Lecture 31 Flashcards

1
Q

How are functional gut disorders defined?

A

Constellation of symptoms but without overt pathology. There is not structural or tissue abnormality.

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2
Q

What causes functional gut disorders?

A

Due to disturbed function:

1) Disturbed motility.
2) Visceral hypersensitivity.
3) Brain-gut dysfunction.
4) Psychosocial factors.

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3
Q

Why is there not a specific diagnostic test for functional gut disorders?

A

Due to there being no overt pathology, there is no diagnostic test. There’s no biochemical abnormality with conventional testing, no histological or radiological features.

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4
Q

What can functional gut disorders affect?

A

Any part of the gut: oesophagus, stomach, SI and LI.

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5
Q

What are examples oesophagus GI disorders?

A

1) Globus - sensation of lump stuck in the throat.

2) Functional heartburn - symptoms of reflux without evidence of GORD or a motility disorder.

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6
Q

What are examples of stomach GI disorders?

A

1) Functional dyspepsia - upper abdomen pain or discomfort without structural abnormality e.g. no ulcer, pancreas or gallbladder pathology.
2) Functional vomiting/cyclical vomiting syndrome - recurrent vomiting; no diagnostic abnormalities and no psychiatric cause.

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7
Q

What are examples of bowel GI disorders?

A

1) Irritable bowel syndrome - abdominal discomfort/bloating associated with defaection and altered bowel habit i.e. constipation/diarrhoea or both.
2) Functional abdominal pain - recurrent or continuous abdominal pain unrelated to defaecation and without disturbed bowel habit; no diagnostic abnormalities.

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8
Q

How can you diagnose functional GI disorder?

A

1) Symptom complex - analogous to diagnosis of migraine.
2) Symptoms of functional gut disorders can be similar to those with serious pathology.
3) Diagnosis of functional gut disorders is a “diagnosis exclusion”.
4) Always consider other GI diagnoses first before making a diagnosis of functional gut disorder.

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9
Q

What is irritable bowel syndrome characterised by?

A

Swinging bowel habit - from constipation to diarrhoea.

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10
Q

What are the symptoms of irritable bowel syndrome?

A

1) Swinging bowel habit.
2) Abdominal pain, which is relieved with defaection.
3) Associated symptoms:
- urgency (incomplete evacuation),
- passage of mucus,
- abdominal bloating and
- excess flatus.

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11
Q

When can irritable bowel syndrome occur?

A

May occur after gastroenteritis (post-infective IBS). Usually people who don’t have a history of IBS.

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12
Q

What is the Rome III criteria for IBS?

A

IBS is a functional disorder characterised by abdominal pain or discomfort and changes in still frequency or consistency.

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13
Q

Describe further the Rome III criteria for IBS?

A

1) At least 3 days per month in the last three months.
2) Onset of symptoms at least 6 months prior to diagnosis.
3) Must be associated with 2 or 3 of the following:
- improves with defecation.
- Onset of pain coincides with changes in stool frequency.
- Onset of symptoms is accompanied by changes in the form or appearance of the stool.

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14
Q

What are the associated symptoms of IBS?

A

1) Fatigue.
2) Other functional GI symptoms:
- functional dyspepsia.
- Early satiety, post-prandial fullness.
- Nausea, vomiting.
3) Backache, headache.
4) Urinary symptoms.
5) Dysmenorrhea, dyspareunia.
6) Palpitations.
7) Poor sleep quality.

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15
Q

What are symptoms that can alert to other possible pathologies?

A

1) Older patient (over 50, even 40+).
2) Short history.
3) Nocturnal diarrhoea/nocturnal pain.
4) Rectal bleeding.
5) Anaemia or iron deficiency.
6) Weight loss.
7) Vomiting.
8) Family history of colon cancer.

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16
Q

How common is IBS?

A

5-12% men.
5-18% women.
But if not strictly based on criteria, more common than this.
It is early onset - early 20-30s.

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17
Q

Describe altered gut motility in IBS?

A

1) Frequency and duration of contractions are either long or short depending on constipation or diarrhoea.
2) Transit time (time for food to meet back passage) is increased or reduced depending on constipation or diarrhoea.
3) Exaggerated response to meal ingestion/stress. Need to go to the toilet.
Simple terms - Exaggerated with diarrhoea, reduced with constipation.

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18
Q

Describe visceral hypersensitivity?

A

1) Balloon distension of colon causes pain in 50-60% of IBS patients compared with 10% of controls. IBS recognise pain at lower threshold of distension compared to controls.
2) People with IBS describe distension as unpleasant or painful.

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19
Q

What is the mechanism of peripheral sensitisation in visceral hypersensitivity?

A

In patients with post-infective IBS, there may be a degree of sensitisation. There was an acute gastroenteritis, which causes inflammation, this will lead to up regulation of nociceptors. This will lead to increased sensitivity to painful stimuli and non-painful stimuli perceived as pain.

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20
Q

What is the mechanism of central sensitisation in visceral hypersensitivity?

A

Central sensitisation is where the pain may radiate beyond the gut e.g headaches.

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21
Q

Describe spinal cord - gate control theory?

A

Pain messages from the periphery and have to enter the spinal cord before entering the brain. Some people with IBS, at the level of spinal cord becomes altered. If the gate is open - reaches the brain. If the gate is closed it doesn’t reach the brain. People with IBS there may be an increased focus on unpleasant stimuli - due to brain focussing on processing pain stimuli.

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22
Q

What are the effect of stress on IBS.

A

The communication between the gut and brain is bi-directional (both ways). Brain can influence motor, sensory, secretory and immune functions of GI tract.

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23
Q

How do you treat IBS?

A

There are 4 types:

1) Conventional.
2) Dietary.
3) Natural.
4) Lifestyle.

24
Q

What is conventional treatment?

A

1) Fibre supplements - if they have constipation. May aggravate symptoms - bloating.
2) Laxatives for constipation - osmotic (preferred) and stimulant laxatives.
3) Anti-Motility drugs for bowel frequency - diarrhoea predominant IBS i.e. loperamide.
4) Low-dose tricyclic antidepressants - Works for neuropathic pain (blocks various neurotransmitters and receptors involved in pain perception) i.e. amitriptyline, nortriptyline.

25
Q

What is dietary management?

A

1) Based on concept of IBS as multiple food sensitivities - intolerance rather than allergy.
2) Diets based on food diaries of foods associated with symptoms.
3) 50-60% response rate - depends on enthusiasm of patient and dietician.
4) Food allergy not likely to have a role in IBS - skin tests and RAST tests do not seem to help.

26
Q

What is the basis of the FODMAP diet?

A

Identifies a number of saccharides fermented in the gut:

1) Oligosaccharides - fructose and galactose.
2) Disaccharides - lactose.
3) Monosaccharides - fructose.
4) Polyols - sorbitol and mannitol.

27
Q

What does the FODMAP diet do?

A

It identifies a number of saccharides that can cause intolerance and excessive fermentation. Shows people what they should avoid eating in IBS. Can exclude a lot of things that are commonly used in peoples diets.

28
Q

What are “natural” options for IBS?

A

Some evidence of benefit for probiotics in IBS. May be strain-dependent.

29
Q

What are other considerations to treat IBS?

A

1) Lifestyle advice:
- regular meals, particularly breakfast.
- Reduce stress levels.
- Adequate sleep.
2) Psychological therapies:
- Many approaches have been shown to be helpful.
- Cognitive behavioural therapy/hypnotherapy.

30
Q

When do symptoms of IBS tend to improve?

A

1) Confident diagnosis.
2) An understanding of the condition.
3) Insight into effect of stress and diet.
4) Been reassured by appropriate investigations.
5) A knowledge that symptoms may remain.
6) Been given encouragement to explore a range of strategies.

31
Q

What do you want to explain to and IBS patient?

A

1) Emphasise structural normality - absence of “disease”.
2) Discuss “over-active gut”.
3) Discuss “over-sensitive gut”: heightened awareness of gut activity and enhanced brain-gut axis.
4) May be a person who tends to express “stress” in bodily symptoms.

32
Q

What does inflammatory bowel disease cover?

A

Covers: Ulcerative colitis and crown’s disease.

Underlying genetic and environmental factors.

33
Q

Describe the genetics involved in IBD?

A

1) First degree relatives of IBD - 3-20x more likely to have IBD than general population.
2) Genetics may be more important in CD than UC.
3) Many genes are involved and not fully elucidate - NOD2 gene on chromosome 16.
4) Very uncommon in certain ethnic groups e.g. maori, pacific island.
5) Despite the role of genes, majority of IBD patients (85%) do not have a family history.

34
Q

Describe the environmental factors involved in IBD?

A

1) Common in western nations. There is improved living standards, so there is less exposure to enteric infections and less “tolerance” of the immune system.
2) Smoking increases risk of crown’s disease.
3) Smoking protective for UC: often develops within a year of stopping smoking. Restarting smoking can lead to a resolution of inflammation.

35
Q

Describe the pathophysiology of IBD?

A

Disruption of integrity of epithelial barrier. This will lead to innate and adaptive immune system becoming deregulated. This will lead to abnormal immune response and triggering of inflammation. Certain microbes in the gut may be pathogenic and imitate IBD.

36
Q

What is the pathology of ulcerative colitis (UC)?

A

1) The disease is limited to the colon.
2) Begins in the rectum and spreads proximally up the colon.
3) Mucosal inflammation - diffuse and granular.
4) No macroscopic ulceration except in severe disease.

37
Q

What is the histology of UC?

A

1) Mucosal inflammation only - chronic inflammatory infiltrate (plasma cells).
2) branching of the crypts and atrophy as well.
3) Neutrophils invade crypts “crypt abscess”.
4) Loss of goblet cells.
5) Paneth cell metaplasia - cells seen in areas which they’re not normally found in e.g. distal colon.

38
Q

What are the clinical features of UC?

A

1) Diarrhoea with blood.
2) Frequent bowel motions and urgency.
3) Abdominal discomfort.
4) Fever, malaise, weight loss (constitutional symptoms).

39
Q

What are the lab tests of UC?

A

1) Inflammation may result in:
- raised ESR/CRP, platelets, neutrophils.
- Mild anaemia.
- Raises ferritin.
2) Bleeding, if prolonged may result in:
- Iron deficiency - low ferritin/with or without anaemia.

40
Q

What is toxic megacolon?

A

Complication of severe UC. The inflammation is so severe that the colon doesn’t move and ends up atonic, and starts to dilate.

41
Q

What is the pathology of Crohn’s disease?

A

1) Occurs in any part of GI tract - ileum and colon.
2) “discontinuous inflammation” - the inflammation is in patches.
3) Transmural inflammation - Starts as small ulcers on the mucosa (pathos ulcers).
- Progress to deep penetrating ulcers with fissuring.
- Mucosa swollen cobblestone appearance.

42
Q

What is the histology of CD?

A

1) Transmural inflammation i.e. across the entire depth of the intestinal wall.
2) Non-Caveating/non-necrotising granulomas. There are other conditions that give granulomas i.e. sarcoidosis.

43
Q

What is a granuloma?

A

Area/nodule of inflammation made up of giant cells - a giant cell is formed by the fusion of epithelioid cells (activated macrophages).

44
Q

What are the clinical features of CD?

A

The presentation depends on part of GI tract involved and clinical sub-type:

1) inflammatory.
2) stricturing.
3) fistulising.
3) perianal.

45
Q

Describe the clinical features of inflammatory CD in the large bowel?

A

Colitis:

  • Similar symptoms to UC.
  • Diarrhoea with blood.
46
Q

Describe the clinical features of inflammatory CD in the small bowel?

A

Ileitis:

  • Abdominal pain.
  • Malabsorption - bile salt malabsorption -> water diarrhoea, steatorrhea.
47
Q

Describe the clinical features of inflammatory CD in the stomach/duodenum?

A

Gastritis/duodenitis:

-Dyspepsia.

48
Q

Describe the clinical features of stricturing CD?

A

Stricture can result in:
-Abdominal pain and distension (1 hour after eating).
-Vomiting.
-Bowel not opening.
Initially inflammatory i.e. due to oedema, over time becomes fibrotic i.e. due to scarring.

49
Q

Describe the clinical features of fistulising CD?

A

Fistula is an abnormal connection/tract between the gut and another organ.

1) Enterocutaneous fistula - SI and skin.
2) Enteroenteric fistula - SI and SI.
3) Enterocolic fistula - SI and colon.
4) Rectovaginal fistula - rectum and fistula.

50
Q

Describe clinical perianal CD?

A
  • Perianal abscess.
  • Perianal fistula.
  • Anal fissure.
51
Q

What are the lab tests in CD?

A

1) Inflammation may result in:
- Raised ESR/ECP, platelets, neutrophils.
- Mild anaemia.
- raised ferritin.
2) Bleeding, if prolonged, may result in:
- iron deficiency - low ferritin with or without anaemia.
3) Malabsorption from SI may result in:
- Iron deficiency.
- B12 deficiency.

52
Q

What are extra-intestinal manifestations of IBD?

A

Symptoms of the IBD, outside the gut e.g:

  • iritis
  • pyoderma gangrenosum.
  • erythema nodosum.
53
Q

How do you treat IBD?

A

1) 5-aminosalicylates (5-ASA). It has mild anti-inflammatory action.
2) Steroids.
3) Immunosuppression e.g. azathioprine, 6-mercaptopurine.
4) Biologics (anti-tumour necrosis factor) e.g. infliximab, adalimumab.

54
Q

What are the principles of surgery in regards to IBD?

A

Used when there is failure of medical treatment - resect diseased bowel e.g. colectomy.
In UC, colectomy is curative where as CD there is no cure.

55
Q

What are the complications that mean surgery needs to happen in patients with IBD?

A
  • Bowel obstruction.
  • Perforation.
  • Fistula.
  • Abscess.