Case Study One:
Annie Wong, a 6-year-old girl, is experiencing painful and frequent urination and moderate lower abdominal pain. Annie was brought by her parents to the nearest Emergency Department (ED). In the ED, her temperature was recorded to be 39°C. Urine sample was collected and sent to pathology by the nursing team. The ED physician suspects Annie has a urinary tract infection (UTI) and orders Bactrim 40 mg sulfamethoxazole and 8 mg trimethoprim per mL (0.5mL per kg), PO BD. To provide effective pain relief to Annie, the ED physician also orders an opioid derivative OxyNorm Liquid [oxycodone 0.1mg per kg, PO STAT].
- Discuss a common pathogen for UTI in young girls in relation to how it causes infection.
- Discuss the mechanism of action of oxycodone in providing analgesia and its role in pain transmission.
- After taking the oxycodone, Annie experienced nausea and vomiting. Describe the physiology of vomiting and provide a rationale for the trigger of Annie’s vomiting in this scenario.
- Subsequently, the ED physician ordered Bactrim 40 mg PO BD. What is the action of Bactrim in terms of its target?
Case Study two:
Mrs Sandy Bilby is a 62-year-old woman living in a tropical region of Australia who has sub-optimally controlled type 2 diabetes mellitus (DM) of > 10 years. Her past medical history includes chronic atrial fibrillation (AF), ischaemic heart disease, severe left ventricular heart failure with an implantable defibrillator inserted 3 years ago, stage III chronic kidney disease, and a history of a stroke with good neurological recovery. Sandy is also obese, with a body mass index (BMI) of 39.7 kg/m2. For the past 4 years, Sandy has been taking insulin glargine and glulisine. Her recent HbA1C was 9.6 per cent and she has diabetic retinopathy and peripheral neuropathy.
Sandy presented complaining of a rash over her abdomen for the last 3-4 weeks. Over the last 10 days the lesions spread to her lower limbs with evolution in some areas to 2 cm with painful and tender lumps and blister with scant discharge. On physical assessment, there were multiple itchy and mildly warm-to-touch lesions over her trunk and all four extremities. The rash was at different stages of evolution and in some areas, there were erythematous plaques with overlying necrotic crust and superficial ulceration. Sandy was afebrile but looked unwell with bilateral leg oedema, increased jugular venous pressure (JVP), and crackles auscultated over her lung bases.
Sandy’s initial blood cultures were positive with gram-positive bacilli, which was subsequently identified as mycobacterium chelonae. She was initially commenced on triple intravenous antibiotic therapy: tobramycin, clarithromycin and ciprofloxacin.
- Outline and describe the pathophysiology of diabetes mellitus and peripheral neuropathy
- Briefly describe what complications are associated with peripheral neuropathy and wound healing
- Describe what factors would delay wound healing in this scenario and provide evidence-based strategies to maximise wound healing
- Discuss the mechanism of action of insulin glargine and glulisine in providing blood glucose control
