In the assessment of a foot ulcer in a patient with diabetes presenting to the emergency department (ED), which ONE of the following features is MOST LIKELY to be associated with underlying osteomyelitis?
Answer: D: The diagnosis of underlying osteomyelitis associated with a diabetic foot ulcer can be difficult. A diabetic foot ulcer extending deep down to the bone is highly likely to be associated with underlying osteomyelitis. This can be determined with sterile surgical probing of the ulcer, if necessary under an appropriate anaesthetic.
Wound swabs taken from diabetic foot ulcers usually grow colonizing organisms only. It may not be possible to identify deep-seated infection purely from wound swabs, and collection of purulent material from the depth of the ulcer is usually required. It has also been found that there is a relatively high positive likelihood ratio for the diagnosis of osteomyelitis when the foot ulcer is >2 cm.There is no direct association between Charcot’s arthropathy and osteomyelitis.
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Regarding ED management of a lower extremity ulcer in a patient with type 1 diabetes, which ONE of the following is TRUE?
Answer: D: Lower extremity infections in diabetics often start as an ulcer, due either to skin breakdown in pressure areas of the foot, or to minor injury. They have the potential to spread rapidly to limb-threatening or life-threatening infections, and therefore demand careful assessment and initiation of appropriate treatment.
Any ulcer with the following features should be considered as limb-threatening:
If not treated promptly and aggressively these infections often become life threatening with sepsis and septic shock. Intravenous antibiotics should be given without delay on presentation.
Broad-spectrum antibiotics should be used to cover staphylococci and streptococci, gram-negative and anaerobic bacteria. Uncomplicated ulcers are not limb-threatening, and can be managed in the community. If the ulcer is longstanding and is not infected (no surrounding cellulitis or discharge), it does not require antibiotic treatment. When peripheral pulses are not palpable, urgent vascular assessment is needed and revascularization should be considered.
In the diagnosis of alcoholic ketoacidosis, which ONE of the following statements is TRUE?
Answer: C: Alcoholic ketoacidosis typically presents in patients with a history of chronic alcohol abuse. These patients usually present with vomiting and abdominal pain 1–3 days after termination of an alcoholic binge. Prolonged vomiting results in severe dehydration and contraction of the extracellular fluid compartment. This is associated with depletion of carbohydrate stores. While ethanol may have initially functioned as a carbohydrate source for gluconeogenesis, the patient is likely to have been abstinent for several days by the time of the presentation, and most chronic alcoholics have poor glycogen stores.
Unlike in DKA, Glasgow Coma Scale (GCS) is usually normal despite metabolic disturbance; confusion or altered level of consciousness should prompt investigation for other pathology. In severe acidosis, ketone bodies exist largely as betahydoxybutyrate, which is not detected by Ketostix testing.
In the management of alcoholic ketoacidosis, which ONE of the following is TRUE?
Answer: B: While the patient is significantly fluid depleted due to prolonged vomiting, intravenous glucose provides a metabolic substrate, halting ketogenesis and returning the patient to normal.
In contrast, while intravenous saline reduces lactate levels, it may result in elevated beta-hydroxybutyrate levels, paradoxically worsening acidosis. Insulin does not affect resolution. Thiamine (vitamin B1) prevents Wernicke’s encephalopathy and is a cofactor in pyruvate metabolism to glucose.
Regarding examination findings in a patient with adrenal insufficiency, which ONE of the following statements is CORRECT?
Answer: B: Vitiligo is an autoimmune disorder, commonly associated with other organ-specific autoimmune disorders including primary adrenal insufficiency (Addison’s disease).
Hyperpigmentation occurs in the presence of primary adrenal failure when adrenocorticotropic hormone (ACTH) levels are elevated in the absence of negative feedback. Elevated ACTH levels stimulate melanin production in skin and mucosa. The most common cause of secondary adrenal insufficiency is chronic glucocorticoid therapy inhibiting ACTH production, and so suppressing primary adrenal function. A careful drug history should be taken, and any recent illness or stress noted. Other sources of hypothalamic–pituitary dysfunction – including pituitary or hypothalamic tumours, infiltrative disorders, severe head trauma and pituitary necrosis or bleeding – may cause secondary adrenal insufficiency. Cushingoid features are usually not found in a patient with Addison’s disease but may be present in a patient who has been on long-term glucocorticoid therapy.
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