Diabetes mellitus is one of the most complex and most common disorders in the nation

affecting nearly 16 million Americans. But many of them don't realize that they have
diabetes.
So the disorder goes unrecognized until the patient seeks care for another problem
such as blurred vision. Yet because diabetes can affect virtually all body systems. The
patient runs a high risk of developing a life-threatening or debilitating complication even
before the disease is diagnosed. That's why you need to be able to spot the clues that
point to diabetes.
For example, this patient was just admitted to the emergency department. He's lethargic
and confused and his breath has a strong alcohol-like odor. Although you rnight think
alcohol and toxication is the cause of this patient's condition you should also suspect
diabetic ketoacidosis (or DKA) as the cause.

But do you know why? Can you relate this patient's assessment findings to the
pathophysiology of diabetes? And do you know how your interventions can help him
control the disorder?
This video will help you answer these questions with confidence. It will clearly explain
the pathophysiology of diabetes. Show you how to identify and control the disorder and
demonstrate ways to recognize and prevent its complications.

Diabetes mellitus is characterized by:

 Insulin deficiency
 Which alters the metabolism of glucose (the body's main source of energy).

Before you can manage diabetes and its complications you need to understand normal
glucose metabolism.

Normally, insulin is produced in the pancreas by beta cells in the islets of Langerhans.
Insulin lowers the blood glucose in three ways. First, it shifts glucose from the blood
stream into the body's cells by binding to insulin receptors on the cells' membrane.
Once bound insulin and the attached receptor move into a cell creating an entry way for
glucose.
Second, insulin promotes the storage of excess glucose. To do this it activates the
enzyme glucokinase which breaks down glucose into glucose-6-phosphate (or G-6-P).
Then insulin activates glycogen synthase. This enzyme converts G6P into glycogen
which is stored in the liver and muscles.
Third, when the glycogen stores are full insulin stimulates the enzyme lipoprotein lipase
to convert excess glucose into free fatty acids. These fatty acids are absorbed by fat
cells where they combine with glucerol-3-phosphate (or G-3-P) to form triglycerides.

Two types of diabetes mellitus have been identified but each develops differently.

 Type 1 diabetes is characterized by the destruction of all beta cells.

 In idiopathic type 1 diabetes the cause of beta cell destruction is unknown.
 In auto immune type 1 diabetes the immune system recognizes beta cells as foreign and
slowly destroys them.

In both forms of type 1 diabetes insulin production eventually comes to a halt. Without
insulin the patient develops hyperglycemia (or excess blood glucose).

Type 2 diabetes is characterized by:

 Decreased insulin production,

 Cell resistance to insulin, or
 Both

Decreased insulin production usually occurs with age. In fact, the risk of developing type
2 diabetes increases with each decade of life.

Insulin resistance occurs when insulin receptors have difficulty recognizing insulin
molecules. As a result fewer insulin molecules bind to receptor sites allowing fewer
glucose molecules to enter the cells.
Several factors may increase the risk of developing insulin resistance.

 A family history of type 2 diabetes, or

 An ethnic background that's African-American Hispanic or Native American may increase the
risk because of genetic factors,
 Obesity raises the risk because it increases the number of fat cells, and the receptors on fat
cells resist insulin more than the receptors on other cells,
 A sedentary lifestyle can compound the risk because the patient doesn't gain the benefit of
regular exercise which lowers the cells insulin resistance and helps prevent obesity

To compensate for insulin resistance beta cells produce more insulin. At first, this helps glucose
enter the body's cells lowering the blood glucose level. Eventually, the beta cells become
overworked and produce less insulin.
This reduces the amount of glucose that enters the cells causing the blood glucose level
to rise. Without treatment severe complications can occur.

An acute complication DKA typically strikes patients with type 1 diabetes who don't take
insulin as prescribed or who have an illness such as pneumonia.
The stress of illness increases the secretion of hormones such as:

 Epinephrine,
 Norepinephrine, and
 Glucagon

These hormones raise the blood glucose level by increasing glucose production or reducing glucose
movement into muscle cells then glucose builds up in the blood because it can't enter the cells
without insulin. The cells soon become starved for glucose to fuel metabolism.
So the brain, signals the alpha cells in the pancreas to produce the hormone glucagon
which converts glycogen into glucose in the liver. When the glycogen stores are
depleted the liver converts free fatty acids and protein into glucose raising the blood
glucose level even further.
The conversion of free fatty acids into glucose creates ketones as a by-product because
ketones are acidic they disturb the acid-base balance when they accumulate in the
blood.
Eventually, ketone accumulation and hyperglycemia lead to DKA— a type of metabolic
acidosis.

If you suspect DKA in your type 1 diabetic patient, assess him quickly so that you can provide
appropriate critical care.
First measure your patient's blood glucose level. Repeat this measurement at least
every hour until his condition is stable. In DKA, the glucose level may increase to 800
milligrams per deciliter or more.
Also check your patient's urine for ketones which appear in DKA. Remember to recheck
for them every two to four hours or as ordered until they're no longer present in the
urine. Next, obtain blood samples to assess fluid electrolyte and arterial blood gas (or
ABG) levels which you'll review later.

Then check for signs of fluid and electrolyte imbalances.

You're likely to detect signs of dehydration such as:
  Poor skin turgor, and
 Dry skin and mucous membranes

You're also likely to see signs of electrolyte imbalances such as cardiac arrhythmias. In
DKA, severe fluid and electrolyte loss usually results from osmotic diuresis.

When the blood glucose level rises the kidneys try to compensate by excreting excess
glucose which takes water, sodium, potassium, and other electrolytes with it. As large
amounts of fluid move from the intravascular space into the urine, the blood volume
decreases.
At first, this hemo concentration causes falsely elevated electrolyte levels. However,
when the fluid is replaced the blood becomes less concentrated. This makes the
electrolyte levels fall often to below-normal levels.

Next, take the patient's vital signs being alert for Kussmaul's respirations. These rapid
deep respirations develop when the lungs try to remove excess acid by exhaling
additional carbon dioxide. And because the acidosis is caused by ketones the patient's
breath smells sweet and like alcohol.
Also check for low blood pressure and tachycardia. Low blood pressure results from low
blood volume. And tachycardia occurs when the body tries to raise cardiac output while
the blood volume is low.

Now assess for signs of GI complications such as:

 Absent bowel sounds,

 Nausea,
 Vomiting, and
 Abdominal pain or tenderness

GI complications are common in DKA because metabolic acidosis slows intestinal function which
may lead to paralytic ileus or intestinal paralysis. When the test results are ready check the ABG
levels.

DKA typically causes:

 A partial pressure of carbon dioxide (or PC02) of less than 35 millimeters of mercury
indicating the lungs attempt to compensate,
 A bicarbonate level of less than 28 milliequivalent per liter indicating the kidneys attempt to
compensate, and
  A pH of less than 7.35 indicating acidosis

To treat DKA, first replace the lost fluid with normal saline. Administer each liter over 30 to 60
minutes as prescribed.
During fluid replacement, recheck the electrolyte levels every hour and administer
specific electrolytes as needed. If your patient's pH level is below 7 start a bicarbonate
infusion as prescribed. To prevent rebound alkalosis be sure to infuse it slowly.
To lower the patients glucose level expect to administer insulin intravenously. After
administering a bolus of regular insulin begin a continuous infusion of 0.1 to 0.2 units
per kilogram per hour based on the blood glucose level.

During insulin therapy, monitor your patient's glucose level closely. Make sure that it
doesn't fall faster than 100 milligrams per deciliter per hour because this can cause
complications.
How? As glucose moves from the blood into the cells it takes water with it. This may
cause cellular edema and organ swelling. If swelling affects the brain, increased
intracranial pressure may lead to herniation and death.

Also, watch for early signs of hypoglycemia (or low blood glucose) such as diaphoresis,
tachycardia and tremors. In this dangerous complication the blood glucose level falls
below 60 milligrams per deciliter.
When intracellular glucose levels fall the brain signals the alpha cells in the islets of
Langerhans to secrete the hormone glucagon. Glucagon causes glycogenolysis by
triggering enzymes to break glycogen into glucose. Glucagon also causes
gluconeogenesis by stimulating the conversion of protein and free fatty acids into new
glycogen.
The brain also signals the adrenal glands to release epinephrine which prompts the
breakdown of glycogen and fats to glucose.

The release of epinephrine causes the early autonomic signs of hypoglycemia such as:

 Diaphoresis,
 Tremors, and
 Tachycardia
If the blood glucose level continuous to fall the patient develops late, neuroleptic signs of
hypoglycemia including:

 Poor coordination,
 Slowed thinking, and
 Loss of consciousness

If your patient has hypoglycemia, is conscious and can swallow. Provide 15 grams of an easily
absorbed carbohydrate such as 4 ounces of orange juice. Repeat this treatment every 15 minutes
until his hypoglycemia resolves.
If you're hypoglycemic patient is unconscious or can't swallow, administer 25 to 50
grams of dextrose 50% in water by I.V. bolus. If he doesn't have an I.V. access device,
inject glucagons intramuscularly. Remember to turn the patient on his side to prevent
aspiration, because glucagon can cause vomiting.
To prevent hypoglycemia, change the I.V solution to dextrose 5% in water and half-
normal saline. When the patient's glucose level falls below 250 milligrams per deciliter.
If your patient with DKA has abdominal pain, nausea, vomiting and absent bowel
sounds, give him nothing by mouth and prepare to insert a nasogastric tube to relieve
distention.

Once you're patient's condition is stable perform a complete physical assessment. First,
obtain a full description of his symptoms.
You're patient is likely to report:

 Polydypsia (or increased thirst),

 Polyuria ( or excesss urine output ),
 Polyphagia ( or increased hunger ), and
 Weight Loss

All of these classic effects of diabetes are caused by hyperglycemia.

Polydypsia results from dehydration. As excess water is excreted in the urine the fluid
volume decreases. Then the brain's thirst mechanism alerts the patient to drink more
fluid.
Polyuria results from osmotic diuresis. As the blood glucose level rises the kidneys try to
compensate by excreting glucose into the urine. Because glucose is a large molecule. It
pulls water with it. This produces large amount of dilute urine.
Polyphagia stems from cellular glucose deprivation. Because glucose can't enter the
cells, they signal the brain's appetite center to increase food intake. But eating more
food worsens the hyperglycemia by causing more glucose to enter the blood from the
GI tract.

Weight loss is caused by dehydration and fat breakdown. The latter occurs when the
glycogen stores are depleted and the cells desperate for fuel signal the liver to convert
fat to glucose.
Also ask about other signs of hyperglycemia, including:

 Frequent infections,
 Vision disturbances, and
 Paresthesias in the hands and feet

Among diabetic patients, infections occur frequently and typically include infections of the:

 Skin,
 Urinary tract,
 Vagina, and
 Wounds

No one knows exactly why diabetes increases the risk of infection. However, some experts believe
that hyperglycemia impairs phagocytosis which is microorganism destruction by white blood cells.
Others believe that hyperglycemia and acidosis lead to infection by creating an
environment that promotes microorganism over growth.

Diabetes may cause vision disturbances such as blurred vision because hyperglycemia
alters eye structures such as the:

 Lens,
 Aqueous humor, and
 Cornea

Paresthesias occur when excess glucose coats the nerve fibers. Over time the coating interferes
with nerve function causing abnormalities such as:

 Numbness, and
 Tingling in the hands and feet
Finally, assess your patient for signs of chronic complications of diabetes which can affect nearly all
of the body's organs. That's because uncontrolled hyperglycemia damages the arteries that supply
those organs with blood.
Here's how:

 First, hyperglycemia increases the risk of hypertension and hyperlipidemia. In the arteries
these conditions tend to injure the endothelial lining allowing lipids to invade it,
 Second, hyperglycemia and other factors lead to smooth muscle cell proliferation in the
injured arteries this narrows the arterial lumen.
 Third, hyperglycemia makes platelets stickier which increases platelet aggregation at the
injury site. This impedes blood flow even further.

All three events raise the blood pressure and impair blood circulation by increasing
arterial resistance.

Most chronic complications of diabetes are macrovascular or microvascular.

Macrovascular complications result from changes in large blood vessels. To detect
them, assess for signs of:

 Heart disease especially coronary artery disease,

 Cerebrovascular disease such as cerebrovascular accident, and
 Peripheral vascular disease such as arterial occlusive disease which can lead to foot ulcers

Microvascular complications stem from changes in small blood vessels.

To spot them, be alert for signs of:

 Retinal disease,
 Kidney disease, and
 Nerve disorders

To evaluate the effectiveness of treatment prepare your patient for diagnostic tests. When the tests
are completed review the results.
In a diabetic patient the blood glucose test is likely to show a level that exceeds 126
milligrams per deciliter on a fasting glucose test and 200 milligrams per deciliter on a 2-
hour postprandial glucose test.
In a patient without diabetes, the glycosylated hemoglobin test shows that 4 to 7 per
cent of glucose is bound to hemoglobin. In a diabetic patient the test may reveal that 10
to 20 percent of glucose is bound to hemoglobin.
That's because in poorly controlled diabetes the blood glucose level remains higher for
a longer time allowing more glucose to bind to hemoglobin in red blood cells.
The glycosylated hemoglobin test reflects glucose control and treatment compliance
over several months because glucose stays bound to hemoglobin for the red blood cells
for the entire life span which is several months.
The urine ketone test may show ketones in the urine. When accompanied by a high
blood glucose level this is abnormal and signals ketoacidosis.

After reviewing the test results and other findings with the patient's physician, work
together to maximize the effectiveness of the treatment plan. Then discuss the plan with
your patient.
Treatment for diabetes mellitus consist of:

 Drugs,
 Diet, and
 Exercise

A patient with type 1 diabetes typically receives insulin subcutaneously every day to control his blood
glucose level. Because this drug mimics endogenous insulin it promotes glucose storage and helps
prevent the breakdown of glycogen, protein, and fat.
Depending on your patient's response to insulin he may need:

 Rapid-acting,
 Intermediate-acting,
 Long-acting insulin, or
 A combination of insulins

A balanced diet is a vital part of therapy for type 1 diabetes. Your diabetic patient should eat a diet
that provides nutrients from all food groups. Is low in sodium and cholesterol and is high in fiber.
A balanced diet typically includes:

 50 to 55 percent carbohydrates,
 30 to 35 percent fat, and
 10 to 20 percent protein

Your patient also should follow a regular exercise program to enhance the body's use of
insulin.

This patient with type 2 diabetes mellitus was admitted to your unit today for treatment
of pneumonia. During your rounds, you notice that she's lethargic and difficult to arouse.
You suspect that she may have hyperglycemic hyperosmolar nonketotic ( HHNK)
syndrome an acute complication of type 2 diabetes mellitus.
In a type 2 diabetic patient, surgery or another stressor increases the body's need for
insulin. Because such a patient can't produce extra insulin or use it effectively. The cells
don't receive enough glucose for energy.
Insufficient intracellular glucose triggers gluconeogenesis which converts fat and protein
into the glucose that the cells need. But without sufficient insulin to help glucose move
into the cells the blood glucose level climbs.

If untreated HHNK syndrome occurs raising the blood glucose level dramatically.
However, this syndrome does not cause ketosis. That may be because the pancreas
still produces some insulin which prevents the breakdown of fat into ketones.
However, the pancreas doesn't produce enough insulin which means that too little
glucose reaches the cells. And this causes the liver to convert glycogen into glucose
raising the glucose level even higher than in DKA.
That's why HHNK syndrome causes severe dehydration and neurologic dysfunction
killing about half of the patients it strikes.

HHNK syndrome requires critical care and prompt treatment. So if you suspect this
syndrome work quickly to assess the patient and intervene rapidly.

First check the blood glucose and urine ketone levels. In a patient with HHNK syndrome
expect the blood glucose level to exceed 800 milligrams per deciliter.
Next assess the patient for signs of fluid and electrolyte imbalances which occur when
the kidneys excrete water and electrolytes along with glucose. Then replace the lost
fluid by administering normal saline at the prescribed rate.

During fluid replacement therapy monitor the patient's urine output closely. When it
reaches 60 milliliters per hour expect to switch to half-normal saline solution to prevent
hypernatremia.
Plan to administer insulin as prescribed usually at 0.1 units per kilogram per hour. When
the patient's blood glucose level reaches 250 milligrams per deciliter prevent
hypoglycemia by switching to an I.V. solution that contains dextrose. As fluids are
replaced check the electrolyte levels and administer electrolytes if needed.
When the patient's condition is stable perform a complete assessment and review all
test results as you would for a patient recovering from DKA. Be alert for signs of
diabetes and its chronic complications.
Also discuss your findings and the treatment plan with the physician and your patient. If
a balanced diet and regular exercise don't control the blood glucose level your type 2
diabetic patient may need drug therapy. Occasionally, she may need insulin. But
usually, she just needs an oral hypoglycemic drug.
Sulfonylureas such as glyburide stimulate beta cells to produce more insulin. They also
increase cell receptor sensitivity to insulin in peripheral tissues which allows more
insulin to bind with insulin receptors. Both mechanisms let more glucose enter the cells
which lowers the blood glucose level.

Like sulfonylureas, biguanides (such as metformin) increase cell receptor sensitivity to

insulin. In addition, they suppress glycogen formation in the liver, which reduces
gluconeogenesis. Alpha-glucosidase inhibitors such as acarbose delay carbohydrate
breakdown and GI tract absorption which lowers the blood glucose level.
When used in combination therapy these drugs may let the patient receive smaller
dosages of other oral hypoglycemics or insulin.

Whether your patient is recovering from DKA or HHNK syndromes. Individualize her
nursing care. But expect to perform these general nursing interventions:

 Check the patient's blood glucose and urine ketone levels at least every four hours,
 Assess electrolyte and ABG levels as well as the results of other tests,
 Monitor the patients fluid intake and output to evaluate fluid replacement,
 Watch for signs of complications such as hypoglycemia, and
 Ensure that the patient receives a balanced diet

Before your patient is discharged teach her and her family how to control diabetes and prevent
complications.

Be sure to cover:

 Medication use and side effects,

 Diet and exercise changes,
 Blood Glucose and urine ketone testing,
 Signs, symptoms, and treatment of hyperglycemia and hypoglycemia,
 Health maintenance activities such as eye and foot care, and
 Follow-up care
As you have just seen diabetes mellitus as a complex disorder that affects all body systems. If
uncontrolled it can lead to life-threatening complications such as DKA and HHNK syndrome.
By understanding the pathophysiology of diabetes you can:

 Recognize its complications swiftly and accurately,

 Intervene with confidence,
 Evaluate the treatment's effectiveness expertly,
 Help your patient control the disorder

Armed with this knowledge you can provide the best possible care for your patient and
help her live longer and better with diabetes.