Incretin mimetics (Exenatide) Insulin Type: GLP-1 (Glucagon-Like Peptide 1) analogue Administration: Subcutaneous injection can't be given orally Degraded in GIT, Inactivated by protease Dosage: Twice daily before meals in the liver SC injection or IV in emergency Function: Acts as a postprandial regulator by enhancing insulin indication secretion in response to meals and slowing gastric emptying. DM1 Replace absent insulin secretion Additional Benefits: Associated with weight reduction through DM2 Supplement insufficient the induction of satiety. GDM Side Effects: Nausea, vomiting, diarrhea, and constipation MOA (decrease blood glucose levels) ↑ uptake of glucose ↑ glycogenesis, ↓ gluconeogenesis DPP-4 inhibitors Anabolic effect on proteins and fat (Inhibits breakdown of fats ) Alogliptin, linagliptin, saxagliptin, sitagliptin k Entrance into cells oral Inhibits ketone body (KB) formation Function: Combination Prolong the activity of incrtein hormones ↑insulin release in Rapid-acting insulin (Lispro) injection 15 minutes before each response to meals&↓ glucagon release . act as post-prandial meal with: regulator Intermediate-acting insulin (NPH) two times (one injection Doesn’t affect the patient’s weight at breakfast and another one at bedtime). last resort in diabetic patients OR Long-acting (glargine or detemir) insulin at bedtime Sodium-glucose co-transporter 2 (SGLT2) inhibitors Short-acting insulin (regular) injection 30 minutes before each Canagliflozin and dapagliflozin meal AND intermediate-acting insulin (NPH) at bed time . Oral -Pre-mixed insulin combination (NPH/Regular 70:30) two times inhibit SGLT2 that is responsible for glucose reabsorption in daily at breakfast and supper the kidney tubules SO: Decrease reabsorption of glucose Glucagon: Increase urinary glucose excretion Polypeptide hyperglycaemic hormone Decreases reabsorption of sodium: osmotic diuresis Mobilizes hepatic glycogen into blood as glucose -S/E: Female genital mycotic infections (candidiasis), Stimulate glycogenolysis stimulate glycogen phosphorylase hypotention,UTI breakdown glycogen polymer release of glucose-1-phosphate α-Glucosidase inhibitors: Acarbose and miglitol Oral anti-diabetic medications Oral Inhibit α-Glucosidase: brush border enzyme that facilitates Useful in the treatment of DM2 (Not effective in DM1) absorption of carbohydrates like glucose lower postprandial Insulin is added because of the progressive decline in β (disease or glucose levels aging) Do not cause hypoglycemia when used as monotherapy types: Insulin secretagogues & sensitizers -S/E: flatulence, diarrhea and abdominal pain
1 PART TWO EXTRA NOTE Glucocorticoids actions Adverse effects (Chronic use) Stimulate gluconeogenesis hyperglycemia➡ Blood glucose (hepatic glucose production) and should be monitored in DM patients inhibit glucose uptake and utilization Lipid profile: Increase cholesterol Increase fat deposition in face, and triglycerides shoulder, abdomen and back. Stimulate protein catabolism Muscle weakness and slow growth in children CNS Euphoria. behavioral changes Reduction of WBCs Delay wound healing Infections Stimulate gastric acid and pepsin PU production. CVS: ▪ Na reabsorption and water ▪ Hypertension retention. ▪ Hypokalemia ▪Potassium excretion. ▪H+ excretion ▪ Alkalosis Decrease calcium absorption from severe bone loss Osteoporosis GIT and increase renal excretion Consider Ca+2 and vitamin D
Hyperparathyroidism Primary hyperparathyroidism. primary problem in the parathyroid glands too much PTH (cancer) causes hypercalcemia Secondary hyperparathyroidism: Response to hypocalcemia (kidney disease and vitamin D deficiency). Tertiary hyperparathyroidism Causes hypercalcemia due to excess PTH production on the backdrop of all four glands being overactive.
