Pathology of the Small Bowel

Question 1

How is the small intestine folded?

Answer 1

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

Question 2

Describe this picture of small bowel

ADD PICTURE 1

Answer 2

Normal small bowel has villi lined by enterocytes and this forms the brush border, which is microvilli covered

Question 3

Blood supply to the small bowel?

Answer 3

Superior mesenteric artery

Question 4

2 main causes of ischaemia of the small bowel?

Answer 4

1. Mesenteric arterial occlusion, due to:
   Mesenteric artery atherosclerosis
   Thromboemolism from the heart, e.g: in AF
2. 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

Question 5

How does bowel ischaemia usually present?

Answer 5

Usually acute but it can be chronic

Question 6

Which part of the small bowel wall is most sensitive to hypoxia?

Answer 6

Mucosa is the most metabolically active part of the small bowel and thus the most sensitive to the effect of hypoxia

Question 7

Pathogenesis of small bowel ischaemia, in relation to duration of hypoxia?

Answer 7

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

Question 8

How is acute ischaemia classified?

Answer 8

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

Question 9

Describe the outcome of a mucosal infarct

Answer 9

Regeneration with mucosal integrity being restored

Question 10

Describe the outcome of a mural infarct

Answer 10

Repair and regeneration, with a fibrous structure forming

Question 11

Describe the outcome of a transmural infarct

Answer 11

Gangrenic death and perforation, if not resected

Question 12

What type of necrosis is seen in infarctions?

Answer 12

Coagulative necrosis

Question 13

Outcomes/complications of ischaemia of the small bowel?

Answer 13

Resolution

Fibrosis, stricture and obstruction
Chronic ischaemia (assoc. with widespread atherosclerosis and presents as a "mesenteric angina") 

Gangrene, perforation, peritonitis, sepsis and death

Question 14

What is mesenteric angina?

Answer 14

Presents with post-prandial abdominal pain

Question 15

What is Meckel’s diverticulum?

Answer 15

Result of incomplete regression of the vitello-intestinal duct; so, there is an embryological remnant attached to the wall of the distal ileum

Question 16

Problems associated with Meckel’s diverticulum?

Answer 16

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

Question 17

Types of small bowel tumours and occurence?

Answer 17

Primary tumours are rare

Secondary tumours (metastases) are much more common, e.g: from the ovary, colon, stomach

Question 18

What are the types of primary tumours?

Answer 18

Lymphomas
Carcinoid tumours
Carcinomas

Question 19

Types of lymphomas of the small bowel?

Answer 19

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)

Question 20

Describe carcinoid tumours of the small bowel

Answer 20

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

Question 21

Complications of carcinoid tumours of the small bowel?

Answer 21

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

Question 22

Describe carcinoma of the small bowel

Answer 22

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

Question 23

Presentation of appendicitis?

Answer 23

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

Question 24

Causes of acute appendicitis?

Answer 24

Unknown
Faecoliths (hardening of faeces, which can occur in dehydration)
Parasites, e.g: enterobius vermicularis worms
Tumours (rare)

Question 25

What is the pathology of acute appendicitis?

Answer 25

1. Mucosal ulceration, due to increased intra-luminal pressure
2. 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)

Question 26

What must acute inflammation involve?

Answer 26

Must involve the muscle coat

Question 27

Complications of appendicitis?

Answer 27

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

Question 28

What is coeliac disease?

Answer 28

There is a genetically-mediated, abnormal reaction to gliadin, which damages enterocytes and reduces absorbtive capacity

Question 29

3 factors that coeliac disease is strongly associated with?

Answer 29

Strong familial tendency and an assoc. with HLA-B8

Dermatitis herpetiformis (assoc. with HLA-B8)

Other autoimmune disease, e.g: childhood diabetes

Question 30

When does coeliac disease present?

Answer 30

Most common in children but may manifest in adulthood

Question 31

Development of coeliac disease?

Answer 31

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

Question 32

How does normal small bowel compare to a coeliac bowel?

Answer 32

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

Question 33

Characteristic biopsy of coeliac disease?

Answer 33

Flat mucosal surface with total villous atrophy

Increased inflammation in the lamina propria and increased intra-epithelial lymphocytes

Question 34

Cautions with coeliac endoscopy and biopsy?

Answer 34

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

Question 35

Serological markers for coeliac disease?

Answer 35

Anti-TTG (transglutaminase antibodies) - child coeliacs may have very high levels; adults need a biopsy

Anti-endosemial

Anti-gliadin

Question 36

3 immediate effects of coeliac disease?

Answer 36

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

Question 37

Effects of malabsorption?

Answer 37

Weight loss and abdominal bloating

Anaemia (iron, vitamin B12, folate) and vitamin deficiencies

Failure to thrive

This is managed by diet

Question 38

4 long-term complications of coeliac disease?

Answer 38

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)