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Epidemiology of Bowel Diseases

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Title: Epidemiology of Bowel Diseases


1
Epidemiology of Bowel Diseases
  • Melanie Shale
  • Physiology

2
Aim of the session
  • Understand the epidemiology, aetiology and
    pathophysiology of benign and malignant bowel
    disease
  • Constipation
  • Haemorrhoids
  • Diverticular disease
  • Ulcerative colitis
  • Polyps
  • Bowel cancer

3
What is epidemiology?
  • A study of the distribution and determinants of
    health related states and events in populations
    and the control of health problems the study of
    epidemic disease

4
What is Aetiology?
  • A branch of knowledge concerned with causes and
    origins of disease factors of causation or
    those associated with the causation of disease or
    abnormal body states

5
Constipation
  • What are the causes of constipation?
  • Not enough fibre in the diet.
  • Not enough liquids.
  • Lack of exercise.
  • Medications.
  • Irritable bowel syndrome.
  • Changes in life or routine such as pregnancy,
    older age,
  • and travel.
  • Abuse of laxatives.
  • Ignoring the urge to have a bowel movement.
  • Specific diseases such as multiple sclerosis and
    lupus.
  • Poor motility of the colon and rectum.
  • Muscle weakness or pain

6
To understand the physiology associated with
constipation and its consequences, we must review
the defaecation reflex
  • See slides 7 8

7
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8
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9
Haemorrhoids
  • A consequence of chronic constipation
  • Rather than the theory that piles were a form of
    varicose vein, a sliding theory has evolved.
  • The anal canal contains 3 fibro vascular
    cushions that appear in the right anterior,
    right posterior and left lateral positions.
  • They are suspended by a connective tissue
    framework derived from the internal anal
    sphincter and longitudinal muscle. Within each
    cushion is a venous plexus that allow for
    enlargement of the cushion.

10
Pathophysiology of haemorrhoids
  • Age and passing of hard stools (which produces a
    shear stress) results in fragmentation of anal
    tissue.
  • Fragmentation of the connective tissue supporting
    the cushions leads to their descent.
  • Straining increases the venous pressure and
    causes the veins to become engorged.
  • The prolapsed cushion has impaired venous return,
    which results in dilation of the plexus and
    venous stasis.
  • Inflammation occurs with erosion of the cushions
    epithelium, resulting in bleeding.

11
Laxatives?
12
An abdominal massage machine??
13
Treatment for constipation
  • BULK PRODUCERS (Fybogel, methylcellulose)
  • Hydroscopic and absorptive properties produce
    larger, softer stools often easier to pass.
  • OSMOTIC AGENTS (Lactulose)
  • Retain fluid in the bowel by creating osmotic
    gradients because they are poorly absorbed.
  • CHEMICAL STIMULANTS (Senna, picolax).
  • Mild gut stimulation / irritation increases
    motility.

14
Colorectal Cancer
  • A malignant neoplasm arising from the mucosa of
    the large intestine.
  • Colorectal cancer is the third most common
    malignancy in the developed world accounting
    for 20,000 deaths in the UK each year.
  • Colon cancer affects almost equal proportions of
    men and women, most commonly between the ages
    60-80.
  • Rectal cancer is more common in men?
  • The pathogenesis of colorectal cancer involves
    genetic and environmental factors, the most
    important being diet.

15
Causative factors
  • Genetic and environmental factors seem to promote
    mutations that most frequently cause the
    formation of adenomatous polyps.
  • Polyps commonly occur in the rectum and sigmoid,
    decreasing in frequency towards the caecum.
  • About 25 of patients with cancer of the large
    bowel have satellite adenomatous polyps.
  • Risk of malignancy seems to be related to size,
    becoming more invasive.
  • Inflammatory polyps occur in chronic ulcerative
    colitis and crohns disease of the colon.

16
Colonic polyp (sessile).
Histology demonstrated benign tubular adenoma.
17
Colonic polyp (pedunculated).
Histology demonstrated benign tubular adenoma.
18
How cancer develops
  • Believed to be as follows
  • 1) Exposure to the carcinogen
  • 2) Entry of the carcinogen into a cell
  • 3) Initiation
  • The carcinogen alters the cells genetic material
  • 4) Promotion.
  • Acceleration by other carcinogens (promoters)
  • The cell begins to multiply out of control
  • Disrupts normal body functions
  • 5)Progression metastasis / migration

19
Cancer and diet
  • Links have been established between colorectal
    cancer and..
  • Low fibre intake
  • High red and processed meat consumption
  • Charred / BBQ foods
  • High Iron intake (necessary for bacterial growth)
  • Low Ca intake (bind with bile acids could be
    mutogenic by inhibiting detoxification enzymes
    and increasing colon cell proliferation)
  • Low essential fatty acid intake anticancer
    properties
  • Low fruit and veg. intake antioxidant
    properties

20
Diverticular disease
  • Millions of people are estimated to have
    diverticular disease.
  • Symptoms of diverticulitis develop in only 1 in
    5people.
  • It is thought that lifestyle and dietary changes
    in the 20th century have contributed to its rise
    specifically fast paced living with convenience
    foods.
  • The disease is more common among lower income
    groups and may reflect awareness (lack of) of
    fibre.
  • Women have now overtaken men regarding incidence
    -dieting?
  • In countries where the diet is high in fibre and
    low in refined carbohydrates, diverticular
    disease is unknown.

21
Aetiology and geographical distribution
  • In high fibres diets, softer stools and greater
    gut motility mean the stool is evacuated more
    frequently.
  • Many researchers believe that a high intake of
    fibre is also the primary reason for low rates of
    colorectal cancer.
  • In the northern European continents, 30 of
    people aged 60 and over have diverticular
    disease.
  • With individuals living longer, diverticular
    disease is increasing, possibly due to age
    associated colonic weakening.
  • Nearly 2/3 of people will have diverticular
    disease by 80yrs of age.

22
Physiology of Diverticular Disease
  • The development of diverticular is not fully
    understood but it believed to be related to
    segmental spasm of the bowel muscle.
  • The resulting increase in pressure causes mucosal
    extrusion at the weakest points in the colon wall
    next to the intramural blood vessels that
    extend into the submucosa.
  • Muscular hypertrophy is also a common finding in
    the sigmoid, probably to compensate for these
    pressure increases.

23
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25
Openings in the mucosa(green arrows) are the
mouths of diverticuli A smooth elevated
polypoid projection(black triangles) represents
an adenomatous polyp Presence or absence of
malignancy can not be established based on the
gross appearance of this lesion although its
modest size favours a benign lesion
26
Diverticular theories
  • Colonic diverticular occur more frequently in
    Western countries and therefore are caused by the
    highly western refined diet that is deficient in
    dietary fibre.
  • This results in decreased faecal bulk, narrowing
    of the colon and increased intraluminal pressure
    for moving smaller faecal mass.
  • Faecal impaction occurs in the sacs resulting in
    secondary erosion and inflammation and
    diverticulitis can follow.

27
Diverticulitis
  • The cause the inflammation in and around a
    diverticulum is probably mechanical.
  • The stagnation of non-sterile faecal material may
    compromise the blood supply to the thin-walled
    sac and render it susceptible to invasion by
    colonic bacteria, causing inflammatory erosion of
    the mucosal lining.
  • This sequence of events can result in perforation
    into the colonic wall, forming an intramural
    abscess.
  • This increases the likelihood of bowel
    obstruction and peritonitis.

28
Ulcerative Colitis
  • Evidence suggests a genetic predisposition leads
    to an unregulated intestinal immune response to
    environmental, dietary or infectious agent.
  • However, no inciting antigen has been identified.
  • Unlike Crohns disease, current cigarette smoking
    appears to decrease the risk? mechanism not
    known
  • Like Crohns, UC may affect people at any age,
    but the age-onset curve peaks at ages 15-30 and
    50-70yrs.
  • Men and women are equally affected.

29
Pathophysiology of U.C.
  • Changes begin with degeneration of reticulin
    fibres beneath the mucosal epithelium, occlusion
    of subepithelial capillaries and progressive
    infiltration of the lamina propria with plasma
    cells, eosinophils, lymphocvytes, mast cells and
    PMNs.
  • Disease usually begins in the rectosigmoid and
    may extend along the entire colon.

30
Immunological aspects
  • Current interests lie on defects in the mucosal
    gel barrier.
  • The existence of true autoimmunity is uncertain
    and the evidence is conflicting.
  • However, there is perhaps an imbalance between T
    lymphocyte subsets that are responsible for
    secreting pro-inflammatory chemical mediators.

31
Inflammation
  • T cell lymphocytes are normally activated in
    response to an antigen and are normally found in
    the gut wall.
  • In inflammatory bowel disease, the normal
    regulation of their activity is disturbed.
  • Activation of mucosal inflammatory cells also
    leads to the production of inflammatory
    mediators.
  • Prostaglandins, leukotrienes, interferons and
    cytokines are partly responsible for the tissue
    damage observed.
  • For some of these mediators, suppression leads to
    activation of alternative pathways, which allow
    inflammation to continue.

32
U.C. quiescent stage. The quiescent stage shows
evidence of previous damage with short deformed
crypts, loss of crypts but no evidence of an
active inflammatory process. The markedly thick
muscularis mucosa (arrow) is often seen in U.C.
33
Crohns Disease
  • Chronic inflammation of the ileum, ileo-caecal
    region or colon that can spread through the bowel
    wall to neighbouring structures.
  • Tending to affect young people between ages 20
    and 40yrs, it is most common in North America and
    Northern Europe (40 per 100,000 population)
  • Studies have shown that 12-18 of patients with
    Crohns disease have at least one family member
    affected.

34
Causes of Crohns disease
  • The mode of inheritance is complex but it is
    likely that several genes are involved.
  • Susceptibility loci for the disease have been
    reported recently on chromosomes 16, 3, 7 and 12,
    the latter three being shared with ulcerative
    colitis.
  • Several environmental factors have also been
    implicated in addition to claims for initiating
    roles for gut flora, food constituents or
    specific infections (TB).

35
Environmental factors
  • Diet
  • The possible role of diet has been examined with
    particular interest in milk, fibre and sugar.
  • Anecdotally, it has been suggested that some
    patients symptoms improve when avoiding dairy
    products.
  • Infective agents
  • There could be an infective cause for Crohns
    Mycobacterium paratuberculosis and the measles
    virus have aroused considerable interest but no
    definitive relationships have been established
    yet.

36
More environmental factors
  • Smoking
  • Crohns is 2-4 times more common in smokers, this
    being a significant factor in the aetiology of
    the disease.
  • The mechanism however is not known.
  • Stress
  • The effect of stress in causing relapses in IBD
    is controversial but some studies have
    demonstrated an increased risk of symptom
    exacerbation following stressful events (divorce,
    death)

37
Pathophysiology
  • Whatever the initiating factors in Crohns
    disease, there is excessive activation of mucosal
    T cells, leading to trans mural inflammation.
  • This again, is amplified and perpetuated by the
    release of pro-inflammatory soluble mediators
    (see next slide).
  • The knowledge of this inflammatory response
    however, has improved our understanding of the
    possible modes of action of conventional
    treatments and has led to the development of new
    anti-inflammatory agents aimed at specific
    pathophysiological targets.

38
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39
Crohns Linear Longitudinal ulcers(black arrows)
Areas of normal mucosa are seen(green arrow)
40
Crohn's ileitis.
Cobblestone appearance caused by inflammation
deep into bowel wall with muscosal oedema.
41
DIFFERENTIATING BETWEENCROHN'S DISEASE AND
ULCERATIVE COLITIS                              
                                                  
     
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