Types of Diabetes
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1 Anti-Diabetic Drugs Bassim I Mohammad Specialist Physician-Assistant Professor College of Pharmacy/ Al Qadisiyah University Iraq
2 Diabetes Mellitus (Definition) DM is an elevated blood glucose level associated with absent, or inadequate pancreatic insulin secretion, with or without concurrent impairment insulin action
3 Diabetes Mellitus (Classification) TYPE 1: characterized by beta cell destruction and severe or absolute insulin deficiency (immune form) TYPE 2: characterized by tissue resistance to the action of insulin combined with a relative deficiency in insulin secretion TYPE 3: refers to multiple other specific causes of an elevated blood glucose: pancreatectomy, pancreatitis, drug therapy etc) TYPE 4:Gestational diabetes is defined as any abnormality in glucose levels noted for the first time during pregnancy
4 Diabetes Mellitus (Clinical Features) Polyuria Polydipsia Polyphagia Weight loss
5 Criteria for the Diagnosis of Diabetes A1C 6.5% OR Fasting plasma glucose (FPG) 126 mg/dl (7.0 mmol/l) OR 2-h plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT OR A random plasma glucose 200 mg/dl (11.1 mmol/l) ADA. 2. Classification and Diagnosis. Diabetes Care 2015;38(suppl 1):S9; Table 2.1
6 Categories of Increased Risk for Diabetes (Prediabetes)* FPG mg/dl ( mmol/l): IFG OR 2-h plasma glucose in the 75-g OGTT mg/dl ( mmol/l): IGT OR A1C % *For all three tests, risk is continuous, extending below the lower limit of a range and becoming disproportionately greater at higher ends of the range. ADA. 2. Classification and Diagnosis. Diabetes Care 2015;38(suppl 1):S10; Table 2.3
7 DM (Complications) 1) Acute Complications: Diabetic ketoacidosis Nonketotic hyperosmolar coma 2) Chronic Complications: (micro/macrovascular)
8 Diabetes Mellitus (Treatment Strategies) Type 1: Insulin is a must, education and nutrition control Type 2: education, Food control, exercise, OAD (1) Increase insulin secretion; (2) Increase the sensitivity of target organs to insulin; (3) Decrease glucose absorption (4) Insulin needed serious complications or an emergency Gestational Diabetes (Insulin)
9 Diabetes Mellitus (Treatment) Insulin Oral Anti-Diabetic Agents
10 Insulin Chemistry, Physiology Pharmacological Effect Mechanism of action Clinical Uses Types and Preparations and mixtures Delivery systems Complications
11 Insulin (Chemistry and Physiology) Insulin is a small protein contains 51 amino acids arranged in two chains (A and B) linked by disulfide bridges. Proinsulin in the Golgi apparatus of beta cells, packaged into granules, and hydrolyzed into insulin and C-peptide by removal of four amino acids Insulin and C-peptide (has no physiological action) are secreted in equimolar amounts in response to all insulin secretagogues.
12 Insulin (Chemistry and Physiology) Insulin is released from pancreatic beta cells at a low basal rate and at a much higher stimulated rate in response to a variety of stimuli, especially glucose. Oral glucose elicits more insulin secretion than dose IV glucose; because oral administration of glucose elicits gut hormones which augment the insulin response
13 Insulin release Stimulators/ Inhibitors Stimulators Glucose (most important) β-adrenergic stimulation Amino acid Cholecystokinin Elevated intracellular Ca2+ Drugs (eg sulfonylureas) Inhibitors α-adrenergic stimulation inhibits release (most important) Glucagon Somatostation Leptin Hypoxia Drugs ( eg e diazoxide, colchicine)
14 Insulin (Degradation) The liver and kidney are the two main organs that remove insulin from the circulation Endogenous insulin: 60% liver, 40% kidney Exogenous insulin: 60% kidney,40% liver The half-life of circulating insulin (endogenous) is 3 5 minutes Is not teratogenic
15 Insulin (Pharmacological effects) Carbohydrate metabolism: reducing blood glucose levels by glycogenolysis, glycogen synthesis, gluconeogenesis (ketone badies ) Lipid metabolism: fat synthesis, lipolysis, plasma FFA Protein metabolism: active transport of aa, incorporation of amino acids into protein, protein catabolism HR, myocardial contractility, renal blood flow Potassium: k+ uptake into cells
16 Action of Insulin on Various Tissues Liver Muscle Adipose glucose production Glucose transport glucose transport glycolysis glycolysis lipogenesis& lipoprotein lipase activity TG synthesis glycogen deposition intracellular lipolysis Protein synthesis protein synthesis
17 Insulin (Mechanism of action) Insulin binds to specialized receptors (found on the membranes of most tissues particularly target tissues, ie, liver, muscle, and adipose tissue) with high specificity and affinity. Insulin receptor consists of two subnits. An α subunit, which constitutes the recognition site and β subunits, which contains a tyrosine kinase.
18 Insulin (Mechanism of action) The binding of an insulin molecule to the α subunits activates the receptor and through a conformational change, facilitates mutual phosphorylation of tyrosine residues on the β subunits and tyrosine kinase activity. These process results in multiple effects, including increase in glucose uptake (translocation of GLUT 4), increased glycogen synthase activity and increased glycogen formation; multiple effects on protein synthesis, lipolysis, and lipogenesis..etc
19 Effect of insulin on glucose uptake and metabolism. Insulin binds to its receptor (1) which in turn starts many protein activation cascades (2). These include: translocation of Glut-4 transporter to the plasma membrane and influx of glucose (3), glycogen synthesis (4), glycolysis (5) and fatty acid synthesis (6). 19
20 Insulin (Clinical uses) Insulin-dependent patients with diabetes mellitus (type 1 diabetes mellitus) Insulin-independent patients: failure to other drugs Diabetic complications: diabetic, hyperosmotic nonketotic coma Critical (stress) situations of diabetic patients: fever, severe infection, pregnancy, trauma, operation Others: promotion of K+ uptake into the cells, pshychiatric disorders
21 Insulin (Available Preparations) Commercial insulin preparations differ in a number of ways, recombinant DNA production techniques, amino acid sequence, concentration, solubility, and the time of onset and duration of their biologic action
22 Insulin (4 Injectable Available Preparations) 1. Rapid (Ultra-short) acting (very fast onset and short duration) 2. Short-acting (Regular) (rapid onset of action) 3. Intermediate-acting 4. Long-acting (slow onset of action)
23 Insulin (Available Preparations) Rapid acting and short-acting insulins are dispensed as clear solutions at neutral ph and contain small amounts of zinc to improve their stability and shelf life Intermediate-acting NPH insulin have been modified to provide prolonged action and are dispensed as a turbid suspension at neutral ph with protamine in phosphate buffer (neutral protamine Hagedorn [NPH] insulin) Insulin glargine and insulin detemir are clear, soluble long-acting insulins
24 Rapid-acting Insulin Three rapid-acting Insulin analogs Are Commercially Available (Insulin lispro, Insulin aspart, Insulin glulisine) Permit more physiologic prandial insulin replacement because their rapid onset and early peak action more Their duration of action is 4 5 hours, which decreases the risk of late postmeal hypoglycemia Have the lowest variability of absorption (approximately 5%) of all available commercial insulins
25 Short-acting (Regular) Insulin Its effect appears within 30 minutes, peaks between 2-3 hours after subcutaneous injection, and generally lasts 5 8 hours The hexameric nature of regular insulin causes a delayed onset and prolongs the time to peak action After S/C injection, the insulin hexamersare too large and bulky to be transported across the vascular endothelium into the bloodstream. As the hexamers break down into dimers and finally monomers. This results in three rates of absorption of the injected insulin, with the final monomeric phase having the fastest uptake out of the injection
26 Short-acting (Regular) Insulin Clinically, when regular insulin is administered at mealtime, the blood glucose rises faster than the insulin with resultant early postprandial hyperglycemia and an increased risk of late postprandial hypoglycemia. Therefore, regular insulin should be injected or more minutes before the meal to minimize the mismatching
27 Short-acting (Regular) Insulin The delayed absorption, dose-dependent duration of action, and variability of absorption ( 25%) of regular human insulin frequently results in a mismatching of insulin availability with need, and its use is declining It is particularly useful for IV therapy in the management of DKA and when the insulin requirement is changing rapidly, such as after surgery or during acute infections. Limitations of regular insulin, namely, highly dose dependent PKs and PDs profiles, and variability in absorption
28 Intermediate-acting NPH (neutral protamine Hagedorn, or isophane) Insulin NPH insulin is an intermediate-acting insulin is a suspension of crystalline zinc insulin combined with protamine (a polypeptide). The conjugation with protamine delays its onset of action and prolongs it effectiveness. Has an onset of approximately 2 5 hours and duration of 4 12 hours and is usually mixed with regular, lispro, aspart, or glulisine insulin The action of NPH is highly unpredictable, and its variability of absorption is over 50%
29 Long-acting Insulin (Glargine) Insulin glargine is a soluble, peakless (ie, having a broad plasma concentration plateau), long-acting insulin analog Achieves a maximum effect after 4 6 hours. This maximum activity is maintained for hours or longer. Glargine is usually given once daily Should not be mixed with other insulins (separate syringes must be used)
30 Profile of Insulin Glargine vs NPH NPH Glargine 30
31 Long-acting Insulin (Insulin detemir) This insulin is the most recently developed long-acting insulin analog Has the most reproducible effect of the intermediate- and long-acting insulins, and its use is associated with less hypoglycemia than NPH insulin Has a dose-dependent onset of action of 1 2 hours and duration of action of more than 12 hours. It is given twice daily to obtain a smooth background insulin level.
32 Mixtures (combinations) Of Insulins Because NPH insulins require several hours to reach adequate therapeutic levels, their use in diabetic patients usually requires supplements of rapid- or short-acting insulin before meals. These are often mixed together in the same syringe before injection. Insulin lispro, aspart, and glulisine can be acutely mixed (ie, just before injection) with NPH insulin without affecting their rapid absorption. Premixed formulations of 70%/30% NPH/regular continue to be available. These preparations have all the limitations of regular insulin, namely, highly dose dependent PKs and PDs profiles, and variability in absorption
33 Insulin Delivery Systems Standard Delivery (conventional disposable syringes) Portable Pen Injectors Continuous Subcutaneous Insulin Infusion Devices ( Insulin Pumps) Inhaled Insulin (dry powder formulation) used in adult, peak level reached 15 minutes and last for 3 hours (faster onset and shorter duratio than SC )
34 Insulin Delivery Systems
35 Complications of Insulin Therapy 1) Hypoglycemia: is the most common complication of insulin therapy. They usually result from (Overdose of insulin, Excessive (unusual) physical exercise, meal is missed) Mild Hypoglycemia and conscious patient treated by dextrose tab, glucose gel or any sugar containing food or beverages Severe hypoglycemia and disoriented or unconscious patient best treated by IV ml of 50% glucose over 2-3 minutes. Alternatively SC or IM 1mg of glucagon. If patient still stuporus or glucagon not available, small amount of honey or syrup can be inserted into buccal pouch.
36 Complications of Insulin Therapy 2) Immunopathology of Insulin Therapy: Local or systemic allergic reactions Immune insulin resistance, A low titer of circulating IgG anti-insulin antibodies that neutralize the action of insulin to a negligible extent develops in most insulin-treated patients. 3) Lipodystrophy at Injection Sites (with new prparation, atrophy less, hypertrophy more) 4) Weight gain
37 Promising
38 Thank You
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