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GASTROENTEROLOGY 2 > UPPER GI TRACT > Flashcards

UPPER GI TRACT Flashcards

1
Q

What anatomical structures contribute to the effectiveness of the lower oesophageal sphincter (LOS)?

A
  • 3-4 cm oesophagus within abdomen
  • Diaphragm surrounds LOS and contracts around sphincter
  • Phrenoesophageal ligament
  • Angle of His
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2
Q

What is the phrenoeophageal ligament?

A

Extension of inferior diaphragmatic fascia
Has superior and inferior limbs:
- Superior attaches lower oesophagus
- Inferior attaches cardia of stomach

Allows for individual movement of diaphragm for respiration and oesophagus for swallowing

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3
Q

What is the angle of His?

A

Acute angle between abdominal oesophagus and fundus of stomach at oesophageal junction

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4
Q

What are the stages of swallowing?

A

Oral phase:

  • Chewing and saliva prepare bolus
  • Both sphincters closed

Pharyngeal phase:
- UOS open, LOS opens by receptive relaxation reflex (vasovagal reflex)

Upper oesophageal phase:

  • UOS closes
  • Superior circular muscle rings contract and inferior rings dilate
  • Sequential contractions of longitudinal muscle

Lower oesophageal phase:
- LOS closes as food passes through

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5
Q

How is oesophageal motility determined?

A

By measuring pressure at different points via manometry

Tube passed through nose to oesophagus

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6
Q

What pressure are peristaltic waves?

A

~ 40 mmHg

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7
Q

What is the resting pressure of the LOS?

A

~ 20 mmHg

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8
Q

What happens to pressure in LOS during receptive relaxation?

A

Decrease < 5 mmHg

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9
Q

What mediates receptive relaxation?

A

Inhibitory noncholinergic nonadrenergic (NCNA) neurone of myenteric plexus

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10
Q

What is an absence of stricture caused by?

A

Abnormal oesophageal contraction:

  • Hypermotility - achalasia
  • Hyopmotility - scleroderma
  • Disordered coordination - corkscrew oesophagus

Failure of protective mechanisms for reflux:
- Gastro oesophageal reflux disease (GORD)

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11
Q

What is dysphagia?

A

Difficulty swallowing
Different types e.g. for solids/fluids, intermittent/progressive, precise/vague in appreciation
Localisation is important

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12
Q

What is odynophagia?

A

Pain on swallowing

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13
Q

What is regurgitation?

A

Return of oesophageal contents from above an obstruction

Can be functional or mechanical

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14
Q

What is reflux?

A

Passive return of gastroduodenal contents to the mouth

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15
Q

What is hypermotility also know as?

A

Achalasia

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16
Q

How does achalasia occur?

A

Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall. Causes decreased activity of inhibitory NCNA neurones

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17
Q

Describe the 2 types of achalasia

A

Primary - unknown aetiology

Secondary - diseases which cause oesophageal motor abnormalities similar to primary achalasia

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18
Q

What are some examples of secondary achalasia?

A

Chagas’ disease
Protozoa infection
Amyloid/Sarcoma/Eosinophilic oesophagitis

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19
Q

What is the proposed model of achalasia pathophysiology?

A 
Environmental trigger
Genetic predisposition
Causing
Non autoimmune inflammatory infiltrates
Extracellular turnover/wound repair/fibrosis
And
Loss of immunological tolerance
Apoptosis of neurones
Humoral response
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20
Q

What occurs in achalasia?

A

Increased resting LOS pressure than normal because receptive relaxation sets in late and is too weak.

During the reflex phase pressure in the LOS is much higher than stomach so food can’t get through it

Swallowed food collects in oesophagus causing increased pressure and dilation.

Overtime the propagation of peristaltic waves cease

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21
Q

What are the symptoms of achalasia?

A

Weight loss
Dysphagia
Regurgitation
Pain

Could lead to oesophagitis, pneumonia and increases risk of oesophageal cancer

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22
Q

Why can achalasia lead to pneumonia?

A

Aspiration of stomach contents into lungs which can contain bacteria

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23
Q

By how much does the risk of oesophageal cancer increase in a patient with achalasia and why?

A

28 fold

Aspiration of stomach acid which can cause oesophageal metaplasia

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24
Q

Describe the onset of achalasia

A

Insidious onset with symptoms for years prior to seeking help

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25
Q

What are the treatments for achalasia?

A

Pneumatic dilation

Surgery: Heller’s myotomy, dor fundoplication

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26
Q

Describe how pneumatic dilation is carried out

A

Guide wire inserted and balloon put into LOS.

Balloon then inflated to expand the LOS and then removed. Can tear muscle fibres in some cases

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27
Q

What is the efficacy of pneumatic dilation?

A

71-90% of patients respond initially but many subsequently relapse

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28
Q

Describe a Heller’s myotomy

A 
Continuous myotomy (muscle cut) of 6cm oesophagus and 3cm of stomach
Vertical cut
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29
Q

Describe dor fundoplication

A

Anterior fundus folded over oesophagus and sutured to right side of myotomy

Surgical treatment for achalasia

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30
Q

What are the risks of surgery to treat achalasia

A

Oesophageal and gastric perforation
Division of splenic nerve
Splenic injury

31
Q

What is scleroderma and what occurs?

A

Autoimmune disease causing hypomotility in early stages due to neuronal defects causing atrophy of oesophageal smooth muscle

Peristalsis in the distal portion ultimately ceases together
LOS resting pressure decreases
Gastroesophageal reflux disease develops
- Often associated with CREST syndrome

32
Q

What is the treatment for scleroderma?

A

Exclude organic obstruction e.g. tumour
Improve force of peristalsis with prokinetics

If peristaltic failure occurs, usually irreversible

33
Q

What is corkscrew oesophagus?

A

Diffuse oesophageal spasm with uncoordinated contractions

34
Q

How can you identify corkscrew oesophagus?

A

Dysphagia and chest pain
Pressures around 400-500 mmHg
Marker hypertrophy of circular muscle
Barium dye shows corkscrew oesophagus

35
Q

What is the treatment for corkscrew oesophagus?

A

May respond to forceful pneumatic dilation of cardia

Results not as predictable

36
Q

Where are oesophageal perforations likely to occur?

A

Cricopharyngeal constriction
Aortic and bronchial constriction
Diaphragmatic/sphincter constriction
Places with pathological narrowing e.g. cancers, foreign bodies, physiological dysfunction

37
Q

What are the aetiology (causes) of oesophageal perforation?

A 
Iatrogenic (OGD) > 50%
Spontaneous (Boerhaave's) - 15%
Foreign body - 12%
Trauma - 9%
Intraoperative - 2%
Malignant - 1%
38
Q

When are iatrogenic oesophageal perforations more common?

A

In presence of diverticula or cancer

39
Q

What is Boerhaave’s and what does it cause to occur?

A

Spontaneous sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure - rupture of oesophagus

Vomiting against a closed glottis
Left posterolateral aspect of distal oesophagus usually gives way

40
Q

What is the incidence of Boerhaave’s?

A

3.1 per 1000000

41
Q

What are some common foreign bodies which cause oesophageal perforation?

A 
Disk batteries (electrical burns if embeds in mucosa)
Magnets
Sharp objects
Dishwasher tablets
Acid/Alkali
42
Q

How does oesophageal perforation by trauma usually present?

A

Neck: usually penetrating
Thorax: usually blunt force

Dysphagia
Blood in saliva
Haematemesis
Surgical emphysema (air trapped under skin - crackling when you touch it)

43
Q

What are some investigations that can be done for a patient suspected with oesophageal perforation?

A

Chest X ray
CT scan
Swallow (gastrograffin contrast)
OGD (Oesophago-Gastro-Duodenoscopy)

OGD should only be done when absolutely needed due to risk of perforation

44
Q

What is the primary management of oesophageal perforation?

A

Surgical emergency (2x mortality if 24 hr delay diagnosis)

IV fluids
Broad spectrum antibiotics/antifungals
ITU/HDU level care
Bloods
Tertiary referral centre
45
Q

What definitive managements of oesophageal perforation should be done?

A

Operative management should be default:

  • Primary repair is optimal
  • Oesophagectomy

Conservative management with covered metal stent only when very small perforation that hasn’t leaked

46
Q

What are bodies protective mechanisms against reflux?

A

LOS usually closed as a barrier

Following reflux:

  • Volume clearance (oesophageal peristalsis reflex)
  • pH clearance (saliva buffers low pH)
  • Epithelium (barrier)
47
Q

What is LOS pressure increased by?

A 
Acetylcholine
Alpha-adrenergic agonists
Hormones
Protein-rich food
Histamine
High intra-abdominal pressure
48
Q

What is LOS pressure decreased by?

A 
Beta-adrenergic agonists
Hormones
Dopamine
Nitric oxide
PGI2
PGE2
Chocolate
Acid gastric juice
Fat
Smoking
49
Q

When might normal sporadic reflux occur?

A

Pressure on full stomach
Swallowing
Transient sphincter opening throughout day

50
Q

What causes GORD?

A

Volume clearance - abnormal peristalsis
pH clearance - decreased saliva/buffering capability (smoking)
Decreased sphincter pressure
Increased transient sphincter opening (air/CO2 from fizzy drinks)
Hiatus hernia
Defective mucosal protective mechanism

51
Q

What can GORD lead to?

A
  • reflux oesophagitis
  • epithelial metaplasia
  • carcinoma
52
Q

What is a sliding hiatus hernia?

A

Phrenoesophageal ligament gives way and part of stomach slides up past diaphragm where the LOS usually is

53
Q

What is a rolling/paraoesophageal hiatus hernia?

A

Defect in diaphragm and portion of stomach slips up past the diaphragm via defect

54
Q

What are some investigations that can be undertaken in a patient with GORD

A

OGD (exclude cancer, confirm oesophagitis/Barrett’s)
Oesophageal manometry
24hr oesophageal pH recording (frequency of reflux)

55
Q

What are the treatments for GORD?

A 
Lifestyle changes (smoking, weight loss...)
PPIs

Surgical:

  • Dilation peptic strictures
  • Laparoscopic Nissen’s fundoplication
56
Q

How does laparoscopic Nissen’s fundoplication work?

A

Hiatus is closed

Fundus wrapped around oesophagus to provide further reinforcement

57
Q

What do the cardia and pyloric region of the stomach produce?

A

Mucus only

58
Q

What do the body and fundus of the stomach produce?

A

Mucus, HCl, pepsinogen

59
Q

What does the antrum of the stomach produce?

A

Gastrin

60
Q

Name the different types of gastritis

A

Erosive and haemorrhagic gastritis
Nonerosive chronic gastritis
Atrophic gastritis
Reactive gastritis

61
Q

What is the cause of erosive and haemorrhagic gastritis and what does it cause?

A

Numerous causes

Forms acute ulcers which can lead to reactive gastritis

62
Q

What is nonerosive chronic gastritis?

A

Occurs in the antrum
Caused by Helicobacter pylori
Treat with antibiotics

63
Q

What is atrophic gastritis and what does it lead to?

A

Occurs in fundus
Autoantibodies attacks parts/products of parietal cell
Parietal cell atrophy

Decreased acid secretion potentially causing cancer
Decreased IF secretion causing pernicious anemia

64
Q

Name the causes of erosive and haemorrhagic gastritis

A 
NSAIDs
Alcohol
Multi-organ failure
Burns
Trauma
Ischaemia
65
Q

Why might patients with nonerosive chronic gastritis also develop reactive gastritis?

A

Helicobacter pylori infection causes gastric and duodenal ulcers which in turn can cause this

66
Q

Which 2 types of gastritis can cause epithelial metaplasia and thus carcinoma?

A

Reactive gastritis

Atrophic gastritis

67
Q

What stimulates the release of gastric secretion?

A

Ach of vagal PNS fibres
Endocrine gastrin
Paracrine histamine

68
Q

What inhibits the release of gastric secretion?

A

Endocrine secretin
Paracrine somatostatin
Paracrine/autocrine PGs, TGF-alpha, adenosine

69
Q

How is the stomach mucosal adapted to protect against the acidic environment and thus gastric ulcer formation?

A

Mucus film
HCO3- secretion to buffer (prostaglandins propagate this)
Epithelial barrier
Mucosal blood perfusion (takes away any H+ that does make it through)

70
Q

What mechanisms are in place to repair epithelial damage/wound healing due to ulcer?

A

Migration - adjacent epithelial cells flatten to close gap via sideward migration along BM

Cell growth - stimulated by EGF, TGF-alpha, IGF-1, GRP and gastrin

Acute wound healing:

  • BM destroyed - leukocytes/macrophages attracted and phagocytose necrotic cells, angiogenesis…
  • Epithelial closure by restitution and cell division
71
Q

What are the gastric outcomes of a H. Pylori infection?

A

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

72
Q

What are the treatments for ulcers?

A

Medical:

  • PPI/H2 blocker
  • Antibiotics for 7-14 days

Elective surgery (rare - most heal in 12 weeks)

73
Q

What do you do if ulcer hasn’t healed after 12 weeks?

A

Change medication and observe for another 12 weeks
Check serum gastrin
OGD for biopsy of all 4 quadrants of ulcer if still refractory to rule out malignancy

74
Q

List negatives for surgery to treat an ulcer

A

Complications:

  • Haemorrhage
  • Obstruction
  • Perforation

Intractability
Continuous requirement of steroid/NSAID therapy

GASTROENTEROLOGY 2 (7 decks)

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