17. Gastroenterology II: ulcerative colitis & Crohn's disease Flashcards
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
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)
CROHN’S
Dental Relevance
non-specific lesions
- Aphthous ulcers
- Angular Cheilitis (swollen corners)
- Glossitis (sore tongue)
- Dental Caries
- Gingivitis/Periodontitis
UC
presentation
- painless, bloody diarrhoea with mucus
- Associated with fevers and remissions to near normal
- ulcerative patches accompanied by polyps
- UC can mimic diverticulitis
- polyps can be pre-malignant
- polyps and diverticulitis are not directly associated to UC BUT can coexist and be differential diagnosis
UC vs CROHN’S
CROHN’S
UC
- less fat wrapping
- bowel wall = less thickened than crohns
- loss of striations
- surviving mucosa can have small bumps = pseudopolyps
UC
- histology
(MAKE Q)
- primarily involve mucosal layer only
- crypt distortion + abscess = common
- absence of goblet cells
UC
treatment
– high protein, high fibre diet, 5-ASA
(5- amino salicyclic acid), sulphasalazine & mesalazine, thioprines, corticosteroids,
* Surgery may be required if longstanding
* Complications/Risks:
Colorectal Cancer due to chronic inflammation
UC
Macroscopic
changes
Reddened mucosa
Shallow ulcers
Pussy exudate
Inflamed and
easily bleeds
- loss of microvascular pattern
- bowel lumen = more open
UC
extra GI UC issues?
*Occular
- episcleritis
- uveitis
*Renal
- stones
- hydronephrosis
- UTI
*Dermatological
- erythema nodosum
*ORAL
- stomatis
- aphthous ulcers
*Hepato-billiary
- gall stones
*Vascular
*Skeletal
- spondylitis
- peripheral arthritis
UC
Extraintestinal Manifestations
Occular
EYES Crohn’s UC
Uveitis 5% 2%
Episcleririts 7% 6%
Conjunctivitis 7% 6%
UC
Extraintestinal Manifestations
Joints
Type 1 Arthropaty
(Pauci)
Type 2 Arthropathy
(Poly)
Arthralgia
Ankylosing Spondylitis
Inflammatory back pain
UC
Extraintestinal Manifestations
skin
SKIN Crohn’s UC
Erythema Nodosum 4% 1%
Pyoderma Gangrenosum 2% 1%
UC
Extraintestinal Manifestations
liver/ billary
LIVER/BILLARY Crohn’s UC
Sclerosing cholangitis 1% 5%
Gall stones Increased Normal Fatty liver Common Common Hepatitis/ Cirrhosis Uncommon
- Kidney stones in Crohn’s
oxalate stones post resection - Anaemia
B12 deficiency in Crohn’s - Venous thrombosis
- Other autoimmune diseases
NOTE
Sclerosing cholangitis = scarring enclosing of biliary tree
UC
Dental Relevance
- Oral manifestations:
- Pyostomatitis vegetans
- benign, multiple small white and yellow
pustules, erythematous/oedematous
background. ‘snail track’ ulcers.
- M>F 3:1
- 20-60years
- Labial attached gingivae, soft/hard palate,
buccal mucosa, sulcus.
- Intestinal symptoms usually precede PV.
UC
other oral conditions going along with
(make Q)
- Aphthous ulcers
- Tongue coating
- Gingivitis
- Periodontitis
- Halitosis
- Acidic taste
- Cutaneous manifestations
Cutaneous Manifestations of Ulcerative Colitis EGs
- erythema nodosum
- vasculitis
- pyodermatitis
- pyoderma gangrenosum
IBD (EG UC + CD)
what Q’s to ask when making a diagnoses
What else to ask?
Rashes
Mouth ulcers
Joint/back pain
Eye problems
Family history
Smoking status
Clinical finals: IBD Investigations
- Bedside
Stool culture: exclude infection
Sigmoidoscopy - Bloods
FBC : anaemia and likely raised WCC
Haematemics: type of anaemia
Inflammartory markers
LFT: hypoalbuminaemia is present in severe
disease, hepatic manifestations
Blood cultures: if septicaemia is suspected in
the acute presentation
Serological: pANCA (UC) - Imaging
Plain AXR: helpful in acute attacks
~ Thumb printing
~ Lead pipe sign
Barium follow-through in Crohn’s
CT
CXR
Perforation
USS
Treating IBD
- Induce remission
Steroids – oral or IV
Enteral nutrition
Azathioprine / 6MP (Crohns) - Maintain remission
Aminosalicylates (UC)
Azathipreine/ 6MP
Methorexate - Biologics generally for Crohn’s only
Infliximab, adalimumab
Test for TB first! - surgical management
CARCINOMA OF THE COLON
- predisposing factors?
- site?
- presentation?
1
* Predisposing factors: Neoplastic polyps, UC FH,
familial polyposis coli, previous cancer
2
* Site 45% rectum, 25% sigmoid, 15% caecum and ascending colon
3
* Presentation: depends on site
– Left colon: bleeding PR, COBH and tenesmus
– Right colon: anaemia, weight loss & abdo pain
– Both: obstruction, perforation,
haemorrhage / fistulae
– Troisier’s sign – Virchow’s Node
IBS – the most common
first diagnosis of many
GI disorders….
Can mask other
inflammatory
conditions /grumbling
appendicitis,
endometriosis & many more..
