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BRS 1b > Upper GI > Flashcards

Upper GI Flashcards

1
Q

Where does the oesophagus begin?

A

C5

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2
Q

At what vertebral level dies the oesophagus pass through the diaphragm at the oesophageal hiatus?

A

T10

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3
Q

What is the oesophagus?

A

A muscular tube connecting the pharynx to the cardia of the stomach, behaving as a conduit for food

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4
Q

What type of muscle comprises the upper cervical oesophagus?

A

Skeletal muscle

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5
Q

What type of muscle comprises the middle and upper thoracic oesophagus?

A

Skeletal and smooth muscle

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6
Q

What type of muscle comprises the lower thoracic oesophagus?

A

Smooth muscle

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7
Q

In what state does the lower oesophageal sphincter tonically exists in?

A

Exists in a constricted state

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8
Q

What reflex causes the LOS to open?

A

Receptive relaxation, facilitating the passage of substrate into the cardia of the stomach

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9
Q

What diaphragmatic structure surrounds the LOW?

A

The left and right crus of the diaphragm

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10
Q

During inspiration what happens to the LOS?

A

The diaphragmatic sling would constrict the oesophagus forming a functional sphincter that prevents gastric reflex when intra-abdominal pressure rises

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11
Q

Which ligament attaches the oesophagus to the diaphragm?

A

Intact phrenoesphageal ligament

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12
Q

The upper limb of the phrenoesophageal ligament resides where?

A

Superior to the surface of the diaphgram

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13
Q

Where does the lower limb of the phrenoesophgeal ligament reside?

A

Cardia region of the stomach

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14
Q

What is the function of the phrenoesophageal ligament?

A

Allows the independent movement of the diaphragm an oesophagus during respiration and swallowing

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15
Q

What is the acute angle between the cardia, at the entrance of the stomach and the oesophagus?

A

Angle of His

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16
Q

What is the purpose of the angle of His?

A

Prevents reflux of duodenal bile, enzymes and gastric acid from entering the oesophagus

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17
Q

What are the four stages of swallowing?

A

Stage 0: Chewing, and saliva prepares bolus

Stage I: Pharyngeal phase

Stage II: Upper oesophageal phase

Stage III: Lower oesophageal phase

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18
Q

In what state are the UOS and lOS in during chewing?

A

Both are constricted

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19
Q

What is the pharyngeal phase?

A

The pharyngeal musculature guides food bolus towards oesophagus

UOS opens reflexly

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20
Q

In what state are both the UOS and LOS in during the pharyngeal phase?

A
  • Upper oesophagus sphincter opens reflexly.

* LOS opened by vasovagal reflex (receptive relaxation).

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21
Q

What is the upper oesophageal phase?

A
  • Upper sphincter closes
  • Superior circular muscle rings contract and inferior rings dilate promoting peristaltic movements.
  • Sequential contractions of longitudinal muscles (act antagonistically, contracting ahead of the bolus.
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22
Q

What state is the UOS during the upper oesophageal phase?

A

Closed

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23
Q

What happens during the lower oesophageal phase?

A

Lower sphincter closes as food passes through

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24
Q

What is the resting pressure of the LOS?

A

20mmHg

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25
Q

What happens to the LOS pressure during receptive relaxation?

A

Pressure decreases to <5mmHg, opening the sphincter, to allow substrate to pass through into the stomach

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26
Q

Which neurones mediate receptive relaxation of the LOS?

A

Inhibitory noncholinergic noradrenergic NCNA neurones of the myenteric plexus within the muscularis layer

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27
Q

How is receptive relaxation of the LOS mediated?

A

Receptive relaxation is induced by the stimulation of NCNA fibres, opening the LOS, by inhibiting contraction

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28
Q

What is dysphagia?

A

Difficulty in swallowing

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29
Q

What is odynophagia?

A

Pain on swallowing

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30
Q

What is regurgitation?

A

Refers to the return of oesophageal contents from above an obstruction (functional or mechanical).

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31
Q

What is reflux?

A

Passive return of gastroduodenal contents to the mouth.

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32
Q

What terms describes hypomotility of the oesophagus?

A

Achalasia

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33
Q

What is achalasia?

A

Achalasia refers to the absence of ganglion cells within the Auerbach’s myenteric plexus in the LOS wall.
• Loss of NCNA inhibitory neurones therefore receptive relaxation to facilitate the movement of bolus into the cardia of the stomach is impaired – the LOS remains in the constricted state

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34
Q

Which type of neurones are absent in achalsia?

A

Inhibitory NCNA neurones

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35
Q

What happens to the LOS in achalasia?

A

Remains in a constricted state due to a loss of receptive relaxation

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36
Q

What are the oesophageal motor abnormalities that resemble achalasia (secondary(?

A

Chaga’s disease
Protozoa infection
Amyloid/sarcoma/eosinophillic oesophagitis

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37
Q

Which autoimmune cells are recruited causing a loss of immunological tolerance and autoimmune inflammation?

A

Th1 cells release cytokines

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38
Q

Which types of antibodies stimulates neuronal apoptosis in achalasia?

A

Antimyenteric antibodies – loss of NCNA inhibitory neurones

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39
Q

What happens to the resting pressure of the LOS in hypermotility?

A

The resting pressure increases due to loss of inhibitory NCNA neurones, maintains an excessively constricted state

  • This causes delayed receptive relaxation that is inadequate (reflux phase pressure is LOS is markedly higher than the stomach)
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40
Q

What is the main consequence of hyper-motility of the oesophagus?

A

Swallowed food accumulates within the oesophagus, increasing pressure throughout, leading to oesophageal dilation

Peristaltic waves ceases

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41
Q

What happens to peristaltic waves in hyper-motility of the oesophagus?

A

Ceases

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42
Q

What type of onset does achalasia have?

A

Insidious onset, with persistent symptoms prior to treatment

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43
Q

How is oesophageal dilation detected?

A

Upon barium swallow

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44
Q

What happens to the risk of developing oesophageal cancer in patients with achalasia?

A

Increases 28-fold (0.34% annual incidence)

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45
Q

What are the presentations of achalasia?

A

Weight loss, oesophagitis, and risk of pneumonia, due to aspiration into the lungs

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46
Q

What is pneumatic dilatation?

A

A wire connected with a deflated balloon descending through the LOS, and is inflated, for the treatment of achalasia

• Circumferential stretching (+tearing of muscle fibres) – reduces the resting pressure of the LOS and promotes relaxation of the stricture.

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47
Q

What is the main non-surgical treatment recommended for achalasia?

A

Pneumatic dilatation

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48
Q

What are the surgical interventions for achalasia?

A

Heller’s myotomy
and
Dor fundolipication

Peroral endoscopic myotomy (POEM)

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49
Q

What is Heller’s myotomy?

A

Heller’s myotomy: A continuous myotomy performed for 6cm on the oesophagus & 3cm onto the stomach. Laparoscopic scissors to cut the muscularis layer, exposing the mucosal layer such that the fundus is wrapped around the exposed mucosa.
• Dor fundoplication – anterior fundus folded over oesophagus and sutured to the right side of myotomy.

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50
Q

What are the risks associated with Heller’s myotomy?

A
  • Oesophageal and gastric perforation (10-16%)
  • Division of vagus nerve – rare
  • Splenic injury (1-5%).
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51
Q

What is peroral endoscopic myotomy (POEM)?

A
  1. Endoscope enters into the dilated oesophagus, whereby a mucosal incision is made.
  2. Formation of a submucosal tunnel, accessing the muscularis layer
  3. Myotomy
  4. Closure of mucosal incision.
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52
Q

What is scleroderma?

A

An autoimmune disorder characterised by fibroblast activation, producing elevated amounts of collagen

Hypomotility in early stages due to neuronal defects - atrophy of oesophageal smooth muscle

Disruption of peristalsis in the distal portion of the oesophagus

Decreased resting pressure f the LOS - this potentates the likeliness of developing GORD (CREST syndrome is associated), as the LOS i uncontracted

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53
Q

What is the greatest risk associated with scleroderma?

A

Gastro-oesophageal reflux

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54
Q

What happens to smooth muscle in scleroderma?

A

Muscular atrophy - disrupting peristalsis

55
Q

What is the main treatment of GORD?

A

Exclude organic obstruction

Prokinetics improve force of peristalsis (cisapride)

Peristaltic failure is irreversible

56
Q

Which pro-kinetic is administered to improve the force of peristalsis?

A

Cisapride

57
Q

What is the characteristic appearance of disordered coordination of peristaltic contractions of the oesophagus?

A

Corkscrew oesophagus

58
Q

What is a corkscrew oesophagus?

A

Marked hypertrophy of the circular smooth muscle, generating peristalsis pressures exceeding 400-500mmHg

59
Q

How is a corkscrew appearance detected?

A

Barium swallow and OGD

60
Q

What are the main symptoms of uncoordinated contractions of the oesophagus?

A

Dysphagia and chest pain

61
Q

What is an example of a vascular abnormality causing dysphagia?

A

Dysphagia lusoria

62
Q

What is dysphagia lusoria?

A

Aberrant right subclavian artery traversing behind the oesphagus, compressing it against the trachea

63
Q

What are the three anatomical constrictions of the upper GI tract?

A

Cricopharyngeal constriction

Aortic and bronchial constriction

Diaphragmatic and sphincter constriction

64
Q

What is the main cause of oesophageal perforation?

A

Iatrogenic (OGD) >50%

65
Q

What are the 6 main causes of oesophageal perforation?

A

Iatrogenic

Spontaneous (Boerhaave’s)

Foreign body

Trauma

Intraoperative

Malignant

66
Q

What is Boerhaave’s?

A

Results from a full-thickness tear in the oesophageal wall due to a sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure.

  • Manifests as vomiting against a closed glottis.
  • Distal oesophageal rupture leads to left-sided effusion.
67
Q

What are the presentations of oesophageal perforation>?

A
  • Pain – 95%
  • Fever – 80%
  • Dysphagia – 70%
  • Emphysema -35%
68
Q

What is a gastrograffin swallow?

A

Water soluble swallow, revealing an uncontained leakage from the oesophagus in oesophageal perforation.

69
Q

What are the main investigations for an oesophageal perforation?

A
  • Chest X-ray
  • CT
  • Swallow (gastrograffin)- Water soluble swallow reveals uncontained leakage from the oesophagus
  • OGD
70
Q

What is the management of an oesophageal perforation?

A 
•	IV fluids
•	Broad spectrum antibiotics & Antifungals
•	Nil by mouth (NBM) 
•	ITU/HDU level care
•	Bloods (Including G&S)
Followed by operative management
71
Q

What is the main operative management for an oesophageal perforation?

A

Primary repair- adventitia is removed providing access to the muscular layer in order to repair the mucosa - stitch

Vascularised pedicle flap
Gastric fundus buttressing (Dor)
Chest drains are required

72
Q

What are the are implications for placing an oesophageal stent in a patient with oesophageal perforation?

A

Operative management should be default unless:
• Minimal contamination
• Contained
• Unfit
Therefore, consider conservative management with covered metal stent.

73
Q

How do you conservatively manage a patient with an oesophageal perforation?

A

Placing an oesophageal stent to keep the oesophagus open

74
Q

What is the definitive solution for an oesophageal perforation?

A

Oesphagetctomy is a definitive solution with reconstruction (mobilising the stomach to re-join to the first viable oesophagus)

75
Q

What are the main protective mechanisms against reflux?

A

LOS remains in a constricted state

Volume clearance
pH clearance
Distal epithelium

76
Q

What is sporadic reflux?

A

Reflux upon swallowing

Transient sphincter opening (reduces the LOS pressure)

Sudden unexpected pressure on a full stomach

77
Q

What is volume clearance?

A

Oesophageal persistaltis reflex ensures that rhythmically regurgitated bolus is returned to the stomach

78
Q

What is pH clearance?

A

After swallowing, the pH in the distal oesophagus decreases, however in a stepwise manner, saliva is swallowed, exhibiting a buffering effect

79
Q

What mechanisms can fail, leading to a failure of protective mechanisms?

A

Decrease in LOS pressure
Increased frequency of transient sphincter opening
Reduces saliva production
Abnormal peristalsis - reduces volume clearance

80
Q

What term describes reduced saliva production?

A

Xerostomia - disturbs pH clearance leading to increased irritation of the mucosal oesophageal lining

81
Q

What is a sliding hiatus hernia?

A

In a sliding hiatal hernia, the stomach is distended through the diaphragm superiorly, increasing gastric acid reflux into the distal oesophagus and gastroesophageal junction.

82
Q

What is a rolling hiatus hernia?

A

In a rolling hiatus hernia, the gastroesophageal junction is intact, the herniated portion of the stomach is alongside the oesophagus.
• Surgical emergency because the stomach can become ischaemic.
• Barium swallow shows barium in the fundus of the stomach superior to the diaphragm.

83
Q

Why is a rolling hiatus hernia a surgical emergency?

A

Because the herniated stomach is constricted by the diaphragm- potentiating the risk of ischaemia

84
Q

What investigations are conducted for patients with suspected GORD?

A

OGD - exclude cancer

Reveals oesophagitis, peptic strictures, and Barret’s oesopahgus

85
Q

What lifestyle changes are recommended in patients with GORD?

A

Smoking cessation, weight loss and etOh

86
Q

What drug is typically prescribed to patients with GORD?

A

Omeprazlole (PPI)

87
Q

What are the surgical interventions for patients with GORD?

A

Dilatation peptic strictures

Laparasopic Nissen’s fundoplication

88
Q

What is laproscopic Nissen’s fundoplication?

A

The dissection and closure of the hiatus, tightening the right and left crus of the diaphragm

89
Q

What is predominantly secreted from the cardiac and pyloric regions of the stomach?

A

Mucous (glands comprised primarily of mucous secreting cells)

90
Q

What is predominantly secreted from the body and fundus of the stomach?

A

Mucuous, HCl and pepsinogen

91
Q

Which cells secrete pepinsogen?

A

Chief cells

92
Q

What are the main secretory cells of the stomach?

A

Parietal cells
Chief cells
Enteroendocrine cells

93
Q

Which enteroendocrine is predominantly secreted from the pyloric antrum?

A

Gastrin

94
Q

Where are parietal cell primarily located?

A

Within the middle region of the gastric glands, differentiated epithelial cells.

95
Q

What do parietal cells secrete?

A

HCl and intrinsic factor

96
Q

What is the function performed by secreted HCl in the stomach?

A

Regulates pH acidity, in order for the activation of pepsinogen into pepsin

Regulates bacteria as a defensive mechanism

Denatures proteins to increase availability for enzymatic digestion

97
Q

What is the function of intrinsic factor?

A

A glycoprotein necessary for the absorption of Vitamin b12 in the small intestine

98
Q

Where are chief cells predominantly located?

A

Within the basal regions of the gastric glands, secreting pepsinogen

99
Q

What is pepsinogen?

A

A zymogen form of pepsin, requiring activation by HCl

100
Q

Where are mucous neck cells located?

A

In the upper part of the stomach

101
Q

What is secreted from mucous neck cells?

A

Mucin, an alkaline mucous, that entraps bicarbonate ions

102
Q

What is the pH of the epithelial surface?

A

6-7

103
Q

What is the pH of the gastric lumen?

A

1-2

104
Q

What is gastritis?

A

Defined as the histological presence of gastric mucosal inflammation

105
Q

What are the four main forms of gastritis?

A

Erosive
Haemorrhagic
Nonerosive, chronic active
Atrophic (fundal gland)

106
Q

What is erosive and haemorrhagic gastritis?

A

Acute ulcerations - gastric bleeding and perforations

107
Q

What are the main causes of erosive and haemorrhagic gastritis?

A 
NSAIDs
Alcohol
Multi-organ failure
Truma
Ischaemia
108
Q

What is the main cause of non-erosive gastritis?

A

helicobacter pylori

and increased gastrin secretion

109
Q

Where does H.pylori favourably proliferate within?

A

Pyloric antrum due to relative alkalinity, disrupts the mucous barrier

110
Q

What effect does increased gastrin secretion have on gastritis?

A

Increased gastric acid release from parietal cells, potentiating as a duodenal ulcer

111
Q

What is atrophic (fundal gland) gastritis?

A

Auto-antibodies to parietal cells and intrinsic factor resulting in inflammatory infiltration and atrophy of the mucosa

112
Q

What are the implications associated with parietal cell atrophy?

A

Decreased gastric acid and IF secretion (achlorhydria and B12 deficiency, manifests as pernicious anaemia)

113
Q

What type of anaemia is concerned with B12 deficiency secondary to parietal cell atrophy?

A

Pernicious anaemia

114
Q

What are the risk of impaired gastric acid secretion from parietal cells in atrophic gastritis?

A

There is a loss of negative feedback, thus G-cell hyperplasia, as a compensatory mechanism -forming a gastronoma

115
Q

How is gastric secretion neurally regulated?

A

ACh release, a post-ganglionic transmitter of vagal parasympathetic fibres

116
Q

Which hormone is released from G cells of the antrum?

A

Gastrin

117
Q

Which hormone exerts a paracrine effect on parietal cells?

A

Histamine

118
Q

Which endocrine hormone inhibits HCl and gastric motility?

A

Secretin

119
Q

Which paracrine hormone inhibits gastric secretion?

A

Somatostatin

120
Q

Which paracrine & autocrine hormone exhibits an inhibitory effect on gastric secretion?

A

Prostaglandins (E2, I2), TNF-alpha, and adenosine

121
Q

Which receptor do ACh act on, parietal cells?

A

M1 receptors

122
Q

What effect does prostaglandins have on bicarbonate release from epithelial cells?

A

Increased bicarbonate release, forming an alkaline mucous layer (Protective of gastric acid within the lumen)

123
Q

Which factor regulates the tight junctions between gastric epithelium?

A

Epidermal growth factor (EGFR)

124
Q

How are ulcers healed and the epithelium repaired?

A

Adjacent epithelium cells flatten to close gap via sideward migration along the basement membrane

The gab is closed by cell growth stimulated by EGF, TGF-alpha, IGF-1, GRP and gastrin, covering defect is restored through cell division

125
Q

What responses occur during acute wound healing of ulcers?

A

Destruction of the basement membrane releases DAMPs that promote leukocyte and macrophage attraction

Phagocytosis of necrotic cells, angiogenesis and regeneration of the extracellular matrix after repair of basement membrane

• Epithelial closure by restitution and cell division.

126
Q

Which enzyme is released from H. pylori?

A

Urease - catalysing the hydrolysis of urea to form carbon dioxide and ammonia

127
Q

Which molecules assist H. pylori adherence to the mucous layer?

A

BabA and liposaccharides

128
Q

Which molecule disrupts the tight junctions between cells, secreted by H.pylori?

A

CagA

129
Q

Which molecule is secreted by H.pylori inducing apoptosis?

A

VacA

130
Q

How does damage to the mucosal layer promote ulcer formation by H.pylori?

A

Secretes mucinase, protease and lipases

131
Q

How can aspirin induce ulcer formation?

A

Inhibits cyclo-oxygenase activity, decreasing prostaglandin synthesis, this reduces bicarbonate secretions into the alkaline mucosal layer.

132
Q

What is the main clinical outcome of a H.pylori infection?

A

Asymptomatic or chronic gastritis

133
Q

What are the four clinical outcomes due to H.pylori infections?

A

1) Asymptomatic or chronic gastritis
2) Chronic atrophic gastritis, intestina metaplasia
3) Gastric or duodenal ulcer
4) Gastric cancer ,MALT lymphoma

134
Q

What are the main treatments involved with ulcers?

A

PPI
H2 blockers

Triple therapy (amoxicillin, clarithromycin and pantoprazole for 1-2 weeks )

BRS 1b (62 decks)

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