Disorders of Upper GI Tract

Question 1

What type of muscle is found in the oesophagus

Answer 1

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

Question 2

at what level does oesophagus start and end

Answer 2

C5 - upper esophageal sphincter

T10 - diaphragm/LOS

Question 3

explain the structure of the LOS

Answer 3

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

Question 4

when are the upper and lower esophageal sphincters open and closed

Answer 4

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

Question 5

how is normal swallowing measured

Answer 5

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

Question 6

explain the manometry of normal swallowing

Answer 6

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

Question 7

explain how the lower oesophageal sphincter opens

Answer 7

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)

Question 8

what is dysphagia

Answer 8

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)

Question 9

what is odynophagia

Answer 9

pain on swallowing

Question 10

what is regurgitation

Answer 10

return of oesophageal contents from above an obstruction

can be functional (no physical blockage) or mechanical (physical blockage)

Question 11

what is reflux

Answer 11

passive return of gastroduodenal contents to mouth

Question 12

what is the difference between reflux and regurgitation

Answer 12

reflux - return of gastroduodenal contents into mouth (passive)

regurgitation - return of oesophageal contents from above an obstruction

Question 13

summarise pathological problems of oesophagus

Answer 13

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

Question 14

what is oesophageal hypermotility

Answer 14

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

Question 15

what causes achalasia

Answer 15

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

Question 16

what are the physiological effects of achalasia

Answer 16

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

Question 17

what are the symptoms of achalasia

Answer 17

weight loss

trouble swallowing - dysphagia

regurgitation

retrosternal pain

Question 18

what are the potential complications of achalasia

why

Answer 18

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)

Question 19

describe the course of achalasia

Answer 19

insidious onset - patients can have symptoms of parasternal pain, weight loss, regurgitation for years prior to seeking help

without treatment → progressive dilation of esophagus

Question 20

what does this x ray show

what would cause this

Answer 20

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

Question 21

how is achalasia treated

Answer 21

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

Question 22

what causes oesophgeal hypomotility

Answer 22

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

Question 23

what is the effect of sceleroderma on the body

Answer 23

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

Question 24

how is scleroderma treated

Answer 24

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

Question 25

what is a cause of disordered coordination of swallowing

Answer 25

corkscrew oesophagus uncoordinated contractions → marked hypertrophy of circular muscle in oesophagus → which generate very high pressures around 400-500mmHg

Question 26

what are the symptoms of corkscrew oesophagus how is it diagnosed

Answer 26

dysphagia and chest pain corkscrew oesophagus can be seen on barium swallow + oesophago-gastro-duodenoscopy

Question 27

how is corkscrew oesophagus treated

Answer 27

forceful pneumatic dilatation of cardia but response to this treatment is not as predictable as achalasia

Question 28

where are the anatomical constrictions of the oesophagus how are these clinically relevant

Answer 28

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

Question 29

where are the anatomical constrictions of the oesophagus how are these clinically relevant

Answer 29

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

Question 30

what can cause esophageal perforation

Answer 30

\>50% are iatrogenic due to OGD 15% are spontaneous (Boerhaave's) 12% are due to foreign bodies 9% are due to trauma 2% are intraoperative 1% are malignancy

Question 31

why is it important to only do necessary investigations

Answer 31

can end up causing more damage with unnecessary investigations OGD are responsible for over 50% of oesophageal perforations, therefore make sure you definitely need to do one first

Question 32

when do iatrogenic perforations of the oesophagus occur how likely are they during procedures

Answer 32

usually during oesphago-gastro-duodenoscopy - more common in presence of diverticula (can get lost in a diverticulum and accidentally go through it and into chest) or cancer (can perforate easily) incidence of perforation: 0.03% of OGD 0.1-2% of stricture dilatation 1-5% of sclerotherapy 2-6% of achlasia dilatation OGD is most common cause of iatrogenic perforation, but the perforation risk is lower compared to other procedures in which there is more intervention

Question 33

what happens during a spontaneous esophageal perforation

Answer 33

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

Question 34

how can foreign bodies cause esophageal perforation

Answer 34

people swallowing objects: disk batteries → can cause electrical burns if they embed in mucosa magnets sharp objets dishwasher tablets an acidic or alkali liquid burning through

Question 35

what types of trauma cause oesphageal perforation

Answer 35

in the neck → penetrating trauma in the thorax → blunt force trauma

Question 36

how is oesphageal perforation caused by trauma diagnosed

Answer 36

can be difficult to diagnose: dysphagia blood in saliva haematemesis surgical emphysema - air in subcutaneous tissue, crepitus (crackling) on palpitation

Question 37

how does esophageal perforation usually present

Answer 37

95% → pain 80% → fever 70% → dysphagia 35% → surgical emphysema

Question 38

what investigations are done with suspected oesophageal perforation

Answer 38

chest x ray CT gastrografin - contrast to show where perforation is exactly OGD - but only if definitely necessary

Question 39

how is esophageal perforation managed when first diagnosed why is this important

Answer 39

**surgical emergency - mortality doubles if there is 24hr delay in diagnosis/care** nil by mouth IV fluids broad spectrum antibiotics and antifungals on ITU/HDU level care Bloods - including group and save referred to tertiary centre

Question 40

what is the definitive management for oesophageal perforation

Answer 40

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

Question 41

how does the LOS influence reflux

Answer 41

when LOS is closed it acts as a barrier against reflux LOS pressure determines how well it acts as a barrier: higher pressure → inhibits reflux lower pressure → promotes reflux

Question 42

what factors influence LOS pressure

Answer 42

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

Question 43

what are the protective mechanisms following reflux why are these necessary

Answer 43

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

Question 44

what happens in GORD

Answer 44

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

Question 45

what is a hiatus hernia

Answer 45

**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

Question 46

how is GORD diagnosed

Answer 46

symptoms - dyspepsia, dysphagia, regurgitation perform OGD to exclude cancer → if you find oesophagitis peptic strictures or barretts oesophagus these confirm GORD if patients are very symptomatic → perform oesophageal manometry and 24 oesophageal recordings to record the reflux + find out how serious it is

Question 47

how is GORD treated

Answer 47

**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

Question 48

what does the stomach produce

Answer 48

cardia and pyloric region → only mucus body and fundus → mucus, HCL, pepsinogen antrum → gastrin

Question 49

label the stomach

Answer 49

Question 50

what are the different types of gastritis

Answer 50

erosive and hemorrhagic gastritis - can occur anywhere in stomach nonerosive chronic active gastritis - antrum atrophic (fundal gland) gastritis - fundus reactive gastritis

Question 51

what causes erosive and hemorrhagic gastritis what are the consequences of this disease

Answer 51

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

Question 52

what causes nonerosive chronic active gastritis how is it treated what are the consequences of this disease

Answer 52

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

Question 53

what causes nonerosive chronic active gastritis how is it treated what are the consequences of this disease f

Answer 53

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

Question 54

what causes atrophic (fundal gand) gastritis what are the consequences of this

Answer 54

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

Question 55

how is gastric secretion controlled

Answer 55

important to protect from ulcers

Question 56

why is the role of prostaglandins in gastric secretion important to remember

Answer 56

PGE2 and PGI2 inhibit gastric secretion NSAIDs inhibit cyclooxygenase → reduced prostaglandin production → reduced inhibition of gastric secretion → more gastric secretions present, can cause ulcers also prostaglandins increase HCO3- production by gastric epithelial cells which buffers H+ → NSAIDS → compromised mucosal barrier → ulcers

Question 57

how is the gastric mucosa protected from gastric secretion

Answer 57

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

Question 58

how does gastric ischaemia cause ulcers

Answer 58

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

Question 59

how is the gastric mucosa protected from ulcer formation

Answer 59

control of gastric secretion - stimulated and inhibited by neural, endocrine + paracrine mechanisms, (PG, somatostatin and secretin inhibit secretions) mucosal protection - mucus film, HCO3- as buffer, epithelial barrier due to tight junctions, good mucosal blood perfusion mechanisms to repair epithelial cell defects + wounds → migration and then rapid cell growth stimulated by growth factors to close gaps and acute wound healing when basement membrane is destroyed

Question 60

how does the gastric mucosa repair itself why is this necessary

Answer 60

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

Question 61

how do ulcers form draw diagram

Answer 61

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

Question 62

what would an ulcer in a young person who does not smoke, drink, on NSAIDS or stressed suggest

Answer 62

young and no risk factors = potential cause is gastrinoma rare neuroendocrine tumours which secrete large amounts of gastrin → increased gastric secretions → ulcer

Question 63

what are the clinical outcomes of people who have H.pylori infection

Answer 63

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

Question 64

how are gastric ulcers treated

Answer 64