Download Chapter 49 Endocrine III – Diabetes Mellitus

Chapter 49 Endocrine III – Diabetes Mellitus
Definition
- A chronic multisystem disease related to
o Abnormal insulin production
o Impaired insulin utilization
- Leading cause of
o End-stage renal disease
o Adult blindness
o Non-traumatic lower limb amputations
- Major contributing factor
o Heart disease
o Stroke
Prevalence
- 20.8 million People with diabetes in the U.S.
- 41 million people with prediabetes
Etiology and Pathophysiology
- Theories link cause to single/ combination of these factors
o Genetic
o Autoimmune
o Viral
o Environmental
- Two most common types
o Type 1
o Type 2
- Other types
o Gestational
o Prediabetes
o Secondary diabetes
- Normal insulin metabolism
o Produced by the  cells
 Islets of Langerhans
o Released continuously into bloodstream in small increments with larger amounts
released after food intake
 Stabilizes glucose range to 70-120 mg/dl
-
Insulin
o Promotes glucose transport from bloodstream across cell membrane to cytoplasm of
cell
o Decreases glucose in the bloodstream
o Stimulates storage of glucose as glycogen in liver and muscle
o Inhibits gluconeogenesis
o Enhances fat deposition
o ↑ Protein synthesis
o Insulin-dependent tissues
 Skeletal muscle and adipose tissue
o Insulin-independent tissues
 Brain
 Blood
 Liver
-
Counterregulatory hormones
o Glucagon, epinephrine, growth hormone, cortisol
 Oppose effects of insulin
 Increase blood glucose levels
 Provide a regulated release of glucose for energy
 Help maintain normal blood glucose levels
Type 1 Diabetes Mellitus
- Formerly known as “juvenile onset” or “insulin-dependent” diabetes
- Most often occurs in people under 30 years of age
- Peak onset between 11 and 13 years of age
Causes
- Inherited Tendency
- Viral Infections
- Body Autoimmune System
Etiology and Pathophysiology
- Progressive destruction of pancreatic  cells by body’s own T cells
o Autoantibodies cause a reduction of 80% to 90% of normal  cell function before
manifestations occur
 Result in an absolute deficit of insulin
Onset of Disease
- Long preclinical period
o Antibodies present for months to years before symptoms occur
- Manifestations develop when pancreas can no longer produce insulin
o Rapid onset of symptoms
 Present at ER with ketoacidosis
o History of recent, sudden weight loss
o Classic symptoms
 Polydipsia
 Polyuria
 Polyphagia
Treatment
- Insulin replacement
o Will require exogenous insulin to sustain life
Acute complications
- Hypoglycemia
o Most frequently encountered complication of Type I
- Diabetic ketoacidosis (DKA)
o Occurs in absence of exogenous insulin
o Life-threatening condition
o Results in metabolic acidosis
Type 2 Diabetes Mellitus
- Most prevalent type of diabetes
o Over 90% of patients with diabetes
- Usually occurs in people over 35 years of age
o Prevalence increases with age
Causes
- Excess Body Weight
- Family History
- Age
Etiology and Pathophysiology
- 80% to 90% of patients are overweight
o Most powerful risk factor
- Genetic basis
o Genetic mutations
 Lead to insulin resistance
 Greater in some ethnic populations
 Increased rate in African Americans, Asian Americans, Hispanic
Americans, and Native Americans
o Native Americans and Alaskan Natives: Highest rate of diabetes
in the world
- Four major metabolic abnormalities
o 1. Insulin resistance
 Body tissues do not respond to insulin
 Insulin receptors either unresponsive or insufficient in number
o Results in hyperglycemia
o 2. Pancreas
 ↓ ability to produce insulin
 β cells fatigued from compensating
 β-cell mass lost
o 3. Inappropriate glucose production from liver
 Liver’s response of regulating release of glucose is haphazard
 Not considered a primary factor in development of type 2
o 4. Alteration in production of hormones and adipokines
 Play a role in glucose and fat metabolism
 Contribute to pathophysiology of type 2 diabetes
Onset of Disease
- Gradual onset
o Person may go many years with undetected hyperglycemia
Clinical Manifestations
- Nonspecific symptoms
o May have classic symptoms of type 1
o Fatigue
o Recurrent infections
o Recurrent vaginal yeast or monilia infections
o Prolonged wound healing
o Visual changes
Treatment
- Increase insulin sensitivity
- Increase insulin production
- Augment insulin levels via exogenous administration
Acute complications
- Hypoglycemia
- Hyperosmolar hyperglycemic non-ketotic syndrome
o Life-threatening
 Osmotic fluid/electrolyte loss from hyperglycemia may become severe
 Hyperosmolar coma
Prediabetes
- Known as impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
o IGT: Fasting glucose levels higher than normal (>100 mg/dl but <126 mg/dl)
o IFG: 2-hour plasma glucose higher than normal (between 140 and 199 mg/dl)
- Not high enough for diabetes diagnosis
o Increase risk for developing type 2 diabetes
 If no preventive measure taken—usually develop diabetes within 10 years
-
-
Long-term damage already occurring
o Heart, blood vessels
 Usually present with no symptoms
Must watch for diabetes symptoms
o Polyuria
o Polyphagia
o Polydipsia
Gestational Diabetes
- Develops during pregnancy
o Detected at 24 to 28 weeks of gestation
 OGTT
o Usually normal glucose levels at 6 weeks postpartum
o Increased risk for cesarean delivery, perinatal death, and neonatal complications
o Increased risk for developing Type 2 in 5 to 10 years
Treatment
- Nutritional therapy
- Insulin
Secondary Diabetes
- Results from:
o Another medical condition
 Cushing syndrome
 Hyperthyroidism
 Pancreatitis
 Parenteral nutrition
 Cystic fibrosis
 Hematochromatosis
o Treatment of a medical condition that causes abnormal blood glucose level
 Corticosteroids (Prednisone)
 Thiazides
 Phenytoin (Dilantin)
 Atypical antipsychotics (clozapine)
- Usually resolves when underlying condition treated
Diagnostic Studies
- Three methods of diagnosis
o Fasting plasma glucose level >126 mg/dl
o Random or casual plasma glucose measurement ≥200 mg/dl plus symptoms
o Two-hour OGTT level ≥200 mg/dl using a glucose load of 75 g
- Hemoglobin A1C test
o Useful in determining glycemic levels over time
o Monitors success of treatment
 Shows the amount of glucose attached to hemoglobin molecules over RBC life
span
 90 to 120 days
o
o
o
Regular assessments required
 Recommended 3-4 times annually
Ideal goal
 ADA ≤7.0%
 American College of Endocrinology <6.5%
Normal A1C reduces risk of retinopathy, nephropathy, and neuropathy
 Calculated
 HbA1c = (46.7 +Plasma Glucose) / 28.7
Plasma Glucose = (28.7 * HbA1c) - 46.7
HbA1c
4.0
4.1
4.2
4.3
4.4
4.5
4.6
4.7
4.8
4.9
Glucose
68
71
74
77
80
82
85
88
91
94
HbA1c
5.0
5.1
5.2
5.3
5.4
5.5
5.6
5.7
5.8
5.9
Glucose
97
100
103
105
108
111
114
117
120
123
HbA1c
6.0
6.1
6.2
6.3
6.4
6.5
6.6
6.7
6.8
6.9
Glucose
125
128
131
134
137
140
143
146
148
151
HbA1c
7.0
7.1
7.2
7.3
7.4
7.5
7.6
7.7
7.8
7.9
Glucose
154
157
160
163
166
169
171
174
177
180
HbA1c
8.0
8.1
8.2
8.3
8.4
8.5
8.6
8.7
8.8
8.9
Glucose
183
186
189
192
194
197
200
203
206
209
HbA1c
9.0
9.1
9.2
9.3
9.4
9.5
9.6
9.7
9.8
9.9
Glucose
212
214
217
220
223
226
229
232
235
237
HbA1c
10.0
10.1
10.2
10.3
10.4
10.5
10.6
10.7
10.8
10.9
Glucose
240
243
246
249
252
255
258
260
263
266
HbA1c
11.0
11.1
11.2
11.3
11.4
11.5
11.6
11.7
11.8
11.9
Glucose
269
272
275
278
280
283
286
289
292
295
HbA1c
12.0
12.1
12.2
12.3
12.4
12.5
12.6
12.7
12.8
12.9
Glucose
298
301
303
306
309
312
315
318
321
324
HbA1c
13.0
13.1
13.2
13.3
13.4
13.5
13.6
13.7
13.8
13.9
Glucose
326
329
332
335
338
341
344
346
349
352
Goals of diabetes management
- Decrease symptoms
- Promote well-being
- Prevent acute complications
- Delay onset and progression of long-term complications
Patient teaching
- Self-monitoring of blood glucose
- Nutritional therapy
- Drug therapy
- Exercise
Drug Therapy
- Insulin
o Exogenous insulin
 Insulin from an outside source
 Required for type 1 diabetes
 Prescribed for patient with type 2 diabetes who cannot control blood
glucose by other means
- Types of insulin
o Human insulin
 Only type used today
 Prepared through genetic engineering
o Insulins differ in regard to onset, peak action, and duration
 Characterized as rapid-acting, short-acting, intermediate-acting, long-acting
 Different types of insulin may be used for combination therapy

-
-
-
Rapid-acting: Lispro (Humalog), aspart (Novolog), and glulisine (Apidra)
 Injected 0 to 15 minutes before meal
o Onset of action 15 minutes
 Short-acting: Regular
 Injected 30 to 45 minutes before meal
o Onset of action 30 to 60 minutes
 Intermediate-acting: NPH
 Long-acting: Glargine (Lantus), detemir (Levemir)
 Injected once a day at bedtime or in the morning
o Released steadily and continuously
 No peak action
 Cannot be mixed with any other insulin or
solution
Storage of insulin
o Do not heat/freeze
o In-use vials may be left at room temperature up to 4 weeks
o Extra insulin should be refrigerated
o Avoid exposure to direct sunlight
Administration of insulin
o Cannot be taken orally
o Subcutaneous injection for self-administration
o Fastest absorption from abdomen, followed by arm, thigh, buttock
 Abdomen -- Preferred site
o Do not inject in site to be exercised
 Why?
Insulin pump
o Continuous subcutaneous infusion
o Battery-operated device
o Connected via plastic tubing to a catheter inserted into subcutaneous tissue in
abdominal wall
o Potential for tight glucose control
Problems with insulin therapy
- Hypoglycemia
o Episodes are caused by an excess of the medications used to lower blood glucose
relative to food intake and activity level
o More than 50% of all episodes of severe hypoglycemia occur during the night
o Exercise with failure to increase carbohydrates or reduce insulin
o Concomitant use of sulfa antibiotics with sulfonylureas
- Somogyi effect
o Rebound effect in which an overdose of insulin causes hypoglycemia
 Counterregulatory hormones released
- Dawn phenomenon
o Characterized by hyperglycemia present on awakening in the morning
 Due to release of counterregulatory hormones in predawn hours
 Growth hormone/cortisol possible factors
Drug Therapy
- Oral Agents
o Not insulin
o Work to improve mechanisms by which insulin and glucose are produced and used by
the body
 Work on three defects of type 2 diabetes
 Insulin resistance
 Decreased insulin production
 Increased hepatic glucose production
 Sulfonylureas
 Meglitinides
 Biguanides
 α-Glucosidase inhibitors
 Thiazolidinediones
- Sulfonylureas
o ↑ Insulin production from pancreas
o ↓ Chance of prolonged hypoglycemia
 10% experience decreased effectiveness after prolonged use
 Examples
o Glipizide (Glucotrol)
o Glimepiride (Amaryl)
- Meglitinides
o Increase insulin production from pancreas
o Taken 30 minutes before each meal up to time of meal
 Should not be taken if meal skipped
 Examples
o Repaglinide (Prandin)
o Nateglinide (Starlix)
Biguanides
o Reduce glucose production by liver
o Enhance insulin sensitivity at tissues
o Improve glucose transport into cells
 Do not promote weight gain
 Example
o Metformin (Glucophage)
- α-Glucosidase inhibitors
o “Starch blockers”
 Slow down absorption of carbohydrate in small intestine
 Example
o Acarbose (Precose)
- Thiazolidinediones
o Most effective in those with insulin resistance
 Improves insulin sensitivity, transport, and utilization at target tissues
 Examples
o Pioglitazone (Actos)
o Rosiglitazone (Avandia)
-
-
Incretin mimetic
o Synthetic peptide
 Stimulates release of insulin from  cells
 Suppresses glucagon secretion
 Reduces food intake
 Slows gastric emptying
 Not to be used with insulin
 Example
o Byetta
-Adrenergic blockers
o Mask symptoms of hypoglycemia
o Prolong hypoglycemic effects of insulin
Nutritional Therapy
- Cornerstone of care for person with diabetes
o Most challenging for many people
 Recommended that diabetes nurse educator and registered dietitian with
diabetes experience be members of team
- American Diabetes Association (ADA)
o Guidelines indicate that within context of an overall healthy eating plan, person with
diabetes can eat same foods as person who does not have diabetes
- Overall goal
o Assist people in making changes in nutrition and exercise habits that will lead to
improved metabolic control
- Type 1 diabetes mellitus
o Meal plan based on individual’s usual food intake and is balanced with insulin and
exercise patterns
o Insulin regimen managed day to day
- Type 2 diabetes mellitus
o Emphasis based on achieving glucose, lipid, and blood pressure goals
o Calorie reduction
- Food composition
o Nutrient balance of diabetic diet is essential
o Carbohydrates and monounsaturated fats should provide 45% to 65% of total energy
intake
 ↓ Carbohydrate diets are not recommended for diabetics
o Glycemic index (GI)
 Term used to describe rise in blood glucose levels after consuming
carbohydrate-containing food
 Should be considered when formulating a meal plan
o Fats should comprise no more than 25% to 30% of meal plan’s total calories
 <7% from saturated fats
o
o
Protein should contribute <10% of total energy consumed
 Intake should be significantly less than general population
Alcohol
 High in calories
 No nutritive value
-
 Promotes hypertriglyceridemia
 Detrimental effects on liver
 Can cause severe hypoglycemia
Diet teaching
o Dietitian initially provides instruction
 Should include patient’s family and significant others
Exercise
- Essential part of diabetes management
o ↑ Insulin receptor sites
o Lowers blood glucose levels
 Several small carbohydrate snacks can be taken every 30 minutes during
exercise to prevent hypoglycemia
o Contributes to weight loss
o Best done after meals
- Exercise plans should be started after medical clearance
o Slowly with gradual progression
o Should be individualized
- Monitor blood glucose levels before, during, and after exercise
Monitoring Blood Glucose
- Self-monitoring of blood glucose (SMBG) enables patient to make self-management decisions
regarding diet, exercise, and medication
- Important for detecting episodic hyperglycemia and hypoglycemia
- Supplies immediate information about blood glucose levels
o What are the steps to checking a FSBG?
Acute complications of DM
- Hypoglycemia
- DKA
- HHS or HHNK
Acute intervention
- Hypoglycemia
o Low blood glucose
 Occurs when Too much insulin in proportion to glucose in the blood
 Blood glucose level less than 70 mg/dl
o Common manifestations
 Confusion
 Irritability
 Diaphoresis
 Tremors
 Hunger
 Weakness
 Visual disturbances
 Can mimic alcohol intoxication
o
Untreated can progress to loss of consciousness, seizures, coma, and death
o
Causes
 Mismatch in timing food intake and peak action of insulin or oral hypoglycemic
agents
o
o
o
o
o
-
Hypoglycemic unawareness
 Person does not experience warning signs/symptoms, increasing risk for
decreased blood glucose levels
 Related to autonomic neuropathy
 May also be caused by β-blockers
At first sign
 Check blood glucose
 If <70 mg/dl, begin treatment
 If >70 mg/dl, investigate further for cause of signs/symptoms
o If monitoring equipment not available, treatment should be
initiated
Treatment
 If alert enough to swallow
 15 to 20 g of a simple carbohydrate
o 4 to 6 oz fruit juice
o Regular soft drink
 Avoid foods with fat
o Decrease absorption of sugar
Do not overtreat
 Recheck blood sugar 15 minutes after treatment
 Repeat until blood sugar >70 mg/dl
 Patient should eat regularly scheduled meal/snack to prevent rebound
hypoglycemia
 Check blood sugar again 45 minutes after treatment
 If no improvement after 2 or 3 doses of simple carbohydrate or patient not alert
enough to swallow
 Administer 1 mg of glucagon IM or subcutaneously
o Side effect: Rebound hypoglycemia
 Have patient ingest a complex carbohydrate after recovery
In acute care settings
 20 to 50 ml of 50% dextrose IV push
Diabetic ketoacidosis (DKA)
o Caused by profound deficiency of insulin
 Characterized by
 Hyperglycemia
 Ketosis
 Acidosis
 Dehydration
 Most likely occurs in type 1
o Precipitating factors
 Illness
 Infection
 Inadequate insulin dosage
 Undiagnosed type 1
 Poor self-management
o
o
o
o
 Neglect
When supply of insulin insufficient
 Glucose cannot be properly used for energy
 Body breaks down fats stores
 Ketones are by-products of fat metabolism
o Alters pH balance, causing metabolic acidosis
 Ketone bodies excreted in urine
 Electrolytes become depleted
Signs and symptoms
 Lethargy/weakness
 Early symptoms
 Dehydration
 Poor skin turgor
 Dry mucous membranes
 Tachycardia
 Orthostatic hypotension
 Abdominal pain
 N/V
 Kussmaul respirations
 Rapid deep breathing
o Attempt to reverse metabolic acidosis
 Sweet fruity odor
Laboratory findings
 Blood glucose > 300 mg/dl
 Arterial blood pH below 7.30
 Serum bicarbonate level <15 mEq/L
 Ketones in blood and urine
Treatment
 Correct fluid/electrolyte imbalance
 Fluid replacement is the priority intervention
 IV infusion 0.45% or 0.9% NaCl
o Restore urine output
o Raise blood pressure
 When blood glucose levels approach 250 mg/dl
 5% dextrose added to regimen
o Prevent hypoglycemia
 Potassium replacement
 Acidosis leads to hyperkalemia but as the glucose levels and pH levels
are corrected hypokalemia can occur
 Sodium bicarbonate
 If pH <7
 Insulin therapy
 Withheld until fluid resuscitation has begun
o Bolus followed by insulin drip
 Must be administered via IV pump
 Frequent FSBG checks
 Minimum hourly until stable
-
Hyperosmolar hyperglycemic syndrome (HHS)
o Life-threatening syndrome
 High mortality rate
 ~ 15%
o Less common than DKA
 Often occurs in patients over 60 years of age with type 2
o Patient has enough circulating insulin so ketoacidosis does not occur
 Produces fewer symptoms in earlier stages
 Neurologic manifestations occur due to ↑ serum osmolality
o Usually history of
 Inadequate fluid intake
 Increasing mental depression
 Polyuria
 Laboratory values
 Blood glucose >400 mg/dl
 Increase in serum osmolality
 Absent/minimal ketone bodies
o Therapy similar to DKA
 Except HHS requires greater fluid replacement
 Renal status
 Cardiopulmonary status
- Assessment in DKA and HHS
- Level of consciousness
- Signs of potassium imbalance
o Cardiac monitoring
- Vital signs
Stress of illness and surgery
- ↑ Blood glucose level
Continue regular meal plan
- ↑ Intake of noncaloric fluids
- Continue taking oral agents and insulin
o Frequent monitoring of blood glucose
 Ketone testing if glucose >240 mg/dl
- Patients undergoing surgery or radiologic procedures requiring contrast medium should hold
their metformin day of surgery and 48 hours
o Begun after serum creatinine has been checked and is normal
Ambulatory and home care
- Overall goal is to enable patient or caregiver to reach an optimal level of independence
o Insulin therapy and oral agents
 Education on proper administration, adjustment, and side effects
 Assessment of patient’s response to therapy
o Personal hygiene
 Regular bathing with emphasis on foot care
o Medical identification and travel card
 Must carry identification indicating diagnosis of diabetes
Chronic Complications
- Angiopathy
o Macrovascular


-
-
Diseases of large and medium-sized blood vessels
 Occur with greater frequency and with an earlier onset in diabetics
o Development promoted by altered lipid metabolism common to
diabetes
 Tight glucose control may delay atherosclerotic process
Risk factors
 Obesity
 Smoking
 Hypertension
 High-fat intake
 Sedentary lifestyle
Patients with diabetes should be screened for dyslipidemia at diagnosis

Angiopathy
o Microvascular
 Result from thickening of vessel membranes in capillaries and arterioles
 In response to chronic hyperglycemia
o Is specific to diabetes unlike macrovascular
 Areas most noticeably affected
 Eyes (retinopathy)
 Kidneys (nephropathy)
 Skin (dermopathy)
o Clinical manifestations usually appear after 10 to 20 years of
diabetes
Diabetic retinopathy
o Microvascular damage to retina
 Result of chronic hyperglycemia
 Most common cause of new cases of blindness in people 20 to 74 years
of age
 Earliest and most treatable stages often produce no changes in vision
 Must have annual dilated eye examinations
-
-
-
Diabetic nephropathy
o Associated with damage to small blood vessels that supply the glomeruli of the kidney
 Leading cause of end-stage renal disease
o Critical factors for prevention/delay
o Tight glucose control
o Blood pressure management
 Angiotensin-converting enzyme (ACE) inhibitors
 Used even when not hypertensive
 Angiotensin II receptor antagonists
o Yearly screening
 Microalbuminuria in urine
 Serum creatinine
Diabetic neuropathy
o 60% to 70% of patients with diabetes have some degree of neuropathy
 Nerve damage due to metabolic derangements of diabetes
o Sensory neuropathy
 Distal symmetric
 Most common form
o Affects hands and/or feet bilaterally
 Characteristics
o Loss of sensation, abnormal sensations, pain, and paresthesias
o Usually worse at night
o Foot injury and ulcerations can occur without the patient having
pain
o Can cause atrophy of small muscles of hands/feet
 Treatment
 Tight blood glucose control
 Drug therapy
o Prevent transmission of pain signals
 Topical creams
 Tricyclic antidepressants
 Selective serotonin and norepinephrine reuptake
inhibitors
 Antiseizure medications
Autonomic neuropathy
o Can affect nearly all body systems
 Complications
 Gastroparesis
o Delayed gastric emptying
 Cardiovascular abnormalities
 Sexual function
 Neurogenic bladder
-
Complications of feet and lower extremities
o Foot complications
 Most common cause of hospitalization in diabetes
 Result from combination of microvascular and macrovascular diseases
 Risk factors
 Sensory neuropathy
 Peripheral arterial disease
 Other contributors
 Smoking
 Clotting abnormalities
 Impaired immune function
 Autonomic neuropathy
-
Infection
o Diabetics more susceptible to infections
 Defect in mobilization of inflammatory cells
 Impairment of phagocytosis by neutrophils and monocytes
 Loss of sensation may delay detection
o Treatment must be prompt and vigorous
-
Gerontologic Considerations
Prevalence increases with age
Hypoglycemia unawareness is more common
Must consider patient’s desire for treatment and coexisting medical problems
o Recognize limitations in physical activity, manual dexterity, and visual acuity