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MRCS B pathology > Oesophageal/gastric pathology > Flashcards

Oesophageal/gastric pathology Flashcards

1
Q

Name some causes for dysphagia

A

Intramural:
-Food bolus/bezour

Intramural
-Pharyngeal pouch
-Plummer vinson syndrome
-Achalasia
-Schatzki ring
-Tumour

Extramural:
-Neurological: stroke/guillain-barre

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2
Q

How will different causes of dysphagia present?

A

Achalasia: chest pain, regurgitation, progressive dysphagia to solids and liquids

Pharyngeal pouch: halitosis, regurgitation, aspiration and chest infection

Barrett’s: GORD

Cancer: weight loss, cachexia

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3
Q

What are main features of achalasia?

A

Loss of myenteric plexus (between longitudinal/circular muscles)

Lower oesophagus does not dilate

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4
Q

How would you investigate achalasia?

A

-Barium swallow
-OGD
-Manometry

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5
Q

How could you manage achalasia?

A

-Botox
-Heller’s cardiomyotomy (results in reflux)

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6
Q

What are the main features of oesophageal web (plummer vinson syndrome)

A

Triad: oesophageal web, dysphagia, iron deficiency anaemia

Other features: beefy red tongue, koilonychia, splenomegaly

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7
Q

What factors are responsible for maintaining integrity of lower oesophageal sphincter?

A

1) lower gastro-mucosal folds
2) angle of his
3) intra-abdominal portion oesophagus (increased pressure)
4) R crus diaphragm

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8
Q

Describe the metaplastic process in Barrett’s transformation in the oesophagus

A

Protective mechanism: body adapted to change of cell type in response to acid in oesophagus

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9
Q

Risk factors for barrett’s

A

Smoking
hiatus hernia
eating large meals late at night

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10
Q

What is the clinical definition of barrett’s oesophagus?

A

Metaplastic change: columnar metoplasia lower 1/3rd
Oesophagus: up to 1cm acceptable. >1cm abnormal

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11
Q

What are the main histological subtypes of gastric cancer and why are they important?

A

Gastric
Intestinal metaplasia–> goblet cells (worse prognosis)

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12
Q

What are theInvestigation/ management options for barrett’s metaplasia?

A

Lifestyle, PPI
24 hr ph monitoring (gold standard for GORD)
Manometry
OGD + biopsy –> 4 biopsies every 2cm from go junction

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13
Q

What surveillance is required for barrett’s

A

Metaplasia <3cm from GO junction: OGD every 3-5 yrs
Metaplasia >3cm more frequent OGD (every 2 years)

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14
Q

What are the management options for low grade dysplasia?

A

6 month –> annual OGD until -ve

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15
Q

What are the management options for high grade dysplasia?

A

Submucosal resection/ablation

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16
Q

Name premalignant conditions of oesophagus

A

pharyngeal pouch
plummer visnon
achalasia
Scleroderma
Gord (barrett’s)

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17
Q

Risk factors for oesophageal ca

A

Advancing age
HPV (squamous cell)
Thoracic radiation
GORD

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18
Q

What are the type of oesohpageal carcinomas?

A

Squamous most common wordlwide –> upper 2/3rd oesohpagus

Adenocarcinoma most common uk –> lower 1/3rd oesophagus

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19
Q

What are the management principles of treating patients with oesophageal carcinomas?

A

Optimise–> nutrition
Neoadjuvant radiotherapy (if squamous)

Surgery
-Lower 1/3rd: Ivor lewis (laparotomy, R side thoracotomy, resect lower part, anastamosis in mediastinum
-Middle 1/3rd: mckewan oesohpagectomy (laparotomy, right thoracotomy, anastamosis in the neck)
-Upper 1/3rd Radiotherapy

20
Q

What are the key complications following oesophageal surgery?

A

-Thoracic duct injury (lymph in drain)–> low fat diet
-Lungs: pneumonia, pneumothorax
-Mediastinitis
-Phrenic nerve injury
-Dietary deficiency (PEG, TPN)
-Subclavian injury, brachial plexus injury

21
Q

Which is the most common site for gastric cancers

A

Pylorus (50%)
Lesser curvature (25%)

22
Q

What are the risk factors of gastric cancer?

A

Genetic: FAP, HNPCC, Blood group A

Modifiable: Cigarette, alcohol, H pylori

Gastric conditions: Autoimmune gastritis, pernicious anaemia, peptic ulcer

23
Q

What are the main types of gastric cancers?

A

Adenocarcinoma
GIST
Lymphoma
Gastrinoma
Carcinoid
Linitis plastica

24
Q

What is triple thearpy for H pylori?

A

Clarithromicin, amox, PPI

25
Q

How are gastruc cancers managed?

A

-Neoadjuvant chemo
-Gastrectomy: partial or total
-Pylorus/antrum: partial
In middle: total

26
Q

What are the main complications following gastric surgery for cancers?

A

Dumping syndrome
B12 deficiency (parietal cells, intrinsic factor)
Malabsorption

27
Q

What is H Pylori?

A

-Helicobactor pylori is a gram-negative, microaerophilic spiral bacterium
-stomach

28
Q

How does h pylori become colonised in the stomach?

A

-Is able to detect ph
-Uses flagella to swim away from acidic luminal contents
-Adheres to more neutral epithelial lining

To avoid being carried away in the lumen, H pylori is able to detect pH and uses its flagella
to swim away from the acidic contents of the lumen and adheres to the more neutral epithelial
lining of the stomach.

29
Q

How does H Pylori survive the acidic conditions in the stomach?

A

-Produces urease
-Urea –> CO2 + ammonia
-Ammonia + H + –> ammonium, neutralises gastric acid

H. pylori produces the enzyme urease. This converts urea to carbon dioxide and ammonia.
The ammonia then binds with H+ to form ammonium which neutralizes gastric acid.

30
Q

How does H Pylori cause gastritis and ulcers?

A

-Proteases and phospholipases
-ammonia from breakdown of urea
-Damage to gastric mucosa
-Leads to further damage due to loss of protective mechanisms from gastric acid

H. Pylori produces certain proteases and phospholipases and these, together with the toxic
ammonia produced from the breakdown of urea, damage the gastric mucosa leading to
inflammation.

Ulcers result when the protective mucosal layer is so damaged by inflammation that it is
unable to combat the acid production in the stomach, leading to further tissue destruction and
ulceration

31
Q

What is the lifetime risk of developing peptic ulcer disease with h pylori?

A

10 - 20%

32
Q

How can patients with H. Pylori present?

A

-Epigastric pain
-nausea
-dyspepsia
-bloating
-haematemesis and melaena

33
Q

Is everyone infected by the bacterium symptomatic?

A

No, 80% of individuals are asymptomatic

34
Q

Are there any other complications associated with H Pylori infection?

A

Gastric neoplasias
-gastric adenocarcinomas
-gastric mucosa-associated lymphoid tissue lymphomas

35
Q

What is the lifetime risk of H. Pylori associated gastric neoplasia?

A

1-2%

36
Q

How is H pylori diagnosed?

A

Via the CLO campylobacter-like organism) test which is dependent on urease production by
H Pylori
.
A gastric mucosal biopsy is taken during gastroscopy and is placed into a medium consisting
of urea and an indicator such as phenol red. Urease produced by H Pylori converts urea to
ammonia which increases the pH changing the colour from yellow to red, hence a positive
test.

37
Q

What is the eradication therapy?

A

7-day twice-daily course of treatment consisting of a:
Full-dose PPI + metronidazole 400 mg and clarithromycin 250 mg OR
amoxicillin 1 g and clarithromycin 500 mg

38
Q

A patient presents with dyspepsia to their general practice. Under what circumstances would
you refer for an endoscopy?

A

ALARM Symptoms

Anaemia
Loss of weight
Anorexia
Recent onset of progressive sympsoms
Malaena or haematemesis
Swallowing difficulty

Urgent specialist referral for endoscopic investigation is indicated for patients of any age with
dyspepsia when presenting with any of the following:
-chronic gastrointestinal bleeding
-progressive unintentional weight loss
-progressive difficulty swallowing
-persistent vomiting
-iron deficiency anaemia
-epigastric mass

Routine endoscopic investigation of patients of any age, presenting with dyspepsia and
without alarm signs, is not necessary. However, in patients aged 55 years and older with
unexplained and persistent recent-onset dyspepsia alone, an urgent referral for endoscopy
should be made.

39
Q

Name some important aetiological factors in peptic ulcer disease

A

Infection with Heliobacter pylori
NSAIDs
Steroids
Stress
Smoking and alcohol

40
Q

Is H. Pylori more strongly associated with gastric or duodenal ulcers?

A

More commonly duodenal ulcers (95%) compared with gastric ulcers (80%)

41
Q

Describe how food consumption relates to pain for gastric ulcers versus duodenal ulcers

A

Duodenal ulcers: pain typical before meals and relieved by eating
Gastric ulcers: pain often related to meals

42
Q

What are the main complications of peptic ulcer disease?

A

Bleeding
Perforation
Gastric outflow obstruction secondary to scarring/inflammation
Small risk of malignant transformation (but common risk factors for both mailganacy and
PUD e.g. H. Pylori, smoking, alcohol etc.)

43
Q

Which vessel is most commonly implicated in a bleed from a duodenal ulcer?

A

The gastroduodenal artery as it runs posteriorly to the duodenum

44
Q

From where does the gastroduodenal artery arise and what are its main terminal branches?

A

The gastroduodenal artery arises from the common hepatic branch of the celiac trunk
Its two main terminal branches are the right gastroepiploic artery and the superior
pancreatoduodenal artery

45
Q

What non surgical treatments are available for peptic ulcer disease?

A

Modification of behaviour e.g. NSAID use, smoking & alcohol
H. Pylori eradication therapy
Proton pump inhibitors and H2 receptor antagonists
Antacids and alginates

46
Q

What are Billroth I and Billroth II operations?

A

Billroth I: partial gastrectomy with simple re-anastomosis
Billroth II: partial gastrectomy with the duodenal stump oversewn (leaving a blind loop) and
anastomosis is to the proximal jejunum

47
Q

Vagotomies can also be used for peptic ulcer disease. What is the action of the vagus nerve
on the stomach?

A

The vagus nerve releases acetylcholine which increases the release of acid, gastrin and
histamine and decreases somatostatin release. It also increases gastric emptying.

MRCS B pathology (14 decks)

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