Session 7 Flashcards
Summarise the basics of the large intestine
- Caecum to anal canal
- Columnar epithelium
- Removes water from all the indigestible gut contents (proximal) which turns chyme into a semi solid
- Production of certain vitamins
- Microbiome- contains lots of commensal bacteria
- Acts as temporary storage until defaecation (distal) - if too quick then not enough time to absorb enough water causing diarrhoea.
- Colonic mucosa does not get majority of its nutrients from blood, instead derives short chain fatty acids from the fermentation of dietary fibre. The by-products of this fermentation process include CO2, methane and hydrogen gas
Describe the position of the large intestine and rectum in the body
- Ascending and descending colon are secondary retro-peritoneal
- Transverse colon is intra peritoneal and has its own mesentery (transverse mesocolon)
- Sigmoid colon has its own mesentery but as a result can twist (sigmoid volvulus) and cause necrosis, obstruction etc
- Rectum:
- Upper 1/3- intra-peritoneal
- Middle 1/3 – retroperitoneal
- Lower 1/3- no peritoneum
Describe the arterial blood supply to the colon
Midgut component - Superior mesenteric artery (SMA) L1 Jejunal and Ileal arteries supply jejunum and ileum from
SMA
- Ileo-colic artery - Caecum
- Right colic artery - ascending colon
- Middle colic artery - transverse colon
Marginal artery is an artery made up of the anastomoses of the terminal ends of these branches along periphery of colon.
Hindgut component- Inferior mesenteric artery (IMA) L3 (comes off slightly to the left)
- Left colic- descending colon
- Sigmoid- descending colon
- Superior rectal artery- upper 1/3 rectum
These also form marginal artery.
As inferior mesenteric artery enters pelvis it becomes superior rectal artery
Describe the venous drainage of the colon
- Midgut drains into superior mesenteric vein (SMV) which joins with splenic vein to become portal vein
- Hindgut drains into Inferior mesenteric vein (IMV) which drains into splenic vein which drains into the portal vein
- Rectum:
- Upper 1/3 drains into superior rectal vein (IMV in pelvis)
- Middle and lower 1/3s drain into systemic venous system (bypassing liver)
- Site of portosystemic anastomosis. If pressure becomes high enough in the portal system then blood in vessels draining into the portal vein will bypass the liver through these anastomoses. These are often thin walled vessels and aren’t used to this kind of pressure so they can become dilated can become varices. .
What are the structural differences between the large and small intestine?
- Large intestine much shorter (6 feet vs 20 feet)
- Large intestine is much wider (average 6cm vs 3cm)
- Large intestine as crypts not villi
- External longitudinal muscle is incomplete in large intestine - Three distinct bands (teniae coli)
- Haustra are sacculations caused by contraction of teniae coli Epiploic appendices are only found in large bowel.
Describe water absorption in the colon
- Facilitated by ENaC on apical membrane, like principle cells of the late distal convoluted tubule, induced by aldosterone. Water follows Na out of the lumen. Na exchanged for K.
- Approx 1500 mls of water enter colon/day
- <100 mls excreted in faeces
- Most absorption in proximal colon
- Much tighter tight junctions in the large intestine allows bigger ion gradient to form as there’s less back diffusion of ions. This allows absorption of smaller amounts of water.
What is Inflammatory bowel disease?
- Group of conditions characterised by idiopathic inflammation of the GI tract
- Affect function of the gut
- 2 common types
- Crohn’s disease
- Ulcerative colitis (young adults)
Prevalence peaks at young adult age (late teens, early 20s) and late 40s/early 50s
Less common: • Diversion colitis • Pouchitis • Microscopic colitis
Where in the colon is affected by Crohn’s disease?
Crohn’s disease
- Affects anywhere in GI tract, isolated areas
- Ileum (mainly terminal portion) involved in most cases
- Transmural - Can affect entire wall of bowel
- Skip lesions - Tissue can be diseased then normal then diseased again
Where in the colon is affected by Ulcerative colitis?
Ulcerative colitis (UC)
- Begins in rectum
- Can extend to involve entire colon
- Continuous pattern (no skip lesions)
- Mucosal inflammation rather than entire gut wall
Pan colitis - whole colon affected. Doesn’t affect ileum (maybe a tiny bit at terminal ileum if really bad)
What are the causes of Crohn’s and ulcerative colitis?
Causes
- Genetic as shown by 1st degree relative increased risk and identical twins concordance 70%
- Gut organisms unhealthy (altered interaction)
- Immune response
Possible triggers:
Antibiotics
Infections
Smoking can make bowel better in UC but worse in Crohn’s.
Diet
What are the gross pathological features of crohns?
- Skip lesions
- Hyperaemia - affected bowel is red/inflamed
- Mucosal oedema
- Discrete superficial ulcers
- Deeper ulcers
- Transmural inflammation
- Thickening of bowel wall caused by repeated damage and then healing and scarring can lead to narrowing of lumen
- Cobblestone appearance caused by linking ulcers
- Fistulae: Between Bowel – bowel/bladder/vagina/skin
What are the microscopic pathological features of crohns?
- Granuloma formation (pathognomonic -definitive of that disease)
- Organised collection of epithelioid macrophages
How do we investigate crohns?
- Bloods - Anaemia
- CT /MRI scans - Bowel wall thickening, obstruction and extramural problems more easily seen
- Barium enema/follow through (oral) - Used less as you don’t want it to leak - Strictures/fistulae seen
Endoscopy not really used and can only really see up to the duodenum
Colonoscopy - Gross pathological changes- can be seen during endoscopy - • Skip lesions (non-continuous sections of disease) • Cobblestone appearance • Fistulae • Strictures
What are the pathological changes seen in ulcerative colitis?
- 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
- Pseudopolyps can develop after repeated episodes of inflammation then healing. Non neoplastic
- More common in UC (vs Crohn’s)
- Loss of haustra - inflammation reduces the appearance of haustra on imaging
How do we investigate Ulcerative colitis?
- Bloods - Anaemia, Serum markers
- Stool cultures
- Colonoscopy
- Plain abdominal radiographs
- Barium enema (mild cases only)
- CT/MRI Less useful in diagnosing uncomplicated UC as its mucosal so might not show up very well
What is intermediate colitis?
Even after diagnostic evaluation, 10% have disorders that cannot be classified as UC and Crohn’s have common features so they’re diagnosed with indeterminate colitis.
What are the distinguishing features between UC and Crohns?
Give a table showing different pathological features between crohns and UC
Give a table showing the different endoscopic changes beween crohns and uc
Describe the radiological feature of crohns
Barium follow through- you can sometimes see long strictures then dilation then more strictures
• ‘String sign of kantour’
Describe the radiological changes seen in UC
Double contrast enema - air and barium so barium sticks to surface more
- Featureless descending and sigmoid colon Seen to be lacking haustral markings and can see “lead pipe colon” - straight and smooth
- Continuous lesions without skipping
- Whole colon
- Mucosal inflammation causes granular appearance
What are the medical treatments for crohns and UC?
Stepwise approach
- Aminosalicylates ◦ For flares and remission
- Corticosteroids ◦ Flares only
- Immunomodulators ◦ Fistulas/ maintenance of remission
What are the surgical treatments for crohns and UC?
Crohn’s
- Not curative
- Strictures/fistulas
- As little bowel removed as possible as doesn’t cure it
UC
• Curable as confined to colon (colectomy)
This is done when inflammation not settling, or when precancerous changes or toxic megacolon (vast distension causes risk of perforation) are seen
Define diarrhoea
Definition- diarrhoea is a symptom and occurs in many conditions
- Loose or watery stools
- More than 3 times a day
- Acute diarrhoea (less than 2 weeks)
Describe the pathophysiology of diarrhoea
- Unwanted substance in gut stimulates secretion and motility to get rid of it- diarrhoea
- Primarily down to epithelial function (secretion) rather than increased gut motility (although this does occur)
- The end product is too much water in stool
- Colon can overwhelmed and cannot absorb the quantity of water it receives from ileum
- There is normally 99% absorption of water from gut leaving only 100 mls in stool/day
What are the two broad causes of diarrhoea?
Secretory- Electrolyte transport is messed up
Osmotic- the gut lumen contains too much osmotic material
What are diverticula? What is diverticulosis? Why do we get diverticula?
- Diverticula are when outpouchings of mucosa and submucosa herniate through the muscularis layers
- Diverticulosis is asymptomatic diverticula
- Occurs in the colon (85% in sigmoid colon)
- Occurs along where nutrient vessels (vasa recta) penetrate the bowel wall
- Thought to be causes by increased intra-luminal pressure (low fibre diet, constipation, increased intra-luminal pressure as you move down colon as stools are more formed)
What is the rectum?
These are the last sections of the GI tract
- Involved in defaecation
- 12-15cm long passes through the pelvic floor
- Has a continuous band of outer longitudinal muscles - unlike the taeniae coli of the rest of the colon
- Curved shape anterior to sacrum
- Parts of it are covered in peritoneum
- Parts are extra-peritoneal
- Temporary storage of faeces prior to defaecation
- Stretching of rectum stimulates urge to defaecate
Describe the blood supply and drainage of the rectum and anal canal
Blood supply to rectum is from several arteries that form a plexus
- Superior rectal artery -continuation of Inferior mesenteric artery
- Middle rectal artery- branches of internal iliac
- Inferior rectal- pudendal artery
Venous drainage
- Potential for porto-systemic anastomosis if portal pressure becomes too high.
- Portal drainage through superior rectal vein
- Systemic drainage through internal iliac vein. Anastomoses between these two
What forms the anal sphincter complex?
•Internal involuntary sphincter
◦ Thickening of circular smooth muscle
- This is under autonomic control (80% of resting anal pressure)
- External anal sphincter is striated muscle
- Deep section, superficial section and subcutaneous section
Upper anal canal:
- Mixes with fibres from levator ani
- Joins with pubo-rectalis to form sling
- Nerve supply from pudendal nerve
- 20% of resting pressure
How does defaecation occur?
Where is the dentate line and what resides around it?
Anal canal contains the Dentate line
◦ Junction of hindgut and proctodaeum (ectoderm)
Above the dentate line
- Visceral pain receptors
- Columnar epithelium
Below the dentate line
- Somatic pain receptors
- Stratified squamous epithelia
What are anal cushions?
- The anus contains a complex venous plexus - confluence of blood vessels, more venous but with arterial connections which swell to make these inflatable cushions.
- Divided into 3+ areas of tissues called anal cushions
- Play a role in anal continence
- Present from birth and a normal finding
