Diabetes Flashcards
what are the most common diabetic symptoms and why do they occur
- polyuria – too much glucose in blood plasma and eventually starts seeping through kidney filtration in to urine; glucose attracts water
- sudden weight loss – difficulty metabolizing carbohydrates and use fats as fuel substrate
- wounds that won’t heal
- polydipsia (thirsty) – losing water through urination due to increased urination of glucose
- polyphagia (hungry) - metabolizing fats as fuel substrate
- blurry vision
- N/T in stocking distribution
- vaginal infections and sexual problems
describe the anatomical location of diabetic dysfunction in type I
insulin deficiency occurring in pancreas (Islets of Langerhans that secrete insulin)
-tx with insulin
describe the anatomical location of diabetic dysfunction in type II
“relative” insulin deficiency, DEC sensitivity/INC resistance to insulin in muscles but often adequate insulin resistance
-tx diet and exercise and then metformin
how does insulin work
- insulin binds to insulin receptor, which causes a conformational change to the Glut-4 receptor
- the Glut-4 receptor moves to the surface of the cell and glucose moves through it
describe type I pathophys
insulin receptors and glut-4 transporter system are intact, but there is inadequate insulin secretion usually b/c of autoimmune destruction of pancreatic cells
describe type II pathophys
insulin release may be normal (or slightly increased/decreased in some cases) but there is a resistance to its action at the receptor/Glut-4 pathway
proposed mechanisms:
-cellular resistance to insulin increases with obesity
-decreased beta cell responsiveness to plasma glucose levels
-abnormal glucagon secretion
-islet of langerhorn dysfunction (decrease/abnormal pancreas beta cells)
-amyloid formation in pancreas to destroy islet cells
what is the gold standard for assessing “long-term” glycemic control
- HBA1c test: hemoglobin greater than 6.5%
- monitors long-term glycemic control b/c average lifespan of an RBC is 3 mon and once glycosylated it remains so
what happens to molecules when glucose binds to them (glycation)
- molecules become denatured from oxidative stress
- cross-linking of connective tissue that impairs normal structure and function of tissues
what are the major consequences of advanced glycation end products
- cardiovascular disease
- diabetic neuropathy, nephropathy, retinopathy
- CNS disease
what are the macrovascular diseases (large vessel diseases-arteries and arterioles) that occur due to DM
most pts have HTN and dyslipidemia, but they also develop artherosclerosis much faster as well, both in coronary arteries and peripheral arteries
how does retinopathy occur with DM
microvascular disease-endothelial basement membrane is damages due to glycation and oxidative stress, causes microneurvsms and hemorrhages that lead to patchy loss of visual field
how does nephropathy occur with DM
microvascular disease-glomerular basement membrane is damaged, increasing it’s permeability to large molecules such as protein, glucose, and albumin
-these large molecules leave in to urine and get diuresis (loss of fluid volume) b/c of glucose attraction to water
how do neuropathies occur with DM
due to a combination of microvascular ischemia of the nerve projections and the oxidative stress on the nerve cells themselves leading to neuronal damage (loss of myelin, disruption of normal neural cell metabolism, impaired ability to maintain normal membrane potentials, etc.)
-bilateral and symmetrical effects
how do autonomic neuropathies occur with DM
HR and vascular tone become dysregulated, causing:
- resting sinus tachycardia (vagus nerve damage and loss of parasympathetic influence to slow HR)
- inability of HR to increase normally during exertion (chronotropic incompetence) b/c of sympathetic nerve damage
if DM patient using fat and protein for fuel, what can happen?
- cause metabolic acidosis due to production of ketones
- body compensates by increasing ventilation (hyperpnea)
