Endocrine disease

18 Endocrine disease



Questions




Question 1


Is growth hormone deficiency in childhood commonly associated with panhypopituitarism?



Question 2


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!



Question 3


Why, in Sheehan’s syndrome, is there an anterior pituitary involvement more than a posterior one?



Question 4


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?



Question 5


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?



Question 6


Does IM testosterone increase levels of serum thyroid-stimulating hormone (TSH)?



Question 7


For some time now I have been confused regarding tests for acromegaly.


1. Which is best – screening or diagnosing test in these patients?

2. Your book says the ‘glucose tolerance test [GTT] is diagnostic’. Does this mean GTT with growth hormone (GH) evaluation or that a patient who is clinically an acromegalic with a positive GTT (diabetic) can be labelled as acromegalic?

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.



Question 8


Does acromegaly cause depression?



Question 9



1. Breathlessness can be a feature of acromegaly. What are the characteristics of this breathlessness?

2. If a patient presents with headaches due to acromegaly, what are the likely characteristics of these headaches?


Question 10


Why does hypothyroidism cause a transudative pleural effusion?



Question 11


What is the significance of the thyroid-releasing horomone (TRH) test in differentiating various causes of hypothyroidism?



Question 12


Is retention of urine/incomplete voiding related to hypothyroidism? If so, how?



Question 13


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?



Question 14


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?



Question 15


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?



Question 16



1. Does the absence of bradycardia exclude hypothyroidism?

2. How often is hypothyroidism accompanied by bradycardia?


Question 17


Should patients with hypo- or hyperthyroidism be given iodine supplements?



Question 18


Is Hashimoto’s thyroiditis associated with dementia?



Question 19


Please explain the causes of, and suggest recommended treatments for, euthyroid and hypothyroid states.



Question 20


What is the role of propranolol in the management of a 35-year-old male thyrotoxic patient who is also hypertensive?



Question 21


What else could we use instead of propranolol in thyrotoxicosis with bronchial asthma?



Question 22


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?



Question 23


What dose of Synacthen is equivalent to adrenocorticotrophic hormone (ACTH)?



Question 24


I want to know the mechanism that causes anaemia in Addison’s disease. I am unable to find the real cause.



Question 25


What causes hypercalcaemia in Addison’s disease?



Question 26


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?



Question 27


Does alternate-day therapy with steroids decrease their efficacy compared with daily therapy?



Question 28


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?



Question 29


How does a phaeochromocytoma give rise to Raynaud’s phenomenon?



Question 30


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?



Question 31


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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Dec 4, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Endocrine disease

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