Oesophageal Disorders Flashcards

1
Q

what is the length of the osophagous

A

25cm in legnth

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2
Q

where does the osophagous begin

A

lower level of cricoid cartilage (C6)

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3
Q

where does the osophagous terminate

A

T11-12 where it enters the stomach

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4
Q

what is the upper part of the osophagous made from

A

upper 3-4cm striated muscle

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5
Q

what is around 20cm of the osophagous made from

A

smooth muscle

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6
Q

what type of epithelium is the lining of the osophagous made from

A

stratified squamous epithelium

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7
Q

what is the function of the osophagous

A

Transport of food/liquid from mouth to stomach – active process

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8
Q

how does the osophagous work to move food bolus downwards

A

Oesophageal peristalsis produced by oesophageal circular muscles and propels swallowed materials distally into the stomach

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9
Q

what does esophageal peristalsis coordinate with

A

lower oesophageal sphincter (LOS) relaxation

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10
Q

Contraction in the oesophageal body (peristalsis) and relaxation of the LOS is mediated by what nerve

A

vagus nerve

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11
Q

what is the Lower Oesophageal Sphincter (LOS)

what factor contribute to the integrity of the LOS

A

Physiological sphincter

High resting pressure in distal smooth muscle

Striated muscle of right crus of diaphragm

“Mucosal Rosette” formed by acute angle (of His) at GOJ

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12
Q

when should the LOS be open

A

when food or liquid is passed into the stomach

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13
Q

what is the most common symptom of oesophageal disease

A

heartburn

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14
Q

how do patients with oesophageal disease describe their symptoms

A

retrosternal discomfort or burning

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15
Q

what may retrosternal discomfort or burning be associated with

A

Waterbrash, Cough

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16
Q

what is heartburn

A

Heartburn is a consequence of reflux of acidic &/or
bilious gastric contents into the oesophagus

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17
Q

what can reduce the LOS pressure

A

Certain drugs/foods, (e.g. alcohol, nicotine, dietary xanthines)

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18
Q

what does reduced LOS pressure result in

A

increased reflux / heartburn

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19
Q

what does persistent reflux and heartburn lead to

A

gastro-oesophageal reflux disease (GORD) which can in turn cause long-term complications

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20
Q

dysphagia

A

Subjective sensation of difficulty in swallowing foods and/or liquids

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21
Q

Odynophagia

A

pain with swallowing (may accompany dysphagia)

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22
Q

what must we ask the patient

A

Enquire about: - Type of food (solid vs liquid)
- Pattern (progressive, intermittent)
- Associated features (weight loss, regurgitation, cough

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23
Q

what are causes os oesophageal dysphagia

A

-benign stricture
-malignant stricture (oesophageal cancer)
-motility disorders (eg achalasia, presbyoesophagus)
-eosinophilic oesophagitis
-extrinsic compression (eg in lung cancer)

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24
Q

what investigations are done for oesophageal disease

A

ENDOSCOPY
Oesophago-Gastro-Duodenoscopy (OGD)
Upper GI Endoscopy (UGIE)

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25
Q

ENDOSCOPY

A

simple, effective, safe in experienced hands – diagnostic endoscopy takes 2-3 mins

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26
Q

what can also be done as an investigation for oesophageal disease

A

Contrast radiology (barium swallow)

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27
Q

BA SWALLOW

A

primary indication is investigation of dysphagia (however endoscopy is the preferred test)

May still be used in “high” dysphagia to exclude a pharyngeal pouch or post-cricoid web prior to endoscopy

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28
Q

Oesophageal Physiology: pH - metry

A

Nasal catheter containing pH sensors at both sphincters (UOS and LOS) sphincters is placed in oesophagus

Alternative is endoscopic placement of BRAVO pH probe

pH studies – used in investigation of refractory heartburn/reflux

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29
Q

Oesophageal Physiology: Manometry

A

Nasal catheter containing multiple pressure sensors is placed in oesophagus

Manometry - used in investigation of dysphagia / suspected motility disorder (usually after endoscopy) -assesses sphincter tonicity, relaxation of sphincters and oesophageal motility.

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30
Q

hyper motility example

A

diffuse oesophageal spasm

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31
Q

hyper motility appearance on barium swallow

A

“Corkscrew appearance”

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32
Q

symptoms of hypermotility

A

-Severe, episodic chest pain +/- dysphagia
-Often confused with angina/MI

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33
Q

cause of hyper motility

A

Cause unclear (idiopathic)

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34
Q

manometry results for hyper motility

A

Manometry shows exaggerated,
uncoordinated, hypertonic contractions
-Rx smooth muscle relaxants

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35
Q

what is hypomotiity associated with

A

connective tissue disease,
diabetes, neuropathy

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36
Q

what does hypo motility cause

A

Causes failure of LOS mechanism leading to
heartburn and reflux symptoms

37
Q

ACHALASIA

A

Functional loss of myenteric plexus ganglion
cells in distal oesophagus and LOS

38
Q

what is the incidence of achalasia

A

1-2/100,000
Male:Female incidence = 1:1

39
Q

what is the onset for achalasia

A

usually 3rd - 5th decade

40
Q

cardinal feature of achalasia

A

failure of LOS to relax
Result: functional distal obstruction of oesophagus

41
Q

symptoms of achalasia

A

progressive dysphagia for solids and liquids
weight loss
Chest pain (30%)
Regurgitation and chest infection

42
Q

treatment of achalasia

A

Pharmacological - Nitrates,
Calcium Channel blockers

Endoscopic - Botulinum Toxin
Pneumatic balloon dilation

Radiological - Pneumatic balloon
dilation

Surgical - Myotomy

43
Q

COMPLICATIONS of achalsia

A

Aspiration pneumonia and lung disease
Increased risk of squamous cell oesophageal carcinoma

44
Q

what percentage of adults experience daily GORD symptoms

A

7% adults

45
Q

Many patients with frequent, pathological episodes of acid/bile reflux do not experience

A

any symptoms!!

46
Q

symptoms of GORD

A

heartburn, cough, water brash, sleep disturbance

47
Q

risk factors for GORD

A

Pregnancy, obesity, drugs lowering LOS pressure, smoking, alcoholism, hypomotility

48
Q

are men or women more effected by GORD

A

Men > Women

49
Q

what ethnicities are most affected by GORD

A

Caucasian > Black > Asian

50
Q

how is typical reflux syndrome diagnosed

A

on the basis of the characteristic symptoms, without diagnostic testing.

51
Q

is endoscopy a good way to diagnose GORD

A

Endoscopy is a poor diagnostic test. Most patients (>50%) with reflux symptoms have no visible evidence of oesophageal abnormality when endoscopy is performed.

52
Q

when must endoscopy be performed

A

in the presence of ‘alarm’ features suggestive of malignancy (eg dysphagia, weight loss, vomiting)

53
Q

GORD without abnormal anatomy

A

↑ Transient relaxations of the LOS
Hypotensive LOS
Delayed gastric emptying
Delayed oesophageal emptying
↓Oesophageal acid clearance
↓ Tissue resistance to acid/bile

54
Q

GORD due to Hiatus Hernia

A

Anatomical distortion of the OG junction
(many patients have both)

55
Q

what are the two main types of hiatus hernia

A

Sliding and Para-oesophageal

56
Q

sliding hiatus hernia

A

the stomach intermittently slides up into the chest through a small opening in the diaphragm.

57
Q

Para-oesophageal hiatus hernia

A

occurs when the lower part of the esophagus, the stomach, or other organs move up into the chest.

58
Q

GORD pathophysiology

A

Mucosa exposed to
acid-pepsin and bile

Increased cell loss
and regenerative activity
(ie inflammation)

Erosive oesophagitis

59
Q

GORD complications

A

Ulceration (5%)

Stricture (8-15%)

Glandular metaplasia (Barrett’s oesophagus)

Carcinoma

60
Q

Barrett’s Oesophagus

A

Intestinal metaplasia related to prolonged acid exposure in distal oesophagus

Change from squamous to mucin-secreting columnar (ie gastric type) epithelial cells in lower oesophagus

61
Q

what is Barretts oesophagus abprecusor to

A

dysplasia/ adenocarcinoma

62
Q

does Barretts oesophagus affect men or women more

A

Men&raquo_space; women

63
Q

what is the cancer rate of Barretts oesophagus

A

Cancer rate ~0.3% per yr

64
Q

Barrett’s Oesophagus
HIGH GRADE DYSPLASIA

A

Risk of developing oesophageal cancer 6%/year

65
Q

treatment for Barretts oesophagus high grade dysplasia

A

Endoscopic Mucosal Resection (EMR)
Radio-Frequency Ablation (RFA)
Oesophagectomy rarely (mortality ~10%)

66
Q

treatment of GORD

A

Mainly empirical (i.e. without investigation) in absence of alarm features

Lifestyle measures

Pharmacological
Alginates (Gaviscon)
H2RA (Ranitidine)
Proton Pump Inhibitor (e.g. Omeprazole, Lansoprazole)

67
Q

what are the pharmacological treatment measures of GORD

A

Alginates (Gaviscon)
H2RA (Ranitidine)
Proton Pump Inhibitor (e.g. Omeprazole, Lansoprazole)

68
Q

GORD treatment for refractory disease/symptoms
following investigation

A

Anti-reflux surgery
(Fundoplication – full / partial wrap)

69
Q

are benign tumours rare in oesophageal cancer

A

they are rare

70
Q

what are the two types of carinoma for oesophageal cancer

A

Squamous Cell Carcinoma

Adenocarcinoma

71
Q

five oesophageal cancer facts

A

5th in World Cancer Mortality Rank

Men>Women 3:1

Median Age 65 years – age decreasing

Western Europe/USA Adenocarcinoma > Squamous

Rest of World Squamous&raquo_space; Adenocarcinoma

72
Q

presentation of oesophageal cancer

A

Progressive dysphagia (90%)
Anorexia and Weight loss (75%)
Odynophagia
Chest pain
Cough
Pneumonia (tracheo-oesophageal fistula)
Vocal cord paralysis
Haematemesis

73
Q

squamous cell carcinoma features

A

Often large exophytic occluding tumours

Occur in proximal and middle third of oesophagus

74
Q

what precedes squamous cell carcinomas

A

Preceded by dysplasia and carcinoma in situ

75
Q

where is there a high incidence of squamous cell carcinoma

A

Southern Africa, China, Iran

76
Q

what are significant risk factors for squamous cell carcinoma

A

tobacco and alcohol significant risk factors
?diet related (vitamin deficiency)

77
Q

what is squamous cell carcinoma associated with

A

Achalasia, Caustic strictures, Plummer-Vinson Syndrome

78
Q

where does adenocarcinoma occur

A

distal oesophagus

79
Q

what is adenocarcinoma associated with

A

Barrett’s oesophagus (progresses through dysplasia to cancer)

80
Q

what are predisposing factors of adenocarcinoma

A

obesity, male sex, middle age, caucasian,

81
Q

oesophageal cancer when does it usually present

A

Usually presents late and tumours have commonly spread to regional nodes and/or liver at presentation

82
Q

what does the oesophagus lack unlike the rest of the GIT

A

No peritoneal (serosal) lining in mediastinum – local invasion (heart, trachea, aorta) often limits surgery

THIS MEANS THAT TUMOUR INVASION INTO ADJACENT STRUCTURES CAN OCCUR MORE EASILY
The Lamina propria (which is in the mucosal layer) has a rich lymphatic supply – in the remainder of the GIT lymphatic vessels are mainly submucosal

THIS MEANS THAT LYMPH NODE INVOLVEMENT OFTEN OCCURS EARLY IN OESOPHAGEAL TUMOURS

83
Q

oesophageal cancer Metastases

A

Hepatic, brain, pulmonary, bone

84
Q

survival rate for oesophageal cancer

A

Prognosis poor: 5 yr survival < 10%

85
Q

diagnostic investigations for osophageal cancer

A

Diagnosis by Endoscopy & Biopsy

86
Q

how is staging done for oesophageal cancer

A

CT Scan- CT scan of chest, abdomen and pelvis for distant metastasis
Endoscopic ultrasound
PET Scan
Bone Scan

Disease staging by
TNM classification

Laparoscopy may be needed where there is suspicion of peritoneal spread on CT or EUS such as in the presence of small volume ascites.

87
Q

osophageal cancer treatment

A

Only potential cure is surgical oesophagectomy +/- adjuvant (after) or neoadjuvant (before) chemotherapy
Limited to patients with localised disease, without co-morbid disease, usually <70 years of age
Significant morbidity and mortality assoc with oesophagectomy (mortality ~ 10%)
Long post operative recovery
Require nutritional support
Combined chemo and radiotherapy now offer some prospect of improved long-term survival (ie > 1year) in patients with locally advanced inoperable disease - ? may ultimately offer non-surgical “cure”

Most have incurable disease at presentation
Symptom palliation (mainly dysphagia) is often overriding priority

OPTIONS:
Endoscopic
(stent, laser/APC, PEG)
Chemotherapy
Radiotherapy
Brachytherapy

87
Q

Eosinophilic Oesophagitis

A

Chronic immune-/allergen-mediated condition defined clinically by symptoms of oesophageal dysfunction, and pathologically by an eosinophilic infiltration of the oesophageal epithelium (≥15 eosinophils per high-power microscopy field on oesophageal biopsy) in the absence of secondary causes of local or systemic eosinophilia.

Incidence and prevalence are increasing

More commonly seen in children and young adults

Males > females

88
Q

Eosinophilic Oesophagitis

A

Presentation: Dysphagia & Food bolus obstruction
Endoscopic findings:

Treatment:
- topical/swallowed corticosteroids
- dietary elimination
- endoscopic dilatation