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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
ENDOSCOPY
simple, effective, safe in experienced hands – diagnostic endoscopy takes 2-3 mins
26
what can also be done as an investigation for oesophageal disease
Contrast radiology (barium swallow)
27
BA SWALLOW
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
28
Oesophageal Physiology: pH - metry
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
29
Oesophageal Physiology: Manometry
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.
30
hyper motility example
diffuse oesophageal spasm
31
hyper motility appearance on barium swallow
“Corkscrew appearance”
32
symptoms of hypermotility
-Severe, episodic chest pain +/- dysphagia -Often confused with angina/MI
33
cause of hyper motility
Cause unclear (idiopathic)
34
manometry results for hyper motility
Manometry shows exaggerated, uncoordinated, hypertonic contractions -Rx smooth muscle relaxants
35
what is hypomotiity associated with
connective tissue disease, diabetes, neuropathy
36
what does hypo motility cause
Causes failure of LOS mechanism leading to heartburn and reflux symptoms
37
ACHALASIA
Functional loss of myenteric plexus ganglion cells in distal oesophagus and LOS
38
what is the incidence of achalasia
1-2/100,000 Male:Female incidence = 1:1
39
what is the onset for achalasia
usually 3rd - 5th decade
40
cardinal feature of achalasia
failure of LOS to relax Result: functional distal obstruction of oesophagus
41
symptoms of achalasia
progressive dysphagia for solids and liquids weight loss Chest pain (30%) Regurgitation and chest infection
42
treatment of achalasia
Pharmacological - Nitrates, Calcium Channel blockers Endoscopic - Botulinum Toxin Pneumatic balloon dilation Radiological - Pneumatic balloon dilation Surgical - Myotomy
43
COMPLICATIONS of achalsia
Aspiration pneumonia and lung disease Increased risk of squamous cell oesophageal carcinoma
44
what percentage of adults experience daily GORD symptoms
7% adults
45
Many patients with frequent, pathological episodes of acid/bile reflux do not experience
any symptoms!!
46
symptoms of GORD
heartburn, cough, water brash, sleep disturbance
47
risk factors for GORD
Pregnancy, obesity, drugs lowering LOS pressure, smoking, alcoholism, hypomotility
48
are men or women more effected by GORD
Men > Women
49
what ethnicities are most affected by GORD
Caucasian > Black > Asian
50
how is typical reflux syndrome diagnosed
on the basis of the characteristic symptoms, without diagnostic testing.
51
is endoscopy a good way to diagnose GORD
Endoscopy is a poor diagnostic test. Most patients (>50%) with reflux symptoms have no visible evidence of oesophageal abnormality when endoscopy is performed.
52
when must endoscopy be performed
in the presence of ‘alarm’ features suggestive of malignancy (eg dysphagia, weight loss, vomiting)
53
GORD without abnormal anatomy
↑ Transient relaxations of the LOS Hypotensive LOS Delayed gastric emptying Delayed oesophageal emptying ↓Oesophageal acid clearance ↓ Tissue resistance to acid/bile
54
GORD due to Hiatus Hernia
Anatomical distortion of the OG junction (many patients have both)
55
what are the two main types of hiatus hernia
Sliding and Para-oesophageal
56
sliding hiatus hernia
the stomach intermittently slides up into the chest through a small opening in the diaphragm.
57
Para-oesophageal hiatus hernia
occurs when the lower part of the esophagus, the stomach, or other organs move up into the chest.
58
GORD pathophysiology
Mucosa exposed to acid-pepsin and bile Increased cell loss and regenerative activity (ie inflammation) Erosive oesophagitis
59
GORD complications
Ulceration (5%) Stricture (8-15%) Glandular metaplasia (Barrett’s oesophagus) Carcinoma
60
Barrett’s Oesophagus
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
what is Barretts oesophagus abprecusor to
dysplasia/ adenocarcinoma
62
does Barretts oesophagus affect men or women more
Men >> women
63
what is the cancer rate of Barretts oesophagus
Cancer rate ~0.3% per yr
64
Barrett’s Oesophagus HIGH GRADE DYSPLASIA
Risk of developing oesophageal cancer 6%/year
65
treatment for Barretts oesophagus high grade dysplasia
Endoscopic Mucosal Resection (EMR) Radio-Frequency Ablation (RFA) Oesophagectomy rarely (mortality ~10%)
66
treatment of GORD
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
what are the pharmacological treatment measures of GORD
Alginates (Gaviscon) H2RA (Ranitidine) Proton Pump Inhibitor (e.g. Omeprazole, Lansoprazole)
68
GORD treatment for refractory disease/symptoms following investigation
Anti-reflux surgery (Fundoplication – full / partial wrap)
69
are benign tumours rare in oesophageal cancer
they are rare
70
what are the two types of carinoma for oesophageal cancer
Squamous Cell Carcinoma Adenocarcinoma
71
five oesophageal cancer facts
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 >> Adenocarcinoma
72
presentation of oesophageal cancer
Progressive dysphagia (90%) Anorexia and Weight loss (75%) Odynophagia Chest pain Cough Pneumonia (tracheo-oesophageal fistula) Vocal cord paralysis Haematemesis
73
squamous cell carcinoma features
Often large exophytic occluding tumours Occur in proximal and middle third of oesophagus
74
what precedes squamous cell carcinomas
Preceded by dysplasia and carcinoma in situ
75
where is there a high incidence of squamous cell carcinoma
Southern Africa, China, Iran
76
what are significant risk factors for squamous cell carcinoma
tobacco and alcohol significant risk factors ?diet related (vitamin deficiency)
77
what is squamous cell carcinoma associated with
Achalasia, Caustic strictures, Plummer-Vinson Syndrome
78
where does adenocarcinoma occur
distal oesophagus
79
what is adenocarcinoma associated with
Barrett’s oesophagus (progresses through dysplasia to cancer)
80
what are predisposing factors of adenocarcinoma
obesity, male sex, middle age, caucasian,
81
oesophageal cancer when does it usually present
Usually presents late and tumours have commonly spread to regional nodes and/or liver at presentation
82
what does the oesophagus lack unlike the rest of the GIT
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
oesophageal cancer Metastases
Hepatic, brain, pulmonary, bone
84
survival rate for oesophageal cancer
Prognosis poor: 5 yr survival < 10%
85
diagnostic investigations for osophageal cancer
Diagnosis by Endoscopy & Biopsy
86
how is staging done for oesophageal cancer
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
osophageal cancer treatment
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
Eosinophilic Oesophagitis
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
Eosinophilic Oesophagitis
Presentation: Dysphagia & Food bolus obstruction Endoscopic findings: Treatment: - topical/swallowed corticosteroids - dietary elimination - endoscopic dilatation

Alimentary System (44 decks)

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