Endocrine System-DIABETES

Objectives• At the end of this lesson, the SPN will be able to:• 1. Describe the pathophysiology of type 1 and type 2 DM• 2. Describe the risk factors associated with type1 and type 2 DM• 3. Describe the s/s of type 1 and type 2 DM• 4. Describe the diagnostic tests associated with DM• 5. Describe the various treatments used for DM including insulin, oral

medications and diet to name a few• 6. Differentiate between DKA and HHS• 7. Describe hypoglycemia and its treatment• 8. Describe the complications associated with diabetes

ANATOMY REVIEW• The pancreas has 2 portions-

• 1. An exocrine portion that secretes digestive enzymes that are carried through a duct to the duodenum

• 2. An endocrine portion that secretes hormones into the blood. This endocrine portion consists of over 1 million small groups of cells, called pancreatic islets or islets of Langerhans. The islets of Langerhans contains both alpha cells and beta cells

ALPHA CELLS• Secrete the hormone glucagon• Glucagon is secreted by alpha cells in response to a low concentration

of glucose in the blood• Glucagon’s principal action is to raise blood glucose levels• It does this by mobilizing glucose and fatty acids from their storage

forms• It also stimulates the liver to break down glycogen into glucose and to

manufacture glucose from noncarbohydrate sources such as proteins and fats

BETA CELLS• Beta cells in the islets of Langerhans secrete the hormone insulin in response

to a high concentration of glucose in the blood• The action of insulin is opposite to glucagon• Insulin promotes cellular uptake and use of glucose for energy• It stimulates the liver and muscle to remove glucose from the blood and store

it as glycogen• When the liver has stored all the glycogen possible, glucose is converted to fat

or adipose • Insulin inhibits the manufacture of glucose from noncarbohydrate sources• As a result of these actions, insulin decreases the blood glucose concentration

DIABETES MELLITUS• Diabetes Mellitus(DM) (diabetes:”like a sieve or siphon”; mellitus:

“sweet or related to honey”)• Is a systemic metabolic disorder that involves improper metabolism of

carbohydrates, fats, and proteins• In people with diabetes, the body’s insulin supply is either absent or

deficient, or target cells resist the action of insulin

Types of Diabetes Mellitus• There are 2 broad categories of DM, type 1 and type 2– The type of diabetes that was known as type I diabetes mellitus, juvenile-

onset diabetes mellitus, or insulin -dependent diabetes mellitus(IDDM) is now type 1 diabetes– The type of diabetes that was known as type II non-insulin dependent

diabetes mellitus(NIDDM) or adult- onset diabetes is now known as type 2 diabetes

Latent Autoimmune Diabetes of Adulthood (LADA)• A variation of type 1 diabetes that has recently been identified. Is

known as type 1.5 Diabetes Mellitus• LADA is a slow progression variation of type 1 diabetes mellitus and is

often misdiagnosed as type 2• Is most common in patients over the age of 35

Risk Factors • Type 1-• If an immediate relative has type 1 diabetes• Children are at higher risk if dad has diabetes rather than mom• If a parent develops diabetes before age 11• Caucasians-especially those of northern European heritage vs.

southern European heritage• An autoimmune response

Risk Factors• Type 2• African American, Hispanic American, Asian American, Native American or

Pacific Islander• You have a parent or sibling with type 2 diabetes• You are generally physically inactive• You’ve already been told you have pre-diabetes• You had gestational diabetes or a baby that weighed more than 9 pounds• Your blood pressure is 140/90 or above• Your triglyceride level is above 250mg/dL or your HDL is below 35• You are a woman with PCOS(Polycystic Ovary Syndrome)• Overweight

Pathophysioplogy• Type 1 Diabetes Mellitus– Results from an autoimmune response, which destroys the beta cells of the

islets of Langerhans in the pancreas– The end result is that insulin is no longer produced– Insulin deficiency causes hyperglycemia and a breakdown of fats and proteins–Without insulin to move glucose into the cells, the cells begin starving so they

burn fats and protein for their energy source– During the burning of fats, ketosis develops, a toxic accumulation of ketone

bodies(by-products from the burning of fatty acids)

Pathophysiology- type 1 DM Con’t.• When blood glucose exceeds the level the kidneys can process,

glucose spills into the urine, and glycosuria(excess glucose in the urine occurs)• The body’s state of hyperglycemia and glycosuria cause the three

primary manifestations of type 1 DM: polyuria, polydipsia, and polyphagia

Pathophysiology-type 1 Con’t. • Hyperglycemia acts as an osmotic diuretic• This causes polyuria(increased urine output)• The increased urinary output leads to dehydration• The mouth becomes dry and thirst sensors are activated, causing the

person to drink increased amounts of fluid (polydipsia)• Because glucose cannot enter the cell without insulin, energy

production decreases. This decrease in energy stimulated hunger, and the person eats more food (polyphagia)

Pathophysiology-Type 1 Con’t.• Despite increased food intake, the person loses weight• Malaise and fatigue accompany the decrease in energy

• Summary- State of absolute insulin deficiency. Usually occurs before childhood and adolescence but may occur at any age. Autoimmune destruction of beta cells. The patient is prone to ketoacidosis and is insulin dependent. (If the patient does not receive insulin, he or she will die!!!)

Pathophysiology- Type 2 DM• Is often undiagnosed for years. People are unaware of its presence

until health care is sought for another problem • Is characterized by hyperglycemia due to insufficient insulin

production and insulin resistance• The inadequate insulin supply cannot lower blood glucose levels

through the usual uptake of glucose by muscle and fat cells. However, sufficient insulin is produced to prevent the breakdown of fats; therefore, ketosis does not develop

Pathophysiology-Type 2 Con’t.• The hyperglycemia found in type 2 is less severe than that of type 1, so

only polyuria and polydipsia are seen• Infection -due to accumulated glucose in the tissues which provides a

breeding ground for bacterial infections• Blurred vision- due to high glucose levels which cloud the lens of the

eye • Paresthesias- due to high glucose levels which destroy peripheral

nerves• Fatigue results from an inadequate amount of glucose being available

to feed the cells

Pathophysiology- Type 2 DM• SUMMARY-State of insufficient insulin to prevent ketoacidosis but

insufficient to lower blood glucose levels. Usually occurs after age 30. Most patients are obese. May become insulin requiring but not insulin dependent. (If the patient does not receive insulin, he or she will become ill but will not die!)

Manifestations of Type 1 and Type2 Diabetes Mellitus--SUMMARY• Type 1• Polyuria• Polydipsia• Polyphagia• Weight loss• Fatigue• Malaise

• Type 2• Polyuria• Polydipsia• Recurrent infections• Obesity• Fatigue• Blurred vision• Paresthesias

Pre- Diabetes• Pre-diabetes is a condition in which blood glucose levels are higher

than normal, but not high enough to be classified as full-blown diabetes• Those with pre-diabetes are at increased risk for developing type 2

diabetes within a decade unless they adopt a healthier lifestyle that includes weight loss and more physical activity• A newer finding is the link between prediabetes and a condition

called Metabolic Syndrome

Metabolic Syndrome• A diagnosis of metabolic syndrome occurs when at least 3 of the

following criteria are met:– Elevated waist circumference(>40 inches in men and 35 inches in women– Triglyceride level >150mg/dl or higher– HDL < 40 mg/dl for men and < 50 mg/dl in women– Blood pressure > 130/85– Fasting glucose level >110mg/dl or higher** Other risk factors for metabolic syndrome are physical inactivity, aging,

hormonal imbalance, and genetic predisposition

DIAGNOSTICS• 1. Fasting Blood Sugar(FBS): After an 8 hour fast, blood is drawn. The

adult normal range is 70-99. The range of 100-125 is pre-diabetes. A value greater than 126 is considered abnormal. ***A patient must have 2 abnormal readings on 2 separate occasions in order to be diagnosed with diabetes.***• 2. Oral Glucose Tolerance Test(OGTT)- Usually not done when a

patient presents with clinical manifestations as well as 2 abnormal FBS.

Diagnostics Con’t• 3. Serum Insulin-absent in type 1 ; normal to high in type 2• 4. Postprandial Blood Sugar(PPBS)- A fasting patient is given either a

measured amount of carbohydrate liquid solution or a measured amount of foods containing carbohydrates, fats, and proteins. A blood sample will be drawn 2 hours after completion of the meal. A level >160 may indicate the presence of DM

Diagnostics Con’t.• 5. Fingerstick-blood sample is obtained and put in a monitoring

device that is used to check blood glucose. You do it in the clinical setting all the time!!• 6. Glycosylated hemoglobin- Also known as A1C- Should be drawn 2-

4 times a year. The A1C reflects one’s average blood glucose for the past 2 to 3 months. The A1C measures glucose that clings to hemoglobin molecules in red blood cells. The higher the glucose levels in the blood, the more glucose clings to the hemoglobin, and thus the higher the A1C. A1C is measured in %. Normal is 4-6%. The ADA-recommended treatment goal for A1C is < 7%.

A1C=approximate average of blood glucose levels over the most recent 3 months

Diagnostics Con’t.• 6. C-Peptide Test-C-peptide is secreted by the kidneys. Levels of C-

peptide correlate with insulin levels and provide a reliable indication of how well the beta cells secrete insulin. Normal values are 0.5 to 2ng/ml(nanograms per milliliter). The patient with type 1 DM is unable to produce insulin therefore, will have decreased levels of C-peptide. Patients with type 2 DM will have normal or higher than normal levels.• THIS IS A GOOD TEST TO DIFFERENTIATE BETWEEN TYPE 1 AND TYPE

2 DM!!!

Treatment of DM• Treatment of the client with diabetes focuses on maintaining blood

glucose at levels as nearly normal as possible through medications, diet, and exercise• 1.Self monitoring of blood glucose-allows the person with diabetes

to monitor and achieve metabolic control. It is also useful when the person is ill, pregnant or has symptoms of hypoglycemia and hyperglycemia. • Self monitoring of blood glucose should be done 3 or more times a

day for diabetics taking insulin. For those who do not use insulin, testing is recommended 2 to 3 times a week.

Treatment of DM Con’t.• Self monitoring of blood glucose requires the use of a lancet, a blood

glucose monitoring machine and a test strip. This is the equipment we use in the clinical setting.• 2. GlucoWatch Biographer- is worn as a watch. This device measures

the glucose value in the client’s perspiration and reports values every 10 minutes for up to 13 hours. When readings are too low or too high, an alarm sounds.

Treatment of DM-Con’t. • 3. Urine testing for Ketones and Glucose-At one time was the only

available method for evaluating diabetic management. Results are unpredictable and cannot measure hypoglycemia. This method is primarily used for pregnant moms.

Treatment of DM- Meds- Insulin• People with type 1 DM must have insulin. People with type 2 DM are

usually able to control glucose levels with an oral antidiabetic medication, but they may require insulin when control is inadequate• Insulin is derived from pork pancreas or made in the lab. • Insulins are available in rapid-acting, short-acting, intermediate-

acting, and long-acting preparations• The appropriate insulin dose is highly individualized• Let us now look at the handout and review the different types of

insulin

Insulin Sliding Scale

• This means that your insulin is prescribed so that your dose or doses are selected on the basis of your blood sugar results.

• Only Fast acting and Rapid acting insulins are used for sliding scale!!!• For instance, at mealtimes, your prescription for regular insulin could be something like this: • Regular insulin: • • o Units for blood sugar less than 180 • • 4 Units for blood sugar 181-240 • • 6 Units for blood sugar 241-320 • • 8 Units for blood sugar 321-400 • • 10 Units for blood sugar greater than 401 and call the physician

• Take regular insulin 1/2 hour before your meal or as suggested by your doctor or diabetes educator. • EXAMPLES • 1. It’s 1/2 hour before dinner. You test your blood sugar and it’s 191.

Look at the ranges on the above sliding scale and find the one that includes 191. Then look to see how much regular insulin you should take. In this example, it’s 4 units of regular insulin

Insulin Sliding Scale

Glucose Level (mg/dL) Humalog Insulin

<70 Administer 15 gm. Of rapid acting sugar, wait 15 minutes and re-assess BS. Repeat until BS>70.

150-200 2 units SQ

201-250 4 units SQ

251-300 6 units SQ

301-350 8 units SQ

351-400 10 units SQ

>400 15 units SQ and notify MD.

Exercises• Based on the sliding scale provided, how much insulin would you

administer???• 1. Administer 6 units before lunch QD in addition to the sliding scale. At

lunch, you get a FS value of 250.• 2. Breakfast FS value of 333• 3. Dinner FS value of 277. In addition you need to administer 18 units of

NPH insulin. What is the total number of units this pt. is to receive? How will you draw up the insulin?• 4. Breakfast FS of 55• 5. Lunch FS of 322

Afrezza (Inhaled Insulin)• Available in 4 unit and 8 unit cartridges• Must be used in combination with long-acting insulin in patients with

type I DM• Not recommended in patients who smoke or who have recently

stopped smoking• Increased risk of acute bronchospasm in patients with chronic lung

disease

Treatment of DM- Medications• Special injection products such as insulin pens and jet injectors are

available. • Insulin pens use an insulin cartridge with a disposable needle. It is

useful for patients who need only 1 type of insulin or need to travel form their home• Jet injectors shoot insulin through the skin in the subcutaneous tissue.

High cost and bruising limit their use.

Treatment of DM- GLP-1 RA’s (Glucagon like Peptide Receptor Agonists)• Action: Increases insulin secretion in response to carbohydrates. Acts

similarly to natural gut hormone. Prevents excessive hepatic glucose production by suppressing glucagon release. Given by injection only.• Side Effects: nausea, diarrhea, increased risk of pancreatitis, DO NOT

use in patients with a family history of thyroid cancer• Slows gastric emptying. Reduced food intake; increased satiety.

Promotes weight loss• Drugs: Byetta (Exenatide), Victoza (Liraglulide), Bydureon, Tanzeum

(Albiglutide), Trulicity( dulaglutide)• Decreases A1C by 0.5- 1.5 %

Treatment of DM- Medications• Regular insulin can be delivered through a continuous subcutaneous

insulin infusion (CSII) device, also called an insulin pump. The CSII has a small external pump, about the size of a pager, that holds a syringe connected to a subcutaneous needle by tubing. • The patient places the needle into the SQ tissue-usually the abdomen • The device delivers a constant amount of programmed insulin

throughout each 24-hour period• It also delivers a bolus of insulin manually (e.g. before meals).

Treatment of DM- Oral Meds• There are 9 different oral drug groups that are used in treating DM. they are:

– 1. Sulfonylureas– 2. Meglitinides– 3. Biguanides– 4. Thiazolidinediones– 5. DPP-4 Inhibitors (Dipeptidyl- Peptidase 4 Inhibitors)– 6. Alpha- Glycosidase Inhibitors– 7. SGLT-2 Inhibitors– 8. Fixed Combinations– 9. Others

**We will look at each group. I will only discuss action, side effects and special considerations since each individual drug has its own dosage range

Oral Meds- Sulfonylureas• ACTION: stimulates pancreas to release more insulin right after a meal and

then over many hours.• SIDE EFFECTS: potential for hypoglycemia, weight gain, increased risk of

cardiovascular disease. Instruct patient to avoid ETOH while taking this drug.• DRUGS: Should be given with meals except Glucotrol which should be given

30 minutes pre-meal– Micronase(glyburide)– Diabeta(glyburide)– Glucotrol(glipizide)– Glucotrol XL(glipizide extended release)– Amaryl(Glimepiride)

Sulfonylureas Con’t.• Should be used with caution in the following patients:• Sulfa allergies• Liver damage• Renal impairment• ETOH abuse

• Improves A1C by 1-2%

Oral Meds- Meglitinides• ACTION: Stimulates pancreas to release more insulin right after a

meal. Has a rapid onset and shorter duration• SIDE EFFECTS: Potential for hypoglycemia• DRUGS: Should be given 0-30 minutes pre-meal.If a meal is skipped, a

dose needs to be skipped. If a meal is added, you add a dose up to 4 doses/day– Prandin(repaglinide)– Starlix(nateglinide)

Decreases A1C by 1-1.5%.

Oral Meds- Biguanides• ACTION: Reduces the amount of glucose the liver releases between meals• Side Effects: Gas, diarrhea, upset stomach, nausea, abdominal pain. In rare cases,

lactic acidosis may occur in people with abnormal liver or kidney function. All drugs should be taken with meals to avoid GI upset• **Use with caution in pts. with renal disease, ETOH abuse, and the elderly (> age 80)• Lowers A1C by 1-1.5%. No hypoglycemia. May promote weight loss• Drugs:

– Glucophage(metformin)– Glucophage XR (metformin sustained release)– Fortamet(metformin extended release)– Riomet(metformin oral solution)

Oral Meds- Thiazolidinediones• Action: Makes the body more sensitive to the effects of insulin• Side Effects: Weight gain, fluid retention, osteopenia, increase in CHF in

those at risk. Liver function tests should be done at regular intervals. Instruct the patient to call the physician immediately if the following side effects occur: nausea, vomiting, fatigue, loss of appetite, SOB, severe edema, dark urine. New warning regarding increased risk of bladder cancer• Decreases A1C by 1-1.5%. Takes 6-12 weeks for maximum effectiveness.• Drugs: Take the same time daily

– Avandia(rosiglitazone)**May cause myocardial ischemia in some patients**– Actos(pioglitazone) 15 -45 mg/daily

Oral Meds- DPP-4 INHIBITORS• Action: Improves the level of the body’s insulin after a meal and lowers the

amount of glucose made by your body.• Often prescribed in combination with metformin. • No hypoglycemia and weight neutral• Side Effects: Stuffy nose, sore throat, occasional diarrhea and stomach discomfort• Drugs: Take 1 time a day at the same time

• Januvia(sitagliptin phosphate)• Onglyza (Saxaglipton)• Tradjenta (Linaglipton)• Nesina (Alogliptin)

• Decreases A1C by 0.5-1.0%

Oral Meds- Starch Blockers or Alpha-Glucosidase Inhibitors• Action: Delays absorption and breakdown of carbohydrates from

intestines• Side Effects: gas, diarrhea, stomach upset • Decreases A1C by 0.5%• Drugs: These drugs need to be taken with the first bite of your meal.

Take 3 times a day• Glyset(miglitol)• Precose(acarbose)

SGLT-2 inhibitors (sodium-glucose co-transporter 2 inhibitors)• Action: Blocks glucose reabsorption by the kidney. Increasing

glucosuria• Side Effects: May cause genitourinary infections, volume depletion,

hypotension, dizziness, transient increase in K⁺ or creatinine. May cause increase in LDL• No hypoglycemia, decrease in BP, decrease in weight• Drugs:• Invokana (Canagliflozin)• Farxiga (Dapaglifiozin)• Jardiance(Empagliflozin)

SYMLIN (Pramlintide Acetate)• Synthetic analog of human amylin• Amylin is a natural occurring hormone excreted by the beta cells

which helps control glucose after eating. • Prescribed for patients with type I and type II DM using insulin • Side Effects: hypoglycemia, nausea• Contraindicated in patients with gastroparesis, hypoglycemia

unawareness

Oral Meds- Combination Drugs• Action: Combines the action of each pill used in combination. May

decrease the number of pills you need to take• Drugs: Take 1-2 times a day with meals• Glucovance(glyburide and metformin)• Metaglip(glipizide and metformin)• Avandamet(rosiglitazone and metformin)

Colesevelam (Welchol)• Lipid lowering and glucose lowering effects• Side Effects: Constipation, indigestion, nausea. Do not use if

triglycerides are >500. Increased risk for pancreatitis• Lowers A1C by 0.5%

Bromocriptine (Cycloset)• Used for DM type II only. Dopamine receptor agonist• Action: Reduces blood glucose independent of the pancreas. • Must be taken within 2 hours of waking• Do not use with lactating patients, patients with syncopal migraines,

patients with hypotension

Nutrition Therapy• The caloric needs for a patient with diabetes is dependent on age,

activities, lean muscle mass, size , and basal metabolic rate• It is recommended that carbohydrates provide 50-60% of the calories.

Approximately 40 to 50% should be from complex carbohydrates(starches). The remaining 10-20% of carbohydrates could be from simple sugar• Fats should be limited to 30% of total calories, and proteins should

provide from 15 to 20% of total calories

Nutrition Therapy- Con’t.• It is important that meals and snacks be composed of similar

nutrients and calories and eaten at regular times each day• Small meals plus 2 or 3 snacks may be more helpful in maintaining a

steady blood glucose level than three large meals a day

Carbohydrate Counting• Carb counting is the newest method for teaching a diabetic client how

to control blood sugar with food• The starch and bread category, milk, and fruits have all been put

under the heading of “carbohydrates”• This means that these food groups can be interchanged within one

meal• One would still have the same number of servings of carbohydrates,

but it would not be the typical number of starches or fruits and milk that one usually eats

Carb Counting Con’t• An example of Carb Counting:• A patient decides to have four carbohydrates for breakfast(2 breads, 1 fruit,

and 1 milk). If there is no milk available, a bread or fruit must be eaten in place of the milk

Diets based on Exchange Lists• The method of diet therapy most commonly used for diabetic clients

is that based on exchange lists• The exchange lists were developed by the ADA• Foods are categorized by type• The foods within each list contain approximately equal amounts of

calories, carbohydrates, protein, and fats. • This means that any food on a particular list can be substituted for

any other food on that particular list and still provides the client with the prescribed types and amounts of nutrients and calories

Fiber• The therapeutic value of fiber in the diabetic diet has become

increasingly evident• High-fiber intake appears to reduce the amount of insulin needed

because it lowers blood glucose• It also appears to lower the blood cholesterol and triglyceride levels

Alternative Sweeteners• Sucralose is a new sweetener made from a molecule of sugar• Aspartame is an artificial sweetener made from amino acids and does

not require insulin for metabolism

Dietetic Foods• Can be misleading to the client• Often the containers of foods will contain the same ingredients as

containers of food prepared for the general public, but the cost is typically higher for the dietetic foods• The most important thing a person who has diabetes can do is to read

ALL food labels

Alcohol• Alcohol is not recommended for diabetic clients• Some patients who use oral hypoglycemic agents cannot tolerate

alcohol• When used, alcohol must be included in the diet plan

Exercise• Exercise is extremely important for diabetic patients• It reduces blood glucose levels by increasing glucose used by the

muscles. This potentially decreases the need for insulin• Patients with diabetes should consult their primary health care

providers before beginning or changing an exercise program• Patients who exercise need to use proper footwear, inspect the feet

daily and after exercise, and avoid exercise in extreme heat or cold• Exercise should be avoided during periods of poor glucose control

Acute Complications of Diabetes Mellitus• Diabetic Ketoacidosis, Hyperosmolar Hyperglycemic state, and

hypoglycemia are the primary acute complications of diabetes mellitus• These can be life threatening and require immediate medical

treatment. We will look at these each individually.

DIABETIC KETOACIDOSIS (DKA)• Is a life-threatening illness occurring primarily in type 1 diabetics but

may occur in type 2 diabetes when insulin deficiency exists• RISK FACTORS:

• A patient with undiagnosed or untreated diabetes• A patient who is sick, has an infection, or has excessive physical or emotional stress

Pathophysiology-DKA• Without insulin, glucose cannot enter the cell, which stimulates the

liver to increase glucose production, leading to hyperglycemia• The excess glucose acts as an osmotic diuretic causing polyuria, and

eventually leads to dehydration and sodium and potassium loss• Because glucose cannot be used for energy, the fat stores break

down, resulting in continued hyperglycemia and burning of fatty acids. This causes the formation of ketones

Pathophysiology of DKA Con’t.• When more ketones are produced than the cell can useand the

kidneys can excrete, ketoacidosis develops• Ketoacidosis alters acid-base balance, causing metabolic acidosis• The increased buildup of ketones depresses the CNS leading to coma

and death if left untreated

Signs and symptoms of DKA• Dehydration- thirst, warm dry skin, poor turgor, dry MM, rapid weak pulse,

hypotension• Metabolic Acidosis-N/V, lethargy to coma, Acetone (fruity, alcohol-like)

breath odor• Other Manifestations: Abdominal pain, Kussmaul’s respirations(rapid, deep

respirations; a compensatory response to prevent a further decrease in pH• Laboratory Findings:

– Blood Glucose: >250 mg/dl– Blood and Urine ketones: positive– ABG: pH <7.3

Treatment of DKA• The patient may be hospitalized when the person has a blood glucose

value greater than 250mg/dl and ketones in the urine• Fluids(for dehydration)-if the patient is alert and conscious, may be

given orally. Unconscious patients require IV fluids. Be prepared to administer0.9% normal saline to replace sodium losses. After 2-3 hours, the IV solution is changed to 0.45% normal saline to prevent hypernatremia. When the blood glucose levels reach 250mg/dl, dextrose is added to prevent hypoglycemia.• Potassium may be added to an IV if the patient has a low potassium

level.

Treatment of DKA Con’t. • Regular insulin is used to treat the client’s hyperglycemia. ***The

degree of hyperglycemia and ketosis determines whether insulin is given by the subcutaneous route or IV route. Typically, a continuous insulin infusion is started and maintained until the ketoacidosis is resolved.

HYPEROSMOLAR HYPERGLYCEMIC STATE(HHS)• Occurs in people with type 2 DM• This condition develops slowly over several hours to days• It is a serious , life-threatening medical emergency that has a higher

mortality rate than DKA.• Infection, surgery, and dialysis are a few of the factors that can trigger

HHS

Pathophysiology-HHS• The state of extreme hyperglycemia leads to osmotic diuresis and

results in severe dehydration, especially of the brain.• The manifestations result from the effects of hyperglycemia and

dehydration• **Ketoacidosis does not occur like it does in DKA, because the type 2

diabetic has sufficient insulin

HHS- Signs and Symptoms• DEHYDRATION-extreme thirst, warm, dry skin with poor turgor, dry mucous

membranes, rapid, weak pulse, hypotension• NEUROLOGIC- Depressed level of consciousness to coma, Grand mal

seizures• OTHER MANIFESTATIONS-Abdominal discomfort may be present, rapid,

shallow breathing• LAB FINDINGS- Blood Glucose > 600 mg/dL

Blood and Urine Ketones-Negative Arterial blood Ph- Normal Serum Osmolality- > 340 mOsm/L

TREATMENT OF HHS• Similar to that of DKA, namely correcting fluid and electrolyte

imbalances, and providing insulin to lower hyperglycemia• IV fluids-0.9%normal saline are given, followed by 0.45% normal

saline to correct the fluid and sodium losses• Insulin is administered to reduce the severe hyperglycemia• **When blood glucose levels reach 250mg/dL, the insulin is

discontinued , because, in contrast to DKA, ketosis is not present

Nursing Care for DKA and HHS• For both DKA and HHS, the nurse is responsible for measuring VS ,

monitoring the level of consciousness, monitoring IV infusions, strict I & O, and notifying the physician of the client’s response to treatment

HYPOGLYCEMIA• Can occur in people with type 1 DM and people with type 2 who are

treated with oral antidiabetic agents. It may be caused by too much insulin intake, overdose of oral antidiabetic agents, too little food, or excess physical activity.• The onset is sudden, and blood glucose is usually less than 50mg/dL

Pathophysiology-Hypoglycemia• The brain requires a constant supply of glucose, so a hypoglycemic

episode alters brain function.• The symptoms of hypoglycemia result from activation of the

autonomic nervous system and from impaired cerebral function.• Severe untreated hypoglycemia may lead to death

Hypoglycemia Signs and Symptoms-Caused by Responses of the Autonomic Nervous System

• Hunger• Nausea• Anxiety• Pale, cool skin• Sweating

• Shakiness• Irritability• Rapid Pulse• Hypotension

Hypoglycemia Signs and Symptoms-Caused by Impaired Cerebral Function• Strange or Unusual Feelings• Headache• Difficulty in thinking• Inability to concentrate• Change in emotional behavior• Slurred speech

• Blurred vision• Decreasing levels of

consciousness• Seizures• Coma

Hypoglycemia-Lab Findings• Blood Glucose <70 mg/dL• Blood and Urine Ketones Negative• Plasma pH Normal• Serum osmolality Normal

Hypoglycemia-Treatment• Hypoglycemia may occur at any time, but it most often develops

before meals or in the middle of the night. Mild hypoglycemia is usually recognized and self managed, but severe hypoglycemia requires treatment by health care providers

Treatment-Mild Hypoglycemia• Blood glucose between 60 and 70 mg/dL• Immediate treatment is necessary • People should take about 15 grams of a rapid-acting sugar. Examples

of fast-acting glucose are:– 3 glucose tablets–½ cup of fruit juice or regular soda– 8 oz. of skim milk– 6 to 8 Life Savers candies– 2 to 3 tsp of sugar or honey

Treatment-Mild Hypoglycemia Con’t. • If the manifestations continue, the 15/15 rule should be followed:–Wait 15 minutes, then monitor blood glucose; if it remains below 70, eat

another 15 grams of carbohydrate.– This procedure can be repeated until blood glucose levels return to normal

– **PEOPLE WITH DIABETES SHOULD ALWAYS CARRY A RAPID-ACTING CARBOHYDRATE SOURCE.

Treatment- Severe Hypoglycemia• Patients who have a blood glucose value less than 60 are often

hospitalized.• If the patient is conscious and alert, 10 to 15 grams of an oral

carbohydrate may be given• When the patient is unconscious, 25 to 50 ml of 50% dextrose is given

intravenously , followed by an intravenous solution of 5% dextrose in water(D5W)• IV glucose acts the fastest to raise blood glucose levels

Treatment-Severe Hypoglycemia Con’t.• When it is available, glucagon 1 mg may be given SQ or IM to

stimulate the release of glycogen• Because glucagon has a short action period, a carbohydrate snack is

given to prevent a recurrence of hypoglycemia• Glucagon should be included in the patient’s emergency kit and family

members should be taught how and when to administer it

OTHER ALTERATIONS IN BLOOD GLUCOSE LEVELS• SOMOGYI EFFECT- Is a morning rise in blood glucose to

hyperglycemic levels following an episode of nighttime hypoglycemia. The morning hyperglycemia is thought to be caused by the release of counterregulatory hormones• Patients with Somogyi effect are taught to monitor their blood

glucose levels and assess for manifestations of nocturnal hypoglycemia: tremors, night sweats, and restlessness.• The treatment focuses on increasing the bedtime snack or decreasing

the evening dose of intermediate-acting insulin

Other Alterations in Blood Glucose Levels Con’t.• Dawn Phenomenon- Is a rise in blood glucose levels between 5 A.M.

and 9 A.M. • The exact cause is unknown but may be related to nighttime release

of growth hormone.• Treatment may include increasing the insulin dose or changing the

injection time of the intermediate –acting insulin from dinnertime to bedtime