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66 Diabetic

66: Diabetic Ketoacidosis (dka) And Hyperosmolar Hyperglycemic State (hhs)

66: Diabetic Ketoacidosis (dka) And Hyperosmolar Hyperglycemic State (hhs)

In this episode I’ll discuss diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). Subscribe on iTunes, Android, or Stitcher Definition Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the most serious acute complications of diabetes. These diabetic crises cause thousands of deaths annually in the US. DKA and HHS differ clinically according to the presence of ketoacidosis and the degree of hyperglycemia. In DKA metabolic acidosis is often the major finding. The serum glucose is below 800 mg/dL and usually in the 350-500 mg/dL range. DKA usually evolves rapidly. In HHS, there is little or no ketoacidosis and the serum glucose concentration frequently exceeds 1000 mg/dL. HHS usually evolves over a period of several days. Overlap between DKA and HHS occurs in more than one-third of patients. Pathogenesis Insulin deficiency/resistance and glucagon excess are responsible for the development of DKA and HHS. The deficiency in insulin (either absolute or relative deficiency) is more severe in DKA compared with HHS. In HHS the residual insulin secretion and its systemic activity minimizes the development of ketoacidosis but is not adequate to control hyperglycemia. In patients with absolute or relative insulin deficiency, DKA and HHS are usually precipitated by a stressor such as infection or discontinuation of / inadequate insulin therapy. Treatment The treatment of DKA and HHS involves the correction of fluid and electrolyte abnormalities, followed by the administration of insulin. Specific treatment protocols include: ADA guidelines, Joslin protocol, and Yale New Haven. The order of treatment is essential. A patient in DKA or HHS is already volume-depleted. Insulin forces glucose as well as potassium and water into cells. Therefor Continue reading >>

Is Low Blood Glucose (hypoglycemia) Dangerous?

Is Low Blood Glucose (hypoglycemia) Dangerous?

Low blood glucose or hypoglycemia is one of the most common problems associated with insulin treatment, but it can also happen to people with diabetes taking pills. In general, hypoglycemia is defined as a blood glucose level below 70 mg/dl. Low blood glucose is usually unpleasant, with the most common symptoms including feeling shaky, sweaty and having one's heart pound. The most common reasons for hypoglycemia are too much diabetes medicine, too little food or a delayed meal, or too much or unplanned activity. A less common, but occasional cause for hypoglycemia, is drinking alcoholic beverages. Most hypoglycemia is mild with recognizable symptoms. If quickly and appropriately treated, it is more of an inconvenience than a cause for alarm. However, severe hypoglycemia that causes mental confusion, antagonistic behaviors, unconsciousness, or seizures is a reason for alarm. We define severe hypoglycemia as the point at which you are not able to independently treat yourself. It is dangerous and to be avoided! Not because hypoglycemia, in itself, is fatal. That is very, very rare. What is dangerous is what might happen as a result of the hypoglycemia. The biggest danger is a motor vehicle accident caused, for example, by passing out at the wheel, swerving into on-coming traffic, hitting a tree, or running stop signs. Sometimes people are seriously injured in other types of accidents related to hypoglycemia, such as falling down stairs. It is equally important to avoid unconsciousness and seizures caused by hypoglycemia, not only because of the increased risk for accidents, but because of the potential for brain damage related to repeated severe hypoglycemia. Guidelines for managing hypoglycemia Recognize symptoms (physical, emotional, mental) and that these symptoms are v Continue reading >>

Hypoglycemia: What Do You Feel In Your Body? What Do You Feel In Your Mind?

Hypoglycemia: What Do You Feel In Your Body? What Do You Feel In Your Mind?

A word of caution about the values used below. This study was conducted using people without diabetes. Some people with diabetes experience symptoms at higher glucose levels than the study suggests. Other people with diabetes appear to function well with blood sugars in the 30’s and 40’s (mg/dl). Therefore, the values in the study should only be used as an approximation. This study also used plasma glucose levels. Your values done at home might be 20 percent lower or higher than these lab values. For example, epinephrine release in someone without diabetes would begin at about 63mg/dl with a home blood glucose meter. More caution: Many people with long-standing type 1 diabetes completely lose some of these responses. The glucose counter-regulation system becomes impaired sometime during the first few years of diabetes. This impairment is unusual in that it seems to be hypoglycemia-specific: the ability of glucagon and epinephrine to respond to other stimuli is basically unchanged, but is reduced or absent when dealing with hypoglycemia. The cause of this is not known, but it is closely linked with the lack of insulin production. SIDE BAR: HYPOGLYCEMIA, What Happens As Your Blood Glucose Levels Fall*: at 69 mg/dl Epinephrine is released into the bloodstream at 68 mg/dl Glucagon release begins at 67 mg/dl The brain conserves glucose by reducing glucose uptake at 66 mg/dl The body releases the growth hormone Somatotropin, which tells the body to reduce its use of glucose and burn fat instead at 58 mg/dl Cortisol, a steroid that promotes the conversion of glycogen into glucose at 54 mg/dl Full-on hypoglycemic body symptoms may start including shaking, pounding heart, nervousness, sweating, tingling and hunger at 49 mg/dl Thinking becomes impaired. The Mind symptoms star Continue reading >>

Payperview: Iga Nephropathy Complicating Diabetic Glomerulosclerosis - Karger Publishers

Payperview: Iga Nephropathy Complicating Diabetic Glomerulosclerosis - Karger Publishers

IgA Nephropathy Complicating Diabetic Glomerulosclerosis von Orfila C.a De Lepert J.-C.a van Modesto A.b van Pipy B.a Suc J.-M.b Tel. +33 5 61 32 29 67, Fax +33 5 61 32 22 93, E-Mail [email protected] I have read the Karger Terms and Conditions and agree. A retrospective study was done on 66 diabetic patients who had renal biopsies performed during 19791994. This review shows 10 patients who presented IgA nephropathy associated with diabetic nephropathy. Six patients had insulin-dependent diabetes mellitus and 4 patients non-insulin-dependent diabetes mellitus. All patients presented with proteinuria and 7 had hematuria. Four patients presented with renal impairment. Histologic evaluation disclosed the presence of thickened glomerular basement membranes and increased mesangial matrix in all cases, associated with nodular sclerosis in 8 cases. By immunofluorescence, diffuse mesangial IgA deposits were observed in all cases. The high incidence of the coexistence of IgA nephropathy and diabetes seems not merely coincidental. Structural and/or functional abnormalities of the glomerular basement membranes might facilitate the development of immune complex glomerular diseases. In patients with diabetes, the appearance of urinary abnormalities and/or deterioration in renal function altered the clinical history of diabetic nephropathy. The disorders are clinically suggestive of the presence of nondiabetic renal disease and raised the possibility of another pathogenetic mechanism. Epstein SE, Becker EL: Acute glomerulonephritis in an adult with longstanding of diabetes mellitus. Ann Intern Med 1961;54:97103. Urizar RE, Schwartz A, Top F, Vernier RL: Nephrotic syndrome in children with diabetes mellitus of recent onset. N Engl J Med 1969;28:173181. Warms PC, Rosenbaum B Continue reading >>

Type 2 Diabetes And The Diet That Cured Me

Type 2 Diabetes And The Diet That Cured Me

Why me? At 59 I was 10st 7lb, 5ft 7in, and had never been overweight. I ran and played cricket regularly and didn't drink alcohol excessively. Yet at a routine check-up I was told that I had type 2 diabetes. In 10 years I could be dependent on insulin, it could affect my sight, feet, ears, heart and I had a 36% greater chance of dying early. In type 1 diabetes, the body produces none of the insulin that regulates our blood sugar levels. Very high glucose levels can damage the body's organs. Patients with type 2 diabetes, however, do produce insulin - just not enough to keep their glucose levels normal. Because I was fit and not overweight (obesity is a major risk factor in type 2 diabetes; however, a number of non-obese people, particularly members of south Asian communities, are also prone to it), my doctor told me I could control my condition with diet alone. Desperate for information, I headed to the web, where I found a report about a research trial at Newcastle University led by Professor Roy Taylor. His research suggested type 2 diabetes could be reversed by following a daily 800-calorie diet for eight weeks. When our bodies are deprived of normal amounts of food they consume their own fat reserves, with the fat inside organs used up first. The idea of Taylor's diet is to use up the fat that is clogging up the pancreas and preventing it from creating insulin, until normal glucose levels return. With my GP's blessing and a home glucose-testing kit, I began my experiment. The diet was strict: three litres of water a day, three 200-calorie food supplements (soups and shakes) and 200 calories of green vegetables. Thanks to my doctor's dietary guidance, and running three times a week, I had already lost a stone. Yet my glucose levels were still above 6mmol/L (millimols Continue reading >>

P66shc: A Novel Biomarker Of Tubular Oxidative Injury In Patients With Diabetic Nephropathy

P66shc: A Novel Biomarker Of Tubular Oxidative Injury In Patients With Diabetic Nephropathy

p66Shc: A novel biomarker of tubular oxidative injury in patients with diabetic nephropathy Scientific Reports volume 6, Articlenumber:29302 (2016) | Download Citation Increased p66Shc expression has been associated with diabetic nephropathy (DN). However, whether p66Shc can serve as a potential biomarker for tubular oxidative injury in DN is unknown. We measured the expression of p66Shc in peripheral blood monocytes (PBMs) and renal biopsy tissues from DN patients and then analysed the relationship between p66Shc expression and the clinical characteristics of patients with DN. Patients were divided into 4 groups (class IIa, class IIb, class III and the control group). qPCR, Western blotting and immunohistochemistry were performed. The results showed that both p66Shc and p-p66Shc expression significantly increased in PBMs and kidney tissues of DN patients. Moreover, Spearmans correlation and multiple regression analyses were carried out. A positive relationship between the p66Shc expression and oxidative stress was found. p66Shc and oxidative stress were significant predictors of the degree of tubular damage. In addition, p66Shc expression was positively correlated with the concentrations of -NAG, UACR and 8-OHdG, low-density lipoprotein and blood glucose levels, and duration of diabetes in patients with DN from class IIa to class III. These data indicated that increased expression of p66Shc may serve as a therapeutic target and a novel biomarker of DN. Diabetic nephropathy (DN) is a severe microangiopathic complication in patients with both type 1 and type 2 diabetes mellitus. A number of risk factors have been associated with the progression of DN, including glomerular hypertension, proteinuria, hyperlipidaemia and genetic predisposition 1 . Studies carried out over Continue reading >>

Diabetes Mellitus

Diabetes Mellitus

"Diabetes" redirects here. For other uses, see Diabetes (disambiguation). Diabetes mellitus (DM), commonly referred to as diabetes, is a group of metabolic disorders in which there are high blood sugar levels over a prolonged period.[7] Symptoms of high blood sugar include frequent urination, increased thirst, and increased hunger.[2] If left untreated, diabetes can cause many complications.[2] Acute complications can include diabetic ketoacidosis, hyperosmolar hyperglycemic state, or death.[3] Serious long-term complications include cardiovascular disease, stroke, chronic kidney disease, foot ulcers, and damage to the eyes.[2] Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced.[8] There are three main types of diabetes mellitus:[2] Type 1 DM results from the pancreas's failure to produce enough insulin.[2] This form was previously referred to as "insulin-dependent diabetes mellitus" (IDDM) or "juvenile diabetes".[2] The cause is unknown.[2] Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses a lack of insulin may also develop.[9] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is excessive body weight and insufficient exercise.[2] Gestational diabetes is the third main form, and occurs when pregnant women without a previous history of diabetes develop high blood sugar levels.[2] Prevention and treatment involve maintaining a healthy diet, regular physical exercise, a normal body weight, and avoiding use of tobacco.[2] Control of blood pressure and maintaining proper foot care are important for people with t Continue reading >>

Frontiers | From Diabetes Care To Diabetes Curethe Integration Of Systems Biology, Ehealth, And Behavioral Change | Endocrinology

Frontiers | From Diabetes Care To Diabetes Curethe Integration Of Systems Biology, Ehealth, And Behavioral Change | Endocrinology

Front. Endocrinol., 22 January 2018 | From Diabetes Care to Diabetes CureThe Integration of Systems Biology, eHealth, and Behavioral Change 1Netherlands Organization for Applied Scientific Research (TNO), Department of Microbiology and Systems Biology, Leiden, Netherlands 2Netherlands Organization for Applied Scientific Research (TNO), Department of Child Health, Leiden, Netherlands 3Leiden University Medical Center (LUMC), Department of Public Health and Primary Care, Leiden, Netherlands 4Netherlands Organization for Applied Scientific Research (TNO), Department of Work Health Technology, Leiden, Netherlands 5Department of Health, Medical and Neuropsychology, Leiden University Medical Centre, Leiden University, Leiden, Netherlands 6Department of Psychiatry, Leiden University Medical Centre, Leiden University, Leiden, Netherlands 7Leiden University Medical Center (LUMC), Department of Internal Medicine, Leiden, Netherlands From a biological view, most of the processes involved in insulin resistance, which drives the pathobiology of type 2 diabetes, are reversible. This theoretically makes the disease reversible and curable by changing dietary habits and physical activity, particularly when adopted early in the disease process. Yet, this is not fully implemented and exploited in health care due to numerous obstacles. This article reviews the state of the art in all areas involved in a diabetes cure-focused therapy and discusses the scientific and technological advancements that need to be integrated into a systems approach sustainable lifestyle-based healthcare system and economy. The implementation of lifestyle as cure necessitates personalized and sustained lifestyle adaptations, which can only be established by a systems approach, including all relevant aspects (pers Continue reading >>

Viewer Comments: Diabetes - Symptoms And Signs

Viewer Comments: Diabetes - Symptoms And Signs

Viewer Comments are not a substitute for professional medical advice, diagnosis, or treatment. Never delay or disregard seeking professional medical advice from your physician or other qualified health provider because of something you have read on eMedicineHealth. The opinions expressed in the comments section are of the author and the author alone. eMedicineHealth does not endorse any specific product, service or treatment. If you think you have a medical emergency, call your doctor or 911 immediately. This is a brilliant article and I have learnt more in the last 20 minutes reading it than in the three months since being diagnosed. I am 54 years old and thought I had bad flu virus and went to the doctor. He sent me for blood tests. He found I had type 2 and high blood pressure. I have been off work for three months and I am feeling better. I am a 66 year old male and in good health, at least I thought so until I was diagnosed with Type II diabetes. My first signs that I might have something wrong came after playing golf on a really hot day. We finished playing around 3:00pm and while sitting around waiting for food I experienced a cold sweat and lightheadedness. I was told to lie on the floor, a doctor in the room took my pulse and asked a few questions and I began to feel better. EMS was called and they checked me out but did not find anything, really. I felt better after eating. I went to the doctor who did some follow up with a cardiologist who said my blood sugar was a little elevated and my blood pressure and cholesterol needed attention. At this time, I noticed that I was getting really thirsty, and of course urinating frequently. I chalked this up to old age. A few weeks later the same thing after another golf outing. At this point I knew that something was am Continue reading >>

Incidence Of End-stage Renal Disease Attributed To Diabetes Among Persons With Diagnosed Diabetes United States And Puerto Rico, 20002014

Incidence Of End-stage Renal Disease Attributed To Diabetes Among Persons With Diagnosed Diabetes United States And Puerto Rico, 20002014

Incidence of End-Stage Renal Disease Attributed to Diabetes Among Persons with Diagnosed Diabetes United States and Puerto Rico, 20002014 Weekly / November 3, 2017 / 66(43);11651170 The incidence of end-stage renal disease attributed to diabetes (ESRD-D) in the U.S. population with diagnosed diabetes began to decline in the mid-1990s. During 20002014, the age-standardized incidence of ESRD-D has continued to decline significantly in the United States and in most states, the District of Columbia, and Puerto Rico. No state experienced an increase in rates. What are the implications for public health practice? Continued awareness of diabetes and interventions to reduce the prevalence of risk factors for kidney failure, improve diabetes care, and prevent type 2 diabetes might sustain the decline in ESRD-D incidence rates in the population with diagnosed diabetes. During 2014, 120,000 persons in the United States and Puerto Rico began treatment for end-stage renal disease (ESRD) (i.e., kidney failure requiring dialysis or transplantation) (1). Among these persons, 44% (approximately 53,000 persons) had diabetes listed as the primary cause of ESRD (ESRD-D) (1). Although the number of persons initiating ESRD-D treatment each year has increased since 1980 (1,2), the ESRD-D incidence rate among persons with diagnosed diabetes has declined since the mid-1990s (2,3). To determine whether ESRD-D incidence has continued to decline in the United States overall and in each state, the District of Columbia (DC), and Puerto Rico, CDC analyzed 20002014 data from the U.S. Renal Data System and the Behavioral Risk Factor Surveillance System. During that period, the age-standardized ESRD-D incidence among persons with diagnosed diabetes declined from 260.2 to 173.9 per 100,000 diabetic popu Continue reading >>

Novel Curcumin Analog C66 Prevents Diabetic Nephropathy Via Jnk Pathway With The Involvement Of P300/cbp-mediated Histone Acetylation

Novel Curcumin Analog C66 Prevents Diabetic Nephropathy Via Jnk Pathway With The Involvement Of P300/cbp-mediated Histone Acetylation

Volume 1852, Issue 1 , January 2015, Pages 34-46 Novel curcumin analog C66 prevents diabetic nephropathy via JNK pathway with the involvement of p300/CBP-mediated histone acetylation First time to show that C66 prevents DN via epigenetic mechanism First time to show that C66 prevents DN via inactivation of JNK-mediated epigenetic modification First to show that C66 treatment can provide a sustained prevention of DN C66 is stronger curcumin analogue, with high effectiveness at low dose range. Glomerulosclerosis and interstitial fibrosis represent the key events in development of diabetic nephropathy (DN), with connective tissue growth factor (CTGF), plasminogen activator inhibitor-1 (PAI-1) and fibronectin 1 (FN-1) playing important roles in these pathogenic processes. To investigate whether the plant metabolite curcumin, which exerts epigenetic modulatory properties when applied as a pharmacological agent, may prevent DN via inhibition of the JNK pathway and epigenetic histone acetylation, diabetic and age-matched non-diabetic control mice were administered a 3-month course of curcumin analogue (C66), c-Jun N-terminal kinase inhibitor (JNKi, sp600125), or vehicle alone. At treatment end, half of the mice were sacrificed for analysis and the other half were maintained without treatment for an additional 3months. Renal JNK phosphorylation was found to be significantly increased in the vehicle-treated diabetic mice, but not the C66- and JNKi-treated diabetic mice, at both the 3-month and 6-month time points. C66 and JNKi treatment also significantly prevented diabetes-induced renal fibrosis and dysfunction. Diabetes-related increases in histone acetylation, histone acetyl transferases' (HATs) activity, and the p300/CBP HAT expression were also significantly attenuated by Continue reading >>

6 Lifestyle Changes To Control Your Diabetes

6 Lifestyle Changes To Control Your Diabetes

Working closely with your doctor, you can manage your diabetes by focusing on six key changes in your daily life. 1. Eat healthy. This is crucial when you have diabetes, because what you eat affects your blood sugar. No foods are strictly off-limits. Focus on eating only as much as your body needs. Get plenty of vegetables, fruits, and whole grains. Choose nonfat dairy and lean meats. Limit foods that are high in sugar and fat. Remember that carbohydrates turn into sugar, so watch your carb intake. Try to keep it about the same from meal to meal. This is even more important if you take insulin or drugs to control your blood sugars. 2. Exercise. If you're not active now, it’s time to start. You don't have to join a gym and do cross-training. Just walk, ride a bike, or play active video games. Your goal should be 30 minutes of activity that makes you sweat and breathe a little harder most days of the week. An active lifestyle helps you control your diabetes by bringing down your blood sugar. It also lowers your chances of getting heart disease. Plus, it can help you lose extra pounds and ease stress. 3. Get checkups. See your doctor at least twice a year. Diabetes raises your odds of heart disease. So learn your numbers: cholesterol, blood pressure, and A1c (average blood sugar over 3 months). Get a full eye exam every year. Visit a foot doctor to check for problems like foot ulcers and nerve damage. 4. Manage stress. When you're stressed, your blood sugar levels go up. And when you're anxious, you may not manage your diabetes well. You may forget to exercise, eat right, or take your medicines. Find ways to relieve stress -- through deep breathing, yoga, or hobbies that relax you. 5. Stop smoking. Diabetes makes you more likely to have health problems like heart disease Continue reading >>

Vitamin D Supplementation And Bone Health In Adults With Diabetic Nephropathy: The Protocol For A Randomized Controlled Trial

Vitamin D Supplementation And Bone Health In Adults With Diabetic Nephropathy: The Protocol For A Randomized Controlled Trial

Vitamin D supplementation and bone health in adults with diabetic nephropathy: the protocol for a randomized controlled trial Mager et al.; licensee BioMed Central Ltd.2014 Suboptimal vitamin D status is highly prevalent in Northern communities, particularly in those patients with chronic diseases such as diabetes and chronic renal disease. Emerging literature suggests that adherence to daily vitamin D supplementation may be an important factor influencing vitamin D status and overall bone health, but compliance with therapies for bone health is a major challenge. It is unknown what level of vitamin D supplementation will ameliorate or improve suboptimal vitamin D status in patients with diabetic nephropathy or contribute to improved bone health, particularly for those living in northern climates. The study purpose was to examine two different strategies of vitamin D3 supplementation; daily dosing of 2000IU per day verses monthly dosing of 40,000IU per month on markers of vitamin D status, bone health and to examine whether adherence, quality of life and patient satisfaction with the supplementation strategy differs between the two vitamin D strategies in adults diagnosed with diabetic nephropathy. The need for RCTs assessing higher doses of vitamin D3 supplementation at varying frequencies of administration and its impact on bone health in adults with diabetes and chronic kidney disease are needed. Vitamin D supplementationBone healthDiabetesKidney disease Suboptimal vitamin D status (25(OH)D <75nmol/L) is associated with the development and progression of both diabetes and chronic kidney disease (CKD) [ 1 ]. Within the general North American population 16-52% have suboptimal vitamin D status; the prevalence of vitamin D insufficiency increases to 86% in the diabetic Continue reading >>

Possible Contribution Of Adipocytokines On Diabetic Neuropathy.

Possible Contribution Of Adipocytokines On Diabetic Neuropathy.

Diabetes Res Clin Pract. 2004 Dec;66 Suppl 1:S121-3. Possible contribution of adipocytokines on diabetic neuropathy. Diabetes and Endocrine Division, Department of Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki-shi, Okayama-ken 701 0192, Japan. [email protected] Neuropathy is one of the typical features of chronic complications of diabetes mellitus. Recent analyses indicate that subjects with impaired glucose tolerance (IGT) already have disturbance of peripheral nerve function. To test the role of adipocytokines, that tend to be abnormal in IGT subjects, on diabetic neuropathy, we analyzed the relationship between plasma adipocytokine levels (TNFalpha, adiponectin, and leptin) and nerve conduction velocity in 105 type 2 diabetic subjects (M/F = 66/39, age = 60.8 +/- 11.8 years, BMI = 24.7 +/- 5.0kg/m2). Adipocytokines were measured by ELISA, and motor conduction velocity (MCV) and sensory conduction velocity (SCV) in median, ulnar, and tibial nerve were measured by electrical stimulation. Motor conduction velocity and SCV were corrected by age to be 1.0 as the normal value, and the average of three nerves were used to be the representative value. Relationship between corrected MCV or corrected SCV as a dependent variable and the duration of diabetes, HbA1C, BMI, TNFalpha, adiponectin, and leptin concentrations as independent variables were analyzed by multiple regression. Duration of diabetes and HbA1C were highly related with both corrected MCV (P < 0.02 and P < 0.001) and SCV (P < 0.02 and P < 0.05) by this analysis. Only corrected SCV was related significantly with TNFalpha (P < 0.05), and close to significantly with leptin (P = 0.059) concentrations. These results indicate that increased plasma glucose levels and duration of diabetes are Continue reading >>

What To Do If Your Blood Sugar Is Too Low

What To Do If Your Blood Sugar Is Too Low

You'll need to test your blood sugar if you think you have hypoglycemia.(ARTIGA PHOTO/CORBIS)Although type 2 diabetes is characterized by blood sugar that is too high, some people take insulin and others medications (such as sulfonylureas) that can occasionally drive blood sugar too low. When blood sugar is too lowgenerally less than 70 mg/dLit's called hypoglycemia, and it can become a medical emergency. (The normal range for fasting blood sugar is 70 to 99 mg/dL, though it varies somewhat with age, and is lower during pregnancy and in children.) You can lose consciousness Hypoglycemia is more likely to occur when you start taking a new medication (it can take practice to match your food intake to your insulin dose, for example) or if you exercise more than usual. As blood sugar drops to low levels, you may feel: Shaky Irritable Sweaty This can occur within 10 to 15 minutes, and in extreme cases you can even lose consciousness and experience seizures if you don't consume some glucose (though hypoglycemia is usually mild in people with type 2 diabetes, and readily fixed by drinking juice or eating other sugar-containing items, such as glucose tablets or four to six pieces of hard candy). Hypoglycemia"My blood sugar was really plummeting" Watch videoMore about blood sugar monitoring You'll need to test your blood sugar to confirm that you're having hypoglycemiasome people become irritable if blood sugar is too high, so it's not always obvious. If you drink sugar-containing juice, or some other form of carbohydrate, it should bring blood sugar back into the normal range. You can also purchase glucose pills or gels in the pharmacy that can get blood sugar back on track. “You should always have a glucose source in the car,” says Yvonne Thigpen, RD, diabetes program coor Continue reading >>

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