INTRODUCTION

Insulin, a hormone produced by the pancreas, controls the level of

glucose in the blood by regulating the production & storage of
glucose. In the diabetic state, the cells may stop responding to insulin
or the pancreas may stop producing insulin entirely. Normally a
certain amount of glucose circulates in the blood. The major sources
of this glucose are absorption of ingested food in the gastrointestinal
tract & formation of glucose by the liver from food substances.

Definition

The term diabetes, without qualification, usually refers to diabetes

mellitus, which roughly translates to excessive sweet urine (known as
"glycosuria"). Several rare conditions are also named diabetes. The
most common of these is diabetes insipidus in which large amounts of
urine are produced (polyuria), which is not sweet (insipidus meaning
"without taste" in Latin).

The term "type 1 diabetes" has replaced several former terms,

including childhood-onset diabetes, juvenile diabetes, and insulin-
dependent diabetes mellitus (IDDM). Likewise, the term "type 2
diabetes" has replaced several former terms, including adult-onset
diabetes, obesity-related diabetes, and non-insulin-dependent diabetes
mellitus (NIDDM). Beyond these two types, there is no agreed-upon
standard nomenclature. Various sources have defined "type 3
diabetes" as: gestational diabetes,[4] insulin-resistant type 1 diabetes
(or "double diabetes"), type 2 diabetes which has progressed to
require injected insulin, and latent autoimmune diabetes of adults.

occurs when a person's blood glucose levels are higher than normal
but not Classification

Most cases of diabetes mellitus fall into three broad categories:

1. Type 1
2. Type 2
3. Gestational diabetes.
A few other types are described.
1. Type 1 diabetes

Main article: Diabetes mellitus type 1

Type 1 diabetes mellitus is characterized by loss of the insulin-

producing beta cells of the islets of Langerhans in the pancreas
leading to insulin deficiency. This type of diabetes can be further
classified as immune-mediated or idiopathic. The majority of type 1
diabetes is of the immune-mediated nature, where beta cell loss is a T-
cell mediated autoimmune attack. There is no known preventive
measure against type 1 diabetes, which causes approximately 10% of
diabetes mellitus cases in North America and Europe. Most affected
people are otherwise healthy and of a healthy weight when onset
occurs. Sensitivity and responsiveness to insulin are usually normal,
especially in the early stages. Type 1 diabetes can affect children or
adults but was traditionally termed "juvenile diabetes" because it
represents a majority of the diabetes cases in children.

2. Type 2 diabetes

Main article: Diabetes mellitus type 2

Type 2 diabetes mellitus is characterized by insulin resistance which

may be combined with relatively reduced insulin secretion. The
defective responsiveness of body tissues to insulin is believed to
involve the insulin receptor. However, the specific defects are not
known. Diabetes mellitus due to a known defect are classified
separately. Type 2 diabetes is the most common type.

In the early stage of type 2 diabetes, the predominant abnormality is

reduced insulin sensitivity. At this stage hyperglycemia can be
reversed by a variety of measures and medications that improve
insulin sensitivity or reduce glucose production by the liver.

3. Gestational diabetes

Main article: Gestational diabetes

Gestational diabetes mellitus (GDM) resembles type 2 diabetes in

several respects, involving a combination of relatively inadequate
insulin secretion and responsiveness. It occurs in about 2%–5% of all
pregnancies and may improve or disappear after delivery. Gestational
diabetes is fully treatable but requires careful medical supervision
throughout the pregnancy. About 20%–50% of affected women
develop type 2 diabetes later in life.

Even though it may be transient, untreated gestational diabetes can

damage the health of the fetus or mother. Risks to the baby include
macrosomia (high birth weight), congenital cardiac and central
nervous system anomalies, and skeletal muscle malformations.
Increased fetal insulin may inhibit fetal surfactant production and
cause respiratory distress syndrome. Hyperbilirubinemia may result
from red blood cell destruction. In severe cases, perinatal death may
occur, most commonly as a result of poor placental perfusion due to
vascular impairment. Labor induction may be indicated with
decreased placental function. A cesarean section may be performed if
there is marked fetal distress or an increased risk of injury associated
with macrosomia, such as shoulder dystocia.

A 2008 study completed in the U.S. found that the number of

American women entering pregnancy with preexisting diabetes is
increasing. In fact the rate of diabetes in expectant mothers has more
than doubled in the past 6 years. This is particularly problematic as
diabetes raises the risk of complications during pregnancy, as well as
increasing the potential that the children of diabetic mothers will also
become diabetic in the future.

4. Other types

Pre-diabetes indicates a condition that high enough for a diagnosis of

type 2 diabetes. Many people destined to develop type 2 diabetes
spend many years in a state of pre-diabetes which has been termed
"America's largest healthcare epidemic.

Some cases of diabetes are caused by the body's tissue receptors not
responding to insulin (even when insulin levels are normal, which is
what separates it from type 2 diabetes); this form is very uncommon.
Genetic mutations (autosomal or mitochondrial) can lead to defects in
beta cell function. Abnormal insulin action may also have been
genetically determined in some cases. Any disease that causes
extensive damage to the pancreas may lead to diabetes (for example,
chronic pancreatitis and cystic fibrosis). Diseases associated with
excessive secretion of insulin-antagonistic hormones can cause
diabetes (which is typically resolved once the hormone excess is
removed). Many drugs impair insulin secretion and some toxins
damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity,
malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10
code E12), was deprecated by the World Health Organization when
the current taxonomy was introduced in 199

Causes

The cause of diabetes depends on the type. Type 2 diabetes is due

primarily to lifestyle factors and genetics.

Type 1 diabetes is also partly inherited and then triggered by certain

infections, with some evidence pointing at Coxsackie B4 virus. There
is a genetic element in individual susceptibility to some of these
triggers which has been traced to particular HLA genotypes (i.e., the
genetic "self" identifiers relied upon by the immune system).
However, even in those who have inherited the susceptibility, type 1
diabetes mellitus seems to require an environmental trigger

OTHER CAUSES

 Genetic defects of β-cell  Endocrinopathies

Function o Growth hormone excess
o Maturity onset (acromegaly)
diabetes of the young o Cushing syndrome
(MODY) o Hyperthyroidism
o Mitochondrial DNA o Pheochromocytoma
mutations o Glucagonoma
 Genetic defects in insulin  Infections
processing or insulin action o Cytomegalovirus
o Defects in proinsulin infection
conversion o Coxsackievirus B
o Insulin gene mutations  Drugs
o Insulin receptor o Glucocorticoids
 mutations o Thyroid hormone
 Exocrine Pancreatic Defects o β-adrenergic agonists
o Chronic pancreatitis
o Pancreatectomy
o Pancreatic neoplasia
o Cystic fibrosis
o Hemochromatosis
o Fibrocalculous
pancreatopathy

Risk Factors

 Family history of diabetes ( i.e. parents or siblings with

diabetes)
 Obesity ( i.e. over desired body weight)
 Race/ ethnicity
 Age above 45 years
 Previously identified impaired fasting glucose or impaired
glucose tolerance
 Hypertension
 HDL cholesterol level above 35mg/dl or triglyceride level above
250mg/dl.
 History of gestational diabetes or delivery of baby of 9lbs
Pathophysiology

Insulin is secreted by beta cells, which are one of four types of cells
in the islets of largerhens in the pancreas. Insulin is an anabolic or
storage hormone. When a person eats meal insulin secretion increases
& moves glucose from the blood into muscle, liver & fat cells. In
those cells insulin:

 Transport & metabolizes glucose for energy.

 Stimulates storage of glucose in the liver & muscle.
 Signals the liver to stop the release of glucose.
 Enhances storage of dietary fat in the adipose tissue.
 Accelerates transport of amino acids into cells.

During fasting periods the pancreas continuously releases a

small amount of insulin, another pancreatic hormone called glucagon
by the alpha cells of the islet of langerhens is released when blood
glucose levels decrease & stimulate the liver to release stored glucose.
The insulin & the glucagon together maintain a constant level of
glucose in the blood by stimulating the release of glucose from the
liver.

Initially the liver produces glucose through the breakdown of

glycogen. After 8 to 12 hours without food the liver forms glucose
from the breakdown of noncarbohydrate substances, including amino
acids (gluconeogenesis).
Pathogenesis of type 2 diabetes

Impaired insulin GI absorption of

secretion from glucose
pancreas

Hyperglycemia

Increased basal Decreased

hepatic glucose insulin
production stimulated
glucose uptake

Pathogenesis of diabetes type 2

The two main problems related to insulin in type 2 are

1. Insulin resistance
2. Impaired insulin secretion
 Insulin resistance refers to decreased tissue sensitivity to insulin.
Normally insulin binds to special receptors on cell surface &
initiates a series reaction involved in glucose metabolism. In
diabetes type 2 these intracellular reactions are diminished thus
rendering insulin less effective at simulating glucose uptake by
the tissues & at regulating glucose release by the liver. The
exact mechanism that leads to insulin resistance & impaired
insulin secretion in type 2 diabetes are unknown, although
genetic factors are thought to play a role.
Clinical Manifestation

Clinical manifestation of all types of diabetes include the three Ps: -

1. Polyuria
2. Polydipsia
3. Polyphagia.

Polyuria (increased urination) & polydipsia (increased thirst) occur as

a result of the excess loss of fluid associated with osmotic dieresis.
The patient also experiences polyphagia resulting from the catabolic
state induced by insulin deficiency & the breakdown of fats &
proteins. Other symptoms include: -

 Fatigue
 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 & Diagnosis

Assessment

History

 Symptoms should be related to the diagnosis of diabetes:

 Symptoms of hyperglycaemia.
 Symptoms of hypoglycaemia.
 Its frequency, timing, severity & resolution
 Results of blood glucose monitoring.
 Status symptoms & management of chronic complications of
diabetes:
 Eye, kidney, nerve, genitourinary & sexual, bladder &
gastrointestinal.
 Cardiac, peripheral vascular, foot complications associated
with diabetes.
 Compliance with prescribed dietary management plan.
 Adherence to prescribed exercise regimen.
 Compliance with prescribed pharmacologic treatment.
 Use of tobacco, alcohol & prescribed & over the counter
medications/drugs.
 Lifestyle, culture, psychosocial & economic factors that may
affect diabetes treatment.

Physical examination

 Blood pressure (sitting & standing to detect orthostatic

changes).
 Body mass index
 Fundoscopic examination
 Foot examination (lesion, sign of infection, pulse).
 Skin examination (lesions & insulin injection sites).
 Neurologic examination
  Vibratory & sensory examination using monofilament.
 Deep tendon reflexes.
 Oral examination.

Laboratory examination

 HgbA1c
 Fasting lipid profile
 Test for microalbiminuria
 Serum creatinine level
 Urinalysis
 Electrocardiogram

Need for referrals

 Ophthalmology
 Podiatry
 Dietician
 Diabetes educator
 Others if indicated

Criteria for diagnosis of diabetes mellitus.

 Symptoms of diabetes plus casuals plasma glucose

concentration equal to or greater than 200mg/dl. Casual is
defined as any time of day without regards to time since last
meal. The classic symptoms of diabetes include polyuria,
polydipsia & unexplained weight loss.
Or
 Fasting blood glucose greater than or equal to 126mg/dl. Fasting
is defined as no caloric intake for at least 8 hours.
Or
 2-hours post load glucose equal to or greater than 200mg/dl
during an oral glucose tolerance test. The test should be
performed as described by the world health organization using a
glucose load containing the equivalent of 75g anhydrous glucose
dissolved in water.
 In the absence of unequivocal hyperglycemia with acute
metabolic deconmpensation these criteria should be confirmed
by repeat testing on a different day. The third measure is not
recommended for routine clinical use.

Glycosylated hemoglobin and Glucose tolerance test

2006 WHO Diabetes diagnosis criteria
Condition 2 hour glucose Fasting glucose
mmol/l(mg/dl) mmol/l(mg/dl)
Normal <7.8 (<140) <6.1 (<110)
Diabetes mellitus ≥11.1 (≥200) ≥7.0 (≥126)

Diabetes mellitus is characterized by recurrent or persistent

hyperglycemia, and is diagnosed by demonstrating any one of the
following

 Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL).

 Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a
75 g oral glucose load as in a glucose tolerance test.
 Symptoms of hyperglycemia and casual plasma glucose
≥ 11.1 mmol/L (200 mg/dL).
 Glycated hemoglobin (Hb A1C) ≥ 6.5%

A positive result, in the absence of unequivocal hyperglycemia,

should be confirmed by a repeat of any of the above-listed methods
on a different day. It is preferable to measure a fasting glucose level
because of the ease of measurement and the considerable time
commitment of formal glucose tolerance testing, which takes two
hours to complete and offers no prognostic advantage over the fasting
test. According to the current definition, two fasting glucose
measurements above 126 mg/dL (7.0 mmol/L) is considered
diagnostic for diabetes mellitus.

People with fasting glucose levels from 100 to 125 mg/dL (5.6 to
6.9 mmol/L) are considered to have impaired fasting glucose. Patients
with plasma glucose at or above 140 mg/dL (7.8 mmol/L), but not
over 200 mg/dL (11.1 mmol/L), two hours after a 75 g oral glucose
load are considered to have impaired glucose tolerance. Of these two
pre-diabetic states, the latter in particular is a major risk factor for
progression to full-blown diabetes mellitus as well as cardiovascular
disease.

Medical Management

There are five components of diabetes mellitus management:

i. Nutrition management
ii. Exercise
iii. Monitoring
iv. Pharmacologic therapy
v. Education

Nutritional
Management

Education
Exercise
MAN

Pharmacological
Monitoring
Therapy
Nutritional management

Evidenced based nutritional principles & recommendations for

the treatment & prevention of diabetes & related complications 2003.

 Providing all essential food constituents necessary for optimal

nutrition (vitamins & minerals).
 Meeting energy needs.
 Achieving & maintaining a reasonable weight.
 Preventing wide daily fluctuation in blood glucose levels with
glucose levels as close as normal as is safe & practical to
prevent or reduce the risk for complications.
 Decreasing serum lipid levels, if elevated to reduce the risk for
macrovascular disease.

Meal planning

For all patients with diabetes, the meal plan must consider the
patient’s food preferences, lifestyle, usual eating times & ethnic &
cultural background.

Guidelines for dietary recommendations

 Combining starchy foods with protein & fat containing foods

tends to slow their absorption & lower the glycemic response.
 In general eating food that are whole results in a lower glycemic
response than eating chopped, pureed or cooked foods.
 Eating whole fruit instead of drinking juice decreases the
glycemic response because fibre in the fruits slows absorption.
 Adding foods with sugars to the diet may produce a lower
glycemic response if these foods are eaten with foods that are
more slowly absorbed.

Other dietary concern

 Alcohol consumption: the main danger of alcohol consumption

by a diabetic patient is hypoglycaemia, especially for patients
 who take insulin. Alcohol may decrease the normal
physiologic reactions in the body that produce glucose.
 Sweeteners: using sweeteners is acceptable for patient with
diabetes, especially if it assists in overall dietary adherence.
Moderation in the amount of sweetener used is encouraged to
avoid potential adverse effect.

Exercise

Benefits

 Exercise lowers the blood glucose level by increasing the

uptake of glucose by body muscles & by improving insulin
utilization.
 It improves muscle tone.
 Exercise also alters blood lipid levels.
 Increasing levels of high density lipoproteins & decreasing
total cholesterol & triglyceride levels.

Exercise precaution

 Patient who have blood glucose level exceeding 250mg/dl &

who have ketones in the urine should not begin exercising until
urine test is negative & the blood glucose level is close to
normal.
 The patient who requires insulin should be taught to eat a 15g
carbohydrate snack or snacks of complex carbohydrates with a
protein before engaging in moderate exercise, to prevent
hypoglycaemia.
 To avoid post exercise hypoglycaemia especially after
strenuous or prolonged exercise, the patient may need to eat a
snack at the end of the exercise session & at bed time & monitor
the blood glucose level.

Exercise recommendation

 People with diabetes should exercise at same time & in

same amount each day.
  Regular exercise rather than sporadic should be
encouraged.
 Exercise recommendation must be altered as necessary for
patient with diabetic complications such as retinopathy,
autonomic neuropathy, sensorimotor neuropathy & vascular
disease.

MONITORING BLOOD GLUCOSE LEVEL

Self monitoring of blood glucose(SMBG)

An older style portable blood glucose meter. A blood
sample is applied to an inserted strip (see image above) and color
changes caused by reaction with blood glucose are measured by the
meter.

Relying on their own perceptions of symptoms of

hyperglycemia or hypoglycemia is usually unsatisfactory as mild to
moderate hyperglycemia causes no obvious symptoms in nearly all
patients. Other considerations include the fact that, while food takes
several hours to be digested and absorbed, insulin administration can
have glucose lowering effects for as little as 2 hours or 24 hours or
more (depending on the nature of the insulin preparation used and
individual patient reaction). In addition, the onset and duration of the
effects of oral hypoglycemic agents vary from type to type and from
patient to patient.

Candidates
 For every one with diabetes, self monitoring of glucose is very
important for managing self care. It is a key component of treatment
for any intensive insulin therapy regimen & for diabetes management
during pregnancy. It is recommended for patients with:

 Unstable diabetes
 A tendency for severe ketosis or hypoglycaemia
 Hypoglycaemia without warning symptoms

For patient not using insulin therapy, SMGB is helpful for

monitoring the effectiveness of exercise, diet & oral anti diabetic
agents. It can also help motivate patients to continue with treatment.
For patient with type 2 diabetes, SMBG is recommended during
periods of suspected hyperglycemia or hypoglycemia.

Personal (home) glucose monitoring

Control and outcomes of both types 1 and 2 diabetes may be

improved by patients using home glucose meters to regularly measure
their glucose levels. Glucose monitoring is both expensive (largely
due to the cost of the consumable test strips) and requires significant
commitment on the part of the patient. The effort and expense may be
worthwhile for patients when they use the values to sensibly adjust
food, exercise, and oral medications or insulin. These adjustments are
generally made by the patients themselves following training by a
clinician.

Regular blood testing, especially in type 1 diabetics, is helpful

to keep adequate control of glucose levels and to reduce the chance of
long term side effects of the disease. There are many (at least 20+)
different types of blood monitoring devices available on the market
today; not every meter suits all patients and it is a specific matter of
choice for the patient, in consultation with a physician or other
experienced professional, to find a meter that they personally find
comfortable to use. The principle of the devices is virtually the same:
a small blood sample is collected and measured. In one type of meter,
the electrochemical, a small blood sample is produced by the patient
using a lancet (a sterile pointed needle). The blood droplet is usually
collected at the bottom of a test strip, while the other end is inserted in
the glucose meter. This test strip contains various chemicals so that
when the blood is applied, a small electrical charge is created between
two contacts. This charge will vary depending on the glucose levels
within the blood. In older glucose meters, the drop of blood is placed
on top of a strip. A chemical reaction occurs and the strip changes
color. The meter then measures the color of the strip optically.

Self-testing is clearly important in type I diabetes where the use of

insulin therapy risks episodes of hypoglycaemia and home-testing
allows for adjustment of dosage on each administration. However its
benefit in type 2 diabetes is more controversial as there is much more
variation in severity of type 2 cases. [26] It has been suggested that
some type 2 patients might do as well with home urine-testing alone.
The best use of home blood-sugar monitoring is being researched.

Benefits of control and reduced hospital admission have

been reported. However, patients on oral medication who do not self-
adjust their drug dosage will miss many of the benefits of self-testing,
and so it is questionable in this group. This is particularly so for
patients taking monotherapy with metformin who are not at risk of
hypoglycaemia. Regular 6 monthly laboratory testing of HbA1c
(glycated haemoglobin) provides some assurance of longterm
effective control and allows the adjustment of the patient's routine
medication dosages in such cases. High frequency of self-testing in
type 2 diabetes has not been shown to be associated with improved
control. The argument is made, though, that type 2 patients with poor
long term control despite home blood glucose monitoring, either have
not had this integrated into their overall management, or are long
overdue for tighter control by a switch from oral medication to
injected insulin.

HbA1c test

A useful test that has usually been done in a laboratory is the

measurement of blood HbA1c levels. This is the ratio of glycosylated
hemoglobin in relation to the total hemoglobin. Persistent raised
plasma glucose levels cause the proportion of these molecules to go
up. This is a test that measures the average amount of diabetic control
over a period originally thought to be about 3 months (the average red
blood cell lifetime), but more recently thought to be more strongly
weighted to the most recent 2 to 4 weeks. In the non-diabetic, the
HbA1C level ranges from 4.0-6.0%; patients with diabetes mellitus
who manage to keep their HbA1C level below 6.5% are considered to
have good glycemic control. The HbA1c test is not appropriate if
there has been changes to diet or treatment within shorter time periods
than 6 weeks or there is disturbance of red cell aging (e.g. recent
bleeding or hemolytic anemia) or a hemoglobinopathy (e.g. sickle cell
disease). In such cases the alternative Fructosamine test is used to
indicate average control in the preceding 2 to 3 weeks.

Ongoing monitoring

Main article: Blood glucose monitoring

Recently, devices have been manufactured which provide

ongoing monitoring of glucose levels on an automated basis during
the day, for example:

1. The Minimed Paradigm REAL-Time by Minimed, is a blood

glucose monitoring device that provides blood glucose
measurements to be made every five minutes. The patient can
thus adjust an insulin infusion pump immediately and mimic the
"feed-back" mechanism of a pancreas.
2. The US Food and Drug Administration has also approved a non-
invasive blood glucose monitoring device, the GlucoWatch G2
Biographer. This allows checking blood glucose levels, while
puncturing the skin as little as twice a day. Once calibrated with
a blood sample, it pulls body fluids from the skin using small
electrical currents, taking six readings an hour for as long as
thirteen hours. It has not proven to be reliable enough, or
convenient enough to be used in lieu of conventional blood
monitoring. Other non-invasive methods like radio waves,
ultrasound and energy waves are also being tested.

Frequency of SMBG
  For most patients who require insulin, SMBG is recommended
two or three times daily.
 For patients who take insulin before each meal, SMBG is
required at least three times daily before meals to determine
each dose.
 Patient not receiving insulin may be instructed to assess their
blood glucose levels at least two or three times per week,
including a 2 hour post prandial test.
 For all patients testing is recommended whenever
hypoglycaemia or hyperglycemia is suspected.
 Patient must increase the frequency of SMBG with changes in
medications, activity or diet & with stress or illness.

Urine testing for glucose

Before urine glucose testing was the only way to monitor diabetes
on daily basis. Today it use is limited to patient who cannot or will
not perform self monitoring of blood glucose ( SMBG).

Testing for ketones

Ketones in the urine signal that control of type 1 diabetes is

deteriorating & the risk of DKA is high. When there is almost no
effective insulin available, the body starts to break down stored fats
for energy. Ketone bodies are the by-products of this fat breakdown
& they accumulate in blood & in the urine.

Ketone testing should be performed whenever patients with type 1

diabetes have glucosuria or persistently elevated blood glucose levels.

Pharmacologic therapy

1. INSULIN THERAPY
Indication
 Body loses the ability to produce insulin in type 1 diabetes,
exogenous insulin must be administered.
 In type 2 diabetes insulin must be administered on a long
term basis to control glucose levels if diet & oral agents
fail.
  Some patient requires insulin temporarily during illness,
infection, pregnancy, surgery or some other stressful
events.

Categories of insulin

Time course Agent Onset Duration

1. Rapid acting  Lispro 10-15min 3hrs

(humalog)
 Aspart 4-6 hrs
(novolog)

2. short acting  Regular ½-1 hr 4-6 hrs

3.intermediate acting  NPH (neutral 2-4 hrs 16-20hrs

protamine
hegadorn)

4.long acting  Ultralente 6-8hrs 20-30 hrs

5.very long acting  Glargine 1hr 24hrs

Insulin regimens

Insulin regimens vary from one to four injections per day. Usually
there is a combination of short acting insulin & short acting insulin.
Normally functioning pancreas continuously secretes small amount of
insulin during the day & the night. In addition when ever blood
glucose rises after ingestion of food there is a rapid burst of insulin
secretion in proportion to the glucose rising effect of the food.

1. Conventional regimen
With this type of simplified regimen e.g. one or more injections
of a mixture of short & intermediate acting insulin per day.
2. Intensive regimen
The second approach is to use a more complex insulin regimen
to achieve as much control over blood glucose levels as is safe
& practical. This regimen allows patients more flexibility to
change in their eating & activity patterns with stress & illness &
as needed for variations in the prevailing glucose level.

Complication of insulin therapy

 Local allergic reactions

Redness, swelling, tenderness & indurations or a 2 to 4 cm
wheal may appear at the injection site 1 to 2 hrs after the insulin
administration. These reactions appear at the beginning of the
therapy & disappear with continued use of insulin.
 Systemic allergic reactions
Systemic allergic reactions to insulin so rare. When they do
occur there is an immediate local skin reaction that gradually
spreads into generalized urticaria (hives). The treatment is
desensitization with small doses of insulin administered in
gradually increasing amount using a desensitizing kit.
 Insulin lipodystrophy
Lipodystrophy is loss of subcutaneous fat & appears as slight
dimpling or more serious pitting of subcutaneous fat. The use of
human insulin has almost eliminated this disfiguring
complication. Lipodystrophy the development of fibrofatty
masses at the injection site is caused by the repeated use of an
injection site. If the insulin is injected into scared areas,
absorption may be delayed, this one of the reason that rotation
of injection sites is so important.
 Insulin resistance
 Most of the patient at one time or another have some degree of
insulin resistance. This may occur for various reasons, the most
common being obesity, which can be overcome by weight loss.
Clinical resistance has been defined as a daily insulin
requirement of 200 units or more.
Treatment administering a more concentrated insulin
preparation, such as U500 which is available by special order.
Occasionally, prednisone is needed to block the production of
antibodies. This may be followed by a gradual reduction iin
insulin requirement.

 Morning hyperglycemia

Characteristic Treatment

1. Insulin warning

Progressive rise in blood Increase evening dose of

glucose from bedtime to intermediate or long acting
morning. insulin.
2. Dawn phenomenon

Relatively normal blood Change time of injection of

glucose until about 3am, when evening time, intermediate
the level begins to rise. acting insulin from dinnertime
to bed time.
 3. Somogyi effect
Normal or elevated blood Decrease evening dose of
glucose at bedtime, a intermediate acting insulin, or
decrease at 2-3 am to increase bedtime snacks.
hypoglycemic levels & a
subsequent increase caused
by the production of counter
regulatory hormones.

ALTERNATIVE METHODS OF INSULIN DELIVERY

 Insulin pens
 Jet injectors
 Insulin pumps
 Implantable & inhalant insulin delivery

2. Oral antidiabetic agents

Oral antidiabetic agents may be effective for patients who have

type2 diabetes that cannot be treated by diet & exercise alone.

 Sulfonylureas:
This exerts its primary action by directly stimulating the
pancreas to secrete insulin. Therefore a functioning pancreas is
necessary for these agents to be effective & they cannot be used
in patient with type 2 diabetes. These agents improve insulin
action at the cellular level & may also directly decrease glucose
production by the liver. The sulfonylurea can be divided into
first & second generation categories.
 Biguanides:
Metformin produces its antidiabetic effect by facilitating
insulin’s action on pheripheral receptors sites. Therefore it can
be used only in presence of insulin. Biguanides have no effect
on pancreatic beta cells. Biguanides used with a sulfonylurea
may enhance the glucose lowering effect more than either
medication used alone. Lactic acidosis is a potential & serious
complication of Biguanide therapy the patient must be
monitored closely when therapy is initiated or when dosage
changes.
 Alpha glucosidase inhibitors:
Used in type 2 diabetes mellitus. They work by delaying
the absorption of glucose in the intestinal system, resulting in
the lower postprandial blood glucose level. They can be used
alone with dietary treatment as monotherapy or in combination
with sulfonylurea, acarbose & miglitol do not enhance insulin
secretion. The advantage of oral alpha inhibitors is that they are
not systemically absorbed & are safe to use. Their side effects
are diarrhea & flatulence. These effect can be minimized by
starting at a very low dose & increasing the dose gradually.
 Thiazolidinediones:
They are indicated for patient who takes insulin injections &
be may affect liver function therefore liver function studies must
be performed at baseline & at frequent intervals.
 Meglitinides:
Lowers blood glucose level by stimulating insulin release
from the pancreatic beta cell. Its effectiveness depends upon the
presence of functioning beta cells. Therefore repaglinide is
contraindicated in patient with type 1 diabetes. Repaglinide has
a fast action & a short duration. It should be taken before meal
to stimulate the release of insulin in response to that meal. It is
also indicated for use in combination with metformin in patient
whose hyperglycemia cannot be controlled by exercise, diet &
either metformin or repaglinide alone.
AGE RELATED CHANGES THAT MAY AFFECT DIABETES &
ITS MANAGEMENT.

Sensory changes

 Decreased vision
 Decreased smell
 Taste changes
 Decreased proprioception
 Diminished thirst

Gastrointestinal changes

 Dental problems
 Appetite changes
 Delayed gastric emptying
 Decreased bowel motility

Activity/exercise pattern changes

 More sedentary

Renal function changes

 Decreased function
 Decreased drug clearance

Affective/cognitive changes

 Medication/meals omitted or taken erractically

Socio economic factors

 Fat diets
 Loneliness/living alone
 Lack of money/ lack of support system

Chronic diseases

 Hypertension
  Arthritis
 Neoplasms
 Acute/chronic infection

Potential drug interactions

 Use of another person’s medications

 Consulting multiple physicians for different illnesses
 Alcohol use/abuse.

NURSING MANAGEMENT

Education: an outline of survival information includes

1. Simple pathophysiology
2. Treatment modalities
3. Recognition, treatment & prevention of acute complications.
4. Pragmatic information
 Where to buy & store insulin, syringes & glucose
monitoring supplies
 When & how to reach the physician.
5. Teaching patients to self administer insulin
 Preparing the insulin
 Withdrawing insulin
 Selecting & rotating the injection site
 Preparing the skin
 Inserting the needle

COMPLICATIONS OF DIABETES MELLITUS

1. Acute complications.
2. Long term complications.

Acute complications
 There are three major acute complication of diabetes related to
short term imbalances in blood glucose levels:

1. Hypoglycaemia
2. Diabetic ketoacidosis
3. Hyperglycaemic hyperosmolar nonketotic syndrome

Hypoglycaemia:

Hypoglycaemia occurs when blood glucose falls to less than 50 to 60

mg/dl. It can be caused due to too much insulin or oral antidiabetic
agents, too little food, or excessive physical activity. It can occur at
any time of the day or night. It often occurs before meals are delayed
or snacks are omitted.

Diabetic ketoacidosis:

Diabetic ketoacidosis is caused by an absence or markedly inadequate

amount of insulin. This deficit in available insulin results in disorders
in the metabolism of carbohydrate, protein & fat. The three main
clinincal features of DKA are hyperglycemia, dehydration &
electrolyte loss & acidosis.

Hyperglycaemic hyperosmolar nonketotic syndrome

Hyperglycaemic hyperosmolar nonketotic syndrome is a serious

condition in which hyperosmolarity & hyperglycemia predominate
with alterations of the sensorium. At the same time, ketosis is minimal
or absent. The basic biochemical defects is lack of effective insulin.
The patient’s persistent hyperglycemia causes osmotic dieresis,
resulting in losses of water & electrolytes.

Long term complications.

Long term complication are seen in both type1 & type 2 diabetes
but usually do not occur within 5 to 10 years of diagnosis. Evidence
of these complication may be present at the time of the diagnosis of
type 2 diabetes mellitus as the patient may have had undiagnosed
diabetes for many years.

Macrovascular complications

Diabetic macrovascular complications results from changes inthe

medium to large blood vessels. Blood vessel walls thicken, sclerose &
become occluded by plaque that adheres to the vessel walls.
Eventually blood flow is blocked. The three main type of
macrovacular complications that occur more frequently in the diabetic
population are:

 Coronary artery disease

 Cerebrovascular accidents
 Peripheral vascular disease

Microvascular complications

Although macrovascular atherosclerotic changes are seen in both

diabetic & nondiabetic patients, the microvascular chages are unique
to diabetes. Diabetic microvascular complication is characterised by
capillary basement membrane thickening. Areas affected by these
changes are:

 Retinopathy: deterioration of the small blood vessels that

nourish the retina
 Nephropathy: renal disease secondary to diabetic microvascular
changes in the kidney, is a common complication of diabetes.
People with kidney account for nearly half of new cases of end
stage renal disease.
 Pheripheral neuropathies: diabetic neuropathies refers to a group
of nerves, including peripheral (sensorimotor), autonomic &
spinal nerves.
 Diabetes insipidus

Definition:
Diabetes insipidus is a disorder of the posterior lobe of the pituitary
gland characterised by a deficiency of antidiuretic hormone or
vasopressine.

Etiology
 Infection of central nervous system.
 Secondary to head trauma, brain tumor, surgical ablation or
irradiation of pituitary gland.
 Failure of renal tubules to respond to ADH

Clinical manifestation
 Enormous daily output of very dilute, water like urine with a
specific gravity of 1.001 to 1.005 occurs.
 Urine contains no abnormal substance such as glucose or
albumin.
 Because of intense thirst, the patient tends to drink 2 to 20 litres
of fluid daily & craves for cold water.

Assessment & diagnostic findings

 Fluid deprivation test is carried out by withholding fluids for 8-
12 hrs or until 3% to 5% of the body weight is lost.
 Plasma & urine osmolality studies are performed
 Concurrent measurement of plasma levels of ADH

Medical management
Objectives of therapy are:

 To replace ADH
 To ensure adequate fluid replacement
 To identify & correct the underlying intracranial pathology.
Pharmacologic therapy

 Desmopressin, a synthetic vasopressine without the vascular

effects of natural ADH, is particularly available because of its
longer duration of action & lesser side effects.
 Intramuscular administration of ADH or vasopressin tannate in
oil.
 Clobitrate, a hypolipidemic agent has fouond to have
antidiuretic effect on patient with diabetes insipidus.

Nursing management
Nursing management of the patient with diabetes can involve
treatment of a wide variety of physiologic disorders, depending on the
patient’s health status & whether the patient is newly diagnosed or
seeks care for an unrelated health problem. Nursing management of
the newly diagnosed patient & the patient with diabetes as a
secondary diagnosis. All the diabetic patient must master the concepts
& skill necessary for long term management of diabetes & its
potential complications a solid educational foundation is necessary for
competent self care & is an ongoing focus of nursing care.

 Encouragement & support while undergoing studies for a

possible cranial lesion.
 Inform patient & family about follow up care & emergency
measures.
 Vasopressin should be administered with caution if the patient
has coronary artery disease because medication causes
vasoconstrictions.
SPECIAL ISSUES IN DIABETES CARE.
The patient with diabetes undergoing surgery.

During periods of physiologic stress such as surgery, blood glucose

levels tends to rise as a result of an increase in the level of stress
hormones such as epinephrine, norepinephrine, glucagon, cortisol &
growth hormone. If hyperglycemia is not controlled during surgery
the resulting osmotic dieresis may lead to excessive loss of fluid &
electrolytes. There are various approaches to managing glucose
control during the perioperative period. Frequent capillary glucose
monitoring is essential throughout the preoperative & postoperative
periods, regardless of the method used for glucose control.

During the post operative period, diabetic must also be closely

monitored for cardiovascular complication because of the increased
prevalence of artherosceloris in patient with diabetes, wound
infections & skin breakdown. Maintaining adequate nutrition & blood
glucose control promotes wound healing.

Management of hospitalised diabetic patients

Hyperglycemia during hospitalization

Hyperglycemias may occur in the hospitalised patient as a result

of the original illness that led to the need for hospitalisation. In
addition, a number of other factors may contribute to hyperglycemia
such as: -

 Changes in the usual treatment regimen.

 Medication e.g. glucocorticoids such as prednisone which are
used in the treatment of a variety of inflammatory disorders.
 IV dextrose, which may be part of the maintenance fluids or
may be used for the administration of antibiotics & other
medications.
 Overly vigorous treatment of hypoglycaemia
 Mismatched timing of meals & insulin.

Hypoglycemia during hospitalization

 Nurses must assess the pattern of glucose values & avoid giving
doses of insulin that repeatedly lead to hypoglycemia.
Successive doses of insulin should be administered no more
frequently than every 3 to 4 hours. For the patient receiving
NPH or lente insulin before breakfast & dinner the nurse must
use caution in administering supplemental doses of regular
insulin at lunch & bedtime. To avoid hypoglycaemia the nurse
should arrange for a snacks to be given to the patient if meals
are going to be delayed because of procedures, physical therapy
or other activities.

Conclusion
Diabetes mellitus is a group of metabolic disease characterised by
elevated levels of glucose in the blood resulting from the defects in
insulin secretion, insulin action or both. The primary goal of treatment
for patient with diabetes include controlling blood glucose levels &
preventing acute & long term complications. Thus the nurse who
cares for diabetic patients must assist them to develop self care
management skills.
Bibliography

1. Basvanthappa BT. Medical Surgical Nursing. (1 ST Edition).New

Delhi: Jaypee Brother Medical Publishers.
2. Black, Joyce.M & Jane(2004). Medical Surgical Nursing. (8 th
Edition). Missouri; Elsevier
3. Black, Joyce.M & Jane(2005). Medical Surgical Nursing. (7 th
Edition). Missouri; Elsevier
4. Phipps,WilmaJ , Frances, et.al (2003).Medical Surgical
Nursing.( 7 th Edition).Philadelphia; Elsevier.
5. Smeltzer, Suzanne C & Brenda (2005). T.B of Medical Surgical
Nursing. (10th Edition). Philadelphia; Lippincott Williams &
Wilkins.
6. Smeltzer, Suzanne c & Brenda (2008). T.B of Medical Surgical
Nursing. (11th Edition). Philadelphia; Lippincott Williams &
Wilkins.
7. Diabetes mellitus. www.wikipedia.com
8. Diabetes management. www.wikipedia.com
9. Diabetic complications. www.wikipedia.com
 SANDIPANI ACEDEMY
PENDRI (MASTURI) BILASPUR C.G.

M.Sc. NURSING 1ST YEAR

SUBJECT :- CHILD HEALTH NURSING

SEMINAR ON :- DIABETES MELLITUS & DIABETES

INSIPIDUS

SUBMITTED TO :- SUBMITTED BY:-

MRS R. S. RAMYA RUBINA RASHMI MASIH

M.Sc. NURSING 1st YEAR

 Content

Introduction

Definition

Classification

Risk factors

Causes

Pathophysiology

Clinical manifestation

Assessment & diagnostic findings

Medical Management

Nursing management

Complications

Conclusion

Bibliography
 NURSING PROCESS FOR DIABETIC PATIENT

Nursing Outcomes Planning Implementation Evaluat

Assessment diagnosis ion
Client has Alteration Client will  Assess the  Assessed Client
increased in glucose have client client blood
thirst & metabolism normal condition. condition glucose
polyuria. related to glucose has is
increased level as increased reduced
blood evidenced blood .
glucose by glucose
level as glucometer level.
manifested reading.  Administer  Administere
by oral anti d insulin as
glucometer diabetic prescribed.
reading. drug or
insulin as
prescribed
by
physician.
 Teach  Taught
patient & about
relatives dietary
about management
dietary
manageme
nt.
 Explained  Explained
about about
exercise. exercise.
 Nursing Outcomes Planning Implementation Evaluat
Assessment diagnosis ion
Altered Alteration Client will  Provide  Provided Client
sleep & in sleeping have comfort extra pillows had
rest. pattern less adequate devices. & air normal
than body rest & sleep  Administer cushions. rest &
requirement as drug  Proper sleep.
related to evidenced timely. positioning
disease by  Explain is given.
condition. observation. about  Promoted
importance timely rest
of sleep & & sleep.
rest.  Provided
warm drinks
before sleep.

Nursing Outcomes Planning Implementation Evaluat

Assessment diagnosis ion
Thermomet Alteration Client will  Reduce  Provided Clients’
er reading body have body cold body
of 101f. temperature normal temperatur sponging. temper
, body e by  Removed ature
hyperpyrex temperature method of: excessive reduced
ia related to as 1. Conducti clothings. to 99f.
infectious evidenced on.  Switched on
process. by 2. Convecti fan.
thermomete on.  Provided
r reading 3. Evaporati drinks.
within on.  Administere
normal 4. Radiation d
limit. inj.paraceta
mol.

Nursing Outcomes Planning Implementation Evaluat

Assessment diagnosis ion
Move & Activity Client will  Provide  Provided Client
maintain intolerance be able to active & active & is able
posture. related to maintain passive passive to
disease normal exercise. exercise. maintai
 condition. posture &  Instruct  Provided n
movement. about comfortable normal
normal bed. posture
body  Advised to &
posture & participate movem
movement. in activities ent.
of daily
living.

Nursing Outcomes Planning Implementation Evaluat

Assessment diagnosis ion
Inadequate Fluid Client will  Administer  Administere Adequa
maintenanc volume have intravenou d te fluid
e of fluid. deficit, normal s fluid. intravenous volume
hypovolemi fluid  Maintain fluid. is
a related to volume as intake &  Maintained maintai
disease manifested output & intake & ned.
condition. by all vital output
improved
 skin recordings. record.
turgidity.  Assessed
skin
turgidity.
 Monitored
vital signs.
 Assessed
electrolyte
level.

Nursing Outcomes Planning Implementation Evaluat

Assessment diagnosis ion
Eat Alteration Client will  Advise to  Advised to Clients
inadequatel in have take take nutritio
y nutritional normal nutritious nutritious nal
pattern less nutritional diet. diet. status
than body pattern as  Explain  Explained is
requirement evidenced importance importance improv
related to by of of ed.
loss of observation carbohydra carbohydrat
appetite. & te diet. e diet.
verbalisatio  Advise to  Advised to
n. take plenty take plenty
 of water. of water.
 Advise to  Advised to
take food take food of
of likings. likings.
 Explain Explained
relative to relative to
give good give good
atmospher atmosphere
e during during meal
meal time. time.

Nursing Outcomes Planning Implementation Evaluat

Assessment diagnosis ion
Knowledge Knowledge Client will  Explain in  Explained Client
deficit. deficit have detail about have
regarding adequate about disease adequat
disease knowledge disease condition. e
condition as condition  Mentioned knowle
as evidenced & its about dge
manifested by manageme medical regardi
by verbalizatio nt. management ng
verbalizatio n.  Explained disease
n. about conditi
dietary on.
management
 Clarified all
doubts.