Acute Coronary Syndrome Moderate Risk Acute Coronary Syndrome Management Low Risk Acute Coronary Syndrome Management Myocardial Infarction Stabilization Post Myocardial Infarction Medications Cardiac Rehabilitation Angina Pectoris Heart Failure Causes NYHA Heart Failure Classification Diastolic Heart Failure Systolic Dysfunction Atrial Fibrillation Acute Management Atrial Fibrillation Anticoagulation Coronary Artery Disease Prevention in Diabetes Hypertension in Diabetes Mellitus CHAD Score Hypertension in the Elderly Isolated Systolic Hypertension Hypertension Criteria Hypertension Evaluation History Hypertension Management Hypertension Risk Stratification Resistant Hypertension Hypertension Management for Specific Comorbid Diseases Hypertension Management for Specific Emergencies Bacterial Endocarditis HDL Cholesterol LDL Cholesterol Triglyceride VLDL Cholesterol Hypercholesterolemia Hypertriglyceridemia AntiHyperlipidemic Hypertensive Disorders of Pregnancy Preeclampsia Prevention Congenital Heart Disease Hypertension in Children Medication Causes of Hypertension ACE Inhibitor Angiotensin 2 Receptor Blocking Agent Dihydropyridine Calcium Channel Blocker Nifedipine Selective Aldosterone Receptor Antagonist Niacin HMG-CoA Reductase Inhibitor Cardiac Risk Cardiac Risk Management Exercise Stress Test Stress Myocardial Perfusion Imaging Preoperative Cardiovascular Evaluation Eagle's Cardiac Risk Assessment Revised Cardiac Risk Index ACC-AHA Preoperative Cardiac Risk Assessment ACP Preoperative Cardiac Risk Assessment Syncope Subclavian Steal Syndrome Periodontitis Oral Health Cellulitis Necrotizing Soft Tissue Infection Group A Streptococcal Cellulitis Vibrio Cellulitis Gram-Negative Toe Web Infection Impetigo Skin Infections in Diabetes Mellitus Erythralgia Blister Skin Ulcer Cutaneous Candidiasis Onychomycosis Alopecia Areata Skin Abscess Skin Infection Intertrigo Nail Discoloration Terry's Nail Ingrown Toenail Hyperpigmentation Carotenemia Incision and Drainage Cryotherapy Skin Conditions in Diabetes Mellitus Acanthosis Nigricans Diabetic Dermopathy Granuloma Annulare Necrobiosis Lipoidica Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus Metabolic Syndrome Diabetes Mellitus Complications Diabetic Ketoacidosis Diabetic Ketoacidosis Management in Adults Diabetic Ketoacidosis Management in Children Hyperosmolar Hyperglycemic State Diabetic Education Diabetes Mellitus Glucose Management Diabetes Mellitus Control in Hospital Diabetes Resources Diabetic Retinopathy Unintentional Weight Loss Unintentional Weight Loss Causes Hypoglycemia Serum Glucose Glucose Challenge Test Glucose Tolerance Test 2 hour Hemoglobin A1C Sex Hormone Binding Globulin Endocrinology Links Diabetic Neuropathy Neonatal Hypoglycemia Obesity Risk Gestational Diabetes Gestational Diabetes Management Gestational Diabetes Perinatal Mortality Diabetes Mellitus Preconception Counseling Obesity in Children Systemic Corticosteroid Medication Causes of Hyperglycemia GlucoWatch Biographer Symlin Inhaled Insulin Somogyi Phenomena Glucophage Human Growth Hormone Orlistat Diabetic Foot Care Nutrition in Diabetes Mellitus Type 2 Diabetic Nephropathy Klinefelter Syndrome Hypogonadotropic Hypogonadism Pubertal Delay Exercise in Diabetes Mellitus Perioperative Diabetes Management Obesity Surgery Night Sweats Acute Otitis Externa Bacterial Otitis Externa Necrotizing Otitis Externa Hearing Loss Sensorineural Hearing Loss Vocal Cord Paralysis Thrush Manual Cerumen Removal Sinus XRay Acute Suppurative Sialoadenitis Rhinosinusitis Tinnitus Burning Mouth Syndrome Taste Dysfunction Loss of Smell Dry Mouth Salivary Gland Enlargement Tongue Pain Dysequilibrium Atrophic Glossitis Animal Bite Infected Animal Bite Human Bite Heat Illness Risk Factors Burn Management Trauma in Pregnancy Bacterial Conjunctivitis Central Retinal Artery Occlusion Open Angle Glaucoma Cataract Ischemic Optic Neuritis Vitreous Hemorrhage Laser In-Situ Keratomileusis Floaters Light Flashes Acute Vision Loss Health Concerns in the Elderly Infections in Older Adults Medication Use in the Elderly Failure to Thrive in the Elderly Fall Prevention in the Elderly Irritable Bowel Syndrome Constipation Causes Chronic Diarrhea Traveler's Diarrhea Esophageal Dysmotility Gastroesophageal Reflux Hemochromatosis Pancreatic Cancer Hepatitis C Nonalcoholic Fatty Liver Serum Angiotensin Converting Enzyme Liver Function Test Abnormality Lactase Deficiency Acute Pancreatitis Chronic Pancreatitis Osmotic Laxative Hepatotoxic Medication Traveler's Diarrhea Prophylaxis Pruritus Ani Perirectal Abscess Gastroparesis Whipple Procedure Upper Gastrointestinal Bleeding Dyspepsia Causes Nausea Causes Contraception HAIR-AN Syndrome Polycystic Ovary Disease Menopause Endometrial Cancer Risk Factor Candida Vulvovaginitis Anovulatory Bleeding Oral Contraceptive Female Sexual Dysfunction Cancer Survivor Care Serum Protein Electrophoresis Perioperative Anticoagulation Cardiovascular Manifestations of HIV HIV Presentation Hepatitis in HIV HIV Related Neuropathy Stavudine Emerging Infection Methicillin Resistant Staphylococcus Aureus Fever of Unknown Origin Candidiasis Neutropenic Fever Hepatitis B Vaccine Influenza Vaccine Postherpetic Neuralgia Fluoroquinolone Third Generation Fluoroquinolone Sulfonamide Travel Preparation Travel Immunization Influenza Dengue Legionella Acute Exacerbation of Chronic Bronchitis Pneumonia in the Elderly Pneumonia Churg-Strauss Syndrome Tuberculin Skin Test Cystic Fibrosis Isoniazid Lung Transplantation in Cystic Fibrosis Active Tuberculosis Treatment Medical Literature Autonomic Dysfunction Bell's Palsy Facial Nerve Paralysis Causes Dementia Agitation in Dementia Ischemic Stroke Stroke Pathophysiology CVA Management Multiple Sclerosis Down Syndrome Cranial Nerve 3 Coma Exam Hemiplegia Giant Cell Arteritis Spinal Headache CSF Protein Altered Level of Consciousness Causes Guillain Barre Syndrome Restless Leg Syndrome Triptan Prevention of Ischemic Stroke Nerve Conduction Velocity Paresthesia Causes Peripheral Neuropathy Asymmetric Peripheral Neuropathy Peripheral Neuropathy Tremor Neonatal Distress Causes Newborn History Newborn Exam Neonatal Jaundice Causes Respiratory Distress Syndrome in the Newborn Late Pregnancy Loss Preterm Labor First Trimester Bleeding Fetal Macrosomia Hyperemesis Gravidarum Medications in Pregnancy Ritodrine Terbutaline Pregnancy Risk Assessment Probe-to-Bone Test Shoulder History Dupuytren's Disease Septic Bursitis Spinal Infection Osteomyelitis Causes Vertebral Osteomyelitis Patellar Tendinopathy Meralgia Paresthetica Frozen Shoulder Exertional Compartment Syndrome Hip Pain Low Back Pain Red Flag Carpal Tunnel Syndrome Adolescent Health Bullying Ephedrine Ginseng Myoinositol Nonsteroidal Anti-inflammatory Lab Markers of Malnutrition Nutrition Guidelines Glycemic Index Non-nutritive Sweetener Conenzyme Q10 Mortality Statistics Adult Health Maintenance Screening DOT Examination Family History Refugee Health Exam Automobile Safety Substance Abuse Evaluation Alcohol Detoxification in Ambulatory Setting Major Depression Major Depression Differential Diagnosis Anorexia Nervosa Antabuse Selective Serotonin Reuptake Inhibitor Antipsychotic Medication Clozapine Olanzapine Psychosis Insomnia Causes Renal Artery Stenosis Idiopathic Cyclic Edema Acute Kidney Injury Risk Chronic Renal Failure Acute Glomerulonephritis Nephrotic Syndrome Serum Osmolality Hypomagnesemia Drug Dosing in Chronic Kidney Disease Hyperkalemia due to Medications Hyperkalemia Causes Prevention of Kidney Disease Progression Intravenous Contrast Related Acute Renal Failure Osteoporosis Evaluation Antiphospholipid Antibody Syndrome Systemic Lupus Erythematosus Polymyositis Differential Diagnosis Septic Joint Gouty Arthritis Fibromyalgia Charcot's Joint Charcot Foot Complex Regional Pain Syndrome Osteoarthritis Methotrexate Joint Injection Rheumatoid Arthritis Fatigue Causes Impairment Evaluation Pre-participation History Exercise Exercise in the Elderly Walking Program Scuba Diving Procedural Sedation and Analgesia Peripheral Arterial Occlusive Disease Peripheral Vascular Disease Management Venous Insufficiency Wound Decubitus Ulcer Foot Wound Leg Ulcer Causes Wound Repair Fishhook Removal Ankle-Brachial Index Preoperative Examination Gallstone Acalculous Cholecystitis Cholecystectomy Small Bowel Obstruction Bowel Pseudoobstruction Abdominal Muscle Wall Pain Abdominal Wall Pain Causes Hydrocolloid Dressing Suture Material Surgical Antibiotic Prophylaxis Male Infertility Testicular Failure Bladder Cancer Urinary Tract Infection Recurrent Cystitis Acute Bacterial Prostatitis Acute Pyelonephritis Erectile Dysfunction Erectile Dysfunction Causes Erectile Dysfunction Management Urinary Incontinence Overflow Incontinence Urine pH Urine Specific Gravity Enuresis Proteinuria in Children Balanitis Peyronie's Disease Benign Prostatic Hyperplasia Vasectomy Counseling Proteinuria Causes Targeted Cancer Therapy Acute Paronychia Chronic Paronychia Urinary Retention Decreased Visual Acuity Gastrointestinal Manifestations of Diabetes Mellitus Shoulder Osteoarthritis Vitiligo Cardiomyopathy Heart Transplant Contraceptive Selection in Diabetes Mellitus Periodontal Bleeding Perioperative Antiplatelet Therapy Charlson Comorbidity Index Constipation Causes in the Elderly Chronic Osteomyelitis Abnormal Gait and Balance Causes in the Elderly Calcium Channel Blocker Overdose Diverticular Bleeding Framingham Cardiac Risk Scale Cardiac Risk in Diabetes Score Outpatient Bleeding Risk Index Four Year Prognostic Index Diabetes Screening ABCD2 Score Urine Microalbumin Hearing Loss in Older Adults Preoperative Guidelines for Medications Prior to Surgery Contrast-Induced Nephropathy Risk Score Hyperlipidemia in Diabetes Mellitus Diamond and Forrester Chest Pain Prediction Rule Coronary Risk Stratification of Chest Pain Diabetes Sick Day Management Urinary Tract Infection in Geriatric Patients Insulinlike Growth Factor 1 Avascular Necrosis of the Femoral Head Family Practice Notebook Updates 2014 Emergency Care in ESRD Medication Compliance Slit Lamp Sulfonamide Allergy Health Care of the Homeless CHADS2-VASc Score Tuberculosis Risk Factors for progression from Latent to Active Disease Family Practice Notebook Updates 2015 Wound Infection Asymptomatic Bacteriuria Toxic Shock Syndrome Tetanus ASA Physical Status Classification System Family Practice Notebook Updates 2016 Solid Organ Transplant Calcineurin Inhibitor Cardiac Pacemaker Infection DAPT Score Acute Maculopathy Medication Causes of Delirium in the Elderly Family Practice Notebook Updates 2017 Major Bleeding Risk With Anticoagulants Severe Asymptomatic Hypertension Chronic Wound Family Practice Notebook Updates Stable Coronary Artery Disease Nocturia Polyuria Hyperhidrosis Causes Pneumaturia Anemia in Older Adults Type 2 Diabetes Mellitus in Children
The tuberculosis skin test is based on the fact that infection with M. tuberculosis produces a delayed-type hypersensitivity skin reaction to certain components of the bacterium. The standard recommended tuberculin test is administered by injecting 0.1mL of 5 TU (tuberculin units) PPD into the top layers of skin of the forearm. "Reading" the skin test means detecting a raised, thickened local area of skin reaction, referred to as induration. The area of induration (palpable, raised, hardened area) around the site of injection is the reaction to tuberculin.
Type 2 diabetes can be prevented with lifestyle changes. People who are overweight and lose as little as 7 percent of their body weight and who increase physical activity (for example, walking 30 minutes per day) can decrease their risk of diabetes mellitus by more than 50%. Metformin and acarbose, drugs that are used to treat diabetes, may reduce the risk of diabetes in people with impaired glucose regulation.
The problem with sugar, regardless of type, is the sheer amount of it that’s found in the Standard American Diet (SAD), which is the typical eating plan many people in the United States — as well as those in an increasing number of modernized countries — have developed a taste for. When consumed in excess, foods in this category can lead to heart disease, stroke, and other serious health issues. “Often, foods with added sugar also contain fat,” explains Grieger, noting that these components go hand in hand when it comes to the risk for insulin resistance, the hallmark of type 2 diabetes.
Insulin-dependent diabetes mellitus is believed to result from autoimmune, environmental, and/or genetic factors. Whatever the cause, the end result is destruction of insulin-producing pancreatic beta cells, a dramatic decrease in the secretion of insulin, and hyperglycemia. Non-insulin-dependent diabetes mellitus is presumably heterogeneous in origin. It is associated with older age, obesity, a family history of diabetes, and ethnicity (genetic components). The vast majority of those with non-insulin-dependent diabetes are overweight Kahn (2003). This form of the disorder has a much slower rate of progression than insulin-dependent diabetes. Over time the ability to respond to insulin decreases, resulting in increased levels of blood glucose. The pancreatic secretion of insulin increases in an attempt to compensate for the elevated levels of glucose. If the condition is untreated, the pancreatic production of insulin decreases and may even cease.
About 84 million adults in the US (more than 1 out of 3) have prediabetes, and about 90% do not know they have it until a routine blood test is ordered, or symptoms of type 2 diabetes develop. For example, excessive thirst, frequent urination, and unexplained weight loss. If you have prediabetes also it puts you at risk for heart attack, stroke, and type 2 diabetes.
Jump up ^ Sattar N, Preiss D, Murray HM, Welsh P, Buckley BM, de Craen AJ, Seshasai SR, McMurray JJ, Freeman DJ, Jukema JW, Macfarlane PW, Packard CJ, Stott DJ, Westendorp RG, Shepherd J, Davis BR, Pressel SL, Marchioli R, Marfisi RM, Maggioni AP, Tavazzi L, Tognoni G, Kjekshus J, Pedersen TR, Cook TJ, Gotto AM, Clearfield MB, Downs JR, Nakamura H, Ohashi Y, Mizuno K, Ray KK, Ford I (February 2010). "Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials". Lancet. 375 (9716): 735–42. doi:10.1016/S0140-6736(09)61965-6. PMID 20167359.
Schedule a yearly physical exam and regular eye exams. Your regular diabetes checkups aren't meant to replace regular physicals or routine eye exams. During the physical, your doctor will look for any diabetes-related complications, as well as screen for other medical problems. Your eye care specialist will check for signs of retinal damage, cataracts and glaucoma.
Doctors, pharmacists, and other health-care professionals use abbreviations, acronyms, and other terminology for instructions and information in regard to a patient's health condition, prescription drugs they are to take, or medical procedures that have been ordered. There is no approved this list of common medical abbreviations, acronyms, and terminology used by doctors and other health- care professionals. You can use this list of medical abbreviations and acronyms written by our doctors the next time you can't understand what is on your prescription package, blood test results, or medical procedure orders. Examples include:
The genes identified so far in people with type 2 include many that affect the insulin-producing beta cells of the pancreas, says Craig Hanis, PhD, a professor at the Human Genetics Center at the University of Texas Health Science Center in Houston. And yet he emphasizes that why people get type 2 isn't at all clear yet: "What it tells us is that diabetes is a complicated disease."

Accelerated atherosclerosis is the main underlying factor contributing to the high risk of atherothrombotic events in DM patients. CAD, peripheral vascular disease, stroke, and increased intima-media thickness are the main macrovascular complications. Diabetics are 2–4 times more likely to develop stroke than people without DM.2 CVD, particularly CAD, is the leading cause of morbidity and mortality in patients with DM.4 Patients with T2DM have a 2- to 4-fold increase in the risk of CAD, and patients with DM but without previous myocardial infarction (MI) carry the same level of risk for subsequent acute coronary events as nondiabetic patients with previous MI.5 Furthermore, people with diabetes have a poorer long-term prognosis after MI, including an increased risk for congestive heart failure and death.


Over recent decades, and particularly in the past five years, researchers have found dozens of genes with links to diabetes. The count stands at about 50 genes for type 1 and 38 for type 2. The numbers have risen quickly in recent years because of advances in the gene-sequencing technology used to conduct genome-wide association studies. This technique involves taking the genetic compositions of a group of people with a disease and comparing them en masse to the genomes of people who don't have the disease.
Type 2 diabetes is typically a chronic disease associated with a ten-year-shorter life expectancy.[10] This is partly due to a number of complications with which it is associated, including: two to four times the risk of cardiovascular disease, including ischemic heart disease and stroke; a 20-fold increase in lower limb amputations, and increased rates of hospitalizations.[10] In the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of nontraumatic blindness and kidney failure.[24] It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia.[25] Other complications include acanthosis nigricans, sexual dysfunction, and frequent infections.[23]
Education: People with diabetes should learn as much as possible about this condition and how to manage it. The more you know about your condition, the better prepared you are to manage it on a daily basis. Many hospitals offer diabetes education programs and many nurses and pharmacists have been certified to provide diabetes education. Contact a local hospital, doctor, or pharmacist to find out about programs and diabetes educators in your area.
Jump up ^ Palmer, Suetonia C.; Mavridis, Dimitris; Nicolucci, Antonio; Johnson, David W.; Tonelli, Marcello; Craig, Jonathan C.; Maggo, Jasjot; Gray, Vanessa; De Berardis, Giorgia; Ruospo, Marinella; Natale, Patrizia; Saglimbene, Valeria; Badve, Sunil V.; Cho, Yeoungjee; Nadeau-Fredette, Annie-Claire; Burke, Michael; Faruque, Labib; Lloyd, Anita; Ahmad, Nasreen; Liu, Yuanchen; Tiv, Sophanny; Wiebe, Natasha; Strippoli, Giovanni F.M. (19 July 2016). "Comparison of Clinical Outcomes and Adverse Events Associated With Glucose-Lowering Drugs in Patients With Type 2 Diabetes". JAMA: the Journal of the American Medical Association. 316 (3): 313–24. doi:10.1001/jama.2016.9400. PMID 27434443.

When it comes to diabetes, there's no real answer yet. Yes, science has begun to uncover the roots of this disease, unearthing a complex interplay of genes and environment—and a lot more unanswered questions. Meanwhile, there's plenty of misinformation to go around. (How often have you had to explain that diabetes doesn't happen because someone "ate too much"?)
Excessive hunger goes hand-in-hand with fatigue and cell starvation. Because the cells are resistant to the body's insulin, glucose remains in the blood. The cells are then unable to gain access to glucose, which can trigger hunger hormones that tell the brain that you are hungry. Excessive eating can complicate things further by causing blood sugars to increase.

The classic presenting symptoms of type 1 diabetes mellitus are discussed below. For some children, the first symptoms of diabetes mellitus are those of diabetic ketoacidosis. This is a serious and life-threatening condition, requiring immediate treatment. Ketoacidosis occurs due to a severe disturbance in the body’s metabolism. Without insulin, glucose cannot be taken up into cells. Instead fats are broken down for energy which can have acid by-products.  
Intensive blood sugar lowering (HbA1c<6%) as opposed to standard blood sugar lowering (HbA1c of 7–7.9%) does not appear to change mortality.[74][75] The goal of treatment is typically an HbA1c of 7 to 8% or a fasting glucose of less than 7.2 mmol/L (130 mg/dl); however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy.[59][76][77] Despite guidelines recommending that intensive blood sugar control be based on balancing immediate harms with long-term benefits, many people – for example people with a life expectancy of less than nine years who will not benefit, are over-treated.[78]
The ketogenic, or keto, diet calls for dramatically increasing your fat intake and consuming a moderate amount of protein and a very low amount of carbs, with the aim of kicking your body into a natural metabolic state called ketosis, in which it relies on burning fat rather than carbs for energy. Ketosis is different from diabetic ketoacidosis, a health emergency that occurs when insulin levels are low in conjunction with high levels of ketones. (37) Ketones are by-products of metabolism that are released in the blood when carb intake is low.

Since cardiovascular disease is a serious complication associated with diabetes, some have recommended blood pressure levels below 130/80 mmHg.[89] However, evidence supports less than or equal to somewhere between 140/90 mmHg to 160/100 mmHg; the only additional benefit found for blood pressure targets beneath this range was an isolated decrease in stroke risk, and this was accompanied by an increased risk of other serious adverse events.[90][91] A 2016 review found potential harm to treating lower than 140 mmHg.[92] Among medications that lower blood pressure, angiotensin converting enzyme inhibitors (ACEIs) improve outcomes in those with DM while the similar medications angiotensin receptor blockers (ARBs) do not.[93] Aspirin is also recommended for people with cardiovascular problems, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes.[94]
You may be able to manage your type 2 diabetes with healthy eating and being active, or your doctor may prescribe insulin, other injectable medications, or oral diabetes medicines to help control your blood sugar and avoid complications. You’ll still need to eat healthy and be active if you take insulin or other medicines. It’s also important to keep your blood pressure and cholesterol under control and get necessary screening tests.

In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.
Fatigue and muscle weakness occur because the glucose needed for energy simply is not metabolized properly. Weight loss in type 1 diabetes patients occurs partly because of the loss of body fluid and partly because in the absence of sufficient insulin the body begins to metabolize its own proteins and stored fat. The oxidation of fats is incomplete, however, and the fatty acids are converted into ketone bodies. When the kidney is no longer able to handle the excess ketones the patient develops ketosis. The overwhelming presence of the strong organic acids in the blood lowers the pH and leads to severe and potentially fatal ketoacidosis.
How does type 2 diabetes progress over time? Type 2 diabetes is a progressive disease, meaning that the body’s ability to regulate blood sugar gets worse over time, despite careful management. Over time, the body’s cells become increasingly less responsive to insulin (increased insulin resistance) and beta cells in the pancreas produce less and less insulin (called beta-cell burnout). In fact, when people are diagnosed with type 2 diabetes, they usually have already lost up to 50% or more of their beta cell function. As type 2 diabetes progresses, people typically need to add one or more different types of medications. The good news is that there are many more choices available for treatments, and a number of these medications don’t cause as much hypoglycemia, hunger and/or weight gain (e.g., metformin, pioglitazone, DPP-4 inhibitors, GLP-1 agonists, SGLT-2 inhibitors, and better insulin). Diligent management early on can help preserve remaining beta cell function and sometimes slow progression of the disease, although the need to use more and different types of medications does not mean that you have failed.

^ Jump up to: a b c d Inzucchi, SE; Bergenstal, RM; Buse, JB; Diamant, M; Ferrannini, E; Nauck, M; Peters, AL; Tsapas, A; Wender, R; Matthews, DR (March 2015). "Management of hyperglycaemia in type 2 diabetes, 2015: a patient-centred approach. Update to a Position Statement of the American Diabetes Association and the European Association for the Study of Diabetes". Diabetologia. 58 (3): 429–42. doi:10.1007/s00125-014-3460-0. PMID 25583541.


Type II is considered a milder form of diabetes because of its slow onset (sometimes developing over the course of several years) and because it usually can be controlled with diet and oral medication. The consequences of uncontrolled and untreated Type II diabetes, however, are the just as serious as those for Type I. This form is also called noninsulin-dependent diabetes, a term that is somewhat misleading. Many people with Type II diabetes can control the condition with diet and oral medications, however, insulin injections are sometimes necessary if treatment with diet and oral medication is not working.
A population-based, nationwide cohort study in Finland examined the short -and long-term time trends in mortality among patients with early-onset and late-onset type 1 diabetes. The results suggest that in those with early-onset type 1 diabetes (age 0-14 y), survival has improved over time. Survival of those with late-onset type 1 diabetes (15-29 y) has deteriorated since the 1980s, and the ratio of deaths caused by acute complications has increased in this group. Overall, alcohol was noted as an important cause of death in patients with type 1 diabetes; women had higher standardized mortality ratios than did men in both groups. [38]
Some patients with type 2 DM can control their disease with a calorically restricted diet (for instance 1600 to 1800 cal/day), regular aerobic exercise, and weight loss. Most patients, however, require the addition of some form of oral hypoglycemic drug or insulin. Oral agents to control DM include sulfonylurea drugs (such as glipizide), which increase pancreatic secretion of insulin; biguanides or thiazolidinediones (such as metformin or pioglitazone), which increase cellular sensitivity to insulin; or a-glucosidase inhibitors (such as acarbose), which decrease the absorption of carbohydrates from the gastrointestinal tract. Both types of diabetics also may be prescribed pramlintide (Symlin), a synthetic analog of human amylin, a hormone manufactured in the pancreatic beta cells. It enhances postprandial glucose control by slowing gastric emptying, decreasing postprandial glucagon concentrations, and regulating appetite and food intake; thus pramlintide is helpful for patients who do not achieve optimal glucose control with insulin and/or oral antidiabetic agents. When combinations of these agents fail to normalize blood glucose levels, insulin injections are added. Tight glucose control can reduce the patient’s risk of many of the complications of the disease. See: illustration
Treatment of pituitary diabetes insipidus consists of administration of vasopressin. A synthetic analogue of vasopressin (DDAVP) can be administered as a nasal spray, providing antidiuretic activity for 8 to 20 hours, and is currently the drug of choice. Patient care includes instruction in self-administration of the drug, its expected action, symptoms that indicate a need to adjust the dosage, and the importance of follow-up visits. Patients with this condition should wear some form of medical identification at all times.
Being too heavy gets the bulk of the blame for triggering type 2 diabetes. According to the National Institutes of Health, about 85 percent of people with type 2 diabetes are overweight or obese. But consider that the remaining 15 percent are not. Consider, too, that roughly two-thirds of overweight people and a third of those who are obese will never develop diabetes. In other words, normal-weight and thin people also develop type 2, while heavy people won't necessarily. Clearly, there is more to the connection between lifestyle and type 2 diabetes than just body size.
Injections of insulin may either be added to oral medication or used alone.[24] Most people do not initially need insulin.[13] When it is used, a long-acting formulation is typically added at night, with oral medications being continued.[23][24] Doses are then increased to effect (blood sugar levels being well controlled).[24] When nightly insulin is insufficient, twice daily insulin may achieve better control.[23] The long acting insulins glargine and detemir are equally safe and effective,[98] and do not appear much better than neutral protamine Hagedorn (NPH) insulin, but as they are significantly more expensive, they are not cost effective as of 2010.[99] In those who are pregnant insulin is generally the treatment of choice.[23]
Dietary factors also influence the risk of developing type 2 DM. Consumption of sugar-sweetened drinks in excess is associated with an increased risk.[46][47] The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk.[45] Eating lots of white rice, and other starches, also may increase the risk of diabetes.[48] A lack of physical activity is believed to cause 7% of cases.[49]
Jump up ^ McBrien, K; Rabi, DM; Campbell, N; Barnieh, L; Clement, F; Hemmelgarn, BR; Tonelli, M; Leiter, LA; Klarenbach, SW; Manns, BJ (6 August 2012). "Intensive and Standard Blood Pressure Targets in Patients With Type 2 Diabetes Mellitus: Systematic Review and Meta-analysis". Archives of Internal Medicine. 172 (17): 1–8. doi:10.1001/archinternmed.2012.3147. PMID 22868819.
Hypoglycemia. Hypoglycemia or “insulin shock” is a common concern in DM management. It typically develops when a diabetic patient takes his or her normal dose of insulin without eating normally. As a result, the administered insulin can push the blood sugar to potentially dangerously low levels. Initially the patient may experience, sweating, nervousness, hunger and weakness. If the hypoglycemic patient is not promptly given sugar (sugar, cola, cake icing), he or she may lose consciousness and even lapse into coma. Questions and Answers about Diabetes and Your Mouth Q: If I have diabetes, will I develop the oral complications that were mentioned? A: It depends. There is a two-way relationship between your oral health and how well your blood sugar is controlled (glycemic control). Poor control of your blood sugar increases your risk of developing the multitude of complications associated with diabetes, including oral complications. Conversely, poor oral health interferes with proper glucose stabilization. Indeed, recent research has shown that diabetic patients who improve their oral health experience a modest improvement in their blood sugar levels. In essence, “Healthy mouths mean healthy bodies.” Q: What are the complications of diabetes therapy that can impact my oral health? A: One of the most worrisome urgent complications associated with diabetes management is the previously described hypoglycemia or insulin shock. In addition, many of the medications prescribed to treat diabetes and its complications, such as hypertension and heart disease, may induce adverse side effects affecting the mouth. Common side effects include dry mouth, taste aberrations, and mouth sores. Q: I have type-2 diabetes. Are my dental problems different than those experienced by people with type-1 diabetes? A: No. All patients with diabetes are at increased risk for the development of dental disease. What is different is that type-2 disease tends to progress more slowly than type-1 disease. Thus, most type-2 diabetes patients are diagnosed later in life, a time in which they are likely to already have existing dental problems. Remember, there is no dental disease unique to diabetes. Uncontrolled or poorly controlled diabetes simply compromises your body’s ability to control the existing disease.
A healthy meal plan for people with diabetes is generally the same as healthy eating for anyone – low in saturated fat, moderate in salt and sugar, with meals based on lean protein, non-starchy vegetables, whole grains, healthy fats, and fruit. Foods that say they are healthier for people with diabetes generally offer no special benefit. Most of them still raise blood glucose levels, are more expensive, and can also have a laxative effect if they contain sugar alcohols.

Can you “exercise your way” out of this problem? Sometimes you can; however, the key is exercising properly. For younger patients, it is best to exercise briefly and intensely. Within the first 20 minutes of intense exercise, your body burns its sugar stores, which are hanging out in liver and muscle again. After that, you start burning fat. Although this sounds good; and to some extent it is, if you spend hours running or exercising excessively, you train your body to burn fat efficiently, which subsequently lead to also training your body to store fat efficiently.
Good metabolic control can delay the onset and progression of diabetic retinopathy. Loss of vision and blindness in persons with diabetes can be prevented by early detection and treatment of vision-threatening retinopathy: regular eye examinations and timely intervention with laser treatment, or through surgery in cases of advanced retinopathy. There is evidence that, even in developed countries, a large proportion of those in need is not receiving such care due to lack of public and professional awareness, as well as an absence of treatment facilities. In developing countries, in many of which diabetes is now common, such care is inaccessible to the majority of the population.
There is evidence that certain emotions can promote type 2 diabetes. A recent study found that depression seems to predispose people to diabetes. Other research has tied emotional stress to diabetes, though the link hasn't been proved. Researchers speculate that the emotional connection may have to do with the hormone cortisol, which floods the body during periods of stress. Cortisol sends glucose to the blood, where it can fuel a fight-or-flight response, but overuse of this system may lead to dysfunction.
It is a considerable challenge to obtain the goals of the intensively treated patients in the DCCT with the vast majority of people with diabetes given the more limited health care resources typically available in routine practice. If diabetes control can be improved without significant damage to quality of life, the economic, health, and quality of life savings associated with a reduction in complications in later life will be vast. Although some people who have had poorly controlled diabetes over many years do not develop complications, complications commonly arise after 15–20 years of diabetes and individuals in their 40s or even 30s may develop several complications in rapid succession. However, up until the early 1980s, patients had no way of monitoring their own blood glucose levels at home. Urine glucose monitoring only told them when their blood glucose had exceeded the renal threshold of approximately 10 mmol/L (i.e., was far too high), without being able to discriminate between the too high levels of 7–10 mmol/L or the hypoglycemic levels below 4 mmol/L. Clinics relied on random blood glucose testing and there were no measures of average blood glucose over a longer period. Since the 1980s there have been measures of glycosylated hemoglobin (GHb, HbA1, or HbA1c) which indicate average blood glucose over a six to eight week period and measures of glycosylated protein, fructosamine, which indicates average blood glucose over a two-week period. Blood-glucose meters for patients were first introduced in the early 1980s and the accuracy and convenience of the meters and the reagent strips they use has improved dramatically since early models. By the late 1990s blood-glucose monitoring is part of the daily routine for most people using insulin in developed countries. Blood-glucose monitoring is less often prescribed for tablet- and diet-alone-treated patients, financial reasons probably being allowed to outweigh the educational value of accurate feedback in improving control long term. The reduced risk of hypoglycemia and diabetic ketoacidosis in NIDDM patients not using insulin means that acute crises rarely arise in these patients though their risk of long-term complications is at least as great as in IDDM and might be expected to be reduced if feedback from blood-glucose monitoring were provided.
Over time, a prolonged exposure to high blood sugar can damage the nerves throughout the body — a condition called diabetic neuropathy. Some people may not have any symptoms of the damage, while others may notice numbness, tingling, or pain in the extremities. “At the beginning, [diabetic neuropathy] usually starts in the feet and then it progresses upward,” says Dr. Ovalle. Although most common in people who have had type 2 diabetes for 25 years or more, it can occur in people who have prediabetes as well. In some studies, almost 50 percent of unexplained peripheral neuropathy [in the extremities], whether painful or otherwise, turns out to be caused by prediabetes or diabetes, says Dr. Einhorn.
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