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Acute Ulcers

*Ulcus acutum*

For medical students2 min readUpdated 2026-10-10

Acute ulcers are tissue defects that occur due to aggressive factors or systemic pathologies. In pathology, they are classically divided into primary ulcers, associated with direct injury, and secondary ulcers, developing as a consequence of other diseases.

Primary ulcersCaused by the direct action of acids, alkalis, microorganisms, or extreme temperatures.
Secondary ulcersA consequence of GI ischemia, severe stress, endocrinopathies, or medication use.
Vessel arrosionDestruction of a blood vessel wall leading to massive hemorrhage.
Steroid ulcersSpecific drug-induced defects with an extremely high tendency for perforation.

Primary Acute Ulcers: Direct Tissue Injury

In pathology, primary acute ulcers are viewed as the result of direct contact between a damaging agent and body tissues.

Localization of the Pathological Process Localization of these defects varies widely. Primarily, they can form on the body surface. Within internal organs, the pathological process affects various segments of the gastrointestinal tract, including:

Etiology of Primary Ulceration Causes of primary defects are always linked to aggressive external factors. Key factors include the direct action of chemicals (acids and alkalis), pathogenic microorganisms, and thermal factors (extreme temperatures).

Morphology and Outcomes The morphological picture is characterized by pronounced purulent-necrotic changes. The ratio of these processes varies; the predominance of the purulent or necrotic component strictly depends on the specific etiology of the injury. The outcome of a primary acute ulcer is healing, which is invariably accompanied by the formation of dense scars.

Secondary Acute Ulcers: Systemic Body Response

Unlike primary ulcers, secondary acute ulcers are not formed through direct contact with an aggressive substance, but rather act as a complication or consequence of other severe systemic conditions.

Main Causes (Etiology):

  1. GI ischemia: disruption of normal blood supply to the gastrointestinal tract wall.
  2. Stress: severe physiological stress responses triggering a cascade of pathological changes.
  3. Endocrinopathies: various disorders of the endocrine system.
  4. Medication effects: intake of specific drug classes that negatively affect tissues.

Outcome of Secondary Lesions Interestingly, the outcome of secondary ulcers differs from primary ones. Despite the severity of the underlying conditions, the ulcerated defects themselves typically resolve with simple tissue healing, often without forming the dense scars seen in primary injuries.

Life-Threatening Complications of Ulcer Disease

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. Pathology highlights two main life-threatening states.

1. Vessel Arrosion Progression of the purulent-necrotic process deep into the organ wall can lead to the destruction (arrosion) of a blood vessel. The inevitable result is hemorrhage. A classic example is massive gastrointestinal bleeding requiring emergency medical intervention.

2. Perforation If the pathological process involves all layers of a hollow organ wall, transmural destruction—perforation—occurs. As a result, luminal contents spill into the body cavities. Pathology emphasizes that this complication is highly characteristic of specific drug therapies, namely steroid ulcers.

Mnemonic

To easily remember the etiology of secondary ulcers, use the mnemonic ESIM: Endocrinopathies, Stress, Ischemia (GI), Medications.

Frequently asked questions

What microscopic zones are distinguished in the base of an acute ulcer?

A zone of fibrinoid necrosis is identified in the base of an acute gastric ulcer. The formation of this zone is a key step in the pathogenesis of the transition from an acute to a chronic ulcer. Due to necrotic debris, epithelial repair via foveolized epithelial sliding becomes ineffective, as the epithelium is shed without a subepithelial scaffold.

What eponymous types of stress ulcers are distinguished in pathology?

Pathology identifies two main eponymous types of stress gastroduodenal ulcers:

  • Cushing ulcers — multiple acute ulcers occurring in traumatic brain injuries, brain hemorrhages, and neurosurgical procedures. Their mechanism is linked to HCl 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, leading to reduced mucosal defense mechanisms.
Which drug groups most commonly cause secondary acute ulcers?

NSAIDs are cited as ulcerogenic drugs causing erosive and ulcerative lesions, including agents with strong ulcerogenic potential such as indometacin, ketoprofen, naproxen, diclofenac, piroxicam, and ibuprofen. Steroid-induced ulcers, prone to perforation, are also well documented.

What is the pathogenesis of acute ulcers in GI ischemia?

GI ischemia serves as an etiologic factor for secondary acute ulcers. Ischemia and tissue acidosis reduce mucosal defense mechanisms—primarily by lowering bicarbonate levels—while mucosal hypoperfusion slows down regeneration.

In which parts of the digestive tract can primary acute ulcers be located?

According to classification, primary lesions can affect almost all segments. They occur in the esophagus, stomach, and intestines—including the small intestine (and duodenum) and large intestine. Additionally, 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 component (purulent or necrotic) predominates depends entirely on the etiology—the specific factor (acid, alkali, microorganisms, or temperature) that caused the injury.

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 usually resolve with simple tissue healing.

What is the primary danger associated with steroid ulcers?

Steroid ulcers, arising as a complication of drug therapy, have a marked tendency toward perforation, which means transmural rupture of the hollow organ wall.

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