Type 2 Diabetes Mellitus
Type 2 diabetes mellitus is a disease
that is becoming more common in association with the increase in obesity in the
population. The overall UK prevalence is around 2% of the population, rising
with age, and is higher in certain ethnic groups including African–Caribbeans
(around 5%) and South Asians (>10%). Diagnosis of diabetes depends on the
demonstration of a raised non-fasting blood glucose of greater than 11 mmol/L.
If there is doubt, a fasting sample should obtained. The guidelines for the
diagnosis of DM are shown in Table 41.1. Impaired glucose tolerance is an
important condition with a high risk of developing Type 2 DM and an increased
risk of macrovascular disease compared to the normal population.
Treatment is of Type 2 diabetes is by
dietary measures, life-style changes and oral hypoglycaemic agents where
necessary. Although patients with Type 2 diabetes do not develop ketosis and do
not require insulin for survival, some may be treated with insulin to optimize
glycaemic control.
Type 2 diabetes mellitus
Type 2 diabetes mellitus is the most
common form of diabetes, accounting for approximately 85% of diabetic patients.
It is characterized by insulin resistance coupled with relative insulin
deficiency. The mechanism of insulin resistance in Type 2 diabetes remains
unclear. Although numerous genetic abnormali- ties of the insulin receptor have
been identified, in some cases in association with profound insulin resistance
syndromes, these are rare and do not explain hyperinsulinaemia seen in the vast
majority of patients with Type 2 diabetes. The consequence of prolonged
hyperinsulinaemia is the development of insulin deficiency. There is a strong
genetic predisposition to Type 2
DM with high levels of concordance
between identical twins and high prevalence in certain ethnic communities,
particularly individuals of South Asian or African–Caribbean origin. However,
environmental factors also play a key role, such that obese individuals have a
much higher rate of insulin resistance and Type 2 DM.
Patients may present with symptoms of
hyperglycaemia such as thirst and polyuria although more commonly
hyperglycaemia is diagnosed during routine investigations or in patients with
cardiovascular disease, urinary tract or skin infections. Investigations reveal
elevated blood glucose and glycated haemoglobin concentrations, usually
associated with dyslipidaemia. Residual insulin secretion means that
individuals with Type 2 diabetes do not develop ketoacidosis, although they may
present as an emergency with hyperosmolar non-ketotic coma (HONK) induced by
prolonged hyperglycaemia and subsequent dehydration and hypernatraemia. These
patients require careful management with fluid replacement and small doses of
insulin to restore euvolaemia and euglycaemia prior to establishment on diet
and oral hypoglycaemic therapy.
Historically, Type 2 diabetes has
occurred more commonly in patients over the age of 40 years. However, with the
rising incidence of obesity in western populations and its earlier onset, it is
now encountered with increasing frequency in young adults and children.
Treatment of Type 2 diabetes
The primary objective is to control
plasma levels of glucose and lipids and to lower blood pressure if it is
raised. Patients should be encouraged to lose weight and give up smoking, since
these are additional risk factors for hypertension and cardiovas- cular
disease, both more common in Type 2 diabetes.
Initially, dietary advice is given.
The aim is to achieve normal blood glucose concentrations with control of
hyperlipidaemia and blood pressure. Seventy-five per cent of these patients
will be overweight or obese and initially the treatment of choice is diet,
which aims to reduce the patient’s weight to the ideal level. When an
appropriate weight for the patient has been achieved, the diet may be adjusted
to maintain it at the desired level. Regular exercise, tailored to the
patient’s abilities, should be encouraged as this helps to increases insulin
sensitivity and reduce blood glucose levels. If lipid levels and blood pressure
are not controlled then the early introduction of lipid-lowering therapies,
usually in the form of statins and antihypertensives, is required. In the
absence of good glycaemic control by dietary measures, oral hypoglycaemics are
introduced. Initial therapy is usually in the form of sulphonylureas, such as
gliclazide or glipizide, which promote insulin secretion, or the biguanide
metformin which alters peripheral glucose metabolism. Newer therapies may be
added, such as the thiazolidinediones, which reduce peripheral insulin
resistance, and acarbose, which inhibits α-glucosidase and lowers postprandial
glucose concentrations. Insulin may be required to achieve good glycaemic
control in patients with Type 2 diabetes when there has been prolonged poor
control and/or symptoms of insulin deficiency supervene. Clinical management of
Type 2 diabetes requires a multidis ciplinary approach.
Gestational diabetes. Patients with a predisposition to Type 2 diabetes
may present during pregnancy, usually with asymptomatic hyperglycaemia
diagnosed routinely. It is vital to achieve excellent glycaemic control to
prevent complications in the newborn and these subjects require detailed
monitoring and insulin therapy, sometimes in large doses. Unless diet and
lifestyle changes are introduced after the pregnancy a high percentage
(>75%) of these women will go on to develop Type 2 diabetes in later life.
Macrovascular complications are the major cause of death in people with Type 2
diabetes, accounting for 50% of deaths in this group (Table 41.2). The relative
risk for cardiovascular disease is two to three times higher in men and three
to four times higher in women with diabetes than age-matched controls.
Diabetics are three times more likely to have a stroke and 15 times more likely
to undergo lower limb amputation than non-diabetic subjects. In the long term,
patients with Type 2 diabetes may also develop microvascular complications such
that diabetic nephropathy is now the second most common cause of end-stage
renal disease in the UK.
The diabetic foot
Foot disease in diabetics may be
caused by peripheral vascular disease or by neuropathy but commonly there is an
element of both (Figs 41a and b). Impaired vascular supply coupled with
external pressure from shoes or at pressure points predisposes to tissue
necrosis and the formation of ischaemic ulcers and digital gangrene. Ischaemic
feet are characterized by weak or absent pulses, pale, cool skin and poor
capillary return. Peripheral neuropathy causes weakness of the dorsal
interossei muscles allowing unopposed action of the long flexors in the foot
and subsequent clawing of the toes. There is a redistribu- tion of pressure
throughout the foot allowing ulceration to develop over the metatarsal heads.
The loss of pain and joint position sensation contributes to the problem as
external irritants (such as stones in the shoes) may go unnoticed by the
patient, leading to breakdown of the skin and the onset of ulceration. Neuropathic
feet are warm with bounding pulses and dry skin.
Management of foot disease in diabetes
is critical to maintaining mobility and prevention of ulceration, gangrene and possible
amputation.
