Upper GI tract disorders

Question 1

What are the embryological foregut structures?

Answer 1

The embryological foregut structures include the oesophagus, stomach, duodenum (to D2), liver, gallbladder, pancreas, and spleen.

Question 2

Which artery supplies blood to the embryological foregut structures?

Answer 2

The coeliac artery supplies blood to most of the embryological foregut structures.

Question 3

What is the primary nerve supply for most embryological foregut structures?

Answer 3

The vagus nerve provides significant autonomic nerve supply to most of the embryological foregut structures.

Question 4

What structures help maintain the function of the lower oesophageal sphincter (LOS)?

Answer 4

The lower oesophageal sphincter (LOS) is maintained by the diaphragmatic crura, which are muscle fibers of the diaphragm.

Question 5

Besides the diaphragmatic crura, what else contributes to the function of the lower oesophageal sphincter (LOS)?

Answer 5

While not essential, gravity can assist in the function of the lower oesophageal sphincter (LOS). Additionally, the normal anatomical position of the stomach in the abdomen helps maintain LOS function.

Question 6

What influences stimulate the production of acid by gastric parietal cells?

Answer 6

Acid production by gastric parietal cells is influenced by both autonomic and hormonal factors.

Question 7

How is acid production in gastric parietal cells stimulated?

Answer 7

Acid production in gastric parietal cells can be stimulated both directly and indirectly.

Question 8

What is the effect of proton pump inhibitors (PPI) on acid suppression?

Answer 8

Proton pump inhibitors directly inhibit “the proton pump” in gastric parietal cells, leading to a significant reduction in acid secretion (over 95%).

Question 9

What are some side effects associated with proton pump inhibitors (PPI)?

Answer 9

Side effects of proton pump inhibitors are rare but may include diarrhea and an increased risk of gastrointestinal infection.

Question 10

How does an H2 receptor antagonist work to reduce acid secretion?

Answer 10

An H2 receptor antagonist reduces histamine stimulation, which helps to decrease acid production in gastric parietal cells.

Question 11

What is Gastro-oesophageal reflux disease (GORD)?

Answer 11

Gastro-oesophageal reflux disease (GORD) is a condition characterised by the reflux of gastric contents into the oesophagus.

Question 12

How common is GORD?

Answer 12

GORD is very common, affecting a significant number of individuals.

Question 13

What are the causes of GORD?

Answer 13

GORD is caused by the failure of the “gatekeeper,” which refers to the lower oesophageal sphincter (LOS) not closing fully or experiencing frequent non-physiological temporary relaxations. Additionally, the diaphragmatic sphincter and increased intra-abdominal pressure can contribute to GORD.

Question 14

What factors contribute to the failure of the “gatekeeper” in Gastro-oesophageal reflux disease (GORD)?

Answer 14

Some factors that contribute to the failure of the “gatekeeper” (lower oesophageal sphincter) in GORD include hiatus hernia, obesity, smoking, pregnancy, excess alcohol consumption, ascites, older age, and lifestyle factors such as meals and stress.

Question 15

What are some lifestyle factors that can exacerbate GORD?

Answer 15

Lifestyle factors such as stress, excess alcohol consumption, and smoking can worsen GORD symptoms.

Question 16

Is Helicobacter pylori infection associated with GORD?

Answer 16

Helicobacter pylori infection is not typically associated with GORD. However, it can contribute to other digestive disorders like gastritis and peptic ulcers.

Question 17

Are many individuals with Gastro-oesophageal reflux disease (GORD) asymptomatic?

Answer 17

Many individuals with GORD are asymptomatic, meaning they do not experience any noticeable symptoms.

Question 18

What are some common symptoms of GORD?

Answer 18

Common symptoms of GORD include dyspepsia (acid reflux), heartburn, a burning discomfort in the chest or throat, reflux of acid into the mouth, upper abdominal or chest pain, a sensation of a “globus” (a lump in the throat), respiratory symptoms, persistent nausea with or without vomiting, and poor dentition.

Question 19

How is Gastro-oesophageal reflux disease (GORD) mostly diagnosed?

Answer 19

GORD is mostly diagnosed based on clinical assessment and evaluation of symptoms.

Question 20

What are some diagnostic tests used for GORD?

Answer 20

Diagnostic tests for GORD may include endoscopy (to visualize the oesophagus and stomach), oesophageal manometry (to measure pressure and function of the oesophagus), pH studies (to assess acid levels in the oesophagus), faeces or breath testing for H. pylori infection, and X-ray contrast swallow or meal (to evaluate the movement and function of the oesophagus).

Question 21

What are some management strategies for Gastro-oesophageal reflux disease (GORD)?

Answer 21

Management of GORD typically involves lifestyle advice such as dietary and positional modifications. Acid suppression therapy is a common approach and includes using proton pump inhibitors (PPIs) as the mainstay of treatment. H2 receptor antagonists may also be used, although they primarily reduce acid levels and do not directly address reflux. If relevant, Helicobacter pylori eradication may be recommended.

Question 22

When is surgery considered as a management option for GORD?

Answer 22

Surgery is typically reserved for cases where medical treatment fails or long-term medical management is undesirable. Proof of reflux, often confirmed through pH studies, is usually required before considering surgical intervention. Surgery, such as fundoplication, aims to restore normal anatomy and improve symptoms.

Question 23

What is a hernia?

Answer 23

A hernia is the protrusion of all or part of a viscus (organ) through its coverings and into an abnormal position.

Question 24

What is a hiatus hernia?

Answer 24

A hiatus hernia is the protrusion of the stomach through the diaphragm and into the chest. It occurs when part of the stomach pushes up into the chest cavity through the opening in the diaphragm called the hiatus.

Question 25

What are the two types of hiatus hernia?

Answer 25

Hiatus hernias can be categorized as "sliding" or "rolling." In a sliding hiatus hernia, the junction between the oesophagus and the stomach and a portion of the stomach slide up into the chest. In a rolling hiatus hernia, a part of the stomach rolls up through the diaphragm beside the oesophagus.

Question 26

What percentage of hiatus hernias are sliding hiatus hernias?

Answer 26

Sliding hiatus hernias account for approximately 85-95% of all hiatus hernia cases.

Question 27

What happens in a sliding hiatus hernia?

Answer 27

In a sliding hiatus hernia, the gastroesophageal junction (GOJ) becomes mobile, and part or all of the stomach enters the chest cavity. This results in a loss of the diaphragmatic sphincter effect, allowing negative thoracic pressure to pull gastric contents into the oesophagus.

Question 28

How do sliding hiatus hernias typically present?

Answer 28

Sliding hiatus hernias are mostly asymptomatic. However, they can manifest as gastroesophageal reflux disease (GORD) symptoms, such as heartburn, regurgitation, and acid reflux. Dysphagia (difficulty swallowing) can also occur.

Question 29

What percentage of hiatus hernias are rolling hiatal hernias (paraoesophageal hernias)?

Answer 29

Rolling hiatal hernias, also known as paraoesophageal hernias, account for approximately 5-15% of all hiatus hernia cases.

Question 30

What is the characteristic feature of a rolling hiatal hernia?

Answer 30

In a rolling hiatal hernia, the gastroesophageal junction (GOJ) remains fixed in its normal position below the diaphragm. However, the gastric fundus serves as the lead point of the hernia and protrudes into the chest cavity.

Question 31

How do rolling hiatal hernias typically present?

Answer 31

Rolling hiatal hernias often do not cause symptoms and are frequently asymptomatic. However, they can manifest as chronic, non-specific symptoms that are difficult to diagnose, including abdominal pain, early satiety (feeling full quickly), anaemia, dysphagia (difficulty swallowing), and, in rare cases, strangulation (1% risk) where the blood supply to the herniated portion becomes compromised.

Question 32

What are the management options for hiatus hernia?

Answer 32

Managing hiatus hernia can include conservative, medical, and surgical approaches.

Question 33

What does conservative management of hiatus hernia involve?

Answer 33

Conservative management of hiatus hernia includes lifestyle modifications such as weight loss, avoiding large meals, elevating the head of the bed, and avoiding triggering foods and beverages that can worsen symptoms.

Question 34

What is the medical management of hiatus hernia?

Answer 34

Medical management typically involves the use of medications such as proton pump inhibitors (PPIs) or H2 receptor antagonists to reduce acid production and alleviate symptoms of gastroesophageal reflux.

Question 35

When is surgical intervention considered for hiatus hernia?

Answer 35

Surgical intervention may be considered if conservative and medical measures fail or if there are complications such as recurrent or severe reflux, complications from reflux (e.g., strictures or Barrett's esophagus), or a large hernia. The surgical procedure aims to reduce the hernia, close the defect in the diaphragm, and is often combined with a fundoplication to reinforce the lower esophageal sphincter.

Question 36

What is Barrett's oesophagus?

Answer 36

Barrett's oesophagus is characterized by the metaplastic replacement of the normal oesophageal squamous epithelium with columnar epithelium, specifically intestinal metaplasia.

Question 37

What percentage of the population is affected by Barrett's oesophagus?

Answer 37

Barrett's oesophagus affects approximately 1-2% of the population.

Question 38

What is the main cause of Barrett's oesophagus?

Answer 38

Barrett's oesophagus is primarily caused by chronic reflux of stomach acid into the oesophagus, known as gastroesophageal reflux disease (GERD).

Question 39

How is Barrett's oesophagus diagnosed?

Answer 39

During an endoscopy, Barrett's oesophagus is diagnosed by identifying columnar epithelium in the lower oesophagus.

Question 40

Is Barrett's oesophagus considered a premalignant condition?

Answer 40

Barrett's oesophagus is considered a premalignant condition, as it carries an increased risk for developing dysplasia (abnormal cell changes) and progressing to adenocarcinoma (a type of cancer) in the oesophagus.

Question 41

What is the sequence of changes in Barrett's oesophagus leading to adenocarcinoma?

Answer 41

The sequence of changes in Barrett's oesophagus leading to adenocarcinoma involves metaplasia (replacement of normal squamous epithelium with columnar epithelium), dysplasia (abnormal cell changes), and eventually, the development of adenocarcinoma.

Question 42

What are some risk factors associated with Barrett's oesophagus?

Answer 42

Risk factors for Barrett's oesophagus include being male, older age, a history of reflux (gastroesophageal reflux disease or GERD), obesity, smoking, and a family history of the condition.

Question 43

What is the natural history of Barrett's oesophagus?

Answer 43

In Barrett's oesophagus, there is a progression from low-grade dysplasia (LGD) to high-grade dysplasia (HGD) and eventually to invasive cancer in some cases. However, not all cases progress; some may revert to non-dysplastic mucosa. The risk of developing cancer increases with the presence of HGD.

Question 44

What is the likelihood of developing invasive cancer if Barrett's oesophagus detects high-grade dysplasia (HGD)?

Answer 44

Up to half of individuals with high-grade dysplasia (HGD) already have invasive cancer. The risk of developing cancer is significant in this stage.

Question 45

How likely is the progression from low-grade dysplasia (LGD) to high-grade dysplasia (HGD) or cancer in Barrett's oesophagus?

Answer 45

Some low-grade dysplasia (LGD) cases in Barrett's oesophagus may progress to high-grade dysplasia (HGD) and eventually to cancer. However, most cases of LGD will not progress or may even revert to non-dysplastic mucosa.

Question 46

What are some factors that contribute to the progression of Barrett's oesophagus?

Answer 46

Multiple factors can contribute to the progression of Barrett's oesophagus, including an increased prevalence of p53 tumor suppressor gene mutation. The progression rates are approximately 5% for non-dysplastic mucosa, 10-20% for LGD, and over 60% for HGD.

Question 47

What is the management approach for Barrett's oesophagus without dysplasia?

Answer 47

Metaplasia without dysplasia in Barrett's oesophagus typically requires surveillance only. Regular monitoring and endoscopic examinations are performed to detect any progression or development of dysplasia.

Question 48

What is the management approach for Barrett's oesophagus with low-grade dysplasia (LGD)?

Answer 48

Barrett's oesophagus with low-grade dysplasia (LGD) often involves surveillance with periodic endoscopic examinations. The frequency of surveillance may vary based on individual factors and guidelines.

Question 49

How is the management of high-grade dysplasia (HGD) in Barrett's oesophagus?

Answer 49

High-grade dysplasia (HGD) in Barrett's oesophagus requires complex multidisciplinary team (MDT) management. Treatment options may include radiofrequency ablation (using heat energy to remove abnormal cells), endoscopic removal of affected tissue with or without ablation, surgical interventions, and ongoing proton pump inhibitor (PPI) therapy.

Question 50

What is radiofrequency ablation in the context of Barrett's oesophagus management?

Answer 50

Radiofrequency ablation is a treatment approach that uses heat energy to destroy and remove abnormal cells in the oesophagus affected by high-grade dysplasia (HGD) in Barrett's oesophagus. This procedure aims to eliminate or reduce the risk of cancer development.

Question 51

When is surgery considered as a management option for Barrett's oesophagus?

Answer 51

Surgery may be considered for Barrett's oesophagus with high-grade dysplasia (HGD) or in cases where endoscopic treatments are not feasible or unsuccessful. Surgical interventions aim to remove the affected tissue and restore normal anatomy.

Question 52

What is the role of proton pump inhibitor (PPI) therapy in Barrett's oesophagus management?

Answer 52

Proton pump inhibitor (PPI) therapy is commonly prescribed as part of the management plan for Barrett's oesophagus. PPIs help reduce acid reflux and provide symptom relief. They may also contribute to the regression of dysplasia in some cases.

Question 53

What can chronic gastritis potentially lead to?

Answer 53

Chronic gastritis can lead to the development of gastric ulcers or even gastric cancer if left untreated.

Question 54

What is the main cause of gastritis?

Answer 54

The main cause of gastritis is infection with Helicobacter pylori bacteria. H. pylori infection is a common and significant factor in the development of gastritis.

Question 55

Besides Helicobacter pylori infection, what are some other causes of gastritis?

Answer 55

Other causes of gastritis include smoking, ingestion of irritants (such as certain medications or substances), autoimmune disorders, other infections, inflammatory conditions, and stress.

Question 56

How can gastritis be managed?

Answer 56

The management of gastritis involves several approaches, including removing the causal agent if possible (e.g., treating H. pylori infection), implementing lifestyle modifications (such as quitting smoking), and using acid suppression therapy, often with proton pump inhibitors (PPIs), to reduce gastric acid secretion and provide symptom relief.

Question 57

How do NSAIDs (non-steroidal anti-inflammatory drugs) affect the body?

Answer 57

NSAIDs work by reversibly inhibiting cyclo-oxygenase (COX) enzymes. COX-1 produces prostaglandins that protect the gastrointestinal (GI) tract, while COX-2 produces prostaglandins involved in pain and inflammation.

Question 58

What happens when NSAIDs inhibit COX enzymes?

Answer 58

Inhibition of COX enzymes by NSAIDs reduces the production of protective prostaglandins in the GI tract. This can result in decreased gastric mucous and bicarbonate production, reduced gastric mucosal blood flow, and impaired protection and repair of the gastric mucosa.

Question 59

Why is gastric protection (such as proton pump inhibitors or PPIs) important with long-term NSAID use?

Answer 59

Long-term use of NSAIDs can significantly increase the risk of gastrointestinal complications, including gastric ulcers and bleeding. Therefore, it is important to consider gastric protection, such as proton pump inhibitors (PPIs), to reduce acid secretion and minimize the risk of NSAID-induced gastric damage.

Question 60

What are the main causes of peptic ulceration?

Answer 60

Peptic ulceration is commonly caused by Helicobacter pylori (H. pylori) infection and the use of non-steroidal anti-inflammatory drugs (NSAIDs). H. pylori is a major contributor to peptic ulcers, while NSAIDs account for a significant portion of other cases.

Question 61

How has the incidence of peptic ulceration changed over time?

Answer 61

The incidence of peptic ulceration has decreased with the introduction of H2 receptor antagonists and proton pump inhibitors (PPIs). These medications have played a significant role in reducing ulcer formation and promoting healing.

Question 62

What are some rarer causes of peptic ulceration?

Answer 62

Apart from H. pylori infection and NSAID use, other rarer causes of peptic ulceration include stress ulceration (typically occurring in critically ill patients), malignancy (such as stomach cancer), Zollinger-Ellison syndrome (a rare hormonal disorder), and certain medications that can induce ulcers as a side effect.

Question 63

What is Zollinger-Ellison syndrome?

Answer 63

Zollinger-Ellison syndrome is a rare neuroendocrine tumor primarily originating from the G cells, most commonly found in the pancreas. It is characterized by the uncontrolled and excessive secretion of gastrin, leading to increased activity of gastric parietal cells and the development of multiple ulcers in the upper gastrointestinal (UGI) tract.

Question 64

What is the prevalence of Zollinger-Ellison syndrome?

Answer 64

Zollinger-Ellison syndrome is a rare condition, with an estimated prevalence of 1 in 100,000 people. It is considered to be a relatively uncommon neuroendocrine tumor.

Question 65

How is Zollinger-Ellison syndrome diagnosed?

Answer 65

The diagnosis of Zollinger-Ellison syndrome involves imaging studies, such as CT or MRI scans, to detect the presence of the tumor, usually in the pancreas. Additionally, blood tests are conducted to measure gastrin levels, which are typically elevated in individuals with Zollinger-Ellison syndrome.

Question 66

What are gastric ulcers?

Answer 66

Gastric ulcers are peptic ulcers that primarily occur in the stomach, most commonly along the lesser curve of the stomach. They are characterized by open sores or lesions in the stomach lining.

Question 67

What is a notable association of gastric ulcers?

Answer 67

Gastric ulcers are more likely to be associated with gastric cancer compared to duodenal ulcers. Regular surveillance and monitoring are important for individuals with gastric ulcers to detect potential malignancy.

Question 68

What are duodenal ulcers?

Answer 68

Duodenal ulcers are peptic ulcers that occur in the first part of the duodenum, known as D1. They are four times more common than gastric ulcers and are characterized by open sores or lesions in the lining of the duodenum.

Question 69

How does chronic peptic ulcer typically present?

Answer 69

Chronic peptic ulcers present with symptoms such as upper abdominal pain. In the case of gastric ulcers, the pain often increases 2-3 hours after a meal due to increased gastric acid secretion. In contrast, duodenal ulcer pain tends to reduce after eating, as food intake stimulates the release of pancreatic juices that help neutralize gastric acid.

Question 70

What are some additional symptoms associated with peptic ulcers?

Answer 70

Peptic ulcers can lead to iron deficiency anemia due to chronic bleeding. Weight changes may also occur due to the association between pain and food intake. Some individuals may experience gradual weight loss, while others may gain weight to alleviate pain through increased food intake.

Question 71

How does acute peptic ulcer present?

Answer 71

Acute peptic ulcers can manifest with acute upper gastrointestinal (UGI) bleeding. This can be observed as hematemesis (vomiting of fresh or "coffee-ground" blood) or melena (dark, tarry stools). In some cases, rectal bleeding may also occur. Perforation of the ulcer can lead to peritonitis, which is characterized by severe abdominal pain and systemic illness.

Question 72

How is peptic ulcer diagnosed?

Answer 72

The diagnosis of peptic ulcer involves a combination of history, physical examination, and specific diagnostic tests. Endoscopy is commonly performed to directly visualize the ulcers and obtain biopsies for further evaluation. Helicobacter pylori testing, such as a stool test or rapid urease test with gastric biopsy (CLO test), is also conducted to determine if the infection is present.

Question 73

What are the treatment options for peptic ulcer?

Answer 73

Treating peptic ulcer typically involves a combination of medications and lifestyle modifications. Proton pump inhibitors (PPIs) are commonly prescribed to reduce gastric acid production and promote healing. If Helicobacter pylori infection is detected, eradication therapy, which includes a combination of antibiotics and acid-suppressing medications, may be recommended. Removing or avoiding causal agents, such as NSAIDs or other irritants, is important for management.

Question 74

What is the mortality rate associated with bleeding from the esophagus, stomach, or duodenum?

Answer 74

Bleeding from the esophagus, stomach, or duodenum carries a mortality rate of approximately 2-10%. Prompt intervention is crucial to manage and control the bleeding to minimize the risk of complications and improve outcomes.

Question 75

How is bleeding from varices managed?

Answer 75

Variceal bleeding accounts for approximately 11% of cases. The primary goals in managing variceal bleeding are to stop the bleeding and reduce portal pressure. This can be achieved through medication, such as beta-blockers, which help lower portal pressure. Radiological or endoscopic interventions may also be performed to control the bleeding and manage the underlying cause.

Question 76

How is non-variceal bleeding managed?

Answer 76

Non-variceal bleeding comprises the majority, around 89%, of cases. The main objectives in managing non-variceal bleeding are to stop the bleeding and address the underlying cause. Medications such as proton pump inhibitors (PPIs) are commonly used to suppress gastric acid production and promote healing. Radiological or endoscopic interventions may also be employed to control the bleeding and treat the source of bleeding.

Question 77

What can happen if an ulcer erodes into the gastroduodenal artery (GDA)?

Answer 77

The gastroduodenal artery (GDA) passes behind the first part of the duodenum (D1). In some cases, a posterior ulcer can erode into the GDA, leading to bleeding. If the bleeding is observed during an endoscopy, it can be treated directly. However, if the bleeding is not visible endoscopically, radiological embolization or surgical intervention may be necessary to manage the bleeding.

Question 78

How are perforated peptic ulcers managed?

Answer 78

Perforated peptic ulcers may sometimes be managed without surgery, particularly if the omentum (a fold of tissue in the abdomen) spontaneously seals the hole. However, surgery is typically required in cases such as posterior (retroperitoneal) duodenal ulcers or if the perforation does not heal spontaneously. The surgical procedure involves closure of the ulcer, and an "omental patch" may be used to reinforce the closure. High-dose proton pump inhibitors (PPIs) are often prescribed to reduce gastric acid production and promote healing.

Question 79

What are some key facts about Helicobacter pylori?

Answer 79

Helicobacter pylori is a bacterium that was discovered in 1980. It is considered a global pandemic, meaning it is widespread worldwide. H. pylori is a gram-negative bacterium. It is most commonly acquired during childhood as a new infection. H. pylori cannot survive in acidic conditions but produces urease, an enzyme that converts urea to ammonia and carbon dioxide. This process raises the pH of its surrounding environment. Interestingly, most individuals colonized with H. pylori show no symptoms, with over 70% being asymptomatic.

Question 80

What are some pathogenic factors of Helicobacter pylori?

Answer 80

Helicobacter pylori produces various pathogenic factors that contribute to its virulence. Some strains' cytotoxin-associated gene A (CagA) is associated with inflammation and an increased risk of ulcers and cancer. Vacuolating toxin A (VacA) is another factor produced by H. pylori that causes cell damage. Additionally, multiple other factors contribute to the development of gastritis, peptic ulceration (70-85% of gastric ulcers and 90-95% of duodenal ulcers), gastric cancer (adenocarcinoma), and mucosa-associated lymphoid tissue (MALT) lymphoma (92-98% of cases).

Question 81

When is testing for Helicobacter pylori recommended, and when is it not routinely necessary?

Answer 81

Testing for Helicobacter pylori is recommended in uncomplicated but unresponsive dyspepsia, before NSAID use if there were previous ulcer(s), and in unexplained iron deficiency anaemia (after malignancy has been excluded). However, routine testing is unnecessary for predominantly gastroesophageal reflux disease (GORD) symptoms within two weeks of proton pump inhibitor (PPI) treatment and following treatment in certain contexts.