DIABETES MELLITUS

ADWOA GYAMFUA ANSAH-ADU

 LEARNING OBJECTIVES
By the end of the course, the learner would be able to:
Explain the relationship between the clinical features
and the pathophysiology of Diabetes Mellitus
Educate clients to adhere to lifestyle modifications.
Differentiate between the signs of Hypoglycemia and
Hypoglycemia.
 Describe the dietary modifications used in the
management of persons with diabetes II.
Plan and give health talk on Diabetes I & II to a
selected group.
Objectives continues
Select a Diabetic patient and utilize the nursing process
approach to care him or her.( Affective –high(6),
Psychomotor- Medium(3))
Manage diabetic patients during sick periods. (Cognitive-
High(5).
Interpret results of diagnostic investigations on blood glucose
test.( cognitive- Medium(3).
Describe the management of diabetes Mellitus I &II and
Preventive practices. (Cognitive- low (2).
Guide patients on how to self administer insulin.
( Affective- high(6).
 What is Diabetes Mellitus
Diabetes mellitus is a
 group of metabolic diseases characterized
by high blood glucose levels, that result from defects in insulin
secretion, or action, or both.

Diabetes mellitus (DM) refers to

 a group of common metabolic
disorders characterized by an elevation of glucose in the blood.
(hyperglycemia).

Diabetes is a chronic metabolic disorder in which the body

cannot metabolize carbohydrates, fats, and proteins because of a
lack of, or ineffective use of the hormone insulin.
Incidence
Based on current trends, More than 360 million
individuals will have diabetes by the year 2030.
Although the prevalence of both type 1 and type 2 DM
is increasing worldwide.
The prevalence of type 2 DM is rising much more
rapidly because of increasing obesity and reduced
activity levels as countries become more
industrialized.
Types of Diabetes Mellitus
Type 1 Diabetes Mellitus
Type 1 diabetes mellitus was formerly known as insulin
dependent diabetes mellitus and juvenile diabetes mellitus.
Little or no endogenous insulin, requiring injections of insulin to
control diabetes and prevent ketoacidosis.
Five percent to 10% of all diabetic patients have type 1.
Etiology: autoimmune, viral, and certain histocompatibility
antigens as well as a genetic component
Most commonly seen in patients under age 30 but can be seen in
older adults.
 Type 2 Diabetes Mellitus
Type 2 diabetes mellitus was formerly known as non-insulin
dependent diabetes mellitus or adult onset diabetes mellitus.
Caused by a combination of insulin resistance and relative
insulin deficiency
Approximately 90% to 95% of diabetic patients have type 2.
 Etiology: strong hereditary component, commonly
associated with obesity.
Found primarily in adults over age 30; however, may be
seen in younger adults and adolescents who are overweight.
 Risk factors for DM II
Family history of diabetes (i.e., parent or sibling with type 2
diabetes)
 Obesity (BMI 25 kg/m2)
 Habitual physical inactivity
 Race/ethnicity (e.g., African American, Latino, Native
American, Asian American, Pacific Islander)
Previous history of gestational diabetes Mellitus or delivery of
baby >4 kg (>9 lb)
HDL cholesterol level less than 35 mg/dL (0.90 mmol/L)
and/or a triglyceride level greater than 250 mg/dL (2.82
mmol/L)
 Polycystic ovary syndrome
Diabetes Associated with other conditions

Certain drugs can decrease insulin activity resulting in

hyperglycemia—corticosteroids, thiazide diuretics,
estrogen, phenytoin.
Disease states affecting the pancreas or insulin
receptors—pancreatitis, cancer of the pancreas,
Cushing's disease or polycystic ovary disease.
Gestational Diabetes Mellitus
Glucose intolerance may develop during pregnancy.
Insulin resistance is related to the metabolic changes of
late pregnancy, and the increased insulin requirements
may lead to impaired glucose tolerance( IGT). Most
women revert to normal glucose tolerance post-partum
but have a substantial risk (30–60%) of developing
DM 2 later in life.
PATHOPHYSIOLOGY
Type I
There is a marked deficiency in the production of
insulin by the pancreatic beta cells leading to fasting
hyperglycemia. Postprandial hyperglycemia results
after meals.
If the concentration of glucose in the blood is
sufficiently high, the kidneys may not reabsorb all the
filtered glucose and so glucose appears in
urine( glucosuria)
Glucosuria is accompanied by excess fluid and
electrolyte loss (osmotic diuresis)
As a result of excess fluid loss, there is polyuria and
polydipsia.
Insulin deficiency impairs the metabolism of proteins
and fats leading to weight loss
Patients may experience increased
appetite( polyphagia), fatique and weakness
Glyconeogenesis and Gluconeogenesis occur
unrestrained contributing further to hyperglycemia
Fat breakdown occurs accumulating ketone bodies
causing diabetic ketoacidosis( DKA) which causes
abdominal pain,nausea,vomiting, hyperventilation, fruity
odour of the breath,altered level of consciousness, coma
and death.
Pathophysiology continues
Type II
The problems associated with type II DM are insulin
resistance and impaired insulin secretion.
Insulin resistance results due to a decrease in insulin
binding to receptors on cell surfaces to enable glucose
metabolism to occur in the cell.
To over come the build up of glucose in the blood, there
must be an increase in the amount of insulin secreted. If
the beta cells are unable to meet up with the increased
demand for insulin, type II Diabetes develops.
Even though there is impaired secretion of insulin,
there is enough to prevent the breakdown of fat and
prevent ketoacidosis
There is however, hyperosmolar nonketotic
syndrome.
Type II is mostly common in obese individuals.
Clinical features
Type I:
Fast onset because no insulin is being produced
 Increased appetite (polyphagia) because cells are starved for
energy, signals a need for more food
Increased thirst (polydipsia) from the body attempting to rid
itself of glucose
 Increased urination (polyuria) from the body attempting to
rid itself of glucose
Weight loss since glucose is unable to enter cells
 Frequent infections as bacteria feeds on the excess glucose
 Delayed healing because elevated glucose levels in the blood
hinders healing process
Type II:
 Slow onset because some insulin is being produced
 Increased thirst (polydipsia) from the body attempting to rid itself of
glucose
 Increased urination (polyuria) from the body attempting to rid itself of
glucose
 nfection as microorganisms feeds on the excess glucose
Delayed healing because elevated glucose levels in the blood hinder the
healing process

Gestational:
 Asymptomatic
 Some patients may experience increased thirst (polydipsia) from the
body
attempting to rid itself of glucose
Acute complications
Hyperglycemia
Hypoglycemia
Fluid and electrolyte imbalance
Ketoacidosis
Hyperosmolar state

 
 Chronic complications of diabetes
Over time, diabetes can lead to
 Diabetic retinopathy ( blindness), 
Diabetic nephropathy (kidney failure)
 Nerve damage from diabetes is called diabetic neuropathy
Diabetic nerve damage can affect the nerves that are
important for penile erection, causing erectile and loss of
sensation.

These types of damage are the result of damage to small

vessels
referred to as micro vascular disease.
 Diabetes is also an important factor in accelerating the
hardening and narrowing of the arteries (atherosclerosis),
leading to strokes, coronary heart disease, Claudication
and other large blood vessel diseases. This is referred to
as macrovascular disease

Because of poor blood circulation, diabetic foot injuries

may not heal. Sometimes, minor foot injuries can lead to
serious infection, ulcers, and even gangrene, necessitating
surgical amputation of toes, feet, and other infected parts.
Diagnostic evaluation
Symptoms of diabetes plus
 random blood glucose concentration
(11.1 mmol/L (200 mg/dL)
Fasting plasma glucose (7.0 mmol/L (126 mg/dL)
Two-hour plasma glucose 11.1 mmol/L (200 mg/dL)
during an oral glucose tolerance test (OGTT) two
hours after ingesting 75 grams oral glucose.
Urine ketones, urine protein, Blood urea electrolyte
and cretinine, blood lipid profile, ECG
Further test
Blood glucose test
Gylcated hemoglobin (HbA1c) twice or thrice a year
( 6% or higher)
Eye test and other test stated above annually or
frequently if levels are abnormal
Treatment
The objectives of long- term diabetes treatment are to
relieve symptoms and maintain fasting
( 4-6mmol/L) and 2 hour post meal ( 4-8) blood glucose
levels within the normal limits.
Prevent acute diabetic complications such as
hypoglycemia, ketoacidosis and hyperosmolar state.
Prevent chronic complications such as such as
blindness, limb amputation, kidney disease, nerve
damage, strokes and so on
Non Pharmacologic treatment
Diabetic diet
Avoid free or refined sugar
Complex carbohydrates are to be encouraged
(the diet should be of 60% carbohydrate, 15% protein
and 25% fat
Exercise within the individual’s limit should be done. It
helps in the utilization of glucose by the tissues and
control blood glucose level.
 Treatment for type II
Maintain ideal body weight through diet and exercise.
Regular monitoring of blood glucose.
Administer oral sulfonylureas to stimulate secretion of
insulin from the pancreas eg. glimepiride .glibenclamide,
giclazide and Tolbutamide oral 250mg -1g,8-12hrly
Administer oral biguanides to reduce blood glucose by

increasing peripheral insulin sensitivity: metformin oral
500mg-1g 12hrly with meal or soon after meals
Administer thiazolidinediones to sensitize peripheral tissues

to insulin: rosiglitazone

Insulin
 may be administered if the patient does not respond
to diet, exercise and hypoglycemic agents.
Treatment for type I
Insulin is administered in type I is the 1st line treatment
Diet
Exercise.
Insulin Regimens

NPH Only
Used alone only in type 2 diabetes when patients are
capable of producing some exogenous insulin as a
supplement for better glucose control.
Traditionally was used in the morning
Bedtime dosage can be helpful in controlling early
morning hyperglycemia.
NPH can also be given twice daily (morning and bedtime)
to eliminate afternoon hypoglycemia yet provide night-
time coverage. Typically, 2/3 to ¾ of the daily dosage is
given before breakfast and 1/3 to ¼ is given at bedtime.
 NPH/Regular or NPH/Immediate-acting Insulin

Short-acting regular insulin or immediate-acting lispro (Humalog),

glulisine (Apidra) or aspart (NovoLog) insulin is added to NPH to
promote postprandial glucose control.
Short- or immediate-acting insulin added to morning NPH controls
glucose elevations after breakfast.
Increased blood glucose levels after supper can be controlled by
the addition of short- or immediate-acting insulin before supper.
NPH and regular, lispro, glulisine, or aspart insulin given before
breakfast and before supper is termed a “split-mix” regimen,
providing 24-hour insulin coverage. However, there is an increased
risk of nocturnal hypoglycemia (2 to 3 AM) when NPH is given
before supper.
Intensive Insulin Therapy
Designed to mimic the body's normal insulin responses to
glucose.
Uses multiple (4 to 5) daily injections of insulin.
Detemir (Levemir) or glargine (Lantus) insulin is used for
basal insulin control.
Regular insulin acts as a premeal bolus given 30 minutes
before each meal. Lispro, glulisine, or aspart insulin may
be used instead of regular and is taken within 1 to 15
minutes before eating.
14-hour insulin coverage designed in this way can be
flexible to accommodate mealtimes and physical activity.
Sliding Scale Versus Algorithm Therapy
Sliding scale therapy uses regular or immediate-acting
insulin to retrospectively correct hyperglycemia.
Algorithm therapy prospectively determines regular or
immediate-acting insulin dosages, taking into account
meal content, premeal blood glucose level, and physical
activity.
Individualization of insulin dosages is the most important
aspect of sliding scale and algorithm therapy.
Nursing diagnoses

 Risk for imbalanced nutrition: less than what body

requires
 Risk for injury related to sensory alterations
 Risk for delayed surgical recovery
 Knowledge deficit on disease process
 Body image disturbance
 Anxiety related to unknown outcome of the condition.
INTERVENTION
Educate the patient about:
The disease and the importance of maintaining normal
glucose levels.
Demonstrate blood glucose monitoring.
Diet and food choices, including portion sizes.
Encourage exercise.
Discuss coping skills to reduce stress.
Teach self-injection of insulin (Type I).
Urge smoking cessation.
Self-care.
Prevention of complications, such as hyperglycemia and
hypoglycemia.
 Teach importance of daily medications.
 Explain hypoglycemia signs and symptoms and interventions.
Sweating, lethargy, confusion, hunger, dizziness, weakness
(Type I).
 Teach the management of hypoglycemia: glucose tablets, or 4
ounces of
fruit juice, several hard candies, or a small amount of a
carbohydrate.
Explain the signs and symptoms of hyperglycemia: fatigue,
headache, blurry vision, dry itchy skin.

 Teach glucagon injection for hypoglycemic events.