medicine

diabetes

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 18:24:00 +0000

Introduction

An understanding of the pathophysiology of diabetes rests upon knowledge of the basics of carbohydrate metabolism and insulin action. Following the consumption of food, carbohydrates are broken down into glucose molecules in the gut. Glucose is absorbed into the bloodstream elevating blood glucose levels. This rise in glycemia stimulates the secretion of insulin from the beta cells of the pancreas. Insulin is needed by most cells to allow glucose entry. Insulin binds to specific cellular receptors and facilitates entry of glucose into the cell, which uses the glucose for energy. The increased insulin secretion from the pancreas and the subsequent cellular utilization of glucose results in lowered of blood glucose levels. Lower glucose levels then result in decreased insulin secretion.

If insulin production and secretion are altered by disease, blood glucose dynamics will also change. If insulin production is decreased, glucose entry into cells will be inhibited, resulting in hyperglycemia. The same effect will be seen if insulin is secreted from the pancreas but is not used properly by target cells. If insulin secretion is increased, blood glucose levels may become very low (hypoglycemia) as large amounts of glucose enter tissue cells and little remains in the bloodstream.

Following meals, the amount of glucose available from carbohydrate breakdown often exceeds the cellular need for glucose. Excess glucose is stored in the liver in the form of glycogen, which serves as a ready reservoir for future use. When energy is required, glycogen stores in the liver are converted into glucose via glycogenolysis, elevating blood glucose levels and providing the needed cellular energy source. The liver also produces glucose from fat (fatty acids) and proteins (amino acids) through the process of gluconeogenesis. Glycogenolysis and gluconeogenesis both serve to increase blood glucose levels. Thus, glycemia is controlled by a complex interaction between the gastrointestinal tract, the pancreas, and the liver.

Multiple hormones may affect glycemia. Insulin is the only hormone that lowers blood glucose levels. The counter-regulatory hormones such as glucagon, catecholamines, growth hormone, thyroid hormone, and glucocorticoids all act to increase blood glucose levels, in addition to their other effects.

Type 1 Diabetes

The underlying pathophysiologic defect in type 1 diabetes is an autoimmune destruction of pancreatic beta cells. Following this destruction, the individual has an absolute insulin deficiency and no longer produces insulin. Autoimmune beta cell destruction is thought to be triggered by an environmental event, such as a viral infection. Genetically determined susceptibility factors increase the risk of such autoimmune phenomena.

The onset of type 1 diabetes is usually abrupt. It generally occurs before the age of 30 years, but may be diagnosed at any age. Most type 1 diabetic individuals are of normal weight or are thin in stature. Since the pancreas no longer produces insulin, a type 1 diabetes patient is absolutely dependent on exogenously administered insulin for survival. People with type 1 diabetes are highly susceptible to diabetic ketoacidosis. Because the pancreas produces no insulin, glucose cannot enter cells and remains in the bloodstream. To meet cellular energy needs, fat is broken down through lipolysis, releasing glycerol and free fatty acids. Glycerol is converted to glucose for cellular use. Fatty acids are converted to ketones, resulting in increased ketone levels in body fluids and decreased hydrogen ion concentration (pH). Ketones are excreted in the urine, accompanied by large amounts of water. The accumulation of ketones in body fluids, decreased pH, electrolyte loss and dehydration from excessive urination, and alterations in the bicarbonate buffer system result in diabetic ketoacidosis (DKA). Untreated DKA can result in coma or death.

Many patients with type 1 diabetes are initially diagnosed with the disease following a hospital admission for DKA. In a known diabetic patient, periods of stress or infection may precipitate DKA. More often, however, DKA results from poor daily glycemic control. Patients who remain severely hyperglycemic for several days or longer due to inadequate insulin administration or excessive glucose intake are prone to developing DKA.
Type 2 Diabetes

About 90% of diabetic Americans have type 2 diabetes. The prevalence of type 2 diabetes is higher in African Americans, Native Americans, Hispanics, and Pacific Islanders than it is in Caucasians. Most type 2 diabetes patients are overweight, and most are diagnosed as adults. The genetic influence in type 2 diabetes is greater than that seen with type 1. While concordance rates between monozygous twins for type 1 diabetes are about 30 to 50%, the rate is approximately 90% for type 2 diabetes. Although the genetic predisposition to type 2 diabetes is strong, no single genetic defect has been found. In addition to genetic influences, acquired risk factors for type 2 diabetes include obesity, advancing age, and an inactive lifestyle.

The underlying pathophysiologic defect in type 2 diabetes does not involve autoimmune beta-cell destruction. Rather, type 2 diabetes is characterized by the following three disorders: (1) peripheral resistance to insulin, especially in muscle cells; (2) increased production of glucose by the liver; and, (3) altered pancreatic insulin secretion. Increased tissue resistance to insulin generally occurs first and is eventually followed by impaired insulin secretion. The pancreas produces insulin, yet insulin resistance prevents its proper use at the cellular level. Glucose cannot enter target cells and accumulates in the bloodstream, resulting in hyperglycemia. The high blood glucose levels often stimulate an increase in insulin production by the pancreas; thus, type 2 diabetic individuals often have excessive insulin production (hyperinsulinemia). Over the years, pancreatic insulin production usually decreases to below normal levels. In addition to hyperglycemia, type 2 diabetic patients often have a group of disorders that has been called "insulin resistance syndrome" or syndrome X.

Obesity contributes greatly to insulin resistance, even in the absence of diabetes. In fact, weight loss is a cornerstone of therapy for obese type 2 diabetic patients. Insulin resistance generally decreases with weight loss. Obesity also may explain the dramatic increase in the incidence of type 2 diabetes among young individuals in the United States in the past 10 to 20 years. Once considered a disease of adults, type 2 diabetes has increased among America's youth in direct correlation with the increase in the average weight of children and young adults during that time period.

Type 2 diabetes usually has a slow onset and may remain undiagnosed for years. Approximately half of those who have type 2 diabetes are unaware of their disease. Unfortunately, the insidious nature of the disease allows prolonged periods of hyperglycemia to begin exerting negative effects on major organ systems. By the time many type 2 diabetic patients are diagnosed, diabetic complications have already begun. Type 2 diabetic patients do not require exogenous insulin for survival since they still produce insulin. However, insulin injection is often an integral part of medical management for type 2 diabetes. Unlike type 1 diabetic patients, individuals with type 2 diabetes are generally resistant to DKA because their pancreatic insulin production is often sufficient to prevent ketone formation. Severe physiologic stress may induce DKA in those with type 2 diabetes. Long periods of severe hyperglycemia may result in hyperosmolar nonketotic acidosis. Hyperglycemia results in the urinary excretion of large amounts of glucose, with attendant water loss. If fluids are not replaced, the dehydration can result in electrolyte imbalance and acidosis.
Gestational Diabetes

Gestational diabetes occurs in approximately 4% of pregnancies in the United States. It usually develops during the third trimester and significantly increases perinatal morbidity and mortality.11 The proper diagnosis and management of gestational diabetes improves pregnancy outcomes. As with type 2 diabetes, the pathophysiology of gestational diabetes is associated with increased insulin resistance. Most patients with gestational diabetes return to a normoglycemic state after parturition; however, about 30 to 50% of women with a history of gestational diabetes will develop type 2 diabetes within 10 years.
Impaired Glucose Tolerance and Impaired Fasting Glucose
The conditions known as impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) represent metabolic states lying between diabetes and normoglycemia. People with IFG have increased fasting blood glucose levels but usually have normal levels following food consumption. Those with IGT are normoglycemic most of the time but can become hyperglycemic after large glucose loads. IGT and IFG are not considered to be clinical entities; rather, they are risk factors for future diabetes. The pathophysiology of IFG and IGT is related primarily to increased insulin resistance whereas endogenous insulin secretion is normal in most patients. Approximately 30 to 40% of individuals with IGT or IFG will develop type 2 diabetes within 10 years after onset.

Global Prevalence of Diabetes
Estimates for the year 2000 and projections for 2030

OBJECTIVE—The goal of this study was to estimate the prevalence of diabetes and the number of people of all ages with diabetes for years 2000 and 2030.

RESEARCH DESIGN AND METHODS—Data on diabetes prevalence by age and sex from a limited number of countries were extrapolated to all 191 World Health Organization member states and applied to United Nations’ population estimates for 2000 and 2030. Urban and rural populations were considered separately for developing countries.

RESULTS—The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% in 2000 and 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. The prevalence of diabetes is higher in men than women, but there are more women with diabetes than men. The urban population in developing countries is projected to double between 2000 and 2030. The most important demographic change to diabetes prevalence across the world appears to be the increase in the proportion of people >65 years of age.

CONCLUSIONS—These findings indicate that the “diabetes epidemic” will continue even if levels of obesity remain constant. Given the increasing prevalence of obesity, it is likely that these figures provide an underestimate of future diabetes prevalence.

* IDF, International Diabetes Federation
* WHO, World Health Organization

The number of people with diabetes is increasing due to population growth, aging, urbanization, and increasing prevalence of obesity and physical inactivity. Quantifying the prevalence of diabetes and the number of people affected by diabetes, now and in the future, is important to allow rational planning and allocation of resources.

Estimates of current and future diabetes prevalence have been published previously (1–3). Since these reports appeared, further epidemiological data have become available for several countries in Africa and the Middle East and for India. The sources of these data are identified in Table 1.

This report provides estimates of the global prevalence of diabetes in the year 2000 (as used in the World Health Organization [WHO] Global Burden of Disease Study) and projections for 2030. It provides a sequel to the report describing estimates of the global burden of diabetes in 1990 (2) using newer data and different methods for estimating age-specific prevalence. As before, the estimates are based on demographic changes alone with the conservative assumption that other risk factor levels such as obesity and physical activity remain constant (in developed countries) or are accounted for by urbanization (in less developed countries). The current estimates include all age-groups, and age-specific data are presented (online appendix [available at http://care.diabetesjournals.org]) to allow comparison with previous estimates that were for adults only (2). As most data sources do not distinguish between type 1 and type 2 diabetes in adults, it is not possible to present data separately for subtypes of diabetes.
Previous SectionNext Section
RESEARCH DESIGN AND METHODS

Diabetes prevalence data for adults (≥20 years of age) were derived from studies meeting the following criteria: a defined, population-based sample and diagnosis of diabetes based on optimal WHO criteria (a venous plasma glucose concentration of >11.1 mmol/l 2 h after a 75-g glucose tolerance test). The exceptions to the latter criterion were the study in China, for which a test meal was used (4), and the study in Tanzania (5), in which fasting glucose alone gave a higher prevalence of diabetes than a previous study that used the optimal WHO criteria.

Prevalence estimates for type 1 diabetes for people <20 years of age for individual countries were estimated from available incidence data using methods described in the International Diabetes Federation (IDF) Diabetes Atlas 2000 (6). Population-based data are not available for type 2 diabetes in people <20 years of age, and this group has been excluded from these estimates. Age- and sex-specific estimates for diabetes prevalence were extrapolated to other countries using a combination of criteria including geographical proximity, ethnic, and socioeconomic similarities applied by the authors with the advice of the WHO regional officer and other experts. Table 1 shows the studies used and the countries to which data were extrapolated. Surveys were generally performed on middle-aged populations, and data are more limited at younger and older ages. Data on diabetes prevalence are usually presented in broad age bands, which suggest a biologically implausible step-like increase in diabetes prevalence with increasing age. DISMOD II software (available from http://www3.who.int/whosis) was used to produce smoothed, age-specific estimates of diabetes prevalence from the available data from each study. Further details on DISMOD II have been published elsewhere (7). In summary, age- and sex-specific diabetes prevalence (derived from the studies listed in Table 1), remission (assumed to be zero), and estimates of relative risk of mortality among people with diabetes (see below) were entered into models. The model output provides estimates of prevalence, incidence, and mortality that are consistent with one another (7). Estimates of relative risk of all-cause mortality among people with diabetes, by age and sex, were derived from the limited number of cohort studies that provide this information (8–10). Estimated relative risks for all-cause mortality ranged between 1 (for the oldest age-group, ≥80 years of age) and 4.1 (for 20–39 years of age) for men and between 1 (for ≥80 years of age) and 6.7 (for 20–39 years of age) for women. Further information on the estimation of age-specific relative risks is available in the draft Global Burden of Disease 2000 documentation (11). Mortality data were derived from developed countries (U.K., Sweden, and U.S.). As no information was available for developing countries, the same relative risks were assumed to apply. Data are required to test the validity of this assumption. Survival is unlikely to be better in developing countries than developed countries, and any bias in the approach we have taken would lead to conservative estimates of incidence of diabetes in developing countries but would not affect estimates of prevalence. Estimates of incidence and mortality are not presented in this report but are available from the authors and from the draft Global Burden of Disease 2000 documentation (11). The prevalence estimates were applied to population estimates for individual countries for 2000 and 2030, which were produced by the United Nations Population Division (12). Conventional, albeit simplistic, definitions of developed countries (Europe including former socialist economies, North America, Japan, Australia, and New Zealand) and less developed countries (all other countries) were used. In keeping with previous estimates, prevalence of diabetes was assumed to be similar in urban and rural areas of developed countries (2). For developing countries, urbanization was used as a proxy measure of the increased risk of diabetes associated with altered diet, obesity, decreased physical activity, and other factors such as stress, which are assumed to differ between urban and rural populations. For most developing countries, the prevalence of diabetes in rural areas was assumed to be one-half that of urban areas, based on the ratio observed in a number of population studies and as used in previous estimates (1). For some populations in developing countries (small islands and populations for which prevalence data were derived from studies combining urban and rural populations), a single estimate of diabetes prevalence was used. In the current estimates, on the advice of local experts, the prevalence of diabetes in rural areas was assumed to be one-quarter that of urban areas for Bangladesh, Bhutan, India, the Maldives, Nepal, and Sri Lanka (13). To facilitate comparisons with previous estimates, the regional grouping of countries originally used in the World Development Report 1993 (14) and the Global Burden of Disease 1990 study was retained. Data on population size and estimated numbers of people with diabetes for individual countries were combined to give regional estimates of diabetes prevalence. Previous SectionNext Section RESULTS Detailed information on the estimated number of people with diabetes, population size, and prevalence for individual countries is given in the online appendix. The regional summaries are shown in Table 2. Assuming that age-specific prevalence remains constant, the number of people with diabetes in the world is expected to approximately double between 2000 and 2030, based solely upon demographic changes. The greatest relative increases will occur in the Middle Eastern Crescent, sub-Saharan Africa, and India. The greatest absolute increase in the number of people with diabetes will be in India. Most of the expected population growth between 2000 and 2030 will be concentrated in the urban areas of the world (15). The most striking demographic change in global terms will be the increase in the proportion of the population >65 years of age (see Table 2).

The importance of age on the prevalence of diabetes is illustrated in Fig. 1, which shows sex-specific estimates of diabetes prevalence by age. Globally, diabetes prevalence is similar in men and women but it is slightly higher in men <60 years of age and in women at older ages. Overall, diabetes prevalence is higher in men, but there are more women with diabetes than men (data available from the authors). The combined effect of a greater number of elderly women than men in most populations and the increasing prevalence of diabetes with age is the most likely explanation for this observation. In developing countries, the majority of people with diabetes are in the 45- to 64-year age range, similar to the finding reported previously (2). In contrast, the majority of people with diabetes in developed countries are >64 years of age. By 2030, it is estimated that the number of people with diabetes >64 years of age will be >82 million in developing countries and >48 million in developed countries. The age distribution of the number of people with diabetes in developed and developing countries is illustrated in Fig. 2.

The 10 countries estimated to have the highest numbers of people with diabetes in 2000 and 2030 are listed in Table 3. The “top three” countries are the same as those identified for 1995 (2) (India, China, and U.S.). Bangladesh, Brazil, Indonesia, Japan, and Pakistan also appear in the lists for both 2000 and 2030. The Russian Federation and Italy appear in the list for 2000 but are replaced by the Philippines and Egypt for 2030, reflecting anticipated changes in the population size and structure in these countries between the two time periods.
Previous SectionNext Section
CONCLUSIONS

The number of cases of diabetes worldwide in 2000 among adults ≥20 years of age is estimated to be ∼171 million. This figure is 11% higher than the previous estimate of 154 million (2). Estimates of total population size and proportion of people >64 years of age in 2000 used in the previous report were higher than those used in this report, and therefore demographic changes cannot account for the discrepancy. The higher prevalence is more likely to be explained by a combination of the inclusion of surveys reporting higher prevalence of diabetes than was assumed previously and different data sources for some countries. The IDF Diabetes Atlas 2000 used different and less stringent criteria for the inclusion of studies to estimate prevalence of diabetes for 20- to 79-year-old individuals in the 172 IDF member countries (∼90% of the population of the world) (6). It was estimated that there were 151 million people with diabetes in this subpopulation in 2000. Despite methodological differences, this was similar to the present estimate for a comparable population of 147 million. The IDF has subsequently released estimates of the numbers of people with diabetes for 2003 and forecasts for 2025 of 194 million and 334 million, respectively (16).

Even if the prevalence of obesity remains stable until 2030, which seems unlikely, it is anticipated that the number of people with diabetes will more than double as a consequence of population aging and urbanization. In the light of the observed increase in prevalence of obesity in many countries of the world and the importance of obesity as a risk factor for diabetes, the number of cases of diabetes in 2030 may be considerably higher than stated here. Increasing evidence of effective interventions, including changes in diet and physical activity or pharmacological treatment to reduce prevalence of diabetes, provides an impetus for wider introduction of preventive approaches (17–19). Furthermore, improved survival may contribute to increasing prevalence of diabetes in the future especially in developed countries (20).

As with previous similar studies, these estimates are limited by a paucity of data, particularly for Eastern Europe and Southeast Asia, and by the assumptions required to generate the estimates. It is possible that individual studies are not representative of the whole country in which they were performed, and it is likely that extrapolation of results to neighboring countries may give inaccurate estimates of diabetes prevalence. A new approach to estimating age-specific prevalence of diabetes was used for the present estimates. For the estimates prepared for the Global Burden of Disease Study 1990, logistic regression models with a linear factor for age were used when data for all age-groups were not available (2). The IDF estimates for 2000 included a quadratic regression model for diabetes with age (6), which can result in a marked reduction in diabetes prevalence at the oldest ages. DISMOD II mod-els showed a flattening or modest reduction of diabetes prevalence in the oldest ages, which appears to be more consistent with the pattern observed in the limited number of studies giving information on diabetes prevalence in the oldest age-groups.

A conservative approach to calculating estimates was taken throughout this study. Given that several of the surveys were performed more than a decade ago, it is probable that this has generated underestimates of diabetes prevalence. Until more modern and nationally representative data are available, this approach provides a guide to the lower limits of the extent of the diabetes epidemic. It is anticipated that estimates will be updated periodically as new information becomes available.

In summary, these data provide an updated quantification of the growing public health burden of diabetes across the world. The human and economic costs of this epidemic are enormous. Mortality from communicable diseases and infant and maternal mortality in less-developed countries are declining. In association with increasing diabetes prevalence, this will inevitably result in increasing proportions of deaths from cardiovascular disease in these countries, as well as increased prevalence and associated consequences of other complications of diabetes. A concerted, global initiative is required to address the diabetes epidemic.

Investigations for Diabetes Mellitus

Glucose is essentially used as a screening parameter. Values are highly diet dependent and drug intake influence the results. The main advantage is that it is one of the most standardised parameters, that even patients can self determine the results by home monitoring metres. Glucose can be estimated chemically and enzymatically. If the fasting blood glucose value is more than 126 mg/dl or the random blood glucose value is more than 200 mg/dl, then it is considered to be a case of diabetes.

Glucose Tolernce Test: (GTT)

This test is used to measure the glucose tolerance in a person. The blood is drawn at intervals of 30 mins each. The first sample is fasting, at 30 mins, 60 min, 120 mins and 180 mins. In all five samples are collected.

The most important role of GTT is to help in the investigation of symptomless glycosuria. It also helps in diagnosing minor cases of DM. A diminished GTT indicates the decreased ability of the body to utilise glucose, thus in turn helping in the diagnosis of diabetes mellitus. An increased GTT indicates the ability to utilise more glucose. It leads to decreased endocrine activity. Seen in hypothyroidism, hypoadrenalism, and hypopituitrism.

Glycosylated Haemoglobin

Of all the glycated forms of Hb, HbA1c is the most stable. More than 80 per cent of the glycated form is the HbA1c. Hence, its measurement is taken to be the ideal parameter to understand the “Long term diabetic control”. This is the most important tool for monitoring diabetes. This test refers to the hemoglobin component formed by interaction with glucose, since half life of RBCs is approximately 120 days; a single HbA1c determination can give information about glycemic control in the preceding 8-12 weeks.

It is estimated by HPLC method, which is considered to be gold standard. The advantage is that this test does not require any dietary preparations, has low sensitivity but high specificity compared to oral glucose tolerance test.

Microalbumin (MAU)

MAU as the name suggests, is the first warning signal to an impending “Nephropathy” - if attention is not paid to keep diabetes under control. Microalbumin is present in 25 per cent of patients with type I disease and 36 per cent patients with type II disease. Patients with microalbuminuria have a greater risk for developing renal failure, vascular damage and risk for cardiovascular damage. It can be estimated by immunoturbidometry and nephelometry: 30 – 40 per cent of Type I {IDDM} diabetes mellitus develop diabetic nephropathy with a strong rise in incidence after 15 years duration of diabetes.

Insulin

This test is used for determination of concentration of bioavailable insulin in the patients. Total insulin exists in free and bound form. In patients without insulin antibodies, total and free levels are similar, but in patients with insulin antibodies total insulin levels are dependant on the binding capacity of the circulating endogenous insulin antibody and availability of insulin to bind to antibody sites. This test is used to determine dosage of IDDM with insulin antibodies. Free insulin measurement helps in interpreting blood sugar concentration and its relationship to insulin injections in insulin treated pts with insulin antibodies. Elevated blood glucose with low free insulin level indicates insufficient insulin for adequate control. Low blood glucose with high free insulin level indicates the need to change the dosage

Insulin Antibodies

Most common antibodies are IgG, IgM, IgA & IgE Abs have been reported. These antibodies are generally seen in pre-Type I DM as well as DM pts with exogenous bovine or human porcine insulin. Widespread use of human insulin & improved purity of animal insulin has led to significant decrease in insulin antibodies.

Free Insulin

Increased levels of free insulin are seen:

* Exogenous insulin
* Insulinoma
* Insulin resistance
* Type II DM.

Proinsulin

Proinsulin is produced in beta cells of pancreas and cleaved into insulin and C-peptide before release into circulation. Only 2-3 percent of proinsulin escapes the conversion and is secreted into blood. Proinsulin is produced in beta cells of pancreas and cleaved into insulin and C-peptide before release into circulation.

Increased levels are seen in

* Insulinomas
* Severe hypoglycemic hypoinsulinomas
* Hyperproinsulinemia.

Proinsulin inhibits hepatic production of glucose thus useful in type II DM.TG & HDL concentrations improve with proinsulin It is used as agonist with insulin due to longer elimination time ½ life and lower metabolic rate. Thus Proinsulin serves as analogue to insulin to retard the complications of Type II DM.

GAD Antibodies

GAD-65 Antibodies: GAD is known as Glutamic Acid Decarboxylase. They are detected in approximately 90 per cent of patients who are newly diagnosed of Type I DM and 80 per cent of pre-diabetic individuals and first degree relative of patients with IDDM.

C-Peptide

C-peptide is cleaved from proinsulin and released into circulation in the course of insulin biosynthesis. C-peptide is used for assessment of pancreatic islet cell function. Type II DM is associated with abundant C-peptide secretion whereas Type I DM has little or no C-peptide.

diabetes and organ damage:-

Diabetes Damage
What are the organs that can be damaged by Diabetes?

Uncontrolled Diabetes damages organs like eyes, kidneys and the nerves. Blood circulation can be a problem with diabetes because high blood sugar, high blood pressure, overweight and high cholesterol associated with Diabetes cause stiffening of arteries and slow down circulation.

How to assess Diabetic eye disease?

Diabetes damage to eyes can be to the extent to blindness and early detection and timely treatment can prevent that. At the beginning you may not have symptoms, so the only way is to check the eye (the back of eye called retina). If you have Diabetes and are seeing an eye specialist you must tell that you have Diabetes. The specialist will do the required check.

Foot care in people with Diabetes

Problem with feet is very common in case of uncontrolled Diabetes. The problem is threefold here:

1. Nerve damage due to diabetes, so that you don"t feel in case of injury
2. Poor circulation so that healing is poor
3. Infection, because of uncontrolled sugar. Infection can spread very quickly in Diabetes and can give rise to general sepsis. It is important to seek expert opinion as soon as you see some problem.

Regular foot care is very important. Particular care should be taken to keep the feet clean and dry. You should cut the nails regularly and apply moisturiser cream to prevent dryness and cracking which can the entry point for infection.

What are the warning signs of foot problem in Diabetes?

There are certain features when patient with Diabetes should consult doctor without wasting time. They are redness, unusual pain, ulcer or cut, swelling and change of colour in feet. Delay in getting treatment may lead to gangrene. Pain in legs after walking and improvement with rest is called claudication (similar to angina of the heart) is a sign of lack of blood supply in the legs and should be checked on urgent basis.

How to check for Diabetic Kidney?

Kidney damage due to diabetes will not show any early symptoms and that is why a routine yearly check is necessary. The simple things are to check urine for protein and blood. Protein starts leaking in urine when the kidneys are affected with Diabetes. More and more leak of protein by the kidney leads to kidney failure. We have treatment available now for reducing this leakage and protecting the kidneys. Ultrasound scan of the kidney is NOT helpful for diagnosis of Diabetic kidney disease.

Damage caused by Diabetes, if not diagosed early can lead to serious problems. Thus, complete body checkup is very important for a Diabetes patient.

diabetes and pregnency:-

You have type 1 or type 2 diabetes and you are pregnant or hoping to get pregnant soon. You can learn what to do to have a healthy baby. You can also learn how to take care of yourself and your diabetes before, during, and after your pregnancy.

Pregnancy and new motherhood are times of great excitement, worry, and change for any woman. If you have diabetes and are pregnant, your pregnancy is automatically considered a high-risk pregnancy. Women carrying twins-or more-or who are beyond a certain age are also considered to have high-risk pregnancies. High risk doesn't mean you'll have problems. Instead, high risk means you need to pay special attention to your health and you may need to see specialized doctors. Millions of high-risk pregnancies produce perfectly healthy babies without the mom's health being affected. Special care and attention are the keys.
Taking Care of Your Baby and Yourself

Keeping your blood glucose as close to normal as possible before you get pregnant and during your pregnancy is the most important thing you can do to stay healthy and have a healthy baby. Your health care team can help you learn how to use meal planning, physical activity, and medications to reach your blood glucose goals. Together, you'll create a plan for taking care of yourself and your diabetes.

Pregnancy causes a number of changes in your body, so you might need to make changes in the ways you manage your diabetes. Even if you've had diabetes for years, you may need changes in your meal plan, physical activity routine, and medications. In addition, your needs might change as you get closer to your delivery date.

How Diabetes Can Affect You and Your Baby

High blood glucose levels before and during pregnancy can

* worsen your long-term diabetes complications, such as vision problems, heart disease, and kidney disease
* increase the chance of problems for your baby, such as being born too early, weighing too much or too little, and having low blood glucose or other health problems at birth
* increase the risk of your baby having birth defects
* increase the risk of losing your baby through miscarriage or stillbirth

However, research has shown that when women with diabetes keep blood glucose levels under control before and during pregnancy, the risk of birth defects is about the same as in babies born to women who don't have diabetes.

Glucose in a pregnant woman's blood passes through to the baby. If your blood glucose level is too high during pregnancy, so is your baby's glucose level before birth.
Your Diabetes, Before and During Your Pregnancy

As you know, in diabetes, blood glucose levels are above normal. Whether you have type 1 or type 2 diabetes, you can manage your blood glucose levels and lower the risk of health problems.

A baby's brain, heart, kidneys, and lungs form during the first 8 weeks of pregnancy. High blood glucose levels are especially harmful during this early part of pregnancy. Yet many women don't realize they're pregnant until 5 or 6 weeks after conception. Ideally, you will work with your health care provider to get your blood glucose under control before you get pregnant.

If you're already pregnant, see your health care provider as soon as possible to make a plan for taking care of yourself and your baby. Even if you learn you're pregnant later in your pregnancy, you can still do a lot for your baby's health and your own.

The checklist below can help you make a plan for a safe and healthy pregnancy. More information on each topic then follows. Your health care team can help you with tasks that are difficult for you. Tackle one thing at a time to keep from being overwhelmed.
My Diabetes Care Plan for Pregnancy

Things I can do to get ready for a healthy pregnancy and continue to do during my pregnancy

Planning Ahead

* I'll get my diabetes under control 3 to 6 months before I try to get pregnant.
* If I'm already pregnant, I'll see my health care provider right away.

My Health Care Team

* I'll make sure I have the right team of health care providers.
* I'll meet with members of my team.

My Blood Glucose Levels

* I'll set goals with my health care team for my daily blood glucose levels.
* I'll set a goal with my health care team for my A1C test result.
* I'll learn how and when to check my blood glucose on my own.
* I'll learn what to do if my blood glucose is too low.
* I'll make sure my family or friends know how to give me glucagon for low blood glucose.
* I'll learn what to do if my blood glucose is too high.

My Ketone Levels

* I'll learn how and when to check my urine or blood for ketones.
* I'll learn what to do if I have ketones in my urine or blood.

My Checkups

I'll get the recommended checkups and laboratory tests for

* blood pressure
* eye disease
* heart and blood vessel disease
* nervous system disease
* kidney function
* thyroid disease
* average blood glucose level-the A1C test

Smoking

* If I smoke, I'll quit.

My Meal Plan

* I'll see a dietitian or diabetes educator about what, when, and how much to eat.
* I'll ask whether I need vitamin and mineral supplements and will take them as directed.
* I'll skip alcoholic beverages.

My Physical Activity Routine

* I'll talk with my health care team about what physical activities are safe for me.
* I'll make a plan with my health care team for regular physical activity.

My Medications

* I'll talk with my health care team about my diabetes medications-what kinds, how much, how to take them, and when to take them.
* I'll talk with my health care team about my other medications-what to keep taking and what to stop taking.

Changes in My Daily Routine

*

I'll make a plan for taking care of myself when I'm ill-what to do about food, insulin, blood glucose testing, and ketone testing.
* I'll make a plan for what I need to have with me when I'm away from home-for several hours or for a longer trip.

Planning Ahead

Before you get pregnant, talk with your health care team about your wish to have a baby. Your team can work with you to make sure your blood glucose levels are on target. If you have questions or worries, bring them up. If you're already pregnant, see your doctor right away.
My Health Care Team

Regular visits with health care providers who are experts in diabetes and pregnancy will ensure you get the very best care. Your team may include

*

a medical doctor who specializes in diabetes care, such as an endocrinologist or a diabetologist. You will continue to need monitoring and advice on glucose control throughout your pregnancy and after.
*

an obstetrician-gynecologist, or "OB/GYN," who has managed pregnancies of women with diabetes. Ask for a referral if your current gynecologist does not also deliver babies, as not all gynecologists do. When calling around to find an OB/GYN, ask about experience with women with diabetes. Maternal-fetal medicine specialists, also called perinatologists, have special training to take care of women with high-risk pregnancies. You will see your OB/GYN regularly throughout your pregnancy.
*

a nurse educator or nurse practitioner, who provides prenatal care and advice on managing diabetes.
*

a registered dietitian to help with meal planning. A good diet-for glucose control and nutrition-has never been more important than now. The phrase "You're eating for two" is not about quantity as much as food choices.
*

specialists who diagnose and treat diabetes-related complications, such as ophthalmologists and optometrists for vision problems, nephrologists for kidney disease, and cardiologists for heart disease. If you are already experiencing complications from diabetes, you'll need those conditions monitored throughout your pregnancy as well.
*

a social worker or psychologist to help you cope with stress, worry, and the extra demands of pregnancy. You may already have this kind of support, or you may suddenly need it. If anxiety mounts, do not hesitate to mention your uneasiness to your OB/GYN. Ask for a referral if you need more help working through issues.
*

a pediatrician-a doctor who cares for children. You might want to ask friends, family, or your health care team for recommendations. Many pediatricians visit their newest patients at the hospital soon after their arrival.
*

a neonatologist-a doctor who cares for newborn babies. The hospital will assign a neonatologist if urgent care for your baby is needed at the hospital.

You are the most important member of the team. Your health care providers can give you expert advice. But you'll be responsible for the day-to-day actions needed to keep your diabetes under control.
My Blood Glucose Levels

Daily Blood Glucose Levels

You'll check your blood glucose levels using a blood glucose meter several times a day. Most health care providers recommend testing at least four times a day. Ask your health care provider when you should check your blood glucose levels and check off the answers using the chart below.

I should check my blood glucose levels

* fasting-when I wake up, before I eat or drink anything
* before each meal
* 1 hour after the start of a meal
* 2 hours after the start of a meal
* before bedtime
* in the middle of the night-for example, at 2 or 3 a.m.

The daily goals recommended by the American Diabetes Association for most pregnant women are shown below. Write down the goals you and your health care team have chosen.
When Plasma Blood Glucose
(mg/dL) My Goals
Before meals and when you wake up 80 to 110
2 hours after the start of a meal Below 155

Source: American Diabetes Association. Preconception care of women with diabetes. Diabetes Care. 2004;27(Supplement 1):S76-78.

See the chart below for goals recommended by the American College of Obstetricians and Gynecologists.
When Plasma Blood Glucose
(mg/dL) My Goals
Fasting 105 or less
Before meals 110 or less
1 hour after the start of a meal 155 or less
2 hours after the start of a meal 135 or less
During the night Not less than 65

Source: American College of Obstetricians and Gynecologists (ACOG) Committee on Practice Bulletins. ACOG Practice Bulletin Number 60: Pregestational diabetes mellitus. Obstetrics and Gynecology. 2005;105(3):675-685.

You can keep track of your blood glucose levels using My Daily Blood Glucose Record. Write down the results every time you check your blood glucose. Your blood glucose records can help you and your health care team decide whether your diabetes care plan is working. You also can use this form to make notes about your insulin and ketones.

The A1C Test

Another way to see whether you're meeting your goals is to have an A1C blood test.

Results of the A1C test show your average blood glucose levels during the past 2 to 3 months. Write the goal you and your health care team have chosen below.
Goal for My A1C Test
Source of Recommendation Target Number My Goal
American Diabetes Association 4 to 6 percent-normal*
or
Less than 1 percent above the upper limits of normal*
American College of Obstetricians and Gynecologists No higher than 6 percent

*Normal values vary according to laboratory; check with your doctor.

Low Blood Glucose

When you're pregnant, you're at increased risk of having low blood glucose, also called hypoglycemia. When blood glucose levels are too low, your body can't get the energy it needs. Usually hypoglycemia is mild and can easily be treated by eating or drinking something with carbohydrate. But left untreated, hypoglycemia can make you pass out

Although hypoglycemia can happen suddenly, it can usually be treated quickly, bringing your blood glucose level back to normal. Low blood glucose can be caused by

* meals or snacks that are too small, delayed, or skipped
* doses of insulin that are too high
* increased activity or exercise

Low blood glucose also can be caused by drinking too much alcohol. However, women who are trying to get pregnant or who are already pregnant should avoid all alcoholic beverages.

Using Glucagon for Severe Low Blood Glucose

If you have severe low blood glucose and pass out, you'll need help to bring your blood glucose level back to normal. Your health care team can teach your family members and friends how to give you an injection of glucagon, a hormone that raises blood glucose levels right away.

High Blood Glucose

High blood glucose, also called hyperglycemia, can happen when you don't have enough insulin or when your body isn't able to use insulin correctly. High blood glucose can result from

* a mismatch between food and medication
* eating more food than usual
* being less active than usual
* illness
* stress

In addition, if your blood glucose level is already high, physical activity can make it go even higher. Symptoms of high blood glucose include

* frequent urination
* thirst
* weight loss

Talk with your health care provider about what to do when your blood glucose is too high-whether it happens once in a while or at the same time every day for several days in a row. Your provider might suggest a change in your insulin, meal plan, or physical activity routine.
My Ketone Levels

When your blood glucose is too high or if you're not eating enough, your body might make chemicals called ketones. Ketones are produced when your body doesn't have enough insulin and glucose can't be used for energy. Then the body uses fat instead of glucose for energy. Burning fat instead of glucose can be harmful to your health and your baby's health. Harmful ketones can pass from you to your baby. Your health care provider can teach you how and when to test your urine or blood for ketones.

If ketones build up in your body, you can develop a condition called ketosis. Ketosis can quickly turn into diabetic ketoacidosis, which can be very dangerous. Symptoms of ketoacidosis are

* stomach pain
* frequent urination or frequent thirst, for a day or more
* fatigue
* nausea and vomiting
* muscle stiffness or aching
* feeling dazed or in shock
* rapid deep breathing
* breath that smells fruity

Checking Your Urine or Blood Ketone Levels

Your health care provider might recommend you test your urine or blood daily for ketones and also when your blood glucose is high, such as higher than 200 mg/dL.

You can prevent serious health problems by checking for ketones as recommended. Ask your health care team about when to check for ketones and what to do if you have them. Then check off the instructions below and fill in the blanks.

I should test my urine or blood for ketones

* every day before breakfast
* when I'm sick
* when my blood glucose is _____________ or higher
* other times: _________________________________

If you use an insulin infusion pump, your health care provider might also recommend that you test for ketones when your blood glucose level is unexpectedly high.

Your health care provider might teach you how to make changes in the amount of insulin you take or when you take it. Or your provider may prefer that you call for advice when you have ketones.
My Checkups

Pregnancy can make some diabetes-related health problems worse. Your health care provider can talk with you about how pregnancy might affect any problems you had since before pregnancy. If you plan your pregnancy enough in advance, you may want to work with your health care provider to arrange for treatments, such as laser treatment for eye problems, before you get pregnant. Your diabetes-related health conditions can also affect your pregnancy.

Have a complete checkup before you get pregnant or at the start of your pregnancy. Your doctor should check for

* high blood pressure, also called hypertension
* eye disease, also called diabetic retinopathy
* heart and blood vessel disease, also called cardiovascular disease
* nerve damage, also called diabetic neuropathy
* kidney disease, also called diabetic nephropathy
* thyroid disease

You'll also get regular checkups throughout your pregnancy to check your blood pressure and average blood glucose levels and to monitor the protein in your urine.
Smoking

Smoking can increase your chance of having a stillborn or premature baby. Smoking is also especially harmful for people with diabetes. If you smoke, talk with your health care provider about how to quit.
My Meal Plan

If you don't already see a dietitian, now would be an excellent time to start. Your dietitian can help you learn what to eat, how much to eat, and when to eat. Together, you'll create a meal plan tailored to your needs, usual schedule, food preferences, medical conditions, medications, and physical fitness routine.

Many women need changes in their diet, such as extra calories and protein, during pregnancy. You might need to see your dietitian every few months during pregnancy as your needs change. Eating a well-balanced diet helps ensure that you and your baby are healthy.

How Much to Eat

Talk with your dietitian about how many servings to have at each meal and snack. Your dietitian can also provide advice about portion sizes. Your meal plan will be based on how many calories you need for pregnancy and your goals for weight gain during the pregnancy. For most women whose weight is in the normal range before pregnancy, gaining 25 to 35 pounds is recommended. If you're underweight or overweight at the start of your pregnancy, your weight goal may differ. For overweight women, the recommended weight gain is no more than 15 pounds.

Vitamin and Mineral Supplements

Your health care team will tell you whether you need to take a vitamin and mineral supplement before and during pregnancy. Many pregnant women need supplements because their diets don't supply enough of the following important vitamins and minerals:

* iron-to help make extra blood for pregnancy and for the baby's supply of iron
* folic acid-to prevent birth defects in the brain and spinal cord
* calcium-to build strong bones

Alcoholic Beverages

You should avoid alcoholic beverages while you're trying to get pregnant and throughout pregnancy. When you drink, the alcohol also goes to your baby. Alcohol can lead to serious, lifelong problems for your baby.

Artificial Sweeteners

Artificial sweeteners can be used in moderate amounts. If you choose to use sweeteners, talk with your dietitian about how much to have.
My Physical Activity Routine

Daily physical activity can help you reach your target blood glucose levels. It can also help you reach your blood pressure and cholesterol target levels, relieve stress, improve muscle tone, strengthen your heart and bones, and keep your joints flexible. Talk with your health care team about moderate physical activity, such as walking or swimming. Consider whether you have any health problems and which exercises would be best for you. Your health care team may advise you to avoid exercises that increase your risk of falling, such as downhill skiing.

A sensible goal for most women is to aim for 30 minutes or more of activity, most days of the week. If you've been active before pregnancy, you may be able to continue with a more moderate version of your usual exercise routine. But if you haven't been active, start with an activity such as walking. Vigorous physical activity, such as walking briskly, can lead to low blood glucose. Pregnant women sometimes do not have the typical signs of low blood glucose.

My Medications

Medications for Diabetes

During pregnancy, the safest diabetes medication is insulin. Your health care team will work with you to make a personalized plan for your insulin routine. If you've been taking diabetes pills to control your blood glucose levels, you'll need to stop taking them. Researchers have not yet determined whether diabetes pills are safe for use throughout pregnancy. Instead, your health care team will show you how to take insulin.

If you're already taking insulin, you might need a change in the kind, the amount, and how or when you take it. The amount of insulin you take is likely to increase as you go through pregnancy because your body becomes less able to respond to the action of insulin, a condition called insulin resistance. Your insulin needs may double or even triple as you get closer to your delivery date. Insulin can be taken in several ways. Your health care team can help you decide which way is best for you.

Other Medications

Some medications are not safe during pregnancy and should be discontinued before you get pregnant. Tell your health care provider about all the medications you currently take, such as those for high cholesterol and high blood pressure. Your provider can tell you which medications to stop taking.
Changes in My Daily Routine

Sick Days

When you're ill, your blood glucose levels can rise rapidly. Diabetic ketoacidosis, a dangerous condition for you and your baby, can occur. Talk with your health care team about what you should do if you get sick. Be sure you know

* what to do if you're nauseated or vomiting
* how often you should check your blood glucose
* how often you should check your urine or blood for ketones
* when you should call your health care provider

Being Away from Home

When you're away from home-for several hours or for a longer trip-you'll want to be prepared for problems. Make sure you always have the following with you:

* a snack or a meal
* food or drinks to treat low blood glucose
* your diabetes medicines and supplies
* your blood glucose meter and supplies
* your glucagon kit
* your health care team's phone numbers for emergencies

Checking Your Baby's Health During Pregnancy

You are likely to have tests all through your pregnancy to check your baby's health. Your health care team can tell you which of the following tests you'll have and when you might have them. Your health care provider might also suggest other tests. If certain diseases or conditions run in your family, you might meet with a genetic counselor. The counselor may recommend tests based on your family history and can explain the risk of certain conditions for your baby.
Maternal Blood Screening Test

The maternal blood screening test is also called the multiple marker screen test, the triple screen, or quad screen. It measures several substances in your blood. Results can tell you whether your baby is at risk for spinal cord and brain problems, Down syndrome, and other birth defects. If the results show an increased risk for problems, additional tests such as ultrasound or amniocentesis can provide more information.
Ultrasound

Ultrasound uses sound waves to provide a picture of areas inside the body. The picture produced by ultrasound is called a sonogram. Ultrasound can show the baby's size, position, structures, and sex. It can also help estimate age, evaluate growth, and show some types of birth defects.
Fetal Echocardiogram

The fetal echocardiogram uses ultrasound to check for problems in the structures of the baby's heart.
Amniocentesis

Amniocentesis uses a thin needle inserted through the abdomen into the uterus to obtain a small amount of the fluid that surrounds the baby. Cells from the fluid are grown in a lab and then analyzed. Amniocentesis can help tell whether your baby has health problems and if your baby's lungs have finished developing. Developed lungs are needed for the baby to breathe without help after delivery.
Chorionic Villus Sampling (CVS)

CVS involves a thin needle inserted into the placenta to obtain cells. Cells then are analyzed to look for health problems. Ultrasound is used to guide the needle into the placenta, either through the vagina and cervix or through the abdomen and uterus. The placenta is composed of tissue and blood vessels that develop to attach the baby to the mother's uterus so the developing baby can get nutrition from mom.
Kick Counts (Fetal Movement Counting)

Counting kicks is an easy way to keep track of your baby's activity. You'll count how many times the baby moves during a certain period of time.
Nonstress Test

A fetal monitor checks whether your baby's heart rate increases as it should when the baby is active.
Biophysical Profile

Ultrasound checks your baby's muscle tone, breathing, and movement to obtain a biophysical profile. Ultrasound also estimates the amount of amniotic fluid surrounding the baby.
Contraction Stress Test

This test measures the baby's heart rate during contractions using a fetal monitor. The results can help your doctor decide whether the baby needs to be delivered early.
About Labor and Delivery
Timing of Delivery

Your health care team will consider your health, your baby's health, and the state of your pregnancy in deciding how and when delivery should occur. Some doctors prefer to deliver babies of women with diabetes 1 or 2 weeks before their due dates to lower the risk of problems. Your doctor may recommend inducing labor before your due date or delivering the baby surgically using a cesarean section, also called a c-section. However, most women with diabetes have the option of delivering vaginally. You'll want to talk with your health care team about your options well ahead of time.

The factors your health care team will consider in deciding what type of delivery is best for you and your baby may include

* your baby's size and position
* your baby's lung maturity
* your baby's movements
* your baby's heart rate
* the amount of amniotic fluid
* your blood glucose and blood pressure levels
* your general health

Blood Glucose Control During Labor and Delivery

Keeping your blood glucose levels under control helps ensure your baby won't have low blood glucose after birth. Because you'll be physically active when you're in labor, you may not need much insulin. Hospital staff will check your blood glucose levels frequently. Some women take both insulin and glucose, as well as fluids, through an intravenous (IV) line during labor. Infusing insulin and glucose directly into your bloodstream through a vein provides good control of blood glucose levels. If you are using an insulin pump, you might continue to use it throughout labor.

If you are having a c-section, your blood glucose levels may increase because of the stress of surgery. Your health care team will closely monitor your blood glucose levels and will likely use an IV for insulin and glucose to keep your levels under control.
After Your Baby Arrives
About Breastfeeding

Breastfeeding is highly recommended for the babies of women with diabetes. Breastfeeding provides the best nutrition and helps your baby stay healthy.
Your Meal Plan

If you're breastfeeding, you might need more calories each day than you needed during your pregnancy. Your dietitian can provide personalized recommendations and answer any questions you have about what, when, and how much to eat.
Your Medications

After you've given birth, you might need less insulin than usual for several days. Breastfeeding can also lower the amount of insulin you need. Diabetes pills are not recommended during breastfeeding.
Low Blood Glucose

You'll be at increased risk for low blood glucose, especially if you're breastfeeding. You might need to have a snack before or after you breastfeed your baby. Your health care team may suggest that you check your blood glucose more often than usual.

diabetes and hypertension:-

Diabetes and high blood pressure are closely related diseases. They occur together so frequently that they are officially considered to be “comorbidities” (diseases likely to be present in the same patient). Unfortunately, diabetes makes high blood pressure more difficult to treat, and high blood pressure makes diabetes even more dangerous.
How Are Diabetes and Hypertension Related?

Diabetes and high blood pressure tend to occur together because they share certain physiological traits –- that is, the effects caused by each disease tend to make the other disease more likely to occur. In the case of diabetes and high blood pressure, these effects include:

* Increased Fluid Volume -- diabetes increases the total amount of fluid in the body, which tends to raise blood pressure
* Increased Arterial Stiffness -- diabetes can decrease the ability of the blood vessels to stretch, increasing average blood pressure
* Impaired Insulin Handling -- changes in the way the body produces and handles insulin can directly cause increases in blood pressure

Though these common biological traits partially explain why diabetes and high blood pressure are such a common pair, in many cases, the two diseases are likely to occur together simply because they share a common set of risk factors. Some important shared risk factors are:

* Body Mass -- Being overweight significantly increases the risk of both diabetes and high blood pressure.
* Diet -- High fat diets rich in salt and processed sugars are known to contribute to the development of organ problems that can lead to both diabetes and high blood pressure
* Activity Level -- A low level of physical activity makes insulin less effective (which can lead to diabetes) and can contribute to the development of stiff blood vessels, increasing the risk of high blood pressure.

Preventive strategies for both high blood pressure and diabetes usually focus on these specific risk factors.
How Common is Hypertension in People with Diabetes?

Data from one large, widely referenced study on type 1 diabetes showed:

* 5% of patients have high blood pressure within 10 years
* 33% have high blood pressure within 20 years
* 70% have high blood pressure by age 40

In studies of type 2 diabetes, data has shown that almost 75% of patients with kidney problems (a common complication) had high blood pressure. In those with type 2 diabetes but no kidney problems, the rate of high blood pressure was about 40%. Overall, when averaged across diabetes type and age range, about 35% of all people with diabetes have high blood pressure.

Common Infections in Diabetes

- Infections are of particular concern for diabetics. People with diabetes are more susceptible to developing infections, as high blood sugar levels can weaken the patient's immune system defenses. In addition, some diabetes-related health issues, such as nerve damage and reduced blood flow to the extremities, increase the body's vulnerability to infection.

What Kinds of Infections Are Diabetics Most Likely to Get?

People with diabetes are especially prone to foot infections, yeast infections, urinary tract infections and surgical site infections.

A diabetic's insulin injection sight can be a possible infection source. Injections provide a potential gateway for certain immune-suppressing agents to enter the blood. For example, common bacteria such as Staphylococcus aureus can enter the blood system and cause what is known as a staph infection.

In addition, yeast cells (Candida albicans) that occur naturally in the mucous membranes (e.g., mouth, vagina, nose) can enter the blood system at the injection sight. These Candida cells then interfere with the normal infection-fighting action of white blood cells. With white blood cells impaired, Candida can replicate unchecked, causing yeast infections. High blood sugar levels contribute to this process.

Other Sources of Diabetes-Related Infection

Diabetic neuropathy (nerve damage) causes problems with sensation, particularly in the feet. This lack of sensation sometimes means foot injuries go unnoticed. Untreated injuries can lead to infection. Some types of neuropathy can also lead to dry, cracked skin, which allows a convenient entry point for infection into the body.

People with diabetes often have low blood flow to the extremities. With less blood flow, the body is less able to mobilize normal immune defenses and nutrients that promote the body's ability to fight infection and promote healing.

Why Are Infections Risky for People With Diabetes?

People with diabetes are more adversely affected when they get an infection than someone without the disease, because diabetics have weakened immune defenses. Studies have shown that diabetics (even those who have minimally elevated blood sugar levels) experience worse outcomes with infections. Diabetic patients in hospitals do not necessarily have a higher mortality rate due to infections, but they do face longer hospitalization and recovery times.

What Can Be Done to Avoid Infections?

One of the most important things that a person with diabetes can do to avoid infections is to practice careful foot care. In addition to wearing shoes and socks to avoid minor bumps and scrapes, the feet should be examined daily for any blisters, cuts, scrapes, sores or other skin problems that could allow an infection to develop. Meticulous foot and skin care is needed to ensure that minor cuts and scrapes do not turn into ulcerated infections that can migrate to the bloodstream and cause major problems.

Good urinary hygiene, especially for women, can help minimize the possibility of developing urinary tract infections. This includes proper toilet hygiene, prompt urination after sexual intercourse, regular emptying of the bladder and ample fluid intake.

Yeast infections can often be avoided by good vaginal care. This may include the avoidance of spermicides and douches. Eating foods with active cultures, such as yogurt containing acidophilus, can be helpful for preventing yeast infections.

Watch for Symptoms of Infection

Early diagnosis and prompt treatment of infections are important. People with diabetes should be vigilant about paying attention to any changes in their bodies that could signal an infection.

Some examples of body changes that diabetics should be alerted to can include a rise in body temperature or change in blood sugars; foul-smelling vaginal discharge; pain with urination, or cloudy, bloody or foul-smelling urine; difficulty or painful swallowing; changes in bowel habits; and warmth or redness at any cut or scrape, including minor trauma locations and surgical sites. Any of these symptoms should be noted and mentioned to the patient's healthcare team.

Diagnosing and Treating Infections

A health care provider may perform one or more tests to diagnose infection, including blood tests, microscopic examination of secretions, urine dipstick tests, x-rays and physical examination.

Healthcare providers may prescribe oral or topical antibiotics to treat some infections. Careful blood sugar control is important during any infection to promote healing and prevent further complications related to the infection.

Diabetics should keep the following questions in mind when discussing any possible infections with their healthcare providers:

* For what symptoms should I call the doctor's office?
* How should I manage my medications (including oral and insulin) during an infection?
* Do antibiotics interact with any of my other medications?

oral glucose tolerance test:-

The glucose tolerance test is a laboratory method to check how the body breaks down (metabolizes) sugar.
How the Test is Performed

The most common glucose tolerance test is the oral glucose tolerance test (OGTT). You cannot eat or drink anything after midnight before the test. For the test, you will be asked to drink a liquid containing a certain amount of glucose. Your blood will be taken before you do this, and again every 30 to 60 minutes after you drink the solution. The test takes up to 3 hours.

The intravenous glucose tolerance test (IGTT) is rarely used. In this test, glucose is injected into your vein for 3 minutes. Blood insulin levels are measured before the injection, and again at 1 and 3 minutes after the injection, although the timing may vary.
How to Prepare for the Test

Make sure you eat normally for several days before the test.

Do not eat or drink anything for 8-10 hours before the test. You cannot eat during the test.

Ask your health care provider if you are using medications that can interfere with the test results.
How the Test Will Feel

Some people feel nauseated or sweaty after drinking the glucose for the test.

When the needle is inserted to draw blood, some people feel moderate pain. Others feel only a prick or stinging sensation. Afterward, there may be some throbbing.
Why the Test is Performed

Glucose is the sugar the body uses for energy. Patients with untreated diabetes have high blood glucose levels. Glucose tolerance tests are one of the tools used to diagnose diabetes.

Above-normal blood glucose levels can be used to diagnose type 2 diabetes or high blood glucose during pregnancy (gestational diabetes). Insulin levels may also be measured. (Insulin is the hormone produced by the pancreas that moves glucose from the bloodstream into cells.)

The oral glucose tolerance test is used to screen pregnant women for gestational diabetes between 24 and 28 weeks of pregnancy. It may also be used in cases where the disease is suspected, despite a normal fasting blood glucose level.
Normal Results

Normal blood values for a 75-gram oral glucose tolerance test used to check for type 2 diabetes:

* Fasting: 60 -100 mg/dL
* 1 hour: less than 200 mg/dL
* 2 hours: less than 140 mg/dL. Between 140 - 200 mg/dL is considered impaired glucose tolerance (sometimes called "prediabetes"). This group is at increased risk for developing diabetes. Greater than 200 mg/dL is a sign of diabetes mellitus.

Normal blood values for a 50-gram oral glucose tolerance test used to screen for gestational diabetes:

* 1 hour: equal to or less than 140 mg/dL

Normal blood values for a 100-gram oral glucose tolerance test used to screen for gestational diabetes:

* Fasting: less than 95 mg/dL
* 1 hour: less than 180 mg/dL
* 2 hour: less than 155 mg/dL
* 3 hour: less than 140 mg/dL

Note: mg/dL = milligrams per deciliter

Normal value ranges may vary slightly among different laboratories. Talk to your doctor about the meaning of your specific test results.

The examples above show the common measurements for results for these tests. Some laboratories use different measurements or may test different specimens.
What Abnormal Results Mean

Greater than normal levels of glucose may mean you have diabetes or gestational diabetes.

However, high glucose levels may be related to another medical problem (for example, Cushing syndrome).
Risks

Veins and arteries vary in size from one patient to another and from one side of the body to the other. Obtaining a blood sample from some people may be more difficult than from others.

Other risks associated with having blood drawn are slight but may include:

* Excessive bleeding
* Fainting or feeling light-headed
* Hematoma (blood accumulating under the skin)
* Infection (a slight risk any time the skin is broken)

Considerations

Factors that may affect the test results:

* Acute stress (for example, from surgery or an infection)
* Vigorous exercise

Several drugs may cause glucose intolerance, including:

* Beta-blockers (for example, propranolol)
* Certain psychiatric medications
* Corticosteroids (for example, prednisone)
* Oral contraceptives (birth control pills)
* Thiazide diuretics (for example, hydrochlorothiazide)

Before having the test, let your health care provider know if you are taking any of these medications.
Alternative Names

Oral glucose tolerance test

Diabetes Diet

Diet plays a significant role in controlling the diabetes. The diabetic diet may be used alone or else in combination with insulin doses or with oral hypoglycemic drugs. Main objective of diabetic diet is to maintain ideal body weight, by providing adequate nutrition along with normal blood sugar levels in blood. The diet plan for a diabetic is based on height, weight, age, sex, physical activity and nature of diabetes. While planning diet, the dietician has to consider complications such as high blood pressure, high cholesterol levels.

With respect to the above factors, a dietician will assess calories to be given, like scheming the carbohydrates, proteins, fats, type of carbohydrate, amount of fiber and so on.

Exchange meal plan is a diet program which balances the amount of carbohydrate that we intake per day. Glucose is a sugar released from carbohydrate so, if we want to control blood sugar we have to limit the consumption of simple carbohydrate. Carbohydrate foods are given as value per portion, known as the exchange. This plan helps us to decide on the type of food to be taken, the amount of food and also the time to eat. You can plan for more flexible meals as you get more knowledge about the diet for a diabetic, may be like the counting carbohydrate meal plan or constant carbohydrate. But there is no common diet that works for everyone. Nor is there any particular diet that works perfectly for any diabetic over a long period. While planning diabetes diet we should adhere to certain important factors, they are as follows:

* Fiber should be at least 1.4 oz / day
* Instead of 3 heavy meals, we should go for 4-5 small mid intervals
* Replace bakery products and fast foods by simple whole cooked cereals, and don't eat carbohydrates 2 hours before bedtime
* Consume fresh fruit and vegetables at least 5 exchange/ day

Diabetics always need to take care of their diet and also about the food they eat. Care has to be taken because all foods contain not only carbohydrate, but also some energy value. Protein and fat available in the food are converted to glucose in the body. This glucose has some effect on the blood sugar level, which has to be taken care of. Furthermore, you needn’t have to eat only the bland boring diet. Instead, you can eat more fruits, vegetables and whole grains. All it means is that you need to select foods that are high in nutrition and low in calories.

A simple step to eat low carbohydrate and low fat diet is to follow Sample Diabetic Diet or Diabetes Plate Method. In order to follow the food guide pyramid for diabetes in all the meals it is essential to visualize the diabetes plate. A sample diabetic diet produces a picture in our brain for the ideal proportion of nutrient intake. This lies especially true for type 2 diabetics, who are in most cases overweight. The problem does not lie is what you eat but off course in the quantity you eat. The diabetes portion plate helps a diabetic to see how much quantity/space the particular food group should occupy on his meal plate. It is nothing but a balanced diabetes diet. This Diet can be used by all the individuals who are overweight and willing to keep diabetes and other heart problems at bay.

How to make Diabetic Portion/Sample Plate

1. Divide your plate in ½, and the second half into two equal ¼.

2. Fill the first half with your favorite non starchy Veggies like Lettuce, Broccoli, Spinach, Peppers, Carrots, Green beans, Tomatoes, Celery, Cabbage, and Mushrooms etc. (Note: Restrict the quantity of corn, peas, potatoes, yams and winter squash.)

3. The ¼ of plate with Meat/Protein like Chicken, Beef, fish, Eggs, Tofu, Cottage cheese, Lamb, Turkey etc.

4. The remaining ¼ with brown rice, bread, Potatoes, Crackers, Peas Soup, Cereal, Tortillas, Beans, Yams, Lentils etc.

5. One serving of non fat, sugar-free yoghurt or milk.

6. One serving of fruit like Guava, Apple, Berries or any Citrus.
Why Sample Diabetic Diet?

* Even Distribution of carbohydrate throughout the day to maintain your blood sugar level in target range.
* It helps to lower down the intake of carbohydrate i.e starches, fat/cholesterol.
* Contains more Fibre, antioxidants, photochemical s and quality protein which are essential part of nutritionally sound diet. This would eventually show complete breakdown of starches.
* It is an easy way to promote weight loss with no extra efforts. Weight loss leads to increase insulin sensitivity.

Sample Diabetic Diet or Diabetes plate method can be beneficial for :-

* Working professionals with busy lifestyles.
* Adult or Senior citizens
* Newly diagnosed diabetics or diabetics with depression.
* Low literate diabetics who understand only thumb rule.
* A diabetic with uncontrolled or dancing blood sugar levels.
* Overweight, obese or anyone willing to loss body weight.
* Person with Cognitive difficulty or mentally challenged.
* Rigid or stubborn person who don’t believe in diet planning.

* For breakfast, take cholesterol-lowering oatmeal
* Have nuts rich in mono unsaturated fat, such as pecans, walnuts, and almonds
* Eat pasta, stews and leafy salads along with beans-- kidney beans, chick peas, and dry beans, navy beans and peas which can reduce LDL "bad"; cholesterol
* Fat free milk, yogurt, and cheese to be taken
* Eggs whites to be included
* White meat chicken and Fish and shellfish (not battered) are good
* Increase intake of dry beans and peas
* Have at least 20 to 25 grams of raw onion daily
* Add wheat bran to your wheat flour (50% wheat flour + 50% wheat bran). This helps increase fiber in your diet
* You can also add flaxseed and fenugreek seeds into the wheat flour
* Increase fiber intake in the form of raw fruits, vegetables, whole cereals etc
* Intake of cinnamon, garlic, onion, bitter melon, guar gum is known to considerably reduce blood glucose level

* Don't fry foods instead bake, boil, poach or sauté in a nonstick pan. Steam or microwave vegetables. Buy tuna packed in water, not oil
* Eat less high-fat red meat and more low-fat turkey and fish. Avoid organ meats
* Limit the use of condiments such as ketchup, mustard and salad dress ion--they're high in salt and can be high in sugar, too
* Rinse processed foods in water and, wherever possible, choose fresh foods over canned
* Limit your salt (sodium content)
* Read labels carefully. Soy sauce, brine and MSG, for example, contain a lot of sodium
* Don't select ready to eat and junk foods items available to you
* Don't smoke and stop alcohol consumption
* Don't skip meals and medicine times

Most of the food items contain carbohydrate, protein and fat. Cereals are rich in carbohydrate, lentils, lean meat, chicken and fish are rich in protein while oils, nuts and milk creams are rich in fat. Fat foods are high in calories; 1g of it provides 9 calories, while 1g carbohydrate or 1g protein gives only 4 calories.

Carbohydrate is easily digested than fat and protein. The rise in blood glucose after a meal is due to absorption of glucose from a carbohydrate digestion and increase in production of glucose by liver. Sucrose (cane sugar), sweets and syrups cause a rapid rise in blood glucose than whole cereals like finger millet and wheat products.

In people with no diabetes, the rise in blood glucose after a meal comes down to the pre-meal level with in 2 hrs. In diabetes, the rise in blood glucose after a meal is not only higher but the fall to pre-meal level is slower (3-4 hrs). Therefore, snacks in between meals or frequent meals at short intervals tend to cause progressive increase in blood glucose in people with diabetes.

Glucose is constantly needed to provide ready energy for the proper functioning of brain, heart, kidneys, liver and blood cells. When glucose is not available from ingested food, our liver produces from its store of carbohydrate (glycocen) and body stores of fats and proteins. The liver produces about 0.1058 oz of glucose/lbs body weight in a day. For example the liver of a man or woman weighing 154 lbs produces 7.0547 oz of glucose in a day. The production of glucose by the liver is kept in a check by small amounts of insulin secreted by the pancreas.

These considerations and the modality of your treatment (tablets/insulin) are taken into account for formulating your diet management during diabetes and meal timings. The dietician would give your information on your diet.
The general guidelines on diet are:

In a typical day’s meals and snacks, you should have 1500-1800 calories with – 60% contribution from the carbohydrate, 20% from fat and 20% from proteins. You may need extra weight reduction. If you are on calorie-restricted diet, make sure to take 50-60% of calories as complex carbohydrate (whole cereals) to prevent any feeling of weakness.

* You should eat a variety of food items everyday. Do not skip meals. Avoid snacks, unless you are advised to (example during insulin treatment). Don’t over eat.
* Eat fruits and vegetables. Use less oil in cooking. Avoid fried foods, milk cream or food items cooked in coconut milk.
* Avoid ready to eat food preparations, sweets and sugary drinks (canned beverages) that provide empty calories (no vitamin or essential minerals).
* Keep a regular check on your weight – maintain it within the estimated limit.
* Check your hemoglobin and proteins in blood samples at 6 months or 1 year’s interval, Suitable correction in diet format or supplementation may become necessary.
* Despite a good control of blood glucose, if your blood lipids are high, you will need lipid lowering drugs regularly. Some times your doctor may advice you lipid-lowering drugs from the beginning of your diabetes treatment.
* Match your mealtime to the form of insulin and insulin injection schedules as explained by your doctor or the diabetes nurse.

Diabetes Symptoms

Symptoms of type 1 diabetes are often dramatic and come on very suddenly.

* Type 1 diabetes is usually recognized in childhood or early adolescence, often in association with an illness (such as a virus or urinary tract infection) or injury.
* The extra stress can cause diabetic ketoacidosis.
o Symptoms of ketoacidosis include nausea and vomiting. Dehydration and often-serious disturbances in blood levels of potassium follow.
o Without treatment, ketoacidosis can lead to coma and death.

Symptoms of type 2 diabetes are often subtle and may be attributed to aging or obesity.

* A person may have type 2 diabetes for many years without knowing it.
* People with type 2 diabetes can develop hyperglycemic hyperosmolar nonketotic syndrome.
* Type 2 diabetes can be precipitated by steroids and stress.
* If not properly treated, type 2 diabetes can lead to complications such as blindness, kidney failure, heart disease, and nerve damage.

Common symptoms of both type 1 and type 2 diabetes include:

* Fatigue, constantly tired: In diabetes, the body is inefficient and sometimes unable to use glucose for fuel. The body switches over to metabolizing fat, partially or completely, as a fuel source. This process requires the body to use more energy. The end result is feeling fatigued or constantly tired.
* Unexplained weight loss: People with diabetes are unable to process many of the calories in the foods they eat. Thus, they may lose weight even though they eat an apparently appropriate or even an excessive amount of food. Losing sugar and water in the urine and the accompanying dehydration also contributes to weight loss.
* Excessive thirst (polydipsia): A person with diabetes develops high blood sugar levels, which overwhelms the kidney's ability to reabsorb the sugar as the blood is filtered to make urine. Excessive urine is made as the kidney spills the excess sugar. The body tries to counteract this by sending a signal to the brain to dilute the blood, which translates into thirst. The body encourages more water consumption to dilute the high blood sugar back to normal levels and to compensate for the water lost by excessive urination.
* Excessive urination (polyuria): Another way the body tries to rid the body of the extra sugar in the blood is to excrete it in the urine. This can also lead to dehydration because a large amount of water is necessary to excrete the sugar.
* Excessive eating (polyphagia): If the body is able, it will secrete more insulin in order to try to manage the excessive blood sugar levels. Moreover, the body is resistant to the action of insulin in type 2 diabetes. One of the functions of insulin is to stimulate hunger. Therefore, higher insulin levels lead to increased hunger. Despite increased caloric intake, the person may gain very little weight and may even lose weight.
* Poor wound healing: High blood sugar levels prevent white blood cells, which are important in defending the body against bacteria and also in cleaning up dead tissue and cells, from functioning normally. When these cells do not function properly, wounds take much longer to heal and become infected more frequently. Long-standing diabetes also is associated with thickening of blood vessels, which prevents good circulation, including the delivery of enough oxygen and other nutrients to body tissues.
* Infections: Certain infections, such as frequent yeast infections of the genitals, skin infections, and frequent urinary tract infections, may result from suppression of the immune system by diabetes and by the presence of glucose in the tissues, which allows bacteria to grow. These infections can also be an indicator of poor blood sugar control in a person known to have diabetes.
* Altered mental status: Agitation, unexplained irritability, inattention, extreme lethargy, or confusion can all be signs of very high blood sugar, ketoacidosis, hyperosmolar hyperglycemia nonketotic syndrome, or hypoglycemia (low sugar). Thus, any of these merit the immediate attention of a medical professional. Call your health care professional or 911.
* Blurry vision: Blurry vision is not specific for diabetes but is frequently present with high blood sugar levels.

* Experiencing diabetes symptoms: this may mean that the person's blood sugar level is not being controlled despite treatment
* Blood sugar levels, when tested, are consistently high (more than 200 mg/dL): Persistently high blood sugar levels are the root cause of all of the complications of diabetes.
* The patient's blood sugar level is often low (less than 70 mg/dL): this may mean that the diabetes management strategy is too aggressive. It also may be a sign of infection or other stress on the body's organs such as kidney failure, liver failure, adrenal gland failure, or the concomitant use of certain medications.
* An injury to the foot or leg, no matter how minor: even the tiniest cut or blister can become very serious in a person with diabetes. Early diagnosis and treatment of problems with the feet and lower extremities, along with regular diabetic foot care, are critical in preserving the function of the legs and preventing amputation.
* Low-grade fever (less than 101.5 F or 38.6 C): Fever is a sign of infection. In patients with diabetes, many common infections can potentially be more dangerous for them than for other people. Note any symptoms, such as painful urination, redness or swelling of the skin, abdominal pain, chest pain, or cough, that may indicate where the infection is located.
* Nausea or vomiting, but can keep liquids down: The health care professional may adjust medications while the patient is sick, and will probably recommend an urgent office visit or a visit to the emergency department. Persistent nausea and vomiting can be a sign of diabetic ketoacidosis, a potentially life-threatening condition, as well as several other serious illnesses.
* Small sore(s) (ulcer) on the foot or le:. Any non-healing sore or ulcer on the feet or legs of someone with diabetes needs to be seen by a medical professional right away. A sore less than 1 inch across, not draining pus, and not exposing deep tissue or bone, can safely be evaluated by a health care professional, as long as the patient does not have fever and their blood sugar levels are under control.

When you call a health care professional, tell them that you or someone you know has diabetes and are concerned.

* The patient will probably be referred to a nurse who will ask questions and make a recommendation about what to do.
* Be prepared for this conversation. Have a list of medications, medical problems, allergies to medicines, and a blood sugar diary handy by the phone.
* The nurse may need any or all of this information to decide both the urgency of the patient's condition and how best to recommend treatment for the problem.

Diabetic emergencies

The following situations can become 911 medical emergencies and warrant an immediate visit to a hospital emergency department.

* The person with a severe diabetic complication may travel to the emergency department by car or ambulance.
* A companion should go along to speak for the person if the person is not able to speak for himself or herself with the emergency care professional.
* Bring a list of medical problems, medications, allergies to medications, and the person's blood sugar diary to the emergency department. This information will help the emergency care professional diagnose the problem and treat it appropriately.

The following are signs and symptoms of diabetic complications that warrant emergency care.

* Altered mental status: Lethargy, agitation, forgetfulness, or just strange behavior can be a sign of very low or very high blood sugar levels. If a person has diabetes with an altered mental status:
o Try giving them some fruit juice (about 6 ounces) or cake icing if the person is awake enough to swallow normally without choking. Avoid giving things such as hard candy that can lodge in the throat. The health care provider can prescribe glucose wafers or gels that melt under the tongue.
o Does not wake up and behave normally within about 15 minutes, call 911.
o Is not a known diabetic, these symptoms can be signs of stroke, drug intoxication, alcohol intoxication, oxygen starvation, and other serious medical conditions. Call 911 immediately.
* Nausea or vomiting: If the patient is known to have diabetes and cannot keep food, medications, or fluids down at all, they may have diabetic ketoacidosis, hyperosmolar hyperglycemic nonketotic syndrome, or another complication of diabetes. If the person:
o Has not already taken the latest insulin dose or oral diabetes medicine, do not take it without talking to a medical professional.
o Already has low blood sugar levels, taking additional insulin or medication will drive the blood sugar level down even further, possibly to dangerous levels.
* Fever above 101.5 F (38.6 C): If the primary health care professional cannot see the patient right away, seek emergency care for a person with diabetes with a high fever. Note any other symptoms such as cough, painful urination, abdominal pain, or chest pain.
* High blood sugar level: If the patient's blood sugar level is above 400 mg/dL, and the primary health care professional cannot see them right away, go to the closest emergency department. Very high blood sugar levels can be a sign of diabetic ketoacidosis or hyperosmolar hyperglycemic nonketotic syndrome, depending on the type of diabetes the person has. Both of these conditions can be fatal if not treated promptly.
* Large sores or ulcers on the feet or legs: If the person has diabetes, a non-healing sore larger than 1 inch in diameter can be a sign of a potentially limb-threatening infection.
o Other signs and symptoms that merit immediate care are exposed bone or deep tissue in the wound, large areas of surrounding redness and warmth, swelling, and severe pain in the foot or leg.
o If left untreated, such a sore may ultimately require amputation of the limb.
* Cuts or lacerations: Any cut penetrating all the layers of skin, especially on the legs, is a potential danger to a person with diabetes. Proper wound care, although important to anyone's recovery, is especially important in diabetics to assure proper wound healing.
* Chest pain: If the person has diabetes, take very seriously any pain in the chest, particularly in the middle or on the left side, and seek medical attention immediately.
o People with diabetes are more likely than non-diabetic people to have a heart attack, with or without experiencing chest pain.
o Irregular heartbeats and unexplained shortness of breath may also be signs of heart attack.
* Severe abdominal pain: Depending on the location, this can be a sign of heart attack, abdominal aortic aneurysm (widening of the large artery in the abdomen), diabetic ketoacidosis, or interrupted blood flow to the bowels.
o All of these are more common in people with diabetes than in the general population, and are potentially life-threatening.
o People with diabetes also get other common causes of severe abdominal pain such as appendicitis, perforated ulcer, inflammation and infection of the gallbladder, kidney stones, and bowel obstruction.
o Severe pain anywhere in the body is a signal for timely medical attention.

Diabetes Medications

Currently there are five classes of oral diabetes medications, all of which help in lowering blood glucose levels. These different classes of diabetes medications can be used in combination or with insulin to achieve control the blood sugar.
Classes and actions of medications:

*

Sulfonylureas stimulate the pancreas to make more insulin. The second- and third-generation ones are the best.
*

Biguanides shut off the liver's excess glucose production
*

Alpha-Glucosidase Inhibitors slow absorption of carbs in the intestine
*

Thiazolidinediones increase the body's sensitivity to insulin
*

Meglitinides stimulate the pancreas to make more insulin

Class Generic Name Brand Name Comments How
Sulfonylureas Chlorpropamide
first-generation Diabinese Use with caution in the elderly. May cause lows With meal
Tolazamide
first-generation Tolinase May cause lows With meal
Glyburide
second-
generation Micronase
Diabeta
Glynase Pres Tab Take 1 to 2 times a day.
May cause lows With meal
Glipizide
second-
generation Glucotrol
Glucotrol XL Take 2 times a day or once with (XL).May cause lows 30 minutes before a meal
Glimepiride
third-generation Amaryl Take 1 time a day. May cause lows With meal
Biguanides Metformin Glucophage Not used with congestive heart, renal or liver problems. Check creatinine clearance if over 65 years of age. With meal
Alpha-Glucosidase Inhibitors Acarbose
Miglitol Precose
Glyset May have side effects in the gastrointestinal
tract. With first bite of food
Thiazolidinediones Rosiglitazone
Pioglitazone Avandia
Actos May reduce effectiveness of birth control pills.
Check liver enzymes as directed. Take at same time each day
Meglitinides Repaglinide Prandin Take with each meal. May cause lows Before meals

These medications along with a balanced diet and exercise plan help control blood glucose levels. Medications should be taken at the same time each day or as directed by a health care provider.

Types of INSULINS available for clinical use:

The types of insulin available for clinical use in India can be classified on the basis of their source, strength and time-characteristic of their activity.

Classification based on Source

The insulins available for routine clinical use are the beef, porcine and human insulins.

The beef and porcine insulins are extracted from the pancreas of cows and pigs respectively

Human insulins are made by genetic engineering or by the chemical modification of porcine insulin i.e., by substituting alanine with threonine in the B30 position.

Beef insulins differ from human insulin in three amino acids, whilst porcine insulin differs from human insulin in only one amino acid. Thus, porcine amino acids are less immunogenic than beef insulins.

But the beef insulins continue to be widely used in view of their relatively lower costs.

Human insulins are pure and have the same amino acid structure as that of native insulin.

Human insulins are replacing the other insulins in most developed countries, but its cost is the inhibiting factor to its widespread acceptability in most developing countries.

The insulins available now are the "pure" varieties and contain negligible amounts of contaminants.

Classification based on Strength

The vast majority of the insulins used in India are of the U-40 strength ( 40 units of insulin/ml.

Most of the countries in the world have switched over to the use of U-100 ( 100 units of insulin /ml) insulins.

U-100 insulin are also available for use in India especially for use with insulin delivery devices such as "pens".

Classification based on Time Characteristic of Activity.

This classification is based on

* how soon the insulin starts working (onset)
* when it works the hardest (peak time)
* how long it lasts in your body (duration).

However, each person responds to insulin in his or her own way. That is why onset, peak time, and duration are given as ranges.

It is important that each person have a clear understanding of the characteristics of each type of insulin that he/she is taking. When blood sugar levels are not well controlled at certain times during the day, or if reactions are occurring, the knowledge of the action and characteristics of each insulin being taken will help to determine where changes need to be made.

The insulins available for clinical use can be classified as

Rapid acting:

Insulin analogs have been developed by modifying the amino acid sequence of the insulin molecule. This modification alters the time characterisitics of activity. The only insulin analog available in India is the rapid acting Lispro. It reaches the blood within 15 minutes after injection. It peaks 30 to 90 minutes later and may last as long as 4-5 hours.

Short acting;

Short-acting (regular) insulin usually reaches the blood within 30 minutes after injection. It peaks 2 to 4 hours later and stays in the blood for about 4 to 8 hours.

Intermediate acting;

Intermediate-acting (NPH and lente) insulins reach the blood 2 to 6 hours after injection. They peak 4 to 14 hours later and stay in the blood for about 14 to 20 hours.

Intermediate-acting insulins include lente and NPH. Insulin preparations with a predetermined proportion of NPH mixed with regular, such as 70% NPH to 30% regular, or a 50/50 mix are called intermediate acting for purposes of classification, although their activity characteristics would be different from either only NPH/Lente or only Regular insulins.

Long acting;

Long-acting (ultralente) insulin takes 6 to 14 hours to start working. It has no peak or a very small peak 10 to 16 hours after injection. It stays in the blood between 20 and 24 hours.

diabetic ketacidosis:-

Diabetic ketoacidosis is a problem that occurs in people with diabetes. It occurs when the body cannot use sugar (glucose) as a fuel source because there is no insulin or not enough insulin. Fat is used for fuel instead.

Byproducts of fat breakdown, called ketones, build up in the body.
Causes

People with type 1 diabetes do not have enough insulin, a hormone the body uses to break down sugar (glucose) in the blood for energy. When glucose is not available, fat is broken down instead.

As fats are broken down, acids called ketones build up in the blood and urine. In high levels, ketones are poisonous. This condition is known as ketoacidosis.

Blood glucose levels rise (usually higher than 300 mg/dL) because the liver makes glucose to try to combat the problem. However the cells cannot pull in that glucose without insulin.

Diabetic ketoacidosis is often the first sign of type 1 diabetes in people who do not yet have other symptoms. It can also occur in someone who has already been diagnosed with type 1 diabetes. Infection, injury, a serious illness, or surgery can lead to diabetic ketoacidosis in people with type 1 diabetes. Missing doses of insulin can also lead to ketoacidosis in people with diabetes.

People with type 2 diabetes can develop ketoacidosis, but it is rare. It is usually triggered by a severe illness. Hispanic and African-American people are more likely to have ketoacidosis as a complication of type 2 diabetes.
Symptoms

Symptoms can include:

* Deep, rapid breathing
* Dry skin and mouth
* Flushed face
* Fruity smelling breath
* Nausea and vomiting
* Stomach pain

Other symptoms that can occur include:

* Abdominal pain
* Breathing difficulty while lying down
* Decreased appetite
* Decreased consciousness
* Dulled senses that may worsen to a coma
* Fatigue
* Frequent urination or thirst that lasts for a day or more
* Headache
* Muscle stiffness or aches
* Shortness of breath

Exams and Tests

Ketone testing may be used in type 1 diabetes to screen for early ketoacidosis. The ketones test is done using a urine sample. Ketone testing is usually done:

* When the blood sugar is higher than 240 mg/dL
* During an illness such as pneumonia, heart attack, or stroke
* When nausea or vomiting occur
* During pregnancy

Other tests for ketoacidosis include:

* Amylase blood test
* Arterial blood gas
* Blood glucose test
* Blood pressure measurement
* Potassium blood test

This disease may also affect the results of the following tests:

* CO2
* CSF collection
* Magnesium blood test
* Phosphorus blood test
* Potassium urine test
* Sodium blood test
* Sodium urine test
* Urine pH

Treatment

The goal of treatment is to correct the high blood sugar level with insulin. Another goal is to replace fluids lost through urination and vomiting.

Most of the time, you will need to go to the hospital, where the following will be done:

* Insulin replacement
* Fluid and electrolyte replacement
* The cause of the condition (such as infection) will be found and treated

You may be able to spot the early warning signs and make changes at home before the condition gets worse. It is important to stay in close touch with your doctor.
Outlook (Prognosis)

Acidosis can lead to severe illness or death. Improved therapy for young people with diabetes has decreased the death rate from this condition. However, it remains a big risk in the elderly, and in people who fall into a coma when treatment has been delayed.
Possible Complications

* Fluid buildup in the brain (cerebral edema)
* Heart attack and death of bowel tissue due to low blood pressure
* Kidney failure

When to Contact a Medical Professional

This condition can become a medical emergency. Call your health care provider if you notice early symptoms of diabetic ketoacidosis.

Go to the emergency room or call the local emergency number (such as 911) if you have:

* Decreased consciousness
* Fruity breath
* Nausea
* Trouble breathing
* Vomiting

Prevention

People with diabetes should learn to recognize the early warning signs and symptoms of ketoacidosis. In people with infections or who are on insulin pump therapy, measuring urine ketones can give more information than glucose measurements alone.

Insulin pump users need to check often to see that insulin is still flowing through the tubing, and that there are no blockages, kinks, or disconnections.

Thyroid Ophthalmopathy (Graves’ Disease)

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:19:00 +0000

Signs and Symptoms
Thyroid eye disease, Graves’ ophthalmopathy, dysthyroid ophthalmopathy, and Graves’ disease are all synonymous terms connoting a process clinically characterized by eyelid retraction, proptosis, conjunctival exposure, ocular injection, ocular chemosis, corneal compromise, extraocular muscle infiltration and fibrosis with the potential for compressive optic neuropathy. It is the most common cause of bilateral, symmetric proptosis in adults.

Interestingly, ocular findings may occur independently from dysthyroid function. Euthyroid Graves’ disease is a condition where the characteristic ophthalmic manifestations of thyroid eye disease exist in the presence of a clinically and biomedically normal thyroid gland.

Most patients with ocular Graves’ disease manifest systemic hyperthyroidism. Up to 80 percent of patients with systemic hyperthyroidism develop some eye signs. Systemic signs of hyperthyroidism include weight loss despite increased appetite, nervousness, palpitations, tachycardia while at rest, systemic hypertension, and hyperreflexia. Conversely, lethargy, bradycardia and weight gain despite decreased appetite are signs of hypometabolism and potential hypothyroidism.

In 1969, the American Thyroid Association adopted the formal classification of Ocular Graves’ disease, represented by the pneumonic NOSPECS. The disease process passes through 6 stages: (0) No signs or symptoms present, (I) Only symptoms of ocular irritation (dryness, tearing, foreign body sensation), (II) Soft tissue involvement (periorbital edema), (III) Proptosis, (IV) Extraocular muscle involvement (ophthalmoplegia), (V) Corneal involvement (dense punctate epitheliopathy, infiltration and ulceration), (VI) Sight loss with or without visual field compromise secondary to compressive optic neuropathy. However, because the disease is recognized as variable, the formal classification was revised in 1974 to range from no manifestations to mild, moderate or severe manifestations.

The common, clinically diagnostic eye signs include: von Graefe’s sign (superior lid lag upon down gaze), Dalrymple’s sign (eyelid retraction), Stellwag’s sign (infrequent blinking), and Ballet’s sign (palsy of one or more extraocular muscles).

Pathophysiology
Graves’ disease is a multisystem disorder of unknown etiology, characterized by one or more of the following three clinical entities: (1) hyperthyroidism associated with diffuse hyperplasia of the thyroid gland; (2) infiltrative ophthalmopathy; and (3) infiltrative dermopathy (pretibial myxedema).

The histopathologic features of the malady include an infiltration of the thyroid gland, skin, extraocular muscles and orbital fat by lymphocytes, macrophages, plasma cells, mast cells and mucopolysaccharides. These changes are characteristic of, but not limited to, an immunologically mediated mechanism.

Management
The diagnosis of Graves’ disease can often be made easily based on symmetrical exophthalmos (exophthalmometry >22mm or asymmetry greater than 3mm) and lid retraction in the
presence of known hyperthyroidism. If symptoms are present and a systemic etiology has not been investigated, consultation with an endocrinologist and laboratory testing for thyroid hormones T3 (triiodothyronine), T4 (tetra-iodothyronine) and TSH (thyroid stimulating hormone) are indicated. Neuroimaging of the orbits in patients with exophthalmos and positive forced duction testing allows clinicians to distinguish extraocular muscle infiltration from inflammatory or infectious myositis.

The systemic management of patients with ocular Graves’ disease lies in the domain of the endocrinologist. Agents that block the synthesis of thyroid hormone such as propylthiouracil (Tapazole) or decrease hypermetabolic symptoms such as propranolol (Inderal) have been proven effective. Systemic steroids, immunosuppressive agents like azathioprine, cyclosporin or cyclophosphamide in combination with orbital irradiation have shown promise in advanced cases. Today, surgical orbital decompression procedures are a last resort.

Since the primary concern proptosis and lid retraction presents is corneal exposure, ocular management is predominantly supportive. Typically, moistening the cornea with artificial tear drops and ointments is effective. Moisture shields that can be attached to the temples of spectacles help to preserve tears and retard tear evaporation. Punctal occlusion may be effective. Cases that involve moderate to severe keratopathy may require prophylactic topical antibiotics. Visual fields should be performed on patients with advanced stage disease, monitoring for the first sign of sight or field loss. Evaluation is usually every three to six months and is based upon severity.

Clinical Pearls

Since a variety of neuro-ophthalmic entities deserve consideration in diseases where there is proptosis or malposition of the eyelid (myasthenia gravis, illusory ptosis of the opposite eyelid, neoplasm, arteriovenous malformation, carotid cavernous fistula, infection, inflammation), forced duction testing (positive in Graves’) and neuroimaging (MRI or CT revealing enlarged EOM bellies with tendon sparing, diagnostic of Graves’) should be done. If myasthenia gravis is suspected, a Tensilon test should be ordered.

Beware of glaucoma in patients with Graves’ ophthalmopathy. The infiltrated muscles can cause globe compression with secondary IOP elevation as well as compressive optic neuropathy.

STAVUDINE (d4T)

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:17:00 +0000

Antiviral Activity

Used in the treatment of HIV-1 infection in combination with at least two additional antiretroviral agents
Active against susceptible HIV strains

Pregnancy Risk Factor

Category C

Contraindication/Precaution

Hypersensitivity to stavudine or to any of its components
HIV-infected mothers should not breast-feed in order to avoid transmission to a non-infected newborn
Do not use in the presence of bone marrow depression
Use caution in the presence of impaired liver/renal function
Use caution in the presence of peripheral Neuropathy, lactic acidosis/severe hepatomegaly with Steatosis

Mechanism of Action

Inhibits viral DNA synthesis by causing DNA chain termination because stavudine lacks the 3'-hydroxyl group necessary for DNA elongation
Also inhibits cellular DNA polymerase beta and gamma, and markedly reduces the synthesis of mitochondrial DNA

Pharmacodynamics/Kinetics

Metabolism:
Not elucidated yet in humans
Half-life:
1.25 hours
Elimination:
Renal (40%)

Dosage

Children :

< 30 kg of body weight: 1 mg/kg PO q12h 30-60 kg of body weight: 30 mg PO bid Adults: < 60 kg of body weight: 30 mg PO bid ³ 60 kg of body weight: 40 mg PO bid Dosage In Renal Failure Creatinine clearance (ml/min): 10-25: 20 mg PO q24h (15 mg if less then 60 kg) 26-50: 20 mg PO q12h (15 mg if less then 60 kg) >50: unchanged
Dialysis
Hemo: 20 mg q24h (³60 kg) or 15 mg q24h (<60 kg)
CAPD: N/A

CYCLOSERINE

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:16:00 +0000

Antibacterial activity

Used in combination with other antituberculosis medications in the treatment of pulmonary tuberculosis caused by Mycobacterium tuberculosis after failure with the primary medications (isoniazid, aminosalicylic acid, streptomycin, ethambutol, and rifampin) or when these cannot be used because of toxicity or development of resistant tubercle bacilli
Also used in the treatment of atypical mycobacterial infections, such as Mycobacterium avium complex

Pregnancy Risk Factor

Class C

Contraindication/Precaution

Do not use in the presence of:
hypersensitivity to cycloserine or any component
epilepsy
depression
severe anxiety, or psychosis
sever renal insufficiency
excessive concurrent use of alcohol
Do not use if nursing
Safety of the use of cycloserine in infants and children has not been established.

Mechanism of Action

Inhibits bacterial cell wall synthesis by competing with amino acid (D-alanine) for incorporation into the bacterial cell wall; bacteriostatic or bactericidal

Pharmacodynamics

Metabolism: liver
Half-life: 10 hours, changes with renal function
Elimination: excreted in urine and some in feces

Dosage

Children: (max 1000 mg/day)

Safety of the use of capreomycin sulfate in infants and children has not been established.
But 10-20 mg/kg/day PO div bid for 18-24 months have been used

Adults: (max 1000 mg/day)

250 mg PO q12h for 14 days then
0.5-1 g/day div bid for 18-24 months
always administered in combination with at least 1 other antituberculosis agent

Dose VS renal function

Cr. clearance (ml/min):
<10: give q36-48h 10-50: give q24h >50: unchanged

Dialysis
Hemo: N/A
CAPD: N/A

PENICILLIN G

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:14:00 +0000

Antibacterial Activity

Effective against gram-positive cocci
Effective against most anaerobe
Not effective against gram-negative aerobe or b-lactamase producing organisms

Pregnancy Risk Factor

Category B

Contraindication/Precaution

Hypersensitivity to penicillin G or any penicillins or any component
Use caution with patient who are allergic to cephalosporin, they could have an hypersensibility to penicillins
Use caution if seizure disorder
Use caution if impaired renal function or other nephrotoxic agents are used

Mechanism of Action

Selective inhibitors of bacterial cell wall synthesis, by binding to penicillins binding proteins (PBP'S)

Pharmacodynamics/Kinetics

Metabolism:
liver (partially)
Half-life:
0.5 hour, change with renal function.
Elimination:
excreted in urine

Dosage

Children:

Body weight < 2000 g 0-7 days old: 50000 u IV q12h 8-28 days old: 75000 u IV q8h Body weight > 2000 g
0-7 days old: 50000 u IV q8h
8-28 days old: 50000 u IV q6h
> 28 days old: 50000 u IV q6h

Adults:

0.5-4 million u IV q4h

Dosage In Renal Failure

Creatinine clearance (ml/min):
10: give 20-50% of normal dose
10-50: give 75% of normal dose
50-80: unchanged
>80: unchanged
Dialysis
Hemo: after dialysis: give 20-50% of normal dose
CAPD: give 20-50% of normal dose

CROTAMITON

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:12:00 +0000

Antibacterial Activity

Use for the eradication of scabies (Sarcoptes scabiei) and for symptomatic treatment of pruritic skin

Pregnancy Risk Factor

Category C

Contraindication/Precaution

Hypersensitivity to crotamiton or any component
Do not used on inflamed or raw skin
Avoid contact with face, eyes, mucous membranes, and urethral meatus
Safety and effectiveness in pediatric patients have not been established

Mechanism of Action

Mechanism of action unknown

Pharmacodynamics/Kinetics

Metabolism:
N/A
Half-life:
N/A
Elimination:
N/A

Dosage

Children and Adults:

Scabicide:
apply from chin to toes qd for 2 days, bathe 48h after last application
Pruritus:
apply to affected area prn

Dosage In Renal Failure

Creatinine clearance (ml/min):
N/A
Dialysis
Hemo: N/A
CAPD: N/A

CLOXACILLIN

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:10:00 +0000

Antibacterial Activity

Effective against Gram-positive cocci including the b-lactamase producers
Effective against some streptococci
Not effective against gram-negative & anaerobes

Pregnancy Risk Factor

Category B

Contraindication/Precaution

Hypersensitivity to cloxacillin or any penicillins or any component
Use caution with patient who are allergic to cephalosporin, they could have an hypersensibility to penicillins
Use caution if impaired liver/renal function

Mechanism of Action

Selective inhibitors of bacterial cell wall synthesis, by inhibiting to penicillins binding proteins (PBP'S)

Pharmacodynamics/Kinetics

Metabolism:
Partially by the kidney
Half-life:
0.5-1.5 hours, change with renal/hepatic function.
Elimination:
mostly excreted in urine, and some in feces

Dosage

Children: (max 4g/day)

> 28 days old: 50-100 mg/kg/d IV/PO div qid

Adults:

250-500 mg q6h IV/PO

Dosage In Renal Failure

Creatinine clearance (ml/min):
10: unchanged
10-50: unchanged
50-80: unchanged
>80: unchanged
Dialysis
Hemo: N/A
CAPD: N/A

CLOTRIMAZOLE

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:09:00 +0000

Antifungal activity

Effective treatment for topical candidiasis, Tinea corporis/cruris/pedis/versicolor
Active against Candida sp., tinea versicolor due to Malassezia furfur, Trichophyton rubrum, Trichophyton mentagrophytes, Epidermophyton floccosum, and Microsporum canis.

Pregnancy Risk Factor

Class B

Contraindication/Precaution

Hypersensitivity to clotrimazole , or any component
Only for topical use (not ophthalmic)
Use caution if nursing mother
Safety and effectiveness of clotrimazole lozenges (troches) in children <3 years of age have not been established Mechanism of Action Binds to phospholipids in the fungal cell membrane altering cell wall permeability resulting in loss of essential intracellular elements Pharmacodynamics Metabolism: N/A Half-life: N/A Elimination: excreted in urine and feces Dosage Topical 1% cream/lotion/solution Children and Adults: Cover affected and immediately surrounding skin Tinea multiple forms: apply bid Candidiasis cutaneous: apply bid Oral (Troches) Children > 3 years and adults:
TX: 10 mg PO 5x/day for 14 days
Prophylaxis: 10 mg PO 3x/day

Vaginal:

Children >12 years and Adults:
cream: apply intra-vaginaly qhs for 7 days
vaginal suppository: 100 mg/day for 7 days or 500 mg single dose

Dose VS renal function

Cr. clearance (ml/min):
N/A

Dialysis
Hemo: N/A
CAPD: N/A

CLOFAZIMINE

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:07:00 +0000

Antibacterial Activity

Used in the treatment of dapsone-resistant leprosy, multibacillary dapsone-sensitive leprosy, erythema nodosum leprosum and Mycobacterium avium-intracellulare (MAI) infections

Pregnancy Risk Factor

Category C

Contraindication/Precaution

Hypersensitivity to clofazimine or any component
Use with caution in patients with GI problems
Use with caution if nursing
Dosages of clofazimine of more than 100 mg daily should be given for as short a period as possible and only under close medical supervision
Safety and effectiveness in children have not been established

Mechanism of Action

Binds preferentially to mycobacterial DNA to inhibit mycobacterial growth; also has some anti-inflammatory activity through an unknown mechanism

Pharmacodynamics/Kinetics

Metabolism:
liver, partially
Half-life:
terminal: 8 days
in tissue: 70 days
Elimination:
excreted in feces

Dosage

Children:

Treatment of leprosy:

Safety and effectiveness in children have not been established
Several cases of children treated with clofazimine have been reported in the literature.
1 mg/kg PO qd in combination with dapsone and rifampin

Adults:

Dapsone-resistant leprosy:
100 mg PO qd in combination with one or more antileprosy drugs for 36 months then
100 mg PO qd as single drug
Dapsone-sensitive multibacillary leprosy:
100 mg PO qd in combination with two or more antileprosy drugs for at least 24 months and continue until negative skin smears are obtained, then institute single drug therapy with appropriate agent
Erythema nodosum leprosum:
100-200 mg PO qd for up to 3 months or longer then
taper dose to 100 mg PO qd
Pyoderma gangrenosum:
300-400 mg PO qd for up to 12 months

Dosage In Renal Failure

Creatinine clearance (ml/min):
N/A
Dialysis
Hemo: N/A
CAPD: N/A

IODOCHLORHYDROXYQUIN/CLIOQUINOL

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:05:00 +0000

Antibacterial activity

Used in the topical treatment of tinea pedis, tinea cruris, and skin infections caused by dermatophytic fungi (ringworm)

Pregnancy Risk Factor

Class C

Contraindication/Precaution

Do not use if hypersensitivity to clioquinol or any component

Mechanism of Action

Chelates bacterial surface and trace metals needed for bacterial growth

Pharmacodynamics

Metabolism: N/A
Half-life: 11-14 hours
Elimination: excreted in urine

Dosage

Children and Adults:

Apply to skin bid-tid; do not use for longer than 7 days

Dose VS renal function

Cr. clearance (ml/min):
N/A

Dialysis
Hemo: N/A
CAPD: N/A

CLINDAMYCIN

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:03:00 +0000

Antibacterial Activity

Cover gram-positives and most anaerobes

Pregnancy Risk Factor

Category B

Contraindication/Precaution

Hypersensitivity to clindamycin or any component
Can cause pseudomembranous colitis and reversible liver enzyme elevation, do not give if previous pseudomembranous colitis or hepatic impairment

Mechanism of Action

Inhibits protein synthesis by reversibly binding to 50S ribosomal subunits

Pharmacodynamics/Kinetics

Metabolism:
liver
Half-life:
1.6-5.3 hours, average: 2-3 hours
Elimination:
others or unknown

Dosage

Children: IV

Body weight < 2000 g 0-7 days old: 5 mg/kg IV q12h 8-28 days old: 5 mg/kg IV q8h Body weight > 2000 g
0-7 days old: 5 mg/kg IV q8h
8-28 days old: 5 mg/kg IV q6h
> 28 days old: 7.5 mg/kg IV q6h or 5-6 mg/kg PO q8h

Adults:

PO: 150-300 mg q6h
IV: 300-900 mg q6-8h (max 2.7 g DIE)

Dosage In Renal Failure

Creatinine clearance (ml/min):
<10: unchanged 10-50: unchanged 50-80: unchanged >80: unchanged

CLARITHROMYCIN

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:02:00 +0000

Antibacterial Activity

Effective against bacteria lacking cell wall (eg. mycoplasma, legionella, chlamydia)
Effective against gram-positive aerobes
Effective against gram-negative aerobes except: campylobacter, pasteurella and some H. influenza
Poor anaerobic coverage

Pregnancy Risk Factor

Category C

Contraindication/Precaution

Hypersensitivity to clarithromycin or macrolides or any component
Not to used be if concomitant cisapride, terfenadine or astemizole usage
Use caution if impaired liver/renal function

Mechanism of Action

Prevents translocation of polypeptide chain by binding to the P site of the ribosomal 50s subunit

Pharmacodynamics/Kinetics

Metabolism:
liver
Half-life:
5-7 hours, changes with renal function.
Elimination:
mostly excreted in feces (bile), and some in uurine

Dosage

Children:

> 28 days old: 7.5 mg/kg PO q12h (max 1 g/d)

Adults:

PO: 250-500 mg q12h

Dosage In Renal Failure

Creatinine clearance (ml/min):
<10: give 50-75% of usual dose 10-50: give 75% of usual dose 50-80: unchanged >80: unchanged
Dialysis
Hemo: dose post-dialysis: 75% of usual dose x1
CAPD: none

CIPROFLOXACIN

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 12:00:00 +0000

Antibacterial activity

Enteric gram-negative bacilli.
Limited gram-positive coverage.
No anaerobic coverage.

Pregnancy Risk Factor

Class C

Contraindication/Precaution

Hypersensitivity to ciprofloxacin, other quinolones or any component
Do not use if pregnancy/lactating patient
Use caution if CNS/seizure disorder

Mechanism of Action

Prevents supercoiling of nucleic acids of bacteria.

Pharmacodynamics

Metabolism: Partially metabolized in the liver.
Half-life: 4 hours.
Elimination: 50% renal, 40% biliary.

Dosage

Children: (with exception of Cystic Fibrosis, not approved under 18 years old)

> 28 days old: 20-30 mg/kg/d PO div bid (max 1.5 g/d)

Adults:

PO: 250-750 mg q12h
IV: 200-400 mg q8-12h

Ophthalmic:

Children/adults:
1-2 drops q2h while awake for 2 days then
1-2 drops q4h while awake for 5 days

Dose VS renal function

Cr. clearance: ml/min
<10: q24h 10-50: PO: 250-500 mg q12h; IV: q12-24h 50-80: unchanged >80: unchanged
Dialysis
Hemo: 50% of normal dose q12h
CAPD: 50% of normal dose q8h

CINOXACIN

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:59:00 +0000

Antibacterial activity

Enteric gram-negative bacilli.
Limited gram-positive coverage.
No anaerobic coverage.
Has less intrinsic bactericidal activities compare to other quinolones

Pregnancy Risk Factor

Class C

Contraindication/Precaution

Hypersensitivity to cinoxacin, other quinolones or any component
Do not use if pregnancy/lactating patient
Use caution if CNS/seizure disorder
Not recommended in children <18 years of age. Mechanism of Action Prevents supercoiling of nucleic acids of bacteria. Pharmacodynamics Metabolism: Partially metabolized in the liver. Half-life: 1.5 hours, changes with renal function Elimination: renal Dosage Children: not approved under 18 years old Adults: 250 mg PO q6h or 500 mg PO q12h (qd for prophylaxis) Dose VS renal function Cr. clearance: ml/min <10: 250 PO q24h (do not use if anuria) 10-50: 250 PO q12-24h 50-80: 250 mg PO q8h >80: unchanged
Dialysis
Hemo: post dialysis dose of 50% normal dose q12h
CAPD: 50% of normal dose q8h

Hypertension

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:56:00 +0000

Signs and Symptoms
The patient with hypertension tends to be older and the prevalence of the disease increases with age. However, 2 percent of children have hypertension while another 5 percent are borderline. Black adults have a higher incidence of hypertension than Caucasian adults and typically a more severe form of the disease. Risk factors for the development of hypertension include a positive family history of hypertension or cardiovascular disease, diabetes, hypercholesterolemia, obesity, sedentary lifestyle, high sodium intake, high dietary fat intake, alcohol use, smoking, and a stressful lifestyle.

Hypertension is defined as systolic blood pressure (BP) exceeding 140mmHg and/or diastolic BP exceeding 90mmHg measured at least twice on separate days. About 90 percent of cases are due to essential hypertension, while the remaining cases are secondary to another disease, such as renal parenchymal disease or pheochromocytoma. There is also isolated systolic hypertension and isolated diastolic hypertension.

Hypertension is manifested within the eye as both hypertensive retinopathy and hypertensive ocular complications. Hypertensive ocular complications include retinal vessel occlusion, ocular ischemic syndrome, non-arteritic anterior ischemic optic neuropathy, internuclear ophthalmoplegia, cranial nerve palsy, nystagmus and midbrain syndrome, and amaurosis fugax and transient ischemic attack.

Pathophysiology
Essential hypertension develops from renal system dysfunction. The kidney is a filtering organ that retains vital blood components and excretes excess fluid. If too much fluid is retained, BP rises. If too little fluid is retained, BP decreases. Arterial pressure within the renal artery triggers a feedback loop. The kidneys excrete sodium, which osmotically draws fluid into the excretory system in a process called pressure diuresis. This causes a decrease in blood fluid volume and arterial pressure.

As pressure within the renal artery decreases, the kidneys reflexively secrete an enzyme called renin. This enzyme causes the formation of a protein called Angiotensin I. Angiotensin I directly stimulates the kidneys to retain sodium and fluid. Angiotensin I is converted in the lungs, via the enzyme angiotensin converting enzyme (ACE) to Angiotensin II. Angiotensin II is a potent vasoconstrictor which increases total peripheral vascular resistance and hence elevates BP.

As BP elevates, the whole system begins again with pressure diuresis. In healthy individuals, this feedback loop maintains a constant blood pressure with only minor fluctuations. In patients with essential hypertension, this feedback loop fails for undiscovered reasons. The result is a higher than normal level of pressure within the renal artery necessary for pressure diuresis to occur.

Hypertension plays a significant role in the development of arteriosclerosis and atherosclerosis. Hypertension reduces the elasticity of vessels allowing lipids to deposit in the form of atheromas, which in turn leads to thrombus formation and possible emboli formation. This impedes blood flow and leads to ischemic disease.

Coronary heart disease is the leading cause of death in hypertensive patients. Ventricular hypertrophy occurs as a result of increased cardiac output in the face of systemic vascular resistance. Eventually, the heart is unable to maintain this constant output and the hypertrophied muscle outstrips its oxygen supply.

Cerebrovascular disease is a serious complication of hypertension. Hypertension is the leading cause of stroke. Hypertension-mediated atherothrombotic lesions are the cause.

Hypertension-induced arteriosclerosis may also result in atrophy of the renal glomeruli and tubules. This results in a malignant form of hypertension, and renal failure is also a frequent cause of death.

Management
Reducing morbidity and mortality is the main goal in hypertension management. Blood pressure reduction is done in a step-wise approach, often beginning with non-pharmacologic methods that include weight loss, and dietary and lifestyle modifications.

Should non-pharmacological methods prove unsuccessful, there are four families of drugs from which to choose:

1. Diuretics (reduce blood volume by inhibiting sodium and water retention)

2. Beta blockers (decrease cardiac output)

3. Calcium antagonists (induce vasodilation)

4. ACE inhibitors (decrease peripheral vascular resistance)

Medications from each family may be combined in order to achieve the desired pressure reduction.

Clinical Pearls

Hypertensive complications are mediated through arteriosclerosis and atherosclerosis.

Weight reduction is the most potent non-pharmacological method of hypertension management.

Diabetes Mellitus

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:53:00 +0000

Signs and Symptoms
Diabetes mellitus is the most common endocrine disorder, and is defined as a group of disorders that exhibit a defective or deficient insulin secretory process, glucose underutilization, and hyperglycemia. Possible systemic signs and symptoms include polyuria (increased frequency of urination), polydipsia (increased thirst), polyphagia (increased appetite), glycosuria, weakness, weight loss, neuropathy, and nephropathy. Ophthalmic signs and symptoms may include chronic conjunctival injection, changes in corneal curvature, large fluctuations in refraction, premature cataractogenesis, nonproliferative and proliferative retinopathy and cranial nerve III, IV or VI palsy.

Type 1 diabetes, formerly known as insulin-dependent diabetes (IDDM) is also referred to as juvenile-onset or ketose prone DM, usually begins by age 20 and is defined by a severe, absolute lack of insulin caused by a reduction in the beta-cell mass of the pancreas. This may be the result of autoimmune processes and may involve genetic susceptibility.

Type 2 diabetes, formerly known as non-insulin-dependent diabetes (NIDDM), sometimes referred to as adult-onset DM, usually begins after age 40 as a multifactorial disease that may involve improper insulin secretion, malfunctioning insulin and/or insulin resistance in peripheral tissues. Approximately 10 percent of diabetic cases are type 1 and approximately 90 percent are Type 2.

Pathophysiology
The pancreas plays a primary role in the metabolism of glucose by secreting the hormones insulin and glucagon. The Islets of Langerhans secrete insulin and glucagon directly into the blood. Inadequate secretion of insulin, inadequate structure or function of insulin or its receptors results in impaired metabolism of glucose, carbohydrates, proteins and fats, characterized by hyperglycemia and glycosuria. Hyperglycemia is the most frequently observed sign of diabetes and is considered the etiologic source of diabetic complications both in the body and in the eye.

Glucagon is a hormone that opposes the action of insulin. It is secreted when blood glucose levels fall. Glucagon increases blood glucose concentration partly by breaking down glycogen in the liver. Following a meal, glucose is absorbed into the blood. In response to increased blood glucose levels, insulin is secreted causing rapid uptake, storage, or use of glucose by the tissues of the body. Unused glucose is stored as glycogen in the liver. Between meals, when blood glucose is at minimal levels, tissues continue to require an energy source to function properly. Stored glycogen, via glucagon, is converted to glucose by a pathway known as glycogenolysis. Gluconeogenesis is the production of glucose in the liver from noncarbohydrate precursors such as glycogenic amino acids.

Elevated glucose levels result in the formation of sorbitol (a sugar alcohol) via the aldose reductase pathway. Since sorbitol cannot readily diffuse through cell membranes, cell edema and changes in function can ensue. With respect to the eye, this contributes to the evolution of premature cataractogenesis (nuclear sclerotic, senile and snowflake posterior subcapsular cataracts) and sight threatening diabetic retinopathy (compromising the pericytes that line capillary walls).

An additional complication of hyperglycemia is nonenzymatic glycosylation. Nonenzymatic glycosylation is the binding of excess glucose to the amino group of proteins in the tissues. As a possible result, at the level of the capillary membranes, altered cell function may lead to the development of microaneurysms, vascular loops, and vessel dilation, allowing blood leakage. Platelet aggregation secondary to these changes initiates tissue hypoxia. These changes result in the system wide accumulation of edema and in the eye, increase the potential for retinal sequelae.

Glycemic control over the course of the disease has been shown to reduce the risk of developing debilitating organ disease and retinopathy. Blood glucose levels are of even greater importance in diabetic pregnant women, as hyperglycemia during pregnancy may initiate swift and severe progression of diabetic retinopathy. Other concurrent systemic variables that may potentiate the onset of diabetic retinopathy include hypertension, nephropathy, cardiac disease, autonomic neuropathy and ocular findings such as elevated intraocular pressure and myopia.

Management
The easiest method of treating Type 2 diabetes is with diet control. Dietary regulation is set by basing the caloric intake on the patient’s ideal body weight, selecting adequate sources of protein and carbohydrate, while maintaining a reasonable distribution of foods. When hyperglycemia persists despite dietary changes, oral hypoglycemic agents become necessary. These agents can be prescribed in small doses, adjusting the dosage to larger levels to achieve tighter control, as necessary.

Insulin is always required for Type 1 and is an option for recalcitrant cases involving Type 2 diabetes. Conventional therapy involves the administration of an intermediate-acting insulin (NPH or lente), once or twice a day, with or without small amounts of regular insulin.

Clinical Pearls

Large changes in refraction may be the first sign of diabetic disease. Often, myopic or hyperopic shifts are created as the lens swells, secondary to sorbitol effects, resulting in large refractive changes, in what were otherwise noted as "stable eyes."

Albinism

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:52:00 +0000

Signs and Symptoms
Albinism affects approximately 1 in 20,000 individuals, producing pigmentary deficiency, abnormal crossings of the temporal fibers in the optic chiasm, nystagmus, photophobia, variable visual acuity and, frequently, strabismus. The main subdivisions of albinism include oculocutaneous, ocular, and albinoidism (absence of pigment in localized areas; the pigment in the skin, hair and eyes is less than normal but does not affect the individual as severely as the oculocutaneous or ocular types). The literature reports as many as 20 variants of oculocutaneous albinism alone.

Oculocutaneous as well as ocular albinos exhibit similar ocular and visual dysfunction. The oculocutaneous albino patient manifests reduced acuity, photophobia, strabismus, significant refractive error with astigmatism, transillumination of the iris and globe, nystagmus, blonde fundus with visible choroidal vasculature, and macular hypoplasia. A super-normal EOG and ERG is also present.

Transillumination of the iris and globe results from insufficient uveal pigmentation and poor development of the retinal pigment epithelium. This leads to a funduscopic picture of a blond fundus with extensive areas of hypopigmentation and clearly visible underlying choroidal vasculature. The pigment of the RPE acts as a sink for incoming light. When the RPE is underdeveloped, light scatters within the eye, producing the subjective complaint of photophobia.

The level of visual acuity varies among albino patients according to the amount of ocular pigmentation present and the concomitant level of macular development. Ocular albinos have variable amounts of uveal pigmentation and the potential to have the best acuity (20/25 to 20/300) among albinos. Oculocutaneous albinos exhibits less pigmentation than their ocular albino counterparts and tend to have lower acuity levels (20/80 to 20/400).

Systemically, albino patients may exhibit difficulties with healing and infection, as well as bleeding (Chédiak-Higashi syndrome and Hermansky-Pudlak respectively). Clinicians should ask questions in the history regarding bruising, nosebleeding and healing.

Pathophysiology
Albinism is a disorder of amino acid metabolism that results in a congenital hypopigmentation of ocular and systemic tissues. Cellular pigmentation is dependant upon a cell’s ability to manufacture and sequester the pigment melanin. This is accomplished within organelles called melanosomes which reside inside cells called melanocytes. The melanocytes that originate in the neural crest provide pigment for the skin (including eyelids), hair, uvea, conjunctiva, stroma of the iris, ciliary body and choroid. The melanocytes that supply pigment for the retinal pigment epithelium (RPE) are derived from neuroectoderm. Inside the melanosome, melanin is synthesized from the amino acid tyrosine through the actions of the enzyme tyrosinase. On the basis of the results of either the tyrosine hair bulb test or electron microscopy of the hair bulb or skin, oculocutaneous albinos are classified as tyrosinase-positive or tyrosinase-negative.

Tyrosinase-positive and -negative oculocutaneous albinos possess an autosomal recessive inheritance pattern. Oculocutaneous albinism results from incomplete melanization of the cellular melanosomes. In tyrosinase-negative oculocutaneous albinism, the congenital inactivity of the enzyme tyrosinase prevents the cell’s use of tyrosine in the formation of the pigment melanin. In tyrosinase-positive oculocutaneous albinism, tyrosinase activity is normal, but there is an inability of the cells to sequester the synthesized melanin into the melanosomes.

An autosomal recessive subtype of tyrosinase positive oculocutaneous albinism commonly seen in Puerto Rico is the Hermansky-Pudlak syndrome. Here, patients exhibit hemorrhagic diathesis (a tendency toward easy bruising and bleeding) due to a platelet dysfunction along with normal tyrosinase activity.

Another autosomal recessive subtype of oculocutaneous albinism is the Chédiak-Higashi syndrome. Here, patients may have a silvery sheen to their skin, and blue to brown irides. Normal tyrosinase activity within hair bulbs shows increased susceptibility to infection, hepatosplenomegaly, lymphadenopathy and a predisposition to development of a lymphoma-like condition.

Ocular albinism, in contrast to oculocutaneous albinism, exhibits pigmentary dilution due to abnormalities in melanosome synthesis rather than inadequate melanization. Ocular albinism is transmitted through either an X-linked or autosomal recessive mode. The hair and skin of the ocular albino tends to show a much greater pigmentation than that of the oculocutaneous albino, often falling into a normal pigmentation range. The uveal pigmentation of the ocular albino is variable and may range from very hypopigmented to a nearly normal pigmentation level.

Both ocular and oculocutaneous albinism exhibit a hypoplastic macula. Orderly retinal morphogenesis depends on the organizing influence of the adjacent retinal pigment epithelium. The insufficient uveal pigmentation and poor development of the RPE in the albinotic patient provides a developmentally unstable substrate for normal retinal organization. Hence, the albinotic macula is always hypoplastic and the albinotic patient has secondarily reduced acuity. This maldevelopment of the macula explains the pendular nystagmus of the albino patient, as the albino eye constantly searches for a clear image.

SYPHILIS

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:50:00 +0000

SIGNS AND SYMPTOMS
Syphilis is a multi-system, multi-symptom disorder that occurs primarily through sexual transmission, though the disease can be spread through blood transfusion and direct contact with an infected lesion. Patients tend to be younger, with a history of unprotected sex. Elderly patients may manifest late-stage syphilis left untreated many years before.

In cases of congenital syphilis, the patient may manifest Hutchinson's triad (interstitial keratitis, deafness and malformed teeth), osteochondritis (inflammation of both bone and cartilage), chorioretinitis, hepatosplenomegaly (enlargement of the liver and spleen), and anorexia.

In the primary stage of acquired syphilis, the patient develops a painless chancre at the site of inoculation, as well as regional lymphadenopathy. While primarily genital, chancres may develop on the eyelid and conjunctiva. Other ocular signs in the primary stage include conjunctivitis, blepharitis, and alopecia.

In the secondary stage of acquired syphilis, the patient will develop malaise, lymphadenopathy, fever, maculopapular skin lesions on the palms and soles, joint pain, headache, and loss of appetite. Ocular signs are most common in secondary syphilis and include episcleritis, anterior uveitis, uveitic glaucoma, neuroretinitis, chorioretinitis, ischemic retinal vasculopathy, and infectious optic neuropathy.

In the third stage of acquired syphilis, focal endarteritis causes the formation of gummas (granulomatous lesions), which can involve the eye and adnexa, and the central nervous and cardiovascular systems. At this stage, neurosyphilis can manifest with acute meningitis, cranial neuropathies, optic atrophy, pupil abnormalities, paresis, and tabes dorsalis (degeneration of the dorsal columns of the spinal cord resulting in loss of coordination, reflexes and sensation, and ataxic gait).

PATHOPHYSIOLOGY
Syphilis is caused by the spirochete bacteria, Treponema pallidum. It is transmitted through mucous membranes or open skin-to-skin contact, primarily through sexual intercourse. Transmission can also occur through blood transfusion.

After infection, a period of incubation ensues. The organism enters the lymphatic system and bloodstream and disseminates soon after contact. Shortly after infection, a chancre forms at the site of inoculation. The chancres spontaneously heal after two to eight weeks, and the patient enters the secondary stage of syphilis. In individuals with an intact immune system, the disease enters a period of latency. Inflammation and regional vasculopathy account for the signs and symptoms.

After a period of latency (which may extend four or more years in an untreated or undertreated individual), the patient enters the tertiary stage. Focal granulomatous lesions known as gummas develop and can affect virtually any organ system. The resultant dysfunction caused by these gummas accounts for the dysfunction seen in tertiary syphilis. Approximately 10 percent of untreated patients develop neurosyphilis. Since the organism has a predilection for the dorsal spinal cord and intercalated neurons, these patients can develop an ataxic gait and loss of sensation from the lower limbs, and light-near dissociated pupils, which are often miotic (Argyll Robertson pupils). If left untreated, dysfunction of the central nervous and cardiovascular systems can lead to progressive dementia and death.

MANAGEMENT
Serologic testing to detect host antibodies is the mainstay of diagnosis. Tests that detect cardiolipin-lecithin-cholesterol antibodies but are non-specific for Treponema pallidum include the venereal disease research laboratory (VDRL) and rapid plasma reagin (RPR) which indicate current activity of disease. False-positive results are possible on these tests.

Tests specific for antibodies to Treponema pallidum include the fluorescent treponemal antibody absorption (FTA-ABS) and microhemagglutination assay for Treponemal pallidum (MHA-TP). These tests indicate whether or not antibodies are present from a previous syphilitic infection, but do not indicate current disease activity. There is a lower incidence of false-positive results with these specific tests. When you suspect syphilis, order both a specific and a non-specific test. In cases where serologic results are uncertain, these tests can be performed using cerebrospinal fluid.

Treatment of syphilis involves systemic IV or IM penicillin. Alternatives for penicillin-sensitive patients include doxycyline, tetracycline, ceftriaxone, and chloramphenicol. In neurosyphilis, there is no acceptable substitute, and patients must be desensitized to penicillin prior to treatment.

CLINICAL PEARLS

Syphilis is a great mimic. Always keep this condition in mind when encountering patients with cranial neuropathies, optic neuropathies, anterior uveitis, chorioretinitis, retinal vascular occlusion, and chronic anterior segment inflammation.
Manifestations of syphilis can be complicated by concurrent HIV infection. Always consider HIV infection in patients with syphilis. Further, concurrent infections with gonorrhea and chlamydia frequently occur, and should also be investigated.
Nearly 45 percent of males manifesting bilateral tonic pupils will test positive for syphilis.
Lyme disease, another spirochetal disease, is also a great mimic and behaves very similar to syphilis. In fact, Lyme disease can cause false-positive readings on both specific and non-specific tests for syphilis.

SICKLE CELL DISEASE

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:48:00 +0000

SIGNS AND SYMPTOMS
Ocular symptoms are uncommon in the early stages of the disease. Systemically, symptoms include painful crises of abdominal and musculoskeletal discomfort.

Ocular signs include comma-shaped vessels in the bulbar conjunctiva, iris atrophy, iris neovascularization, dull-gray fundus appearance, retinal venous tortuosity, nonproliferative retinal hemorrhages in the subretinal, intraretinal or preretinal position. Further signs include black sunbursts (retinal pigment epithelial hyperplasia secondary to deep retinal vascular occlusions), glistening refractile deposits in the retinal periphery (hemosiderin-laden macrophages), salmon patch hemorrhages (orange-pink-colored intraretinal hemorrhage), angioid streaks (breaks in Bruch's membrane radiating from the optic nerve), venous occlusion, artery occlusion, peripheral neovascularization (seafan retinopathy) with subsequent vitreous hemorrhage and tractional retinal detachment.

PATHOPHYSIOLOGY
Hemoglobinopathies are among the more commonly inherited diseases in humans. Hemoglobinopathies result when there is altered structure, function or production of hemoglobin. Hemoglobin is the principle protein of the erythrocyte, responsible for binding and facilitating oxygen transmission to tissues. In the four variations of sickle cell disease, systemic and ocular tissues become deprived of oxygen and undergo pathologic changes.

Normal erythrocytes, containing normal hemoglobin, appear as flexible, pliable, biconcave discs. Erythrocytes affected by sickling disease lose their biconcave shape and their ability to efficiently move through the circulatory system. The "sickled" cells become rigid, restrict blood flow, produce clots and cause tissues to become hypoxic.

Variations in the alteration of the amino acid sequence on the globin chain produce variations in the disease's expression. The four forms of the disease are often referred to by their genotype: sickle cell trait (AS), sickle cell anemia (SS), sickle cell disease (SC) and sickle cell thalasemia (SThal).

Systemically, the sickle cell anemia variation (SS) produces the most symptoms. With respect to the eye, the sickle cell disease mutation (SC) produces the most effects. Overall, the sickle cell trait expression (AS) produces the fewest complications.

MANAGEMENT
The treatment goal for sickle cell retinopathy is to reduce the risk of, prevent or eliminate retinal neovascularization. Follow patients with asymptomatic sickle cell disease biannually with ocular examinations and dilated retinal evaluation. Since visual loss can result from both nonproliferative (subretinal neovascularization secondary to angioid streaks) and proliferative retinal disease, refer the patient to the retinologist when you see these retinal findings. Treat proliferative disease with fluorescein angiography and panretinal photocoagulation. Cryotherapy has not been proven to be efficacious and is associated with high complication rates.

CLINICAL PEARLS

Proliferative sickle cell retinopathy breaks down into five stages:
Stage 1: peripheral retinal arteriolar occlusions
Stage 2: peripheral arterio-venous anastamoses
Stage 3: neovascular fronds known as sea fans
Stage 4: vitreous hemorrhage as tractional forces and vitreous collapse tear fragile neovascular membranes
Stage 5: advanced disease, identified by severe vitreous traction and retinal detachment

Other causes of peripheral neovascularization include sarcoidosis, diabetes, retinal venous occlusion, Eales' disease, leukemia and ocular ischemic syndrome. However, the characteristic sea fan frond is diagnostic of sickle retinopathy.

For patients with suspicious findings, laboratory tests for sickle cell disease include the Sickledex, Sickle Prep and plasma hemoglobin electrophoresis.

Oral carbonic anhydrase inhibitors should be avoided. They may exacerbate the sickling of blood cells.

SARCOIDOSIS

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:45:00 +0000

SIGNS AND SYMPTOMS
Sarcoidosis is a systemic granulomatous disease of unknown etiology. Clinical findings may include a debilitating, febrile illness with cough and dyspnea, fatigue, bilateral hilar lymphadenopathy (visible upon plain film radiograph), erythema nodosum, alveolitis, acute polymyositis, arthritis, musculoskeletal anomalies, lacrimal or salivary gland infiltration or sarcoid nodules of the skin. It occurs most frequently in young adults (20 to 40 years), has a predilection for women and for races of color.

Patients diagnosed with systemic sarcoidosis have nearly 20 percent incidence of ocular involvement. The most prevalent ocular sign is unilateral, anterior, granulomatous uveitis. Less common presentations include unilateral nongranulomatous uveitis, bilateral intermediate uveitis, and bilateral chronically smoldering low-grade granulomatous ocular inflammation (Lofgren's syndrome).

The common clinical ocular findings associated with sarcoid uveitis include decreased or hazy vision, pain, photophobia, lacrimation, conjunctival injection, cells and flare in the anterior chamber, granulomatous iritis with large "mutton fat" keratic precipitates scattered over the back surface of the corneal endothelium, iritis spill over leading to anterior vitritis, true vitritis with white exudative debris in the region of the ora serrata (snowball or snowbank retinopathy) with retinal vasculitis (candle wax drippings) and phlebitis (venous sheathing).

Nodules of the iris stroma (Busacca nodules), nodules of the pupillary border (Koeppe nodules), conjunctival granulomas, band keratopathy, posterior synechiae, cataract formation, secondary glaucoma, retinal hemorrhage, retinal neovascularization, cystoid macular edema, venous occlusion, optic disc swelling, optic nerve infiltration, compressive optic neuropathy, proptosis and extra ocular muscle palsy are all documented findings.

PATHOPHYSIOLOGY
Studies underscore that lymphocytes interact with macrophages. Some postulate that CD4+ T-helper 1 cells, in concert with macrophages, produce a cascade of cytokines and chemotactic factors which result in tissue changes and granulomatous lesions that affect many tissues and allow for the multi-system, multi-symptom nature of this disease. The clinical features of sarcoidosis mimic those of rheumatologic diseases, with increasing reports of coexistent autoimmune disease; however, no one has decisively determined an association.

MANAGEMENT
Manage the ocular signs and symptoms of sarcoidosis by the findings. Manage uveitis aggressively with topical cycloplegics (e.g. homatropine 5%, scopolamine 0.25%, or atropine 1%, BID), topical steroids such as Vexol (rimexolone 1%) and Pred Forte (prednisolone acetate 1%), Q1H to QID if necessary, oral steroidal or nonsteroidal anti-inflammatories. In recalcitrant cases, you may attempt periocular subtenon steroid injections of Kenalog 40 (triamcinolone) every three to four weeks. Antimetabolites such as methotrexate and cyclosporin-A have been used effectively in patients intolerant to steroids. Add topical aqueous suppressants if intraocular pressure control is required. Topical nonsteroidal anti-inflammatory agents such as Acular (Ketorolac tromethamine) and Voltaren (diclofenac sodium), QID, may be attempted if you detect cystoid macular edema. Allow the retinologist to manage peripheral retinal neovascularization and pars planitis with panretinal photocoagulation and oral or injected steroids respectively.

The primary care physician can lead systemic management. Referral for laboratory testing across the autoimmunologic, rheumatologic, infectious and inflammatory spectrum is essential, especially for atypical uveitis or optic neuropathy. Obtain or suggest to the PCP testing for anemia, leukemia, syphilis, HIV, lupus, Lyme disease, tuberculosis, arthritis, ankylosing spondylitis and hypertension. The initial battery could include complete blood count (CBC with differential), fluorescent treponemal antibody absorption test (FTA-Abs), reactive plasma reagin (RPR), purified protein derivative with anergy panel (PPD with anergy panel), anti-nuclear antibody (ANA), angiotensin converting enzyme (ACE), Lyme titre, rheumatoid factor (RF), sickle prep, chest x-ray (CXR) and sacroiliac joint films. Tests that indicate sarcoidosis most specifically are the chest x-ray, ACE and gallium scan.

CLINICAL PEARLS

Diagnose sarcoidosis through clinical (laboratory tests and biopsy) and radiologic evidence. Up to 90 percent of patients with ocular sarcoid have abnormal chest radiographs. Lung biopsy by tracheobronchial fiber optic techniques is 90 percent accurate. Biopsy of an enlarged, potentially infiltrated lacrimal gland or conjunctival granuloma is an acceptable alternative and can be handled by most general ophthalmologists.

A simple but effective practice management tool: a dictated letter to the primary care physician explaining the ocular problem, the management, the request for lab studies and the progress reports.

Vitritis without retinitis, vasculitis or phlebitis should be considered large reticulum cell sarcoma until proven otherwise. The minimum initial work up for this form of intermediate uveitis includes, but is not limited to, CBC with differential, FTA-Abs, RPR, PPD, ANA, ACE, Lyme titre, RF and CXR.

MYASTHENIA GRAVIS

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:44:00 +0000

SIGNS AND SYMPTOMS
Patients with myasthenia gravis typically present with symptoms of variable ocular fatigue and weakness. The common ocular findings include ptosis, droopy eyelids that appear worse at the end of the day, orbicularis weakness, limitation of ocular motility, paradoxical lid retraction, Cogan's lid twitch (transient eyelid retraction following an extended period of down gaze), exposure keratitis and intermittent diplopia.

A small percentage of patients possess a form of the disease known as ocular myasthenia. Here, the signs and symptoms remain strictly confined to the extraocular muscles. The pupil is never involved in MG.

Systemic symptoms include intermittent fatigue of the limbs, weakness of the facial muscles and difficulty breathing, chewing, talking and swallowing. In a small percentage of patients, dysthyroidism may also be present, resulting in the mixture of ptosis and exophthalmos. Thymic neoplasia (thymoma) is an associated finding in patients over 65. Associated disorders such as diabetes mellitus, lupus erythematosus and rheumatoid arthritis occur in 20 percent of MG patients.

PATHOPHYSIOLOGY
Myasthenia gravis (MG) is an autoimmune disease that destroys key components of the neuromuscular system responsible for governing muscular activity. It has a prevalence of approximately 1 in 20,000 persons. Females are more likely to experience early onset disease (under age 50) by a ratio of 7:3. Females reach their peak incidence by the third decade while males reach their peak incidence in the fifth decade.

Up to 75 percent of patients with myasthenia present with some type of ocular symptom. Ninety percent of patients with myasthenia gravis will develop ocular signs or symptoms, and 80 percent of patients who present with ocular involvement progress to have involvement of additional muscle groups within two years of the initial presentation.

Signs and symptoms may be initiated, exacerbated or mimicked by medications such as D-penicillamine, antibiotics (polymyxn B, neomycin, gentamicin, streptomycin), beta blockers and anticonvulsants.

MANAGEMENT
Patients who report neurological signs or symptoms require a through review of family history, illnesses, systems, medications and behaviors. Inspect and measure the palpebral apertures of patients with positional lid anomalies.

In office tests for the optometrist include:

1. asking the pertinent history

2. testing the pupils

3. assessing the orbicularis function by asking the patient to squeeze their eyelids shut while you attempt to open them forcibly

4. attempt to elicit diplopia by eliminating the occlusive effects of ptosis

5. attempt to elicit superior rectus or levator fatigue by asking the patient to sustain upgaze while you observe for unexpected eyelid droop

6. attempt to elicit the Cogan's lid twitch sign by asking the patient to look into downgaze for an extended period, then to gaze up

7. apply an ice pack to the eyelid for five to 15 minutes, reevaluating the ptosis and/or ocular motility for improved position following the ice packs removal

8. ask the patient to close their eyes for 30 minutes (sleep test), reevaluating the ocular motility and/or ptosis for improved position upon awakening. Diagnosis may also be assisted by evaluating old photographs for appearance.

The quintessential method of diagnosing MG is the endrophonium hydrochloride (Tensilon) injection test. An additional laboratory test used for diagnosing MG is the acetylcholine antibody receptor test. Medical management of MG should be handled by the neurologist or neuro-ophthalmologist.

CLINICAL PEARLS

MG should always be a consideration in cases of non-restrictive, pupil sparing CN III, IV and VI nerve palsy as well as unilateral and bilateral internuclear ophthalmoplegia.

Laboratory testing is an important consideration for patients diagnosed with MG because of its association with other systemic autoimmune diseases. Pertinent studies include fasting blood sugar (FBS: diabetes), thyroid function tests (ASH, T3, T4), antinuclear antibody (ANA: lupus), rheumatoid factor (RF: arthritis) and in suspicious cases, radiological testing of the thymus gland. A purified protein derivative (PPD: tuberculosis) should be completed because steroid regimens, used to treat MG have the potential to activate or worsen dormant disease.

Patients should always be educated to report difficulties with breathing or swallowing.

GIANT CELL ARTERITIS

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:41:00 +0000

SIGNS AND SYMPTOMS
The patient is invariably elderly, with the mean age of 75 years. Incidence increases with advancing age. An associated condition, known as polymyalgia rheumatica (PMR), involves pain and stiffness of the muscles of the proximal limbs, particularly upon waking. In fact, PMR is likely within the same spectrum as giant cell arteritis (GCA). There is a 2:1 female to male ratio, and a higher incidence in whites.

Systemic manifestations may include malaise, weight loss and anorexia, headache in the temporal or occipital region, pulseless and indurated temporal artery, night sweats, tongue necrosis and oral ulceration, dental abscess, scalp pain, scalp necrosis and jaw claudication when eating. Other systemic manifestations include depression, mental disturbance, breast masses, gynecological disorders, persistent flu-like illness, chronic pharyngitis, vertigo, muscle aches, cardiac arrhythmia, congestive heart failure, and myocardial infarction.

Ocular manifestations include anterior ischemic optic neuropathy (AION), posterior ischemic optic neuropathy (PION), central retinal artery occlusion (CRAO), cilioretinal artery occlusion, ophthalmic artery occlusion, amaurosis fugax, diplopia and opthalmoplegia. Further ocular manifestations are tonic pupil, Horner's syndrome, ocular hypotony, chronic uveitis, episcleritis and scleritis, conjunctivitis, ocular ischemic syndrome, visual hallucinations, posterior chiasmal field loss, cortical blindness, and ocular ischemic syndrome.

PATHOPHYSIOLOGY
GCA is an idiopathic inflammation of medium and large arteries where the muscular wall of these vessels is infiltrated by monocytes, histiocytes, plasma cells, and multinucleate giant cells. Significant infiltration can lead to vessel occlusion with resultant ischemia and dysfunction of the organ system fed by the vessel. GCA is a multi-system, multi-symptom disorder-virtually any vessel within the body may be involved.

The degree of ischemia tolerated varies by system, and symptoms often appear for a period of months before diagnosis. In the eye, ischemia often manifests by amaurosis fugax, intermittent diplopia and ophthalmoplegia prior to complete occlusion of the posterior ciliary, retinal or ophthalmic arteries. When ocular symptoms occur, there is a much shorter time interval to severe permanent vision loss.

MANAGEMENT
Optimal management of giant cell arteritis means recognizing GCA as a potential cause of the above mentioned findings in an elderly patient. Once recognized, order a Westegren erythrocyte sedimentation rate (ESR) to confirm suspicions. The ESR is a non-specific index of illness, but is frequently elevated in cases of GCA. If the ESR is elevated, then refer for a temporal artery biopsy in order to conclusively diagnose GCA. Remember, however, that a small number of GCA cases do not manifest an elevated ESR. In these cases, the findings and systemic history become more diagnostically important.

GCA requires systemic steroids to preserve vision and reduce morbidity. However, do not withhold steroids pending biopsy results. If exam findings and ESR indicate GCA, then start steroids immediately. Biopsy results, though, will not be affected for several weeks after you initiate steroid therapy.

The dosage of steroids is controversial. Rheumatologists recommend low doses of prednisone, typically 10-20mg per day. However, it is argued that rheumatologists see patients with milder forms of the disease. When vision loss ensues, the patient should receive 1-2mg IV methylprednisolone for several days, with high dose (80-120mg) daily oral prednisone tapered over several weeks. Afterwards, these patients must be maintained on low dose oral prednisone for two to four years.

CLINICAL PEARLS

Vision loss from GCA is an emergency. Untreated, progression to the fellow eye occurs in a high number of cases within hours to days. Frequently, vision loss in GCA is devastating and irreversible. Don't wait until the second eye is involved to take action. You must have an emergency plan in your office in order to handle this disease.

You must consider GCA in elderly patients with AION, PION, amaurosis fugax, intermittent diplopia, CRAO, and cilioretinal occlusion and manage accordingly.

In cases of retrobulbar optic neuropathy in an elderly patient, don't be fooled into diagnosing retrobulbar optic neuritis (as seen in multiple sclerosis) as this is a disease of younger patients. Consider PION, which is typically caused by GCA and tends to involve the fellow eye.

In cases where there are multiple clinical presentations, such as combined cilioretinal artery occlusion and AION, bilateral AION, bilateral CRAO, or CRAO and contralateral tonic pupil (among others), then aggressively investigate GCA in the elderly patient.

Giant cell arteritis and its visual manifestations should not be handled by a primary care optometrist, or even a general ophthalmologist. As the prognosis is grim and morbidity high, these patients should be managed by a neurologist (or neuro-ophthalmologist) specifically skilled in the treatment of GCA. Identify such an individual well in advance, since time is crucial once the GCA patient enters your office.

Pituitary Adenoma

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:40:00 +0000

Signs and Symptoms
Pituitary adenomas typically present during early adulthood, equally affecting males and females. There are no outstanding reported risk factors. The clinical presentation of pituitary adenoma varies depending on the location and severity of the tumor.

Prolactinomas, the most common form of pituitary tumor, cause amenorrhea (the loss of menstruation), galactorrhea (the spontaneous flow of milk from the breast), and infertility in females. They cause hypogonadism, decreased libido and impotence in males. Tumors that secrete excess growth hormone cause gigantism in children and acromegaly in adults. Adrenocorticotropic hormone (ACTH) secreting adenomas produce Cushing’s disease (hyperadrenalism). Symptomatic pituitary adenomas comprise 12 to 15 percent of all intracranial tumors, and must be differentiated from non-neoplastic mass lesions.

Visual symptoms vary and include bitemporal visual field loss more dense from the superior to inferior, color desaturation, diplopia as well as ophthalmoplegia tumors expand into the cavernous sinus. The funduscopic sign of long-standing chiasmal compression is primary optic atrophy (secondary to retrograde axonal degeneration). Severe optic atrophy indicates a poor prognosis for visual recovery following surgical decompression. (For visual field printout, see "Understanding Visual Fields and the Visual Pathways" page 56.)

Pathophysiology
The pituitary gland is situated within the sella turcica of the sphenoid bone, at the base of the skull. The anterior lobe of the pituitary gland secretes six hormones: thyroid stimulating hormone (TSH), ACTH, follicle stimulating hormone (FSH), leutenizing hormone, growth hormone (GH), and prolactin. The posterior pituitary gland secretes vasopressin and oxytocin.

Pituitary adenomas typically are slow growing, benign neoplasms of epithelial origin. In most circumstances they arise from the adenohypophysis (the anterior lobe of the pituitary gland) and are capable of producing both systemic and visual signs. Approximately 8 mm to 13 mm above the pituitary gland is the optic chiasm. The nasal retinal fibers of each eye (temporal visual field) cross at this point, proceeding into the contralateral optic tract.

Upwardly growing pituitary tumors, which reach appropriate sizes, impinge on the anterior notch of the chiasm at its lowest lying aspect. This produces the bitemporal hemianopsia with increased density superiorly. Since tumor growth is usually asymmetrical, the field loss between two eyes is also typically asymmetrical.

Diseases affecting the pituitary gland produce two types of disturbances: mechanical and hormonal. Mechanical disturbances occur whenever a tumor compresses adjacent structures. Hormonal manifestations result when hyper-or hyposecretions occur. Pituitary adenomas are further differentiated by size. Microadenomas have little impact on the visual system or gland function and are defined as intrasellar adenomas that measure up to one centimeter in diameter without sellar enlargement. Macroadenomas present with mass effect symptoms such as headaches and measure larger than one centimeter with generalized sellar enlargement. Macroadenomas include (in order of most common to least common): non-secreting adenomas, prolactin secreting (chromaphobe) adenomas, growth hormone secreting (acidophil) adenomas, ACTH secreting (basophil) adenomas and FSH or TSH secreting adenomas.

Secreting tumors are usually diagnosed by general physicians and endocrinologists. Non-secreting tumors are often diagnosed by eye care practitioners because they produce visual symptoms in the absence of systemic signs.

Management
Surgical therapy, medicinal therapy or radiotherapy are the three treatment options for pituitary adenomas. Since the late 1970s, the transphenoidal surgical approach has been the preferred procedure for removal of tumors. Surgery is indicated if there is evidence of tumor enlargement, especially when growth is accompanied by compression of the optic chiasm, cavernous sinus invasion, or the development of pituitary hormone deficiencies. Visual improvement following treatment is often dramatic, with the greatest degree of improvement occurring within the first few months. Perimetry and MRI occupy an important role in the post treatment monitoring of patients. Medicinal treatment is limited to prolactinomas. Bromocriptine, a dopamine agonist, is useful in shrinking the sizes of these tumors. Low dose therapy of Bromocriptine is maintained for life. If the drug therapy is discontinued, there is often regrowth and enlargement of the adenoma. Conventional radiotherapy is usually added adjunctively to prevent tumor regrowth.

Clinical Pearls

In pregnant women, bitemporal visual field loss and headache may signal pituitary apoplexy (rapid degeneration with hemorrhagic necrosis of the pituitary gland). Pituitary apoplexy is a potentially life-threatening condition. Any woman with sudden onset of headache and suspicious visual symptoms (confirmed by perimetry) should be referred for a MRI with or without lumbar puncture to rule out subarachnoid hemorrhage from the this type of tumor. Women with pituitary adenomas and MRI evidence of subarachnoid bleeding should deliver by cesarean section to avoid risk of apoplexy during delivery. Postpartum hemorrhage can cause infarction of the pituitary gland leading to hypopituitarism (Sheehan’s syndrome).

Pseudotumor Cerebri

noreply@blogger.com (Unknown) — Mon, 28 Nov 2011 11:37:00 +0000

Signs and Symptoms
Pseudotumor cerebri (PTC) is encountered most frequently in young, overweight women between the ages of 20 and 45. Headache is the most common presenting complaint, occurring in more than 90 percent of cases. Dizziness, nausea, and vomiting may also be encountered, but typically there are no alterations of consciousness or higher cognitive function. Tinnitus, or a "rushing" sound in the ears, is another frequent complaint. Visual symptoms are present in up to 70 percent of all patients with PTC, and include transient visual obscurations, general blurriness, and intermittent horizontal diplopia. These symptoms tend to worsen in association with Valsalva maneuvers and changes in posture. Reports of ocular pain, particularly with extreme eye movements, have also been noted.

Funduscopic evaluation of patients with PTC demonstrates bilaterally swollen, edematous optic nerves consistent with true papilledema. Ophthalmoscopy may reveal striations within the nerve fiber layer, blurring of the superior and inferior margins of the neural rim, disc hyperemia, and capillary dilatation. More severe presentations involve engorged and tortuous retinal venules, peripapillary hemorrhages and/or cotton wool spots, and circumferential retinal microfolds (Paton’s lines). Chronic papilledema mayresult in atrophy of the nerve head, with associated pallor and gliosis. Most cases of true papilledema will not present with a relative afferent pupillary defect, although visual field deficits may be present. The most common visual field defect associated with PTC is an enlarged blind spot, followed by a nasal deficit, typically affecting the inferior quadrants. Other field losses seen in PTC include arcuate defects, nasal step, generalized constriction, and least commonly, cecocentral scotoma.

Pathophysiology
Pseudotumor cerebri is a syndrome disorder defined clinically by four criteria: (1) elevated intracranial pressure as demonstrated by lumbar puncture; (2) normal cerebral anatomy, as demonstrated by neuroradiographic evaluation; (3) normal cerebrospinal fluid composition; and (4) signs and symptoms of increased intracranial pressure, including papilledema.

While the mechanism of PTC is not fully understood, most experts agree that the disorder results from poor absorption of cerebrospinal fluid by the meninges surrounding the brain and spinal cord. The subsequent increase in extracerebral fluid volume leads to elevated intracranial pressure. However, because the process is slow and insidious, there is ample time for the ventricular system to compensate and this explains why there is no dilation of the cerebral ventricles in PTC. Increased intracranial pressure induces stress on the peripheral aspects of the brain, including the cranial nerves. Stagnation of axoplasmic flow in the optic nerve (CN II) results in papilledema and transient visual obscurations; when the abducens nerve (CN VI) is involved, the result is intermittent nerve palsy and diplopia.

Many conditions and factors have been proposed as causative agents of PTC, including excessive dosages of some exogenously administered medications (e.g., vitamin A, tetracycline, minocycline, naladixic acid, corticosteroids), endocrinologic abnormalities, anemias, blood dyscrasias, and chronic respiratory insufficiency. However the majority of cases remain idiopathic in nature.

Management
All patients presenting with suspected papilledema or other manifestations of intracranial hypertension warrant prompt medical evaluation and neurologic testing. Current protocol dictates that patients presumptively diagnosed with papilledema must undergo neuroimaging via computed tomography or, preferably, magnetic resonance imaging within 24 hours. These tests are meant to rule out space-occupying intracranial mass lesions, and therefore should be ordered with contrast media unless otherwise contraindicated. In cases of PTC, neuroimaging typically displays small to normal-sized cerebral ventricles with otherwise normal brain structure. Patients with unremarkable radiographic studies should be subsequently referred for neurosurgical consultation and lumbar puncture. (Lumbar puncture should not be ordered until neuroimaging is found negative for space-occupying mass due to risk for herniation of brainstem through foramen magnum secondary to mass during lumbar puncture.) Additional medical testing includes serologic and hematologic studies.

Therapy for patients with PTC varies, but in most instances initiate systemic medications as a first line treatment. Typically, the drug of choice for the initial management of PTC is oral acetazolamide (Diamox), although other diuretics including chlorthalidone (Hygroton) and furosemide (Lasix) may also be used effectively. Corticosteroid therapy is considered controversial in the management of PTC. While a short-term course of oral or intravenous dexamethasone may be helpful in initially lowering intracranial pressure, it is not considered to be an effective long-term therapy because of the potential for systemic and ocular complications.

For patients in whom conventional medical therapy fails to alleviate the symptoms and prevent pathologic decline, surgical intervention is the only definitive treatment. Cerebrospinal fluid shunting procedures are commonly employed in recalcitrant cases of PTC, but are successful in only 70 to 80 percent of cases. Optic nerve sheath decompression has also been advocated as a method

CIDOFOVIR

noreply@blogger.com (Unknown) — Sat, 19 Nov 2011 15:48:00 +0000

Antibacterial activity

Active against CMV
Active against others herpes viruses (but not approved for their Tx)

Pregnancy Risk Factor

Class C

Contraindication/Precaution

Cidofovir is indicated for the treatment of CMV retinitis in patients with acquired immunodeficiency syndrome (AIDS) only
IV prehydratation and administration of probenecid MUST be used with each cidofovir infusion
Hypersensitivity to cidofovir, or any component
Do not use with nursing mothers
Must monitor renal function and adjust dosage accordingly
Monitor neutrophil counts, could cause granulocytopenia
Safety and effectiveness in children have not been studied.
Use caution if renal dysfunction or if other nephrotoxic agents present

Mechanism of Action

Suppresses CMV replication by selective inhibition of viral DNA synthesis.

Pharmacodynamics

Metabolism: N/A
Half-life: ~3 hours, changes with renal function
Elimination: excreted in urine

Dosage

Cidofovir is indicated for the treatment of CMV retinitis in patients with acquired immunodeficiency syndrome (AIDS) only
IV prehydratation and administration of probenecid MUST be used with each cidofovir infusion

Children and Adults:

Safety and effectiveness in children have not been studied.

Administration to children should be undertaken only after careful evaluation and only if the potential benefits of treatment outweigh the risks.

Administer with probenecid - 2 g PO 3 hours prior to each cidofovir dose and 1 g at 2 and 8 hours after completion of the infusion (total: 4 g)

Induction:
(5 mg/kg IV (administer over 1 hrs) qwk with probenecid) for 2 weeks
Maintenance:
5 mg/kg IV (administer over 1 hrs) q2wks with probenecid

Dose VS renal function

Induction, Cr. clearance (ml/min) :
<19: 0.5 mg/kg IV qwk 20-29: 1 mg/kg IV qwk 30-40: 1.5 mg/kg IV qwk 41-55: 2 mg/kg IV qwk >55: unchanged

Maintenance, Cr. clearance (ml/min) :
<19: 0.5 mg/kg IV q2wk 20-29: 1 mg/kg IV q2wk 30-40: 1.5 mg/kg IV q2wk 41-55: 2 mg/kg IV q2wk >55: unchanged

Dialysis
Hemo: N/A
CAPD: N/A