Primary acute ulcers: direct tissue damage
In pathological anatomy, primary acute ulcers are viewed as the result of direct contact between a damaging agent and the body's tissues.
Localization of the pathological process The localization of such defects is quite diverse. First of all, they can form directly on the body surface. Speaking of internal organs, the pathological process affects various parts of the digestive tract. These include:
- Esophagus;
- Stomach;
- Small intestine;
- Duodenum;
- Large intestine.
Etiology of primary ulceration The causes of primary defects are always associated with aggressive external exposure. The main factors include the direct action of chemicals (various acids and alkalis), the influence of pathogenic microorganisms, and thermal factors (exposure to extreme temperatures).
Morphology and outcome The morphological picture is characterized by the development of pronounced purulent-necrotic changes. It is important to note that the ratio of these processes is not constant: the predominance of the purulent or, conversely, necrotic component strictly depends on the specific etiology that caused the damage. The outcome of a primary acute ulceration is healing, which is invariably accompanied by the formation of dense scars.
Secondary acute ulcers: systemic response of the body
Unlike primary ones, secondary acute ulcers are formed not due to direct contact with an aggressive substance, but act as a complication or consequence of other severe systemic conditions.
Main causes (etiology):
- GI ischemia: impairment of the normal blood supply to the gastrointestinal wall.
- Stress: severe stress reactions of the body that trigger a cascade of pathological changes.
- Endocrinopathies: various disorders in the endocrine system.
- Medication impact: intake of certain groups of drugs that adversely affect tissues.
Outcome of secondary lesions Interestingly, the outcome of secondary ulcers differs from that of primary ones. Despite the severity of the conditions causing them, the ulcer defects themselves usually end in simple tissue healing, often without forming the severe scars seen in primary injuries.
Severe complications of the ulcerative process
Any acute ulcer, regardless of its origin (primary or secondary), poses a serious threat to the patient's life due to the risk of severe complications. In pathological anatomy, two main life-threatening conditions are distinguished.
1. Vascular erosion The progression of the purulent-necrotic process deep into the organ wall can lead to the destruction (erosion) of a passing blood vessel. The logical outcome of this is the development of hemorrhage. A classic example is massive gastric hemorrhage requiring emergency medical intervention.
2. Perforation If the pathological process encompasses all layers of the hollow organ wall, transmural destruction occurs—perforation. As a result, the organ contents spill outward. Pathological anatomy emphasizes that this complication is highly characteristic of specific drug exposure, namely, steroid ulcers.
Briefly: answers to topical questions
What microscopic zones are distinguished in the base of an acute ulcer?
The base of an acute gastric ulcer shows a zone of fibrinoid necrosis. The formation of this zone is a key stage in the pathogenesis of the transition from an acute ulcer to a chronic form. Due to the presence of necrotic masses, tissue repair via the migration of foveolar epithelium becomes ineffective, as the epithelium is sloughed off without a subepithelial basement.
What eponymic types of stress ulcers are distinguished in pathological anatomy?
Pathological anatomy distinguishes two main eponymic types of stress gastroduodenal ulcers.
- Cushing ulcers — multiple acute ulcers occurring in traumatic brain injuries, brain hemorrhages, and neurosurgical operations. Their mechanism of formation is associated with gastric acid hypersecretion due to increased vagus nerve (n. vagus) tone.
- Curling ulcers — acute ulcers developing in extensive burns as a manifestation of burn disease. Their pathogenesis is driven by tissue ischemia and acidosis, which leads to a decrease in the protective properties of the mucosa.
Which drug groups most commonly cause secondary acute ulcers?
Sources point to NSAIDs as ulcerogenic drugs causing erosive and ulcerative lesions, including agents with pronounced ulcerogenic effects: indomethacin, ketoprofen, naproxen, diclofenac, piroxicam, and ibuprofen. Steroid ulcers, which are characterized by perforation, are also described.
What is the pathogenesis of acute ulcers in GI ischemia?
GI ischemia is indicated as an etiological factor for secondary acute ulcers. Sources also note that tissue ischemia and acidosis reduce mucosal protective properties, primarily due to lowered bicarbonate levels, while mucosal microvascular hypoperfusion slows down regeneration.
To easily remember the etiology of secondary ulcers, use the acronym EMSI: Endocrinopathies, Medication impact, Stress, Ischemia (GI).
Class and exam questions
In which parts of the digestive tract can primary acute ulcers be localized?
According to classification, primary lesions can affect virtually all segments. They are found in the esophagus, stomach, and intestines—the small intestine (including the duodenum) and large intestine. In addition, they can occur on the body surface.
What determines the morphological picture of a primary ulcer?
Purulent-necrotic changes form the basis of the morphology. However, which specific component (purulent or necrotic) predominates in the lesion entirely depends on the etiology—that is, the factor (acid, alkali, microorganisms, or temperature) that caused the damage.
How do the outcomes of primary and secondary acute ulcers differ?
Primary acute ulcers typically heal with scar formation due to deep direct tissue damage. Secondary lesions, on the other hand, usually end in simple tissue healing.
What is the danger of steroid ulcers?
Steroid ulcers, arising as a consequence of medication impact, have a pronounced tendency toward complications such as perforation. This implies a transmural rupture of the hollow organ wall.
What else to study on this topic
- Detailed analysis of purulent-necrotic changes depending on specific etiology (acids, alkalis, microorganisms, thermal factors)
- Mechanisms of scar formation during the healing of primary ulcer defects
- Pathogenesis of secondary ulcers against the background of GI ischemia and severe stress
- The effect of endocrinopathies on mucous membranes and ulcer formation
- Morphological picture of blood vessel erosion and the development of gastric hemorrhage
- Features of hollow organ wall perforation in steroid ulcers
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