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Cell Pathology II > Gastrointestinal Pathology > Flashcards

Gastrointestinal Pathology Flashcards

1
Q

What are the 6 functions of the GIT?

A

Ingestion
Secretion
Mixing and Propulsion
Digestion
Absorption
Defecation

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2
Q

What are the 4 different types of diseases affecting the GIT?

A

Structural defects
Infectious agents
Cellular responses
Neoplasms

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3
Q

What are the 3 different layers associated with the structure of the GIT?

A

Mucosa (epithelium, lamina propria, muscularis mucosae)
Submucosa and the muscularis propria

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4
Q

What are the different functional types of mucosa associated with the GIT?

A

Protective - mouth and anus
Secretory - stomach/tubular
Absorptive - villi and crypts
Absorptive/Protective - straight tubular glands

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5
Q

What is the malignant tumour of the mouth/oral cavity?

A

Squamous cell carcinoma (95%)
- Late diagnosis; 5yr survival ~ 50%

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6
Q

What type of epithelium is present in the pharynx?

A

Stratified Squamous

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7
Q

Which bacteria is most likely to cause pharyngitis?

A

Streptococcus

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8
Q

What are the two most common diseases/disorders of the salivary glands?

A

Obstruction, inflammation (mumps) - blocked duct
Tumours

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9
Q

What type of epithelium is present in the oesophagus?

A

Stratified Squamous

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10
Q

What are 4 examples of structural disorders of the oesophagus?

A
  • achalasia
  • hiatus hernia
  • diverticula
  • laceration
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11
Q

What is dysphagia?

A

Difficulty Swallowing

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12
Q

What is Barrett’s oesophagus?

A

This is where the flat pink lining of the oesophagus which connects the mouth to the stomach becomes damaged by acid reflux causing the lining to thicken and become red.
- Metaplasia

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13
Q

What is another name for reflux oesophagitis?

A

GERD
- most common GI outpatient diagnosis in the US

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14
Q

What are some possible causes to reflux oesphagitis?

A
  • sphincter defect/hernia
  • increased intra-abdominal pressure (surgery, pregnancy, obesity)
  • alcohol, medications
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15
Q

What damage does reflux oesophagitis do at the cellular level?

A

Acid with squamous epithelium leads to cell injury; cell loss at the lumen and an increased basal proliferation.
Basal zone hyperplasia and elongation of connective tissue papillae

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16
Q

How can Barrett’s Metaplasia be diagnosed?

A
  • endoscopic; evidence of columnar lining above the GE junction.
  • histologic evidence
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17
Q

What kind of metaplasia can occur with Barrett’s Metaplasia?

A

Intestinal (glandular with goblet cells) metaplasia within the oesophageal squamous mucosa

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18
Q

What are two examples of benign oesophagheal tumours?

A

Leiomyoma, squamous papilloma

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19
Q

What are the two types of malignant oesphageal tumours?

A
  • squamous cell carcinoma
  • adenocarcinoma
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20
Q

Which area of the oesophagus does Barrett’s Metaplasia / Adenocarcinoma usually affect?

A

The lower 1/3 of the oesophagus

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21
Q

What type of mucosa is present in the stomach?

A

Tubular glandular

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22
Q

What is an example of a congenital abnormality associated with the stomach?

A
  • pyloric stenosis
    Hypertrophy of the circular muscle at pylorus
    Obstruction outflow, projectile vomiting
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23
Q

Acute gastritis is usually ___ in nature?

A

Transient

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24
Q

Chronic gastritis is usually ___ in nature?

A

Chronic, inflammatory changes leading eventually to mucosal atrophy and intestinal metaplasia - usually in the absence of erosions

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25
What is a common cause of chronic gastritis?
H.Pylori, autoimmune disorders and chemical damage
26
Autoimmune Gastritis is caused by?
Antibodies to parietal cells and intrinsic factor.
27
Loss of parietal cells leads to?
Glandular atrophy, loss of HCL secretion and a failure to stimulate gastrin release leading to hypergastrinaemia.
28
Lack of IF cells lead to?
Vit B12 deficiency, anaemia (macrocytic and pernicious anaemia)
29
H. Pylori is which type of bacteria?
It is a common, gram negative, non sporing, curved (seagull) shaped bacterium. It secretes urease
30
H.Pylori is a urease secreing bacterium what does this lead to in the stomach?
Urea breaks down leading to an increase in ammonia and in the local pH.
31
How can H.Pylori be diagnosed?
- urea breath test (gold standard) - antibody test - stool test - gastric biopsy - Urease/CLO test
32
What is PUD associated with? (peptic ulcer disease)
Chronic mucosal ulceration affecting the duodenum/stomach H.Pylori
33
What are some complications associated with PUD?
- scarring - breach of vessel - perforation - malignant transformation RARE
34
What is the definition of a polyp?
Any mass or nodule that projects above the level of the surrounding mucosa.
35
What are the two different types of polyps?
Hyperplastic (75%) - antrum or body, dysplasia risk Adenoma (10%) - occur anywhere, adenocarcinoma risk
36
What are the three types of gastric tumours?
- Gastric adenocarcinoma (most common) - Primary gastric lymphoma - MALToma, H/Pylori - Stromal GIST = tyrosine kinase mutation, surgical resection, tyrosine kinase inhibitors
37
What is the second most common fatal malignancy in the world, accountable for 10% of deaths?
Gastric adenocarcinoma
38
What are some of the symptoms and causes of gastric adenocarcinoma?
Symptoms: chronic gastritis, dysphagia, nausea, weight loss, different bowel habits Causes: diet - high salt, smoked foods, h.pylori, genetics - CDH1 gene
39
What is seen in the intestinal type of gastric adenocarcinoma?
- gland formations - mucus secreting cells - moderately differentiated - well demarcated border
40
What is seen with diffuse type gastric adenocarcinoma?
- signet ring cells - poor differentiation - chains of single cells infiltrating wall - little gland formation - poorly demarcated invasion margin
41
What are the six parts of the large intestine?
- cecum - ascending colon - transverse colon - descending colon - sigmoid colon - rectum
42
What structures are present in the colonic mucosa?
- flat, no villi - vertical crypt - goblet cells (mucous secreting) - tubular glands - thick muscle layers - absorptive cells
43
What is a diverticulum?
An abnormal hollow pouch communicating with the lumen structure from which it has arisen
44
What is Meckel diverticulum and the rule of 2's?
A tubular diverticulum in the ileum. Rule of 2's: - 2% pop - 2 feet from ileocaecal junction - 2 inches long - 2M:F
45
What is meconium ileus?
A small intestine obstruction - viscous meconium - seen in 15% of CF
46
What is Hirschsprung disease?
This is where there is a lack of coordinated peristalsis/aganglionosis. Leading to constipation and repeat obstruction. Rectum and distal colon are usually affected
47
Hirschsprung disease is usually presented in which type of patients, what is the diagnosis process and the treatment?
It is seen in neonates as a failure to pass the meconium. Diagnosis occurs by a resection and the treatment is surgical resection or anastomosis.
48
What is the definition of malabsorption?
Defective absorption of fats, fat and water soluble vitamins, proteins, carbohydrates, electrolytes, minerals and water.
49
What is one of the main causes of malabsorption in the developed world?
Coeliac disease
50
Coeliac disease is a type of autoimmune disease, what is its sensitivity to and what are the results of prolonged exposure to this type?
It is an immune mediated enteropathy and is caused by sensitivity to the gliadin portion of gluten. Its mechanisms of toxicity are unknown T cell mediated chronic inflammation reaction Prolonged interaction with gluten leads to villus atrophy and crypt hyperplasia on the duodenal or jejunal biopsy.
51
What genes are affected in coeliac disease?
HLA-DQ2 DQ8
52
What is the clinical morphology of coeliac disease?
Villus atrophy and crypt hyperplasia on duodenal or jejunal biopsy +/- intraepithelial lymphocytes.
53
What are the serological results of coeliac disease?
Anti-gliadin Anti-endomysial Anti-tissue transglutaminase
54
What are the two main inflammatory diseases of the intestine?
Crohn's Disease Ulcerative colitis (of which 10% of cases are indeterminate)
55
What is the strong genetic predisposition to Crohn's disease?
NOD2 smokers also have an increased risk
56
Where in the alimentary tract can crohn's disease affect?
Any part of the alimentary tract with possible skip regions.
57
What structures are seen in the GIT of Crohn's Disease patients?
- strictures - cobblestone appearance - fissures --> perforation - thickened wall (fibrosis, inflammation, luminal narrowing) - crypt distortion - ulceration - noncaseating granuloma - transmural inflammation - thickening of the wall
58
What type of disorder is ulcerative colitis?
Relapsing inflammatory disorder Affecting the rectum and the variable length of the contiguous colon
59
What is the main genetic predisposition to ulcerative colitis?
HLA-DR2
60
What types of structures are seen in ulcerative colitis?
red granular mucosa and then smooth atrophic mucosa. - continuous lesions - broad based ulcers, polyps, mucosal bridges - crypt abscess
61
Where does ulcerative colitis begin?
In the rectum and involves continuous colonic involvement.
62
What are two vascular disorders of the bowel?
Occlusive Ischaemia (obstruction to blood supply - thrombus or embolism) Non-occlusive ischaemia (inadequate blood supply, hypotension, dehydration, shock or vasoconstriction)
63
Acute Intestinal Infarction morphology can occur in three stages ranging from transient, ulcerated possibly leading to hemorrhage and then possible gangrene.
1. Mucosal 2. Mural - into submucosa, but not through MP 3. Transmural - through the MP --> gangrene
64
What are some of the risk factors of ischemic bowel disease and what are the complications and presentations?
50 yr plus with a history of cardiac or vascular disease Presentation: severe and sudden abdominal pain and tenderness, possible nausea, vomiting and/or blood diarrhea Complications: strictures, gangrene, perforation and death.
65
What is diverticula?
It is the herniations of the mucosa into the intestinal wall.
66
Diverticular disease is most commonly sigmoid, what are the common areas for outpouching?
colonic mucosa + submucosa
67
What are some of the complications of diverticular disease?
- Diverticulitis - Haemorrhage - Fistulae
68
Are tumours of the small intestine more often benign or malignant?
Normally benign - adenomas or stromal for example only about ~1% of tumours are malignant.
69
What are the 2 types of polyps of the colon and rectum?
Non-neoplastic and neoplastic
70
What is the most important clinical feature of a polyp?
Its size as it can lead to malignancy.
71
What are two familial syndromes which contribute to one's risk of developing colorectal cancer?
FAP - familial adenomatous polyposis HNPCC - hereditary non-polyposis colon cancer
72
What is a polyp?
It is any mass or nodule which projects above the level of the surrounding mucosa.
73
What are the two different structures a polyp can take?
- sessile: no stalk - pedunculated: stalk present
74
Non-neoplastic polyps can be which types and what are these types most commonly associated with?
- Inflammatory: IBD - Hyperplastic: increases with age, rectum, low to no malignancy potential
75
Neoplastic polyps can be of which three types and what do neoplastic polyps possibly develop into?
Neoplastic polyps develop into adenomas and possible adenocarcinomas. - tubular (most) - raspberry, with stalk - vilous (10%) - no stalk - tubulovillous (15%)
76
How do carcinomas develop?
From adenomas molecular cascade of gene defects...activation of oncogenes, loss/mutation of TSG and defective DNA repair genes.
77
Familial Adenomatous polyposis (FAP) is caused by mutations of which gene? what is the minimum number of polyps needed for diagnosis?
APC gene 100 polyps minimum
78
FAP if left untreated can lead to what? What is the classical amount of colonic adenomas seen in FAP?
If left untreated will lead to colorectal adenocarcinoma, before 50. 500-2500 colonic adenomas.
79
Hereditary non-polyposis colon cancer is called which and is due to mutations in which two common genes?
Lynch syndrome MSH2, MLH1
80
Colorectal cancer is which place of malignancy deaths?
Second of both sexes
81
Where are the majority of colorectal carcinomas?
50% in the rectum 30% in the sigmoid colon
82
What is the progression of spread in colorectal carcinoma?
direct lymph lungs liver bone
83
TMN has 4 different stages, what are the distinguishing factors of these stages?
1 - invades submucosa 2 - tumour invades into put not through the muscularis propria 3 - tumour invades the adjacent organs 4 - tumour invades adjacent organs
84
Bowelscreen age range?
55-74 yrs every 2 years. Faecal test - detects presence of blood
85
Appendicitis is as a result of which type of inflammation?
Acute suppurative inflammation
86
What type of tumours are found in the anus/anal canal?
- papilloma - carcinoma: adenocarcinoma, basaloid and squamous - melanoma

Cell Pathology II (6 decks)

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