GIT Diseases II - PUD Flashcards
Define Peptic Ulcer Disease (PUD).
Peptic Ulcer Disease is a group of disorders characterised by circumscribed lesions of the mucosa of the upper GIT.
It is also a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the GIT wall.
What are the 2 types of peptic ulcers?
i. Gastric ulcer - affects the lining of the stomach.
ii. Duodenal ulcer - affects the lining of the duodenum
The most common symptom of both gastric and duodenal ulcers is _______.
Epigastric pain, which is gnawing, burning sensation in the epigastrium, usually after meals.
It occurs shortly after meals in GU and 2-3 hours after meals in DU.
Mucosal injury and peptic ulcer occur when the balance between the aggressive factors and the GIT defensive mechanisms is disrupted.
True or False?
True.
What are the defensive mechanisms (protective factors) of the gastroduodenal mucosa?
i. Thick mucus secretion by mucosa
ii. Mucosal blood flow, which removes acids that damage the epithelium
iii. Alkaline and neutral biliary juice
iv. Tight intercellular junction
v. Rapid continual epithelium renewal
vi. Prostaglandins, which inhibit acid secretion, maintain blood flow and stimulate mucus and bicarbonate production
What are the aggressive factors involved in the development of PUD?
Extrinsic factors:
i. NSAIDs
ii. H. pylori infection
iii. Alcohol
iv. Tobacco smoking
Intrinsic factors
vii. Bile salts
viii. Gastric acid
ix. Pepsin
Briefly discuss H. pylori in the pathogenesis of PUD.
- The bacterium infects the GI mucosa and produces an enzyme called urease which breaks down urea into ammonia and carbon dioxide. This ammonia, which shields the bacterium from the stomach’s acidity, also damages the protective mucous layer.
It also produces some enzymes such as haemolysins, fucosidase, and neuraminidase, which may be involved in tissue damage. - H. pylori also alters Gastrin homeostasis (hypergastrinemia), affecting gastric acid secretion and causing hyperacidity by:
i. decreasing antral D cells which secrete somatostatin, which is responsible for inhibiting gastrin
ii. direct stimulation of gastrin cells by cytokines produced during bacteria cytotoxin-induced inflammation
Briefly discuss NSAIDs in the pathogenesis of PUD.
- NSAIDs promote back diffusion of hydrogen ions into the mucosa
- NSAIDs cause mucosal injury due to their acidity
- They inhibit prostaglandins (PGE2 and PGI2) by inhibiting the enzymes COX-1 and COX-2
Gastric ulcers are classified according to ________, and staging is done based on ________.
-the Johnson classification
-the location of the lesion
Describe stage I gastric ulcer.
They are located near the incisura angularis on the lesser curvature, close to the border between the antrum and body of the stomach.
Gastric acid secretion is usually normal or decreased.
Describe stage III gastric ulcer.
It is prepyloric i.e. above the pylorus.
Gastric acid secretion is usually normal or increased.
Describe stage IV gastric ulcer.
it is located near the gastroesophageal junction.
Gastric acid secretion is usually normal or decreased.
Describe stage II gastric ulcer.
It’s a combination of stomach and duodenal ulcer.
Gastric acid secretion is usually normal or increased.
Describe stage V gastric ulcer.
It is found all over the stomach, and is drug-induced.
What are the 3 distinct causes of PUD.
i. H. pylori
ii. NSAIDs such as aspirin
iii. Hypersecretion of HCl as in Zollinger-Ellison syndrome
Mention 7 risk factors that predispose an individual to PUD.
- Previous history of PUD
- Genetic factors
- Corticosteroids: concurrent use of corticosteroids with NSAIDS
- Cigarette smoking
- Advanced age
- Associated disorders such as hyperparathyroidism, alcoholic cirrhosis, emphysema, rheumatoid arthritis
- Stress
What are the clinical manifestations of PUD?
i. Epigastric pain (dyspepsia)
ii. Nausea
iii. Vomiting
iv. Heartburn
v. Bloating and Belching
vi. Anorexia
vii. Weight loss.
Compare and contrast gastric ulcer and duodenal ulcer.
i. Epigastric pain occurs shortly after meal (45-60 mins) in GU, but 2-4 hours after meal in DU.
ii. Nocturnal pain (around 2 a.m.) occurs in DU but rarely ever occurs in GU.
iii. Food usually triggers pain in GU but relieves pain in DU
iv. GU patients tend to lose weight while DU patients tend to gain weight
v. H. pylori is present in 70% of GU cases, while it is present in almost all DU cases.
What are the complications of PUD?
i. Haemorrhage
ii. Chronic iron deficiency anaemia
iii. Pyloric stenosis
iv. Perforation
The selected treatment for PUD depends on:
i. Etiology
ii. Whether it is new or recurrent
iii. The presence of complications
Mention 6 goals of PUD therapy.
- To relieve dyspeptic symptoms
- To reduce acid secretion
- To promote epithelial healing
- To prevent complications
- To prevent recurrence
- To eradicate H. pylori infection.
Mention 5 non-pharmacological approaches to PUD management.
- Avoid exposure to exacerbating factors e.g. spicy foods, caffeine
- Reduce psychological stress
- Avoid smoking
- Avoid alcohol consumption
- Surgical intervention
What are the goals of pharmacotherapy in PUD?
i. To eradicate H. pylori infection
ii. To reduce morbidity
iii. To prevent complications
What are the classes of pharmacological agents used in PUD?
- Acid-antisecretory agents:
- H2 receptor antagonists e.g. Cimetidine, Ranitidine
- PPIs e.g. Omeprazole, Esomeprazole
- Potassium competitive acid blockers (PCASBs): competitively block H+ ions from back diffusing into the mucosa e.g. Vonoprazan - Mucosa protectants or cytoprotective agents e.g. Bismuth, Misoprostol, Sucralfate and antacids.
These agents stimulate mucus production and enhance blood flow through the GI lining. They also work by forming a coating that protects the ulcerated tissue. - Agents that eradicate H. pylori
