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DIABETES MELLITUS|Types of diabetes mellitus|Pathophysiology of diabetes mellitus|Diabetes mellitus symptoms|Medical world

Diabetes mellitus

INTRODUCTION

This is the most common endocrine disorder; the primary sign is hyperglycaemia which is accompanied by varying degrees of disruption of carbohydrate and fat metabolism. DM is caused by complete absence of, relative deficiency of or resistance to the hormone insulin.


CLASSIFICATION OF DIABETES MELLITUS

Box 1.1 shows the classification of diabetes. Primary DM is categorised as type 1 or type 2.

Primary
  • Type 1 diabetes mellitus
  • Type 2 diabetes mellitus

  • Secondary

    due to other situations, e.g:

  • acute or chronic pancreatitis
  • some drug therapy, e.g. corticosteriods
  • other endocrine disorders involiving hormones that increase plasma glucose levels, e.g. growth hormone, thyroid hormones, cortisol.

  • Gestational diabetes

    this develops during pregnancy and may disappear after delivary but often recurs in later life. it is associated with birth of heavier than normal and stillborn babies, and deaths shortly after birth.


    n secondary DM, the disorder arises as a result of other conditions, and gestational diabetes develops in pregnancy. The incidence of type1 and 2 DM, especially type 2, is rapidly increasing worldwide.


    Table 1.2 shows some distinguishing features of type 1 and 2 DM.

    ... Type 1 Type 2
    Age of onset usually childhood Adulthood and later life
    Body weight at onset Normal or low Obese
    Onset of symptoms Weeks Months/years
    Main course Autoimmune Obesity,lack of exercise
    Insulin requirments 100% of cases Up to 20% of cases
    Ketoneuria Yes No
    Complications at diagnosis No Up to 25%
    Family history Rare Common


    TYPES OF DIABETES MELLITUS

    Type 1 diabetes mellitus

    Previously known as insulin-dependent diabetes Mellitus, this occurs mainly in children and young adult; the onset is usually sudden and can be life threatening there is severe deficiency or absence of insulin secretion due to destruction of β-islet cells of the pancreas. Treatment with injection of insulin is required. There is usually evidence of an autoimmune mechanism that destroys β-islet cells. Genetic predisposition and environmental factors, including viral infections, are also implicated.


    Type 2 diabetic 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: predominantly affecting middle-aged and older adults
  • Genetics factors

  • Its onset is gradual, often over many years, and it frequently 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 into cells. Treatment involves diet and/or drugs, although sometimes insulin injection and required.


    CLINICAL FEATURES

  • Drowsiness
  • Confusion
  • Speech
  • Difficulty
  • Sweating
  • Trembling
  • Anxiety and a rapid pulse.

  • PATHOPHYSIOLOGY

    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 sam as in the the blood and, although diabetes raises the renal threshold for glucose, it is not all reabsorbed by the tubules. The glucose remaining in the filtrate raises its volume of urine is increased (polyuria) this result its electrolyte imbalance and execration of urine of high specific gravity. Polyuria leads to dehydration, extreme thrist (polydipsia) and increased fluid intake.



    Weight loss

    The cells are essentially staved of glucose because, in the absence of insulin, they are unable to extract it from the bloodstream, leading to derangement of energy metabolism as cell must use alternative pathways to produce the energy they need. This result in weight loss due to:

  • Gluconeogenesis from amino acids and body protein, causing muscle wasting, tissue breakdown and further increases in blood glucose
  • Catabolism of body fat, releasing some of its energy and excess production of ketone bodies.
  • This is very common in type 1 DM and sometimes occurs I type 2 DM.

  • Ketosis and ketoacidosis

    This nearly always affects people with type 1 DM. In the absence of insulin to promote normal intracellular glucose metabolism, alternative energy sources must be used instead and increased breakdown of fat occurs. This leads to excessive production of weakly acidic ketone bodies, which can be used for metabolism by the liver. Normal buffering system maintain PH balance so long as the levels of ketone bodies are not excessive. Ketosis develops as ketone bodies accumulate. Execration of ketones is via the urine and/or the lungs giving the breath a characteristics smell of acetone or 'pear drops'.

    Ketoacidosis develops owing to increased resistance to insulin due to some added stress, such as pregnancy, infection, infraction, or cerebrovascular accident. It may occur when insufficient insulin is administrated during times of increased requirement. Severe and dangerous ketoacidosis may occur without loss of consciousness. 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 due to accumulation of ketoacids
  • Increasing hyperglycaemia
  • Hyperventilation as the lungs excrete excess hydrogen ions as CO2
  • Confusion , coma and death.

  • COMPLICATIONS OF DIABETES MELLITUS

    Acute complications of diabetes mellitus

    Diabetic ketoacidosis

    The effects and consequence of diabetic ketoacidosis are

    Hypoglycaemia coma

    This occurs when insulin administered is in excess of that needed to balance the food intake and expenditure of energy. Hyperglycaemia is of sudden onset and may be 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.


    Long-term complications of diabetes mellitus

    These increase with the severity and duration of hyperglycaemia and represent significant causes of morbidity and mortality in people with both type 1 and type 2 diabetes.


    Cardiovascular disturbance

    Diabetes mellitus is a significant risk factors for cardiovascular disorders. Blood vessels abnormalities 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 1 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 infraction

  • Stroke
  • Peripheral vascular disease

  • Diabetic microangiopathy

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

  • Peripheral vascular disease, progressive to gangrene and diabetic 'foot'
  • Diabetic retinopathy and visual impairment
  • Diabetic retinopathy and chronic renal failure
  • Peripheral neuropathy causing sensory deficits and motor weakness, especially when myelination is affected.

  • Infection

    DM predisposes to infection, especially by bacteria and fungi, possibly because phagocyte activity is depressed by insufficient intracellular glucose. Infection may cause:

  • Boils and carbuncles
  • Vaginal candidiasis
  • Pyleonephritis
  • Diabetic foot
  • Renal failure

    This is due to diabetic nephropathy and is a common cause of death.


    Visual impairment and blindness

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


    Diabetic foot

    Many factors commonly present in DM contribute to the development of this serious situation. Disease of large and small blood vessels impairs blood blood supply to and around the extremities. If peripheral neuropathy is present, sensation is reduced. A small injury to the foot may go unnoticed, especially hen there is visual impairment. In DM healing is slower and injuries easily worsen if aggravated, e.g. by chafing shoes, and often become infected. An ulcer may form and the healing process is lengthy, if at all. In severe cases the injured area ulcerates and enlarged, and may become gangrenous, sometimes to the extent that amputation is required.

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