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Diabetes Mellitus and Hypoglycemia

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1 Diabetes Mellitus and Hypoglycemia
Chapter 46 Diabetes Mellitus and Hypoglycemia 1

2 Learning Objectives Describe the role of insulin in the body.
Explain the pathophysiology of diabetes mellitus and hypoglycemia. Describe the signs and symptoms of diabetes mellitus and hypoglycemia. Explain tests and procedures used to diagnose diabetes mellitus and hypoglycemia. Discuss treatment of diabetes mellitus and Explain the difference between type 1 and type 2 diabetes mellitus.

3 Learning Objectives Differentiate between acute hypoglycemia and diabetic ketoacidosis. Describe the treatment of a patient experiencing acute hypoglycemia or diabetic ketoacidosis. Describe the complications of diabetes mellitus. Identify nursing interventions for a patient diagnosed with diabetes mellitus or hypoglycemia. with ketoacidosis.

4 Diabetes Mellitus 4

5 Pathophysiology Chronic disorder of impaired metabolism with vascular and neurologic complications Key feature is elevated blood glucose, called hyperglycemia Blood glucose level normally regulated by insulin, a hormone produced by beta cells in the islets of Langerhans located in the pancreas The ingestion of carbohydrates triggers the secretion of a larger volume of insulin. What is the difference in endogenous and exogenous insulin? 5

6 Type 1 Absence of endogenous insulin
Formerly called juvenile-onset diabetes because it most commonly occurs in juveniles and young adults An autoimmune process, possibly triggered by a viral infection, destroys beta cells, the development of insulin antibodies, and the production of islet cell antibodies (ICAs) Affected people require exogenous insulin for the rest of their lives 6

7 Type 2 Inadequate endogenous insulin and body’s inability to properly use insulin Beta cells respond inadequately to hyperglycemia; results in chronically elevated blood glucose Continuous high glucose level in the blood desensitizes the beta cells; they become less responsive to the elevated glucose More common in adults; increasing in children Controlled by diet and exercise; may require oral hypoglycemic agents or exogenous insulin 7

8 Role of Insulin Glucose
Insulin stimulates active transport of glucose into cells If insulin absent, glucose remains in the bloodstream Blood becomes thick, which increases its osmolality Increased osmolality stimulates the thirst center Increased fluid does not pass into body tissues; high serum osmolality retains fluid in the bloodstream As blood passes through the kidneys, some glucose eliminated Osmotic force created by glucose draws extra fluid and electrolytes with it, causing abnormally increased urine volume The patient may take in more food but, unfortunately, cannot use the extra glucose without insulin. Weight loss occurs despite increased appetite and food ingestion. What are the three “P’s” related to symptoms of DM? 8

9 Role of Insulin Fatty acids
Promotes fatty acid synthesis and conversion of fatty acids into fat, which is stored as adipose tissue Also spares fat by inhibiting breakdown of adipose tissue and mobilization of fat and by inhibiting the conversion of fats to glucose Without adequate insulin, fat stores break down and increased triglycerides are stored in the liver Increased fatty acids in the liver can triple the production of lipoproteins; promotes atherosclerosis Why do people with DM have a high incidence of cardiovascular disease? 9

10 Role of Insulin Protein
Enhances protein synthesis in tissues and inhibits the conversion of protein into glucose Amino acids are admitted into cells; enhances rate of protein formation while preventing protein degradation Without adequate insulin, protein storage halts; large amounts of amino acids dumped into the bloodstream High levels of plasma amino acids place people with diabetes at risk for development of gout Changes in protein metabolism lead to extreme weakness and poor organ functioning 10

11 Etiology An autoimmune malfunction may cause complete destruction of the islets of Langerhans in the pancreas, creating type 1 diabetes Islet cell antibodies are identified in more than 80% of all people with type 1 diabetes at the time of diagnosis 11

12 Figure 46-1 12

13 Risk Factors Obesity Sedentary lifestyle Family history of diabetes
Age 40 years and older History of gestational DM History of delivering infant weighing more than 10 lb African American (33% higher risk for type 2 DM) Latin American/Hispanic (>300% higher risk for type 2 DM) American Indians (33%-50% higher risk for type 2 DM) 13

14 Risk Factors Metabolic syndrome Thought to be a precursor to diabetes
Impaired glucose tolerance, high serum insulin, hypertension, elevated triglycerides, low HDL cholesterol, altered size and density of LDL cholesterol Believed that metabolic syndrome is a chronic low-grade inflammatory process affecting endothelial tissue Long-term effects: atherosclerosis, ischemic heart disease, left ventricular hypertrophy, type 2 DM Research directed at learning how to detect this syndrome early and what interventions might slow or arrest the progress What is Syndrome X? 14

15 Long-Term Complications

16 Microvascular Complications
Retinopathy Pathological changes in the retina that are associated with DM Nephropathy Kidney damage Among people 25 to 74 years of age, DM is the leading cause of blindness. What are the two types of diabetic retinopathy? Signs and symptoms that suggest impending eye problems are the presence of spots (“floaters”) in the field of vision, seeing “cobwebs,” or sudden visual changes. Diabetes is the most common cause of end-stage renal disease (ESRD) in the United States. Factors that contribute to the development of nephropathy (kidney damage) include poor control of blood glucose, hypertension, long-standing diabetes, and genetic susceptibility. 16

17 Macrovascular Complications
Accelerated atherosclerotic changes in the person with diabetes Associated with coronary artery disease (CAD), cerebral vascular accidents (CVA or stroke), and peripheral vascular disease (PVD) What vessels are affected by atherosclerosis? Individuals with diabetes have a 2- to 4-fold increased risk for heart disease and stroke, which accounts for 65% of the deaths in people with diabetes. Treatment for macrovascular disease is directed toward weight loss and exercise. 17

18 Long-Term Complications

19 Neuropathic Complications
Neuropathy: pathologic changes in nerve tissue Mononeuropathy affects a single nerve or group of nerves Polyneuropathy involves both sensory and autonomic nerves Autonomic neuropathy affects the sympathetic and parasympathetic nervous systems Almost 30% of individuals older than age 40 with diabetes have impaired sensation in as least one area of the foot. What percentage of people who have had DM for more than 25 years experience neuropathies? 19

20 Hypoglycemic Unawareness
The usual symptoms of tachycardia, palpitations, tremor, sweating, and nervousness may be absent Patient may suddenly have changes in mental status as the first sign of hypoglycemia What is hypoglycemic unawareness attributed to? 20

21 Long-Term Complications
Foot complications of diabetes May have foot problems associated with neuropathy, inadequate blood supply, or a combination Mechanical irritation Thermal injury Chemical irritation The patient may have a foot injury but fail to recognize it in the absence of pain. What is the best treatment for foot complications? 21

22 Long-Term Complications: Prevention
Diabetes Control and Complications Trial (DCCT): intensive treatment of type 1 DM delayed the onset or slowed the progress of diabetic retinopathy, nephropathy, and neuropathy Outcome of United Kingdom Prospective Diabetes Study (UKPDS): similar benefits of tight control with type 2 DM Tight control means that the blood glucose is maintained in the normal range with carefully balanced drugs, diet, and exercise. What medications are recommended for patients with increased cardiovascular risks? 22

23 Long-Term Complications: Prevention
ADA recommends Blood pressure: <130 systolic, <80 diastolic Total cholesterol: <200 mg/dL LDL: <100 mg/dL HDL: >45 mg/dL for men (>55 mg/dL for women) Triglyceride: <150 mg/dL 23

24 Acute Emergency Complications

25 Acute Hypoglycemia Dangerous drop in blood glucose Causes
Taking too much insulin, not eating enough food or not eating at the right time, an inconsistent pattern of exercise Gastroparesis, renal insufficiency, and certain drugs including aspirin and beta-adrenergic blockers What glucose levels are considered moderate hypoglycemia? 25

26 Acute Hypoglycemia Signs and symptoms
Adrenergic: shakiness, nervousness, irritability, tachycardia, anxiety, lightheadedness, hunger, tingling or numbness of the lips or tongue, and diaphoresis Neuroglucopenia: drowsiness, irritability, impaired judgment, blurred vision, slurred speech, headaches, and mood swings progressing to disorientation, seizures, and unconsciousness 26

27 Acute Hypoglycemia Treatment
Give patient 10 to 15 g of quick-acting carbohydrates Repeat every minutes until blood glucose is >70 mg/dL for adults, 80 to 100 mg/dL for older adults and children If patient is unable to swallow, an IM or subcutaneous injection of 1 mg of glucagon or an IV dose of 50 mL of 50% dextrose should be given as ordered or per protocol What are examples of quick-acting carbohydrates? 27

28 Diabetic Ketoacidosis (DKA)
Life-threatening emergency caused by a relative or absolute deficiency of insulin Early signs and symptoms Anorexia, headache, and fatigue As condition progresses, classic symptoms of polydipsia, polyuria, and polyphagia develop If untreated, patient becomes dehydrated, weak, and lethargic with abdominal pain, nausea, vomiting, fruity breath, increased respiratory rate, tachycardia, blurred vision, and hypothermia What sequence of events occurs with DKA? The patient with ketoacidosis has hyperglycemia (300 mg/dL); ketonuria; and acidosis, with a pH of less than 7.3 or a bicarbonate level of less than 15 mEq/L. 28

29 Diabetic Ketoacidosis (DKA)
Late signs Air hunger (Kussmaul’s respirations), coma, and shock Death can result without prompt medical care 29

30 Diabetic Ketoacidosis (DKA)
Treatment aimed at correction of three main problems Dehydration Electrolyte imbalance Acidosis 30

31 Hyperglycemic Hyperosmolar Nonketotic Syndrome
Patient goes into a coma from extremely high glucose levels (>600 mg/dL) There is no evidence of elevated ketones Pancreas produces enough insulin to prevent breakdown of fatty acids and formation of ketones, but not enough to prevent hyperglycemia Persistent hyperglycemia causes osmotic diuresis, resulting in loss of fluid and electrolytes Dehydration and hypernatremia develop May be caused by the same factors that trigger ketoacidosis Hyperglycemic hyperosmolar nonketotic syndrome may be caused by the same factors that trigger ketoacidosis. It also can be brought about by total parenteral nutrition or dialysis. Why can intravenous solutions that contain high amounts of glucose cause HHNS? 31

32 Medical Diagnosis One or more of the following criteria on two separate occasions is considered DM Polyuria, polydipsia, polyphagia, unexplained weight loss plus random glucose level >200 mg/dL Fasting serum glucose level >126 mg/dL (after at least an 8-hour fast) Two-hour postprandial glucose level >200 mg/dL during oral glucose tolerance test (OGTT) under specific guidelines. Test must use a glucose load of 75 g of anhydrous glucose dissolved in water 32

33 Medical Diagnosis Prediabetes
Individuals with impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) Individuals should receive education on weight reduction and increasing physical activity What fasting glucose levels indicate IFG? IGT? 33

34 Medical Diagnosis Oral glucose tolerance test
Diet of 150 to 300 g carbohydrate for 3 days before test Night before test, patient fasts after midnight Morning of test, blood drawn for fasting serum glucose Patient then given a drink (Glucola) containing 75 g of carbohydrates and instructed to remain quiet Blood drawn at 30 minutes and 1 hour after the ingestion of glucose. After these two samples, blood is drawn at hourly intervals until the test is completed How can the need for multiple venipunctures be eliminated? 34

35 Medical Treatment Nutritional management
Medical nutrition therapy (MNT) is an important part of diabetes management; should be included in diabetes self-management education Because of complexity of nutritional management, a registered dietitian should be part of the diabetes management team, and the individual with diabetes should be included in decision making What are the goals of medical nutrition therapy? To maintain weight, a caloric intake of 28 calories/kg of body weight is required. To reduce weight, the caloric intake is calculated based on 15 to 20 calories/kg body weight. Patient teaching should include sample menus that include as many favorite foods as possible. 35

36 Medical Treatment Exercise Effective adjunct for people with diabetes
Aids in weight loss, improves cardiovascular conditioning, improves insulin sensitivity, and promotes a sense of well-being Exercising muscle uses glucose at 20 times the rate of a muscle at rest and does not require insulin Exercise is known to improve low-density lipoproteins, serum glucose, blood pressure, some blood coagulation parameters, and triglycerides. What is largely responsible for maintaining glucose levels during exercise? It is important for individuals with diabetes to monitor blood glucose levels before and after exercise. 36

37 Insulin Therapy All patients with type 1 disease need insulin injections; some patients with type 2 disease may eventually need insulin Insulins classified by source and course of action Source: human, pork, or beef (beef is being phased out) Course of action: rapid acting, short acting, intermediate acting, and long acting All rapid-acting and short-acting insulins are clear The other insulins are cloudy “Human” insulin causes fewer problems than that from animal sources. Which type of insulin is being phased out in the US? 37

38 Figure 46-2 38

39 Insulin Therapy Route Oral: insulin cannot be given orally because it is rendered useless in the gastrointestinal tract Subcutaneously: all insulins can be given subcutaneously Intravenously: ONLY regular insulin can be given intravenously Inhalation: a form of insulin that can be taken by inhalation has recently been approved, but it is not yet widely used 39

40 Insulin Therapy Concentrations U-100 insulin has 100 units/mL
Most commonly used U-500 insulin has 500 units/mL Used only in emergencies and for patients who are extremely insulin resistant U-40 insulin has 40 units/mL Not available in the United States 40

41 Insulin Therapy Premixed insulin products
Contain both Regular and NPH insulin 70% NPH and 30% Regular insulin 50% NPH and 50% Regular insulin 75% NPH and 25% Lispro 41

42 Insulin Therapy Dosing schedules Conventional therapy
Typically uses a combination of a short-acting and an intermediate- or long-acting insulin Intensive therapy To achieve tight control; may require 3 or 4 injections daily Continuous subcutaneous insulin infusion Patient has indwelling subcutaneous catheter connected to an external portable infusion pump; pump delivers Regular insulin continuously Exogenous insulin is administered in an effort to mimic the action of a normal pancreas. What is a major problem with conventional therapy? The preprandial (before meal) doses are adjusted for the caloric content of the meal with intensive therapy. 42

43 Insulin Therapy Insulin mixing Insulin injection
Two types can be mixed in one syringe to avoid two injections Insulin injection Site rotation helps prevent lipohypertrophy or lipoatrophy Absorption rate varies with different body sites American Diabetes Association recommends rotating sites within one anatomic area rather than moving among all areas See Figure 46-3 What are the steps for mixing two types of insulin in the same syringe? The rate of absorption from the abdomen is approximately 50% faster than from the thighs. 43

44 Figure 46-3 44

45 Insulin Therapy Insulin pump
Needle is inserted subcutaneously in an appropriate part of the anatomy Pump is programmed to deliver a steady trickle of insulin throughout the day and can provide a bolus of insulin at mealtimes Consists of a battery-driven syringe with a long piece of tubing (usually made of Teflon) that is attached to a small needle. One advantage of the external insulin pump is that patients do not have to use intermediate- or long-acting insulins, with their uncertain peaks and valleys. What is an “artificial pancreas?” 45

46 Figure 46-4 46

47 Insulin Therapy Intranasal route Insulin catheter
Only 10% of the drug is absorbed through the nasal mucosa, making it relatively expensive to use Nasal irritation is a frequent side effect Only Regular insulin is given intranasally Insulin catheter Indwelling subcutaneous catheters may be placed in the abdomen to permit repeated insulin injections without repeated needlesticks 47

48 Oral Hypoglycemic Agents
If patients with type 2 DM unable to control blood glucose with nutrition and exercise, physician may prescribe oral hypoglycemics Sulfonylureas (three generations), alpha-glucosidase inhibitors, biguanides, thiazolidinediones, D-phenylalanines, meglitinides Combination oral medications ACTOplus met (pioglitazone and metformin), Avandamet (rosiglitazone and metformin), Avandaryl (rosiglitazone and glimepiride), Glucovance (glyburide and metformin), Metaglip (glipizide and metformin) What interventions may be required if the blood glucose rises above 300 mg/dL? 48

49 Self-Monitoring of Blood Glucose
Allows patients to monitor blood glucose levels to regulate their diet, exercise, and medication regimens to remain euglycemic Portable electronic glucose meters have largely replaced other methods of self-monitoring The self-monitoring of blood glucose levels is seen as the greatest breakthrough in managing diabetes since the advent of insulin. What should premeal plasma glucose levels be? Bedtime glucose levels? 49

50 Glycosylated Glucose Levels
Glycosylated hemoglobin (HbA1c) reflects glucose levels over the past few months Fructosamine levels reflect those over several weeks 50

51 Complications of Therapy
Hypoglycemia A person injects too much insulin, does not eat enough, eats at the wrong time, or exercises inconsistently: glucose levels may suddenly drop Somogyi phenomenon Rebound hyperglycemia in response to hypoglycemia Dawn phenomenon An increase in fasting blood glucose levels between 5 and 9 AM that is not related to hypoglycemia The Somogyi phenomenon should be suspected when a patient reports awakening with a headache, and complains of restless sleep, nightmares, enuresis (involuntary voiding during sleep), and nausea and vomiting. How can the Somogyi phenomenon be confirmed? 51

52 Assessment Ketoacidosis: ketonuria, Kussmaul’s respirations, orthostatic hypotension, hypertension, nausea, vomiting, lethargy, or change in level of consciousness Hypoglycemic patient: expect to find tachycardia, anxiety, trembling, and decreasing level of consciousness Be alert for indications of hyperosmolar nonketotic coma 52

53 Assessment Attempt to determine the following Type of diabetes
Hypoglycemic agents: name, dosage, when last dose was taken Food and fluid intake for the past 3 days Relevant laboratory values: blood glucose, blood pH, bicarbonate levels, electrolytes, and osmolality and urine osmolality 53

54 Health History Chief complaint and history of present illness
Signs/symptoms that prompted patient to seek medical care Past medical history Type and duration of DM Name and dosage of prescribed medications and when they were last taken If patient monitors blood glucose, record type of equipment used, testing schedule, recent test results Family history Diabetes, heart disease, stroke, hypertension, hyperlipidemia 54

55 Health History Review of systems
Description of the patient’s general health Changes in skin moisture or turgor Inquire whether the patient has had floaters, diplopia (double vision), or blurred vision, or has seen white halos around objects Abdominal symptoms: diarrhea, abdominal bloating, and gas Problems passing or holding urine If any pain in the legs, note when it occurs Numbness, tingling, or burning in the extremities Changes in mental alertness or seizures 55

56 Health History Functional assessment
Explore factors that can affect patient’s ability to perform self-care, including literacy, financial resources such as health insurance, and family support The impact of diabetes on the patient’s life should be explored, including self-concept, social relationships, and employment. Why would a patient be asked for a 24-hour dietary history? 56

57 Health History Physical examination
Level of consciousness, posture and gait, and apparent well-being Vital signs, height, and weight Skin color, warmth, turgor, and lesions noted Inspect eye grounds for evidence of diabetic retinopathy or cataracts Be alert for a sweet, fruity odor to the patient’s breath that is common with ketoacidosis Carefully assess the feet Test gait, balance, and motor coordination 57

58 Interventions Ineffective Health Maintenance
Ineffective Therapeutic Regimen Management Risk for Deficient Fluid Volume Risk for Injury Activity Intolerance Chronic Pain Disturbed Sensory Perception or Impaired Skin Integrity Disturbed Thought Processes Ineffective Coping 58

59 Hypoglycemia 59

60 Pathophysiology Develops when the blood glucose level falls to less than 45 to 50 mg/dL Symptoms occur at different blood levels according to individual tolerances and how rapidly the level falls Hypoglycemia may result from causes other than the pharmacologic treatment for diabetes. What does regulation of blood glucose depend on? The causes of hypoglycemia may be divided into three categories: exogenous, endogenous, and functional 60

61 Causes Exogenous hypoglycemia
Results from outside factors acting on the body to produce a low blood glucose Include insulin, oral hypoglycemic agents, alcohol, or exercise 61

62 Causes Endogenous hypoglycemia
Occurs when internal factors cause an excessive secretion of insulin or an increase in glucose metabolism These conditions may be related to tumors or genetics 62

63 Causes Functional hypoglycemia
From a variety of causes, including gastric surgery, fasting, or malnutrition 63

64 Signs and Symptoms Glucose level falls rapidly, causes epinephrine, cortisol, glucagon, and growth hormone to be secreted in an attempt to increase glucose levels Symptoms: weakness, hunger, diaphoresis, tremors, anxiety, irritability, headache, pallor, and tachycardia A blood glucose level that falls over several hours: symptoms attributed to lack of essential glucose to brain tissue Symptoms: confusion, weakness, dizziness, blurred or double vision, seizure, and in severe cases, coma 64

65 Medical Diagnosis The diagnosis of hypoglycemia not associated with diabetes can be based on fasting blood glucose, OGTT, intravenous glucose tolerance test, and 72-hour inpatient fasting Whipple’s triad The presence of symptoms Documentation of low blood glucose when symptoms occur Improvement of symptoms when blood glucose rises 65

66 Medical Treatment In an unconscious patient who has diabetes, hypoglycemia should be suspected until it is ruled out 50 mL of 50% glucose solution should be administered immediately The patient with a milder form of hypoglycemia Treated with 15 g carbohydrate If the patient’s condition does not improve, another 15 g of carbohydrate should be given after 10 minutes 66

67 Medical Treatment Prevention of hypoglycemia by proper food intake
The diet is directed by the underlying cause If overproduction of insulin after carbohydrate ingestion, a low-carbohydrate, high-protein diet Restriction of carbohydrates to no more than 100 g/day is recommended Simple sugars avoided; complex carbohydrates encouraged Patients may tolerate smaller, more frequent meals. Alcohol should be avoided In an unconscious patient who has diabetes, hypoglycemia should be suspected until it is ruled out. What is the recommended amount of carbohydrates per day? 67

68 Assessment Present illness: shakiness, nervousness, irritability, tachycardia, anxiety, lightheadedness, hunger, tingling or numbness of the lips or tongue, nightmares, and crying out during sleep Note when episodes occur in relation to meals and particular food intake The past medical history documents diabetes, previous gastric surgery, abdominal cancer, or adrenal insufficiency Medications, paying particular attention to hypoglycemic agents 68

69 Assessment Note hypoglycemic agents, prescribed dose, and the time last dose taken Functional assessment: information about current diet, exercise, alcohol intake, and the effects of symptoms on daily activities Important aspects of the physical examination include general behavior, appearance, pulse, and blood pressure 69

70 Interventions Deficient Knowledge Risk for Injury Impaired Adjustment

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