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DM, Insulin, & Orals
Various questions about diabetes, insulins, and oral hypoglycemics
| Question | Answer |
|---|---|
| Diabetes Mellitus | Group of metabolic disorders of fat, carb, and protein metabolism that result from defects in insulin secretion, action, or both |
| Type I DM | Insulin Dependent DM; Autoimmune disease that kills insulin-producing beta-cells of the pancrease; develops very quickly; gets worse over time; absolute insulin deficiency |
| Incidence of DM | 7-10% of population; 5% of these are Type I |
| Short Term Consequences of poor control | polyuria, poydipsia, polyphagia, ketonuria, fatigue, malnourishment, stomach pain, N/V, blurred vision, more prone to infections |
| Long Term Consequences of Poor Control | Retinopathy, Neuropathy, Nephropathy; ANS Problems (orthostatic hypotension, GI Problems, ED, circulatory problems, atherosclerosis |
| Mechanism of Action of Insulin | 1) Increases uptake of glucose via GLUT4 transporter; 2) Decreases gluconeogenesis in liver; 3) Increases uptake of AAs and thus protein formation; 4) increase fat (inhibits lipolysis, promotes storage of fat); 5) Increases glycogen production |
| Human Secretion of Insulin | Secretes pulses of 5-8 units of insulin after ingestion of each meal, along with a basal level of 0.5-1.0 Units continually; This is the basis for insulin therapy |
| PK of Rapid Acting Insulin | Onset: 15min; Peak: 30min-1h; Duration: 3h; Includes Aspart, lispro, & glulisine |
| PK of Short Acting Insulin | Regular Insulin; Onset: 30min; Peak: 2-5h; Duration: 5-8h |
| PK of Intermediate Acting Insulin | Protamine (NPH) and Lente (Zinc); Onset: 2h; Peak: 6h; Duration: 20h |
| PK of Long Acting Insulins | Glargine (Lantus) and Debmir (Levemir); Onset: 2+ hours; Peak: Little or no peak; Duration: 24h |
| Usual Dose of Insulin for Healthy Type I DM | 0.5-0.8 Unit per kg |
| Twice Daily Dosing Regimen | 2/3 of dose in morning, 1/3 in evening before meals; Of each dose, 2/3 should be NPH and remainder regular insulin |
| Fasting Glucose Goal | <100mg/dL |
| Goal for Post-Prandial Glucose | <140-180mg/dL |
| Goal for HbA1C | <6.5-7% |
| Symptoms of mild hypoglycemia | (50-60mg/dL and below; happen quickly) sweating, nervousness, tachycardia, hunger, heart palpitations, tremor, anxiety, tingling around mouth |
| Symptoms of moderate hypoglycemia | (Between 20 and 50mg/dL) headache, mood changes (irritability, difficulty concentrating, drowsiness, confusion, agitation), weakness, slurred speech, dizziness, nightmares, night sweats |
| Symptoms of severe hypoglycemia | (Usually below 20mg/dL) Fainting and loss of consciousness; potentially fatal if severe and prolonged |
| Dose of insulin during honeymoon phase | 0.2-0.5 Units/kg |
| Dose of insulin during ketosis, illness, or rapid growth | 1-1.5 Units/kg |
| Which insulins can be given IV? | Lispro, aspart, and regular |
| Which insulins can be mixed? | Can mix NPH with Regular, Lispro, Aspart, and glulisine; Can mix Lente with Ultralente only; Detemir and Glargine cannot be mixed with anything |
| Which insulins are clear? | Rapid Acting (lispro, aspart, glulisine), regular insulin, detemir, and lantus |
| Which insulins are cloudy? | NPH, Lente, and Ultralente |
| How is insulin dose usually increased? | 2-3 Unit increments every 3-4 days |
| If fasting levels are high... | increase basal insulin by 2-4 Units |
| If post-prandial levels are high... | increase bolus dose by 2-4 units |
| Hospitalized Patient --> Ambulatory Patient... | Lowers insulin requirement by 6-8 units/day |
| A 1mg% reduction in HbA1C is a result of _________ | A 35-50mg% average reduction in glucose levels |
| Risk Factors for Type II DM | Family history, weight >20% IBW, inactivity, Poor diet/exercise habits, non-europeans |
| MOA of Sulfonylureas | Bind SU receptors --> Close ATP-dependent K+ channels --> Causes buildup of Na+ and subsequent release of insulin |
| Most common side effect of Sulfonylureas | Hypoglycemia --> they will still release insulin, even if glucose isn't high; Also weight gain is common |
| Classes of Insulin releasing oral meds | Sulfonylureas and meglitinides |
| Brand and Generic Name of meglitinides | Repaglinide (Prandin) and Nateglinide (Starlix) |
| MOA of Meglitinides | Increase the release of insulin, but are not SUs |
| Classes of insulin assisting oral meds | Alpha Glucosidase inhibitors |
| Brand and Generic Names of Alpha-glucosidase inhibitors | Acarbose (Precose) and miglitol (Glyset) |
| MOA of Alpha-glucosidase inhibitors | Reversibly inhibit alpha-glucosidase enzyme --> Slows the breakdown and thus absorption of carbohydrates in the gut |
| Most common side effect of alpha-glucosidase inhibitors (and how to avoid it) | GI Upset; Avoid by titrating up |
| Dosing/Administration tips for a-glucosidase inhibitors | Take with first bite of meal; If hypoglycemia occurs, take glucose, dextrose, or milk (not carbs or sucrose) |
| Classes of Insulin Sensitizing Oral meds | Biguanides and Thiazolidinediones (TZDs) |
| Brand and Generic Biguanide | Metformin (Glucophage, Fortamet) |
| Brand and generic of TZDs | Pioglitazone (Actos) and Rosiglitazone (Avandia) |
| MOA of Metformin | Unknown; theories: 1) Decrease hepatic glycogenolysis and gluconeogenesis; 2) Increase muscle uptake of glucose. 3) increases insulin sensitivity |
| Common SEs of Metformin | GI Upset (titrate dose up to minimize), metallic taste, bloating, possible lactic acidosis (esp. in elderly and those with renal or hepatic disease or alcohol consumption) |
| MOA of TZDs | Decrease insulin resistance by binding to PPAR and increasing intracellular action (Glucose is better utilized) |
| Do TZDs cause hypoglycemia? | No |
| Common SEs of TZDs | Weight gain, N/V, stomach pain, respiratory infections (possible liver disease) |
| HCTZ and its effect on DM | Decreases BP, acts as diuretic --> Causes K depletion --> Decreases amount of insulin released |
| ACE Inhibitos and DM | Nephroprotection (decreases afferent arteriole pressure in kidney) |
| Beta-Blockers and DM | Hypoglycemia tends to cause rapid heartbeat, tremors, and sweating --> B-Blockers mask these signs |
| Best Control of Type I DM | Basal-Bolus Therapy --> Requires multiple injections --> Basal every 12-24 hours, bolus before meals, or an insulin pump to mimic endogenous release |
| Exercise Guidelines | Test Glucose before, during, and after exercise; For moderate exercise, decrease previous dose by 30-50%; Have 10-15 grams of glucose handy; inject into abdomen; watch for post-exercise hypoglycemia (can occur 8-15 hours afterward) |
| Exercise Guidelines--If glucose is greater than 240 | DO NOT EXERCISE --> Will likely increase glucose further |
| Symptoms of Hyperglycemia | polyuria, polydipsia, polyphagia, dehydration, fatigue, stomach pain, nausea, loss of appetite, vomiting, blurred vision, acetone breath, difficulty breathing, potential loss of consciousness to coma (sever DKA) |
| Best Intial Choice for Treatment of Type II DM | Probably Metformin --> No hypoglycemia, weight loss, improvement in lipids |
| Treatment of Type II DM if FPG >300mg/dL | Orals are not potent enough, patient should be on insulin |
| What if FPG is >400mg/dL | Patient needs to be hospitalized and monitored closely |
| Step Therapy | Initial Agent --> Monitor response and compliance --> Increase to ceiling dose --> Add second agent of a different MOA (try to avoid two meds with same SEs, e.g. metformin and acarbose--increased GI effects) |
| Step Therapy--What if two oral agents are enough? | Go to insulin or combine one oral agent with insulin (usually bedtime insulin, oral day (BIDS--Bedtime Insulin, Daily Sulfonylurea); Usually a long acting insulin (Lantus); Some discussion about adding 3rd agent |
| Type II DM Patient with renal or hepatic dysfunction | Switch to insulin -- Orals cause too much of a problem |
| Best oral with renal problems | TZDs (primarily metabolized by liver) -- Avoid SUs and metformin; ACE Inhibitors or ARBs are advised (nephroprotective) |
| Best oral with hepatic problems | Short acting meglitinides -- Avoid metformin and especially TZDs |
| Titration Schedule for A-Glucosidase Inhibitors | Increase by 50mg/day every 1-3 weeks; OR 25 TID c food, increase every 4-8 weeks to 50-100mg TID with meals |
| Titration Schedule for Metformin | Initial dose 500 mg bid with increases every week up to 2000 mg/day |
| How long does it take to see a response with TZDs? | May require 8-12 weeks for maximal effect |
| Pramlintide--What is the brand name and classification? | Brand: Symlin; New class of agents called amylinomimetics |
| Actions of Pramlintide (Symlin) | 1) Inhibits glucagon secretion normally seen after meals (Glucagon acts to further raise glucose); 2) slows gastric emptying, thereby lowing glucose spike, and 3) increases satiety |
| Adminstration of Symlin | SQ TID before meals; Type I 15-60mcg; Type II: 60-120mcg |
| Frequent side effects of Symlin | Nausea, vomiting, anorexia, headache; more frequent in Type I; helped by titrating up; if nausea at 30mcg, D/C |
| Are Symlin and Byetta approved for Type I and Type II DM? | Symlin: Type I and II; Byetta: Type II Only |
| Drug Interactions of Symlin | Slows absorption of oral drugs taken 1h before or 2h after; Recommended not to take with other agents that slow GI emptying (e.g. anticholinergics) |
| Results of Symlin | Better control of post-prandial glucose, less swing in blood glucose, less insulin required, increase in satiety means less weight gain or weight loss |
| Exenatide--What is the brand name and classification? | Byetta; Classified as an incretinmimetic |
| MOA of Byetta | 1) Inhibits secretion of glucagon following a meal, 2) slows gastric emptying, 3) promotes satiety, 4) Restore first phase insulin spike and increased second phase as well, and 5) promotes growth of beta cells in animals [1-3 are same as Symlin) |
| Results of Byetta | moderate lowering of fasting glucose, marked lowering of post-prandial glucose |
| Co-Administration of Byetta with insulin, orals | Not yet approved for use with insulin; can be added to metformin and SUs (watch for hypoglycemia, may need to lower SU dose) |
| Byetta Dose | 5-10mcg SQ BID, AM and before supper, within 60 minutes of eating |
| Byetta Side Effects | Dose related nausea, vomiting, diarrhea (nausea 44% AT 10mcg dose -- declines with continued use) |
| Blood Pressure Goal | <130/80 mmHg |
| Renal Threshold | 180mg/dL; After this threshold, glucose begins to spill into the urine (glucosuria) |
| LDL Goal | <100 mg/Dl |
| HDL Goal | Men >40; Women >50mg/dL |
| Triglyceride Goal | <150 mg/dL |
| Metabolic Syndrom | AKA Syndrome X; Association between insulin resistance, hypertension, and dyslipidemia |
| Indications for Exubera (Inhaled Insulin) | Type I DM (in conjunction with Basal insulin); Type II DM (can be used alone, with insulin, or with oral agents); Approved for use in Adults only |
| Contraindications for Exubera | Unstable or poorly controlled chonic long disease (bronchitis, asthma, emphysema), smokers, or those who have quit smoking for less than 6 months |
| How do onset and duration of Exubera compare to SQ insulin? | More closely resembles endogenous insulin released after meals; Peaks in 49 minutes (SQ: 105min); Duration: 2-3h (SQ: 5-8h) |
| Dosage and Administration of Exubera | Administer no more than 10 minutes before meal: Usual Starting Dose: 0.05mg/kg, round down to nearest whole number |
| Absorption of Exubera | Absorbed as quickly as rapid acting insulin analogs |
| Drug of Choice during pregnancy | Insulin; Does not cross placenta and has established safety record for mother and fetus; |
| Which oral meds cause hypoglycemia? | Sulfonylureas and meglitinides (meglitinides cause less hypoglycemia due to short half-life) |
| Glucocrticoids and DM | Glucocorticoids tend to increase blood glucose |
| Atypical Antipsychotics (e.g. Risperidone) | Tend to counter effects of insulin and thus decrease glucose uptake by cells |
| Oral Contraceptives and DM | OCs tend to decrease efficacy of oral hypoglycemics |
| Symptoms of Lactic Acidosis | Weakness, malaise, shortness of breath |
| Mechanisms of Insulin Resistance | 1) High glucose concentrations are toxic to pancreatic beta cells --> Decrease B-cell function and insulin production 2) Fat cells are more resistant to insulin |
| Alcohol and Diabetes | Alcohol causes hypoglycemia; high caloric intake (causes hyperglycemia) |
| Effects of Diabetes on Fetus | 2-4x increase for birth defects/malformations; Increased risk for spontaneous abortions; increased risk for still birth; Macrosomia (increased birth weight) |
| Insulin Regimen and Testing Frequency during pregnancy | Test BG 5-7 times daily; intense insulin therapy is best (3-4 injections/day) |
| 1st Trimester Insulin Requirement | Insulin requirement decreased by 10-20% (fetus is rapidly gowthing and utilizing glucose) |
| 2nd Trimester Insulin Requirement | Insulin requirement begins to increase and dose may need to be adjusted every 5-10 days |
| 3rd Trimester Insulin Requirement | Largest insulin requirement; may be twice the dose required before pregnancy; insulin is antagonized by hormones |
| Risk Factors for GDM | Age >25, overweight, non-European, family history of DM or GDM, history of glucose problems, history of diabetes, history of problematic pregnancy, gave birth to child >9 lbs |
| Preconception Measures for Females with DM | Obtain good glycemic control, use contraceptive until glucose is controlled, pre-natal vitamins, screen for ischemic heart disease, screen for retinopathy, neuropathy, nephropathy |
| Use of Oral Hypoglycemics during pregnancy | Should avoid orals, especially metformin and TZDs; glyburide and glipizide may be OK; Insulin is BEST (regular, aspart, lispro, NPH) |
Created by:
dfsaly2