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By Z. Mitch. Cumberland College. 2017.

Although it is uncertain whether the bacteria themselves produce additional airway damage purchase 25 mg benadryl free shipping, heavy bacterial loads correlate with increased 7 INFECTIOUS DISEASE 69 inflammation. Workup, although beneficial to rule out other potential causes of lung dysfunction, is not necessary for diagnosis. An 18-year-old college student comes to the student health clinic for evaluation of fever and cough. Headache, sore throat, runny nose, and fatigue began 5 days ago. Fever and cough began 2 days ago and steadily increased. The cough is hacking, occurs frequently, and produces small amounts of clear spu- tum with occasional flecks of purulent material and blood. The patient has a history of childhood asth- ma, occasional marijuana use, and acne. He takes no oral medications and has no known drug allergies. On physical examination, the patient appears ill but not toxic. Pulse oximetry, measured while the patient is breathing room air, is 98%. Chest x-ray reveals segmental opacities in the right and left lower lobes. Sputum Gram stain shows abundant polymorphonuclear cells without microorganisms.

What interventions would be appropriate in the treatment of this patient? Continue with observation and repeated neurologic examinations cheap 25mg benadryl amex; repeat assessment with the GCS periodically; and consider imaging with a CT scan to rule out contusions B. Continue with observation and repeated neurologic examinations; repeat assessment with the GCS periodically; and obtain an MRI C. Admit the patient for prolonged observation; obtain a CT scan to rule out contusions; and start I. Admit the patient to the ICU; obtain an MRI; and consider intraven- tricular monitoring of intracranial pressure (ICP) Key Concept/Objective: To understand the appropriate treatment of mild traumatic brain injury (MTBI) With an incidence of 180 per 100,000 people, MTBI is more common than any other neu- rologic diagnosis except migraine. MTBI is defined as any traumatic brain injury/concus- sion with loss of consciousness of 0 to 30 minutes, a GCS score of 13 to 15 on admission, posttraumatic amnesia or confusion lasting less than 24 hours, and no evidence of contu- sion or hematoma on CT. Although the emergency department evaluation and manage- ment of MTBI is controversial, the principal concern is with identifying evolving surgical lesions such as hematomas and contusions. In addition to history and examination, CT has become the mainstay of evaluation. Prolonged or deteriorating mental status or the presence of neurologic signs or other risk factors are still indications for CT scanning, observation, or both after MTBI. MRI promises to be very useful in the long-term manage- ment of moderate and severe TBI, as well as in the documentation of brain pathology in patients with milder injury. However, it is often impractical and not cost-effective in the acute setting. This patient has MTBI, and observation for a few hours and possibly a CT scan to rule out contusions are appropriate. He does not have severe enough trauma to warrant admission or invasive monitoring of his ICP. A 46-year-old woman is brought to the emergency department by EMS after being involved in a car acci- dent.

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Increasingly discount benadryl 25mg mastercard, patients with a metabolic myopathy present with significant symptoms of myalgia or myoglobinuria and have normal or minimally abnormal basic muscle histology, yet biochemical tests reveal signif- icant enzyme abnormalities that would otherwise be missed. However, even the most astute muscle pathologist is dependent on accurate clinical informa- tion to decide which of the numerous biochemical studies are most appropri- ate. Pathological evaluation of muscle should be performed even where genet- ic analysis is available because it provides information about the severity of the disease, characterizes the presence or absence of a specific protein, and provides a clinical correlate for an available treatment. As discussed below, even the presence of a specific gene mutation may produce widely varying biochemical changes in muscle due to the presence of gene modifying effects. Regulation of gene Characterizing the molecular genetics of muscle has become increasingly defects in muscle important in understanding the pathogenesis of myopathy. Most gene defects have been described in the following chapters. The resulting clinical profile is dependent not only on the gene, but also on whether the disorder is autosomal recessive or dominant, the chromosomal localization, size of the gene defect, exon number, the type of gene promoter or enhancer, transcription characteris- tics, and the number and extent of deletions. A further important effect is that of compensatory or modifying alleles e. A mutation of the same gene can cause widely differing clinical phenotypes. For example, the same mutation of the dysferlin gene may cause either type 2B limb-girdle dystrophy or Miyoshi’s distal myopathy. In the mitochondrial myopathies, or disorders of β-oxidation, combinations of gene defects coding for specific enzymes can significantly modify the clinical phenotype. Unfortunately, the exponential increase in knowledge of genetic defects in specific muscle disorders has not been matched by the diagnostic availability of these tests.

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