WBR0295
| Author | [[PageAuthor::Ogheneochuko Ajari, MB.BS, MS [1] (Reviewed by Yazan Daaboul, M.D.)]] |
|---|---|
| Exam Type | ExamType::USMLE Step 1 |
| Main Category | MainCategory::Pathophysiology |
| Sub Category | SubCategory::Head and Neck |
| Prompt | [[Prompt::A 42-year-old man presents to the emergency department (ED) with fever and facial redness, pain, and edema for the past 2 days. The patient recalls that his symptoms started after he accidentally cut his face while shaving 5 days ago. In the ED, his temperature is 38.4 °C (101.1 °F), blood pressure is 130/84 mmHg, and heart rate is 100/min. Physical examination is remarkable for a tender, edematous, and erythematous skin lesion on the left side of the face that has clearly demarcated margins. Which of the following statements is true about the pathogenesis of erythema in this patient's condition?]] |
| Answer A | AnswerA::It is due to histamine-mediated vasoconstriction of arterioles |
| Answer A Explanation | AnswerAExp::The redness and warmth is due to histamine-mediated vasodilation of arterioles, not due to vasoconstriction of arterioles. |
| Answer B | AnswerB::It is due to histamine-mediated vasodilation of venules |
| Answer B Explanation | AnswerBExp::The redness and warmth is due to histamine-mediated vasodilation of arterioles, not due to vasodilation of venules. |
| Answer C | AnswerC::It is due to histamine-mediated vasodilation of arterioles |
| Answer C Explanation | AnswerCExp::In inflammation, redness and warmth are a result of histamine-mediated vasodilation of arterioles. |
| Answer D | AnswerD::It is due to histamine-mediated increase in the permeability of venules |
| Answer D Explanation | AnswerDExp::Edema associated with inflammation is due to histamine-mediated increase in the permeability of venules. |
| Answer E | AnswerE::Bradykinin-mediated effect on nerve endings that have been sensitized by PGE2. |
| Answer E Explanation | AnswerEExp::Pain is due to the effect of bradykinin and other pain mediators on nerve endings that have been sensitized by PGE2. |
| Right Answer | RightAnswer::C |
| Explanation | [[Explanation::Facial erysipelas is a clinical diagnosis characterized by an acute-onset of fever, facial pain, erythema, and edema. Patients often complain of a tender skin lesion that has clearly demarcated margins. While patients with uncomplicated erysipelas are treated as out-patients, hospitalization is required for pediatric patients (due to high risk of sepsis) or for adults patients who present with facial involvement or complicated disease. This patient is presenting with symptoms and signs of acute inflammation, which is a transient and early physiological response to this patient's facial infection. During inflammation, blood supply and capillary permeability in the involved region significantly increases to facilitate the migration of leukocytes from the blood vessels into the interstitial space of the inflamed tissue. During inflammation, cytokines and chemical mediators are released that result in small vessel and leukocytic responses. Clinically, inflammation is characterized by 5 important features:
In inflammation, redness and warmth are a result of histamine-mediated vasodilation of arterioles, whereas edema is a result of the increase in histamine-mediated venular permeability. Pain is due to the effect of bradykinin and other pain mediators on nerve endings that have been sensitized by PGE2. The distinction between these features and the mechanism by which they manifest is important. |
| Approved | Approved::Yes |
| Keyword | WBRKeyword::Histamine, WBRKeyword::Infection, WBRKeyword::Rubor, WBRKeyword::Rash, WBRKeyword::Inflammation, WBRKeyword::Erythema, WBRKeyword::Erysipelas, WBRKeyword::Histamine, WBRKeyword::Cytokines, WBRKeyword::Redness |
| Linked Question | Linked:: |
| Order in Linked Questions | LinkedOrder:: |