-a rise in blood glucose

between 4 AM - 8 AM

that is NOT a response to

HYPOGLYCEMIA

-can occur in Type 1 & Type 2 DM

-possibly related to nocturnal increases in growth

hormone which decrease peripheral uptake of glucose

-a combination of HYPOGLYCEMIA during the night with a REBOUND MORNING RISE in blood glucose to HYPERGLYCEMIC levels

-stimulates counterregulatory hormones

which inhibit peripheral glucose use

which may cause insulin resistance  for 12-48 hours

- the breakdown of fatty acids, producing ketones as a by-product of metabolism

-BG > 250-300 mg/dL--a severe metabolic complication of uncontrolled diabetes that if untreated, leads to diabetic coma and death

 -symptoms: metabolic acidosis (ABG), ketones in the serum, dehydration, electrolyte imbalance--low potassium levels; thirst, weakness, dry skin, rapid pulse, hypotension, urination, fruity breath, abdominal pain, vomiting

-treatment: fluid and electrolyte replacement and intravenous unsulin therapy

-usually affects Type 1

-predisposing factors: infection, stress, lack of insulin

*Late- severe lethargy, coma, Kussmaul’s breathing.(deep & rapid)

-a metabolic complication of of uncontrolled Type 2 diabetes, similar to DKA, but without ketosis and acidosis

-treatment involves fluid and electrolyte replacement as well as intravenous unsulin therapy

*BS >  600 mg/dL

Usually affects patients with Type 2 than have an underlying infection

Main precipitating factor: dehydration

Manifestations:  negative for ketones,  negative for acidosis

(+++) dehydration , altered  CNS function (seizures, confusion, coma)

Those most at risk to diabetic ketoacidosis are

people who are sick, have an infection,

or who decrease/omit insulin doses

-the most common precipitator of DKA & HNKS is some type of phisical or emotional stress

-produced by alpha cells in the pancreas

-stimulates the breakdown of glycogen in the liver,

the formation of carbohydrates in the liver, and the breakdown of lipids in both the liver and adipose tissue

 -primary function is to decrease glucose oxidation and to increase blood glucose levels

-prevents blood glucose from decreasing below a certain level when the body is fasting or between meals

-usually iniitiated when bg ~ 70

breakdown of liver glycogen

formation of glucose from fats and proteins

Type 2 DM is by far the most common

-accounting for at least 90% of all cases in the US

 •Resulting in increase blood glucose levels

~Insulin resistance implies  decreased tissue sensitivity to insulin

4 Major Classifications: Type 1: (5-10%), Type 2: (90-95%)

Gestational: (2-5% of all pregnancies), Other Specific Types

-produced by beta cells in the pancreas

-facilitates the movement of glucose across cell

membranes into cells, thus decreasing blood glucose levels

-prevents excessive breakdown of glycogen in the liver and in muscle, facilitates the formation of lipid while inhibiting the breakdown of stored fats, and helps to move amino acids into cells for protein synthesis

-produced by delta cells in the pancreas

-believed to be a neurotransmitter that inhibits the production of both glucagon and insulin

Type 1 DM results from destruction

of beta cells in the pancreas,

the only cells in the body that make insulin

Type 1 DM (also called juvenile or insulin dependent)

-the autoimmune process which slowly destroys beta cell production

of insulin usually occurs over a long preclinical period

with the onset of hyperglycemia occurring when

80-90% of beta cell function is lost, resulting in severe insulin deficiency

-onset 11-13 years of age

-lean body type

-positive antibody in islet cells

-Type 1 DM most often occurs in childhood and adolescence, but it may occur at any age, with a rapid onselt of symptoms

-Genetic predisposition plays a role and triggers can be exposure

to a virus or chemical toxin > autoimmune response

Type 2 DM 

develops during pregnancy;

having gestational DM predisposes a woman to developing Type II DM in later years; hyperglycemia can occur during pregnancy due to secretion of placental hormones;

this can occur in as many as 18% of pregnant women

-3 P's: Polyuria - excessive urination

          Polydipsia - excessive thirst

         Polyphagia - excessive hunger

-recent weight loss (but client my be overweight)

-fatigue

Also:

-ketoacidosis (on initial presentation in 30-40% of cases)

-short duration of symptoms

-initial period of decreased insulin requirement,

then need of insulin for survival  

-blood glucose monitoring

-insulin

-dietary management, balancing carbohydrate        intake to insulin

-exercise

-obesity (waist circumference >35 for females/>40 for males)

-coronary heart disease

-dyslipidemia (triglycerides >150 / HDL <50 females & <40 males)

-hypertension (blood pressure >130/85)

-microalbuminuria (spilling of protein into the urine)

-increased risk for thrombotic (blood clotting) events such as stroke (cerebrovascular accident)

-peripheral vascular disease 

-for Type 2 DM, the ADA recommends the use of aspirin for prevention of coronary artery disease & antihyperlipidemic drug therapy

What are the clinical manifestations of Type 2 DM?

-symptoms are about the same as Type 1 DM, but polyphagia and weight loss are uncommon

-onset >30/40 years old

-obesity

-increasing in younger children

-insidious onset (may take several years to have symptoms)

-isulin resistance with normal or decreased insulin secretion

-other manifestations that result from hyperglycemia include blurred vision, fatigue, paresthesias, and recurrent skin infections 

-acanthosis nigricans (skin condition characterized by areas of dark, velvety discoloration in body folds and creases), long duration of symptoms, lipid disorders, hypertension, androgen-mediated problems (acne, hirsutism, menstrual disturbances, polycystic ovary disease), excessive weight gain and fatigue caused by insulin resistance

-diet with decreased calories and low-fat foods

-decrease sedentary activity time,

or increase routine physical activity

-blood glucose monitoring

-oral medication (metformin) to improve insulin sensitivity

-occurs in people who have Type 2 DM

-characterized by a plasma osmolarity of 340 or greater (normal range is 280-300), greatly elevated blood glucose levels, and altered levels of consciousness/seizures

-results in severe dehydration, including the brain

-is a serious, life-threatening medical emergency

-mortality is high--even higher than DKA

-establishing & maintaining adequate ventilation

-correcting shock with adequate IV fluids

-if pt. is comatose, instituting nasogastric suction to prevent aspiration

-maintaining fluid volume with isotonic IV fluids or colliod solutions, administering potassium IV to replace losses

-administering insulin to reduce blood glucose, usually until levels reach 250 (because there is no ketosis)

-also known as insulin shock, insulin reaction, "the lows"

-blood glucose <45-60

-give 15g of a rapid-acting sugar orally

(3 glucose tablets, 1/2 cup fruit juice/soda,

8 oz skim milk, 5 Life Savers candies,

3 lg marshmallows, 3 tsp sugar/honey)

after giving 15g of sugar to treat hypoglycemia, wait 15 minutes and monitor bg levels, and if it is still low, administer another 15g of sugar and repeat until bg level is normal

disease of the kidneys characterized by the presence of albumin in the urine, hypertension, edema, and progressive renal insufficiency

-in the US, this disorder accounts for 44% of new cases of end-stage renal disease requiring dialysis or transplantation

-changes in the retina that occur in the person with diabetes due to alterations in blood flow, retinal ischemia and loss of vision

-is the leading cuse of blindness in people between

20-74 years of age (12,000 - 24,000 new cases per year)

-3 stages: I nonproliferative retinopathy

II & III proliferative retinopathy

somatic/sensory neuropathy: 

–cold feet, pain numbness/tingling, fatigue on lower extremities

–may lead to infection, ulceration and gangrene of feet

Drugs used to treat peripheral neuropathy:

-Analgesics (pain killers)

-TCS's (tricyclic antidepressants): amitryptyline/Elavil, doxepin/Sinequan

-SNRI (serotonin-norepinephrine reuptake inhibitor antidepressant):  duloxetine/Cymbalta

-Anti-seizure drugs: pregabalin/Lyrica

Prevention & Treatment: control BG, do not smoke, routine assessment of feet q visit, proper foot wear, avoiding foot trauma, do not self-treat foot problems, foot care teaching *do not cut toenails* see podiatrist

-combination of antidepressant medications and psychotherapy focused on restoring logical thinking and problem-solvingskills

-correcting misconceptions about depression

-identifying individual strengths in managing diabetes

-acknowledging negative feelings that may be expressed

-suggesting problem-solving behaviors to better manage the disease

Visceral neuropathies:

Sweating disorder (anhydrosis--reduced or no sweating)

Bladder dysfunction (Urinary retention)

GI dysfunction (Delayed gastric emptying and constipation)

Sexual dysfunction (Impotence)

Cardiovascular dysfunction (Orthostatic hypotension)

DM affects an estimated 25.6 million people in the United States and is the 7th leading cause of death.

 One third of these cases are undiagnosed.

 It lowers life expectancy by 15-20 years.

 Increase heart disease 2 to 4 times and is leading cause of death from CVD, MI, Stroke and Peripheral Vascular Disease

 Leading cause of amputations, blindness and end stage renal disease

 Healthy People 2020 lists 16 objectives related to diabetes.

        —HgbA1c  at or > 6.5%

glycosylated hemoglobin

Glycosylated Hgb is useful in determining blood glucose control for the previous 90-120 days. What is the rationale behind this test? Glucose attaches to Hgb and remains attached throughout the life span of the RBC (90-120 days). When blood glucose is elevated over time, the amount of glucose attached to the Hgb molecule increases and remains attached to the red blood cells  for the life of the cell.  The normal hemoglobin A 1 c is between 4 and 6. 

3.Hgba1c is 5.7% to 6.4%

Secondary Diabetes:

Development of DM may also be secondary to another medical condition such as Cushing’s Syndrome or hyperthyroidism or the result of treatment of a medical condition that causes abnormal blood glucose levels (for example TPN--Total Parenteral Nutrition/ high Dextrose based IV infusion, Steroids)

Gestational Diabetes usually is discovered in the 2nd or 3rd trimester of pregnancy. Urine dip sticks done at every visit to monitor for glucose, ketones and other abnormalities that could occur.  To detect his alteration early in pregnancy all women who are pregnant are screened at 24- 28 weeks, especially if there is are risk factors for GDM in previous pregnancies or obesity. The client receives a 50 gram oral GTT.  If the BG is greater than 140 mg/dL at one hour, a three hour GTT is then performed.

–For a Type 1 DM who is pregnant the Glycosylated Hemoglobin (HbA1c) will give indicative information of how glucose is managed

For treatment, medications may include oral hypoglycemic agents and insulin which must be carefully regulated and adjusted as pregnancy progresses.  Glucose testing will continue and teaching of the S/S of hypo and hyperglycemia are reinforced.  Office visits may be more frequent with urine and weights evaluated at each visit.  Fetal surveillance may be required with the use of ultrasound and non-stress tests (determine the longevity of the placenta). Delivery is around week 39 and is based on the biophysical profile to reduce the risks for stillbirth caused by a premature placental aging.  

 —If GD is Dx in third trimester oral agent may be used 

A1c (glycosylated hemoglobin)

random glucose

fasting glucose (preferred)

Oral Glucos Tolerance Test (OGTT)

diet, exercise, meds

(triad of diabetes treatment)

hypoglycemia

allergic reaction (local)

systemic(rare)

lipodystrophy (pitting it dimpling in skin)

Dawn’s phenomenon

Somogyi’s phenomenon

Continue to take insulin even if unable to eat.

Monitor BG Q 4hrs, check ketones w/ every void, do not skip insulin

replace food and fluids (warm jello, Gatorade, fruit juice)

know when to call health care provider…when ketones present and

when BG is < 60 or >250, when unable to eat for 24 hrs and if diarrhea and vomiting for 6 hrs or more

1st Gen: chlorpropamide/Diabinese

2nd Gen: glyburide/Diabeta (Book: glipizide/Glucotrol, glimerpiride/Amaryl)

-MOA: stimulates the pancreas to secrete insulin

-Complications: hypoglycemia, weight gain, skin rash, nausea, epigastric fullness, heartburn

-oldest group of oral antidiabetic drugs still being used

-these are used in the early stages of Type 2 DM and are not used for Type 1

-can be used with metformin but should not be used with insulin

Metformin (this is the only drug in its class)

-has to be taken with food

-mechanism of action: decrease hepatic production of glucose, augments glucose uptake by muscle and fat tissue

-complications: diarrhea, GI distress, and lactic acidosis--especially in renal patients, it lowers GI absorptions of carbs

*needs to be held 48 hrs before and after IV contrast or radiologic procedures 

-used for Type 2, not Type 1; may be combined with insulin

-also used in pre-diabetes

-contraindicated in pts with renal disease/dysfunction, because Metformin can accumulate, increasing the risk of development of lactic acidosis

"Thiazolidine-diones" (glitazones):

Avandia/rosiglitazone (Book: was removed from market in 2011 due to cardiac problems, can only be obtained through specialized manufacturer programs)

Actos/pioglitazone (the only TZD currently availabe and is widely used)

-MOA: enhance sensitivity of insulin receptors, stimulate glucose uptake/ storage in the muscles, and inhibit hepatic gluconeogenesis

-Complications: weight gain, fluid retention/peripheral edema, heart failure, reduced bone mineral density/increased risk of fracture, may cause a rise in liver enzymes

-slow onset of activity ver several weeks 

-may be combined with metformin & solfonylurea, can also be used with insulin

Precose/acarbose & Glyset/miglitol: Starch blockers

MOA: bind to alpha-glucosidase enzymes in the small intestine and inhibit the ability of enzymes to  breakdown complex CHO into simpler starches and in turn into glucose; this action delays absorption of sugar into the blood from the gut and helps prevent sudden surges of glucose after eating, thus preventing postprandial hyperglycemia

Complications: abdominal discomfort, gas, diarrhea; may cause rise in liver enzymes

-must be taken with food, impractical for directly lowering fasting blood sugar; used for Type 2, not for Type 1

-contraindicated for IBD (inflammatory bowel disease), malabsorption syndromes, or intestinal obstructions

Prandin/repaglinide, Starlix/nateglinide (note: end in glinide)

-MOA: stimulate sudden and short lived surges of insulin from the pancreas

-Complications: hypoglycemia and weight gain

-can be used with metformin & TZD's, but not with sulfonylureas or insulin 

*These drugs became available in the US in 1998; they are similar to sulfonylureas only they are shorter-acting; since they require glucose to work, they are taken 30 minutes before or right after meals

Anti-hypertensives:

• ACE--angiotensin converting enzyme--inhibitors: (-prils); dry cough, dizziness, angioedema; these lower b/p and preserve kidneys
• ARB's--angiotensin receptor blockers: (-sartans/Divan); cause dizziness, hypotension
• CCB--calcium channel blockers: (verapamil, diltiazam, amlodipine, felodipine, nefedipine); cause dizziness, headache, swelling ankles
• diuretics

-Antiplatelet agents: Plavix and Aspirin

-Lipid-lowering drugs: Niacin & -statins* (*cause nausea, diarrhea, constipation, muscle and joint pain which could lead to rhabdomyolysis--breakdown of muscle tissue that leads to the release of muscle fiber contents into the blood--these substances are harmful to the kidney); other serious side effect is liver damage

*Note: for meds lowering b/p, teach dizziness side effects/precautions;

These drugs are contraindicated in those over age 80 and  in those with impaired hepatic function or excessive alcohol intake.

It is necessary to emphasize to all diabetic patients  that oral agents are only effective in controlling diabetes if balanced with the correct diet and exercise regimens.

The patient with diabetes has an increased risk for gingivitis and periodontal disease and therefore will benefit from regular dental visits. Almost one-third of people with diabetes have severe periodontal disease with loss of attachment of the gums to the teeth measuring 5 millimeters or more.

Sick day management (when a diabetic is sick, BG levels increase):

-Monitor BG every 4 hours & check ketones with every void

-Pts with Type 2 can develop ketosis--it is possible to have + ketones with  normal or near normal BG levels

-Do not skip insulin!

-Replace food/fluids: 50 grams carbs/meal, 15 gms of carbs/hour while awake, Gatorade 1 cup, 6 saltine crackers, 1/2 cup vanilla ice cream,     chicken noodle soup 1 cup, regular gelatin ½ cup 

-Must see a health care provider if he is too sick to eat or vomiting and cannot keep food down; have frequent diarrhea; have moderate to large ketones in the urine; has BG under 60 or stays over 300; or if he feels short of breath, sleepy, or have trouble concentrating

Immunizations:

-Annual influenza vaccine to all diabetic patients ≥6 months of age             -Pneumococcal polysaccharide vaccine to all diabetic patients ≥2 years old  -A one-time re-vaccination is recommended for individuals >64 years of age previously immunized when they were <65 years of age if the vaccine was administered >5 years ago

-More aggressive antibiotic treatment due to higher risk for infections

Hospitalized patients may be placed on insulin

Surgical patient may require prophylaxis

Mild Hypoglycemia: BG <70  *Requires immediate attention*

Due to: insulin excess, sulfonylurea agents, alcohol and other drugs, increased activity/exercise, lack of food; Onset is always rapid

Symptoms of Hypo-glycemia: 

*Some patients do not experience the warning signs and symptoms of hypoglycemia. This absence of signs and symptoms is called hypoglycemic unawareness. Those that have hypoglycemic unawareness are those that are elderly, have long-standing Type I DM, and those that are on beta adrenergic blockers for tx of hypertension.

-At the first sign of hypoglycemia, blood glucose should be checked.

-If it is < 70, treatment is initiated with 15 g of simple carbohydrates

-Blood glucose is rechecked in 15 minutes and treatment is repeated if glucose is still < 70

15 g of carbohydrates:

½ cup pure fruit juice

6 oz. regular soda

4 cubes or 2 packets of sugar

3 (5 g) glucose tablets

1 tube of prepackaged glucose gel

1 cup reduced fat milk

2 tbsp raisins

1 tbsp syrup 

10 rolled hard candy (LifeSavers) 

Some textbooks classify hypoglycemia as mild if the BG is between 40 and 60 and the patient is alert and awake.

Moderate: -If the BG is between 20 and 40 and the patient is awake, the patient is given 30g of carbs instead of 15g

-Whether the hypoglycemia is mild or moderate, the BG is rechecked after 15 minutes and treatment is repeated depending on the BG 

-If the patient is not alert enough to swallow, 1mg of glucagon SQ or IM may be given

Severe: -If the patient has severe hypoglycemia  (<20) while in the hospital (or if unconscious), 1 amp of 50mL Dextrose 50% (25g) maybe given by IV push; IV push rate  for D50 is 10 mL/minute  and may be followed by an IV infusion of D5W

-the patient usually regains consciousness in one minute

-after a hypoglycemic episode, the patient needs to be given protein snacks such as peanut butter or cheese to prevent a similar episode

-Glucagon is available in powder form. It must be reconstituted with the accompanying diluent  immediately before use. Glucagon causes nausea so placing the patient in side-lying position after an injection of glucagon will prevent him from aspirating if he does vomit

-requires immediate attention

-untreated for a length of time will cause complications

*When a person has type 1  or type 2DM,  illness, stress, infection can exacerbate the hyperglycemia and put the patient in a severe metabolic state

There are 2 forms of hyperglycemia:

     -diabetic ketoacidosis (DKA)

     -hyperglycemic hyperosmolar  non-ketotic syndrome (HHNS)

-FLUID VOLUME DEFICIT

-Altered Electrolyte balance

-Impaired Thought Processes

-Risk for altered tissue perfusion

Another concept to consider in the diabetic diet is the glycemic index.  GI is the direct impact of food on BG levels. Some of the factors that influence GI include type of starch, viscosity of fiber, cooking, processing, acid content, protein content, fat content, and sugar content. Foods that have high GI are also called “gushers” They are quickly digested carbs, promote rapid spikes in BG, and promote fat storage. Low GI foods are “tricklers”

They are preferred over “gushers”.

-Glucose: renal threshold for glucose differs among individuals

-Ketone: (+ ) indicates impending diabetic ketoacidosis

perform test: -during acute illness or stress; BG >250; pregnant; s/s of HKA

-Renal function: 24-hour urine 

*Urine maybe checked for glucose or ketones. An estimate of the amount of glucose in the urine maybe done by dipstick method and read for color changes after one minute. Urine glucose does not reflect blood glucose at time of test. Also individuals vary in their renal threshold for glucose. Older people will not spill glucose into their urine until their blood glucose reaches close to 200 mg. That makes urine testing for glucose inaccurate for determination of blood glucose.

The ADA recommends that all clients with DM be taught to monitor their blood glucose,especially those on insulin. SMBG using a blood glucose meter is recommended to be done at least 3x/day or more especially for Type I patients since their bodies do not regulate the insulin after it is injected.

SMBG’s are to be done when there are modifications in therapy whether it is a change in diet, drug regimen, or exercise regimen. They need to be done when the patient is ill or pregnant or feeling s/s of low or high blood glucose. SMBG’s are usually done before breakfast-, before lunch, before dinner, and before bed time (4 befores). They are not used to Diagnose but to manage and help the patient be more informed of their blood sugars.

There are many currently available blood glucose monitoring machines and most health insurance policies cover the cost of these. Each machine has specific instructions that need to be learned by the patient. These devices should not be shared and used by only person. It is better to avoid the middle pad of the finger for needle sticks. 

–FDA & CDC recommendation (Aug. 2010)

-Children or siblings of Type I patients who are + for islet cell cytoplasmic antibodies have a 50% chance of developing Type I

Even then, screening is not recommended in siblings until clinical trials demonstrate efficacy and safety of treatment (insulin, sulfonylurea, immunosuppressant)  to prevent or delay the development of DM

Keep in mind that the incidence of Type I is “low”

Type II  incidence is high and many millions are undiagnosed; It is recommended that screening be done at age 45 using fasting BG or OGTT; if results are normal, the test is done every 3 years; if the individual is considered high-risk, screening is done at a younger age and/or more frequently

Who is considered high-risk for DM?

4.  Those with HTN

Triad of Treatment: Diet, Exercise, & Medication

GOALS: To normalize insulin activity & blood sugar levels with proper nutrition, exercise, medication, education, and monitoring.

HgbA1c-  < 7% & BG=WNL

To lower risk for complications

*The hallmarks of diabetes management include nutrition, exercise, anti-diabetes medications, education, and monitoring. The immediate goal is to normalize blood glucose levels which in turn will lower the risk for complications.

Within the first 12 weeks of diagnosis, the patient is to receive a minimum of 10-12 hours of instruction which is essential for successful diabetes management. 

Nutrition is the cornerstone of care for the diabetic. The meal plan for diabetics  should be balanced and include all food groups. The emphasis is on blood glucose control, NOT weight loss. There is no “ideal” diet.

In some Type II patients, diet alone is sufficient for glucose control. Reduction in caloric intake is essential for overweight or obese patients and 10-20 lb loss regardless of initial weight or 5-10% of initial body weight is desirable.

In Type I, diet alone is not enough for glucose control. Along with insulin injections, they need to have equal distribution of carbohydrates. Snacks arevery important.

Focus: healthy food choices & balanced meal plans

Specific nutritional goals: -Achieve optimum serum lipid levels by reduction of total fat --especially saturated fats andprovide adequate calories for maintaining or attaining reasonable weights with moderate caloric restriction

Carbohydrates: 50-60%

Proteins: 10-20%   (10% if  (+)  diabetic nephropathy)

Fats: 20-30%   (Avoid saturated fats and trans fats; decrease cholesterol to <300 mg/day)

Fiber: 25-30 g/day 

The general dietary recommendations for diabetics is the same for the general population.

Fifteen to 20% of total daily calories should come from proteins.

Fats compose 20 to 30% and should be non-saturated fats.

Cholesterol intake should be less than 300 mg/day. 

CHO in the form of whole grains, fresh fruits/vegetables should constitute the remaining percentage of calories. Simple sugar in moderation is okay.

Fiber requirements are the same as for the general population.

-a system to identify the caloric content of a food based on the number of carbohydrate, fat, and protein grams that are in that food.  There are six main exchange lists- bread/starch, vegetable, milk, meat, fruit, and fat. Foods within one group (in the portion specified) contain equal numbers of calories and are approx equal in grams of protein, fat, and carbohydrate. To make it simpler for the average person, one serving of meat maybe compared to a deck of cards or the palm of a woman’s hand.

One half cup of vegetables is the size of half a tennis ball; 1 cup of broccoli is about the size of a light bulb; a cup of pasta/rice is about the size of a clenched fist.

2 starchs  = choice of 2 slices of bread, one hamburger bun,  OR 1 cup cooked pasta

One serving of carbohydrate

Apple 2 inches in diameter

One slice of bread

Vegetables/meat are counted as 1/3 of a carbohydrate serving

Portions sizes

3 oz beef, chicken or fish equals the palm of your hand.

1 cup of pasta OR rice

1 cup of broccoli

[image]

1/2 plate of low calorie vegetables

Not more than 3-4 oz lean meat or other protein (size of a deck of cards)

Not more than 1/4 plate whole grain carbs with fiber (size of a woman's fist

 Moderation defined as

No more than 2 drinks /day (males) and one drink/day (females)

                                       Can cause hypoglycemia 

*Alcohol precautions for diabetics are the same as for the general public as long as the diabetes is well-controlled. The key word is  Moderation : which means no more than 2 drinks per day for men and one for women. One drink is approx 135 calories. The preferred alcoholic bev for diabetics is light beer. The effect of ETOH on the BG is dependent on both the amount ingested and relationship to food intake. Alcohol is NOT metabolized to glucose and inhibits gluconeogenesis therefore if ETOH is consumed without food by people on insulin/hypoglycemics, it can cause hypoglycemia.

So diabetics need to take alcohol with food. They also must use sugar-free mixes, and drink dry light wines.

Sweeteners are deemed safe for diabetics. They do not raise blood glucose. Remember anything artificial from chemicals can have risks so it is important to educate the clients to refrain from all sugars in general.

“Sugar-free” foods are not “free” foods to be eaten in unlimited quantities; they still have calories and usually no nutritional value.  It is important to read food lables

Do not skip meals!

Pace food intake throughout the day

Eating 5 meals a day and an evening snack is better

*patients with diabetics are not to skip meals.  For better blood glucose control, food intake must be paced throughout the day. Eating 5 meals instead of 3 has many advantages.

*lowers blood glucose and reduces Cardio-Vascular risk factors

*increases the uptake of glucose by the muscles and inproves utilization of insulin

promotes weight loss, lower BP, improve CV status, lower risk for depression and cancer; In normal clients, BG remain constant during exercise; thebody’s able to transfer energy from the liver and pancreas by regulating the amounts of insulin and glucagon released to the muscles during exercise. Regular exercise can decrease the need for insulin in Type I patients and reverse insulin resistance or increase insulin sensitivity in Type II patients. It also helps reduce triglyceride and LDL cholesterol levels and blood pressure. The physiologic differences that characterize DM have an impact on the way body responds to exercise. In Type 2 pts. with controlled diabetes, the physiologic response to exercise is pretty normal. The patients benefit in the sense that their endogenous insulin works better. The physiologic effects of aerobic exercise on insulin sensitivity lasts up to 48 hours so exercise 30 minutes every other day is sufficient. 

Have a physical exam prior to exercise regimen

Walking & low-impact aerobics are recommended

Use proper footwear

Exercise same time and in same amount/day

Slow gradual increase  in time period is recommended

Take a snack (15 grams carbs)  and 8 oz of fluid/ 30 minutes

*Have  extra fast-acting carbohydrate source handy

Monitor BG before, during, and after exercise

Retinopathy: rigorous aerobic or resistance exercise may be contraindicated because of the risk of triggering vitreous hemorrhage or retinal detachment

*No jarring motions (jogging) & those that increase vascular pressure

Neuropathy: encourage non–weight-bearing activities such as swimming, bicycling, or arm exercises 

Prevent post-exercise hypoglycemia:Added carbohydrate should be ingested if pre-exercise glucose levels are <100 mg/dl; exercise is rigorous  or prolonged

Type 1 pts are high-risk for post-activity delayed onset hypoglycemia

*The liver takes up to 48 hours to replenish glycogen stores

Avoid exercise: during peak insulin action, poor glucose control, extreme heat or cold

Caution when: BG >300 (negative ketones);   BG >250 (positive ketones)

*Insulin is required in Type I DM. It may also be given to Type II patients with moderate to severe forms of DM.

Concentrations/strength: U-100 and U-500

 Grouped according to speed of action (onset,  peak,  & duration differ)

Insulin was first discovered in 1921 and was made from beef/pork pancreas. Insulin made from an animal source is now hardly used in the US because biosynthetic human insulin is now available. Genetically engineered insulin analogs have been produced to mimic physiologic insulin response.

Insulin is destroyed by gastric juices so they are not given orally. Current research is investigating using non-injectable types of insulin. The standard insulin concentration used in the US is U-100 which means there are 100 units of insulin in 1 cc. The U-500 insulin is reserved for those who need > 200 u of insulin. 

lispro (Humalog),  aspart (Novolog),  glusisine (Apidra)

ONSET: 5- 15 minutes; PEAK: 30-90 minutes; DURATION: 5 hours or <

Used as BOLUS insulin (mealtime coverage)

Rapid-acting insulin is clear and colorless and is within  15 minutes of mealtime. They are rapid acting analogs, having profile much like endogenous insulin, which makes them easier to dose and less likely to cause hypoglycemia.

Regular: ®Humulin R, Novolin R

ONSET: 0.5-1 hour; PEAK: 2-4  hours; DURATION: 4-6 hours

Used as BOLUS (mealtime coverage)

*the only one that can be given by the IV route, if this is route needed

All insulins are given subcutaneously. When given at about 7:30 in the morning, the patient should have a meal in about 30 minutes. Its peak effects will be seen in midmorning or between 9:30 and 11:30. 

NPH (N): Humulin N, Novolin N, NPH insulin

ONSET: 2 hours; PEAK: 6-8 hours; DURATION: 12-16 hours

Used as BASAL insulin

Using regular insulin as the base, zinc and protamine are added to make NPH insulin. NPH stands for neutral protamine hagedorn. Only zinc is added to make lente insulin. These additives prolong the action of regular insulin and makes it appear cloudy. They are foreign substances that can cause allergic reactions. Intermediate insulins are usually given once a day or twice a day because of their prolonged actions. 

glargine (Lantus), detemir (Levemir)

Clear, Onset: 2-4 hours; Peakless; Duration 24 hrs

*Not to be mixed with other insulins.

*Used as BASAL insulin

Basal insulin is the foundational insulin that the pancreas produces 24 hours a day whether a person eats or not. Long-acting basal insulins begin working in 1-2 hours but are released slowly so they can last up to 24 hours, providing that foundational insulin that is needed around the clock.

Two different types of insulin are commonly prescribed in combination to mimic normal insulin secretion: 

• Humalog 75/25 is 75% intermediate acting insulin and 25% rapid acting insulin.
• Humulin 70/30 is 70% intermediate and 30% short-acting. insulin
• contains 70% NPH, and 30% regular
• ONSET: 0.5 hour; PEAK: 2-12 hours; DURATION: 24 hours

A patient may have orders for both NPH and regular insulin and the patient or nurse may combine them in one syringe for injection, if compatible with each other.

*Fixed combination insulins are used to minimize the inconvenience in mixing 2 insulins.

Contains 500 units of regular insulin per mL

Humulin R U-500 is 5x more potent than U-100 regular insulin. 

According to the FDA, Humulin R U-500 takes effect within 30 minutes, has a peak similar to that observed with U-100 regular human insulin (2-4 hrs) and has a relatively long duration of activity following a single dose (up to 24 hours) as compared with U-100 regular insulins.

No specific syringe for U-500; Use a tuberculin syringe

Dosed in  volume not in units; If pt. needs 250 units- the label will  be written as 0.5 mL

Not given IV or IM

Onset and peak like U-100 but has longer  duration (similar to basal insulin)

Sliding Scale: Sample MD order: 

Check capillary blood glucose  ac (before eating) and hs (at bedtime)

Give regular insulin subcutaneously on a sliding scale

BG 0-250 = 0  units regular insulin;  BG 251-300 = 2 units regular insulin

BG 301-400= 4 units regular insulin;  > 400 = call MD 

*(The type of insulin used for the sliding scale is short-acting or rapid-acting insulin)

Correction Dose: Sample MD order: BG minus 120 divided by 20 = units of insulin  (round^)

The correction dose is another alternative for prescribing coverage. It is a formula written by the physician for tight glycemic control specific for that client.

Because the abdomen does not have a lot of blood vessels and provides for constant and most rapid absorption, it is the preferred site for injection.

*Massaging the area is not necessary.

Because human instead of animal source-insulins are now widely used and because rotating sites cause variable rates of absorption, there is now no need to rotate sites. Instead, patients are advised to rotate the injection within one particular site (e.g. on the abdomen for about 2 weeks)

Wait 5 seconds before WD  needle to prevent leakage at the site – one drop of insulin leaked is = about 5 units (may vary with size of needle)

In a cool place; once opened, insulin may be kept at room temperature for up to 30 days or at 36-46 degrees F up to 3 months; insulin is never stored in freezers; syringes prefilled with insulin are  stable up to 30 days in the refrigerator; they are stored vertically to prevent the needles from clogging.

Every patient on insulin needs to be taught about signs and symptoms of hypo- and hyper-glycemia and about self-monitoring of blood glucose using a meter. The patient must also understand that insulin regimens are individualized.

Theinsulin pumpoffers a more physiologically correct dose of insulin.  Currently 90% of patients use lispro (a rapid-acting insulin) in their pump. The rate of delivery is programmed for basal rate or maintenance dose and then at mealtimes, the patient programs the pump to deliver a bolus dose. Assuming the physician’s order is 1 unit of insulin for each 15 grams of carbohydrate and the patient is planning to have 45 grams of carbohydrate for lunch, then he gives himself a 3 unit bolus dose of insulin. The pump is connected to a catheter inserted into the subcutaneous tissue of the abdomen, The site is changed Q 2-3 days and the pump is refilled with insulin. Not all clients are candidates for insulin pumps. The client must be extra compliant, highly-motivated and mature. 

Allergic reactions -

Local: Redness, swelling, induration; Disappear with  continued use

Systemic: Rare - Treatment is desensitization

Lipodystrophy - 

hypertrophy: due to frequent use of same injection site; regress if not used for 6 months 

Lipoatrophy: loss of fat, dimpling or pitting of SubCutaneous tissue (rarely seen)

Humalog (human analog)

rapid acting insulin

onset 5-15 min

peak 30-90 min

duration 5 hours or less

used as bolus for mealtime or sliding scale

Intermediate insulin

Humulin N and Novilin N

onset 2hrs

peak 6-8hrs

duration 12-16hrs

basal insulin

(cloudy due to zinc, protamine)

clear to cloudy

change your needles?

Long acting insulin

onset 2-4 hrs

no peak

duration 24hrs

#1 point - not to be mixed with other insulins

used as basal insulins

5 times more concentrated than Regular(short acting) insulin

someone who needs more than 200 untis of insulin at one time

Measured in volume (ml)

cannot use any unit syringe U-100 syringe

must use TB syringe

the 3 P’s, weight loss, malaise, fatigue, increased freq of infections, rapid onset, insulin dependent, early onset. 

• What are the 3 major treatment interventions for DM?

Diet

Exercise

Medications