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P11- GI pathology for dentists Flashcards

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1
Q

Name 2 inflammatory conditions.

A
  • Inflammatory bowel disease

- Coeliac disease

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2
Q

Name 2 inflammatory bowel diseases.

A
  • Crohn disease

- Ulcerative colitis

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3
Q

What is an inflammatory bowel disease ?

A

Chronic condition due to inappropriate mucosal immune activity

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4
Q

who are inflammatory bowel disease more common in?

A
  • developed nations and males
  • higher incidence in Ashkenazi jews
  • frequently present in young adulthood
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5
Q

Describe the pathogenesis of inflammatory bowel disease.

A
  • Hygiene hypothesis
  • Thought due to combination of defects in host response to intestinal microbes, intestinal epithelial function and immune responses
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6
Q

Describe the genetic pathogenesis of inflammatory bowel disease.

A

increased risk with affected family members (Crohn – 50% concordance monozygotic twins and ass with NOD2 gene)

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7
Q

Describe the immune response of the inflammatory bowel disease.

A

association with certain types of T helper cells and interleukin receptors, treated immunosuppression

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8
Q

Describe the epithelial defect of inflammatory bowel disease.

A

barrier dysfunction, abnormal Paneth cell granules

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9
Q

Describe the microbes of inflammatory bowel disease.

A

more limited flora thought to have greater impact

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10
Q

what can help the microbes in the inflammatory bowel disease?

A

antibiotics

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11
Q

What impact does smoking have on inflammatory bowel diseases?

A

Crohn - smoking makes the disease worse

Ulcerative colitis - smoking can help

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12
Q

Describe the Crohn vs UC features.

A 
Crohn 
•  Anywhere in GI tract
•  Skip lesions !!!!
•  Thick wall
•  Strictures
•  Deep, knife-like ulcers
•  Moderate pseudopolyps
•  Transmural inflammation
•  Granulomas (35-50%)
•  Fistulae/sinuses
•  Recurrence after surgery
UC
•  Limited to colon and rectum 
•  Continuous disease !!!!
•  Thin wall
•  No strictures
•  Superficial, broad based ulcers 
•  Marked pseudopolyps
•  Mucosal inflammation
•  No granulomas
•  No fistulae/sinuses
•  No recurrence after surgery
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13
Q

What can be seen histologically in Crohn’s disease?

A
  • Crypt abcess -neutrophiles leaked out

- Granuloma -aggregate of histiocytes

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14
Q

what are the oral manifestations of Crohn’s?

A

– oral lesions may precede in 30%
− oral ulcers and ‘cobblestone mucosa’
similar to elsewhere in GI tract − recurrent aphthous ulcers

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15
Q

what are the oral manifestations of UC?

A
  • Recurrent aphthous ulcers

- Pyostomatitis vegatans

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16
Q

what is Coeliac disease?

A

Immune mediated disease due to ingestion gluten containing cereals

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17
Q

what is the prevalence of coeliac disease?

A

1% prevalence in countries of mostly caucasian European descent

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18
Q

Who does coeliac disease normally present in?

A

30-60 years

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19
Q

what is coeliac disease in association with?

A

HLA-DQ8, dermatitis herpetiformis and other auto-immune diseases

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20
Q

Describe the pathogenesis of coeliac disease.

A
  • Gliadin (component of gluten) triggers immune system
  • activation of intra- epithelial lymphocytes
  • Tissue damage
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21
Q

What is the histology of coeliac disease?

A
  • Villous atrophy
  • Crypt hyperplasia
  • Increased intra-epithelial lymphocytes
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22
Q

What are the oral manifestations of coeliac disease?

A
  • Enamel defects
  • Delayed eruption
  • Recurrent aphthous ulcers
  • Angular cheilitis
  • Atrophic glossitis
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23
Q

what 4 types of cancers are in this lecture?

A 
•  Oral squamous cell carcinoma
•  Oesophageal :
- squamous cell carcinoma
- adenocarcinoma 
•  Colo-rectal carcinoma
•  Anal carcinoma
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24
Q

who is oral squamous cell sarcoma (SCC) most common in?

A
  • More common in men

* Increasing incidence with age

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25
What is the multifactorial aetiology of oral SCC?
smoking, alcohol, HPV, betel nut, genetics, chronic irrita*on
26
what is the pathogenesis of oral SCC?
successive genetic alterations due to activation/inactivation of oncogenes/ tumour suppression genes
27
what is the morphology of an oral SCC?
Can present as white patch, speckled patch, red patch, verrucous-like or ulceration
28
what is the histology of an oral SCC?
- begins as dysplastic lesion :squamous cells breach basement membrane - can be poor, moderate or well differentiated - must show keratin or prickle cells
29
what are the majority of oesophageal cancers?
Majority are SCC and adenocarcinoma
30
what is the most common type of oesophageal cancer?
SCC commonest worldwide, but adenocarcinoma increasing in western society
31
who is oesophageal cancer more common in?
More common in men and with increasing age
32
where is an SCC most common in the oesophagus?
in the middle third
33
what is the aetiology of a SCC in the oesophagus?
smoking, alcohol, oesophageal injury, achalasia, Plummer-Vinson syndrome, mediastinal radiotherapy
34
what is the pathogenesis of an oesophageal SCC similar to?
oral SCC
35
what does oesophageal SCC look like macroscopic?
polypoidal/exophytic or ulcerated and diffusely infiltrative
36
where is a adneocarcinoma most common in the oesophagus?
distal third
37
what is the aetiology of a adenocarcinoma in the oesophagus?
GORD, smoking, obesity, previous radiotherapy
38
what is the pathogenesis of adenocarcinoma in the oesophagus?
stepwise accumulation of genetic abnormalities, usually arises in area of Barrek oesophagus
39
what does oesophageal adenocarcinoma look like macroscopic?
similar to SCC
40
what does an oesophageal adenocarcinoma look like histologically?
mucin producing intestinal type glands, signet cells or small poorly differentiated cells which invade beyond muscularis mucosa
41
what is the commonest GI malignancy and the 4th most common malignancy in the UK?
colo-rectal carcinoma
42
who is most affected by colo-rectal carcinoma?
- Increased incidence with age | - males and females almost equally affected
43
what is the aetiology of cold-rectal carcinoma?
diet and genetics
44
What is the pathogenesis of cold-rectal carcinoma?
stepwise accumulation of multiple genetic defects, 2 pathways (classic adenoma-carcinoma sequence, DNA mismatch repair deficiency), arise from adenomatous polyps
45
Describe the presentation of cool-rectal carcinoma?
* Polypoidal or ulcerated mass * Histology similar to adenocarcinoma elsewhere in GI tract, elicits strong desmoplastic stromal response, dirty necrosis in gland lumen * Can metastasis to the head and neck region – asymptomatic, lump/swelling, paraesthesia, tooth mobility
46
what are the two types of anal cancer?
Glandular or squamous
47
what are the risk factors of anal cancer?
HPV, smoking, immunosuppression, chronic inflammation, age, gender
48
what is anal cancer associated with?
condyloma accuminatum
49
what is the pathogenesis of anal cancer?
- Normal - dysplasia - carcinoma
50
Name 3 syndromes discussed in this lecture.
* Gardner syndrome * Peutz-Jeghers syndrome * Plummer-Vinson syndrome
51
Describe what garner syndrome is.
* Rare – autosomal dominant, but 1/3 spontaneous mutations | * Mutation on long arm of chromosome 5 (APC gene)
52
What is the presentation of Gardner syndrome?
familial adenomatous polyposis, osteomas of skull/paranasal sinuses/mandible, desmoid tumours, epidermoid cysts, thyroid carcinoma, dental abnormalities
53
When is the 1st polyp of Gardner syndrome?
teenager
54
what percentage of people will develop colo-rectal cancer after garner syndrome?
100% will develop colo-rectal cancer, often before 30s
55
Describe what pout-jeghers syndrome is.
* Rare - autosomal dominant, few sporadic cases | * Often present 10-15 years
56
what is the pathogenesis of peutz-jeghers syndrome?
associated with loss of function mutation in LBK1/STK11 gene
57
what is the presentation of peutz-jeghers syndrome?
hamartomatous polyps commonly in small intestine, intusseption and obstruction, adenocarcinoma of GI tract, thyroid, breast, genital tract, pancreas, lung, bladder
58
what are the oral manifestations of pout-jeghers syndrome?
dark blue/brown macules peri-oral, labial/buccal mucosa and tongue
59
what is plummer-vinson syndrome?
Most common in middle aged caucasians of N. European descent
60
what is the pathogens of plummer-vinson syndrome?
Nutritional factors (Fe deficiency anaemia), autoimmune, genetic, infection
61
what is the presentation of Plummer-vinson syndrome?
oesophageal webs proximal oesophagus, oesophageal rings distal oesophagus, symptoms of anaemia, nail changes, brikle hair
62
what are the oral manifestations of plummer-vinson syndrome?
glossitis, angular cheilitis, SCC
63
what is plummer-vinson syndrome associated with?
Associated with coeliac disease, pernicious anaemia, Crohn disease, diverticular disease, colo-rectal tumours
64
what is cirrhosis?
Long term damage to liver leading to scarring fibrosis
65
what is the aetiology of cirrhosis?
alcohol abuse, NAFLD, viral hepatitis, autoimmune disease, genetic diseases, drugs
66
what is the pathogenesis of cirrhosis?
death of hepatocytes, ECM deposition, vascular reorganisa*on and proliferation of remaining hepatocytes
67
what is the presentation of cirrhosis?
non-specific, jaundice, portal hypertension, clonng dysfunction, hepatocellular carcinoma
68
what are the oral manifestations/complications of cirrhosis?
* Jaundiced mucosa * Prolonged bleeding * Glossitis (alcoholic cirrhosis) * Impaired drug metabolism
69
what are the take nom messages of this lecture?
* The oral cavity is part of the GI tract * Many of the conditions affecting the GI tract can have oral manifesta*ons * Risk factors for oral cancer the same as cancers elsewhere – possibility of synchronous tumours * Knowledge of the medical history can have diagnostic and treatment implications

Pathology (9 decks)

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