesophagus → increased pressure throughout oesophagus + oesophagus dilatation (can be seen on barium swallow)
over time propagation of peristaltic waves stops
what are the symptoms of achalasia
weight loss
trouble swallowing - dysphagia
regurgitation
retrosternal pain
what are the potential complications of achalasia
why
oesophagitis → trapped food
pneumonia - due to frequent regurgitation of oesophageal contents which contain bacteria → can then enter lung
x28 increase in risk of oesophageal cancer (very rare cancer)
describe the course of achalasia
insidious onset - patients can have symptoms of parasternal pain, weight loss, regurgitation for years prior to seeking help
without treatment → progressive dilation of esophagus
what does this x ray show
what would cause this
oesophageal dilation
inability of food to pass into stomach so accumulates in oesophagus
achalasia → loss of inhibitory NCNA neurons in aurebach myenteric plexus in LOS wall → reduced relaxation of LOS
could be primary or secondary
pressure of LOS does not decrease enough during receptive relaxation to allow passage of food into stomach
how is achalasia treated
easiest treatment:
pneumatic dilatation - inflate balloon in LOS → circumferential stretching + sometimes tearing of muscle fibres in LOS → restores patency of LOS
71-90% of patients respond initially but then relapse
definitive treatment = surgery
Heller’s myotomy → muscularis layer of 6cm of oesophagus above LOS and 3cm of stomach below LOS is cut → this leaves mucosa exposed
then Dor fundoplication - anterior fundus is folded over exposed esophagus and sutured to right side of myotomy
risks of surgery: gastric or oesophageal perforation = 10-16% splenic injury (due to moving stomach) = 1-5% division of vagus nerve = rare
what causes oesophgeal hypomotility
scleroderma - autoimmune disease
in its early stages leads to hypomotility as it causes neuronal defects → atrophy of esophageal smooth muscle → eventually peristalsis in distal oesophagus stops completely
there is decreased resting pressure of LOS
what is the effect of sceleroderma on the body
causes neuronal defects → smooth muscle atrophy → peristalsis in distal oesophagus stops
muscle atrophy → decreased tone of of LOS → decreased resting pressure of LOS → gastroesophageal reflux disease developing
CREST syndrome: associated with scleroderma
Calcium deposits in soft tissue
Raynauds phenomenon - constriction of peripheral blood vessels
Esophageal dysmotility
Sclerodactyly - thickening of skin on digits of hands and feet
Telangiectasia - dilated capillaries → red marks on skin
how is scleroderma treated
exclude organic obstruction → make sure there is no malignancy
give prokinetics e.g. Cisapride - to improve force of peristalsis
once peristaltic failure has occurred it is usually irreversible
what is a cause of disordered coordination of swallowing
corkscrew oesophagus
uncoordinated contractions → marked hypertrophy of circular muscle in oesophagus → which generate very high pressures around 400-500mmHg
what are the symptoms of corkscrew oesophagus
how is it diagnosed
dysphagia and chest pain
corkscrew oesophagus can be seen on barium swallow + oesophago-gastro-duodenoscopy
where are the anatomical constrictions of the oesophagus
how are these clinically relevant
cricopharyngeal constriction - near where it starts at the level of the cricoid cartilage, around C5/6
aortic and bronchial constriction - where the aorta crosses in front at T4/5 and where left main bronchus cross in front at T5/T6
diaphragmatic constriction - where it passes through diaphragm, at T10
where are the anatomical constrictions of the oesophagus
how are these clinically relevant
cricopharyngeal constriction - near where it starts at the level of the cricoid cartilage, around C5/6
aortic and bronchial constriction - where the aorta crosses in front at T4/5 and where left main bronchus cross in front at T5/T6
diaphragmatic constriction - where it passes through diaphragm, at T10, same level as LOS
perforations are most likely to occur at these 3 areas
there can also be pathological narrowing due to cancer, foreign body, or physiological dysfunction
what happens during a spontaneous esophageal perforation
spontaneous perforation also called boerhaave’s
sudden increase in intra-oesophageal pressure with negative intrathoracic pressure → vomiting against a closed glottis → full thickness tear in oesophagus, most likely at the left posterolateral aspect of the distal oesophagus
quite rare - 3.1 per 1,000,000
but responsible for 15% of perforations in general
what investigations are done with suspected oesophageal perforation
chest x ray
CT
gastrografin - contrast to show where perforation is exactly
OGD - but only if definitely necessary
what is the definitive management for oesophageal perforation
operative management:
primary repair of esophagus → stitching layers of wall back together
rarely oesophagetomy → only if oesophagus is very damaged, stomach is then joined to patent proximal oesophagus
if perforation is very minor it can be managed conservatively with metal stent but surgery should be default management
what factors influence LOS pressure
NCNA (non-cholinergic non-adrenergic) neurons → receptive relaxation of LOS = reduces LOS pressure
therefore acetylcholine and alpha-adrenergic agonists increase LOS pressure and prevent reflux
what are the protective mechanisms following reflux
why are these necessary
protective mechanisms:
volume clearance → esophageal peristalsis reflex - when there is sporadic reflux, this triggers a peristaltic reflex which clears any reflux contents in the oesophagus back into the stomach
pH clearance → saliva buffers the acidic pH of the reflux contents when they re-enter the oesophagus
epithelium of distal oesophagus - has barrier properties
these are mechanisms necessary because sporadic reflux is normal
sudden pressure on LES from full stomach
reflux on swallowing (when LES opens)
transient sphincter opening - spontaneous LES opening which is induced without swallowing
what happens in GORD
there is failure of the protective mechanisms following reflux - can be due to a number of reasons
increased frequency of transient sphincter opening → e.g. due to drinking fizzy drinks
abnormal peristalsis e.g. due to achalasia → decreased volume clearance
reduced saliva production e.g. in sleep or xerostomia → reduces pH clearance
reduced buffering capacity of saliva e.g. due to smoking → reduced pH clearance
defective mucosal protection e.g. due to alcohol → reduced barrier epithelium
hiatus hernia
overall lead to reflux oesophagitis → epithelial metaplasia → carcinoma
what is a hiatus hernia
sliding hiatus hernia:
phrenoesophageal ligament gives way → distal oesophagus (gastro-oesophageal junction) and cardia of stomach become distended through diaphragm superiorly into chest (no longer intra-abdominal)
contributes to GORD as there is increased reflux from stomach into distal esophagus
rolling hiatus hernia:
upward movement of gastric fundus through diaphragm to lie alongside a normally positioned gastro-oesophageal junction
surgical emergency - can become strangulated → ischaemia → necrotic → perforated organ
how is GORD treated
medically:
lifestyle changes - weight loss, stop smoking, reduce alcohol
manage with PPIs e.g. omeprazole
surgically (rarely needed):
dilatation of peptic strictures
laparoscopic NIssen’s fundoplication → dissection + closure of oesophageal hiatus (tightens it), and then wrap fundus around distal oesophagus and suture to reinforce sphincter action, make sure to not suture too tight as then patient can’t swallow
what does the stomach produce
cardia and pyloric region → only mucus
body and fundus → mucus, HCL, pepsinogen
antrum → gastrin
label the stomach
what are the different types of gastritis
erosive and hemorrhagic gastritis - can occur anywhere in stomach
nonerosive chronic active gastritis - antrum
atrophic (fundal gland) gastritis - fundus
reactive gastritis
what causes erosive and hemorrhagic gastritis
what are the consequences of this disease
can occur anywhere in body
many causes:
NSAIDS, alcohol
multi-organ failure, burns
trauma, stress
ischaemia (gastritis can be secondary to gastritis)
most common cause of acute ulcers → which either cause massive gastric bleeding or stomach wall perforation
what causes nonerosive chronic active gastritis
how is it treated
what are the consequences of this disease
H.pylori → easily treated → amoxicillin, clarithromycin, pantoprazole all 3 for 1-2 weeks
usually only affects antrum
increased gastrin secretion due to H.pylori → increased acid secretion → ulcers
used to cause gastric ulcers and duodenal ulcers which then perforated or caused bleeding but now it doesn’t as the H.pylori is easily treated before this all can occur
can also cause reactive gastritis
what causes atrophic (fundal gand) gastritis
what are the consequences of this
autoantibodies to parts or products of parietal cells (parietal cells normally secrete IF and HCl)
decreased acid secretion → increased gastrin secretion → g cell hyperplasia → epithelial hyperplasia → carcinoma
(g cells produce gastrin which then normally acts on parietal and ECL to increased HCl secretion)
increased gastrin secretion → ECL cell hyperplasia → carcinoid (neuroendocrine tumours)
decreased intrinsic factor production → decreased cobalamine(B12) absorption → pernicious anaemia, increased MCV, macrocytes, anisopoikilocytosis
how is gastric secretion controlled
important to protect from ulcers
how is the gastric mucosa protected from gastric secretion
mucus film - epithelial cells produce mucus → layer 0.5-1cm thick → protects against H+ and pepsin
HCO3- secretion by epithelial cells → buffers H+
epithelial barrier → tight junctions on apical membrane → prevents H+ penetration
mucosal blood perfusion → if H+ ions do get past epithelial barrier they are quickly taken away by basolateral blood flow
these are all important to protect the mucosa from ulcers forming
how does gastric ischaemia cause ulcers
normally good mucosal blood perfusion means that any H+ ion which are able to pass through mucus film + epithelial barrier are taken away quickly on the basolateral side via blood supply
however when there is ischaemia this doesn’t happen → ulcer formation
how does the gastric mucosa repair itself
why is this necessary
cells are destroyed but basement membrane is intact:
migration - epithelial cells flatten and then migrate sideways to close gap
rapid cell growth - stimulated by EGF, TGF-alpha, IGF1, GRP and gastrin
when cells and basement membrane destroyed in acute wounds:
leukocyte + macrophage attraction → phagocytosis of necrotic cells
rapid angiogenesis + repair of basement membrane, then ECM is regenerated
epithelial closure by restitution & cell division
how do ulcers form
draw diagram
barrier function of epithelia is disturbed or there is increased chemical aggression → epithelial damage → wound forms which is unable/doesn’t heal → ulcer → which can then bleed and perforate
can be due to:
H.Pylori - disturbs barrier + invades mucosa
increased secretion of gastric juice - NSAIDS decrease PG which normally inhibit secretions, smoking also increases secretions
decreased HCO3- secretion - NSAIDS inhibit PG which normally stimulate secretion
decreased ability of cell formation (wound repair) - smoking causes this
decreased blood perfusion - stress, ischaemia, trauma → mucosa is not protected as substances which invade are not taken away
what would an ulcer in a young person who does not smoke, drink, on NSAIDS or stressed suggest
young and no risk factors = potential cause is gastrinoma
rare neuroendocrine tumours which secrete large amounts of gastrin → increased gastric secretions → ulcer
what are the clinical outcomes of people who have H.pylori infection
over 80% will be asymptomatic or have chronic gastritis
15-20% have chronic atrophic gastritis or intestinal metaplasia and gastric or duodenal ulcers
<1% get gastric cancer and MALT lymphoma
how are gastric ulcers treated
