Diabetes Mellitus - Acute complications o Hyperglycemia: elevated glucose Leads to polyuria (excess urination), polydipsia (excess thirst), polyphagia (loss of calories so excess eating) o Hypoglycemia: decreased glucose Complication from insulin treatment and oral hypoglycemic agents Occurs during exercise and fasting as well o Diabetic Ketoacidosis In absence of insulin, lipolysis stimulated, this provides fatty acids which are converted to ketone bodies in liver Hyperglycemia and ketone bodies found in type 1 diabetes mostly Can also occur in type 2 during infections and sever trauma, not as common as type 1 Get increased respiration, polyuria, nausea and acetone breath, vomiting, abdominal pain in children Treat with ER and IV fluid therapy and insulin o Hyperosmolar Coma Occurs in absence of ketosis in type 2 Usually due to decreased fluid intake Higher incidence of coma than ketoacidosis due to more severe hyperglycemia and dehydration (10 times higher) Hypoglycemia (Insulin Shock) - Drug-induced o Stimulation of sympathetic nervous system (adregenergic), which can be from too much insulin: brain and nervous system react. - Non-drug related: o Fasting hypoglycemia Exercise o Reactive/Post-prandial Induced by a meal o Symptoms are adrenergic in nature, so get shaking, sweating and palpitations o All symptoms are related to adrenaline o Also see confusion, irritability, headaches, abnormal behaviour, weakness, diplopia o Nocturnal hypoglycemia Occurs mostly in insulin-dependent individuals Night sweats, nightmares (symptoms usually due to excess insulin) - Renal Failure, Insulinoma, GH deficiency Types of Comas in Diabetes Mellitus - Hyperglycemic Coma o Blood glucose is greater then insulin o Symptoms are weak and rapid pulse, skin is dry and warm, intense thirst, acetone breath, respiration increased, seizures, and altered consciousness o Get patient to the ER - Non Ketotic Hyperglycemia Coma (NKHHC) o Symptomatic hyperglycemia, inadequate fluid intake, dehydrated, osmotic diuresis o There are CNS alterations, extreme hyperglycemia without marked hyperketonemia and mild metabolic acidosis o Get patient to the ER - Hypoglycemic Coma
o Insulin excess gives insulin shock o Patients pulse is full and rapid, skin is cold and clammy, intense hunger, decreased respiration, irritable, confusion, and seizures o Treat by giving sugar Chronic Complications of Diabetes Mellitus Seen On Ophthalmoscopy (if that is even the word, I think its Fundoscopy, but you get the point) - Cotton wool patches on the eye = infarction resulting in nerve cell damage, hemorrhage, can be caused by hypertensive retinopathy o Associated with cataracts and glaucoma o See exudates (fat/protein) which accumulate in back of eye - Damaged Disk = papilledema (acute swelling from excess pressure) o Pressure is on CN 2 (optic), this pushes disk forwards o Signs also seen in brain tumor - Enlarged Cup = glaucoma (decreased vessels around optic disk) - Papular Eruptive Xanthoma = lipid problem (usually LDL) o If eruption, must act quickly o May be secondary to diabetes, liver problems, and may be hormone related Other Conditions related to Diabetes Mellitus - Skin tags = evident in the years before type 2 is diagnosed. Normal finding, but seems to be a link between skin tags and blood sugar, especially over the age of 35 - Ulcers o Venous/Stasis Ulcer Medial and lateral aspect of malleoli Superficial ulcer, some pain Warm to touch due to stasis, venous blood stays in the area Heels are purple due to blood leaking into tissue Minimal pulse and sensation Can have atrophy blanche = scarring and healing from venous stasis related to previous ulceration o Arterial Ulcer Dorsum of foot and tips of toes and over tibia Absent foot pulse Deep ulcer and painful o Neuropathic Ulcers Develop at pressure sites, and bottom of foot Decreased sensation of big toe, of foot, and joint position sense Will lose sense of fine touch Achilles reflex will be diminished Pulses are reduced, don’t feel pain Chronic Complications of Diabetes Mellitus o Microvascular Disease Retinopathy, Nephropathy o Macrovascular Disease Atherosclerosis o Insulin Resistance Syndrome (Syndrome X) Obese or sedentary people with type 2 or family history of type 2 diabetes Hypertension, hyperinsulinemia, dyslipidemia, hyper or normoglycemia Progress to coronary artery disease/stroke
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Clinical manifestations are diabetic nephropathy, ocular disease, peripheral neuropathy, infections, gallstones, xanthomas, impotence and foot ulcers o Hyperglycemia With excess glucose, it can bind more to cells not requiring insulin like nerves, lens of eye, kidney and blood vessels leading to many problems o Protein Glycosylation Glucose binds to proteins in proportion to hyperglycemia which can lead to cross linking with blood vessel walls and this can lead to hypertension because of decreased elasticity o Sorbitol Accumulation Accumulation of sorbitol (made from glucose) occurs because of prolonged high glucose levels, this leads to influx of water and swelling and cell damage o Lipid Glycosylation Glycosylated LDL’s don’t bind to LDL receptor in liver and so LDL is now available for depositing in arterial wall, so increased TG levels and this contributes to hypertension
Lab Tests - Glucose Tolerance Test o Looks at how well the body can produce insulin in response to a challenge with lots of sugar. o Good test for people with hypoglycemic symptoms - Skin Prick Test o Need to know when person ate, so not exact, and on glucose tolerance curve diabetes type 2 would be represented by staying high for a longer period of time on the curve - Glycosylated Hemoglobin o Estimates plasma glucose for past 3 months o 97-98% of hemoglobin in adults is HbA o Normal glycosylation of blood is 4-5.9% in diabetes can se 13-20% HbA1C - Urinary Ketones and Urinary Glucose o Ketonuria = can occur in starvation states, high protein diets, and alcoholism o Gluosuria = not well controlled DM, disease of renal tubules (seen in gestational diabetes) Diabetes Mellitus - Increased glucose metabolism - Hyperglycemia in fasting state - Caused by defective or deficient insulin secretion and/or insulin receptor defects (type II) Classification of Diabetes - Type I (insulin dependent DM) o Not producing any insulin, islet cells of pancreas are destroyed o Produce ketones o Seen usually in younger onset (juvenile diabetes) o Have HLA islet cell antibody - Type II (Non-insulin dependent DM) o No ketosis, Have some insulin, More mature onset o No islet cell antibodies o Decreased sensitivity of beta cells to glucose and eventual loss of beta cells Type A = have defect in insulin receptor Type B = have Ab to insulin receptor - Type III (Gestational DM) o History of DM in family, previous infant of more then 9 lbs, unexplained still births, previous miscarriages o Mother has anti-insulin hormone, secreted by placenta (human chorionic somatomammotropin). More glucose is available to the baby so it grows larger
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Type IV (Secondary DM) o Conditions and syndromes associated with impaired glucose tolerance o Chronic pancreatitis, hormonal tumors