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Year 3 - Medicine > Gastroenterology - Luminal Disease > Flashcards

Gastroenterology - Luminal Disease Flashcards

1
Q

What are the two main types of inflammatory bowel disease?

A
  • Crohn’s disease
  • Ulcerative colitis
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2
Q

Features of Crohn’s disease?

A

Crow’s NESTS:

No blood or mucus
Entire GI tract involved
Skip lesions on endoscopy
Terminal ileum most affected and Transmural inflammation
Smoking is a risk factor

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3
Q

Features of ulcerative colitis?

A

U-C-CLOSEUP

Continuous inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis

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4
Q

Presentation of IBD.

A
  • diarrhoea
  • abdominal pain
  • passing blood
  • weight loss
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5
Q

Which blood tests should be considered in a patient with a change in bowel habit, and why?

A

FBCs - anaemia or raised platelet count

U&Es - deranged electrolytes or AKI, due to GI losses

CRP - inflammatory marker (although normal CRP doesn’t exclude IBD)

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6
Q

Which stool tests should be considered in a patient with a change in bowel habit, and why?

A

Stool cultures - exclude infective colitis

Faecal calprotectin - raised in active disease, but negative in remissive disease

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7
Q

Which imaging modalities should be considered in a patient with a change in bowel habit, and why?

A

AXR - useful if clinical suspicion of toxic megacolon

Endoscopy (OGD and colonoscopy) with biopsy is diagnostic for IBD.

Imaging with ultrasound, CT and MRI can be used to look for complications such as fistulas, abscesses and strictures.

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8
Q

How can remission be induced in Crohn’s disease?

A

Steroids (e.g. oral prednisolone or IV hydrocortisone)

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9
Q

How can remission be maintained in Crohn’s disease?

A

Azathioprine and mercaptopurine are standard maintenance therapy.

Alternatives include methotrexate and infliximab.

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10
Q

When is surgical intervention considered in Crohn’s disease?

A

When the disease only affects the distal ileum it is possible to surgically resect this area, and it prevents further flares of the disease.

Surgery can also be used to treat strictures and fistulas, secondary to Crohn’s disease.

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11
Q

How can remission be induced in ulcerative colitis?

A

Aminosalicylate (e.g. mesalazine) first line in mild-moderate disease.

In severe disease IV corticosteroids (e.g. hydrocortisone) used.

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12
Q

How is remission maintained in Crohn’s disease?

A

Aminosalicylate (e.g. mesalazine)

Azathioprine and mercaptopurine also useful in maintenance therapy.

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13
Q

When is surgery considered for ulcerative colitis treatment?

A

As ulcerative colitis only affects the rectum and colon, a panproctocolectomy will remove the disease.

The patient is left with either a permanent ileostomy or an ileo-anal anastamosis, the latter of which allows normal defaecation by the patient.

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14
Q

Why are patients admitted to hospital with acute IBD prescribed heparin?

A

High risk of VTE as IBD flares are prothrombotic diseases

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15
Q

What is irritable bowel syndrome?

A

A set of symptoms where there is no identifiable organic disease, diagnosed upon a basis of clinical symptoms.

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16
Q

Presentation of irritable bowel syndrome.

A
  • diarrhoea
  • constipation
  • fluctuating bowel habit
  • abdominal pain
  • bloating
  • worse after eating
  • improved by opening bowels
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17
Q

NICE criteria for diagnosing irritable bowel syndrome:

A

Other pathology should be excluded:

Normal FBC, ESR and CRP blood tests
Faecal calprotectin negative to exclude inflammatory bowel disease
Negative coeliac disease serology (anti-TTG antibodies)
Cancer is not suspected or excluded if suspected

Symptoms should suggest IBS:

Abdominal pain / discomfort:
- Relieved on opening bowels, or
- Associated with a change in bowel habit

AND 2 of:
- Abnormal stool passage
- Bloating
- Worse symptoms after eating
- PR mucus

18
Q

How is irritable bowel syndrome managed?

A

Conservative measures include adequate fluid intake, regular small meals, reduced processed foods, and limited caffeine and alcohol intake.

First line medications:
- loperamide for diarrhoea
- linaclotide for constipation
- hydroscine butylbromide for cramps (antispasmodic)

Cognitive Behavioural Therapy (CBT) and antidepressants are also an option to help patients psychologically manage the condition and reduce distress associated with symptoms.

19
Q

Pathophysiology of coeliac disease.

A

Immunological exposure to gliadin component of gluten triggers an autoimmune inflammation within the small bowel, particularly the jejenum.

Inflammation causes atrophy of the intestinal villi, resulting in malabsorption of nutrients and the development of symptoms.

20
Q

Presentation of coeliac disease.

A

Coeliac disease if often asymptomatic, so requires a low threshold for diagnosis.

  • diarrhoea
  • fatigue
  • weight loss
  • mouth ulcers
  • anaemia (iron deficiency, B12 deficiency)
  • dermatitis herpetiformis (itchy, blistering skin rash on abdomen)
21
Q

Give the genetic associations for coeliac disease.

A

HLA-DQ2 gene (90%

HLA-DQ8 gene

22
Q

Which autoantibodies are associated with coeliac disease?

A
  • anti-TTG (IgA)
  • anti-EMAs (IgA)
  • anti-DGPs

NB: Anti-TTG and anti-EMA antibodies are IgA. Some patients have an IgA deficiency. When you test for these antibodies, it is important to test for total Immunoglobulin A levels because if total IgA is low because they have an IgA deficiency, then the coeliac test will be negative even when they have coeliacs. In this circumstance, you can test for the IgG version of anti-TTG or anti-EMA antibodies or simply do an endoscopy with biopsies.

23
Q

How is coeliac disease diagnosed?

A
  • raised anti-TTG
  • raised anti-EMA
  • IgA to exclude IgA deficiency

Endoscopy and intestinal biopsy show:
- crypt hypertrophy
- villous atrophy

24
Q

Coeliac disease is associated with which other autoimmune conditions?

A
  • T1DM
  • thyroid disease
  • autoimmune hepatitis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis
25
Q

Complications of untreated coeliac disease?

A
  • vitamin deficiency
  • anaemia
  • osteoporosis
  • small bowel adenocarcinoma
  • small bowel lymphoma
26
Q

How is coeliac disease treated?

A

Lifelong gluten free diet (e.g. avoid wheat, barley, oats) is curative.

Relapse will occur on consuming gluten again.

Checking anti-TTG and anti-EMA can be helpful in monitoring the disease.

27
Q

What is dysphagia?

A

Difficulty swallowing

28
Q

What is oesophageal dysphagia, and what does it indicate?

A

Patient are able to get the food to leave the mouth, then it gets stuck, indicating a problem with the oeseophageal phase of swallowing.

This is due to either physical obstruction (e.g. tumour, stricture) or neuromuscular problems (e.g. achalasia, dysmotility).

29
Q

What is oro-pharyngeal dysphagia, and what does it indicate?

A

Patients struggle to get the food to leave the mouth, indicating a problem with the oro-pharyngeal phase of swallowing.

This is due to problems coordinating the muscles that move the bolus to the back of the mouth, for example in neurological disease subsequent to a stroke.

30
Q

What is gastro-oeseophageal reflux disease (GORD)?

A

Acid from the stomach refluxes through the lower oesophageal sphincter into the oesophagus, irritating the lining.

31
Q

Presentation of GORD.

A
  • heartburn
  • acid regurgitation
  • retrosternal or epigastric pain
  • bloating
  • nocturnal cough
  • hoarse voice
32
Q

What are the red flag symptoms that warrant urgent referral for endoscopy?

A
  • dysphagia at any age
  • aged over 55
  • weight loss
  • upper abdominal pain / reflux
  • treatment resistant dyspepsia
  • nausea and vomiting
  • anaemia
  • thrombophilia
33
Q

What lifestyle advice can be given to help manage the symptoms of GORD?

A
  • reduce caffeine and alcohol intake
  • weight loss
  • avoid smoking
  • smaller, lighter meals
  • stay upright after meals
34
Q

How is GORD medically managed?

A

Acid neutralising medication prn. (e.g. Gaviscon or Rennie)

Proton pump inhibitors (e.g. omeprazole, lansoprazole)

H2 receptor antagonist (e.g. ranitidine) is alternative to PPI.

35
Q

How is GORD surgically managed?

A

Surgery for reflux is called laparoscopic fundoplication.

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

36
Q

What is Helicobacter pylori?

A

A gram negative aerobic bacteria, which lives in the stomach and causes damage to the epithelial lining, resulting in gastritis, ulcers and increasing the risk of stomach adenocarcinoma.

37
Q

Describe the virulence of H. pylori.

A

H-pylori is able to force its way into the gastric mucosa, causing breaks and exposing the epithelial cells underneath to acid.

H. pylori also produces ammonia to neutralise stomach acid, and also directly damages epithelial cells.

38
Q

How is H. pylori tested for?

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.

  • 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.

39
Q

How is H. pylori eradicated?

A

Triple therapy:

  1. PPI (e.g. omeprazole)
  2. Amoxcillin (1/52)
  3. Clarithromycin (1/52)

The urea breath test can be used to confirm eradication after treatment, however is not routine.

40
Q

Pathophysiology of Barrets oeseophagus?

A

Constant reflux in the lower oesophageal epithelium causes metaplasia from squamous to columnar epithelium.

When this change happens people generally get an improvement of reflux symptoms, as columnar epithelial lining is more protected against stomach acid.

41
Q

What are the complications of Barrets oesopagus?

A

Considered a premalignant condition, with a large number of patients going on to develop adenocarcinoma of the oesophagus.

Patients are monitored for adenocarcinoma using regular endoscopy.

42
Q

Treatment of Barrets oeseophagus?

A

PPI (e.g. omeprazole).

Early evidence suggests treatment with regular aspirin can reduce the rate of adenocarcinoma developing, however unlicensed use.

Year 3 - Medicine (33 decks)

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