Ross & Wilson Anatomy and Physiology in Health and Illness (106 page)

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Authors: Anne Waugh,Allison Grant

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Type II diabetes mellitus

Previously known as non-insulin-dependent diabetes mellitus (NIDDM), this is the most common form of diabetes, accounting for about 90% of cases. The causes are multifactorial and predisposing factors include:

•
obesity

•
sedentary lifestyle

•
increasing age: affecting middle-aged and older people

•
genetic factors.

It often goes undetected until signs are found on routine investigation or a complication occurs. Insulin secretion may be below or above normal. Deficiency of glucose inside body cells occurs despite hyperglycaemia and a high insulin level. This may be due to insulin resistance, i.e. changes in cell membranes that block the insulin-assisted movement of glucose into cells. Treatment involves diet and/or drugs, although sometimes insulin injections are required.

Secondary diabetes

This may develop as a complication of:

•
acute and chronic pancreatitis

•
some drugs, e.g. corticosteroids, phenytoin, thiazide diuretics

•
secondary to other endocrine disorders involving hypersecretion of hormones which increase plasma glucose levels, e.g. growth hormone, thyroid hormones, cortisol, adrenaline (epinephrine).

Gestational diabetes

This develops during pregnancy and may disappear after delivery; however, diabetes often recurs in later life. Raised plasma glucose levels during pregnancy predispose to the birth of heavier than normal and stillborn babies, and deaths shortly after birth.

Effects of diabetes mellitus

Raised plasma glucose level

After eating a carbohydrate-rich meal the plasma glucose level remains high because:

•
cells are unable to take up and use glucose from the bloodstream, despite high plasma levels

•
conversion of glucose to glycogen in the liver and muscles is diminished

•
there is gluconeogenesis from protein, in response to deficiency of intracellular glucose.

Glycosuria and polyuria

The concentration of glucose in the glomerular filtrate is the same as in the blood and, although diabetes raises the renal threshold for glucose, it is not all reabsorbed by the tubules (
p. 335
). The glucose remaining in the filtrate raises its osmotic pressure, water reabsorption is reduced and the volume of urine is increased (polyuria). This results in electrolyte imbalance and excretion of urine of high specific gravity. Polyuria leads to dehydration, extreme thirst (polydipsia) and increased fluid intake.

Weight loss

In diabetes, cells fail to metabolise glucose in the normal manner, effectively becoming starved. This results in weight loss due to:

•
gluconeogenesis from amino acids and body protein, causing muscle wasting, tissue breakdown and further increases blood glucose

•
catabolism of body fat, releasing some of its energy and excess production of ketone bodies.

Ketosis and ketoacidosis

In the absence of insulin to promote normal intracellular glucose metabolism, alternative energy sources must be used instead and increased breakdown of fat occurs (see
Fig. 12.43, p. 310
). This leads to excessive production of weakly acidic ketone bodies, which can be used for metabolism by the liver. Normal buffering systems maintain pH balance so long as the levels of ketone bodies are not excessive.
Ketosis
(see
p. 310
) develops as ketone bodies accumulate. Excretion of ketones is via the urine (ketonuria) and/or the lungs giving the breath a characteristic smell of acetone or ‘pear drops’.

When worsening ketosis swamps the compensatory buffer systems, control of acid–base balance is lost; the blood pH falls and
ketoacidosis
occurs. The consequences if untreated are:

•
increasing acidosis (↓ blood pH) due to accumulation of ketoacids

•
increasing hyperglycaemia

•
hyperventilation as the lungs excrete excess hydrogen ions as CO
₂

•
acidification of urine – the result of kidney buffering

•
polyuria as the renal threshold for glucose is exceeded

•
dehydration and hypovolaemia (↓ BP and ↑ pulse) – caused by polyuria

•
disturbances of electrolyte balance accompanying fluid loss, hyponatraemia (↓ plasma sodium) and hypokalaemia (↓ plasma potassium)

•
confusion, coma and death.

Acute complications of diabetes mellitus

Diabetic ketoacidosis

This nearly always affects people with type I diabetes. Ketoacidosis develops owing to increased insulin requirement or increased resistance to insulin due to some added stress, such as pregnancy, infection, infarction, or cerebrovascular accident. It may occur when insufficient insulin is administered by a diabetic person during times of increased requirement. Severe and dangerous ketoacidosis may occur without loss of consciousness; the effects and consequences of diabetic ketoacidosis are outlined above.

Hypoglycaemic coma

This occurs in type I diabetes when insulin administered is in excess of that needed to balance the food intake and expenditure of energy. Hypoglycaemia is of sudden onset and may be the result of:

•
accidental overdose of insulin

•
delay in eating after insulin administration

•
drinking alcohol on an empty stomach

•
strenuous exercise.

It may also arise from an insulin-secreting tumour, especially if it produces irregular bursts of secretion. Because neurones are more dependent on glucose for their energy needs than are other cells, glucose deprivation causes disturbed neurological function, leading to coma and, if prolonged, irreversible damage.

Common signs and symptoms of hypoglycaemia include drowsiness, confusion, speech difficulty, sweating, trembling, anxiety and a rapid pulse. This can progress rapidly to coma without treatment.

Long-term complications of diabetes mellitus

These increase with the severity and duration of hyperglycaemia and represent significant causes of morbidity (poor health) and mortality (death) in people with both type I and type II diabetes.

Cardiovascular disturbances

Diabetes mellitus is a significant risk factor for cardiovascular disorders. Changes in blood vessels (angiopathies) may still occur even when the disease is well controlled.

Diabetic macroangiopathy

The most common lesions are atheroma and calcification of the tunica media of the large arteries. In type I diabetes these changes may occur at a relatively early age. The most common consequences are serious and often fatal:

•
ischaemic heart disease, i.e. angina and myocardial infarction (
p. 120
)

•
stroke (
p. 175
)

•
peripheral vascular disease.

Diabetic microangiopathy

This affects small blood vessels and there is thickening of the epithelial basement membrane of arterioles, capillaries and, sometimes, venules. These changes may lead to:

•
peripheral vascular disease, progressing to gangrene and ‘diabetic foot’

•
diabetic retinopathy (see
p. 205
)

•
diabetic nephropathy (
p. 345
)

•
peripheral neuropathy (
p. 181
), especially when myelination is affected.

Infection

Diabetic people are highly susceptible to infection, especially by bacteria and fungi, possibly because phagocyte activity is depressed by insufficient intracellular glucose. Infection may cause:

•
complications in areas affected by peripheral neuropathy and changes in blood vessels, e.g. in the feet when sensation and blood supply are impaired

•
boils and carbuncles

•
vaginal candidiasis (thrush)

•
pyelonephritis (
p. 345
).

Renal failure

This is due to diabetic nephropathy (
p. 347
) and is a common cause of death in those with diabetes.

Blindness

Diabetic retinopathy (
p. 205
) is the commonest cause of blindness in adults between 30 and 65 years in developed countries. Diabetes also increases the risk of early development of cataracts (
p. 204
) and other visual disorders.