Presentation on theme: "Nursing 3703 Pharmacology By Linda Self"— Presentation transcript:
1 Nursing 3703 Pharmacology By Linda Self Antidiabetic DrugsNursing 3703PharmacologyBy Linda Self
2 Diabetes MellitusChronic systemic disease characterized by metabolic and vascular abnormalitiesDisorder of carbohydrate metabolismResults from inadequate production or underutilization of insulin
3 Diabetes Mellitus Characterized by glucosuria and hyperglycemia Two forms—Type 1 and Type 2Type 1—patient secretes no insulin. Cause is felt to be autoimmune.Type 2- patient secretes insufficient amounts of insulin and insulin receptors are resistant to existent circulating insulinType 1 hereditary. Triggered by viral infection that inflames the beta cells of the pancreas. Exact mechanism is not known.
4 Diabetes MellitusSymptoms: hyperglycemia, glucosuria, polyuria, polydipsia, polyphagia, and possibly itching.Fasting blood glucose is higher than 126Manifested by: weight loss, weakness, increased frequency of infections, poly’s
5 Diabetes MellitusWithout intervention, significant complications will ensue.Include: retinopathies, glaucoma, neuropathies, cardiovascular disease.PVD. Increased incidence of toxemia of pregnancy.
6 Pathophysiology Insulin secreted by beta cells Insulin binds with and activates 80% of cellsLiver, muscle, and fat cells are primary tissues for insulin actionWith insulin receptor binding, cell membranes permeable to glucose into the cells
7 Pathophysiology cont.Increased cell permeability also allows for amino acids, fatty acids and electrolytes to enter cellsChanges cause anabolism and inhibit catabolismAnabolism includes use and storage of glucose, amino acids, and fatty acids.
8 Pathophysiology cont. Carbohydrate metabolism Insulin increases glucose transport into liver, skeletal muscle, adipose tissue, the heart, and even uterus.Must be present for muscle and fat tissues to use glucose for energyInsulin regulates glucose metabolism to produce energy for cellular functionsIf excess glucose is present after need is met, it is converted to glycogen and stored or converted to fat and stored.The excess glucose transported to liver cells is converted to fat only after glycogen stores are saturated. Liver is especially important in restoring blood sugar levels by breaking down glycogen or by forming new glucose.
9 Pathophysiology cont. Fat Metabolism Insulin promotes glucose into fat cells where it is broken downOne of breakdown products is A-glycerophosphate, combines with fatty acids which ultimately forms triglyceridesThis is the mechanism by which insulin promotes fat storageActually, insulin transport of glucose into fat cells results first in alpha-glycerophosphate which combines with fatty acids and produces alpha-glycerophosphate, This then is converted to triglycerides.
10 Fat MetabolismWhen insulin is lacking, fat is released into the bloodstream as free fatty acids.Blood concentrations of triglycerides, cholesterol and phospholipids are also increasedThus the high lipid concentration probably contributes to the accelerated atherogenesis seen in diabetics. Some of the free fatty acids may be converted to ketones, resulting in ketosis.
11 Protein MetabolismInsulin increases the total amount of body protein by increasing transport of amino acids into cells and synthesizing protein within the cellsInsulin potentiates the effects of growth hormoneLack of insulin causes protein breakdown into amino acidsThese amino acids are not replaced by synthesis of new proteins; thus, protein wasting occurs resulting in weakness, weight loss and abnormal functioning of many body organs
12 Endogenous Insulin Glucose is the major stimulus of insulin secretion Oral glucose is more effective than intravenous glucose because glucose in digestive tract increases the release of gastrin, secretin, chlecystokinin, and gastric inhibitory peptideAlso stimulates vagal activity
14 Endogenous Insulin Factors that inhibit insulin secretion include: HypoxiaHypothermiaStimulation of alpha adrenergic 2 receptors
15 Classification of Two Types of Diabetes Type 1 diabetes results from an autoimmune disorder that destroys pancreatic beta cellsUsually has sudden onsetAssociated with high incidence of complicationsRequires exogenous insulin10% of those with diabetes are type I
16 Diabetic Ketoacidosis (DKA) Life-threatening complication occurs with insulin deficiencyGlucose cannot be used by body cells for energy so fat is mobilized for this purposeMobilized fat is then extracted by liver and broken down into glycerol and fatty acidsFatty acids further broken down into ketones
17 DKA Accumulation of ketones results in acidemia Attempts to buffer acidic H+occurs by ionic exchange, intracellular potassium exits cells. H+ ions enter cells. Result is excretion of potassium in urine.Kidneys attempt to buffer by excreting ketonesPulmonary attempt to buffer by Kussmaul breathing
18 Clinical S/S of DKA Kussmaul breathing Nausea and vomiting Thirst Polydipsia, polyphagia and polyuriaHypotensionTachycardiashock
19 Type 2 Diabetes Mellitus Characterized by hyperglycemia and insulin resistanceResults from increased production of glucose by liver and decreased uptake of glucose in liver, muscle and fat cellsInsulin resistance—higher than usual concentrations of insulin are required
20 Type 2 Diabetes Mellitus Occurs at any ageGradual onsetLess severe symptoms initiallyEasier to controlMore MIs and strokes90% of those with diabetes are Type 2multifactorial
21 Hyperosmolar hyperglycemia nonketotic coma (HHNC) Occurs in Type 2 DiabetesBecause patient has some endogenous insulin, no ketosis developsBlood sugars can be >Can result in hypovolemic shock, renal problems, stroke, coma and even death
22 Metabolic Syndrome or Syndrome X Comprised of a set of risk factors which include:Central abdominal adiposity (men waist size greater than 40 inches, women greater than 35 inchesFasting triglycerides greater > or equal to 150 mg/dlHDL cholesterol (less than 40 in men, less than 50 mg/dl in women
23 Metabolic Syndrome cont. 4. Blood pressure greater than or equal to 130/855. Fasting glucose greater than or equal to 110mg/dLAlso possess prothrombotic and proinflammatory tendenciesIn US, 20% of adults (47 million) have metabolic syndrome with prevalence approaching 50% in elderly. Seen more often in those who are overweight. Root cause is poor eating habits and sedentary lifestyle.
24 Metabolic Syndrome cont. All factors are interrelatedObesity and lack of exercise tend to lead to insulin resistanceInsulin resistance has a negative effect on lipid production. Increase VLDL, LDL, TG and decreasing the HDL.Insulin resistance leads to increased insulin and glucose levels in blood.Increased glucose and insulin in blood affect kidneys by holding onto sodium which then increases BP and can lead to hypertension. Also chronically elevated glucose levels damage blood vessels and organs.
25 Hypoglycemic DrugsInsulin lower glucose levels by increasing glucose uptake by cellsIndicated for Type 1 DM, often in Type 2 DM, in those with chronic pancreatitis, in those on TPN, to treat hyperkalemia (infusion with dextrose and insulin)Available insulins are pork and human
26 Age-Related considerations Type 1 DM in childrenConsistent diet, blood glucose monitoring, insulin injections and exerciseBlood sugar control essential to maintain normal growth and developmentInfections and illnesses can cause wide fluctuations
27 Type 1 DM in children cont. Children highly susceptible to dehydrationRotation of sites is very importantAvoiding hypoglycemia is a major goal in infants and young children d/t damaging effects on growth and development
28 Type 1 DM in childrens/s of hypoglycemia include: hunger, sweating, tachcardia, irritability and lethargy.
29 Age related considerations in older adults Close monitoring of blood glucose levelsVisual impairment may affect their ability to self administer medicationMay have renal insufficiency so caution w/certain antidiabetic meds a concernCaution with metformin if renal impairmentGlitazones can predispose to fluid retention and heart failure
30 InsulinHuman insulin is chemically identical to endogenous insulin but it is not derived from the human pancreasCannot be given orallyInsulins differ in onset and duration of action. Ultra-short, short, intermediate and long acting.
31 Rapid acting insulinInsulin lispro (Humalog) or insulin aspart (Novolog) are very shorting acting insulinsMore effective in decreasing post-prandial hyperglycemiaLess likely to cause hypoglycemia before the next mealOnset is 15’, peaks in 1-3 hours, duration is 3-5 hours
32 Insulin cont. Short acting Insulins Regular Iletin II, Humulin R, Novolin RMay be given sub Q or IVMay be given as a continuous IV dripThe only insulin that may be given IVOnset is ½-1 hour, peak is 2-3 hours and duration is 5-7 hours
33 Intermediate-acting Insulins Isophane insulin suspension (NPH, NPH Iletin II, Humulin N, Novolin N)Onset is hours, peaks in 8-12 hours and duration is 18-24
34 Long-acting Insulin Extended insulin zinc suspension Onset is 4-8 hours, peaks in hours and duration is 36+ hours
35 Insulins cont. Insulin Mixtures NPH 70/30 (Humulin or Novolin 70/30) Durations of actions same as individual components
36 Insulins cont. Insulin Analogs Lispro and aspart as previously describedInsulin glargine (Lantus)-once daily at bedtime. Onset is 1.1 hours, peak is none, duration is 24 hoursMust not be diluted or mixed with any other insulin or solutions
37 Oral Hypoglycemic Drugs Five types used to treat Type 2 DMSulfonylureas—oldest. Increase release of insulin. Also decrease production of glucose in the liver, increase the number of insulin receptors and increase peripheral use of glucose. Effective only if have functioning beta cells.Primary side effect is hypoglycemia
38 Sulfonylureas cont. First generation are essentially obsolete Use 2nd generation agentsAre glipizide (Glucotrol), glyburide (Diabeta)and glimepiride (Amaryl)Can be used with metformin, glitazones, insulin or acarbonesCaution w/renal or hepatic impairment. Not used in pregnancy.
39 Alpha glucosidase Inhibitors Acarbose (Precose) and miglitol (Glyset) inhibit alpha-glucosidase enzymes (maltase, amylase, sucrase) in GI tract. Delays absorption of complex CHO and simple sugarsCan be combined therapy w/insulin or w/sulfonylureaContraindicated in cirrhosis, malabsorption, severe renal impairment
40 Alpha-glucosidase Inhibitors Take at beginning of each mealCan cause bloating and diarrhea
41 BiguanidesMetformin (Glucophage) increases the use of glucose by muscle and fat cells, decreases hepatic glucose production, and decreases intestinal absorption of glucoseDoes not cause hypoglycemiaMay be used alone or in combinationContraindicated in liver or renal impairment. Can result in lactic acidosis.
42 Biguanides cont.Must check renal function before beginning this medicationCaution with parenteral radiographic contrast media containing iodine. May cause renal failure and has been associated with lactic acidosis.
43 GlitazonesPioglitazone (Actos) and rosiglitazone (Avandia) are also called thiazolidinediones or TZDsAre insulin sensitizersDecrease insulin resistance. Stimulate receptors on muscle, fat, and liver cells. Results in increased uptake of glucose in periphery and decreased production by the liver.
44 GlitazonesContraindicated in patients with liver disease or who have ALT levels > 2.5 of normalMay be used as monotherapy or in combination with insulin, metformin (Glucophage) or a sulfonylureaCaution in patients with heart failureEnsure baseline LFTs are performed
45 MeglitinidesNateglinide and repaglinide are nonsulfonylureas that lower blood sugar by stimulating pancreatic secretion of insulinMonotherapy or in combination with metforminShould be taken before or up to 30 minutes before a meal. Dosage and frequency is flexible depending on food intake.
46 Herbals and Dietary Supplements that affect blood glucose levels Bee pollen, gingko biloba and glucosamine are thought to increase blood sugars or may potentially affect beta-cell function and insulin secretions (see p. 378)Basil and bay leaf may cause hypoglycemiaChromium may increase production of insulin receptors and increase insulin effectiveness
47 DKA IV fluids to rehydrate No use of hypotonic solutions at this time Potassium supplementationIV insulin drip with gradual lowering of blood sugarsJudicious administration of sodium bicarbonate
49 Diabetic management “pearls” When mixing insulins, draw up the regular insulin firstTid glucose monitoring is highly recommendedAllow mild hyperglycemia for the patient undergoing surgery—treat with short acting insulinsFor elective surgery, schedule patient early in day to avoid prolonged fasting
50 “Pearls” Use U-100 syringes for U-100 vials In patients with insulin pumps, use regular insulin or insulin aspart. Generally will deliver one unit per hour w/bolus insulin before mealsTight glycemic control can reduce the complications of diabetes.Use ACE inhibitors to delay nephropathyLimit dietary intake of protein
51 “Pearls” Glitazones must suspect r/t hepatotoxicity Metformin cautiously with liver and renal impairment. Concern that with hepatotoxicity, because risks of lactic acidosis are increased.Rotate sites of injection of insulin to avoid development of lipodystrophy
52 “Pearls”Absorption of injected insulin in abdomen is not uniform with injections in arms or legs
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