Upper GI Tract

Question 1

Where does the oesophagus start and end ?

Answer 1

Start-C5
End-T10

Question 2

Name the 2 Oesophageal sphincters ?

Answer 2

Lower Oesophageal Sphincter-LOS
Upper Oesophageal Sphincter-UOS

Question 3

What are the 4 anatomical contributions to the Lower Oesophageal Sphincter ?

Answer 3

LOS is more of a physiological sphincter, with a number of contributing anatomical contributions;
1- Distal 3-4cm of oesophagus in abdomen.
2-Diaphragm surrounds the LOS.
3- Intact Phrenoesophageal ligament.
4-Angle of His.

Question 4

How does the distal 3-4 cm of the oesophagus being in the abdomen contribute to LOS function?

Answer 4

If you get an increase in intra-abdominal pressure you get an increase in LOS pressure as well.

Question 5

How does the diaphragm surrounding the LOS contribute to its function ?

Answer 5

The left and right crux act like scissors when the diaphragm contracts, they contract against the sphincter.

Question 6

What is the role of the phrenoesophageal ligament in the function of the LOS ?

Answer 6

You need to have an intact phrenoesophageal ligament, this is an extension of the inferior diaphragmatic fascia, with two limbs one that goes superiorly and attaches to the lower part of the oesophagus the other goes inferiorly and attaches to the cardia of the stomach, this allows individual movement of the diaphragm during respiration and the oesophagus when you swallow.

Question 7

What is the structure known as ?

Answer 7

Angle of His, an acute angle between the abdominal oesophagus and the fundus of the stomach, at the oesophago-gastric junction. This prevents reflux disease by the fundus expanding and combressing the oesophagus when someone has had a large meal.

Question 8

How many stages are there in normal swallowing?

Answer 8

4

Question 9

What is stage 0 of normal swallowing ?

Answer 9

Oral phase - chewing and saliva prepares bolus, both the oesophageal sphincters are constricted

Question 10

What is stage 1 of normal swallowing ?

Answer 10

Pharyngeal phase - pharyngeal musculature guides food bolus towards oesophagus, the UOS opens reflexly. The LOS is opened by vasovagal reflex (receptive relaxation reflex).

Question 11

What is stage 2 of normal swallowing ?

Answer 11

Upper Oesophageal phase - the UOS closes and superior circular muscle rings contract whilst inferior rings dilate, with sequential contractions of longitudinal muscle.

Question 12

What is stage 3 of normal swallowing ?

Answer 12

Lower oesophageal phase - LOS closes as food passes through.

Question 13

How do you measure normal swallowing ?

Answer 13

Manometry, this is where a tube is passed throught he nose down the oesophagus that measures pressure of contractions.

Question 14

What are normal peristaltic waves ?

Answer 14

40mmHg

Question 15

What is the normal pressure of the LOS ?

Answer 15

20mmHg

Question 16

What happens to the pressure at the LOS during receptive relaxation ?

Answer 16

Decreases to <5mmHg this is mediated by inhibitory noncholinergic nonadrenergic NCNC neurons of myenteric plexus.

Question 17

What are 3 causes of functional oesophageal disorders ?

Answer 17

1. Absence of a stricture.
2. Abnormal oesophageal contraction.
3. Failure of protective mechanisms for reflux.

Question 18

What is an example of Abnormal oesophageal contraction ?

Answer 18

• Hypermotility
• Hypomotility
• Disordered Coordination

Question 19

What is an example of failure of the protective mechanisms for reflux ?

Answer 19

GastroOesophageal Reflux disease GORD

Question 20

What term is used for difficulty in swallowing ?

Answer 20

Dysphagia, it is important to localise the dysphagia as well as what type ( to solids or liquids), if it is getting better or worse.

Question 21

What is the term for pain on swallowing?

Answer 21

Odynophagia

Question 22

What term describes the return of oesophageal contents from above an obstruction?

Answer 22

Regurgitation, is it functional or mechanical.

Question 23

What term describes passive return of gastroduodenal contents into the mouth ?

Answer 23

Reflux

Question 24

Give an example of hypermotility ?

Answer 24

Achalasia

Question 25

What is Achalasia ?

Answer 25

Increased resting pressure of LOS, due to loss of ganglion cells in Auerbachs myenteric plexus in LOS walls. Therefore you have a decreased activity of inhibitory NCNA neurones.

Question 26

What happens in Achalasia ?

Answer 26

Receptive relaxation sets in too late and is too weak, so during reflex phase the pressure in the LOS is higher than in the stomach. So swallowed food collects in the oesophagus causing increased pressure throughout, with dilation of the oesophagus. it gets to a point where propagation of peristaltic waves ceases. ![]()

Question 27

What is the disease course of Achalasia ?

Answer 27

Insidious onset, without treatment it can lead to progressive oesophageal dilation of the oesophagus. You also have an increased risk of Oesophageal cancer by 28 fold.

Question 28

What are the treatment options for Achalasia ?

Answer 28

* Pneumatic dilation - weakens the LOS by circumferential stretching and in some casesmuscle tearing. 71-90% of patients respond initially but many relapse. * Heller's Myotomy - A continuous myotomy carried out on 6cm on the oesophagus and 3 cm onto the stomach, this is a more permanent solution. Involves Dor fundoplication - this is where the anterior fundus is folded over the oesopagus and sutured to the right side of myotomy. Risks include; oesophageal and gastric perforation 10-16%, division of the vagus nerve (rare) and splenic injury 1-5%.

Question 29

What is an example of Hypomotility ?

Answer 29

Scleroderma

Question 30

What is Scleroderma ?

Answer 30

Autoimmune disease - results due to neuronal defects, so you get atrophy od smooth muscle of oesophagus and peristalsis in the distal portion ultimately ceases altogether. The decreased resting pressure of the LOS can develop GORD, which can be associated with CREST syndrome.

Question 31

What is CREST syndrome ?

Answer 31

* Calcinosis in soft tissue * Raynaud's phenomenon - constriction of peripheral blood vessels, leads to problems with hands. * Esophageal problems * Scerodactyly- thickening of digits of hands and toes * Telengiactasia- dilated or broken blood vessels near the surface of the skin.

Question 32

What is the treatment for Scleroderma ?

Answer 32

* Exclude organic obstruction * Imrove force of peristalsis with prokenetics (cisapride), not very effective. * Unfortunately once peristaltic failure occurs it is usually irreversible.

Question 33

What is an example of Disordered coordination of the Oesophagus ?

Answer 33

Corkscrew Oesophagus

Question 34

What is Corkscrew Oesophagus ?

Answer 34

Diffuse oesophageal spasm, presents as dysphagia and chest pain. Pressures can reach 400-500mmHg, with marked hypertrophy of circular muscle. Treatment may involve Pneumatic dilation but results are not predictable/favourable.

Question 35

Where do you get Oesophageal Perferation ?

Answer 35

3 main areas of anatomic constriction; 1. Cricopharyngeal constriction 2. Aortic and Bronchial constriction 3. Diaphragmatic and sphincter constriction

Question 36

How do you get oesophageal perforations?

Answer 36

* Latrogenic (OGD)\>50% * Spontaneous (Boerhaave's) - 15% * Foreign Body - 12% * Trauma - 9% * Intraoperative - 2% * Malignant - 1%

Question 37

How do you get Oesophageal perforation latrogenically ?

Answer 37

Usually at OGD (Oesophago-Gastro-Duodenoscopy), more common in the presence of diverticula or cancer.

Question 38

How do you get Oesophageal perforation due to Boerhaave's?

Answer 38

Often described as spontaneous perforation, a sudden increase in intra-oesophageal pressure with negative intra thoracic pressure. You are essentially vomiting against a closed glottis. Incidence is 3.1 per 100,000. Perforation at left posterolateral aspect of the distal oesophagus.

Question 39

What are examples of foreign objects that cause oesophageal perforation?

Answer 39

Disk batteries, Magnets, Sharp objects, Dishwasher tablets

Question 40

How do you get oesophageal perforation via trauma ?

Answer 40

Neck- penetrating, Thorax- Blunt force. Can be difficult to giagnose, dysphagia, blood in saliva, surgical emphysema, Haematemesis. surgical emphysema is air under the skin and sound likes crackling when walking on snow.

Question 41

What is the presentation of Oesophageal perforation?

Answer 41

Pain, Fever, Dysphagia, Emphysema. Do CXR, CT, OGD, swallow gastrograffin.

Question 42

What is the management of oesophageal perforation ?

Answer 42

It is a surgical emergency, there is a 2X mortality if surgery is delayed by 24 hours. NBM, IV Fluids, Broad spectrum antibiotics. ITU level care. Mangement can be conservative with a metal stent, but primary repair is optimal and oesophagectomy is definitive.

Question 43

What increases LOS pressure and thereby inhibits reflux?

Answer 43

Acetylcholine, α-adrenergic agonists, hormones, protein rich food, histamine, high intra-abdominal pressure, Prostaglandin F2α.

Question 44

What decreases LOS pressure and thereby promotes reflux?

Answer 44

Vasoactive intestinal peptide VIP, ß-adrenergic agonists, hormones, dopamine, NO, PG12, PGE2 both vasodilator local hormones, chocolate, acid gastric juice, fat, smoking.

Question 45

What causes normal sporadic reflux?

Answer 45

* Pressure on full stomach * swallowing * transient sphincter opening

Question 46

What are 3 protective mechanisms following reflux?

Answer 46

* Volume clearance - oesophageal peristalsis reflex * pH clearance - saliva * Epithelium - barrier protects

Question 47

What protective mechanisms fail in GORD?

Answer 47

* Decreases sphincter pressure. * Increased transient sphincter opening. * Abnormal peristalsis leading to reduced volume clearance. * Decreased volume clearance due to decreased saliva production e.g. in sleep and xerostomia, as well as decrased buffering capacity of saliva e.g. smoking. * Hiatus Hernia * Defective mucosal protective mechanism, e.g. alcohol. All of these factors lead to Reflux esophagitis and can lead to epithelial metaplasia and possibly carcinoma.

Question 48

What type of hernia is this?

Answer 48

Sliding hiatus hernia

Question 49

What type of hernia is this?

Answer 49

Rolling Hiatus hernia

Question 50

How do you diagnose & treat GORD?

Answer 50

* Diagnosis - OGD to exclude cancer, oesophagitis, peptic stricture, Barrets oesophagus. As well as Oesophageal monometry and possibly 24hr oesophageal ph recording. * Treatment - Non surgical; Lifestyle changes e.g. wt loss, smoking, EtOh, as well as PPI's. Surgical involves Dilation peptic strictures, Laparoscopic Nissen's fundoplication.

Question 51

What does the Cardia and Pyloric region of the stomach produce?

Answer 51

Mucus only.

Question 52

What do the Body&Fundus of the stomach produce?

Answer 52

Mucus, HCl, Pepsin.

Question 53

What does the Antrum produce?

Answer 53

Gastrin.

Question 54

What are the 4 main types of Gastritis?

Answer 54

* Erosive & haemorrhagic gastritis * Nonerosive, chronic active gastritis * Atrophic (fundal gland) gastritis * Reactive gastritis

Question 55

What are the causes of Erosive & haemorrhagic gastritis?

Answer 55

NSAIDs, alcohol, multiorgan failure, burns, trauma, ischaemia. This can happen anywhere in the stomach and lead Acute Ulcer formation which leads to gastric bleeding and perforation.

Question 56

What type of gastritis can Helicobacter pylori lead to ?

Answer 56

Nonerosive, chronic active gastritis in the Antrum. Treated with triple dose of antibiotics (amoxicillin, clarithromycin, pantoprazole) for 7-14 days.

Question 57

How can chroic active antral gastritis lead to reactive gastritis?

Answer 57

Icreased gastrin production causes normal/increased acid secretion which forms chronic gastric & duodenal ulcer formation which leads to reactive gastritis that can develop into epithelial metaplasia and carcinoma.

Question 58

What happens in Atrophic gastritis ?

Answer 58

Occurs in the Fundus, Autoantibodies attack parts/products of parietal cells this lease to parietal cells atrophy. This causes decreases acid secretion & IF Secretion, leading to carcinod/carcinoma formation and Pernicious anaemia respectively.

Question 59

What stimulates Gastric secretion ?

Answer 59

* Neural - ACh, postganglionic transmitter of vagal parasympathetic fibres. * Endocrine - Gastrin, from G cells of antrum. * Paracrine - Histamine from ECL cells & mast cells of gastric wall.

Question 60

What inhibits gastric secretion ?

Answer 60

* Endocrine - Secretin, from small intestine. * Paracrine - Somatostatin. * Paracrine & Autocrine - PGs (E2 & I2) TGF-alpha and adenosine.

Question 61

What are 4 mechanisms for Mucosal protection ?

Answer 61

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Question 62

What are the mechanisms for Epithelial repair and wound healing ?

Answer 62

1. Migration - Adjacent epithelial cells flatten to close th egap via sideward migration along the basement membrane. 2. Gap closed by cell growth - Stimulated by EGF, TGF-alpha, IGF-1, GRP & gastrin. 3. Acute wound healing - Basement membrane destroyed, so leukocytes and macrophages are attracted in order to phagocytose necrotic cells; angiogenesis; regeneration of ECM after repair of BM. Restitution and cell division leads to epithelial closure.

Question 63

Why do you get ulcers?

Answer 63

* Helicobacter pylori * increased secretion of gastric juices * decreased carbonate secretion & therefore decreased mucosal protection dur to inhibition of prostaglandin synthese by NSAIDs. * decreased cell formation * decreased blood perfusion due to stress, smoking, psychogenic components.

Question 64

What are the consequences of *H.Pylori?*

Answer 64

* Asymptomatic \>80% * Chronic atrophic gastritis/ Intestinal metaplasia 15-20% * Gastric/ Duodenal ulcer 15-20% * Gastric cancer, MALT lymphoma\<1%

Question 65

What are the treatments for *H.Pylori* ?

Answer 65

* Primarily medical- PPI or H2 blocker, Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days). * Elective Surgical Rx, Rare - most uncomplicated ulcers heal within 12 weeks. If don’t, change medication, observe additional 12 weeks. Check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome]). OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory. * Surgical indications; Intractability (after medical therapy), Relative: continuous requirement of steroid therapy/NSAIDs. Complications; Haemorrhage, Obstruction, Perforation.