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Year 3 Gastrointestinal > Oesophagus > Flashcards

Oesophagus Flashcards

1
Q

What is the definition of GORD?

A

Gastro-oesophageal reflux disease: inflammation of the oesophagus caused by reflux of gastric acid and/or bile.

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2
Q

What is the pathology of GORD?

A

Disruption of mechanisms that prevent reflux.

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3
Q

What are the causes of GORD? (x5, x2, x4, x1, x1)

A

o MECHANICAL: Lower oesophageal sphincter hypotension, hiatus hernia, oesophageal dysmotility (e.g. from systemic sclerosis (an autoimmune condition leading to replacement of normal organ-specific tissue with connective tissue)), absent mucosal rosette (redundant mucosal folds at gastro-oesophageal junction), obtuse angle of junction

o PHYSIOLOGICAL: Delayed gastric emptying, gastric acid hypersecretion.

o LIFESTYLE: Obesity, smoking, alcohol, pregnancy.

o Drugs (tricyclics, anticholinergics, nitrates).

o H. pylori.

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4
Q

What are the population-level risk factors of GORD? (x3)

A

Caucasian, male, old.

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5
Q

What does an acute angle of junction look like? How does it lead to GORD? Newborns?

A

Acute angle of junction is referred to the Angle of His and concerns the angle between the cardia and oesophagus. Acute prevents gastric contents from entering oesophagus. In new-borns, this is underdeveloped and obtuse (almost vertical with the stomach), so reflux is common.

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6
Q

How does LOS hypotension lead to GORD?

A

Hypotensive LOS is characterized by reduced basal tone so that the pressure gradient between the gastric fundus and the LOS is less than 10 mmHg. This may cause free reflux of gastric acid into the oesophagus.

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7
Q

What is hiatus hernia?

A

Part of stomach herniates above the diaphragm.

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8
Q

How does hiatus hernia lead to GORD?

A

Reduces function of the LOS (diaphragm surrounds sphincter and supports its contraction).

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9
Q

What is the function of the mucosal rosette and its relation to GORD?

A

Mucosal rosette is formed when the angle at the gastro-oesophageal junction is ACUTE. They form a weak anti-reflux valve. Therefore, when not present i.e. when the angle is obtuse, reflux can occur.

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10
Q

What is the epidemiology of GORD?

A

Common, prevalence is 5-10% in adults.

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11
Q

What are the symptoms of GORD? (x6 (x5))

A

o PAIN: Substernal (behind sternum) burning discomfort or ‘heartburn’ aggravated by lying supine, bending, large meals and drinking alcohol. This symptom is also known as dyspepsia or indigestion. Relieved by antacids.

o Waterbrash: sudden flow of saliva

o Regurgitation of gastric contents

o Tooth erosion

o Odynophagia – painful swallowing e.g. from oesophagitis or ulceration

o Symptoms of aspiration e.g. voice hoarseness, laryngitis, nocturnal cough, wheeze and pneumonia (rare)

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12
Q

What are the complications of GORD? (x6 +5)

A

Oesophageal ulceration, peptic stricture (this is actually oesophageal stricture), Barrett’s oesophagus, oesophagitis, oesophageal adenocarcinoma, and iron deficiency anaemia. Complications of aspiration – hoarseness, laryngitis, nocturnal cough, wheeze, pneumonia.

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13
Q

What are the signs of GORD?

A

Usually normal. Occasionally epigastric tenderness, wheeze on chest auscultation and dysphonia.

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14
Q

What is dysphonia?

A

Abnormal voice.

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15
Q

What are the investigations for GORD? (x5)

A

o Upper GI endoscopy: biopsy and cytological brushings to confirm the presence of oesophagitis and exclude the possibility of malignancy

o Barium swallow: to detect hiatus hernia

o CXR: INCIDENTAL finding of hiatus hernia (i.e. not routine)

o 24hr oesophageal pH monitoring: pH probe placed in lower oesophagus; determines the temporal relationship (timing between a factor and an outcome which can be used to assign causality to a relationship) between symptoms and oesophageal pH.

o Manometry can help with diagnosis alongside 24hr pH monitoring (measures strength and muscle coordination of oesophagus when you swallow)

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16
Q

When are patients sent for endoscopy for their GORD? Indications? (x2)

A

When they are over 55 years old with alarm symptoms OR have treatment-refractory GORD.

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17
Q

What are alarm symptoms?

A

Follow the anagram, ALARMS: Anaemia (iron deficiency), loss of weight, anorexia, recent onset/progressive symptoms, melaena/haematemesis, swallowing difficulty.

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18
Q

How is oesophagitis identified endoscopically?

A

Longitudinal mucosal breaks.

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19
Q

How is GORD managed with advice? (x5)

A

Weight loss, elevating head of bed, avoid provoking factors e.g. large meals in the evening and alcohol, stop smoking, lower fat meals.

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20
Q

Why are lower fat meals advised?

A

Fatty meals result in increased time for gastric emptying. Delayed emptying is a risk factor for GORD.

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21
Q

How is GORD managed medically?

A

PPIs, antacids and H2 receptor blockers +/- alginates. H2 receptor blockers added to treatment regime for refractory symptoms.

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22
Q

What drugs should be avoided for GORD? (x3)

A

Those that affect oesophageal motility (nitrates, anticholinergics), relax the LOS (Ca2+ channel blockers), and damage the mucosa (NSAIDs, K+ salts, bisphosphonates).

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23
Q

How is GORD managed endoscopically?

A

Surveillance for Barrett’s oesophagus annually.

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24
Q

How is GORD managed surgically? Indications? (x2)

A

Laparoscopic Nissen fundoplication - the upper part of the stomach is wrapped around the lower oesophageal sphincter to strengthen the sphincter and prevent acid reflux and to repair a hiatal hernia. For those with symptoms despite optimal medical management or in those intolerant of medication.

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25
Q

What is the prognosis of GORD: Responsiveness to lifestyle measures? Drug withdrawal? Endoscopy findings?

A

50% respond to lifestyle measures alone. In patient who require drug therapy, withdrawal is often associated with relapse. 20% undergoing endoscopy have Barrett’s.

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26
Q

What is hiatus hernia?

A

Herniation of part of the gastric cardia through the oesophageal aperture of the diaphragm.

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27
Q

What are the two types of hiatus hernia?

A

Sliding and rolling (or paraoesophageal).

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28
Q

What is the prevalence of sliding and rolling hiatus hernia?

A

Sliding is 80% and rolling is 20%.

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29
Q

What is sliding hiatus hernia?

A

The gastro-oesophageal junction slides up into the chest. In these cases, reflux is common as the lower oesophageal sphincter becomes less competent.

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30
Q

What is rolling hiatus hernia?

A

Gastro-oesophageal junction remains in the abdomen, but a bulge of stomach herniates up into the chest, alongside the oesophagus. As the G-O junction remains intact, acid reflux is uncommon.

31
Q

What are the aetiologies of hiatus hernia? (x3)

A
  1. Widening of the diaphragmatic hiatus, 2. Pulling up of the stomach due to oesophageal shortening. 3. Pushing up of the stomach due to increased intra-abdominal pressures.
32
Q

What are the causes and risk factors for hiatus hernia? (x10)

A

o Heavy lifting or bending over

o Frequent or hard coughing

o Violent vomiting

o Straining on defecation i.e. the Valsalva manoeuvrer

o Obesity

o Age

o Pregnancy

o Ascites

o Genetics

o Chronic oesophagitis leading to shortening of the oesophagus

33
Q

What is the epidemiology of hiatus hernia: Incidence? Symptomatic? Where? Gender?

A

Common, 30% of patients over the age of 50. Of these, 9% are symptomatic. Higher incidence in the Western world. Most common in women than men.

34
Q

What are the signs/symptoms of hiatus hernia? (x5)

A

o Pain: heartburn or retrosternal burning sensation from reflux

o Flatulence

o Dysphagia, though rare

o Shortness of breath from effect of hernia on diaphragm

o Heart palpitations from irritation on vagus nerve.

35
Q

What are the investigations for hiatus hernia? (x3)

A

o Not routinely investigated; picked up only incidentally.

o Endoscopy: but not reliably.

o CT scan: can be picked up reliably.

o CXR: presents as a gastric bubble.

36
Q

How is hiatus hernia identified on CXR?

A

Gastric bubble behind cardiac shadow.

37
Q

How is hiatus hernia managed conservatively? (x3)

A

Lose weight, elevate head of bed, don’t lay down after meals.

38
Q

How is hiatus hernia managed medically?

A

Medication can be used to treat GORD.

39
Q

How is hiatus hernia managed surgically?

A

Laparoscopic Nissen fundoplication.

40
Q

What are the indications for surgical management of hiatus hernia?

A

Symptomatic despite aggressive medical therapy, or patient suffering complications especially oesophageal stricture.

41
Q

Why is surgical management of hiatus hernia often avoided?

A

Operative mortality is 1-2% due to complications including gas bloat syndrome, dysphagia and achalasia, AND strangulation risk (a complication that indicates surgical management) drops dramatically after 65 years.

42
Q

What are the complications of hiatus hernia? (x4)

A

GORD and its associated complications, strangulation (in cases of rolling hernia) leading to obstruction, iron deficiency anaemia, volvulus.

43
Q

What is the prognosis of hiatus hernia?

A

Only 9% are symptomatic.

44
Q

What is Barrett’s oesophagus?

A

Metaplasia of the normal stratified squamous epithelium of the distal oesophagus to a columnar epithelium.

45
Q

What are the causes of Barrett’s oesophagus?

A

Chronic GORD.

46
Q

What are the risk factors of Barrett’s oesophagus?

A

Same as GORD.

47
Q

What is the epidemiology of Barrett’s oesophagus: Gender? Ethnicity? Age? GORD? Prevalence?

A

More common in men (10:1), Caucasians, and increased prevalence with age. 3-5% with GORD develop Barrett’s oesophagus. Screening studies in asymptomatic patients have indicated 6% general population prevalence.

48
Q

What are the signs/symptoms of Barrett’s oesophagus? ((x5))

A

Barrett’s oesophagus does not cause symptoms, but it is associated with heartburn, dysphagia, haematemesis, weight loss, odynophagia.

49
Q

What are the investigations for GORD?

A

Endoscopic biopsy and visible columnarisation (see photo)

50
Q

What is the endoscopic variation in Barrett’s oesophagus? (x2)

A

May be patchy or continuous; may be the whole oesophagus or distal cms.

51
Q

When is endoscopy indicated for patients suspected of having Barrett’s oesophagus?

A

With chronic uncontrollable GORD and multiple risk factors including over the age of 50, obese, man, Caucasian, family history etc.

52
Q

What are the complications of Barrett’s oesophagus?

A

Metaplastic columnar epithelium is at risk of transitioning to dysplasia leading to oesophageal adenocarcinoma.

53
Q

What are the risk factors for malignant transformation of Barrett’s oesophagus? (x3)

A

Increased age, male, long segment of oesophagus involved.

54
Q

How is Barrett’s oesophagus managed? (x2)

A

o 2-3-year endoscopic surveillance for dysplasia in patients with extensive disease. If low-grade dysplasia is detected, it should be confirmed by repeat examination after 6 months.

o If high-grade dysplasia or intramural (within walls) carcinoma is detected, endoscopic resection or mucosal radiofrequency ablation is recommended.

55
Q

What is mucosal radiofrequency ablation?

A

Needle probe inserted inside tumour and radiofrequency waves passed into the tumour resulting in increased temperature within the tumour and destruction.

56
Q

What is the prognosis of Barrett’s oesophagus?

A

Risk of progression to adenocarcinoma is 6-7 per 1000 per year. However, mortality of oesophageal adenocarcinoma in the gastro-oesophageal junction is over 85%.

57
Q

What is achalasia?

A

An oesophageal motility disorder characterised by loss of peristalsis and failure of relaxation of the lower oesophageal sphincter (LOS).

58
Q

What is the aetiology of achalasia?

A

Degeneration of ganglion cells of the myenteric plexus in the oesophagus.

59
Q

What is the cause of achalasia? ((x2))

A

Unknown. Though a small proportion are secondary to oesophageal carcinoma and Chagas’ disease (parasitic infection with Trypanosoma cruzi seen in Central and South America).

60
Q

What is the epidemiology of achalasia: Incidence? Age? Gender?

A

Annual incidence is 1 in 100 000. Usual presentation age = 25-60 years. No gender discrepancy.

61
Q

What are the symptoms of achalasia? (x6)

A

o GRADUAL (insidious) ONSET of intermitted dysphagia

o Difficulty belching (flatus absent)

o Regurgitation (particularly at night)

o Heartburn

o Chest pain (atypical/cramping, retrosternal)

o Weight loss

62
Q

What are the complications of achalasia? (x3)

A

o Aspiration pneumonia

o Malnutrition and weight loss

o Increased risk of oesophageal malignancy (15x that of the general population (on average 15 years after diagnosis))

63
Q

What are the signs of achalasia? (x2)

A

You may see signs of COMPLICATIONS: aspiration pneumonia - coarse crackles in right middle lung as this is the easiest route for aspirates, and weight loss.

64
Q

What are the investigations for achalasia? (x5)

A

o CXR: widened mediastinum and double right heart border (indicating dilated oesophagus), an air-fluid level in the upper chest, and absence of the normal gastric air bubble.

o BARIUM SWALLOW: dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped)

o ENDOSCOPY: to exclude malignancy which can mimic achalasia

o MANOMETRY: elevated resting LOS pressure, incomplete LOS relaxation, absence of peristalsis in the distal (smooth muscle portion) of the oesophagus.

o SEROLOGY: for antibodies against T. cruzi if Chagas’ disease if suggested by epidemiology and symptoms.

65
Q

What is Mallory-Weiss tear?

A

Bleeding from a laceration in the mucosa at the gastro-oesophageal junction.

66
Q

What are the aetiologies/risk factors of Mallory-Weiss tear? (x5)

A

o Severe vomiting from alcoholism

o Severe vomiting from bulimia

o Food poisoning leading to retching and vomiting

o NSAID use

o Hyperemesis gravidarum – severe morning sickness in pregnancy

67
Q

What is the epidemiology of Mallory-Weiss tears: Age?

A

Between 30 and 50 years.

68
Q

What are the symptoms of Mallory-Weiss tears? (x4)

A

o Presents as an episode of hematemesis after violent retching or vomiting

o Melena

o Light-headedness or dizziness

o Abdominal pain from the vomiting

o No epigastric or upper GI pain

69
Q

What are the signs of Mallory-Weiss tears?

A

No specific signs though there may be signs of anaemia from blood loss.

70
Q

What are the investigations for Mallory-Weiss tears?

A

Endoscopy

71
Q

How is Mallory-Weiss managed? (x2)

A

o In most cases, bleeding stops spontaneously after 24-48 hours

o Resuscitation – maintain airway, high-flow oxygen and correct fluid losses

o ENDOSCOPIC CAUTERISATION or EPINEPHRINE INJECTION to stop the bleeding. Very rarely, embolization of the arteries supplying the region.

72
Q

What are the complications of Mallory-Weiss tears? (x3 types)

A

o VOMITING: hypokalaemia, aspiration pneumonia, perforation

o BLEEDING: hypovolaemic shock, anaemia

o COMORBIDITIES: myocardial ischaemia, hepatitis, renal disease and diabetes.

73
Q

What is the prognosis of Mallory-Weiss tear?

A

Usually very good as most stop bleeding spontaneously.

Year 3 Gastrointestinal (29 decks)

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