CCP 63: Change in bowel habit

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CCP 63: Change in bowel habit
Structure and function of the small intestine
The small bowel is the main site for digestion and absorption. 3 parts with distinctive
histological appearance:
 Duodenum – C-shaped around pancreas and is retroperitoneal therefore less
mobile. Contains submucosal Brunner’s glands
 Jejunum – numerous plicae circulares and villi and diffuse lymphoid tissue
 Ileum – Less vascular with thinner walls, and more Peyer’s patchs and MALT
Jejunum and ileum held by mesentry therefore mobile
Goblet cells become increasingly common from D to I as does bacterial flora
The mucosa of the small intestine is designed for absorption with a huge surface area
provided by plicae circulares (circular folds), villi (broad in D, leaf-life in J and
finger-like in I) which contain enterocytes with microvilli. Enterocytes have a very
high turnover and are replaced by stem cells in the crypts of Lieberkuhn
The submucosa contains Meissner’s plexus, MALT and vessels
The muscularis externa has an inner circular layer and outer longitudinal layer with
Auerbach’s plexus in between
Finally the outer layer is the serosa
Blood supply to the proximal ½ of duodenum is via the celiac trunk (foregut) whilst
the rest of the small intestine is via the superior mesenteric artery (mid-gut) which
leaves the abdominal aorta at the level of L1
Venous drainage is via the superior mesenteric vein to the portal vein to the liver
The small intestine completes digestion with enzymes and hormones:
 Carbohydrate – pancreatic amylase
 Protein – pancreatic protease
 Fat – bile acids
 Vitamins A, D, E and K with fat, others e.g. B12 with intrinsic factor
 Water – more in the jejunum
 Sodium, potassium, calcium and iron
Motility is maintained by segmentation (mix chyme together) and peristalsis (move
towards large bowel)
Structure and function of the large intestine
Role is to concentrate faeces by absorbing water, and then expel them out of the anus.
It is gathered into a series of pouch-like folds called haustrations which are
differentiated from s. intestine on x-ray because they do not extend across the entire
width of the large intestine.
Tissue layers are the same as the small intestine but woth thicker muscle walls and
larger lumens, as well as taeniae coli (bands of longitudinal muscle)
The large intestine contains no villi or plicae circulares
Contains:
 Caecum and appendix
 Ascending, transverse and descending colon
 Sigmoid colon – highly mobile therefore most prone to volvulus and also has
the weakest walls with high pressure therefore prone to perforation
 Rectum
 Anus
Blood supply is from the superior mesenteric atery (mid-gut) up until the distal 1/3 of
the transverse colon which is supplied by the inferior mesenteric artery (hind-gut)
The large intestine flora contains many species of bacteria which defend against
pathogenic bacteria, a process easily disrupted by administering antibiotics. The flora
also convert conjugated bilirubin to urobilinogen and then to stercobilinogen to be
excreted in the faeces
Colonic mucosa contains many goblet cells which secrete mucus to lubricate the
colon and therefore prevent trauma.
Motility of the large intestine occurs via segmentation and peristalsis and is controlled
by sympathetic (decreased motility) and parasympathetic (increased motility) activity
Index conditions
Colorectal carcinoma
The second most common cancer in the UK, and more common in the western world
due to diet high in animal fat and low in fibre leading to slow transit time in the
intestine.
Risk factors include familial polyposis coli and inflammatory bowel disease
The cancer is caused by a series of genetic mutations including the APC tumoursuppressor gene on chromo 5, K-ras and p53.
Classified using the Duke’s classification:
 A – confined to bowel wall
 B – Extends through muscularis propria but not lymph nodes
 C1 – All layers affected including proximal lymph nodes
 C2 - Higher lymph nodes affected
Histologically, signet ring cells are also seen due to excess mucin production
Hereditary non-polyposis colorectal cancer (HNPCC) is an AD condition where the
cancer develops from flat adenomas – occur by age of 40
Symptoms of large bowel cancer
 Altered bowel habit with loose bowel motions the most common
 Anaemia, weight loss, abdo pain
 Left-sided lesions (i.e. rectosigmoid) rectal bleeding/obstruction
Investigations:
 FBC for anaemia
 Faecal occult blood
 Barium enema and flexible sigmoidoscopy
Management
 Surgical resection with end-to-end anastomosis
 Dukes B and C – chemotherapy and/or radiotherapy
Screening – for those aged 60 – 74, faecal occult blood test every 2 years and positive
results are referred to colonoscopy
Inflammatory Bowel Disease
Inflammatory response to environmental conditions, usually in genetically
predisposed individuals
Increased risk of colonic cancer
Ulcerative Colitis
Limited to colon
Bloody diarrhoea, Colicky abdo pain, urgency, tenesmus
Extra-intestinal manifestations:
 Eyes – uveitis, conjunctivitis, episcleritis
 Bile buct – sclerosing cholangitis
 Bones – ankylosing spondylitis
 Joints – Seronegative arthritis
 Skin – Erythema nodulosum, pyoderma gangrenosum
Investigation – endoscopy with mucosal biopsy:
 Superficial, continuous ulceration
 Crypt abscesses
 Barium enema – ‘lead-pipe’ colon
IBD is a relapsing-remitting disease – flares are often caused by environmental factors
which may cause inflammatory response to bowel flora. Non-smoking, NSAIDs and
stress are causes
The most worrying complication is toxic megacolon – severe inflammation involves
the smooth muscle leading to paralysis and dilatation of more than 5cm on x-ray
Management – the aims of management is induction and maintenance of remission:
 Corticosteroids during flares e.g. oral pred 40mg per day
 If ineffective – use azathioprine
 Mesalazine – maintain remission
If UC is affecting QoL or not responding to treatment, colectomy is indicated
Crohn’s Disease
Involves anywhere from mouth to anus, most commonly terminal ileum and proximal
bowel
Abdo pain and weight loss, but may cause colonic symptoms
Extra-intestinal manifestations
Investigation – CRP correlates to disease activity. Endoscopy and biopsy:
 Patchy transmural ulceration and skip lesions
 Granulomas
Complications include strictures, abscesses and fistulae.
Crohn’s has a stronger genetic component than UC and is more common in smokers
Management – colonic disease management is the same as for UC
 Bowel resection for strictures
Toddler’s diarrhoea
Persistent loose stools in a well, thriving child
Caused by a delay in intestinal motility with intermittent, explosive ‘carrots and peas’
diarrhoea
The diarrhoea will ease with age or from addressing the diet of the child
Irritable Bowel Syndrome
Can be diarrhoea or constipation – predominant, or present as a mixed picture.
Typically presents in women aged 20-40
Symptoms
 RIF abdo pain – relieved by defecation/flatus
 Abdo distension and feeling of ‘bloating’
 Anxiety/depression
Diagnosis is clinical, and management involves reassurance (that the disease will not
progress to a more serious condition) and lifestyle advice
Bacterial infection is the most common cause of diarrhoea worldwide – especially
travellers! Usually spreads faecal-oral route and contaminated food.
Symptoms are diarrhoea, abdo pain and fever/vomiting
Investigations – FBC may show leucocytosis. Stool culture.
Common pathogens are E. coli, shigella and salmonella
Management is with rehydration and appropriate antibiotics
C.difficile is responsible for outbreaks on hospitals, particularly after antibiotic
treatment and in elderly – treated with metronidazole or vancomycin
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