BRS YR2 > Upper GI tract > Flashcards

Upper GI tract Flashcards

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1
Q

At what vertebrae does the trachea start and end?

A

C5 and T4

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2
Q

Where does the diaphragm sit?

A

T10

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3
Q

What is Stage 0 of swallowing?

A

Oral Phase

  • chewing and saliva prepare bolus
  • both oesophageal sphincters constricted
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4
Q

What is Stage 1 of swallowing?

A

Pharyngeal Phase

  • pharyngeal musculature guides bolus towards the oesophagus
  • upper oesophageal sphincter opens reflexively
  • lower oesophageal sphincter opens due to vasovagal reflex (receptive relaxation reflex)
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5
Q

What is Stage 2 of swallowing?

A

Upper Oesophageal Phase

  • upper sphincter closes
  • superior circular muscles contract while inferior rings dilate
  • sequential contractions of longitudinal muscle
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6
Q

What is Stage 3 of swallowing?

A

Lower Oesophageal Phase

- lower sphincter closes as food passes through

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7
Q

How is oesophageal motility measured?

A

pressure measurements (manometry)

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8
Q

What is the approximate pressure measurement of peristaltic waves?

A

around 40mmHg

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9
Q

What is the lower oesophageal sphincter’s resting pressure?

A

around 20 mmHg

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10
Q

What is the approximate change in the oesophageal sphincter’s pressure during receptive relaxation?

A

decreases by <5mmHg

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11
Q

What is the lower oesophageal sphincter mediated by?

A

inhibitory noncholinergic nonadrenergic (NCNA) neurons of the myenteric plexus

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12
Q

What is the absence of a stricture caused by?

A
  • abnormal oesophageal contraction (hyper-motility, hypo-motility, disordered co-ordination)
  • failure of protective mechanisms for reflux (GORD)
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13
Q

What are the different types of dysphagia?

A
  • solids or fluids
  • intermittent or progressive
  • precise or vague
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14
Q

What is important when someone is complaining of dysphagia?

A

localisation

cricopharyngeal sphincter or distal

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15
Q

What is odynophagia?

A

pain on swallowing

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16
Q

What is regurgitation?

A

return of oesophageal contents from above an obstruction (functional or mechanical)

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17
Q

What may cause mechanical regurgitation?

A

obstructions eg: tumours

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18
Q

What is reflux?

A

passive return of gastroduodenal contents to the mouth

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19
Q

What is the biological characteristics of Achalasia?

A

loss of ganglion cells in Aurebach’s myenteric plexus in the lower oesophageal sphincter wall, leading to decreased activity of inhibitory NCNA neurones.

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20
Q

What is Achalasia?

A

the absence of peristalsis, and impaired relaxation of the lower oesophageal sphincter

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21
Q

What causes primary achalasia?

A

unknown aetiology

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22
Q

What causes secondary achalasia?

A

diseases that cause similar oesophageal motor abnormalities

  • Chagas’ Disease
  • Protozoa Infection
  • Anyloid/Sarcoma/Eosinophilic Oesophagitis
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23
Q

What happens in the development of Achalasia?

A
  • increased resting pressure of the lower oesophageal sphincter
  • receptive relaxation sets in too late, and is too weak as the pressure in the LOS is much higher than the stomach, so food does not pass through
  • swallowed food contents collects in the oesophagus causes increased pressure throughout with dilation of the oesophagus
  • propagation of peristalic waves cease
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24
Q

What are the symptoms of Achalasia?

A
  • weight loss
  • dysplasia
  • regurgitation
  • oesophagitis
  • pneumonia due to aspiration
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25
Is Achalasia a disorder of hyper or hypomotility?
hypermotility
26
What is the course of Achalasia?
- insidious onset (symptoms for years before help) | - without treatment leads to progressive oesophageal dilation of the oesophagus
27
What does Achalasia predispose you to?
- increased risk of oesophageal cancer by 28-fold
28
What are the possible treatment options for Achalasia?
- Pneumatic Dilation - Peroral Endoscopic Myotomy surgery: - Heller's Myotomy and then, Dor fundoplication
29
What is pneumatic dilation?
- weakening of the LOS by circumferential stretching and in some cases - tearing muscle fibres
30
What is the efficacy of pneumatic dilation?
71-90% respond initially, many subsequently relapse
31
What is Heller's Myotomy?
a continuous myotomy performed for 6cm of the oesophagus and 3cm of the stomach
32
What is Dor Fundoplication?
anterior fundus folded over the oesophagus and sutured to the right side of myotomy
33
What are the risks associated with Heller's Myotomy and Dor Fundoplication?
- oesophageal and gastric perforation (10-16%) - splenic injury (1-5%) - division of the vagus nerve (rare)
34
What happens in a Peroral Endoscopic Myotomy?
- mucosal incision - creation of submucosal tunnel - myotomy - closure of mucosal incision
35
What is Scleroderma?
autoimmune disease that is usually irreversible
36
What are the biological effects of Scleroderma?
- hypo-motility in it's early stages due to neuronal defects leading to atrophy of the smooth muscle of the oesophagus - peristalsis in the distal portion ultimately ceases - decreased resting pressure on the LOS - GORD develops
37
What is Scleroderma associated with?
CREST syndrome
38
What is CREST syndrome?
- Calcinosis - Reynauds phenomenon - Esophageal Dysmotility - Sclerodactyly - Telangiectasia
39
How do you treat Scleroderma?
- exclude organic obstruction (no malignancy) - improve force of peristalsis with prokinetics (cisapride) - low efficacy - once peristaltic failure occurs, usually irreversible
40
What is corkscrew oesophagus?
diffuse oesophageal spasm - inco-ordinate contractions - marked hypertrophy of circular muscle - pressures of 400-500mmHg
41
What symptoms can corkscrew oesophagus present with?
- dysphagia | - chest pain
42
What is the treatment of corkscrew oesophagus?
may respond to forceful pneumatic dilation - results are not as predictable
43
What vascular abnormalities cause dysphagia?
- dysphagia lusoria | - double aortic arch
44
Where do oesophageal perforations tend to occur?
- Cricopharyngeal constriction - Aortic and bronchial constriction - Diaphragmatic and 'sphincter' constriction
45
What can cause oesophageal perforations?
- Iatrogenic (investigation caused) >50% - Spontaneous 15% - Foreign body 12% - Trauma 9% - Intraoperative 2% - Malignant 1%
46
When do Iatrogenic oesophageal perforations tend to occur?
- usually at OGD | - more common: diverticula, cancer
47
What can cause an Iatrogenic Oesophageal perforations?
- OGD 0.03% - Stricture dilation 0.1-2% - Slcerotherapy 1-5% - Achlasia dilation 2-6%
48
What tends to cause spontaneous oesophageal perforations?
Boerhaave's
49
What happens in a spontanous (Boerhaave's) oesophageal perforation?
- sudden increase in intra-oesophageal pressure with negative intra thoracic pressure - vomiting against a closed glottis - tends to happen at the left posterolateral aspect of the distal oesophagus
50
What common foreign bodies tend to cause a oesophageal perforation?
- disk batteries (electrical burns if impacts in the mucosa) - magnets - sharp objects - dishwasher tablets - acid/alkali
51
What can cause a trauma induced oesophageal perforation?
- NECK penetrating trauma | - THORAX blunt force (very rare)
52
How do trauma induced oesophageal perforations present?
- Dysphagia - Blood in saliva - Haematemesis - Surgical empysema
53
How does a surgical empysema present?
air under the skin | crackling sensation on touch
54
What can cause a intraoperative oesophageal perforation?
- Hiatus hernia repair - Heller's cardiomyotomy - Pulmonary surgery - Thyroid surgery
55
What tends to cause malignant oesophageal perforations?
advanced cancers
56
What can be used to treat an oesophageal perforation?
- radiotherapy - stenting - dilation
57
What is the prognosis for a malignant oesophageal perforation?
poor
58
How do oesophageal perforations present?
- pain (95%) - fever (80%) - dysphagia (70%) - emphysema (35%)
59
What investigations would you run on a suspected oesophageal perforation?
- chest x-ray - CT - swallow test (gastrograffin) - OGD
60
What is the initial management plan for a oesophageal perforation?
- nil by mouth - IV fluids - broadspectrum ABx and antifungals - ITU/HDU care - Bloods (incl. G+S) - tertiary referral centre
61
Why are oesophageal perforations considered a surgical emergency?
2 x increase in mortality if 24hr delay in diagnosis
62
What needs to be known about an oesophageal perforation?
- transmural or intramural? - where and on which side? - how big? - well defined or diffuse leak?
63
What should be the default management?
operative management
64
When should operative management NOT be default?
- minimal contamination - contained (no leak) - unfit
65
What is the conservative management option for those where operative solutions CANNOT be used?
covered metal stent
66
What is the optimal surgical management of a oesophageal perforation?
primary repair - vascularised pedicle flap - gastric fundus butressing drains
67
What is the definitive surgical option to treat an oesophageal perforation?
oesophagectomy | - reconstruction or oesophagostomy and delayed reconstruction
68
What structural part of the body acts as a barrier against reflux?
LOS
69
What causes normal sporadic reflux?
- pressure on a full stomach - swallowing - transient sphincter opening
70
What are the mechanisms used to protect from reflux?
- volume clearance (oesophageal peristalsis reflex) - pH clearance (saliva) - Epithelium (barrier properties)
71
What can prevent/inhibit reflux?
increased pressure in the LOS - protein - histamine - high intra-abdominal pressure
72
What can promote reflux?
decreased pressure in the LOS - chocolate - gastric acid - fat - smoking
73
What are examples of the protective measures failing and causing GORD?
- reduced LOS pressure - increased transient sphincter opening (carbonated drinks) - reduced saliva production - reduced buffering capacity of saliva (smoking) - abnormal peristalsis - hiatus hernia - defective mucosal protective mechanism (alcohol)
74
How can GORD lead to malignancy?
- increased reflux - reflux esophagitis - epithelial metaplasia - carcinoma
75
What is a sliding hiatus hernia?
- distal oesophagus ligament snaps | - stomach moves into the thorax, through the diaphragm
76
What is a rolling/paraoesophageal hiatus hernia?
- fundus of stomach moves through the diaphragm into the thorax - blood flow compromised, ischaemia
77
What investigations should be done when GORD is suspected?
- endoscopy exclude cancer, oesophagitis, peptic stricture and Barretts oesophagus confirmed - oesophageal manometry - 24-hour oesophageal pH recording
78
What medical options are there to treat GORD?
lifestyle changes - weight loss - no smoking PPIs
79
What are the surgical options available to treat GORD?
- dilation of peptic strictures | - laparoscopic Nissen's fundoplication
80
What are the functions of the stomach?
- break down food - release food at a steady rate into the duodenum - kill parasites and certain bacteria
81
What is produced in the Cardia and Pyloric regions?
mucus only
82
What is produced in the body and fundus of the stomach?
- mucus - HCl - Pesinogen
83
What is produced in the antrum of the stomach?
Gastrin
84
What is the pH at the epithelial surface?
6-7
85
What is the pH at the lumen of the stomach?
1-2
86
What is Mucins?
gel coating of the epithelium, traps carbonate ions
87
How much stomach acid is produced daily, and what is it made of?
- 2L/day | - 150mM H+ (3 mill x blood contents)
88
What can cause erosive and hemorrhagic gastritis?
- NSAIDs - Alcohol - Trauma - Ischaemia - Multi-organ failure - burns
89
Where does erosive and haemorrhagic gastritis present?
anywhere in the stomach
90
How does erosive and haemorrhagic gastritis present?
gastric bleeding and perforation of the stomach wall
91
What causes nonerosive, chronic active gastritis?
H. pylori infections
92
Where does nonerosive, chronic active gastritis occur?
limited to the antrum
93
How you manage nonerosive, chronic active gastritis?
triple Rx: amoxicillin, clarithromycin, pantoprazole for 7-14 days
94
Where does atrophic (fundal gland) gastritis occur?
the fundus of the stomach
95
What causes atrophic (fundal gland) gastritis?
- autoantibodies that attack the parietal cells in the stomach (eg: gastrin receptor, carbonic anhydrase...) - parietal cell atrophy - decreased gastric acid and IF secretion - G-cell hyperplasia - epithelial metaplasia
96
What can atrophic (fundal gland) gastritis cause?
- decreased IF secretion - reduced cobalamine absorption - cobalamine deficiency - pernicious anaemia
97
What can cause reactive gastritis?
- acute ulcers
98
What can reactive gastritis cause?
epithelial metaplasia | eventually: carcinoma
99
What is a carcinoid?
neuro-endocrine tumours
100
What stimulates gastric secretion?
- ACh - Gastrin - Histamine
101
What produces gastrin?
G cells of the antrum
102
What produces histamine?
ECL cells and mast cells of the gastric wall
103
What releases ACh?
post ganglionic receptor of vagal parasympathetic fibres
104
What inhibits gastric secretion?
- secretin - somatostatin - PGs (E2 and I2), TGF-alpha, adenosine
105
What produces secretin?
released from the small intestine
106
What is somatostatin?
somatotropin release-inhibiting hormone
107
What are the forms of mucosal protection?
- mucus film - carbonate secretion - epithelial barrier - mucosal blood perfusion
108
How does carbonate secretion protect the gastric wall?
buffers H+ | propogated by prostaglandins
109
How does the epithelial barrier protect the gastric wall?
tight junctions prevent H+ penetration.
110
What is the danger of epithelial wall ischaemia?
increased penetration of H+
111
What are the 2 mechanisms of epithelial repair?
- migration | - gap closed by cell growth
112
How does migration repair the epithelium?
adjacent epithelial cells flatten to close the gap via sideward migration along the basement membrane
113
What stimulates epithelial repair via cell growth?
- EGF - TGF-alpha - IGF-1 - GRP - gastrin
114
When does acute wound healing of the epithelium occur?
when the basement membrane is destroyed
115
What happens during acute wound healing when the basement membrane is destroyed?
- attraction of leukocytes and macrophages - phagocytosis of necrotic cells - angiogenesis - regeneration of ECM after BM repair - epithelial closure by restitution and cell division (granulation, angiogenesis and BM restitution)
116
What factors aid ulcer formation?
- H pylori - increased gastric juice secretion - reduced carbonate secretion - reduced cell formation - reduced blood perfusion
117
What does urease on H pylori do?
- neutralise gastric acid | - gastric mucosal injury (ammonia)
118
What do exotoxins from H pylori do?
- vacuolating toxin (vacA) | - gastric mucosal injury
119
What do secretary enzymes from H pylori do?
(mucinase, protease and lipase) | - gastric mucosal injury
120
What do the effectors (cagA ...) released by H pylori do?
- IL-8 induction | - host cell growth and apoptosis inhibition
121
What do the lipopolysaccharides on H pylori do?
- adhere to host cells | - inflammation
122
What symptoms do 80% of the population with H pylori experience?
asymptomatic or chronic gastritis
123
What symptoms do 15-20% of the population with H pylori experience?
- chronic atrophic gastritis - intestinal metaplasia - gastric or duodenal ulcer
124
What symptoms do <1% of the population with H pylori experience?
- gastric cancer | - MALT lymphoma
125
What are the medical treatments available for ulcers?
- PPI or H2 blocker | - Triple Rx (amoxicillin, clarithromycin and pantoprazol) for 7-14 days
126
When is surgery required?
rarely - most uncomplicated resolve in 12 weeks - if not, change meds and observe for an additional 12 weeks - check serum gastrin - OGD (biopsy)
127
Why is serum gastrin checked if an ulcer has not healed in 24 weeks?
antral G-cell hyperplasia or gastrinoma (Zollinger-Ellison syndrome)
128
Why is an OGD done if an ulcer has not healed in 24 weeks?
- to biopsy all 4 quadrants of the ulcer | - rule out malignant ulcer if refractory
129
What are the surgical indications for ulcer treatment?
- intractability (after medical therapy) - haemorrhage - obstruction - perforation - relative: continuous requirement of steroid therapy/NSAIDS
130
What are the possible surgical causes of upper abdomen pain?
- PUD/GORD - Pancreatitis - Biliary pathology - Abdominal wall - Vascular - Small bowel - Large bowel
131
What are the possible non-surgical causes of upper abdomen pain?
- cardiac - GI - MSK - Diabetes - Dermatological
132
What is the first investigations done when presenting with upper abdomen pain?
- chest x-ray | - abdomen x-ray
133
What blood marker can exclude a diagnosis of pancreatitis?
Normal amylase
134
What is the most likely organ to perforate?
The duodenum
135
What is Rigler’s sign?
Free intraperitoneal air (both inside and outside the bowel) - clear bowel wall
136
When is Rigler’s sign the clearest?
Transverse x-ray plane
137
What labs would indicate gallstone pancreatitis?
- increased amylase | - abnormal LFTs
138
What is the management plan for gallstone pancreatitis?
NJ or IV food, aim is pancreatic rest
139
What is the first line scan done to see gallstone pancreatitis?
USS Abdomen
140
What blood tests suggest that a stone is still present/hasn’t passed?
LFTs remain deranged
141
What does a HIDA scan look for?
Functional problems
142
What is intraabdominal collection?
Improper ‘washing out’ leads to bacterial build up and pus development
143
How do you treat intraabdominal collection?
- drainage | - IV ABx
144
How does intraabdominal collection present on blood tests?
- elevated WCC and CRP
145
What symptom makes a small/large bowel obstruction unlikely?
Due to peritonitis
146
How can pain on inhalation cause pneumonia?
- breathing causes pain - therefore there’s no air filling the lungs - then fluid fills the lung instead - leading to an infection
147
What type of perforations are quite rare?
Stomach perforations
148
What should be looked for when a stomach perforation occurs?
Cancer
149
What do posterior gastric ulcers tend to cause?
Bleeding
150
What do anterior gastric ulcers tend to cause?
Perforations
151
What does free air below the diaphragm (subdiaphragmatic) indicate?
An abdominal perforation
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