Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Structural defects
Infectious agents
Cellular responses
Neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What type of epithelium is present in the pharynx?

A

Stratified Squamous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which bacteria is most likely to cause pharyngitis?

A

Streptococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Obstruction, inflammation (mumps) - blocked duct
Tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What type of epithelium is present in the oesophagus?

A

Stratified Squamous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are 4 examples of structural disorders of the oesophagus?

A
  • achalasia
  • hiatus hernia
  • diverticula
  • laceration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is dysphagia?

A

Difficulty Swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is another name for reflux oesophagitis?

A

GERD
- most common GI outpatient diagnosis in the US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some possible causes to reflux oesphagitis?

A
  • sphincter defect/hernia
  • increased intra-abdominal pressure (surgery, pregnancy, obesity)
  • alcohol, medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can Barrett’s Metaplasia be diagnosed?

A
  • endoscopic; evidence of columnar lining above the GE junction.
  • histologic evidence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are two examples of benign oesophagheal tumours?

A

Leiomyoma, squamous papilloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two types of malignant oesphageal tumours?

A
  • squamous cell carcinoma
  • adenocarcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

The lower 1/3 of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of mucosa is present in the stomach?

A

Tubular glandular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Acute gastritis is usually ___ in nature?

A

Transient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is a common cause of chronic gastritis?

A

H.Pylori, autoimmune disorders and chemical damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Autoimmune Gastritis is caused by?

A

Antibodies to parietal cells and intrinsic factor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Loss of parietal cells leads to?

A

Glandular atrophy, loss of HCL secretion and a failure to stimulate gastrin release leading to hypergastrinaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Lack of IF cells lead to?

A

Vit B12 deficiency, anaemia (macrocytic and pernicious anaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

H. Pylori is which type of bacteria?

A

It is a common, gram negative, non sporing, curved (seagull) shaped bacterium.
It secretes urease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

H.Pylori is a urease secreing bacterium what does this lead to in the stomach?

A

Urea breaks down leading to an increase in ammonia and in the local pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How can H.Pylori be diagnosed?

A
  • urea breath test (gold standard)
  • antibody test
  • stool test
  • gastric biopsy
  • Urease/CLO test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is PUD associated with? (peptic ulcer disease)

A

Chronic mucosal ulceration affecting the duodenum/stomach
H.Pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are some complications associated with PUD?

A
  • scarring
  • breach of vessel
  • perforation
  • malignant transformation RARE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the definition of a polyp?

A

Any mass or nodule that projects above the level of the surrounding mucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the two different types of polyps?

A

Hyperplastic (75%) - antrum or body, dysplasia risk
Adenoma (10%) - occur anywhere, adenocarcinoma risk

36
Q

What are the three types of gastric tumours?

A
  • Gastric adenocarcinoma (most common)
  • Primary gastric lymphoma - MALToma, H/Pylori
  • Stromal GIST = tyrosine kinase mutation, surgical resection, tyrosine kinase inhibitors
37
Q

What is the second most common fatal malignancy in the world, accountable for 10% of deaths?

A

Gastric adenocarcinoma

38
Q

What are some of the symptoms and causes of gastric adenocarcinoma?

A

Symptoms: chronic gastritis, dysphagia, nausea, weight loss, different bowel habits

Causes: diet - high salt, smoked foods, h.pylori, genetics - CDH1 gene

39
Q

What is seen in the intestinal type of gastric adenocarcinoma?

A
  • gland formations
  • mucus secreting cells
  • moderately differentiated
  • well demarcated border
40
Q

What is seen with diffuse type gastric adenocarcinoma?

A
  • signet ring cells
  • poor differentiation
  • chains of single cells infiltrating wall
  • little gland formation
  • poorly demarcated invasion margin
41
Q

What are the six parts of the large intestine?

A
  • cecum
  • ascending colon
  • transverse colon
  • descending colon
  • sigmoid colon
  • rectum
42
Q

What structures are present in the colonic mucosa?

A
  • flat, no villi
  • vertical crypt
  • goblet cells (mucous secreting)
  • tubular glands
  • thick muscle layers
  • absorptive cells
43
Q

What is a diverticulum?

A

An abnormal hollow pouch communicating with the lumen structure from which it has arisen

44
Q

What is Meckel diverticulum and the rule of 2’s?

A

A tubular diverticulum in the ileum.
Rule of 2’s:
- 2% pop
- 2 feet from ileocaecal junction
- 2 inches long
- 2M:F

45
Q

What is meconium ileus?

A

A small intestine obstruction
- viscous meconium
- seen in 15% of CF

46
Q

What is Hirschsprung disease?

A

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
Q

Hirschsprung disease is usually presented in which type of patients, what is the diagnosis process and the treatment?

A

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
Q

What is the definition of malabsorption?

A

Defective absorption of fats, fat and water soluble vitamins, proteins, carbohydrates, electrolytes, minerals and water.

49
Q

What is one of the main causes of malabsorption in the developed world?

A

Coeliac disease

50
Q

Coeliac disease is a type of autoimmune disease, what is its sensitivity to and what are the results of prolonged exposure to this type?

A

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
Q

What genes are affected in coeliac disease?

A

HLA-DQ2
DQ8

52
Q

What is the clinical morphology of coeliac disease?

A

Villus atrophy and crypt hyperplasia on duodenal or jejunal biopsy +/- intraepithelial lymphocytes.

53
Q

What are the serological results of coeliac disease?

A

Anti-gliadin
Anti-endomysial
Anti-tissue transglutaminase

54
Q

What are the two main inflammatory diseases of the intestine?

A

Crohn’s Disease
Ulcerative colitis (of which 10% of cases are indeterminate)

55
Q

What is the strong genetic predisposition to Crohn’s disease?

A

NOD2
smokers also have an increased risk

56
Q

Where in the alimentary tract can crohn’s disease affect?

A

Any part of the alimentary tract with possible skip regions.

57
Q

What structures are seen in the GIT of Crohn’s Disease patients?

A
  • strictures
  • cobblestone appearance
  • fissures –> perforation
  • thickened wall (fibrosis, inflammation, luminal narrowing)
  • crypt distortion
  • ulceration
  • noncaseating granuloma
  • transmural inflammation
  • thickening of the wall
58
Q

What type of disorder is ulcerative colitis?

A

Relapsing inflammatory disorder
Affecting the rectum and the variable length of the contiguous colon

59
Q

What is the main genetic predisposition to ulcerative colitis?

A

HLA-DR2

60
Q

What types of structures are seen in ulcerative colitis?

A

red granular mucosa and then smooth atrophic mucosa.
- continuous lesions
- broad based ulcers, polyps, mucosal bridges
- crypt abscess

61
Q

Where does ulcerative colitis begin?

A

In the rectum and involves continuous colonic involvement.

62
Q

What are two vascular disorders of the bowel?

A

Occlusive Ischaemia (obstruction to blood supply - thrombus or embolism)
Non-occlusive ischaemia (inadequate blood supply, hypotension, dehydration, shock or vasoconstriction)

63
Q

Acute Intestinal Infarction morphology can occur in three stages ranging from transient, ulcerated possibly leading to hemorrhage and then possible gangrene.

A
  1. Mucosal
  2. Mural - into submucosa, but not through MP
  3. Transmural - through the MP –> gangrene
64
Q

What are some of the risk factors of ischemic bowel disease and what are the complications and presentations?

A

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
Q

What is diverticula?

A

It is the herniations of the mucosa into the intestinal wall.

66
Q

Diverticular disease is most commonly sigmoid, what are the common areas for outpouching?

A

colonic mucosa + submucosa

67
Q

What are some of the complications of diverticular disease?

A
  • Diverticulitis
  • Haemorrhage
  • Fistulae
68
Q

Are tumours of the small intestine more often benign or malignant?

A

Normally benign - adenomas or stromal for example
only about ~1% of tumours are malignant.

69
Q

What are the 2 types of polyps of the colon and rectum?

A

Non-neoplastic and neoplastic

70
Q

What is the most important clinical feature of a polyp?

A

Its size as it can lead to malignancy.

71
Q

What are two familial syndromes which contribute to one’s risk of developing colorectal cancer?

A

FAP - familial adenomatous polyposis
HNPCC - hereditary non-polyposis colon cancer

72
Q

What is a polyp?

A

It is any mass or nodule which projects above the level of the surrounding mucosa.

73
Q

What are the two different structures a polyp can take?

A
  • sessile: no stalk
  • pedunculated: stalk present
74
Q

Non-neoplastic polyps can be which types and what are these types most commonly associated with?

A
  • Inflammatory: IBD
  • Hyperplastic: increases with age, rectum, low to no malignancy potential
75
Q

Neoplastic polyps can be of which three types and what do neoplastic polyps possibly develop into?

A

Neoplastic polyps develop into adenomas and possible adenocarcinomas.
- tubular (most) - raspberry, with stalk
- vilous (10%) - no stalk
- tubulovillous (15%)

76
Q

How do carcinomas develop?

A

From adenomas
molecular cascade of gene defects…activation of oncogenes, loss/mutation of TSG and defective DNA repair genes.

77
Q

Familial Adenomatous polyposis (FAP) is caused by mutations of which gene?
what is the minimum number of polyps needed for diagnosis?

A

APC gene
100 polyps minimum

78
Q

FAP if left untreated can lead to what?
What is the classical amount of colonic adenomas seen in FAP?

A

If left untreated will lead to colorectal adenocarcinoma, before 50.
500-2500 colonic adenomas.

79
Q

Hereditary non-polyposis colon cancer is called which and is due to mutations in which two common genes?

A

Lynch syndrome
MSH2, MLH1

80
Q

Colorectal cancer is which place of malignancy deaths?

A

Second of both sexes

81
Q

Where are the majority of colorectal carcinomas?

A

50% in the rectum
30% in the sigmoid colon

82
Q

What is the progression of spread in colorectal carcinoma?

A

direct
lymph
lungs
liver
bone

83
Q

TMN has 4 different stages, what are the distinguishing factors of these stages?

A

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
Q

Bowelscreen age range?

A

55-74 yrs every 2 years. Faecal test - detects presence of blood

85
Q

Appendicitis is as a result of which type of inflammation?

A

Acute suppurative inflammation

86
Q

What type of tumours are found in the anus/anal canal?

A
  • papilloma
  • carcinoma: adenocarcinoma, basaloid and squamous
  • melanoma

Cell Pathology II (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions