Upper GI Tract

Question 1

What vertebral level does the oesophagus start and end at?

Answer 1

Starts at C5 ends at T10

Question 2

What are some anatomical advantages the LOS has

Answer 2

Distal 3-4cm is in the abdomen
Diaphragm surrounds it
Angle of His allows expansion after a heavy meal

Question 3

What are the 4 phases of swallowing? Describe them briefly

Answer 3

Oral phase: chewing and saliva prepare bolus, both sphincters are constricted
Pharyngeal phase: musculature guides bolus to oesophagus, upper sphincter opens reflexly, LOS opened by vasovagal reflex (receptive relaxation reflex)
Upper oesophageal phase: upper sphincter closes, superior muscle rings contract, inferior rings dilate
Lower oesophageal phase: LOS closes as food passes through

Question 4

What reflex opens the LOS? What is its name?

Answer 4

The vasovagal reflex aka receptive relaxation reflex

Question 5

How is the motility of the oesophagus measures?

Answer 5

Manometry

Question 6

What is the pressure of normal peristaltic waves?

Answer 6

40 mmHg

Question 7

What is the resting pressure of the LOS?

Answer 7

20 mmHg

Question 8

What is the pressure of the LOS when it relaxes?

Answer 8

5 mmHg

Question 9

What mediates the relaxation of the LOS?

Answer 9

Inhibitory noncholinergic noradrenergic neurons of the myenteric plexus

Question 10

Define dysphagia?

Answer 10

Difficulty swallowing

Question 11

How do we describe dysphagia?

Answer 11

Is it during solid or fluid intake
Is it intermittent or progressive
Is it precise or vague

Question 12

What are the 2 localisations for dysphagia?

Answer 12

Cricopharyngeal sphincter

Distal

Question 13

Define odynphagia

Answer 13

Pain on swallowing

Question 14

Define regurgitation and what are the 2 types

Answer 14

Return of oesophageal contents from above an obstruction

Can be functional or mechanical

Question 15

Define reflux

Answer 15

Passive return of gastroduodenal contents to the mouth

Question 16

What is the other name for hypermotility in the oesophagus?

Answer 16

Achalasia

Question 17

Why does achalasia arise?

Answer 17

Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall leading to reduced activity of inhibitory NCNA neurones

Question 18

What are secondary causes of achalasia?

Answer 18

Diseases causing oesophageal motor abnormalities eg
Chagas’ Disease
Protozoa infection
Amyloid/Sarcoma/Eosinophilic Oesophagitis

Question 19

Describe what happens in achalasia?

Answer 19

Theres increased resting pressure of the LOS
Receptive relaxation is too weak
In reflex LOS pressure is higher then in the stomach
Swallowed food collects in the oesophagus and there is increased pressure and dilation
Peristaltic waves decrease

Question 20

What type of onset does achalasia have?

Answer 20

Insidious

Question 21

What happens if achalasia isnt treated?

Answer 21

Progressive oesophageal dilation

Question 22

What does achalasia increase risk of?

Answer 22

Oesophageal cancer

Question 23

What is the main non surgical treatment for achalasia?

Answer 23

Pneumatic dilation. it weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres

Question 24

What are the surgical treatments for achalasia?

Answer 24

Heller’s myotomy= myotomy for 6 cm of oesophagus and 3cm of stomach
Dor fundoplication= the anterior fundus is folded over the oesophagus and sutured to the right side of the myotomy

Question 25

What type of disease is sclerodoma?

Answer 25

Autoimmune

Question 26

Why does hypomotility arise and what does it lead to?

Answer 26

Its due to neuronal defects and leads to atrophy of smooth muscle

Question 27

What condition develops if there is hypomotility?

Answer 27

GORD

Question 28

How is hypomotility treated?

Answer 28

Exclude organic obstruction Improve force of peristalsis with prokinetics (cisapride) Once peristaltic failure occurs its usually irreversible

Question 29

What is corkscrew oesophagus?

Answer 29

Diffuse oesophageal spasm and incoordinate contractions leading to dysphagia and chest pain

Question 30

What is the pressure in corkscrew oesophagus?

Answer 30

400-500 mmHg

Question 31

Where is hypertrophy in corkscrew oesophagus?

Answer 31

In the circular muscle

Question 32

How is corkscrew oesophagus treated?

Answer 32

It may be responsive to forceful pneumatic dilation of the cardia

Question 33

What is dysphagia lusoria?

Answer 33

Vascular compression of the oesophagus from an aberrant right subclavian artery

Question 34

Describe the path of the right subclavian artery from where it arises to where it goes

Answer 34

Arises from the thoracic aorta and goes posterior to the oesophagus

Question 35

How is dysphoria lusoria treated?

Answer 35

Surgically

Question 36

What are the 3 areas of constriction in the upper GI tract?

Answer 36

Cricopharyngeal constriction Aortic and bronchial constriction Diaphragmatic and sphincter constriction

Question 37

What might cause pathological constriction in the upper GI tract?

Answer 37

Cancer, foreign body and physiological dysfunction

Question 38

What is the most common cause of oesophageal perforation?

Answer 38

Latrogenic from OGD (over 50% of perforation is due to this)

Question 39

What are some other causes of oesophageal perforation?

Answer 39

``` Spontaneous (boerhaave's) Foreign bodies Trauma Intraoperative Malignant ```

Question 40

What is Boerhaave's?

Answer 40

A cause of oesophageal perforation: Sudden increase in in intra-oesophageal pressure with negative intra thoracic pressure Results in vomiting against a closed glottis

Question 41

How does oesophageal perforation present?

Answer 41

Pain Fever Dysphagia Emphysema

Question 42

How is oesophageal perforation diagnosed?

Answer 42

CXR CT Swallow OGD

Question 43

How is oesophageal perforation managed?

Answer 43

Operative management is default unless there is minimal contamination Primary management is NDM, IV fluids, broad spectrum antibiotics/antifungals, bloods

Question 44

How is oesophageal perforation managed conservatively?

Answer 44

Via covered metal stent

Question 45

How is surgical management of oesophageal perforation done?

Answer 45

Primary repair with a vascularised pedicle flap is optimal | Oesophagectomy is a definitive solution with reconstruction

Question 46

How does LOS act as a barrier against reflex?

Answer 46

it is closed to prevent contents from the stomach coming back up

Question 47

When does sporadic reflux occur?

Answer 47

When theres pressure on full stomach When swallowing When the transient sphincter is opening

Question 48

What are the protective mechanisms after reflux?

Answer 48

``` Volume clearance= oesophageal peristalsis reflux pH clearance (saliva) Epithelium, it has barrier properties ```

Question 49

What does failure of protective mechanisms cause?

Answer 49

GORD | Sliding or rolling hiatus hernia

Question 50

What does non surgical management of GORD involve?

Answer 50

``` OGD to exclude cancer Oesophageal manometry 24 hr oesophageal pH recording Lifestyle changes eg weight loss, smoking etc PPIs ```

Question 51

What does surgical management of GORD involve?

Answer 51

Dilation peptic strictures | Laparoscopic Nissen’s fundoplication

Question 52

What are the functions of the stomach?

Answer 52

Breaks food into smaller particles (acid & pepsin) Holds food, releasing it in controlled steady rate into duodenum Kills parasites & certain bacteria

Question 53

What does the cardia and pylorus of the stomach produce?

Answer 53

Mucus only

Question 54

What does the body and fundus of the stomach produce?

Answer 54

Mucus, Hcl, pepsinogen

Question 55

What does the antrum of the stomach produce?

Answer 55

Gastrin

Question 56

How much acid does the stomach produce everyday?

Answer 56

2L

Question 57

What is the pH of the stomach at the epithelial and lumen?

Answer 57

``` Epithelium= 6-7 Lumen= 1-2 ```

Question 58

What is erosive and haemorrhagic gastritis?

Answer 58

When an acute ulcer causes gastric bleeding and perforation

Question 59

What is nonerosive, chronic gastritis? What stomach region is it associated with?

Answer 59

Associated with the antrum | Due to helicobacter pylori

Question 60

What is atrophic gastritis? What stomach region is it associated with?

Answer 60

Associated with the fundus Autoantibodies attack parts and products of parietal cells causing parietal atrophy leading to reduced acid and IF secretion

Question 61

What are the 4 types of gastritis?

Answer 61

Erosive and haemorrhagic Nonerosive, chronic Atrophic Reactive

Question 62

Where does stimulation come from when regulating gastric secretion?

Answer 62

Neural cells: Ach postganglionic transmitter of vagal parasympathetic fibres Endocrine: Gastrin (G cells of antrum) Paracrine: Histamine (ECL cells & mast cells of gastric wall)

Question 63

Where does inhibition come from when regulating gastric secretion?

Answer 63

Endocrine: Secretin (small intestine) Paracrine: Somatostatin (SIH) Paracrine & autocrine: PGs (E2 & I2), TGF-α & adenosine

Question 64

What are the 3 mechanisms that repair epithelial defects from ulcers?

Answer 64

Migration Gap closed by cell growth Acute wound healing

Question 65

What is migration in relation to repairing epithelial defects?

Answer 65

Adjacent epithelial cells flatten to close gap via sideward migration along the basement membrane

Question 66

What is gap closed cell growth in relation to repairing epithelial defects stimulated by?

Answer 66

EGF, TGF-α, IGF-1, GRP & gastrin

Question 67

What is acute wound healing in relation to repairing epithelial defects?

Answer 67

BM destroyed and epithelial closure by restitution & cell division

Question 68

What are some mechanisms by which the basement membrane may be destroyed?

Answer 68

Leukocytes & macrophages; phagocytosis of necrotic cells; angiogenesis; regeneration of ECM after repair of BM

Question 69

What are some reasons ulcers form?

Answer 69

``` Infection by helicobacter pylori Increased secretion of gastric juice Reduced HCO3- secretion Reduced cell formation Reduced blood perfusion ```

Question 70

What are some of the clinical outcomes of infection by h pylori? How common are they?

Answer 70

Asymptomatic or chronic gastritis (80%) Chronic atrophic gastritis intestinal metaplasia (15-20%) Gastric or duodenal ulcer (15-20%) Gastric cancer/MALT lymphoma (< 1%)

Question 71

How are ulcers treated?

Answer 71

Primarily via PPI or H2 blocker and triple antibiotics for 7-14 days They are rarely managed surgically as they usually heal by themselves in 12 weeks