1. Endocrine System-DIABETES

2. 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

3. 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

4. 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

5. 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

6. 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

7. 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

8. 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

9. 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

10. 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

11. 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)

12. 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

13. 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)

14. 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!!!)

15. 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

16. 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

17. 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!)

18. Manifestations of Type 1 and Type2 Diabetes Mellitus--SUMMARY
Polyuria
Polydipsia
Polyphagia
Weight loss
Fatigue
Malaise
Type 2
Polyuria
Polydipsia
Recurrent infections
Obesity
Fatigue
Blurred vision
Paresthesias

19. 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

20. 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

21. DIAGNOSTICS
1. Fasting Blood Sugar(FBS): After an 8 hour fast, blood is drawn. The adult normal range is The range of 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.

22. 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

23. 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%.

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

25. 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!!!

26. 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.

27. 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.

28. 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.

29. 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

30. 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
• 6 Units for blood sugar
• 8 Units for blood sugar
• 10 Units for blood sugar greater than 401 and call the physician

31. 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 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

32. 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.
2 units SQ
4 units SQ
6 units SQ
8 units SQ
10 units SQ
>400
15 units SQ and notify MD.

33. 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

34. 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

35. 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.

36. 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 %

37. 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).
What are the advantages of CSII?—normal glucose control and greater lifestyle flexibility.
Disadvantages-increased risk for ketoacidosis from a malfunctioning pumpand infection at the needle site

38. 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

39. 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)

40. 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%

41. 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%.

42. 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)

43. 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) mg/daily

44. 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 %

45. 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)

46. 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)

47. 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

48. 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)

49. 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%

50. 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

51. 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

52. 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

53. 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

54. 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

55. 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

56. 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

57. 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

58. 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

59. 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

60. 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

61. 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.

62. 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

63. 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

64. 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

65. 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

66. 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.

67. 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.

68. 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

69. 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

70. 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

71. 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

72. 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

73. 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

74. 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

75. Hypoglycemia Signs and Symptoms-Caused by Responses of the Autonomic Nervous System
Hunger
Nausea
Anxiety
Pale, cool skin
Sweating
Shakiness
Irritability
Rapid Pulse
Hypotension

76. 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

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

78. 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

79. 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

80. 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.

81. 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

82. 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

83. 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

84. 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