peptic ulcer disease Flashcards
1
Q
peptic ulcers
A
- sore that develop in the lining of the stomach/lower oesophagus/small intestine
- ulcers can penetrate the entire wall resulting in leakage of luminal content into abdominal cavity
- more common in men than women
2
Q
peritonitis
A
- when ulcer perforation allows bacteria that live in your stomach to infect the lining of the abdomen (peritoneum)
- infection can spread into blood (sepsis) reaching other areas causing organ failure if untreated
3
Q
peptic ulceration symptoms
A
- epigastric pain (relieved by antacids)
- nocturnal pain (spasms in leg muscles when sleeping)
- vomiting
4
Q
causes of peptic ulcer disease
A
- H. pylori
- NSAIDs/steroids
- pepsin
- smoking/alcohol
- bile acids
- stress
- genetics
5
Q
mucosa
A
- lined with goblet cells that secrete alkaline mucus that forms a layer over luminal surface
- protein content and alkalinity of mucus neutralises
H+ in the epithelium - mucus forms a chemical barrier between acidic contents of lumen and cell surface
6
Q
defence mechanisms from body to combat ulceration
A
- mucus
- bicarbonate
- mucosal blood flow
- prostaglandins
7
Q
duodenal mucosa
A
- forms gel layer which is impermeable to acid and pepsin
- other cells secrete bicarbonate which aids in buffering acid that lies near the mucosa
8
Q
prostaglandins
A
- type E (PGE)
- increases the production of bicarbonate and the mucous layer
9
Q
H. pylori
A
- infects lower part of stomach (antrum) causing inflammation of the gastric mucosa which leads to duodenal/gastric ulcer
- resides within gastric mucosa
- high activity of the enzyme urease which enables it to colonise the stomach
- stimulates increased gastrin release thereby increased acid secretion causing direct damage to mucosa
10
Q
NSAIDs
A
- impair mucosal resistance but do not alter acid secretion
- patients with an ulcer caused by NSAID discontinue the NSAID and be given a H2 antagonist
- if patient cannot stop NSAID then PPI should be given to heal ulcer
11
Q
H. pylori mechanism of action
A
- using its flagella to burrow into mucus lining of stomach to reach epithelial cells where pH is neutral
- it adheres to the cells by producing adhesions that bind to lipids and carbohydrates in the membrane
- uses chemotaxis to avoid areas of low pH and neutralises the acid in its environment by producing large amounts of urease
- urease breaks down the urea present in the stomach to carbon dioxide and ammonia
12
Q
urea breath test
A
patients swallow capsule containing urea made from an isotope of carbon and CO2 exhaled by patients is measured for the isotope and if detected the patient is H. pylori positive
13
Q
stool antigen test (SAT)
A
enzyme immunoassay (EIA) designed to detect H. pylori in faecal specimens by measuring H. pylori antigen released from organisms lining the stomach wall as the antigen is only detected if H. pylori is present
14
Q
fundus
A
- thin walled upper portion of stomach
- secretes mucus, pepsinogen, HCl
15
Q
antrum
A
- lower part of the stomach
- thicker layer of smooth muscle responsible for mixing and grinding stomach contents
- contain endocrine cells that secrete hormone gastrin