4.2 Peptic Ulcer Disease Flashcards
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?
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)
Define peptic ulcer disease
What is a ulcer in the stomach vs the duodenum known as?
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
What are the 2 most common causes of PUD?
Give 2 other causes
1) H.Pylori
2) NSAIDS
Other causes:
- acid
- diet; spicy food and lots of caffeine
- alcohol, smoking, stress
- Zollinger Ellison syndrome
What is Zollinger Ellison syndrome?
A gastrin secreting tumour in the pancreas, leads to continued production of acid within the stomach
List 4 common symptoms of an “upset stomach”
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
The following are symptoms of an upset stomach, explain what each is
1) Dyspepsia:
2) Haematemesis
3) Melaena
4) Acid Brash
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)
Define Gastritis and what is its relationship to ulcers and therfore PUD?
Gastritis is mucosal inflammation which leads to mucosal breakdown
Can form: Fissues ➞ Erosion ➞ Ulcers
Eventually this mucosal breakdown can lead to PUD
As H. Pylori can be a causitive agent of PUD what can be said about its treatment?
It is a bacteria, hence H.Pylori and consequently PUD caused by H.Pylor can be treated effectivly by antibiotics
Give 4 structural features of Helicobacter pylori and Is it transmissible? (MUG FAM)
- motile
- urease producing
- gram negative
- flagellated
- a?
- microaerophilic (requires little O2)
- spiral cocbacillus
YES it is transmissible
Where specifically does H.Pylori attach and what 2 damaging substances does it produce?
Adheres to gastric mucosa and produces urease and cytotoxins
What are the 2 ways in which H.Pylori is able to survive in the acid environment of the stomach?
1) uses chemotaxis to avoid areas of low pH
2) H. pylori produces large amount of urease
Explain how urease produced by H. Pylori aids the bacteria and effects the gut
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
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?
- proteases and phospholipases
- vacuolating cytotoxin A (VacA)
- CagA
These damage epithelial cells, disrupt tight junctions and cause apoptosis
The Cytotoxin associated gene (CagA) can act as a potential carcinogen!!
Not everyone infected with H.pylori presents in the same way…
Give 5 various “phenotypes” H.Pylori can produce?
- gastritis only
- Intermittent Gastric ulcers
- Intermittent Duodenal ulcers
- gastric cancer
- MALT lymphoma (a/w HP CagA virulence factor, early eradication of H.Pylori can treat progression)
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
1) Antrum predominant: duodenal ulcer risk
2) Antrum & body: largly asymptomatic
3) Body predominant: gastric ulcer AND cancer risk
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?
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.
How does the inflammatory response caused by H.Pylori in antrum cause massive acid secretion?
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
If H.Pylori only colonises the gastric mucosa (stomach) how does it lead to duodenal ulceration?
What is a serious consequence of this?
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
Name 3 ways you could diagnose H.pylori
1) Urea breath test
2) Blood test: can look for antibodies
3) Stool test: antibodies
What is the issue with diagnosing H.pylori with a blood test?
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.
What is the danger of a peptic ulcer in the pyloric sphincter?
If large enough can cause a pyloric obstruction and erode blood vessels
How does eating affect individuals suffering from a duodenal vs gastric ulcer?
Gastric: more pain when they eat
Duodenal: less pain when they eat
How can NSAIDs cause PUD?
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
How can we reduce the risk of stomach damage from NSAIDs?
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.
Give 2 occasions where we should NOT prescribe NSAIDs to a patient and explain why?
Give options if we have too?
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)
Name the 4 most common causes of upper GI bleeds
Give 2 other causes
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
List 6 symptoms and 3 signs an individual with an upper GI bleed might have
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
Why is an upper GI bleed extremly dangeous?
Can cause massive blood loss which can progress to HYPOVOLEMIC shock!!
Name four important aspects of a history from a patient with suspected PUD?
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
Give 6 signs of an upper GI bleed that may indicate patient is in shock
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
What 3 steps might you take to immediately manage a patient with an upper GI bleed
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
What is the Blatchford score
Helps identify which patients with upper GI bleeding may be safely discharged from the ER
Score is out of 12
Give 4 parameters of the glasgow-blatchford score (there are 8)
- Hemoglobin
- BUN (blood urea nitrogen)
- Initial systolic BP
- Sex
- Heart rate ≥100
- Melena present
- Recent syncope
- Hepatic disease history
- Cardiac failure present
Why would BUN be raised in an upper GI bleed?
Blood is digested to protein/aa which is metabolised in the liver (urea cycle) into blood urea nitrogen
What does OGD stand for?
oesophago-gastro-duodenoscopy
Give 2 endoscopic managements for an upper GI bleed
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
Give 3 therapeutics that can be provided before an endoscopy?
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
For on-going management of PUD, NSAID usage should be stopped, what can be given as an alternative?
Clopidogrel short term if possible or low dose Aspirin if absolutely necessary (eg. if preventive for vascular events)
How would pain relief be managed in a patient with preveous history of peptic ulcers who ALSO has Rheumatoid arthritis?
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
If patient requires ongoing anti-platelet therpy (eg. for cardiac problems) following treatment of peptic ulcers what must you do?
Reinstate anti-platelet monotherapy after 1 week AND long term PPI cover
What is the major risk for an untreated ulcer and what is the danger of this?
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.
Where would you spot a stomach perforation on a Chest X-ray and why?
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)
