Upper GI Flashcards
1
Q
Where does the oesophagus begin?
A
C5
2
Q
At what vertebral level dies the oesophagus pass through the diaphragm at the oesophageal hiatus?
A
T10
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
4
Q
What type of muscle comprises the upper cervical oesophagus?
A
Skeletal muscle
5
Q
What type of muscle comprises the middle and upper thoracic oesophagus?
A
Skeletal and smooth muscle
6
Q
What type of muscle comprises the lower thoracic oesophagus?
A
Smooth muscle
7
Q
In what state does the lower oesophageal sphincter tonically exists in?
A
Exists in a constricted state
8
Q
What reflex causes the LOS to open?
A
Receptive relaxation, facilitating the passage of substrate into the cardia of the stomach
9
Q
What diaphragmatic structure surrounds the LOW?
A
The left and right crus of the diaphragm
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
11
Q
Which ligament attaches the oesophagus to the diaphragm?
A
Intact phrenoesphageal ligament
12
Q
The upper limb of the phrenoesophageal ligament resides where?
A
Superior to the surface of the diaphgram
13
Q
Where does the lower limb of the phrenoesophgeal ligament reside?
A
Cardia region of the stomach
14
Q
What is the function of the phrenoesophageal ligament?
A
Allows the independent movement of the diaphragm an oesophagus during respiration and swallowing
15
Q
What is the acute angle between the cardia, at the entrance of the stomach and the oesophagus?
A
Angle of His
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
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
18
Q
In what state are the UOS and lOS in during chewing?
A
Both are constricted
19
Q
What is the pharyngeal phase?
A
The pharyngeal musculature guides food bolus towards oesophagus
UOS opens reflexly
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).
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.
22
Q
What state is the UOS during the upper oesophageal phase?
A
Closed
23
Q
What happens during the lower oesophageal phase?
A
Lower sphincter closes as food passes through
24
Q
What is the resting pressure of the LOS?
A
20mmHg
25
What happens to the LOS pressure during receptive relaxation?
Pressure decreases to <5mmHg, opening the sphincter, to allow substrate to pass through into the stomach
26
Which neurones mediate receptive relaxation of the LOS?
Inhibitory noncholinergic noradrenergic NCNA neurones of the myenteric plexus within the muscularis layer
27
How is receptive relaxation of the LOS mediated?
Receptive relaxation is induced by the stimulation of NCNA fibres, opening the LOS, by inhibiting contraction
28
What is dysphagia?
Difficulty in swallowing
29
What is odynophagia?
Pain on swallowing
30
What is regurgitation?
Refers to the return of oesophageal contents from above an obstruction (functional or mechanical).
31
What is reflux?
Passive return of gastroduodenal contents to the mouth.
32
What terms describes hypomotility of the oesophagus?
Achalasia
33
What is achalasia?
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
34
Which type of neurones are absent in achalsia?
Inhibitory NCNA neurones
35
What happens to the LOS in achalasia?
Remains in a constricted state due to a loss of receptive relaxation
36
What are the oesophageal motor abnormalities that resemble achalasia (secondary(?
Chaga's disease
Protozoa infection
Amyloid/sarcoma/eosinophillic oesophagitis
37
Which autoimmune cells are recruited causing a loss of immunological tolerance and autoimmune inflammation?
Th1 cells release cytokines
38
Which types of antibodies stimulates neuronal apoptosis in achalasia?
Antimyenteric antibodies -- loss of NCNA inhibitory neurones
39
What happens to the resting pressure of the LOS in hypermotility?
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)
40
What is the main consequence of hyper-motility of the oesophagus?
Swallowed food accumulates within the oesophagus, increasing pressure throughout, leading to oesophageal dilation
Peristaltic waves ceases
41
What happens to peristaltic waves in hyper-motility of the oesophagus?
Ceases
42
What type of onset does achalasia have?
Insidious onset, with persistent symptoms prior to treatment
43
How is oesophageal dilation detected?
Upon barium swallow
44
What happens to the risk of developing oesophageal cancer in patients with achalasia?
Increases 28-fold (0.34% annual incidence)
45
What are the presentations of achalasia?
Weight loss, oesophagitis, and risk of pneumonia, due to aspiration into the lungs
46
What is pneumatic dilatation?
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.
47
What is the main non-surgical treatment recommended for achalasia?
Pneumatic dilatation
48
What are the surgical interventions for achalasia?
Heller's myotomy
and
Dor fundolipication
Peroral endoscopic myotomy (POEM)
49
What is Heller's myotomy?
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.
50
What are the risks associated with Heller's myotomy?
* Oesophageal and gastric perforation (10-16%)
* Division of vagus nerve – rare
* Splenic injury (1-5%).
51
What is peroral endoscopic myotomy (POEM)?
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.
52
What is scleroderma?
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
53
What is the greatest risk associated with scleroderma?
Gastro-oesophageal reflux
54
What happens to smooth muscle in scleroderma?
Muscular atrophy - disrupting peristalsis
55
What is the main treatment of GORD?
Exclude organic obstruction
Prokinetics improve force of peristalsis (cisapride)
Peristaltic failure is irreversible
56
Which pro-kinetic is administered to improve the force of peristalsis?
Cisapride
57
What is the characteristic appearance of disordered coordination of peristaltic contractions of the oesophagus?
Corkscrew oesophagus
58
What is a corkscrew oesophagus?
Marked hypertrophy of the circular smooth muscle, generating peristalsis pressures exceeding 400-500mmHg
59
How is a corkscrew appearance detected?
Barium swallow and OGD
60
What are the main symptoms of uncoordinated contractions of the oesophagus?
Dysphagia and chest pain
61
What is an example of a vascular abnormality causing dysphagia?
Dysphagia lusoria
62
What is dysphagia lusoria?
Aberrant right subclavian artery traversing behind the oesphagus, compressing it against the trachea
63
What are the three anatomical constrictions of the upper GI tract?
Cricopharyngeal constriction
Aortic and bronchial constriction
Diaphragmatic and sphincter constriction
64
What is the main cause of oesophageal perforation?
Iatrogenic (OGD) >50%
65
What are the 6 main causes of oesophageal perforation?
Iatrogenic
Spontaneous (Boerhaave's)
Foreign body
Trauma
Intraoperative
Malignant
66
What is Boerhaave's?
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
What are the presentations of oesophageal perforation>?
* Pain – 95%
* Fever – 80%
* Dysphagia – 70%
* Emphysema -35%
68
What is a gastrograffin swallow?
Water soluble swallow, revealing an uncontained leakage from the oesophagus in oesophageal perforation.
69
What are the main investigations for an oesophageal perforation?
* Chest X-ray
* CT
* Swallow (gastrograffin)- Water soluble swallow reveals uncontained leakage from the oesophagus
* OGD
70
What is the management of an oesophageal perforation?
```
• IV fluids
• Broad spectrum antibiotics & Antifungals
• Nil by mouth (NBM)
• ITU/HDU level care
• Bloods (Including G&S)
Followed by operative management
```
71
What is the main operative management for an oesophageal perforation?
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
What are the are implications for placing an oesophageal stent in a patient with oesophageal perforation?
Operative management should be default unless:
• Minimal contamination
• Contained
• Unfit
Therefore, consider conservative management with covered metal stent.
73
How do you conservatively manage a patient with an oesophageal perforation?
Placing an oesophageal stent to keep the oesophagus open
74
What is the definitive solution for an oesophageal perforation?
Oesphagetctomy is a definitive solution with reconstruction (mobilising the stomach to re-join to the first viable oesophagus)
75
What are the main protective mechanisms against reflux?
LOS remains in a constricted state
Volume clearance
pH clearance
Distal epithelium
76
What is sporadic reflux?
Reflux upon swallowing
Transient sphincter opening (reduces the LOS pressure)
Sudden unexpected pressure on a full stomach
77
What is volume clearance?
Oesophageal persistaltis reflex ensures that rhythmically regurgitated bolus is returned to the stomach
78
What is pH clearance?
After swallowing, the pH in the distal oesophagus decreases, however in a stepwise manner, saliva is swallowed, exhibiting a buffering effect
79
What mechanisms can fail, leading to a failure of protective mechanisms?
Decrease in LOS pressure
Increased frequency of transient sphincter opening
Reduces saliva production
Abnormal peristalsis - reduces volume clearance
80
What term describes reduced saliva production?
Xerostomia - disturbs pH clearance leading to increased irritation of the mucosal oesophageal lining
81
What is a sliding hiatus hernia?
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
What is a rolling hiatus hernia?
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
Why is a rolling hiatus hernia a surgical emergency?
Because the herniated stomach is constricted by the diaphragm- potentiating the risk of ischaemia
84
What investigations are conducted for patients with suspected GORD?
OGD - exclude cancer
Reveals oesophagitis, peptic strictures, and Barret's oesopahgus
85
What lifestyle changes are recommended in patients with GORD?
Smoking cessation, weight loss and etOh
86
What drug is typically prescribed to patients with GORD?
Omeprazlole (PPI)
87
What are the surgical interventions for patients with GORD?
Dilatation peptic strictures
| Laparasopic Nissen's fundoplication
88
What is laproscopic Nissen's fundoplication?
The dissection and closure of the hiatus, tightening the right and left crus of the diaphragm
89
What is predominantly secreted from the cardiac and pyloric regions of the stomach?
Mucous (glands comprised primarily of mucous secreting cells)
90
What is predominantly secreted from the body and fundus of the stomach?
Mucuous, HCl and pepsinogen
91
Which cells secrete pepinsogen?
Chief cells
92
What are the main secretory cells of the stomach?
Parietal cells
Chief cells
Enteroendocrine cells
93
Which enteroendocrine is predominantly secreted from the pyloric antrum?
Gastrin
94
Where are parietal cell primarily located?
Within the middle region of the gastric glands, differentiated epithelial cells.
95
What do parietal cells secrete?
HCl and intrinsic factor
96
What is the function performed by secreted HCl in the stomach?
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
What is the function of intrinsic factor?
A glycoprotein necessary for the absorption of Vitamin b12 in the small intestine
98
Where are chief cells predominantly located?
Within the basal regions of the gastric glands, secreting pepsinogen
99
What is pepsinogen?
A zymogen form of pepsin, requiring activation by HCl
100
Where are mucous neck cells located?
In the upper part of the stomach
101
What is secreted from mucous neck cells?
Mucin, an alkaline mucous, that entraps bicarbonate ions
102
What is the pH of the epithelial surface?
6-7
103
What is the pH of the gastric lumen?
1-2
104
What is gastritis?
Defined as the histological presence of gastric mucosal inflammation
105
What are the four main forms of gastritis?
Erosive
Haemorrhagic
Nonerosive, chronic active
Atrophic (fundal gland)
106
What is erosive and haemorrhagic gastritis?
Acute ulcerations - gastric bleeding and perforations
107
What are the main causes of erosive and haemorrhagic gastritis?
```
NSAIDs
Alcohol
Multi-organ failure
Truma
Ischaemia
```
108
What is the main cause of non-erosive gastritis?
helicobacter pylori
| and increased gastrin secretion
109
Where does H.pylori favourably proliferate within?
Pyloric antrum due to relative alkalinity, disrupts the mucous barrier
110
What effect does increased gastrin secretion have on gastritis?
Increased gastric acid release from parietal cells, potentiating as a duodenal ulcer
111
What is atrophic (fundal gland) gastritis?
Auto-antibodies to parietal cells and intrinsic factor resulting in inflammatory infiltration and atrophy of the mucosa
112
What are the implications associated with parietal cell atrophy?
Decreased gastric acid and IF secretion (achlorhydria and B12 deficiency, manifests as pernicious anaemia)
113
What type of anaemia is concerned with B12 deficiency secondary to parietal cell atrophy?
Pernicious anaemia
114
What are the risk of impaired gastric acid secretion from parietal cells in atrophic gastritis?
There is a loss of negative feedback, thus G-cell hyperplasia, as a compensatory mechanism -forming a gastronoma
115
How is gastric secretion neurally regulated?
ACh release, a post-ganglionic transmitter of vagal parasympathetic fibres
116
Which hormone is released from G cells of the antrum?
Gastrin
117
Which hormone exerts a paracrine effect on parietal cells?
Histamine
118
Which endocrine hormone inhibits HCl and gastric motility?
Secretin
119
Which paracrine hormone inhibits gastric secretion?
Somatostatin
120
Which paracrine & autocrine hormone exhibits an inhibitory effect on gastric secretion?
Prostaglandins (E2, I2), TNF-alpha, and adenosine
121
Which receptor do ACh act on, parietal cells?
M1 receptors
122
What effect does prostaglandins have on bicarbonate release from epithelial cells?
Increased bicarbonate release, forming an alkaline mucous layer (Protective of gastric acid within the lumen)
123
Which factor regulates the tight junctions between gastric epithelium?
Epidermal growth factor (EGFR)
124
How are ulcers healed and the epithelium repaired?
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
What responses occur during acute wound healing of ulcers?
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
Which enzyme is released from H. pylori?
Urease - catalysing the hydrolysis of urea to form carbon dioxide and ammonia
127
Which molecules assist H. pylori adherence to the mucous layer?
BabA and liposaccharides
128
Which molecule disrupts the tight junctions between cells, secreted by H.pylori?
CagA
129
Which molecule is secreted by H.pylori inducing apoptosis?
VacA
130
How does damage to the mucosal layer promote ulcer formation by H.pylori?
Secretes mucinase, protease and lipases
131
How can aspirin induce ulcer formation?
Inhibits cyclo-oxygenase activity, decreasing prostaglandin synthesis, this reduces bicarbonate secretions into the alkaline mucosal layer.
132
What is the main clinical outcome of a H.pylori infection?
Asymptomatic or chronic gastritis
133
What are the four clinical outcomes due to H.pylori infections?
1) Asymptomatic or chronic gastritis
2) Chronic atrophic gastritis, intestina metaplasia
3) Gastric or duodenal ulcer
4) Gastric cancer ,MALT lymphoma
134
What are the main treatments involved with ulcers?
PPI
H2 blockers
Triple therapy (amoxicillin, clarithromycin and pantoprazole for 1-2 weeks )
