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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

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2
Q

Where are the spincters of the oesophagus found?

A

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

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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

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4
Q

Where is the squamo-columnar junction situated?

A

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

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5
Q

What is Oesophagitis?

A

Inflammation of the oesophagus

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6
Q

What is the classifications of oesophagitis?

A

Acute

Chronic

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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

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8
Q

What is the commenst form of oesophagitis?

A

Reflux oesophagitis

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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)

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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

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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
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12
Q

Whata are the two types of hiatus hernia?

A

Sliding Hiatus Hernia

Paraesophageal hiatus hernia

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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

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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)

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15
Q

What is the cause of Barrett’s oesophagus?

A

Longstanding reflux

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16
Q

Risk factors of Barrett’s oesophagus?

A

Same as for reflux (male, Caucasian, overweight)

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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

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18
Q

What is the histological change in Barrett’s oeophagus?

A

Squamous mucosa replaced by columnar mucosa > “glandular metaplasia

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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”

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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

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21
Q

What is adenocarcinoma?

A

A malignant tumour formed from glandular structures in epithelial tissue

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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

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23
Q

How is neoplasia of the oesophagus detected?

A

Regular endoscopic surveillance is recommended for early detection of neoplasia

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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

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25
What is the disease progression from Barrett's oesophagus too adenocarcinoma?
Barrett's oesophagus --> low grade dysplasia --> high grade dysplasia --> adenocarcinoma
26
What are the two histological types of oesophageal carcinoma?
Squamous cell carcinoma --> originating from the normal oesophageal epithelium Adenocarcinoma --> following on from Barrett's, originating from glandular epithelium
27
Where is incidence of adenocarcinoma highest?
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
28
What is the aetiology of adenocarcinoma?
Barrett’s oesophagus | tobacco, obesity
29
Where is adenocarcinoma found and what is the macroscopic profile? Finally how does spread and staging?
Localisation: Lower oesophagus --> see the barest metaplasia Macroscopy: Plaque-like, nodular, fungating, ulcerated, depressed, infiltrating Spread and staging: Same as squamous cell carcinoma
30
How common is oesophageal carcinoma in the world?
It is the 8th most common cancer
31
What is more common squamous carcinoma or adenocarcinoma in the UK?
Adenocarcinoma?
32
What are the risk factors of Squamous carcinoma?
``` Tobacco and alcohol Nutrition (potential sources of nitrosamines) Thermal injury (hot beverages) HPV Male Ethnicity (black) ```
33
What is the location of squamous carcinoma?
Middle and lower third (
34
What system is used for staging cancer and what does each part mean?
Use the TNM system T--> depth of invasion of the primary tumour N--> Regional lymph nodes M --> distant metastasis
35
What are the different grades of T in the TNM system for Squamous carcinoma and adenocarcinoma staging?
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
What are the different grades of N and M in the TNM system for Squamous carcinoma and adenocarcinoma staging?
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
What are the 4 anatomcal regions of the stomach?
Cardia Fundus Body Antrum
38
What are the 3 histological regions with different functions?
Cardia Body Antrum
39
What type of glands are found in the cardia and antrum of the stomach?
Mucous glands
40
What type of glands are found in the body of the stomach?
Body get specialist glands that produce the enzymes to digest
41
Normally how does a stomach balance beteen the aggressive acid and defences forces?
Surface mucous Bicarbonate secretion Mucosal blood flow Regenerative capacity Prostaglandins
42
What is a cause of increased aggression in the stomach?
``` Excessive alcohol- Drugs --> NSAIDS Heavy smoking Corrosive Radiation Chemotherapy Infection ```
43
What is a cause of impaired defences of the stomach?
``` Ischaemia --> reduction in mucosal blood flow Shock Delayed emptying Duodenal reflux Impaired regulation of pepsin secretion ```
44
Describe the type of bacteria H. Pylori is and its structure?
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
What is the actions of H.pylori?
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
What are the complications of H.pylori?
Gastric ulcer = 2-5% | Duodenal ulcer = 10-15%
47
What is the 3 main aetiology category that causes chronic gastritis?
Autoimmune Bacterial infection Chemical injury
48
What is the pathogenic mechanism of autoimmune chronic gastritis?
Anti-parietal cell and anti-intrinsic factor antibodies | Sensitised T lymphocytes
49
What is the histological findings of autoimmune chronic gastritis?
Glandular atrophy in body mucosa intestinal metaplasia
50
What is the main histological findings of chronic gastritis caused by Bacterial infection?
1) Active chronic inflammation | 2) Multifocal atrophy: Antrum> body intestinal metaplasia
51
What is the pathogenic mechanism for chronic Gastritis causd by NSAIDS and bile reflux?
NSAIDS --> disruption of the mucus layer Bile reflux --> Degranulation of mast cells
52
Histological findings of oedema, vasolidation or paucity of inflammatory cells in chronic gastritis is due to?
Oedema --> NSAIDS Vasolidation --> bile reflux paucity of inflammatory cells --> Alcohol
53
What two cancers can be caused by H.pylori?
Gastric cancer | MALT lymphoma
54
What is peptic ulcer?
Localised defect extending at least into submucosa
55
What are the 3 major sites of peptic ulcers?
``` First part of duodenum Junction of antral and body mucosa Distal oesophagus (GOJ) ```
56
What is the 5 main aetiological factors of peptic ulcers?
``` Hyperacidity H. pylori infection Duodeno-gastric reflux Drugs (NSAIDs) Smoking ```
57
What are the histological findings of acute gastric ulcers?
Full-thickness coagulative necrosis of mucosa (or deeper layers) Covered with ulcer slough (necrotic debris + fibrin + neutrophils) Granulation tissue at ulcer floor
58
What are the histological findings of chronic gastric ulcers?
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
What are the 4 complications of peptic ulcers?
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
Is gastric or duodenal ulcer more common and what is the age distribution?
Duodenal ulcer is more common. Gastric ulcer --> increase with age Duodenal ulcer --> incrase up to 35 yrs
61
What are the acid levels in gastric and duodenal ulcers?
Gastric --> normal or low | Duoednal --> elevated or normal
62
How often does H.pylori caused Gastric and Duodenal ulcers?
Gastric --> 70% the other 30% is caused due to gastric cancer, chemicals, drugs Duodenal -->95-100% ( predominatly in the antrum)
63
What blood groups is gastric ulcer and duodenal ulcers found in?
Gastric --> blood group A Duodenal --> blood group O
64
What is the most common gastric cancer?
Adenocarcinoma
65
What are less frequent gastric cancers?
``` Endocrine tumours MALT lymphomas Stromal tumours (GIST)--> from stromal cells ```
66
How common is gastric adenocarcinoma in the world?
5th most common cacncer in the world
67
What are the causes of gastric adenocarcinoma?
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
What is the assoications with carcinoma of the gastroesophageal junction?
White males - Association with GO reflux - No association with H. pylori / diet - Increased incidence in recent years with overweight individuals
69
What are the associations of carcinoma in the gastric body/atrum?
- Association with H. pylori - Association with diet (salt, low fruit & vegetables) - No association with GO reflux - Decreased incidence in recent years
70
What is the 2 main histological subtypes of gastric cancer and whata are there features?
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
What type of gatric cancer is hereditary and what is teh mutation?
Hereditary diffuse type gastric cancer (HDGC) | Caused by Germline CDH1/E-cadherin mutation
72
What is the TNM staging for gastric cancer?
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
What is Coeliac disease and what is its estimated prevalence?
Sensitivity to Gluten Immune mediated enteropathy Fairly common, estimated prevalence of 0.5% to 1%
74
What are the 2 pathogensis causes of coeliac disease?
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
What is the diagnosis of Coeliac disease?
Commonly affects adults between 30 and 60 years No geneder preference Diagnosis is often difficult Atypical presentations / non specific symptoms Silent disease Positive serology / villous atrophy but no symptoms Latent disease Positive serology but no villous atrophy Symptomatic patients Anaemia, chronic diarrhoea, bloating, or chronic fatigue
76
What other diseases and cancer is coeliac disease associated with?
Disease: Dermatitis herpetiformis - 10% of patients Lymphocytic gastritis and lymphocytic colitis Cancer: Enteropathy-associated T-cell lymphoma  Small intestinal adenocarcinoma 
77
What is the diagnosis of coeliac disease?
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
Treatment for Coeliac disease
Gluten-free diet --> symptomatic improvement for most patients
79
What are the long term consequences of coeliac disease if not treated?
Anaemia, female infertility, osteoporosis, and cancer

Year 2 clinical pathology (21 decks)

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