DIABETES OVERVIEW AND UPDATE 11_11_11 Barb Bancroft_ RN

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DIABETES OVERVIEW AND UPDATE 11_11_11 Barb Bancroft_ RN Powered By Docstoc
					DIABETES OVERVIEW AND
       UPDATE

  Barb Bancroft, RN, MSN, PNP
           Chicago IL
Definitions—new names, new drugs, new lab tests,
 new numbers, and a never-ending supply of new
                 patients

•   (1659) Diabetes—”to siphon”
•   Mellitus—”sweet”
•   Insipidus—”tasteless”
•   Nurse…

• “Taste thy patient’s urine, for if it be sweet…”
   ---Dr. Thomas Willis
    What’s in a name? The evolution…
•   “Sugar diabetes”
•   Juvenile Onset Diabetes Mellitus (JODM)
•   Adult Onset Diabetes Mellitus (AODM)
•   Insulin Dependent Diabetes Mellitus (IDDM)
•   Non-insulin Dependent Diabetes Mellitus (NIDDM)
•   Type I (Roman numeral used)
•   Type II (Roman numeral used)
•   Type 1 (Arabic number)
•   Type 2 (Arabic number)
      And, it’s not thaaaaaat easy
         either…other types…
• Type 1A (autoimmune)
• Type 1B (idiopathic)
• LADA (latent autoimmune diabetes in adults)
  —also referred to as Type 1.5
• MODY (maturity onset diabetes of the
  young)
               Definition
• Chronic disorder of carbohydrate, fat
  and protein metabolism characterized
  in its fully expressed clinical form by an
  absolute deficiency of insulin (Type 1
  diabetes) or a relative insulin
  deficiency (Type 2 diabetes).
• Huh?
                Definition
• Type 1—pancreatic beta cell failure due to
  autoimmune disease (NO or minimal insulin)
  (actually type 1A—most common)
• Type 2—insulin resistance AND pancreatic
  beta cell dysfunction (50% normal insulin
  secretion with dx; after 6 years w/ disease,
  drops to 25%; eventually zero…)
• PLUS…diabetes is a prothrombotic,
  proinflammatory, a proatherosclerotic and a
  proaccelerated proaging disease! So be PRO-
  active in DX and RX!
      RISK FACTORS for DIABETES
•   Who’s sitting in YOUR waiting room?
•   Primary care?
•   OB?
•   Geriatrics?
•   Pediatrics?
•   Who’s laying in that bed in the coronary care
    unit? Stroke unit?
    First question--family history?
• A family history of diabetes—for both type 1
  and type 2
• Type 2—almost all cases have a parent or
  grandparent; identical twin concordance rate
  is 80%
• Type 1—50-90% don’t have a family history;
  identical twin concordance rate is 35-50%;
  5% chance (one in twenty) if sibling has
  T1DM;
 Type 1 diabetes--How many genes?
• In the past five years researchers have found
  dozens of genes with links to diabetes
• Approximately 50 genes for type 1—about
  half are genes that coordinate the HLA
  system that helps the body recognize self vs.
  non-self; explains why other autoimmune
  diseases are associated w/ T1DM
• Celiac disease and Hashimoto’s thyroiditis
 Type 1 diabetes—how many genes?
• Other genes that have been found mediate
  the immune response to viruses (explains the
  viral hypothesis as a possible trigger)
  Type 2 diabetes--how many genes?
• Approximately 38 genes for type 2
• Believed that the known genetic links to type 2
  diabetes probably account for only 6 percent of the
  genetic predisposition
• What does that mean? Either some of the genes
  discovered have a bigger effect than is currently
  believed or that 94% of the genes are still missing
• Genes discovered affect the secretion of insulin
  from the beta cells
    Other risk factors for type 2 diabetes
                  mellitus?
•   Family history of early coronary heart disease
•   Undesirable lipid levels
•   Ethnic groups
•   Hypertension
•   Weight gain
•   Impaired glucose tolerance—metabolic
    syndrome, PCOS, gestational diabetes
    Family history of early coronary
             artery disease
• What’s early?
• 1st degree relative
       Undesirable lipid levels
• HDL less than 40 mg/dl (1.04 mmol/L) in
  men; less than 50 mg/dl (1.3 mmol) in
  women
• Triglycerides greater than 150 mg/dl (1.70
  mmol/L)(New AHA guidelines say 100 mg/dL)
• Think diabetes or hypothyroidism with the
  above lipid profile
• Draw a FBS or HbA1C and a TSH
           Reducing triglycerides
• Fish oil capsules (omega 3s) can also reduce the TG (1
  gm/day lowers TG by 5-10%; statins
  (rosuvastatin/Crestor, specifically) by 30%; diet changes
  by 20%--increased fiber, decreased trans fats, reduce
  added sugars, limiting alcohol)
• EPA (ecosapentanoic acid)
• DHA—docosahexanoic acid)
• 1000 mg/1 gram per day for established CAD
• Higher doses for high TG (platelet problems with higher
  doses)
• READ THE LABEL
• Lovaza (prescription fish oil)
Hypertension—which comes first?
• Greater than 140/90 (persistent 135/80 warrants
  testing for DM) increases the risk of diabetes
• 50-60% have both DM and HTN at diagnosis— “the
  deadly duo”
• In a diabetic patient, a systolic pressure of 130-139
  mmHg with a diastolic pressure of 85-89 mmHg,
  although classified as “high normal”, warrants
  PROMPT treatment
• However, lowering the BP to less than 120/70
  doesn’t appear to improve outcomes
          High risk ethnic groups
• Indian (from India)(#1)
• Asian (#2)
• Hispanic
• Pacific Islanders
• Native American Indians
• Dark skinned individuals have a higher risk of Type 2
  diabetes
• Could it have something to do with vitamin D?
• Beta cells also have vitamin D receptors on their surface,
  and people with vitamin D deficiency are at increased risk
  for type 2
       Age and type 2 diabetes
• 50% of all type 2 diabetics are over 60;
• 18% are 65-75;
• 40% of people over 80 have diabetes
    Type 2 diabetes risk factors
• Weight gain
• 85% are overweight or obese
• (however, 2/3 of all overweight people and
  1/3 of obese patients will never develop
  diabetes)
   What did you weigh as a kid?
The odds that a person who is a normal weight
  at age 18 will develop diabetes later in life
  are 1-in-5 or 1-in-6. However, if you’re very
  obese at age 18, you have a 3-in-4 chance of
  developing diabetes.
50% of all newly diagnosed children with
  diabetes are type 2
WHY?
 Let’s dispel a few “old” myths…#1
• Is a calorie just a calorie just a calorie?
• OLD ANSWER? YES, of course…cut calories?
  Lose weight…
• NEW ANSWER? Not exactly…potatoes have
  been found to pack on the pounds more than
  the same amount of calories in walnuts…
• What kind of potatoes? FRENCH FRIES…then
  chips, soda, red meat, mashed potatoes
• (N Engl J Med June 23, 2011)
     Location, location, location
• Abdominal (visceral)--obesity and insulin
  resistance (fat in the liver and muscle is
  insulin resistant)
• It’s a new organ…it’s metabolically active
• It produces inflammatory mediators such as
  TNF-α, IL-6, C-reactive protein, and
  adiponectin
• Waist greater than 102 cm (40 inches) in
  males and 88 cm (35 inches) in females
• Actually your waist should be ½ your height
          Metabolic syndrome
• DEFINITION: A clustering of risk factors that, in
  the aggregate, sharply increase the risk of
  cardiovascular disease and diabetes
• By the time a diagnosis of diabetes is made, 70-
  90% of patients have metabolic syndrome,
  irrespective of ethnicity or the definition used
• Female to male ratio -- (2:1)
• Weight or body mass index is a major risk
  factor; 5% of normal weight; 22% overweight,
  and 60% of obese individuals have the
  metabolic syndrome
   NCEP--ATP III guidelines for metabolic
                 syndrome
• Central obesity—waist size greater than 40.2 inches in
  men, 34.6 inches in women
• High TG (>150 mg/dL/1.7 mmol/L or greater) or being
  treated for high triglycerides
• Low HDL (less than 40 mg/dL/1.03 mmol/L in men, less
  than 50 mg/dL / 1.30 mmol/L in women)—or being
  treated for low HDL
• Hypertension (≥ 130/85 mm Hg) or being treated for
  HTN
• Fasting glucose ≥ 100 mg/dL/ 5.5 mmol/L or being
  treated for diabetes
• WHO guidelines add microalbuminuria (urinary albumin
  to creatinine ratio 30-300 mg/g.
   Where do you measure waist
              size?
• Official guidelines—locate the top of the
  right iliac crest; Got it? Intersect that point
  with a line dropped vertically from the
  middle of the right armpit is where you place
  the paper tape measure (cloth tape measures
  are too easy to stretch, J)
Other risk factors for Type 2 diabetes
       —Gestational Diabetes
• Gestational diabetes—5-9% of pregnant women in
  U.S.; rates have increased 122% between 1989 and
  2004
• Risk factors—obesity, advanced maternal age (over
  40? 6x greater risk) FH of DM, history of GDM or
  abnormal glucose metabolism,, ethnicity—Indian
  and Pakistani women have a 4x greater risk;
  Middle Eastern and African American women have
  a 2x greater risk; Lower income—higher risk
     Impaired glucose tolerance
• Baby weighing greater than 9 lbs. or a
• Small for Gestational Age (SGA) babies

• Were YOU, as a baby, exposed to
  intrauterine hyperglycemia ?
Polycystic Ovary Syndrome (PCOS)
• First article published in 1922 by 2 French MDs
  entitled: “The Diabetes of Bearded Ladies…”
• Metabolic syndrome is 2-3 x higher in women with
  PCOS
• Type 2 diabetes is 10x higher in women with PCOS
• Liver and muscle tissues are insulin resistant; ovary is
  NOT; hyperinsulinemia triggers androgen production
  with hirsutism and decreased ovulation
• Metformin (Glucophage) increases insulin sensitivity,
  decreases hyperinsulinemia, decreases androgens,
  and improves ovulation
     Abnormal beta cell function—
      increased risk of type 2 DM
• “Oh, I’m so hypoglycemic…”
• ONLY if it’s a documented history of
  hypoglycemia
• Documented with an oral glucose tolerance
  test
• Beta cells are not functioning normally after
  a glucose load, hence beta cell dysfunction
• ~30- 70% risk of developing type 2 DM
     Duodenal exclusion surgery?
• Is the cure for diabetes just a scalpel away? Not so
  fast…Many diabetic patients that have had gastric
  by-pass surgery that bypasses the duodenum and
  the upper small intestine have observed that their
  diabetes disappeared within weeks of the
  procedure—before any substantial weight loss.
  Postprandial hyperglycemia and the return of
  diabetes…
• Gut bacteria and obesity—firmacutes vs.
  bacteriodetes
        What does exercise do?
• Exercise has a role in fat placement
• Exercise reduces insulin resistance; one way it may
  do this is to burn fat out of the muscle
• Because of this, getting enough exercise may stave
  off type 2 diabetes in some cases
   Back to type 2 diabetes--the perfect
              storm…Type 2
• Family history– genes that control the
  amount of insulin produced by the beta cells
  —whether or not the insulin produced can
  overcome the insulin resistance
• Abdominal obesity
• Lifestyle (Lack of physical activity and
  sedentary lifestyle)
What is the best way to reduce belly fat?
              WALKING…
• Ladies…the bad news…
• exercise not only reduces insulin resistance
  it also jump starts weight loss…
           Secondary diabetes
• Exocrine pancreatic disease—cystic fibrosis
• Cushing’s disease or syndrome
• Drugs—corticosteroids, L-dopa, sympathomimetics,
  niacin, glucosamine, thiazide diuretics
• Atypical anti-psychotics--Weight gain= Clozapine
  (Clozaril)(biggest offender) and #2 is Olanzapine
  (Zyprexa); 10 weeks/10 pounds
• Risperidone w/ intermediate weight gain,
  ziprasidone (Geodon) and aripiprazole (Abilify) with
  least weight gain
 Do the statin drugs increase the risk
         of type 2 diabetes?
• Latest findings…yes, BUT the statins’ proven
  power to prevent heart attacks and strokes
  outweighs ANY potential increase in type 2
  diabetes risk
• Study of postmenopausal women—6.4% not
  taking statins developed type 2 DM vs. 9.9%
  among statin users (over an 8 year period)
• Manson J. Harvard Medical School, 1/10/12
            Type 1A diabetes
• Type 1A DM—primarily diagnosed in pre-
  teens or teenagers; onset prior to age 40 in
  the majority of patients;
• Caucasians greater than darker skinned
  individuals
• Finland #1 country in world with Type 1 DM
               Type 1A Diabetes
• Associated with immune response genes and HLA-DR3 and
  HLA-DR4 (99%; 53% with both; only 3% of people without
  T1A DM have both; also DQB1 (genetic background of
  Northern Europeans—Sardinia, Finland)
• Autoimmune attack against beta cells of pancreas (anti-
  glutamic acid decarboxylase antibodies—anti-GAD; ICA {islet
  cell antibodies}; IAA {Insulin autoantibodies})—months to
  years
• Present with 3 p’s—polyuria, polydipsia, polyphagia, and
  weight loss
• Classic presentation is in a Caucasian, blue-eyed, blonde-
  haired kid named…
         Autoimmune disease
• What triggers the autoimmune response in a
  genetically susceptible individual?
• The most likely culprit is one of the childhood
  viruses…cross reaction? Molecular mimicry?
• Coxsackie B? Measles? Influenza A or B?
• Or?
    Triggers of Type 1 diabetes…
• Type 1 diabetes has increased by 5% per year
  since the 1980s
• In addition to viruses…
• 3 other suspects..
                     Too little sun
•   Sunphobia
•   Sunscreen maniac moms
•   SLAP A DERMATOLOGIEST TODAY!!
•   Kids playing inside (the “thumb tribe”)
•   Pushes the immune system in the wrong direction—
•   Abnormal regulatory T cells?
•   2 pathways—TH1 and TH2
•   Taking the TH2 pathway increases the risk of allergies and
    autoimmune disease?
             Too little dirt
• The hygiene hypothesis— GUT bacteria and
  priming the immune system
• Germphobic (mysophobic) *moms
• LET THEM EAT DIRT!
• (*irrational fear of DIRT)
         Too much cow’s milk…
• Decreased risk in babies who are breast fed
• Increased risk in drinking cow’s milk—is there a
  protein that aggravates the immune system and
  triggers diabetes in genetically susceptible
  individuals?
• Large scale clinical trial called TRIGR, testing this
  hypothesis and is scheduled for completion in 2017
 Other autoimmune diseases associated
         with Type 1 diabetes

• Celiac disease—(12.3% of T1DM kids in Denmark
  have celiac disease; 6.4% in US have both—growth
  problems, iron deficiency anemia)—younger the
  age at DX for DM the greater the risk (Diabetes Care
  2006; 29:2452-2456)—share HLA-DQB1 with Type 1
  DM
        Autoimmune disease
• Thyroid disease (Hashimoto’s thyroiditis)
  —4.8% with T1DM and HT); clinical
  presentation; check their TSH
• Pernicious anemia– 2.6%—antibodies to
  intrinsic factor resulting in a B12
  deficiency
   Digression on B12 deficiency…
• B12 deficiency can cause peripheral
  neuropathy which may be falsely attributed to
  the neuropathy of diabetes (check B12 levels
  and check MCV as B12 deficiency can also
  result in a macrocytic anemia)

• Metformin can contribute to B12 deficiency
• PPIs can cause a B12 deficiency
            Laboratory diagnosis
• Hemoglobin A1C—gold standard for measuring long-term
  glycemic control—how does it work? RBC life span
• Glucose binds irreversibly with hemoglobin over the lifespan
  of the RBC
• 50% of glycosylated hemoglobin is from previous month;
  25% from the month before; 25% 3-4 months ago
• Normal range is 4-6%
• *TIGHT control in the Type 2 diabetic does NOT always lead
  to the best outcomes (ADVANCE and ACCORD studies—
  HbA1c’s of 7 are more feasible and provide better outcomes
                Pre-diabetes
• ...one step away. HUH?
• Asymptomatic fasting blood sugars between
  (5.5/100mg/dl)/6.1 (110) to 7.0 mmol
• Used to be called impaired glucose tolerance
• May have metabolic syndrome
 The Geriatric Patient and blood glucose
                 control
• Blood sugars? (may want to keep the HbA1C
  in the 7-8 range)—hypoglycemia can break a
  hip
• Blood pressure? Hypotension can break a hip
• Consider co-morbidities before aggressively
  treating
• Polypharmacy
• Life expectancy?
           Life expectancy?
• Consider co-morbidities before aggressively
  treating—8 years needed benefit of glycemic
  control in reducing microvascular
  complications
• 2-3 years for benefit from BP and lipid
  control for reducing macrovascular
  complications
           What about kids?
• More liberal numbers for kids and
  developing brains who are more vulnerable
  to the effects of hypoglycemia and who may
  not be able to effectively recognize or speak
  about the symptoms of hypoglycemia
        INSULIN and GLUCAGON
• Insulin is a growth hormone—stores fat and sugar and
  stimulates protein synthesis after the meal
• Produced by the beta cells of the pancreas
• Too much insulin? WEIGHT GAIN
• Glucagon is a catabolic hormone produced during the fasting
  state; breaks down stored glycogen
• Produced by the alpha cells of the pancreas
• Too much? WEIGHT LOSS
Right after a meal (The postprandial state)

• The pancreatic beta cells produce insulin
• Insulin triggers glucose to enter cells and to be
  stored as glycogen in the liver and muscle
  (glycogenesis)
• Lipogenesis—insulin transports lipids into
  adipocytes
• Protein synthesis—transports amino acids
  into muscle
• GROWTH
        Postprandial state

• The meal
           CHO, lipids,
           proteins

                          pancreas



                                        Muscle, fat, liver cell insulin
                                        receptors
    Blood vessel            Insulin*    Stores sugar as glycogen
                            Incretins   Stores lipids in fat tissue
                            Amylin*     Stores protein and glucose
                            GLP-1—      in muscle tissue
                            GI tract    Receptor sensitivity/exercise
       During the fasting state
• Between meals and overnight primarily
• The pancreatic alpha cells produce glucagon
• Glucagon triggers glycogenolysis (breaks
  down stored glucose in the liver) to maintain
  a steady state of blood glucose
• Lipolysis—breaks down fat tissue and forms
  free fatty acids
• Gluconeogenesis—turns proteins into sugar
Ketoacidosis (DKA) in Type 1 diabetes
• Type 1 ketoacidosis is a prolonged fasting state
  with an absolute deficiency of insulin;
• Glucagon is working overtime—glycogenolysis;
  lipolysis; and gluconeogenesis
• All contribute to hyperglycemia and osmotic
  diuresis
• fatty acid release (ketones in the urine—osmotic
  diuresis)--ketoacidosis
• A young girl presenting with alternating
  hypoglycemia and DKA – consider an eating
  disorder
    A quick primer on Diabetic Ketoacidosis
                    (DKA)
•   Dehydration (usually 7-10%)
•   Abdominal pain
•   Anorexia, weight loss
•   Kussmaul’s respirations (acidosis)(hyperventilation
    with slow, deep sighing breathing)
•   Tachycardia
•   Weakness, fatigue
•   Fruity breath odor
•   hypotension
•   N or V
•   Confusion, decreased reflexes, coma
   A quick primer on Ketoacidosis
• Dehydration is your biggest concern initially (10-20 mL/kg
  for 1-2 hours)
• GIVE FLUIDS…what kind? NS or RL)
• Then what? Regular insulin IV (0.1 U kg/hr)
• Then what? Check electrolytes and pH
• ICU
• Should bicarb be given?
   Pathophysiology of Type 2 DM
• Early in the disease—as the body becomes resistant
  to insulin, the beta cells in the pancreas must pump
  out more hormone to compensate; people with
  beta cells that can’t keep up with insulin resistance
  can’t move the glucose into the muscle, fat and
  liver cells
• Insulin resistance is characterized by a rise in
  postprandial blood sugars
• Hyperinsulinemia results.
• What are the consequences of hyperinsulinemia?
    Hyperinsulinemia results in…
• Increased triglycerides and decreased HDLs
• Triggers release of angiotensin 2 → aldosterone
• Vasoconstriction and sodium and water retention—
  hypertension
• Stimulate fat storage (CHO to fats)
• Prothrombotic (increased AT2)
• Proinflammatory (increased AT2)
• Triggers endothelial cell dysfunction-fancy way of
  saying, deposits LDL cholesterol and triglycerides
  into the arterial walls
• YIKES!!
              Type 2 diabetes
• Metabolic derangements aren’t usually as severe as
  Type 1
• Few symptoms initially, 2 P’s (no polyphagia),
  weight gain due to hyperinsulinemia
• Other symptoms—fatigue, diplopia, nocturia
  (nocturnal diarrhea)
• Skin infections, vaginal yeast infections, poor
  wound healing (BS >180 mg/dL or 9 mmol/l),
  neuropathy
• “Silent” for a full decade in some individuals
    Oral Drugs—the #1 oral drug
• Metformin (glucophage) does not have any direct
  effect on insulin release from the pancreas—doesn’t
  require insulin to work
• Primary action: DECREASE hepatic glucose
  production; also, decreases glucose absorption via
  the GI tract, and may increase sensitivity of insulin
  receptors
• Problem? GI blues (nighttime dosing/give with food),
  need functioning organs--kidneys and heart
  especially (check serum creatinine before starting
  metformin)
• Se Creatinine--Cut-off is 1.4 (50-90 mmol/L) in
  females and 1.5 (70-120 mmol/L) in males;
      Metformin (Glucophage)
• Other benefits: lowers BP, increases HDL,
  lowers LDL; has been shown to be safe during
  PG (? Use for gestational diabetes?)(N Engl J
  Med May 8, 2008)
• B12 deficiency
• Metformin and gestational diabetes
• Metformin and breast cancer reduction
  (54%)—Diabetes Care December 2010
• Metformin and slowing the aging process
       Oral drugs for type 2 DM…
• 2nd tier: The “Glitazone” sister— pioglitazone (Actos)
  (troglitazone/Rezulin and rosiglitazone/Avandia are
  history)—black box warning for bladder cancer with
  Actos
• Improve muscle receptor sensitivity to insulin with
  secondary effects in the liver
• May slow down the progression of the disease
• Problem? Volume expansion, heart failure,
  dilutional anemia, weight gain (peripheral, not
  central)
• Good news? Reduce triglycerides; reduce fatty liver
  OLD Drugs…are these even worth using anymore?
    Considered third-line therapy…cheap drugs

• Oral sulfonylureas—Glipizide (Glucotrol) and
  glyburide (Diabeta, Micronase, Glynase) (used for
  gestational diabetes)and glimipiride (Amaryl)…
• Increase the secretion of insulin from the pancreas
  and increase receptor sensitivity
• Problem? Weight gain, hypoglycemia, increased
  cardiovascular risk
• glimipiride (Amaryl)—safe use in elderly--decreased
  incidence of hypoglycemia
• Increased risk of cardiovascular events (highest doses
  increased risk vs. metformin; may prevent heart from
  recovering from brief periods of ischemia) (Canadian Medical
  Association Journal January 2006)
      Oral drugs before a meal
• Repaglinide (Prandin)*
• Nateglinide (Starlix)
• Good for elderly to prevent postprandial
  excursions
• Great if your meals are sporadic
• Prandin* (better than Starlix)
               The “gliptins”
• Weight neutral
• Sitagliptan (Januvia) inhibits enzymes in the
  intestine responsible for breaking down
  incretins; incretins potentiate insulin release
• Saxagliptin (Onglyza)
• Newest: linagliptin (Tradjenta)
• Januvia + simvastatin in one pill
       Better…drug combinations
•   Actosplus Met (metformin/pioglitazone)
•   Metaglip (glipizide and metformin)
•   Glucovance (glyburide and metformin)
•   Duetact (pioglitazone HCl and glimepiride)
•   Janumet (sitagliptan and metformin)
•   Kombiglyze (onglyza + metformin)
  Incretin mimetics (April 28, 2005)—
• Exenatide (Byetta)—isolated from saliva of a Gila Monster
• (incretins are responsible for approx. 60% of the post-meal
  insulin secretion, but the action of the incretins is impaired
  in diabetics)
• Type 2 diabetics who are already receiving metformin, a
  sulfonylurea, or both and do not have optimal control
• Acts at the GLP-1 receptor, promoting insulin release
• Weight loss is a + side effect (due to slowing of gastric
  emptying and “feeling full”)
• 2nd generation—liraglutide (Victoza)
                    Insulin
• The discovery of insulin…
• Frederick Banting and his assistant, Charles Best
  experimented on diabetic dogs over the
  summer of 1921, and finally, dog number 92, a
  collie, hopped off the table after an injection
  and wagged her tail—this was the breakthrough
• In the spring of 1922, Elizabeth Hughes,
  daughter of Justice Charles Evans Hughes
  traveled to Toronto to receive insulin; she was
  52 pounds when she arrived
• By the time she died in 1981, at age 74, she
  had received 42,000 insulin shots
 Eli J. Lilly and Company (Indianapolis)
• Won the right to mass produce insulin
• First partnership negotiated among academia,
  individual physicians and the pharmaceutical
  industry
• Chicago played a major role—slaughterhouses
  began sending trainloads of frozen porcine (pig)
  and bovine (cow) pancreas to Lilly’s plant in Indy.
• By 1932 insulin’s price had fallen by 90 percent
                      Insulin
• The pancreas will eventually give out and the oral
  agents will no longer work; over the course of 15
  years, the proportion of patients using oral agents
  alone declines from 65% to 25%, with a
  corresponding increase in those using insulin
• BUT new studies show that insulin should be
  started EARLIER in Type 2 DM…better glucose
  control than w/ oral meds
                        Insulins
• Old “down –on-the-farm” insulins
• Anything with the last name “ine”—bovine, porcine
• Rapid-acting insulins include aspart (Novolog), glulisine
  (Apidra), lyspro (Humalog),
• Regular insulin—Novolin R and Humulin -R
• Intermediate acting insulin—neutral protamine Hagedorn
  (NPH)—Humulin N, Novolin N
• Long-acting insulins include detemir (Levemir), glargine
  (Lantus)
      NPH continues to have some
              usefulness
• Used to provide basal insulin and because it has a
  peak action, they may cover the midday meal;
  onset 4-6 hours, peak at 8-14, duration of 16-20
  hours
• Human NPH with shorter onset (2-4 hours), peak in
  4-10, and duration is 10-16
• SOMOGYI effect at 2-3 a.m.—nocturnal
  hypoglycemia with rebound SNS response and
  subsequent hyperglycemia
• DAWN phenomenon—early morning rise in BS
• Still used but if possible switch to…
                  Switch to…
• LANTUS (insulin glargine) or LEVEMIR (insulin
  detemir)—long-acting basal insulins; they don’t
  have a peak; provide constant levels over 24 hours;
  controls blood sugar as well as NPH given once or
  twice daily with less nocturnal hypoglycemia and
  weight gain
• How do you switch from NPH to Lantus? Easy
• Can you mix other types of insulin with Lantus? NO
• Does Lantus “look” funny? YES, compared to NPH,
  it’s clear
• Lantus and Levemir stabilize endothelial
  cells…HUH? Reduce atherosclerosis risk
 Complications of type 2 diabetes
• Accelerated atherosclerosis--four out of five
  diabetics die from complications of cardiovascular
  disease and atherosclerosis
• Coronary artery disease, cerebrovascular disease,
  peripheral vascular disease—diffuse disease; triple
  vessel CAD
• 10x greater risk of CHF in females with diabetes and
  a 6x greater risk of CHF in males with diabetes
• Risk of stroke is 2.5-4x greater in diabetics
 Protect your heart! Floss your teeth!
• “Floss only the teeth
  you want to keep…”
      Dental care and diabetes
• 1 to 2 periodontal treatments per year
  decreased diabetes costs by 11-12%
• Univ of Michigan School of Public Health
• January 8, 2009, Science Daily
• Neuropathy and dry mouth
• Increased risk of yeast infections
        Peripheral arterial disease
• Atherosclerosis of the aorta, iliac arteries, femoral
  arteries
• Intermittent claudication
• Risk of amputation is 15-40 x higher in the diabetic
• A diabetic foot ulcer precedes amputation 85% of
  the time
• Let’s hear it for WOCNs!
• FOOT CARE!!
 Wound care: What do they do with all of
      that circumcised foreskin?


• Apligraf
• Regranex (PDGF)
• How about honey for wounds??
      Are they on aspirin and/or Plavix
               (clopidogrel)?
• Diabetes is a pro-inflammatory disease!
• Diabetes is a pro-thrombotic disease
• ASA is not for men under 50 and women under 60 UNLESS…
  other risk factors (smoking, HTN, high LDL) are present
• Plavix if allergic to ASA
• Plavix after a coronary event or cerebral event
• Plavix with a stent
• Diabetes Care , June 2010
 Are they on a “Statin” to improve LDL cholesterol
      levels?? And to decrease inflammation?

• If not, why not?
• LDL-levels should be reduced to 70 mg/dL
• Say yes to the “statin” sisters—lova (Mevacor), atorva
  (Lipitor), prava (Pravachol), simva (Zocor), fluva
  (Lescol), rosuva (Crestor), pitavastatin (Livalo)
• Statins are anti-inflammatory, anti-lipid, decrease
  plaque formation, stabilize plaques and prevent plaque
  rupture
• HDL greater than 40 mg/dL in men, greater than 50 in
  women
• Statins may also slow the progression of chronic renal
  disease (Fried)
                  Statin drugs
• Should all diabetics be on statins REGARDLESS of their
  LDL level?
• YES…YES…YES…their anti-inflammatory effects are
  even more beneficial; and even if their LDL level is
  normal, their LDLs tend to be small and dense
  (Pattern B—think BBs floating around in the arteries);
  statins may change the size of LDLs to large and
  LOOSE (Pattern A)!
• Small dense LDLs are even more damaging to artery
  walls
• The reason their LDLs are small and dense is because
  their triglycerides are too high--PAY ATTENTION to
  TG!!
• Fibric acid derivatives (fenofibrate) lower TG and
  increase particle size; extended release niacin also
  increases particle size
                     FYI
• Particle size and particle number can be
  determined by the NMR (nuclear magnetic
  resonance) LipoProfile—cost ~ $100 to $120,
  slightly higher than a lipid profile
• Many insurance companies cover the cost of
  NMR, including Medicare
• Goal for particle number is less than 1000
  nmil/L and goal for LDL size is 20.6 nm or
  greater
  What’s not to love about the statins? Yeah,
              yeah…side effects
• Myalgias **(other causes in elderly patients…)
• Myositis; rhabdomyolysis (rare)
• About 1/20 patients experiences muscle pain
  or weakness
• Reduce the dose, don’t stop the drug
• Change to Crestor? Give the statin every other
  day?
• Check the creatine kinase if muscle aches and
  pains are severe
  Hypertension and the diabetic
• 50-60% of all newly diagnosed diabetics have
  hypertension
• VIGOROUSLY treat hypertension to reduce the
  cardiovascular risks and to reduce the risk of
  nephropathy
• What drugs should be chosen for the treatment of
  hypertension? (Usually 2 are needed) First line
  therapy should be either the…
                  Prils              or         ARBs
•   Captopril (Capoten)                   •   losartan—Cozaar
•   Enalapril (Vasotec)                   •   valsartan—Diovan
•   Lisinopril (Prinivil, Zestril)
•   Perindopril (Aceon)                   •   candesartan—Atacand
•   Moxepril (Univasc)                    •   irbesartan—Avapro
•   Benazepril (Lotensin)                 •   telmisartan—Micardis
•   Quinapril (Accupril)                  •   olmesartan—Benicar
•   Trandolapril (Mavik)                  •   Eprosartan—Tevetan
•   Ramipril (Altace)
                                          •   Azilsartan--Edarbi
• DO NOT USE DURING
  PREGNANCY!!
Side effects of the ACE inhibitors…
• Hypotension
• Hyperkalemia (excreting sodium and water and
  retaining potassium)
• Hypoglycemia
• Cough (gender difference)
• Angioedema (“Does my voice sound funny to
  you?”)
  What should the 2nd anti-hypertensive
                drug be?
• Thiazide diuretic? (may increase BS)
• Beta-blocker if they have tachycardia, angina
  or previous MI (may mask symptoms of
  hypoglycemia)
• Calcium Channel blocker—verapamil or
  diltiazem for renoprotection
• Amlodipine (Norvasc)—another calcium
  channel blocker
Diabetic nephropathy…PREVENTION!!
• Treat high blood pressure!
• Reduce the animal protein in the diet! Especially
  if they have any evidence of renal involvement—
  the amino acids valine and lysine from animal
  meat increase intraglomerular hypertension and
  accelerate kidney damage
• Reduce serum glucose!
• SAY YES to the ACE inhibitors or ARBs—the PRILS
  or SARTANS (something to inhibit Angie and Al
  (Angiotensin and Aldosterone)
               The healthy kidney…
•  Afferent arteriole     PG
  (vasodilated via
  (prostaglandins)
• Blood entering
  glomerulus

•   Glomerulus→filter
                            filter
•  Efferent arteriole
  (vasoconstricted via
  (angiotensin 2)
• Blood exiting           AT2        Toilet
  glomerulus
    The Diabetic Kidney…insulin resistance,
     hyperglycemia, hypertension, animal protein
•   Afferent arteriole
  ( vasodilation by
  ( prostaglandins)
• Blood entering
  glomerulus

•  Glomerulus→filter
•  Efferent arteriole
  ( vasoconstriction via
  ( angiotensin 2)
• Blood exiting
   glomerulus                     Microalbuminuria**
**CVD and microalbuminuria
  Digression on the diabetic diet…
• Diabetic Diet—circa 1917
• “Forty-eight hours after admission to the hospital the
  patient is kept on ordinary diet to determine the
  severity of his diabetes. Then he is starved, and no food
  allowed save whiskey and black coffee. Whiskey is
  given in the coffee: one ounce of whiskey every two
  hours, from 7 a.m. until 7 p.m. This furnishes roughly
  about 800 calories. The whiskey is not an essential part
  of the treatment: it merely furnishes a few calories and
  keeps the patient more comfortable while he is being
  starved.” (Starvation Treatment for Diabetes—1917)
                  Other diets
•   Exchange diet
•   Counting carb diet
•   Glycemic index diet
•   Mediterranean diet
         The Cardiologist’s diet?
• “If it tastes good, spit it out!”




• Say NO to the Old Country Buffet Diet…
 In addition to reducing animal protein, is there
        such a thing as a “diabetic diet”?
• Low calorie (PORTION CONTROL)
• Low-fat (especially trans and saturated fats)
• Low protein (especially ANIMAL protein to protect the
  kidneys)
• High fiber (20-35 grams per day)
• Carbohydrates—what type? Count those carbs!
• One visit to a nutritionist can save $13,872 per person
  over a 4 year period; savings in hospital charges…one
  visit makes a HUGE difference
  What about the Atkin’s diet to lose weight?
               NOOOOOOOO
• The Atkin’s diet is PRO-inflammatory
• Saturated and trans fats
• Increases intraglomerular hypertension
 Know how to estimate portion size…
• One teaspoon of peanut butter is the size of your
  thumb’s first joint
• Roll the dice…cheese portion
• Think baseball or tennis ball size for a portion of fruit
  or pasta
• Think deck of cards or palm of your hand (sans
  fingers) for a portion of meat, fish, or chicken
• Dove soap bar or mouse for the size of a baked
  potato
   Burning calories to lose weight…
• Besides the obvious activities for burning
  calories—walking, biking, hiking, swimming…
• The “little” things mean a lot too…
  When you’re just about ready to take a bite..

• It takes 2 hours and one minute for a 130-pound
  person to walk off the calories in a McDonald’s BIG
  MAC;
• 3 hours and 26 minutes to walk off a Burger King
  Double Whopper, with cheese
Burn more calories than you take in…
• Stand up when talking on the phone…burn an
  extra 15 calories
• Chewing gum…burn an extra 11 calories
• Tighten your rear-end when walking through a
  doorframe…15 extra calories per squeeze
• FIDGET
             Burning calories
• Kiss your honey every a.m. burns 6-12 calories
  depending on the intensity of the kiss
             Burning calories…
• A wild ride in the hay burns 125 to 300 calories
  depending on how wild that ride happens to be!
• New partner or “same old same old”…??
 Helpful hints for burning calories..
• Passionate kiss three times a day…
    +
• Mad, passionate love twice a week…
    =
• 32,000 calories per year, the equivalent of a 9-
  pound weight loss
                        OR...
• Banging your head against the steps for one hour
  burns 150 calories…this is a suggested alternative
  when a wild ride in the hay isn’t an option.
 Diabetic peripheral neuropathy (DPN)—
               FOOT CARE
• Monofilament screening for sensory loss at every
  office visit
• Longest nerves first
• Small fiber loss resulting in the loss of pain, light
  touch, and temperature sensation
• Large fiber loss later—loss of vibration and
  proprioception
• Stocking-glove distribution
    Diabetic peripheral neuropathy— “Now
     where did I put that sewing needle?”
• Tingling or burning
• Walking on hot coals
• Walking on shards of glass—lancinating/shooting pains
• Treatment—analgesics, antidepressants
• Amitriptyline/Elavil,
• (duloxetine/Cymbalta),
• anticonvulsants (pregabalin/Lyrica) or
  (gabapentin/Neurontin)
• Opioids as necessary
• Acupuncture, TENS, magnets (but not with an insulin
  PUMP)
   Metanx as a therapeutic option
• Prescription only medical food, regulated by the
  FDA
• Contains active forms of folate, vitamin B6, and
  vitamin B12
• Nutritional support for improvement in
  symptoms and sensations for DPN
(Said G. Diabetic Neuropathy—A Review. Nature Clinical Practice
   Neurology 6/26/07; Casellini C and Vinik A. Clinical
   Manifestations and Treatment Options for Diabetic
   Neuropathies. Endocrine Practice 11/19/07)
         Autonomic neuropathy
• Evaluated and followed by a cardiologist
• Orthostatic hypotension (also common w/ aging)
• Resting tachycardia is an important sign of the LOSS
  of vagal input
• Silent ischemia and congestive heart failure
• Need a beta-blocker (atenolol {Tenormin)
• metoprolol {Lopressor, Toprol XL}),
  bisoprolol/Monocor/Zebeta
• Metoprolol or carvedilol (Lopressor or Coreg) with
  CHF
        Autonomic neuropathy
• Gastroparesis (wide swings in blood sugar
  with slowed digestion interfering with the
  timing of insulin), early satiety, chronic N &
  vomiting of food digested hours before
• Metoclopramide (Reglan, Maxeran),
  erythromycin, cisapride (special use),
  domperidone (Motilium)(Canada only)
• Gastric pacer
          Erectile dysfunction
• Atherosclerosis and neuropathy are the 2
  major causes
• ED is an accurate indicator of CVD
• The Pfizer riser (and relatives—Levitra and
  Cialis) are effective treatments in 50% of the
  cases
• Injections, implants, and suction devices
• VED not TED
       Autonomic neuropathy
• Impaired bladder emptying with hydroureter,
  hydronephrosis, chronic infection
• Urecholine, DuVoid
Diabetic Retinopathy—number 1 cause of
             blindness in U.S.

• SEE the EYE GUY once a year!
And lastly…TREAT the DEPRESSION!
                 Thank you.

• Barb Bancroft, RN, MSN, PNP
• www.barbbancroft.com
• BBancr9271@aol.com
                      Bibliography
• Bloomgarden ZT, Comi RJ, Kendall DM. New therapies to achieve
  glycemic control and weight loss in T2DM. Patient Care 2006
  (February): 46-53.
• Fogel N, Zimmerman D. Management of Diabetic Ketoacidosis in
  the ED. Clinical Pediatric Emergency Medicine 2009; 10(4).
• Fried LF, Orchard TJ, Kasiske BL. Effect of lipid reduction on the
  progression of renal disease: a meta-analysis. Kidney Int
  2001;59:260-9.
• Gebel E. The other diabetes. Diabetes Forecast 2010 May:46-48.
• Gondeck K. LDL particle number and size. ADVANCE for NPs and
  PAs. January 2012
• Nestler JF. Metformin for the treatment of polycystic ovary
  syndrome. N Engl J Med 2008 Jan 3; 358:47-54
• Nissen SE and Wolski K. Effect of rosiglitazone on the risk of
  myocardial infarction and death from cardiovascular causes. N Engl
  J Med 2007 Jun 14; 356:2457-71.
                    Bibliography
• Psaty BM and Furber CD. Rosiglitazone and cardiovascular
  risk. N Engl J Med 2007 Jun 14; 356:2522-4.
• Ribowsky J. Gestational Diabetes. ADVANCE for NPs & PAs;
  November 2010; 31-48.
• Shah AA, Durso SC. Applying clinical practice guidelines in
  caring for older adults with diabetes. Patient Care 2007
  (February): 18-25.
• Is Avandia a flawed drug or was the big new study flawed?
  Prescriber’s Letter 2007 (July).
                     Bibliography
• Insulin glulisine (Apidra): A New Rapid-Acting Insulin. The
  Medical Letter 2006; 48(1233).
• Sitagliptin (Januvia) for Type 2 Diabetes. The Medical Letter
  2007; 49(1251).
• Sitagliptin/Metformin (Janumet) for Type 2 Diabetes. The
  Medical Letter 2007; (49)1262).
• Expanding the Therapeutic Options for Type 2 Diabetes
  Mellitus. Clinical News 2006 (December supplement).
• Gavi S, Hensley J. Diagnosis and management of type 2
  diabetes in adults: A review of the ICSI guideline. Geriatrics
  (2009);64(6):12-17.
• Gebel E. Why Me? Diabetes Forecast 2010 (October); 44-50.
                    Bibliography
• Sernyak MJ, Leslie DL, Alarcon RD et al. Association of
  diabetes mellitus with the use of atypical neuroleptics in the
  treatment of schizophrenia. Am J Psychiatr 2002;159:561-6.
• Szerszen A, Seminara DP, Castellanos MR. Glucose control in
  the hospitalized elderly—a concern not just for patients with
  diabetes. Geriatrics (2009); 64(6):18-20.
• Umpierrez GE, Palacio A, Smiley D. Sliding Scale Insulin Use:
  Myth or Insanity? The American Journal of Medicine 2007;
  120 (7).
• Umpierrez GE, Isaacs SD, Bazargan N, et al. Hyperglycemia: an
  independent marker of in-hospital mortality in patients with
  undiagnosed hyperglycemia. J of Clin Endoc and Metabol
  (2002); 87(3):978-82.
• Vasconcelos A. Could surgery spell the end of diabetes? New
  Scientist, Sept 2007
LADA (Latent autoimmune diabetes in
    adults)—10% of all diabetics
• Typical age of onset – adult
• Progression to insulin dependence – months to years
• Presence of autoantibodies—yes
• Insulin dependence – within 6 years
• Insulin resistance – some
The presence of autoantibodies distinguishes this type
  from type 2 and no need for insulin within the first six
  months distinguishes it from type 1.
Consider this diagnosis in a “skinny, type 2 diabetic that
  doesn’t respond well to oral drugs”—usually
  misdiagnosed
   MODY—1 to 5% of all diabetics
• Maturity-onset diabetes of the young
• Monogenic (single gene abnormality)—the pancreas
  cannot make enough insulin and/ or a defect in insulin
  secretion; autosomal dominant
• Usually diagnosed before age 25
• 6 different subtypes—some don’t require insulin and
  can be treated with oral medications
• doesn’t progress to ketoacidosis; persistent
  hyperglycemia; continued partial insulin secretion with
  no insulin resistance; mild to moderate hyperglycemia
  with a range of 130 – 250 (7 -14 mmol); absence of ++
  antibodies or other autoimmune diseases
Intrauterine hyperglycemia and future
   risk of Type 2 DM or prediabetes
1) offspring of women with diet-treated gestational
  DM (21% of offspring develop T2DM or
  prediabetes )
2) offspring of genetically predisposed women with
  a normal OGTT (12% develop T2DM or
  prediabetes)
3) Offspring of women with T1DM (11% develop T2
  DM or prediabetes)
4) Offspring of women from the normal population
  (4% develop T2DM or prediabetes)
(Diabetes Care 2008 Feb 01: 31(2):340-6)
    Estimated average glucose—a calculated
               conversion of A1c
•   eAG = 28.7 x A1c – 46.7

•  A1c (%)                         eAG (mg/dL)
 5.5                                97
 6                                  126 (7 mmol)
 7                                  154
 8                                  183
 9                                  212 (11 mmol)
 10                                 240
 11                                 269
 12                                 298
eAG is a running average over the past 3 months of all glucose fluctuations;
   used to help patients correlate their numbers with A1c.
             Symlin (Pramlinitide)
• Amylinomimetic agent for type 1 and type 2 diabetes—
  synthetic analogue of the hormone amylin, which is deficient
  in patients with diabetes
• Acts by slowing gastric emptying, curbing appetite, and
  suppressing postprandial plasma glucagon and hepatic
  glucose output
• Adjunct therapy for patients with T1DM and T2DM who use
  mealtime insulin and have not maintained glycemic control
  despite optimal insulin therapy with or without oral drugs; cut
  mealtime doses by 50% with Symlin
• Improves postprandial blood glucose and promotes weight
  loss

				
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