Endocrine disease

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18 Endocrine disease

Questions

Is growth hormone deficiency in childhood commonly associated with panhypopituitarism?

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!

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

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?

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

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.

Does acromegaly cause depression?

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?

Why does hypothyroidism cause a transudative pleural effusion?

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

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

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?

1. Does the absence of bradycardia exclude hypothyroidism?

2. How often is hypothyroidism accompanied by bradycardia?

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

Is Hashimoto’s thyroiditis associated with dementia?

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?

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

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?

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

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

What causes hypercalcaemia in Addison’s disease?

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?

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

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 does a phaeochromocytoma give rise to Raynaud’s phenomenon?

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?

Is there a difference between impotence and erectile dysfunction and are the treatments different if they are different conditions?

In multiple endocrine neoplasia under screening, you say that family members who are ‘at risk’ should be screened. What does that mean?

You mention that a number of tests can be used in the diagnosis of a phaechromocytoma. Can you say which is the best and do they all need to be done, considering the expense of those investigations?

In a patient who is found to be hypertensive, how should we exclude Conn’s syndrome?

Diabetes mellitus and diabetes insipidus are very different conditions so why are they both called diabetes?

I have a young patient who has hirsutism associated with the polycystic ovary syndrome. She has become desperate about her symptoms, which have not been improved by long-term medical treatment with oestrogens, spironolactone and cyproterone. She has asked about whether surgery would help.

In a previously fertile patient with infertility secondary to testosterone replacement, how soon after stopping testosterone therapy will he become fertile again? Can reduced fertility and hypogonadism be treated other than with testosterone replacement therapy?

Why is the ‘insulin-like growth factor’ (released from the liver in response to the growth hormone) so called, although it opposes the effects of insulin?

Does hyperprolactinaemia cause gynaecomastia?

Is it practical, after a period of time, to try to wean patients on thyroxine treatment for hypothyroidism, if the thyroid gland has not been surgically removed? Should TSH monitoring be used? And after how long from the start of treatment should this be tried?

Why and how does uraemia occur in Addison’s disease?

Growth hormone deficiency in children is usually an isolated defect but pituitary deficiency can occur and should be treated.

Thyroid replacement therapy increases cortisol degradation and basal metabolism. This can precipitate an adrenal crisis if steroids are not given first.

Sheehan’s syndrome is now very rare. There is anterior pituitary involvement rather than posterior because the blood supply to the anterior pituitary is dominant.

Yes, it is normal. Montgomery’s tubercles respond to oestrogens. Hyperpigmentation or overdevelopment are other signs of hyperoestrogenism.

This is a small dose; liver damage is unlikely. Pituitary gonadotrophin secretion inhibition does occur. Testosterone is used in hypothalamic hypogonadism.

Intramuscular testosterone does not affect serum TSH.

1. An undetectable growth hormone level excludes acromegaly. The best diagnostic test is either an oral GTT with measurement of growth hormone levels or a single raised plasma insulin-like growth factor 1 (IGF-1) level.

2. In patients with diabetes mellitus (who therefore have a diabetic GTT) without acromegaly the IGF-1 levels are low, whereas in a diabetics with acromegaly the IGF-1 levels are high. Kumar and Clark is correct.

No; prolonged symptoms can ‘depress’ people, as in any other illness, which can be difficult to diagnose.

1. The breathlessness is usually due to cardiac disease, which is a feature of acromegaly.

2. The headaches are due to pituitary tumours. The headaches are variable. They can be felt behind the eyes or on top of the head.

In hypothyroidism there is generalized water retention and this can produce a pleural effusion that is a transudate.

The TRH test was used to differentiate thyroid from hypothalamic/ pituitary causes of hypothyroidism. It has been replaced by accurate measurement of serum thyroid-stimulating hormone, making the TRH test obsolete.

No; retention of urine is not a feature of hypothyroidism.

Clinical improvement is certainly of value but this should be backed up with TSH and T4 estimations. These should be kept within the normal range. A TSH above 10mmol/L usually requires an increase in levothyroxine. Most patients with hypothyroidism require 150μg of levothyroxine daily.

There seems to be resistance at the pituitary gland as well, so feedback is reduced.

Thyroxine is a small peptide that is absorbed intact, as are many other small peptides. Although some proteins are broken down into peptides and then individual amino acids, many small peptides are absorbed intact.

2. Severe hypothyroidism is often associated with bradycardia (60%) but many cases are now diagnosed on the evidence of high levels of thyroid-stimulating hormone and low serum thyroxine, with few clinical signs.

Iodine would be appropriate where dietary deficiency of iodine still exists. Iodine in the form of potassium iodide (60mg three times daily) is given prior to thyroidectomy for hyperthyroidism but there is little evidence for its beneficial effect!

Rarely; usually there is mental slowness. All dementia patients must be screened for hypothyroidism with a serum thyroid-stimulating hormone.

Euthyroid means normal thyroid function and requires no treatment! Hypothyroid is usually due to an autoimmune cause and low/decreased thyroid function. Levothyroxine is used for replacement therapy.

It means you can treat both conditions with one drug. Instead of disconti nuing propranolol when the patient is euthyroid, continue it to control blood pressure.

Propranolol should not be used in bronchial asthma, as you indicate. A cardioselective beta-blocker such as atenolol or metoprolol can be used with extreme caution. Remember, beta-blockers are mainly given for symptom control until the definitive therapy (e.g. antithyroid drugs, radioactive iodine) has controlled the hyperthyroidism. Thus, some patients do not need beta-blocker therapy.

There is no definite figure for how long steroid therapy needs to be given before secondary adrenal insufficiency occurs. However, it is very unlikely on less than 3 weeks of treatment. You only need to give steroid cover for severe illness or for surgery (see K&C 7e, p. 1016). A stimulation test with adrenocorticotrophic hormone is not normally required.

1mg tetracosactide (Synacthen) is equivalent to 80 units of ACTH in terms of adrenal stimulation.

The normocytic, normochromic anaemia that occurs in patients with Addison’s disease is probably a direct effect of glucocorticoid deficiency. In addition, as most cases are due to autoimmune disease, the anaemia can be due to pernicious anaemia.

Further reading

Burke CW (1985) Adrenocortical insufficiency. Clinics in Endocrinology and Metabolism14: 947-976.

Many factors, including increased bone resorption and increased calcium resorption by proximal tubules, both of which are partly mediated by glucocorticoids. Mild to moderate hypercalcaemia occurs in 6% of patients and is corrected by glucocorticoid replacement therapy which increases renal excretion.

Further reading

Muls E et al. (1982) Etiology of hypercalcemia in a patient with Addison’s diseases. Calcified Tissue International34: 523-526.

The ‘grossly’ elevated cortisol level is still in the nanomolar level. Oral dexamethasone is given as 1 mg.

No; alternate-day therapy is used to try to reduce the side-effects of steroids. Do not use in asthma.

Dietary sodium reduction will raise renin levels, although not invariably. Increased blood pressure (BP) levels have been observed in some hypertensive patients when dietary sodium is reduced. This heterogeneity in BP response has led some authorities to divide patients into ‘salt sensitive’ or ‘salt resistant’. Elderly patients who might have low renin levels often show reduction in BP on sodium restriction. The action of ACE inhibitors in preventing the formation of angiotensin II is more important than the renin effect.

High circulating levels of noradrenaline (norepinephrine) produce vasoconstriction.

Patients with hyperparathyroidism are often asymptomatic. There is, therefore, no good correlation between symptoms and serum calcium levels. In patients with acute hypercalcaemia, often due to malignancy, symptoms usually develop rapidly. You should therefore treat any patient with acute hypercalcaemia with symptoms or any patient with a serum calcium of greater than 3.5mmol/L (normal range is 2.20-2.67mmol/L or 8.5-10.5mg/dL).

This is often an individual decision, which must be made jointly between you and the patient. You should inform the patient of the risks, which are:

• Breast cancer risk increased by 1.5 extra cases per 1000 over 5 years (normal risk is 14 per 1000).

• Venous thrombosis risk increased by 4 extra cases in 1000 cases (normal risk 20 per 1000) over 5 years.

• Stroke incidence rises by 6 extra in 1000 (normal risk number 20 cases).

• The patient must balance these risks against any perceived benefits.

Further reading

Grady D (2006) Management of menopausal symptoms. New England Journal of Medicine355: 2338-2347.

The term ‘impotence’ includes both loss of libido and erectile dysfunction. A lack of libido is a loss of sexual desire leading to erectile dysfunction. The treatment for erectile dysfunction is now a phosphodiesterase type 5 inhibitor, e.g. sildenafil, which can also help with the loss of libido.

Additional measures might be required for loss of libido.

The family members ‘at risk’ are those who have the gene mutation.

The first and most useful screening test is the measurement of urinary catecholamines and metanephrines in two 24-hour urine collections. Normal levels virtually exclude the diagnosis. (Note: many drugs and dietary vanilla interfere with the test.) Following a positive test, imaging, i.e. computed tomography or magnetic resonance imaging, should be performed.

60% of patients with Conn’s syndrome have hypokalaemia along with their hypertension. These patients, along with all hypertensives under 35 years, require investigation. The best screening test is the plasma aldosterone:renin ratio, which is elevated.

Diabetes is derived from a Greek word meaning a siphon. It means excessive urination ‘like the passing of water by a siphon’, which occurs with both conditions.

Wedge resections of ovaries were used in the past with very poor results. Metformin has improved hirsutism in some patients. Presumably she has already tried local therapies.

Further reading

Rosenfield RL (2005) Hirsutism. New England Journal of Medicine353: 2578-2588.

Yes; spermatogenesis recurs in weeks after the drug is stopped; whether the patient becomes fertile again depends on many factors. Luteinizing hormone, follicle-stimulating hormone and pulsatile gonadotrophin-releasing hormone are all used when fertility is required (see K&C 7e, p. 999).

Insulin-like growth factor (IGF) is a polypeptide about the same size as insulin. IGF-1, IGF-II and insulin genes are part of the same family. IGF-I, IGF-II and human proinsulin have some structural similarities, which explain their different activities.

Yes. Gynaecomastia can occur in men with hyperprolactinaemia; rarely galactorrhoea.

No, patients with hypothyroidism need lifetime levothyroxine therapy.

Uraemia is secondary to dehydration.

Related

1000 Questions and Answers from Kumar _ Clarks Clinical Medicine