type 2 diabetes and Type 1 diabetes Flashcards
Diabetes mellitus
A chronic metabolic disorder with characteristic complications associated with hyperglycemia
Hb A1C> 6.5%, Fasting plasma glucose>126, 2 hr plasma glucose > 200 75 oral glucose, Random glucose >200
Pre diabetes
A1c5.7, fasting 100-125, 2 hour plasma 140 oral glucose test
DM short term complications
Short term complications- electrolyte abnormalities, fatigue, poor wound healing, impaired immune defenses, prolonged hospital stay, increased inpatient morbiditiy and mortality, diabetic ketoacidosis, hyperosmolar hyperglycemic state, treatment related hypoglycemia
Long term Complications: Microvascular (retinopathy, nephropathy, neuropathy), macrovasculat (Coronary artery disease, peripheral vascular disease)
Pathogenesis of diabetes mellitus complication
accumulation of advanced glycosylation end products, accumulation of sorbitol, disruption of the hexosamine pathway, disruption of the protein kinase C pathway, activation of the poly (ADP-ribose) polymerase pathway
Increased oxidative stress
Long term glycation of proteins and damage- causing retinopathy via immune attack
Etiology of DM
Type 1- Autoimmune B cell destruction with lack of insulin
Type 2- insulin resistance with relative insulin deficiency
Others- genetic defects in B cell function, exocrine pancreas disesease, endocrinopathies, drug/chemical induced
Gestational- insulin resistance with B cell dysfunciton
T@DM clinical presentation
USUALLY: insidious onset, occurs over 40, Metabolic syndrome, progressive
Acanthosis nigricans
Obesity, people who are obese have really high insulin peaks compared to normal weight
Diabetic emergency
Diabetic ketoacidosis, Hyperosmolar hypergycemia
Pathophysiology of Type 1 DM in kids
Damage to the beta cell, likely by environmental/virus with release of Ag, taken up by Ag presenting cells, causes priming of CD4 T cells
Cytokines and T cell differentiation–> CD8 transformation to systemically destroy the beta cell
Causes release of more antigen, amplifies response
Natural history of Type 1 diabetes
Genetic predisposition–putative environmental trigger, beta cell injury, pre diabetes and then diabetes
Pravelecnce of T1DM increases with age until 19, M>F
White people, Native americans rare
Glucose/insulin curves for normal vs T1DM
Normally After a glucose tolerance test, glucose spikes with insulin and then goes down
In T1DM glucose is already high and then shoots up, but the insulin barely goes up
IV glucose isnt as strong bc GLP is not released (from gut)
Biochemistry of ketoacidosis
Insulin deficiency–> Cellular underutilization of glucose, increased hepatic gluconeogenesis–> hyperglycemia
Hyperglycemia exceeds glomerular T max for glucose, Glycosuria–> osmotic diuresis–> Decreased GFR–> severe hyperglycemia–> intracellular dehydration and impaired consciousness
Dehydration and hemoconcentration–> shock
Lipolysis–> fatty acid transport to hepatocytes–> Carnitine transferase 1–> hepatic mitochondria–> Beta oxidation–> ketoacids–> vomidting and metabolic acidosis
Metabolic acidosis- dont give bicarb,
Electrolyte abnormalities in untreated T1DM
Hyponatremia- osmotic dilution of plasma
Hypokalemia- not a consistent finding
Low carbon dioxide (bicarbonate)-ketoacidosis
Phosphate- decreased phosphate intake and phosphaturia
Treatment of children in DKA
obtain labs- venous blood gases, basic metabolic profile, HbA1C, urine ketones, thyroid studies/antibodies, celiac screen, T1DM antibodies
Assess level of dehydration: Start with normal saline (.9% NaCL) bolus of 20 ml/kG, a second bolus is rarely necessary, start regular insulin drip .1units/kg/hr
Assess electrolyte distrubances to determine what IV fluids to add for hydration (Na, K, glucose, chloride)
Add dextrose to IV Fluids when BG<250/300, hourly labs, hourly neurological checks to assess for cerebral edema treat any possible cerebral edema with mannitol, DO NOT treat DKA with bicarbonate, after pH normalizes and bicarb is >17 may transition to subQ insulin therapy
insulin overdose
insulin overdose causes hypoglycemia (<70), this can cause mild adrenergic symptoms of shakiness, headaches, dizziness, sweatiness, tachycardia, hunger or fatigue
treated with oral fast acting carbs (juice, candy and rechecking blood sugar in 15 minutes)
if pt has moderate hypoglycemia which causes neuro symptoms, pts experience confusion, combativeness, poor coordination slurred speech, treatment usually includes fast acting carbohydrates, frosting sugar gel, given orally or in the buccal mucosa
For sever hypoglycemiap tupor,seizure, and coma– give ER care with glucagon injections
