]> 2026-07-31T14:08:21+00:00 WBR0295 0 en It is due to histamine-mediated vasoconstriction of arterioles The redness and warmth are due to histamine-mediated vasodilation of arterioles, not due to vasoconstriction of arterioles. It is due to histamine-mediated vasodilation of venules The redness and warmth are due to histamine-mediated vasodilation of arterioles, not due to vasodilation of venules. It is due to histamine-mediated vasodilation of arterioles In inflammation, redness and warmth are a result of histamine-mediated vasodilation of arterioles. It is due to histamine-mediated increase in the permeability of venules Edema that is associated with inflammation is due to histamine-mediated increase in the permeability of venules. Bradykinin-mediated effect on nerve endings that have been sensitized by PGE2. Pain is due to the effect of bradykinin and other pain mediators on nerve endings that have been sensitized by PGE2. 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 the facial erysipelas. During acute 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 changes and leukocytic responses. Clinically, acute inflammation is characterized by 5 important features: * Rubor (redness) * Calor (warmth) * Tumor (swelling) * Dolor (pain) * Functio laesa (loss of function) In acute 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 already been sensitized by PGE2. The distinction between the features of acute inflammation and the mechanisms by which they manifest is important.<br/> '''Educational Objective:''' In inflammation, redness and warmth are a result of histamine-mediated vasodilation of arterioles<br/> '''References:''' Rankin JA. Biological mediators of acute inflammation. AACN Clin Issues. 2004;15(1):3-17.<br> MacGlashan D Jr. Histamine: a mediator of inflammation. J Allergy Clin Immunol. 2003;112(4 Suppl):S53-9.<br> First Aid 2014 page 244 Pathophysiology A 42-year-old man presents to the emergency department (ED) with fever and facial redness, pain, and edema for the past day. The patient recalls that his symptoms started 2 days after he accidentally cut his face while shaving. 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? C Head and Neck 2020-10-28T00:05:43Z 2459150.5039699 WBR0295