Pathology of the small intestine Flashcards

1
Q

Both the small and large bowel have lots of immune cells within them. True/ False?

A

False

Only the small intestine has lots of immune cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

from which artery does the small intestine get its blood supply?

A

the superior mesenteric artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the 2 main causes of ischaemia of the small bowel?

A
  1. mesenteric artery occlusion (e.g. due to atherosclerosis or thromboembolism from heart)
  2. non-occlusive perfusion insufficiency (e.g. in shock, strangulation obstructing venous return - such as a hernia/ adhesion, due to drugs e.g. cocaine, hyperviscosity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which layer of the small bowel is most sensitive to hypoxia and why?

A

the mucosa
because it is the most metabolically active part of the bowel wall. the longer the hypoxia duration, the greater the damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

in non-occlusive ischaemia, when does much of the tissue damage occur?

A

after reperfusion
(due to reperfusion injury - which is when the restoration of blood flow allows for increased formation of free radicals - which damage tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the sequence (as duration of ischaemia increases) of outcomes of small intestine ischaemia?

A
  • mucosal infarct (which can be regenerated)
  • mural infarct (which regenerates to form a fibrous stricture - so narrows the lumen)
  • transmural infarct (which is gangrene - a type of necrosis caused by critically insufficient blood supply) (death will occur if gangrene is not resected)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

list some possible outcomes of ischaemia of the small intestines

A
resolution (complete healing)
mesenteric angina (pain after eating due to ongoing poor blood supply)
fibrosis
stricture (narrowing of lumen)
gangrene (transmural infarct)
perforation (hole in the wall of part of the GI tract)
sepsis
death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is Meckel’s diverticulum?

A
a true (involves all 4 layers of the wall) congenital diverticulum. It's a slight bulge in the small intestine, and is present at birth (it's a now functionless remnant of the vitelline duct - which joined the yolk sac to the midgut lumen of the foetus). 
Meckel's diverticulum may cause bleeding, perforation or diverticulitis (which mimicks appendicitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is a diverticulum?

A

outpouching of a hollow (or fluid-filled) structure in the body. Either true or false, depending on which layers of the structure are involved. True diverticulum = when all 4 layers of the wall are included in the outpouching.
False diverticulum = when only the mucosa and submucosa are included in the outpouching, and are covered only by serosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe features of Meckel’s diverticulum? Hint: the number 2

A

this diverticulum is a tubular structure which is:

  • 2 inches long
  • within 2 feet of the ileocaecal valve
  • 2 times as common in males
  • present in 2% of the population
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is diverticulitis?

A

digestive disease in which pouches within the large bowel wall (diverticula) become inflamed. Often results in lower abdominal pain of sudden onset. (Having diverticula that are NOT inflamed is known as having “diverticulosis”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Primary/ secondary tumours of the small intestine are common?

A

secondary e.g. from ovary, stomach, colon

primary e.g. lymphomas, carcinoid tumours, carcinomas are rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which type of lymphoma (Hodgkins or Non Hodgkins) are lymphomas of the small bowel?

A

non-Hodgkins
Specifically, they are MALTomas (MALT lymphomas) - which is a form of lymphoma involving the mucosa-associated lymphoid tissue, often of the stomach. It’s a cancer originating from B cells in the marginal zone of the MALT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is enteropathy-associated T cell lymphoma?

A

a type of T cell lymphoma that affects the small intestine. These cancerous T cells are a possible consequence of refractory cases of coeliac disease or in chronic, untreated cases of Coeliac disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

give some information about carcinoid tumours of the small bowel?

A
rare, commonest site is appendix
small, yello, slow-growing tumours
locally invasive]
can cause obstruction
produces hormones so can cause paraneoplastic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

give some information about carcinoma of the small bowel?

A

rare
associated with Crohn’s disease and Coeliac disease
identical appearance to colorectal carcinoma
presents late
metastases to lymph nodes and liver can occur

17
Q

what is appendicitis?

A

inflammation of the appendix, commoner in children

Causes vomiting, abdominal pain, RIF tenderness, increased WCC

18
Q

what are some causes of appendicitis?

A
  • idiopathic (most cases)
  • faecoliths (faecal impaction due to dehydration)
  • lymphoid hyperplasia
  • parasites
  • tumours (rare)
19
Q

outline the pathology of acute appendicitis?

A

-acute inflammation (neutrophilic infiltrate of the muscularis propria)
-mucosal ulceration
-serosal congestion, exudate
-pus in lumen
(acute inflammation must involve the muscle coat)

20
Q

what are complications of appendicitis?

A
  • peritonitis (spread of infection)
  • rupture (pus extrudes out)
  • abscess (body tries to wall off infection)
  • fistula (an abnormal anastomosis)
  • sepsis (rare in developed world)
21
Q

what is coeliac disease?

A

an autoimmune disorder affecting mainly the small intestine. Occurs in those who are genetically predisposed. Upon exposure to gluten, an abnormal immune response may lead to the production of several different autoantibodies that can affect a number of different organs. In small bowel, this shortens and flattens the villi (damages the enterocytes) - affecting nutrient absorption and often leading to anaemia. Strong association with childhood diabetes (another autoimmune disease).

22
Q

what causes coeliac disease?

A

exposure to the gliadin peptide (component of gluten) in those who are sensitive to it. Reaction is mediated by T cells (IELs).

23
Q

In coeliac disease, is there a change in the number of IELs in the small intestinal wall?

A

Yes, there are more IELs

24
Q

pathology of coeliac disease?

A

gliadin peptide presented to CD4 cells by macrophages in the small intestine
CD4 cells release inflammatory cytokines e.g. IFNg and TNF - which directly damage and destroy epithelial cells in the small intestine, and also stimulate B cells to produce antibodies (IgA, anti-tTG and anti-EMA), also causes killer T cells (CD8) to come and destroy cells undergoing inflammation

25
Q

Coeliac disease begins proximally/ distally in the small intestine?

A

proximally (so duodenal biopsy very sensitive)

The disease extends if untreated

26
Q

metabolic effects of Coeliac disease?

A

malabsorption of sugars, fats (leads to steatohhoea), amino acids, water, electrolytes, reduced intestinal hormone production leads to reduced pancreatic secretion and bile flow (CCK) leading to gallstones
Effects: weight loss, anaemia, abdominal bloating, failure to thrive, vitamin deficiencies
Other complications: T cell lymphomas of the GI tract (nearly always fatal), increased risk of small bowel carcinoma, gallstones, ulcerative-jejenoilleitis