Successful Use of a Single Subcutaneous Continuous Glucose Monitor Sensor for 28 Days in a Patient with Type 1 Diabetes.
R.F. is a 48-year-old white man with type 1 diabetes since age 24. He was initially seen at the Utah Diabetes Center in Salt Lake City on 15 September 2006. The patient had been treated with NPH insulin, 2 units at bedtime; ultralente insulin, 3 units twice a day; and lispro insulin, 2-3 units at each meal. The patient corrected elevated blood glucose levels with 1 unit of lispro for blood glucose readings > 200 mg/dl and about 2 units of lispro for blood glucose readings > 300 mg/dl. His hemoglobin A1c (A1C) was 9.2%, and he described losing control of his diabetes progressively through the years.
The patient often developed nocturnal hypoglycemia, most likely as a result of the combination of NPH and ultralente insulins taken at bedtime, and his blood glucose levels often dropped by 50-80 mg/dl through the night. The fear of nocturnal hypoglycemia and the patient’s inability to control postprandial blood glucose levels were very frustrating to him. He had no evidence of microvascular complications. His blood pressure and lipids have always been within the normal range.
R.F.’s basal insulin regimen was changed to detemir insulin twice daily, and he was also given an insulin-to-carbohydrate ratio to determine lispro doses at mealtimes and a correction scale to aggressively correct hyperglycemia. He also received intensive diabetes education. By 7 April 2007, his A1C was 7.8%, and he had gained much more confidence as his blood glucose levels remained stable through the nights.
The patient then decided to purchase a continuous glucose monitor (CGM) system (Medtronic MiniMed Guardian REAL-Time Continuous Glucose Monitoring System). The patient was instructed on the use of the sensor system by the diabetes education team at the Utah Diabetes Center. He continued to monitor his blood glucose levels four to six times per day. He found that he was able to aggressively dose insulin at meals based on anticipated carbohydrate intake and to correct even mild hyperglycemia throughout the day. His A1C had improved to 5.5% when measured on 11 October 2007.
The patient described replacing the subcutaneous sensor used in his CGM system only every 10-14 days, instead of the recommended 3 days. He reported minimal to no local skin irritation and described the accuracy of the system as excellent, even after using a single sensor for at least 1 week. During his clinic visit on 11 October 2007, he described using his current subcutaneous glucose sensor for 28 consecutive days.
The patient’s CGM data was downloaded, and the weekly sensor reports by week over the 4-week period. The patient typically provided four to six valid calibrations per day with his glucose meter. The mean absolute difference in glucose levels between the CGM readings and the glucose meter results remained excellent, in the 15-19% range for the entire month during which he had worn the same subcutaneous glucose sensor. On exam, the sensor site showed minimal surrounding erythema with no discharge or tenderness.
This case highlights an important consideration in the use of CGM systems and raises questions regarding the longevity of subcutaneous glucose sensors. It is well known that diabetes is associated with numerous vascular complications that are clearly related to the duration and severity of hyperglycemia. With improvements in this patient’s insulin regimen, a decreased in A1C of 1.4 percentage points was achieved. The use of the CGM system allowed the patient to more aggressively treat even mild hyperglycemia and further reduced his hemoglobin A1C by 2.3 percentage points.
The Diabetes Control and Complications Trial demonstrated that intensive therapy resulting in an average A1C of 7.2% reduced the risk of retinopathy by 76%, nephropathy by 50%, and neuropathy by 60% compared to standard therapy resulting in an average A1C of 9.1%.1 In addition, lower A1C values risk of nonfatal myocardial infarction, stroke, or death from cardiovascular disease by 57 %.2 Thus, lowering R.F.’s A1C by more than 3 percentage points was enormously beneficial. His glycemic control was clearly improved by the addition of the CGM system.
This case also raises questions about the longevity of subcutaneous glucose sensors. Currently, the Medtronic Guardian REAL-Time CGM system sensor is FDA-approved for 3 days of continuous wear.3 The DexCom sensor is approved for 7 days of continuous wear, and the FreeStyle Navigator is approved for 5 days of continuous wear.4,5 But can these sensors be worn for longer periods of time than their current FDA approvals and still remain accurate? R.F. wore his sensor for 28 days and maintained a 15-19% mean absolute difference in glucose values. This is similar to the accuracy reported between the Yellow Springs Instrument glucose analyzer and the Guardian REAL-Time readings (mean absolute difference 19.7 ± 18.4%).3
The main barrier to obtaining a CGM system is the initial cost for the system and, more importantly, the resistance of insurance companies to pay for this new technology. The initial out-of-pocket expense ranges from $800-$1,200 with monthly costs for sensors ranging $240 to $450.
However, the total annual economic cost of diabetes in 2007 was estimated to be $174 billion.6 Medical expenditures comprised a large portion of these costs totaling $116 billion, including $58 billion to care for chronic diabetes-related complications.6 In fact, one of every five health care dollars is spent caring for someone with diagnosed diabetes, while one in ten health care dollars is attributed to diabetes.6 As A1C increases, medical costs increase. For every increase of 1 percentage point from 6% to 10%, cumulative charges increase by 4, 10, 20, and 30%, respectively.7 Improvements in long-term glycemic control with CGM, albeit at a significant initial cost, may more than offset the costs of treating the chronic complications of diabetes.
Many of our patients have observed their sensors working accurately for longer periods than the FDA-approved time limits. We have not discouraged this practice. If the practical, functional life of a subcutaneous glucose sensor is generally longer than currently believed, monthly costs associated with CGM will obviously be much lower, increasing access to this important technology for many patients. Studies investigating the possibility of longer sensor life spans are much needed.
There are three CGM systems available for use (Medtronic Guardian REAL-Time Continuous Glucose Monitoring System, FreeStyle Navigator Continuous Glucose Monitoring System, DexCom Seven Continuous Glucose Monitoring System)
Individual subcutaneous glucose sensors are currently approved for 3-day (Medtronic Guardian), 5-day (FreeStyle Navigator), and 7-day (DexCom Seven) use.
The initial cost of a CGM system is roughly $800-1,200 and ongoing monthly costs are $240-350 for continuous use.
Studies are needed to determine whether subcutaneous continuous glucose sensors may remain safe and accurate for longer periods than current FDA-approved time limits.
James J. Chamberlain, MD and Denise Small, PharmD
DiabetesHypertension Management in adults
Evidence review: hypertension as a risk factor for complications of diabetes
Diabetes increases the risk of coronary events twofold in men and fourfold in women. Part of this increase is due to the frequency of associated cardiovascular risk factors such as hypertension, dyslipidemia, and clotting abnormalities. In observational studies, people with both diabetes and hypertension have approximately twice the risk of cardiovascular disease as nondiabetic people with hypertension. Hypertensive diabetic patients are also at increased risk for diabetes-specific complications including retinopathy and nephropathy. In the U.K. Prospective Diabetes Study (UKPDS) epidemiological study, each 10-mmHg decrease in mean systolic blood pressure was associated with reductions in risk of 12% for any complication related to diabetes, 15% for deaths related to diabetes, 11% for myocardial infarction, and 13% for microvascular complications. No threshold of risk was observed for any end point
American Diabetes Association
DiabetesHypertension Management in adults
Evidence for target levels of blood pressure in patients with diabetes
The UKPDS and the Hypertension Optimal Treatment (HOT) trial both demonstrated improved outcomes, especially in preventing stroke, in patients assigned to lower blood pressure targets. Optimal outcomes in the HOT study were achieved in the group with a target diastolic blood pressure of 80 mmHg (achieved 82.6 mmHg). Randomized clinical trials demonstrate the benefit of targeting a diastolic blood pressure of 80 mmHg. Epidemiological analyses show that blood pressures 120/70 mmHg are associated with increased cardiovascular event rates and mortality in persons with diabetes. Therefore, a target blood pressure goal of <130/80 mmHg is reasonable if it can be safely achieved. There is no threshold value for blood pressure, and risk continues to decrease well into the normal range. Achieving lower levels, however, would increase the cost of care as well as drug side effects and is often difficult in practice. Whether even more aggressive treatment would further reduce the risk is an unanswered question, but may be answered by clinical trials now in progress.
American Diabetes Association
DiabetesHypertension Management in Adults
Evidence for non-drug management of hypertension
Dietary management with moderate sodium restriction has been effective in reducing blood pressure in individuals with essential hypertension. Several controlled studies have looked at the relationship between weight loss and blood pressure reduction. Weight reduction can reduce blood pressure independent of sodium intake and also can improve blood glucose and lipid levels. The loss of one kilogram in body weight has resulted in decreases in mean arterial blood pressure of 1 mmHg. The role of very low calorie diets and pharmacologic agents that induce weight loss in the management of hypertension in diabetic patients has not been adequately studied. Some appetite suppressants may induce increases in blood pressure levels, so these must be used with care. Given the present evidence, weight reduction should be considered an effective measure in the initial management of mild-to-moderate hypertension, and these results could probably be extrapolated to the diabetic hypertensive population.
Sodium restriction has not been tested in the diabetic population in controlled clinical trials. However, results from controlled trials in essential hypertension have shown a reduction in systolic blood pressure of 5 mmHg and diastolic blood pressure of 2–3 mmHg with moderate sodium restriction (from a daily intake of 200 mmol [4,600 mg] to 100 mmol [2,300 mg] of sodium per day). A dose response effect has been observed with sodium restriction. Even when pharmacologic agents are used, there is often a better response when there is concomitant salt restriction due to the aforementioned volume component of the hypertension that is almost always present. The efficacy of these measures in diabetic individuals is not known.
Moderately intense physical activity, such as 30–45 min of brisk walking most days of the week, has been shown to lower blood pressure and is recommended in the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC VI). The American Diabetes Association Consensus Development Conference on the Diagnosis of Coronary Heart Disease in People with Diabetes has recommended that diabetic patients who are 35 years of age or older and are planning to begin a vigorous exercise program should have exercise stress testing or other appropriate noninvasive testing. Stress testing is not generally necessary for asymptomatic patients beginning moderate exercise such as walking. Smoking cessation and moderation of alcohol intake are also recommended by JNC VI and are clearly appropriate for all patients with diabetes.
American Diabetes Association
DiabetesHypertension Management in Adults
Evidence for drug therapy of hypertension
There are a number of trials demonstrating the superiority of drug therapy versus placebo in reducing outcomes including cardiovascular events and microvascular complications of retinopathy and progression of nephropathy. These studies used different drug classes, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), diuretics, and ß-blockers, as the initial step in therapy. All of these agents were superior to placebo; however, it must be noted that many patients required three or more drugs to achieve the specified target levels of blood pressure control. Overall there is strong evidence that pharmacologic therapy of hypertension in patients with diabetes is effective in producing substantial decreases in cardiovascular and microvascular diseases.
There are limited data from trials comparing different classes of drugs in patients with diabetes and hypertension. The UKPDS-Hypertension in Diabetes Study showed no significant difference in outcomes for treatment based on an ACE inhibitor compared with a ß-blocker. There were slightly more withdrawals due to side effects and there was more weight gain in the ß-blocker group. In postmyocardial infarction patients, ß-blockers have been shown to reduce mortality.
There are numerous studies documenting the effectiveness of ACE inhibitors and ARBs in retarding the development and progression of diabetic nephropathy. ACE inhibitors have a favorable effect on cardiovascular outcomes, as demonstrated in the MICRO-HOPE study. This cardiovascular effect may be mediated by mechanisms other than blood pressure reduction. It is possible that other drug classes may behave similarly.
Some studies have shown an excess of selected cardiac events in patients treated with dihydropyridine calcium channel blockers (DCCBs) compared with ACE inhibitors. Ongoing trials including the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) study should help to resolve this issue. DCCBs in combination with ACE inhibitors, ß-blockers, and diuretics, as in the HOT study and the Systolic Hypertension in Europe (Syst-Eur) Trial, did not appear to be associated with increased cardiovascular morbidity. However, ACE inhibitors and ß-blockers appear to be superior to DCCBs in reducing myocardial infarction and heart failure. Therefore, DCCBs appear to be appropriate agents in addition to, but not instead of, ACE inhibitors and ß-blockers. Non-DCCBs (i.e., verapamil and diltiazem) may reduce coronary events. In short-term studies, non-DCCBs have reduced albumin excretion.
There are no long-term studies of the effect of -blockers, loop diuretics, or centrally acting adrenergic blockers on long-term complications of diabetes. The -blocker arm of the ALLHAT study was stopped by the data and safety monitoring committee because of an increase in cases of new-onset heart failure in patients assigned to the -blocker. While this could merely represent unmasking of heart failure in patients previously treated with an ACE inhibitor or a diuretic, it seems reasonable to use these as second-line agents when preferred classes have been ineffective or when other specific indications, such as benign prostatic hypertrophy (BPH), are present.
American Diabetes association
DiabetesHypertension Management in Adults
Summary
There is a strong epidemiological connection between hypertension in diabetes and adverse outcomes of diabetes. Clinical trials demonstrate the efficacy of drug therapy versus placebo in reducing these outcomes and in setting an aggressive blood pressure–lowering target of <130/80 mmHg. It is very clear that many people will require three or more drugs to achieve the recommended target. Achievement of the target blood pressure goal with a regimen that does not produce burdensome side effects and is at reasonable cost to the patient is probably more important than the specific drug strategy.
Because many studies demonstrate the benefits of ACE inhibitors on multiple adverse outcomes in patients with diabetes, including both macrovascular and microvascular complications, in patients with either mild or more severe hypertension and in both type 1 and type 2 diabetes, the established practice of choosing an ACE inhibitor as the first-line agent in most patients with diabetes is reasonable. In patients with microalbuminemia or clinical nephropathy, both ACE inhibitors (type 1 and type 2 patients) and ARBs (type 2 patients) are considered first-line therapy for the prevention of and progression of nephropathy. However, other strategies including diuretic and ß-blocker–based therapy are also supported by evidence. Because of lingering concerns about the lower effectiveness of DCCBs (compared with ACE inhibitors, ARBs, ß-blockers, or diuretics) in decreasing coronary events and heart failure and in reducing progression of renal disease in diabetes, these agents should be used as second-line drugs for patients who cannot tolerate the other preferred classes or who require additional agents to achieve the target blood pressure. Other classes, including -blockers, may be used under specific indications (such as symptoms of BPH for -blockers) or other agents have failed to control the blood pressure or have unacceptable side effects. Blood pressure, orthostatic changes, renal function, and serum potassium should be monitored at appropriate intervals.
Treatment decisions should be individualized based on the clinical characteristics of the patient, including comorbidities as well as tolerability, personal preferences, and cost.
Screening and diagnosis
Expert opinion:
Blood pressure should be measured at every routine diabetes visit. Patients found to have systolic blood pressure 130 mmHg or diastolic blood pressure 80 mmHg should have blood pressure confirmed on a separate day.
Orthostatic measurement of blood pressure should be performed to assess for the presence of autonomic neuropathy.
American Diabetes Association
DiabetesHypertension Management in Adults
Treatment
A-Level evidence:
- Patients with diabetes should be treated to a diastolic blood pressure <80 mmHg.
- Patients with a systolic blood pressure of 130–139 mmHg or a diastolic blood pressure of 80–89 mmHg should be given lifestyle/behavioral therapy alone for a maximum of 3 months and then, if targets are not achieved, should also be treated pharmacologically.
- Patients with hypertension (systolic blood pressure 140 mmHg or diastolic blood pressure 90 mmHg) should receive drug therapy in addition to lifestyle/behavioral therapy.
Initial drug therapy may be with any drug class currently indicated for the treatment of hypertension. However, some drug classes (ACE inhibitors, ß-blockers, and diuretics) have been repeatedly shown to be particularly beneficial in reducing CVD events during the treatment of uncomplicated hypertension and are therefore preferred agents for initial therapy. If ACE inhibitors are not tolerated, ARBs may be used. Additional drugs may be chosen from these classes or another drug class. (A)
If ACE inhibitors or ARBs are used, monitor renal function and serum potassium levels. (E)
In patients with type 1 diabetes, with or without hypertension, with any degree of albuminuria, ACE inhibitors have been shown to delay the progression of nephropathy. (A) • In patients with type 2 diabetes, hypertension and microalbuminuria, ACE inhibitors and ARBs have been shown to delay the progression to macroalbuminuria. (A) • In those with type 2 diabetes, hypertension, macroalbuminuria (>300 mg/day), nephropathy, or renal insufficiency, an ARB should be strongly considered. If one class is not tolerated, the other should be substituted.
In patients over age 55 years, with hypertension or without hypertension but with another cardiovascular risk factor (history of cardiovascular disease, dyslipidemia, microalbuminuria, smoking), an ACE inhibitor (if not contraindicated) should be considered to reduce the risk of cardiovascular events.
In patients with a recent myocardial infarction, ß-blockers, in addition, should be considered to reduce mortality.
B-Level evidence:
Patients with diabetes should be treated to a systolic blood pressure <130 mmHg.
C-Level evidence
In patients with microalbuminuria or overt nephropathy, in whom ACE inhibitors or ARBs are not well tolerated, a non-DCCB or ß-blocker should be considered.
Expert consensus
- If ACE inhibitors or ARBs are used, monitor renal function and serum potassium levels.
- In elderly hypertensive patients, blood pressure should be lowered gradually to avoid complications.
- Patients not achieving target blood pressure on three drugs, including a diuretic, and patients with a significant renal disease should be referred to a specialist experienced in the care of patients with hypertension.
American Diabetes Association
If your blood sugar is 70 mg/dL or lower or you feel shaky, nervous or confused, stop exercising and eat or drink something to raise your blood sugar level. Try:
- Two or three glucose tablets
- 1/2 cup of fruit juice
- 1/2 cup of regular (not diet) soda
- Five or six pieces of hard candy
Recheck your blood sugar 15 minutes later. If it’s still too low, have another serving and test again 15 minutes later. Repeat as needed until your blood sugar reaches at least 70 mg/dL. If you haven’t finished your workout, continue once your blood sugar returns to a safe range. Back …
By Mayo Clinic Staff
Feb. 23, 2007 © 1998-2008 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved. A single copy of these materials may be reprinted for noncommercial personal use only. “Mayo,” “Mayo Clinic,” “MayoClinic.com,” “EmbodyHealth,” “Reliable tools for healthier lives,” “Enhance your life,” and the triple-shield Mayo Clinic logo are trademarks of Mayo Foundation for Medical Education and Research.
After exercise: Check your blood sugar again
After exercise, check your blood sugar right away and then several times during the next few hours. Exercise draws on reserve sugar stored in your muscles and liver. As your body rebuilds these stores, it takes sugar from your blood. And the more strenuous your workout, the longer your blood sugar will be affected. Low blood sugar is possible even hours after exercise.
Exercise may seem like enough work on its own. But testing your blood sugar before, during and after you exercise may be just as important as the exercise itself.
By Mayo Clinic Staff
Feb. 23, 2007 © 1998-2008 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved. A single copy of these materials may be reprinted for noncommercial personal use only. “Mayo,” “Mayo Clinic,” “MayoClinic.com,” “EmbodyHealth,” “Reliable tools for healthier lives,” “Enhance your life,” and the triple-shield Mayo Clinic logo are trademarks of Mayo Foundation for Medical Education and Research.
Some Of Diabetes Exercise
Diabetes Exercise: When to monitor your blood sugar
Exercise is an important part of any diabetes treatment plan. To avoid potential problems, check your blood sugar before, during and after exercise.
Diabetes and exercise go hand in hand, at least when it comes to managing diabetes. Exercise can help you improve your blood sugar control, as well as boost your overall fitness and reduce your risk of heart disease and nerve damage.
But diabetes exercise pose special challenges, too. Remember to track your blood sugar before, during and after exercise. Your records will reveal how your body responds to exercise — and help you prevent potentially dangerous blood sugar fluctuations.
Before exercise: Check your blood sugar before your workout
Before jumping into a fitness program, get your doctor’s OK to exercise — especially if you’ve been inactive. Discuss with your doctor which activities you’re contemplating and the best time to exercise, as well as the potential impact of medications on your blood sugar as you become more active.
If you’re taking insulin or medications that can cause low blood sugar (hypoglycemia), test your blood sugar 30 minutes before exercising and once again immediately before exercising. This will help you determine if your blood sugar level is stable, rising or falling — and if it’s safe to exercise. Consider these general guidelines:
Lower than 100 milligrams per deciliter (mg/dL). Your blood sugar may be too low to exercise safely. Eat a small carbohydrate-containing snack such as fruit or crackers before you begin your workout.
100 to 250 mg/dL. You’re good to go. For most people, this is a safe pre-exercise blood sugar range.
250 mg/dL or higher. This is a caution zone. To make sure it’s safe to exercise, test your urine for ketones — substances made when your body breaks down fat for energy. Excess ketones indicate that your body doesn’t have enough insulin to control your blood sugar. If you exercise when you have a high level of ketones, you risk ketoacidosis — a serious complication of diabetes that needs immediate treatment. Instead, wait to exercise until you have a low level of ketones in your urine.
300 mg/dL or higher. Your blood sugar may be too high to exercise safely, putting you at risk of ketoacidosis. Postpone your workout until your blood sugar drops to a safe pre-exercise range.
By Mayo Clinic Staff
Feb. 23, 2007 © 1998-2008 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved. A single copy of these materials may be reprinted for noncommercial personal use only. “Mayo,” “Mayo Clinic,” “MayoClinic.com,” “EmbodyHealth,” “Reliable tools for healthier lives,” “Enhance your life,” and the triple-shield Mayo Clinic logo are trademarks of Mayo Foundation for Medical Education and Research.
Publish By : Alfento P Sinurat S.Si, Apt
Pharmacist
Components of the classical circulating RAS, in particular, renin release from the juxtaglomerular cells of the kidney, undergo a decline in older animals. This includes reductions in renal tissue renin mRNA, juxtaglomerular cell renin content, responsiveness of renin release to various challenges, and plasma renin and angiotensin (Ang) II.The renal vasoconstrictor responses to exogenously administered Ang II are increased in older animals,perhaps resulting from the reductions in the circulating system. In striking contrast, however, kidney Ang II content increases in older animals.This latter finding is not surprising, because all of the components of the RAS are synthesized locally within the kidney, and local production of Ang peptides is regulated independent of the circulating system.Thus, whereas the juxtaglomerular cell renin and its release into the circulation are considered representative of the circulating/hormonal RAS, renal tissue content, tubular fluid, or urinary RAS components are considered representative of the intrarenal RAS.
The concept of differential regulation of the circulating and intrarenal or other tissue RAS is not new. One possibility for these differences relate to the increase in SBP. An increase in arterial pressure during aging may lead to a baromediated reduction in renin release from the kidney, contributing to the decline in the circulating RAS. In contrast, for the intrarenal system, there is evidence that the regulation of tubular renin may be opposite to or at least different from that of the circulation. Although kidney Ang II content may reflect receptor-mediated uptake of the peptide, as well as local synthesis, urinary components representing the intrarenal RAS likely reflect a tubular site of synthesis and regulation. In Ang II–dependent hypertension, Ang peptides increase in the kidney but not in hypertension caused by high salt. For the intrarenal RAS, changes in glomerular filtration rate, either hyperfiltration or loss of nephrons, and reduced glomerular filtration rate may contribute to the independent regulation. In addition, the extent to which the metabolic dysfunction accompanying aging contributes to changes in the kidney is not completely known. The role of each of the above potential contributors to the regulation of the intrarenal RAS are emphasized in this review.
Lewis K. Dahl Memorial Lecture
The Renin-Angiotensin System and Aging
From the Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, NC.
Are You Wielding TheSecret Weapon That Wins The Complications War?
Living with diabetes has far better outcomes when you understand how your glucose issue shuts down your blood circulation.
IF you use that knowledge to help yourself. The complications of diabetes arise from diminishing blood circulation. If you have either Type I or Type II diabetes, your body’s blood flow slowly and insidiously decreases over time. Your heart, kidneys, eyes, skin, nerves, and all other organs exhibit signs of reduced blood circulation. Diabetes complications develop as your circulation gradually worsens. Issues like leg ulcers and foot numbness, heart trouble, even blindness, and kidney failure. The complete list is too horribly familiar. One organ or body part may fail earlier than another. But eventually, diabetic bodies degenerate throughout because circulation is impaired. The key to slowing diabetic degeneration is to delay blood flow loss. Or even better, to restore circulation back toward normal levels.
DiabetesHypertension Complication
Diabetes is a chronic, life long conditiion that requires careful control. Without proper management it can lead to various complications such as cardiovascular disease, kidney failure, blindness and nerve damage.
Short Term DiabetesHypertension Complications :
- Low Blood Sugar (Hypoglycaemia)
A person who takes insulin is going to face the problem of their blood sugar falling to low at some point (Because they have overestimated the insulin they need, have exercised more than anticipated or have not eaten enough). Hypoglycaemia can be corrected rapidly by eating some sugar. If it is not corrected can lead to the person losing consciousness. - Ketoacidosis
When the body breaks down fats, acidic waste product called ketones are produced. The body cannot tolerate large amount of ketones and will try to get rid of them through the urine. However, the body cannot release all the ketones and they build up in your blood, causing ketoacidosis. Ketoacidosis is a severe condition caused by lack of insulin. It mainly affects people with type 1 diabetes. - Lactic Acidosis
Lactic acidosis is the build up of lactic acid in the body. Cells make lactic acid when they use glucose for energy. If too much lactic acid stays in the body, the balance tips and the person begins to feel ill. Lactic acidosis is rare mainly affect people with type 2 diabetes. - Bacteria Infections
People with diabetes are more prone bacterial and fungal infections. Bacterial infections include sties and boils. Fungal infections include athletes foot, ringworm and vaginal infections.
Long Term DiabetesHypertension Complication :
- Eye Disease (Retinopathy)
Eye disease or retinopathy is the leading cause of blindness and visual impairment in adults in developed societies. About 2% of all people who have had for 15 years become blind while about 10 person develop a severe visual impairment.
IDF Fact Sheet on diabetes and eye disease
- Kidney Disease (Nephropathy)
Diabetes is the leading cause of kidney disease (Nephopathy) About one third of all people with diabetes develop kidney disease and apptoximately 20 of people with type 1 diabetes kidney failure.
IDF Fact Sheet on diabetes and kidney disease
- Nerve Disease (Neuropathy)
Diabetes nerve disease or neuropathy affect at least half of all people with diabetes. There are different types of nerve disease which can result in a loss sensation in the feet of sensation in the feet or in some cases the hands, pain in the foot aand problems with functioning of different parts of the body including the heart, the eye, the stomach the bladder and the penis. A lack of sensation in the feet can lead to people with diabetes injuring their feet without realising it. - Disease of the Circulation System
Disease of the circularatory system, or cardiovasculae disease account for 75% of all deaths among people with diabetes of european origin. In the USA, corony heart disease is present in between 8% and 20% of people with diabetes over 45 years of age. Their risk of heart disease is 2-4 times higher than those who do not have diabetes. It is the main cause of disability and death for people with type 2 diabetes in industrilized countries.
IDF Fact Sheet on diabetes and cardiovascular disease
Source International Diabetes Federation.
Dieatary to maintain the healthy and avoid Diabetes Juvenille
Maintaining healthy eating habits in college can sometimes be harder than trying to pass a quantum physics exam. College cafetarias, late-night snackathons and packed schedjules that leave little time for exercising often lead not only to “Freshman Fifteen” wight gain, but to an unhealthy lifestyle that continues aven after graduation.
So how can you avoid some of dietary pitfalls common to your college campus? We spoke with two Certified Diabetes Educators, Lara Rondinelli, RD, LDN, CDE, and Jolene Sutter, MS, RD, CDN as well as some current and former college students who gave their throughs and suggestions on how to incorporate some healthy eating habits into your routine.
Juvenille Diabetes Research Diabetes International
ABOUT GESTATIONAL DIABETES
The investigators in the metformin in Gestational Diabetes mellitus ( alone or with supplemental insulin ) is not associated with increased perinatal complications as compared insulin. Many statement said Metformin is a Logical Threatment for women with gestational diabetes mellitus, but randomized trials to assess the efficacy and safety of its use for this condition are lacking. Of the women assigned to metformin, 92.6% continue to receive metfoemin until delivery and 46.3% received suppmuntal insulin. The rate of primary composite outcome was 32.0 % in the group assign to metformin and 32.2 % In sulin grou p. More women in tthe met formin group and it the group insulin group that they would choose to received (76.6 %vs 27.2%, P0.001. The rates of the secondary outcomes did not significantly between the groups. There were no serious adverse associated wit the use of the of metformin.
Massachusetts Medical Society 2008
American Diabetes Association
Patient with type 2 Diabetes often have many associated disorders, including hypertension (high blood pressure) obesity , hyperlipidemia (Excess fat in the blood) and accelerated atherosclerosis (damage arterires cause by fatty deposits). Diabetes may worsen these disorders. For this reason, it is important to treat both and hyperlipidemia are now includedin all ADA recommendation for Diabetes Managament.
Information About Diabetes
Does safe Thiazolidine for Current Diabetes Threatment?
The thiazolidine (TZDs) enhance insulin action in muscle, fat and others tissues and are known as insulin sensitizer. They require the presence of insulin in order to work, so TZDs are not indicated for type 1 ( Insulin dependent diabetes) and certain other varieties of diabetes.
TZDs are reducing effective in reducing HbA1c. They are also effective in combination with either sulfonyuureas or meformin. Compared to other drugs, it takes a patient a long time to see the benefits the TZDs. For this reason, doses should not to increasesd until after 4-6weeks, the time it normally takes for maximal biological effect on blood lipids. Some TZDs also have beneficial effect on blood lipid. Troglitazone has a lipid lowering effect and increases HDL, or high density lipoprotein
The major side effect, seen with troglitazone the first TZDs to be approved by FDA, is liver damage. The effect observed range from an alevation in liver enzymes, which is reversible, to liver failure which has caused a in small number of patients. Because of this dangerous side effect the FDA in March 2000 removed troglitazone (Rezulin) from the market.Two o ther members the TZD class that have recently approved by the FDA, rosiglitazone and pioglitazone do not appear to cause liver damage. However the FDArequires regular monitoring of liver enzyme level with these drug as well. Other side effects are mild elevations of LDL cholesterol and fluid retention. TZDs do not cause hypoglycaemia when used aloneWhich one the best choice Metformin or Insulin? (For Gestational Diabetes)
Many people said Metformin was not refferenced for Gestational Diabetes because it was scared which have caused dark problems for the threament ….
Top 10 Tips For eating Healty in College
1. Sneaky Snakes
2. Don’t “Do Lunch” Every Day
3. Food Fuel
4. Be the “Designated Driver”
5. Find a Routine That Works
6. Get an “A” in Fitness
7. Channel Your Inner Julia Child
8. Get Creative
9. Stay Balanced
10. When in doubt Ask
Primary Prevention
Identifies and Protect Individual at risk from developing diabetes it therefore has an impact by reducing both the need diabetes care the need to treat diabetes -related complication
Secondary Prevention
Involves the early detection and prevention of complications, therefore reducing the need for threatment
There is now conclusive evidence that good control of blood glucose levels can substantially reduce the risk of developing complication and slow their progression in all types of diabetes. The Management of blood pressure and raised blood lipids is equally imporant
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