Med Surg 1: Diabetes

Diagnostic Studies: 4 methods: 1

1. Fasting plasma glucose (FPG) -level 126 mg/dl -fasting= no sugar for 8 hours -perferred method

Mixing Insulin Steps- 8

1. wash hands 2. Gently rotate NPH insulin bottle 3. Wipe off tops of insulin vials with alcohol sponge 4. Draw back amount of air into the syringe that equals total dose 5. Inject air equal to NPH dose into NPH vial. Remove syringe from vial 6. Inject air equal to regular dose into regular vial 7. Invert regular insulin bottle and withdraw regualr insulin dose 8. Without adding more air to NPH vial, carefully withdraw NPH dose.

DM Type 2: Etiology and Patho (4 steps) 2:

2. Pancreatic B cells "wear out" from compensatory OVERproduction and the mass of B cells are lost... and with it... some level of insulin production.

Diagnostic Studies: 4 methods: 2

2. Random (casual) plasma glucose level ->200 mg/dl plus symptoms -anytime w/o regard to food

DM Type 2: Etiology and Patho (4 steps) 3:

3. Inappropriate glucose production by liver. **Normally the liver properly responds to changing serum glucose by increasing or decreasing glucose availability in an orderly fashion. If glucose high, liver aggregates and stores as glycogen which lowers serum glucose. If glucose low, liver breaks down glycogen to produce glucose which elevates serum glucose.

Diagnostic Studies: 4 methods: 3

3. Two-hour oral glucose tolerance test (OGTT) level -200 mg/dl using a glucose load of 75g *factors can affect accuracy: false high readings if possible- recent card restriction, current acute illness, certain meds (corticosteriods, contraceptives), and restricted activity (bed rest). False lows/negative seen with impaired GI absortion.

Overall goal of ADA (American Diabetic Association)

Assist people in making changes in nutrition and exercise habits that will lead to improved metabolic control: 1. maintain blood glucose levels 2. lipid profiles and BP to decrease cardiac risk 3. modify lifestyle to help prevent and/or treat obesity, dyslipdemia, cardiovascular disease, neuropathy 4. improve health throughout healthy food choices and exercise

Metabolic Syndrome

Associated with Type 2 DM.Cluster of abnormalities that act synergistically to increase the risk of cardiovascular disease: increase insulin resistance, increase insulin levels, increase triglycerides, decrease HDLs, increase LDLs, hypertension. Risk Factors: central obesity, sedentary lifestyle, urban/western

Sedentary Diabetes

Results from another medical condition or due to the treatment of a medical condition that causes abnormal blood glucose levels: Cushing syndrome, hyperthyroidism, parenteral nutrition

Etiology and Pathophysiology: Normal Insulin Metabolism

The pancreas secreted insulin to facilitate movement of glucose into the cell to be stored as glycogen. Other hormones work to increase serum glucose levels by breaking down glycogen into glucose. (cortisol, epinephrine, glucagon, growth hormone). An abnormal increase in any of these hormones can lead to diabetes.

If BS continues or gets worse/pt becomes unconscious

admin 25-50mL of D50 (50% glucose) solution to IV push. Follow the hospital protocol.

What is an assessment??

an assessment is on the lookout for things to do. -an assessment never improves anything bacause it is simply an observation

What is an intervention??

an intervention does those things

Mealtime Insulin- bolus

blood levels rise after meals

Insulin secretion

normally secretes throughout the day and additional insulin as a response to food. And at night, with little serum insulin, the individual cells break down stored glycogen into glucose for energy.

Hypoglycemic unawareness

patients who are unaware of the S&S of hypoglycemia -those with neuropathy -the elderly -B-adrenergic users -These patients are usually not kept in as "tight" a range of control but are managed a little on the high side

Teaching Type 2 DM nutrition

teach regular exercise, lifestyle changes and monitoring

Diabetes Mellitus Definition

A multisystem disease related to an abnormal insulin production, impaired insulin utilization, and both abnormal production and impaired utilization.

Glucose needs to be in the serum for...

**Brain**, liver and blood cells

Hypoglycemic Causes

-ususally a mismatch of food intake and peak insulin action-that is why they (and you) must know the times that these drugs work --too much insulin --too little food --too little exercise -Not just insulin (though insulin males it more likley) -can also happen with oral hypoglycemic meds

Measures to prevent type 2 DM

-weight loss, diet, exercise -most important weight loss-- do some patient teaching!!

Type 1 DM- the nutrition plan

-work with their usual intake (preferences) -take into account their exercise pattern

Balanced Diet

**Alcohol- high in calories without any nutritive value -try to encourage limiting or eliminating -promote hypertriglyceridema -can cause severe hyperglycemia (impact on liver) **Carbohydrates- 45-65% -some use the glycemic index- how quickly metabolized but the quantity is more important **Fats-- 25-30% with <7% from saturated fats **Proteins-- 10%, less than general population

Nursing Implementation: Stress of illness and surgery

*physical and emotional stress increase blood glucose levels (again.. cortisol)- leads to hyperglycemia *if ill or under stress:-continue regular meal plan (cals important during stress) -increase non-caloric fluids -continue taking medications as prescribed -check blood glucose at least every 4 hours -if sugar>240, check ketones -if illness leads to loss of appitite, continue medications and supplement food intake with caloric liquids -if you are caring for a post-op patient be aware of S/S of hypoglycemia

Oral hypoglycemic- a-Glucosidase inhibitors

-"starch blockers" -decrease absorption of carbohydrates by small intestine -Very effective in reducing postprandial serum glucose: 1. take with the first bite of each meal 2. measure effectiveness with 2 hour postprandial levels -ineffective if hyperglycemia outside of meals Drugs: Precose and Glyset

What to do when you suspect HYPOGLYCEMIA

-1st- assess the patient -accucheck -if BS >70, begin assessing for other causes of these signs and symptoms -if signs and symptoms are there.. and there is no BS monitoring equipment around-assume hypoglycemia and intervene accordingly

Prevalence in the US

-25.8 million have it, 79 million with pre-diabetes, 7 million have it and are undiagnosed, 7th leading cause of death. Leading cause of heart disease, stroke adult blindness, and non-traumatic lower limb amputations. Increased risk of stroke and almost 3/4 diabetics have hypertension.

DM Type 1

-<30 years old -Peak prevalence between 11 and 13 y.o -Typically with lean body type

Drug interactions affecting blood glucose levels

-B adrenergic blockers- mask hypoglycemia and prolong the hypoglycemic effects of insulin -Thiazide and loop diuretics can potentiate hyperglycemia by inducing potassium loss

When measuring the effectiveness of the nutritional plan use:

-Blood glucose -hbA1C -Lipid values -Renal tests -Body weight -BP

Somogyi Effect

-Bounce down then bounce up. Art of tweaking -it is a rebound effect, usually at night- maintenance insulin on board and no food intake -Blood glucose level drop -counter regulatory hormones released (lipolysis, glucogenesis) -This produces rebound hyperglycemia and ketosis then pt measures blood glucose in the morning, hyperglycemia appears and insulin dosage (sliding scare) may be increased- HYPOGLYCEMIA ensues -PT reports: headache on awakening, night sweats, nightmares -**Check levels at 0200-0400

Diet Teaching

-Dietitian initially provides instruction: nurse should be ready to work with the dietitian, maybe no access to dietitian- then its the nurse -Should include the patients family and significant others -Make sure the person that cooks is there -The pt must be knowledgeable!

Injection Sites

-Different injection sites absorb at different rates and therefore have varying levels of "peak" Fastest to slowest: Abdomen, arm, high, and butt -Do not inject into site that will be exercised (thigh before run) -rotating within sites

Gestational Diabetes

-During pregnancy (about 4% of pregnancies) -Detected at 24-28 weeks -OGGT (oral glucose tolerance test)-diagnosis -Higher risk of C-section, neonatal death and neonatal complications -most return to normal post pregnancy -increased risk of type 2 in 5-10 years

Clinical Manifestations Type 2

-Gradual onset that are oftern unidentified- person blames increasing age or lack of sleep. Therefore the person may go many years with undetected hyperglycemia. -Could hae classic signs: polyuria, polydipsia, polypagia -More common (and non-specific) sign od type 2 are: fatigue, recurrent infections, prolonged wound healing, recurrent yeast infections, visual changes.

Problems with Insulin Therapy

-Hypoglycemia -Allergic Reactions: true systemic allergy to insulin is rare, usually it is local at injection site, most often body will adjust (2-3 months) or maybe benadryl -Lipodystrophy (atrophy at the injection site): rotate injection sites, if occurs, rest for 6 months and should get better -Somogyi Effect

Insulin Administration

-Insulin: cannot be taken orally (gastric juices inactivate), SQ- most common, inhaled. -Mixing insulin steps (next card...) -Nurses job to do required teaching

Type 2 DM

-Most prevalent type- accounts for 90% -Usuallu occurs in people over 35 yo: incidence increases with age, w/childhood obesity age is getting younger -80-90% of patients are overweight -gentic predisposition: runs in families, greater genetic predisposition for type 2 than type 1 -Ethnic predisposition: Greater in black, Asiain, Latino and Native. Native and AK natives are the highest

Intensive Insulin Therapy

-Multiple daily injections couples with frequent self monitoring of serum glucose -if done correctly, this method has the best chance of achieving near normal glucose levels throughout the day -EBP- tight control= fewer and less severe complications -Basal medication (NPH/long-acting) plus rapid/short (lispro) acting for boluses around meals -DISADVANTAGES: 1. requires 3 or more daily injections, 2. requires 4-6 blood glucose checks daily, 3. this complicated regimen makes it much more likely that pt has a hypoglycemic reaction

Drug Therapy: Oral Agents

-Not insulin- therefore type 2 -work to improve the mechanisms in which insulin and glucose are produced and used by the body -Work in 3 ways: 1. reduce insulin resistance (cell membrane- key and door) 2. increase insulin production (pancreas) 3. reduce hepatic glucose production (liver) -5 Classes

Collaborative Care- What needs to be taught?

-Nutritional therapy -Drug therapy: insulin- all type 1 require and sometimes type 2, oral hypoglycemic meds-most type 2, for some type 2 pts- exercise, diet, maintenance of weight is sufficient- but most require meds. -Exercise -Self monitoring pf glucose

Normal Insulin Metabolism

-Produced by the B cells in the inslet of Langherans of the pancrease. Typically insulin pulses out of the pancreas continuously and increases its secretion when food is consumed. Facilitates normal glucose range of 70 to 120 mg/dl. Promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell. Once in the cell, glucose can be stored as glycogen for "a rainy day"... or any time when input decreases. (sleeping or fasting)

Acute interventions:

-Stress of illness and surgery -hypoglycemia (if in doubt- treat with sugar!!) -Diabetic ketoacidosis (DKA- increase in sugar) -Hyperosmolar hyperglycemic (nonketonic syndrome)

Insulin Pump

-The patient programs and changes sites-Teach -Continuous subQ infusion -Change site every 2-3 days and refilled and reprogrammed -Delivers rapid or short acting insulin 24/7 (at a basal rate) -Bolus may be programmed by user (meals, if exercise) -Advantage- potential for tight control, also lifestyle advantages -Check insertion site for redness- trach -Disadvantage is increased BG montoring- 4-6 times daily

Combination Therapy

-To save "sticks" some mix an intermediate (NPH) with short-acting -Patients can mix themselves or buy pre-mixed -control is not as precise **Do not use this much anymore -it is most precise to use a basal insulin and then a rapid acting bolus around meals

Drug Therapy: Insulin: Exogenous Insulin

-Type 1 require it: maybe 4-5 times daily. -Type 2 may temporarily need it (periods of stress, if it progresses- but usually less frequent)

Pre-diabetes

-also called IGT- Impaired Glucose Tolerance -occurs when the lateration in B cell function is mild -blood glucose higher than normal >100 but <126 -At risk of developing type 2 DM: if no prevent meausures are taken in about 10 yrs. With prevent meausres it may not develop or can be delayed. -long term damage has already begun- esp in heart and blood vessels- can lead invariably to type 2 DM

Oral hypoglycemic- Meglitinide

-also enhance pancreatic production of insulin -they are more rapidly absorbed and eliminated so there is even a more reduced risk of hypoglycemia -Because they are fast, they can be taken right before a meal -Examples: Prandin and Starlix *Teaching: Take anytime from 30 before the meal until right up to the meal. If you you skip the meal, do not take.

Impaired Glucose Tolerance (IGT)

-also signals the intermediate stage of prediabetes -2 hour plasma glucose between 140-199

DM Type 1: Etiology and Patho

-complex interaction of genetic, autoimmune and environmental factors. -Progressive destruction of pancreas B cells -Auto-antibodies cause a reduction of 80% to 90% of normal B cell function before manifestations occur. -Genetic predisposition -Virus exposure??

Signs and Symptoms of HYPOGLYCEMIA

-confusion -irritability -diaphoresis -tremors -hunger -weakness -visual disturbances **If untreated= loss of consciousness, coma, and death

Dawn Effect

-effects most -Hyperglycemia in AM... same reason as above -usually associated with adolescence and young adult when growth hormone is active -What to do-- adjust the timing of the dosage

Type 2 DM- the nutrition plan

-emphasis based on achieving targets for glucose, lipids and BP -calorie and fat reduction (80-90% are overweight) -Not a "set in stone" strategy: want a nutritionally adequate diet-- decreased saturated fats, decreased simple sugars -space meals out -shoot for a 5-7% reduction in weight

Exercise

-essential part of diabetes management -increases insulin sensitivity of cells -lowers blood glucose levels: effects can last up to 48 hrs post exercise, watch for hypoglycemia, ADA recommends 30 mins x 5days per week -decrease insulin resistance (weight loss) -contributes to weight loss *always start a exercise program slowly- after medical clearance

Teaching

-exercise is good-encourage it -if you know you will exercise-should eat prior because of reduced serum glucose that follows -if sustained exercise-take small carbohydrate snacks about every 30mins -monitor serum glucose before, during and after -Remember= too much exercise=stress=cortisol. So consistent exercise

Is confirmed, how do you treat HYPOGLYCEMIA

-give 15-20gm of simple (fast) sugars -reassess in 15 mins, if continues repeat. -When BS >70 follow up with complex carbs and protein (longer lasting) -after 3 checks still low, notify the provider!

Insulin Storage- Rules (know for teaching)

-heat or freezing alter it -vials in current use can be at room temperature for 4 weeks. Nothing below freezing or >86 degrees -Avoid exposure to direct sunlight -Extra insulin in fridge -Traveling patient (cooler OK, no freezing) -Pre-filled syringes: 30 days in fridge, if cloudy (NPH) pre-filled- stored upright with needle up. when ready to use-roll in hands to warn it up and suspend the particles before injecting.

Teaching Type 1 DM nutrition

-if fixed insulin regiman: it is very important to have a routine of time and calories and exercise. -if rapid acting or insulin intensive or pump: all allow the client to be more flexible depending on the circumstances. This client must know exactly how much more or less to give themselves depending on the caloric intake of the particular meal or the specific exercise that is abut to be done.

Long acting (basal) background insulin

-in between meals and at night -24 hour control makes it less likely for DKA -Type 2 that use mealtime are more likely to use this too -Once daily at bedtime or in the morning -Lack a "peak" time-steadily released throughout- so less risk of hypoglycemic reaction Kinds: 1. Glargine (Lantus)- do not dilute or mix, do not prefill and store. 2. Detemir (Levemir)- do not dilute or mix with other insulin

Food Composition

-individual meal plan developed by a dietitian -nutritionally balanced -does not prohibit the consumption of any one type of food -should be balanced

Insulin Syringes

-insulin is U100-1ml=100 units -0.01ml=1 unit -Variety of sizes-smaller is better (easier to see-accuracy) -NEVER RECAP!! -Person using may recap... -Alcohol prep for hosp, at home not required -45-90 degree angle, 90 degrees if more fat -insulin pen- multiple use, change needles between uses

4 identifiable factors in the development of Type 2 DM

-insulin resistance -decrease pancreatic ability to produce insulin -inappropriate liver glucogenesis -altered hormone production

Oral hypoglycemic- Thiazolidinediones

-insulin sensitizers -action: 1. improve insulin sensitivity, transport and utilization at target tissues 2. does not increase insulin production 3. Therefore, by themselves, they do not have a hypoglycemic risk 4. but when used in combination... they can. DISADVANTAGE: can cause edema, no CHF pts (fluid build up-more workload for heart) ADVANTAGE: improved lipid profiles and BP Ex: Avandia

Rapid acting insulin

-lispro (humalog), aspart (Novolog), glulisine, Apidra -Onset- 15mins -most closely mimic postprandial endogenous insulin -take about 15mins before the meal

ONSET of DM Type 1

-long preclinical period (3-9 months or more) -manifestations develop when the pancreas can no longer produce insulin: rapid onset of symptoms, present at ER with impending or actual ketoacidosis -Classic symptoms: weight loss, polyuria, polydipsia, polyphagia -REQUIRES: exogenous insulin- if no, DKA

Nursing Implementation: Hypoglycemia

-low blood sugar (definition- BS<70) -KEY-unlike most of the cells in the body, the brain MUST have glucose to eat -other cells can convert protein and fat into energy but not the brain -it must have glucose

When managing DM focus on: (4)

-medications -nutrition -exercising -monitoring

DKA- Diabetic ketoacidosis

-occurs in the absence of exogenous insulin -life threatening condition -results in metabolic acidosis

Oral hypoglycemic- Sulfonylureas

-often drug of choice for type 2, less chance of hypoglycemia -Action-- increase pancreas production of endogenous insulin -effectiveness-best early in the course of the disease (about 10% of pancreas experience lower effectiveness over time, could be some weight gain) Examples: Glyburide, Glucotrol, Glucotrol, Glucotrol XL, Micronase, Diabeta, Glynase

Self Monitoring of Blood Glucose (SMBG)

-patient training is crucial, try and teach them on the machine they will actually be using -a cornerstone of self management -if they know this they can make decisions about diet and exercise and medication -detects the beginnings of when things may go bad WHEN: usually before meals and at bed but depending on exercise, it could be anytime ELDERLY: make sure the machine is appropriate (maybe needs talking machine, visually impaired, significant other present)

Collaborative Care- GOALS of Diabetic Management

-reduce symptoms -promote well-being -prevent acute complications -prevent long-term complications -delayed long-term complications **Maintain blood glucose levels at normal or near normal. **Keep em stable- in the range. The key is teaching!!

Short acting insulin

-regular insulin -onset 30-60 mins -timing should coincide with absorption of food -take about 30-45 mins before meals

Impaired Fasting Glucose (IFG)

-signals the intermediate stage of prediabetes -fasting >110, <126

DM Type 2: Etiology and Patho (4 steps) 1:

1. Insulin Resistance: -body tissues do not respond to insulin: insulin receptors are either unresponsive or insufficient, glucose impeded from entering the cell, it accumulates in serum... result: hyperglycemia. Early on, the pancreas responds by secreting more insulin (hyperinsulinemia)

5 Classes of Oral Agents

1. Sulfonylureas 2. Meglitinides 3. Biguanides 4. a-Glucosidase inhibitors 5. Thiazolidinediones

Oral hypoglycemic- Biguanides

Action: reduce glucose production by the liver, enhances insulin sensitivity (increase glucose transport) -Used alone or in combination with other drugs -Some advantages: 1. not promote weight gain (insulin and sulfonyureas both do ) 2. used for prediabetics (especially obese) -Metformin (glucophage)-most common oral hypoglycemic... period -Often in combination with other oral hypoglycemic drugs: Glucovalance (w/glyburide), Metaglip (w/glipizide)

DM Type 2: Etiology and Patho (4 steps) 4:

Altered production of hormones- adipokines

Nutrition

Cornerstone of care -Diabetics can eat the same foods as a person who does not have diabetes. -Principles of good nutrition apply

Many Theories as to why...

Genetic, autoimmune, viral, environmental. Regardless... it is a problem with glucose metabolism.

Diagnostic Studies: 4 methods: 4

Glycosylated hemoglobin -hemoglobin A1C -not used as an initial diagnostic test -determines glycemics level over time (glucose attached to hemoglobin) test shows serum glucose over the past 120 days (90-120 days) -IF A1C levels stay at near normal levels there is a much less chance of complications

Some tissues are "insulin dependent"

Have insulin receptors and rely on insulin to move sugar into their cells- skeletal muscle, adipose tissue

Clinical Manifestations Type 1

Onset is rapid so symptoms are usually acute. Classic signs: polyuria (increased serum glucose is an osmotic diuretic), polydipsia (after polyuria-thirsty), polyphagia (cellular malnutrition). Weight loss- the body begins breaking down other sources of energy. Weakness and fatigue, possible DKA.

Types of Insulin

Rapid acting: Short acting: regular Intermediate acting: NPH or Lente Long acting: glargine, detemir