random Flashcards
A 55-year-old smoker presents with weight loss, haemoptysis and confusion. Laboratory results demonstrate:
- Plasma osmolarity243 mmol/l
- Urine osmolality540 mmol/l
- Na+112 mmol/l
- K+3.8 mmol/l
- Urea3.2 mmol/l
- Blood glucose5.2 mmol/l
What is the most likely cause of the hyponatraemia?
- Diabetes insipidus
- Dehydration
- Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
- Pseudohyponatraemia
- Cerebral Salt-Wasting Syndrome
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
A serum sodium of 112 mmol/l is alarming. When faced with a laboratory value with this much derangement, it would be prudent to obtain a further sample to ensure there was no errors with the laboratory analysis.
It is essential to assess if it is a true hyponatraemia or a pseudohyponatraemia. The osmolar gap is very useful for this purpose. The calculated osmolarity = 2*Na + 2*K + urea + blood glucose. In this example, the calculated osmolarity = 240 mmol/l. The measured plasma osmolarity = 243 mmol/l. The osmolar gap = measured serum osmolality - calculated osmolality = 243 - 240 = 3 mmol/l. A normal osmolar gap is < 10 mmol/l. Therefore a normal osmolar gap rules out pseudohyponatraemia.
The next step would be to assess the fluid status of the patient clinically (e.g. assess if the patient is hypervolaemic, hypovolaemic or euvolaemic). This is essential information for forming a differential diagnosis and providing the correct treatment. This information is not available in the question, so the next step would be to analyse the serum and urine osmolarity.
The serum osmolarity is very low. In normal physiology we would expect a low serum osmolarity to trigger a decrease of ADH production thereby resulting in an increased urinary output of low osmolarity urine. In this example the urine osmolarity is inappropriately concentrated suggesting that ADH levels are inappropriately high. This is highly suggestive of SIADH. We would also expect the patient to be euvolaemic which is a defining feature of SIADH.
SIADH is associated with malignancy (especially small cell carcinoma of the lung), pulmonary disorders, CNS disorders and drugs (e.g. carbamazepine, chlorpropamide and cyclophosphamide). To make the diagnosis patients must be clinically euvolaemic with normal thyroid and adrenal function, a low plasma osmolarity and inappropriately high urine osmolarity.
A 69-year-old female with a history of multiple myeloma presents with confusion. Blood tests are taken and the following results are obtained:
Adjusted calcium3.1 mmol/l
What is the most appropriate initial management?
- Oral alendronate + prednisolone
- Oral alendronate
- Oral prednisolone
- Admit for IV pamidronate
- Admit for IV normal saline
Admit for IV normal saline. IV fluid therapy is the first-line management in patients with hypercalcaemia.
Hypercalcaemia: management:
The initial management of hypercalcaemia is rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days
Other options include:
- calcitonin - quicker effect than bisphosphonates
- steroids in sarcoidosis
Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.
You are asked for advice from a local GP. He has received the following blood results for one of his patients, a 50-year-old non-smoker.
- Na+130 mmol/l
- K+4.2 mmol/l
- Bicarbonate23 mmol/l
- Urea4.8 mmol/l
- Creatinine71 µmol/l
Which one of his medications is most likely to explain this result?
- Fluoxetine
- Pioglitazone
- Methotrexate
- Ibuprofen
- Nicorandil
Fluoxetine
SIADH - drug causes: carbamazepine, sulfonylureas, SSRIs, tricyclics
In section 4.3 of the BNF specific mention is made of the risks of hyponatraemia developing in patients who take antidepressants, especially SSRIs such as fluoxetine. The exact mechanism causing hyponatraemia is not fully understood but it is thought to be due to the syndrome of inappropriate ADH section.
A 45-year-old man comes to see you recent as his recent blood tests have shown a total cholesterol of 6.2 mmol/L. You ask him to come in so that you can discuss this further. You calculate his Q-risk score to be 23%.
He smokes 10 cigarettes a day and has been smoking for the past 20 years. His father died of a heart attack aged 50. His past medical history includes asthma.
Which one of the following medications would you ask him to start?
- Atorvastatin 20mg
- Atorvastatin 40mg
- Atorvastatin 80mg
- Simvastatin 10mg
- Simvastatin 20mg
Atorvastatin 20mg is a high-intensity statin and should be started as primary prevention against cardiovascular disease.
Incorrect answers:
- Atorvastatin 80mg is used in secondary prevention.
- Simvastatin 10mg and 20mg are low-intensity statins.
Statin treatment should be combined with lifestyle measures such as increased physical activity, reduction of alcohol intake and adoption of a cardio-protective diet.
A 50-year-old male presents to the GP surgery for a routine review of his diabetes medication. He has a past medical history of type 2 diabetes, migraines, depression and eczema. He is currently taking metformin, atorvastatin, citalopram and propranolol. Blood tests show:
- HbA1c43 mmol/mol (6.1%)
- Hb15 g/dl
- MCV85 fl
- Platelets250 * 109/l
- WBC5 * 109/l
- Na+125 mmol/l
- K+4.1 mmol/l
- Urea5.5 mmol/l
- Creatinine125 µmol/l
What is the most likely cause of the abnormal blood test result?
- Type 2 diabetes
- Atorvastatin
- Upper gastrointestinal bleed
- Metformin
- Citalopram
Citalopram
SSRIs are a cause of SIADH
Citalopram is an selective serotonin reuptake inhibitor (SSRI) antidepressant which are known to be a potential cause of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Raised levels of ADH causes increased reabsorption of water from the collection ducts in the nephrons leading to a dilutional hyponatraemia.
The other options are not causes of hyponatraemia.
A 47-year-old patient is reviewed 3 days following a subarachnoid haemorrhage. Their routine blood tests show the following:
- Na+122 mmol/L(135 - 145)
- K+4.9 mmol/L(3.5 - 5.0)
- Urea7.3 mmol/L(2.0 - 7.0)
- Creatinine113 µmol/L(55 - 120)
They have no symptoms of hyponatraemia. Their observations are unremarkable. On examination, JVP is at 6 cm, there is no peripheral oedema and their chest is clear. They are receiving no fluids currently.
Further follow-up tests are conducted to investigate the abnormality.
- Plasma osmolality↓
- Urine sodium↑
- Urine osmolality↑
What is the most appropriate initial management?
- Fluid restriction
- IV 0.9% NaCl
- IV hydrocortisone
- IV hypertonic saline
- Oral desmopressin
Fluid restriction should be used in euvolemic and hypervolemic hyponatraemic patients who don’t have severe symptoms
Important for meLess important
This patient is most likely presenting with a syndrome of inadequate ADH secretion (SIADH). This can occur due to hypophyseal irritation in a subarachnoid haemorrhage. Water is retained from the urine, resulting in decreased plasma osmolality due to dilution of the blood and more salt than usual is lost into the urine, resulting in an increase in urine sodium and osmolality. The most appropriate initial treatment of SIADH is to fluid restrict to between 500-1000ml per day.
IV 0.9% NaCl may be appropriate for hypovolaemic hyponatraemia. This patient is clinically euvolemic based on the examination findings. Giving further isotonic fluids in SIADH may actually worsen hyponatraemia.
IV hydrocortisone would be appropriate of Addison’s was expected. However, this is more likely to present with hypovolaemia and a raised potassium.
IV hypertonic saline may be appropriate for severe hyponatraemia. This includes levels of under 120 mmol/L or symptomatic hyponatraemia. This is either 1.8% or 3% NaCl depending on the local supply.
Oral desmopressin can be used for diabetes insipidus. However, this would present with polyuria and is ruled out due to the increased urine osmolality in this patient
A 59-year-old man presents to the Acute Medical Unit complaining of back pain. He has a history of hypertension, congestive cardiac failure, type 2 diabetes and prostate cancer.
His blood pressure is well-controlled on amlodipine and ramipril. In addition to this, he takes bisoprolol and eplerenone due to previous issues with lower limb swelling. He takes metformin, and was prescribed sitagliptin two months ago due to an increase in his Hba1c readings. An isotope bone scan four months before had shown metastasis of his prostate cancer to his pelvic girdle, at which point he had commenced monthly goserelin injections.
On examination, you notice pronounced breast tissue bilaterally.
Which of his medications is the most likely cause of this examination finding?
- Eplerenone
- Ramipril
- Metformin
- Sitagliptin
- Goserelin
Goserelin53%
GnRH agonists (e.g. goserelin) used in the management of prostate cancer may result in gynaecomastia
Important for meLess important
This patient has an incidental examination finding of gynaecomastia. Of the medications listed above, goserelin is most strongly linked to causing gynaecomastia.
Goserelin is a gonadotropin releasing hormone (GnRH) agonist. In normal physiology, the pulsatile release of GnRH stimulates testosterone production. When goserelin is given long-term in a non-pulsatile manner, this disrupts the endogenous feedback loops controlling testosterone production, and results in hypoandrogenism. This in turn causes the development of gynaecomastia.
Of note, although both are aldosterone antagonists, a comparison of results from the RALES and EPHESUS trials revealed that eplerenone was much less likely to cause gynaecomastia than spironolactone in heart failure patients (0.5% vs 10%). This is because unlike spironolactone, eplerenone does not inhibit free testosterone binding to androgen receptors on breast tissue.
The other three medications listed are not strongly linked to the development of gynaecomastia.
A 42-year-old woman is started on daily hydrocortisone and fludrocortisone following a diagnosis of Addison’s disease. A week later she presents to her general practitioner as she is waking up 2 hours earlier than she used to in the morning, and is feeling very tired all day.
She denies any other symptoms.
What is the most likely cause of this?
- Fatigue related to Addison’s disease
- Nocturnal hypoglycaemia related to Addison’s disease
- Steroid-induced hypomania
- Steroid-induced insomnia
- Steroid-related mood disturbance
Steroid-induced insomnia.
Corticosteroids may cause insomnia
Important for meLess important
It can be difficult to determine whether a symptom is due to the underlying disease, or due to the treatment of the disease. In this case, since steroids come with a wide variety of side effects, it is important to think about this being the cause. Steroid-induced psychiatric symptoms are likely to come on 3-5 days after starting a new steroid regime, but can also start at any time when taking them, or even when discontinuing them. This woman is describing early morning awakening, with no other symptoms. This is likely to be steroid-induced insomnia, as insomnia can include waking up and not being able to get back to sleep, as well as not being able to fall asleep in the first place.
Fatigue related to Addison’s disease is a common symptom experienced. Sleep cycles can be affected due to the normal diurnal variation in cortisol secretion being lost. However, since she has started treatment, this is unlikely to be the reason for the current insomnia.
Nocturnal hypoglycaemia related to Addison’s disease is a cause of sleep disturbance in those with the condition. However, other symptoms would be expected, such as confusion or nausea in the morning, and the fatigue is unlikely to last all day, as it will get better when breakfast is eaten.
Steroid-induced hypomania may be a cause of sleep cycle disturbance in those taking the drug. However, it would not present with individuals feeling fatigued all day long, as they would by contrast have lots of energy.
Steroid-related mood disturbance may cause early morning awakening as a somatic symptom of depression. However, in the absence of other symptoms of depression, this is unlikely.
