GI: GORD & Diverticular Disease Flashcards

1
Q

What is GORD?

A

Gastro-oesophageal reflux disease (GORD) is where acid from the stomach flows through the lower oesophageal sphincter and into the oesophagus, where it irritates the lining and causes symptoms.

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2
Q

Describe cells lining oesophagus vs stomach

A

Oesophagus –> squamous epithelial lining (more sensitive to the effects of stomach acid)

Stomach –> columnar epithelial lining (more protected against stomach acid)

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3
Q

Causes/triggers of symptoms of GORD?

A
  • Greasy and spicy foods
  • Coffee and tea
  • Alcohol
  • NSAIDs
  • Stress
  • Smoking
  • Obesity
  • Hiatus hernia
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4
Q

Presentation of GORD?

A

Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:

  • Heartburn
  • Acid regurgitation
  • Retrosternal or epigastric pain
  • Bloating
  • Nocturnal cough
  • Hoarse voice
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5
Q

Red flag symptoms in GORD?

A

Patients with symptoms suspicious of cancer get a two week wait referral for further investigation.

Key red flag features:
1) Dysphagia (difficulty swallowing) at ANY AGE gets an immediate 2 week wait referral

2) Aged over 55 (this is generally the cut-off for urgent versus routine referrals)

3) Weight loss

4) Upper abdominal pain

5) Reflux

6) Treatment-resistant dyspepsia

7) Nausea and vomiting

8) Upper abdominal mass on palpation

9) Low haemoglobin (anaemia)

10) Raised platelet count

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6
Q

Why is dysphagia an important symptom?

A

Remember dysphagia as a critical red flag. Any patient presenting with the feeling that food is getting STUCK on the way down needs an urgent two week wait referral for an endoscopy.

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7
Q

1st line investigation in GORD?

A

An oesophago-gastro-duodenoscopy (OGD) –> involves inserting a camera through the mouth down to the oesophagus, stomach and duodenum.

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8
Q

What can an OGD be used to assess for?

A
  • Gastritis
  • Peptic ulcers
  • Upper GI bleeding
  • Oesophageal varices (in liver cirrhosis)
  • Barretts oesophagus
  • Oesophageal stricture
  • Malignancy of the oesophagus or stomach
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9
Q

If a patient has evidence of upper gastrointestinal bleeding (e.g., melaena or coffee ground vomiting, what is next step?

A

They need admission and urgent endoscopy.

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10
Q

Indications for an upper GI endoscopy?

A

1) age > 55 years
2) symptoms > 4 weeks or persistent symptoms despite treatment
3) dysphagia
4) relapsing symptoms
5) weight loss

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11
Q

If endoscopy is negative, what is next step in GORD?

A

24 hour oesophageal pH monitoring

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12
Q

Gold standard test for diagnosis of GORD?

A

24-hr oesophageal pH monitoring

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13
Q

What is a hiatus hernia?

A

A hiatus hernia refers to the herniation of the stomach up through the diaphragm.

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14
Q

How can a hiatus hernia lead to GORD?

A

Normal:
1) The diaphragm opening should be at the lower oesophageal sphincter level and fixed in place
2) A narrow opening helps to maintain the sphincter and stops acid and stomach contents from refluxing into the oesophagus.

GORD:
When the opening of the diaphragm is wider, the stomach can enter through the diaphragm, and the contents of the stomach can reflux into the oesophagus.

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15
Q

What are the 4 types of hiatus hernias?

A

Type 1: sliding

Type 2: rolling

Type 3: combination of sliding and rolling

Type 4: large opening with additional abdominal organs entering the thorax

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16
Q

What is a sliding hiatus hernia?

A

Where the stomach slides up through the diaphragm, with the gastro-oesophageal junction passing up into the thorax.

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17
Q

What is a rolling hiatus hernia?

A

Where a separate portion of the stomach (i.e., the fundus), folds around and enters through the diaphragm opening, alongside the oesophagus.

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18
Q

What is a type 4 hiatus hernia?

A

Type 4 hiatus hernia refers to a large hernia that allows other intra-abdominal organs to pass through the diaphragm opening (e.g., bowel, pancreas or omentum).

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19
Q

Investigations for a hiatus hernia?

A

1) CXR
2) CT scan
3) Endoscopy
4) Barium swallow test

N.B. Hiatus hernias can be intermittent, meaning they may not be seen on investigations.

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20
Q

Lifestyle management options in GORD?

A

1) Reduce tea, coffee and alcohol

2) Weight loss

3) Avoid smoking

4) Smaller, lighter meals

5) Avoid heavy meals before bedtime

6) Stay upright after meals rather than lying flat

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21
Q

Management of GORD?

A

1) Lifestyle changes

2) Reviewing meds e.g. stop NSAIDs

3) Antacids (e.g., Gaviscon, Pepto-Bismol and Rennie) – short term only

4) PPIs e.g. omeprazole and lansoprazole

5) Histamine H2-receptor antagonists (e.g., famotidine)

6) Surgery

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22
Q

Mechanism of PPIs?

A

Proton pump inhibitors (PPI) cause irreversible blockade of H+/K+ ATPase of the gastric parietal cell –> block gastric acid secretion

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23
Q

Adverse effects of long-term PPI use?

A

1) hyponatraemia, hypomagnasaemia

2) osteoporosis –> increased risk of fractures

3) microscopic colitis

4) increased risk of C. difficile infections

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24
Q

If a patient with endoscopically proven oesophagitis has no response after full PPI for 1-2 months, what is next step?

A

if no response then double-dose PPI for 1 month

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25
Q

If a patient with endoscopically proven oesophagitis does have a response after full PPI for 1-2 months, what is next step?

A

if response then low dose treatment as required

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26
Q

Complications of GORD?

A

1) oesophagitis
2) ulcers
3) anaemia
4) benign strictures
5) Barrett’s oesophagus
6) oesophageal carcinoma

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27
Q

What is surgical option for GORD?

A

laparoscopic fundoplication

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28
Q

What does laparoscopic fundoplication involve?

A

This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

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29
Q

Usual medical strategy when someone presents with GORD for the first time?

A

1) Exclude red flags

2) Address potential triggers

3) +/- endoscopy

4) Offer a 1 month trial of a proton pump inhibitor

5) Consider H. pylori testing.

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30
Q

What is H. pylori?

A

Helicobacter pylori (H. pylori) is a gram-negative aerobic bacteria that can live in the stomach.

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31
Q

Complications of H. pylori in the stomach?

A

It causes damage to the epithelial lining, resulting in gastritis, ulcers and an increased risk of stomach cancer.

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32
Q

How does H. pylori cause damage?

A

1) It avoids the acidic environment by forcing its way into the gastric mucosa, using flagella to propel itself.

2) It creates gaps in the mucosa, exposing the epithelial cells underneath to damage from stomach acid.

3) H. pylori produces ammonium hydroxide, which neutralises the acid surrounding the bacteria

4) It also produces several toxins.

5) The ammonia and toxins lead to gastric mucosal damage.

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33
Q

Who should an H. pylori test be offered to?

A

anyone with dyspepsia

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34
Q

Rules of PPIs and H. pylori testing?

A

PPIs must be stopped 2 weeks before H. pylori testing for accurate result.

35
Q

Investigations for H. pylori?

A

1) Stool antigen test

2) Urea breath test using radiolabelled carbon 13

3) H. pylori antibody test (blood)

4) Rapid urease test performed during endoscopy (also known as the CLO test)

36
Q

What does a rapid urease test involve?

A

1) Taking a small biopsy of the stomach mucosa.

2) This is added to a liquid medium containing urea.

3) H. pylori produce urease enzymes that convert urea to ammonia. Ammonia makes the solution more alkaline.

4) A pH indicator (e.g., phenol red) changes colour if the pH rises, giving a positive result.

37
Q

What does the H. pylori eradication regime involve?

A

Triple therapy:
1) PPI
2) two Abx (e.g. amoxicillin and clarithromycin) for 7 days

38
Q

What is Barrett’s oesophagus?

A

When the lower oesophageal epithelium changes from squamous to columnar epithelium (metaplasia).

This is a PRE-MALIGNANT condition.

39
Q

Cause of Barrett’s oesophagus?

A

It is caused by chronic acid reflux into the oesophagus.

40
Q

How may Barrett’s oesophagus affect symptoms?

A

Patients may notice improved reflux symptoms after they develop Barrett’s oesophagus.

41
Q

Barret’s oesophagus is a pre-malignant condition.

What is it a significant risk factor for developing?

A

Oesophageal adenocarcinoma (cancer of the epithelial cells).

42
Q

Describe stepwise progression from Barrett’s oesophagus to cancer

A

1) no dysplasia

2) low-grade dysplasia

3) high-grade dysphasia

4) adenocarcinoma.

43
Q

Treatment of Barrett’s oesophagus?

A

1) Endoscopic monitoring for progression to adenocarcinoma

2) Proton pump inhibitors

3) Endoscopic ablation (e.g., radiofrequency ablation)

44
Q

Purpose of ablation in Barrett’s oesophagus?

A

Ablation can be used to destroy abnormal columnar epithelial cells, which are then replaced with normal squamous epithelial cells.

45
Q

What is Zollinger-Ellison syndrome?

A

A rare condition where a duodenal or pancreatic tumour secretes excessive quantities of gastrin.

46
Q

What hormone is excreted in excess in Zollinger-Ellison syndrome?

A

Gastrin

47
Q

What is gastrin?

A

Gastrin is a hormone that stimulates acid secretion in the stomach.

48
Q

Symptoms of excess gastrin in Zollinger-Ellison syndrome?

A

1) Severe dyspepsia

2) Diarrhoea

3) Peptic ulcers

49
Q

What is multiple endocrine neoplasia type 1 (MEN1)?

A

An autosomal dominant genetic condition which can cause:

1) Gastrin secreting gastrinomas

2) tumours of the parathyroid gland

3) pituitary gland tumours

50
Q

What 3 tumours are seen in MEN1?

A

1) gastrinomas

2) parathyroid tumour

3) pituitary tumour

51
Q

What is the most common cause of vomiting in infancy?

A

Gastro-oesophageal reflux:

Around 40% of infants regurgitate their feeds to a certain extent so there is a degree of overlap with normal physiological processes.

52
Q

Risk factors for gastro-oesophageal reflux in infants?

A

1) preterm delivery

2) neurological disorders

53
Q

Features of gastro-oesophageal reflux in children?

A

1) typically develops before 8 weeks

2) vomiting/regurgitation
- milky vomits after feeds
- may occur after being laid flat

3) excessive crying, especially while feeding

54
Q

Management of gastro-oesophageal reflux in infants?

A

Some options:

  • advise regarding position during feeds - 30 degree head-up
  • infants should sleep on their backs as per standard guidance to reduce the risk of cot death
  • ensure infant is not being overfed (as per their weight) and consider a trial of smaller and more frequent feeds
55
Q

Complications of gastro-oesophageal reflux in children?

A
  • distress
  • failure to thrive
  • aspiration
  • frequent otitis media
  • in older children dental erosion may occur
56
Q

What is a diverticulum?

A

A pouch or pocket in the bowel wall, ranging in size from 0.5 – 1cm.

It consists of the herniation of colonic mucosa through the muscular wall of the colon.

57
Q

What is diverticulosis?

A

Diverticulosis refers to the presence of diverticula, without inflammation or infection.

Also known as diverticular disease when patients experience symptoms.

58
Q

Where is the usual site of diverticular disease?

A

Between the taenia coli where vessels pierce the muscle to supply the mucosa.

59
Q

Define diverticulitis

A

Diverticulitis refers to inflammation and infection of diverticula.

60
Q

Why is the rectum often spared in diverticular disease?

A

Rectum lacks taenia coli.

Rectum has an outer longitudinal muscle layer that completely surrounds the diameter of the rectum, adding extra support.

61
Q

Pathophysiology in diverticular disease:

A

1) The wall of the large intestine contains a layer of muscle called the circular muscle.

2) The points where this muscle layer is penetrated by blood vessels are areas of weakness.

3) Increased pressure inside the lumen over time, can cause a gap to form in these areas of the circular muscle.

4) These gaps allow the mucosa to herniate through the muscle layer and pouches to form (diverticula).

5) In the colon, there are three longitudinal muscles that run along the colon, forming strips or ribbons called teniae coli –> the areas that are not covered by teniae coli are vulnerable to the development of diverticula.

62
Q

What is the most commonly affected section of bowel in diverticulosis?

A

Sigmoid colon

63
Q

Risk factors for diverticulosis?

A
  • Increased age
  • Low fibre diets
  • Obesity
  • Use of NSAIDs (also increases the risk of diverticular haemorrhage)
64
Q

How is diverticulosis often diagnosed?

A

On colonoscopy or CT scans

65
Q

Treatment of asymptomatic diverticulosis?

A

Treatment is not necessary where the patient is asymptomatic.

However, advice regarding a high fibre diet and weight loss is appropriate.

66
Q

What type of laxatives can be offered in diverticulosis if patients have constipation?

A

Bulk forming (e.g. isaphula husk)

67
Q

What type of laxatives should be AVOIDED in diverticulosis?

A

Stimulants e.g. senna

68
Q

Symptoms of diverticulitis (i.e. inflammation in the diverticula)?

A

1) Pain and tenderness in the left iliac fossa / lower left abdomen
2) Altered bowel habit e.g. diarrhoea, constipation
3) Rectal bleeding

Others:
- Fever
- Nausea and vomiting
- Palpable abdominal mass (if an abscess has formed)
- Raised inflammatory markers (e.g., CRP) and white blood cells

69
Q

Management of uncomplicated diverticulitis in primary care?

A

1) Oral co-amoxiclav (at least 5 days)

2) Analgesia (avoiding NSAIDs and opiates, if possible)

3) Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)

4) Follow-up within 2 days to review symptoms

70
Q

Typical Abx of choice in uncomplicated diverticulitis?

A

Oral co-amoxiclav (at least 5 days)

71
Q

Classification of diverticulitis?

A

Class I: para-colonic abscess
Class II: pelvic abscess
Class III: purulent peritonitis
Class IV: faecal peritonitis

72
Q

Potential management in SEVERE cases of diverticulitis?

A
  • Nil by mouth or clear fluids only
  • IV antibiotics
  • IV fluids
  • Analgesia
  • Urgent investigations (e.g., CT scan)
  • Urgent surgery may be required for complications
73
Q

Complications of acute diverticulitis?

A
  • Perforation
  • Peritonitis
  • Peridiverticular abscess
  • Large haemorrhage requiring blood transfusions
  • Fistula (e.g., between the colon and the bladder or vagina)
  • Ileus / obstruction
74
Q

Where is abdo pain located in diverticulitis?

A

Lower left quadrant

75
Q

Where might abdo pain be located in diverticulitis in some Asian patients?

A

Lower right quadrant

76
Q

Investigations in diverticulitis?

A

1) FBC: raised WCC
2) CRP: raised
3) Erect CXR: may show pneumoperitoneum in cases of perforation
4) AXR: may show dilated bowel loops, obstruction or absceses
5) CT: best modality in suspected abscesses

77
Q

Is a colonoscopy indicated in diverticulitis?

A

No - should be avoided initially due to the increased risk of perforation in diverticulitis

78
Q

What is Meckel’s diverticulum?

A

A congenital diverticulum of the small intestine –> it is a remnant of the omphalomesenteric duct

79
Q

What does Meckel’s diverticulum contain?

A

contains ectopic ileal, gastric or pancreatic mucosa.

80
Q

What is the ‘rule of 2s’ in Meckel’s diverticulum?

A

1) occurs in 2% of the population
2) is 2 feet from the ileocaecal valve
3) is 2 inches long

81
Q

Presentation of Meckel’s diverticulum?

A
  • Usually asymptomatic
  • abdominal pain mimicking appendicitis
  • rectal bleeding
  • intestinal obstruction
82
Q

What is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years?

A

Meckel’s diverticulum

83
Q
A