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{{WBRQuestion
{{WBRQuestion
|QuestionAuthor={{Ochuko}}
|QuestionAuthor= {{Ochuko}} (Reviewed by  {{YD}})
|ExamType=USMLE Step 1
|ExamType=USMLE Step 1
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Dermatology
|SubCategory=Head and Neck
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Dermatology
|SubCategory=Head and Neck
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Dermatology
|SubCategory=Head and Neck
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Dermatology
|SubCategory=Head and Neck
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Dermatology
|SubCategory=Head and Neck
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Dermatology
|SubCategory=Head and Neck
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Dermatology
|SubCategory=Head and Neck
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Dermatology
|SubCategory=Head and Neck
|Prompt=A 42-year-old male presents to the ER with a fever, chills, and facial pain, which had began three days prior. Upon further questioning, he states that he accidentally cut his face while shaving. Physical examination reveals a very red and swollen skin lesion with blisters and a raised border that is warm to touch on the left side of the face. Which of the following mechanisms is true about the lesion?
|Prompt=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?
|Explanation=This is a case of Erysipelas of the face due to group A streptococcus. Signs of acute inflammation present in this patient include Rubor (redness), Calor (warm to touch), Tumor (swelling) and Dolor (pain). The infection is associated with a warm skin (calor) and pain (dolor). The redness and warmth experienced by this patient is due to histamine-mediated vasodilation of arterioles
|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 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:
|AnswerA=The redness and warmth is due to histamine-mediated vasoconstriction of arterioles
* Rubor (redness)
|AnswerAExp=The redness and warmth is due to histamine-mediated vasodilation of arterioles and not due to vasoconstriction of arterioles
* Calor (warmth)
|AnswerB=The redness and warmth is due to histamine-mediated vasodilation of venules
* Tumor (swelling)
|AnswerBExp=The redness and warmth is due to histamine-mediated vasodilation of arterioles and not due to vasodilation of venules
* Dolor (pain)
|AnswerC=The redness and warmth is due to histamine-mediated vasodilation of arterioles
* Functio laesa (loss of function)
|AnswerCExp=See explanation
 
|AnswerD=The swelling is due to histamine mediated decrease in permeability of venules
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.
|AnswerDExp=The swelling is due to histamine mediated increase and not a decrease in permeability of venules
|AnswerA=It is due to histamine-mediated vasoconstriction of arterioles
|AnswerE=The pain is caused by PGE2 sensitization of specialized nerve endings to the effects of serotonin
|AnswerAExp=The redness and warmth are due to histamine-mediated vasodilation of arterioles, not due to vasoconstriction of arterioles.
|AnswerEExp=The pain is caused by PGE2 sensitization of specialized nerve endings to the effects of bradykinin
|AnswerB=It is due to histamine-mediated vasodilation of venules
|EducationalObjectives=The tissue redness of Erysipelas is caused by histamine-mediated vasodilation of aterioles.
|AnswerBExp=The redness and warmth are due to histamine-mediated vasodilation of arterioles, not due to vasodilation of venules.
|References=First Aid 2014 page 244
|AnswerC=It is due to histamine-mediated vasodilation of arterioles
|AnswerCExp=In inflammation, redness and warmth are a result of histamine-mediated vasodilation of arterioles.
|AnswerD=It is due to histamine-mediated increase in the permeability of venules
|AnswerDExp=Edema that is associated with inflammation is due to histamine-mediated increase in the permeability of venules.
|AnswerE=Bradykinin-mediated effect on nerve endings that have been sensitized by PGE2.
|AnswerEExp=Pain is due to the effect of bradykinin and other pain mediators on nerve endings that have been sensitized by PGE2.
|EducationalObjectives=In inflammation, redness and warmth are a result of histamine-mediated vasodilation of arterioles
|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
|RightAnswer=C
|RightAnswer=C
|WBRKeyword=Histamine, Infection, Rubor, Rash
|WBRKeyword=Histamine, Infection, Rubor, Rash, Inflammation, Erythema, Erysipelas, Histamine, Cytokines, Redness
|Approved=Yes
|Approved=Yes
}}
}}

Latest revision as of 00:05, 28 October 2020
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 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?]]
Answer A AnswerA::It is due to histamine-mediated vasoconstriction of arterioles
Answer A Explanation AnswerAExp::The redness and warmth are 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 are 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 that is 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 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.
Educational Objective: In inflammation, redness and warmth are a result of histamine-mediated vasodilation of arterioles
References: Rankin JA. Biological mediators of acute inflammation. AACN Clin Issues. 2004;15(1):3-17.
MacGlashan D Jr. Histamine: a mediator of inflammation. J Allergy Clin Immunol. 2003;112(4 Suppl):S53-9.
First Aid 2014 page 244]]

Approved Approved::Yes
Keyword WBRKeyword::Histamine, WBRKeyword::Infection, WBRKeyword::Rubor, WBRKeyword::Rash, WBRKeyword::Inflammation, WBRKeyword::Erythema, WBRKeyword::Erysipelas, WBRKeyword::Histamine, WBRKeyword::Cytokines, WBRKeyword::Redness
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