Large intestine/ iBD Flashcards

1
Q

What is the large intestine made up of? What epithelium does it have?

A
Caecum
Ascending colon 
Transverse colon 
Descending colon
Sigmoid colon 
Rectum 
Anal canal 

Simple Columnar (bar distal anus= simple squamous)

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2
Q

What are the functions of the large intestine?

A

Removes water from all the indigestible gut contents (proximal)

Produces vitamins

Microbiome

Temporary storage until defaecation (distal) T&D C -> rapid peristalsis

Ferments dietary fibre -> short chain fatty acids + CO2/ methane/ H2 gas

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3
Q

Explain the peritoneum of the large intestine

A

Ascending and descending colon are retro-peritoneal

Transverse colon has its own Mesentery (transverse mesocolon) intra-peritoneal

Sigmoid colon has own Mesentery (can form volvulus)

Rectum upper 1/3 intra-peritoneal
Middle 1/3 retroperitoneal
Lower 1/3 no peritoneum

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4
Q

What is the large intestine arterial supply to each part?

A
Midgut component - superior mesenteric artery: 
Ileo-colic -> Caecum 
Right colic -> AC 
Middle colic -> transverse colon 
(Jejunal and Ileal arteries) 

Terminal branches of SMA form anastomoses network around periphery of bowel ‘marginal artery’

Hindgut component - IMA:
Left colic -> Dc
Sigmoid arteries -> SC
Superior rectal A -> upper 1/3 rectum

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5
Q

Venous drainage of the large intestine?

A

Midgut (caecum, AC, TC) -> superior mesenteric vein

Hindgut (DC, SC) -> IMV

Rectum: upper 1/3 -> Superior rectal vein (IMV), middle and lower -> systemic venous system = portosystemic anastomosis (thin walled)

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6
Q

Differences between structure large and small intestine

A

Large: shorter, wider, has crypts not villi, external longitudinal muscle is incomplete - 3 distinct bands (teniae coli) - haustra are sacculations caused by contraction of teniae coli (+ complete circular muscle), has epiploic appendices (fatty tags)

SI doesn’t

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7
Q

How does the colon absorb water?

A

ENaC channel on apical membrane (conc grad set up by NAK pump basolateral and K channel apical)

Induced by aldosterone

1500mls enter colon/ day, <100mls excreted faeces

Most absorption proximal colon

Tighter junctions, less back diffusion of ions

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8
Q

What is inflammatory bowel disease? What are the two most common types? Which age group is most affected?

A

Group of conditions characterised by idiopathic inflammation of the GI tract. Affect function of the gut.

Including:
Crohn’s disease
Ulcerative colitis (young adults)

20yrs (highest) and 60 peaks of IBD

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9
Q

Compare and contrast Crohn’s disease and ulcerative colitis? including presentation and cause

A

Crohn’s: affects anywhere GI tract (ileum normally involved), transmural (isolated area(s)) - skip lesions, affects deep tissue, 25% gross bleeding, perianal disease 75%, transmural inflammation (rare UC), granulomas, fibrosis

UC: begins rectum -> can involve entire colon, continuous pattern, mucosal inflammation (shallow), gross bleeding, perianal disease rare, no fistulaes, no malnutrition, crypt abscesses (rare C)

Both can present with:
Extra- intestinal problems- MSK pain (50%) e.g. arthritis, skin (30%) e.g. erythema nodosum/ pyoderma gangrenosum/ psoriasis, liver/ biliary tree e.g. primary sclerosing cholangitis, eye problems (5%)

Both caused by unclear mechanisms involving: genetic element, gut organisms altered interaction, immune response, trigger e.g. antibiotics, infections, diet

Smoking: cause of Crohn’s but settles UC

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10
Q

Crohn’s disease symptoms and gross/ microscopic pathological

A
  • Unexplained weight loss
  • Tender mass RLQ (terminal ileum inflammation)
  • frequent, recurring diarrhoea
  • low grade fever
  • mildly anaemia

Pathology:

  • skip lesions
  • hyperaemia (XS blood supplied)
  • mucosal oedema
  • discrete superficial ulcers
  • deeper ulcers
  • transmural inflammation
  • thickening wall -> narrowed lumen
  • cobblestone appearance (ulcers between inflamed mucosa)
  • fistulae (connections between 2 epithelial lined surfaces) (also occurs bladder/ vagina/ skin)
  • granulosa formation = pathognomonic (v characteristic Crohn’s)
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11
Q

Investigating Crohn’s

A

Bloods - anaemia

CT/ MRI - bowel wall thickening, obstruction, extramural problems

Barium enema/ follow through (oral) - used less but good for demonstrating strictures/ fistulaes - string sign of Kantour (long stricture)

Colonoscopy or endoscopy - gross pathological changes e.g. skip lesions, cobblestone appearance (severe), fistulae, strictures

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12
Q

Ulcerative colitis symptoms and pathological changes

A
  • Mildly tender abdomen
  • no perianal disease (skin tag/ fistulae/ ulcers)
  • normal temp (unless advanced)
  • weight loss
  • diarrhoea

Pathological:

  • chronic inflammatory infiltrate of lamina propria
  • crypt abscesses (neutrophilic exudate)
  • crypt distortion (irregular shaped glands with dysplasia, darker crowed nuclei)
  • friable mucosa
  • reduced goblet cells
  • pseudopolyps (inflammation then healing, non neoplastic, more common UCS)
  • loss of haustra
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13
Q

Investigating Uc

A

Bloods - anaemia, serum markers

Stool cultures - blood

Colonoscopy

Plain abdo radiographs

Barium enema (mild cases) - double contrast enema lead pipe colon (no haustra)

CT/MRI (less useful for diagnosing uncomplicated Uc)

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14
Q

What is indeterminate colitis?

A

Has features of both ulcerative colitis and Crohn’s disease so cant be classified as one or the other (10% of IBD)

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15
Q

pharmacological Treatment options IBD

A
  1. Aminosalicylates - for flares and remission
  2. Corticosteroids - prednisolone flares only
  3. Immunomodulators fistulaes/ maintenance of remission
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16
Q

Surgical treatments options for Uc and Crohn’s

A

UC:
Curable (colectomy) remove entire colon if inflammation not settling/ precancerous changes/ toxic megacolon (vast distension -> perforate)

Crohn’s:
Not curative. Strictures/ fistulaes have to be removed, as little bowel removed as possible. Multiple surgeries -> adhesions