Upper GI Flashcards

1
Q

What is the anatomy of the oesophagus (C5/6-T10)?

A

Upper oesophageal sphincter
Cervical oesophagus
Upper thoracic oesophagus
Middle thoracic oesophagus
Lower thoracic
oesophagus/oesophagastric junction
Abdominal oesophagus
Lower oesophageal sphincter

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2
Q

Where is the abdominal oesophagus?

A

Between where is reaches the diaphragm and the cardia of the stomach

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3
Q

What does the oesophagus enter at T10?

A

The diaphragm

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4
Q

Where is the trachea in respect to the oesophagus?

A

The trachea is anterior to the oesophagus

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5
Q

Where is the aorta in respect to the oesophagus?

A

The aorta lies on the left hand side of the oesophagus

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6
Q

What muscle is the upper 1/3 of the oesophagus made up of?

A

Skeletal muscle

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7
Q

What muscle is the middle 1/3 of the oesophagus made up of?

A

Skeletal and smooth muscle

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8
Q

What muscle is the lower 1/3 of the oesophagus made up of?

A

Smooth muscle

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9
Q

What is the arteriole blood supply to the superior aspect thoracic oesophagus?

A

Branches of the aorta

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10
Q

What is the arteriole blood supply to the inferior aspect of the thoracic oesophagus?

A

Inferior thyroid artery which are branches of the thyroid cervical trunk

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11
Q

What is the arteriole blood supply to the abdominal oesophagus?

A

Left gastric artery and inferior phrenic artery

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12
Q

What is the venous drainage in the thoracic oesophagus?

A

The azygous vein(systemic circulation)

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13
Q

What is the portal veinous drainage of the lower third of the oesophagus?

A

Left gastric vein which drains into the portal venous system

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14
Q

What is the anatomy of the LOS?

A

Diaphragm surrounds LOS (L+R crux)
Phrenoesophageal ligament
Angle of His (between stomach and oesophagus)

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15
Q

Describe the phrenoesophageal ligament?

A

Extension of inferior diaphragmatic fascia
Consists of upper and lower limbs

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16
Q

What is the upper limb of the phrenoesophageal ligament?

A

Goes superiorly and attaches to lower part of the oesophagus

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17
Q

What is the lower limb of the phrenoesophageal ligament?

A

Goes inferiorly and attaches to cardia of the stomach

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18
Q

What are the 4 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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19
Q

What does the oral stage of swallowing involve?

A

Chewing and saliva prepare bolus
Both oesophageal sphincters constricted

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20
Q

What does the pharyngeal phase involve?

A

Pharyngeal muscles guides food bolus towards oesophagus
UOS opens reflexly
LOS opened by vasovagal reflex (receptive relaxation reflex)

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21
Q

What is the receptive relaxation reflex?

A

Proximal part of the stomach relaxes so more food can be taken in

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22
Q

What coordinates the receptive relaxation reflex?

A

Inhibitory non-cholinergic non-adrenergic neurones of myenteric plexus

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23
Q

What does the upper oesophageal phase involve?

A

UOS closes
Superior circular muscle rings contract and inferior rings dilate
Sequential contractions of longitudinal muscle

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24
Q

What does the lower oesophageal phase involve?

A

LOS closes as food passes through

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25
Q

How is motility of the oesophagus determined?

A

Pressure measurements (manometry)

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26
Q

What is a functional disorder of the oesophagus?

A

Absence of an oesophageal structure (abnormal narrowing of oesophagus)

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27
Q

What are the 2 causes of a functional disorder of the oesophagus?

A

Abnormal oesophageal contraction
Failure of protective mechanisms for reflux

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28
Q

What are examples of abnormal oesophageal contraction?

A

Hypermotility
Hypomotility
Disordered coordination

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29
Q

What is an example of failure off protective mechanisms for reflux?

A

Gastro-oesophageal reflux disease (GORD)

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30
Q

What are the types of dysphagia

A

Solids OR fluids
Intermittent OR progressive
Precise OR vague

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31
Q

What is odynophagia?

A

Pain on swallowing

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32
Q

What is achalasia?

A

Hypermotility due to loss of ganglion cells in the Auerbach’s myenteric plexus in LOS wall
Results in decreased activity of inhibitory NCNA neurones
Increased resting potential of LOS

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33
Q

What is the cause for primary achalasia?

A

Idiopathic

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34
Q

What is the cause of secondary achalasia?

A

Diseases causing oesophageal motor abnormalities similar to primary achalasia

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35
Q

What are examples of diseases causing secondary achalasia?

A

Chagas’ disease
Protozoa infection
Amyloid/sarcoma/eosinophilic oesophagitis

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36
Q

How does achalasia work?

A

Receptive relaxation sets in late or too weak
Swallowed food collects in the oesophagus causing increased pressure in the oesophagus with oesophageal dilatation
Peristaltic waves cease

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37
Q

What is the onset of achalasia?

A

Gradual onset
Can also increase the risk of cancer by 28 fold

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38
Q

How does pneumatic dilatation work as treatment for achalasia?

A

Weakens LOS by circumferential stretching and can tear the muscle fibre in some cases

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39
Q

What are the 2 methods of surgery for achalasia?

A

Heller’s myotomy
Dor fundoplication

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40
Q

What is a myotomy?

A

Cutting of oesophageal muscles

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41
Q

How does Heller’s myotomy work?

A

Myotomy of oesophagus (6cm) and stomach (3cm)

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42
Q

What are the risks of Heller’s myotomy?

A

Oesophageal and gastric perforation
Divides of vagus nerve
Splenic injury

43
Q

What is scleroderma?

A

An autoimmune disease
Hypomotility in early stages due to neuronal defects due to atrophy of smooth muscles

44
Q

How does scleroderma cause hypomotility?

A

Smooth muscles do not function in oesophagus so peristalsis in distal portion completely ceases
Decreased resting pressure of LOS

45
Q

What disease can develop from scleroderma?

A

GORD

46
Q

What are treatments for scleroderma?

A

Exclude organic obstruction
Improve force of peristalsis using prokinetics
Peristaltic failure is usually irreversible

47
Q

What is corkscrew oesophagus?

A

Disordered coordination of the oesophagus from diffuse oesophageal spasm

48
Q

What symptoms do uncoordinated contractions cause?

A

Dysphagia and chest pain

49
Q

What is observed in corkscrew oesophagus?

A

Marked hypertrophy of the circular muscles
Corkscrew oesophagus on barium

50
Q

What is treatment for corkscrew oesophagus?

A

MAY respond to forceful pneumatic dilatation of cardia however results are not as predictable as achalasia

51
Q

Where are the 3 areas of anatomical constriction of the oesophagus?

A

Cricopharyngeal constriction
Aorta and bronchial constriction
Diaphragmatic and ‘sphincter’ constriction

52
Q

What are the 6 causes of oesophageal perforation in order of prevalence?

A

Iatrogenic
Spontaneous (Boerhaave’s)
Foreign body
Trauma
Intraoperative
Malignant

53
Q

What are the main cause of iatrogenic oesophageal perforation?

A

Oesophagogastro duodenoscopy
(More common if diverticula or cancer is present)

54
Q

How does Boerhaave’s oesophageal perforation work?

A

-Sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure
-Usually due to vomiting against a closed glottis
-Perforation at left posterolateral aspect of distal oesophagus

55
Q

What types of trauma can cause oesophageal perforation?

A

Penetrating trauma to the neck
Blunt force trauma to the thorax

56
Q

What symptoms can patients with oesophageal perforation from trauma present with?

A

Dysphagia
Blood in saliva
Haematemesis (vomiting blood)
Surgical emphysema

57
Q

What are the main symptoms patients with oesophageal perforation present with in general?

A

Pain
Fever
Dysphagia
Emphysema

58
Q

What are investigations used for oesophageal perforation?

A

Chest X-Ray
CT scan
Gastrograffin (swallowing)
Oesophagogastro duodenoscopy

59
Q

What is initial management for oesophageal perforation?

A

Nil by mouth
IV fluids
Broad spectrum antibiotics and antifungals
Bloods
ITU/HDU level care
Refer tertiary referral centre

60
Q

What are the surgical options for oesophageal perforation?

A

Primary repair through suturing (optimal)
Oesophagectomy (definitive solution)

61
Q

What are protective mechanisms against reflux?

A

LOS usually closed as a barrier against reflux
Volume clearance= oesophageal peristalsis reflex
pH clearance= saliva
Epithelium= barrier problems

62
Q

What are examples of failure of sphincter function?

A

Reduced sphincter pressure
Transient sphincter opening

63
Q

What are examples of failure of protective mechanisms which reduces pH clearance?

A

Reduced saliva production
Reduced buffering capacity of saliva

64
Q

What are other examples of failure of protective mechanisms?

A

Hiatus hernia
Defective mucosal protective mechanism

65
Q

What are the 2 types of hiatus hernia you can get?

A

Sliding hiatus hernia
Rolling/paraoesophageal hiatus hernia

66
Q

How can GORD progress if untreated?

A

Reflux oesophagitis
Epithelial metaplasia
Carcinoma

67
Q

What are investigations for GORD?

A

Oesophagastro duodenoscopy
Oesophageal manometry
24 hour oesophageal pH recording

68
Q

How does an oesophageal manometry work?

A

Insertion of thin, flexible tube with pressure sensors through the nose into the throat
Sensors measure the pressure and coordination of the muscles

69
Q

What are the 2 categories for treatment of GORD?

A

Medical
Surgical

70
Q

What are examples of medical treatments for GORD?

A

Lifestyle changes
Proton-pump inhibitors

71
Q

What are examples of surgical treatments for GORD?

A

Dilatation peptic strictures
Laparoscopic Nissen’s fundoplication

72
Q

What is dilatation peptic strictures?

A

Dilation of narrowed oesophageal structures (known as oesophageal strictures)

73
Q

What is laparoscopic’s Nissen’s fundoplication?

A

The fundus (upper part) of the stomach is wrapped around the lower part of the esophagus to create a valve-like structure

74
Q

What are the 4 types of gastritis?

A

Erosive and hemorrhagic gastritis
Non-erosive, chronic active gastritis
Atrophic (fundal gland) gastritis
Reactive gastritis

75
Q

What is the main cause of erosive and hemorrhagic gastritis?

A

Acute ulcer= gastric bleeding and perforation

76
Q

What is the main cause of non-erosive, chronic active gastritis?

A

Helicobacter pylori

77
Q

What is the part of the stomach that is targeted non-erosive, chronic active gastritis?

A

Antrum

78
Q

What is the treatment for helicobacter pylori?

A

Triple drug therapy with amoxicillin+clarithromycin+prantoprazle
For 7-14 times for 7 days

79
Q

What is the main cause of atrophic gastritis?

A

Autoantibodies against the parts and products of parietal cells
Results in less acid and intrinsic factor secretion

80
Q

What part of the stomach is damaged by atrophic gastritis?

A

Fundus

81
Q

What causes the stimulation of gastric secretion?

A

Neural= ACh from vagal parasympathetic fibres
Endocrine= Gastrin (G cells of antrum)
Paracrine= Histamine (ECL and mast cells)

82
Q

What causes the inhibition of gastric secretion?

A

Endocrine= secretin (small intestine)
Paracrine= somatostatin (SIH)
Paracrine and autocrine= Prostaglandins, TGF-⍺ and adenosine

83
Q

What are the 4 ways in which the mucosa is protected?

A

Mucus film
Hydrogen carbonate secretion
Epithelial barrier
Mucosal blood perfusion

84
Q

How does a mucus film protect the mucosa?

A

Epithelial cells make mucus
Mucus protects against pepsin and H+ ions

85
Q

How does hydrogen carbonate secretion protect the mucosa?

A

HCO3- buffers against acids
Needs prostaglandins

86
Q

How do epithelial barriers protect the mucosa?

A

Apical membrane and tight junctions are barriers
This prevents penetration of H+ ions

87
Q

How does good mucosal blood perfusion protect the mucosa?

A

Perfusion allows H+ ions which have penetrated to be taken away quickly via the blood
Ischaemia in ulcer so mucosa is open to attack by H+ ions

88
Q

What are the 3 mechanisms of epithelial repair and wound healing?

A

Migration
Gap closed by cell growth
Acute wound healing

89
Q

What is migration?

A

Adjacent epithelial cells flatten to close gap via sideway migration along basement membrane

90
Q

What factors stimulate the gap to close by cell growth?

A

EGF
TGF-⍺
IGF-1
GRP
Gastrin

91
Q

When does acute wound healing work?

A

Basement membrane destroyed

92
Q

How does acute wound healing work?

A

-Attraction of leukocytes and macrophages
-Phagocytosis of necrotic cells
-Angiogenesis
-Regeneration of ECM after repair of basement membrane
-Epithelial closure by restitution and cell division

93
Q

What are the causes of ulcer formation?

A

-Helicobacter pylori
-Non-steroidals and smoking
-Stress (shocks, burns, operation)
-Psychogenic components, smoking and gastrinoma
-Secretion of gastric juice
-Less HCO3- secretion
-Less cell formation
-Less blood perfusion

94
Q

How does helicobacter pylori cause ulcer formation?

A

Disturbs barrier function
Causes gastritis which also disturbs barrier function
Increases H+ and pepsinogen secretion which increases chemical aggression

95
Q

How does non-steroidal and smoking cause ulcer formation?

A

1) Decreased PG synthesis → less mucosal protection → barrier function disturbed
2) Decreased PG synthesis → increased H+ and pepsinogen secretion → increased chemical aggression

96
Q

How does stress cause ulcer formation?

A

Decreased blood perfusion → less mucosal protection → barrier function disturbed

97
Q

How do psychogenic components, smoking and gastrinoma cause ulcers?

A

Increased H+ and pepsinogen secretion → increased chemical aggression

98
Q

What is a gastrinoma?

A

Neuroendocrine tumours that produce gastrin

99
Q

How do all these methods lead to ulcer formation?

A

Chemical aggression and barrier function being disturbed leads to epithelial damage
Epithelial damage → wound → can lead to ulcer if not healed

100
Q

What is Zollinger-Ellison syndrome?

A

Recurrent gastrinoma formation leading to recurrent peptic ulcer formation

101
Q

What are the different clinical outcomes of H Pylori infections?

A

80%= asymptomatic or chromic gastritis
15-20%= chronic atrophic gastritis/intestinal metaplasia/ gastric/duodenal ulcer
<1%= gastric cancer/MALT lymphoma

102
Q

What are indicators for surgery for ulcers?

A

-Interactability= might have symptoms after medical therapy
-Relative= continuous requirements of steroid therapy
-Complications from ulcer

103
Q

What are the 3 complications from ulcer?

A

Haemorrhage
Obstruction
Perforation