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MP322 > MP322 - PEPTIC ULCER DISEASE AND GORD > Flashcards

MP322 - PEPTIC ULCER DISEASE AND GORD Flashcards

1
Q

Peptic ulcers?

A

sores that develop in the lining of the stomach, lower oesophagus, or small intestine

duodenum ulcers more common than gastric ulcers

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2
Q

Causes of peptic ulcers

A
  • stress
  • alcohol
  • diet
  • use of NSAIDs
  • presence of H. Pylori
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3
Q

Treatment of peptic ulcers

A

anti-ulcer therapy
drugs - H2 antagonists and Proton pump inhibitors (PPIs)

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4
Q

current treatment of H. Pylori peptic ulcer

A

triple therapy -
PPI
amoxicillin
clarithromycin or metronidazole

(penicillin allergic)
PPI
clarithromycin
metronidazole

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5
Q

Dyspepsia

A

range of symptoms arising from the upper GI tract, not a diagnosis itself

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6
Q

symptoms of dyspepsia

A
  • upper abdominal pain/discomfort
  • heartburn
  • gastric reflux
  • nausea/vomiting

symptoms typically last 4 weeks or more

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7
Q

How the stomach doesn’t digest itself

A

(1) surface of mucosa is lined with cells that secrete slightly alkaline mucus that forms a thin layer over the luminal surface. both the protein content of mucus and its alkalinity neutralise H+ in the epithelium.
(2) tight junctions between the epithelial cells lining the stomach limit the diffusion of H+ into the underlying tissues
(3) damaged epithelial cells are replaced every few days by new cells by cell division in gastric pits

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8
Q

consequences of NSAIDs use

A
  • inhibition of endogenous prostaglandin synthesis
  • decrease in epithelial mucus, bicarbonate secretion, mucosal blood flow, epithelial proliferation, mucosal resistance to injury
  • lower mucosal resistance increases the incidence of injury by endogenous factors such as acid, pepsin, and bile salts as well as exogenous factors such as NSAIDs, ethanol and other noxious agents
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9
Q

peptic ulcer symptoms

A
  • abdominal discomfort, pain or nausea
  • pain is located in the epigastrium and usually does not radiate
  • pain aggravated by meals, whereas that of a duodenal ulcer is relived
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10
Q

H. Pylori mechanism of action

A
  • avoids acidic environment of the interior stomach (lumen) by using the flagella to burrow into mucus lining of the stomach to reach epithelial cells, where the pH is more neutral
  • can sense the pH gradient in the mucus and move towards the less acidic region (chemotaxis)
  • can neutralise the acid in its environment by producing large amounts of urease
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11
Q

why does H. Pylori produce urease

A
  • breaks down the urea in the stomach into carbon dioxide and ammonia
  • the basic ammonia then neutralises the stomach acid
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12
Q

non-invasive diagnostic testing for H. Pylori

A
  • evaluation of presence of H. Pylori antibodies
  • urea breath test
  • stool antigen test
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13
Q

gastric gland regions in the stomach

A

body, antrum, fundus

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14
Q

body region in the stomach

A

thin-walled upper portion secretes mucus, pepsinogen and HCL

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15
Q

antrum region in the stomach

A
  • lower portion
  • thicker layer of smooth muscle
  • responsible for mixing and grinding stomach contents
  • secretes mucus, pepsinogen and gastrin
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16
Q

fundus region in the stomach

A
  • uppermost portion
  • cells at the opening secrete mucus
  • lining the walls are parietal cells (oxyntic cells), which secrete acid and intrinsic factor, and chief cells which secrete pepsinogen
17
Q

canaliculi

A

an infolding of the outer layer of the luminal membranes of parietal cells, greatly increases the surface area for secretion

18
Q

enterochromaffin-like cells

A
  • in the antrum
  • release the paracrine agent histamine and endocrine cells (D cells) which release the peptide somatostatin
19
Q

acid secretion in the stomach

A

(1) parietal cells activated by acetylcholine or gastrin, increase in intracellular Ca2+ concentration, which stimulates acid secretion from the H+/K+ ATPase (proton pump) on the canalicular surface
(2) enterochromaffin-like cells have receptors for gastrin and acetylcholine, which stimulate histamine release
(3) histamine binds to H2 receptor on the parietal cell, activating adenylyl cyclase, which increases cAMP and activates protein kinases stimulates acid secretion from the H+/K+ ATPase

20
Q

antacids

A
  • weak alkalis
  • partly neutralise free acids in the stomach
    stimulate mucosal repair mechanisms around ulcers by stimulating prostaglandin release
  • used for symptomatic relief
21
Q

Histamine receptor (H2) antagonists

A

cimetidine, ranitidine, nizatidine, famotidine
- act competitively on H2 receptors on gastric parietal cells
- reduce basal acid secretion
- can treat both duodenal and gastric ulcers
- most effective when fasting (at night)

22
Q

adverse effects of H2 antagonists

A
  • diarrhoea
  • headache
  • confusion in elderly
  • gynaecomastia with cimetidine (anti-androgen effect)
  • cimetidine inhibits cytochrome P450 system (drug interactions)
23
Q

Proton pump inhibitors (PPIs)

A

omeprazole, lansoprazole, pantoprazole, esomeprazole
- inhibition of pump almost completely blocks acid secretion
- PPIs are irreversible
- return of acid secretion is dependant on synthesis of new enzymes (H+/K+ ATPase)

24
Q

adverse effects of PPIs

A
  • GI discomfort (e.g. nausea, diarrhoea, vomiting)
  • headache
  • skin rashes
  • long term use may cause gastric atrophy
  • omeprazole has both stimulatory and inhibitory effects on cytochrome P450 system
25
Q

Zollinger-Ellision syndrome

A
  • rare disorder that can cause gastric or duodenal ulcers (multiple) or in the jejunum
  • gastric acid hypersecretion
  • due to gastrin-secreting tumour in the pancreas or duodenum (gastrinoma) that stimulates acid secretion in the stomach
26
Q

Gastro-oesophageal reflux disease (GORD)

A
  • amount of acid secretion is normal
  • functionally incompetent lower oesophageal sphincter
  • reflux of gastric contents (inc. acid and pepsinogen into oesophagus)
27
Q

drugs for treating GORD

A
  • antacids and antacid/alginate combinations
  • H2 receptor antagonists and PPIs
  • drugs acting on oesophageal and/or gastric motility
28
Q

Barrett’s oesophagus

A
  • common in patients with long-term GORD
  • replacement of normal stratified squamous epithelium by columnar epithelium with goblet cells
  • can lead to oesophageal adenocarcinoma

MP322 (6 decks)

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