Diabetes Mellitus Study Guide

Topics: Insulin, Diabetes mellitus, Blood sugar Pages: 14 (3555 words) Published: November 25, 2012

* Chronic multisystem dz , abnormal insulin production / impaired utilization * Disorder of glucose metabolism related to absent/ insuff insulin supply or poor utilization of inslin that’s available * 7th leading cause of death

* leading cause of blindness, ESRD, lower limb amputation * contributing factor for heart dz/ stroke risk 2-4 x higher than without DM * INSULIN – hormone produced by cells in islets of Langerhans of pancreas. Normal – continously into bloodstream ( basal rate), or increased w/ meals (bolus) * Normal glucose range 70-120 mg/dL, average insulin secreted daily 40-50 U 0.6 U/kg * Glucagon, epinephrine, GH, cortisol oppose effects of insulin counterregulatory hormones they blood glucose lebels, stimulate glucose production by liver, movement of glucose into cells. * Insulin released from cells – as precursor / proinsulin thru liver enzymes form insulin & C-peptide ( C-peptide in serum & urine indicator of cell function) * in plasma insulin after meal storage of glucose as glycogen in liver/ muscle, inhibits gluconeogenesis, fat deposition, protein synthesis * Nl overnight fasting release of stored g;ucose from liver, protein from muscle, fat from adipose tissue * Skeletal muscle & adipose tissue receptors for insulin insulin-dependent tissues

Type I Diabetes

* Juvenile onset, insulin-dependent, s/s abrupt but dz process present for several yrs, 5-10%, absent or minimal insulin production, virus/toxins, under 40, 40% before 20 yr * s/s thirst( polydipsia), polyuria, polyphagia ( hunger), fatigue, wt loss, Kussmaul respirations * immune mediated dz; T-cells attack & destroy cells

* genetic predisposition & exposure to virus
* Idiopathic diabetes – not atoimmune, strongly inherited, in small # pt w/ type I DM , African/Asian * Predisposition HLAs human leukocyte antigens when exposed to viral infection cells destroyed * Long preclinical period, s/s develop when pancreas can no longer produce sufficient insulin to maintain nl glucose levels * Req. insulin from outside source exogenous insulin eg. injection * No insulin diabetic ketoacidosis (DKA) life threatening, results in metabolic acidosis * “honeymoon period” – newely diagnosed pts, tx initiated pt experience remissions req little insulin because cells produce suff amount of insulin lasts 3-12 mths then req permanent insulin


* risk for developing diabetes
* glucose levels high but not high enough for diabetes diagnosis * impaired fasting glucose IGF 100-125 mg/dL
* 2 hr oral glucose tolerance test OGTT 140-199 mg/dL
* HgB A1C – 5.7%-6.4% risk for diabetes
* Increased risk for developing DM type II – if no preventive measures develop DM in 10 yrs * Long term damage to body heart, blood vessels occur in prediabetes * Usually no symptoms
* Maintain healthy weight, exercise regularly, healthy diet risk of developing diabetes Type II Diabetes

* Adult onset, non-insulin dependent, 90%
* > 35, overweight, tendency to run n families
* African Am, Asian, Hispanics, Amerian Indians
* Some insulin is produced but either insufficient for body needs / poorly utilized * Gradual onset, many yrs undetected hyperglycemia, 500-1000mg/dL * Early usu. asymptomatic; high risk pt screen annually

* Fatigue, recurrent inf, vaginal yeast inf, candida inf, prolonged wound healing, visual changes * Risk factor obesity ( abdominal/ visceral )
* 4 major metabolic abnormalities
* insulin resistance > tissue no response to insulin / unresp receptors – receptors are located on skeletal muscles, fat & liver * ability of pancreas to produce insulin – fatigued from compensatory prod of insulin, cell mass lost * inappropriate glucose by liver – too much glucose for body needs – type II * altered prod. of hormones & cytokines by adipose tissue (...
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