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FGIDs (functional GI disorders), ABNORMAL GUT MOTILITY & DIARRHOEA -…
FGIDs (functional GI disorders)
classified by GI symptoms in the absence of organic pathology, but not psychomatic/psychiatric
Upper GIT
Oesophagus
functional heartburn
functional chest pain
need to rule out eosinophilic oesophagitis
usually young with intermittent dysphagia, especially with concomitant asthma
rule out with biopsy + endoscopy
need to rule out other major oesophageal disorders
functional dysphagia
Gastric
functional dyspepsia
(non-ulcer)
epigastric pain commonly with N/V or early satiety
abdominal bloating/distension
symptoms overlap with gastroparesis
exclude with gastric emptying study
Lower GIT
IBS
criteria for diagnosis: recurrent abdominal pain (at least 1 day/week in last 3 months) and ≥2 of following:
Related to defecation (improved or worsened)
Associated with change in stool frequency
Associated with change in stool form
Abdominal pain + changed stool pattern (diarrhoea/constipation/alternating)
Exclude endometriosis (lower abdominal pain, related to menstrual cycle, not related to defecation)
functional constipation
functional diarrhoea
differentiate from IBS: these are not associated with pain
exclude IBS or coeliac
functional anorectal disorders
anorectal function testing (only FGID with diagnostic test)
pelvic floor dysfunction
constipation
faecal incontinence
functional anorectal pain
1/3 of community have FGID, and patients can transition in and out of FGID or between FGIDs
complex, multifactorial, polygenic
peripheral: mucosal alterations, ENS dysfunction (luminal triggers)
central: psychological distress, altered brain/spinal cord activation (psychological triggers), brain-gut dysregulation
ABNORMAL GUT MOTILITY & DIARRHOEA
Coeliac Disease
immunologically mediated disease of SI caused by dietary exposure to gluten
wheat (gliadins), barley (hordeins), rye (secalins)
incompletely digested by proteases - large peptides enter lamina propria via transcellular or paracellular pathways
in suspectible individuals, immune response occurs
potential (+ve serology and normal biopsy), asymptomatic, symptomatic, classic, refractory (persistent symptoms and villous atrophy despite adherence to gluten-free diet)
gluten-free diet (lifelong compliance)
non-adherence
ulcerative jejunoileitis
refractory sprue
increased risk of enteropathy-associated T cell lymphoma (EATL)
decreased bone mineral density (osteopenia)
Genetic:
HLA DQ2/8
HLADQ2/8 necessary for coeliac disease but not sufficient alone to develop it
30% of normal population HLADQ2/8 positive
testing positive cannot be used to diagnose; testing negative excludes diagnosis of coeliac disease
HLA testing performed as adjunct only
DQ2 responsible for 90%
screen first degree relatives, patients with associated disorders e.g. T1DM, IBS, etc.
Environmental: gluten
Immunological:
tissue transglutaminase
gut mucosa repair enzyme (crosslinks ECM proteins)
deamidates glutamine in gliadin to glutamate
deamidation by tTG increases affinity of HLADQ2/8 APCs for gliadin
gliadin-transglutaminase complex presented to CD4+ T cells
immune response - TH1 matrix metalloproteinases/gamma-inteferon
tissue damage
villous atrophy which resolves after removal of offending proteins (hallmark feature)
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intraepithelial lymphocytosis
antibody testing (anti-gliadin deamidated, anti-transglutaminase, anti-endomysial) and IgG testing - gluten ingestion required
occurs mostly in white individuals of northern Europe ancestry
diarrhoea, anaemia, fatigue, bloating, etc.
Inflammatory bowel disease
Ulcerative colitis
ex-smoker
confined to colon and only mucosa affected
rectum always involved, and disease spreads proximally from there
confluent inflammation for variable distance
proctitis (just rectum)
rectal bleeding, constipation, tenesmus (sense of incomplete evacuation), urgency
no diarrhoea (stool already formed)
left-sided colitis (up to L colic flexure)
proctitis symptoms + diarrhoea and abdominal cramps
extensive colitis (beyond L colic flexure)
L-sided colitis symptoms + constitutional: fatigue, weight loss, fever
relapsing or chronic continuous
associated with increased bowel cancer risk
surveillance colonoscopy after 8 years and then every 1-5 years
yearly in patients with primary sclerosing cholangitis
diffuse inflammation, neutrophil and plasma cell infiltration, crypt abscesses and architectural distortion
no fistulas and rarely strictures
5-ASA
Pyoderma gangrenosum (ulcerations on lower skins)
Crohn's disease
can affect any part of GIT, but most commonly ileum and/or colon (particularly ascending)
ileocolic most common, followed by only small bowel, only colon
transmural disease i.e. involves both mucosa and submucosa
characterised by deep fissures and ulcers
discontinuous inflammation i.e. 'skip' lesions
strictures and fistulae can occur
granulomas typical (70%)
not in every case but if present, Crohn's > UC
abnormal connection between 2 epithelialised surfaces
perianal, enteroenteric, enterocolonic, enterocutaneous, enterovesical, rectovaginal
perianal - serious if deep (affecting sphincter)
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surgery
lymphocytes and plasma cells
abdominal pain, diarrhoea (if colon involved), constipation (if ileal), bleeding, systemic (weight loss, fever, malaise), impaired nutrition, obstruction
Erythema nodosum (red nodules on shins)
smoking
smoking cessation
relapsing or chronic continuous
Immunosuppressive: corticosteroids (induction) and immunomodulators/biologic agents (maintenance)
Antibiotics used for infectious complications e.g. abscess
non-Mendelian genetic: NOD2 (ileal), IL-23R, ATGI6LI
more prevalent in developed countries, maximal at 15-35 and 50-70 years
uveitis, episcleritis, arthritis, primary sclerosing cholangitis (particularly in UC), cholangiocarcinoma