A patient presents to the ED with a known diagnosis of hypopituitarism. He appears ill but remains slightly tachycardic and normotensive.
Which ONE of the following interventions should take the HIGHEST priority?
Answer: A: Over 95% of cases of hypopitutarism in adults are caused by pituitary adenomas. Other causes include intrasellar and parasellar tumours, inflammatory/ infectious destruction, radiation-induced destruction, traumatic brain injury, subarachnoid haemorrhage and postpartum pituitary necrosis (Sheehan’s syndrome). In hypopituitarism, patients usually have a combination of pituitary hormonal deficiencies (ACTH, TSH, FSH, LH, GH, prolactin, ADH and oxytocin); however, all hormones are rarely involved. Patients may develop a striking pallor, with loss of melanocyte stimulating hormone (MSH) activity caused by reduced ACTH secretion. These patients often have secondary adrenal insufficiency. Unlike in patients with primary adrenal insufficiency, these patients do not present with marked hyperkalaemia or hyponatraemia. The patient usually has a normal serum potassium or mild hyperkalaemia. Aldosterone secretion is normal as well.
Patients with a diagnosis of hypopituitarism may present to the ED appearing unwell, with acute decompensation secondary to an acute stress such as infection, noncompliance with hormone replacement, emotional stress and trauma.
The priorities in the ED intervention for such patients are:
References:
Regarding primary hyperaldosteronism, which ONE of the following statements is TRUE?
Answer: B: Elevated aldosterone levels induce sodium retention and potassium excretion in the urine. The resulting proton shift at cell membrane level results in a metabolic alkalosis with an elevated serum bicarbonate level.
Primary hyperaldosteronism is most commonly due to an adrenal adenoma, less commonly to bilateral adrenal hyperplasia. Excess aldosterone induces elevated blood pressure, which is invariable at presentation. Patients may present with muscle weakness due to hypokalaemia, or polyuria due to nephrogenic diabetes insipidus related to renal tubular damage.
Reference:
In a patient with severe hypercalcaemia due to primary hyperparathyroidism, which ONE of the following statements is TRUE?
Answer: A: In 80–90% of cases causes of hypercalcaemia in patients presenting to the ED include:
Primary hyperparathyroidism
Malignancy (most patients seen in the ED with hypercalcaemia)
Other less common causes include:
Management of hypercalcaemia includes the following steps.
1. Rehydration:
2. Intravenous bisphosphonate:
3. In acute life-threatening hypercalcaemia:
4. IV hydrocortisone:
All of the following features in patients presenting to the ED raise suspicion of an undiagnosed phaeochromocytoma EXCEPT:
Answer: B: Phaeochromocytoma is a catecholamine-producing neuroendocrine tumour. Approximately 80–85% arise from the adrenal medulla and 15–20% from extra adrenal chromaffin tissue. The prevalence of phaeochromocytoma in outpatients with hypertension is 0.1–0.6%. This condition is described as a ‘great mimic’ because similar clinical features are produced by many other clinical conditions. Usually there is a delay of about 3 years between the initial appearance of symptoms and the final diagnosis. Most of the clinical features are produced by the direct actions of catecholamines secreted by the tumours. The following important presentations to the ED may raise the suspicion for a pheochromocytoma:
A patient with type 2 diabetes who is on intensive insulin treatment presents to the ED with uncomplicated hyperglycaemia > 20 mmol/L.
Regarding the initial stat (supplemental) doses of insulin she would receive in the ED, which ONE of the following statements is TRUE?
Answer: D: Patients with type 1 and type 2 diabetes who are on insulin treatment commonly present to the ED with uncomplicated hyperglycaemia for stabilization. These patients routinely are on one of the following insulin regimes:
The regimes belong to two categories:
As a general rule, patients who are eating normally and are not unwell do not require intravenous insulin infusions. The hyperglycaemia can be managed with stat and supplemental subcutaneous insulin, as well as appropriate increases in routine basal and mealtime insulin doses. The initial stat dose and the supplemental doses can be given using either rapid-acting or short-acting (regular) insulin. The rapid-acting preparations are insulin analogues such as insulin lispro (e.g. Humalog), aspart (e.g. NovoRapid) and glulisine, which have many advantages over regular short-acting insulin. They act more like naturally occurring insulin. An example of short-acting insulin is actrapid (see Table below). Because of the rapid onset of action of rapidacting insulin, they can be accurately and easily timed with food intake. They cause fewer episodes of hypoglycaemia. The duration of action of short-acting regular insulins becomes prolonged with increasing dose. The initial stat and supplemental dose of subcutaneous rapid or short-acting insulin should be determined using the patient’s blood glucose level as well as his/her previous total daily insulin dose.
ACTION TIME OF RAPID- AND SHORT-ACTING INSULIN:
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