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Lower gastro-intestinal diseases > IBD: Aetiology, Epidemiology, Pathogenesis and Immunology > Flashcards

IBD: Aetiology, Epidemiology, Pathogenesis and Immunology Flashcards

1
Q

Describe the type of conditions that are classified as Inflammatory Bowel Disease?

A

Inflammatory Bowel Disease encompasses two conditions Crohn’s and Ulcerative Colitis that are characterised by chronic inflammation of the gastrointestinal tract. Both conditions have periods of remission and relapse (flare ups). However even in remission there is an underlying inflammation.

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2
Q

How do extra-intestinal manifestations occur in IBD?

A

IBD is an auto-immune condition where there is over-activation of T cells, macrophages and a large inflammatory infiltration of pro-inflammatory cytokines. These immune cells can spill over into other tissues and into the blood, causing manifestations elsewhere.

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3
Q

Is there any overlap between Crohn’s and Colitis?

A

In 10-15% of IBD it is unable to categorise as one or the other.
This is known as IBD-U (unclassified)

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4
Q

What are the key differences between Crohn’s and Colitis in terms of the location of the inflammation?

A

Inflammation associated with Crohn’s disease can occur anywhere (and is often in patches) in the GI tract from the mouth to the anus.

Ulcerative colitis however only affects the large intestine and the rectum. The inflammation will begin at the rectum and work its way up into the large intestine and is continuous in nature.

Inflammation in Crohn’s disease is transmural meaning that it will penetrate through the layers in the GI wall, potentially causing fistulas whereas in Ulcerative colitis inflammation retained within the mucosal layer.

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5
Q

Compare the incidence of cases of Crohn’s and UC.

A

Crohn’s disease: 5-10 cases per 100,000 of the population

Ulcerative Colitis; 10-20 cases per 100,000 of the population

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6
Q

Compare the prevalence of cases of Crohn’s and UC.

A

Crohn’s disease: 50-100 cases per 100,000 of the population

Ulcerative Colitis: 100-200 cases per 100,000 of the population

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7
Q

Compare the age and gender susceptibility for Crohn’s and UC.

A

Crohn’s disease: More common in females (1:1.2) Mean age of onset: 26 years

Ulcerative colitis: More common in males (1.2:1) Mean age of onset: 34 years

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8
Q

Between what ages is most likely for IBD onset?

A

15-40 years

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9
Q

How many patients with IBD are diagnosed before the age of 21?

A

1/3

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10
Q

How many patients with IBD are diagnosed after 60?

A

15%

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11
Q

When is the second reported incidence peak of IBD?

A

Between 60-69 years

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12
Q

How many people are living with IBD worldwide?

A

6.8 million

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13
Q

How many people are living with IBD in the UK?

A

300,000-500,000 people
(roughly 1/250 people)

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14
Q

Which countries have the highest prevalence of IBD?

A

North America and Western Europe where up to 0.5% of the populations are affected.

Overall prevalence is higher in industrialised countries.

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15
Q

Why is the prevalence of IBD remaining high even when the incidence is reducing?

A

Patients have improved disease outcomes and are now living longer with the condition due to better control of IBD due to medication and monitoring advancements.

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16
Q

When is poor outcomes associated with UC?

A

Although 90% of patients with UC will relapse after their first episode, if there is early relapse or active disease in the first two years following diagnosis of UC, this is associated with poor outcomes.

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17
Q

What is the aetiology of IBD?

A

Genetic predisposition- some individuals are more susceptible to the development of IBD. It is still being researched whether environmental factors such as smoking, diet, infection and drugs actually cause the disease or just exacerbate the symptoms.

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18
Q

What is the link between diet and IBD?

A

There have been some studies to suggest that the Westernised diet can cause IBD. This can include:
Fat intake
Fast food ingestion
Milk and fibre consumption
Total protein and energy intake
Refined carbohydrates

However this evidence is inconclusive and it is more likely that these foods exacerbate the symptoms

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19
Q

Why is a high fibre diet not recommended in relapse of IBD?

A

When there is inflammation such as in IBD, this causes narrowing, making a high fibre meal difficult to process

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20
Q

What are some foods that patients may recognise as the cause of exacerbating symptoms during a flare?

A

Dairy based products
Fried foods
Spicy foods
Caffeine and alcohol

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21
Q

How does dairy based products worsen IBD symptoms?

A

During inflammation the lactase enzyme does not work properly and meaning that dairy based foods cannot be broken down and digested properly leading to diarrhoea.

22
Q

What is the relationship between Crohn’s disease and smoking?

A

People who smoke are twice as likely to develop CD than non-smokers.
40% of people who have Crohn’s disease are smokers.

23
Q

What is the relationship between UC disease and smoking?

A

UC is more common in non-smokers and those who have recently quit,
particularly within the first 2–5 years following cessation. There has been some evidence to suggest that in UC the nicotine found in cigarettes can have a protective effect (nitric oxide acting on smooth muscle) and delay the onset of UC.

24
Q

What is the appropriate management for a smoker with UC?

A

Encourage smoking cessation due to the widespread health benefits but do inform the patient that they may experience an increased number of flares after quitting.

25
Q

What infection is linked to Crohn’s disease?

A

Mycobacterium paratuberculosis
This is the bacterium that causes TB, but we can become exposed to it due to unpasteurised milk etc.
It is more likely that exposure to this bacterium is a secondary cause rather than a primary one.

26
Q

What infection is linked to UC?

A

Can occur after episode of infective diarrhoea (but no particular agent).

Most likely a genetic basis and then the bacterium triggers it.

MMR can be linked to IBD also.

27
Q

What is the link between enteric microflora and IBD?

A

In IBD, where is a inflammatory infiltration this causes tissue disruption and the body begins to lose tolerance to the microflora within the gut.
Therefore it is questioned where probiotics might be beneficial in IBD.

28
Q

What are prebiotics?

A

Non-absorbable sugars that work their way through the gut, good bacteria in the gut metabolise these prebiotics and provide this good bacterium with food.

29
Q

Which drugs are known to exacerbate/worsen IBD?

A

NSAIDs - exacerbate due to inhibiting production of cytoprotective prostaglandins,

Antibiotics - alter the enteric microflora

Contraceptive pill - increase in risk of development due to vascular changes

Isotrenoin- possible risk factor

30
Q

What is the relationship between appendectomy and IBD?

A

Having your appendix out is known to have a protective effect in IBD.

31
Q

What is the relationship between stress and IBD?

A

It has been suggested that there is an association between major life stressors, anxiety and depression and increased risk of IBD. It is thought that stress activates
inflammatory mediators at enteric nerve endings in the gut wall.
In those with established IBD it is believed that anxiety and depression leads to poor outcomes and increased risk of relapse, surgery, hospitalisation.

32
Q

How do genes affect the development of IBD?

A

Genes which correlate to the:
-Disruption of the epithelial barrier integrity (allowing the infiltration of immune cells)

-Deficits in autophagy (cell death, leading to tissue destruction, important in wound healing and resolving inflammation)

-Deficiencies in innate pattern recognition receptors

-Problems with lymphocyte differentiation, especially in Crohn’s disease

33
Q

If you had a microscope to assess the inflammation in IBD, what would you see?

A

Area of non specific granulomas inflammation, pro-inflammatory cells stuck there unable to get rid of whatever is causing the inflammation.
The inflammation is transmural and inflammatory cells such as lymphocytes and plasma cells are seen throughout.

34
Q

What are some of the specific genes linked to the development of IBD?

A

Mutations of the gene CARD15/NOD2 located on chromosome16

The genes OCTNI on chromosome 5 and DLG5 on chromosome10 have also been linked to Crohn’s disease

35
Q

What auto-antibody is present in UC patients?

A

70% of UC patients have the anti-neutrophil cytoplasmic antibodies (antibodies to the cytoplasmic neutrophils)

36
Q

What other auto-immune conditions is IBD linked to?

A

Ankylosing spondylitis, both have HLA-B27 present

37
Q

What races are at an increased risk of IBD?

A

Jewish people have an increased risk of IBD; this is higher among Ashkenazi, American
and European populations compared to those living in Israel.

This confirms that there is a genetic link in IBD, as these people tend to marry within their population and hence have a smaller gene pool.

38
Q

Which ethnicities have lower prevalence of IBD?

A

Prevalence among individuals of African American or Hispanic ethnicity appear to have a lower incidence of IBD than white populations.

39
Q

What is the familial factor rate for IBD?

A

– First-degree relatives of those with IBD have up to 20-fold increase in developing the disease
– 15-fold greater concordance for IBD in identical twins than non-identical twins

40
Q

In regards to the pathophysiology of IBD, what does the excessive inflammation cause?

A

Causes change and remodelling of the gut wall, leading to the destruction of the mucosal cell barrier and infiltration of immune cells (pain, swelling, redness).

41
Q

What are the main immune cells you would expect to find in IBD? What is their role?

A

Macrophages, Lymphocytes, Monocytes. These cells release a lot of pro-inflammatory mediators.

42
Q

What happens with T-regs in IBD?

A

They do not work properly

43
Q

What happens to T cells in Crohn’s disease?

A

They become resistant to apoptosis

44
Q

Describe the areas of inflammation in Crohn’s disease.

A

The affected areas become thickened, oedematous and narrowed (problems for faeces and food to pass through).

45
Q

What are some of the complications of the inflammation in Crohn’s disease?

A

-Archaeological changes in the formation of fissures (crevices) which have a cobblestone appearance.
-Deep ulcers
-Fibrosis (fibroblasts and growth factors)
-Strictures (narrowing)
-Bowel obstruction
-Abscesses
-Perforation

46
Q

Is Crohn’s disease Th1 or Th2 mediated?

A

Th1

47
Q

Is UC Th1 or Th2 mediated?

A

Th2 (IL4,5,6 and 10)

48
Q

At diagnosis which type of colitis are patients diagnosed with?

A

40% proctitis
40% sigmoid and descending colon
20% whole colon

49
Q

What are some of the complications associated with UC inflammation?

A

Crypt abscesses
Mucosal ulceration
Pseudopolyps

50
Q

How would the mucosa look in UC if it was examined under a microscope?

A

Red, inflammed and bleeding easily
Dysplasia can be seen
Inflammatory cells infiltrate the lamina propria and crypts

Lower gastro-intestinal diseases (15 decks)

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