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GASTROENTEROLOGY > 1b Upper GI Tract > Flashcards

1b Upper GI Tract Flashcards

1
Q

Where does the oesophagus run from in terms of vertabrae?

A

C5-T10

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2
Q

What type of muscle does each third of the oesophagus have?

A

Upper = Skeletal
Middle = Skeletal / Smooth
Lower = Smooth

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3
Q

Describe the change in epithelium which when going from the top of the oesophagus to the bottom?

A

Non ketatinizing squamoous epithelium to columnar epithelium

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4
Q

Which bone is the upper oesophageal sphincter related to?

A

Hyoid bone

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5
Q

What is the name of the ligament that attaches the diaphragm to the oesophagus?

A

Phrenoesophageal ligament

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6
Q

What is the function of this ligament? Phrenoesophageal ligament

A

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

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7
Q

What is the angle of His?

A

Acute angle created between the cardia at the entrance to the stomach and the oesophagus

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8
Q

What is the function of the angle of His?

A

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

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9
Q

Which part of the diaphragm surrounds the LOS?

A

LEFT and RIGHT Crux

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10
Q

How much of the distal oesophagus is within the abdomen?

A

3-4 cm

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11
Q

What happens in stage 0 (Oral phase) of swallowing?

A

Chewing and saliva prepare the bolus
UOS and LOS are BOTH CLOSED

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12
Q

What happens in stage 1 (Pharyngeal phase) of swallowing?

A

Pharyngeal musculature guides food bolus towards the oesophagus

UOS opens reflexly
LOS Opened by the vasovagal reflex

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13
Q

Which reflex causes the LOS to open during the pharyngeal phase of swallowing?

A

receptive relaxation reflex

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14
Q

What happens in stage 2 (Upper oesophageal phase) of swallowing?

A

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

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15
Q

What happens in stage 3 (lower oesophageal phase) of swallowing?

A

Lower sphincter closes as food passes through

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16
Q

As the bolus passes through the oesophagus, what happens to the muscles?

A

Superior muscles contract
Inferior muscles dilate in order to make space for the food bolus to pass through

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17
Q

What is manometry and what is it used to do?

A

When a probe is placed into the oesophagus and used to measure the pressure inside it

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18
Q

What is the pressure of normal peristaltic waves

A

About 40 mmHg

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19
Q

What is the LOS resting pressure?

A

About 20 mmHg

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20
Q

What happens to the pressure inside the oesophagus during receptive relaxation?

A

decreases to less than 5

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21
Q

What is the pressure and motility of the oeseophagus mediated by?

A

Inhibitory noncholinergic nonadrenergic neurones of myenteric plexus

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22
Q

What is the Receptive Relaxation of the LOS mediated by?

A

Inhibitory non-cholinergic noradrenergic (NCNA) neurons of myenteric plexus

They prevent constriction and so they induce relaxation

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23
Q

What is the most common reason for a functional disorder of the oesophagus?

A

Stricture

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24
Q

In the absence of the stricture, what is the most common cause of functional disorders of the oesophagus?

A
  1. Abnormal oesophageal contraction
  2. Failure of protective mechanisms for GORD
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25
Q

What is dysphagia?

A

Difficulty in swallowing

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26
Q

What is odynaphagia?

A

pain on swallowing

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27
Q

What is regurgitation?

A

Refers to the return of oesophageal contents from above an obstruction

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28
Q

What is meant by reflux?

A

The passive return of gastroduodenal contents to the mouth

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29
Q

What condition is caused by hypermobility?

A

Achalasia

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30
Q

What causes achalasia?

A

Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall, leading to DECREASED ACTIVITY inhibitory NCNA neurones - therefore more mobility

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31
Q

What is seen on images of the oesophagus in achalasia?

A

Birds beak = tapering of the distal oesophagus

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32
Q

Which conditions could cause oesophageal motor abnormalities similar to PRIMARY ACHALASIA?

A

Chaga’s disease
PROTOZOA INFECTION
Amyloid / Sarcoma / Eosinophillic Oesophagitis

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33
Q

Describe the onset of achalasia?

A

Insidious onset = symptoms for years prior to seeking help, without treatment can lead to progressive oesophageal dilation of oesophagus

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34
Q

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

A

Increased resting pressure

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35
Q

What happens to the receptive relaxation phase in achalasia?

A

Sets in too late, and is to weak

during the reflex phase the pressure in the LOS is markedly higher than stomach

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36
Q

How does achalasia cause dilation of the oesophagus?

A

Swallowed food collects in the oesophagus causing increased pressure throughout with dilation of the eosophagus

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37
Q

What is PD?

A

Pneumatic dilatation

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38
Q

How is PD a treatment for achalasia?

A

Dilator into the LOS, inflated and causes the LOS to expand

PD weakens the LOS by circumferential stretching and tearing of the muscle fibres, therefore less suc

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38
Q

How is PD a treatment for achalasia?

A

Dilator into the LOS, inflated and causes the LOS to expand

PD weakens the LOS by circumferential stretching and tearing of the muscle fibres

LOS is too tight in Achalasia, therefore PD is needed to relax it to allow food to pass through the oesophagus

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39
Q

What happens to the LOS in achalasia?

A

TOO TIGHT

NCNA neurones cause the LOS to relax

Therefore if they are decreased activity in achalasia, the LOS becomes very tight

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40
Q

What is Heller’s myotomy?

A

A continuous myotomy performed for 6cm on the oesophagus and 3cm into the stomach

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41
Q

What is a dor fundoplication?

A

Anterior fundus folded over oesophagus and sutured to right side of myotomy

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42
Q

What is a dor fundoplication used to do?

A

Anti-reflux

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43
Q

What are the risks of surgery on the LOS?

A

Perforation
division of vagus nerve
splenic injury

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44
Q

Which condition causes hypomobility?

A

Scleroderma

45
Q

What does hypomobility lead to?

A

Leads to atrophy of smooth muscle of oesophagus, such that peristalsis in the distal portion ultimately ceases altogether

46
Q

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

A

Decreased

47
Q

What is GORD that develops as a result of scleroderma often associated with?

A

CREST Syndrome

48
Q

What is the treatment for Scleroderma?

A
  1. exclude organic obstruction
  2. Improve force of peristalsis with prokinetics (cisapride)
49
Q

What is corkscrew oesophagus?

A

When there is disordered coordination resulting in diffuce oesophageal spasms

50
Q

What are the symptoms of corkscrew oesophagus?

A

dysphagia and chest pain

51
Q

What happens to the circular muscle in the oesophagus in corkscrew oesophagus?

A

Marked hypertrophy of the muscle

52
Q

What is the treatment of corkscrew oesophagus?

A

May respond to forceful PD of cardia

53
Q

What are the three locations in which oesophageal perforations due to anatomical constriction may occur?

A

Cricopharyngeal
Aortic and bronchial
Diaphragmatic and sphincter

54
Q

What might cause pathological narrowing of the oesophagus?

A

Cancer, foreign body or physiological dysfunction

55
Q

Whats the most common cause of oesophageal perforations?

A

Latrogenic - OGD

56
Q

What does an OGD commonly perforate?

A

Killians triangle4

57
Q

What causes Boerhaave’s perforation?

A

Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure

58
Q

What activity can cause Boerhaave’s perforation?

A

Vomiting against a closed glottis

59
Q

Where does Boerhaave’s perforation occur?

A

Left posterolateral aspect of the distal oesophagus

60
Q

Why is children swallowing disc batteries a large problem?

A

Causes electrical burns if embedded into the mucosa, become logged in the oesophagus and erodes, creating a hole in the oesophagus

61
Q

What signs might suggest trauma causing perforation?

A

Dysphagia
Blood in the Saliva
Haematemesis
Surgical emphysema

62
Q

What imaging is done to identify a oesophageal perforation?

A

CXR
CT
Swallow
OGD

See oesophageal contents leak into the mediastinum on the scan

63
Q

What are the most common symptoms of oesophageal perforation?

A

Chest pain
Fever
Dysphagia
Emphysema

64
Q

What is the initial management of oesophageal perforation?

A

Initial Management = Nil By Mouth, IV Fluids, Broad spectrum A/Bs and Antifungal

65
Q

Why are both a/b’s and antifungals needed to treat oesophageal perforation?

A

Due to the high abundance of fungi in the oesophagus therefore both are needed

66
Q

What is the definitive management of Oesophageal perforation?

A

covered metal stent

67
Q

Why is the LOS usually closed?

A

As a barrier against reflux of harmful gastric juice (pepsin and HCl)

68
Q

What happens to the LOS pressure is high?

A

Reflux is inhibited

69
Q

What happens to raise LOS pressure?

A

ACh
hormones
Histamine
high intra-abdominal pressure
PGF

70
Q

What happens when the pressure of LOS is low?

A

Reflux is promoted

71
Q

What lowers the LOS pressure?

A

VIP
Dopamine
NO
PGI
PGE
Fat
Smoking
B-adrenergic agonists

72
Q

What are the three mechanisms which protect following reflux?

A
  1. Volume clearange - oesophageal peristalsis reflex
  2. pH clearance - saliva
  3. Epitheloium has barrier properties
73
Q

Describe what happens if the protective mechanisms against reflux do not work?

A

Reflux oesophagitis, leads to epithelial metaplasia

This leads to carcinoma

74
Q

Why might the protective mechanisms against reflux fail?

A
  1. Lower sphincter pressure
  2. Lowered saliva production (reduce volume and pH clearance)
  3. Abnormal peristalsis (reduce volume and pH clearance)
  4. hiatus hernia
75
Q

What is a sliding hiatus hernia?

A

When a portion of the stomach slides up through the diaphragmatic hiatus

76
Q

What is a rolling hernia?

A

When the herniated portion of the stomach pushed through the diaphragmatic hiatus but next to the oesophagus

77
Q

What is the purpose of doing a OGD for GORD?

A

To exclude cancer
Oesophagitis, peptic stricture and Barrett’s

78
Q

What are the treatments for GORD / hernia?

A

Lifestyle changes
PPI’s - proton pump inhibitor
Dilation of peptic strictures
Laparoscopic Nissen’s fundoplication

79
Q

What is Nissen’s fundoplication?

A

When a portion of the stomach (fundus) is taken and wrapped around the oesophagus to help prevent reflux

80
Q

What is the funtion of the stomach?

A

Break food into smaller pieces using acid and pepsin
Holds food, releasing it in controlled steady rate into the duodenum
Kills parasites and certain bacteria - using low pH

81
Q

What does the cardia and pyloric region of the stomach secrete?

A

Mucus only

82
Q

What does the body and fundus of the stomach secrete?

A

Mucus, HCl and pepsingogen

83
Q

What does the antrum of the stomach secrete?

A

Gastrin

84
Q

What does gastrin do?

A

Stimulates acid production, works via a negative feedback loop

85
Q

What is the most common cause of gastritis?

A

Helicobacter pylori

86
Q

What is the treatment for non-erosive, chronic active gastritis?

A

Triple treatment = amoxicillin, clarithromycin and pantoprazole for 7-14/7

87
Q

Gastritis affecting the fundus?

A

Atrophic gastritis

88
Q

Gastritis affecting the antrum?

A

Non-erosive, chronic active gastritis

  • increased GASTRIN
  • increased acid secretion
  • Chronic gastric / duodenal ulcer
  • Reactive gastritis
    Can lead to epithelial metaplasia
89
Q

What does atrophic gastritis lead to?

A

Parietal cell atrophy, reduced acid and IF secretion leading to pernicious anaemia

90
Q

Which gastritis forms acute ulcers?

A

Erosive and haemorrhagic gastritis

91
Q

What is the neural stimulant of gastric acid secretion?

A

ACh - post ganglionic transmitter of vagal parasympathetic fibres

92
Q

What is the endocrine stimulant of gastric acid secretion?

A

Gastrin from the G cells of the antrum

93
Q

What is the paracrine stimulant for gastric acid secretion?

A

Histamine (ECL - enterochromaffin like cells and mast cells of gastric wall)

94
Q

What are the inhibitory factors of gastric acid secretion?

A

Secretin
Somatostatin
PGs (E2 and I2), TGF-alpha and adenosine

95
Q

What generates bicarb for mucosal protection?

A

Prostaglandins - also inhibited by NSAID’s, so when taking them, gastric perforation is a complication

96
Q

Describe the mucosal protection against ulcers?

A
  1. Mucus film - thick gel like film which covers the surface of the stomach / duodenum so prevents any acidic stomach contents coming into contact with the epithalial cells
  2. HCO3- secretion - The stomach and duodenum also secrete bicarbonate ions (HCO3-) into the mucus layer. These ions neutralize the acidic environment of the stomach
  3. Epithelial barrier - epithelial cells are tightly lined with extensive tight junctions to prevent the leaking of gastric acid into the submucosa
  4. Mucosal blood perfusion - rich supply of blood vessels, allows for efficient delivery of oxygen and nutrients to the epithelial cells, which helps to maintain their integrity and repair any damage that may occur.
97
Q

How does migration work as a mechanism for epithelial repair and wound healing?

A

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

98
Q

How is the gap in the epithelium of the stomach closed by cell growth?

A

Stimulated by EGF, TGF-alpha, IGF-1 and GRP and gastrin

99
Q

How does acute wound healing occur?

A

attraction of leukocytes & macrophages; phagocytosis of necrotic cells; angiogenesis; regeneration of ECM after repair of BM
epithelial closure by restitution & cell division

100
Q

Describe how ulcer formation occurs?

A
  1. Helicobacter pylori
  2. Increased gastric acid secretion
  3. Decreased bicarb secretion
  4. Reduced cell formation
  5. Reduced cell perfusion = less mucosal protection so barrier function disrupted
101
Q

What is the most common outcome of H. pylori infection?

A

Chronic gastritis

102
Q

What is the medical treatment for stomach ulcers?

A

PPI or H2 blocker
Triple Rx (Amoxicillin, clarithromycin and pantoprazole)

103
Q

What is zollinger-Ellison syndrome?

A

Antral G-cell hyperplasia or gastrinoma

104
Q

What are the surgical indications for the treatment of stomach ulcers?

A

ntractability (after medical therapy)

Relative: continuous requirement of steroid therapy/NSAIDs

Complications:

Haemorrhage

Obstruction

Perforation

105
Q

If an ulcer has not healed in 12 weeks, what should be done?

A

Change medication and observe for another 12 weeks

Check serum gastrin (antral G cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome - too much gastric acid])

106
Q

How do NSAIDs and Smoking lead to ulcer formation?

A

Decrease prostaglandin synthesis → Increased H+ & Pepsinogen secretion → Increased chemical aggresion

107
Q

Which prostaglandins are affected by smoking?

A

Decreased PGI2

Increased PGE2

108
Q

Chronic infection with the parasite Trypanosoma cruzi can cause an oesophageal motor abnormality similar to which commoner functional disorder?

A

Achalasia

109
Q

How does Atrophic arise?

A

Atrophic fundal gastritis = due to auto antibodies against parts of the parietal cell like Gastrin receptor, carbonic anyhdrase, H+ K+ ATPase and intrinsic factor

110
Q

Describe how atrophic gastritis may lead to epithelial metaplasia?

A

reduced acid secretion due to auto antibodies, resulting in an increased release of Gastrin to compensate

This leads to ECL cell hyperplasia and G cell Hyperplasia resulting in carcinoid (ECL) and epithelial metaplasia

111
Q

Describe how atrophic gastritis might lead to pernicious anaemia?

A

reduced intrinsic factor, decreased cobalamine absorption and long term this leads to cobalamine deficiency, resulting in pernicious anaemia - could give hydroxycobalamin injections?

GASTROENTEROLOGY (25 decks)

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