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GI > Pathology of small bowel > Flashcards

Pathology of small bowel Flashcards

1
Q

what are 2 types of ischaemia of the small bowel?

A

1) mesenteric arterial occlusion

2) non-occlusive perfusion insufficiency

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2
Q

what 2 things can lead to mesenteric arterial occlusion?

A
  • mesenteric artery atherosclerosis

- thrombi-embolism from heart (e.g. A. Fib)

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3
Q

what 4 things could lead to non-occlusive perfusion insufficiency?

A
  • shock
  • strangulation obstructing venous return (e.g. hernia, adhesion)
  • drugs e.g. cocaine
  • hyper-viscocity
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4
Q

what is bowel ischaemia usually?

A

= acute but can be chronic

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5
Q

what is the most metabolically active part of the bowel wall?

A

= mucosa is the most metabolically active part

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6
Q

what is the consequence of the mucosa being the most metabolically active part of the bowel wall?

A

= the most sensitive to effects of hypoxia

  • longer period of hypoxia, greater the depth of damage to the bowel wall and the greater the likelihood of complications
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7
Q

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

A

= after re-perfusion

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8
Q

what is acute ischaemia classified by?

A

the degree of infarction (obstruction of the blood supply) caused

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9
Q

describe the 3 areas that are infracted as length of time of ischaemic increases?

A

1) mucosal infarct (regeneration)
2) mural infarct (stricture)
3) transmural infarct (gangrene - death)

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10
Q

what are the complications of ischaemia of small bowel?

A
  • resolution
  • fibrosis, stricture, chronic ischaemia, ‘mesenteric angina’ and obstruction
  • gangrene, perforation, peritonitis, sepsis and death
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11
Q

what is Meckel’s diverticulum?

A

an outpouching or bulge in the lower part of the small intestine.

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12
Q

what is Meckel’s diverticulum a result of?

A

= involute regression of vitello-intestinal duct

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13
Q

describe the structure of Meckel’s diverticulum?

A

= tubular structure

  • 2 inches long
  • 2 foot above IC valve in 2% of people
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14
Q

what may Meckel’s diverticulum contain and what might it cause?

A

Contain
= heterotopic gastric mucosa

Cause
= bleeding, perforation or diverticulitis which mimics appendicitis

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15
Q

describe the symptoms of Meckel’s diverticulum?

A

= asymptomatic, incidental finding

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16
Q

what type of tumours are rare and more common of the small bowel?

A
  • primary tumours = rare

- secondary tumours (metastases) = common

17
Q

give examples of 3 types of secondary tumours (metastases) of small bowel?

A
  • ovary
  • colon
  • stomach
18
Q

give 3 examples of primary tumours of small bowel?

A
  • lymphomas
  • carcinoid tumours
  • carcinomas
19
Q

describe lymphomas of small bowel.

A

= they are rare

  • all Non-hodgkins in type
  • maltomas (B cell) derived
  • enteropathy associated T-cell lymphomas (associated with coeliac disease)

Treatment;

  • surgery
  • chemo
20
Q

describe carcinoid tumours of small bowel.

A

= rare

  • commonest site = appendix
  • small, yellow, slow growing tumours
  • locally invasive
  • can cause inttussuscepttion, obstruction
  • produce hormone like substances
  • if they metastases to liver occur a carcinoid syndrome occurs
  • flushing & diarrhoea
21
Q

describe carcinomas of small bowel.

A

= rare

  • associated with Crohn’s disease and coeliac disease
  • identical to colorectal carcinoma in appearance
  • presents late
  • metastases two lymph nodes and liver
22
Q

what is appendicitis a common cause of and who is it more common in and describe its symptoms?

A

= an acute abdomen

More common = in children, but occurs in adults

Symptoms;

  • vomiting
  • abdominal pain
  • RIF (right iliac fossa)
  • tenderness
  • increased WCC (white cell count)
23
Q

what are 5 causes of acute appendicitis?

A
  • unknown
  • faecoliths (dehydration)
  • lymphoid hyperplasia
  • parasites
  • tumours (rare)
24
Q

describe 4 pathological features of acute appendicitis

A
  • acute inflammation (neutrophils invade appendix wall)
  • mucosal ulceration
  • serosal congestion, exudate
  • pus in lumen
25
Q

what must acute inflammation involve?

A

= the muscle coat

26
Q

what are 5 complications of appendicitis?

A
  • peritonitis
  • rupture
  • abscess
  • fistula
  • sepsis and liver abscess
27
Q

what is coeliac disease?

A

digestive condition where the small intestine becomes inflamed and unable to absorb nutrients.

28
Q

what is coeliac disease caused by?

A

= abnormal reaction to a constituent of wheat flour, gluten, which damages enterocytes and reduces absorptive capacity

  • gliadin a component of gluten is the toxic agent
  • but tissue injury may be a bystander effect of abdominal immune reaction to gliadin

(can present in childhood, middle age and adulthood)

29
Q

how is coeliac disease damage mediated ?

A

T cell lymphocytes which exist within small intestinal epithelium ‘intra-epithelial lymphocytes’ (IELS)

30
Q

what 3 things does coeliac disease have a strong association with?

A

1) HLA-B8
2) dermatitis herpetiform
3) childhood diabetes

31
Q

what is the normal lifespan of an enterocyte?

A

72hours

32
Q

describe what happens to enterocytes in coeliac disease and what does this lead to?

A

= increasing loss of enterocytes due to IEL mediated damage

Leads to;
- loss of villous structure (villous atrophy), loss of surface area, a reduction in absorption and a flat duodenal mucosa

33
Q

describe 2 morphological features of coeliac disease.

A

1) increased inflammation in lamina propria

2) increased intra-epithelial lymphocytes

34
Q

describe how you would pick up coeliac disease clinically and by doing serology.

A

Clinically;

  • mucosa may be endoscopically normal or appear attenuated
  • lesions worse in proximal bowel so duodenal biopsy is very sensitive

Serology = antibodies;

  • anti-TTG
  • anti-endomesial
  • anti-gliadin
35
Q

what are 3 metabolic effects of coeliac disease?

A

1) malabsorption of sugars, fats, amino acids, water and electrolytes
2) malabsorption of fats leading to steatorrhea
3) reduced intestinal hormone production leading to reduced pancreatic secretions and bile flow (CCK) leading to gallstones

36
Q

what are 5 effects of malabsobtion, managed by diet, due to coeliac disease?

A
  • loss of weight
  • anaemia (Fe, Vit B12, folate)
  • abdominal bloating
  • failure to thrive
  • vitamin deficiencies
37
Q

what are 4 other complications of coeliac disease?

A
  • T-cell lymphomas of GI tract
  • increased risk of small bowel carcinoma
  • gall stones
  • ulcerative-jejenoilleitis

GI (43 decks)

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