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1B upper GI tract Flashcards

1
Q

Label these diagrams of oesophageal anatomy

A
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2
Q

What are the 4 anatomical contributions to the lower oesophageal sphincter (LOS)’s effectiveness?

A
  • 3-4cm of the distal oesophagus is within the abdomen so if there’s an increase in intraabdominal pressure there’s also increase in LOS pressure
  • Diaphragm surrounds LOS (left and right crux)- contract like a pair of scissors around LOS when diaphragm contracts and contribute to its effectiveness
  • An intact phrenoesophageal ligament
  • Angle of His
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3
Q

Describe the intact phrenoesophageal ligament

A
  • It’s an extension of inferior diaphragmatic fascia
  • It has 2 limbs:
    • One goes superiorly and attaches to lower part of oesophagus
    • Other goes inferiorly and attaches to cardia of stomach
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4
Q

What is the angle of His?

A

Normally there’s an acute angle between the abdominal oesophagus and fundus of stomach at oesophageal junction that prevents reflux disease

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5
Q

What are the 4 stages of swallowing?

A
  • Stage 0: Oral phase
  • Stage 1: Pharyngeal phase
  • Stage 2: Upper oesophageal phase
  • Stage 3: Lower oesophageal phase
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6
Q

What happens in the oral phase?

A
  • Chewing and saliva prepare bolus
  • Both oesophageal sphincters constricted
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7
Q

What happens in the pharyngeal phase?

A
  • Pharyngeal musculature guides food bolus towards oesophagus
  • Upper oesophageal sphincter opens reflexly
  • LOS opened by vasovagal reflex (receptive relaxation reflex)
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8
Q

What happens in upper oesophageal phase?

A
  • Upper sphincter closes
  • Superior circular muscle rings contract and inferior rings dilate
  • Sequential contractions of longitudinal muscle
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9
Q

What happens in the lower oesophageal phase?

A

Lower sphincter closes as food passes through

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10
Q

How is the motility of the oesophagus determined?

A
  • By pressure measurements (manometry)
  • Peristaltic waves are around 40 mmHg
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11
Q

What is the LOS resting pressure and how does that change during receptive relaxation?

A
  • Resting pressure is 20 mmHg
  • Decreases by <5 mmHg during receptive relaxation
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12
Q

What mediates the LOS resting pressure?

A

Inhibitory noncholinergic nonadrenergic (NCNA) neurones of myenteric plexus

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13
Q

What is a functional disorder of the oesophagus?

A

Absence of an oesophageal stricture (abnormal narrowing of oesophagus)

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14
Q

What are the causes of an oesophagus stricture absence?

A
  • Abnormal oesophageal contraction
  • Failure of protective mechanisms for reflux
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15
Q

What are some examples of abnormal oesophageal contraction?

A
  • Hypermotility
  • Hypomotility
  • Disordered coordination
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16
Q

What is an example of a failure of protective mechanism for reflux?

A

Gastro-Oesophageal Reflux Disease (GORD)

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17
Q

What is dysphagia?

A

Difficulty in swallowing

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18
Q

What is important when describing dysphagia?

A

To describe the localisation- cricopharyngeal sphincter or distal

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19
Q

What types of dysphagia are there?

A
  • For solids and fluids
  • Intermittent or progressive
  • Precise or vague in appreciation
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20
Q

What is odynophagia?

A

Pain on swallowing

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21
Q

What is regurgitation?

A
  • Return of oesophageal contents from above an obstruction
  • May be functional or mechanical
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22
Q

What is reflux?

A

Passive return of gastroduodenal contents to the mouth

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23
Q

Define achalasia

A
  • Hypermotility of oesophagus due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
  • Leads to decreased activity of inhibitory NCNA neurones
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24
Q

What does achalasia lead to?

A
  • Increased resting pressure of LOS
  • Receptive relaxation sets in late and is too weak so during reflex phase the LOS pressure is much higher than stomach
  • Swallowed food collects in oesophagus causing increased pressure throughout with dilation of oesophagus
  • Propagation of peristaltic waves cease
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25
Q

What is primary achalasia?

A
  • Majority of achalasia is primary
  • Aetiology is unknown
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26
Q

What is secondary achalasia?

A

Diseases causing oesophageal motor abnormalities similar to primary achalasia

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27
Q

What are examples of secondary achalasia?

A
  • Chagas’ Disease - chronic infection of a parasite
  • Protozoa infection
  • Amyloid/Sarcoma/Eosinophilic Oesophagitis
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28
Q

What is the course of achalasia?

A
  • Insidious onset- symptoms for years prior to seeking help
  • Without treatment there’s progressive oesophageal dilation of oesophagus
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29
Q

What does achalasia increase the risk of?

A
  • Increases risk of oesophageal cancer by 28 fold
  • Annual incidence is only 0.34%
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30
Q

What are the two main treatments of achalasia?

A
  • Pneumatic dilatation (PD)
  • Surgery
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31
Q

What happens in pneumatic dilatation (PD)?

A

PD weakens LOS by circumferential stretching and in some cases, tearing of muscle fibres- done by inserting balloon and expanding it in LOS

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32
Q

What is the efficacy of PD?

A

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

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33
Q

What happens in surgery for achalasia?

A
  • Heller’s myotomy- a continuous myotomy (cutting of musculature and exposing mucosa) performed for 6cm on the oesophagus and 3cm onto stomach
  • Dor fundoplication then done- anterior fundus folded over oesophagus and sutured to right side of myotomy
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34
Q

What are the risks of surgery for achalasia?

A
  • Oesophageal and gastric perforation- 10-16%
  • Division of vagus nerve- rare
  • Splenic injury- 1-5%
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35
Q

Define scleroderma

A

Autoimmune disease where hypomotility happens in early stages due to neuronal defects leading to atrophy of smooth muscle of oesophagus

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36
Q

What does scleroderma cause?

A
  • Peristalsis in distal portion ultimately ceases fully
  • Decreases resting pressure of LOS
  • GORD develops
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37
Q

What is scleroderma often associated with?

A

CREST syndrome

  • Calcinosis- deposits of calcium in soft tissue
  • Raynaud’s phenomenon- constriction of peripheral blood vessels, can lead to problems with hands
  • Esophageal problems
  • Sclerodactyly- thickening of digits of hands and toes
  • Telangiectasia- dilated or broken blood vessels near surface of skin
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38
Q

What is the treatment for scleroderma?

A
  • Exclude organic obstruction and make sure they don’t have malignancy
  • Improve of peristalsis with prokinetics (cisapride). This doesn’t work too well because once peristaltic failure occurs it’s usually irreversible
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39
Q

What is corkscrew oesophagus?

A
  • Disordered coordination of contraction of oesophagus
  • Leads to dysphagia and chest pain
  • Pressures of 400-500 mmHg
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40
Q

What can we see when investigating corkscrew oesophagus?

A
  • Marked hypertrophy of circular muscle
  • Corkscrew shaped oesophagus on Barium
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41
Q

What is the treatment for corkscrew oesophagus?

A
  • May respond to forceful PD of cardia
  • Results not as predictable as achalasia
42
Q

What three areas of anatomical constriction occur in the oesophagus?

A
  • Cricopharyngeal constriction
  • Aortic and bronchial constriction
  • Diaphragmatic and sphincter constriction
43
Q

What are the causes of oesophageal perforations?

A
  • Iatrogenic (>50%)
  • Spontaneous; Boerhaave’s (15%)
  • Foreign body (12%)
  • Trauma (9%)
  • Intraoperative (2%)
  • Malignant (1%)
44
Q

Where does iatrogenic oesophageal perforation usually happen?

A
  • At OGD
  • More common in presence of diverticula or cancer
  • Most commonly in Killian’s triangle
45
Q

How does Boerhaave’s happen?

A
  • Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
  • Vomiting against a closed glottis occurs
  • 3.1 per 1,000,000
46
Q

Where does Boerhaave’s happen?

A

Usually in left posterolateral aspect of distal oesophagus

47
Q

What foreign bodies can cause oesophageal perforations?

A
  • FoDisk batteries- a growing problem and it causes electrical burns if it embeds in the mucosa
  • Magnets
  • Sharp objects
  • Dishwasher tablets
  • Acid/alkali
48
Q

What types of trauma are there for oesophageal perforations?

A
  • Neck- penetrating force needed
  • Thorax- blunt force needed
49
Q

As oesophageal perforation caused by trauma can be difficult to diagnose, what do we check for?

A
  • Dysphagia
  • Blood in saliva
  • Haematemesis (vomiting blood)
  • Surgical emphysema
50
Q

How do patients with oesophageal perforation present?

A
  • Pain- 95%
  • Fever- 80%
  • Dysphagia- 70%
  • Emphysema- 35%
51
Q

What investigations are done for oesophageal perforation?

A
  • CXR
  • CT
  • Swallow (gastrogaffin contrast given)
  • OGD- only do endoscopy if really needed because it can make it worse
52
Q

How is oesophageal perforation mainly treated?

A

Surgery- it’s a surgical emergency and increased mortality by 2x if 24h delay in diagnosis

53
Q

Describe the initial management of oesophageal perforation

A
  • Nil by mouth (NBM)
  • IV fluids
  • Broad spectrum A/Bs and antifungals
  • Bloods (including G&S)
  • ITU/HDU level care
  • Have to refer to tertiary referral centre
54
Q

What definitive management is there for oesphageal perforation?

A
  • Conservative management with a metal stent covering oesophagus- only if it’s a small contained perforation that hasn’t leaked
  • Operative management should be default as primary repair is optimal
    • Oesophagectomy is the definitive solution and may happen
55
Q

What is a protective mechanism against reflux?

A

LOS usually closed as a barrier against reflux of harmful gastric juice (pepsin & HCl)

56
Q

What is LOS pressure increased by?

A
  • Acetylcholine
  • Alpha adrenergic agonists
  • Hormones
  • Protein-rich food
  • Histamine
  • High intraabdominal pressure
  • PGF2alpha etc
57
Q

What is LOS pressure decreased by?

A
  • VIP (vasoactive intestinal polypeptide)
  • Beta adrenergic agonists
  • hormones, dopamine
  • NO
  • PGI2
  • PGE2
  • chocolate
  • acid gastric juice
  • Smoking etc
58
Q

When does sporadic reflux occur?

A
  • Pressure on full stomach
  • Swallowing
  • Transient sphincter opening
59
Q

What 3 mechanisms protect following reflux?

A
  • Volume clearance- oesophageal peristalsis reflex
  • pH clearance- saliva
  • Epithelium- barrier properties
60
Q

What different ways can GORD protective mechanisms fail?

A
  • Decrease in sphincter pressure
  • Increased transient sphincter opening (happens if you drink too much fizzy drink)
  • Hiatus hernia
  • Abnormal peristalsis leading to decreased volume clearance
  • Decreased saliva production (in sleep, xerostomia) leading to decreased pH clearance
  • Decrease in buffering capacity of saliva (e.g. through smoking) leading to decreased pH clearance
  • Defective mucosal protective mechanism e.g. alcohol
61
Q

What are the two types of hiatus hernia?

A
  • Sliding hiatus hernia- ligament holding distal oesophagus down gives way so whole stomach slides up into chest
  • Rolling/paraoesophageal hiatus hernia- portion of stomach sticks up side- it’s an emergency
62
Q

What happens if a hernia gets strangulated?

A

The blood supply to it is cut off and then the stomach/oesophagus can become ischaemic

63
Q

What investigations are done for GORD?

A
  • OGD to exclude cancer and to look for oesophagitis, peptic stricture and Barrett’s oesophagus
  • Oesophageal manometry (pressure measurement)
  • 24-hr oesophageal pH recording
64
Q

What medical treatment is there for GORD?

A
  • Lifestyle changes (weight loss, smoking cessation, teetotaling)
  • PPIs
65
Q

What surgical treatment is there for GORD?

A
  • Dilation of peptic strictures
  • Laparoscopic Nissen’s fundoplication- stitch up the perforation then wrap fundus around oesophagus and put stitches in
    • If you do it too tight the person can’t swallow
66
Q

What are the functions of the stomach?

A
  • Break food into smaller particles (acid and pepsin)
  • Holds food, releasing it in controlled steady rate into duodenum
  • Kills parasites and certain bacteria
67
Q

What do the cardia and pyloric regions produce?

A
  • Cardia and pyloric region- mucus only
  • Body and fundus- mucus, HCl, pepsinogen
  • Antrum- gastrin
68
Q

What things can cause erosive and haemorrhagic gastritis?

A
  • NSAIDs, alcohol
  • Multi-organ failure, burns
  • Trauma
  • Ischaemia
69
Q

What do erosive and haemorrhagic gastritis cause?

A

Acute ulcer- massive gastric bleeding and perforation

70
Q

Where does erosive and haemorrhagic gastritis occur?

A

Anywhere in stomach

71
Q

What can cause non-erosive, chronic active gastritis?

A

Helicobacter pylori

72
Q

What does non-erosive, chronic active gastritis cause?

A
  • Increase in gastrin
  • Acid secretion is normal or increased
  • Leads to chronic gastric and duodenal ulcer
  • Leads to reactive gastritis → epithelial metaplasia → carcinoma
73
Q

Where does non-erosive, chronic active gastritis occur?

A

Antrum

74
Q

How is non-erosive, chronic active gastritis treated?

A

Triple antibiotics (amoxicillin, clarithromycin and pantoprazole) for 2 weeks

75
Q

What can cause atrophic (fundal gland) gastritis?

A

Autoantibodies against parts and products of parietal cells e.g. gastrin receptor/carbonic anhydrase/H+-K+ ATPase

76
Q

What problems can atrophic gastritis cause?

A
  • Decreased acid secretion → G cell hyperplasia (gastrin secretion) → epithelial metaplasia → carcinoma
  • Decreased acid secretion → increased gastrin to counteract this → ECL (endochromaffin cell like) cell hyperplasia (histamine secretion) → carcinoid (neuroendocrine tumour)
  • Decreased IF secretion → decreased cobalamine (B12) absorption → long term leads to cobalamine (B12) deficiency → pernicious anaemia
77
Q

What do parietal cells produce?

A

Hydrogen ions

78
Q

What do chief cells do?

A

Enrich glands with pepsinogen

79
Q

What are 3 ways of stimulating gastric secretion?

A
  • Neural: ACh acting on M1 receptors through postganglionic transmitter of vagal parasympathetic fibres
  • Endocrine: Gastrin produced by G cells of antrum
  • Paracrine: Histamine made by ECL cells and mast cells of gastric wall on H2 receptors
80
Q

What are three ways of inhibiting gastric secretion?

A
  • Endocrine: Secretin produced by small intestine
  • Paracrine: Somatostatin
  • Paracrine and autocrine:
    • PGs (E2 and I2)
    • TGFalpha
    • adenosine
81
Q

What are four ways in which the mucosa is protected?

A
  • Mucus film
  • HCO3- secretion
  • Epithelial barrier
  • Mucosal blood perfusion
82
Q

How does mucus film protect mucosa?

A
  • Epithelial cells make mucus
  • Mucus protects against Pepsin and H+ ions
83
Q

How does HCO3- secretion protect mucosa?

A
  • HCO3- buffers against action of acids
  • Needs prostaglandins however- if we take non steroidals this attacks COX and decreases production of HCO3-
84
Q

How does epithelial barrier protect mucosa?

A
  • Apical membrane and tight junctions are barriers
  • Prevent penetration of H+ ions
85
Q

How does mucosal blood perfusion protect mucosa?

A
  • Good perfusion means even if H+ ions do get through, they’re quickly taken away by blood
  • This is how ischaemia causes problem in ulcers because there isn’t good mucosal blood perfusion so mucosa is open to attack by H+ ions
85
Q

What are 3 mechanisms of epithelial repair and wound healing?

A
  • Migration
  • Gap closed by cell growth
  • Acute wound healing
86
Q

What is migration in wound healing?

A

Adjacent epithelial cells flatten to close gap via sideward migration along basement membrane (BM)

87
Q

What factors stimulate cell growth in wound healing?

A
  • EGF
  • TGFalpha
  • IGF-1
  • GRP
  • Gastrin
88
Q

Acute wound healing- when and how does this occur?

A

BM destroyed:

  • Attraction of leukocytes and macrophages
  • Phagocytosis of necrotic cells
  • Angiogenesis
  • Regeneration of ECM after repair of BM
  • Epithelial closure by restitution and cell division
89
Q

What are causes of ulcer formation?

A
  • Helicobacter pylori
  • Non steroidals and smoking
  • Stress
  • Psychogenic components, smoking and gastrinoma
  • Secretion of gastric juice
  • Less HCO3- secretion
  • Less cell formation
  • Less blood perfusion
90
Q

How does helicobacter pylori cause ulcer formation?

A
  • Disturbs barrier function
  • Causes gastritis which also disturbs barrier function
  • Increases H+ and pepsinogen secretion which increases chemical aggression
91
Q

How do non steroidals and smoking cause ulcer formation?

A
  • Decreased prostaglandin synthesis → less mucosal protection → barrier function disturbed
  • Decreased prostaglandin synthesis → increased H+ and pepsinogen secretion → increased chemical aggression
92
Q

How does stress (shocks, burns, operation) cause ulcers?

A

Decreased blood perfusion → less mucosal protection → barrier function disturbed

93
Q

How do Psychogenic components, smoking and gastrinoma cause ulcers?

A

Increased H+ and pepsinogen secretion → increased chemical aggression

94
Q

How do ulcers form?

A
  • Chemical aggression and barrier function being disturbed leads to epithelial damage
  • Epithelial damage → wound → can lead to ulcer if not healed
95
Q

What do we look to diagnose if there’s a young person who develops an ulcer with no risk factors?

A

Gastrinomas- neuroendocrine tumours that produce gastrin

These can be caused by Zollinger-Ellison syndrome

96
Q

What are the different clinical outcomes of H pylori infections?

A
  • 80% are asymptomatic or chronic gastritis
  • 15-20% get chronic atrophic gastritis/intestinal metaplasia/gastric or duodenal ulcer
  • <1% get gastric cancer or MALT lymphoma
97
Q

What medical treatment is given to ulcers?

A
  • PPI or H2 blocker
  • Triple antibiotic if h pylori is proven (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
98
Q

What are the elective surgery procedures for gastritis and why is it rarely done?

A
  • 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
  • Rarely done because most ulcers heal within 12 weeks and if they don’t you change medication
99
Q

What are the surgical indications for ulcers?

A
  • Intractability (after medical therapy)- they still have symptoms after therapy so e.g. might have to consider fundoplication
  • Relative- continuous requirement of steroids therapy/NSAIDs
  • Complications from ulcer: haemorrhage, obstruction, perforation

gastro (8 decks)

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