DEFINITION

DIABETES MELLITUS

Is a group of metabolic diseases characterized by elevated

levels of glucose in the blood (hyperglycemia) resulting from
defects in insulin secretion, insulin action, or both.

Normally a certain amount of glucose circulates in the blood.

The major sources of this glucose are absorption of ingested
food in the gastrointestinal (GI) tract and formation of glucose
by the liver from food substances.
INSULIN
A hormone secreted by the beta cells of the islets of
langerhans of the pancreas that is necessary for the metabolism
of carbohydrates, proteins, and fats; a deficiency of insulin
results in diabetes mellitus
A hormone produced by the pancreas, controls the level of
glucose in the blood by regulating the production and storage
of glucose.
 In the diabetic state, the cells may stop responding to insulin
or the pancreas may stop producing insulin entirely.
PREVALENCE RATE
Diabetes- is the 6th leading cause of death among Filipinos
based on the data from the 2013 Philippine health statistics,
and over 6 million Filipinos are diagnosed to have diabetes, as
declared by the Philippine Center for diabetes education
foundation in 2016. 
In the United States, approximately 800,000 new cases of
diabetes are diagnosed yearly
 Diabetes is especially prevalent in the elderly, with up to
50% of people older than 65 suffering some degree of glucose
intolerance
RISK FACTORS
 Family history of diabetes (ie, parents or siblings with
diabetes)

 Obesity (ie, ≥20% over desired body weight or bmi ≥27

kg/m2)

 Race/ethnicity (eg, african americans, hispanic americans,

native americans, asian americans, pacific islanders) age≥45
years
 PREVIOUSLY IDENTIFIED IMPAIRED FASTING GLUCOSE OR
IMPAIRED GLUCOSE TOLERANCE
 HYPERTENSION (≥140/90 MM HG)
 HDL CHOLESTEROL LEVEL ≤35 MG/DL (0.90 MMOL/L)
AND/OR TRIGLYCERIDE LEVEL ≥250 MG/DL (2.8 MMOL/L)
 HISTORY OF GESTATIONAL DIABETES OR DELIVERY OF
BABIES OVER 9 LBS
CLASSIFICATION OF DIABETES
• TYPE 1 DIABETES(PREVIOUSLY REFERRED TO AS
INSULIN-DEPENDENT DIABETES MELLITUS)
• TYPE 2 DIABETES (PREVIOUSLY REFERRED TO
AS NON-INSULINDEPENDENT DIABETES
MELLITUS)
• GESTATIONAL DIABETES MELLITUS
• DIABETES MELLITUS ASSOCIATED WITH
OTHER CONDITIONS OR SYNDROMES
TYPE 1 DIABETES

Type 1 diabetes is characterized by destruction of the

pancreatic beta cells
It is thought that combined genetic, immunologic, and
possibly environmental (eg, viral) factors contribute to beta
cell destruction.
People do not inherit type 1 diabetes itself; rather, they inherit
a genetic predisposition, or tendency, toward developing type
1 diabetes.
This genetic tendency has been found in people with certain
HLA (human leukocyte antigen) types.
HLA refers to a cluster of genes responsible for
transplantation antigens and other immune processes.
-A metabolic disorder characterized by an absence of insulin
production and secretion from autoimmune destruction of the
beta cells of the islets of Langerhans in the pancreas.
Formerly called insulin-dependent, juvenile or type I diabetes.
- 5-10% of all diabetes
 CLINICAL CHARACTERISTICS/IMPLICATION

• Onset any age, but usually young (<30 yrs)

• Usually thin at diagnosis;
• With recent weight loss
• Etiology includes genetic, immunologic, or environmental
factors (eg, virus). Often have islet cell antibodies
• Often have antibodies to insulin even before insulin
treatment little or no endogenous insulin need insulin to
preserve life ketosis-prone when insulin absent acute
complication of hyperglycemia:
• Diabetic ketoacidosis
TYPE 2 DIABETES

• The two main problems related to insulin in type 2 diabetes

are insulin resistance and impaired insulin secretion.
• A metabolic disorder characterized by the relative
deficiency of insulin production and a decreased insulin
action and increased insulin resistance. Formerly called non-
insulin-dependent, adult-onset, or type II diabetes
 CLINICAL IMPLICATION
• Onset any age, usually over 30 years
• Usually obese at diagnosis causes include obesity, heredity, or
environmental factors.
• No islet cell antibodies decrease in endogenous insulin, or increased
with insulin resistance most patients can control blood glucose through
weight loss if obese. Oral antidiabetic agents may improve blood
glucose levels if dietary modification and exercise are unsuccessful.
• May need insulin on a short- or long-term basis to prevent
hyperglycemia
• Ketosis rare, except in stress or infection
• Acute complication: hyperglycemic hyperosmolar nonketotic syndrome
GESTATIONAL DIABETES

• Is any degree of glucose intolerance with its onset during

pregnancy. Hyperglycemia develops during pregnancy
because of the secretion of placental hormones, which
causes insulin resistance.
SIGNS AND SYMPTOMS
• Polyuria (increased urination)
• Polydipsia (increased thirst) occur as a result of the excess
loss of fluid associated with osmotic diuresis.
• Polyphagia (increased appetite) that results from the
catabolic state induced by insulin
• Fatigue and weakness
• Sudden vision changes
• Tingling or numbness in hands or feet
• Dry skin, skin lesions or wounds that are slow to heal,
• Recurrent infections
• The onset of type 1 diabetes may also be associated with
sudden weight loss or nausea, vomiting, or abdominal pains,
if DKA has developed.
 ASSESSMENT AND DIAGNOSTIC FINDINGS

• FASTING PLASMA GLUCOSE (FPG) FASTING

PLASMA
Pre-diabetes: 100-125 mg/dL
Diabetes : >126 mg/dl (7.0 mmol/L)

Fasting is defined as no caloric intake for at least 8 hours.

• RANDOM PLASMA GLUCOSE
Diabetes : >200 mg/dl (11.1 mmol/L)

• GLUCOSE LEVEL 2 HOURS AFTER RECEIVING

GLUCOSE (2-HOUR POSTLOAD)
-Two-hour postload glucose:
Pre-diabetes: 140-199 mg/dL
Diabetes : >200 mg/dl (11.1 mmol/L)

The test should be performed as described by the world

health organization, using a glucose load containing the
equivalent of 75 g anhydrous glucose dissolved in water.
4. HBA1C (glycated hemoglobin)
Pre-diabetes: 5.7-6.4%
Diabetes: > 6.5 %
PHYSIOLOGY
FOOD
INGESTION
GLUCOSE
ABSORPTION IN
SMALL INTESTINE

INSULIN SECRETION
(PANCREAS)

INSULIN BINDS TO
CELL RECEPTORS

GLUCOSE
TRANSPORTER FUSE IN
CELL MEMBRANE

GLUCOSE MOVES
FROM BLOOD TO:
-MUSCLE
-LIVER
-ADIPOSE TISSUES
 PATHOPHYSIOLOGY DIABETES MELLITUS TYPE 1
GENETIC,
IMMUNOLOGIC,
ENVIRONMETAL
FACTORS
BETA CELLS
DESTRUCTION
LACK OF
DECREASED INSULIN
UTILIZATION OF INCREASED
GLUCOSE BY BREAKDOWN OF FAT
MUSCLE, FAT, AND
LIVER INCREASED FATTY
ACIDS
HYPERGLYCEMIA INCREASED KETONE
BODIES
BLURRE POLYURIA ACETONE
D VISION ACIDOSIS
BREATH
DHN POOR APPETITE NAUSEA
NAUSEA VOMITING
WEAKNESS POLYDIPS ABDOMINAL PAIN
HEADACHE IA INCREASINGLY
RAPID RESPIRAIONS
PATHOPHYSIOLOGY OF DIABETES MELLITUS TYPE II AND GDM
INSULIN SECRETION
(PANCREAS)

HORMONES BLOCK INSULIN BINDS TO

BINDING OF INSULIN CELL RECEPTORS
TO RECEPTORS
INSULIN
RESISTANCE:
-OBESITY
-LACK OF
EXERCISE
-HPN
-GENETICS
BETA CELLS COMPEASATE
AND BECOME
DYSFUNCTIONAL
BETA CELLS
DESTRUCTION

IMPAIRED
HYPERGLYCEMI
INSULIN
A
PRODUCTION
 PATHOPHYSIOLOGY
INSULIN HYPERGLYCEMI IMPAIRED
RESISTANCE A INSULIN
PRODUCTION
INCREASED RENAL
THRESHOLD FOR MUSCLES AND ADIPOSE
GLUCOSE TISSUES CANNOT
RECEIVE GLUCOSE
KIDNEY FAILED TO
REABSORB FILTERED
GLUCOSE
ADIPOSE TISSUE- LIPOLYSIS
GLUCOSE MUSCLE- BREAK DOWN OF CHON
EXCRETED IN
URINE
(GLUCOSURIA)
WEIGHT LOSS
POLYURIA +
HUNGER
(POLYPHAGIA)
DEHYDRATION

POLYDIPSIA
 ACUTE COMPLICATIONS
 
1. Diabetic Ketoacidosis - (Type I)

2. Hyperglycemic hyperosmolar non ketotic syndrome

(HHNS) - (Type II)

3. Hypoglycemia
 LONG-TERM COMPLICATIONS OF
DIABETES

1. Macrovascular complication
1. Coronary artery disease
2. cerebrovascular disease
3. peripheral vascular disease

2. Microvascular complication
1. Retinopathy
2. Nephropathy
3. Neuropathy
 MEDICAL MANAGEMENT

 
The main goal of diabetes treatment is to normalize
insulin activity and blood glucose levels to reduce the
development of vascular and neuropathic
complications.

Nutritional therapy, exercise, monitoring,

pharmacologic therapy, and education.
 MEDICAL MANAGEMENT
1. Nutritional Therapy

Nutrition, meal planning, and weight control are the

foundation of diabetes management. The most important
objectives in the dietary and nutritional management of diabetes
are control of total caloric intake to attain or maintain a
reasonable body weight, control of blood glucose levels, and
normalization of lipids and blood pressure to prevent heart
disease.
2. Exercise

Regular exercise is extremely important in diabetes

management because of its effects on lowering blood glucose
and reducing cardiovascular risk factors. Exercise lowers blood
glucose levels by increasing the uptake of glucose by body
muscles and by improving insulin utilization.
3. Monitoring Glucose Levels and Ketones

Blood glucose monitoring is a cornerstone of diabetes

management, and self-monitoring of blood glucose (SMBG)
levels has dramatically altered diabetes care.
 4. PHARMACOLOGIC MANAGEMENT

1. Insulin Therapy

In type 1 diabetes, exogenous insulin must be administered

for life because the body loses the ability to produce insulin. In
type 2 diabetes, insulin may be necessary on a long-term basis
to control glucose levels if meal planning and oral agents are
ineffective.
2. Oral Antidiabetic Agents

Patients who have type 2 diabetes that cannot be treated

effectively with MNT and exercise alone. Sulfonylureas and
meglitinides - increases the secretion of insulin by the
pancreatic beta cells.
3. Other Pharmacologic Therapy

Pramlintide (Symlin) - recently been approved for treatment

of both type 1 and type 2 diabetes. It is used to control
hyperglycemia in adults who have not achieved acceptable
levels of glucose control despite the use of insulin at mealtimes.
It is used with insulin, not in place of insulin.
4. PATIENT EDUCATION

Diabetes mellitus is a chronic illness

that requires a lifetime of special self-
management behaviors.
 HOSPITAL MANAGEMENT

1. Rehydration

In dehydrated patients, rehydration is important for

maintaining tissue perfusion. In addition, fluid replacement
enhances the excretion of excessive glucose by the kidneys.
 HOSPITAL MANAGEMENT

2. Restoring Electrolytes

The major electrolyte of concern during treatment of DKA

is potassium. Although the initial plasma concentration of
potassium may be low, normal, or even high, there is a major
loss of potassium from body stores and an intracellular-to
extracellular shift of potassium.
 HOSPITAL MANAGEMENT

3. Insulin administration

The acidosis that occurs in DKA is reversed with insulin,

which inhibits fat breakdown, thereby stopping acid buildup.
Insulin is usually infused intravenously at a slow, continuous
rate (eg, 5 units/h).
 HOME AND COMMUNITY- BASED CARE

1. Teaching Patients Self-Care

The focus of diabetes education should be patient

empowerment. Patient education should address behavior
change, self-efficacy, and health beliefs.
 HOME AND COMMUNITY- BASED CARE

2. Continuing Care

Many patients with diabetes are seen by home health nurses

for diabetes education, wound care, insulin preparation, or
assistance with glucose monitoring. Even patients who achieve
excellent glucose control and have no complications can expect
to see their primary health care provider at least twice a year for
ongoing evaluation and should receive routine nutrition
updates.
 PRIORITY NURSING PROBLEM

Deficient knowledge regarding disease process, treatment, and

individual care needs.