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Y2 GASTRO > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

How does the upper oesophageal sphincter open vs the lower oesophageal sphincter?

A

UOS = reflexively
LOS = by vasovagal reflex (receptive relaxation reflex)

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2
Q

What are the anatomical contributors from the upper GI tract to the lower oesophageal sphincter?

A

Is the 3-4 cm distal oesophagus within abdomen
• diaphragm surrounds LOS (Lt & Rt crux)
• intact phrenoesophageal ligament
• angle of His
Intraabdominal pressure

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3
Q

what type of muscle makes up the lower thoracic oesophagus/ oesophageal junction?

A

Smooth muscle

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4
Q

At what vertebral level is the angle of His found?

A

T10

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5
Q

What are the four 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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6
Q

What happens during stage 0 of swallowing?

A
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7
Q

How is the motility of the oesophagus determined?

A

determined by pressure measurements (manometry)
• peristaltic waves ~ 40 mmHg
• LOS resting pressure ~ 20 mmHg
> ↓<5 mmHg during receptive relaxation

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8
Q

How is motility of the oesophagus mediated?

A

mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurones of myenteric plexus

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9
Q

What are the common functional disorders of the oesophagus?

A

Absence of a stricture
• Abnormal oesophageal contraction
> Hypermotility
> Hypomotility
> Disordered coordination
• Failure of protective mechanisms for reflux
> Gastro-oesophageal reflux disease (GORD)

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10
Q

What is dysphagia? Why are the 2 descriptive terms for localisation?

A

Difficulty swallowing
Localisation is important - cricopharyngeal sphincter or distal

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11
Q

What is odynophagia?

A

Pain on swallowing

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12
Q

Define regurgitation

A

Regurgitation = return of oesophageal contents from above an obstruction
> may be function or mechanical

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13
Q

Define reflux

A

Reflux = passive return of gastroduodenal contents to the mouth

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14
Q

What causes achalasia?

A

Loss of ganglion cells in Aurebachs myenteric plexus in LOS wall causing decreased activity of inhibitory NCNA neurones

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15
Q

What is the aetiology behind primary achalasia?

A

Unknown

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16
Q

What is the aetiology behind secondary achalasia?

A

Diseases causing oesophageal motor abnormalities similiar to primary achalasia

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17
Q

What effect does achalasia have on the resting pressure of the LOS?

A

Increased

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18
Q

What are 3 examples of secondary achalasia?

A

Chagas’ disease
Protozoa infection
Amyloid/sarcoma/eosinophilic oesophagitis

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19
Q

outline the 8 steps of the proposed model of achalasia pathophysiology

A

Proposed model of achalasia pathophysiology
1. environmental trigger - chronic infections
2. genetic predisposition
3. first stagenon-autoimmune inflammatory infiltrates
4. promotes would repair and fibrosis
5.loss of immunological toleranceleads to autoimmune inflammatory infiltrates
6. apoptosis of neurones
7. humoral response - autoimmune
8. all leads to myenteric neurone abnormalities

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20
Q

What are the symptoms of achalasia?

A

Retrosternal pain, weight loss, dilated oesophagus, aperistalsis, bird beak in barium swallow, increased LOS pressure

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21
Q

what is aperistalsis?

A

Absence of peristalsis- radially symmetrical contraction and relaxation of muscles

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22
Q

What are the two most common complications of achalasia?

A

Oesophagitis, aspiration pneumonia

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23
Q

Give an example of oesophageal hypermotility

A

Achalasia

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24
Q

Give an example of oesophageal hypomotility

A

Scleroderma

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25
Q

Where does iatrogenic oesophageal perforation usually occur

A

At OGD, located above cricopharyngeal muscle

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26
Q

A normal barium swallow rules out achalasia. True or false

A

False, it is a late feature

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27
Q

What are the different types of dysphagia?

A

For fluids or solids, Intermittent or progressive, precise or vague in appreciation

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28
Q

Describe the progression of achalasia

A

> hasinsidious onset- symptoms for years prior to seeking help
without treatment → progressive oesophageal dilatation of oesophagus
• risk of oesophageal cancer increased28-fold

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29
Q

What are the three methods of treatment for achalasia?

A

Pneumatic dilatation
Hellers myotomy and Dor fundoplication

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30
Q

What occurs during pneumatic dilatation to treat achalasia?

A

PD weakens LOS by circumferential stretching, and in some cases tearing of muscle fibres. This helps to restore flow

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31
Q

What is the efficacy of pneumatic dilatation to treat achalasia?

A

71-90% of patients respond initially but many relapse

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32
Q

What treatment is given to treat achalasia after relapse following pneumatic dilatation?

A

Hellers myotomy and Dor fundoplication

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33
Q

What is Hellers myotomy?

A

Continuous myotomy performed for 6cm on opesophagus and 3cm onto cardia of the stomach

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34
Q

What is Dor fundoplication?

A

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

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35
Q

What are the risks associated with a Hellers myotomy and Dor fundoplication?

A

Oesophageal and gastric perforation, division of vagus nerve, splenic injury

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36
Q

What occurs during a peroral endoscopic myotomy to treat achalasia? (POEM)

A

Mucosal incision, creation of submucosal tunnel, myotomy, closure of mucosal incision

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37
Q

What is scleroderma?

A

An autoimmune disease causing early hypomotility due to neuronal defects. This causes atrophy of smooth muscle of oesophagus

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38
Q

What happens to peristalsis in the distal oesophagus during scleroderma?

A

Ceases all together

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39
Q

Scleroderma treatment?

A

Exclude organic obstruction.
Improve force of peristalsis with pro kinetics such as cisapride
Once peristaltic failure occurs is usually irreversible

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40
Q

What is an example of a disordered oesophageal coordination?

A

Corkscrew oesophagus

41
Q

What is corkscrew oesophagus?

A

Incoordinate contractions cause dysphagia and chest pain

42
Q

What is seen in the circular muscle of the oesophagus in corkscrew oesophagus?

A

Marked hypertrophy

43
Q

Corkscrew oesophagus treatment?

A

May respond to forceful pneumatic dilatation, however results not as predictable as achalasia

44
Q

What vascular anomalies cause dysphagia?

A

Dysphagia Lusoria cause by aberrant right subclavian artery
Double aortic arch

45
Q

How does an aberrant right subclavian artery cause dysphagia lusoria?

A

Constricts the oesphagus against the trachea meaning the right subclavian needs to be reconnect at the right position

46
Q

What oesophageal constrictions cause dysphagia?

A

Cricopharyngeal constriction
Aortic and bronchial constrictions
Diaphragmatic and sphincter constriction

47
Q

What are the common causes of oesophageal perforations?

A

Iatrogenic (OGD), spontaneous (Boerhaaves), foreign body, trauma, intraoperative, malignant

48
Q

An iatrogenic oesophageal perforation is more common at GOD in the presence of what?

A

Diverticula or cancer

49
Q

What is Boerhaaves ?

A

A spontaneous oesophageal perforation caused by sudden increase in intra-oesophageal pressure with negative intrathoracic pressure - for example vomitting against a closed epiglottis

50
Q

What foreign body’s often cause oesophageal perforations?

A

Disk batteries, magnets, sharp objects, dishwasher tablets, acid/alkali

51
Q

What inter-operative oesophageal perforations are most common?

A

Hiatus hernia repair, hellers cardiomyotomy, pulmonary surgery, thyroid surgery

52
Q

What are some malignant causes of oesophageal perforations?

A

Advanced cancers, treated with radiotherapy, dilation, stenting, poor prognosis

53
Q

What investigations can be done to investigate oesophageal perforations?

A

CXR, CT, swallow (gastrograffin), OGD

54
Q

What is done to treat oesophageal perforation?

A

Initial management (NBM, IV fluids, broad spectrum ABs and anti fungal)

55
Q

When investigating an oesophageal perforation what questions do we think of?

A

Is the perforation transmural and intramural?
Where is it and on which side?
How big?
Is the leak well defined or diffuse?

56
Q

Failure of protective mechanisms against reflux in the stomach can lead to what?

A

GORD or a hiatus hernia

57
Q

What protective mechanisms are there against reflux in the stomach?

A

LOS usually closed as barrier against reflux of harmful gastric juice
Swallowing
Pressure on full stomach
Transient sphincter opening

58
Q

Following reflux in stomach what protective mechanisms are there? (3)

A

Volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
Epithelium - barrier properties

59
Q

How is oesophageal perforation managed?

A

Operative management - conservative management with covered metal stent
Primary repair is optimal - vascularised pedicle flap, gastric fundus buttressing
Oesophagectomy - definitive solution, reconstruction or oesophagostomy and delayed reconstruction

60
Q

When is operative management for oesophageal perforation not conducted?

A

Minimal contamination or the patient is unfit

61
Q

What mechanisms lead to GORD

A

• reduced sphincter pressure
• transient sphincter opening
• abnormal peristalsis - reduced volume clearance
• reduced saliva production (in sleep, xerostomia)
• buffering capacity of saliva (smoking)
> reduced pH clearance
• hiatus hernia
• defective mucosal protective mechanism (eg alcohol)
→ reflux oesophagitis

62
Q

What are the different types of hiatus hernia?

A

• Sliding
> stomach moves up through the oesophageal hiatus
• Rolling/paraoesophageal
> stomach herniates to the side of the GOJ
> surgical emergency

63
Q

What is a hiatus hernia?

A

Hiatus hernia is the protrusion of intra-abdominal contents into the thoracic cavity through an enlarged oesophageal hiatus of the diaphragm.

64
Q

How is GORD investigated?

A

OGD to exclude cancer or confirm oesophagitis, peptic stricture, and Barrett’s oesophagus
Oesophageal manometry
24hr oesophageal pH recording

65
Q

At what vertebral level does the oesophagus begin and end?

A

Begins at C5 and ends at T10

66
Q

What happens during stage 0 of swallowing?

A

Chewing and saliva prepare bolus
Both oesophageal sphincters constricted

67
Q

What occurs during stage 1 of swallowing? What is this stage called?

A

Pharyngeal phase
Pharyngeal musculature guides food bolus towards oesophagus
UOS opens reflexly
LOS opened by vasovagal reflex

68
Q

What occurs during stage 2 of swallowing?

A

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

69
Q

What occurs during stage 3 of swallowing?

A

LOS closes as food passes through

70
Q

Following a decrease in resting pressure in LOS in scleroderma, what disease often develops and what is often associated?

A

GORD develops, often associated with CREST syndrome

71
Q

What are the functions of the stomach?

A

Breaks food into smaller particles (acid & pepsin)
• Holds food, releasing it in controlled steady rate into duodenum
• Kills parasites & certain bacteria

72
Q

Where in the stomach is mucus secreted?

A

Cardia, pyloric region, body, fundus

73
Q

Where in the stomach is HCl secreted?

A

Body and fundus

74
Q

Where in the stomach is pepsinogen secreted?

A

Body and fundus

75
Q

Where in the stomach is gastrin secreted?

A

Antrum

76
Q

What are the four different types of gastritis?

A

Erosive and haemorrhagic
Nonerosive, chronic active
Atrophic
Reactive

77
Q

What causes erosive and haemorrhagic gastritis?

A

Acute ulcer causing gastric bleeding and perforation

78
Q

Where does nonerosive, chronic active gastritis affect in the stomach and what bacteria is the cause?

A

Antrum
Helicobacter pylori

79
Q

Where does atro phic gastritis affect in the stomach and how, what affect does it have?

A

Affects the fundus (fundal gland)
Autoantibodies vs parts and products of parietal cells
Parietal cell atrophy
Decrease in acid and IF secretion - can lead to pernicious anaemia

80
Q

What neural stimulation regulates gastric secretion?

A

ACh - postganglionic transmitter of Vagal parasympathetic fibres

81
Q

What endocrine stimulation regulates gastric secretion?

A

Gastrin from G cells of antrum

82
Q

What paracrine stimulation regulates gastric secretion?

A

Histamine from ECL cells and mast cells of gastric wall

83
Q

What endocrine inhibition regulates gastric secretion?

A

Secretin from small intestine

84
Q

What paracrine inhibition regulates gastric secretion?

A

Somatostatin

85
Q

What paracrine and autocrine inhibition regulates gastric secretion?

A

Prostaglandins, TGF-alpha and adenosine

86
Q

What four methods of mucosal protection are there in an ulcer?

A

Mucus film, HCO3- secretion, epithelial barrier, mucosal blood perfusion

87
Q

What 3 mechanisms are there for repairing epithelial defects?

A

Migration, gap closed by cell growth, acute wound healing

88
Q

How does migration repair epithelial defects in an ulcer?

A

Adjacent epithelial cells flatten to close gap via side wards migration along BM

89
Q

How does gap closing by cell growth occur to repair epithelial defects due to an ulcer?

A

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

90
Q

How does acute wound healing occur to repair epithelial defects?

A

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

91
Q

What are the four clinical outcomes of infection by H.pylori?

A

Asymptomatic or chronic gastritis
Chronic atrophic gastritis or intestinal metaplasia
Gastric or duodenal ulcer
Gastric cancer or MALT lymphoma

92
Q

What are the first line treatment options for an ulcer?

A

PPI or H2 blocker
Triple Rx amoxicillin, clarithromyocin, pantoprazole
If unsuccessful elective surgical Rx

93
Q

In the elective surgical Rx of ulcer treatment what is checked and what procedure is undergone?

A

Check serum gastrin for Antral G-cell hyperplasia or gastrinoma (Zollinger-Ellison syndrome)
OGD biopsy of all 4 quadrant of ulcer if refractory

94
Q

What are the surgical indications associated with ulcer treatment??

A

• Intractability (after medical therapy) • Relative: continuous requirement of
steroid therapy/NSAIDs • Complications
• Haemorrhage • Obstruction
• Perforation

95
Q

Is conservative management or operative management for an oesophageal perforation the default?

A

Operative management

96
Q

What things can cause increased LOS pressure?

A

Acetylcholine
Alpha-adrenergic agonists
Protein-rich food
Histamine
High Intra-abdominal pressure

97
Q

What things can cause a decrease in LOS pressure and what does this promote?

A

Promotes acid reflux

Vasoactive intestinal peptides (VIP)
Beta-adrenergic agonists
Dopamine
Acid gastric juice
Fatty foods
Chocolate
Ethanol

98
Q

When does sporadic reflux occur?

A

When there is unexpected pressure on a full stomach
When swallowing
When there is transient sphincter opening

99
Q

Following reflux, what three mechanisms act to protect us?

A

Volume clearance - esophageal peristalsis reflex
pH clearance - Saliva acts as a buffer as it enters the esophagus
Barrier properties of the distal epithelium

Y2 GASTRO (10 decks)

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