Back to Endocrine Diseases
Diabetes is a group of metabolic disorders resulting from
a lack of insulin effect upon tissues with consequent development of abnormal
carbohydrate, protein and fat metabolism. Superimposed upon the biochemical
abnormality is a specific microangiopathy, neuropathy, and more frequent
and accelerated macrovascular disease.
Diabetes mellitus is characterized by
chronic hyperglycemia and disturbances of carbohydrate, protein and fat
metabolism. There are several types of the disease of variable etiology.
In recent decades, understanding of underlying causes and pathological
mechanisms leading to diabetes mellitus has progressed considerably. It
has become possible to distinguish clearly among the different forms of
the disease, sometimes tracing the cause to a single defective gene.
According to the World Health Organization, in 2004, more than 150
million people worldwide suffer from some form of diabetes. Even more
alarming, by the year 2025 this number is expected to double. Unlike
many other diseases, such as malaria, diabetes is prevalent everywhere
but more so in economically successful and highly industrialized
countries such as the United States. As of 2002, about 18.2 million
United States nationals suffer from diabetes. For at least 20 years,
diabetes rates in North America have been increasing substantially. The
Centers for Disease Control has termed the change an epidemic. This is a
medically and economically important disease, the National Diabetes
Information Clearinghouse estimates that in the United States alone
diabetes accounts for a total of $132 billion. Diabetes is easily in the
top 10 and perhaps in the top 5 most devastating diseases in the
developed world, and is becoming rapidly more so (see big killers).
Long-term diabetes mellitus can have detrimental effects on numerous
organs of the body. Prolonged high blood glucose levels can produce the
chronic complications of diabetes mellitus. They include:
- Endothelial damage - manifesting as microvascular or macrovascular
- Proliferative retinopathy can lead to blindness;
- Peripheral neuropathy can lead to foot ulcers leading to necrosis and
infection (including gangrene), eventually requiring amputation;
- Nephropathy can cause chronic renal failure requiring dialysis or
- Ischemic heart disease, stroke and neuropathy are other possible
complications -- probably stemming from blood vessel damage.
- High blood pressure -- which is more common in diabetics.
Diabetes mellitus is the most common cause of adult renal failure
worldwide. It is the most common non-accidental cause of amputation in
the US. It is the most common cause of blindness among non-elderly
adults in the US.
Generally, diabetes cannot now be cured (except experimentally in Type 1
diabetics) but it often can be treated effectively and there is emerging
solid evidence that diabetes mellitus Type 2 can be evaded in people
with impaired glucose tolerance6; that is, in those with 'beginning'
Traditionally (after the first use of insulin in 1922), the goal of
treatment was prevention of either hyperglycemic or hypoglycemic coma
and diabetic ketoacidosis. Lack of sufficiently frequent and
sufficiently inexpensive blood glucose monitoring precluded much more
nuanced intervention until the late 1970s. The chronic side effects of
diabetes were not even recognized as preventable until the last few
decades. Until the early 1920s, they couldn't be observed at all -- much
less treated -- because patients didn't survive long enough to suffer
Are you a doctor or a nurse?
Do you want to join the Doctors Lounge online medical community?
Participate in editorial activities (publish, peer review, edit) and
give a helping hand to the largest online community of patients.
Click on the link below to see the requirements:
Doctors Lounge Membership
Several large, long duration, studies since 1980 have made it clear that
the effort needed to keep blood glucose levels as close to normal (ie,
fasting levels below 126 mg/dl adn above 60 pr 70 depending on the
individual patient) is well worth while, and that it is actually
possible in the real world of diabetic patients. The risk of
complications is quite clearly inversely proportional to how well
controlled blood glucose levels are kept. Several studies have recently
shown that the beneficial effect of close control is a long term one as
well. More recent studies in Type 2 diabetes also stress the need for
stringent blood pressure and cholesterol control. Much of the vascular
damage that is associated with diabetes mellitus seems to be due, in
large part, to prolonged uncontrolled high blood pressure, which is
common in diabetics - probably due to insulin resistance or renal
failure / damage or both.
The clinical goal today is to avoid or minimize chronic diabetic
complications, as well as to avoid acute problems due to too high or too
low blood glucose. For Type 1 diabetics, this means injecting insulin;
for Type 2 diabetics, this means diet, exercise, and weight loss, in any
possible combination depending on the patient, followed by medication
(usually oral, but possibly insulin as well).
The management of diabetes is almost always a major ongoing presence in
patients' lives and activities. It need not be more than 'merely'
annoying for most; however, patient participation is so important to
diabetes management that patient education is required for diabetes.
Many treatments are potentially damaging (if not deadly) when
administered improperly. Moreover, there are (and appear to have long
been) a large number of "alternative" treatments for diabetes; some are
dangerous and occasionally deadly in themselves and/or by supplanting
more conventional treatments.
"Diabetes" is a Greek word meaning "a passer through; a siphon".
"Mellitus" comes from the Greek word "sweet". Apparently, the Greeks
named it thus because the excessive amounts of urine that a diabetic
(when in a hyperglycemic state) would excrete attracted flies and bees
because of the glucose content. The ancient Chinese would test for
diabetes by observing whether ants were attracted to a person's urine.
Passing abnormal amounts of urine can be a symptom of several diseases
(most commonly of the kidneys), and the word diabetes is applied to many
of them. The most common are diabetes insipidus and diabetes mellitus.
Until 1922, when insulin was first discovered and made clinically
available, a clinical diagnosis of diabetes was an invariable death
sentence, more or less promptly. Non-progressing Type 2 diabetics almost
certainly often went undiagnosed then; many still do.
The discovery of the role of the pancreas in diabetes is generally
credited to Joseph Von Mering and Oskar Minkowski, two European
researchers who, in 1889, found that when they completely removed the
pancreas of dogs, the dogs developed all the signs and symptoms of
diabetes and died shortly afterward. In 1910, Sir Edward Albert Sharpey-Schafer
in Edinburgh suggested that diabetics were deficient in a single
chemical that was normally produced by the pancreas - he proposed
calling this substance insulin.
The endocrine role of the pancreas in metabolism, and indeed the
existence of insulin, was not fully clarified until 1921, when Frederick
Grant Banting and Charles Herbert Best repeated the work of Von Mering
and Minkowski but went a step further and managed to show that they
could reverse the induced diabetes in dogs by giving them an extract
from the pancreatic islets of Langerhans of healthy dogs. They went on
to isolate the hormone insulin from bovine pancreases at the University
of Toronto in Canada.
This led to the availability of an effective treatment - insulin
injections - and the first clinical patient was treated in 1922. For
this, Banting, et al, received the Nobel Prize in Medicine in 1923. The
two researchers did not patent their discovery and the therapy rapidly
spread around the world.
Causes and types
The role of insulin
Insulin is a hormone that enables blood glucose molecules to enter about
2/3 of the cells of the body (primarily muscle and fat cells). It also
controls many other body mechanisms, from fat processing (in liver and
fat cells), protein synthesis (by controlling amino acid uptake in
cells), and electrolyte balance (by controlling potassium uptake in
cells). It is the central hormone involved in controlling metabolism. It
is produced in the endocrine part of the pancreas, which consists of
very small clumps of specialised cells scattered throughout that organ
(the 'Islets of Langerhans'). Hyperglycemia (too high blood glucose
levels) results if the amount of insulin is not sufficient to cause the
cells to take up the glucose from the blood, or if those cells which
require insulin to absorb glucose no longer respond adequately to it.
Hyperglycemia has two major causes, which may occur together:
Not enough insulin is produced by the pancreas (in Type 1, and in some
The cells of the body have become resistant to insulin action (in Type 2
and even in some Type 1)
Type 1 diabetes is most commonly diagnosed in children and adolescents.
It is an autoimmune disorder, in which the body's own immune system
attacks the glutamate decarboxylase enzyme in the hormone-producing beta
cells of the Islets of Langerhans in the pancreas, preventing them from
producing enough (or any) insulin. The autoimmune attack is generally
triggered by an infection, often by one of the Coxsackie virus family
(group B). The Coxsackie virus expresses the protein P2-C, which is
similar in structure to glutamate decarboxylase and lead to molecular
Some poisons work by selectively destroying the beta cells, thus
producing 'artificial' Type 1 diabetes. Pancreatic trauma or tumor can
also do so.
Currently, Type 1 is almost always treated with insulin injections,
usually using intensive insulinotherapy on a sliding dose scale. Doses
must be fitted to the individual patient's responses, and adjusted
thereafter as required.
About 5-10% of all North American cases of diabetes are Type 1. The
fraction of Type 1 diabetics in other parts of the world differs; this
is likely due to both differences in the rate of Type 1 and differences
in the rate of other Types, most prominently Type 2. Most of this
difference is not currently understood.
Formerly Type 1 diabetes was called "childhood" or "juvenile" diabetes
or and "insulin dependent" (IDDM) diabetes. All are misnomers,
especially since the obesity epidemic of recent years has lead to
increased incidence of Type 2 diabetes in children and adolescents.
Type 2 diabetes is characterized by resistant to insulin in those body
cells requiring insulin to permit uptake of glucose from the blood;
about 2/3 of body cells do. The four main characteristics of this
disease ("the disharmonious quartet") are: (1) decreased insulin
secretion, (2) increased lipolysis, (3) increased hepatic glucose
production (gluconeogenesis), and (4) decreased muscular glucose uptake.
All contribute to the development of hyperglycemia, which often goes
unnoticed for years and may lead to complications (see below) by which
it is finally detected. Type 2 often develops later in life, and is
often accompanied by central obesity, hypertension and combined
dyslipidemia (together termed Metabolic Syndrome X. However, it is
currently believed that obesity is the most significant risk factor. A
person's chances of developing Type 2 diabetes increases by 4 percent
for every pound of excess weight.
It was formerly called any of 'adult-onset' diabetes, 'obesity
related'-diabetes, 'insulin resistant'-diabetes, or 'non-insulin
dependent' (NIDDM) diabetes.
Type 2 diabetes can be secondary to a number of diseases (e.g.
hemochromatosis and polycystic ovary syndrome) and certain types of
medication (e.g. as a side effect of long-term steroid use). About
90-95% of all North American cases of diabetes are Type 2, and about 20%
of the population over the age of 65 suffer from it. The fraction of
Type 2 diabetics in other parts of the world varies substantially,
almost certainly for environmental reasons (probably lifestyle
differences). There is a very strong inheritable genetic connection in
Type 2 diabetes. For example, in late 2000 researchers found that a
variation of the gene Caplain-10, is associated with the development of
Type 2 diabetes. Relatives, especially close ones, with Type 2 are a
considerable risk factor.
Type 2 is initially treated with weight loss, which can restore insulin
sensitivity even when the weight lost is modest. Often, the next step is
treatment with oral antidiabetic drugs (sulphonylureas, metformin, or
thiazolidinediones). When a combination of the above has failed, insulin
therapy may be necessary.
Other specific forms of diabetes, accounting for up to 5% of all
diagnosed cases of diabetes:
- Genetic defect in beta cells.
- Genetically related insulin resistance.
- Diseases of the pancreas.
- Caused by hormonal defects.
- Caused by chemicals or drugs.
- Gestational diabetes mellitus appears in about 2-5% of all
pregnancies. About 20-50% of these women go on to develop Type 2
Both Type 1 and Type 2 diabetes have genetic linkages. Type 1 diabetes
may be triggered by infection, stress, or environmental factors (eg,
substances of one kind or another). There is clearly a genetic element
in the susceptibility of individuals to some of these triggers; it has
been traced to particular HLA genotypes. Even with the susceptibility,
Type 1 does not apparently occur without an environmental trigger. There
is an even stronger genetic link in Type 2 diabetes; those with Type 2
ancestors or relatives have very much higher chances of developing Type
2. It is also often connected to obesity, which is found in
approximately 85% of (North American) patients diagnosed with that form
of the disease. Age is also thought to be a contributing factor, as most
Type 2 patients in the past were older. The exact reasons for these
connections are unknown.
Presentation (signs and symptoms)
In Type 2 diabetes there is almost always a slow onset (years), but in
Type 1, particularly in children, onset may be quite fast (weeks or
Early symptoms of Type 1 diabetes are often polyuria (frequent
urination) and polydipsia (increased thirst and concomitant increased
fluid intake). There may also be weight loss despite normal or increased
eating, increased appetite, and unreduceable fatigue. These may also be
symptoms of Type 2, though usually not until a later, more 'severe'
Thirst develops because of osmotic effects?sufficient excess glucose
(above the 'renal threshold') from the blood is eventually excreted by
the kidneys but this causes fluid loss, which must be replaced.
Acute danger signs for diabetics include the smell of acetone on the
patient's breath (a sign of ketoacidosis), Kussmaul breathing (rapid,
deep breathing), and any altered state of consciousness or arousal
(hostility and mania are both possible, as is confusion). The worst form
of altered consciousness is the so-called "diabetic coma". Early
symptoms of impending diabetic coma are polyuria, nausea, vomiting and
abdominal pain, with lethargy and somnolence a later development,
progressing to unconsciousness and coma and death if continued and
Diabetic ketoacidosis and coma
See also the main article diabetic ketoacidosis and diabetic coma
Diabetic ketoacidosis (DKA) is an acute, dangerous complication diabetes
and always is a medical emergency. If left without prompt proper
treatment diabetic ketoacidosis has substantial mortality.
Pathophysiology of diabetic ketoacidosis
It arises from incomplete fat breakdown. Production of [[fatty acid]]s
from stored lipids is entirely normal during metabolic ketosis, and is
begun when insulin levels are low. It is therefore indirectly controlled
by the blood glucose level (in non-diabetics) and so ultimately, though
still more indirectly, controlled by carbohydrates in the diet. When
glucose is persistently low or absent (and so when fat is being taken
from body stores and converted to fatty acids for energy use, ie
ketosis), glucose is produced from some amino acids after protein
degradation. During glucose production from protein, fat metabolism (ie,
ketosis) becomes abnormal because of competitive interference between
the two processes. Under those conditions, the liver converts the
metabolic chemical acetyl-CoA (an intermediate in ketosis) to ketone
bodies without completing fat processing; these are together quite
acidic, and if present in too high quantities cannot be removed from the
blood fast enough to prevent acidosis. DKA is more common in Type 1
diabetics, probably because they do not secrete significant amounts of
their own insulin. It is much rarer in Type 2 diabetics.
The brain (and a few other tissues, including parts of the kidneys) uses
glucose from the blood regardless of diabetic status (ie, insulin
insufficiency or cellular resistance) as nerve cells do not require
insulin to absorb glucose; but neither it nor most of the rest of the
body is able to survive acidosis if it is 'too severe' or continues 'too
long'. The ketone bodies are acetone, acetoacetate and beta-hydroxybutyrate.
Oddly, only two are, chemically, ketones; the name survives from a time
when the biochemistry was poorly understood.
DKA is usually accompanied by hyperglycemia which also causes osmotic
diuresis, leading to excessive losses of water, sodium and potassium.
These electrolyte imbalances are also dangerous and can cause problems
up to and including death.
A patient with DKA is always acidotic, almost always dehydrated, and
nearly always hyperglycaemic. All are very dangerous conditions and
together are no less so. The patient urgently requires IV fluids and,
almost always, insulin -- typically intravenously. A bicarbonate
infusion may be necessary if the pH of the blood is sufficiently low.
DKA is a medical emergency and requires immediate skilled treatment,
supplies, and facilities; it cannot be adequately handled at home on a
'first aid' basis.
Hyperosmotic diabetic coma
Hyperosmotic diabetic coma has some similar symptoms, but a different
cause. In anyone with very high blood glucose levels (usually considered
to be above 300 mg/dl) water will be osmotically driven out of cells
into the blood. The kidneys will be "dumping" glucose, and the water
necessary to carry it, from the blood. The osmotic effect of the high
glucose levels combined with the (excessive) loss of water will
eventually result in raised serum osmolality. Electrolyte imbalances
often also occur. The combination of changes, if prolonged, will result
in symptoms similar to ketoacidosis, including loss of consciousness. As
with DKA, urgent medical treatment is necessary. It is the diabetic coma
to which Type 2 diabetics are prone.
A complication of treatment (primarily, insulin and sulphonylureas) is
hypoglycemia, meaning excessively low blood sugar levels. The patient is
often agitated (sometimes irrational), sweaty and has all the features
of sympathetic activation of the autonomic nervous system. Consciousness
drops in extreme cases, leading to coma and seizures. A diabetic,
particularly an experienced one, can sometimes recognise the symptoms
early (that is, if no hypoglycemia unawareness is present) and should
always carry something sugary to eat or drink, which can reduce the
symptoms rapidly. If this opportunity has been missed, oral or
intravenous dextrose administration will reverse the symptoms very
quickly. Longstanding hypoglycemia might require hospital admission.
The need for treatment
Diabetes is a chronic disease (the most common such disease) and, as
there is no cure, it can only be managed symptomatically, often by
life-long treatment with medication. Moreover, it can lead to several
serious acute or chronic complications that can make a patient dependent
on dialysis, blind and wheelchair-bound if not managed adequately and
Diabetes mellitus requires complex therapy, education and life-style
modifications to minimize bad outcomes. The goals of diabetes management
are several: not only near-normal glycemic control (and so avoidance of
both acute and chronic hyperglycemia), but also prevention of
hypoglycemia episodes, thus reducing the risk of long-term complications
and preserving quality of life for patients.
Several major studies (involving very large numbers of patients) have
shown, clearly and convincingly and beyond reasonable doubt, that
keeping blood glucose levels as close as possible to 'normal',
nondiabetic, values really does prevent, or delay, chronic diabetic
- Diabetic retinopathy
- Microangiopathic and macroangiopathic damage (atherosclerosis)
Close glucose control should be undertaken with care, as keeping blood
glucose levels 'normally' low in diabetics leaves less room for
medication / diet / exercise error and so increases the possibility of a
(possibly dangerous) hypoglycemic episode (see above).
Treatment depends on the type of diabetes:
Type 1 is generally treated with insulin as a first-line therapy,
sometimes proceeding to an insulin pump. There is no oral treatment for
Type 1 diabetes. Islet transplants are still in their experimental
Type 2 can usually be managed with: a diet and medication. Common
antidiabetic drugs include the biguanides (mainly metformin), the
sulfonylureas (e.g. Orinase?, Diabinase?, and Tolinase? among many
others) and the newer thiazolidinediones (rosiglitazone and pioglitazone).
Some Type 2 diabetics require insulin therapy when diet, exercise,
weight control, and combinations of antidiabetic drugs have failed to
bring the glucose levels down (or have caused intolerable side effects).
Insulin therapy requires close monitoring and a great deal of patient
education. For example, when food intake is reduced, less insulin is
required. The previously satisfactory doseing may now be too much and
cause a hypoglycemic reaction. More exercise decreases insulin
requirements, and vice versa: exercise increases glucose uptake by body
cells nominally under insulin control for glucose uptake. Since there
are many different insulin preparations, since foods vary in their
effect on blood glucose levels (even if they have exactly the same
calories), and since the "glucose absorption"-effect of exercise varies
depending on many factors (including individual patient variations),
getting the right amount and timing of diabetic medication (most
particularly insulin) is not trivial. For most diabetics, it takes time
and effort to "get the hang of it". Adjusting insulin and other diabetic
drugs is an attainable goal for the average patient, but it is not
simple, nor trivially safe either. The consequences of making an error
include death, and so great caution, and expert advice (especially when
beginning drug therapy), are both mandatory. Especially for newly
diagnosed diabetics, medication changes should be done only in
consultation with a physician.
Illness, surgery, and stress also affect glucose levels (eg, several of
the stress hormones force increases in glucose levels), so all diabetics
should be aware that their insulin and other drug routines may have to
change if any of these occur. Previously prepared "sick day rules" may
be a reasonable approach, but must actually be suitable to the diabetic
situation during illness, stress, etc. for that particular patient.
Other risk factors
The presence of hyperglycemia should prompt the search for other risk
factors that can lead to cardiovascular disease, mainly hypertension and
hypercholesterolemia. In both conditions, the presence of diabetes is an
additional reason to intensify treatment.
Results from an important study5 in the journal Lancet suggest that
diabetics should be treated with a statin drug (simvastatin 40 mg or
equivalent), irrespective of their cholesterol levels. The treatment
seems to reduce (by 24-27%) the rate of myocardial infarction, coronary
death, and stroke, as well as the need for peripheral arterial
revascularization procedures. The reason is thought to be an
anti-inflammatory reaction, and not just the modification of cholesterol
levels. The effect seems clear, but the mechanism remains obscure.
Monitoring of blood glucose levels
a simple blood glucose meter Sensible management of diabetes depends
almost entirely on blood glucose testing. This is because mild to
moderate hyperglycemia causes no obvious symptoms in most patients.
Other complicating factors include the fact that, while food takes
several hours to be digested and absorbed, insulin can have glucose
lowering effects for as little as 2 hours or 24 hours or more (depending
on the nature of the insulin preparation used and individual patient
reaction). And, the onset time and duration of the effects of oral
hypoglycemic agents (nearly always pills) vary from type to type and
from patient to patient.
Since blood glucose levels change regularly and rapidly (within hours
and less), portable meters are effectively the only reasonable choice.
Testing only during visits to a clinic, at a doctor's office, or in
hospital is entirely inadequate as a basis for almost every decision
about food, exercise, drug dosage and timing a diabetic patient is
obliged to make.
Regular urine glucose testing is only slightly more useful, except
perhaps for detecting ketones in the early stages of ketoacidosis. It
reflects all glucose levels since the last urination, not only what they
are now. Even in an emergency, this is not likely to be of much help.
There are multiple suppliers of blood glucose meters (all of which must
be approved by the FDA in the US). Differences among them include size
of the blood droplet required, where it can be taken (from a finger, or
a forearm, or ...), whether the blood sample may be applied to a test
strip before or after it is inserted in the meter, length of delay until
results are available, size and packaging of the disposable test strips,
the underlying detection technique (optical reflectance or
electrochemical are the usual techniques), and compatibility with
computer programs for keeping records of readings and other information.
Cost also varies, but not for inherent technical reasons; these are all
machines of quite similar complexity and inherent cost.
a blood test strip The cost per test strip varies quite substantially --
cost differences of more than 3x are found in the US as this is written.
Thus, strips for one meter model may be as much as 1/3 the cost for
strips for another. Cumulative strip costs, over even short periods,
completely swamp all other meter cost issues. Strip cost should be a
major (probably the most important) contributor in the decision of which
meter to choose. How often to test, and what to do with/about the
results should be closely coordinated with medication schedules
(especially for insulin), food, and exercise. At least when beginning to
test, medical supervision is a very sensible, and in many cases
A useful laboratory test of long term diabetic glucose control is the
glycated haemoglobin level (aka, "HbA1c"). Non-diabetics typically have
an HbA1c level of less than 7%. This is a good target for most (but not
all) diabetics; since diabetic situations differ, determining an HbA1c
target should be determined in cooperation with a physician. HbA1c
levels indicate average glucose levels in the recent past (around 3
months in most people as the lifetime of a red blood cell usually
averages 120 days), and so less 'close' blood glucose control. What
HbA1c level indicates poor diabetic control will vary with each patient.
There is now a commercial test kit (in the US, anyway) for doing this at
Short term (acute) problems
Since insulin became available, short term benefits of its sensible use
have been, on the whole, excellent. At the very least, they didn't
inevitably die in the short term as they had inevitably done previously.
Impurities in insulin preparations have been decreasing steadily since
1922, and allergic reactions have decreased with them. Insulin has never
been purer, by and large, than it is now. Insulin use has not become
trivial and side effect reactions to commercial insulin products have
not disappeared, but the situation is better now than it has ever been.
The acute problems of diabetes mellitus, such as DKA, are fully
treatable today. They are not always treated properly, in part because
many people don't pay sufficient attention to their diabetes, or behave
sensibly, and in part because some care givers have not taken into
account the discoveries of the past few years about best treatments for
Long term (chronic) problems
The long-term consequences of diabetes mellitus are another story. Long
term complications of diabetes mellitus include damage to small blood
vessels (microangiopathy), larger blood vessels (macroangiopathy),
kidneys nephropathy, and to the peripheral and autonomic nervous systems
(diabetic neuropathy). Each of these causes its own symptoms, most of
Distinct forms of microangiopathy include damage to the retina of the
eye (diabetic retinopathy) and damage to the kidneys (nephropathy). The
damage in both cases seems to be primarily due to high glucose levels,
probably via assorted reactions between glucose and various proteins
which thereupon change their behaviour and so the behaviour of the
tissue in which the protein is found (eg, small blood vessel walls).
Keeping glucose levels at or near 'normal' reduces the risk of any of
these complications of diabetes mellitus without any question.
There are distinct forms of neuropathy as well. Peripheral sensory
neuropathy affects sensation at first, and primarily, in the feet and
lower legs, and eventually even fingers and hands. Feeling decreases and
with it protective reaction to damage, eg from thumb tacks, blisters,
ill fitting shoes, .... Combined with vascular damage leading to slower
healing, the effect is to greatly increase the risk of trauma (eg, can't
feel the pebble or pin or developing blister), and the risk of spread of
serious infection (eg, infection not noticed (no or reduced pain) and no
measures taken until 'too late'). Autonomic neuropathy can cause
problems with balance, with intestinal operations (ie, digestion), with
balance and coordination, with sexual responses and other reflexes, and
indeed, with 'automatic' compensating adjustments of many kinds.
Several studies have demonstrated that, for both types of diabetes
mellitus, the rate and severity of these long term complication is
substantially reduced, or eliminated, by keeping blood glucose levels at
or near 'normal'. Blood glucose testing is important if only because it
helps with this.
Other investigations include urinanalysis for glucose, ketones
and protein; full blood count; electrolytes; kidney function tests; blood
cholesterol and triglycerides.