Priority List 2's Flashcards

1
Q

Why is the stomach less sensitive to the effects of stomach acid than the oseophagus?

A
  • The oesophagus has a SQUAMOUS epithelial lining making it more sensitive to the effects of stomach acid.
  • The stomach has a COLUMNAR epithelial lining that is more protected against stomach acid.

Also the stomach has a mucosal layer to protect it.

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2
Q

what is dyspepsia and what are the symptoms of GORD (6) ?

A

Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:

Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
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3
Q

What would you do a patient presents to the GP with evidence of a GI bleed?

A

send them for admission and urgent endoscopy

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4
Q

Patients with symptoms suspicious of cancer should have a two-week-wait referral so that endoscopy is performed within 2 weeks.

what are the red flag features? 8

A
  • Dysphagia (difficulty swallowing) at any age gets a two week wait referral
  • Aged over 55 (this is generally the cut off for urgent versus routine referrals)
  • Weight loss
  • Upper abdominal pain / reflux
  • Treatment resistant dyspepsia
  • Nausea and vomiting
  • Low haemoglobin
  • Raised platelet count
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5
Q

what are the 3 medications/ medications types that can be given for GORD

A

Acid neutralising medication when required:

  • Gaviscon
  • Rennie

Proton pump inhibitors (reduce acid secretion in the stomach):
Omeprazole
Lansoprazole

Ranitidine:

  • This is an alternative to PPIs
  • H2 receptor antagonist (antihistamine)
  • Reduces stomach acid
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6
Q

what is the surgery for reflux?

A

Surgery for reflux is called laparoscopic fundoplication. This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

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7
Q

Why is H.pylori damaging?

A
  • It causes damage the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer.
  • It avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it creates in the mucosa exposes the epithelial cells underneath to acid
  • It also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells.
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8
Q

How do you test for H.Pylori

A
  • urea breath test (using radio-labelled carbon 13)
  • stool antigen test
  • rapid urease test (can be preformed during endoscopy)
  • aka CLO test involves taking a small biopsy of the stomach mucosa. Urea is added to this sample. If H. pylori are present, they produce urease enzymes that converts the urea to ammonia. The ammonia makes the solution more alkali giving a positive result on when the pH is tested.
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9
Q

What is involved in the tripple therapy for H.pylori?

A

The eradication regime involves triple therapy with a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) (can use one beginnigng w m instead too) for 7 days.

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10
Q

what is barrett’s oesophagus and why is it a problem

A

Constant reflux of acid results in the lower oesophageal epithelium changing in a process known as metaplasia from a squamous to a columnar epithelium. This change to columnar epithelium is called Barretts oesophagus. When this change happens patients typically get an improvement in reflux symptoms.

Barretts oesophagus is considered a “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus

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11
Q

How is barretts oesophagus managed and treated?

A

They are monitored for adenocarcinoma by regular endoscopy. In some patients there is a progression from Barretts oesophagus (columnar epithelium) with no dysplasia to low grade dysplasia to high grade dysplasia and then to adenocarcinoma.

Treatment of Barretts oesophagus is with proton pump inhibitors (e.g. omeprazole)

Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy is used to destroy the epithelium so that it is replaced with normal cells. This is not recommended in patients with no dysplasia but has a role in low and high grade dysplasia in preventing progression to cancer.

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12
Q

What is a hiatus hernia?

A

Herniation of the stomach up through the diaphragm. The diaphragm opening should be fixed in place at the level of the lower oesophageal sphincter. The narrow opening in the diaphragm helps to maintain the sphincter and stop acid and stomach acid contents refluxing into oesophagus. When this opening is wider than it should be the stomach can enter through the diaphragm and the contents of the stomach can reflux into the oesophageal.

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13
Q

How does a hiatus hernia present.?

A

Presents with dyspepsia (indigestion symptoms) e.g. heart burn, acid reflux, burping, bloating, bad breath.

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14
Q

What are the 4 types of hiatus hernia explained?

A

Look at pics if confused

Type 1: sliding
When the oesophagus slides up taking the top part of the stomach with it. So the gastro-oesophageal junction passes into the thorax

Type 2: rolling
Where a separate portion of the stomach e.g. the fundus folds and enters through the diaphragm, alongside the oesophagus.

  1. Combination of rolling and sliding
  2. large opening with additional organs entering the thorax. Large hernia that allows other intra-abdominal organs to pass through the diaphragm opening e.g. bowel, pancreas or omentum.
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15
Q

How can hiatus hernias be investigated and what is one thing to watch out for?

A

They can be intermittent meaning they may not be seen on investigation.

Hiatus hernias may be seen on:

  • chest x-ray
  • CT scans
  • Endoscopy
  • Barium swallow test
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16
Q

How are hiatal hernias treated?

A

-conservative (with just medical treatment of the reflux).

-surgical repair
If there is a high risk of complications or symptoms that are resistant to medical treatment

Surgery involves laparoscopic fundoplication. (Tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter)

17
Q

are gastric or duodenal ulcers more common? Also how can you differentiate them?

A

duodenal ulcers are more common

stomach ulcers are worse when you eat where as they make duodenal ulcers feel better.
TOM TIP: In your MCQ exams, eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.

gnawing or burning sensation and occurs after meals, shortly after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer. Food or antacids relieve the pain of duodenal ulcers but provide minimal relief of gastric ulcer pain.

18
Q

The stomach mucosa is prone to ulceration when there is break down of the protective layer of the stomach and duodenum and an Increase in stomach acid.

What causes this protective layer to break down (2) and what things can result in increased stomach acid (5).

A

break down of the protective layer of the stomach and duodenum.
- medications (e.g. steriods and NSAIDS)

Increase in stomach acid.

  • Stress
  • Alcohol
  • Caffine
  • smoking
  • spicy food
19
Q

2 examples of medications that break down the protective mucosal layer of the stomach and duodenum.

A

Steroids and NSAIDS

20
Q

What is the presentation of a peptic ulcer (stomach and duodenal ulcer).

A
  • Epigastric discomfort or pain
  • Nausea and vomiting
  • Dyspepsia
  • Bleeding causing haematemesis, “coffee ground” vomiting and melaena
  • Iron deficiency anaemia (due to constant bleeding)
21
Q

What is the investigation and management of peptic ulcers?

A

Peptic ulcers are diagnosed by endoscopy.

During endoscopy a rapid urease test (CLO test) can be performed to check for H. pylori.

Biopsy should be considered during endoscopy to exclude malignancy as cancers can look similar to ulcers during the procedure.

Medical treatment is the same as with GORD, usually with high dose proton pump inhibitors.

Endoscopy can be used to monitoring the ulcer to ensure it heals and to assess for further ulcers.

22
Q

What are complications of peptic ulcers?

A

1.) Bleeding
from the ulcer is a common and potentially life threatening complication.

2.) Perforation
resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).

3.)Scarring and strictures
of the muscle and mucosa. This can lead to a narrowing of the pylorus (the exit of the stomach) causing difficulty in emptying the stomach contents. This is known as pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting, particularly after eating.

23
Q

where does pancreatic carcinoma most commonly occur and what does this result in?

A

normally occurs on the head of the pancreas which can compress the bible Ducts and create an obstructive jaundice .
Pancreatic cancer has a very poor prognosis.

24
Q

Pancreatic cancers tend to spread and metastasise early, where to?

A

particularly to the liver, then to the peritoneum, lungs and bones.

25
Q

How does pancreatic cancer present?

A

Painless obstructive jaundice is a key presenting feature that should make you immediately consider pancreatic cancer (the key differential is cholangiocarcinoma).

presenting with: Yellow skin and sclera
Pale stools
Dark urine
Generalised itching

+ other vague cancer features like abdo pain, weight loss, n&v, new onset diabetes or worsening of type 2 diabetes (because remember the pancreas releases insulin).

TOM TIP: It is worth noting that a new onset of diabetes, or a rapid worsening of glycaemic control type 2 diabetes, can be a sign of pancreatic cancer. Keep pancreatic cancer in mind if a patient in your exams or practice has worsening glycaemic control despite good lifestyle measures and medication.