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Diabetes Mellitus

Normal fasting glucose
less than 100 mg/dl
Impaired Fasting Glucose (IFG)
100 - 125 mg/dl {Pre-Diabetes}
Impaired Glucose Tolerance (IGT)
OGTT level > 140 - 199 mg/dl
after 2 hrs {Pre-diabetes}
young, thin, requires insulin, prone to ketosis, autoimmune B cell destruction, low fasting C-peptide [conc]
Type 1 diabetes
older, obese, doesn't require insulin, not prone to ketosis, peripheral resistance B cell dysfunction, normal-high fasting C-peptide [conc]
type 2 diabetes
Typically occurs in children and adolescents but may occur at any age
Type 1 DM
Exogenous administration of insulin is necessary for survival in patients with type
Type 1 DM
It is an autoimmune disorder: patients develop an absolute lack of insulin due to destruction of beta cells in the pancreatic islets of Langerhans
Type 1 DM
Usually develops in adults although the incidence in children and adolescents is increasing
Type 2 DM
90-95% of patients with diabetes have type
Type 2 DM
Most patients with type 2 disease do not need insulin initially but require it later because of disease progression
There is tissue insensitivity to insulin:
? genetic factors
Aging, sedentary lifestyle
Abdominal-visceral obesity as well as fat deposition on the neck, face, and chest
Polyuria, Fatigue, weakness, Slow wound healing, Polydipsia, Recurrent blurred vision, Peripheral neuropathy, Frequent infections (candidiasis)
general signs/symptoms of Diabetes Mellitus
signs unique to Type 1 DM
weight loss
patients with type 2 DM may be
Excess GH, hypercortisolism, glucagons or somatostatin
secondary Hyperglycemia
Disorders that affect insulin action or insulin secretion
High-dose glucocorticoids, diuretics, phenytoin, niacin
secondary Hyperglycemia (medication induced)
Disorders that affect insulin action or insulin secretion
Individuals have IFG and/or IGT
Individuals have an increased risk of developing DM and/or CV disease
Is associated with the metabolic syndrome (insulin resistance syndrome)
Individuals with IFG and/or IGT may have normal HbA1C levels
______have been demonstrated to prevent or delay the development of type 2 diabetes in persons with IGT
Use of medical nutrition therapy (MNT) to decrease body weight by 5-10% + exercise + pharmacologic agents (selected individuals)
what pharmacologic agents can be helpful in conjunction with medical nutritional therapy for a patient with "pre-diabetes"
statins -> lower lipids
Individuals have an increased risk of developing type 2 DM
Independent risk factor for cardiovascular disease - increases risk of coronary artery disease and stroke
Metabolic Syndrome
for a patient with HTN releated to metabolic syndrome, use
B-blockers and diuretics RAISE LIPID LEVELS
for a patient with dyslipidemia releated to metabolic syndrome, use
Niacin corrects elevated lipids but may increase insulin resistance.
Insulin resistance
Dyslipidemia - elevated triglycerides, decreased HDL, increased LDL (especially small, dense particle LDL)
Metabolic Syndrome - Associated Clinical Abnormalities
Hypercoagulable state (elevated plasminogen activator inhibitor-1, hyperfibrinogenemia, increased platelet aggregation)
Metabolic Syndrome - Associated Clinical Abnormalities
Proinflammatory state (elevated C-reactive protein, endothelial dysfunction)
Metabolic Syndrome - Associated Clinical Abnormalities
Abdominal Obesity:
Waist circumference > 40 in. (males) and > 35 in. (females) who have a BMI of 25-34.9 kg/m2
Metabolic Syndrome - Associated Clinical Abnormalities
Abdominal Obesity
There is an increased risk of type 2 DM, HTN, and CV disease
Can be a marker of increased disease risk even in persons of normal weight (BMI 18.5-24.9 kg/m2)
Some men develop metabolic risk factors when waist circumference is only marginally increased
Central adiposity (see waist circumference)
Increased triglyceride level
Decreased HDL-C level
3 out of 5 must be present before classifying a patient as having the metabolic syndrome
Hyperinsulinemia, through stimulation of arterial smooth muscle proliferation, has been implicated in the development of
atherosclerotic plaque.
who is most likely to develop metabolic syndrome
Hispanics: men 28%, women 37%
Treating the metabolic syndrome may prevent or improve
CVD and type 2 DM.
Hemoglobin A1C (HbA1C)
Degree to which glucose is bound to the A1C component of hemoglobin
Level of blood glucose is ________ to the level of HbA1C
directly proportional
the goal for HbA1C levels is
< 7%
HbA1C normal concentration is about _______% (average American) but the normal range can vary between labs.
4-6 %
HbA1C reflects the concentration of glucose present in the body over a prolonged time period related to the 60-day half-life of _______
HbA1C reflects glucose control over the past ______ weeks
8-12 weeks
Check every ____ months in patients with HbA1C > 7%
3 months >7%
Check every ____ months in patients with HbA1C < 7%
6 months <7%
Measures over 2-3 months instead of day to day
Provides better indicator of severity and presence of disease
Stable value and easy to collect
Hemoglobinopathies may interfere
Conditions that cause RBC turnover can cause false positives
Anemia's, transfusions, pregnancy)
Not useful for acute elevations (Type 1)
Age > 45 years
Low HDL cholesterol (< 35 mg/dl) and/or high triglyceride (> 250 mg/dl)
Family history of diabetes
Obesity (BMI > 25 kg/m2)
Ethnicity: Native-Americans, African-Americans, Hispanics
History of Vascular disease
Risk Factors for Type 2 DM
Low HDL-C and/or high triglycerides as well as obesity (especially abdominal obesity) are 2 of 5 criteria for
the metabolic syndrome
Previously identified impaired fasting glucose (FBS: 100-125 mg/dl) or impaired glucose tolerance
Habitual physical inactivity
History of gestational diabetes mellitus or delivery of a baby weighing > 9 lbs.
Polycystic Ovarian Syndrome
Risk Factors for Type 2 DM
Previously identified IFG and hypertension are 2 of the 5 criteria for
metabolic syndrome
who is at an increased risk for macrovascular complications
fasting glucose is 100-125 mg/dl (Impaired Fasting Glucose)
who should be screened for Type 2 DM
All adults over age 45 years every 3 years
Especially those with BMI > 25 kg/m2
if result of the initial fasting glucose is 100-125 mg/dl (Impaired Fasting Glucose) how frequently should you repeat the screening test for Type 2 DM
if the individual is overweight and has one or more risk factors for DM
screen at a younger age
Test every 2 years starting at age 10 or at onset of puberty
You should begin screening for _____ if a teen is OVERWEIGHT, has HTN, high serum triglycerides, and low a HDL level
Diabetes Mellitus
Fasting blood sugar
Random glucose level with symptoms of DM
Oral Glucose Tolerance Test
3 tests used for the diagnosis of DM
hopw do you confirm a Dx of DM
Any of the 3 diagnostic criteria must be confirmed on a different day to make the diagnosis of diabetes mellitus
The fasting blood sugar test is recommended as the confirmatory test
no caloric intake for at least 8 hrs before testing
glucose tolerance test (GTT)
draw a FBS, have patient drink a measured amount of sugar (75 gms) as a very sweet drink, and then test glucose at least 2 hours later. DM is diagnosed if the 2 hour glucose is >200
GTT may be utilized for patients with a FBS ______ if diabetes is suspected
< 126 mg/dl
FBS >126 mg/dl (no caloric intake for at least 8 hrs)
HbA1c >6.5% (Repeated unless random glucose >200 with symtoms)
Random glucose >200mg/dl with symptoms of diabetes
OGTT: 2hrs plasma glucose >200mg/dl
Diagnosis - Diabetes Mellitus
what is recommended as the confirmatory test for DM Dx
fasting blood sugar test
if HbA1c is >6.5% when do you NOT need to repeat this test
random glucose >200 with symtoms
blood glucose monitoring
diabetes education
patient self monitoring
this test is not reliable for patient self-monitoring
urine tests
The concentration of urine also makes a big difference - if you drink 2 glasses of water the glucose level in your urine will be diluted but the blood glucose will remain stable.
When glucose is elevated, patients c/o being thirsty, dry, and tired but not until the glucose is at
200 mg/dl
some patients get used to the symptoms of elevated glucose levels and may not notice them, even when the levels reach
200s-300s mg/dl
When glucose is low patients become shaky and sweaty but not until the glucose
< 60 mg/dl
the diet of a patient with DM should strive for
Saturated fats should be < 7% , carb intake must be monitored
first line therapies for DM
diet and exercise
If you can get a patient to lose as little as _____% of their body weight, they may get decreased insulin resistance with improved glycemic control.
They may even be able to stop drug therapy at that time. Added benefits of weight loss are lower lipid levels and decreased blood pressure.
Alcohol is not metabolized to glucose and it also inhibits
gluconeogenesis in the liver. Too much may result in hypoglycemia as late as 8-12 hours after consumption. Alcohol should not be a substitute for food and should always be taken with food
Has beneficial effects on carbohydrate metabolism and insulin sensitivity
Decreases triglycerides
Decreases blood pressure
May enhance weight loss
May be helpful in preventing or delaying the onset of type 2 DM
Ideally 150 minutes per week aerobic + resistance training 3 time per week
Beneficial for dealing with carbs, increasing insulin sensitivity, decrease triglycerides, decreases BP, decreases weight
Type 1 DM treatment
Educate patient about the risk of hypoglycemia
Exercise alone decreases blood glucose. The combination of exercise + insulin significantly increases the risk of hypoglycemia
you should order what test on these types of patients:
Diabetic patients > 35 years old
Those w/ Type 2 disease for > 10 years
Those w/ Type 1 disease for > 15 years
Those with any other risk factor for CAD
+ presence of microvascular disease
+ presence of peripheral vascular disease
+ presence of autonomic neuropathy
Order a graded exercise stress test or radionuclide stress test for the following
what medications are used in the treatment of DM
Glycemic controlling agents
Lipid lowering agents
Blood pressure lowering agents
Oral agents:
-Stimulate insulin secretion
-Alter insulin action
-Affect absorption of glucose
glycemic controlling agents
Primary preventive strategy for all diabetics men > 50, women > 60 years old, or all diabetics with any one of the following risk factors for CAD:
Increased lipid levels
Family history of premature CAD
ASA therapy: 75-162 mg daily (EC)
Secondary preventive strategy for all diabetics with a history of any of the following conditions:
Transient ischemic attacks (TIA)
Peripheral vascular disease (PVD)
Non-hemorrhagic stroke
MI, angina, or documented CAD
ASA therapy: 75 - 162 mg daily (EC)
Contraindications to use of ASA
ASA allergy, bleeding tendency, anticoagulant therapy, recent GI bleed, hepatic disease
add these (regardless of labs) to those patients who have
Overt CVD
Without overt CVD, < 40 with 1 or more CVD risk factors
lipid control goal for LDL is____
what if overt CVD is present
< 100
<70 if overt CVD present
lipid control goal for HDL is
> 50
lipid control goal for triglycerides is
blood pressure goal
Lifestyle modifications acceptable for first 3 months only
If BP 130-139/80-89
If BP <140/<90 needs mods + meds
if BP is <140/<90 you need
mods + meds
Treat with ACE/ARB FIRST
Use multiple drugs if needed
a diabetic pt with HTN, what is your first line medication for the HTN
recommended vaccines for DM pts
Flu Vaccine annually
Pneumococcal Vaccine
At time of diagnosis
Repeat dose at age 65 if received prior to 65
when should you consider bariatric surgery for a diabetic pt
Consider if BMI > 35
when should you provide your diabetic pt with DSME (diabetes self monitoring education)
Done at time of diagnosis
Done at least annually
Can be done by you, nurse educator, diabetic educator
tobacco cessation is important and you should
Encourage at each visit, assess and document readiness to quit
Average FPG (mg/dl)
Or Preprandial - goal
90 - 130
Avg Postprandial 2 hr
(mg/dl) - goal
< 160
Avg Bedtime Glucose
(mg/dl) - goal
110 - 150
sustained HbA1C - goal
you should initiate action when Average FPG (mg/dl)
Or Preprandial is
<80 or >140
you should initiate action when Avg Postprandial 2 hr
(mg/dl) is
you should initiate action when Avg Bedtime Glucose
(mg/dl) is
<110 or >160
you should initiate action when sustained HbA1C is
greater than or equal to 7%
Sulfonylureas, Meglitinide analogs &
D-Phenylalanine derivative
stimulate insulin secretion
Metformin, Thiazolidinediones
alter insulin action
Alpha-glucosidase inhibitors
affect absorption of glucose
increases pancreatic insulin secretion (secretagogues)
Sulfonylureas (glipizide, glyburide)
Meglitinide analogs (repaglinide)
D-phenylalanine derivative (nateglinide)
what patient population are secretagogues useful in
non-obese/mildly obese
the first class of pills used to treat DM
useful for patients with postprandial hyperglycemia
Repaglinide and nateglinide
Repaglinide and nateglinide
Advantages: long use history, inexpensive, addresses FPG
Disadvantages: hypoglycemia, weight gain
Contraindications: sulfonylureas in severe liver or renal disease
Suppresses hepatic gluconeogenesis; increases hepatic insulin sensitivity
Metformin (a biguanide)
Metformin (a biguanide) is useful in what patient population
obese, normal renal/liver function
Improves lipid profile, no hypoglycemia, inexpensive, weight neutral
dose-related GI side-effects
lactic acidosis occurs in the setting of renal insufficiency or after use of IV contrast agents (50% mortality rate)
serum creatinine > 1.4 mg/dl (females),
> 1.5 mg/dl (males)
concurrent use of IV contrast agents
alcoholics, > 80 years old (unless creatinine clearance is normal), congestive heart failure (CHF)
when you put a patient on these drugs to sensitize their peripheral tissues to insulin you Must monitor liver function by LFTs as mandated by the FDA
rosiglitazone, pioglitazone
MOA of thiazoladinesdiones:
rosiglitazone, pioglitazone
sensitizes peripheral tissues to insulin
in obese, signs of insulin resistance, normal liver function, renal impairment type patients, you can use
rosiglitazone, pioglitazone
how long can it take before you see benefit from thiazoladinesdiones:
rosiglitazone, pioglitazone
2-4 months
can cause fluid retention
rosiglitazone, pioglitazone are contraindicated in
LFTs > 2.5 times normal
when presrcibing oral therapy agents for DM usually one agent is used, when would two agents be called for (initial therapy)
if there is evidence of MARKED hyperglycemia after medical nutrition therapy and physical activity (failure to meet target goal)
titration of oral therapy agents is done over
2-4 months, reinforce medical nutrition therapy and exercise
after the 2-4 month titration period of oral therapy for DM what do you do
recheck plasma glucose or post-prandial glucose or HbA1C:
If the FBS > 140 mg/dl OR
If the post-prandial glucose > 180 mg/dl OR
HbA1C > 7.0%
ADD a drug in a different class
you have begun your patient on a second oral therapy agent, how long is the titration period
Titrate the dose over 2-4 months, reinforce medical nutrition therapy and exercise
(it's the same as when you initially started them on therapy)
after the 2-4 month titration period of oral therapy for DM of two medications what do you do
After 2-4 more months, recheck the FBS, post-prandial glucose, or HbA1C. If values meet the criteria noted (not in target range yet/goals not met) ADD A THIRD ORAL AGENT OR ADD INSULIN
The third oral agent should be of a different class
There is no benefit of adding 2 different secretagogues in combination
Very-rapid acting:
(Ultra short acting)
Short duration INSULIN
Humalog (lispro)
Novolog (aspart)
Apidra (glulisine)
(short acting) INSULIN
Humulin R (regular)
Not used as often, hypoglycemia, variable absorption
Intermediate acting: INSULIN
Humulin N (NPH)
Not used as often, peak at 9 hours
(Ultra-lente) INSULIN
Lantus (glargine)
Detemir (Levemir)
Becoming initial choice, bedtime, titrated 1-3U every 2-3 days
what are the Usual sites for insulin injection?
Abdomen - except for circular area within 2 inches of navel
Thighs - medial, anterior or lateral
Upper arms near triceps or deltoid
where is an insulin injection most rapidly absorbed
the abdomen
where is an insulin injection absorbed slowest
the buttocks
It's a good idea to have patient rotate the site but keep the same site for the same time each day
AM in abdomen, PM in arm or leg, the bedtime shot in the buttocks
what effects does exercise have on insulin absorption
increases insulin absorption so don't have patient inject insulin into the thigh and then go for a run
Type 2 DM: Guidelines for ADDING Insulin to Oral Therapy
Continue oral agent(s) at the same dose
Add a single evening insulin dose (~10 U):
Suggested starting dose 0.1-0.2 U/kg of IDEAL body weight
NPH insulin or Lantus (glargine) (at bedtime)
when adding insulin to oral therapy, what should you do to the oral therapy agents
Continue oral agent(s) at the same dose
when adding insulin to oral therapy, when should the insulin be injected and how many times daily
Add a single evening insulin dose (~10 U):
NPH insulin or Lantus (glargine) (at bedtime)
Insulin NPH/Regular Insulin (Humulin 70/30)
70% of dose is NPH/30% is Regular***(this is the one referred to above)
[Another example of 70/30: Insulin LISPRO (short-acting) - 70% of dose is lispro PROTAMINE/30% is just lispro]
if needed how frequently should you increase insulin doses
Increase insulin dose weekly as needed:
Increase 4 U if FBS > 140 mg/dl
Increase 2 U if FBS = 120-140 mg/dl
70/30 insulin (evening meal) (OBESE)
Adjust dose by monitoring fasting SMBG (self-monitored blood glucose)
Type 2 DM: Guidelines for ADVANCING Insulin + Oral Therapy
indicated when
the FBS is acceptable but:
The HbA1C > 7% and/or
SMBG before dinner > 180 mg/dl
Type 2 DM: Guidelines for ADVANCING Insulin + Oral Therapy
insulin options
To bedtime NPH, add AM NPH and mealtime regular or lispro
To suppertime 70/30, add morning 70/30
Type 2 DM: Guidelines for ADVANCING Insulin + Oral Therapy
options for the oral therapy agents
Usually discontinue the sulfonylurea agent
Continue metformin for weight control (if applicable)
Regulate dose after conditions of normal daily activity and optimal diet have been achieved
Type 1 DM: Insulin Therapy
Once-daily and split-dose regimens (traditional dosing) are INEFFECTIVE for patients with type 1 DM
Results in nighttime hypoglycemia
3 or 4 dose intensive regimens are recommended
what type of insulin would you want to give a type 1 diabetic before meals
Ultra-short acting insulin analogs (lispro) are recommended as more safe and convenient than Regular insulin before meals
an example of insulin doing for a 70 kg adult
5U(breakfast), 4U(lunch), 6U(dinner) Humalog (lispro) before meals;
8-14 U of Lantus (glargine) at bedtime
what is the insulin of choice for an insulin pump
Lispro (ultra short-acting insulin)
Dawn Phenomenon
Slightly elevated or markedly elevated 0200-0300 glucose
Reduced tissue sensitivity to insulin that develops between 0500 and 0800
Attributed to nocturnal rise in GH secretion
treatment for dawn phenomenon
increase bedtime insulin dose
Somogyi Phenomenon
Low 0200-0300 glucose
Nocturnal hypoglycemia stimulates a surge of epinephrine that produces high glucose levels by 0700 (increases glucose release by the liver)
what is the treatment for Somogyi phenomenon
reduce bedtime insulin
Diabetic ketoacidosis
Hyperosmolar nonketotic syndrome
acute diabetic complications
Microvascular (retina, kidney, peripheral nerves)
Macrovascular (coronary arteries, peripheral vasculature)
chronic diabetic complications
at what glucose level would you start seeing s/s of hypoglycemia
Glucose < 55 mg/dl
Hunger, diaphoresis, anxiety, tremors, tachycardia, palpitations, Behavior/cognitive changes, drowsiness, confusion, blurred vision, headaches, amnesia, seizures, coma
Hypoglycemia Symptoms (Glucose < 55 mg/dl)
Common Causes of Hypoglycemia
Too much insulin - most common complication of insulin therapy
In otherwise healthy individuals, suspect the presence of an insulinoma
Too little food
Too much activity
Alcohol-suppresses glucose release from the liver
Oral hypoglycemic agents
Other medications
Menstrual cycle
Gastroparesis: nerve damage delays stomach emptying and food is absorbed slower
treatment for mild hypoglycemia
2 - 3 glucose tablets/gel
(3 gms each)(Dextrosol)
4-6 oz orange juice
4-6 oz regular soda
1/4 - 1/3 cup of raisins
5 Lifesaver candies
Follow with complex
carbohydrates (a glass of milk or a sandwich)
neurogenic hypoglycemia symptoms
hunger, diaphoresis, anxiety, tremors, tachycardia, palpitations
neuroglycopenic hypoglycemia symptoms
behavior/cognitive changes, drowsiness, confusion, blurred vision, HA, amnesia, seizures, coma
home treatment for Moderate - Severe Hypoglycemia (The Patient is Unresponsive)
glucagon kit:
Contains one ampule (1 mg)
Should be provided to every patient receiving insulin therapy
Patient and family and/or friends should be instructed on use
If the glucagon kit is used and the patient regains consciousness
they should immediately consume simple carbohydrates followed by a snack with complex carbohydrates
If the patient presents to the ER with mental confusion, bizarre behavior, seizures, or coma you should think about
Patients in a deep hypoglycemic coma appear
appear adequately hydrated, are generally flaccid, and have quiet breathing. There is no Kussmaul breathing as with diabetic ketoacidosis.
Moderate-Severe Hypoglycemia ER treatment
Insure an adequate airway
Give IV glucose (50 ml of 50% glucose solution)
Once the patient is conscious, they may sip fruit juice
If IV glucose is not available, give glucagon 1 mg IM
what can be used for a pt in a hypoglycemic coma if IV glucose is not available
give glucagon 1 mg IM
a patient with type 2 DM is suffereing from acute illness, what must you consider
diabetic ketoacidosis
risk factors for DKA
Infection - 30%
Lapse in insulin administration - 15 - 41%
Recent onset diabetes - 17 - 25%
Medical illnesses - 10%
Trauma, alcohol, steroid use - 10 - 20%
Idiopathic - 2 - 25%
Polyuria, polydipsia for 1-2 days, progressing to:
Fatigue, nausea, vomiting
Mental stupor that can progress to coma
Symptoms of DKA
Dehydration in a stuporous patient
Rapid, deep breathing (Kussmaul's respirations)
"Fruity" breath odor (presence of acetone)
Tachycardia, hypotension
May have abdominal pain/tenderness
signs of DKA
Hyperglycemia (glucose > 250 mg/dl) - Due to decreased glucose uptake by tissues + hepatic gluconeogenesis
Ketonemia (elevated serum acetone)
Elevated levels of GH, catecholamines and glucagon cause increased lipolysis from adipose tissue and increased liver ketone production
laboratory findings DKA
Low arterial blood pH (< 7.3)
Low plasma bicarbonate (< 15 mEq/L)
4+ glycosuria
Elevated serum potassium - may not reflect body potassium depletion
Elevated serum osmolality
The increased lipolysis contributes to elevated levels of free fatty acids (FFAs).
These FFAs (in large amounts) become available to the peripheral tissue cells (to be used for energy fuel) and to the liver cells where many of them are converted to ketone bodies
These large amounts of ketone bodies are only partially oxidized by peripheral cells and the remainder build up in the blood, and eventually the urine, and can be measured.
managing DKA:
There is a 4-5 liter fluid deficit in most patients
Failure to provide adequate volume replacement is the most serious therapeutic error that adversely affects recovery
Restore circulating plasma volume:
Most important in the therapy of DKA is the restoration of circulating plasma volume with maintenance of cardiac output and renal function. Fluid by itself decreases the levels of counter-regulatory hormones and increases renal perfusion which will resolve the hyperglycemia and acidemia.
Management of DKA, after you have initiated fluid restoration
Regular insulin 10 U IV after 30 minutes or 0.1 U/kg/hr
The goal is to maintain a glucose level of 250-300 mg/dl to decrease the risk of cerebral edema and hypoglycemia
If acidosis is refractory or the pH < 7.0, give 100 ml bicarbonate over 45 minutes
Management of DKA during 2nd and 3rd hours of fluid resuscitation as soon as the acidosis starts to resolve
Give potassium chloride 10-30 mEq/L during 2nd and 3rd hours of fluid resuscitation as soon as the acidosis starts to resolve
ECG monitoring
Frequent monitoring of serum osmolality
Search for a precipitating cause
DKA Prevention: Sick-Day Guidelines
Test urine ketones every 2-4 hours
The patient is to call if their blood glucose > 250 mg/dl for > 6 hrs The patient is to continue taking insulin
The patient should eat and drink fluids if possible
If the patient can't eat
DKA Prevention: Sick-Day Guidelines
they should drink carbohydrate-containing liquids
Occurs in patients with mild or undiagnosed DM
Most patients are middle-aged or elderly (type 2 diabetics)
Underlying CHF or renal insufficiency is common
Hyperglycemic Hyperosmolar State
etiologies of Hyperglycemic Hyperosmolar State include
Myocardial infarction
Post-operative states
Insidious onset of polyuria, polydipsia and weakness over several days or weeks
Lethargy, confusion, coma Profound dehydration
ABSENCE of Kussmaul's respirations
NO acetone breath odor
Hyperglycemic Hyperosmolar State
High mortality rate due to the insidious organ dysfunction and delayed diagnosis
10 times the mortality rate of DKA!
Hyperglycemic Hyperosmolar State
Severe hyperglycemia - a blood glucose level of 600-2400 mg/dl
Moderate to severe dehydration is common
initially hyponatremia then there is a gradual increase in serum sodium
serum urea nitrogen is elevated
Hyperglycemic Hyperosmolar State
Treatment of Hyperglycemic Hyperosmolar State 1st step
Fluid replacement - very important!
4-6 liters over 8-10 hours is usually required
Hypovolemic: normal saline (0.9%)
Not hypovolemic: 0.45% NS - avoids contributing to the hyperosmolar state
in the treatment of a diabetic patient with HHS
Once the serum glucose < 250 mg/dl, give 5% dextrose in water (D5W), 0.45% saline or 0.9% saline (the goal is to maintain serum glucose levels of
250-300 mg/dl thereby decreasing the risk of cerebral edema and hypoglycemia
what about insulin therapy for a patient in HHS
lower doses than in DKA as the patient may be insulin sensitive
Fluid replacement alone may adequately reduce the hyperglycemia by increasing the GFR and renal excretion of glucose
potassium replacement for patients in HHS
Potassium replacement - 10 mEq/L given during initial IV fluid administration if the serum potassium is not elevated
Look for an underlying cause
Chronic Complications of Diabetes
Macro vascular: Accounts for ____% of deaths in Type 2 diabetics
Coronary artery disease
Peripheral artery disease
Cerebrovascular disease
Background retinopathy
Microaneurysms, hemorrhages, exudates, edema
Preproliferative retinopathy
Cotton-wool spots (arteriolar ischemia)
Proliferative retinopathy
retinal ischemia promotes neovascularization
Therapy: panretinal photocoagulation
Reduces level of growth factor and neovascularization
Acute loss of visual acuity
Fluctuating visual changes
Floating spots
Flashing lights
Ocular pain
Ocular complaints to worry about in patients who have had DM for more than a few years
Question the patient at each visit about any of these symptoms
how often should you screen a type 1 diabetic for microalbuminuria
Type 1 DM: screen 5 years after diagnosis then yearly
how often should you screen a type 2 diabetic for microalbuminuria
screen at time of diagnosis then yearly (after blood glucose has stabilized)
will Routine urine dipstick testing for protein screen for microalbuminuria?
no, it will not
what is the assay of choice for screening for microalbuminuria
A morning spot urine screen for the albumin/creatinine ratio is the assay of choice:
If the spot albumin/creatinine ratio is 30-300 mcg/mg, confirm microalbuminuria with at least 2 of 3 positive collections performed within 3-6 months
what may alter (elevate) urinary protein excretion
Exercise, a UTI, heart failure, or a fever may falsely elevate urinary protein excretion
microalbuminuria management meds:
Used in normotensive type 1 diabetics
Many providers use in type 2 diabetics for its renal-protective effects
ACE inhibitors ("pril" drugs)
blood pressure goals in patients with microalbuminuria
Angiotensin II receptor blockers Cozaar or Hyzaar (losartan)
Maintain BP < 130/80
<120/75 for patients with proteinuria > 1 gram/24 hours
Repeat an A:C (Albumin:Creatinine)ratio every 6 months
Progressive Diabetic Nephropathy
Continued BP control
Protein sparing diet (0.6-0.8 g/kg/day)
Within 5 yrs, 50% of patients have a 50% decline in GFR
In the next 3-4 yrs, 50% will have ESRD - a renal transplant may be required
Remember to think twice before ordering contrast radiographic studies in patients with
diabetic nephropathy
Types of Peripheral neuropathy
Distal symmetric polyneuropathy
Isolated peripheral neuropathy
Painful diabetic neuropathy
Bilateral, symmetrical nerve involvement
"Glove and stocking" distribution
Primarily sensory (with/without motor)
Dullness of vibration, pain, temperature perception
describes what type of peripheral neuropathy
Distal symmetric polyneuropathy Symptoms of numbness, hyperesthesias, paresthesias, pain may progress to sensory loss
Early detection is emphasized:
Distal reflexes
Distal vibratory sensation
Distal light touch perception
how should you treat a patient with Distal Symmetric Polyneuropathy
Tight and stable glucose control will slow the progression
May involve one nerve or several nerves
The onset is acute
The femoral and cranial nerves are most commonly involved
Recovery of all or most function usually occurs in 6-12 weeks
Example: CN III palsy
describes what type of peripheral neuropathy
Isolated Peripheral Neuropathy
Hypersensitivity to light touch
Severe burning pain, especially at night
painful diabetic neuropathy
Elavil (amitriptyline)
Norpramin (desipramine)
Neurontin (gabapentin)
Capsaicin cream
are treatments for?
painful diabetic neuropathy
Autonomic Neuropathy
GI tract: Gastric dysmotility, Gastroparesis, Constipation, Diarrhea
urinary retention or incontinence
erectile dysfunction
Reglan (metoclopramide), Propulsid (cisapride)
are used to treat
lmodium (loperamide)
Lomotil (diphenoxylate)
treatment for
Sildenafil (Viagra) - 50-60% improvement
Intracavernous injection of vasoactive drugs (papaverine)
External vacuum therapy
Implant of penile prostheses treatments for
Erectile dysfunction
macrovascular cardiac complications
Myocardial ischemia/infarction:
Diabetes eliminates female advantage
Macrovascular Complications
TIAs, stroke
Peripheral vascular disease
Management of Macrovascular Complications
Keep BP less than 130/80
ACE inhibitor therapy
Angiotensin II receptor blocker
Remember beta-blockers may mask hypoglycemia
Low-dose aspirin
Tobacco cessation
what do you need to remember about beta-blockers
they may mask hypoglycemia
Management of obesity and dyslipidemia - GOALS
LDL < 100 mg/dl (< 70 mg/dl for pts with CAD)
HDL: > 40 mg/dl (males), > 50 mg/dl (females)
Triglycerides < 150 mg/dl (fasting)
what are the drugs of choice for lipid control in diabetics
the LDL goal for an obese diabetic
the HDL goal for an obese diabetic
the triglyceride goals for an obese diabetic
< 150 mg/dl (fasting)
at risk diabetic foot
oss of protective sensation; absent pedal pulses; foot deformity; history of foot ulcer; prior amputation; smokers; history of retinopathy, nephropathy; those receiving anticoagulant therapy; those who cannot see, feel, or reach their feet
Summary of "P" (Management)
Diabetes education class
Dietary consult
BP, pulse, height, and weight at every visit
Foot exam (including pulse) at every visit, monofilament exam annually FBS, UA, Chem 10, HbA1C at every visit (2-4 times yearly for stable patients)
Goal fasting glucose: 110-120 mg/dl
Goal HbA1C is < 7.0%,
ideally < 6.5% (if they meet criteria)
Serial microalbumin at initial diagnosis and annually (type 2 DM) Lipid profile annually (fasting cholesterol, triglycerides, LDL, HDL)
Ophthalmology referral at diagnosis and annually (type 2 DM)
Pneumovax vaccine (once) and influenza vaccine yearly
Tobacco Cessation
Summary of "P" (Management)
Initiate ACE inhibitor therapy
Daily low-dose aspirin
Oral agent/insulin
Lipid lowering agent
Glucometer, strips and lancets
Baseline ECG
MedicAlert bracelet or necklace and wallet card