17. Gastroenterology II: ulcerative colitis & Crohn's disease Flashcards
(54 cards)
AIMS & OBEJECTIVES
- Overview of lower gastrointestinal
disorders - Oral manifestations of gastrointestinal
diseases - Dental relevance of lower gastrointestinal
disorders
Anatomy of the lower GI tract
what does small + large intestine cosisist of?
- Small Intestine
Duodenum
(D1/2 = point of no return)
Jejunum
Ileum - Large Intestine (Colon)
Cecum
Rectum
Anal Canal
GI TRACT MAIN FUNCTION
- most og GI tract is involved with processing food
- then excreting faeces (via retum + anus)
COELIAC DISEASE
- what is it?
- genetics?
- prevalence
- presents with what bowel habits?
- diagnosis rate?
- bimodal age distribution
1
* Gluten sensitivity – wheat, barley, rye, oats
* Gluten intolerance
2
* Genetic – HLA B8 tissue type
3
* Prevalence 1:1800
4
* Presents with change of bowel habit (COBH)
o Pale, bulky, offensive, greasy stool
o Abdominal colic
o Weakness, weight loss
o Short stature/failure to thrive
5
* Under-diagnosed in most affected people;
o true incidence ~ 1% US & Western
European population
o migration ~ increasingly seen in Africa,
Asia & Middle East
6
* Bimodal age distribution
o 8-12 months and 3-4th decade;
o prevalence in >60 yrs is 20%
COELIAC DISEASE
symptoms (GI + extra-intestinal)
GASTROINTESTINAL
Diarrhea (45-85%)
Flatulence (28%)
Borborygmus (35-72%)
Weight loss (45%)
Weakness, fatigue (80%)
Abdominal pain (30-65%)
Secondary lactose intolerance
Steatorrhea
EXTRA-INTESTINAL
*Anemias (10-15%)
~ especially Fe, B12
~ due to damage to lining = malabsorption
*Neurological Sx (8-14%)
~ tingling, weakness
*Skin disorders (10-20%)
~ itchy skin (image)
*Endocrine disturbances incl
~ infertility
~ impotence
~ amenorrhea
~ delayed menarche
COELIAC DISEASE
diagnosis
1 SEROLOGY
Antibodies to target in serum:
- gliadin
- endomysium
- transglutaminase (ttg)
IgA antibodies to TTG first and best test;
if under 2 years of age may need IgG ab
to TTG
Check total IgA antibodies because 3-5%
patients are IgA deficient
Antiendomesial antibodies have higher
sensitivity than antigliadin abs
antigliadin antibodies can regress with
gluten free diets
ENDOSCOPIC BIOPSY
- if a patient has HLA haplotypes &TTG antibodies with classical symptoms then bx not necessary for dx
-inflamed small gut lining with loss of epithelium integrity
- Pillcam offers biopsy free non-invasive inspection
COELIAC DISEASE
treatment
Gluten restriction curative in 95%
Refractory in 5%
- use corticosteroids, poor outcome
Involve dietician, support groups, on-line recipes,
read labels including medications, cosmetics, etc
Although rare, remember there is increased risk of lymphoma and adenocarcinoma of the pancreas, esophagus, small bowel, biliary tract, including T & B cell non-Hodgkins lymphoma
COELIAC DISEASE
long term effects
- tooth enamel defects - only apply during amelogenesis rather than later on in life
COELIAC DISEASE
dental relevance
- Problems related to malabsorption
– B12, folate, ferritin: glossitis, angular
cheilits, anaemia, burning mouth,
smooth tongue…..
– Vitamin K – bleeding tendency
– Vitamin D – osteomalacia and
rickets in children - Enamel defects may occur in the permanent dentition if the onset is in childhood
Reflection 1
Review the mechanisms and athogenesis of Coeliac disease and gluten sensitivities
Consider the potential malabsorbtions that can occur in coeliac – in particular the Fe Folate & B12 issues and how these impact upon anaemias and also how they manifest as Oral disease?
Reflect upon how exclusion works as a primary
management strategy here & reflect upon other
diseases that might use similar strategies?
- big 2 inflamm bowel disorders
- difference?
1
- Crohn’s disease
- Ulcerative colitis
2
CROHN’s
- can affect any part of bowel
UC
- restricted to colon
- usu distal half rather than proximal
- some colitis disorders have features of both
CROHN’S + UC
epidemiology
1. /100000
2. F:M
3. age
CROHN’S UC
1
Slightly less common Slightly more common
27-106/100,000 80-150/100,000
2
Females: 1.2:1 Males: 1.2:1
3
Younger: 26 Older: 34
CROHN’S + UC
Aetiology
- largely unknown BUT know it’s an autoimmune disease
- Genetics
Polygenic: 16, 12, 6, 14, 5, 19, 1, 3
HLA DRB
Familial (1 in 5) - Host immunology
Defective mucosal immune system
Inappropriate response to intraluminal
bacteria
T-cells and cytokines
CROHN’S + UC
Aetiology : environmental influence?
CROHN’S UC
Good hygiene/ No relation to hygiene
developed countries
Appendicectomy Appendicectomy is
protective
Smokers Non smokers
Breast feeding is Breast feeding is protective protective
CROHN’S + UC
Pathology
CROHN’S UC
- Mouth to anus - Rectum and extends
proximally - Terminal illeum - Proctitis
- Ileocolonic disease - Left sided colitis
Ascending colon Sigmoid and
descending - Skip lesions - Pancolitis
- Pancolitis - Backwash ileitis
Can be large Distal terminal
bowel only illem
NOTE
- pancolitis = inflamm of large bowel in total
- proctitis = inflamm of anal ring and last part of rectum
- backwash ileitis = if earliest (most proximal) part of colon is inflamed, tends to pass irritation back into last part of ileum (important as terminal ileum is part where B12 absorption finally occurs)
- lack of B12
= contributes to anaemia
= oral mucosa stability
CROHN’S
- what is it?
- aetiology?
- age?
1
* Chronic Inflammatory bowel disease :
- Chronic and recurring inflammation of the
GI tract
* First described 1932 Burril Crohn
* Patchy distribution ‘skip lesions’ – terminal ileum
and colon
2
* Aetiology unknown : inflammatory response to
intestinal microbes + environmental factors +
genetic factors
3
* Teens or early twenties, second peak in old age
* Prevalence 1:1300-1:2500
CROHN’S
presentation?
– Intermittent abdominal pain, diarrhoea,
abdominal distension (90%)
– Decreased appetite
– Anaemia and weight loss (50%)
– Fresh blood or melaena passed through rectum (40%)
– Fistulae and perianal sepsis (20%)
– Episodes of flares with asymptomatic intervals
NOTE
- fistulae = epithelium lined tract between one hollow epithelial organ and another
- perianal sepsis = infected fissures in mucosa around anal ring
IMAGE
- thickened wall w/ deep fissures
- fat wrapping
cobble stoning
CROHN’S
3 major phenotypes?
- Stricturing: gradual thickening of intestinal
wall: leads to stenosis/ obstruction - Penetrating: intestinal fistulas between GI
tract and other organs. External fistulas –
skin - Non- Penetrating: anal fissures, abscesses
CROHN’S
macroscopic changes
o Bowel is thickened
o Lumen is narrowed
o Deep ulcers
o Mucusal fissures
o Cobblestone
o Fistulae
o Abscess
o Apthoid ulceration
CROHN’S
Microscopic Changes
- transmural (can form goes from internal to external wall of infected part of gut - why they can form fistulae in other organs)
- Chronic inflammatory cells: transmural
- Lymphoid hyperplasia
- Granulomas
Langhan’s cells
CROHN’S
diagnosis?
– Barium enema: rose thorn, skip lesion, string
sign
– Sigmoidoscopy and biopsy, colonoscopy
– Differential diagnosis includes TB and
sarcoidosis
CROHN’S
treatment?
- symptomatic relief, reduction of
inflammation, increase QOL (quality of life)
– Medical – Glucocorticoids,
Immunomodulators, biologics
– Surgical – Intestinal resection (if too much scarring has occurred)
CROHN’S
Dental Relevance
- Oral manifestations:
- First described: Dudeney 1969.
- Prevalance: Children > Adults
Proximal/ Perianal CD - Precede or Coincide with intestinal disease
- Classification: Specific and Non-Specific
CROHN’S
Dental Relevance
specific lesions
- Specific lesions:
- Diffuse labial and buccal swelling
- Cobblestones
- Mucosal tags
- Linear ulcers
- Mucogingivits (inflamm of gingivitis)
- Granulomatous Cheilitis (swollen lips that
evert)
