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Met3 > Gastroenterology; Upper GI; Dyspepsia & GORD > Flashcards

Gastroenterology; Upper GI; Dyspepsia & GORD Flashcards

1
Q

What is the most common cause of dysepsia? [1]

A

oesophageal cancer

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2
Q

State 7 red flag symptoms when asking about dyspepsia [7]

A
  • dysphagia
  • weight loss (unintentional)
  • persistent vomiting
  • epigastric mass
  • GI bleeding
  • iron deficiency
  • new/ persistent unexplained symptoms > 55y
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3
Q

Define dyspepsia [3]

A

Dyspepsia is a group of symptoms that suggest upper GI disease, according to NICE. Descriptions include:

· Pain or discomfort in the epigastrium (ulcer-like)

· Heartburn/regurgitation of eaten food (GORD-like)

· Bloating, nausea, vomiting and excess wind (dysmotility-like)

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4
Q

A ptx presents with upper GI discomfort but after endoscopy there is no evidence of an ulcer. What is this called? [1]

A

Non-ulcer dyspepsia

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5
Q

State the 4 most common causes of dyspepsia [4]

A
  • No lesions / non-ulcer dyspepsia (75%)
  • Peptic ulcer disease (10-15%)
  • Oesphagitis (15%)
  • Cancer (2%)
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6
Q

State 6 reasons non-ulcer dyspepsia may occur [6]

A

· Disturbance in GI motility

· Disturbance in visceral sensation, i.e. hypersensitivity

· Decreased sense of accommodation by the stomach: stomach is sensitive so feels abnormally distended/quickly full

· Pronounced intenstino-gastric reflexes, may mimic IBS symptoms

· Gastric aid sensitivity

· Psychosocial factors

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7
Q

Name 4 factors that increase the likelyhood of GORD [4]

A
  • Obesity (BMI > 30; increases intra-abdominal pressure)
  • Smoking, alchohol and coffee
  • Drugs (relax LOS): tricyclics, anticholinergics, nitrates, calcium channel blockers
  • Fatty foods
  • Pregnancy

NB: no association with H. pylori.
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8
Q

Describe the pathophysiology of GORD [3]

A
  • High intra-abdominal pressure combined with LOS relaxation and / or abnormalities causes gastric acid, bile, pepsin and pancreatin enzymes are able to reflux back into the oesophagus, causing mucosal injuries
  • Often combined with decreased oesophageal motility, causing decreased oesophageal clearance
  • The gastric acid levels are normal, just in the wrong place
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9
Q

Describe a cause of LOS dysfunction [1]

A

Hiatus hernia: herniation of the stomach up through the diaphragm. Causes the opening from the oesophagus to the stomach to be wider, and more stomach content can reflux into the oesophagus

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10
Q

State 5 causes of GORD

A

GORD:
- Hiatus hernia
- LOS hypotension
- obesity
- pregnancy
- smoking & alcohol
- drugs (tricyclic; anticholinergics; nitrates)

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11
Q

State five drug classes that can cause GORD [5]

A
  • tricyclic
  • anticholinergics
  • nitrates
  • CCBs
  • NSAIDs
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12
Q

Describe symptoms of GORD [5]

A

Heartburn
Retrosternal discomfort after meals
Belching
Halitosis
Acid brash
Increased salivation (mouth fills with saliva)

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13
Q

State 3 extra-oesophageal symptoms of GORD [3]

A

Nocturnal asthma
Chronic cough
Laryngitis
Sinusitis

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14
Q

Describe the 4 different types of hiatus hernia [4]

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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15
Q
A
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16
Q

What type of hernia is this? [1]

A

Type 3: sliding and rolling

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17
Q

What type of hernia is depicted? [1]

A

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

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18
Q

What type of hernia is depicted? [1]

A

Type 1: displacement of GOJ above diaphragm

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19
Q

What type of hernia is depicted? [1]

A

Type 2: rolling - dislocation of fundus

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20
Q

GORD can be clinically diagnosed based on which of following isolated symptoms? [5]

State 3 atypical symptoms [3]

A
  • Heartburn
  • Belching
  • Acid regurgitaton
  • Water brash (xs salivation)
  • Odynophagia (painful swallowing)
  • Nocturnal asthma

Atypical:
- Chest pain
- Epigastric pain
- Chroic aspiration

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21
Q

GORD can lead to macroscopic oesophagitis.

Define macroscopic oesophagitis [1]

A

Ulcerations of the oesophagus

22
Q

Why is GORD developing macroscopic oesophagitis clinically signfiicant? [3]

A
  • Causes strictures
  • Can cause Barrett’s oesophagus: can lead to cancer
23
Q

Describe diagnostic investigations for GORD [3]

A

Therapeutic trial of PPI:
- i.e. 40mg of omeprazole for 2 weeks and if the symptoms are completely resolved on that and no alarm symptoms, this may be a reasonable diagnostic tes

Endoscopy (NB: ~ 50% have no lesions);
- used to create Los Angeles scoring system for oesophagitis

Oesophageal function testing:
- can monitor pH over 24 hours using a small sensor

24
Q

Describe the LA Classification of oesophagitis [4]

A

Grade A
- At least one mucosal break, up to 5 mm, that does not extend between the tops of two mucosal folds

Grade B:
- At least one mucosal break, more than 5 mm long, that does not extend between the tops of two mucosal folds

Grade C:
- At least one mucosal break that is continuous between the tops of two or more mucosal folds but which involve less than 75% of the circumference

Grade D:
- At least one mucosal break which involves at least 75% of the esophageal circumference

25
Q

State the therapeutic management for GORD
- Therapeutics [4]
- Surgery [1]

A

Drugs:
If no red flags: 4 week PPI course:
- omeprazole

Antiacids: Mg trisilicate
Alginates: Gaviscon

Acid suppression:
- PPIs: omeprazole and lansoprazole
- or H2 receptor antagonists: famotidine or ranitidine

Surgery:
- laparoscopic fundoplication: tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter

26
Q

Describe the usual medical strategy when someone presents with GORD [4]

A
  • Exclude red flags
  • Address potential triggers
  • Offer a 1 month trial of a proton pump inhibitor
  • Consider H. pylori testing
27
Q

Anyone with dyspepsia is offered to be tested for which organism? [1]

Describe conditions needed to test for this organism for an accurate result [1]

A

H. pylori

Need 2 weeks without using a PPI before testing for H. pylori for an accurate result.

28
Q

Describe the pathophysiology of H. pyorli cause gastritis, uclers and stomach cancer [3]

A

H. pylori goes into gastric mucosa; exposing epithelial cells below to stomach acid

H. pylori produces ammonium hydroxide; neutralises the acid around the bacteria and also produces toxins

Ammonia & toxins causes gastric mucosal damage

29
Q

Describe how you investigate for H. pylori prescence [4]

A
  • Stool antigen test
  • Urea breath test using radiolabelled carbon 13 (H.pylori converts urea to ammonia: pH tested and if red: positive
  • H. pylori antibody test (blood)
  • Rapid urease (enzyme used by H. pylori) test performed during endoscopy (also known as the CLO test)
30
Q

Which form of Which form of testing for H. pylori is used for diagnosis? [1]

A

The stool test is often used to diagnose Helicobacter pylori, but cannot be used to test for eradication as there is insufficient evidence for this.

31
Q

Which form of testing for H. pylori is used for post-eradication therapy? [1]

A

Urea breath test is the only test recommended for H. pylori post-eradication therapy

32
Q

Which form of testing for H. pylori is used for during endoscopy? [1]

A

CLO testing is a rapid urease test that is done during endoscopy to detect Helicobacter pylori and relies on the fact that the bacteria contain the urease enzyme

. It is approximately 90% sensitive, however it is an invasive test and is not recommended for eradication testing unless a patient requires an endoscopy.

33
Q

Describe the treatment regime if a patient tests postive for H. pylori [6]

How long is treatment for? [1]

A

7 Day treament plan of triple therapy:

PPI:
- omeprazole

Antibiotics (two required):
- amoxicillin
- clathromyocin
- metronidazole (increasing resistance has limited its usefulness)
- Bismuth
- Metoclopramide
- Vasopressin

7 days

34
Q

Describe the pathophysiology of Barrett’s oesophagus (BO) [2]

A

Chronic oesophageal injury from chronic reflux of gatstric contents; causes a change from squamous to columnar epithelium (process is called metaplasia)

35
Q

Describe why BO is a clincially significant disease [2]

A

BO is pre-malignant; high risk of deveoping oesophageal adenocarcinoma (via reflux associated DNA damage)

There can be a stepwise progression from no dysplasia to low-grade dysplasia, high-grade dysphasia, and adenocarcinoma.

36
Q

State 5 risk factors for BO

A

Long standing gastro-oesophageal reflux
Male sex (male-to-female ratio 2:1)
Caucasian ethnicity
Increasing age
Obesity
Smoking
Family history

37
Q

Describe the treatment for

non-dysplastic BO [2]
low-grade dysplasia BO [2]
high-grade dysplasia [3]

A

non-dysplastic BO:
- PPI (omeprazole)
- Anti-reflux surgery (Nissen fundoplication)

low-grade dysplasia BO
- radiofrequency ablation
- consider PPI

high-grade dysplasia
- radiofrequency ablation
- consider PPI
- oesophagectomy

38
Q

Describe what Eosinophilic oesophagitis (EoO) is [2]

A

Chronic, immune-mediated/allergen-mediated clinicopathological condition:

  • oesophageal dysfunction (e.g., dysphagia and food impaction in adolescents and adults, and vomiting, regurgitation, heartburn, abdominal pain)

AND

  • Histologically: eosinophilic infiltration of the oesophageal epithelium of ≥15 eosinophils
39
Q

How do you diagnose EoO? [1]
How do you treat? [2]

A

Diagnose: biopsy
Tx: swallow inhaled steroids; exclusion diet

40
Q

Describe two motility disorders that can cause dysphagia [2]

A

Achalasia: increased tone of LOS; can’t relax

Presbyoesophagus: elderly; peristalsis ineffective

41
Q

What would indicate a patient has neurological dysphagia? [1]

A

More difficult to swallow liquids than solids

42
Q

Describe managment for dyspepsia if H.pylori tests negative [1]

A

2 week PPI treatment

43
Q

Tx for non-ulcer dyspepsia? [1]

A

PPI

44
Q

State 5 extra-oesophageal manifestations of GORD [5]

A
  • middle ear problems
  • chronic sinusitis
  • dental erosions
  • sore throat
  • cough
  • astha
  • aspiration pneumonia
45
Q

What is the gold standard for diagnosing GORD? [2]

A
46
Q

How do PPIs work? [1]

A

PPIs form the cornerstone of GORD treatment.

PPIs prevent acid production within the stomach through inhibition of H+/K+ ATPases in parietal cells.

47
Q

What is the name of the surgery for GORD? [1]

A

Nissen fundoplication.

48
Q

What is the NICE first line treatment for H. pylori? [3]

A

A proton pump inhibitor, plus amoxicillin, and either clarithromycin or metronidazole

49
Q

Achalasia is associated with which type of oesophageal cancer? [1]

Name a significant risk factor for this cancer [1]

A

Squamous cell cancer

Smoking

50
Q

What is the difference in location of adenocarcinoma and squamous cell carcinoma of oesophagus? [2]

A

Adenocarcinoma: Lower third - near the gastroesophageal junction

SSC: Upper two-thirds of the oesophagus

51
Q

A 60-year-old man who is known to have Barrett’s oesophagus is reviewed with the results of his surveillance biopsies. These show high-grade dysplasia but no evidence of carcinoma. He is asymptomatic apart from his gastro-oesophageal reflux disease symptoms which are well controlled on high dose proton pump inhibitor therapy. What treatment is he most likely to be offered?
[2]

A

radiofrequency ablation: preferred first-line treatment, particularly for low-grade dysplasia

endoscopic mucosal resection

52
Q
A

Met3 (52 decks)

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