Diabetes Mellitus

Presented & Modified by:

Asghar Khan

Prepared By: Azizullah

Objectives:
Review the anatomy and physiology of endocrine
pancreas.
Briefly discuss the classification of diabetes mellitus
( DM).
Discuss etiology, pathophysiology, and clinical
manifestation of Type 1 & Type 2 DM.
Identify main differences between type 1& type 2 DM
Identify pathogenesis and manifestation of the acute and
chronic complications of DM
A & P of Endocrine Pancreas:
The pancreas is an elongated
organ, light tan or pinkish in
color, that lies in close
proximity to the duodenum. It
is covered with a very thin
connective tissue capsule
which extends inward as septa,
partitioning the gland into
lobules.
Weighing about 60 grams. It is about 12 to 15 cm
long
Situated in the epigastric and left hypochondriac
regions of the abdominal cavity.
Consists of a broad head, a body and a narrow tail.
The endocrine pancreas consists of about 1-2 million
microscopic units, the islets of Langerhans. That account
1% of the pancreas.
The four most important cell types are;
A (alpha)
B (beta)
D (delta)
PP (Pancreatic polypeptide)
B cells constitute 70% of islet cell population and
secrete insulin, that lowers blood glucose level.
A cells account for 20% and secretes glucagon, that
raises blood glucose level
D cells make up 5-10% and contain somatostatin,
that suppresses the release of insulin and glucagon.
PP cells constitute 1-2% and secrete a hormone of
unknown function pancreatic polypeptide
 Effects of Insulin on Metabolism
Carbohydrate metabolism
Insulin increases glucose transport into skeletal
muscle and adipose tissue.
 Glycogen synthesis (Insulin increases glycogen
synthesis, i.e. extra glucose in the liver, skeletal
muscle and adipose tissue is converted into glycogen
and stored there).
 Glycogenolysis (Insulin decrease the breakdown of
stored glycogen into glucose)
 Gluconeogenesis (Insulin also decreases the
formation of glucose from other substances such as
amino acid, lactic acid and glycerol)
 Effects of Insulin on Metabolism
Lipid Metabolism
 Lipogenesis and  lipolysis (Insulin also
facilitates triglyceride synthesis from glucose in fat
cells and inhibits the intracellular breakdown of
stored triglycerides)
Protein Metabolism
 Protein synthesis (Insulin also inhibits protein
breakdown and increases protein synthesis by
increasing the active transport of amino acids into
body cells)
 Effects of Glucagon on Metabolism
Carbohydrate Metabolism
Stimulation of Glycogenolysis: (Glucagon
initiates glycogenolysis or the breakdown of liver
glycogen as a means of raising blood glucose)

Inhibition of glycogen synthesis: ( Glucagon

inhibits the formation of glycogen from glucose)

Stimulation of gluconeogenesis: (Glucagon also

increases the transport of amino acids into the liver
and stimulates their conversion into glucose, a
process called gluconeogenesis)
 Effects of Glucagon on Metabolism
Lipid Metabolism
Stimulation of lipolysis (Enhances lipolysis in adipose
tissue, liberating fatty acids and glycerol for use in
gluconeogenesis )
Stimulation of ketogenesis
Inhibition of triglyceride synthesis

Protein Metabolism
Stimulation of proteolysis (Increases breakdown of
proteins into amino acids for use in gluconeogenesis)
Increases transport of amino acids into hepatic
cells
 Diabetes Mellitus (DM)
The term diabetes mellitus describes a metabolic
disorder of multiple etiology, characterized by
chronic hyperglycemia with disturbances of
carbohydrate, fat and protein metabolism resulting
from an imbalance b/w insulin availability and
insulin need.
OR
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 (American
 Diabetes Mellitus (DM)
Insulin, 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.
The effects of diabetes mellitus include long-
term damage, dysfunction and failure associated
with microvascular, macrovascular, and
metabolic complications of various organs.
 Prevalence of DM
It is top 5 of the most significant diseases in the
developed world.
In 2012 according to the WHO, at least 271 million
people world wide suffered from DM.

According to ADA 26.8 million with DM, 6.2

million people undiagnosed and about 41 million
would be considered pre-diabetic in USA.

Its incidences are increasing rapidly and it is

estimated that by the year 2030 this number will be
doubled.
 Classification of DM
There are several different types of diabetes
mellitus.
Type 1 Diabetes Mellitus - formerly known as
insulin-dependent diabetes mellitus (IDDM),
childhood diabetes, or juvenile-onset diabetes.

Type 2 Diabetes Mellitus - previously known as

adult-onset diabetes, maturity-onset diabetes, or
non-insulin dependent diabetes mellitus
(NIDDM)
 Classification of DM
Gestational Diabetes. It develops during
pregnancy and may improve or disappear after
delivery, involves a combination of inadequate
insulin secretion and responsiveness, resembling
type 2 diabetes in several respects.
Other specific types. Formerly known as
secondary diabetes, describes diabetes that is
associated with certain other conditions and
syndromes.
 Stages of Glucose Intolerance
The categories of Impaired Glucose Tolerance
(IGT) and Impaired Fasting Plasma Glucose (IFG)
refers to metabolic stages intermediate b/w normal
glucose homeostasis and diabetes, and are labeled
together as prediabetes.
Prediabetes is associated with increased risk for
atherosclerosis, heart diseases and progress to type 2
DM.
 Diagnosis of DM

In order to determine whether or not a patient has pre-

diabetes or diabetes, health care providers conduct
A Fasting Plasma Glucose Test (FPG) or an Oral
Glucose Tolerance Test (OGTT) or HbA1C . Either test
can be used to diagnose pre-diabetes or diabetes.
FPG test, A fasting blood glucose level between 110 and 126
mg/dl signals pre-diabetes.
A person with a fasting blood glucose level of
126 mg/dl or higher has diabetes.
In the OGT test, a person's blood glucose level is measured
after a fast and two hours after drinking a glucose-rich
beverage.
If the two-hour blood glucose level is between 140 and
200mg/dl, the person tested, has pre-diabetes.
If the two-hour blood glucose level is at 200 mg/dl or higher,
the person, tested has diabetes
 Glycated Hemoglobin Testing

• Glycated hemoglobin, also referred to as

glycohemoglobin, glycosylated hemoglobin, HbA1c,
or A1C is a term used to describe hemoglobin into
which glucose has been incorporated.
• It is recommended that persons with diabetes
lower their A1C to 7.0% or even achieve a normal
glycemic level of less than 6.0%.
• The level of A1C present in the blood provides an
index of blood glucose levels over the previous 6
to 12 weeks.
 Other Tests For DM
Capillary Blood Tests
This test is used for self
Monitoring of blood
glucose. The drop of
capillary blood is placed
on or absorbed by reagent
strip, and glucose levels
are determined
electronically using a
glucose meter.
 Other Tests For DM
Urine Test:
• When blood glucose reaches 180-200 mg/100ml,the kidney
begin to excrete glucose into the urine. (renal threshold).
• The level of glucose in urine depends on many factors and
therefore not routinely recommended in recent practice.

Urine Acetone:
The presence of acetone in the urine is called Ketonuria.
Ketonuria is a sign that a diabetes is out of control. Clients
are often told to test for urinary ketones if their blood
glucose level exceeds 240mg/dl.
 Type 1 DM
Type 1 diabetes is characterized by loss of the
insulin-producing beta cells of the islets of
Langerhans of the pancreas leading to a deficiency
or absolute lack of insulin
About 10% of all people with DM have type 1
disease.
Most people with Type1 DM develop the disease
before age 30.
“Less common and more severe condition”
 Etiology
• It is thought that combined genetic, immunologic
and possibly environmental (e.g. viral) factors
contribute to beta-cell destruction.
Genetic
The genetic tendency has been found in people with
certain HLA (human leukocyte antigen) types i.e.
DR3 or DR4).
People who have one of these two HLA type genes
are three to five times more prone to type1 diabetes.
The risk increases 10 to 20 times in people who
have both DR3 and DR4 HLA types (as compared
 Etiology cont..
Auto-Immunity
This is an abnormal response in which antibodies
are directed against normal tissues of the body,
responding to these tissues as if they are foreign.
Autoantibodies against islet cells and against
endogenous (internal) insulin have been detected in
people at the time of diagnosis and even several
years before the development of clinical signs of
type 1 diabetes.
Islet cells antibodies act against beta cells and
destroy these cells.
 Etiology cont..

Environmental Factors
Viruses like Rubella, Mumps and Measles may play
role in causing type 1 diabetes. They trigger
autoimmune process in genetically susceptible
individuals.
Exposure to cow's milk in infancy rather than
maternal milk, may play role, as albumin in cow's
milk react with islet cells of pancreas.
.
 Pathophysiology
• The destruction of the beta cells results in decreased
insulin production.
• Unchecked glucose production by the liver leads to
fasting hyperglycemia.
• In addition, glucose derived from food cannot be stored
in the liver but instead remains in the bloodstream and
contributes to postprandial (after meals) hyperglycemia
• In people with insulin deficiency the breakdown of
stored glucose (glycogenolysis) and production of new
glucose from amino acids and other substrates
(gluconeogenesis) occur in an uncontrolled way and
contribute further to hyperglycemia.
 Pathophysiology

• If the concentration of glucose in the blood exceeds

usually 180 to 200 mg/dl, the glucose then appears
in the urine (glucosuria).
• In addition, fat break-down occurs as an alternate
fuel for energy, resulting in an increased production
of ketone bodies, which are the byproducts of fat
breakdown and causing diabetic keto-acidosis
(DKA).
 Type 2 Diabetes Mellitus (T2DM)
T2DM is a syndrome in which hyperglycemia is
caused by the combination of insulin resistance
(inability of the peripheral tissues to respond to
insulin) and insulin deficiency (a derangement in
insulin secretion with relative to glucose load).
 Etiology:
Genetic factor:
Insulin secretion and action may be altered by many
genes (not yet identified)
• Environmental factor:
• Obesity, Aging, sedentary life style, diet etc
People with upper body obesity (central
obesity) are at great risk for developing T2DM
and metabolic disturbances than person with
lower body obesity.
Fat tissue particularly abdominal fat, is known
to become increasingly resistant to the action of
insulin.
Unexercised muscle tissue also becomes
insulin resistant.
In obese T2DM persons, insulin resistance may
stem from an increased concentration of free fatty
acid (FFA).
This has several consequences;
FFAs act on B cells to stimulate insulin secretion,
which with excessive and chronic stimulation causes
B cells failure (lipotoxicity)
They act at the level of peripheral tissue to cause
insulin resistance and decrease glucose.
Accumulation of FFAs reduce hepatic insulin
sensitivity of the liver, leading to increase hepatic
glucose production and hyperglycemia (especially
Fasting Plasma Glucose level).
 Pathophysiology
• Normally, insulin binds to special receptors on cell
surfaces leading to glucose uptake and glucose
metabolism.
• In type 2 diabetes, due to insulin resistance and
impaired insulin secretion glucose uptake is
diminished and also glucose released by the liver is
increased leading to hyperglycemia.
• Increased amount of insulin must be secreted to
maintain the glucose level at a normal or slightly
elevated level but the beta cells cannot fulfill the
increased demand for insulin, the glucose level rises,
and type 2 diabetes develops.
Insulin resistance in early stage of T2DM

B cells Insulin production to compensate and

maintain blood glucose level (hyperinsulinemia)

In late stage if insulin resistance persists, B cells

either due to genetic defect, fat toxicity or
exhaustion begin to fail resulting in hyperglycemia
 Pathophysiology
• Despite the impaired insulin secretion that is
characteristic of type 2 diabetes, there is enough
insulin present to prevent the breakdown of fat and
the accompanying production of ketone bodies.
• Therefore, DKA (diabetic ketoacidosis) does not
typically occur in type 2 diabetes.
• Uncontrolled type 2 diabetes may, however, lead to
another acute problem, HHNS (Hyperosmolar
Hyperglycemic Nonketotic Syndrome)
 Clinical Manifestation of DM
Hyperglycemia & glycosuria
Polyphagia, polyuria and polydipsia
Weight loss ( common in Type 1 DM)
Ketoacidosis ( common in Type 1 DM)
Blurred vision
Fatigue and weakness
Numbness and paresthesias (tingling sensation)
Skin lesions and other skin infections
Poor wound healing
Candidal infection (pruritus & vulvovaginitis)
 Major Characteristics of Types 1 and 2
Diabetes Mellitus
Features Type 1 DM Type 2 DM
Age at onset Usually <40 Usually >40
Proportion About 10% About 90%
Appearance Acute or subacute Slow or
subacute
of symptoms
Metabolic Frequent Rare
Ketoacidosis
Obesity at onset Uncommon Common
ß-Cells Decreased Variable
 Major Characteristics of Types 1 and 2 Diabetes
Mellitus
Features Type 1 DM
Type 2 DM

Insulin Decreased or absent Variable

Inflammatory Present initially Absent

cells in islets

Family history Uncommon

Common
 Major Characteristics of Types 1 and 2 Diabetes Mellitus

Features Type 1 DM Type 2 DM

HLA Association Yes No

Islets Cells
Antibodies (ICA) Yes Uncommon

Insulin auto-
antibodies (IAA) Yes (younger age) No

• Treatment Insulin and diet Diet exercise,

Weight reduction, Oral
hypoglycemics,
Insulin
 Acute Complications Of DM
The three major acute complication of DM are;
Diabetic Ketoacidosis
Hyperosmolar Hyperglycemic State
Hypoglycemia
Diabetic Ketoacidosis (DKA):
DKA occurs when ketone production by the liver exceeds
cellular use and renal excretion.
It most commonly occurs in a person with type 1 DM
Insulin suppresses lipase activity thereby prevents the
break down of lipids into fatty acids and glycerol.
In the absence of insulin increase in fatty acid levels leads
to ketone production by the liver
It can occur at the onset of the disease, often before the
disease has been diagnosed.
It is often preceded by physical and emotional stress, such
as infection, pregnancy, and extreme anxiety
Stress increases the release of gluconeogenic hormones
and predisposes the person to the development of DKA.
 Diabetic Ketoacidosis (DKA)
The three major metabolic derangements in DKA are
hyperglycaemia, ketosis, and metabolic acidosis.

Hyperglycaemia (blood glucose level >250mg/dL)

Low serum bicarbonate (<15 mEq/L)
Low pH (<7.3) with
Ketonemia & moderate ketonuria
 Other Clinical Manifestations
Dehydration caused by hyperglycemia
Warm, dry skin, dry mucous membrane
Tachycardia, hypotension, acute weight loss
Anorexia, nausea & vomiting
Odor of ketones on the breath
Depression of the CNS and coma
Compensatory rapid , deep respiration (Kussmaul
respiration- is a deep and labored breathing pattern often
associated with severe metabolic acidosis to wash out CO2)
Hyperosmolar Hyperglycemic State (HHS)
HHS is characterized by
Hyperglycemia (blood glucose >600 mg/dL)
Hyperosmolarity (plasma osmolarity >310
mOsm/L)
Dehydration, in the absence of ketoacidosis and
depression of the sensorium (perception).
Most frequently seen in people with T2DM
 Hypoglycemia or an Insulin reaction
Occurs from a relative excess of insulin in the blood
and is characterized by below normal glucose level
(<53 mg/dL)
It occurs most commonly in people treated with
insulin injection and prolonged use of hypoglycemic
agents.
 Signs & Symptoms
• Impaired cerebral function:
Feeling of vagueness, headache, difficulty in
problem solving, slurred speech, impaired
motor function, change in emotional behavior,
seizures, coma
• Autonomic Nervous system responses
Hunger, anxiety, hypotension, sweating, skin
pale and cool, tachycardia
 Chronic complications
Microvascular Disorders
neuropathies, nephropathies and retinopathies.
Macrovascular Disorders
CAD, stroke, and Peripheral Vascular Disease
Foot Ulcer
Formation of abnormal glycoprotein that
accumulate in the basement membrane of small
blood vessels and capillaries and causes
structural defects contribute eyes, kidneys, and
vascular complication.
Decrease in oxygen delivery in small vessels
of microcirculation.
 Dietry Management Of DM
 For all patients with diabetes, the meal plan must
consider the patient’s food preferences, lifestyle,
usual eating times, and ethnic and cultural
background.
 A thorough assessment of the patient’s need for
weight loss, gain, or maintenance is also undertaken
 In most instances, the person with type 2 diabetes
requires weight reduction.
 The priority for a young patient with type 1
diabetes, should be a diet with enough calories to
maintain normal growth and development.
 Dietry Management of DM
 Currently, the American Dietetic Association
recommend that 50% to 60% of calories should be
derived from carbohydrates, 20% to 30% from fat,
and the remaining 10% to 20% from protein.
 The latest nutrition guidelines recommend that all
carbohydrates be eaten in moderation to avoid
high postprandial blood glucose levels.
 The use of fiber in diabetic diet is recommended.
 This type of diet plays a role in lowering total
cholesterol and low-density lipoprotein cholesterol
in
the blood.
 Dietry Management of DM
Combining starchy foods with protein- and fat-
containing foods tends to slow their absorption
and lower the glycemic response.
In general, eating foods that are raw and whole
results in a lower glycemic response than eating
chopped, puréed, or cooked foods.
Eating whole fruit instead of drinking juice
decreases the glycemic response because fiber in
the fruit slows absorption.
 Dietary Management of DM
 Type 1: Eat at consistent times; adjust insulin dose
for amount of food eaten.
 Type 2: Space meals throughout day; moderate
calorie restriction(250-500 kcal less than average
daily intake.)
1. Reduced calorie intake increases sensitivity to
insulin.
2. Moderate weight loss (10-20lbs) decreases
hyperglycemia, hyperlipidemia, and hypertension.
 Exercise
 Exercise lowers the blood glucose level by increasing the
uptake of glucose by body muscles and by improving insulin
utilization.
 It also improves circulation and muscle tone.
 Resistance (strength) training, such as weight lifting, can
increase lean muscle mass, thereby increasing the resting
metabolic rate.
 These effects are useful in diabetes in relation to losing
weight, easing stress, and maintaining a feeling of well-being.
 Exercise also alters blood lipid levels, increasing levels of
high-density lipoproteins and decreasing total cholesterol and
triglyceride levels. This is especially important to the person
with diabetes because of the increased risk of cardiovascular
disease
 Exercise
 Patients who have blood glucose levels exceeding
250 mg/dL and who have ketones in their urine
should not begin exercising until the urine tests
negative for ketones and the blood glucose level is
closer to normal.
 The patient who requires insulin should be taught
to eat a 15-g carbohydrate snack (a fruit exchange)
or a snack of complex carbohydrate with a protein
before engaging in moderate exercise, to prevent
unexpected hypoglycemia
 Medical Management of DM
Oral Antidiabetic Agents:
 Oral antidiabetic agents are indicated for patients
who have type 2 diabetes that cannot be treated by
diet and exercise alone
 Contraindicated during pregnancy.
 Classified into five classes on the basis of their
action namely:
1. Sulfonylureas
2. Biguanides
3. Alpha Glucosidase Inhibitors
4. Thiazolidinediones
 Sulfonylureas
The sulfonylureas can be divided into first and second-
generation categories.
First Generation: Acetohexamide, chlorpropamide
Second Generation: Glipizide, glyburide, glimepiride
Action
 Directly stimulating the pancreas to secrete insulin.
 Improves insulin action at the cellular level and may also
directly decrease glucose production by the liver.
Side effects
 Most commonly GI symptoms and dermatologic reactions.
 Hypoglycemia when excessive dose is used or when the
patient omits or delays meals, reduces food intake, or
increases activity.
 Biguanides
Action
The biguanides e.g. Metformin (Glucophage) increases the
use of glucose by muscle and fat cells, decreases hepatic
glucose production, and decreases intestinal absorption of
glucose..
Side effects
 Lactic acidosis is a potential and serious complication
of biguanide therapy
Contraindications
 Renal impairment (serum creatinine level more than
1.4) , myocardial infarction.
 Hold Metformin for 2 days before any diagnostic
 Alpha Glucosidase Inhibitors
They include acarbonose
Action
 They work by delaying the absorption of glucose
in the intestinal system
 They can be used alone with dietary treatment as
monotherapy or in combination with sulfonylureas,
thiazolidinediones, or meglitinides
Side effects
 Hypoglycemia may occur when used in
combination
 Diarrhea and flatulence.
 Thiazolidinedions
Rosiglitizone and pioglitozone are categorized as
thiazolidinediones
Action
Thiazolidinediones enhance insulin action at the
receptor site and decrease production of glucose by
the liver.
Side effects
 These medications may affect liver function
 Thiazolidinediones can cause resumption of
ovulation in perimenopausal an ovulatory women,
making pregnancy a possibility.
 Meglitinides
This class includes Repaglinide
Action
 Lowers the blood glucose level by stimulating
insulin release from the pancreatic beta cells.
 Also indicated for use in combination with
metformin
Side effects
The principal side effect of repaglinide is hypo-
glycemia; however, this side effect is less severe and
frequent than for a sulfonylurea
 Insulin
Parenteral insulin is obtained from pork and beef
pancreas.
 Indicated for type 1 DM patients
 It was introduced in 1983.
 The concentration of insulin is 100 units/ml.
 Types of Insulin
There are several standard types of insulin:
Rapid acting.
Short acting
Intermediate acting.
Long acting.
Combinations.
 Rapid acting Insulin
Examples: Lispro (Humalog)
 Appearance: a clear liquid solution like water.
Action of Lispro= 5-15 min.
The hypoglycemic drug of choice for diabetics
experiencing acute or chronic diabetic emergencies,
e.g., DKA, HNKC (Hyperosmolar Non Ketotic Coma)
etc.
Lispro acts faster than regular insulin, thus it must not
be administered greater than >5 min before meals.
Route= SC.
 Short Acting Insulin
Example: Regular insulin (Humulin-R).
Appearance: a clear liquid solution like water.
Onset of action = 30min-1hr.
Humulin-R is the only insulin preparation that
can be given IV.
Regular insulin is given 30 min. before meals.
Regular Insulin routes: SC, IV
 Intermediate Acting Insulin
 Examples: Neutral Protamine Hagedorn (NPH),
Humulin N, Lente, Humulin L.
 NPH and Humulin-N contains protamine, a protein

that prolongs the action of insulin.

 Lente and Humulin L contains Zinc that also
prolongs the action of insulin.
 The onset of action:1-2 hrs.
 Duration of action:18-24 hrs.
 Route= SC
 Long acting Insulin
 Examples: Humulin Ultralente, Lantus (an insulin
glargine).
 Long acting insulin absorb slower than other
insulin b/c of its large crystals, which dissolve
slowly and prolongs the action.
 Onset of action: 4-8 hrs and lasts for 24-36 hrs.
 Lantus is an analogue of human insulin
 It is administered once daily HS.
 With Lantus, clients c/o pain at injection site.
 Available with ―Optipen or insulin pen.
 Route= SC.
 Combination Insulin
They are commercially premixed.
 Examples: Humulin 70/30, Humulin 50/50,
Humalog 75/25.
 Insulin
Side-effects: Hypoglycemic reaction, confusion,
agitation, tremors, headache, weakness, lethargy,
fatigue, urticaria, redness, irritation or swelling at
insulin injection site, tachycardia, palpitation,
rebound Hyperglycemia (Somogyi effect),
lipodystrophy, shock.
Contraindications:
Hypersensitivity to beef, pork, zinc, protamine insulin.
 Nursing Management
Patient education:
 Knowledge about nutrition,
 Medication effects and side effects
 Exercise, disease progression, prevention strategies
 Blood glucose monitoring techniques
 Medication adjustment.
 Nursing Diagnoses
Major nursing diagnoses may include the following:
 Risk for fluid volume deficit related to polyuria and
dehydration
 Fluid and electrolyte imbalance related to fluid loss or
shifts
 Deficient knowledge about diabetes self-care skills or
information
 Anxiety related to loss of control, fear of inability to
manage diabetes, misinformation related to diabetes,
fear of diabetes complications
Teaching Survival Skills
1. Simple pathophysiology
a. Basic definition of diabetes (having a high blood
glucose level)
b. Normal blood glucose ranges and target blood
glucose levels
c. Effect of insulin and exercise (decrease glucose)
d. Effect of food and stress, including illness and
infections (increase glucose)
e. Basic treatment approaches
Teaching survival skills

2. Treatment modalities
a. Administration of insulin and oral antidiabetes medications
b. Diet information (food groups, timing of meals)
c. Monitoring of blood glucose and ketones
3. Recognition, treatment, and prevention of acute
complications
a. Hypoglycemia
b. Hyperglycemia
4. Pragmatic information
a. Where to buy and store insulin, syringes, and glucose
monitoring supplies
Nursing Management Cont…

Teaching preventive measures

• Foot care
• Eye care
• General hygiene (e.g. skin care, oral hygiene)
• Risk factor management (e.g. control of blood
pressure and blood lipid levels, and normalizing
blood glucose levels)
Priority Nursing Actions

Hypoglycemic reaction.
1. Check the client’s blood glucose level
2. Give the client 10 to 15 g carbohydrate item such
as half cup of fruit juice to drink.
3. Take the client’s vital signs
4. Retest the blood glucose level
5. Give the client a small snack of carbohydrate and
protein
6. Document the client’s complaint’s, actions taken,
and outcome.
 Nursing Interventions For DKA

1. Restore circulating blood volume and protect against

cerebral, coronary and renal hypoperfusion.
2. Treat dehydration with rapid IV infusion of 0.9% or
0.45% NS as prescribed, 5% dextrose is added to
0.45%NS when the blood glucose comes down to
250 to 300 mg.
3. Treat hyperglycemia with regular insulin IV as
prescribed.
4. Correct electrolyte imbalance (Potassium level may
be elevated as a result of dehydration and acidosis).
5. Monitor potassium level closely because it may
decrease after IV hydration.
Nursing Interventions For HHNS

1. Treatment is similar to that for DKA

2. Treatment includes fluid replacement, correction of
electrolyte imbalances, and insulin administration
3. Fluid replacement in older client must be done
very carefully because of the potential for heart
failure
4. Insulin plays a less critical role in the treatment of
HHNS, rehydration alone may decrease glucose
level.
Client’s Education During Illness

1. Take insulin or oral antidiabetic agents as prescribed

2. Test blood glucose level and test the urine for
ketones every 3 to 4 hours
3. If the usual meal plan cannot be followed, substitute
soft foods for six to eight times a day.
4. If vomiting, diarrhea, or fever occurs, consume
liquids every 30 to 60 min. to prevent dehydration
and to provide calories.
5. Notify physician if glucose 250 to 300 mg/dl, when
ketonuria, when unable to take food or liquids for 4
hrs
Thank You