Diabetes mellitus and other disorders of metabolism

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19 Diabetes mellitus and other disorders of metabolism

Questions

Question 1

I would like to know the exact mechanism of entry of potassium into cells under the influence of insulin.

Question 2

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?

Question 3

What are the latest diagnostic criteria for the diagnosis of diabetes mellitus?

Question 4

What test is recommended for diabetes and can the same be used to diagnose diabetes in a child?

Question 5

What is the value of glycosylated haemoglobin (HbA_1C) in diabetes mellitus?

Question 6

I read in a book that in diabetics the random blood sugar is more important than the fasting; on a medical website I noted that, for a patient with type 2 diabetes, the fasting blood sugar level is more important. What do you say?

Is it acceptable to let the fasting blood sugar remain at approximately 1.5mmol/L above the upper limit in a patient of >60 years with type 2 and presently on oral therapy?

Question 7

In type 2 diabetes, which blood sugar – fasting or random – is more revealing prognostically?

Question 8

Why are the fasting and 2-hour blood glucose levels needed in a diabetic patient being treated with oral antidiabetic drugs?

Question 9

Is it sufficient to use a fasting blood sugar and glycosylated haemoglobin (HbA_1C) level as a guide to modify the insulin or oral antidiabetic dose without considering the 1 and 2 hour postprandial values?

Question 10

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?

Question 11

What does BM mean in relation to blood sugar monitoring?

Question 12

What is the role of urine examination in diabetic control?

Question 13

Diabetes and diet: could the authors of my favourite medical text please advise whether or not it is acceptable to have controlled quantities of refined sugar, providing the total calorie intake is kept under control?

Question 14

Do non-obese patients with impaired fasting glucose, i.e. a glucose level of 6.1-6.9mmol/L, need drug treatment with biguanides if lifestyle modifications fail to normalize?

Question 15

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?

Question 16

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.

Question 17

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.

Question 18

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?

Question 19

What oral antidiabetics are safe in pregnancy?

Question 20

Is it necessary to put all type 2 diabetics on aspirin?

Question 21

In the chapter on diabetes you wrote that you should avoid tablets before age of 40 years in non-insulin-dependent diabetes mellitus (NIDDM). Why is this, because in our country most doctors are prescribing this?

Question 22

1. Should a patient poorly controlled on glibenclamide 15mg a day and metformin 1500mg a day be moved onto insulin?

2. What are the indications for insulin in type 2 diabetics?

Question 23

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?

Question 24

1. Is inhaled insulin a suitable substitute for injectable insulin?

2. Is there, or will there soon be, insulin in the form of a tablet?

Question 25

What are the complications of insulin other than hypoglycaemia and injection?

Question 26

I would like to know the processes that go into administering the Alberti’s/modified Alberti’s regime in patients with uncontrolled diabetes mellitus.

Question 27

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?

Question 28

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 + 10mmol of KCl + 500mL 10% glucose.

Question 29

What is the cut-off point of daily albumin excretion above which a diabetic patient without hypertension should be given an angiotensin-converting enzyme (ACE) inhibitor?

Question 30

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?

Question 31

Do potassium channel activators such as nicorandil have any benefit in the treatment of a diabetic patient with cardiovascular complications?

Question 32

Is a dosage of 2.5mg/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 (see also Chapter 5, question 5)?

Question 33

How does diabetes mellitus cause atherosclerosis?

Question 34

How does diabetes cause renal damage, especially diabetic nephropathy with the presence of microalbuminuria?

Question 35

Type 1 diabetes causes nephropathy in 40% of cases and type 2 causes it in 20% of cases but the most common cause of nephropathy we see is type 2, why?

Question 36

Why is intractable vomiting seen in diabetes mellitus and how can it be managed?

Question 37

Is gabapentin superior to carbamazepine in terms of efficacy in the treatment of painful diabetic neuropathy? What are its side-effects?

Question 38

Why is diabetic ketoacidosis more common in type 1 diabetes?

Question 39

Why is there abdominal pain in diabetic ketoacidosis?

Question 40

Grades of ketonuria are sometimes mentioned. I have not been able to locate a detailed description in textbooks and would be grateful if you could explain the grades of ketonuria or recommend suitable reading material.

Question 41

What false-positive factors could cause ketone bodies to appear in the urine in a non-diabetic patient?

Question 42

Why is tetanus not seen in a diabetic foot wound?

Question 43

Can impaired glucose tolerance cause recurrent lower motor facial palsy?

Question 44

Can long-term diabetes mellitus cause vertigo not accompanied by other brainstem signs?

Question 45

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?

Question 46

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?

Question 47

Why is there immunosuppression in diabetes?

Question 48

Dextrose infusion in quinine induced hypoglycaemia causes more hypoglycaemia, so what is to be used?

Question 49

Does the serum cholesterol level rise with age?

Question 50

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?

Question 51

In the diet of hypercholesterolaemic patients, should milk and other dairy products be restricted?

Question 52

Should a 20-year-old, either male or female, with a blood cholesterol level of 300mg/dL and with hypercholesterolaemic parents, be treated?

Question 53

Why are lipid-lowering drugs (statins) administered at bed time?

Question 54

What is the best statin now and what is your opinion about Crestor 10mg (rosuvastatin) and Lescol XL (fluvastatin sodium)?

Question 55

How long do statins take to achieve their maximum benefit?

Question 56

If, after 4 months of taking simvastatin (20mg daily), a patient with hyperlipidaemia and hypertension has an increased aspartate transferase (AST) of up to 60U/L, with a normal alanine transferase (ALT), what action should I take?

Question 57

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?

Question 58

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?

Question 59

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?

Question 60

Can diabetes mellitus cause Horner’s syndrome? If so, how?

Question 61

Is it typical for a diabetic patient to experience angina during myocardial ischaemia?

Question 62

What are the causes of a flat oral glucose tolerance test (GTT)?

Question 63

Are there any indications for routinely prescribing a statin (simvastatin, for example) in hypertensive and/or diabetic patients as prophylactic therapy?

Question 64

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?

Question 65

In diabetic ketoacidosis there is an overall potassium deficit. Since insulin promotes cellular potassium uptake, potassium should be given along with insulin in the treatment of ketoacidosis since hypokalaemia could potentially cause tachycardia. Why? I realise that hyperkalaemia can cause problems since the concentration gradient and therefore the membrane potential is reduced thus inhibiting proper function, but what is the problem with hypokalaemia? Is it that the membrane potential and the concentration gradient are too large? If so, how is this possible considering that the body may have too little potassium to make the intracellular concentration approach normal, so that although the extracellular concentration is reduced, the intracellular concentration is also reduced?

Question 66

Can diabetes mellitus result in Horner’s syndrome with no other neurological deficit?

Question 67

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?

Answers

Answer 1

Insulin promotes active transport of glucose into the cell (using the glucose transporter GLUT 4) and this is accompanied by potassium transport.

Answer 2

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.

Answer 3

The diagnosis for diabetes mellitus is a fasting plasma glucose greater than 7mmol/L (126mg/dL) or random plasma glucose greater than 11.1mmol/L (200mg/dL). Two abnormal values are required in an asymptomatic patient to indicate impaired glucose tolerance are shown in Box 19.1.

Box 19.1 Definitions

Impaired fasting glucose (IFG)

American Diabetes Association criteria is a plasma glucose level of 5.6-6.9mmol/L (110-126mg/dL)

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)

Note: both IFG and IGT are risk factors for the development of diabetes and cardiovascular disease

Answer 4

The diagnosis is made on:-symptoms of diabetes and a random plasma glucose of > 200mg/dL (11.1mmol/L or a fasting plasma glucose > 126mg/dL (7.0mmol/L). This also applies to children.

Answer 5

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. HbA_1C 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.

Answer 6

Both the random blood sugar and the fasting blood sugar are of some use in the management of type 2 diabetes. However, both are isolated measurements. It is much more useful to get patients to measure their own blood glucose three or four times a day, say at 3-weekly intervals. An alternative is to use the glycosylated haemoglobin level, which is the best guide to overall blood sugar levels over the preceding 3 months. In both type 1 and type 2 diabetes, good control reduces the risk of complications. Your patient should therefore be encouraged to keep a normal blood sugar and a normal level of glycosylated haemoglobin.

Answer 7

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.

Answer 8

It is better to use the glycosylated haemoglobin (HbA_1C) level; the ideal is <7% and the patient does not need to be fasted.

Answer 9

The best approach is for the patient to do blood sugars at home throughout the day, with HbA_1C being performed at the clinic visit.

Answer 10

Two-hour postprandial blood sugar is not as good a measurement as HbA_1C, 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.

Answer 11

BM stands for Boehringer Mannheim, the firm that produces a number of glucose measurement strips.

Answer 12

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.

Answer 13

No, it is not a good idea because refined sugar will produce abrupt swings in glucose level due to rapid absorption. Better to eat an apple!

Answer 14

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.

Answer 15

Impaired glucose tolerance is a risk factor for future diabetes and cardiovascular disease. Therefore, many diabetologists start metformin therapy (Fig. 19.1).

Fig. 19.1 A treatment pathway for type 2 diabetes mellitus.

Answer 16

Fortunately, the Muslim faith does not require insulin-dependent diabetic patients to fast during Ramadan. Some patients do, however, decide they would like to fast.

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 5-7mmol/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 5-8mmol/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.

Answer 17

Pioglitazone and rosiglitazone are the two glitazones available in the UK. They 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.

Answer 18

It makes no difference.

Answer 19

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.

Answer 20

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.

Answer 21

The statement that you should ‘avoid tablets before the age of 40 years’ is a reference to the fact that below 40 years most patients have type 1 diabetes with insulin deficiency and therefore require insulin therapy.

Answer 22

1. Yes – use insulin in all type 2 patients if glycosylated haemoglobin (HbA_1C) 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.

Further reading

Gaede P et al. (2003) Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. New England Journal of Medicine348: 383-393.

Answer 34

The pathogenesis of the renal complications of diabetes mellitus is still not completely understood.

In general, the 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.

Answer 35

You are correct, but there are of course many more cases of type 2 diabetes; hence this is the most common cause.

Answer 36

Delayed gastric emptying has been demonstrated in approximately 50% of unselected usually asymptomatic patients with type 1 diabetes. There is usually evidence of an autonomic neuropathy and often a peripheral neuropathy. There is, however, no good correlation between the motility findings and the symptoms. A few patients do develop severe vomiting. In addition, hyperglycaemia per se inhibits gut motility.

Treatment consists of very good glycaemic control. Metoclopramide, domperidone or erythromycin (this acts on motilin receptors) can also be tried. Hospital admission is occasionally required for dehydration and control of diabetes.

Answer 37

Gabapentin is effective in painful neuropathy, although trials are small. It produces many side-effects (look up your national formulary) but on the whole is well tolerated. It does cause troublesome diarrhoea. Carbamazepine is also effective but less so. Only two drugs have been approved by the US Food and Drug Administration based on phase III RCTs: pregabalin (related to gabapentin) and duloxetine, which inhibit the receptors of serotonin and noradrenaline (norepinephrine).

Answer 38

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.

Answer 39

The cause of abdominal pain in diabetic ketoacidosis is not clear.

Answer 40

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.

Answer 41

Starvation is the main cause. It also occurs after heavy alcohol consumption (starvation is also involved as people do not eat when drinking heavily).

Answer 42

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.

Answer 43

There is some evidence that neuropathies can occur without overt diabetes mellitus.

Answer 44

It depends on 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.

Answer 45

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.

Answer 46

There is good evidence that ACE inhibitors or angiotensin receptor antagonists are renoprotective. Recent guidelines suggest that the antagonists should be used first in type 2 diabetes.

Answer 47

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.

Answer 48

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 50μg SC 6-hourly has been used.

Answer 49

Yes.

Answer 50

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.

Answer 51

Milk and other dairy products should be restricted. However, it is only with severe restriction that a significant effect on cholesterol levels is seen and this is often unacceptable to patients. Some restriction, plus a statin, may be a better option.

Answer 52

Yes, with diet and a statin (Table 19.1).

Table 19.1 Target goals of risk factors for diabetic patients (standards from the American Diabetes Association, 2003)

Parameter	Ideal	Reasonable but not ideal
HbA_1C	<7%	<8%
Blood pressure (mmHg)	<130/80	<140/80
Total cholesterol (mmol/L)	<4.5	<5
LDL	<2.0	<3.0
HDL*	>1.1	>0.8
Triglycerides	<1.7	<2.0

* In women, >1.3 mmol/L. HbA_1C, glycosylated haemoglobin; HDL, high-density lipoprotein; LDL, low-density lipoprotein.

Answer 53

Cholesterol synthesis is maximal in the late evening/early morning, so that giving a statin at night maximizes its effect.

Answer 54

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.

Answer 55

At least 4 weeks.

Answer 56

None; treatment should only be discontinued if transferases are more than three times the upper limit of normal.

Answer 57

Probably forever, as diet modification seldom works.

Answer 58

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 rocess. There is no treatment.

Answer 59

A number of patients with familial hypercholesterolaemia do need an additional drug. Ezetimibe (a cholesterol absorption inhibitor) should be added to a statin.

Answer 60

No. Diabetic neuropathy is described on p. 1055 of Kumar and Clark Clinical Medicine 7th edn, and the sympathetic nervous system can be involved in diabetes. However, Horner’s syndrome is not described.

Answer 61

Diabetic patients classically have ‘silent’ ischaemia or heart attacks due to the accompanying neuropathy. They can, however, have typical angina with chest pain.

Answer 62

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, hich 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.

Answer 63

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 <4mmol/L (150mg/dL).

Answer 64

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.

Answer 65

You are right in that hyperkalaemia is more dangerous than hypokalaemia. However, cardiac arrhythmias do occur with hypokalaemia.

Answer 66

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.

Answer 67

Patients resistant to methotrexate are now treated with anti-TNF therapy, e.g. infliximab.

1000 Questions and Answers from Kumar _ Clarks Clinical Medicine

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