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Antidiabetic Drugs


Antidiabetic Drugs Nursing 3703 Pharmacology By Linda Self Diabetes Mellitus Chronic systemic disease characterized by metabolic and vascular abnormalities Disorder ... – PowerPoint PPT presentation

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Title: Antidiabetic Drugs

Antidiabetic Drugs
  • Nursing 3703
  • Pharmacology
  • By Linda Self

Diabetes Mellitus
  • Chronic systemic disease characterized by
    metabolic and vascular abnormalities
  • Disorder of carbohydrate metabolism
  • Results from inadequate production or
    underutilization of insulin

Diabetes Mellitus
  • Characterized by glucosuria and hyperglycemia
  • Two formsType 1 and Type 2
  • Type 1patient 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 insulin

Diabetes Mellitus
  • Symptoms hyperglycemia, glucosuria, polyuria,
    polydipsia, polyphagia, and possibly itching.
  • Fasting blood glucose is higher than 126
  • Manifested by weight loss, weakness, increased
    frequency of infections, polys

Diabetes Mellitus
  • Without intervention, significant complications
    will ensue.
  • Include retinopathies, glaucoma, neuropathies,
    cardiovascular disease.PVD. Increased incidence
    of toxemia of pregnancy.

  • Insulin secreted by beta cells
  • Insulin binds with and activates 80 of cells
  • Liver, muscle, and fat cells are primary tissues
    for insulin action
  • With insulin receptor binding, cell membranes
    permeable to glucose into the cells

Pathophysiology cont.
  • Increased cell permeability also allows for amino
    acids, fatty acids and electrolytes to enter
  • Changes cause anabolism and inhibit catabolism

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 energy
  • Insulin regulates glucose metabolism to produce
    energy for cellular functions

Pathophysiology cont. Fat Metabolism
  • Insulin promotes glucose into fat cells where it
    is broken down
  • One of breakdown products is A-glycerophosphate,
    combines with fatty acids which ultimately forms
  • This is the mechanism by which insulin promotes
    fat storage

Fat Metabolism
  • When insulin is lacking, fat is released into the
    bloodstream as free fatty acids.
  • Blood concentrations of triglycerides,
    cholesterol and phospholipids are also increased

Protein Metabolism
  • Insulin increases the total amount of body
    protein by increasing transport of amino acids
    into cells and synthesizing protein within the
  • Insulin potentiates the effects of growth hormone
  • Lack of insulin causes protein breakdown into
    amino acids

Endogenous Insulin
  • Glucose is the major stimulus of insulin
  • Oral glucose is more effective than intravenous
    glucose because glucose in digestive tract
    increases the release of gastrin, secretin,
    chlecystokinin, and gastric inhibitory peptide
  • Also stimulates vagal activity

Endogenous Insulin
  • Other hormones that raise blood glucose levels
  • Cortisol
  • Glucagon
  • Growth hormone
  • Epinephrine
  • Estrogen
  • Progesterone

Endogenous Insulin
  • Factors that inhibit insulin secretion include
  • Hypoxia
  • Hypothermia
  • Stimulation of alpha adrenergic 2 receptors

Classification of Two Types of Diabetes
  • Type 1 diabetes results from an autoimmune
    disorder that destroys pancreatic beta cells
  • Usually has sudden onset
  • Associated with high incidence of complications
  • Requires exogenous insulin
  • 10 of those with diabetes are type I

Diabetic Ketoacidosis (DKA)
  • Life-threatening complication occurs with insulin
  • Glucose cannot be used by body cells for energy
    so fat is mobilized for this purpose
  • Mobilized fat is then extracted by liver and
    broken down into glycerol and fatty acids
  • Fatty acids further broken down into ketones

  • Accumulation of ketones results in acidemia
  • Attempts to buffer acidic Hoccurs by ionic
    exchange, intracellular potassium exits cells. H
    ions enter cells. Result is excretion of
    potassium in urine.
  • Kidneys attempt to buffer by excreting ketones
  • Pulmonary attempt to buffer by Kussmaul breathing

Clinical S/S of DKA
  • Kussmaul breathing
  • Nausea and vomiting
  • Thirst
  • Polydipsia, polyphagia and polyuria
  • Hypotension
  • Tachycardia
  • shock

Type 2 Diabetes Mellitus
  • Characterized by hyperglycemia and insulin
  • Results from increased production of glucose by
    liver and decreased uptake of glucose in liver,
    muscle and fat cells
  • Insulin resistancehigher than usual
    concentrations of insulin are required

Type 2 Diabetes Mellitus
  • Occurs at any age
  • Gradual onset
  • Less severe symptoms initially
  • Easier to control
  • More MIs and strokes
  • 90 of those with diabetes are Type 2
  • multifactorial

Hyperosmolar hyperglycemia nonketotic coma (HHNC)
  • Occurs in Type 2 Diabetes
  • Because patient has some endogenous insulin, no
    ketosis develops
  • Blood sugars can be gt800-1000
  • Can result in hypovolemic shock, renal problems,
    stroke, coma and even death

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
  • Fasting triglycerides greater gt or equal to 150
  • HDL cholesterol (less than 40 in men, less than
    50 mg/dl in women

Metabolic Syndrome cont.
  • 4. Blood pressure greater than or equal to 130/85
  • 5. Fasting glucose greater than or equal to
  • Also possess prothrombotic and proinflammatory

Metabolic Syndrome cont.
  • All factors are interrelated
  • Obesity and lack of exercise tend to lead to
    insulin resistance
  • Insulin 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.

Hypoglycemic Drugs
  • Insulin lower glucose levels by increasing
    glucose uptake by cells
  • Indicated 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
  • Available insulins are pork and human

Age-Related considerations
  • Type 1 DM in children
  • Consistent diet, blood glucose monitoring,
    insulin injections and exercise
  • Blood sugar control essential to maintain normal
    growth and development
  • Infections and illnesses can cause wide

Type 1 DM in children cont.
  • Children highly susceptible to dehydration
  • Rotation of sites is very important
  • Avoiding hypoglycemia is a major goal in infants
    and young children d/t damaging effects on growth
    and development

Type 1 DM in children
  • s/s of hypoglycemia include hunger, sweating,
    tachcardia, irritability and lethargy.

Age related considerations in older adults
  • Close monitoring of blood glucose levels
  • Visual impairment may affect their ability to
    self administer medication
  • May have renal insufficiency so caution w/certain
    antidiabetic meds a concern
  • Caution with metformin if renal impairment
  • Glitazones can predispose to fluid retention and
    heart failure

  • Human insulin is chemically identical to
    endogenous insulin but it is not derived from the
    human pancreas
  • Cannot be given orally
  • Insulins differ in onset and duration of action.
    Ultra-short, short, intermediate and long acting.

Rapid acting insulin
  • Insulin lispro (Humalog) or insulin aspart
    (Novolog) are very shorting acting insulins
  • More effective in decreasing post-prandial
  • Less likely to cause hypoglycemia before the next
  • Onset is 15, peaks in 1-3 hours, duration is 3-5

Insulin cont.
  • Short acting Insulins
  • Regular Iletin II, Humulin R, Novolin R
  • May be given sub Q or IV
  • May be given as a continuous IV drip
  • The only insulin that may be given IV
  • Onset is ½-1 hour, peak is 2-3 hours and duration
    is 5-7 hours

Intermediate-acting Insulins
  • Isophane insulin suspension (NPH, NPH Iletin II,
    Humulin N, Novolin N)
  • Onset is 1-1.5 hours, peaks in 8-12 hours and
    duration is 18-24

Long-acting Insulin
  • Extended insulin zinc suspension
  • Onset is 4-8 hours, peaks in 10-30 hours and
    duration is 36 hours

Insulins cont.
  • Insulin Mixtures
  • NPH 70/30 (Humulin or Novolin 70/30)
  • Durations of actions same as individual components

Insulins cont.
  • Insulin Analogs
  • Lispro and aspart as previously described
  • Insulin glargine (Lantus)-once daily at bedtime.
    Onset is 1.1 hours, peak is none, duration is 24
  • Must not be diluted or mixed with any other
    insulin or solutions

Oral Hypoglycemic Drugs
  • Five types used to treat Type 2 DM
  • Sulfonylureasoldest. 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

Sulfonylureas cont.
  • First generation are essentially obsolete
  • Use 2nd generation agents
  • Are glipizide (Glucotrol), glyburide (Diabeta)and
    glimepiride (Amaryl)
  • Can be used with metformin, glitazones, insulin
    or acarbones
  • Caution w/renal or hepatic impairment. Not used
    in pregnancy.

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 sugars
  • Can be combined therapy w/insulin or
  • Contraindicated in cirrhosis, malabsorption,
    severe renal impairment

Alpha-glucosidase Inhibitors
  • Take at beginning of each meal
  • Can cause bloating and diarrhea

  • Metformin (Glucophage) increases the use of
    glucose by muscle and fat cells, decreases
    hepatic glucose production, and decreases
    intestinal absorption of glucose
  • Does not cause hypoglycemia
  • May be used alone or in combination
  • Contraindicated in liver or renal impairment. Can
    result in lactic acidosis.

Biguanides cont.
  • Must check renal function before beginning this
  • Caution with parenteral radiographic contrast
    media containing iodine. May cause renal failure
    and has been associated with lactic acidosis.

  • Pioglitazone (Actos) and rosiglitazone (Avandia)
    are also called thiazolidinediones or TZDs
  • Are insulin sensitizers
  • Decrease insulin resistance. Stimulate receptors
    on muscle, fat, and liver cells. Results in
    increased uptake of glucose in periphery and
    decreased production by the liver.

  • Contraindicated in patients with liver disease or
    who have ALT levels gt 2.5 of normal
  • May be used as monotherapy or in combination with
    insulin, metformin (Glucophage) or a sulfonylurea
  • Caution in patients with heart failure
  • Ensure baseline LFTs are performed

  • Nateglinide and repaglinide are nonsulfonylureas
    that lower blood sugar by stimulating pancreatic
    secretion of insulin
  • Monotherapy or in combination with metformin
  • Should be taken before or up to 30 minutes before
    a meal. Dosage and frequency is flexible
    depending on food intake.

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 hypoglycemia
  • Chromium may increase production of insulin
    receptors and increase insulin effectiveness

  • IV fluids to rehydrate
  • No use of hypotonic solutions at this time
  • Potassium supplementation
  • IV insulin drip with gradual lowering of blood
  • Judicious administration of sodium bicarbonate

  • Treatment similar to that of DKA

Diabetic management pearls
  • When mixing insulins, draw up the regular insulin
  • Tid glucose monitoring is highly recommended
  • Allow mild hyperglycemia for the patient
    undergoing surgerytreat with short acting
  • For elective surgery, schedule patient early in
    day to avoid prolonged fasting

  • 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 meals
  • Tight glycemic control can reduce the
    complications of diabetes.
  • Use ACE inhibitors to delay nephropathy
  • Limit dietary intake of protein

  • 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

  • Absorption of injected insulin in abdomen is not
    uniform with injections in arms or legs