What is stress ulcer?
A stress ulcer, also known as stress-related mucosal damage (SRMD) or stress-related gastric mucosal injury, is a type of peptic ulcer that develops in the lining of the stomach or duodenum (the first part of the small intestine) as a result of severe physiological stress. These ulcers typically occur in individuals who are critically ill, such as those hospitalized in intensive care units (ICUs), and are often associated with conditions such as severe trauma, major surgery, severe burns, sepsis, or shock.
The exact mechanism by which stress ulcers develop is not fully understood, but several factors are believed to contribute to their formation:
- Decreased Blood Flow: During periods of severe stress, the body may redistribute blood flow away from the gastrointestinal tract to vital organs such as the heart, lungs, and brain. This reduction in blood flow to the stomach and duodenum can lead to ischemia (lack of oxygen) and damage to the mucosal lining, predisposing it to ulcer formation.
- Increased Gastric Acid Secretion: Stress and critical illness can stimulate the release of stress hormones such as cortisol and catecholamines (e.g., epinephrine), which can increase gastric acid secretion and decrease mucosal blood flow, further contributing to mucosal injury and ulcer formation.
- Disruption of Mucosal Barrier: Severe physiological stress can disrupt the protective mucosal barrier of the stomach and duodenum, which normally helps to prevent damage from gastric acid and other digestive enzymes. Disruption of this barrier allows gastric acid and other irritants to come into direct contact with the mucosal lining, leading to ulcer formation.
- Impaired Mucosal Repair: Critical illness and severe stress can impair the body’s ability to repair and regenerate the mucosal lining of the stomach and duodenum, prolonging the duration of mucosal damage and increasing the risk of ulcer formation.
What is the relationship between stress ulcer and oxidative stress?
The relationship between stress ulcers and oxidative stress is multifaceted and involves several mechanisms that contribute to the development and progression of stress-induced mucosal damage. Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses, leading to cellular damage. In the context of stress ulcers, oxidative stress can exacerbate mucosal injury and impair the healing process through various mechanisms:
- Ischemia-Reperfusion Injury: During periods of severe stress, such as critical illness or shock, there may be transient reductions in blood flow (ischemia) to the gastrointestinal mucosa. When blood flow is restored (reperfusion), it can lead to the generation of ROS and oxidative stress in the affected tissues. Ischemia-reperfusion injury contributes to mucosal damage and ulcer formation, particularly in the stomach and duodenum, where the mucosa is highly susceptible to ischemic injury.
- Increased Gastric Acid Secretion: Stress and critical illness can stimulate the release of stress hormones such as cortisol and catecholamines (e.g., epinephrine), which can increase gastric acid secretion. Elevated gastric acid levels can lead to mucosal damage and ulcer formation, and oxidative stress may further exacerbate this process by impairing mucosal defense mechanisms and increasing susceptibility to acid-induced injury.
- Disruption of Mucosal Barrier: Oxidative stress can disrupt the integrity of the gastrointestinal mucosal barrier, which normally acts as a protective barrier against gastric acid, bile salts, and other irritants. Disruption of this barrier allows harmful substances to penetrate the mucosa and cause tissue damage, promoting ulcer formation.
- Impaired Mucosal Repair: Oxidative stress can impair the body’s ability to repair and regenerate the mucosal lining of the stomach and duodenum following injury. ROS can directly damage mucosal cells and impair cellular repair mechanisms, prolonging the duration of mucosal damage and delaying ulcer healing.
- Inflammatory Response: Stress ulcers trigger an inflammatory response in the gastrointestinal mucosa, characterized by the release of pro-inflammatory cytokines, activation of immune cells, and recruitment of inflammatory mediators. Inflammatory processes generate ROS and reactive nitrogen species (RNS), leading to oxidative stress and further exacerbating mucosal injury and ulcer formation.
Overall, oxidative stress plays a significant role in the pathogenesis and progression of stress ulcers by exacerbating mucosal damage, impairing mucosal repair mechanisms, and promoting inflammation.