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Related Concept Videos

Peptic Ulcer01:27

Peptic Ulcer

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Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the...
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Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

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Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
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Peptic Ulcer Disease II: Pathophysiology01:28

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Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
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Increased Body Temperature01:25

Increased Body Temperature

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A body temperature above  38°C  (100.4 °F) is known as fever or pyrexia, and a person with fever is termed 'febrile.' Typically, the hypothalamus, a part of the brain that acts as the body's thermostat, regulates body temperature through a thermoregulatory setpoint. It receives signals from cold and warm thermal receptors throughout the body and adjusts the body's temperature accordingly. Fever occurs when this hypothalamic setpoint is altered, usually in...
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Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

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Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal...
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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
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A Metadata Extraction Approach for Clinical Case Reports to Enable Advanced Understanding of Biomedical Concepts
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Febrile ulceronecrotic Mucha-Habermann disease.

F-X Lejuste1, C Michaux, C Lehners

  • 1Service de Chirurgie Plastique Reconstructrice et Esthétique, Centre Hospitalier de Luxembourg, Luxembourg, Luxembourg.

BMJ Case Reports
|October 16, 2013
PubMed
Summary

Mucha-Habermann disease, a rare inflammatory skin condition, can present with severe necrotic lesions mimicking erysipelas. Early diagnosis is crucial to avoid misdiagnosis and unnecessary surgical interventions.

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Area of Science:

  • Dermatology
  • Pathology

Background:

  • Mucha-Habermann disease is a rare inflammatory skin condition and a variant of pityriasis lichenoides et varioliformis acuta.
  • The etiology of Mucha-Habermann disease remains uncertain, and no standard treatment is established.

Observation:

  • A 64-year-old woman presented with facial erysipelas that progressed to a necrotizing ulcerative lesion.
  • Associated symptoms included local edema and headache, prompting a skin biopsy.
  • The biopsy confirmed pityriasis lichenoides et varioliformis acuta.

Findings:

  • Corticosteroid treatment rapidly stabilized the patient's skin lesions.
  • After six months, only a small area of frontal hypopigmentation remained.

Implications:

  • This case highlights the importance of considering Mucha-Habermann disease in patients with necrotic lesions and rapidly expanding cutaneous signs.
  • Timely diagnosis can prevent unnecessary debridement and extensive scarring.
  • Raising awareness among medical and surgical specialists is essential for managing this rare condition.