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Pathology > P11- GI pathology for dentists > Flashcards

P11- GI pathology for dentists Flashcards

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
Q

What is the multifactorial aetiology of oral SCC?

A

smoking, alcohol, HPV, betel nut, genetics, chronic irrita*on

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26
Q

what is the pathogenesis of oral SCC?

A

successive genetic alterations due to activation/inactivation of oncogenes/ tumour suppression genes

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27
Q

what is the morphology of an oral SCC?

A

Can present as white patch, speckled patch, red patch, verrucous-like or ulceration

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28
Q

what is the histology of an oral SCC?

A
  • begins as dysplastic lesion :squamous cells breach basement membrane
  • can be poor, moderate or well
    differentiated
  • must show keratin or prickle cells
29
Q

what are the majority of oesophageal cancers?

A

Majority are SCC and adenocarcinoma

30
Q

what is the most common type of oesophageal cancer?

A

SCC commonest worldwide, but adenocarcinoma increasing in western society

31
Q

who is oesophageal cancer more common in?

A

More common in men and with increasing age

32
Q

where is an SCC most common in the oesophagus?

A

in the middle third

33
Q

what is the aetiology of a SCC in the oesophagus?

A

smoking, alcohol, oesophageal injury, achalasia, Plummer-Vinson syndrome, mediastinal radiotherapy

34
Q

what is the pathogenesis of an oesophageal SCC similar to?

A

oral SCC

35
Q

what does oesophageal SCC look like macroscopic?

A

polypoidal/exophytic or ulcerated and diffusely infiltrative

36
Q

where is a adneocarcinoma most common in the oesophagus?

A

distal third

37
Q

what is the aetiology of a adenocarcinoma in the oesophagus?

A

GORD, smoking, obesity, previous radiotherapy

38
Q

what is the pathogenesis of adenocarcinoma in the oesophagus?

A

stepwise accumulation of genetic abnormalities, usually arises in area of Barrek oesophagus

39
Q

what does oesophageal adenocarcinoma look like macroscopic?

A

similar to SCC

40
Q

what does an oesophageal adenocarcinoma look like histologically?

A

mucin producing intestinal type glands, signet cells or small poorly differentiated cells which invade beyond muscularis mucosa

41
Q

what is the commonest GI malignancy and the 4th most common malignancy in the UK?

A

colo-rectal carcinoma

42
Q

who is most affected by colo-rectal carcinoma?

A
  • Increased incidence with age

- males and females almost equally affected

43
Q

what is the aetiology of cold-rectal carcinoma?

A

diet and genetics

44
Q

What is the pathogenesis of cold-rectal carcinoma?

A

stepwise accumulation of multiple genetic defects, 2 pathways (classic adenoma-carcinoma sequence, DNA mismatch repair deficiency), arise from adenomatous polyps

45
Q

Describe the presentation of cool-rectal carcinoma?

A
  • 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
Q

what are the two types of anal cancer?

A

Glandular or squamous

47
Q

what are the risk factors of anal cancer?

A

HPV, smoking, immunosuppression, chronic inflammation, age, gender

48
Q

what is anal cancer associated with?

A

condyloma accuminatum

49
Q

what is the pathogenesis of anal cancer?

A
  • Normal
  • dysplasia
  • carcinoma
50
Q

Name 3 syndromes discussed in this lecture.

A
  • Gardner syndrome
  • Peutz-Jeghers syndrome
  • Plummer-Vinson syndrome
51
Q

Describe what garner syndrome is.

A
  • Rare – autosomal dominant, but 1/3 spontaneous mutations

* Mutation on long arm of chromosome 5 (APC gene)

52
Q

What is the presentation of Gardner syndrome?

A

familial adenomatous polyposis, osteomas of skull/paranasal sinuses/mandible, desmoid tumours, epidermoid cysts, thyroid carcinoma, dental abnormalities

53
Q

When is the 1st polyp of Gardner syndrome?

A

teenager

54
Q

what percentage of people will develop colo-rectal cancer after garner syndrome?

A

100% will develop colo-rectal cancer, often before 30s

55
Q

Describe what pout-jeghers syndrome is.

A
  • Rare - autosomal dominant, few sporadic cases

* Often present 10-15 years

56
Q

what is the pathogenesis of peutz-jeghers syndrome?

A

associated with loss of function mutation in LBK1/STK11 gene

57
Q

what is the presentation of peutz-jeghers syndrome?

A

hamartomatous polyps commonly in small intestine, intusseption and obstruction, adenocarcinoma of GI tract, thyroid, breast, genital tract, pancreas, lung, bladder

58
Q

what are the oral manifestations of pout-jeghers syndrome?

A

dark blue/brown macules peri-oral, labial/buccal mucosa and tongue

59
Q

what is plummer-vinson syndrome?

A

Most common in middle aged caucasians of N. European descent

60
Q

what is the pathogens of plummer-vinson syndrome?

A

Nutritional factors (Fe deficiency anaemia), autoimmune, genetic, infection

61
Q

what is the presentation of Plummer-vinson syndrome?

A

oesophageal webs proximal oesophagus, oesophageal rings distal oesophagus, symptoms of anaemia, nail changes, brikle hair

62
Q

what are the oral manifestations of plummer-vinson syndrome?

A

glossitis, angular cheilitis, SCC

63
Q

what is plummer-vinson syndrome associated with?

A

Associated with coeliac disease, pernicious anaemia, Crohn disease, diverticular disease, colo-rectal tumours

64
Q

what is cirrhosis?

A

Long term damage to liver leading to scarring fibrosis

65
Q

what is the aetiology of cirrhosis?

A

alcohol abuse, NAFLD, viral hepatitis, autoimmune disease, genetic diseases, drugs

66
Q

what is the pathogenesis of cirrhosis?

A

death of hepatocytes, ECM deposition, vascular reorganisa*on and proliferation of remaining hepatocytes

67
Q

what is the presentation of cirrhosis?

A

non-specific, jaundice, portal hypertension, clonng dysfunction, hepatocellular carcinoma

68
Q

what are the oral manifestations/complications of cirrhosis?

A
  • Jaundiced mucosa
  • Prolonged bleeding
  • Glossitis (alcoholic cirrhosis)
  • Impaired drug metabolism
69
Q

what are the take nom messages of this lecture?

A
  • 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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