DIABETES MELLITUS

DEFINITION:
• is a group of metabolic diseases characterized by increased levels
of glucose in the blood (hyperglycemia) resulting from defects in insulin
secretion, insulin action, or both.
PATHOPHYSIOLOGY
• Insulin

> is a hormone secreted by beta cells, which are one of four types of
cells in the islets of Langerhans in the pancreas.
> is an anabolic, or storage, hormone.
> insulin secretion increases and moves glucose from the blood into
muscle, liver, and fat cells. In those cells, insulin has the following
actions:
• Transports and metabolizes glucose for energy
• Stimulates storage of glucose in the liver and muscle (in the form of
• glycogen)
• Signals the liver to stop the release of glucose
• Enhances storage of dietary fat in adipose tissue
• Accelerates transport of amino acids (derived from dietary protein)
• into cells
• Inhibits the breakdown of stored glucose, protein, and fat
CLINICAL CHARACTERISTICS AND
MANIFESTATIONS
• Type 1
(previously classified as Juvenile
Diabetes, ketosis-prone diabetes
and insulin dependent diabetes
mellitus IDDM)
• onset at any age but usually
very young (<30 y.o)
• Usually thin at diagnosis; recent
weight loss.
• Etiology includes genetic,
immunologic and environmental
factors (e.g. virus
• Little or no endogenous insulin
• Type 2
(previously classified as Adult-
onset diabetes, Maturity-onset
diabetes, Ketosis-resistant
diabetes, stable diabetes, and
non-insulin-dependent diabetes
NIDDMI)
• Onset at any age usually at <30
y.o
• usually obese at diagnosis
• Causes includes obesity,
heredity and environmental
factors
• decrease in endogenous insulin,
or increased with insulin
resistance.
Other Clinical Manifestations includes:
> 3 P’s
- Polyphagia
- Polydipsia
- Polyuria
- Other symptoms includes: fatigue and weakness, sudden vision
changes, tingling or numbness in hands or feet, dry skin, skin lesions or
wounds that are slow to heal, and recurrent infections,
ASSESSMENT AND DIAGNOSIS
• History
>Symptoms related to the diagnosis of diabetes:
- Symptoms of Hyperglycemia
- Symptoms of Hypoglycemia
> Results of blood glucose monitoring
> Use of Tobacco, alcohol and prescribed and over-the-counter
medication/drugs.
> Lifestyle, cultural, psychosocial and economic factors that may affect
diabetes treatment.
• Physical Examination
> Blood pressure (sitting and standing to detect Orthostatic changes)
> Body mass index (height and weight)
> Foot examination (Lesions, signs of infection, pulses)
> Skin Examination using monofilament Deep tendon reflexes
• Laboratory Examination
> HgB > Serum Creatinine Level
> Fasting lipid profile > Urinalysis
> Test for microalbuminuria > Electrocardiogram
CRITERIA
1) Symptoms of Diabetes plus plasma glucose concentration equal to
or greater than 200mg/dL (11.1 mmol/L)

2) Fasting plasma glucose greater than or equal to 126mg/dL (7.0

mmol/L). Fasting is defined as no caloric intake for at least 8 hrs.

3) Two-hour postload glucose equal to or greater than 200mg/dL

(11.1mmol/L) during an oral glucose tolerance test. The test should be
performed as prescribed using a glucose load containing the equivalent
of 75 g anhydrous glucose dissolved in water.
MEDICAL MANAGEMENT
• Administration of Insulin
> Rapid acting (lispro, asparr, glulisine)
> Short acting (regular – Humalog R, Novolin R)
> Intermediate acting (NPH )
> Very long acting (Glargine, Detemir)
> Premixed
> Inhaled
• OHA (Oral Antidiabetic Agents)
• Amputation of infected leg/gangrenous tissue
NURSING MANAGEMENT
• Patient Education
> developing a diabetes education plan
> organizing information
> educating patients about survival skills (must be learned by newly
diagnosed type 1 or type 2 patients who are receiving insulin)
• Management of glucose
> blood glucose targets are 140 – 180 mg/dL
> Insulin (subcutaneous or IV)
> Appropriate timing of blood glucose checks, meal consumptions,
and insulin dose are all crucial for glucose control and to avoid
hypoglycemia.
• Assessing readiness to learn
> the nurse should assess the patient (and px family) readiness to
learn. Most patients are in denial
> low literacy level
> limited financial resources
> Cultural beliefs that may impact adherence to a regimen
• Educating experienced patients
• Determining education methods
• Educating patients to self-administer Insulin
> Storing insulin
- whether short or long acting preparation, vials not in use,
including spare vials or pens should be refrigerated.
• Mixing insulins
> when rapid or short acting insulins are to be given simultaneously
with longer acting insulins, usually mixed with t he same syringe.
• Selecting and rotating the injection site
> four main areas are; Abdomen, upper arm (posterior surface),
thighs (anterior surface), and hips.
> the patient should not use the exact same site.
DM COMPLICATIONS
• HYPOGLYCEMIA
- low sugar in the blood. (less than 70mg/dL)
• Manifestations
➢sweating, tremor, tachycardia, palpitations, nervousness, hunger.
➢ Moderate; inability to concentrate, headache, lightheadedness,
confusion, numbness of the lips and tongue, slurred speech, double
vision, drowsiness.
➢ Severe; disoriented behavior, seizures, difficulty arousing from sleep, or
loss of consciousness.
• Management
> Treating with carbohydrates
> Initiating emergency measures
- injection of glucagon 1mg (for px who are unconscious)
> Providing patient education
- consistent pattern of eating, administering insulin and
exercising.
- snacks between meals.
• DIABETIC KETOACIDOSIS
- caused by an absence or markedly inadequate amount of
insulin.
- 3 main causes of DKA
1. Decrease or missed dose of Insulin.
2. Illness / Infection
3. Undiagnosed and untreated diabetes
➢Prevention: “Sick day rules”
- Most important concept in this is to NEVER eliminate insulin doses when nausea and
vomiting occur. Instead, patient should take the usual insulin dose
 - Drinking of fluids every hours is important to prevent
dehydration .
- blood glucose and urine ketones must be assessed every 3 – 4
hrs.
➢Manifestations
- Hyperglycemia of DKA (the 3 P’s), and marked fatigue. Patient
may experience blurred vision, headache, weakness, orthostatic
hypotension, weak rapid pulse.
- Ketosis and acidosis of DKA lead to anorexia, nausea, vomiting and
abdominal pain, px may also have Acetone breath (fruity odor),
Kussmauls respirations.
- Mental Status: Alert, lethargic or comatose.
• Management
- Rehydration
> maintaining tissue perfusion, fluid replacement
enhances the excretion of excessive glucose by the
kidneys.
> 6 – 10 L of fluid to replace fluid losses.
> 0.9 % Sodium Chloride (NSS), Half-Strength NS
(0.45%)
- Restoring electrolytes
- Reversing Acidosis
• HYPERGLYCEMIC HYPEROSMOLAR SYNDROME
- metabolic disorder of type 2 diabetes resulting from a relative
insulin deficiency initiated by an illness that raises the demand
for insulin.
➢Manifestations
- Hypotension, profound dehydration (dry mucous membranes,
poor skin turgor), tachycardia and variable neurologic signs
(alterations of consciousness, seizures, hemiparesis)
• ASSESSMENT
- Range of laboratory tests, blood glucose, electrolytes, BUN, complete
blood count, serum osmolality, and arterial blood gas analysis ( blood
glucose lvl is usually 600-1200mg/dL and the Osmolality exceeds 320
mOsm/kg.
- Mental status changes, Focal Neurologic deficits and hallucinations are
common.
• NURSING DIAGNOSES
- Risk for deficit fluid volume related to polyuria and dehydration.
- Risk for electrolyte imbalance related to fluid loss or shifts.
- Deficit knowledge about diabetes self-care skills or information.
- Anxiety related to loss of control, fear or inability to manage diabetes,
misinformation related to diabetes, fear of diabetes complications.