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BRS YR2 > Upper GI tract > Flashcards

Upper GI tract Flashcards

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
Q

Is Achalasia a disorder of hyper or hypomotility?

A

hypermotility

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26
Q

What is the course of Achalasia?

A
  • insidious onset (symptoms for years before help)

- without treatment leads to progressive oesophageal dilation of the oesophagus

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27
Q

What does Achalasia predispose you to?

A
  • increased risk of oesophageal cancer by 28-fold
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28
Q

What are the possible treatment options for Achalasia?

A
  • Pneumatic Dilation
  • Peroral Endoscopic Myotomy
    surgery:
  • Heller’s Myotomy and then, Dor fundoplication
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29
Q

What is pneumatic dilation?

A
  • weakening of the LOS by circumferential stretching and in some cases - tearing muscle fibres
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30
Q

What is the efficacy of pneumatic dilation?

A

71-90% respond initially, many subsequently relapse

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31
Q

What is Heller’s Myotomy?

A

a continuous myotomy performed for 6cm of the oesophagus and 3cm of the stomach

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32
Q

What is Dor Fundoplication?

A

anterior fundus folded over the oesophagus and sutured to the right side of myotomy

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33
Q

What are the risks associated with Heller’s Myotomy and Dor Fundoplication?

A
  • oesophageal and gastric perforation (10-16%)
  • splenic injury (1-5%)
  • division of the vagus nerve (rare)
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34
Q

What happens in a Peroral Endoscopic Myotomy?

A
  • mucosal incision
  • creation of submucosal tunnel
  • myotomy
  • closure of mucosal incision
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35
Q

What is Scleroderma?

A

autoimmune disease that is usually irreversible

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36
Q

What are the biological effects of Scleroderma?

A
  • 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
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37
Q

What is Scleroderma associated with?

A

CREST syndrome

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38
Q

What is CREST syndrome?

A
  • Calcinosis
  • Reynauds phenomenon
  • Esophageal Dysmotility
  • Sclerodactyly
  • Telangiectasia
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39
Q

How do you treat Scleroderma?

A
  • exclude organic obstruction (no malignancy)
  • improve force of peristalsis with prokinetics (cisapride) - low efficacy
  • once peristaltic failure occurs, usually irreversible
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40
Q

What is corkscrew oesophagus?

A

diffuse oesophageal spasm

  • inco-ordinate contractions
  • marked hypertrophy of circular muscle
  • pressures of 400-500mmHg
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41
Q

What symptoms can corkscrew oesophagus present with?

A
  • dysphagia

- chest pain

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42
Q

What is the treatment of corkscrew oesophagus?

A

may respond to forceful pneumatic dilation - results are not as predictable

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43
Q

What vascular abnormalities cause dysphagia?

A
  • dysphagia lusoria

- double aortic arch

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44
Q

Where do oesophageal perforations tend to occur?

A
  • Cricopharyngeal constriction
  • Aortic and bronchial constriction
  • Diaphragmatic and ‘sphincter’ constriction
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45
Q

What can cause oesophageal perforations?

A
  • Iatrogenic (investigation caused) >50%
  • Spontaneous 15%
  • Foreign body 12%
  • Trauma 9%
  • Intraoperative 2%
  • Malignant 1%
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46
Q

When do Iatrogenic oesophageal perforations tend to occur?

A
  • usually at OGD

- more common: diverticula, cancer

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47
Q

What can cause an Iatrogenic Oesophageal perforations?

A
  • OGD 0.03%
  • Stricture dilation 0.1-2%
  • Slcerotherapy 1-5%
  • Achlasia dilation 2-6%
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48
Q

What tends to cause spontaneous oesophageal perforations?

A

Boerhaave’s

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49
Q

What happens in a spontanous (Boerhaave’s) oesophageal perforation?

A
  • 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
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50
Q

What common foreign bodies tend to cause a oesophageal perforation?

A
  • disk batteries (electrical burns if impacts in the mucosa)
  • magnets
  • sharp objects
  • dishwasher tablets
  • acid/alkali
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51
Q

What can cause a trauma induced oesophageal perforation?

A
  • NECK penetrating trauma

- THORAX blunt force (very rare)

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52
Q

How do trauma induced oesophageal perforations present?

A
  • Dysphagia
  • Blood in saliva
  • Haematemesis
  • Surgical empysema
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53
Q

How does a surgical empysema present?

A

air under the skin

crackling sensation on touch

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54
Q

What can cause a intraoperative oesophageal perforation?

A
  • Hiatus hernia repair
  • Heller’s cardiomyotomy
  • Pulmonary surgery
  • Thyroid surgery
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55
Q

What tends to cause malignant oesophageal perforations?

A

advanced cancers

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56
Q

What can be used to treat an oesophageal perforation?

A
  • radiotherapy
  • stenting
  • dilation
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57
Q

What is the prognosis for a malignant oesophageal perforation?

A

poor

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58
Q

How do oesophageal perforations present?

A
  • pain (95%)
  • fever (80%)
  • dysphagia (70%)
  • emphysema (35%)
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59
Q

What investigations would you run on a suspected oesophageal perforation?

A
  • chest x-ray
  • CT
  • swallow test (gastrograffin)
  • OGD
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60
Q

What is the initial management plan for a oesophageal perforation?

A
  • nil by mouth
  • IV fluids
  • broadspectrum ABx and antifungals
  • ITU/HDU care
  • Bloods (incl. G+S)
  • tertiary referral centre
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61
Q

Why are oesophageal perforations considered a surgical emergency?

A

2 x increase in mortality if 24hr delay in diagnosis

62
Q

What needs to be known about an oesophageal perforation?

A
  • transmural or intramural?
  • where and on which side?
  • how big?
  • well defined or diffuse leak?
63
Q

What should be the default management?

A

operative management

64
Q

When should operative management NOT be default?

A
  • minimal contamination
  • contained (no leak)
  • unfit
65
Q

What is the conservative management option for those where operative solutions CANNOT be used?

A

covered metal stent

66
Q

What is the optimal surgical management of a oesophageal perforation?

A

primary repair
- vascularised pedicle flap
- gastric fundus butressing
drains

67
Q

What is the definitive surgical option to treat an oesophageal perforation?

A

oesophagectomy

- reconstruction or oesophagostomy and delayed reconstruction

68
Q

What structural part of the body acts as a barrier against reflux?

69
Q

What causes normal sporadic reflux?

A
  • pressure on a full stomach
  • swallowing
  • transient sphincter opening
70
Q

What are the mechanisms used to protect from reflux?

A
  • volume clearance (oesophageal peristalsis reflex)
  • pH clearance (saliva)
  • Epithelium (barrier properties)
71
Q

What can prevent/inhibit reflux?

A

increased pressure in the LOS

  • protein
  • histamine
  • high intra-abdominal pressure
72
Q

What can promote reflux?

A

decreased pressure in the LOS

  • chocolate
  • gastric acid
  • fat
  • smoking
73
Q

What are examples of the protective measures failing and causing GORD?

A
  • 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
Q

How can GORD lead to malignancy?

A
  • increased reflux
  • reflux esophagitis
  • epithelial metaplasia
  • carcinoma
75
Q

What is a sliding hiatus hernia?

A
  • distal oesophagus ligament snaps

- stomach moves into the thorax, through the diaphragm

76
Q

What is a rolling/paraoesophageal hiatus hernia?

A
  • fundus of stomach moves through the diaphragm into the thorax
  • blood flow compromised, ischaemia
77
Q

What investigations should be done when GORD is suspected?

A
  • endoscopy
    exclude cancer, oesophagitis, peptic stricture and Barretts oesophagus confirmed
  • oesophageal manometry
  • 24-hour oesophageal pH recording
78
Q

What medical options are there to treat GORD?

A

lifestyle changes
- weight loss
- no smoking
PPIs

79
Q

What are the surgical options available to treat GORD?

A
  • dilation of peptic strictures

- laparoscopic Nissen’s fundoplication

80
Q

What are the functions of the stomach?

A
  • break down food
  • release food at a steady rate into the duodenum
  • kill parasites and certain bacteria
81
Q

What is produced in the Cardia and Pyloric regions?

A

mucus only

82
Q

What is produced in the body and fundus of the stomach?

A
  • mucus
  • HCl
  • Pesinogen
83
Q

What is produced in the antrum of the stomach?

84
Q

What is the pH at the epithelial surface?

85
Q

What is the pH at the lumen of the stomach?

86
Q

What is Mucins?

A

gel coating of the epithelium, traps carbonate ions

87
Q

How much stomach acid is produced daily, and what is it made of?

A
  • 2L/day

- 150mM H+ (3 mill x blood contents)

88
Q

What can cause erosive and hemorrhagic gastritis?

A
  • NSAIDs
  • Alcohol
  • Trauma
  • Ischaemia
  • Multi-organ failure
  • burns
89
Q

Where does erosive and haemorrhagic gastritis present?

A

anywhere in the stomach

90
Q

How does erosive and haemorrhagic gastritis present?

A

gastric bleeding and perforation of the stomach wall

91
Q

What causes nonerosive, chronic active gastritis?

A

H. pylori infections

92
Q

Where does nonerosive, chronic active gastritis occur?

A

limited to the antrum

93
Q

How you manage nonerosive, chronic active gastritis?

A

triple Rx: amoxicillin, clarithromycin, pantoprazole for 7-14 days

94
Q

Where does atrophic (fundal gland) gastritis occur?

A

the fundus of the stomach

95
Q

What causes atrophic (fundal gland) gastritis?

A
  • 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
Q

What can atrophic (fundal gland) gastritis cause?

A
  • decreased IF secretion
  • reduced cobalamine absorption
  • cobalamine deficiency
  • pernicious anaemia
97
Q

What can cause reactive gastritis?

A
  • acute ulcers
98
Q

What can reactive gastritis cause?

A

epithelial metaplasia

eventually: carcinoma

99
Q

What is a carcinoid?

A

neuro-endocrine tumours

100
Q

What stimulates gastric secretion?

A
  • ACh
  • Gastrin
  • Histamine
101
Q

What produces gastrin?

A

G cells of the antrum

102
Q

What produces histamine?

A

ECL cells and mast cells of the gastric wall

103
Q

What releases ACh?

A

post ganglionic receptor of vagal parasympathetic fibres

104
Q

What inhibits gastric secretion?

A
  • secretin
  • somatostatin
  • PGs (E2 and I2), TGF-alpha, adenosine
105
Q

What produces secretin?

A

released from the small intestine

106
Q

What is somatostatin?

A

somatotropin release-inhibiting hormone

107
Q

What are the forms of mucosal protection?

A
  • mucus film
  • carbonate secretion
  • epithelial barrier
  • mucosal blood perfusion
108
Q

How does carbonate secretion protect the gastric wall?

A

buffers H+

propogated by prostaglandins

109
Q

How does the epithelial barrier protect the gastric wall?

A

tight junctions prevent H+ penetration.

110
Q

What is the danger of epithelial wall ischaemia?

A

increased penetration of H+

111
Q

What are the 2 mechanisms of epithelial repair?

A
  • migration

- gap closed by cell growth

112
Q

How does migration repair the epithelium?

A

adjacent epithelial cells flatten to close the gap via sideward migration along the basement membrane

113
Q

What stimulates epithelial repair via cell growth?

A
  • EGF
  • TGF-alpha
  • IGF-1
  • GRP
  • gastrin
114
Q

When does acute wound healing of the epithelium occur?

A

when the basement membrane is destroyed

115
Q

What happens during acute wound healing when the basement membrane is destroyed?

A
  • 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
Q

What factors aid ulcer formation?

A
  • H pylori
  • increased gastric juice secretion
  • reduced carbonate secretion
  • reduced cell formation
  • reduced blood perfusion
117
Q

What does urease on H pylori do?

A
  • neutralise gastric acid

- gastric mucosal injury (ammonia)

118
Q

What do exotoxins from H pylori do?

A
  • vacuolating toxin (vacA)

- gastric mucosal injury

119
Q

What do secretary enzymes from H pylori do?

A

(mucinase, protease and lipase)

- gastric mucosal injury

120
Q

What do the effectors (cagA …) released by H pylori do?

A
  • IL-8 induction

- host cell growth and apoptosis inhibition

121
Q

What do the lipopolysaccharides on H pylori do?

A
  • adhere to host cells

- inflammation

122
Q

What symptoms do 80% of the population with H pylori experience?

A

asymptomatic or chronic gastritis

123
Q

What symptoms do 15-20% of the population with H pylori experience?

A
  • chronic atrophic gastritis
  • intestinal metaplasia
  • gastric or duodenal ulcer
124
Q

What symptoms do <1% of the population with H pylori experience?

A
  • gastric cancer

- MALT lymphoma

125
Q

What are the medical treatments available for ulcers?

A
  • PPI or H2 blocker

- Triple Rx (amoxicillin, clarithromycin and pantoprazol) for 7-14 days

126
Q

When is surgery required?

A

rarely

  • most uncomplicated resolve in 12 weeks
  • if not, change meds and observe for an additional 12 weeks
  • check serum gastrin
  • OGD (biopsy)
127
Q

Why is serum gastrin checked if an ulcer has not healed in 24 weeks?

A

antral G-cell hyperplasia or gastrinoma (Zollinger-Ellison syndrome)

128
Q

Why is an OGD done if an ulcer has not healed in 24 weeks?

A
  • to biopsy all 4 quadrants of the ulcer

- rule out malignant ulcer if refractory

129
Q

What are the surgical indications for ulcer treatment?

A
  • intractability (after medical therapy)
  • haemorrhage
  • obstruction
  • perforation
  • relative: continuous requirement of steroid therapy/NSAIDS
130
Q

What are the possible surgical causes of upper abdomen pain?

A
  • PUD/GORD
  • Pancreatitis
  • Biliary pathology
  • Abdominal wall
  • Vascular
  • Small bowel
  • Large bowel
131
Q

What are the possible non-surgical causes of upper abdomen pain?

A
  • cardiac
  • GI
  • MSK
  • Diabetes
  • Dermatological
132
Q

What is the first investigations done when presenting with upper abdomen pain?

A
  • chest x-ray

- abdomen x-ray

133
Q

What blood marker can exclude a diagnosis of pancreatitis?

A

Normal amylase

134
Q

What is the most likely organ to perforate?

A

The duodenum

135
Q

What is Rigler’s sign?

A

Free intraperitoneal air (both inside and outside the bowel) - clear bowel wall

136
Q

When is Rigler’s sign the clearest?

A

Transverse x-ray plane

137
Q

What labs would indicate gallstone pancreatitis?

A
  • increased amylase

- abnormal LFTs

138
Q

What is the management plan for gallstone pancreatitis?

A

NJ or IV food, aim is pancreatic rest

139
Q

What is the first line scan done to see gallstone pancreatitis?

A

USS Abdomen

140
Q

What blood tests suggest that a stone is still present/hasn’t passed?

A

LFTs remain deranged

141
Q

What does a HIDA scan look for?

A

Functional problems

142
Q

What is intraabdominal collection?

A

Improper ‘washing out’ leads to bacterial build up and pus development

143
Q

How do you treat intraabdominal collection?

A
  • drainage

- IV ABx

144
Q

How does intraabdominal collection present on blood tests?

A
  • elevated WCC and CRP
145
Q

What symptom makes a small/large bowel obstruction unlikely?

A

Due to peritonitis

146
Q

How can pain on inhalation cause pneumonia?

A
  • breathing causes pain
  • therefore there’s no air filling the lungs
  • then fluid fills the lung instead
  • leading to an infection
147
Q

What type of perforations are quite rare?

A

Stomach perforations

148
Q

What should be looked for when a stomach perforation occurs?

149
Q

What do posterior gastric ulcers tend to cause?

150
Q

What do anterior gastric ulcers tend to cause?

A

Perforations

151
Q

What does free air below the diaphragm (subdiaphragmatic) indicate?

A

An abdominal perforation

BRS YR2 (70 decks)

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