Diabetes Mellitus

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Unformatted text preview: t baby) o family history of type 2 DM o low birth weight of mother (organs - pancreas may not have developed well) Gestational Diabetes • insulin resistance in the second trimester o increase in fat deposition increases insulin resistance o pregnancy hormones increase insulin resistance estrogen, lactogen, progesterone increased uptake of glucose by fetus o beta cells can’t meet demand hyperglycemia • most women regain normal blood glucose levels after delivery • insulin resistance – normal part of pregnancy – body makes sure infant has enough glucose o normal pregnancy – body can produce enough insulin to compensate o gestational diabetes – beta cells can’t produce enough insulin – can’t compensate for insulin resistance Effect of Poor Glycemic Control in Pregnancy • for the mother: o increased risk of infection, diabetic ketoacidosis, premature labour, delivery complications, hypertension, death o increased risk of macro and micro vascular complications o for those with GDM: increased risk of developing T2DM later in life • effects on the infant: o increased risk of congenital defects (if blood glucose is elevated at conception) o hyperinsulinemia, hyperglycemia macrosomia (due to high blood glucose) o material ketosis cognitive impairment (ketones can cross the placenta) o stillbirth, premature delivery o fetal programming more likely to develop type 2 DM more likely to be obese what fetus is exposed to can change gene expression (turns genes on or off) Reducing these effects • aim for excellent glycemic control • those with pre- existing diabetes should improve glucose control prior to conception • switch antihyperglycemic agents to exogenous insulin Pathophysiology Long- term Complications • stroke • heart disease • nerve damage • kidney disease • blindness • dementia Microvascular Complications • retinopathy o too much glucose can damage capillaries in retina o night blindness, blindness • nephropathy o microalbuminuria – if capillaries in kidney are damaged, albumin can leak out into urine o can lead to end stage renal disease as diabetes progresses Macrovascular Complications • coronary artery disease • stroke • peripheral vascular disease o clots can form in the peripheral vascular system – may require amputation • metabolic effects of DM result in atherogenic body response: o platelet dysfunction, increased fibrinogen, increased viscosity and clotting of the blood, dyslipidemia, leukocyte dysfunction, macrophage dysfunction leading to greater foam cell production, increased oxidation of LDL, dense atherogenic LDL, hypertension • most people with diabetes end up dying of heart disease Other Complications • neuropathy o pain or loss of feeling in various parts of the body o infections, amputations (body doesn’t heal as well) o can cause changes in digestion, bowel and bladder function, sexual response, perspiration (due to nerve damage) How do high blood glucose levels lead to complications? 1. glycosylation of protein • sugar molecules bind to proteins – changes structure and function • glycosylation of proteins in blood vessel wall cause the artery wall to thicken or even rupture small vessels • stroke, atherosclerosis, increased risk of heart disease, damage to small blood vessels in eyes and kidney • sugar molecules attach to protein – changes protein shape and function o proteins on surface of cell important in cell signalling and function 2. polyol accumulation • high blood glucose excess uptake into non- insulin dependent cells (brain, eyes, kidneys, nerves) • excess...
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This document was uploaded on 03/03/2014.

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