Summary

This document contains questions and answers about insulin regimens. It covers basal and bolus insulin, adverse effects of not having insulin, and the use of insulin in appropriate doses. It also details the purpose of bolus insulin, and which insulins are considered long-acting and short-acting. Further details on insulin injection sites and side effects are also included.

Full Transcript

1. Which insulin regiments can lower HgA1c a. Basal bolus b. Intensive insulin replacement reduced A1C improved long-term outcomes i. Multiple daily injections of insulin ii. Continuous subcutaneous administration via an insulin pump 2. What is an ad...

1. Which insulin regiments can lower HgA1c a. Basal bolus b. Intensive insulin replacement reduced A1C improved long-term outcomes i. Multiple daily injections of insulin ii. Continuous subcutaneous administration via an insulin pump 2. What is an adverse e ect of not having insulin? a. Lack of insulin can result in i. Hyperglycemia ii. Ketoacidosis – acidic, fruity breath, high bs, losing weight, lipids and triglycerides are high. Nausea vomiting abdominal pain iii. Tissue catabolism iv. Hypertriglyceridemia 3. What does the basal dose of insulin do? Basal insulin suppresses hepatic glucose production and when used in appropriate doses should maintain near normoglycemia in the fasting state 4. What is the purpose of bolus insulin in a basal bolus program? Bolus insulin (prandial/premeal) covers the extra requirements after food is absorbed, thereby decreasing postprandial glucose excursions. 5. Which insulin are considered “basal” i.e. long-acting? i. NPH ii. Long-acting insulin analogs (longer duration of action, flatter, more constant plasma levels 1. Insulin glargine 100U and 300U 2. Insulin detemir 3. Insulin degludec 100 U and 200 U iii. Continuous delivery or rapid-acting insulin via a pump 6. Which insulins are considered “bolus,” i.e., short-acting? a. Regular b. Rapid-acting analogs (quicker onset and peak, shorter duration of action, less weight gain and lower A1C and less hypoglycemia) i. Lispro (U-100, U-200) ii. Aspart iii. Faster aspart iv. Glulisine 7. What is the onset of lispro insulin? 15 to 30 min 8. What is the duration of action of insulin glargine? 20 to more than 24 hours 9. What is the general percent of basal and bolus insulin needed in a newly diagnosed type 1 diabetic? 50% basal and 50% prandial 10. What are factors that need to be considered when dosing insulin? Carbohydrate intake and higher doses required during pregnancy, puberty, and medical illness. If a patient gets sick we will have to increase their insulin doses. 11. What is the total daily dose of insulin when starting U/Kg, what is the typical dose once stabilized x-x u/kg? 0.5 U/kg when starting. 0.4-1 U/kg when stabilized. 12. What factors should be considered for bolus (prandial) insulin? a. Controls postprandial glucose b. Well timed i. Pharmacokinetics of formulation 1. Regular, rapid-acting, inhaled 2. Pre-meal glucose level 3. Carbohydrate consumption a. If carb counting is e ective estimates of fat and protein content should be incorporated 4. Anticipated activity (muscle utilization of glucose) – are they laying around or going for a jog. If going out for a jog we might decrease the insulin intake 13. Where should insulin be injected, benefits of rotating sites, and what e ects IM insulin injection absorption? Sites of injection Subcutaneous Abdomen Thigh Buttock Upper arm Rotate sites To Avoid liphohypetrophy IM Absorption is different from SQ Influenced by activity Unpredictable levels So avoid IM if at all possible 14. What are five factors that are associated with Type II diabetes? (i.e. insulin resistance) Insulin resistance Impaired insulin secretion Elevated glucose production by the liver Insulin's ability to decrease glucose production by the liver is decreased Lean patients with Type 2 B-cells function issue Overweight patients (majority of patients with Type 2) Impairment of the target cells (impaired insulin sensitivity in muscle) 15. What lifestyle factors are associated with Type II diabetes? a. Diabetes self-management, education, support, avoidance of clinical inertia, and social determinants of health b. Established/high-risk atherosclerotic CV disease/HF/CKD i. Include agents that reduce cardiorenal risk c. Pharmacologic approaches i. Adequate e icacy ii. Maintain treatment goals d. Weight management 16. MOA of metformin Decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity (increases peripheral glucose uptake and utilization) 17. Metformin severe ADE i. GI NVD, flatulence, dyspepsia, abdominal pain (rapid dose escalation, IR formulation, chronic asymptomatic gastritis) ii. Lactic acidosis (increases with increased serum levels, kidney impairment, hepatic impairment, decreased tissue perfusion, >65 y/o, contrast, excess alcohol, hypoxic states) iii. Vitamin B12 deficiency interferes with absorption of B12 (duration of therapy, higher dosages, inadequate B12 stores, >65 y/o 18. Metformin contraindications? Several drug interactions, severe renal impairment (CrCl 12 years adult dosing b. Acquired hypothyroidism often caused by autoimmune thyroiditis Geriatric i. Increased incidence ii. More prone to ADE 1. Start with a low dose and titrated a. Symptom improvement b. TSH –goal is the higher end of normal Pregnancy c. Untreated i. Miscarriage ii. Preterm delivery iii. Maternal hypertension iv. Preeclampsia v. LBW vi. Still birth vii. Child, impaired intellectual development d. If treated prior to pregnancy, increase the dose by 20-50% to maintain TSH

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