Endocrine disease Flashcards
(102 cards)
1
Q
Is growth hormone deficiency in childhood commonly associated with
panhypopituitarism?
A
Growth hormone deficiency in children is usually an isolated defect but
pituitary deficiency can occur and should be treated.
2
Q
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!
A
Thyroid replacement therapy increases cortisol degradation and basal
metabolism. This can precipitate an adrenal crisis if steroids are not given
first.
3
Q
Why, in Sheehan’s syndrome, is there an anterior pituitary involvement
more than a posterior one?
A
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.
4
Q
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?
A
Yes, it is normal. Montgomery’s tubercles respond to oestrogens.
Hyperpigmentation or overdevelopment are other signs of
hyperoestrogenism.
5
Q
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?
A
This is a small dose; liver damage is unlikely. Pituitary gonadotrophin
secretion inhibition does occur. Testosterone is used in hypothalamic
hypogonadism.
6
Q
Does IM testosterone increase levels of serum thyroid-stimulating
hormone (TSH)?
A
Intramuscular testosterone does not affect serum TSH.
7
Q
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?
A
- 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.
8
Q
Does acromegaly cause depression?
A
No; prolonged symptoms can ‘depress’ people, as in any other illness,
which can be difficult to diagnose.
9
Q
- 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?
A
- 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.
10
Q
Why does hypothyroidism cause a transudative pleural effusion?
A
In hypothyroidism there is generalized water retention and this can
produce a pleural effusion that is a transudate.
11
Q
What is the significance of the thyroid-releasing horomone (TRH) test in
differentiating various causes of hypothyroidism?
A
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.
12
Q
Is retention of urine/incomplete voiding related to hypothyroidism? If
so, how?
A
No; retention of urine is not a feature of hypothyroidism.
13
Q
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?
A
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.
14
Q
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?
A
There seems to be resistance at the pituitary gland as well, so feedback
is reduced.
15
Q
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?
A
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.
16
Q
- Does the absence of bradycardia exclude hypothyroidism?
2. How often is hypothyroidism accompanied by bradycardia?
A
- 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.
17
Q
Should patients with hypo- or hyperthyroidism be given iodine
supplements?
A
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!
18
Q
Is Hashimoto’s thyroiditis associated with dementia?
A
Rarely; usually there is mental slowness. All dementia patients must be
screened for hypothyroidism with a serum thyroid-stimulating hormone.
19
Q
Please explain the causes of, and suggest recommended treatments for,
euthyroid and hypothyroid states.
A
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.
20
Q
What is the role of propranolol in the management of a 35-year-old male
thyrotoxic patient who is also hypertensive?
A
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.
21
Q
What else could we use instead of propranolol in thyrotoxicosis with
bronchial asthma?
A
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.
22
Q
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?
A
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.
23
Q
What dose of Synacthen is equivalent to adrenocorticotrophic hormone
(ACTH)?
A
1 mg tetracosactide (Synacthen) is equivalent to 80 units of ACTH in
terms of adrenal stimulation
24
Q
I want to know the mechanism that causes anaemia in Addison’s disease.
A
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.
25
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
26
```
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
27
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.
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 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
29
How does a phaeochromocytoma give rise to Raynaud’s phenomenon?
High circulating levels of noradrenaline (norepinephrine) produce
vasoconstriction.
30
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).
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?
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.
32
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.
33
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.
34
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.
35
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.
36
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.
37
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.
38
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
39
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
40
Does hyperprolactinaemia cause gynaecomastia?
Yes. Gynaecomastia can occur in men with hyperprolactinaemia; rarely
galactorrhoea.
41
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?
No, patients with hypothyroidism need lifetime levothyroxine therapy.
42
Why and how does uraemia occur in Addison’s disease?
Uraemia is secondary to dehydration.
43
I would like to know the exact mechanism of entry of potassium into
cells under the influence of insulin.
Insulin promotes active transport of glucose into the cell (using the glucose
transporter GLUT 4) and this is accompanied by potassium transport.
44
I am seeing an increasing number of diabetic patients in primary care
who have elevated fasting blood glucose readings but postprandial
measurements that are normal or only slightly high. Does this indicate
insulin resistance in these patients? What is the reason for this trend?
We can see no reason for the change that is occurring in your primary
care practice. The difference between fasting and postprandial
measurements might be related to insulin resistance in type 2 diabetes
but it also relates to changes in lifestyle, i.e. food intake and exercise.
45
What are the latest diagnostic criteria for the diagnosis of diabetes
mellitus?
The diagnosis for diabetes mellitus is a fasting plasma glucose greater
than 7 mmol/L (126 mg/dL) or random plasma glucose greater than
11.1 mmol/L (200 mg/dL).
46
What test is recommended for diabetes and can the same be used to
diagnose diabetes in a child?
on:-symptoms of diabetes and a random plasma
glucose of 200 mg/dL (11.1 mmol/L or a fasting plasma glucose
126 mg/dL (7.0 mmol/L). This also applies to children.
47
What is the value of glycosylated haemoglobin (HbA1C) in diabetes
mellitus?
Glycosylation of haemoglobin results in the formation of a covalent bond
between the glucose molecule and the terminal valine of the beta chains of
the haemoglobin molecule. The rate at which this occurs is related to the
prevailing glucose concentration. HbA1C is expressed as a percentage
of the normal haemoglobin, and normal is 4–6.2%. This test provides
an index of the average blood glucose concentration over the life of the
haemoglobin molecule, about 6 weeks. It therefore gives a more general
picture of the blood glucose level than a single blood glucose.
48
In type 2 diabetes, which blood sugar – fasting or random – is more
revealing prognostically?
Any high blood sugar, whether fasting or random, indicates diabetes but
single tests, e.g. in the clinic, are of limited value. Help your patients to
do their own blood testing at home.
49
Why are the fasting and 2-hour blood glucose levels needed in a diabetic
patient being treated with oral antidiabetic drugs?
It is better to use the glycosylated haemoglobin (HbA1C) level; the ideal is
7% and the patient does not need to be fasted.
50
Is it sufficient to use a fasting blood sugar and glycosylated haemoglobin
(HbA1C) level as a guide to modify the insulin or oral antidiabetic dose
without considering the 1 and 2 hour postprandial values?
The best approach is for the patient to do blood sugars at home
throughout the day, with HbA1C being performed at the clinic visit.
51
What is the value of the 2-hour postprandial blood sugar level above
which the dose of an oral antidiabetic should be increased if this value is
exceeded several times despite dietary modification?
Two-hour postprandial blood sugar is not as good a measurement as
HbA1C, which should be less that 7%. If the level is higher, the oral
diabetic therapy should be increased if possible. However, do not
hesitate to start insulin therapy sooner rather than later.
52
What does BM mean in relation to blood sugar monitoring?
BM stands for Boehringer Mannheim, the firm that produces a number of
glucose measurement strips.
53
What is the role of urine examination in diabetic control?
Glycosuria occurs when the blood glucose level exceeds the renal
threshold. This threshold varies, and fluid intake affects urine glucose
concentration. A negative urine does not distinguish between hypo-,
normo- or even slight hyperglycaemia. For these reasons, diabetic control
is monitored using blood samples obtained at regular intervals by the
patient. However, in a stable type 2 diabetic whose urine is always
negative and occasional blood glucose tests are normal, urine tests can be
used if the patient refuses to do regular blood tests.
54
Do non-obese patients with impaired fasting glucose, i.e. a glucose level
of 6.1–6.9 mmol/L, need drug treatment with biguanides if lifestyle
modifications fail to normalize?
Impaired fasting glucose carries the same risks of cardiovascular disease
and future onset of diabetes as impaired glucose tolerance. So, yes,
metformin is used in these patients.
55
Do non-obese patients with impaired glucose tolerance (but not fulfilling
the criteria for diabetes mellitus) need drug treatment with biguanides if
lifestyle modifications fail to normalize their post-prandial blood glucose
measurements?
Impaired glucose tolerance is a risk factor for future diabetes and
cardiovascular disease. Therefore, many diabetologists start metformin
therapy
56
It is the Muslim month of fasting currently. I would be grateful if you
could advise on how to adjust the insulin regimen of a type 1 diabetic
patient, for example a 21-year-old girl who is on subcutaneous Actrapid
(short-acting soluble insulin) 22 units t.d.s.
One regimen is for the patient to run on a bed-time injection of insulin
glargine. This long-acting insulin acts over approximately 24 hours and
will often provide sufficient basal insulin to carry the patient through
from bed time to the evening of the next day. The size of the insulin
glargine (basal) injection is adjusted during the year to get pre-breakfast
blood glucose readings of 5–7 mmol/L.
On top of the basal insulin, the patient injects a rapid-acting, rapidly
disappearing insulin whenever he or she eats. During the year this will
be three times a day. During Ramadan it will be twice a day (before
sunrise and after sunset).
The meal-time insulin is adjusted to the size of the meal on the plate,
aiming to get a home blood glucose reading of 5–8 mmol/L 2 hours
postprandially. Trial and error is needed for each patient to be able to
‘guestimate’ how much insulin goes with a meal of a given size. This
regimen is also used in shift workers.
57
I would like to know more about the use of the glitazone group in type 2
diabetes: its action, side-effects, precautions taken on using them.
act by reducing peripheral insulin resistance. The current
recommendations are that glitazones should be used in patients who are
unable to take metformin and a sulphonylurea, or for those whose blood
sugar remains high on this combination.
There are rare reports of liver dysfunction, and monitoring of liver
biochemistry is necessary every 2 months for the first year. These drugs
can also cause salt and water retention, giving oedema and rosiglitazone
which has been linked with increased cardiac events.
58
In a patient receiving oral antidiabetics, should the drug be administered
just after taking the blood sample for fasting blood glucose level (and
before a meal), or just prior to the sample being taken?
It makes no difference.
59
What oral antidiabetics are safe in pregnancy?
Glibenclamide was shown in one trial to be safe in pregnancy; it does not
cross the human placenta. However, most diabetologists do not use oral
therapy in pregnancy
60
Is it necessary to put all type 2 diabetics on aspirin?
No, it is not always necessary. However, the group of patients over
50 years of age with a coronary heart disease risk greater than 15 over
the next 10 years will include many people who are diabetics, and they
should be given low-dose aspirin
61
1. Should a patient poorly controlled on glibenclamide 15 mg a day and
metformin 1500 mg a day be moved onto insulin?
2. What are the indications for insulin in type 2 diabetics?
1. Yes – use insulin in all type 2 patients if glycosylated haemoglobin
(HbA1C) is 9.0%. It is better to start insulin therapy early than to wait.
2. Failure of control using oral agents, including the glitazones. Weight
gain is a problem with insulin therapy.
62
What happens to the insulin-secreting capacity of a type 2 diabetic
placed on insulin therapy earlier than recommended? Can the external
supply of insulin improve the functional capacity of the insulin-secreting
cells, to some extent by providing some rest to these cells?
Beta-cell function steadily decreases in type 2 diabetes. No improvement
in functional capacity of beta-cells would occur with insulin therapy
63
What are the complications of insulin other than hypoglycaemia and
injection?
Antibodies can be demonstrated in
the serum but rarely cause a problem. Patients can react to the protamine
added to make long-acting insulins. Weight gain can be a problem and
needs to be monitored. Many patients feel hungry on insulin and a
reduction in dose may be required.
64
Is there any role for steroids in the management of resistant diabetes
mellitus (daily insulin requirement exceeding 100 units/day)? Don’t they
make glycaemic control worse?
There is no role for steroids, even in resistant diabetes.
65
```
What is the importance of potassium chloride (KCl) in the treatment of a
diabetic patient (pre-operative care)? The formula in the text is explained
as 16 U of insulin 10 mmol of KCl 500 mL 10% glucose.
```
Insulin therapy drives K
into the cell and hypokalaemia can result.
Hence always give K
20 mmol/L of 0.9% saline.
66
What is the cut-off point of daily albumin excretion above which a
diabetic patient without hypertension should be given an angiotensinconverting
enzyme (ACE) inhibitor?
30–300 mg in 24 hours is called microalbuminuria. In type 1 diabetes, if
microalbuminuria is persistent despite good glycaemic and lipid control,
an ACE inhibitor should be used. In type 2 diabetes, an ACE receptor
blocker is preferred.
67
What is the urinary concentration or 24-hour urine albumin content above
which angiotensin-converting enzyme (ACE) inhibitors should be started
in diabetic patients? Does an albumin (in microgram)/creatinine (in
milligrams) ratio above 30 in the morning sample indicate a need for this?
Frank proteinuria, i.e. 300 mg/day, should be treated with an ACE
inhibitor/antagonist after good glycaemic and lipid control has been
instituted. A ratio of 30 would also indicate the necessity for treatment
68
Is a dosage of 2.5 mg/day of methyltestosterone, as a component in
some multivitamin formulae, safe to give to diabetics or will it make the
diabetes more difficult to control
2. 5 mg methyltestosterone is a very small dose and should be safe in
diabetics. It is, however, difficult to see an indication for this therapy
69
How does diabetes mellitus cause atherosclerosis?
● Endothelial dysfunction.
● Abnormalities of coagulation, particularly in the fibrinolytic pathway.
● Plaque composition: there is increased lipid and macrophages in
plaques in diabetes mellitus which increase the risk of rupture.
● Platelet activation leading to aggregation.
70
How does diabetes cause renal damage, especially diabetic nephropathy
with the presence of microalbuminuria?
conversion of glucose to sorbitol via the polyol pathway
seems to play a central role as this leads to vascular permeability and
structural defects in capillaries.
In the kidney, the glomerular filtration rate (GFR) is initially
increased out of proportion to plasma flow owing to an elevation in the transglomerular pressure gradient. The raised glomerular pressure might
promote transglomerular passage of proteins as well as glycosylate
end products. This could lead to proliferation of mesangial cells and
accumulation of matrix products in the basement membrane. These are
the first changes seen pathologically when microalbuminuria occurs.
These changes eventually lead to glomerular sclerosis with progressive
loss of glomeruli and more marked proteinuria.
71
Why is intractable vomiting seen in diabetes mellitus and how can it be
managed?
Delayed gastric emptying has been demonstrated in approximately 50%
of unselected usually asymptomatic patients with type 1 diabetes.
Tx good glycaemic control. Metoclopramide,
domperidone or erythromycin
72
Is gabapentin superior to carbamazepine in terms of efficacy in the
treatment of painful diabetic neuropathy? What are its side-effects?
Gabapentin is effective in painful neuropathy
73
Why is diabetic ketoacidosis more common in type 1 diabetes?
In type 1 diabetes there is no or very low insulin available. In type 2,
insulin is present although there is resistance to its action. This is the
reason for diabetic ketoacidosis in type 1 diabetes
74
Why is there abdominal pain in diabetic ketoacidosis?
who knows
75
Grades of ketonuria
In ketoacidosis, stix testing of the urine will show very high ketone
levels (grade III). This is occasionally useful if you have any doubt of the
diagnosis. Low levels of ketonuria (grade I) are seen in starvation.
You can also measure ketone levels in the serum; again high ketone
levels are seen in ketoacidosis
76
What false-positive factors could cause ketone bodies to appear in the
urine in a non-diabetic patient?
Starvation is the main cause. It also occurs after heavy alcohol consumption
77
Why is tetanus not seen in a diabetic foot wound?
The diabetic foot ulcer is not usually caused by trauma where the tetanus
bacillus can be picked up. It is usually the result of neuropathy and/or
ischaemia
78
Can impaired glucose tolerance cause recurrent lower motor facial palsy?
neuropathies can occur without overt
| diabetes mellitus
79
Can long-term diabetes mellitus cause vertigo not accompanied by other
brainstem signs?
the cause of the vertigo. If the vertigo is due to a brainstem
vascular lesion associated with diabetes mellitus, nystagmus is
frequently present. Transient vertigo occurs with hypoglycaemia without
the neurological signs.
80
We know that type 2 diabetes mellitus provokes left ventricular diastolic
dysfunction. Does chronic stable angina, associated with type 2 diabetes
mellitus, further increase the prevalence of left ventricular diastolic
dysfunction?
Type 2 diabetes is associated with coronary artery disease, which usually
produces left ventricular systolic dysfunction with some degree of
diastolic dysfunction. In chronic stable angina, the diastolic dysfunction is
usually stable except after exercise when ‘demand ischaemia’ occurs due
to increased oxygen demand when there is a decreased coronary flow.
81
Is there adequate evidence for choosing an angiotensin-converting
enzyme (ACE) inhibitor or antagonist for the initial management of
raised blood pressure in type 2 diabetes, or is it now advisable to choose
any tolerated antihypertensive?
ACE inhibitors or angiotensin receptor
| antagonists are renoprotective
82
Why is there immunosuppression in diabetes?
Type 1 diabetes is an immune mediated disease and there is some
immunosupression. It has been shown that treatment with an
immunosuppressive drug prolongs beta cell survival, although this is
not used in clinical practice
83
Dextrose infusion in quinine induced hypoglycaemia causes more
hypoglycaemia, so what is to be used?
Quinine overdose can cause hypoglycaemia but dextrose (10%) infusion
can be used and will prevent severe hypoglycaemia in most cases.
The mechanism of the hypoglycaemia is increased insulin secretion.
Intramuscular glucagon might be of short-term help and Octreotide 50 μg
SC 6-hourly has been used
84
Does the serum cholesterol level rise with age?
yes
85
Please explain the significance of having normal total high-density
lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol but a
raised lipoprotein (a) [Lp(a)] in a normotensive, non-smoking patient?
LP(a) is associated with an increased risk of coronary heart disease, but
in the patient you describe, who has a normal cholesterol, nothing should
be done.
86
Should a 20-year-old, either male or female, with a blood cholesterol
level of 300mg/dL and with hypercholesterolaemic parents, be treated?
Yes, with diet and a statin
87
Why are lipid-lowering drugs (statins) administered at bed time?
Cholesterol synthesis is maximal in the late evening/early morning, so
that giving a statin at night maximizes its effect.
88
What is the best statin now and what is your opinion about Crestor 10 mg
(rosuvastatin) and Lescol XL (fluvastatin sodium)?
There is no best statin. When prescribing drugs it is usually wise to use
the drug you know best, not to go immediately for the newest.
89
How long do statins take to achieve their maximum benefit?
At least 4 weeks
90
If, after 4 months of taking simvastatin (20 mg daily), a patient with
hyperlipidaemia and hypertension has an increased aspartate transferase
(AST) of up to 60 U/L, with a normal alanine transferase (ALT), what
action should I take?
None; treatment should only be discontinued if transferases are more
than three times the upper limit of normal
91
How long should the statins be continued once the lipid profile returns to
normal? Can we stop the statins once normal levels are attained and then
continue with diet modification?
Forever
92
What is the exact mechanism of corneal arcus? What is its clinical
significance? What is its relationship to hyperlipidaemia? Is there any
effective treatment in medicine or alternative medicine to remove
corneal arcus?
Lipid/cholesterol deposits in the cornea produce an arcus. In the young,
it is said to be associated with hyperlipidaemia but the exact relationship
is unclear. It has no significance in the elderly as it is a degenerative
process. There is no treatment
93
What is the best drug to be added to a statin in a case of familial
hypercholesterolaemia not responding to lifestyle and diet modification
plus a statin?
A number of patients with familial hypercholesterolaemia do need an
additional drug. Ezetimibe (a cholesterol absorption inhibitor) should be
added to a statin
94
Is it typical for a diabetic patient to experience angina during myocardial
ischaemia?
Diabetic patients classically have ‘silent’ ischaemia or heart attacks due to
the accompanying neuropathy. They can, however, have typical angina
with chest pain.
95
What are the causes of a flat oral glucose tolerance test (GTT)?
A flat oral GTT occurs when there is malabsorption of glucose. It was
used in the 1950s and 1960s as a test to show malabsorption. However,
it was replaced by tests using non-metabolized sugars, such as xylose,
which were more reliable. More recently, absorption tests have been
superseded by imaging, antibody tests and histology of the small
intestine to diagnose malabsorptive conditions such as coeliac disease
96
Are there any indications for routinely prescribing a statin (simvastatin, for
example) in hypertensive and/or diabetic patients as prophylactic therapy?
Most patients with hypertension and diabetes will require a statin but
before starting this agent you should encourage lifestyle changes, e.g.
stopping smoking, taking regular exercise and reducing fat in the diet.
Use statins to keep serum cholesterol to 4 mmol/L (150 mg/dL).
97
What are the causes of vomiting and other gastrointestinal tract problems
in type 2 diabetes mellitus? What is the correct treatment for a patient
with nausea and vomiting, already taking hypoglycaemic agents and
antihypertensives?
Vagal damage can lead to gastroparesis but this is usually in type 1
diabetes. There is no correct treatment for nausea and vomiting; meal
changes and antiemetics are the best approaches
98
potassium should be given along
with insulin in the treatment of ketoacidosis since hypokalaemia could
potentially cause tachycardia.
You are right in that hyperkalaemia is more dangerous than
hypokalaemia. However, cardiac arrhythmias do occur with
hypokalaemia
99
Can diabetes mellitus result in Horner’s syndrome with no other
neurological deficit?
Diabetes mellitus is of course a risk factor for atherosclerosis, which can
present with, for example, aortic or carotid dissection both associated
with Horner’s syndrome
100
Which drug is best recommended for a diabetic patient with rheumatoid
arthritis resistant to methotrexate, and requiring frequent pushes with
intramuscular depot preparations of methylprednisolone?
Patients resistant to methotrexate are now treated with anti-TNF therapy,
e.g. infliximab
101
Impaired glucose tolerance (IGT)
Fasting plasma glucose 7 mmol/L (126 mg/dL). At 2 h following a 75-g
glucose load: 7.8–11 mmol/L (140–200 mg/dL)
102
```
Target goals of risk factors for diabetic patients
HbA1c
BP
Total cholesterol
LDL
HDL
TG
```
```
7%
130/80
4.5
2.0
1.1
1.7
```
