Lagr Intestine/inflammatory Bowel Disease Flashcards

1
Q

Give an overview of the large intestine

A
  • Caecum to anal canal
  • Columnar epithelium
  • Removes water from all the indigestible gut contents (proximal)
  • Turns chyme into a semi solid
  • Production of certain vitamins
  • Microbiome- contains lots of commensal bacteria - Half of vit K + others produced by bacteria in the gut
  • Acts as temporary storage until defaecation (distal)
  • Colonic mucosa does not get majority of nutrients from blood
  • Short chain fatty acids derived from the fermentation of dietary fibre
  • The by-products of this fermentation process include CO2, methane and hydrogen gas
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2
Q

Describe the peritoneum of the colon

A
  • Ascending and descending colon is retro-peritoneal (secondary)
  • Transverse colon has its own mesentery (transverse mesocolon)
  • Sigmoid colon has its own mesentery
  • Rectum:
  • Upper 1/3- intra-peritoneal
  • Middle 1/3 – retroperitoneal
  • Lower 1/3- no peritoneum
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3
Q

Describe the arterial supply of the midgut component o the colon

A

Midgut component- Superior mesenteric artery (SMA)
• Ileo-colic - goes into rLq- Caecum
• Right colic- ascending colon
• Middle colic- transverse colon prod 2/3
Right colic divides into ascending and descending branch. Ileocolic also have an ascending and descending. These anastamose at the periphery and go al the way around the edge. This is the marginal artery = sum of anastamoses of the branches of the SMA

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4
Q

Descrive the arterial supply to the hindgut component of the colon

A

Hindgut component- Inferior mesenteric artery (IMA)
• Left colic- descending colon
• Sigmoid- descending colon
• Superior rectal artery- upper 1/3 rectum (continuation of IMA)
Left colic goes round and anastamioses with middle colic to give marginal

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5
Q

Describe the venous drainage of the colon

A
  • Midgut drains into superior mesenteric vein (SMV) - Where SMV ad splenic vein meet - portal vein continues from there
  • Hindgut drains into Inferior mesenteric vein (IMV) - drains into splenic
  • Rectum:
  • Upper 1/3 drains into superior rectal artery (IMV)
  • Middle and lower 1/3s drain into systemic venous system
  • Site of portosystemic anastomosis
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6
Q

Compare teh large intestine vs small

A
  • Large intestine much shorter (6 feet vs 20 feet)
  • Large intestine is much wider (average 6cm vs 3cm)
  • Has crypts not villi
  • External longitudinal muscle is incomplete
  • Three distinct bands called the teniae coli
  • Haustra are sacculations caused by contraction of teniae coli
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7
Q

Describe water absorption on the colon

A
  • Facilitated by ENaC
  • Like principle cells of the late distal convolute\ tubule
  • NaK ATPase Induced by aldosterone - Na out, o basolateral surface, then more comes in via ENaC
  • Approx 1500 mls of water enter colon/day
  • <100 mls excreted in faeces
  • Most absorption inn proximal colon
  • Much tighter tight junctions
  • Allows bigger gradient to form
  • Less back diffusion of ions
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8
Q

What is inflammatory bowel disease and what are the.2 main types

A
  • Group of conditions characterised by idiopathic inflammation of the GI tact
  • Affect function of the gut
• 2 common types
— Crohn’s disease
— Ulcerative colitis (young adults)
  - Diversion colitis 
  - Pouchitis 
  - Microscopic colitis
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9
Q

Where do chronic disease and UC affect

A

Crohn’s disease
• Affects anywhere in GI tract
• Ileum involved in most cases
• Transmural - potentially right though thickness of the Boswell
• Skip lesions - parts of the bowel, so some normal parts

Ulcerative colitis (UC) 
• Begins in rectum
• Can extend to involve entire colon. Can only rly affect colon 
• Continuous pattern - no skips
• Mucosal inflammation
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10
Q

What are the symptoms

A
  • Extra-intestinal problems
  • MSK pain (up to 50%)
  • Arthritis
  • Skin (up to 30%)
  • Erythema nodosum (painful tender lumps on limbs) /pyoderma gangrenosum /psoriasis
  • Liver/biliary tree
  • Primary Sclerosing Cholangitis (PSC)
  • Eye problems (up to 5%)
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11
Q

What are the abuses of chronic and up

A
Causes
• Genetic
• 1st degree relative increased risk • Identical twins concordance 70%
• Gut organisms (altered interaction)
• Immune response
• ? Trigger
• Antibiotics
• Infections
• Smoking
• Diet
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12
Q

Describe teh typica presentation of chronic

A
  • 22 year old female
  • 6/52 hx of 5x loose stools/day
  • Tender mass (RLQ) - terminal ileum
  • Mild perianal inflammation/ulceration - fistula
  • Low grade fever
  • Mildly anaemic
  • Non bloody
  • Weight loss
  • Right lower quadrant pain
  • Some joint pains (lower limbs)
  • Smoke
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13
Q

Describe the gross appearance of chronic

A
• Skip lesions 
• Hyperaemia 
• Mucosal oedema 
• Discrete superficial ulcers 
• Deeper ulcers 
• Transmural inflammation
- Thickening of bowel wall
- Narrowing of lumen
•Cobblestone appearance
•Fistulae
•Bowel – bowel/bladder/vagina/skin - fecal material can move through to here 
Deep linear ulcers cris crossing.. could be oedematous?
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14
Q

Describe th histology of chronic

A

• Granuloma formation (pathognomonic)
• Organised collection of epithelioid macrophages
Ss

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15
Q

Describe the investigations for chronic

A
  • Bloods
  • Anaemia
  • CT /MRI scans
  • Bowel wall thickening
  • obstruction
  • good for extramural problems
  • Barium enema/follow through
  • Used less
  • Strictures/fistulae
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16
Q

What can ve seen in a colonoscopy for chron s

A

Colonoscopy • Gross pathological changes- can be seen during endoscopy
• Skip lesions (non-continuous sections of disease)
• Cobblestone appearance
• Fistulae
• Strictures

17
Q

Describe the tyicalprsentaio of us

A
  • 8/52 hx 6 x bloody stools/day
  • Mucus in stools
  • Weight loss
  • Mild lower abdominal pain/cramping
  • Painful red eye
  • Mildly tender abdomen
  • No perianal disease
  • Normal temp
18
Q

Describe teh histology of chronic

A

• Chronic inflammatory infiltrate of lamina propria • Crypt abscesses (neutrophilic exudate in crypts)
• Crypt distortion (bottom image)
— Irregular shaped glands with dysplasia
— Darker crowded nuclei
• Reduced numbers of goblet cells
Risk of colonic cancer ss

19
Q

Describ the changes seen in ur in colonoscopy

A

Pseudopolyps can develop after repeated episodes
• Inflammation then healing
• Non neoplastic
• More common in UC (vs Crohn’s)

Loss of haustra
• Inflammation reduces the appearance of haustra on imaging

20
Q

What are th investigation in uc

A
  • Bloods
  • Anaemia
  • Serum markers
  • Stool cultures
  • Colonoscopy
  • Plain abdominal radiographs
  • Barium enema (mild cases only)
  • CT/MRI
  • Less useful in diagnosing uncomplicated UC
21
Q

What is indeterminate colitis

A

Difficulty distinguishing them
• Even after diagnostic evaluation, 10% have
disorders that cannot be classified (indeterminate
colitis).

22
Q

Compare the distinguishing characteristics in chronic and up

A

Ss

23
Q

Compare the pathological features of chronic and up

A

Ss

24
Q

Compare the endoscopic changes in chronic and up

A

Ss

25
Q

Describ ethe radiological futures I Caron’s

A

Barium follow through- you can sometimes see long strictures
• ‘String sign of kantour’
Ss

26
Q

Describe teh radiological features of ur

A
Double contrast enema 
• Featureless descending and sigmoid colon
— Lacking haustral markings 
— Lead pipe colon
• Continuous lesions without skipping 
• Whole colon 
• Mucosal inflammation
• Causes granular appearance
27
Q

What is the stepwise treatment option ss

A
Stepwise approach
1. Aminosalicylates
◦ Sulfasalazine (5-ASA preparations)
- For flares and remission
2. Corticosteroids 
◦ Prednisolon- Flares only 
3. Immunomodulators
◦ Azathioprine
-Fistulas/ maintenance of remission
28
Q

What are the surgical treatment options

A
Crohn’s
• Not curative
• Strictures/fistulas
• As little bowel removed as possible 
Can lad to short bowel syndrome - cant absorb enough.
Repeated surgery’s lead to adhesions  
UC
• Curable (colectomy) - can leave small terminal pouch to maintain continence 
• Inflammation not settling 
• Precancerous changes 
• Toxic megacolon