Upper GI tract

Question 1

anatomical contributions to LOS

Answer 1

3/4cm distal oesophagus within abdomen

Diaphragm surrounds LO

An intact phrenoesophageal ligament: has 2 limbs: 1 attached to the oesophagus and other attached to diaphragm- allows movement of oesophagus and diaphragm

Angle of His- between abdominal oesophagus and fundus of stomach- stops acid reflux

Question 2

stages of swallowing

Answer 2

4 (0-3)
oral
pharyngeal
upper oesophageal
lower oesophageal

Question 3

how to determine motility of oesophagus

Answer 3

manometry- pressure measurements

Question 4

functional disorders of the oesophagus

Answer 4

• abnormal oesophageal contraction (hypomobility, hypermobility and disordered coordination)
• failure of protective mechanisms of reflux

Question 5

dysphagia

Answer 5

difficulty in swallowing

Question 6

What do we call pain on swallowing?

Answer 6

odynophagia

Question 7

regurgitation

Answer 7

return of oesophageal content from above an obstruction (functional or mechanical)

Question 8

reflux

Answer 8

passive return of gastroduodenal contents to the mouth

Question 9

is reflux the same as vomiting?

Answer 9

no

Question 10

example of oseophageal hypermotility and causes?

Answer 10

achalasia
- Due to loss of ganglion cell in Aurebach’s myenteric plexus
Primary cause aetiology is unknown
Secondary cause:
-Diseases causing oesophageal motor abnormalities similar to primary achalasia
• Chagas’ Disease
• Protozoa infection
• Amyloid/Sarcoma/Eosinophilic Oesophagitis

Question 11

features of achalaisa hypermotility

Answer 11

• increased resting pressure of LOS
• receptive relaxation sets in late and is too weak -> during reflex phase, pressure in LOS is markedly higher than stomach
• swallowed food collects in the oesophagus causing increased pressure throughout with dilation of the oesophagus
• Propagation of peristaltic wave ceases

Question 12

disease course of achalasia

Answer 12

• insidious onset: symptoms for years without seeking help
• without treatment you get progressive oesophageal dilation
• oesophageal cancer risk increased 28-fold

Question 13

treatment of achalasia

Answer 13

pneumatic dilation (PD) to stretch muscles of the LOS:
-uses endoscopy, guide wire with PD
-balloon inserted and inflated to expand LO
- restored flow in LO
Efficacy of 90%, but usually relapses

Question 14

surgical treatment of achalasia and risks?

Answer 14

• heller’s myotomy : myotomy (muscle cut) for 6cm of oesophagus and 3cm of stomach
• Dor fundopilation: anterior fundus folded over oesophagus and sutured to right side of myotomy

Risks include:

• Esophageal and gastric perforation
• Division of vagus nerve
• splenic injury

Question 15

What is an example of a cause of oesophageal hypomotility ?

Answer 15

Scleroderma-autoimmune disease
Hypomotility in its early stages due to neuronal defects → atrophy of smooth muscle of oesophagus
Peristalsis in the distal portion ultimately ceases
Decreased resting pressure of LOS
Leads to development of GORD- often associated with CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia)

Question 16

treatment of scleroderma

Answer 16

Exclude organic obstruction
Improve force of peristalsis with prokinetics
Once peristaltic failure occurs, this is usually irreversible - may have to have oesophagus removed

Question 17

conditions causing disordered coordination

Answer 17

corkscrew oesophagus
Incoordinate contractions → dysphagia & chest pain
• Pressures of 400-500 mmHg
• Marked hypertrophy of circular muscle
• Corkscrew oesophagus seen on Barium x-ray scan

Question 18

treating corkscrew oesophagus

Answer 18

forceful PD of cardia

results not as predictable as achalasia

Question 19

What are causes of oesophageal perforation (most common to least common?

Answer 19

latrogenic - usually due to OGD (Oesophago-Gastro-Duodenoscopy)
Spontaneous (Boerhaave's)
Foreign body
Trauma
Intraoperative
Malignant

Question 20

what causes spontaneous oesophageal perforation

Answer 20

aka. Boerhaave’s
Sudden increase in intraesophageal pressure with negative intrathoracic pressure
Vomiting against a closed glottis
Usually left posterolateral aspect of distal oesophagus

Question 21

foreign bodies causing oesophageal perforation

Answer 21

Disk batteries is growing problem- cause electrical burns if impact in mucosa

• magnets
• sharp objects
• dishwasher tablets
• acid/alkali

Question 22

oesophageal perforation from trauma signs

Answer 22

Neck - caused by penetrating trauma
Thorax - caused by blunt force

Symptoms:

• dysphagia
• blood in saliva
• haematemsis
• surgical emphysema

Question 23

surgeries that can cause oesophageal perforation

Answer 23

• hiatus hernia repair
• hellers myotomy
• pulmonary surgery
• thyroid surgery

Question 24

investigating oesophageal perfortion

Answer 24

• CXR
• CT
• Swallow (gastrograffin)
• OGD

Question 25

initial management of oesophageal perforation

Answer 25

``` NBM (nil by mouth) IV fluids Broadspec AB and antifungal Bloods ICU/ HDU level care tertiary care (specialist) referral ```

Question 26

definitive management of the oesophageal perforation

Answer 26

Perforation is a surgical emergency (2x increase in morality if 24hr delay in diagnosis) ``` Operative management is default unless: -there's minimal contamination -it's contained -patient unfit In this case you can use conservative management with a covered metal stent ```

Question 27

why is LOS normally closed?

Answer 27

barrier against reflux to protect from gastric juice

Question 28

is sporadic reflux normal?

Answer 28

yes, occurs when: pressure on full stomach swallowing transient sphincter opening (spontaneous)

Question 29

3 mechanisms for protection following reflux

Answer 29

- volume clearance (oesophageal peristalsis reflex) - pH clearance (saliva) - epithelial barrier properties

Question 30

what are failed protective mechanisms against reflux and what can this cause?

Answer 30

Decreased sphincter pressure Transient sphincter opening Decreased saliva production- leads to decreased pH clearance Decreased buffering capacity of saliva (e.g. by smoking) - leads to decreased pH clearance Abnormal peristalsis- leads to decreased volume clearance Hiatus hernia Defective mucosal protective mechanism These can lead to GORD -> reflux oesophagitis -> epithelial metaplasia -> carcinoma

Question 31

what often happens with GORD?

Answer 31

sliding hiatus hernia- Ligament gives way and stomach slides up

Question 32

rolling hiatus hernia

Answer 32

Bit of stomach squeezes through next to oesphagus

Question 33

how to investigate GORD

Answer 33

``` OGD - exclude other cause like cancer - look for oesophagitis, peptic stricture and barrett's oesophagus Oesophageal manometry 24 hr oesophageal pH recording ```

Question 34

types of gastritis

Answer 34

- erosive and hemorrhagic - nonerosive chronic active gastritis - atrophic gastritis - reactive gastritis

Question 35

What are causes of nonerosive, chronic active gastritis, what does it lead to and what is treatment?

Answer 35

helicobacter pylori in the antrum Leads to increased gastrin and inc/normal acid secretion -> gastric and duodenal ulcer -> reactive gastritis -> epithelial metaplasia -> carcinoma Treatment: triple therapy - amoxicillin and clarithromycin and a PPI for up to 14 days

Question 36

cause of atrophic gastritis

Answer 36

autoantibodies attacking gastric receptor/ carbonic anhydrase/ H+/K+NATPase/ IF Atrophic gastritis leads to dec pepsinogen, dec acid secretion (-> inc gastrin -> ECL cell hyperplasia -> carcinoid OR G-cell hyperplasia -> carcinoma) and dec IF secretion (-> dec cobalamin absorption -> cobalamin deficiency -> pernicious anaemia)

Question 37

What are causes of erosive and hemorrhagic gastritis and what does it lead to?

Answer 37

``` NSAIDs Alcohol Multi-organ failure Trauma Ischaemia ``` Leads to acute ulcer- gastric bleeding and perforation

Question 38

methods of mucosal protection (4)

Answer 38

1. mucus film 2. HCO3- secretion 3. Epithelial barrier 4. mucosal blood perfusion

Question 39

What are the stages of epithelial repair and wound healing?

Answer 39

Migration Gap closed by cell growth Acute wound healing

Question 40

How does H Pylori cause virulence? (8)

Answer 40

Urease: to neutralise gastric acid Flagella: for mobility and chemotaxis Lipopolysaccharides: adhere to host cells and inflammation Outer proteins: Adhere to host cell Exotoxins: vacuolating toxin for gastric mucosal injury Secretory enzymes: mucinase, protease, lipase for gastric mucosal injury Type IV secretion system: for injection of effectors Effectors: for actin remodelling, IL-8 induction, host cell growth and apoptosis inhibition

Question 41

neural stimulation of gastric secretion?

Answer 41

ACh -> postganglionic transmitter of vagal parasympathetic fibres

Question 42

endocrine stimulation of gastric secretion?

Answer 42

Gastrin (G cells of antrum)

Question 43

paracrine stimulation of gastric secretion?

Answer 43

Histamine (from ECL cells & mast cells of gastric wall)

Question 44

endocrine inhibition of gastric secretion?

Answer 44

Secretin (small intestine)

Question 45

paracrine inhibition of gastric secretion?

Answer 45

Somatostatin (SIH)

Question 46

paracrine and autocrine inhibition of gastric secretion?

Answer 46

Prostaglandins (E2 & I2), TGF-α & | adenosine

Question 47

What occurs in the migration stage of epithelial repair and wound healing

Answer 47

• Adjacent epithelial cells flatten to close gap | via sideward migration along BM

Question 48

gap closed by cell stage of epithelial repair and wound healing

Answer 48

• Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin

Question 49

acute wound healing by cell stage of epithelial repair and wound healing

Answer 49

- BM destroyed - attraction of leukocytes & macrophages; phagocytosis of necrotic cells; angiogenesis; regeneration of ECM after repair of BM - epithelial closure by restitution & cell division.

Question 50

What factors contribute to ulcer formation? | look at slide on this and slide after!!

Answer 50

- helicobater pylori - secretion of gastric juice increased - HCO3- secretion decreased - cell formation decreased - blood prefusion decreased

Question 51

primarily medical treatment ulcer

Answer 51

- PPI or H2 blocker • Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days)

Question 52

Elective Surgical Rx for ulcers

Answer 52

``` 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 [ZollingerEllison syndrome]) • OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory ```

Question 53

surgical indication ulcers

Answer 53

- Intractability (after medical therapy) - Haemorrhage -Obstruction -Perforation -Relative: continuous requirement of steroid therapy/NSAIDs

Question 54

main disorders of the stomach (8)

Answer 54

``` • Failure of protective mechanisms • Gastrooesophageal reflux (GORD) • Hiatus hernia • Gastritis • Failure in regulation of gastric secretion, mucosal protection & epithelial repair • GIT ulcer formation • H. pylori • Treatment ```

Question 55

What happens in the oral phase of swallowing?

Answer 55

* Chewing & saliva prepare bolus | * Both oesophageal sphincters constricted

Question 56

What happens in the pharyngeal phase of swallowing?

Answer 56

• Pharyngeal musculature guides food bolus towards oesophagus • Upper oesophageal sphincter opens reflexly • LOS opened by vasovagal reflex (receptive relaxation reflex)

Question 57

What happens in the upper oesophageal phase of swallowing?

Answer 57

• Upper sphincter closes • Superior circular muscle rings contract & inferior rings dilate • Sequential contractions of longitudinal muscle

Question 58

What happens in the lower oesophageal phase of swallowing?

Answer 58

• Lower sphincter closes as food passes through

Question 59

What is the pressure of a normal oesophagus during a peristaltic wave?

Answer 59

40 mmhg

Question 60

What is the lower oesophageal resting pressure normally and how does this change with receptive relaxation?

Answer 60

20 mmhg | decreased by 5 mmhg during receptive relaxation

Question 61

What mediates the pressure within the oesophagus?

Answer 61

Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus

Question 62

How is dysphagia classified?

Answer 62

Location: cricopharyngeal sphincter or distal | Type of dysphasia: solids or fluids/ intermittent or progressive/ precise or vague in precision

Question 63

What is an endoscopic treatment of achalasia?

Answer 63

Peroral endoscopic myotomy (POEM): 1. Mucosal incision mae 2. Submucosal tunnel is creates 3. Myotomy 4. Closure of mucosal tunnel

Question 64

What are iatrogenic causes of oesophageal perforation?

Answer 64

Usually occurs at OGD Incidence (low to high) OGD alone Stricture dilatation Sclerotherapy Achalasia dilatation

Question 65

How do you treat malignancies that cause esophageal perforation?

Answer 65

• Radiotherapy • Dilatation • Stenting Has poor prognosis

Question 66

What are symptoms of oesophageal perforation?

Answer 66

Pain Fever Dysphagia Emphysema

Question 67

What surgery would be used to repair an oesophageal perforation?

Answer 67

Primary repair is optimina: • +/- Vascularised pedicle flap • +/- Gastric fundus buttressing (e.g. Dor) Oesophagaectomy is a definitive soloution: - With reconstruction or oesophagostomy & delayed reconstruction

Question 68

What are things that can increase LOS pressure and what is their effect?

Answer 68

Acetylcholine, α-adrenergic agonists, hormones, protein-rich food, histamine, high intra-abdominal pressure, PGF2α, etc. Inhibit reflux

Question 69

What are things that can decrease LOS pressure and what is their effect?

Answer 69

VIP, β-adrenergic agonists, hormones, dopamine, NO, PGI2 , PGE2 , chocolate, acid gastric juice, fat, smoking, etc. Promote reflux

Question 70

What are treatments of GORD?

Answer 70

Medical: - lifestyle changes (wt loss, smoking) - PPIs Surgical: - Dilatation peptic strictures - Laparoscopic Nissen’s fundoplication (close where stomach enters diaphragm and wrap fundus around oesophagus)

Question 71

What are the clinical outcomes of a H Pylori infection?

Answer 71

``` Asymptomatic or chronic gastritis e.g. Chronic atrophic gastritis Intestinal metaplasia Gastric or duodenal ulcer Gastric cancer e.g MALT lymphoma ```