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Gastrointestinal 2 > Dyspepsia > Flashcards

Dyspepsia Flashcards

1
Q

What is meant by dyspepsia?

A

Indigestion - Dyspepsia describes symptoms such as discomfort, bloating and nausea, which are thought to originate from the upper gastrointestinal tract.

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2
Q

What are common oesophageal symptoms of dyspepsia?

A

Heartburn
Odynophagia
Dysphagia

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3
Q

What are common gastroduodenal symptoms of dyspepsia?

A

Epigastric pain or discomfort
Nausea + vomitting
Bloating / Belching

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4
Q

What are common general symptoms of dyspepsia?

A

Appetite

Weight changes

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5
Q

Odynophagia

A

Pain when swallowing

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6
Q

What are the clinical signs of dyspepsia?

A 
Often minimal clinical signs:
Pallor
Enlarged cervical lymph nodes
Abdominal tenderness
Abdominal masses
Abdominal scars
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7
Q

What is the common cause of oesophageal dyspepsia?

A

GORD

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8
Q

GORD

A

Gastro-oesophageal reflux disease

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9
Q

What are some of the gastroduodenal causes of dyspepsia?

A

Peptic ulceration
Gastric cancer
Functional dyspepsia

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10
Q

What other other causes that can cause dyspepsia separate from the gastrointestinal tract.

A

Biliary diseases such as gallstones
Pancreatic diseases
Heart diseases

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11
Q

What are the ‘ alarm’ features of dyspepsia?

A
  • Weight loss
  • Anaemia
  • Vomiting
  • Haematemesis and/or melaena
  • Dysphagia
  • Palpable abdominal mass
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12
Q

Haematemesis

A

Haematemesis is the vomiting of blood, either bright or altered blood (so-called ‘coffee grounds’ vomitus), due to the action of acid on the blood.

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13
Q

Melaena

A

Melaena is the passage of black tarry stools containing blood.

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14
Q

Summary of GORD - read not memorise.

A

Heartburn describes retrosternal, burning discomfort, often rising up into the chest and sometimes accompanied by regurgitation of acidic or bitter fluid into the throat. These symptoms often occur after meals, on lying down or with bending, straining or heavy lifting. They are classical symptoms of gastro-oesophageal reflux but up to 50% of patients present with other symptoms, such as chest pain, belching, halitosis, chronic cough or sore throats. In young patients with typical symptoms and a good response to dietary changes, antacids or acid suppression investigation is not required, but in patients over 55 years of age and those with alarm symptoms or atypical features urgent endoscopy is necessary.

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15
Q

What investigations are carried out for a patient with dyspepsia?

A

Oesophagoduodenogastroscopy

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16
Q

What hormones, neurotransmitters and substrates are involved in gastric acid secretion and what is their effect?

A
  • histamine (a stimulatory local hormone)
  • gastrin (a stimulatory peptide hormone)
  • acetylcholine (a stimulatory neurotransmitter)
  • prostaglandins E 2 and I 2 (local hormones that inhibit acid secretion)
  • somatostatin (an inhibitory peptide hormone)
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17
Q

How does somatostatin affect gastric acid secretion?

A

Exerts paracrine inhibitory actions on gastrin release from G cells, histamine release from ECL cells, as well as directly on parietal cell acid output.

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18
Q

How do Prostaglandins affect gastric acid secretion?

A

Prostaglandins E 2 and I 2 inhibit acid, stimulate mucus and bicarbonate secretion, and dilate mucosal blood vessels.

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19
Q

Which prostaglandins inhibit gastric acid secretion?

A

E2 and I2

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20
Q

What are the pre-disposing factors for GORD?

A 
Obesity
Smoking
Alcohol
Fatty / Spicy foods
Lying flat
Pregnancy
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21
Q

How may GORD affect the oesophagus?

A

May cause oesophagitis - inflammatory reaction caused by acid.

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22
Q

What is the treatment for GORD?

A

Lifestyle changes - weight loss, head elevation in bed.
Antacids / Alginates
Acid suppressors - proton pump inhibitors / H2 receptor antagonist.
Surgery - Nissen fundoplication.

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23
Q

What do alginates do?

A

Alginates are believed to increase the viscosity and adherence of mucus to the oesophageal mucosa.

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24
Q

What is the pathogenesis of GORD?

A

Abnormal relaxation of the lower oesophageal sphincter.

Hiatus hernia - where part of the stomach is about the diaphragm.

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25
Q

What is Barrett’s oesophagus?

A

Intestinal metaplasia - change in the squamous epithelium that lines the oesophagus to columnar epithelium.

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26
Q

Barrett’s oesophagus affects 5-15% of patients affected with GORD.

A

Barrett’s oesophagus affects 10% of patients affected with GORD. - Understood.

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27
Q

Barrett’s oesophagus increases of the risk of developing what?

A

Oesophageal adenocarcinoma

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28
Q

How is Barrett’s oesophagus diagnosed?

A

This requires multiple systematic biopsies to maximise the chance of detecting intestinal metaplasia and/or dysplasia.

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29
Q

What is a peptic ulceration?

A

An ulcer in the stomach / duodenum most are benign but gastric ulcers may be malignant.

30
Q

What are the main causes of peptic ulcers?

A

Helicobacter pylori infection
NSAID’s or asprin
Zollinger Ellison syndrome

31
Q

How is peptic ulceration managed?

A
  1. Exclude malignancy if a gastric ulcer by biopsy.
  2. Stop NSAID’s / Asprin if possible.
  3. Acid suppression (usually proton pump inhibitor).
  4. H.pylori infection eradication if present.
  5. Check ulcer healing in 6-8 weeks.
32
Q

What are the complications of peptic ulceration?

A
  1. Haemorrhage - haematemesis / malaena
  2. Perforation - severe abdominal pain with guarding / rigidity.
  3. Gastric outlet obstruction
33
Q

How does Helicobacter pylori cause peptic ulcers?

A

The H. pylori bacteria weakens the protective mucous coating of the stomach and duodenum, thus allowing acid to get through to the sensitive lining beneath. Both the acid and the bacteria irritate the lining and cause a sore, or ulcer.

34
Q

How are NSAID’s associated with peptic ulcer formation?

A

Treatment with NSAIDs is associated with peptic ulcers due to impairment of mucosal defences.

35
Q

What are the methods for diagnosing a H.pylori infection?

A

Serology - however lacks specificity as cannot differentiate a past infection from a current one.

13C-urea breath test.

Faecal antigen test.

36
Q

What is the treatment for H.pylori infection?

A

Triple therapy - 1 high dose proton pump inhibitor and 2 antibiotics.

e.g amoxicillin + clarithromyocin + omeprazole

37
Q

What is meant by gastritis?

A

Inflammation associated with mucosal injury.

38
Q

Zollinger-Ellison syndrome

A

Zollinger-Ellison syndrome is a rare condition in which gastrinomas form in your pancreas / duodenum.
These gastrinomas secrete large amounts of the hormone gastrin causing the stomach to produce excess acid.

39
Q

What can the excess gastric acid secreted due to Zollinger-Ellison syndrome lead to?

A

Unusual / severe peptic ulcerations
Oesophagitis
Diarrhoea and malabsorption

40
Q

How is Zollinger-Ellison syndrome diagnosed?

A

Fasting serum gastrin concentration is elevated - can also be raised with PPI or H.pylori.
Biopsy.

41
Q

Multiple endocrine neoplasia type 1 (MEN1)

A

Hereditary condition associated with tumors of the endocrine (hormone producing) glands.

42
Q

Where do tumours seen in MEN1 most commonly affect?

A

The most common tumours seen in MEN1 involve the parathyroid gland, islet cells of the pancreas, and pituitary gland.

43
Q

What is the treatment for Zollinger-Ellison syndrome?

A

High dose acid suppression

Resection of the gastrinoma

44
Q

Functional (non-ulcer) dyspepsia

A

It means that no known cause can be found for the symptoms. That is, other causes for dyspepsia such as duodenal ulcer, stomach ulcer, acid reflux and oesophagitis, inflamed stomach (gastritis) and eosinophilic oesophagitis are not the cause.

45
Q

What are the complications of gastric adenocarcinomas?

A

They have non-specific symptoms and present late.
Surgery is curative when diagnosed early.
Has a poor response to radio/chemotherapy.

46
Q

What virulence factors does H.pylori produce?

A

Cytotoxin associated gene A (cagA)

Exotoxin vacuolating cytotoxin A (vacA)

47
Q

Explain the pathogenesis of cagA produced by H.pylori.

A

CagA interferes with the attachments between adjacent epithelial cells. This induces an inflammatory immune response causing gastritis.

48
Q

What gastric cancers has H.pylori been linked to?

A 
Gastric adenocarcinoma
MALT lymphoma (mucosa-associated lymphoid tissue)
49
Q

What does vacA produced by H.pylori do?

A

Cause epithelial cell death

50
Q

How does H.pylori increase HCl secretion?

A

The inflammation caused by H.pylori causes G cells to secrete more gastrin resulting in parietal cells secreting more HCl.

51
Q

What are some of the symptoms that result from H.pylori infection?

A

Heartburn
Shortness of breath
Loss of appetite

52
Q

What cells line the oesophagus?

A

The oesophagus has a squamous epithelial lining making it more sensitive to the effects of stomach acid.

53
Q

What cells line the stomach?

A

The stomach has a columnar epithelial lining that is more protected against stomach acid.

54
Q

What are the key red flags that indicate the need for referral for endoscopy in GORD?

A 
Dysphagia (difficulty swallowing) at any age gets a two week wait referral
Aged over 55 (this is generally the cut off for urgent versus routine referrals)
Weight loss
Upper abdominal pain / reflux
Treatment resistant dyspepsia
Nausea and vomiting
Low haemoglobin
Raised platelet count
55
Q

Management of GORD

A

Lifestyle advice

Reduce tea, coffee and alcohol
Weight loss
Avoid smoking
Smaller, lighter meals
Avoid heavy meals before bed time
Stay upright after meals rather than lying flat
Acid neutralising medication when required:

Gaviscon
Rennie
Proton pump inhibitors (reduce acid secretion in the stomach)

Omeprazole
Lansoprazole
Ranitidine - This is an alternative to PPIs
H2 receptor antagonist (antihistamine)
Reduces stomach acid
56
Q

H. pylori is what type of bacteria?

A

H. pylori is a gram negative aerobic bacteria.

57
Q

Pathogenesis of H. pylori

A

It lives in the stomach. It causes damage the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it creates in the mucosa exposes the epithelial cells underneath to acid.

It also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells. Other chemicals produced by the bacteria also damage the epithelial lining.

58
Q

Diagnosis of H. pylori

A

We offer a test for H. pylori to anyone with dyspepsia. They need 2 weeks without using a PPI before testing for H. pylori for an accurate result.

Tests

Urea breath test using radiolabelled carbon 13
Stool antigen test
Rapid urease test can be performed during endoscopy.
A rapid urease test is also known as a CLO test (Campylobacter-like organism test). It is performed during endoscopy and involves taking a small biopsy of the stomach mucosa. Urea is added to this sample. If H. pylori are present, they produce urease enzymes that converts the urea to ammonia. The ammonia makes the solution more alkali giving a positive result on when the pH is tested.

59
Q

What is the eradication therapy for H. pylori?

A

The eradication regime involves triple therapy with a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.

60
Q

What is Barretts oesophagus?

A

Constant reflux of acid results in the lower oesophageal epithelium changing in a process known as metaplasia from a squamous to a columnar epithelium. This change to columnar epithelium is called Barretts oesophagus. When this change happens patients typically get an improvement in reflux symptoms.

61
Q

Barret’s oesophagus outcome and management:

A

Barretts oesophagus is considered a “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus (3-5% lifetime risk with Barretts). Patients identified as having Barretts oesophagus are monitored for adenocarcinoma by regular endoscopy. In some patients there is a progression from Barretts oesophagus (columnar epithelium) with no dysplasia to low grade dysplasia to high grade dysplasia and then to adenocarcinoma.

62
Q

Treatment for Barretts:

A

Treatment of Barretts oesophagus is with proton pump inhibitors (e.g. omeprazole). There is new evidence that treatment with regular aspirin can reduce the rate of adenocarcinoma developing however the is not yet in guidelines.

Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy is used to destroy the epithelium so that it is replaced with normal cells. This is not recommended in patients with no dysplasia but has a role in low and high grade dysplasia in preventing progression to cancer.

63
Q

There is a protective layer in the stomach comprised of mucus and bicarbonate secreted by the stomach mucosa. This protective layer can be broken down by:

A

Medications (e.g. steroids or NSAIDs)

Helicobacter pylori

64
Q

How do peptic ulcers present?

A

Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding causing haematemesis, “coffee ground” vomiting and melaena
Iron deficiency anaemia (due to constant bleeding)

65
Q

How does eating indicate location of the ulcer?

A

Eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

66
Q

How are peptic ulcers managed?

A

Peptic ulcers are diagnosed by endoscopy. During endoscopy a rapid urease test (CLO test) can be performed to check for H. pylori. Biopsy should be considered during endoscopy to exclude malignancy as cancers can look similar to ulcers during the procedure.

Medical treatment is the same as with GORD, usually with high dose proton pump inhibitors. Endoscopy can be used to monitoring the ulcer to ensure it heals and to assess for further ulcers.

67
Q

What complications can present as a result of peptic ulcers?

A

Bleeding from the ulcer is a common and potentially life threatening complication.

Perforation resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).

Scarring and strictures of the muscle and mucosa. This can lead to a narrowing of the pylorus (the exit of the stomach) causing difficulty in emptying the stomach contents. This is known as pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting, particularly after eating.

68
Q

Common causes of upper GI bleeds:

A

Oesophageal varices
Mallory-Weiss tear, which is a tear of the oesophageal mucous membrane
Ulcers of the stomach or duodenum
Cancers of the stomach or duodenum

69
Q

How do upper GI bleeds present?

A

Haematemesis (vomiting blood)
“Coffee ground” vomit. This is caused by vomiting digested blood that looks like coffee grounds.
Melaena, which is tar like, black, greasy and offensive stools caused by digested blood
Haemodynamic instability occurs in large blood loss, causing a low blood pressure, tachycardia and other signs of shock. Bear in mind that young, fit patients may compensate well until they have lost a lot of blood.

Epigastric pain and dyspepsia in peptic ulcers.
Jaundice for ascites in liver disease with oesophageal varices.

70
Q

Why does urea rise in GI bleeds?

A

The reason urea rises in upper GI bleeds is that the blood in the GI tract gets broken down by the acid and digestive enzymes. One of the breakdown products is urea and this urea is then absorbed in the intestines.

71
Q

Management of an Upper GI bleed:

ABATED

A

A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 large bore cannula)
T – Transfuse
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

In Oesophageal varicies add Terlipressin and prophylactic broad spectrum antibiotics.

Gastrointestinal 2 (24 decks)

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