Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI Pathology > 2. Oesophageal disorders > Flashcards

2. Oesophageal disorders Flashcards

1
Q

Oesophagus anatomy:

  1. Where does it begin & end?
  2. What kind of muscle is it made out of?
  3. What kind of epithelial lining does it have?
A
  1. Begins at lower level of cricoid cartilage (C6), terminates at T11-T12 where it enters the stomach.
  2. Upper 3-4cm = striated muscle. Remainder (lower 2/3) = smooth muscle
  3. Stratified squamous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Physiology and function of oesophagus:

  1. What kind of process is the transport of food/liquid from mouth to stomach?
  2. What produces peristalsis?
  3. Contraction in the oesophageal body (peristalsis) and relaxation of the LOS is mediated by which nerve?
A
  1. Active
  2. Oesophageal peristalsis produced by oesophageal circular muscles and propels swallowed materials distally into the stomach
  3. Vagus nerve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. T/F: High resting pressure in distal smooth muscle
    of oesophagus.
  2. What forms the mucosal rosette?
A
  1. True

2. the angle (of His) at gastroesophageal junction (GOJ)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the symptoms of oesophageal disease?

A

Heartburn

dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  1. Where does the patient feel heartburn?
  2. Heartburn maybe associated with?
  3. What causes heartburn?
A
  1. Retrosternal discomfort/burning
  2. Water brash (a sudden flow of saliva), cough
  3. reflux of acidic &/or bilious gastric contents into the oesophagus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. What kind of drugs/foods can increase reflux/heartburn?
  2. What worsens heartburn?
  3. What can heartburn be confused with?
A
  1. Alcohol, nicotine, dietary xanthines can reduce the LOS pressure resulting in increased reflux/heartburn
  2. often worst lying down at night, when gravity promotes reflux, or on bending or stooping.
  3. Pain can be confused with pain of ischaemic heart disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Persistent reflux & heartburn can lead to what?

A

Gastro-oesophageal reflux disease (GORD).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Define dysphagia.

2. where can dysphagia occur?

A
  1. subjective sensation of difficulty in swallowing foods and/or liquids
  2. Oropharyngeal, oesophageal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define Odynophagia.

A

pain with swallowing (may accompany dysphagia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What would you ask during history from a patient presenting with dysphagia?

A

-Difficulty in swallowing type of food (e.g. solid vs liquid)
-Pattern (progressive vs intermittent)
-Associated features (e.g. weight loss, regurgitation, cough)
E.g. intermittent slow progression with a history of heartburn suggests a benign peptic stricture; relentless progression over a few weeks suggests a malignant stricture. The slow onset of dysphagia for solids and liquids at the same time suggests a motility disorder (e.g. achalasia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is regurgitation?

A

effortless reflux of oesophageal contents into the mouth and pharynx. Uncommon in normal subjects, it occurs frequently in patients with gastro-oesophageal reflux disease or organic stenosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes oesophageal dysphagia?

A

-benign stricture
-malignant stricture (oesophageal cancer)
-motility disorders (e.g. achalasia, presbyoesophagus:
abnormal shape of oesophagus e.g. more wavy)
-eosinophilic oesophagitis (allergic inflammatory condition)
-extrinsic compression (e.g. in lung cancer).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List investigations done for oesophageal disease. Indicate why they are used.

A
  • Endoscopy (aka oesophago-gastro-duodenoscopy (OGD) or upper GI endoscopy (UGIE): used in investigation of dysphagia or reflux symptoms with alarm features.
  • Contrast barium swallow X-ray: primary indication is investigation of dysphagia (however endoscopy is the preferred test) is an alternative. May still be used in “high” dysphagia to exclude a pharyngeal pouch or post-cricoid web prior to endoscopy
  • pH-metry: Nasal catheter containing pH sensors at both sphincters (UOS and LOS) is placed in oesophagus. Alternative is endoscopic placement of BRAVO pH probe. pH studies – used in investigation of refractory heartburn/reflux episodes (pH<4).
  • Manometry: Nasal catheter containing multiple pressure sensors is placed in oesophagus. Used in investigation of dysphagia/ suspected motility disorder (usually after endoscopy). Assesses sphincter tonicity, relaxation of sphincters and oesophageal motility.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

List motility disorders.

A

hypermotility e.g. diffuse oesophageal spasm
Hypomotility
Achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Regarding hypermotility e.g. diffuse oesophageal spasm:

  1. What are the symptoms?
  2. What is it confused with often?
  3. What is the cause?
  4. What does investigations show?
  5. What is the treatment?
A
  1. Severe, episodic chest pain, +/- dysphagia.
  2. Angina/MI
  3. Unclear (idiopathic)
  4. On Ba swallow: oesophagus has corkscrew appearance. Manometry shows exaggerated, uncoordinated, hypertonic contractions.
  5. Smooth muscle relaxants.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Regarding hypomotility:

  1. What other diseases is it associated with?
  2. What are the symptoms & what causes it?
A
  1. Connective tissue disease, diabetes, neuropathy

2. Causes failure of LOS mechanism leading to heartburn & reflux symptoms.

17
Q

Regarding achalasia:

  1. What causes it?
  2. What is the cardinal feature & the consequence of it?
  3. what is the aetiology?
  4. What are the symptoms?
A
  1. For most cases cause = unknown. In some cases functional loss of myenteric plexus ganglion cells (specifically inhibitory neurons) in distal oesophagus & LOS.
  2. Failure of LOS to relax resulting in functional distal obstruction of oesophagus (food doesn’t enter stomach).
  3. Not really known but inflammatory response suspected as ganglion cells often surrounded by lymphocytes.
  4. Progressive dysphagia for solids & liquids.
    - Weight loss
    - Chest pain behind sternum (30%)
    - Regurgitation & chest infection (aspiration pneumonia = complication)
18
Q

Achalasia:

Which investigations are performed?

A
  1. Manometry: measure the muscle pressure along it at different points. Shows absence of peristalsis (contractions) of the oesophagus and failure of relaxation of the LOS.
  2. Barium swallow shows lack of peristalsis and often synchronous contractions in the body of the oesophagus, sometimes with dilatation. The lower end shows a ‘bird’s beak’ due to failure of the sphincter to relax.
  3. Chest X-ray shows a dilated oesophagus, sometimes with a fluid level seen behind the heart. The fundal gas shadow is absent.
  4. Endoscopy to exclude adenocarcinoma.
19
Q

Achalasia:

  1. Complications?
  2. Treatment?
A
  1. Aspiration pneumonia & lung disease. Increased risk of squamous cell oesophageal carcinoma.
  2. Pharmacological: Nitrates, Ca channel blockers to relax the smooth muscle to make swallowing easier.
    Endoscopic: Botulinum toxin, and balloon dilation: relax smooth muscle.
    Radiological: Pneumatic balloon dilation: stretch ring of muscle.
    Surgical: Myotomy - muscle fibres in the ring of muscle that lets food into your stomach are cut.
20
Q

Gastro-Oesophageal Reflux Disease:

  1. What causes GORD?
  2. What are the symptoms?
  3. Which risk factors predisposes you to GORD?
A
  1. Due to pathological acid (and bile) exposure in lower oesophagus.
  2. heartburn, cough, water brash, sleep disturbance. Many patients with frequent, pathological episodes of acid/bile reflux do not experience any symptoms!
  3. Pregnancy, obesity, drugs lowering LOS pressure, smoking, alcoholism, hypomotility
21
Q

How is GORD diagnosed?

A

Typically diagnosed based on characteristic symptoms without needing diagnostic testing.
Endoscopy = poor diagnostic test. Most patients (>50%) with reflux symptoms have no visible evidence of oesophageal abnormality when endoscopy is performed.
Perform endoscopy if ALARM symptoms (dysphagia, weight loss, vomiting) present as that indicates malignancy.
Oesophageal pH studies and manometry

22
Q

Outline GORD aetiology.

A
  1. GORD without abnormal anatomy:
    - increase in transient relaxations of the LOS
    - Hypotensive LOS
    - Delayed gastric emptying
    - Delayed oesophageal emptying
    - decrease in oesophageal acid clearance
    - decrease in tissue resistance to acid/bile
  2. GORD due to Hiatus Hernia: Anatomical distortion of the OG junction
    (many patients have both)
23
Q

Describe main types of hiatus hernia.

A
  1. Sliding hiatus hernia: The oesophageal–gastric junction and part of the stomach ‘slide’ through the hiatus so that it lies above the diaphragm.
  2. Para-oesophageal hiatus hernia: Part of the fundus of the stomach prolapses through the hiatus alongside the oesophagus.
    Obesity and aging predisposes it.
24
Q

Describe pathophysiology of GORD.

A
  • Mucosa exposed to acid-pepsin and bile
  • Increased cell loss and regenerative activity (i.e. inflammation)
  • Erosive oesophagitis (inflammation of the lining of the oesophagus)
25
Q

List complications of GORD.

A

Ulceration
Stricture
Glandular metaplasia (Barrett’s oesophagus)
Carcinoma

26
Q

What is Barrett’s oesophagus? Outline treatment for it.

A
  • Intestinal metaplasia related to prolonged acid exposure in distal oesophagus. Change from squamous to mucin-secreting columnar (i.e. gastric type) epithelial cells in lower oesophagus.
  • Precursor to dysplasia/ adenocarcinoma
  • High grade dysplasia: can develop into oesophageal cancer. Treatment: Endoscopic Mucosal Resection (EMR), Radio-Frequency Ablation (RFA), Oesophagectomy rarely (mortality ~10%)
27
Q

What is the treatment for GORD?

A
  1. Mainly empirical (i.e. without investigation) in absence of alarm features:
    - Lifestyle measures (reduce weight, sleep with pillows)
    - Pharmacological:
    > Alginate containing antacids (Gaviscon) - form a gel or ‘foam raft’ with gastric contents to reduce reflux.
    > H2RA (Ranitidine): used for acid suppression
    > Proton Pump Inhibitor (e.g. Omeprazole, Lansoprazole) - inhibit gastric H+/K+-ATPase, reducing acid secretion.
  2. For refractory disease/symptoms following investigation:
    - Perform anti-reflux surgery (Fundoplication – full / partial wrap: fundus wrapped around lower oesophagus acting like a valve)
28
Q

What type of oesophageal cancer more common in the West?

A
  • Western Europe/USA: Adenocarcinoma > Squamous

- Rest of World: Squamous&raquo_space; Adenocarcinoma

29
Q

How does oesophageal cancer present?

A
  • Progressive dysphagia (90%)
  • Anorexia and Weight loss (75%)
    Odynophagia
    Chest pain
    Cough
    Pneumonia (tracheo-oesophageal fistula)
    Vocal cord paralysis
    Haematemesis
30
Q

Squamous cell carcinoma:

  1. T/F: often large exophytic occluding tumours.
  2. Where does it occur in the oesophagus?
  3. What are the risk factors?
  4. What is it associated with?
A
  1. True. Exophytic: tumour growing outward from epithelium rather than inward (endophytic).
  2. Occur in proximal and middle 1/3 of oesophagus. Preceded by dysplasia and carcinoma in situ.
  3. Significant risk factors = tobacco and alcohol. Diet related (vitamin deficiency)? Low socio-economic status
  4. Associated with Achalasia, Caustic strictures, Plummer-Vinson Syndrome
31
Q

Adenocarcinoma:

  1. Where does it occur?
  2. What is it associated with?
  3. What are the predisposing factors?
A
  1. Occurs in distal oesophagus
  2. Associated with Barrett’s oesophagus (progresses through dysplasia to cancer)
  3. Predisposing factors: obesity, male sex, middle age, Caucasian
32
Q
  1. Where does oesophageal cancer metastasise to?

2. Why does oesophageal cancer spread to surrounding tissues easily?

A
  1. Metastases - Hepatic, brain, pulmonary, bone
  2. Oesophagus lacks a serosal layer - unlike the rest of the GIT: so invasion into adjacent structures is easy.
    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 so lymph node involvement occurs early in oesophageal tumours.
33
Q

How would you diagnose and stage oesophageal cancer?

A
  1. Diagnosis by Endoscopy and Biopsy. Can do contrast barium swallow.
  2. Staging:
    - CT Scan of chest, abdomen and pelvis for distant metastasis. If metastatic/unfit then no further staging required. If resectable/fit then:
    > Endoscopic ultrasound for loco regional staging (T, N staging)
    > PET Scan gives M stage
    - Bone Scan
    - Laparoscopy needed if suspicion of peritoneal spread on CT/EUS such as in the presence of small volume ascites.
  3. Disease staging by TNM classification.
34
Q

How is oesophageal cancer treated?

A
  1. Most have incurable disease at presentation so symptom palliation (mainly dysphagia) is often overriding priority.
  2. If resectable/fit:
    - surgical oesophagectomy (cancer removed and stomach pulled up into chest) +/- adjuvant (after) or neoadjuvant (before) chemotherapy: only potential cure, but limited to patients with localised disease.
    - Chemotherapy and Radiotherapy if inoperable or concerns about fitness and no metastatic disease.
  3. If metastatic/unfit:
    - Endoscopic (stent, laser/APC, PEG)
    - Palliative radiotherapy/chemotherapy
  4. Other options: Brachytherapy
35
Q

What is 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.

36
Q

Eosinophilic Oesophagitis:

  1. Presentation?
  2. How is it diagnosed?
  3. What are the treatment options?
A
  1. Presentation: Dysphagia and Food bolus obstruction
  2. Endoscopy
  3. Treatment:
    • topical/swallowed corticosteroids
    • dietary elimination
    • endoscopic dilatation

GI Pathology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions