METABOLIC & ENDOCRINE: DIABETES

DIABETES  After 8 to 12 hours without food, the

liver forms glucose from the
 Risk Factors: breakdown of non-carbohydrate
 Family history of diabetes (ie, parents or substances, including amino acids
siblings with diabetes) (gluconeogenesis).
 Obesity (ie, > 20% over desired body
weight or BMI > 27 kg/m2) A. Type 1 Diabetes
 Race/ethnicity (eg, African Americans  Characterized by the destruction of the
(less potassium), Hispanic Americans, pancreatic beta cells.
Native Americans, Asian Americans,  Combined genetic, immunologic, and
Pacific Islanders) possibly environmental factors are thought
 Age > 45 y/o (impaired pancreatic islet to contribute to beta-cell destruction.
function)  Destruction of the beta cells results in
 Previously identified impaired fasting decreased insulin production, increased
glucose or impaired glucose tolerance glucose production by the liver, and fasting
 Hypertension (> 140/90 mm Hg) hyperglycemia.
 HDL cholesterol level < 35 mg/dL (0.90  Glucose from food cannot be stored in the
mmol/L) and/or triglyceride level > 250 liver but instead remains in the
mg/dL (2.8 mmol/L) bloodstream and contributes to postprandial
 History of gestational diabetes or delivery (after meals) hyperglycemia.
of babies over 9 lb  If the concentration of glucose in the blood
 Insulin exceeds 180 to 200 mg/dL glucose appears
 A hormone secreted by beta cells. in the urine (glycosuria).
 An anabolic, or storage hormone.  When excess glucose is excreted in the
 Has the following actions: urine, it is accompanied by excessive loss of
 Transports and metabolizes glucose fluids and electrolytes (osmotic diuresis).
for energy Note: Excessive amount of glucose enters
 Stimulates storage of glucose in the the renal tubules, it draws a large amount of
liver and muscle (in the form of water that ends up producing a significant
glycogen) amount of urine.
 Signals the liver to stop the release of  Insulin normally inhibits glycogenolysis and
glucose gluconeogenesis, causing the opposite in
 Enhances storage of dietary fat in type 1 diabetes.
adipose tissue  Fat breakdown results in an increased
 Accelerates transport of amino acids production of ketone bodies (a highly acidic
(derived from dietary protein) into substance).
cells Note: Liver breakdown fat for energy use
 Inhibits the breakdown of stored since glucose is not converted to energy
glucose, protein, and fat  Diabetic ketoacidosis (DKA)
 Initially, the liver produces glucose  A metabolic derangement that occurs
through the breakdown of glycogen most commonly in persons with type 1
(glycogenolysis). diabetes.
 METABOLIC & ENDOCRINE: DIABETES
 Results from a deficiency of insulin; normal or slightly elevated level. This is
formation of highly acidic ketone bodies called metabolic syndrome, which
causing metabolic acidosis. includes hypertension,
 The breath has a characteristic fruity hypercholesterolemia, and abdominal
odor due to the presence of ketoacids. obesity.

B. Type 2 Diabetes
 There is enough insulin present to
 Affects approximately 95% of adults with prevent the breakdown of fat and the
the disease. accompanying production of ketone
 The two main problems are: bodies. Therefore, DKA does not typically
occur in type 2 diabetes. However,
 Insulin resistance
 Decreased tissue sensitivity to uncontrolled type 2 diabetes may lead to
insulin. another acute problem—hyperglycemic
 May also lead to metabolic hyperosmolar nonketotic syndrome
syndrome (hypertension,  Common symptoms are fatigue, irritability,
hypercholesterolemia, abdominal polyuria, polydipsia, poorly healing skin
obesity, and other abnormities. wounds, vaginal infections, or blurred
vision.
 Impaired insulin secretion
 DKA does not typically occur in  Long-term diabetes complications include
type 2 diabetes. eye disease, peripheral neuropathy,
 If uncontrolled, may lead to peripheral vascular disease.
hyperglycemic hyperosmolar C. Gestational Diabetes
syndrome (HHS).
 Pathophysiology  Any degree of glucose intolerance with its
 Insulin resistance and Impaired insulin onset during pregnancy
secretion.  Hyperglycemia develops because of the
 Intracellular reactions are diminished secretion of placental hormones, which
 Increased glucose production by the liver, causes insulin resistance.
 Decreased insulin-stimulated glucose uptake  Women considered to be at high risk or
by the muscles average risk should have either an oral
 Glucose remains in the bloodstream glucose tolerance test (OGTT) or a glucose
 Increased amounts of insulin must be challenge test (GCT) followed by OGTT in
secreted women who exceed the glucose threshold
 Metabolic syndrome (hypertension, value of 140 mg/dL.
hypercholesterolemia, and abdominal  OGTT - blood sample will be taken from a
obesity) vein in the arm to test the starting blood
 Type 2 diabetes sugar level.
 Hyperglycemic Hyperosmolar Non- ketotic  The client will then drink a mixture of
glucose dissolved in water.
Syndrome
 The client will get another blood glucose
 To overcome insulin resistance and to
test 2 hours later (1 hr for pregnant
prevent the buildup of glucose in the blood,
women).
increased amounts of insulin must be
 Below 140 mg/dL: normal blood sugar
secreted to maintain the glucose level at a
 METABOLIC & ENDOCRINE: DIABETES
 Between 140 and 199: Impaired  Clinical Manifestations In General
glucose tolerance, or Pre-diabetes  Depend on the patient’s level of
 200 or higher: Diabetes hyperglycemia.
 GCT - measures the body's response to  Classic clinical manifestations include the
glucose. “three Ps”: Polyuria (increased urination),
 The client drinks a sugary solution. Polydipsia (increased thirst that occur as a
 One hour later, the client’s blood sugar result of the excess loss of fluid associated
level is measured. with osmotic diuresis), and Polyphagia
 A blood sugar level below 140 mg/dL (increased appetite)
(7.8 mmol/L) is considered normal.  Other symptoms include fatigue and
 A blood sugar level of 140 mg/dL (7.8 weakness, sudden vision changes, tingling
mmol/L) or higher might indicate or numbness in hands or feet, dry skin, skin
gestational diabetes. lesions or wounds that are slow to heal, and
 Initial management includes dietary recurrent infections.
modification and blood glucose  The onset of type 1 diabetes may also be
monitoring. associated with sudden weight loss or
 If hyperglycemia persists, insulin is nausea, vomiting, or abdominal pains, if
prescribed. DKA has developed.
 Goals for blood glucose levels during
pregnancy are 95 mg/dL or less before  Assessment and Diagnostic Findings
meals and 120 mg/dL or less 2 hours  An abnormally high blood glucose level is
after meals. the basic criterion for the diagnosis of
 After delivery, blood glucose levels in diabetes.
women with gestational diabetes usually  Fasting plasma glucose (FPG)
return to normal.
 Random plasma glucose
 However, many women who have had
gestational diabetes develop type 2
 Criteria for the Diagnosis of Diabetes
diabetes later in life (35% to 60%).
Mellitus
D. Latent Autoimmune Diabetes of Adults 1. Symptoms of diabetes plus casual plasma
(LADA) glucose concentration equal to or greater
than 200 mg/dL (11.1mmol/L). Casual is
 A slow-progressing form of autoimmune defined as any time of day without regard to
diabetes. time since last meal. The classic symptoms
 Patients with LADA are not insulin- of diabetes include polyuria, polydipsia, and
dependent in the initial 6 months of disease unexplained weight loss.
onset. 2. Fasting plasma glucose: greater than or
 Clinical manifestation of LADA shares the equal to 126 mg/dL (7.0mmol/L). Fasting
features of types 1 and 2 diabetes. is defined as no caloric intake for at least 8
hours.
 Prevention 3. Two-hour post load glucose: equal to or
 Type 2 diabetes can be prevented with greater than 200 mg/dL (11.1 mmol/L)
appropriate changes in lifestyle. during an oral glucose tolerance test. The
test should be performed as described by the
World Health Organization, using a glucose
 METABOLIC & ENDOCRINE: DIABETES
load containing the equivalent of 75 g  To maintain the pleasure of eating by
anhydrous glucose dissolved in water. In the only limiting food choices when
absence of unequivocal hyperglycemia with indicated by scientific evidence
acute metabolic decompensation, these  Meal Planning and Related
criteria should be confirmed by repeat Education:
testing on a different day. The third measure  Must consider the patient’s food
is not recommended for routine clinical preferences, lifestyle, usual
use. eating times, and ethnic and
cultural background.
 Medical Management  Helps prevent hypoglycemic
 The main goal of diabetes treatment is to reactions and maintain overall
normalize insulin activity and blood blood glucose control.
glucose levels to reduce the development of  Initial education addresses the
complications. importance of consistent eating
 The therapeutic goal for diabetes habits, the relationship of food
management is to achieve normal blood and insulin, and the provision of
glucose levels (euglycemia) without an individualized meal plan.
hypoglycemia while maintaining a high  In-depth follow-up education
quality of life. then focuses on management
 Diabetes management has five components: skills, such as eating at
nutritional therapy, exercise, monitoring, restaurants; reading food labels;
pharmacologic therapy, and education. and adjusting the meal plan for
1. Nutritional Therapy exercise, illness, and special
 To achieve and maintain: occasions.
a. Blood glucose levels in the  Caloric Requirements:
normal range or as close to  Calorie-controlled diets are
normal as is safely possible planned by first calculating a
b. A lipid and lipoprotein profile person’s energy needs and
that reduces the risk for vascular caloric requirements based on
disease age, gender, height, and weight.
c. Blood pressure levels in the  An activity element is then
normal range or as close to factored in to provide the actual
normal as is safely possible number of calories required for
 To prevent, or at least slow, the rate weight maintenance.
of development of the chronic  To promote a 1 to 2 lb weight
complications of diabetes by loss per week, 500 to 1000
modifying nutrient intake and calories are subtracted from the
lifestyle daily total.
 To address individual nutrition  The calories are distributed into
needs, taking into account personal carbohydrates, proteins, and fats,
and cultural preferences and and a meal plan is then
willingness to change developed, taking into account
the patient’s lifestyle and food
preferences.
 METABOLIC & ENDOCRINE: DIABETES
 Caloric Distribution: to the food exchange list and
 Carbohydrates - recommended emphasizes portion control of
is higher in carbohydrates (50- total servings of carbohydrate at
60%) than in fat (20% to 30%) meals and snacks.
and protein (10% to 20%).  Glycemic Index - used to
 Fats - reducing the total describe how much a given
percentage of calories from fat food increases the blood
sources to less than 30% of total glucose level compared with an
calories and limiting the amount equivalent amount of glucose.
of saturated fats to 10% of total 1. Combining starchy foods with
calories. protein- and fat-containing
 Protein - The meal plan may foods tends to slow their
include the use of some non- absorption and lower the
animal sources of protein (e.g., glycemic index.
legumes, whole grains) to help 2. In general, eating foods that
reduce saturated fat and are raw and whole results in a
cholesterol intake. lower glycemic index than
 Fiber – Soluble fiber—in foods eating chopped, puréed, or
such as legumes, oats, and some cooked foods (except meat).
fruits. Insoluble fiber is found in 3. Eating whole fruit instead of
whole-grain breads and cereals drinking juice decreases the
and in some vegetables. glycemic index, because fiber
 Food Classification Systems: in the fruit slows absorption.
 Exchange Lists - There are six 4. Adding foods with sugars to
main exchange lists: the diet may result in a lower
bread/starch, vegetable, milk, glycemic index if these foods
meat, fruit, and fat. Foods within are eaten with foods that are
one group (in the portion more slowly absorbed.
amounts specified) contain equal  Other Dietary Concerns:
numbers of calories and are 1. Alcohol Consumption
approximately equal in grams of o Alcohol is absorbed before
protein, fat, and carbohydrate. other nutrients and does not
 Nutrition Labels - Food require insulin for absorption.
manufacturers are required to o Large amounts can be
have the nutrition content of converted to fats, increasing
foods listed on their packaging. the risk for DKA.
The label includes information o Alcohol may decrease the
about how many grams of normal physiologic reactions
carbohydrate are in a serving of in the body that produce
food. glucose.
 Healthy Food Choices - An 2. Sweeteners
alternative to counting grams of o The use of artificial sweeteners
carbohydrate is measuring is acceptable, especially if it
servings or choices. It is similar
 METABOLIC & ENDOCRINE: DIABETES
assists in overall dietary  Inspect feet daily after exercise.
adherence.  Avoid exercise in extreme heat
o There are two main types of or cold.
sweeteners: nutritive and non-  Avoid exercise during periods
nutritive. The nutritive of poor metabolic control.
sweeteners contain calories,  Stretch for 10 to 15 minutes
and the Non-nutritive before exercising
sweeteners have few or no 3. Monitoring Glucose Levels and
calories in the amounts Ketones
normally used.  SMBG - a method of capillary
o Misleading Food Labels - blood glucose testing in which the
Foods labeled ―sugarless‖ or patient pricks their finger and applies
―sugar-free‖ may still provide a drop of blood to a test strip that is
calories equal to those of the read by a meter
equivalent sugar-containing  Recommended that SMBG
products if they are made with occurs when circumstances call
nutritive sweeteners. for it.
o Foods labeled “dietetic” are  Some common sources of error
not necessarily reduced-calorie include improper application of
foods. blood (e.g., drop too small),
2. Exercise damage to the reagent strips
 Extremely important in diabetes caused by heat or humidity, the
management because of its effects on use of outdated strips, and
lowering blood glucose and reducing improper meter cleaning and
cardiovascular risk factors. maintenance.
 The nurse instructs the patient to:  Nurses play an important role in
 Exercise three times each week providing initial education about
with no more than 2 consecutive SMBG techniques.
days without exercise.  For most patients who require
 Perform resistance training insulin, SMBG is
twice a week if you have type 2 recommended two to four
diabetes. times daily (usually before
 Exercise at the same time of day meals and at bedtime).
(preferably when blood glucose  For patients who take insulin
levels are at their peak) and for before each meal, SMBG is
the same duration each session. required at least three times
 Use proper footwear and, if daily before meals to determine
appropriate, other protective each dose.
equipment (i.e., helmets for  Patients are asked to keep a
cycling). record or logbook of blood
 Avoid trauma to the lower glucose levels so that they can
extremities, especially if you detect patterns.
have numbness due to peripheral  Testing is done at the peak action
neuropathy. time of the medication to
 METABOLIC & ENDOCRINE: DIABETES
evaluate the need for dosage  Insulin injections are given two
adjustments. or more times daily to control the
 Testing for Glycated Hemoglobin - blood glucose level.
also referred to as glycosylated  SMBG is a cornerstone of insulin
hemoglobin, HgbA1C, or A1C therapy. Insulin dose required
 A measure of glucose control for is determined by the level of
the past 3 months. glucose in the blood.
 When blood glucose levels are a. Preparations - vary according to
elevated, glucose molecules three main characteristics: time
attach to hemoglobin in red course of action, species
blood cells. (source), and manufacturer.
 The longer the amount of b. Insulin Regimens - vary from 1
glucose in the blood remains to 4 injections per day
above normal, the more glucose  Usually, there is a
binds to hemoglobin and the combination of a short-acting
higher the glycated hemoglobin insulin and a longer-acting
level becomes. insulin.
 This complex (hemoglobin  There are two general
attached to the glucose) is approaches to insulin
permanent and lasts for the life therapy: conventional and
of an individual red blood cell, intensive.
approximately 120 days.  There are no set guidelines as
 Testing for Ketones - Ketones (or to which insulin regimen
ketone bodies) accumulate in the should be used for which
blood and urine patient
 Ketones in the urine signal that  Conventional Regimen –
there is a deficiency of insulin simplified insulin
and control of type 1 diabetes is regimen.
deteriorating.  for the terminally
 The patient may use a urine ill, the older adult
dipstick to detect ketonuria. The who is frail and has
reagent pad on the strip turns limited self-care
purple when ketones are present abilities.
4. Pharmacologic Therapy  Intensive Regimen -
 In the absence of adequate insulin, complex insulin regimen.
pharmacologic therapy is essential.  Allows the patient more
 Insulin Therapy flexibility to change the
 In type 1 diabetes, exogenous insulin doses from day to
insulin must be given for life. day in accordance with
 In type 2 diabetes, insulin may changes in eating and
be necessary on a long-term basis activity patterns.
to control glucose levels.  The risk of severe
hypoglycemia increases
threefold in patients
 METABOLIC & ENDOCRINE: DIABETES
receiving intensive mimic the functioning of the
treatment. normal pancreas.
c. Complications of Insulin  Oral Antidiabetic Agents
Therapy  For patients who have type 2
 Systemic Allergic diabetes that cannot be treated
Reactions: the treatment is effectively with MNT and
desensitization. exercise alone.
 Insulin Lipodystrophy: a  Other Pharmacologic Therapy
localized reaction, in the  Pramlintide (Symlin) - a
form of either lipoatrophy or synthetic analogue of human
lipohypertrophy, occurring amylin. It acts to slow the rate
at the site of insulin at which food leaves the
injections. stomach and reduces appetite.
 Resistance to Injected  Exenatide (Byetta, Byduron) -
Insulin: Patients may derived from a hormone that is
develop insulin resistance produced in the small intestine
and require large insulin and has been found to be
doses. Immune antibodies deficient in type 2 diabetes.
develop and bind the insulin.  It is normally released after food
 Morning Hyperglycemia: is ingested to delay gastric
caused by several factors: the emptying and enhance insulin
dawn phenomenon, the secretion.
Somogyi effect, or insulin 5. Nursing Management
waning. 1. Managing Glucose Control in the
 The dawn phenomenon: Hospital Setting
thought to result from 2. Providing Patient Education
nocturnal surges in growth  Pathophysiology:
hormone secretion. a. Basic definition of diabetes
 Somogyi effect: nocturnal (having a high blood glucose
hypoglycemia followed by level)
rebound hyperglycemia. b. Normal blood glucose ranges
d. Methods of Insulin Delivery and target blood glucose levels
c. Effect of insulin and exercise
 Insulin Pens: Insulin is
(decrease glucose)
delivered by dialing in a dose
d. Effect of food and stress,
or pushing a button for every
including illness and infections
1- or 2- unit increment given.
(increaseglucose)
 Jet Injectors: deliver insulin
e. Basic treatment approaches
through the skin under
 Treatment modalities:
pressure in an extremely fine
a. Administration of insulin and
stream.
oral antidiabetes medications
 Insulin Pumps: involves the
b. Meal planning (food groups,
use of small, externally
timing of meals)
worn devices that closely
 METABOLIC & ENDOCRINE: DIABETES
c. Monitoring of blood glucose
and urine ketones
5. Mixing Insulins
 Recognition, treatment, and
 When rapid- or short-acting
prevention of acute
insulins are to be given
complications:
a. Hypoglycemia simultaneously with longer-acting
b. Hyperglycemia insulins, they are usually mixed
together in the same syringe.
 Pragmatic information:
a. Where to buy and store insulin,  The ADA recommends that the
syringes, and glucose regular insulin be drawn up first
monitoring supplies 6. Withdrawing Insulin
b. When and how to contact the  Instruct patients to inject air into
primary provider the bottle of insulin equivalent to
the number of units of insulin to be
3. Storing Insulin
 Should be refrigerated. withdrawn.
 Extremes of temperature should be 7. Selecting and Rotating the Injection
avoided; insulin should not be Site
allowed to freeze and should not  The four main areas for injection
be kept in direct sunlight or in a are the abdomen, upper arms
(posterior surface), thighs (anterior
hot car.
 The insulin vial in use should be surface), and hips.
kept at room temperature to  The speed of absorption is
greatest in the abdomen and
reduce local irritation at the
injection site. decreases progressively in the arm,
 Cloudy insulins should be thigh, and hip, respectively.
 Systematic rotation of injection
thoroughly mixed.
 Bottles of intermediate-acting sites within an anatomic area is
insulin should also be inspected for recommended to prevent localized
flocculation (frosted, whitish changes in fatty tissue
coating inside the bottle). (lipodystrophy)
 The patient should be encouraged
4. Selecting Syringes
to use all available injection sites
 currently, three sizes of U-100
insulin syringes are available: within one area rather than
 1-mL syringe, 100-unit randomly rotating sites from area
to area.
capacity
 0.5-mL syringe, 50-unit  The patient should try not to use
capacity the exact same site more than once
in 2 to 3 weeks.
 0.3-mL syringe, 30-unit
capacity  If the patient is planning to
exercise, insulin should not be
 Most insulin syringes have a
disposable 27- to 29-gauge needle injected into the limb that will be
that is approximately 0.5 in long. exercised.
8. Preparing the Skin - allow the skin
to dry after cleansing with alcohol
before injection.
 METABOLIC & ENDOCRINE: DIABETES
9. Inserting the Needle - for a normal or  Assessment and Diagnostic Findings:
overweight person, a 90-degree angle  The hypoglycemia may not be detected
is the best insertion angle. until moderate or severe CNS
 Aspiration is not necessary impairment occurs.
 Affected patients must perform SMBG on
 Acute Complications of Diabetes a frequent regular basis, especially before
1. Hypoglycemia (Insulin Reactions) driving or engaging in other potentially
 Occurs when the blood glucose falls to less dangerous activities.
than 70 mg/dL.  Management:
 Severe hypoglycemia: < 40 mg/dL 1. Treating with Carbohydrates -
 It can occur when there is too much insulin Immediate treatment must be given when
or oral hypoglycemic agents, too little food, hypoglycemia occurs.
or excessive physical activity.  The usual recommendation is for 15 g of
 It often occurs before meals, especially if a fast-acting concentrated source of
meals are delayed or snacks are omitted. carbohydrate.
 Clinical Manifestations:  It is not necessary to add sugar to juice,
 May be grouped into two categories: even if it is labeled as unsweetened juice
adrenergic symptoms and central
2. Initiating Emergency Measures - In
nervous system (CNS) symptoms.
emergency situations, for adults who are
 In mild hypoglycemia: the sympathetic
unconscious and cannot swallow, an
nervous system is stimulated, resulting
injection of glucagon 1mg can be given
in a surge of epinephrine and
either subq or IM.
norepinephrine. This causes symptoms
such as sweating, tremor, tachycardia,  After injection of glucagon, the patient
palpitation, nervousness, and hunger. may take as long as 20 minutes to
 In moderate hypoglycemia: the drop in regain consciousness.
blood glucose level deprives the brain  A concentrated source of carbohydrate
cells of needed fuel for functioning. followed by a snack should be given to
Signs of impaired function of the CNS the patient on awakening to prevent
may include inability to concentrate, recurrence of hypoglycemia (glucagon
headache, lightheadedness, confusion, onset is 8 to 10 minutes, and its action
memory lapses, numbness of the lips and lasts 12 to 27 minutes).
tongue, slurred speech, impaired  The patient should be turned to the side
coordination, emotional changes, to prevent aspiration in case the patient
irrational or combative behavior, double vomits.
vision, and drowsiness.  For patients who are unconscious or
 In severe hypoglycemia: CNS function cannot swallow, 25 to 50 mL of dextrose
is so impaired that the patient needs the 50% in water (D50W) may be
assistance of another person for administered IV.
treatment of hypoglycemia. Symptoms  Providing Patient Education
may include disoriented behavior,
seizures, difficulty arousing from sleep,
or loss of consciousness.
 METABOLIC & ENDOCRINE: DIABETES
2. Diabetic Ketoacidosis 2. Another effect of insulin deficiency or
deficit is the breakdown of fat (lipolysis)
 Caused by an absence or markedly into free fatty acids and glycerol.
inadequate amount of insulin.  The free fatty acids are converted into
 The three main clinical features of DKA are as ketone bodies by the liver.
follows:  Ketone bodies are acids; their
 Hyperglycemia accumulation in the circulation due to
 Dehydration and electrolyte loss lack of insulin leads to metabolic
 Acidosis acidosis.
 Clinical Manifestations:  Assessment and Diagnostic Findings:
 The hyperglycemia of DKA leads to  Blood glucose levels may vary between
polyuria, polydipsia (increased thirst), 300 and 800 mg/dL.
and marked fatigue.  Some patients have lower glucose values,
 In addition, the patient may experience and others have values of 1000 mg/dL or
blurred vision, weakness, and headache. higher (usually depending on the degree
 Patients with marked intravascular of dehydration).
volume depletion may have orthostatic  Evidence of ketoacidosis is reflected in
hypotension. low serum bicarbonate (0 to 15 mEq/L)
 Volume depletion may also lead to frank and low pH (6.8 to 7.3) values.
hypotension with a weak, rapid pulse.  Low partial pressure of carbon dioxide
 The ketosis and acidosis of DKA lead to (PCO2 10 to 30 mm Hg) reflects
gastrointestinal symptoms, such as respiratory compensation (Kussmaul
anorexia, nausea, vomiting, and respirations) for the metabolic acidosis.
abdominal pain.  Accumulation of ketone bodies is
 The patient may have acetone breath (a reflected in blood and urine ketone
fruity odor). measurements.
 In addition, hyperventilation (with very  Increased levels of creatinine, blood
deep, but not labored, respirations) may urea nitrogen (BUN), and hematocrit
occur. may also be seen with dehydration.
 Pathophysiology:  Management:
1.Without insulin, the amount of glucose 1. Rehydration
entering the cells is reduced, and the  The patient may need as much as 6
production and release of glucose by the to 10 L of IV fluid to replace fluid
liver are increased. losses caused by polyuria,
 In an attempt to rid the body of the hyperventilation, diarrhea, and
excess glucose, the kidneys excrete vomiting.
the glucose along with water and  Initially, 0.9% sodium chloride
electrolytes (e.g., sodium, potassium). (normal saline [NS]) solution is
 This osmotic diuresis, which is given at a rapid rate, usually 0.5 to
characterized by excessive urination 1 L per hour for 2 to 3 hours.
(polyuria), leads to dehydration and  After the first few hours, half-
marked electrolyte loss. strength NS solution is the fluid of
choice for continued rehydration,
 METABOLIC & ENDOCRINE: DIABETES
provided the blood pressure is stable potentially fatal) decreases in serum
and the sodium level is not low. potassium levels.
 Plasma expanders may be
necessary to correct severe 3. Hyperglycemic Hyperosmolar Syndrome
hypotension that does not respond to  A metabolic disorder of type 2 diabetes
IV fluid treatment. resulting from a relative insulin deficiency
2. Restoring Electrolytes - major concern initiated by an illness that raises the demand
during treatment of DKA is potassium. for insulin.
 The plasma concentration of  This is a serious condition in which
potassium tends to be high hyperosmolarity and hyperglycemia
(hyperkalemia) from disruption of predominate, with alterations of the
the cellular sodium-potassium pump sensorium (sense of awareness).
(in the face of acidosis).
 Ketosis is usually minimal or absent.
 Rehydration leads to increased
 The basic biochemical defect is the lack of
plasma volume and subsequent
effective insulin.
decreases in the concentration of
 Persistent hyperglycemia causes osmotic
serum potassium.
diuresis, which results in losses of water and
 Rehydration also leads to increased
electrolytes. To maintain osmotic
urinary excretion of potassium.
equilibrium, water shifts from the
 Insulin administration enhances the
intracellular fluid space to the extracellular
movement of potassium from the
fluid space.
extracellular fluid into the cells.
 With glycosuria and dehydration,
 Potassium replacement - 40 mEq
hypernatremia and increased osmolarity
per hour may be needed for several
occur
hours.
 Frequent (every 2 to 4 hours  Clinical Manifestations:
initially) ECGs and laboratory  Hypotension
measurements of potassium are  Profound dehydration (dry mucous
necessary during the first 8 hours of membranes, poor skin turgor)
treatment.  Tachycardia
3. Reversing Acidosis  Variable neurologic signs (e.g., alteration
 Insulin - inhibits fat breakdown, of consciousness, seizures, hemiparesis)
thereby ending ketone production.  Assessment and Diagnostic Findings:
 Regular insulin, the only type of  Blood glucose (usually 600 to 1200
insulin approved for IV use, may be mg/dL)
added to IV solutions.  Electrolytes
 Insulin must be infused  BUN
continuously until subcutaneous  Complete blood count
administration of insulin can be  Serum osmolality (exceeds 320
resumed. mOsm/kg)
 Bicarbonate infusion to correct  Arterial blood gas analysis
severe acidosis is avoided during  Management:
treatment of DKA because it  The overall approach to the treatment
precipitates further, sudden (and of HHS is similar to that of DKA: fluid
 METABOLIC & ENDOCRINE: DIABETES
replacement, correction of electrolyte claudication (pain in the buttock, thigh,
imbalances, and insulin administration. or calf during walking)
 Other therapeutic modalities are  Management:
determined by the underlying illness and  The focus of management is an
the results of continuing clinical and aggressive modification and
laboratory evaluation. reduction of risk factors.
 After recovery from HHS, many patients  This involves prevention and
can control their diabetes with MNT treatment of the commonly accepted
alone or with MNT and oral antidiabetic risk factors for atherosclerosis.
medications.  MNT and exercise are important in
 Insulin may not be needed once the acute managing obesity, hypertension, and
hyperglycemic complication is resolved. hyperlipidemia.
 Frequent SBGM is important in  The use of medications to control
prevention of recurrence of HHS. hypertension and hyperlipidemia is
 Nursing Management: indicated.
 Maintaining fluid and electrolyte  Smoking cessation is essential.
balance
 Increasing knowledge about diabetes 2. Microvascular Complications
management  Diabetic microvascular disease (or
 Decreasing anxiety microangiopathy) is characterized by
 Monitoring and managing potential capillary basement membrane
complications (fluid overload, thickening.
hypokalemia, cerebral edema)  Two areas affected by these changes are
 Long-Term Complications Of Diabetes the retina and the kidneys.
1. Macrovascular Complications  Retinopathy
 Result from changes in the medium to  Occurs in both type 1 and type 2
large blood vessels. diabetes.
 Blood vessel walls thicken, sclerose, and  Caused by changes in the small
become occluded by plaque that adheres blood vessels in the retina.
to the vessel walls.  Retinopathy has three main
 Coronary artery disease, cerebrovascular stages: non-proliferative
disease, and peripheral vascular disease (background), pre-proliferative,
are the three main types of and proliferative.
macrovascular complications in diabetes.  Clinical Manifestations:
 MI is twice as common in men with  Retinopathy is a painless
diabetes and three times as common in process.
women with diabetes.  Blurry vision secondary to
 People with diabetes have twice the risk macular edema occurs in
of developing cerebrovascular disease some patients.
and an increased risk of death from  Symptoms indicative of
stroke. hemorrhaging include
 Signs and symptoms of peripheral floaters or cobwebs in the
vascular disease include diminished visual field, sudden visual
peripheral pulses and intermittent changes including spotty or
 METABOLIC & ENDOCRINE: DIABETES
hazy vision, or complete loss stressed, allowing blood proteins
of vision. to leak into the urine.
 Assessment and Diagnostic  As a result, the pressure in the
Findings: blood vessels of the kidney
 Diagnosis is by direct increases.
visualization of the retina  Clinical Manifestations:
through dilated pupils with an  Signs and symptoms of
ophthalmoscope or with a kidney dysfunction
technique known as  Frequent hypoglycemic
fluorescein angiography. episodes (decreased
 Medical Management: catabolism of insulin)
 The first focus of  Assessment and Diagnostic
management of retinopathy is Findings:
on primary and secondary  The urine should be
prevention. checked annually for the
 Other strategies that may presence of microalbumin.
slow the progression of  If the microalbuminuria
diabetic retinopathy include exceeds 30 mg/24 hours on
control of hypertension, two consecutive random
control of blood glucose, urine tests, a 24- hour urine
and cessation of smoking. sample should be obtained
 For advanced cases of and tested.
diabetic retinopathy, the  Tests for serum creatinine
main treatment is argon and BUN levels should be
laser photocoagulation. The conducted annually
laser treatment destroys  Management:
leaking blood vessels and  Control of hypertension
areas of neovascularization. (the use of angiotensin-
 Vitrectomy - a surgical converting enzyme [ACE]
procedure in which vitreous inhibitors, such as captopril
humor filled with blood or [Capoten]), because control
fibrous tissue is removed of hypertension may also
with a special drill-like decrease or delay the onset of
instrument and replaced with early proteinuria
saline or another liquid.  Prevention or vigorous
 Nephropathy treatment of urinary tract
 Kidney disease secondary to infections
diabetic microvascular changes  Avoidance of nephrotoxic
in the kidney. medications and contrast dye
 If blood glucose levels are  Adjustment of medications as
elevated consistently for a kidney function changes
significant period of time, the  Low-sodium diet
kidney’s filtration mechanism is  Low-protein diet
 METABOLIC & ENDOCRINE: DIABETES
 In chronic or ESKD, two  Autonomic Neuropathies
types of treatment are  Neuropathy of the autonomic
available: dialysis nervous system results in a broad
(hemodialysis or peritoneal range of dysfunctions affecting
dialysis) and transplantation almost every organ system of the
from a relative or a cadaver. body.
3. Peripheral Neuropathy  Clinical Manifestations:
 Diabetic neuropathy refers to a group  Three manifestations of
of diseases that affect all types of autonomic neuropathy are related
nerves, including peripheral to the cardiac, gastrointestinal,
(sensorimotor), autonomic, and spinal and renal systems.
nerves.  Cardiovascular symptoms
 Peripheral neuropathy most commonly range from a fixed, slightly
affects the distal portions of the nerves, tachycardic heart rate and
especially the nerves of the lower orthostatic hypotension to silent,
extremities. or painless, myocardial ischemia
 It affects both sides of the body and infarction.
symmetrically and may spread in a  Delayed gastric emptying may
proximal direction. occur with typical GI symptoms
of early satiety, bloating, nausea,
 Clinical Manifestations: and vomiting (―Diabetic‖
 Initial symptoms may include constipation or diarrhea).
paresthesias (prickling, tingling, or  Urinary retention, a decreased
heightened sensation) and burning sensation of bladder fullness,
sensations (especially at night). and other urinary symptoms of
 As the neuropathy progresses, the neurogenic bladder result from
feet become numb. autonomic neuropathy.
 A decrease in proprioception and a 1. Hypoglycemic Unawareness
decreased sensation of light touch - Autonomic neuropathy
may lead to an unsteady gait. affecting the adrenal
 Decreased sensations of pain and medulla is responsible for
temperature place patients with diminished or absent
neuropathy at increased risk for adrenergic symptoms of
injury and undetected foot infections. hypoglycemia.
 Deformities of the foot may also 2. Sudomotor Neuropathy – a
occur; neuropathy-related joint decrease or absence of
changes are sometimes referred to as sweating (anhidrosis) of the
Charcot joints. extremities, with a
 On physical examination, a decrease compensatory increase in
in deep tendon reflexes and upper body sweating.
vibratory sensation is found. 3. Sexual Dysfunction -
 Management: erectile dysfunction,
 Intensive insulin therapy decreased libido and lack of
 Pain management orgasm.
 METABOLIC & ENDOCRINE: DIABETES
4. Foot and Leg Problems
 Between 50% and 75% of lower
extremity amputations are performed on
people with diabetes.
 Complications of diabetes that contribute
to the increased risk of foot problems
and infections include the following:
1. Neuropathy - Sensory neuropathy
leads to loss of pain and pressure
sensation, and autonomic neuropathy
leads to increased dryness and
fissuring of the skin.
2. Peripheral vascular disease - Poor
circulation of the lower extremities
contributes to poor wound healing and
the development of gangrene.
3. Immunocompromise:
Hyperglycemia impairs the ability of
specialized leukocytes to destroy
bacteria.