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Metabolic Diseases

Diabetes Mellitus


Diabetes mellitus (DM) is the most common and possibly one of the oldest metabolic disorders in the world. It is characterised by multi-system dysfunction due to an elevated blood sugar level. Susruta has described this disorder in his medical text.



Types of Diabetes

There are two broad types of diabetes mellitus:

i. Primary or type I Insulin Dependent Diabetes Mellitus (IDDM), which develops before the age of forty.
This is often seen in children too. It is almost certain that the disease is auto-immune in nature and that there is a genetic predisposition. The body's defense mechanism attacks the pancreas and destroys the islets, and the level of endogenous insulin is very low. The situation is similar to rheumatoid arthritis. An environmental factor of viral etiology is also thought to play an important role in the genesis of the disease. The situation can be summarised as: genetic predisposition -->> environmental insulitis -->> activation of auto immunity -->> destruction of the cells of the pancreas -->> diabetes.

ii. Type II Non-Insulin Dependent Diabetes Mellitus (NIDDM), which is the most common form of the disease and accounts for 90% of all diabetics.
This usually begins after middle age. There are three sub-types: non-obese, obese, and maturity-onset diabetes of the young (MODY). Endogenous insulin is adequate but, in the face of stress, may fail. The defect here can be either one of the beta cells failing to produce enough insulin or an impaired tissue sensitivity to insulin.
There can also be secondary diabetes which is caused by (i) pancreatic disease due to damage to cells of the gland; (ii) drugs like diuretics and steroids which can increase the blood sugar level; (iii) hormonal abnormalities — over functioning of the pituitary and adrenal glands; (iv) insulin receptor abnormalities; and (v) genetic disorders.
In IDDM, by the time diagnosis is made, 90% of the beta cells are destroyed. Little progress has been made in the pathogenesis of NIDDM.



Symptoms

The patient usually complains of passing a larger than normal volume of urine, with increasing frequency every day. The osmotic effect of increased levels of blood glucose causes more thirst and hunger. These classic symptoms, however, are not the normal presentation. Usually the disease is discovered on routine examination. Sometimes the patient suffers a frozen shoulder and this can be a manifestation of diabetes. Lethargy, weight loss and easy susceptibility to infections, particularly of the skin (like a simple boil or a fungal infection), excessive hunger, craving for sweets and sweating are some of the other symptoms.

Diabetes may co-exist with other disease states. In this situation, it might be the diabetic condition that has made the patient prone to infection. Tuberculosis is the most common clinical condition which may also be present. Some others are malignancy, HIV infection, surgical stress, a heart attack, febrile illnesses and renal disease.

Normally, the fasting level of blood glucose is less than 90 mg/dL and the post-prandial (2 hour) level is less than 120 mg/dL. If the post-prandial sugar level is between 150 and 200 mg, the condition is labelled as an impaired tolerance and, if above 200, it is frank diabetes.



Complications of diabetes

Acute complications include ketoacidosis, a state of metabolic stress with overproduction of chemicals called ketone bodies. The patient suffers nausea, vomiting, dehydration and, if untreated, coma supervenes. This is always treated with insulin and replacement of electrolytes. The fluid deficit is around three to five litres. Any kind of stress — mental tension, a major infection or even a mere boil, fever, etc. can precipitate an acute increase in blood sugar level. Mental stress is the commonest situation that raises blood sugar level. Stress drives the adrenal glands and this raises the blood sugar. Stress also prevents orderly secretion from the pancreas, which is unable to handle the extra load. Eventually, the majority of diabetic patients suffer long-term complications which can be prevented if adequate precautions are taken to stem the disease in the early stages by a healthy diet and, more importantly, by the inculcation of a daily exercise schedule.



Long term complications of diabetes

Cardiovascular problems: The rate of progression of atherosclerosis is rapid due to the elevated blood sugar. Blockage of peripheral blood vessels creates intermittent claudication (pain when walking, which varies from patient to patient) in the legs. Silent heart attacks (due to narrowed coronary vessels) are the rule because of damage to the cardiac nerves that normally transmit the pain sensation of angina. Sudden rhythm changes in the electrical conduction of the nerves of the heart can cause what are known as arrhythmias. These may manifest as a medical emergency with the heart coming to a total standstill. Sudden death due to autonomic cardiac dysfunction is well known. Hypotension and sudden fainting due to autonomic imbalance are also common.

Eye complications: Diabetic retinopathy is one of the leading causes of blindness. The basic reason is hypoxia to the blood vessels which causes the various forms of retinopathy. The eye lesions are classified into background retinopathy and proliferative type. Because of hypoxia, there occurs increased capillary permeability, venous dilatation, leakage of protein and lipids, infarcts in the retina called `cotton wool spots' which are nothing but areas of dead tissue, bulging of the lining of blood vessels and haemorrhages.

New vessels may form due to hypoxia. The stimulus for new vessel formation is lack of oxygen. These new vessels affect vision and cause traction on the retina and subsequent retinal detachment. Photo-coagulation is the treatment for neo-vascularisation. Some loss of peripheral vision may occur. About 85% of patients develop eye -complications.

Diabetic Nephropathy: Renal disease due to diabetes is a leading cause of mortality. The minute blood vessels undergo thickening and deposition of albumin and globulin material occurs. Atherosclerosis is rapid in the diabetic kidney. The cells of the kidneys shrink due to loss of blood supply, resulting in an ischaemic shrunken kidney. There is loss of albumin in the urine to the extent of more than 30 mg to 300 mg per day. Recurrent kidney infections are also common. There is no specific therapy for diabetic renal disease. Renal transplantation offers a solution if renal failure occurs, but there may be other associated complications that may offer poor results. Associated hypertension has to be aggressively treated.

Diabetic Neuropathy: This affects every part of the nervous system with the exception of the brain. There is de-myelination of the nerves due to ischaemic changes in the minute blood vessels that supply the nerves. Loss of nerve function causes symptoms like sensory and motor disturbances, severe pain, and altered sensation in the area of the nerve, the so-called diabetic polyneuropathy. The nerves innervating the joints are damaged. Pain in the joints due to wrong usage goes unnoticed as the nerves that transmit such pain to the cerebral cortex and spinal cord are damaged by excess blood sugar. This results in trauma to the joints, with the affected joints becoming deformed and 'dead'.

Sudden paralysis of any of the cranial nerves can occur. Spinal nerves are also affected, leading to pain in the muscle innervated (diabetic amyotrophy). Sometimes the affected area can also burn like fire.

Gastrointestinal Conditions: Autonomic dysfunction (imbalance between sympathetic and parasympathetic systems) affects the gastro-intestinal tract, resulting in delayed gastric emptying, constipation or diarrhoea. The impaired colonic motility causes stagnation of bowel contents and colonisation by pathogenic bacteria and infection. This diarrhoea responds to the antibiotic tetracycline but the mechanism is ill understood. Bladder dysfunction or impotence can occur.

Skin Disorders: Diabetic foot ulcers are a dreaded problem. The elevated blood sugar leads to altered and defective protein synthesis and abnormal collagen formation, and the tissue formed is easily susceptible to trauma. Blockage to the minute blood vessels also causes ischaemic necrosis of the skin and gangrene can result with added infection. This leads to easy breakdown of skin and formation of ulcers; and, since the nerves are damaged, the pain is not noticed even if there is gross infection. Healing of wounds is delayed due to poor circulation and low resistance of the tissues in a high sugar medium. The skin on the surface of the shin is affected by certain specific lesions. The deposition of lipid-laden macrophages on the buttocks, back of the elbows and knees constitute what are known as xanthomas.



Causes of complications

This is not known for sure. A substance called sorbitol, a metabolite of glucose formed by activation of different chemical reactions, acts as a tissue toxin and is thought to be responsible for all lesions. A second mechanism is the formation of altered proteins in the body. The lipoproteins are also affected. Altered collagen traps this changed lipoprotein in the vessel walls. Thus blockage of vessels is accelerated. The lipid fractions in the blood are raised. Hyperviscosity, with abnormal aggregation of platelets, occurs.



Medical Management

Patient education is very important. Physicians must spend time to explain that this is a controllable situation and one need not despair. Patients too often do not comply. They abuse their diet and yet expect the blood sugar to remain under control. Firstly, a strict dietary regimen is very important. Secondly, exercise is very valuable. A diabetic may manage without medication, but he or she cannot manage without exercise and a healthy diet. Exercises like jogging and cycling increase the rate of entry of sugar into the cells and improve insulin sensitivity. As the cells are metabolically very active during exercise, they consume greater amounts of sugar and the blood levels of sugar reduce. The quantity and type of exercise needed varies from patient to patient and has to be monitored.

The goal of therapy is to maintain blood glucose to as near normal as possible. This is associated with fewer complications in the long run. The danger of low blood sugar during therapy has to be carefully tackled. Self-monitoring of glucose is convenient though regular hospital check-ups are important. There are a variety of user-friendly gadgets for home monitoring. Periodic laboratory check-ups are essential for counter checks.

Control through diet
Dietary modification depends upon the type of food the patient is exposed to; and the correct balance of proteins, fats and carbohydrate is to be taught. Generally, a low fat, high protein diet with normal carbohydrate intake is advised. If the patient does not exercise regularly, carbohydrate content is to be reduced. Protein is important unless renal disease is present. A young active diabetic needs around 1800 to 3000 kcal per day. The elderly diabetic needs around 1000 to 1800 kcal, and an obese middle-aged patient needs 1000 to 1600 kcal.

In most diabetic diets, calories derived from carbohydrate is around 45% to 55%, from protein 15% to 20%, and from fat 30% to 35%. This is not a strict classification and there are any number of modifications possible from patient to patient. The intake of protein may be around 60 to 110 gm. That of fat is around 50 to 150 gm and of carbohydrate around 200 gm. For obese patients, reduction in weight is important as blood sugar level improves with loss of weight.

Strict monitoring of this regimen is necessary. A measured diet is healthier than an unmeasured one. Fibre lowers the absorption of sugar from the intestine and reduces post-prandial increase in blood sugar. Beans, legumes, guar gum and bran help to control and reduce absorption of the LDL type of cholesterol. Though artificial sweeteners can be used, they are better avoided as they are chemicals. Non-vegetarian food, with its high fat content, is not recommended. Alcohol is strictly prohibited.

Medication
The treatment of IDDM is primarily by insulin. There are several kinds of insulin — short-acting, ultra short, intermediate and long-acting — which are used as the situation warrants. For example, if the sugar has to be normalised very rapidly, short-acting types may be used. Insulin lowers sugar in all kinds of diabetes. This delivery should be similar to endogenous natural pancreatic insulin; but then, man can never duplicate nature. At best a mechanical pseudo-imitation can be manufactured. The release of insulin is influenced by the state of mind which, in turn, influences sleep and so many other mental and physiological factors which regulate insulin release which no machine can sense and adjust.

The delivery of insulin can be by a syringe, by a jet injection or by portable infusion pumps. Treatment with insulin does have problems. Hypoglycaemia is the most common dysfunction. Each method of delivery has its inherent problems. For example, when portable infusion pumps are used, signs of infection must be carefully watched for. The areas where insulin has been injected can atrophy, causing skin problems. The body can develop allergy, resistance, antibodies to the insulin delivered; and increased dosage of insulin may be needed as the disease progresses. Insulin from human sources is less irritative to the body, less stimulative to antibody systems and is better tolerated than most other kinds.

Drugs used to treat diabetes, like tolbutamide, glibenclamide, glipizide, glyburide, glicazide, etc (the sulphonylureas), lower blood glucose in patients capable of endogenous insulin production. These are indicated for type II diabetes and in non-pregnant adults and most types of secondary diabetes. They stimulate the islets to release insulin and possibly decrease insulin resistance. Side effects include hypoglycaemia, rash, nausea and an increased risk of cardiovascular mortality. Drugs are the first line method of treatment if the situation allows it. In the elderly, who cannot try other modalities of treatment, these are very helpful.

Even for the middle-aged with maturity onset diabetes, it might be easy to reduce the sugar levels with a drug or insulin and then switch over to, or add, the important component of exercise. In the long run, unless the tool of exercise is introduced, metabolic control is not satisfactory in all the types of diabetes.

Role of exercise
The effect of exercise in IDDM and NIDDM stems from the fact that exercising muscles increase their uptake of glucose 10 to 20 times, depending upon the duration and intensity. High intensity exercise reduces blood glucose and fatty acids are used for energy. Exercise training enhances the action of drugs and increases insulin sensitivity. If the patient is obese, the development of such sensitivity takes a longer time. Blood sugar must be fairly under control before this is begun.

Vigorous exercise training helps normalise blood sugar, either alone or in combination with dietary modification and drugs. For type I diabetics, regular exercise is important. This improves cardiac function and lowers excess lipids. Individual monitoring of the response to exercise is important. If exercise sessions are intense, it is advisable to decrease insulin dosage and raise carbohydrate content. If any complication is present, like peripheral neuropathy, irritative exercises like jogging which can cause foot damage should be avoided as the patient cannot feel the pain due to the nerves being damaged by excess blood sugar.

Heavy meals should be eaten one to two hours before strenuous physical activity. This avoids the coincidence of meal and insulin effect. If the patient has any other existing complications like retinopathy or renal disease, he or she should avoid strenuous exertion to prevent rise in systolic blood pressure which can damage the weakened arteries.



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