Brainscape's Knowledge GenomeTM

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


See full index

Year 2 clinical pathology > Week 6 Upper Tract GI > Flashcards

Week 6 Upper Tract GI Flashcards

1
Q

What is the length of the oesophageus and what is it normally lined with?

A

25 cm long muscular tube mostly lined by squamous epithelium

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

Where are the spincters of the oesophagus found?

A

Sphincter at upper end (cricopharyngeal) and lower end (gastro-oesophageal junction)

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

What part of the oesophagus is lined by glandular mucosa?

A

Distal 1.5-2 cm are situated below the diaphragm and lined by glandular (columnar) mucosa

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

Where is the squamo-columnar junction situated?

A

The squamo-columnar junction is usually located at 40 cm from the incisor teeth

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

What is Oesophagitis?

A

Inflammation of the oesophagus

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

What is the classifications of oesophagitis?

A

Acute

Chronic

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

What is the aetiology of oesophagitis?

A

Infectious–> not common unless you are immunocompromised
Bacterial, viral (HSV1, CMV), fungal (candida)

Chemical
Ingestion of corrosive substances
Reflux of gastric contents –> gastro reflux disease most common type

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

What is the commenst form of oesophagitis?

A

Reflux oesophagitis

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

What is the cause of reflux oesophagitis?

A

Caused by reflux of gastric acid (gastro-oesophageal reflux) and/or bile (duodeno-gastric reflux)

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

What are the risk factors of Reflux oesophagitis?

A

Defective lower oesophageal sphincter

Hiatus hernia  part of the stomach will herniate through the diaphragm to the thorax

Increased intra-abdominal pressure

Increased gastric fluid volume due to gastric outflow stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the main clinical symptom of reflux oesophagitis and what is the possible complications?

A

Heart burn is the main symptom.

Ulceration 
Haemorrhage 
Perforation 
Benign stricture (segmental narrowing) 
Barrett’s oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Whata are the two types of hiatus hernia?

A

Sliding Hiatus Hernia

Paraesophageal hiatus hernia

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

What are the symptoms of sliding and paraesophageal hiatus hernia?

A

Sliding –> reflux symptoms

Para-oesophageal hernia –> strangulation which can lead to a lack of blood to that area and can get necrosis

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

What are the epithelial changes that takes place in reflux oesophagitis?

A

Squamous epithelium –> Basal cell hyperplasia, elongation of papillae, increased cell desquamation

Lamina propria –>Inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the cause of Barrett’s oesophagus?

A

Longstanding reflux

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

Risk factors of Barrett’s oesophagus?

A

Same as for reflux (male, Caucasian, overweight)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the macroscopic features of Barretts oeophagus?

A

Proximal extension of the squamo-columnar junction = caused by metaplasia = change from normal squamous lining to a columnar lining in the stomach –> this is trying to combat the acid content

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

What is the histological change in Barrett’s oeophagus?

A

Squamous mucosa replaced by columnar mucosa > “glandular metaplasia

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

What are the types of columnar mucosa in Barrett’s oeophagus?

A

Get a type of gastric epithelium that represents
Gastric cardia type
Gastric body type

Intestinal type = “specialised Barrett’s mucosa”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the importance of specialised barrett’s mucosa in terms of diagnosis?

A

Characteristic feature of Barrett’s oesophagus = Confirm diagnostic when you find this in the oesophageal tube

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

What is adenocarcinoma?

A

A malignant tumour formed from glandular structures in epithelial tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Barret’s oesophagus increases the risk of what disease?

A

Barret’s oesophagus is a premalignant condition with an increased risk of developing adenocarcinoma of the oesophagus

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

How is neoplasia of the oesophagus detected?

A

Regular endoscopic surveillance is recommended for early detection of neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a treatment if you get adenocarcinoma of the oesophagus?

A

Replacement of the esophagostomy= remove it and then replace with colon

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

What is the disease progression from Barrett’s oesophagus too adenocarcinoma?

A

Barrett’s oesophagus –> low grade dysplasia –> high grade dysplasia –> adenocarcinoma

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

What are the two histological types of oesophageal carcinoma?

A

Squamous cell carcinoma –> originating from the normal oesophageal epithelium

Adenocarcinoma –> following on from Barrett’s, originating from glandular epithelium

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

Where is incidence of adenocarcinoma highest?

A

Risen in industrial country due to increase in number of overweight people.
There is a ratio of 7;1 for males/female preponderance.
Hight incidence among caucasions

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

What is the aetiology of adenocarcinoma?

A

Barrett’s oesophagus

tobacco, obesity

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

Where is adenocarcinoma found and what is the macroscopic profile?
Finally how does spread and staging?

A

Localisation:
Lower oesophagus –> see the barest metaplasia

Macroscopy:
Plaque-like, nodular, fungating, ulcerated, depressed, infiltrating

Spread and staging:
Same as squamous cell carcinoma

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

How common is oesophageal carcinoma in the world?

A

It is the 8th most common cancer

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

What is more common squamous carcinoma or adenocarcinoma in the UK?

A

Adenocarcinoma?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the risk factors of Squamous carcinoma?

A 
Tobacco and alcohol
Nutrition (potential sources of nitrosamines)
Thermal injury (hot beverages)
HPV
Male
Ethnicity (black)
33
Q

What is the location of squamous carcinoma?

A

Middle and lower third (

34
Q

What system is used for staging cancer and what does each part mean?

A

Use the TNM system
T–> depth of invasion of the primary tumour
N–> Regional lymph nodes
M –> distant metastasis

35
Q

What are the different grades of T in the TNM system for Squamous carcinoma and adenocarcinoma staging?

A

pT1: tumour invades lamina propria, muscularis mucosae or submucosa
pT2: tumour invades muscularis propria thick muscle layer
pT3: tumour invades adventitia through the muscularis propria
pT4: tumour invades adjacent structures move outside the eosophageus

36
Q

What are the different grades of N and M in the TNM system for Squamous carcinoma and adenocarcinoma staging?

A

pN0: no regional lymph node metastasis
pN1: regional lymph node metastasis in 1 or 2 nodes
pN2: regional lymph node metastasis in 3 to 6 nodes
pN3: regional lymph node metastasis in 7 or more nodes

M0: no distant metastasis
M1: distant metastasis

37
Q

What are the 4 anatomcal regions of the stomach?

A

Cardia
Fundus
Body
Antrum

38
Q

What are the 3 histological regions with different functions?

A

Cardia
Body
Antrum

39
Q

What type of glands are found in the cardia and antrum of the stomach?

A

Mucous glands

40
Q

What type of glands are found in the body of the stomach?

A

Body get specialist glands that produce the enzymes to digest

41
Q

Normally how does a stomach balance beteen the aggressive acid and defences forces?

A

Surface mucous
Bicarbonate secretion
Mucosal blood flow Regenerative capacity Prostaglandins

42
Q

What is a cause of increased aggression in the stomach?

A 
Excessive alcohol- 
Drugs --> NSAIDS
 Heavy smoking
 Corrosive 
Radiation
 Chemotherapy 
Infection
43
Q

What is a cause of impaired defences of the stomach?

A 
Ischaemia --> reduction in mucosal blood flow 
 Shock
 Delayed emptying
 Duodenal reflux
Impaired regulation of pepsin secretion
44
Q

Describe the type of bacteria H. Pylori is and its structure?

A

Gram negative spiral shaped bacterium
2.5-5.0 micrometres long
4 to 6 flagellae
Lives on the epithelial surface protected by the overlying mucus barrier

45
Q

What is the actions of H.pylori?

A

Damages the epithelium leading to chronic inflammation of the mucosa

More common in gastric antrum than body

Results in glandular atrophy lead to replacement fibrosis over time and intestinal metaplasia

46
Q

What are the complications of H.pylori?

A

Gastric ulcer = 2-5%

Duodenal ulcer = 10-15%

47
Q

What is the 3 main aetiology category that causes chronic gastritis?

A

Autoimmune
Bacterial infection
Chemical injury

48
Q

What is the pathogenic mechanism of autoimmune chronic gastritis?

A

Anti-parietal cell and anti-intrinsic factor antibodies

Sensitised T lymphocytes

49
Q

What is the histological findings of autoimmune chronic gastritis?

A

Glandular atrophy in body mucosa intestinal metaplasia

50
Q

What is the main histological findings of chronic gastritis caused by Bacterial infection?

A

1) Active chronic inflammation

2) Multifocal atrophy: Antrum> body intestinal metaplasia

51
Q

What is the pathogenic mechanism for chronic Gastritis causd by NSAIDS and bile reflux?

A

NSAIDS –> disruption of the mucus layer

Bile reflux –> Degranulation of mast cells

52
Q

Histological findings of oedema, vasolidation or paucity of inflammatory cells in chronic gastritis is due to?

A

Oedema –> NSAIDS
Vasolidation –> bile reflux
paucity of inflammatory cells –> Alcohol

53
Q

What two cancers can be caused by H.pylori?

A

Gastric cancer

MALT lymphoma

54
Q

What is peptic ulcer?

A

Localised defect extending at least into submucosa

55
Q

What are the 3 major sites of peptic ulcers?

A 
First part of duodenum
Junction of antral and body mucosa
Distal oesophagus (GOJ)
56
Q

What is the 5 main aetiological factors of peptic ulcers?

A 
Hyperacidity
H. pylori infection
Duodeno-gastric reflux
Drugs (NSAIDs)
Smoking
57
Q

What are the histological findings of acute gastric ulcers?

A

Full-thickness coagulative necrosis of mucosa (or deeper layers)

Covered with ulcer slough (necrotic debris + fibrin + neutrophils)

Granulation tissue at ulcer floor

58
Q

What are the histological findings of chronic gastric ulcers?

A

Clear-cut edges overhanging the base

Extensive granulation and scar tissue at ulcer floor

Scarring often throughout the entire gastric wall with breaching of the muscularis propria

Bleeding

59
Q

What are the 4 complications of peptic ulcers?

A

Haemorrhage (acute and/or chronic –> anaemia)

Perforation –> peritonitis –> through the full thickness of the wall

Penetration into an adjacent organ (liver, pancreas)

Stricturing –> hour-glass deformity

60
Q

Is gastric or duodenal ulcer more common and what is the age distribution?

A

Duodenal ulcer is more common.

Gastric ulcer –> increase with age
Duodenal ulcer –> incrase up to 35 yrs

61
Q

What are the acid levels in gastric and duodenal ulcers?

A

Gastric –> normal or low

Duoednal –> elevated or normal

62
Q

How often does H.pylori caused Gastric and Duodenal ulcers?

A

Gastric –> 70% the other 30% is caused due to gastric cancer, chemicals, drugs

Duodenal –>95-100% ( predominatly in the antrum)

63
Q

What blood groups is gastric ulcer and duodenal ulcers found in?

A

Gastric –> blood group A

Duodenal –> blood group O

64
Q

What is the most common gastric cancer?

A

Adenocarcinoma

65
Q

What are less frequent gastric cancers?

A 
Endocrine tumours
MALT lymphomas
Stromal tumours (GIST)--> from stromal cells
66
Q

How common is gastric adenocarcinoma in the world?

A

5th most common cacncer in the world

67
Q

What are the causes of gastric adenocarcinoma?

A

Diet (smoked/cured meat or fish, pickled vegetables)

Helicobacter pylori infection

Bile reflux (e.g. post Billroth II operation)

Hypochlorhydria (allows bacterial growth)

~1% hereditary

68
Q

What is the assoications with carcinoma of the gastroesophageal junction?

A

White males

  • Association with GO reflux
  • No association with H. pylori / diet
  • Increased incidence in recent years with overweight individuals
69
Q

What are the associations of carcinoma in the gastric body/atrum?

A
  • Association with H. pylori
  • Association with diet (salt, low fruit
    & vegetables)
  • No association with GO reflux
  • Decreased incidence in recent years
70
Q

What is the 2 main histological subtypes of gastric cancer and whata are there features?

A

Diffuse types (signet ring cell carcinoma) –> worse prognosis . Poorly differentiated. Scattered growth. Cadherin loss/mutation

Intestinal type ( tubular adenocarcinoma) 
-well or moderately differentiated
May undergo intestinal metaplasia and adenoma steps
71
Q

What type of gatric cancer is hereditary and what is teh mutation?

A

Hereditary diffuse type gastric cancer (HDGC)

Caused by Germline CDH1/E-cadherin mutation

72
Q

What is the TNM staging for gastric cancer?

A

pT1: intramucosal or submucosal
pT2: into muscularis propria
pT3: through muscularis propria into subserosa
pT4: through serosa (peritoneum)or into adjacent organs

pN0: no lymph node metastases
pN1: 1 to 2 lymph node metastases
pN2: 3 to 6 lymph node metastases
pN3: more than 6 lymph node met.

M0: no distant metastases
M1: distant metastases present

73
Q

What is Coeliac disease and what is its estimated prevalence?

A

Sensitivity to Gluten

Immune mediated enteropathy

Fairly common, estimated prevalence of 0.5% to 1%

74
Q

What are the 2 pathogensis causes of coeliac disease?

A

Reaction to GLIADIN

Alcohol soluble component of gluten
Contains most of the disease-producing components
Induces epithelial cells to express IL-15

CD8+ Intraepithelial lymphocytes (IELs)

IL15 produced by the epithelium  activation / proliferation of CD8+ IELs
These are cytotoxic and kill enterocytes
CD8+ IELs do not recognise gliadin directly
Gliadin-induced IL15 secretion by epithelium is the mechanism

75
Q

What is the diagnosis of Coeliac disease?

A

Commonly affects adults between 30 and 60 years

No geneder preference

Diagnosis is often difficult
Atypical presentations / non specific symptoms
Silentdisease
Positive serology / villous atrophy but no symptoms
Latentdisease
Positive serology but no villous atrophy
Symptomatic patients
Anaemia, chronic diarrhoea, bloating, or chronic fatigue

76
Q

What other diseases and cancer is coeliac disease associated with?

A

Disease:
Dermatitis herpetiformis - 10% of patients
Lymphocytic gastritisandlymphocytic colitis

Cancer:
Enteropathy-associated T-cell lymphoma
Small intestinal adenocarcinoma

77
Q

What is the diagnosis of coeliac disease?

A

Non-invasive serologic tests usually performed before biopsy

The most sensitive tests–> serology test
IgA antibodies to tissue transglutaminase (TTG)
IgA or IgG antibodies to deamidated gliadin
Anti-endomysial antibodies - highly specific but less sensitive

Tissue biopsy is diagnostic (2nd biopsy after GFD) –> Gold standard

78
Q

Treatment for Coeliac disease

A

Gluten-free diet –> symptomatic improvement for most patients

79
Q

What are the long term consequences of coeliac disease if not treated?

A

Anaemia, female infertility, osteoporosis, and cancer

Year 2 clinical pathology (21 decks)

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