Common disorder characterised by insulin resistance and relative insulin deficiency. Most patients are asymptomatic and are diagnosed through screening (abnormal fasting plasma glucose, haemoglobin A1c, and/or oral glucose tolerance test).[1] Strong risk factors include older age, overweight/obesity, physical inactivity, prior gestational diabetes, pre-diabetes, non-white ancestry, family history of diabetes, or polycystic ovary syndrome. Modification of cardiovascular risk factors (e.g., hypertension and dyslipidaemia) are important treatment considerations, along with glycaemic control to prevent microvascular complications.
Characterised by absolute insulin deficiency. Most cases result from autoimmune pancreatic beta-cell destruction in genetically susceptible individuals. Usually presents with acute symptoms or ketoacidosis in childhood or adolescence. Lifelong insulin therapy is required.
Defined as any degree of glucose intolerance with onset or first recognition occurring during pregnancy.[4] It is usually recognised at 24 to 28 weeks of gestation on the basis of abnormal glucose tolerance testing. Strong risk factors include advanced maternal age (>40 years), obesity, personal history of gestational diabetes or macrosomia of previous child, polycystic ovary syndrome, non-white ancestry, and family history of diabetes mellitus.[5][6][7] It is uncommon for patients to present with symptoms (e.g., urinary tract infections or vulvovaginal candidiasis). Occasionally it may be difficult to distinguish GD from undiagnosed pre-existing type 2 diabetes. Infrequently, type 1 diabetes may present during pregnancy. Medical nutrition therapy is central to control of GD and most women are adequately treated with diet alone.
DKA and hyperosmolar hyperglycaemic states are acute metabolic emergencies.[8] Successful treatment includes correction of volume depletion, hyperglycaemia and ketosis/acidosis, electrolyte imbalances, and comorbid precipitating events (e.g., infection), along with frequent monitoring.
Severe hyperglycaemia, hyperosmolality, and volume depletion, in the absence of severe ketoacidosis.[8] Occurs most commonly in older patients with type 2 diabetes, with high mortality. Treatment includes correction of fluid deficit and electrolyte abnormalities, and intravenous insulin.
Coronary artery disease and stroke are the most common manifestations, and account for most deaths in people with diabetes. Modification of cardiovascular risk factors (e.g., hypertension and dyslipidaemia) are important long-term treatment issues.
Defined as increased urinary albumin excretion (30-299 mg/24 hour, historically called microalbuminuria; and ≥300 mg/24 hour, historically called macroalbuminuria or clinical albuminuria) associated with either diabetic retinopathy or greater than 10 years duration of type 1 diabetes mellitus.[1] Symptoms may be absent until the disease is advanced. Treatment includes intensive control of hyperglycaemia and hypertension.[9] Lipid reduction, low-protein diet, and smoking cessation may also be beneficial.
The most common chronic complication in diabetes, characterised by peripheral or autonomic nerve dysfunction. Peripheral neuropathy may present as loss of sensation, painless ulcers on pressure points, or pain, although many patients are asymptomatic. Treatment has traditionally focused on control of hyperglycaemia as a means of slowing progression or delaying onset, on targeting potential pathogenetic mechanisms, and on pain reduction; drug therapy may be used depending on variant of neuropathy.
Include ulcers and infections. Prevention and/or healing of diabetic foot ulcers helps to prevent infections and thereby minimizes the risk of limb loss.
Consequence of chronic progressive diabetic microvascular leakage and occlusion. Sight-threatening signs include macular oedema, ischaemia, or traction; vitreous haemorrhage; or retinal detachment. Main goals of therapy are to improve glycaemic, lipid, and blood pressure control and to ensure that disease is arrested before visual loss occurs.
Refers to identification and treatment of hyperglycaemia in hospital, in patients with either pre-existing diabetes or new-onset hyperglycaemia. The development of hyperglycaemia during acute medical or surgical illness may not be a physiological or benign condition but rather a marker of poor clinical outcomes and increased mortality. Effective management of hyperglycaemia often includes basal-bolus insulin protocols.
Cluster of common abnormalities, including insulin resistance, impaired glucose tolerance, abdominal obesity, reduced high-density lipoprotein-cholesterol levels, elevated triglycerides, and hypertension. However, this syndrome is not universally accepted as more clinically useful than assessment of individual cardiovascular risk factors.[10][11]
Characterised by polydipsia, polyuria, increased thirst, and hypotonic urine. Central DI is due to defective synthesis or release of arginine vasopressin (AVP). Nephrogenic DI is due to renal insensitivity to AVP. Either type may be associated with hypernatraemia. Treatment goals are correction of water deficits and reduction in ongoing excessive urinary losses.
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This overview has been compiled using the information in existing sub-topics.
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