UPPER GI TRACT Flashcards

(74 cards)

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
What are the treatments for achalasia?
Pneumatic dilation | Surgery: Heller's myotomy, dor fundoplication
26
Describe how pneumatic dilation is carried out
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
27
What is the efficacy of pneumatic dilation?
71-90% of patients respond initially but many subsequently relapse
28
Describe a Heller's myotomy
``` Continuous myotomy (muscle cut) of 6cm oesophagus and 3cm of stomach Vertical cut ```
29
Describe dor fundoplication
Anterior fundus folded over oesophagus and sutured to right side of myotomy Surgical treatment for achalasia
30
What are the risks of surgery to treat achalasia
Oesophageal and gastric perforation Division of splenic nerve Splenic injury
31
What is scleroderma and what occurs?
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
What is the treatment for scleroderma?
Exclude organic obstruction e.g. tumour Improve force of peristalsis with prokinetics If peristaltic failure occurs, usually irreversible
33
What is corkscrew oesophagus?
Diffuse oesophageal spasm with uncoordinated contractions
34
How can you identify corkscrew oesophagus?
Dysphagia and chest pain Pressures around 400-500 mmHg Marker hypertrophy of circular muscle Barium dye shows corkscrew oesophagus
35
What is the treatment for corkscrew oesophagus?
May respond to forceful pneumatic dilation of cardia | Results not as predictable
36
Where are oesophageal perforations likely to occur?
Cricopharyngeal constriction Aortic and bronchial constriction Diaphragmatic/sphincter constriction Places with pathological narrowing e.g. cancers, foreign bodies, physiological dysfunction
37
What are the aetiology (causes) of oesophageal perforation?
``` Iatrogenic (OGD) > 50% Spontaneous (Boerhaave's) - 15% Foreign body - 12% Trauma - 9% Intraoperative - 2% Malignant - 1% ```
38
When are iatrogenic oesophageal perforations more common?
In presence of diverticula or cancer
39
What is Boerhaave's and what does it cause to occur?
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
What is the incidence of Boerhaave's?
3.1 per 1000000
41
What are some common foreign bodies which cause oesophageal perforation?
``` Disk batteries (electrical burns if embeds in mucosa) Magnets Sharp objects Dishwasher tablets Acid/Alkali ```
42
How does oesophageal perforation by trauma usually present?
Neck: usually penetrating Thorax: usually blunt force Dysphagia Blood in saliva Haematemesis Surgical emphysema (air trapped under skin - crackling when you touch it)
43
What are some investigations that can be done for a patient suspected with oesophageal perforation?
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
What is the primary management of oesophageal perforation?
Surgical emergency (2x mortality if 24 hr delay diagnosis) ``` IV fluids Broad spectrum antibiotics/antifungals ITU/HDU level care Bloods Tertiary referral centre ```
45
What definitive managements of oesophageal perforation should be done?
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
What are bodies protective mechanisms against reflux?
LOS usually closed as a barrier Following reflux: - Volume clearance (oesophageal peristalsis reflex) - pH clearance (saliva buffers low pH) - Epithelium (barrier)
47
What is LOS pressure increased by?
``` Acetylcholine Alpha-adrenergic agonists Hormones Protein-rich food Histamine High intra-abdominal pressure ```
48
What is LOS pressure decreased by?
``` Beta-adrenergic agonists Hormones Dopamine Nitric oxide PGI2 PGE2 Chocolate Acid gastric juice Fat Smoking ```
49
When might normal sporadic reflux occur?
Pressure on full stomach Swallowing Transient sphincter opening throughout day
50
What causes GORD?
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
What can GORD lead to?
- reflux oesophagitis - epithelial metaplasia - carcinoma
52
What is a sliding hiatus hernia?
Phrenoesophageal ligament gives way and part of stomach slides up past diaphragm where the LOS usually is
53
What is a rolling/paraoesophageal hiatus hernia?
Defect in diaphragm and portion of stomach slips up past the diaphragm via defect
54
What are some investigations that can be undertaken in a patient with GORD
OGD (exclude cancer, confirm oesophagitis/Barrett's) Oesophageal manometry 24hr oesophageal pH recording (frequency of reflux)
55
What are the treatments for GORD?
``` Lifestyle changes (smoking, weight loss...) PPIs ``` Surgical: - Dilation peptic strictures - Laparoscopic Nissen's fundoplication
56
How does laparoscopic Nissen's fundoplication work?
Hiatus is closed | Fundus wrapped around oesophagus to provide further reinforcement
57
What do the cardia and pyloric region of the stomach produce?
Mucus only
58
What do the body and fundus of the stomach produce?
Mucus, HCl, pepsinogen
59
What does the antrum of the stomach produce?
Gastrin
60
Name the different types of gastritis
Erosive and haemorrhagic gastritis Nonerosive chronic gastritis Atrophic gastritis Reactive gastritis
61
What is the cause of erosive and haemorrhagic gastritis and what does it cause?
Numerous causes | Forms acute ulcers which can lead to reactive gastritis
62
What is nonerosive chronic gastritis?
Occurs in the antrum Caused by Helicobacter pylori Treat with antibiotics
63
What is atrophic gastritis and what does it lead to?
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
Name the causes of erosive and haemorrhagic gastritis
``` NSAIDs Alcohol Multi-organ failure Burns Trauma Ischaemia ```
65
Why might patients with nonerosive chronic gastritis also develop reactive gastritis?
Helicobacter pylori infection causes gastric and duodenal ulcers which in turn can cause this
66
Which 2 types of gastritis can cause epithelial metaplasia and thus carcinoma?
Reactive gastritis | Atrophic gastritis
67
What stimulates the release of gastric secretion?
Ach of vagal PNS fibres Endocrine gastrin Paracrine histamine
68
What inhibits the release of gastric secretion?
Endocrine secretin Paracrine somatostatin Paracrine/autocrine PGs, TGF-alpha, adenosine
69
How is the stomach mucosal adapted to protect against the acidic environment and thus gastric ulcer formation?
Mucus film HCO3- secretion to buffer (prostaglandins propagate this) Epithelial barrier Mucosal blood perfusion (takes away any H+ that does make it through)
70
What mechanisms are in place to repair epithelial damage/wound healing due to ulcer?
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
What are the gastric outcomes of a H. Pylori infection?
Asymptomatic/chronic gastritis > 80% Chronic atrophic gastritis/intestinal metaplasia 15-20% Gastric/duodenal ulcer 15-20% Gastric cancer/MALT lymphoma < 1%
72
What are the treatments for ulcers?
Medical: - PPI/H2 blocker - Antibiotics for 7-14 days Elective surgery (rare - most heal in 12 weeks)
73
What do you do if ulcer hasn't healed after 12 weeks?
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
List negatives for surgery to treat an ulcer
Complications: - Haemorrhage - Obstruction - Perforation Intractability Continuous requirement of steroid/NSAID therapy