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
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)
CROHN’S
Dental Relevance
non-specific lesions
- Aphthous ulcers
- Angular Cheilitis (swollen corners)
- Glossitis (sore tongue)
- Dental Caries
- Gingivitis/Periodontitis
Orofacial Granulomatosis (OFG)
MAKE Q’s
- Orofacial signs/ symptoms similar to CD
- Prevalance : children and young adults
- Concurrent CD 40% children diagnosed
with OFG - Cinnamon & Benzoates free diet : Benefit
70% cases
UC
1. what is it
2. aetiology
3. runs in the family?
1
* Chronic inflammatory bowel disease
* First described: Sir Samuel Wilks 1859
* Diffuse mucosal inflammation of the colon
with backwash involvement of the terminal
ileum:
Rectum always involved
2
* Aetiology unknown :
* Hypothesis – dysregulated interaction mucosal
immunology and intestinal microflora + genetic
predisposition
- Strong Family history…. Jewish Origin
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
diagnosis
–Colonoscopy and Biopsy:
- Exudates, ulcerations, loss of vascular pattern,
friability, continuous granularity (fragile - bleed
when touch). Superficial
inflammation with loss of haustration
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
Microscopic Changes
- mucosal
- Chronic inflammatory cells: lamina propria
- Goblet cell depletion
- Crypt abscess
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
can surgery help UC and crohn’s?
Surgery can be curative for ulcerative colitis
80% of Crohn’s have resections but generally little help (condition is throughout bowel)
Indications for surgery in Ulcerative Colitis
Acute:
Failure of medical treatment for 3 days
Toxic dilatation
Haemorrhage
Perforation
Chronic:
Poor response to medical treatment
Excessive steroid use
Non compliance with medication
Risk of cancer
(main risk indicators for surgery)
I CHOP
- Infection
- Carcinoma
- Haemorrhage
- Obstruction
- Perforation
UC + crohn’s prognosis
UC
1/3 Single attack
1/3 Relapsing attacks
1/3 Progressively worsen requiring colectomy
within 20 years
Crohn’s
Varied prognosis, new biological agents
improving
Cancer
Both have increased risk of colon cancer,
though UC>Crohn’s
Screening colonoscopy done every 2 years
after 10 years disease and every year after 20
years disease
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
Functional Bowel Disorders
- Diverticular disease
– Herniation of bowel mucosa through the
bowel wall
– Inflammation results in diverticulitis
– Treatment: high fibre diet +/- surgery - Irritable bowel syndrome
– Intermittent diarrhoea, abdominal pain and
bloating, relieved by bowel action
– Psychological factors important, some cases
relate to food intolerances
Differential diagnoses
Coeliac disease
IBS
Ischaemic colitis
Diverticular disease
Appendicitis
Polyps
Haemorrhoids
Know the side effects of steroids!
Know the difference between colostomy and ileostomy!
IBS – the most common
first diagnosis of many
GI disorders….
Can mask other
inflammatory
conditions /grumbling
appendicitis,
endometriosis & many more..
Final reflection 2
- Review i rritable bowel s yndrome / disease & how i ts presentation can mimic other c onditions?
- Reflect upon the oral and c utaneous presentations of these c onditions
- Review the differences between UC & Crohns disease
- Reflect on the drugs and mechanisms used t o treat both UC & Crohns & how they can i mpact on oral ca re – eg Steroids, anti-inflammatories, Immuno-suppressing agents etc
- Reflect on how IBS can mimic many other i ntra a bdominal conditions?
(watch last 5 minutes of lecture to finish adding info to cards) (card 49 - 52 need to complete - info only from slides rn)
