Diabetes is a disorder of metabolism- the way our bodies use digested food for grpwth and energy. Most of the food we eat is broken down into glucose, the form of sugar in the blood. Glucose is the main source of fuel in the body.
After digestion glucose passes into the blood stream, where it is used by cells for growth and energy. Insulin is a hormone produced by the Beta cells (B cells) of pancreas, a large gland behind the stomach. When we eat the pancreas is supposed to automatically produce the right amount of insulin to move the glucose from the blood into our body cells. In people with diabetes, however the pancreas either produces little or no insulin or the cells do not respond appropriately to the insulin that is produced. Glucose builds up in the blood, overflows into the urine and passes out of the body. Thus the body loses its main source of fuel even though the blood contains large amounts of glucose.
Diabetes is classified on the basis of the pathogenesis process that leads to hyperglycemia. The two broad categories of DM are designated type 1 and type 2. Type 1A DM results from auto immune beta cell destruction, which leads to insulin deficiency. Individuals with type 1 B DM lack immunologic markers indicative of an auto immune destructive process of beta cells. However they develop insulin deficiency by unknown mechanism and are ketosis prone. Many of these individuals are either African- American or Asian in heritage.
Patients with type 1 diabetes appear to have a genetic susceptibility to develop diabetes; they are susceptible to a variety of triggers (viral, environmental, or toxin) that stimulate immunologic destruction of B cells. Individuals with genetic susceptibility have normal beta cells mass at birth but begin to loose beta cells secondary to auto immune destruction that occurs over months to years. After 80-90% of beta cells are destroyed, hyperglycemia develops and diabetes is diagnosed. In studies of identical twin pairs in which one twin has type 1 diabetes, antibodies to the islet cell (ICA) and to insulin (IAA) may be positive for several years in the non diabetic twin before overt diabetes develops. Autoantibodies of glutamate deccarboxylase (GAD65 –AA) are also found and may be an extremely good marker of type 1 DM. as B cell mass declines, insulin secretion decreases until the available insulin is no longer adequate to maintain normal blood glucose levels. Although the specific genes related to type I diabetes have not been found, patients with type I diabetes are more likely to express DR3 and/or DR4 class II HLA molecules. (About 90-955 of patients with type I diabetes compared with 50 to 60 % in the general population have these HLA haplotypes.
Type II diabetes has a powerful genetic predisposition( 90-100% concordance in identical twin pairs), although the exact genetic basis is not known yet. It is likely that more than one pathogenic mechanism will be found. Many patients with type II diabetes are asymptomatic and their diabetes is either diagnosed during screening for diabetes or when the patient is seen for unrelated medical problem. These patients exhibit peripheral insulin resistance along with insufficient pancreatic B cell secretion of insulin. As hyperglycemia develops glucotoxicity occurs, which further decreases insulin secretion. The liver also is resistant to the inhibitory effect of insulin, and as a result, hepatic gluconeogenesis is not adequately suppressed, leading to fasting hyperglycemia. (Dennis L.Kasper, Anthony s. Fauci, Dan L. Longo 2005)
The worldwide prevalence of type I and II DM is increasing worldwide.
The prevalence of type I DM is equal among males and females, but is more common in whites than in non-whites. Data from WHO ‘s multinational project for childhood diabetics indicate that type I Dm is rare in most African, American Indian, and Asian populations. However some northern European countries, including Finland and Sweden, have high rates of type I DM. The reason for these differences is unknown.
The prevalence of type II DM is expected to rise more rapidly in future because of increasing obesity and reduced activity levels. Most patients who develop type II diabetes are obese, and obesity itself is associated with insulin resistance, which further worsens the diabetic state. Type II diabetes is becoming increasingly common because more people are living longer (diabetes increases with age). It is also occurring ore frequently in younger people, as more individuals are exposed to high-calorie Western diets, leading to childhood obesity. The prevalence is similar in men and women throughout most age ranges but is slightly greater in men> 60 years. The onset of type II DM occurs, on average, at an earlier age in ethnic groups other than non-Hispanic whites.
The experts suggest that high risk factors for diabetes include;
Being more than 20% above ideal body weight or having a BMI of > 27.
Having a mother , father, brother or sister with diabetes.
Being African American, Alaska native, American Indian, Asian American, Hispanic American, or Pacific Islander American.
Giving birth to a baby weighing more than 9 pounds or having diabetes during pregnancy.
Having blood pressure at or above 140/90 (mmHg).
Having abnormal blood lipid levels, such as high density Lipoprotein (HDL) cholesterol less than 35mg/dl or triglycerides > 250 mg/dl.
Having abnormal glucose tolerance when previously tested for diabetes.
Subjective and Objective findings:
The classical symptoms of increased thirst, increased or frequent urination especially at night and weight loss are prominent in type I diabetes, but are often absent with type II patients, many of whom are asymptomatic or have non specific complaints such as chronic fatigue and malaise. Uncontrolled diabetes is associated with blurred vision, increased susceptibility to infection in the form of boils and genital candidiasis, and complains of pruritus vulva and balanitis.
Patients with type I DM often have no objective findings attributable to diabetes, but weight loss is common. In the fulminating case with ketoacidosis, the striking features are those of salt and water depletion, with loss of skin turgor, furred tongue and cracked lips, tachycardia, hypotension, and reduced intraocular pressure. Breathing may be deep and sighing, the breath is usually fetid and fruity smell of acetone may be present. Mental apathy, confusion or a reduced conscious level may be present.
The Objective findings in patients with type II DM at presentation depend on the mode of presentation. More than 70% are overweight, and obesity may be central (truncal or abdominal) in distribution. Hypertension is present in 50% of patients with type II DM. Although hyperlipidemia is also common, skin lesions such as xanthelasma and eruptive xanthomata are relatively rare. Unusually sometimes patients present with long term complications of diabetes. They may complain of paresthesia, pain and muscle weakness in the legs with signs of peripheral neuropathy or foot ulceration, or deterioration of vision from cataract or retinopathy. Signs of macro vascular disease are common and may include diminished or impalpable pulses in feet, bruits over the carotid or femoral arteries and ischemic toes. Cutaneous features of diabetes include a dermopathy with trophic brownish scars on the shins and the much rarer necrobiosis lipoidica diabeticorum. (Dennis L.Kasper, Anthony s. Fauci, Dan L. Longo 2005)
When the symptoms suggest diabetes you should test urine for glucose and ketones. If possible the test for urinary glucose should be performed on urine passed 1-2 hours after a meal since this will detect more cases of diabetes than fasting urine specimen. Glucosuria always warrants full assessment. Ketonuria may be found in normal people who have been fasting or exercising vigorously for long periods or vomiting or have been eating a diet high in fat and low in carbohydrates. Ketonuria is therefore not a pathognomonic of diabetes but, if associated with glucosuria, the diagnosis of diabetes is practically certain. In addition to urinanalysis measurement of fasting (FBS) and random (RBS) blood sugar levels of patient should be checked. The criteria for labeling a patient as diabetic is that his two fasting blood sugar values should be of 126mg/dl or greater, one random blood sugar level of 200mg/dl. If the fasting glucose meet these criteria and oral glucose tolerance test is not required. If the patient has no diabetic symptoms diagnosis should not be based on a single glucose value. If there is any doubt, the 2-hour value in an OGTT should be used (look for a blood sugar level of 200mg/dl in a three hours 75gm glucose tolerance test, one value at two hours). If the fasting blood sugar concentration is between 115 and 140mg/dl, hemoglobin A1c level should be measured. Patient with the FPS concentration between 115 and 140mg/dl probably have an abnormality of glucose metabolism and should be followed carefully for the development of treatable diabetes. For monitoring the long term control hemoglobin A1c is measured intermediately. A level of greater than 7.0% indicates the presence of diabetes that requires treatment. (Dennis L.Kasper, Anthony s. Fauci, Dan L. Longo 2005)
Raised blood sugar has been associated with various disorders of insulin target tissues (liver muscle, and adipose tissue) other secondary causes of hyperglycemia include endocrine disorders-often specific endocrine tumors-associated with excess production of growth hormone, glucocorticoids, catecholamines, glucagons, or somatostatin. A rare syndrome of extreme insulin resistance associated with acanthosis nigricans in home a circulation immunoglobulin binds to insulin receptors and reduces there affinity to insulin.
Medications such as thiazide diuretics, phenytoin and high dose glucocorticoids can produce hyperglycemia that is reversible one the drug are discontinued. Chronic pancreatitis reduces the number of functioning B cells and can result in a metabolic derangement very similar to that of genetic type 1 diabetes except that a concomitant reduction in pancreatic A cells may reduce glucagons secretion so that relatively lower doses of insulin replacement are needed.
Insulin dependent diabetes is occasionally associated with Addison’s disease and autoimmune thyroiditis. This occurs more commonly in women.
Non-diabetic glucosuria is a benign asymptomatic condition wherein glucose appears in the urine despite the normal amount of glucose in the blood. As many as fifty percent of pregnant women normally have demonstrable sugar in the urine especially during the third and fourth month. This sugar is practically always glucose except during the late weeks of pregnancy, when lactose may be present.
Warning Signs or “Red Flags”
Elevated blood sugar
Not eating and/or not taking your insulin
Unexplained elevated blood sugar without obvious signs of illness
Unable to eat for long periods of time due to medical tests or surgery
Diabetes mellitus is the chronic disease that requires ongoing medical care as well as patient and family education both to prevent and to reduce the risk of long term complications. Patient’s motivation and education on drugs, diet and other issues mentioned below is the key to success. Aim to avoid complications which include hypoglycemia as well as long term consequences of hyperglycemia.
Monitoring blood or urine glucose and adapting treatment accordingly.
Explain to the patient that when he is ill more, not less insulin is needed. Recognition and treatment of hypoglycemia (for example sweet/ sugar candies) is essential.
Regular follow up and regular exercise decreases insulin resistance and decreases risk of myocardial infarction. A well balanced nutritious diet remains a fundamental element of therapy aiming at weight reduction by caloric restrictions. Healthy eating includes decreased saturated fats, decreased sugar, increased starch/carbohydrates, and moderate protein. If renal impairment or micro albuminuria than restrict protein and consider ACE inhibitors.
Strict plasma glucose control does reduce CNS, renal and retinal damage.
Strict blood pressure control is as effective in reducing micro vascular disease, but also reduces macrovascular disease and motility. This emphasizes the importance of the global assessment of an individual risk- glucose, blood pressure, cholesterol, and smoking history. Never treat DM in isolation treat the patient as the whole.
The patient in the given case history as evidenced by her past body weight and current weight loss of 10 pounds, proteinuria , glucosuria, no urinary ketones heralds that she is suffering from type II diabetes. After confirming the diagnosis by measuring her FBS and RBS drug treatment should be started. Along with that her serum cholesterol and lipoprotein levels should also be checked. Her kidney function should be tested by ordering for serum creatinine level. Metfromin (a biguanide) should be started in the dose of 500- 1000 mg orally at an interval of eight hours. As this drug causes hepatic and renal impairment, special precautions should be taken. Aspirin and Statins decreases the overall cardiovascular risks. Aspirin should be given in a dose of 75 mg /day and the simvastatin (statin) in a dose of 20 mg/day. Patient should be asked for follow-up visit after 7 weekdays. At this time her blood sugar level is rechecked and patient is reassessed. The dose adjustment may take sometimes and a number of visits are required. Once the dose is adjusted and required response has began patient could be asked for self monitoring of her blood sugar at home. If she finds any fluctuation or abnormal result she should see her care provider at once.
Dennis L.Kasper, Anthony s. Fauci, Dan L. Longo (2005). Harrison’s Principles of Internal medicine.