Pathology- the small bowl Flashcards

(43 cards)

1
Q

What is the small bowl

A

the small intestine

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2
Q

what is the innermost cell of the small bowl

A

enterocytes lined with villi

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3
Q

what is the main function of the villi

A

absroption

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4
Q

what is the blood supply to the small bowl

A

entire supply from superior mesenteric

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5
Q

what can cause ischaemia of the small bowl

A

mesenteric artery occlusion

non occlusive perfusion insufficiency

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6
Q

what can cause mesenteric artery occlusion

A

mesenteric artery atherosclerosis

thromboembolism from heart (e.g. A fib)

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7
Q

what can cause a non occlusive perfusion insufficiency

A

shock (when haemorrhaging as brain, heart and lungs a priority)

strangulation obstructing venous return (e.g. hernia or adhesion)

drugs (e.g. cocaine, causes spasm of intestinal wall)

hyperviscosity

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8
Q

what pain is associated with ischaemia of the small bowl

A

acute pain as usually acute, can by chronic

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9
Q

why is the mucosa the area most affected by an infarction (the effects of hypoxia)

A

as it is the most metabolically active area

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10
Q

what increases with the period of hypoxia

A

the greater the dept of the damage to the bowl wall and likelyhood of complications

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11
Q

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

A

after reperfusion

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12
Q

what is a possible outcome from the following

  • mucosa infarct
  • mural infarct
  • transmural infarct
A

different types of infarct occur as the length og time of ischaemia increases. the outcomes also get worse

  • regeneration
  • stricture (abnormal narrowing caused by firbous scarring during healing)
  • gangrene (when infarct goes through the bowl)
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13
Q

what are the complications of ischaemia of the small bowl

A

mucosa
resolution

mural
fibrosis, stricture, chronic ischaemia, mesenteric angina, obstruction,

transmural
gangrene, perforation, peritonitis, sepsis, death

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14
Q

what is meckel’s diverticulum

A

is a result of imcomplete regression of vitello-intestinal duct (embryological feature)

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15
Q

describe meckels diverticulum

A

Tubular structure, 2 inches long, 2 foot above IC (illeocecal) valve in 2% of people

May contain heterotopic gastric mucosa

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16
Q

what can a mekels diverticulum cause

A

bleeding, perforation or diverticulitis which mimicks appendicitis, peptic ulcers

Commonly assymptomatic, incidental finding

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17
Q

what tumours are most common in the small bowel

A
primary tumours rare 
secondary tumours (metastases from ovary, colon and stomach) more common 
primary tumours include 
-lymphomas
-carcinoid tumours
-carcinomas
(in order of commonness)
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18
Q

what type are the lymphomas of the bowel

A

non hodkins in type

19
Q

how are lymphomas of the bowel treated

A

surgery and chemotherapy

20
Q

where is the most common site for a carcinoid tumour in the small bowl

21
Q

describe carcinoid tumours of the bowel

A

small, yellow, small growing, locally invasive, produces hormone like substances, if metastases to liver causes a carcinoid tumour producing flushing, diarrhoea and head aches

22
Q

what cancer is associated with coeliac disease

23
Q

describe carcinomas of the small bowel

A

rare, presents late, metastases to lymph nodes and liver occur

24
Q

what bowl cancer is associated to crohns and coeliac disease

A

carcinoma (as they are predisposed to rarer cancers)

25
what are the symptoms of an appendicitis
vomiting, abdominal pain, right illiac fossa, increased white cell count
26
what can cause an cute appendicitis
unknown (most common), faecoliths (dehydration), lymphoid hyperplasia, parasites, tumours (rare)
27
describe the pathology of an acute appendicitis
Acute inflammation (neutrophils)- must involve a muscle coat Mucosal ulceration Serosal congestion, exudate Pus in lumen
28
what happens to the wall of the appendix during an acute appendicitis
is thickened, neutrophils invade it, inflammation
29
what are the complications of an appendicitis
peritonitis, rupture, abscess, fistula, sepsis and liver abscess
30
how can an acute appendicitis cause a liver abscess
can spread to liver via portal system causing abscess of liver
31
what is coeliac disease caused by
an abnormal reaction to a constituent of wheat flour, gluten, which damages enterocytes and reduces absorptive capacity- damages villi
32
when can coeliac disease present
any time
33
what is coeliac disease strongly associated with
HLA-B8, dermatitis herpeformis, childhood diabetes
34
what is the suspected auto antigen (toxic agent) in coeliac disease
gliadin (component of gluten) -tissue injury may be a bystander effect of abnormal immune reaction to Gliadin
35
what is T cells role in coeliac disease
Mediated by T-cell lymphocytes which exist within the small intestinal epithelium ‘intraepithelial lymphocytes’ (IELS)
36
what is the normal lifespan of an enterocyte
72 hours
37
how is coeliac disease seen in the gut
increasing loss of enterocytes due to IEL mediated damage This leads to loss of villous structure, loss of surface area, a reduction in absorbtion and a flat duodenal mucosa (e.g. flat mucosal biopsy with total villous atropy)
38
what is the morphology of coeliac disease
increased inflammation in lamina propria, increased intraepithelial lmphocytes
39
what part of the bowl is usually worse in coeliac disease
proximal
40
what antibodies will be found in someone with coeliac disease
anti-TTG, anti-endomesial, anti glandin
41
what are the metabolic effects of coeliac disease
Malabsorbtion of sugars, fats, amino acids, water and electrolytes Malabsorbtion of fats leads to steatorrhea (excessive fat in poo) Reduced intestinal hormone production leads to reduced pancreatic secretion and bile flow (CCK) leading to gallstones
42
what are the clinical effects of malabsorption
weight loss, anaemia, abdominal bloating, failure to thrive, vitamin deficiencies
43
what are 4 rare complications of coeliac disease
T-cell lymphomas of GI tract Increased risk of small bowel carcinoma Gall stones Ulcerative-jejenoilleitis