18 Endocrine disease
Questions
I would like to ask why, when treating hypopituitarism, an adrenal crisis occurs if thyroid replacement is given before steroid replacement therapy? And what is the underlying mechanism? Thank you!
Is the cyclic presence of Montgomery tubercles, where they reduce and later increase, in a nulliparous woman’s breast normal? And, if so, what is the cause?
Does methyltestosterone, if given in a daily dose of 2.5mg per day, cause liver cell injury or hypothalamic gonadal suppression? Can this drug be prescribed for other cases with hypothalamic hypogonadism, usually being given by intramuscular injection or implant?
For some time now I have been confused regarding tests for acromegaly.
Incidentally, a lot of people around me are similarly confused and others have been following the latter saying that ‘Kumar and Clark say so’. Please clarify.
What is the significance of the thyroid-releasing horomone (TRH) test in differentiating various causes of hypothyroidism?
It is stated that a little overtreatment might be required for hypothyroidism, i.e. slightly raised thyroxine (T4) and suppressed thyroid-stimulating hormone (TSH). Is the clinical improvement the best criteria or is there an optimum/maximum level that one should watch out for when monitoring TSH and T4?
Why is thyroid-stimulating hormone (TSH) normal or increased in patients with peripheral resistance to tri-iodothyronine (T3) and thyroxine (T4)? The thyroid hormone levels are high in these patients, so the TSH should drop lower: why doesn’t it?
Thyroxine is a peptide hormone used to treat thyroid deficiency and other thyroid disorders. It is taken orally. Peptides are broken down into amino acids before being absorbed. What factors cause the thyroxine to remain stable in the digestive tract so that it is absorbed without being digested?
Please explain the causes of, and suggest recommended treatments for, euthyroid and hypothyroid states.
What is the role of propranolol in the management of a 35-year-old male thyrotoxic patient who is also hypertensive?
At what dose, and for how long, would steroid therapy give rise to secondary adrenal insufficiency? For adrenal insufficiency due to long-term steroid use, when should we start to give a cortisone supplement? How should we monitor these patients?
I want to know the mechanism that causes anaemia in Addison’s disease. I am unable to find the real cause.
In the diagnosis of Cushing’s disease using the high-dose dexametha-sone suppression test, how can the exogenous steroid suppress adrenocorticotrophic hormone (ACTH) when the grossly elevated serum cortisol levels fail to do so?
Regarding the renin-angiotensin-aldosterone axis, it states that dietary sodium excess suppresses renin secretion. Then why are we asking hypertensives to restrict sodium intake? Also if we are using angiotensin-converting enzyme (ACE) inhibitors, the plasma renin activity increases due to loss of feedback inhibition. Wouldn’t that be counterproductive?
How well do symptoms of hypercalcaemia correlate with serum calcium levels. Can I ignore an asymptomatic patient with a serum calcium of 3.7mmol/L but have to give treatment to a symptomatic patient who has a serum calcium of 3.3mmol/L?
A 64-year-old woman tells me she has been on hormone replacement therapy (HRT) – oestrogen only following a hysterectomy – for 7 years. She wants to continue with this therapy as she thinks it helps her. How long should I continue prescriptions?
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