Pathology of the Small Bowel Flashcards
How is the small intestine folded?
Surface is folded into villi to increase surface area and then into microvilli to further increase this
Also, the plicae circulares extend around the entire circumference of the SI
Describe this picture of small bowel
ADD PICTURE 1
Normal small bowel has villi lined by enterocytes and this forms the brush border, which is microvilli covered
Blood supply to the small bowel?
Superior mesenteric artery
2 main causes of ischaemia of the small bowel?
- Mesenteric arterial occlusion, due to:
Mesenteric artery atherosclerosis
Thromboemolism from the heart, e.g: in AF - Non-occlusive perfusion insufficiency, due to:
Shock
Strangulation obstructing the venous return, e.g: due to a hernia or adhesion
Certain drugs, e.g: cocaine, can cause spasm of the superior mesenteric artery
How does bowel ischaemia usually present?
Usually acute but it can be chronic
Which part of the small bowel wall is most sensitive to hypoxia?
Mucosa is the most metabolically active part of the small bowel and thus the most sensitive to the effect of hypoxia
Pathogenesis of small bowel ischaemia, in relation to duration of hypoxia?
Longer the period of hypoxia, the greater the depth of the damage to the bowel wall and so there is a greater likelihood of complications; the mucosa can regenerate if the obstruction is removed but smooth muscle cannot
So, if hypoxia lasts a long time, mucosa will no longer be able to regenerate
How is acute ischaemia classified?
According to the degree of infarction caused, which depends on the length of time of the ischaemia :
Mucosal infarct
Mural infarct
Transmural infarct (gangrene)
Progression from mucosal infarct increases chance of a poorer outcome:
Regeneration
Stricture
Gangrene
Describe the outcome of a mucosal infarct
Regeneration with mucosal integrity being restored
Describe the outcome of a mural infarct
Repair and regeneration, with a fibrous structure forming
Describe the outcome of a transmural infarct
Gangrenic death and perforation, if not resected
What type of necrosis is seen in infarctions?
Coagulative necrosis
Outcomes/complications of ischaemia of the small bowel?
Resolution
Fibrosis, stricture and obstruction Chronic ischaemia (assoc. with widespread atherosclerosis and presents as a "mesenteric angina")
Gangrene, perforation, peritonitis, sepsis and death
What is mesenteric angina?
Presents with post-prandial abdominal pain
What is Meckel’s diverticulum?
Result of incomplete regression of the vitello-intestinal duct; so, there is an embryological remnant attached to the wall of the distal ileum
Problems associated with Meckel’s diverticulum?
The diverticulum may become inflamed and the symptoms mimic that of appendicitis
It often contains heterotopic gastric mucosa and this may lead to local ileal peptic ulceration
It is commonly asymptomatic and an incidental finding
Types of small bowel tumours and occurence?
Primary tumours are rare
Secondary tumours (metastases) are much more common, e.g: from the ovary, colon, stomach
What are the types of primary tumours?
Lymphomas
Carcinoid tumours
Carcinomas
Types of lymphomas of the small bowel?
They are rare and all are non-Hodgkins in type:
Maltomas (B-cell origin) are the most common
Enteropathy associated T-cell lymphomas (assoc. with coeliac disease)
Describe carcinoid tumours of the small bowel
Rare but the commonest site is the appendix; they produce hormone-like substances
They are small, yellow and slow-growing tumours that are locally invasive
Complications of carcinoid tumours of the small bowel?
Can cause obstruction and intussusception (inversion of a part of the intestine)
If metastases to the liver occur, a carcinoid syndrome occurs resulting in flushing and diarrhoea
Describe carcinoma of the small bowel
Rare but is assoc. with Crohn’s disease and coeliac disease; it is identical to colorectal carcinoma in appearance
Presents late and can metastasise to lymph nodes and to the liver
The most common site of adenomatus lesions is at the ampulla of Vater; this can progress to adenocarcinoma and is more common in patients with FAP
Presentation of appendicitis?
Common cause of an acute abdomen and is associated with vomiting, abdominal pain (umbilical initially and then right iliac fossa tenderness) and increased white cell count
It is more common in children but can occur in adults
Causes of acute appendicitis?
Unknown
Faecoliths (hardening of faeces, which can occur in dehydration)
Parasites, e.g: enterobius vermicularis worms
Tumours (rare)
What is the pathology of acute appendicitis?
- Mucosal ulceration, due to increased intra-luminal pressure
- An inflammatory infiltrate invades the appendix wall (acute appendicitis), causing a local peritonitis
Serosal congestion and a yellow surface exudate will be seen on the appendix; there will be pus in the lumen and thickened walls (this irritates the parietal peritoneum and causes the sharp, RIF pain)
What must acute inflammation involve?
Must involve the muscle coat
Complications of appendicitis?
Peritonitis - bacterial organisms can leak out of the appendix
Rupture
Abscess
Fistula - formation of an abnormal passageway between 2 epithelial surfaces
Sepsis and liver abscess
What is coeliac disease?
There is a genetically-mediated, abnormal reaction to gliadin, which damages enterocytes and reduces absorbtive capacity
3 factors that coeliac disease is strongly associated with?
Strong familial tendency and an assoc. with HLA-B8
Dermatitis herpetiformis (assoc. with HLA-B8)
Other autoimmune disease, e.g: childhood diabetes
When does coeliac disease present?
Most common in children but may manifest in adulthood
Development of coeliac disease?
Gliadin stimulates an auto-immune reaction and tissue injury is a bystander effect; it is mediated by T lymphocytes within the small intestine epithelium, AKA intra-epithelial lymphocytes
How does normal small bowel compare to a coeliac bowel?
Normal lifespan of enterocytes is about 72 hours and then they are shed
In coeliac disease, there is increased loss of enterocytes due to intra-epithelial lymphocyte mediated damage; this leads to loss of villous structure, loss of surface area, a reduction in absorption and a flat duodenal mucosa
Characteristic biopsy of coeliac disease?
Flat mucosal surface with total villous atrophy
Increased inflammation in the lamina propria and increased intra-epithelial lymphocytes
Cautions with coeliac endoscopy and biopsy?
Mucosa may be endoscopically normal or appear attenuated
Lesions will be worse in the proximal bowel so a duodenal biopsy is very sensitive; absolute confirmation is only possible if there is a return of features to normal after several weeks on a gluten-free diet
Serological markers for coeliac disease?
Anti-TTG (transglutaminase antibodies) - child coeliacs may have very high levels; adults need a biopsy
Anti-endosemial
Anti-gliadin
3 immediate effects of coeliac disease?
Malabsorbtion of sugars, fats, amino acids, water and electrolytes leads to impaired nutrition
Malabsorbtion of fats, leading to steatorrhea (excretion of abnormal quantities of fat with the faeces, leading to bulky and pale stool)
Reduced intestinal hormone production (CCK) leads to reduced pancreatic secretion and bile flow, leading to gallstones
Effects of malabsorption?
Weight loss and abdominal bloating
Anaemia (iron, vitamin B12, folate) and vitamin deficiencies
Failure to thrive
This is managed by diet
4 long-term complications of coeliac disease?
Increased risk of enteropathy assoc. T-cell lymphomas of the GI tract
Increased risk of small bowel carcinoma
Gallstones
Ulcerative-jejunoilleitis (GI tract breaks down into ulcers)
