| Flap 1 | Flap 2 |
| Group of diseases characterized by hyperglycemia | Diabetes Mellitus |
| Hyperglycemia can be d/t defects in | Insulin secretion, Insulin action, Both |
| Disproportionately affected populations | Elderly & minorities |
| Insulin functions r/t glucose | Transport, Metabolism, Stimulates storage, Inhibits breakdown, Signals liver to stop release |
| Storage sites of glucose | Liver & muscles |
| Other functions of insulin | Enhances storage of dietary fat in adipose tissue, Transport of amino acids into cells, Inhibits breakdown of protein and fat |
| Type 1 DM d/t | Autoimmune destruction of Beta cells in pancreas |
| 2 factors causing Type 2 DM | Decreased sensitivity to insulin (resistance), Impaired beta cell function |
| DM that can be controlled by diet | Type 2 DM |
| Fasting blood glucose > | 126 mg/dL |
| Random glucose > | 200 mg/dL |
| Three P's r/t Clinical Manifestation of DM | Polyuria, Polydipsia, Polyphagia |
| Polydipsia vs. Polyphagia | Dip:excessive thirst, Phagia:excessive eating |
| Abd r/t Type 1 DM d/t | Diabetic Ketoacidosis |
| Vascular & neuropathic complications can be decreased with | Intensive control |
| Dietary goals r/t DM | Optimal nutrition, Meet energy needs, Reasonable weight, Prevent wide glucose fluctuations, Decrease serum lipids |
| Diabetic ketoacidosis(DKA) caused by | Type I diabetes |
| Main causes r/t DKA | Noncompliance w/insulin regimen, Illness/infection, Undiagnosed/untreated diabetes |
| Hyperglycemic Hyperosmolar Nonketonic Syndrome(HHNS) caused by | Type II diaetes |
| Can Pts move from type II diabetes to gestational diabetes and vice versa | Yes |
| Can type I Pts move to other forms of DM | No |
| Complication r/t Diabetes can occur in anyone w/ | Type I and Type II diabetes, Not only Pts using insulin |
| Glucagon function | Stimulates liver to release glucose |
| Pathophysiology effects r/t Type I diabetes | Decreased insulin production, Rampant glucose production by liver, Fasting hyperglycemia, Glucose not stored in liver |
| Excess glucose secretion in urine r/t Fluid and electrolytes | Excessive loss of fluids and electrolytes |
| Ketone bodies are byproducts of | Fat breakdown |
| S/Sx r/t DKA | Abd pain, N/V, Hyperventilation, Acetone breath(fruity odor) |
| Insulin problems r/t Type II diabetes | Insulin resistance, Impaired insulin secretion |
| Insulin resistance r/t Tissue sensitivity to insulin | Decreased tissue sensitivity |
| Primary treatment r/t Type II diabetes | Weight loss |
| Causes insulin resistance r/t Gestational diabetes | Placental hormone secretion |
| Main goal r/t Diabetes treatment | Normalize insulin activity and blood glucose levels, Reduce development of complications |
| Fasting is no caloric intake over | 8 hours |
| Control of total caloric intake is associated with | Reversal of hyperglycemia r/t Type II diabetes |
| Moderate alcohol intake r/t Men & women | M:2/day, W:1/day |
| Nutritive sweeteners vs. Sucrose r/t Blood sugar elevation | Nutritive sweeteneres cause less elevation |
| Non-nutritive sweeteners r/t Safety to diabetics | FDA approved them safe |
| Time to evaluate for dosage adjustments vs. Time to evaluate basal/bolus insulin r/t Self-monitoring of blood glucose | Measure at peak action time for dosage adjustments, Measure before meals to evaluate basal/bolus insulin |
| Time r/t Determing bolus doses of regular/lispro insulin | 2 hours after meals |
| Glycated hemoglobin(A1C) reflects | Average blood glucose levels over the last 2-3 months |
| A1C binds to | RBC's for the cells entire life |
| Most common method for self-testing of ketone bodies | Urine testing |
| Rapid-acting vs. Short-acting vs. Intermediate-acting vs. Very long-acting r/t Insulin names | R:Lispro, S:Regular, I:NPH, V:Lantus |
| Rapid-acting vs. Short-acting vs. Intermediate-acting vs. Very long-acting r/t Onset period | R:15 min, S:30 min, I:2 hrs, V:1 hr |
| Basal insulin function | Maintain blood glucose levels regardless of meals |
| Insulin type r/t Basal insulin | Intermediate-acting insulin (NPH), Lantus is also approved |
| Only insulin approved for IV use | Regular |
| Regular insulin vs. NPH insulin | R:clear and drawn into syringe first |
| Mixing w/other insulins r/t Lantus | No mixing |
| Insulin regimens goal | Mimic normal pattern of insulin secretion d/t food intake and activity patterns |
| Pt requirements r/t Complex insulin regimens | Commitment, Intensive education, Close follow-up w/health care team |
| Risk of hypoglycemic reactions r/t Complex insulin regimens | Risk of MORE reactions |
| Conventional vs. Intensive insulin regimens | C:simplified regimen, I:achieve as much control over blood glucose levels as possible |
| Conventional vs. Intensive insulin regimens r/t Flexibility of meal & activity patterns | C:Patterns should not vary, I:Pt has flexibility on a daily basis |
| Risks of complications & severe hypoglycemia r/t Intensive insulin regimens | Decreased risk of complications, Increased risk of severe hypoglycemia |
| Appropriate candidiates r/t Conventional insulin regimens | Terminally ill, Frail elderly, Pts unwilling to comply w/intensive regimen |
| Inappropriate Pts r/t Intensive regimens | Nervous system disorders, Recurring severe hypoglycemia, Irreversible diabetic complications, Cerebrovascular and/or cardiovascular disease, Ineffective self-care skills |
| Insulin regimen r/t Kidney transplant Pts | Intensive regimen |
| Complications r/t Insulin therapy | Local/systemic allergic reactions, Insulin lipodystrophy, Insulin resistance, Morning hyperglycemia |
| Do local allergic reaction to insulin ever disappear | Yes, w/continued use |
| Lipoatrophy vs. Lipohypertrophy | L-atrophy:loss of SC fat, L-hypertrophy:development of fibrofatty masses at injection sites |
| Measurement r/t Clinical insulin resistance | Daily insulin requirement > 200 units |
| 3 types of Morning hyperglycemia | Dawn phenomenon, Insulin waning, Somogyi effect |
| Dawn phenomenon vs. Insulin waning vs. Somogyi effect | D:blood glucose levels rise after 0300 d/t surges in growth hormone secretion, I:progessive increase in blood glucose from bedtime - morning, S:nocturnal hypoglycemia following by rebound hyperglycemia |
| Insulin waning prevention | Administer evening dose of NPH to bedtime |
| Alternative methods r/t Insulin delivery | Insulin pen, Jet injector, Insulin pump, Implantable insulin delivery, Pancreatic cell transplants |
| Absorption r/t Jet injectors | Faster absorption |
| Needle/catheter changing schedule | At least every 3 days |
| Insulin pump placement r/t Cougars, Milfs, Hotties et cetera | Front/side of bra, Garter belt on thigh |
| Most common risk r/t Insulin pump therapy | DKA unless type II |
| First skills taught r/t Newly diagnosed diabetics | Needle insertion & insulin injection |
| Insulin storage | Room temp if bottle is being used, Refrigerated if not in use |
| Storage r/t Prefilled syringes | Needle in an upright position to avoid clogging of needle |
| Absorption rates(Fastest to slowest) r/t Injections sites | Abd(fastest), arm, thigh, hip(slowest) |
| Injection site r/t Exercise | Injected into limb not being exercised |
| Hypoglycemia r/t Blood glucose level | Less than 60 mg/dL |
| Hypoglycemia causes | Too much insulin or physical activity, Too little food |
| Mild vs. Moderate vs. Severe hypoglycemia r/t Manefestations | Mild:adrenergic symptoms(sweating, tremor, tachycardia, hunger), Moderate:adrenergic symptoms plus some CNS impairities, S:extremely impaired CNS function(Pt needs assistance) |
| Immediate treatment r/t Hypoglycemia | 15g fast-acting concentrated CHO |
| Emergency treatment r/t Hypoglycemia | 1 mg glucagon |
| Time r/t Snacking | Peak insulin activity |
| 3 main clinical feature r/t DKA | Hyperglycemia, Dehydration/electrolyte loss, Acidosis |
| DKA treatment factors that reduce serum K levels | Rehydration, Insulin administration |
| Necessary first step when preparing IV insulin drip | Flush insulin through tubing and discard first 50 mL, Initial fluid contain a decreased insulin concentration |
| Precipitating events r/t HHNS | Acute illness, Medications exacerbating hyperglycemia, Recent history of polyuria w/adequate fluid intake |
| Ketosis & acidosis r/t HHNS | Generally do not occur |
| Manifestations r/t HHNS | Hypotension, Severe dehydration, Tachycardia, Variable neurologic signs |
| Initial treatments r/t DKA & HHNS | Fluid replacement, Correct electrolyte imbalances, Insulin administration |
| Cause r/t Diabetic retinopathy | Changes in blood vessels of retina |
| Manifestation r/t Proliferative retinopathy | New blood vessels growing from retina to vitreous |
| Visual loss r/t Diabetic retinopathy is d/t | Vitreous hemorrhage, Retinal detachment, Both |
| Deep tendon reflexes and Vibratory sensation r/t Peripheral neuropathy | Both decrease |
| Autonomic neuropathy affects | Almost every organ system in body |
| Autonomic neuropathy r/t Adrenergic symptoms of hypoglycemia | Symptoms are diminshed/absent |
| Subtle sign r/t Hypoglycemia | Numbness around mouth, Difficulty concentrating |
| Manifestations r/t Sudomotor neuropathy | Decreased/absence of sweating in extremities, Increased upper body sweating |
