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Year 2 - BRS > 6.1 - Upper GI tract > Flashcards

6.1 - Upper GI tract Flashcards

1
Q

At what vertebral level does the oesophagus start and end?

A

Starts at C5, ends at T10 (where it pierces the diaphragm) - approx 25cm tube

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2
Q

Where are the trachea and aorta found in comparison to the oesophagus?

A
  • trachea anterior
  • aorta to the left
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3
Q

What are the two sphincters of the oesophagus?

A
  • upper oesophageal sphincter (UOS)
  • lower oesophageal sphincter (LOS)
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4
Q

What are the three muscle types found along the oesophagus?

A
  • upper 1/3 - skeletal
  • middle 1/3 - skeletal/smooth
  • bottom 1/3 - smooth
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5
Q

What is the arterial supply to the thoracic and abdominal oesophagus?

A
  • thoracic - branches of aorta
    • superior aspect also supplied by inferior thyroid artery (branches of thyrocervical trunk)
  • abdominal - left gastric artery and inferior phrenic artery
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6
Q

What is the venous drainage of the thoracic and abdominal oesophagus?

A
  • thoracic - drained by azygous vein (systemic circulation)
  • abdominal - drained by portal vein (portal circulation)
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7
Q

What are the four anatomical contributions to the effectiveness of the lower oesophageal sphincter?

A
  • 3-4cm distal oesophagus within abdomen (so if increase in intra-abdominal pressure = increase in LOS pressure)
  • diaphragm surrounds LOS (left and right crux) - contracts like a pair of scissors around LOS when diaphragm contracts
  • an intact phrenoesophageal ligament
  • angle of His
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8
Q

What is the phrenoesophageal ligament?

A
  • fibrous band connecting oesophagus to diaphragm (extension of inferior diaphragmatic fascia)
  • two limbs:
    • superior attaches to lower part of oesophagus
    • inferior attaches to cardia of stomach
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9
Q

What is the Angle of His?

A

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

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10
Q

What are the four 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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11
Q

What happens in stage 0 - oral phase?

A
  • chewing and saliva prepare bolus
  • both oesophageal sphincters constricted
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12
Q

What happens in stage 1 - pharyngeal phase?

A
  • pharyngeal musculature guides food bolus towards oesophagus
  • upper oesophageal sphincter opens reflexly
  • LOS opened by vasovagal reflex (receptive relaxation reflex)
  • circular muscles dilate (allow bolus down), longitudinal muscles propel bolus down
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13
Q

What happens in stage 2 - upper oesophageal phase?

A
  • upper sphincter closes
  • superior circular muscle rings contract and inferior rings dilate (LOS dilates)
  • sequential contractions of longitudinal muscle
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14
Q

What happens in stage 3 - lower oesophageal phase?

A

Lower sphincter closes as food passes through

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15
Q

How is motility of the oesophagus determined?

A
  • oesophageal motility determined by pressure measurements (manometry)
  • peristaltic waves are around 40 mmHg
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16
Q

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

A
  • resting pressure is 20 mmHg
  • decreases to <5 mmHg during receptive relaxation (when it opens during pharyngeal phase)
  • mediated by inhibitory noncholinergic noradrenergic (NCNA) neurones of myenteric plexus (between circular and longitudinal muscles in distal oesophagus)
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17
Q

What is a functional disorder of the oesophagus?

A

Absence (?? should be presence) of an oesophageal stricture (abnormal narrowing of oesophagus)

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18
Q

What can (oesophageal strictures) be caused by?

A
  • abnormal oesophageal contraction
    • hypermotility
    • hypomotility
    • disordered coordination
  • failure of protective mechanisms for reflux
    • gastro-oesophageal reflux disease (GORD)
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19
Q

What is dysphagia?

A

Difficulty in swallowing

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20
Q

What is important when describing dysphagia?

A

Localisation is important to describe - cricopharyngeal sphincter or distal

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21
Q

What types of dysphagia are there? (3)

A
  • for solids or fluids
  • intermittent or progressive
  • precise or vague in appreciation
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22
Q

What is odynophagia?

A

Pain on swallowing

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23
Q

What is regurgitation (GIT)?

A
  • return of oesophageal contents from above an obstruction
  • may be functional or mechanical
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24
Q

What is reflux?

A

Passive return of gastroduodenal contents to the mouth

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25
Q

What is achalasia?

A
  • hypermotility of oesophagus due to loss of ganglion cells in Auerbach’s myenteric plexus in LOS wall
  • leads to decreased activity of inhibitory NCNA neurones (so LOS cannot relax/open)
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26
Q

What is the pathophysiology of achalasia? (What does it lead to?)

A
  • loss of NCNA = loss of inhibitory effects = increased resting pressure of LOS
  • receptive relaxation sets in late and is too weak - so during reflex phase pressure in LOS is markedly higher than stomach (LOS cannot open properly)
  • swallowed food collects in oesophagus causing increased pressure throughout with dilation of oesophagus
  • propagation of peristaltic waves cease
  • leads to bird beak appearance + oesophageal dilation on barium swallow

Can be associated with weight loss, trouble swallowing, pain –> eosphagitis and aspiration pneumonia

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27
Q

What is primary achalasia?

A

Majority of achalasia is primary, aetiology is unknown

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28
Q

What is secondary achalasia?

A
  • diseases causing oesophageal motor abnormalities similar to primary achalasia:
    • Chagas’ Disease
    • protozoa infection
    • amyloid/sarcoma/eosinophilic oesophagitis
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29
Q

What is the disease course of achalasia?

A
  • insidious onset - symptoms for years prior to seeking help
  • without treatment: progressive oesophageal dilation of oesophagus
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30
Q

What does achalasia increase the risk of?

A
  • increases risk of oesophageal cancer by 28-fold
  • annual incidence only 0.34%
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31
Q

What are the two main treatments for achalasia?

A
  • pneumatic dilatation (PD)
  • surgery
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32
Q

What happens in pneumatic dilatation (PD)?

A
  • PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres
    • done by inserting balloon and expanding it in LOS
  • efficacy: 71-90% of patients respond initially but many patients subsequently relapse
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33
Q

What happens in surgery for achalasia?

Done when PD fails/recurrence

A
  • Heller’s myotomy - a continuous myotomy (cutting of musculature and exposing mucosa - disrupt longitudinal muscle, keep circular intact) performed for 6cm on oesophagus and 3cm onto the stomach
  • Dor fundoplication (done after) - 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? (3)

A
  • oesophageal and gastric perforation (10-16%)
  • division of vagus nerve - rare
  • splenic injury (1-5%)
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35
Q

What is scleroderma (in context of oesophageal motility)?

A

Autoimmune disease where hypomotility happens in its early stages due to neuronal defects leading to atrophy of smooth muscle of oesophagus (LOS too relaxed)

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36
Q

What does scleroderma lead to/cause (GIT)? (3)

A
  • peristalsis in the distal portion (of oesophagus) ultimately ceases altogether
  • decreased resting pressure of LOS
  • GORD develops - reflux through open LOS
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37
Q

What is scleroderma often associated with?

A

CREST syndrome

38
Q

What is the treatment for scleroderma?

A
  • exclude organic obstruction (and make sure no malignancy)
  • improve force of peristalsis with prokinetics (cisapride)
    • does not work too well as once peristaltic failure occurs, it is usually irreversible
39
Q

What is corkscrew oesophagus (diffuse oesophageal spasm)?

A
  • disordered coordination of contraction of oesophagus
  • leads to dysphagia and chest pain
  • pressures of 400-500 mmHg (compared to normal pressures ~20 mmHg)
40
Q

What can we see on endoscopy when investigating corkscrew oesophagus/diffuse oesophageal spasm?

A
  • marked hypertrophy of circular muscle
  • corkscrew-shaped oesophagus on barium swallow
41
Q

What is the treatment for corkscrew oesophagus?

A
  • may respond to forceful PD (pneumatic dilatation) of cardia
  • results not as predictable as achalasia
42
Q

What are the three areas of anatomical constriction of the oesophagus?

Prone to perforations

A
  • cricopharyngeal constriction
  • aortic and bronchial constriction
  • diaphragmatic and ‘sphincter’ constriction
  • (pathological narrowing can occur e.g. cancer, foreign body, physiological dysfunction = prone to perforation)
43
Q

What are the causes of oesophageal perforations? (6)

A
  • iatrogenic (OGD) >50%
  • spontaneous (Boerhaave’s) - 15%
  • foreign body - 12%
  • trauma - 9%
  • intraoperative - 2%
  • malignant - 1%

I Smell Fruit To Ingest, Mother

44
Q

When does iatrogenic oesophageal perforation occur?

A
  • usually at OGD
  • more common in presence of diverticula or cancer

Usually at Killian’s triangle (oblique inferior constrictor + cricopharyngeus muscle junction)

45
Q

What is the incidence of iatrogenic oesophageal perforation?

A
  • OGD = 0.03%
  • stricture dilatation = 0.1-2%
  • sclerotherapy = 1-5%
  • achalasia dilatation = 2-6%
46
Q

How does spontaneous oesophageal perforation (Boerhaave’s) happen?

A
  • sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure
  • vomiting against closed glottis occurs
  • 3.1 per 1,000,000

Usully secondary to alcohol intake

47
Q

Where does spontaneous (Boerhaave’s) oesophageal perforation usually occur?

A

Usually in left posterolateral aspect of distal oesophagus

2cm above gastro-oesophageal junction

48
Q

What foreign bodies can cause oesophageal perforation? (5)

A
  • disk batteries - growing problem, causes electrical burns if it embeds in the mucosa
  • magnets
  • sharp objects
  • dishwasher tablets
  • acid/alkali (can cause burning, stricture, perforation)
49
Q

What two types of trauma can cause oesophageal perforation?

A
  • neck - penetrating force needed
  • thorax - blunt force needed
50
Q

What do we look for to diagnose trauma-induced oesophageal perforation? (4)

A
  • dysphagia
  • blood in saliva
  • haematemesis
  • surgical emphysema
51
Q

How do oesophageal perforations present? (4)

A
  • pain 95%
  • fever 80%
  • dysphagia 70%
  • emphysema 35%
52
Q

What investigations are done for oesophageal perforations? (4)

A
  • CXR
  • CT
  • swallow (gastrograffin contrast given)
  • OGD (only do if necessary as it can make it worse)
53
Q

What is the primary management of oesophageal perforation?

A

Surgery - surgical emergency, mortality increased by 2x if 24h delay in diagnosis

54
Q

Describe the initial management of oesophageal perforation? (6)

A
  • nil by mouth (NBM)
  • IV fluids (rehydrate)
  • broad spectrum antibiotics and antifungals
  • bloods (include G&S)
  • ITU/HDU level care
  • refer to tertiary referral centre

Usually done for iatrogenic causes as tend not to be full-thickness perforations, unlike Boerhaave’s

55
Q

What definitive management is there for oesophageal perforation? (2)

A
  • conservative management (with a metal stent covering oesophagus) - only if small, contained perforation that has not leaked - covered metal stent
  • operative management should be default as primary repair is optimal
    • oesophagectomy is the definitive solution

Sponges can be used to block off hole and drain fluid

56
Q

What is a protective mechanism against reflux?

A

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

57
Q

What is LOS pressure increased by? (7)

A
  • acetylcholine
  • alpha adrenergic agonists
  • hormones
  • protein-rich food
  • histamine
  • high intra-abdominal pressure
  • PGF2alpha etc
  • (inhibits reflux)
58
Q

What is LOS pressure decreased by? (11)

A
  • VIP (vasoactive intestinal polypeptide)
  • beta adrenergic agonists
  • hormones
  • dopamine
  • NO
  • PGI2
  • PGE2
  • chocolate
  • acid gastric juice
  • fat
  • smoking etc
  • (promotes reflux)
59
Q

When does sporadic reflux occur (normal)? (3)

A
  • pressure on full stomach
  • swallowing
  • transient sphincter opening
60
Q

What three mechanisms protect following reflux?

A
  • volume clearance - oesophageal peristalsis reflex
  • pH clearance - saliva (neutralises acid)
  • epithelium - barrier properties
61
Q

What different ways can protective mechanisms fail in GORD? (7)

A
  • decrease in sphincter pressure
  • increased transient sphincter opening
  • hiatus hernia
  • abnormal peristalsis leading to decreased volume clearance
  • decreased saliva production (in sleep, xerostomia) leading to decreased pH clearance
  • decreased buffering capacity of saliva (e.g. through smoking) = decreased pH clearance
  • defective mucosal protective mechanism e.g. alcohol
62
Q

What happens when the GORD protective mechanisms fail?

A

Reflux oesophagitis –> potential epithelial metaplasia –> potential carcinoma

63
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 oesophagus/chest
  • rolling/paraoesophageal hiatus hernia - portion of stomach sticks up side = emergency
64
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

65
Q

What investigations are done for GORD? (3)

A
  • OGD - to exclude cancer and to look for oesophagitis, peptic stricture and Barrett’s oesophagus
  • oesophageal manometry
  • 24-hr oesophageal pH recording
65
Q

What is the medical treatment for GORD? (2)

A
  • lifestyle changes (weight loss, smoking cessation, no alcohol)
  • PPIs
66
Q

What is the surgical treatment for GORD? (2)

A
  • dilatation of peptic strictures
  • laparoscopic Nissen’s fundoplication - stitch up perforation, wrap fundus around oesophagus, put stitches (not too tight or cannot swallow)
67
Q

What are the functions of the stomach? (3)

A
  • breaks food into smaller particles (acid and pepsin)
  • holds food, releasing it in controlled steady rate into duodenum
  • kills parasites and certain bacteria
68
Q

What parts of the stomach produce what?

A
  • cardia and pyloric region - mucus only
  • body and fundus - mucus, HCl, pepsinogen
  • antrum - gastrin

Closest to oesophagus (proximal) = cardia
Main bit: fundus –> body –> antrum
Distal end: pyloric region

69
Q

What are the four types of gastritis?

A
  • erosive and haemorrhagic gastritis (ischaemia –> acute ulcer)
  • nonerosive, chronic, active gastritis (H. pylori)
  • atrophic (fundal gland) gastritis (autoimmune)
  • reactive gastritis (meds and external factors etc)
70
Q

What are the causes of erosive and haemorrhagic gastritis? (4)

A
  • NSAIDs, alcohol
  • multi-organ failure, burns
  • trauma
  • ischaemia
71
Q

What does erosive and haemorrhagic gastritis cause?

A

Acute ulcer - massive gastric bleeding and perforation, anywhere in stomach

72
Q

What can cause nonerosive, chronic, active gastritis?

A

Helicobacter pylori infection –> increased gastrin, acid secretion normal/increased –> chronic gastric and duodenal ulcer –> reactive gastritis –> epithelial metaplasia –> carcinoma

73
Q

Where does nonerosive, chronic, active gastritis occur?

A

Antrum

74
Q

How can we treat nonerosive, chronic, active gastritis?

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
  • decreased acid secretion –> G cell hyperplasia (gastrin secretion) –> epithelial metaplasia –> carcinoma
  • decreased acid secretion –> increased gastrin to counteract this –> ECL cell hyperplasia (histamine secretion) –> carcinoid (neuroendocrine tumour)
  • decreased IF secretion –> decreased cobalamine absorption –> long term leads to cobalamine (B12) deficiency –> pernicious anaemia
  • parietal cell atrophy
76
Q

Where does atrophic (fundal gland) gastritis occur?

A

Fundus

77
Q

What are three ways of stimulating gastric secretion?

A
  • neural - ACh (acts 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)
78
Q

What are three ways of inhibiting gastric secretion?

A
  • endocrine - secretin (produced by small intestine)
  • paracrine - somatostatin (SIH)
  • paracrine & autocrine - PGs (E2 and I2), TGFalpha, adenosine
79
Q

What are four ways in which the mucosa is protected from H+?

A
  • mucus film - epithelial cells make mucus, protects against pepsin and H+
  • HCO3- secretion - HCO3- buffers against acids, needs prostaglandins (NSAIDs decrease production)
  • epithelial barrier - apical membrane and tight junctions prevent penetration of H+
  • mucosal blood perfusion - good perfusion means any H+ quickly taken away by blood (ischaemia causes issue in ulcers)
79
Q

What are the three mechanisms/steps of epithelial repair and wound healing?

A
  • migration - adjacent epithelial cells flatten to close gap via sideward migration along BM
  • gap closed by cell growth - EGF, TGF-a, IGF-1, GRP, gastrin
  • acute wound healing - BM destroyed and repaired, leukocytes/macrophages and phagocytosis, angiogenesis, ECM regeneration, epithelial closure
80
Q

What happens in migration (mechanisms repairing epithelial defects)?

A

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

81
Q

What stimulates the gap to close by cell growth (mechanisms repairing epithelial defects)? (5)

A
  • EGF
  • TGF-alpha
  • IGF-1
  • GRP
  • gastrin
82
Q

When and how does acute wound healing occur (mechanisms repairing epithelial defects)?

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
83
Q

What are the causes of ulcer formation? (5)

A
  • Helicobacter pylori
  • secretion of gastric juice
  • less HCO3- secretion
  • less cell formation
  • less blood perfusion
84
Q

How do the causes of ulcer formation lead to ulcers?

A
  • chemical aggression and barrier function being disturbed –> epithelial damage
  • epithelial damage –> wound –> can lead to ulcer if not healed
85
Q

What are the different clinical outcomes of H. pylori infections?

A
  • 80% asymptomatic or chronic gastritis
  • 15-20% chronic atrophic gastritis/intestinal metaplasia/gastric or duodenal ulcer
  • <1% gastric cancer/MALT lymphoma
86
Q

What are the medical treatments (primarily done) for ulcers? (2)

A
  • PPI or H2 blocker
  • triple antibiotic therapy (amoxicillin, clarithromycin, pantoprazole) for 7-14 days (if H. pylori proven)
87
Q

What are the elective surgery procedures for ulcers (and why are they 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 as most uncomplicated ulcers heal within 12 weeks, and if not you change medication and observe for another 12 weeks
88
Q

What are the surgical indications for ulcer treatment? (3)

A
  • intractability (after medical therapy) - still have symptoms so might consider fundoplication
  • relative - continuous requirement of steroid therapy/NSAIDs (impair HCO3- secretion = ulcers)
  • complications from ulcer (haemorrhage, obstruction, perforation)

Year 2 - BRS (84 decks)

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