55 terms



Terms in this set (...)

A. Describe the etiology, pathophysiology and clinical manifestations of Type 1 Diabetes Mellitus (DM).
More common in young persons but can occur at any age

Signs and symptoms abrupt, but disease process may be present for several years

Accounts for 5%-10% of all types of diabetes

Environmental factors-Virus, toxins


Islet cell antibodies-Often present at onset

Endogenous insulin-Minimal or absent

Thin, normal, or obese

Thirst, polyuria, polyphagia, fatigue, weight loss

Prone at onset or during insulin deficiency

Nutritional therapy-Essential

Insulin-Required for all

Vascular and neurologic complications-Frequent
A. Describe the etiology, pathophysiology and clinical manifestations of Type 2 Diabetes Mellitus (DM).
Usually age 35 yr or older but can occur at any age
Incidence is increasing in children

Insidious, may go undiagnosed for years
Accounts for 90%-95% of all types of diabetes

Environmental factors-obesity, lack of exercise

Primary defect-Insulin resistance, decreased insulin production over time, and alterations in production of adipokines

Islet cell antibodies- absent

Endogenous insulin-Possibly excessive; adequate but delayed secretion or reduced utilization; secretions diminish over time

Obese or normal

Symptoms: Frequently none, fatigue, recurrent infections

Ketosis: Resistant except during infection or stress

Nutritional therapy-Essential

Insulin-Required for some

Vascular and neurologic complications-Frequent
B. Correlate the American Diabetes Association recommendations for patients with diabetes with current nursing care.
The American Diabetes Association and the Endocrinologists are the data gatherers for best practice.

This helps us to provide evidence-based care as nurses and helps us teach about glucose monitoring, medications, exercise and stress
C. Interpret and analyze the laboratory testing used for diagnosis and management of patients with diabetes. Fasting blood glucose
Dx above 126 mg/dL
(normal is below 100)
(prediabetes is about 100 but below 126)
C. Interpret and analyze the laboratory testing used for diagnosis and management of patients with diabetes. Oral glucose tolerance test
2 hour glucose values >200 mg/dL
C. Interpret and analyze the laboratory testing used for diagnosis and management of patients with diabetes. Random glucose
greater than 200 mg/dL with symptoms: three P's, weight loss
(three P's: polydipsia, polyphagia, polyuria)
C. Interpret and analyze the laboratory testing used for diagnosis and management of patients with diabetes. Prediabetes
at an increased risk for developing diabetes. In this condition the blood glucose levels are high but not high enough to meet the diagnostic criteria for diabetes. This group has impaired fasting glucose (IFG) or impaired glucose tolerance (IGT).
IGT: Impaired glucose tolerance
2 hours after a meal, plasma glucose is 140-199 mg/dL; 200 mg/dL or higher during an oral glucose tolerance test
IFG: Impaired fasting glucose
fasting blood glucose is greater than 100 mg/dL, but less than 126 mg/dL
C. Interpret and analyze the laboratory testing used for diagnosis and management of patients with diabetes. Glycosylated hemoglobin (HbA1c)
increased (less than 6.5% is considered good control)
indicates control for the past 120 days
C. Interpret and analyze the laboratory testing used for diagnosis and management of patients with diabetes.
The presence of C-peptide in serum and urine is a useful indicator of β-cell function.
Normal level is:
Fasting: 0.78-1.89 ng/mL or 0.26-0.62 nmol/L (SI units)
1 hour after glucose load: 5-12 ng/mL


C-peptide levels, more accurately reflect islet cell function as opposed to insulin levels in the following situations:

•Patients with diabetes who are treated with exogenous insulin and who have antiinsulin antibodies.
•Patients who secretly administer insulin to themselves (factitious hypoglycemia). Insulin levels will be elevated. Direct insulin measurement in these patients tends to be high because the insulin measured is the self-administered exogenous insulin. But C-peptide levels in that same specimen will be low because exogenously administered insulin suppresses endogenous insulin (and C-peptide) production.
•Diabetic patients who are taking insulin. This is done to see if the diabetic patient is in remission and may not need exogenous insulin.
•Distinguishing type I from type II diabetes. This is particularly helpful in newly diagnosed diabetics. A person whose pancreas does not make any insulin (type I diabetes) has low levels of insulin and C-peptide. A person with type II diabetes has a normal or high level of C-peptide.
C. Interpret and analyze the laboratory testing used for diagnosis and management of patients with diabetes.
insulin antibodies, islet cell auto andibodies, glutamic acid decarboxylase (GAD), Tyrosine phosphatases
Insulin autoantibody [IAA], Islet cell antibody [ICA], Glutamic acid decarboxylase antibody [GAD Ab], Tyrosine phosphatases

Sixty percent to 80% of first-degree relatives with both ICA and IAA will develop IDDM within 10 years. GAD Ab provides confirmatory evidence. The presence of these antibodies identifies which gestational diabetic will eventually require insulin permanently.

Type I diabetes mellitus (DM) is insulin-dependent (IDDM). It is becoming increasingly recognized that this disease is an organ-specific form of autoimmune disease that results in destruction of the pancreatic islet cells and their products. These antibodies are used to differentiate type I DM from type II non-insulin-dependent DM. Nearly 90% of type I diabetics have one or more of these autoantibodies at the time of their diagnosis. Type II diabetics have low or negative titers.

Normal findings <1:4 titer; no antibody detected

the presence of insulin antibodies is diagnostic of factitious hypoglycemia from surreptitious administration of insulin. This antibody panel is also used in surveillance of patients who have received pancreatic islet cell transplantation. Finally, these antibodies can be used to identify late onset type I diabetes in those patients previously thought to have type II diabetes.
D. Describe nursing management and collaborative care of patients with prediabetes and diabetes mellitus using the nursing process. Assessment
History and physical examination

Blood tests, including fasting blood glucose, postprandial blood glucose, A1C, lipid profile, blood urea nitrogen and serum creatinine, electrolytes, TSH

Urine for complete urinalysis, microalbuminuria, and acetone (if indicated)

Blood pressure

ECG (if indicated)

Funduscopic examination—dilated eye examination

Dental examination

Neurologic examination, including monofilament test for sensation to lower extremities

Ankle-brachial index (ABI) (if indicated)

Foot (podiatric) examination

Monitoring of weight
D. Describe nursing management and collaborative care of patients with prediabetes and diabetes mellitus using the nursing process. Diagnosis
1.A1C ≥6.5%.

2.Fasting plasma glucose (FPG) level ≥126 mg/dL (7.0 mmol/L).
Fasting is defined as no caloric intake for at least 8 hours.

3.Two-hour plasma glucose level ≥200 mg/dL (11.1 mmol/L) during an OGTT, using a glucose load of 75 g.

4.In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight loss) or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).
D. Describe nursing management and collaborative care of patients with prediabetes and diabetes mellitus using the nursing process. Interventions



Stress Management
Interventions- food
Total carbohydrate
• Minimum of 130 g/day.
• Include carbohydrate from fruits, vegetables, whole grains, legumes, and low-fat milk.
• Monitor by carbohydrate counting, exchanges, or experienced-based estimation.
• Glycemic index may provide additional benefit.
• Sucrose-containing food can be substituted for other carbohydrates in the meal plan.
• Fiber intake at 14 g/1000 kcal (same as general population).
• Sugar alcohols and nonnutritive sweeteners are safe when consumed within FDA daily intake levels.

• 15%-20% of total calories.
• High-protein diets are not recommended for weight loss.

• Limit saturated fat to <7% of total calories.
• Trans fat should be minimized.
• Dietary cholesterol <200 mg/day.
• ≥2 servings of fish per week to provide polyunsaturated fatty acids.
Interventions- Activity
You should include the following information in the exercise teaching plan for patients with diabetes.

1. Exercise does not have to be vigorous to be effective. The blood glucose-reducing effects of exercise can be attained with exercise such as brisk walking.
2. The exercises selected should be enjoyable to foster regularity.
3. It is important to have properly fitting footwear.
4. The exercise session should have a warm-up period and a cool-down period. The exercise program should be started gradually and increased slowly.
5. Exercise is best done after meals, when the blood glucose level is rising.
6. Exercise plans should be individualized and monitored by the health care provider.
7. It is important to self-monitor blood glucose levels before, during, and after exercise to determine the effect exercise has on blood glucose level at particular times of the day.
•Before exercise, if blood glucose ≤100 mg/dL, eat a 10- to 15-g carbohydrate snack. After 15 to 30 min, retest blood glucose levels. Do not exercise if less than 100 mg/dL.
•Before exercise, if blood glucose ≥250 mg/dL in a person with type 1 diabetes and ketones are present, vigorous activity should be avoided.
8. Delayed exercise-induced hypoglycemia may occur several hours after the completion of exercise.
9. Taking a glucose-lowering medication does not mean that planned or spontaneous exercise cannot occur.
10. It is important to compensate for extensive planned and spontaneous activity by monitoring blood glucose level to make adjustments in the insulin dose (if taken) and food intake.
Interventions- Medications
Drug therapy
• Insulin
• Oral and other agents
• Enteric-coated aspirin (81-162 mg/day)
• Angiotensin-converting enzyme (ACE) inhibitors
• Angiotensin II receptor blockers (ARBs)
• Antihyperlipidemic drugs (see Table 34-6)
Interventions- Stress management
This area is often overlooked, but stress can be a cause of high blood sugar
E. Describe the role of nutrition and exercise in management of diabetes.
This is the most important factor in managing Diabetes
F. Discuss drug therapy in the treatment of DM.
1. Insulin
aspart (Novolo) rapid, 15 min onset, peak 60-90 min (3-4h) EAT
lispro (Humalog) rapid, 15 min onset, peak 60-90 min (3-4h) EAT
glulisine (Apidra) rapid, 15 min onset, peak 60-90 min (3-4h) EAT
regular -short acting Peak 2-3 hr (3-6h) (SQ, IV, IM) only reg IV

NPH -Intermediate action Peak 4-10 hr (10-16h) SQ
detemir (Levemir) - long acting(24h) no pronounced peak, onset 1-2 hr
glargine (Lantus) - long acting(24h) NO DEFINITE PEAK, onset 1-2 hr
(long acting are only SQ)

F. Discuss drug therapy in the treatment of DM.
2. Oral Agents
alpha-glucosidase inhibitor
Drugs that slow the absorption of carbs
Precose 75-300 mg in 3 doses lasts 2 hours
Glyset 25 to 100 mg in 3 doses lasts 2-3 hours
Take with firs bite of food at meal
F. Discuss drug therapy in the treatment of DM.
2. Oral Agents
Drugs that decrease glucose production in the LIVER and sensitize the body to insulin
Glucophage 500-2500 mg/2 doses lasts 12 hr
Glucophage XR 500-2000 mg/once/day
Riomet 500-2550 liquid lasts 12 hrs
Fortamet 1150-2000 mg once/day
May upset stomach
Take right after eating
Usu. 7-10 days to adjust GI system
F. Discuss drug therapy in the treatment of DM.
2. Oral Agents
incretin enhancers:
GLP-1 agonists
Drugs that increase or mimic the action of GLP-1 hormone
(makes you feel full, shuts down glucagon (slowing down liver sugar), slows stomach emptying (better digestion)
Byetta lasts for up to 10 hours, give 2xdaily
Victoza lasts for 24 hrs, give 1xday
Bydureon last for 7 days 1xweek
DPP-4 inhibitors (INCREASES GLP-1)
(DPP-4 is an enzyme that breaks down GLP-1)
*alogliptin +metformin
*alogliptin + pioglitazone
*sitagliptin + metformin
*onglyza +metformin
Don't use with insulin or SFU
F. Discuss drug therapy in the treatment of DM.
2. Oral Agents
Drugs that stimulate the pancreatic beta cells to make more insulin
use alone or with metformin
Up to 15-30 min before meals; 2, 3, or 4×/day preprandially
• Skip dose if meal skipped; add dose if meal added
F. Discuss drug therapy in the treatment of DM.
2. Oral Agents
drugs that stimulate the PANCREATIC beta cells to make more insulin
- also improve sensitivity to insulin and shut down liver sugar production
(may wear out beta cells more quickly)
**Most common drug to cause HYPOGLYCEMIA
Micronase, Dose 1.25-20 mg in 1-2 doses in 24 hours
DiaBeta, Dose 1.25-20 mg in 1-2 doses in 24 hours
Glynase PresTab, Dose 1.5-12 mg in 1-2 doses in 24 hours
Glucotrol (2.5 to 40 mg in 1-3 doses in 24 hrs)
Glucotrol XL (do not break in half) (5-20 mg in 1 dose in 24 hrs)
Amaryl (can use with insulin) (1-8 mg in 1 dose in 24 hrs)
F. Discuss drug therapy in the treatment of DM.
2. Oral Agents
drugs that sensitize the body to insulin
(will gain weight if not changing diet-actually will hurt in the end)
*teach that this should only be taken by patient that is on a regular exercise and food regimin
Actos 15 or 30 mg/day with a sulfonylurea, metformin, or insulin; decrease sulfonylurea dose if hypoglycemia occurs; decrease insulin dose by 10%-25% if hypoglycemia occurs or if plasma glucose is <100 mg/dl, max 45 mg/day
Liver fn tests prior to starting for ALT baseline, periodically,
discontinue if ALT>2.5
F. Discuss drug therapy in the treatment of DM.
2. Oral Agents
dopamine agonist
drugs that increase AM dopamine level
give within first 2 hours of waking, or metabolic cascade won't get a good start
(because dopamine response is suppressed, body says "I already have enough storage")
Improves glycemic control
by decreasing lipolysis in adipose tissue
decreasing postprandial hepatic glucose output
decreasing insulin resistance
F. Discuss drug therapy in the treatment of DM.
2. Oral Agents
SGLT2 inhibitor
drugs that decrease the reabsoption of glucose in the kidney (stops from going back into blood stream)
Invokana PO 100 mg-300 mg/day
(brand new drug for 2013)

Hypotension:Use with caution: patients on ACE-I or ARBS BP meds

Renal: don't use if eGFR 45 or less

*Hyperkalemia: Use with caution: Patients on K+ sparing diuretics, ACE-I, ARBS (lisinopril, losartin)

HYPOGLYCEMIA: with concomitant use of insulin, insulin secretagogues, -sulfonylureas (TANK FASTER)

DEHYDRATION- important to hydrate, may have false high BG, monitor blood volume

Genital mycotic infection- mostly in females (yeast)
G. Contrast pharmacodynamics of diabetic medications.
Sulfonureas and meglitinides
-both stimulate beta cells to make more insulin

Thiazolidinediones and biguanides
-sensitize body to insulin

Dopamine agonist
-increase AM dopamine level

SGLT2 inhibitor
-decrease reabsorption of glucose in kidney

GLP-1 agonists, DPP-4 inhibitors (incretin enhancers)
-Drugs that increase or mimic the action of GLP-1 hormone

-decrease glucose production in the liver and sensitize the body to insulin

Alpha-glucosidase inhibitor
-slow the absorption of carbs
H. Review techniques for the administration of insulin.
roll cloudy (NPH)
clear to cloudy
rotate injection sites within major site

• Before loading the syringe, disperse insulin suspensions (ie, NPH insulin preparations) by rolling the vial gently between the palms. Vigorous agitation causes frothing and must be avoided. If granules or clumps remain after mixing, discard the vial.

• Except for NPH insulin, all preparations are formulated as clear, colorless solutions, and hence can be administered without resuspension. If a preparation becomes cloudy or discolored, or if a precipitate develops, discard the vial.

• Before loading the syringe, swab the bottle cap with alcohol.

• Eliminate air bubbles from the syringe and needle after loading.

• Cleanse the skin (with alcohol or soap and water) prior to injection.

• Usual sites of injection are the abdomen, upper arm, and thigh. To minimize variability in responses, make all injections in just one of these areas. Injections in the abdomen provide the most consistent insulin levels and effects.

• Rotate the injection site within the general area employed (eg, the abdomen).

• Allow about 1 inch between sites. If possible, use each site just once a month.
I. Recognize the significance of cultural background relating to risk for DM.
genetic link (one or both parents)
Native American, Hispanic, African American
55 yrs or older
J. Review steps to include when teaching clients the proper use of glucose monitors.
Self-monitoring of blood glucose (SMBG) is a cornerstone of diabetes management. By providing a current blood glucose reading, SMBG enables the patient to make self-management decisions regarding diet, exercise, and medication. SMBG is also important for detecting episodic hyperglycemia and hypoglycemia.

Portable blood glucose monitors (meters) are used at the hospital bedside and by patients who perform SMBG. A wide variety of blood glucose monitors are available (Fig. 49-8). Disposable lancets are usually used to obtain a small drop of capillary blood (usually from a finger stick) that is placed onto a reagent strip. After a specified time, the monitor displays a digital reading of the blood glucose. The technology of SMBG is a rapidly changing field with newer and more convenient systems being introduced every year. Newer systems allow the user to collect blood from alternative sites such as the forearm or palm. Alternate site testing is not recommended with rapidly changing blood glucose readings or when symptoms of low blood glucose are present.

Continuous glucose monitoring (CGM) systems provide another route for monitoring glucose. The CGM systems available include the (1) DexCom Seven by DexCom, (2) MiniMed Paradigm REAL-Time System by Medtronic (3) Guardian REAL-Time by Medtronic, and (4) FreeStyle Navigator by Abbott. Using a sensor inserted subcutaneously under the skin, the systems display glucose values continuously with updated values occurring every 1 to 5 minutes. The sensor is inserted by the patient using an automatic insertion device. Data are sent from the sensor to a transmitter, which displays the glucose value on either an insulin pump (MiniMed Paradigm REAL-Time System and Guardian Real-Time) or a pager-like receiver (DexCom Seven and FreeStyle Navigator).
K. Identify the pathophysiology and clinical manifestations of acute complications of diabetes mellitus.
arise from events associated with hyperglycemia and insufficient insulin

Diabetic ketoacidosis (DKA), also referred to as diabetic acidosis and diabetic coma, is caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration. It is most likely to occur in people with type 1 diabetes but may be seen in type 2 in conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin. Precipitating factors include illness and infection, inadequate insulin dosage, undiagnosed type 1 diabetes, poor self-management, and neglect.

Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion (Fig. 49-12). HHS is less common than DKA. It often occurs in patients over 60 years of age with type 2 diabetes. Common causes of HHS in a patient with type 2 diabetes are infections of the urinary tract, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes. The main difference between HHS and DKA is that the patient with HHS usually has enough circulating insulin so that ketoacidosis does not occur.

Hypoglycemia, or low blood glucose, occurs when there is too much insulin in proportion to available glucose in the blood. This causes the blood glucose level to drop to less than 70 mg/dL (3.9 mmol/L). Once plasma glucose drops below 70 mg/dL (3.9 mmol/L), neuroendocrine hormones are released and the autonomic nervous system is activated. Suppression of insulin secretion and production of glucagon and epinephrine provide defense against hypoglycemia. Epinephrine release causes manifestations that include shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor. Because the brain requires a constant supply of glucose in sufficient quantities to function properly, hypoglycemia can affect mental functioning. These manifestations are difficulty speaking, visual disturbances, stupor, confusion, and coma. Manifestations of hypoglycemia can mimic alcohol intoxication. Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death.

Hypoglycemic unawareness is a condition in which a person does not experience the warning signs and symptoms of hypoglycemia until the glucose levels reach a critical point. Then the person may become incoherent and combative or lose consciousness. This is often related to autonomic neuropathy of diabetes that interferes with the secretion of counterregulatory hormones that produce these symptoms. Elderly patients and patients who use β-adrenergic blockers are also at risk for hypoglycemic unawareness.
K. Identify the pathophysiology and clinical manifestations of chronic complications of diabetes mellitus.
Chronic complications of diabetes are primarily those of end-organ disease from damage to blood vessels (angiopathy) secondary to chronic hyperglycemia (Fig. 49-13). Angiopathy is one of the leading causes of diabetes-related deaths, with about 68% of deaths due to cardiovascular disease and 16% due to strokes.

These chronic blood vessel dysfunctions are divided into two categories: macrovascular complications and microvascular complications.

Dermopathy (skin)
Neuropathy (foot and lower extremities)

cerebrovascular, cardiovascular, and peripheral vascular disease
Several theories exist as to how and why chronic hyperglycemia damages cells and tissues.
Possible causes include (1) the accumulation of damaging by-products of glucose metabolism, such as sorbitol, which is associated with damage to nerve cells; (2) the formation of abnormal glucose molecules in the basement membrane of small blood vessels such as those that circulate to the eye and kidney; and (3) a derangement in red blood cell function that leads to a decrease in oxygenation to the tissues.
L. Differentiate between the diagnosis, assessment, interventions, and evaluations of patients experiencing complications of diabetes such as:
1. Somogyi effect
A rebound effect in which an overdose of insulin induces hypoglycemia. Usually occurring during the hours of sleep, the Somogyi effect produces a decline in blood glucose level in response to too much insulin. Counterregulatory hormones are released, stimulating lipolysis, gluconeogenesis, and glycogenolysis, which in turn produce rebound hyperglycemia and ketosis. The danger of this effect is that when blood glucose levels are measured in the morning, hyperglycemia is apparent and the patient (or the health care professional) may increase the insulin dose. The Somogyi effect is associated with the occurrence of undetected hypoglycemia during sleep, although it can happen at any time.

The patient may report headaches on awakening and may recall having night sweats or nightmares. If the Somogyi effect is suspected as a cause for early morning high blood glucose, the patient may be advised to check blood glucose levels between 2:00 and 4:00 AM to determine if hypoglycemia is present at that time. If it is, the insulin dosage affecting the early morning blood glucose is reduced.
L. Differentiate between the diagnosis, assessment, interventions, and evaluations of patients experiencing complications of diabetes such as:
2. Dawn phenomenon
The dawn phenomenon is characterized by hyperglycemia that is present on awakening in the morning due to the release of counterregulatory hormones in the predawn hours. It has been suggested that growth hormone and cortisol are possible factors in this occurrence. The dawn phenomenon affects the majority of people with diabetes and tends to be most severe when growth hormone is at its peak in adolescence and young adulthood.

The treatment for dawn phenomenon is an adjustment in the timing of insulin administration or an increase in insulin. Your assessment must include insulin dose, injection sites, and variability in the time of meals or insulin administration. In addition, ask the patient to measure and document bedtime, nighttime (between 2:00 and 4:00 AM), and morning fasting blood glucose levels on several occasions. If the predawn levels are less than 60 mg/dL (3.3 mmol/L) and signs and symptoms of hypoglycemia are present, the insulin dosage should be reduced. If the 2:00 to 4:00 AM blood glucose is high, the insulin dosage should be increased. In addition, counsel the patient on appropriate bedtime snacks.
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
1. Diabetic ketoacidosis
• Dry mouth
• Thirst
• Abdominal pain* symptom of acidosis
• Nausea and vomiting
• Gradually increasing restlessness, confusion, lethargy
• Flushed, dry skin
• Eyes appear sunken
• Breath odor of ketones
• Rapid, weak pulse
• Labored breathing (Kussmaul respirations)-rapid and deep
• Fever
• Urinary frequency
• Serum glucose >250 mg/dL (13.9 mmol/L)
• Glucosuria and ketonuria


• Ensure patent airway.
• Administer oxygen via nasal cannula or non-rebreather mask.
• Establish IV access with large-bore catheter.
• Begin fluid resuscitation with 0.9% NaCl solution 1 L/hr until BP stabilized and urine output 30-60 mL/hr.
• Begin continuous regular insulin drip 0.1 U/kg/hr.
• Identify history of diabetes, time of last food, and time/amount of last insulin injection.

Ongoing Monitoring

• Monitor vital signs, level of consciousness, cardiac rhythm, oxygen saturation, and urine output.
• Assess breath sounds for fluid overload.
• Monitor serum glucose and serum potassium.
• Administer potassium to correct hypokalemia.
• Administer sodium bicarbonate if severe acidosis (pH <7.0).
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
2. Hyperosmolar hyperglycemic syndrome
Same as DKA, but glucose levels >600 mg/dL
No metabolic acidosis (no kussmaul respirations), very high serum osmolarity
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
3. Hypoglycemia

History (if possible) and physical examination
Blood glucose—stat

Collaborative Therapy

Determine cause of hypoglycemia (after correction of condition)

Conscious Patient
Administration of 15-20 g of quick-acting carbohydrate (e.g., 4-6 oz of regular soda, 8-10 LifeSavers, 1 tbs syrup or honey, 4 tsp jelly, 4-6 oz orange juice, 8 oz low-fat milk, commercial dextrose products [per label instructions])

Repetition of treatment in 15 min (if no improvement)
Administration of additional food of longer-acting combination carbohydrate plus protein or fat (e.g., crackers with peanut butter or cheese) after symptoms subside, if next meal is longer than 1 hr away
Immediate notification of health care provider or emergency service (if patient outside hospital) if symptoms do not subside after two or three administrations of quick-acting carbohydrate

Worsening Symptoms or Unconscious Patient
Subcutaneous or intramuscular injection of 1 mg glucagon
IV administration of 25-50 mL of 50% glucose
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
4. Macrovascular complications
peripheral vascular disease

target BP of less than 130/80
ADA goals for diabetics:
LDL cholesterol goal of less than 100 mg/dL
triglycerides less than 150 mg/dL
HDL cholesterol >40 mg/dL in men and >50 mg/dL in women
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
5. Microvascular complications
result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia.

microvascular complications are specific to diabetes.

microangiopathy: usu. eyes (retinopathy), the kidneys (nephropathy), and the skin (dermopathy)

clinical manifestations usually do not appear until 10 to 20 years after the onset of diabetes
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
5. Microvascular complications- retinopathy
retinopathy is the most common cause of new cases of blindness in people ages 20 to 74 years

The earliest and most treatable stages of diabetic retinopathy often produce no changes in the vision. Because of this, the patient with type 2 diabetes should have a dilated eye examination by an ophthalmologist or a specially trained optometrist at the time of diagnosis and annually thereafter for early detection and treatment. A person with type 1 diabetes should have the dilated eye examined within 5 years after the onset of diabetes and then repeated annually

Laser photocoagulation therapy reduces vision loss in proliferative retinopathy or macular edema and in some cases of nonproliferative retinopathy

advanced proliferative retinopathy- vitrectomy (aspiration of blood, membrane, and fibers from the inside of the eye through a small incision just behind the cornea)

Glaucoma occurs as a result of the occlusion of the outflow channels secondary to neovascularization. This type of glaucoma is difficult to treat and often results in blindness.

Cataracts develop at an earlier age and progress more rapidly in people with diabetes.
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
5. Microvascular complications- nephropathy
Diabetic nephropathy is a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney. It is the leading cause of end-stage renal disease (ESRD) in the United States (chronic hyperglycemia)
kidney disease can be significantly reduced when near-normal blood glucose control is achieved and maintained

screened for nephropathy annually with a measurement of the albumin-to-creatinine ratio in a random spot urine collection for albumin. A serum creatinine is also needed. Serum creatinine measurements provide an estimation of the glomerular filtration rate and thus the degree of kidney function

patients with diabetes who have microalbuminuria or macroalbuminuria, either angiotensin-converting enzyme (ACE) inhibitor drugs (e.g., lisinopril [Prinivil, Zestril]) or angiotensin II receptor antagonists (e.g., losartan [Cozaar]) should be used. Both classifications of these drugs are used to treat hypertension and have been found to delay the progression of nephropathy in patients with diabetes

HTN significantly accelerates nephropathy

Tight blood glucose control is also critical to the prevention and delay of diabetic nephropathy
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
5. Microvascular complications- neuropathy
pathophysiologic processes of diabetic neuropathy are not well understood. Several theories exist, including metabolic, vascular, and autoimmune elements.

The prevailing theory suggests that persistent hyperglycemia leads to an accumulation of sorbitol and fructose in the nerves that causes damage by an unknown mechanism. The result is reduced nerve conduction and demyelinization.

Ischemia in blood vessels damaged by chronic hyperglycemia that supply the peripheral nerves is also implicated in the development of diabetic neuropathy.

Neuropathy can precede, accompany, or follow the diagnosis of diabetes

Control of blood glucose is the only treatment for diabetic neuropathy, being effective in many, but not all cases

Sensory neuropathy is a major risk factor for lower extremity amputation in the person with diabetes.

Autonomic neuropathy can affect nearly all body systems and lead to hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention.

Erectile dysfunction (ED) in diabetic men is well recognized and common, often being the first manifestation of autonomic failure
M. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetic mellitus.
5. Microvascular complications- neuropathy- PAD (Peripheral Artery Disease)
PAD increases the risk for amputation by causing a reduction in blood flow to the lower extremities.

When blood flow is decreased, oxygen, white blood cells, and vital nutrients are not available to the tissues.

Therefore wounds take longer to heal and the risk for infection increases.

Signs of PAD include intermittent claudication, pain at rest, cold feet, loss of hair, delayed capillary filling, and dependent rubor (redness of the skin that occurs when the extremity is in a dependent position).

The disease is diagnosed by history, ankle-brachial index (ABI), and angiography.

Management includes control or reduction of risk factors, particularly smoking, high cholesterol intake, and hypertension. Bypass or graft surgery is indicated in some patients.

Proper care of the feet is essential for the patient with PAD
Diabetes - FOOT care
1. Wash feet daily with a mild soap and warm water. First test water temperature with hands.

2. Pat feet dry gently, especially between toes.

3. Examine feet daily for cuts, blisters, swelling, and red, tender areas. Do not depend on feeling sores. If eyesight is poor, have others inspect feet.

4. Use lanolin on feet to prevent skin from drying and cracking. Do not apply between toes.

5. Use mild foot powder on sweaty feet.

6. Do not use commercial remedies to remove calluses or corns.

7. Cleanse cuts with warm water and mild soap, covering with clean dressing. Do not use iodine, rubbing alcohol, or strong adhesives.

8. Report skin infections or nonhealing sores to health care provider immediately.

9. Cut toenails evenly with rounded contour of toes. Do not cut down corners. The best time to trim nails is after a shower or bath.

10. Separate overlapping toes with cotton or lamb's wool.

11. Avoid open-toe, open-heel, and high-heel shoes. Leather shoes are preferred to plastic ones. Wear slippers with soles. Do not go barefoot. Shake out shoes before putting on.

12. Wear clean, absorbent (cotton or wool) socks or stockings that have not been mended. Colored socks must be colorfast.

13. Do not wear clothing that leaves impressions, hindering circulation.

14. Do not use hot water bottles or heating pads to warm feet. Wear socks for warmth.

15. Guard against frostbite.

16. Exercise feet daily either by walking or by flexing and extending feet in suspended position. Avoid prolonged sitting, standing, and crossing of legs.
Physiological activity of insulin-Carbohydrate metabolism
• Increases glucose transport across cell membrane in most cells including muscle and fat
• Within liver and muscle, promotes glycogenesis, the storage form of glucose
• Inhibits gluconeogenesis and glycogenolysis in the liver, thus sparing amino acids and glycerol for protein and fatty acid synthesis
Physiological activity of insulin-Fat metabolism
• Increases triglyceride synthesis
• Increases fatty acid transport into adipose tissue
• Inhibits lipolysis of triglycerides stored in adipose tissue
• Stimulates fatty acid synthesis from glucose and other substrates
Physiological activity of insulin-Protein metabolism
• Increases amino acid transport across cell membrane of muscle and liver
• Augments protein synthesis
• Inhibits proteolysis
Gestational diabetes
criteria for high risk are severe obesity, prior history of gestational diabetes, presence of glycosuria, diagnosis of polycystic ovary syndrome, and strong family history of type 2 diabetes.

Women with average risk for gestational diabetes are to have an OGTT at 24 to 28 weeks of gestation.
Women with gestational diabetes have a higher risk for cesarean delivery, perinatal death, and neonatal complications.

Although most women with gestational diabetes will have normal glucose levels within 6 weeks postpartum, their risk for developing type 2 diabetes in 5 to 10 years is increased.

Nutritional therapy is considered to be the first-line therapy. If nutritional therapy alone does not achieve desirable fasting blood glucose levels, insulin therapy is usually indicated.

Gestational diabetes and management of the pregnant patient with diabetes is a specialized area not covered in detail in this chapter.
Metabolic syndrome
is characterized by insulin resistance, elevated insulin levels, high levels of triglycerides, decreased levels of high-density lipoproteins (HDLs), increased levels of low-density lipoproteins (LDLs), and hypertension.

Risk factors for metabolic syndrome include, but are not limited to, central obesity, sedentary lifestyle, urbanization/Westernization, and certain ethnicities (Native Americans, Hispanics, and African Americans).

Overweight individuals with metabolic syndrome can prevent or delay the onset of diabetes through a program of weight loss and regular physical activity.
Pink panther and Hockenberry BG targets
Under 5 yo: 80-200
5-11: 70-180
12 and older: 70-150
<7 ADA, <6.5 AACE
70-130 mg/dL AACE <110
<180 mg/dL AACE <140