Endocrine disease Flashcards
Is growth hormone deficiency in childhood commonly associated with
panhypopituitarism?
Growth hormone deficiency in children is usually an isolated defect but
pituitary deficiency can occur and should be treated.
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!
Thyroid replacement therapy increases cortisol degradation and basal
metabolism. This can precipitate an adrenal crisis if steroids are not given
first.
Why, in Sheehan’s syndrome, is there an anterior pituitary involvement
more than a posterior one?
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.
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?
Yes, it is normal. Montgomery’s tubercles respond to oestrogens.
Hyperpigmentation or overdevelopment are other signs of
hyperoestrogenism.
Does methyltestosterone, if given in a daily dose of 2.5 mg 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?
This is a small dose; liver damage is unlikely. Pituitary gonadotrophin
secretion inhibition does occur. Testosterone is used in hypothalamic
hypogonadism.
Does IM testosterone increase levels of serum thyroid-stimulating
hormone (TSH)?
Intramuscular testosterone does not affect serum TSH.
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?
- 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. - 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.
Does acromegaly cause depression?
No; prolonged symptoms can ‘depress’ people, as in any other illness,
which can be difficult to diagnose.
- Breathlessness can be a feature of acromegaly. What are the
characteristics of this breathlessness? - If a patient presents with headaches due to acromegaly, what are the
likely characteristics of these headaches?
- The breathlessness is usually due to cardiac disease, which is a feature
of acromegaly. - The headaches are due to pituitary tumours. The headaches are
variable. They can be felt behind the eyes or on top of the head.
Why does hypothyroidism cause a transudative pleural effusion?
In hypothyroidism there is generalized water retention and this can
produce a pleural effusion that is a transudate.
What is the significance of the thyroid-releasing horomone (TRH) test in
differentiating various causes of hypothyroidism?
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.
Is retention of urine/incomplete voiding related to hypothyroidism? If
so, how?
No; retention of urine is not a feature 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?
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 10 mmol/L usually requires an increase
in levothyroxine. Most patients with hypothyroidism require 150 μg of
levothyroxine daily.
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?
There seems to be resistance at the pituitary gland as well, so feedback
is reduced.
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?
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.
- Does the absence of bradycardia exclude hypothyroidism?
2. How often is hypothyroidism accompanied by bradycardia?
- No.
- 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.
Should patients with hypo- or hyperthyroidism be given iodine
supplements?
Iodine would be appropriate where dietary deficiency of iodine still
exists. Iodine in the form of potassium iodide (60 mg three times daily)
is given prior to thyroidectomy for hyperthyroidism but there is little
evidence for its beneficial effect!
Is Hashimoto’s thyroiditis associated with dementia?
Rarely; usually there is mental slowness. All dementia patients must be
screened for hypothyroidism with a serum thyroid-stimulating hormone.
Please explain the causes of, and suggest recommended treatments for,
euthyroid and hypothyroid states.
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.
What is the role of propranolol in the management of a 35-year-old male
thyrotoxic patient who is also hypertensive?
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.
What else could we use instead of propranolol in thyrotoxicosis with
bronchial asthma?
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.
At what dose, and for how long, would steroid therapy give rise to
secondary adrenal insufficiency? For adrenal insufficiency due to longterm
steroid use, when should we start to give a cortisone supplement?
How should we monitor these patients?
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.
What dose of Synacthen is equivalent to adrenocorticotrophic hormone
(ACTH)?
1 mg tetracosactide (Synacthen) is equivalent to 80 units of ACTH in
terms of adrenal stimulation
I want to know the mechanism that causes anaemia in Addison’s disease.
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.
What causes hypercalcaemia in Addison’s disease?
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
In the diagnosis of Cushing’s disease using the high-dose dexamethasone suppression test, how can the exogenous steroid suppress adrenocorticotrophic hormone (ACTH) when the grossly elevated serum cortisol levels fail to do so?
The ‘grossly’ elevated cortisol level is still in the nanomolar level. Oral
dexamethasone is given as 1 mg
Does alternate-day therapy with steroids decrease their efficacy
compared with daily therapy?
No; alternate-day therapy is used to try to reduce the side-effects of
steroids. Do not use in asthma.
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 angiotensinconverting
enzyme (ACE) inhibitors, the plasma renin activity increases
due to loss of feedback inhibition. Wouldn’t that be counterproductive?
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
How does a phaeochromocytoma give rise to Raynaud’s phenomenon?
High circulating levels of noradrenaline (norepinephrine) produce
vasoconstriction.
How well do symptoms of hypercalcaemia correlate with serum calcium
levels. Can I ignore an asymptomatic patient with a serum calcium of
3.7 mmol/L but have to give treatment to a symptomatic patient who has
a serum calcium of 3.3mmol/L?
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 3.5 mmol/L (normal range is
2.20–2.67 mmol/L or 8.5–10.5 mg/dL).
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?
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.
Is there a difference between impotence and erectile dysfunction and are
the treatments different if they are different conditions?
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.
In multiple endocrine neoplasia under screening, you say that family
members who are ‘at risk’ should be screened. What does that mean?
The family members ‘at risk’ are those who have the gene mutation.
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?
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.
In a patient who is found to be hypertensive, how should we exclude
Conn’s syndrome?
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 mellitus and diabetes insipidus are very different conditions so
why are they both called diabetes?
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.
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.
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.
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?
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 gonadotrophinreleasing
hormone are all used when fertility is required
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?
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
Does hyperprolactinaemia cause gynaecomastia?
Yes. Gynaecomastia can occur in men with hyperprolactinaemia; rarely
galactorrhoea.
