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You are a Physician's Assistant in the Emergency Room. A 19-year-old female is admitted in an unconscious state. Your quick evaluation of the patient yields stiff neck and positive Kernig's signs (i.e., leg cannot be extended while the patient is laying on her back), which are classical indications of meningitis (an infection in the central nervous system). The attending clinician suspects bacterial meningitis and so starts empirical therapy (i.e., antibiotic therapy presuming that this is a bacterial infection). Cerebrospinal fluid (CSF) collected from her spinal cord is sent for emergency evaluation and the results are received in less than an hour. The results indicate the presence of gram- negative diplococcus bacteria and the presence of many pus cells with intracellular bacteria. Your preliminary assessment of the function of the complement proteins in her serum indicates that the classical activation pathway appears to be intact; however when you add the bacteria to her serum ex vivo (i.e., in a tube in the lab), the bacteria are not killed. When the patient is stabilized the doctor receives the transcript of her past medical history, which includes a similar episode 2 years ago. Which of the following complement pathway component defects most likely led to this patient's condition? O C5-C9 complex deficiency O C2/C4 deficiency O Complement receptor deficiency De O Mannose binding lectin (MBL) deficicency Decay accelerating factor (DAF) deficiency

You are a Physician's Assistant in the Emergency Room. A 19-year-old female is admitted in an unconscious state. Your quick evaluation of the patient yields stiff neck and positive Kernig's signs (i.e., leg cannot be extended while the patient is laying on her back), which are classical indications of meningitis (an infection in the central nervous system). The attending clinician suspects bacterial meningitis and so starts empirical therapy (i.e., antibiotic therapy presuming that this is a bacterial infection). Cerebrospinal fluid (CSF) collected from her spinal cord is sent for emergency evaluation and the results are received in less than an hour. The results indicate the presence of gram- negative diplococcus bacteria and the presence of many pus cells with intracellular bacteria. Your preliminary assessment of the function of the complement proteins in her serum indicates that the classical activation pathway appears to be intact; however when you add the bacteria to her serum ex vivo (i.e., in a tube in the lab), the bacteria are not killed. When the patient is stabilized the doctor receives the transcript of her past medical history, which includes a similar episode 2 years ago. Which of the following complement pathway component defects most likely led to this patient's condition? O C5-C9 complex deficiency O C2/C4 deficiency O Complement receptor deficiency De O Mannose binding lectin (MBL) deficicency Decay accelerating factor (DAF) deficiency

Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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You are a Physician's Assistant in the Emergency Room. A 19-year-old female is admitted in an unconscious state. Your quick evaluation of the patient yields stiff neck and positive Kernig's signs (i.e., leg cannot be extended while the patient is laying on her back), which are classical indications of meningitis (an infection in the central nervous system). The attending clinician suspects bacterial meningitis and so starts empirical therapy (i.e., antibiotic therapy presuming that this is a bacterial infection). Cerebrospinal fluid (CSF) collected from her spinal cord is sent for emergency evaluation and the results are received in less than an hour. The results indicate the presence of gram- negative diplococcus bacteria and the presence of many pus cells with intracellular bacteria. Your preliminary assessment of the function of the complement proteins in her serum indicates that the classical activation pathway appears to be intact; however when you add the bacteria to her serum ex vivo (i.e., in a tube in the lab), the bacteria are not killed. When the patient is stabilized the doctor receives the transcript of her past medical history, which includes a similar episode 2 years ago. Which of the following complement pathway component defects most likely led to this patient's condition? O C5-C9 complex deficiency O C2/C4 deficiency O Complement receptor deficiency De O Mannose binding lectin (MBL) deficicency Decay accelerating factor (DAF) deficiency
Transcribed Image Text:You are a Physician's Assistant in the Emergency Room. A 19-year-old female is admitted in an unconscious state. Your quick evaluation of the patient yields stiff neck and positive Kernig's signs (i.e., leg cannot be extended while the patient is laying on her back), which are classical indications of meningitis (an infection in the central nervous system). The attending clinician suspects bacterial meningitis and so starts empirical therapy (i.e., antibiotic therapy presuming that this is a bacterial infection). Cerebrospinal fluid (CSF) collected from her spinal cord is sent for emergency evaluation and the results are received in less than an hour. The results indicate the presence of gram- negative diplococcus bacteria and the presence of many pus cells with intracellular bacteria. Your preliminary assessment of the function of the complement proteins in her serum indicates that the classical activation pathway appears to be intact; however when you add the bacteria to her serum ex vivo (i.e., in a tube in the lab), the bacteria are not killed. When the patient is stabilized the doctor receives the transcript of her past medical history, which includes a similar episode 2 years ago. Which of the following complement pathway component defects most likely led to this patient's condition? O C5-C9 complex deficiency O C2/C4 deficiency O Complement receptor deficiency De O Mannose binding lectin (MBL) deficicency Decay accelerating factor (DAF) deficiency
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