DM – Diabetes Mellitus
What is it?
A disease caused by deficiency in the production and/or action of insulin, which leads to acute symptoms and characteristic chronic complications.
The disorder involves the metabolism of glucose, fats and proteins and has severe outcomes both when its onset is rapid and when it’s slow. Currently, it constitutes a public health problem for the number of people presenting the illness, especially in Brazil.
It presents several clinical forms, being classified as:
Type I DM –
Caused by the obstruction of the beta-cells of the pancreas, usually as a result of na auto-immune disease, leading to total insulin deficiency.
Type II DM-
Caused predominantly by a state of resistance to insulin action associated with a relative deficiency in its secretion.
Other forms of DM-
Condition associated to genetic disorders, infections, pancreatic diseases, use of medications, drugs, or further endocrine diseases.
Circumstances in which the diagnosis is made during pregnancy in a patient without previous glucose elevation.
How does it develop?
As can be observed in the item above (clinical forms), various are the causes of DM.
In type I DM, the underlying cause is an autoimmune disease that damages irreversibly the insulin-producing pancreatic cells (beta cells). Thus, in the first months after the disease onset, several antibodies are detected in the patient’s blood, the most important being the anti-pancreatic isle antibody, the antibody to beta-cell enzymes (anti-glutanic acid decarboxilase antibodies – antiGAD, e.g.) and insulin antibodies.
In type II DM occur several mechanisms of resistance to insulin action, the main one being obesity, which is present in most patients.
In patients with other DM forms, what occurs in general is an anatomic lesion of the pancreas, resulting from diverse toxic aggressions either by alcohol, drugs, medications or infections, among others.
What does one experience?
DM symptoms result from glycemia elevation and chronic complications that develop in the long run.
The symptoms of glycemia elevation are:
|increased urine volume|
|increased number of urinations|
|appearance of an urge to urinate at night|
|fatigue, weakness, dizziness|
These symptoms tend to progressively worsen and may lead to severe complications, namely, diabetic ketoacidosis (in type I DM) and hyperosmolar coma (in type II DM).
The symptoms of complications involve visual, cardiac, circulatory, digestive, renal, urinary, neurologic, skin, and orthopedic complaints, amongst others.
A decompensated DM patient shows a blurred sight and refraction difficulty. Long-term complications involve reduction in visual accuracy and dark vision which can be associated to cataract or alterations in the retina called diabetic retinopathy. Diabetic retinopathy may lead to a significant compromise of the retina, even causing dettachment thereof, vitreal hemorrhage and blindness.
Diabetic patients show a higher prevalence of arterial hypertension, obesity and fat alterations. For these reasons, and, mainly, if there’s smoking associated, a heart disease may occur. The heart disease can involve the coronary arteries, the heart muscle, and the conduction system of the heart’s electric stimuli. As the patient usually also presents some degree of alteration of the heart nerves, cardiac alterations may not elicit any symptoms, being found out only in presence of more severe symptoms such as myocardial infarction, heart failure and arrhythmias.
The same factors associated to other complications make more frequent circulatory alterations that manifest themselves by the arteriosclerosis of several blood vessels. Frequent are the complications that obstruct main vessels as the carotid, aorta, iliac arteries and several others in the extremities. These changes are particularly important in the lower limbs (legs and feet), leading to a set of alterations that make up the so-called “diabetic foot”. This involves, in addition to circulatory changes, the peripheral nerves (peripheral neuropathy), fungal and bacterial infections and pressure ulcers. These alterations to amputation of the lower limbs, with grave impairment of life quality.
Diabetic patients can show compromise of the digestive tract innervation, with decrease in its motions, most notably at the level of the stomach and large intestine. These changes can cause symptoms of abdominal distension and vomiting with food residues and diarrhea. Diarrhea is characteristically nocturnal, and occurs without significant abdominal pain, often associated with the inability to retain the feces (fecal incontinence).
The compromise of the kidneys in the diabetic patient slowly evolves without provoking symptoms. When symptoms occur, usually they already imply a significant loss of renal function. These symptoms are: swelling of the feet, increase in arterial pressure, anemia, and loss of proteins via urine (proteinuria).
Diabetic patients can present difficulty emptying out their bladder as a result of loss of its innervation (neurogenic bladder). This change can bring about loss of renal function and works as a factor for urinary infection maintenance. In men, this alteration can be associated with erection difficulties and sexual impotence, in addition to aggravating symptoms related to prostate enlargement.
The compromise of the diabetic patient’s nerves may bring about acute neuritis (acute paralysis) in the nerves of face, eyes, and extremities. Chronic neuritis affecting the nerves of upper and lower limbs may also occur, causing progressive loss of vibratory sensitivity, tenderness to heat and touch. These alterations are the main factor for the appearance of modifications in the articular position and in the skin that appear in the foot sole, and may lead to ulcer formation (perforating plantar affliction). The most characteristic signs of neuropathy presence are the loss of sensitivity in hands and feet, and the emergence of deformities such as the loss of the plantar arch and “praying hands”, as well as complaints of tingling and shifts from cold to hot flashes in the feet and legs, chiefly at night.
Diabetic patients show a greater sensitivity for fungal skin infections (tinea corporis, intertrigo) and nail infections (onicomycosis). In the areas affected by neuropathy, formation of plaques and thickened skin, called hyperkeratosis, takes place, which can be the early manifestation of a perforation plantar ulcer.
The loss of sensitivity in the extremities leads to a number of deformities as flat feet, hammertoes, and degeneration of heels and knees (Charcot’s joint).
How does the doctor diagnose it?
The diagnosis can be presumed in patients presenting the classic symptoms and signs of the disease, namely: excessive thirst, increased urine volume and greater number of urinations (including the appearance of an urge to urinate at night), excessive hunger, and weight loss. As a large number of people don’t show these symptoms over a long period of time and, yet, have the disease already, an early diagnosis is recommended.
The laboratory diagnosis of DM is established by measuring glycemia in the serum and plasma, after a 8 to 12-h fast. As a result of the fact that a high rate of patients with type II DM discovers the disease too late, already with severe chronic complications, an early diagnosis and the monitoring of the disease are recommended in many situations. Screening the whole population is disputable though.
Risk factors for DM:
There are situations when risk factors for DM are present, as shown below:
|age 45 or older|
|family history of DM (parents, children, siblings)|
|low HDL-c or elevated triglycerides|
|coronary artery disease|
|previous gestational disease|
|children weighing over 4 kg, repeat miscarriages, or children’s death within the first days of life|
|use of medicines that elevate glucose (cortisones, thiazidic diuretics, and beta-blockers).|
These aim at attaining normal glycemia both at fast and after meals and managing associated metabolic alterations.
The treatment of a DM patient involves at least 4 important aspects:
|Diet program –||it’s the key element in the treatment of any kind of diabetic patient. The general goal is to help the individual to make changes in their dietary habits, allowing a suitable metabolic management. Also, the nutritional treatment must contribute to normalize glycemia, decrease cardiovascular risk factors, supply calories enough for maintaining a healthy bodyweight, prevent acute and chronic complications and promote the patient’s general health. To meet these goals, diet should be balanced as any healthy person’s , being customized according to each patient’s peculiarities, including age, gender, functional status, physical activity, associated diseases, and cultural, socioeconomic status.
Composition of the diet program
The diet must include 50-60% of carbohydrates, 30% of fats and 10-15% of proteins. Carbohydrates should preferably be complex and ingested at 5-6 portions a day. Fats must include at most 10% of saturated fats, which means that fatty meats, fried foods, whole daily products, sauces and creams rich in fats and sautéed foods or foods spiced with excess oil must be avoided. Proteins should correspond to 0.8-1.0 kg of the ideal bodyweight per day, which corresponds as a rule to 2 portions of meat a day. Additionally, the diet must be rich in fibers, vitamins and mineral salts, which is obtained by the consumption of 2-4 portions of fruits, 3-5 portions of vegetables, giving preference to whole foods. The habitual use of alcoholic beverage isn’t recommended, especially for obese patients with elevation of triglycerides and poor metabolic management. In general, 2 glasses of wine, one can of beer, or 40 ml of whiskey can be drunk twice a week, accompanied by some food, as alcohol can induce a reduction in sugar (hypoglycemia).
|Physical activity||All patients must be encouraged to practice regular physical activity, which can be a 30-40 min walk or equivalent exercises. Advice for getting started with a physical activity must include a suitable medical evaluation with the purpose of checking out the presence of neuropathies or cardiorespiratory alterations that could contraindicate physical activity and provoke further risk to the patient.|
|Medications, oral hypoglycemiant agents||These are useful drugs for managing type II DM patients, being contraindicated for type I. For obese and hypoglycemic patients, usually the initial medication can be metformine, sultonylurea or thiazolidinedione. Insulin is the key drug for type I DM patients, also being very important to type II DM patients that haven’t responded to treatment with oral hypoglycemiant agents.|
|Screening||Screening, detection and treatment of chronic DM complications must always be carried out according to several recommendations. This approach is indicated at 5 years of the diagnosis of type I DM, at the moment of the type II diagnosis, and subsequently on a yearly basis. This investigation includes eye bottom examination with dilated pupils, 24-h microalbuminuria or in sample, serum creatine and exercise stress test. A proper analysis of the lipid profile, the investigation of deep sensitiveness of the feet must be performed with mofilament and diapason, and a thorough exam of peripheral pulses must be carried out at every patient visit. Once complications have been detected, there are specific treatments which are further detailed in other articles on this site.|
How to prevent it?
DM prevention can only be undertaken in type II and forms associated with other pancreatic alterations. In type I DM, as this develops from autoimmune changes, these can be identified prior to sugar elevation in the blood. This early diagnosis cannot be confused with prevention though, as prevention isn’t available yet.
In type II DM, as a number of risk factors are well known, patients that carry these alterations can be monitored periodically and advised to adopt behaviors and measures that will remove them off the risk group.
That’s how patients with family history of DM must be oriented to:
|maintain a normal weight|
|perform regular physical activities|
|control arterial pressure|
|avoid medicines that may potentially damage the pancreas (cortisone, thiazidic diuretics.|
These measures, adopted early, can result in the non-appearance of DM in a genetically predisposed person, or lead to a delay in its onset and in the severity of its complications.