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Path: inflamm diseases of bowel (i) (Hirschsprung's disease (signs…
Path: inflamm diseases of bowel (i)
Large intestine normal anatomy
1-1.5 m long
caecum -> ascending colon -> transverse colon -> descending colon -> sigmoid colon -> rectum -> anus
SMA supplies caecum to splenic flexure (splenic flexure = furthest away - watershed area - vulnerable)
IMA supplies remainder of colon to upper 2/3 of rectum
haemorrhoid branches of the int iliac or int pudendal art supply the lower 1/3 of rectum
mucosa
crypts + suface epithelium
no villi
surface epithelium in covered by columnar absorptive cells
goblet cells in crypts - secrete mucin
paneth cells in caecum + ascending colon - immune defence
endocrine cells - products modulate digestive functions
lamina propria
muscularis mucosae
submucosa = loose connective tissue with plexus of Meissner (regulates configuration of the luminal surface, glandual secretions, electrolytes + water transport, local blood flow)
Muscular propria
inner circular later
outer longitudinal layer
myenteric plexus of Auerbach (responsible for peristalsis)
serosa
mesothelial cells
fibrous tissue
perimuscular tissue in rectum
Hirschsprung's disease
congenital megacolon
1 in 5000-8000 live births
Male preponderance (4:1)
more frequent in patients with other anomalies (occurs in 10% of Down's)
most commonly involve rectum + sigmoid
arrested migration of neural crest cells into bowel wall
absence of ganglion cells in muscle wall (Auerbach's plexus) + submucosa (Meissner's plexus)
aganglionic aperistaltic narrow segment
causes functional obstruction + dilatation of the unaffected proximal colon (megacolon)
50% of familial cases + 15% of sporadic cases have mutations in RET gene
signs
failure to pass meconium
constipation
abdo distension
vomitting
complications
proximal innervated colon may become massively dilated, rupture/perforate + lead in infection + enterocolitis
mortality = 5%
tx = resection of involved bowel
Necrotising enterocolitis
affects neonates
acute necrotising inflamm of small + large bowel
most common in premature infants or low birth weight
presents any time in 1st 3 months - usually day 2-4
combo of ischaemia, colonisation by pathogenic organisms (infection), excess protein in lumen + functional immaturity of gut
Antibiotic-associated colitis (pseudomembranous colitis)
acute colitis characterised by an adherent inflamm exudate (pseudomembrane) composed of mucus, fibrin + inflamm debris
yellow
looks like volcano eruption (mushroom cap)
following course of broad-spectrum antibiotics - microbiota destroyed
C diff colonisation - cytotoxins produced - diarrhoea
Dx = cytotoxin detection in stool
Tx = metronidazole, vancomycin
Idiopathic IBD
Chronic, relapsing inflamm intestinal disorders of unknown cause
Crohn's + UC
incidence rising
possible factors
genetic susceptibly
intestinal flora
abnormal T cell response
emotional stress
diet
final common pathway = inflamm
impaired integrity of mucosa - mucosal destruction
loss of absorptive function
increased secretory function
thus tx is directed towards immune down-regulation
Intestinal obstruction
more common in small bowel (smaller lumen)
mechanical causes
congenital (atresia, imperforate anus etc)
acquired
volvulus
adhesions
hernia
intussusception
stenosis
Crohn's
ischaemia
diverticular disease
mass
functional causes
paralytic ileus (muscle paralysis - often post-op)
myopathy
neuropathy
Hirschprung's