diabetes overview and update l.
Skip this Video
Loading SlideShow in 5 Seconds..
Download Presentation

Loading in 2 Seconds...

play fullscreen
1 / 102


  • Uploaded on

DIABETES OVERVIEW AND UPDATE. Barb Bancroft, RN, MSN, PNP BBancr9271@aol.com www.barbbancroft.com. Historical highlights…in the old days…. Diabetes—”to siphon” Mellitus—”sweet” Nurse… “ Taste thy patient’s urine, for if it be sweet…” ---Dr. Thomas Willis.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'DIABETES OVERVIEW AND UPDATE' - daniel_millan

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
diabetes overview and update


Barb Bancroft, RN, MSN, PNP



historical highlights in the old days
Historical highlights…in the old days…
  • Diabetes—”to siphon”
  • Mellitus—”sweet”
  • Nurse…
  • “Taste thy patient’s urine, for if it be sweet…”

---Dr. Thomas Willis

when i was in nursing school it was called sugar diabetes the evolution of the name
When I was in Nursing School…it was called “sugar diabetes”…the evolution of the name…

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)

definition of diabetes mellitus
Definition of Diabetes Mellitus
  • Chronic disorder of carbohydrate, lipid, and protein metabolism characterized in its fully expressed clinical form by an absolutedeficiency of insulin (Type 1 diabetes) or a relative insulin deficiency (Type 2 diabetes).
  • Huh?
  • Type 1—no insulin
  • Type 2—insulin resistance
  • PLUS…it’s a PROthrombotic, PROinflammatory, and PROatherosclerotic disease! So be PRO-active in DX and RX!
  • Is this a cardiovascular disease?
type 2 diabetes the numbers
Type 2 diabetes—the numbers
  • 1.5 million new cases diagnosed per year in the U.S.
  • Over 20 years of age: 20.8 million Americans (9.6%); 1/3 have no clue
  • Over 60 years of age: 10.3 million or 20.9% of all people
  • Usual onset after 40; 70% increase in incidence under 40 in last decade
  • Under 20 years of age: 176,500 or 0.22% of the population; 1 in every 400-600 kids with Type 1
  • 2 million adoloescents (1 in 6 overweight adolescents) aged 12-19 have prediabetes
  • 50% of all new cases of Pediatric diabetes are TYPE 2…not Type 1…
who s at risk who s sitting in your waiting room
Who’s at risk? Who’s sitting in YOUR waiting room?
  • Genetic risk for Type 1 and for Type 2 diabetes—family history, sibling or parent
  • How many genes?
family history
Family history
  • Family history of early coronary artery disease
  • What is meant by early?
  • Greater than 140/90 increases the risk of diabetes
  • 50-60% of newly diagnosed patients also have HTN at diagnosis
  • An interesting note: A family history of hypertension in a child with Type 1 diabetes increases their risk of developing nephropathy
high risk ethnic groups
High risk ethnic groups
  • African American
  • Native American
  • Asian American
  • Hispanic American
  • Pacific Islander
  • Indian (from India)
impaired glucose tolerance
Impaired glucose tolerance
  • Gestational diabetes
  • Baby weighing greater than 9 lbs.
  • Were YOU, as a baby, exposed to hyperglycemia en utero?
what did you weigh as a kid
What did you weigh as a kid?

The odds that a person who is normal weight at age 18 will develop diabetes later in life are 1-in-5 or 1-in-6. However, if a child is very obese at age 18, they have a 3-in-4 chance of developing diabetes. The lifetime risk of developing diabetes, based on a body mass index at age 18, is as follows:

bmi and risk of type 2 t2 diabetes
BMI and risk of Type 2 (T2)diabetes
  • A BMI under 25 (normal BMI)—risk of T2 diabetes for women is 17%; risk of diabetes for men is 20%
  • A BMI between 25-29—risk of T2 diabetes for women is 35%; risk of diabetes for men is 30%
  • A BMI between 30-34—risk of T2 diabetes for women is 55%; risk of diabetes for men is 57%
  • A BMI greater than 35—risk of T2 diabetes for women is 74%; risk of diabetes for men is 70%

(CDC—Diabetes Branch, May 2006)(June 2006, ADA)

within a single ethnic group
Within a single ethnic group…
  • Diet (high calorie, high fat)
  • Lifestyle (Lack of physical activity and sedentary lifestyle)
  • Both play a major role in obesity and insulin resistance with DM
abdominal obesity as a risk factor
Abdominal obesity as a risk factor
  • Abdominal obesity and insulin resistance
  • Visceral fat is an endocrine organ and is metabolically active
  • It is insulin resistant
  • Produces inflammatory mediators such as TNF-α and IL-6,
  • Waist greater than 38 inches in females increases the risk by 6-fold
  • What should we look like?
other conditions that increase the risk of type 2 diabetes pcos and documented hypoglycemia
Other conditions that increase the risk of Type 2 diabetes—PCOS and documented hypoglycemia
  • Polycystic ovary syndrome


  • Polycystic ovary syndrome (PCOS)—5-10% of women of reproductive age; increasing at the same rate as Type 2 DM and metabolic syndrome in U.S.
  • Anovulation, irregular menses, androgen excess, insulin resistance, increased CV risk and Type 2 DM
  • Rx: Metformin and “glitazones” decrease insulin resistance: WORD TO THE WISE: These oral drugs also decrease the efficacy of COCs and increase ovulation—need 2 forms of birth control unless pregnancy is the goal
  • History of hypoglycemia (documented with OGTT)
undesirable lipid levels
Undesirable lipid levels
  • HDL less than 35 mg/dL
  • Triglycerides greater than 150 mg/dL
  • Think diabetes or hypothyroidism with the above lipid profile
  • Draw a FBS and a TSH
type 1 diabetes
Type 1 diabetes
  • Type 1 DM—primarily diagnosed in pre-teens or teenagers; onset prior to age 40 in the majority of patients;
  • Caucasians greater than African-Americans
  • Finland #1 country in world with Type 1 DM
  • 1 in 150 kids by the age of 15
type 1 diabetes19
Type 1 Diabetes
  • Associated with immune response genes and HLA-DR3 and HLA-DR4
  • Autoimmune attack against specific components of the islet beta cellsof the pancreas (anti-glutamic acid decarboxylase antibodies—anti-GAD; anti-islet cell antibodies)
  • Usually present with 3 p’s (loss—polyuria, polydipsia, polyphagia), and weight loss
  • Classic presentation is in a Caucasian, blue-eyed, blonde-haired kid
type 1 diabetes20
Type 1 diabetes
  • What triggers the autoimmune response?
  • The most likely culprit is one of the childhood viruses…
  • Coxsackie B? Measles? Influenza A or B?
other conditions associated with type 1 diabetes
Other conditions associated with Type 1 diabetes
  • Autoimmune diseases are more common
  • Celiac disease
  • Thyroid disease
  • Pernicious anemia
secondary diabetes
Secondary diabetes
  • Exocrine pancreatic disease—cystic fibrosis
  • Cushing’s disease or syndrome
  • Drugs—corticosteroids, L-dopa, beta-blockers, atypical anti-psychotics (especially Clozapine/Clozaril and Olanzapine/Zyprexa), sympathomimetics, niacin, glucosamine, thiazide diuretics
  • Hospital critical care--stress
hyperglycemia in the hospital setting
Hyperglycemia in the hospital setting…
  • Inpatient hyperglycemia in people with or without diabetes is associated with an increased risk of complications and mortality, a longer hospital stay, a higher admission rate to the ICU, and higher hospitalization costs
  • Control is challenging…what is the best way to control hyperglycemia in the hospital setting?
  • Basal/bolus therapy is more efficient than sliding scale which is associated with poorer glycemic control and an increase risk of hypoglycemia

(Umpierrez GE, Palacio A, Smiley D. Sliding Scale Insulin Use: Myth or Insanity? The Am J of Med 2007 (July): 120 (7).

laboratory tests
Laboratory Tests
  • Prediabetes…one-step away… HUH?
  • 54 million Americans with prediabetes
  • Asymptomatic fasting blood sugars between 100 mg/dL and 125 mg/dL
  • Used to be called impaired glucose tolerance
  • May have metabolic syndrome
central obesity and the metabolic syndrome insulin resistance syndrome
Central obesity and the metabolic syndrome (insulin resistance syndrome)
  • What is the metabolic syndrome? (Previously known as syndrome X)
  • 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
  • 1 million adolescents have metabolic syndrome
  • What is the definition of metabolic syndrome?
Definition varies by group: NCEP ATP III guidelines: Metabolic syndrome or IRS (insulin resistance syndrome)
  • Central obesity—waist size greater than 40.2 inches in men, 34.6 inches in women
  • High TG (>150 mg/dL),
  • Low HDL (less than 40 mg/dL in men, less than 50 mg/dL in women)
  • Hypertension (≥ 130/85 mm Hg)
  • Fasting glucose ≥ 110 mg/dL (or greater than 100 mg/dL)
  • Metabolic syndrome is present when any 3 of these risk factors are present
  • PCOS (polycystic ovary syndrome is a form of metabolic syndrome/IRS)
laboratory diagnosis
Laboratory diagnosis
  • Fasting plasma glucose—after 8 hours without caloric intake
  • A.M. specimens greater than or = to 126 mg/dL (previous was 140 mg/dL)
  • Random glucose of greater than or equal to 200 mg/dL
  • Postprandial glucose excursions with subsequent hypoglycemia—patient with early diabetes can present with this picture—give glucometer to take home and measure
  • Postprandial glucose excursions are also associated with an increased risk of CV disease…
laboratory diagnosis29
Laboratory diagnosis
  • Hemoglobin A1C—gold standard for measuring long-term glycemic control—how does it work? RBC life span
  • 50% of glycosylated hemoglobin is from previous month; 25% from the month before; 25% 3-4 months ago
  • Normal range is 4-6%; each percent equals 20-22 mg/dL of plasma glucose (6% is TOO HIGH—but is considered normal range by laboratory)
  • HbA1C of 4% is the equivalent of a FPG of 80-88 mg/dL; 10% = 200-220 mg/dL
  • What does the ADA recommend for HbA1C for adults? (Less than 7) Clinical endocrinologists for adults? (Less than 6.5)
hemoglobin a1c for kids ada guidelines
Hemoglobin A1c for kids (ADA guidelines)
  • Guidelines for kids—less than 8.5 but greater than 7.5 for toddlers and preschoolers 0-6 years of age
  • Less than 8 for kids 6-12
  • Less than 7.5 for adolescents and young adults (13-19)
  • 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
  • The DCCT data certainly showed that tighter blood glucose controls increase the risk of serious hypoglycemia BUT also decrease the risk of long-term complications
hemoglobin a1c for older adults
Hemoglobin A1C for older adults
  • More complex because of co-morbidities (example aggressive control of BP + BS may increase the risk of falls)
  • How aggressive should we be?
  • LIGHT mnemonic is useful
  • L—life expectancy: estimate average life expectancy based on age and health status
  • I—impact of geriatric syndromes and other co-morbidities
  • G—goals of care and patient preferences
  • H—help the patient prioritize and develop a care plan
  • T—Time required to benefit from the therapeutic intervention
six syndromes to consider in older patients with diabetes
Six syndromes to consider in older patients with diabetes
  • Polypharmacy—drug burden and drug-drug and drug-disease interactions are very common
  • Depression—increased prevalence and incidence; interferes with self-management
  • Cognitive impairment—screen yearly and more often in patients having difficulty with disease management and self-care (check TSH and B12); is dementia more common in diabetics?
six syndromes to consider in older patients with diabetes33
Six syndromes to consider in older patients with diabetes
  • Urinary incontinence—from glucosuria, neurogenic bladder, stool impaction, UTI, vaginal yeast infection
  • Falls—
  • Undertreated pain—may not mention or may just blame it on normal aging; may not describe neuropathic pain in the usual terms of tingling, burning, but use terms such as aching, discomfort
basic physiology pathophysiology
Basic physiology/pathophysiology
  • Insulin is a growth hormone—stores fat and sugar and stimulates protein synthesis after the meal
  • Too much? WEIGHT GAIN; hypoglycemia
  • Glucagon is a catabolic hormone produced during the fasting state; breaks down stored glycogen
  • Too much? WEIGHT LOSS; hyperglycemia
the fasting state
The fasting state
  • The pancreas produces glucagon for glycogenolysis (break down stored sugar 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
  • Type 1 ketoacidosis is a prolonged fasting state; absolute deficiency of insulin; glucagon is working overtime; weight loss; glycogenolysis and lipolysis with hyperglycemia and fatty acid release (ketones); ketones and glycosuria cause a significant osmotic diuresis (significant dehydration)
symptoms of dka diabetic ketoacidosis
Symptoms of DKA (Diabetic Ketoacidosis)
  • Dehydration
  • Abdominal pain
  • Anorexia, weight loss
  • Kussmaul’s respirations (acidosis)
  • Tachycardia
  • Weakness, fatigue
  • Fruity breath odor
  • hypotension
  • N and/or V
  • Confusion, decreased reflexes, coma
treatment of dka
Treatment of DKA
  • Dehydration is your first priority
  • GIVE FLUIDS…what kind?
  • Then what? Regular insulin IV
  • Then what? Check electrolytes and bicarb
pathophysiology of type 2 dm
Pathophysiology of Type 2 DM
  • Early in the disease—insulin resistance is characterized by a subnormal receptor response to insulin (partially due to abdominal obesity)
  • Abnormal beta cell response with an abnormal release of insulin to glucose—too much released resulting in hyperinsulinemia and hypoglycemia in the postprandial state
  • What are the consequences of hyperinsulinemia?
  • Increased TG and decreased HDLs
  • Sodium and water retention—HTN
  • Stimulate fat storage (CHO to fats)
  • Prothrombotic
  • Proinflammatory
  • Triggers endothelial cell dysfunction
  • YIKES!!
type 2 diabetes
Type 2 diabetes
  • Metabolic derangements aren’t usually as severe as Type 1; as insulin resistance continues, serum glucose levels gradually increase; with increasing glucose levels the pancreas responds by increasing insulin output resulting in hyperinsulinemia
  • Few symptoms initially, 2 P’s (no polyphagia), weight gain due to hyperinsulinemia
  • Other symptoms—fatigue, diplopia, nocturia
  • Skin infections, vaginal infections, poor wound healing, neuropathy
  • Cardiovascular complications may be the first presenting symptoms—MI, PAD, Stroke
  • “Silent” for a full decade in some individuals
some new physiology
Some new physiology…
  • You eat a meal…and then?
  • The intestine releases incretin hormones known as GLP-1 (glucagon-like peptide 1) and GIP (glucose-dependent insulinotropic polypeptide) throughout the day, with an increase right after the meal (postprandial increase)
  • The incretin hormones influence the pancreas to increase the synthesis and release of insulin and decrease the synthesis and release of glucagon
  • Drugs that affect incretin—Exenatide (Byetta); symlin (Amlin); sitagliptin (Januvia)
and then what
And then what?
  • Insulin acts on insulin receptors in the liver, skeletal muscle tissue and adipose tissue to trigger the entry of sugar into the cells
  • (Obesity decreases the number of insulin receptors; exercise increases the receptor sensitivity)—HENCE, the strong recommendation to LOSE weight and exercise!
  • The liver stores extra glucose as glycogen and releases it as necessary to keep the blood sugar levels in the normal range throughout the day and night
  • The liver does most of its work at night
  • Clinical implications of giving metformin at night (Metformin blocks the breakdown of glycogen to glucose)—the whole dose
how do you treat it the usual suspects oral drugs
How do you treat it? The usual suspects…(oral drugs)
  • By decreasing the production of glucose by the liver—Metformin (glucophage)
  • By increasing insulin sensitivity in the tissues (the glitazones—rosi- and pio-)—Avandia and Actos; metformin (glucophage)
  • By increasing insulin secretion from the pancreas and increasing insulin receptor sensitivity (the oral sulfonylureas)
  • By giving oral drugs that reduce postprandial excursions of glucose (repaglinide/Prandin, nateglinide/Starlix)
  • By inhibiting enzymes in the intestine responsible for breaking down incretins that potentiate insulin release (sitagliptin/Januvia)
  • By mimicking hormones (incretins) that trigger insulin release from the pancreas (exenatide/Byetta)
oral drugs the 1 bestseller
Oral Drugs…the #1 bestseller
  • 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, need functioning organs--kidneys and heart especially (check serum creatinine before starting metformin)
  • Se Creatinine--Cut-off is 1.4 in females and 1.5 in males
  • Other benefits: lowers BP, increases HDL, lowers LDL
  • B12 deficiency—longer the use and the higher the dose, the greater the risk
digression the importance of b12
Digression: the importance of B12
  • B12 is necessary for the healthy production of RBCs and for the maintenance of the central and peripheral nervous system (cognitive function in the CNS and normal PNS function)
  • B12 deficiency is the one of the top 3 causes of peripheral neuropathy in the U.S. and the #1 cause of nutritional dementia in the U.S.
  • B12 is stored in the liver for 5 years or so
  • 39% of the population over 50 has a B12 deficiency
  • PPIs and Metformin decrease B12
  • B12 and peripheral neuropathy in the diabetic
  • Supplements? How much?
  • Can you overdose on B12? The one dreaded side effect is…
oral drugs for type 2 dm
Oral drugs for type 2 DM…
  • The “Glitazone” sisters—rosi (Avandia), pio (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
  • The bad news? Do these drugs increase the risk of cardiovascular events?
  • Can you use this class of drugs in the patient with heart failure?
old drugs are these even worth using anymore considered third line therapy
OLD Drugs…are these even worth using anymore? Considered third-line therapy…
  • Oral sulfonylureas—Glipizide (Glucotrol) and glyburide (Diabeta, Micronase, Glynase) and glimipiride (Amaryl)…
  • Increase the secretion of insulin from the pancreas and increase receptor sensitivity
  • Problem? Weight gain, hypoglycemia, increased cardiovascular risk) (highest doses increased risk vs. metformin; may prevent heart from recovering from brief periods of ischemia) (Canadian Medical Association Journal January 2006)
  • glimipiride (Amaryl)—safe use in elderly--decreased incidence of hypoglycemia
drug combinations
Drug combinations
  • Glucovance (glyburide and metformin)
  • Avandamet (rosiglitazone and metformin)
  • Metaglip (glipizide and metformin)
  • Actosplus Met (metformin/pioglitazone)
  • Avandaryl (rosiglitazone/glimepiride)
  • Duetact

(pioglitazone HCl and glimepiride)

  • Sitagliptin/metformin (Janumet)
other drugs
Other drugs
  • Repaglinide (Prandin)
  • Nateglinide (Starlix)
  • Good for elderly to prevent postprandial excursions
  • Great if your meals are sporadic
exenatide byetta incretin mimetic
Exenatide (Byetta)—incretin mimetic
  • incretins are responsible for approx. 60% of the post-meal insulin secretion; however, the action of the incretins is impaired in diabetics
  • Byetta is an incretin mimetic; acts at the GLP-1 receptor in the pancreas that promotes insulin release
  • Type 2 diabetics who are already receiving metformin, a sulfonylurea, or both and do not have optimal control
  • Weight loss is a + side effect due to early satiety (10-15 lbs to 40-50 lbs)
  • Take less than an hour before a.m. and p.m. meals (nausea)
sitagliptin phosphate januvia merck
Sitagliptin phosphate (Januvia)(Merck)
  • DPP-4 inhibitor…huh?
  • Dipeptidyl-peptidase-4 is an enzyme responsible for the inactivation of the incretin hormones GLP-1 and GIP (glucose-dependent insulinotropic polypeptide). These hormones are released from the intestine throughout the day, with an increase postprandially; they potentiate insulin synthesis and release by pancreatic beta cells and decrease glucagon release by pancreatic alpha cells, lowering blood sugar
  • Costly…$171.90 per month vs. generic Metformin $50-75/month); oral sulfonylureas are $10-40/month); glitazones are ~$100-115/month
  • Janumet (combination with metformin)
pramlintide acetate symlin
Pramlintide acetate (Symlin)
  • Amylinomimetic agent for type 1 and type 2 diabetes—synthetic analogue of the hormone amylin (released after meals), 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 T2DM who use mealtime insulin and have not maintained glycemic control despite optimal insulin therapy with or without oral drugs
  • Improves postprandial blood glucose and promotes weight loss
  • Taken just before the meal (multiple shots w/ insulin)
  • 36% of type 2 DM use insulin today; within 5 years of diagnosis, 50% require insulin
  • Weight gain can be significant– 5 to 10 kg in first year; daytime insulin promotes weight gain; night time insulin does not
  • Insulin dose needed varies from 0.2 units to 2 units per day; no correlation with age, gender, duration, race or HbA1c level
  • Most serious side effect is HYPOGLYCEMIA
  • Rapid-acting insulins include aspart (Novolog), glulisine (Apidra), lyspro (Humalog)
  • regular insulin—Humulin R, Novolin R
  • Intermediate acting—NPH; Humulin N, Novolin N
  • Long-acting insulins include detemir (Levemir), glargine (Lantus)
  • Mixtures
  • 50% lispro protamine, 50% insulin lispro = Humalog Mix 50/50
  • 70% NPH/30% regular = Humulin 70/30; Novolin 70/30
  • 75% lispro protamine/25% lispro = Humalog Mix 75/25
  • 70% aspart protamine/30% aspart = NovoLog Mix 70/30
rapid acting insulins
  • Lyspro/Lispro (Humalog); Aspart (NovoLog); glulisine (Apidra)
  • quicker absorption and quicker onset of action; duration of action is shorter, and higher peak concentrations compared to regular insulin
  • Less nocturnal episodes of hypoglycemia than regular insulin
  • Closer administration to meal times within 5-10 minutes; even shortly after the meal if necessary
  • Peak 1-2 hours; duration 3-4 hours
  • Closer approximation to physiologic insulin release
  • Lower peak postprandial glucose excursions
intermediate acting insulin
Intermediate-acting insulin
  • NPH (Humulin N and Novolin N)
  • Used to provide basal insulin and because they have a peak action, they may cover the midday meal; onset 2-4 hours, peak at 4-10 duration of 10-16 hours
  • Is there a problem?
if they are still on nph
If they are still on NPH…
  • Somogyi effect and NPH at dinner—peaks at 2-3 a.m. and causes nocturnal hypoglycemia
  • Patient wakes up in a sweat and with tachycardia
  • Immediately checks blood sugar and it’s normal or high, secondary to a sympathetic nervous system response
  • DON’T increase the dinner dose!!
  • Change the dinner dose to a nighttime dose or decrease the dinner dose and increase the snack at bedtime
  • Or better yet…
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 stabilizes endothelial cells…HUH?
complications of type 2 diabetes
Complications of type 2 diabetes
  • Is diabetes a cardiovascular disease?
  • Accelerated atherosclerosis--four out of five diabetics die from complications of cardiovascular disease and atherosclerosis
  • Considered a “risk equivalent” of heart disease
  • Proinflammatory, prothrombotic, proatherosclerotic
  • Endothelial dysfunction with increased deposition of fat in the large arteries
  • Coronary artery disease, cerebrovascular disease, peripheral vascular disease—diffuse disease; triple vessel CAD
coronary artery disease and angina
Coronary artery disease and angina…
  • 4 out of 5 diabetics die of complications of cardiovascular disease
  • Estrogen does NOT protect the premenopausal diabetic woman from heart disease
  • If a diabetic woman under 50 years of age presents with signs and symptoms of heart disease, take her seriously!
frontoparietal stroke
Frontoparietal stroke
  • “Brain attacks”

and TIAs

  • Internal carotids
  • Circle of Willis
  • Risk of stroke is 2.5-4x greater in diabetics
peripheral arterial disease
Peripheral arterial disease
  • Atherosclerosis of the aorta, iliac arteries, femoral arteries
  • Intermittent claudication
  • Diabetes raises the risk of amputation 14x for men 35-44; 17x for men 45-54;
  • Raises the risk for amputation 20x for women between 35-44; 28x for women between 45-54
  • 50% die within 3

years of amputation

are they on a statin to improve ldl cholesterol levels and to decrease inflammation
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)
  • Statins are anti-inflammatory, anti-lipid, decrease plaque formation, stabilize plaques, prevent plaque rupture
  • Strive for an LDL-cholesterol of 70 mg/dL; HDL greater than 40 in men, greater than 50 in women
  • Should all diabetics be on statins REGARDLESS of their LDL level?
are they on aspirin and or plavix clopidogrel
Are they on aspirin and/or Plavix (clopidogrel)?
  • If not, why not?
  • Diabetes is a pro-inflammatory disease!
  • Diabetes is a pro-thrombotic disease
  • ASA for daily use as soon as diagnosed
  • Plavix if allergic to ASA
  • Plavix after a coronary event or cerebral event
before you start the statins
Before you start the statins…
  • Check liver function tests (AST)
  • Check CK
  • Consider checking the TSH in women
  • Caution patients to NOT drink grapefruit juice if they are on lovastatin (Mevacor), simvastatin (Zocor), and atorvastatin (Lipitor)
  • They can drink grapefruit juice with the other statins (Pravachol, Crestor, Lescol)
  • Try not to use Lopid (to reduce TG) with the statins
  • Keep triglycerides below 150 mg/dL (may need to add fenfibrate (Tricor) or gemfibrozil (Lopid)
  • Keep HDL’s above 50 mg/dL—HOW?
  • May need to add NIACIN (keep eye on blood sugars)
  • FISH OIL capsules for high TG—2-4 grams/day
  • Vytorin—Zocor and Zetia (ezetimibe)
  • What’s Zetia?
  • When would you use Vytorin?
  • Advicor (niacin + lovastatin)
hypertension more pearls
Hypertension…more pearls
  • In a diabetic patient, BP control exerts a more positive impact on CV events than BS control!
  • Blood glucose control that achieves levels of glycosylated hemoglobin of about 7% has less impact on cardiovascular disease than does BLOOD PRESSURE control that maintains diastolic pressure at about 85 mmHg.
  • A systolic pressure of 130-139 mmHg with a diastolic pressure of 85-89 mmHg, although classified as “high normal”, warrants PROMPT treatment in the diabetic patient.
  • “Pre-hypertension” is 120-139 over 80-89 mg/Hg
hypertension and the diabetic
Hypertension and the diabetic
  • Which comes first, the chicken or the egg?
  • Does diabetes CAUSE hypertension, or does hypertension CAUSE diabetes?
  • 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? First line therapy should be either the…
prils ace inhibitors or the arbs angiotensin receptor blockers
“Prils” (ACE inhibitors)…or the ARBs (angiotensin receptor blockers)
  • Block the production of angiotensin 2 reduces blood pressure, decreases remodeling of the heart, reduces preload and afterload (reducing the workload of the heart), and decreases intraglomerular hypertension and renal disease (more later)
  • May also PREVENT Type 2 diabetes
  • Reducing angiotensin is anti-inflammatory!
prils the ace inhibitors brazilian pit viper
“Prils”—The ACE inhibitors (Brazilian pit viper)
  • Captopril (Capoten)
  • Enalapril (Vasotec)
  • Lisinopril (Prinivil, Zestril)
  • Perindopril (Aceon)
  • Moxepril (Univasc)
  • Benazepril (Lotensin)
  • Quinapril (Accupril)
  • Trandolapril (Mavik)
  • Ramipril (Altace)
  • HUH?…..
sartans arbs
  • Angiotensin receptor blockers (bypass ACE) and work by blocking the tissue receptors
  • Who are they? The “Sartan Sisters”…
  • losartan—Cozaar
  • valsartan—Diovan
  • candesartan—Atacand
  • irbesartan—Avapro
  • telmisartan—Micardis
  • olmesartan—Benicar
  • Less side effects—may substitute if cough is unbearable
most diabetics need more than 1 drug to treat hypertension
Most diabetics need more than 1 drug to treat hypertension
  • ACE inhibitor
  • ARB
  • Diuretic
  • Calcium channel blockers
dietary changes to reduce blood pressure the dash diet
Dietary changes to reduce blood pressure—the DASH diet
  • Increase potassium containing foods (4700 mg/day)
  • Decrease sodium containing foods (stop eating out of the box or can; decrease processed foods)—less than 2400 mg/day
  • Increase low-fat calcium containing foods—greater than 1200 mg/day
can dietary changes lower cholesterol and protect the heart
Can dietary changes lower cholesterol and protect the heart?
  • The Mediterranean diet with nuts, fiber, fish, vegetables, fresh fruits, olive oil, and vino, lots of vino
  • Lowers the markers of inflammation (Environmental Nutrition, July 2004;27(7)
is there such a thing as a diabetic diet
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)
  • High fiber (20-35 grams per day)
  • Carbohydrates—what type?
  • Glycemic index of foods??
what about the atkin s diet to lose weight
What about the Atkin’s diet to lose weight?
  • The Atkin’s diet is PRO-inflammatory
  • Saturated and trans fats
  • Nephrotoxic
know how to estimate portion size
Know how to estimate portion size…
  • One teaspoon of peanut butter is the size of your thumb’s first joint
portion control
Portion control…
  • 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
should a diabetic drink to lower cholesterol
Should a diabetic drink to lower cholesterol ?
  • Only if BS and TG are under control
  • Discuss with health care professional
  • Alcohol has a cholesterol lowering effect and an anti-inflammatory effect
  • 1-7 drinks per week has an anti-inflammatory effect
  • What constitutes “1 drink”?
diabetic peripheral neuropathic pain dpnp
Diabetic peripheral neuropathic pain (DPNP)
  • 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 —loss of vibration and proprioception
  • Stocking-glove distribution
diabetic peripheral neuropathy now where did i put that sewing needle
Diabetic peripheral neuropathy—”Now where did I put that sewing needle?”
  • Tingling, numbness, or burning pain— “ I feel like I’m walking on hot coals.”
  • Stabbing pain– “I feel like I’m walking on shards of glass.”
treating diabetic peripheral neuropathic pain
Treating diabetic peripheral neuropathic pain
  • Analgesics (NSAIDS)—neuropathy has an inflammatory component; however, most patients are already on aspirin—mixing ASA and an NSAID increases the risk for gastric bleeding
  • Antidepressants—duloxetine (Cymbalta)** is FDA approved for treating both depression and diabetic peripheral neuropathy; amitryptiline (Elavil) may be used in small doses @ night for neuropathy (remember that escalating the dose of Elavil escalates the anti-cholinergic side effects)
treating diabetic peripheral neuropathic pain87
Treating diabetic peripheral neuropathic pain
  • Anticonvulsants—gabapentin (Neurontin), pregabalin (Lyrica), and carbamazepine (Tegretal),
  • Antiarrhythmics (oral lidocaine)
  • TENS
  • Magnet therapy for just feet (but not with an insulin PUMP)
  • Α-Lipoic Acid—600 mg daily; has been shown to reduce symptoms in some patients with DN; available as a nonprescription dietary supplement and thus is not regulated; use a reputable company for all dietary supplements

(Ziegler D et al. Oral treatment with alpha lipoic acid improves symtpomatic diabetic polyneuropathy: The SYDNEY 2 trial. Diabetes Care 2006 Nov; 29:2365-70.

autonomic neuropathy
Autonomic neuropathy
  • Evaluated and followed by a cardiologist
  • Orthostatic hypotension
  • Resting tachycardia is an important sign of the LOSS of vagal input
  • Silent ischemia and congestive heart failure
autonomic neuropathy90
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), erythromycin, cisapride (special use)
  • Tegaserod (Zelnorm)
erectile dysfunction
Erectile dysfunction
  • Atherosclerosis and neuropathy are the 2 major causes
  • 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 neuropathy92
Autonomic neuropathy
  • Impaired bladder emptying with hydroureter, hydronephrosis, chronic infection
  • Urecholine, DuVoid
the healthy kidney
The healthy kidney…
  • Afferent arteriole

(vasodilated via


  • Blood entering


  • Glomerulus→filter
  • Efferent arteriole

(vasoconstricted via

(angiotensin 2)

  • Blood exiting






the diabetic kidney hyperglycemia
The Diabetic Kidney…hyperglycemia
  • Afferent arteriole

(  vasodilation by

(  prostaglandins)

  • Blood entering


  • Glomerulus→filter
  • Efferent arteriole

(  vasoconstriction via

(  angiotensin 2)

  • Blood exiting



clinical significance of microalbuminuria
Clinical significance of microalbuminuria
  • Microalbuminuria ≥ 20μg/min or A/C ratio ≥ 30 mg/g
  • “window” to the health of the vascular system
  • Assume that vascular disease is already present when microalbuminuria is present
diabetic nephropathy prevention
Diabetic nephropathy…PREVENTION!!
  • Treat high blood pressure!
  • Reduce the animal protein in the diet!
  • Reduce serum glucose!
  • SAY YES to the ACE inhibitors or ARBs—the PRILS or SARTANS (something to inhibit Angie and Al (Angiotensin and Aldosterone)
  • If they are NOT on a PRIL or SARTAN…the question is:
diabetic retinopathy
Diabetic Retinopathy
  • Non-proliferative—macular edema, microaneurysms, small intraretinal hemorrhages, exudates
  • Blot hemorrhages, cotton-wool exudates
  • Proliferative stage with neovascular growth; scar tissue and retinal detachment
  • Control blood sugars!
  • SEE the EYE GUY once a year!
and lastly treat the depression
And lastly…TREAT the DEPRESSION!
  • Depression and compliance
  • Before discharge, evaluate for depression
  • 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).
  • Umpierrez GE, Palacio A, Smiley D. Sliding Scale Insulin Use: Myth or Insanity? The American Journal of Medicine 2007; 120 (7).
  • Bloomgarden ZT, Comi RJ, Kendall DM. New therapies to achieve glycemic control and weight loss in T2DM. Patient Care 2006 (February): 46-53.
  • 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.
  • Psaty BM and Furber CD. Rosiglitazone and cardiovascular risk. N Engl J Med 2007 Jun 14; 356:2522-4.
  • 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).
  • Brown AF, Mangione CM, Saliba D, et al. Guidelines for improving the care of the older person with diabetes mellitus. J Am Geriatr Soc.2003; 51(suppl 5):S265-S280)
  • Dargie HJ, Hildebraindt PR, Riegger GA, et al. A randomized placebo-controlled trial assessing the effects of rosiglitazone on echocardiographic function and cardiac status in type 2 diabetic patients with NYHA Functional Class I or II Heart Failure. J Am Coll Cardiol. 2007;49(16):1696-1704.
ada contacts
ADA Contacts
  • Diabetes.org
  • Diabetes.org/research
  • To locate an ADA/NCQA Recognized provider of diabetes care in your area Call 1-800-342-2383.
  • Just for kids…diabetes.org/youthzone
  • ADA fundraising events—America’s Walk for Diabetes annual national walk event; call 1-888-342-2383.