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2- pathology of small bowel Flashcards

1
Q

where is small bowel?

A

runs from gastric pylorus to ileocaecal valve
small bowel = small intestine

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2
Q

is duodenum, jejunum and ileum intraperitoneal or retroperitoneal?

A
  • duodenum is retroperitoneal (apart from 1st part which is intraperitoneal)
  • jejunum + ileum is intraperitoneal
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3
Q

is walls of jejunum or ileum thicker?

A

wall of jejunum are thicker due prominent mucosal folds (plicae circulares)

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4
Q

what is purpose of villi in mucosa of small intestine?

A

location for digestion and absorption of nutrients from food (into columnar cells)

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5
Q

what is function of crypts in small intestine?

A

secrete ions, water, immunoglobulins and antimicrobial peptides into the lumen

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6
Q

where is absorption of vitamin b12?

A

terminal ileum (it’s joined by intrinsic factor in stomach)

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7
Q

where is iron/folate absorbed?

A

duodenal and proximal jejunum

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8
Q

what is coeliac disease?

A

=abnormal immune response to gluten leading to inflammation & damage of small intestine

  • immune mediated disorder
  • triggered by ingestion of gluten
  • associated with other autoimmune disease like type 1 diabetes, thyroiditis, sjogren syndrome, IgA nephropathy
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9
Q

what are clinical presentations of coeliac disease?

A

all pretty non specific - diarrhoea, bloating, fatigue, anemia, vitamin malabsorption

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10
Q

what are clinical presentations of coeliac disease in children?

A

irritability, failure to thrive, weight loss, abdominal distension, diarrhoea, anorexia

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11
Q

what is dermatitis herpetiformis?

A

itchy, blistering skin lesions in 10% of patients with coeliac
= caused by the deposit of immunoglobulin A (IgA) in the skin

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12
Q

what can be measured in coeliac disease to help diagnose?

A
  • IgA antibodies like specifically tissue transglutaminase (tTG) & endomysial
  • gliadin
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13
Q

what is major risk of coeliac disease if it’s not well maintained?

A

Increased risk of malignancy – specifically enteropathy associated T cell lymphoma

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14
Q

what is gliadin?

A

= component of gluten - it’s the suspected toxic agent which triggers abnormal immune reaction (antibodies formed and cause activation of T cells that go to duodenum and damage epithelium and enterocytes, destroying + reducing absorptive capacity)

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15
Q

what is histologically different of coeliac disease?

A

the villi aren’t big nice projections - sort of flattened

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16
Q

what are characteristic features histologically of coeliac disease?

A
  • loss in villous height (flat), intraepithelial lymphocytes (top cell layer has a lot of dark cells within it)
  • at base of crypts big hyperplastic cells trying to regenerate damage

*lymphocytes infiltrate in epithelium

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17
Q

what is management of coeliac disease?

A

gluten free diet →resolution of symptoms, reduction in antibody titre →restores normal small bowel microscopic appearance within 6-24 months

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18
Q

what are different ways mesenteric vessels can be blocked causing small bowel ischaemia?

A
  • Thrombosis due to atherosclerosis obstructing blood flow causing ischaemia
  • vasculitis = inflammation of blood vessels, triggered by autoimmune diseases, neoplasia, cirrhosis, trauma, compression of portal drainage
  • Emboli = origin from atheromas in aorta/cardiac mural thrombi
19
Q

what can cause intestinal hypoperfusion which can lead to small bowel ischaemia?

A

Intestinal hypoperfusion can also occur due to cardiac failure, shock, dehydration or vasoconstrictive drugs e.g. adrenaline

20
Q

what is macroscopic appearance of ischaemia of small bowel?

A

dusky serosa (external surface of unopened intestine) & dark coloured mucosa due to haemorrhage (internal intestinal surface)

21
Q

what is summary of what happens in ischaemic small intestine?

A

attenuation of villous epithelium →atrophy →fibrosis of lamina propria →ulceration →haemorrhage →necrosis →eventually involves all layers

*once muscularis propria gone = bowel no longer viable

22
Q

what is complication of ischaemia of small bowel - if not removed in time?

A

fibrosis →stricture →obstruction (fills with gas) →chronic ischaemia “mesenteric angina” →gangrene, gets thin →perforation which gets peritonitis →sepsis which can lead to death

23
Q

what are primary tumours of small bowel? and how common?

A

they’re rare and examples = lymphomas, neuroendocrine neoplasms (carcinoid) , carcinoma

24
Q

what are lymphomas of small bowel?

A

All are non-Hodgkins type
* MALTomas (mucosal associated lymphoid tissue): B cell derived
* Enteropathy associated T cell lymphoma: associated with coeliac

25
Q

what is MALToma?

A

= if autoimmune inflammatory condition and not well controlled then increases risk of MALToma, not unique to small intestine can also happen in stomach, skin, lung, breast, salivary gland, thyroid,
skin, lung, breast + stomach is most common (H.pylori)
* Memory B cell origin

26
Q

what is macroscopic appearance of MALToma?

A

haemorrhage, stricture, nodules, ulceration

27
Q

what is microscopic appearance of MALToma?

A

medium sized B cells, pale cytoplasm, irregular nuclei,
dispersed chromatin, inconspicuous nucleoli

28
Q

what is enteropathy associated T cell lymphoma?

A
  • complication of refractory coeliac disease (still symptoms of coeliac even when no gluten for 12 months at least)
  • perefers intestine but also in lymph nodes
29
Q

what is macroscopic view of enteropathy associated T cell lymphoma?

A

ulcerated lesion

30
Q

what is microscopic view of enteropathy associated T cell lymphoma?

A

mucosa flat, lymphocytes in epithelium, dense inflammatory cell infiltrate, neoplastic lymphocytes, nuclei appear angulated and irregular, prominent nucleus

31
Q

what is neuroendocrine neoplasms of small bowel?

A
  • Rare
  • Commonest site = appendix
  • Small bowel: derived from serotonin producing enterochromaffin cells
  • they form masses in mesentery – cause buckling/tethering of bowel
  • Carcinoid syndrome (specific set of symptoms): diarrhoea, flushing, right heart fibrosis
32
Q

what is macroscopic appearance of neuroendocrine neoplasms of small bowel?

A

bright yellow coloured nodule

33
Q

what is microscopic appearance of neuroendocrine neoplasms of small bowel?

A

nested growth, salt & pepper chromatin, cytoplasmic granularity, palisading of tumour cells +/- rosette formation →salt + pepper view

34
Q

what is primary carcinoma of small bowel?

A
  • rare
  • Associated with Crohn’s & coeliac
  • Identical to colorectal carcinoma
  • Late presentation
  • Metastases to lymph nodes and liver
35
Q

what is macroscopic appearance of primary carcinoma of small bowel?

A

plaque like growth, polypoidal, constricting “apple core” lesions

36
Q

what is microscopic appearance of primary carcinoma of small bowel?

A

complex glands, nuclear pleomorphism, pseudostratification, loss of polarity, “dirty” necrosis →looks same as in colon

37
Q

what is appendicitis?

A

= commonest cause of acute abdomen (more common in children/adolescents)

38
Q

what is clinical presentation of appendicitis?

A

periumbilical pain radiating to RIF, anorexia, N+V, diarrhoea, fever, raised CRP/WCC

39
Q

what is macroscopic view of appendicitis?

A

congested, erythematous, fibrinopurulent exudate, friable

40
Q

what is microscopic view of appendicitis?

A

acute inflammation involving some/all layers of appendiceal wall; necrosis (gangrenous), haemorrhage, abscess formation, peritonitis

41
Q

what are complications of appendicitis?

A
  • rupture
  • peritonitis
  • abscess
  • fistula
  • sepsis
  • liver abscess
42
Q

what are tumours of appendix?

A

rare

  • neuroendocrine neoplasm = commonst

macro = bright yellow
micro = nests, monotonous round cells, salt + pepper chromatin

43
Q

what is enterobius vermicularis?

A

= worms (pinworm infection)
- parasitic infection
- pruritus ani (intense chronic itching affecting peri-anal skin)

44
Q

what is macroscopic and microscopic appearance of enterobius vermicularis?

A
  • Macro: congestion, fibrinopurulent exudate,may see parasite
  • Micro: ranges from normal to

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