4.2 Peptic Ulcer Disease

Question 1

What epithelium is found in the stomach and what provides it protection?

What is cells are found in the upper 2/3s vs the lower 1/3 and what do these secrete?

Answer 1

Simple columnar epithelium protected by a mucus bicarbonate barrier

Upper2/3rds: Pariteal cells (HCl) and chief cells (pepsinogen)

Lower1/3rd: mucus cells (HCO3- mucus) and G-cells (gastrin)

Question 2

Define peptic ulcer disease

What is a ulcer in the stomach vs the duodenum known as?

Answer 2

Peptic ulcer disease (PUD) refers to painful sores or ulcers in the lining of the stomach or the duodenum

Ulcer in stomach = gastric ulcer

Ulcer in duodenum = duodenal ulcer

Question 3

What are the 2 most common causes of PUD?

Give 2 other causes

Answer 3

1) H.Pylori
2) NSAIDS

Other causes:

• acid
• diet; spicy food and lots of caffeine
• alcohol, smoking, stress
• Zollinger Ellison syndrome

Question 4

What is Zollinger Ellison syndrome?

Answer 4

A gastrin secreting tumour in the pancreas, leads to continued production of acid within the stomach

Question 5

List 4 common symptoms of an “upset stomach”

Answer 5

1) Dyspepsia
2) Anorexia
3) Nausea
4) Vomiting
5) Hematemesis; vomiting blood
6) Malena
7) Heartburn
8) Acid brash
9) Abdominal pain
10) Gastro-oesophageal reflux

Question 6

The following are symptoms of an upset stomach, explain what each is

1) Dyspepsia:
2) Haematemesis
3) Melaena
4) Acid Brash

Answer 6

1) Dyspepsia: indigestion, refers to discomfort/pain in upper abdomen
2) Haematemesis: vomiting blood
3) Melaena: black, tarry, offensive stool, presents within 2-6hrs of an upper GI bleed and can last 48hrs following
4) Acid Brash: bad taste caused by stomach acid entering mouth and mixing with saliva (not vomiting)

Question 7

Define Gastritis and what is its relationship to ulcers and therfore PUD?

Answer 7

Gastritis is mucosal inflammation which leads to mucosal breakdown

Can form: Fissues ➞ Erosion ➞ Ulcers

Eventually this mucosal breakdown can lead to PUD

Question 8

As H. Pylori can be a causitive agent of PUD what can be said about its treatment?

Answer 8

It is a bacteria, hence H.Pylori and consequently PUD caused by H.Pylor can be treated effectivly by antibiotics

Question 9

Give 4 structural features of Helicobacter pylori and Is it transmissible? (MUG FAM)

Answer 9

1. motile
2. urease producing
3. gram negative
4. flagellated
5. a?
6. microaerophilic (requires little O2)
7. • spiral cocbacillus

YES it is transmissible

Question 10

Where specifically does H.Pylori attach and what 2 damaging substances does it produce?

Answer 10

Adheres to gastric mucosa and produces urease and cytotoxins

Question 11

What are the 2 ways in which H.Pylori is able to survive in the acid environment of the stomach?

Answer 11

1) uses chemotaxis to avoid areas of low pH
2) H. pylori produces large amount of urease

Question 12

Explain how urease produced by H. Pylori aids the bacteria and effects the gut

Answer 12

1) Urease breaks down the urea present in the stomach into CO2 + NH3 (ammonia). The ammonia is basic so neutralises stomach acid (and is toxic to epithelial cells)
2) Urease is also highly immunogenic which causes local inflammation in the gut ➞ can progress to chronic infection

Question 13

Give 3 other proteins secreted by H.Pylori that harm the gut linings and explain how

What gene is present within H.Pylori that can be very dangerous and why?

Answer 13

1. proteases and phospholipases
2. vacuolating cytotoxin A (VacA)
3. CagA

These damage epithelial cells, disrupt tight junctions and cause apoptosis

The Cytotoxin associated gene (CagA) can act as a potential carcinogen!!

Question 14

Not everyone infected with H.pylori presents in the same way…

Give 5 various “phenotypes” H.Pylori can produce?

Answer 14

1. gastritis only
2. Intermittent Gastric ulcers
3. Intermittent Duodenal ulcers
4. gastric cancer
5. MALT lymphoma (a/w HP CagA virulence factor, early eradication of H.Pylori can treat progression)

Question 15

H.pylori infection + presentation is based on the location which the bacteria colonises.

What the most likley presentation is if H.p colonises:

1) Antrum predominant
2) Antrum & body
3) Body predominant

Answer 15

1) Antrum predominant: duodenal ulcer risk
2) Antrum & body: largly asymptomatic
3) Body predominant: gastric ulcer AND cancer risk

Question 16

Why does H.Pylori colonize different areas of the gut?

What can be said about people who produce high vs low amounts of stomach acid?

Answer 16

The location of colonization of H. pylori depends on the acidity of the stomach

In people producing large amounts of acid, H. pylori colonizes pyloric antrum (exit to duodenum) to avoid the acid-secreting parietal cells at the fundus (entrance to stomach)

In people producing normal or reduced amounts of acid, H. pylori can also colonize the rest of the stomach.

Question 17

How does the inflammatory response caused by H.Pylori in antrum cause massive acid secretion?

Answer 17

1) inflammation induces G cells in antrum to secrete gastrin
2) gastrin travels through bloodstream to parietal cells in the fundus and causes increased gastric acid secretion (HCl)
3) increased acid causes furthur inflammation ➞ more activation of G-cells etc… ➞ vicious cycle

Question 18

If H.Pylori only colonises the gastric mucosa (stomach) how does it lead to duodenal ulceration?

What is a serious consequence of this?

Answer 18

Increased acid secretion due to inflammation eventually causes duodenal cap (first part of duodenum, continuation of pylorus) to become damaged over time.

Hence H.p can progress into the duodenum and can eventually cause metaplasia of both gastric duodenum mucosa

Question 19

Name 3 ways you could diagnose H.pylori

Answer 19

1) Urea breath test
2) Blood test: can look for antibodies
3) Stool test: antibodies

Question 20

What is the issue with diagnosing H.pylori with a blood test?

Answer 20

Antibodies can stay in the blood for a long time, so it can be difficult to identify whether the antibodies are from a previous infection and if the antibiotics given were effective.

Question 21

What is the danger of a peptic ulcer in the pyloric sphincter?

Answer 21

If large enough can cause a pyloric obstruction and erode blood vessels

Question 22

How does eating affect individuals suffering from a duodenal vs gastric ulcer?

Answer 22

Gastric: more pain when they eat

Duodenal: less pain when they eat

Question 23

How can NSAIDs cause PUD?

Answer 23

The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of this mucus is stimulated prostaglandins

NSAIDs block cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins

Hence causes decreased stomach protection ➞ leads to peptic ulcer formation and PUD

Question 24

How can we reduce the risk of stomach damage from NSAIDs?

Answer 24

Use COX-2 selective anti-inflammatories eg. celecoxib

These preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halves the risk of NSAID-related gastric ulceration.

Question 25

Give 2 occasions where we should NOT prescribe NSAIDs to a patient and explain why?

Give options if we have too?

Answer 25

1) If they are already infected with H.p because H.p and NSAIDs are synergistic (work togther, increases risk). H.p should try and be eradicated first before prescribing NSAIDs
2) In the elderly (majority GI bleeds > 65 were on NSAIDs or aspirin). If NSAIDs must be prescribe in elderly, PPI’s should also be given (decrease acid secretion)

Question 26

Name the 4 most common causes of upper GI bleeds

Give 2 other causes

Answer 26

1) Peptic ulcers; slow bleed
2) Gastroduodenal erosions
3) Oesophagitis
4) Mallory Weiss Tear: persistent vomiting for >24 hours (for any reason) can cause a tear in the stomach lining

Others:

• oesophageal varicies
• vascular malformations
• upper GI malignancy
• rare causes

Question 27

List 6 symptoms and 3 signs an individual with an upper GI bleed might have

Answer 27

Symptoms:

• hematemesis (coffee-ground vomit)
• melaena (black, tarry stools)
• dizziness (especially postural)
• fainting
• abdominal pain
• cool and clammy peripheries (with delayed CRT)
• low urine output

Signs:

• Low JVP
• hypotension
• tachycardia

Question 28

Why is an upper GI bleed extremly dangeous?

Answer 28

Can cause massive blood loss which can progress to HYPOVOLEMIC shock!!

Question 29

Name four important aspects of a history from a patient with suspected PUD?

Answer 29

1) Previous peptic ulceration/upper GI symptoms
2) Current medication + OTC analgesics (ie. aspirin)
3) Bleeding disorders; impt to consider for use of warfarin, asprin and clopidogrel
4) Previous drug use and alcohol intake

Question 30

Give 6 signs of an upper GI bleed that may indicate patient is in shock

Answer 30

1) cool & clammy
2) raised capillary refill time
3) tachycardic
4) systolic BP <100mmHg
5) postural drop (esp younger pts with significant blood loss)
6) urine Output < 30ml/hr

Question 31

What 3 steps might you take to immediately manage a patient with an upper GI bleed

Answer 31

1) Take them off any contributing drugs; NSAIDs, aspirin, clopidogrel, etc
2) Send for endoscopy
3) If they are in shock give blood! If blood is unavailble give crystalloids and saline

Question 32

What is the Blatchford score

Answer 32

Helps identify which patients with upper GI bleeding may be safely discharged from the ER

Score is out of 12

Question 33

Give 4 parameters of the glasgow-blatchford score (there are 8)

Answer 33

• Hemoglobin
• BUN (blood urea nitrogen)
• Initial systolic BP
• Sex
• Heart rate ≥100
• Melena present
• Recent syncope
• Hepatic disease history
• Cardiac failure present

Question 34

Why would BUN be raised in an upper GI bleed?

Answer 34

Blood is digested to protein/aa which is metabolised in the liver (urea cycle) into blood urea nitrogen

Question 35

What does OGD stand for?

Answer 35

oesophago-gastro-duodenoscopy

Question 36

Give 2 endoscopic managements for an upper GI bleed

Answer 36

1) Injection sclerotherapy: injection into vessel which causes it to shrink and close off
2) Diathermy: burning vessel to promote clot (good for bleeds thay can be visualised)
3) Variceal ligation: used in oesophageal varicosoties, vessels are tied off
4) Laser therapy: use of a laser
5) Endoscopic clipping: metal clip inserted to close off bleeding vessel

Question 37

Give 3 therapeutics that can be provided before an endoscopy?

Answer 37

1) PPIs: reduces acid-dependent protease clot lysis
2) Antifibrinolytics (eg. Tranexamic acid) Not often used in UK
3) Prokinetics: medications that help control acid reflux

Question 38

For on-going management of PUD, NSAID usage should be stopped, what can be given as an alternative?

Answer 38

Clopidogrel short term if possible or low dose Aspirin if absolutely necessary (eg. if preventive for vascular events)

Question 39

How would pain relief be managed in a patient with preveous history of peptic ulcers who ALSO has Rheumatoid arthritis?

Answer 39

Consider COX-2 inhibitors if no cardiac disease

In patients that >65 use ibuprofen non-selective NSAID with lowest GI side effect co-prescribed with PPIs

Question 40

If patient requires ongoing anti-platelet therpy (eg. for cardiac problems) following treatment of peptic ulcers what must you do?

Answer 40

Reinstate anti-platelet monotherapy after 1 week AND long term PPI cover

Question 41

What is the major risk for an untreated ulcer and what is the danger of this?

Answer 41

Perforation

This causes HCl to leak out of the stomach into the cavity causing the alterations in the body pH. This can lead to death of cells and can also cause air within stomach to leak out into peritoneal cavity.

Question 42

Where would you spot a stomach perforation on a Chest X-ray and why?

Answer 42

Porforation can cause air to leak out of stomach and enter peritoneal cavity. Hence, when patient is upright; air will rise and a gastric bubble can be seen sitting above the diaphragm (skinny half moons)