CASE REPORT ON DIABETES MELLITUS

I. INTRODUCTION
HISTORY OF THE DISEASE
1552 BC Written on a 3rd Dynasty Egyptian papyrus, physician Hesy-Ra mentions
frequent urination as a symptom. This is the earliest known record of diabetes.
1500 BC Ancient Hindu writings note that ants are attracted to the urine of people
with a mysterious emaciating disease.
500 BC The first descriptions of sugar in the urine and its occurrence in obese
individuals.
250 BC Apollonius of Memphis is credited with coining the term diabetes, meaning
to go through, or siphon, for a disease that drains patients of more fluid than they can
consume.
1st Century AD The Greeks describe the disease as a melting down of the flesh and
limbs into urine.
164 AD Greek physician, Galen of Pergamum, diagnoses diabetes as a kidney
ailment.
Up to 11th Century Since the urine of people with diabetes is thought to be sweet
tasting, diagnosis is often made by water tasters who drink the urine of those
suspected of having diabetes. Mellitus, the Latin word for honey, is added to the term
diabetes.
16th Century Paracelsus identifies diabetes as a serious general disorder.
For thousands of years, no one knows how to live with diabetes, let alone
treat or cure it. Children with diabetes often die within days of onset and older
people deal with devastating complications. Remedies range from herbs to
bleeding.
1776 Dobson finds a substance like brown sugar in appearance and taste when
diabetic urine evaporates. He also notes a sweetish taste of sugar in the blood of
diabetics. He observes that, for some people, diabetes is fatal in less than five weeks

and, for others, is a chronic condition. This is the first time that a distinction between
Type 1 and Type 2 has been made.
1797 Rollo applies the first significant dietary approach to the treatment of diabetes.
He successfully treats a patient using a high fat and protein diet after observing that
sugar in the urine increases after eating starchy food.
1798 Rollo documents excess sugar in the blood, as well as the urine.
Early 1800s Researchers develop the first chemical tests to indicate and measure
the presence of sugar in the urine.
1848 Bernard discovers that glycogen is formed by the liver and speculates that this is
the same sugar found in the urine of diabetics. This is the first linking of diabetes and
glycogen metabolism.
Late 1850s The French physician, Priorry, advises diabetes patients to eat extra large
quantities of sugar as a treatment.
1869 Langerhans, a German medical student, announces the pancreas contains two
types of cells one set secretes the normal pancreatic fluids, while the function of the
other is unknown. Later, these cells are identified as the islets of Langerhans, which
help produce the hormone insulin.
1870s French physician, Bouchardat, notices the disappearance of sugar in the urine
of his diabetes patients during the food rationing in Paris during the Franco-Prussian
War and formulates the idea of individualized diets.
1889 Minkowski and von Mering, at the University of Strasbourg, France, remove the
pancreas from a dog to determine the effect on digestion and discover that diabetes
develops.
In 1897, the average life expectancy for a 10-year-old child with diabetes is
about 1 year. Diagnosis at age 30 carries a life expectancy of about 4 years. A
newly diagnosed 50-year-old might live 8 more years.
1908 Zuelzer extracts a pancreatic substance and injects it into five diabetes
patients. Although sugar in the urine is reduced or disappears, the side effects of
treatment are extreme and unacceptable.

1909 de Meyer of Belgium proposes the name insulin (Latin: insula, island) for the
unknown pancreatic substance.
1911 Benedict devises a new method to measure urine sugar (Benedicts Solution).
1900-1915 Diabetes treatment includes: the oat-cure (daily allowance is
approximately eight ounces of oatmeal mixed with eight ounces of butter, eaten every
two hours), the milk diet, the rice cure, potato therapy, opium, and overfeeding to
compensate for the loss of fluids and weight.
1913 Allens book, Studies Concerning Glycosuria and Diabetes, stimulates a
revolution in diabetes therapy.
1910-1920 Allen and Joslin are considered the two leading diabetes specialists in the
United States. Joslin believes that diabetes is the best of the chronic diseases
because it was clean, seldom unsightly, not contagious, often painless and susceptible
to treatment.
1916 Allen promotes a strict diet regimen, which is soon widely adopted. Allen
believes that the diabetics body cannot use food, so he limits the amount of food
allowed patients. Patients were admitted to the hospital and given only whiskey mixed
with black coffee (or clear soup for teetotalers) every two hours from 7 am to 7 pm. This
diet is followed until there is no sign of sugar in the urine usually 5 days or less. A
strict diet follows. Outcomes are better than ever seen before for those with Type 2
diabetes. Unfortunately, those patients with Type 1 commonly die during the treatment,
likely from starvation. A few young people do survive and become the first insulin users.
1919 Allen publishes Total Dietary Regulation in the Treatment of Diabetes, with
exhaustive case records and observations of 76 of his 100 diabetes patients. He
becomes the director of diabetes research at the Rockefeller Institute.
1920 Banting conceives of the idea of insulin after reading Moses Barrons The
Relation of the Islets of Langerhans to Diabetes with Special Reference to Cases of
Pancreatic Lithiasis in the journal: Surgery, Gynecology and Obstetrics. With help from

Best, Collip and Macleod, Banting continues experimenting with different pancreatic
extracts on de-pancreatized dogs.
1921 Paulescu, a distinguished Romanian scientist, publishes an article describing his
successful isolation of pancreine insulin.
1921 Insulin is discovered. A de-pancreatized dog is successfully treated with
insulin.
1921 Banting presents The Beneficial Influences of Certain Pancreatic Extracts on
Pancreatic Diabetes, summarizing his work at a session of the American Physiological
Society at Yale University.
1922 In Toronto, one of Collips insulin extracts is tested on a human being, a 14-yearold boy named Leonard Thompson. This test is considered a success by the end of the
following February.
1922 Eli Lilly and the University of Toronto strike a deal for the mass production of
insulin in North America.
1923 Banting and his colleague, Macleod, are awarded the Nobel Prize in Physiology
or Medicine. Banting shares his award with Best; Macleod shares his with Collip.
While insulin can prevent early death from diabetic coma, insulin treatment
does not prevent the chronic, disabling and sometimes deadly complications of
the disease.
1923 Eli Lilly begins commercial production of insulin. The Toronto group calls the
substance insulin; Eli Lilly calls their product Isletin Insulin.
1925 Home testing for sugar in the urine is introduced. Eight drops of urine is mixed in
a test tube with 6 cc of Benedicts solution provided by the doctor. The tube is put into
boiling water for five minutes. The color of the liquid indicates the presence of sugar:
greenish (light sugar), yellow (moderate) or red/orange (heavy).

1930s Insulin is further refined. Protamine zinc insulin, a long acting insulin that
provides greater flexibility for diabetics, is introduced. (It actually remained on the
market until several years ago.)
1936 Research by Himsworth (UK) divides diabetics into two types based on insulin
sensitivity.
1940s The connection is made between diabetes and long-term complications such
as kidney and eye disease.
1944 A uniform insulin syringe is developed and diabetes management becomes
more standardized.
By 1945, a newly diagnosed 10-year-old has a life expectancy of 45 years; a
30-year-old has 30.5 more years; and a 50-year-old might have 16 more years to
live.
1948 Joslin writes about the unknown diabetic in Postgraduate Medicine. Although a
million people are known to have diabetes, he speculates a million more have it but
dont know it. He is the first expert to emphasize that insulin alone cannot solve all
diabetes-related issues.
Late 1940s Helen Free develops the dip-and-read urine test (Clinistix), allowing
instant monitoring of blood glucose levels.
1950s Specialists still recommend against marriage for people with hereditary
diabetes.
1951 Lawrence and Bornstein measure the amount of insulin in the blood. They find
that older and obese patients with diabetes do have insulin, but those who are young
have none.

1955 Oral drugs that help lower blood glucose levels are introduced.
1959 Two major types of diabetes are recognized: Type 1 (insulin-dependent)
diabetes and Type 2 (non-insulin-dependent) diabetes.
1960s Home testing for glucose levels in the urine increases the level of control for
people with diabetes.
1964 The first strips for testing blood glucose are used. A drop of blood is placed on
the paper strip for 1 minute, and then washed off. Comparing the color to a color chart
provides a rough indication of blood glucose levels.
1965 Instant glucose is developed.
1966 Doctors at the University of Manitoba perform the first pancreas transplant.
1970 First blood glucose meter (Ames) is introduced. It is intended for use in doctors
offices and costs around $500.
1970 Insulin pumps are developed.
The development of testing equipment and supplies provides patients with
much greater control and flexibility in the management of their diabetes.
1970 Laser therapy is used to help slow or prevent blindness resulting from diabetes.
1973 U-100 insulin is introduced.
1976 HbA1c test is introduced.
1978 Testing of the first recombinant DNA insulin is announced.
Until this date manufacturers of insulin have had to stockpile animal
pancreatic tissue. This changes dramatically with the development of DNA
technology that allows the manufacturing of a genetically engineered human
type of insulin.
1978 The National Diabetes Information Clearinghouse (NDIC) is established to
increase knowledge and understanding about diabetes among patients, health care
professionals and the general public.
1983 The first biosynthetic human insulin is introduced.

1983 Reflolux, later known as Accu-Chek, is introduced allowing relatively easy

and accurate blood glucose self-monitoring.
1986 Insulin pen delivery system is introduced.
1990 Defeat Diabetes Foundation established to address the issue of prevention,
which was not being met by existing diabetes related organizations.
1993 The landmark clinical trial Diabetes Control and Complications Trial (DCCT)
publishes its report. The study clearly demonstrates that more active self-management
through nutrition, activity and monitoring of glucose levels (and adjustments) delays the
onset and progression of long-term complications in Type 1 individuals. The study
results shows proper management reduces risk complications significantly for eye
disease (76%), kidney disease (50%) and nerve disease (60%).
1993 Instant Glucose tablets are introduced.
1996 The FDA approves the first recombinant DNA human insulin analogue, lispro
(Humalog).
1990-1997 External insulin pumps allow closer control and freedom from multiple
injections. More sophisticated insulin analogues are introduced which offer faster action,
less risk of reactions and more flexibility for diabetes management.
More than 300 insulin analogues have been identified, including 70 animal insulins, 80
chemically modified insulins and 150 biosynthetic insulins. These allow physicians the
ability to customize treatment, reduce side effects and have improved outcomes.

2003 The names Insulin Dependent Diabetes Mellitus (IDDM) for Type 1 and Non
Insulin Dependent Diabetes Mellitus (NIDDM) for Type 2 diabetes are formally dropped.

The life expectancy for people with diabetes in 2004 is still lower than that
for the general population by about 15 years.

2014 26 million Americans have diabetes and 1 in 3 of them dont know it. Another 79
million Americans are categorized as pre-diabetic and are at risk of developing
diabetes in the next ten years if they dont make appropriate lifestyle changes.
Source: http://www.defeatdiabetes.org/diabetes-history/#sthash.WSZqtssF.dpuf

II. DISCUSSION OF THE DISEASE

A. DEFINITION OF THE DISEASE
Diabetes mellitus is a syndrome consisting of metabolic, vascular, and
neuropathic components that are interrelated. It is defined as a group of metabolic
diseases that are characterized by hyperglycemia resulting from defects in insulin
secretion, insulin action, or both. Insulin is a hormone produced by the pancreas that is
essential for carbohydrate metabolism and is also for metabolism for both fats and
proteins. The lack of insulin action leads to alterations in carbohydrate, fat, and protein
metabolism. Insulin works together with glucose in the bloodstream to help it enter the
body's cells to be burned for energy. If the insulin isn't functioning properly, glucose
cannot enter the cells. This causes glucose levels in the blood to rise, creating a
condition of high blood sugar or diabetes, and leaving the cells without fuel.
The following are the three main types of diabetes: Type 1 diabetes (also known
as insulin-dependent diabetes mellitus); Type 2 diabetes (also known as non-insulin
dependent diabetes mellitus); and gestational diabetes mellitus (GDM).
Type 1 Diabetes
In Type 1 diabetes the pancreas produces little or no insulin. It has also been
previously referred to as "juvenile onset diabetes" or "insulin dependent diabetes
mellitus" (IDDM) because it often begins in childhood. It may be autoimmune condition
wherein there is pancreatic islet cell destruction leading to absolute lack of insulin. It is
not known what causes this autoimmune reaction to occur, but it is believed that certain
viruses or environmental factors, as well as genetic factors are involved. There is also
some evidence to suggest that dietary factors and stress play a part in the development
of the condition.

 Type 2 Diabetes
Type 2 diabetes has also been previously referred to as "adult onset diabetes"
because it develops more commonly in people over 40 years of age or "non-insulin
dependent diabetes mellitus" (NIDDM). In Type 2 diabetes the pancreas still produces
insulin; however it may not produce enough insulin to meet the body's needs due to
sluggish production, rapid destruction, inhibition, or inactivation of insulin combined with
insulin resistance. It is the most common form of diabetes affecting approximately 90%
of all people with diabetes. There is a strong hereditary component to Type 2 diabetes.
It is also related very strongly to obesity - the greater the degree of obesity, the greater
the risk of developing the condition. Age is also an important factor, with the condition
most commonly occurring after the age of 40 years. It is thought that as people age,
beta cells become less efficient and the cells in the body become less able to use the
insulin made by the pancreas.
Gestational Diabetes Mellitus
This is an uncommon form of diabetes that can occur during pregnancy. It is first
diagnosed during pregnancy, and is primarily a temporary intolerance to carbohydrate,
which returns to normal after the birth. It involves insulin resistance; the hormones of
pregnancy can cause insulin resistance in women genetically predisposed to developing
this condition. However the condition usually disappears after the pregnancy. It can
manifest as either Type 1 or Type 2 diabetes.

Women who have had gestational

diabetes are at greater risk of developing Type 2 diabetes later in life.

B. RISK FACTORS
Type 1 Diabetes
Although the exact cause of type 1 diabetes is unknown, factors that may signal an
increased risk include:
Non-modifiable Risk Factors:

o Family history - Your risk increases if a parent or sibling has type 1 diabetes.
o Genetics - The presence of certain genes indicates an increased risk of
developing type 1 diabetes.
o The presence of damaging immune system cells (autoantibodies) Sometimes family members of people with type 1 diabetes are tested for the
presence of diabetes autoantibodies. If you have these autoantibodies, you
have an increased risk of developing type 1 diabetes. But not everyone who
has these autoantibodies develops diabetes.
o Age - Although type 1 diabetes can appear at any age, it appears at two
noticeable peaks. The first peak occurs in children between 4 and 7 years old,
and the second is in children between 10 and 14 years old.
o Geography - Certain countries, such as Finland and Sweden, have higher
rates of type 1 diabetes.

Modifiable Risk Factors:

o Dietary factors - These include low vitamin D consumption, early exposure to
cow's milk or cow's milk formula, and exposure to cereals before 4 months of
age. None of these factors has been shown to directly cause type 1 diabetes.
o Environmental factors - Circumstances such as exposure to certain viruses
such as the Epstein-Barr virus, Coxsackie virus, mumps virus and
cytomegalovirus likely play some role in type 1 diabetes.
Type 2 Diabetes
Non-modifiable Risk Factors:
o Family history Risk increases if a parent or sibling has type 2 diabetes
o Race - Although it's unclear why, people of certain races including blacks,
Hispanics, American Indians and Asian-Americans are more likely to develop
type 2 diabetes than whites are.
o Age - Glucose tolerance deteriorates with increasing age, due to a combination
of decreasing insulin secretion and increasing resistance to insulin. Risk
increases as a person gets older. This may be because a person tends to

exercise less, lose muscle mass and gain weight as he/she ages. But type 2
diabetes is also increasing dramatically among children, adolescents and
younger adults.
Modifiable Risk Factors:
o Obesity increased risk of developing metabolic syndrome, formerly called
syndrome X. The components of this syndrome include obesity, hypertension
and insulin resistance. The more fatty tissue you have, the more resistant your
cells become to insulin.
o Poor diet Increase in refined foods containing high levels of sugars, fats, and
salts), and a decrease in the intake of dietary fiber is described as poor nutrition.
Accompanied by reduced physical activity coupled with poor nutritional factors,
heightens the risk of multiple chronic diseases, such as diabetes, obesity, and
heart disease.
o Inactivity - The less active you are, the greater your risk of type 2 diabetes.
Physical activity helps you control your weight, uses up glucose as energy and
makes your cells more sensitive to insulin.
o Gestational diabetes - If you developed gestational diabetes when you were
pregnant, your risk of developing prediabetes and type 2 diabetes later
increases. If you gave birth to a baby weighing more than 9 pounds (4
kilograms), you're also at risk of type 2 diabetes.
o Polycystic ovary syndrome - For women, having polycystic ovary syndrome
a common condition characterized by irregular menstrual periods, excess hair
growth and obesity increases the risk of diabetes
o Degree of modernization/'westernization this can be seen on population who
lives in a traditional lifestyle and changed into western lifestyle. Westernization
include a life lifestyle in which less energy is expended (due to use of motorized
transport and other labor-saving devices), and a diet that higher in
carbohydrates, fat but lower in fiber.
Gestational Diabetes Mellitus

Non- Modifiable Risk Factors:

o Age - If a woman is older than 25 is more at risk of having GDM.
o Family or personal health history The risk of a woman developing GDM
increases when she has Prediabetes - is a condition in which your blood sugar
level is higher than normal, but not high enough to be classified as diabetes. Left
untreated, prediabetes often progresses to type 2 diabetes. Another risk of
having GDM is when you have history of GDM with your last pregnancy and if
you have delivered a macrosomic baby (baby weighing more than 9 pounds (4.1
kilograms), or if you had an unexplained stillbirth.
o Nonwhite race. For reasons that aren't clear, women who are black, Hispanic,
American Indian or Asian are more likely to develop gestational diabetes.

Modifiable Risk Factors:

o Weight - You're more likely to develop gestational diabetes if you're significantly
overweight with a body mass index (BMI) of 30 or higher.

C. SIGNS AND SYMPTOMS

The development of type 1 diabetes is usually sudden and dramatic while the
symptoms can often be mild or absent in people with type 2 diabetes, making this type
of diabetes hard to detect. Individuals can experience different signs and symptoms of
diabetes, and sometimes there may be no signs. Some of the signs commonly
experienced include:
o Hyperglycemia This is a result of the inability of glucose to enter the cell so it
accumulates in the blood.
o Polyuria (frequent urination) - The hyperglycemia created an osmotic gradient
that attracts water out of the cell into the interstitial spaces and then to the
vascular space to dilute the hyperosmolar glomerular filtrate. Osmotic diversion
of water occurs

o Polydipsia (excessive thirst) This is caused by urinary fluid losses and since
the bloodstream now lacks water, this leads to increased thirst.
o Polyphagia (excessive hunger or increased appetite) - In uncontrolled
diabetes where blood glucose levels remain abnormally high (hyperglycemia),
glucose from the blood cannot enter the cells - due to either a lack of insulin or
insulin resistance - so the body cant convert the food you eat into energy. This
lack of energy causes an increase in hunger.
o Glycosuria The renal threshold for glucose exceeds and spills in the
glomerular filtrate.
o Weight loss - In people with diabetes, insufficient insulin prevents the body from
getting glucose from the blood into the body's cells to use as energy. When this
occurs, the body starts burning fat and muscle for energy, causing a reduction in
overall body weight.
o Fatigue - When there is not enough insulin, or the insulin isnt working effectively,
it means the sugar in our blood cannot get into our cells and therefore our cells
do not receive the energy they need. As a result, we feel fatigued. High blood
glucose slows blood circulation so cells cant get the oxygen and nutrients they
need.
o Lack of interest and concentration A constant supply of glucose to the brain
is needed in order to maintain normal brain functioning.
o A tingling sensation or numbness in the hands or feet The cause is usually
peripheral neuropathy, or nerve damage in the arms, legs, hands, and feet. This
results from high blood glucose levels damaging nerves and blood vessels.
o Blurred vision - High blood sugar causes the lens of the eye to swell, which
changes your ability to see.
o Frequent infections - Because of the extra glucose in your urine it provides an
excellent source of food for any bacteria or germs. This increases your risk of
getting bladder or kidney infections.
o Slow-healing wounds - An elevated blood sugar level stiffens the arteries and
causes narrowing of the blood vessels. Narrowed blood vessels lead to
decreased blood flow and oxygen to a wound. Without sufficient nutrients and
oxygen, a wound heals slowly.
o Vomiting and stomach pain (often mistaken as the flu) Diabetes affects the
vagus nerve which controls how quickly your stomach empties. When it's

damaged, your digestion slows down and food stays in your body longer than it
should. This is a condition called gastroparesis. It can make you feel queasy and
vomit.

D. PATHOPHYSIOLOGY
Exhaustion/ destruction of beta cells
Altered pancreatic insulin production
Decreased insulin production/ no insulin production

Decreased absorption of glucose by the cells/ no glucose absorption

Glucose is unable to enter the cells
Glucose remains in the blood stream
Increased serum glucose level

Sluggish flow
of blood
Impaired
delivery of blood
components

Serum osmolarity
Blood
viscosity
Blood flow to
the organs
and

Inadequate
inflammator
y response

Tissue perfusion
in nerves

Microorganism
would enter
the body at
any route

Nerve hypoxia

Tissue perfusion
of kidney
Impaired removal
of waste from
blood
Glucose level
exceeds
renal
threshold
Impaired
renal
function

Nerve damage

Infection occurs

Inadequat
e
nutritional
Weight
support
loss
Poor
wound
healing

Excessive glucose is
converted into sorbitol
which accumulate in
the nerves
Sorbitol impairs
motor nerve
conduction

Permeability
of the renal
cell wall

Osmotic
pressure
Water from
cell
towards
the blood
Dehydration
Stimulation of
osmoreceptor
s

Glucose Glucose intake

concentration
of cells
in urine
Reabsorption
of glucose in
renal tubule

Energy for
normal cell
function
Cell
starvation
occurs

Osmotic
pressure
Water
reabsorptio

Stimulation of
hunger
mechanism

Polyuria

Polydipsia

Polyphagia

Impaired
filtration of
macro cells
and particles
Glycosuria

Muscles
and fats
breakdown

Fatigue

Tingling,
numbness

E. COMPLICATIONS
DIABETES MELLITUS
Diabetes can cause both acute (sudden onset) and chronic (long-term)
complications. Complications will be worsened by diabetes that is poorly managed.
Acute Complications

Hypoglycemia
This is a situation where there are abnormally low levels of glucose in the blood.
It can occur when excessive amounts of diabetic medications have been given, when
not enough food has been eaten, or when too much exercise has been undertaken.
Because cells rely on glucose for fuel in order to function, hypoglycemia can affect the
proper functioning of the cells - particularly the cells in the nervous system. This can
lead to initial symptoms such as nervousness, dizziness, weakness, confusion, blurred
vision and tremors. The first signs of hypoglycemia must be treated quickly in order to
prevent symptoms becoming severe. This involves eating or drinking something sugary
e.g. orange juice, and glucose tablets.

If left untreated, hypoglycemia can cause

seizures and coma. This situation requires urgent treatment in hospital.

Ketoacidosis
Some people with Type 1 diabetes can develop a complication called diabetic
ketoacidosis. Ketoacidosis develops when the body doesn't have enough insulin to
break down glucose and use it as fuel, so it breaks down fat to use for fuel instead.
When fat is broken down acids called ketones are produced. If too much fat is broken
down at any one time, excessive amounts of ketones may be released, causing the
blood to become acidic. Ketonuria occurs in an attempt to compensate but may cause
significant dehydration. This can lead to symptoms such as vomiting, headache,
drowsiness, a rapid pulse and abdominal pain. There may also be an acetone smell on
the persons breath. If left untreated, and in severe cases, diabetic ketoacidosis can
lead to coma and death. If ketoacidosis is suspected, urgent medical treatment should
be sought.

Chronic Complications
Chronic complications essentially occur as a result of damage to blood vessels.
Diabetes can cause the small blood vessels to weaken and break, and the large blood

vessels to harden, narrow and become blocked with fatty deposits (a process known as
atherosclerosis). The resultant poor circulation, compounded by the fact that people
with diabetes are more prone to infections, can lead to various complications. Chronic
diabetic complications occur when diabetes has remained uncontrolled over a period of
many years.

However, most of the following complications can be minimized or

prevented by good control of the diabetes.

Circulatory problems
Atherosclerosis and damage to the large blood vessels can impede the
circulation of blood around the body - particularly affecting to the heart, brain and lower
limbs. This is compounded by the fact that people with diabetes are more prone to high
blood pressure and high blood cholesterol levels.

When circulation to the heart is

affected (cardiovascular disease) there is an increased risk of angina and heart attack.
When circulation to the brain is affected (cerebrovascular disease) there is an increased
risk of stroke. When circulation to the lower legs is affected it is known as peripheral
vascular disease (PVD). This can cause pain in the lower legs, known medically as
claudication. PVD can also slow the healing of small injuries of the lower legs. This can
lead to the development of infections, ulcers and in some cases, gangrene. In severe
cases, surgery to repair blood vessels or to amputate diseased tissue is required.
Nerves Disease/Neuropathy
Diabetes can damage the nerves - particularly the nerves of the lower legs and
sometimes the hands. The nerve damage can cause symptoms such as decreased
sensation, numbness, burning, tingling and pain in the affected area. When damage to
the nerves is caused by diabetes it is referred to as diabetic neuropathy. Medications to
help relieve the pain caused by diabetic neuropathy may be given.

Medications

commonly used in the treatment of epilepsy and depression are sometimes used for this
purpose.

Decreased sensation in the lower legs can make it difficult for the person to

know when an injury occurs.

In order to prevent the complications of diabetic

neuropathy, it is important for people with diabetes to take particular care to check their
feet regularly, keep them clean and protect them from injury.

Eye Disease/ Retinopathy

In people with diabetes, the many tiny blood vessels in the retina can weaken or
break. This can affect the retina's ability to work properly and can cause blood to leak
into the eyeball, clouding the vision. This process is known as diabetic retinopathy.
Diabetic retinopathy and cataracts do not tend to occur until diabetes has been present
for many years. It is therefore recommended that people with diabetes are screened for
these conditions by having their eyes checked every 1 - 2 years by an eye specialist
(ophthalmologist). This allows for early detection and appropriate treatment.
Kidney Disease/ Nephropathy
The kidneys filter wastes from the blood and excrete them in the urine. When the
delicate filtering structures and blood vessels within the kidneys are damaged, the
kidneys are unable to function effectively and kidney failure can occur. When this is
caused by diabetes it is referred to as diabetic nephropathy. Severe kidney failure may
need to be treated with dialysis and in some cases a kidney transplant (sometimes
combined with a pancreas transplant). The kidneys play an important role in regulating
blood pressure.

Damage caused by diabetes can lead to high blood pressure

(hypertension), which in turn can compound the kidney damage. Medications and/or a
low salt diet may be prescribed to treat the high blood pressure. People with diabetes
are also at greater risk of developing urinary tract infections (UTIs). These can also
cause damage to the kidneys if the infection reaches the kidneys themselves.
Teeth and gum problems
People with diabetes are at greater risk of developing infections of the teeth and
gums. It is therefore important that particular care is paid to the health of teeth and
gums. It is also recommended that people with diabetes have regular check-ups with
their dentist.
Impotence
A side effect of blood vessels damage and the resultant poor circulation can be
impotence in men. This may also be compounded by the treatment for other diabetes-

related conditions such as high blood pressure.

If impotence is experienced, it is

important to discuss this with a specialist.

F. MANAGEMENT
a) MEDICAL MANAGEMENT
The goal of diabetes management is to keep blood glucose levels as close to
normal as safely possible. Since diabetes may greatly increase risk for heart
disease and peripheral artery disease, measures to control blood pressure and
cholesterol levels are an essential part of diabetes treatment as well.
People with diabetes must take responsibility for their day-to-day care. This
includes monitoring blood glucose levels, dietary management, maintaining physical
activity, keeping weight and stress under control, monitoring oral medications and, if
required, insulin use via injections or pump.

Pharmacologic Management:
Insulin Therapy
People with type 1 diabetes require multiple insulin injections each day to
maintain safe insulin levels. Insulin is often required to treat type 2 diabetes too. Using
an insulin pump is an alternative to injections. The pump is about the size of a pager
and is usually worn on your belt. Insulin is delivered through a small tube (catheter) that
is placed under the skin (usually in the abdomen).
There are four major types of insulin:
o
o
o
o

Rapid-acting
Short-acting
Intermediate-acting
Long-acting

Common Types of Human Insulin

Preparation
Onset (hr)
Peak effect
Duration of Effect
(hr)
(hr)
Lispro (Humalog)
immediate
30mins-1
3-4
Regular (Humulin-R)
30mins-1
2-4
5-7
Lantus
1
5
24
Humulin-N
1-2
4-12
24+
Humulin-L
1-3
6-14
24+
Humulin-U
6
16-18
36+
Your doctor will determine your dose and how often you need to take insulin.
There is no standard insulin dose as it depends on factors such as your body weight,
when you eat, how often you exercise and how much insulin your body produces.
Oral Anti-Diabetic Medication
Sometimes blood sugar levels remain high in people with type 2 diabetes even
though they eat in a healthy manner and exercise. When this happens, medications
taken in pill form may be prescribed. The medications work in several different ways.
These include improve the effectiveness of the body's natural insulin, reduce blood
sugar production, increase insulin production and inhibit blood sugar absorption. Oral
diabetes medications are sometimes taken in combination with insulin.
Oral medication either makes the pancreas produce more insulin, helps decrease
insulin requirements by the body or reduces gluconeogenesis by the liver.
a. Sulfonylureas
- work by stimulating the pancreas to release more insulin and are onlyeffective
when there is some pancreatic beta-cell activity still present. Non-obese patients
with Type 2 diabetes are usually started on sulfonylureas.
- a common side effect is hypoglycemia. It may cause weight gain and is
therefore not suitable for obese patients.
First generation:

Chlorpropamide (Diabinase)

Tolazamide (Tolinase)

Tolbutamide (Orinase)

Dymelor (Acetohexamide)

Second Generation:

Gimepiride (Amaryl)

Gpizide (Glucotrol)

Gyburide (DiaBeta)

Gliclazide (Diamicron)

b. Biguanides
- prevent the production of glucose in the liver. The term biguanide refers to a
group of oral type 2 diabetes drugs that work by preventing the production of
glucose in the liver, improving the body's sensitivity towards insulin and reducing the
amount of sugar absorbed by the intestines.
- common side effects include abdominal discomfort, diarrhea, nausea or
vomiting, loss of appetite, and metallic taste.\
E.g. Metformin (Fortamet, Glucophage, Glumetza, Riomet)
c. Alpha-Glucosidase Inhibitors
- work in the small intestine to slow the digestion of carbohydrates and
delay glucose absorption. They work by inhibiting intestinal enzymes that digest
carbohydrates, thereby reducing carbohydrate digestion after a meal, which
lowers postprandial blood glucose elevation in diabetics.
-common side effects include abdominal pain, diarrhea and flatulence.
E.g. Arbose (Precose)
Miglitol (Glyset)

d.Thiazolidinediones
- work by making the body's cells more sensitive to insulin, so less insulin is
needed to move glucose from the blood into the cells. This leads to a reduction of
blood glucose levels.
E.g. Pioglitazone (Actos)
Rosiglitazone (Avandia)
e. Dipeptidyl Peptidase 4 Inhibitors (DPP-4 Inhibitor)
E.g. Saxagliptin (Onglyza)
Alogliptin (Nessina)
Linagliptin (Tradjenta)
Sitagliptin (Januvia)

Non-pharmacologic Management:
Regulation of Nutrition and Exercise
1. Planning what you eat and following a balanced meal plan.
2. Exercising regularly (unless contraindicated by another condition)
3. Monitoring your blood glucose and blood pressure levels at home.

Generally it is recommended that foods containing refined sugars be avoided.

This includes foods such as chocolate, jam, soft drinks, sweet biscuits, cakes, pastries
and some fruit juices. Natural carbohydrates, which can be converted to energy, are
recommended. This includes foods such as fruit, vegetables, wholemeal bread and
cereals. The diet should also be low in fat and high in dietary fiber. Alcohol contains a lot
of sugar so intake should be minimized. Having a regular eating pattern is also
important as this helps to keep blood glucose levels balanced. In some cases, having
snacks between meals may be recommended. Again this helps to balance blood
glucose levels. It is recommended that people with diabetes seek dietary advice from a
dietician and that they follow an individualized food plan.

Regular exercise is important in maintaining balanced blood glucose levels.

Exercise also helps to maintain a healthy body weight and control high blood
pressure and high blood cholesterol levels. This in turn helps to reduce the risk of
related health conditions such as cardio-vascular disease (heart attacks and strokes). It
should be remembered however that excessive and/or prolonged exercise can cause
the blood glucose levels to drop too low. It is therefore recommended that any exercise
undertaken is regular and moderate.

Stress Management
When the body is stressed, the blood glucose levels are more difficult to control. It is
therefore important that stress is adequately managed. It is recommended that people
with diabetes do not smoke. Smoking plays a part in increasing the risk of developing
many diabetic complications. Illness can also make blood glucose levels more difficult to
control. If blood glucose levels become unstable due to illness, it is important to consult
a doctor - particularly if vomiting occurs.

b) SURGICAL MANAGEMENT

METABOLIC AND BARIATRIC SURGERY

Nearly all individuals who have bariatric surgery show improvement in their
diabetic state. Metabolic and bariatric surgery is the most effective treatment for T2DM
among individuals who are affected by obesity and may result in remission or
improvement in nearly all cases.
Types of Metabolic and Bariatric Surgeries:
ROUX-EN-Y GASTRIC BYPASS
Roux-en-y Gastric Bypass is a surgery that alters the GI tract to cause food to
bypass most of the stomach and the upper portion of the small intestine. The operation
results in significant weight-loss and causes remission of T2DM in 80 percent of
patients and improvement of the disease in an additional 15 percent of patients.
Improvement or remission of diabetes with gastric bypass occurs early after
surgery and before there is significant weight-loss. The weight-loss independent
mechanisms of diabetes improvement after gastric bypass are partially explained by
changes in hormones produced by the gut after the surgery, and this is an active area of
research in the field of metabolic and bariatric surgery.

SLEEVE GASTRECTOMY
Sleeve Gastrectomy (Vertical gastrectomy) is an operation that removes a large
portion of the stomach and, in doing so, causes weight-loss. The remaining stomach is
narrow and provides a much smaller reservoir for food.
Sleeve gastrectomy also appears to have some weight-loss independent effects on
glucose metabolism and also causes some changes in gut hormones that favor
improvement in diabetes. Diabetes remission rates after sleeve gastrectomy are also
very high (more than 60%) and, in some studies, similar to results seen after gastric
bypass.

 ADJUSTABLE GASTRIC BAND

The Adjustable Gastric Band is a weight-loss procedure that involves the placement
of a band around the upper portion of the stomach.
Remission of diabetes occurs in approximately 45-60 percent of patients. The
remission or improvement of diabetes, however, is secondary to the weight-loss
produced by the procedure, and there does not appear to be any other mechanism for
diabetes improvement in band patients. In other words, patients who have diabetes and
who are unsuccessful in losing weight with the AGB will unlikely see any improvement in
the diabetes.

DUODENAL SWITCH
The Duodenal Switch is a malabsorptive procedure performed far less frequently
than the gastric bypass, sleeve gastrectomy or the adjustable gastric band due to the
complexity of the procedure and the greater risk of complications. Studies find, however,
that the operation is most effective in inducing early and sustained remission or
improvement of T2DM (more than 85 percent remission rates with weight-loss
independent effects)

III. NURSING CARE PLANS

ACTUAL PROBLEMS:
DEFICIENT FLUID VOLUME
Assessment
S:

O:
Decreased
urine output
Sudden
weight loss
Poor
skin
turgor
Dry skin or
mucous
membrane
Weak
and
thready
Pulse
With the ff. vital
signs:
T: 36.5
P: 71
R: 16
Bp: 120/80

Nursing
Diagnosis
Deficient Fluid
Volume related
to osmotic
diuresis

Objectives
Short term:
After 3 hours of
nursing interventions
the client will be able
to demonstrate an
behaviors to monitor
and prevent the
development of
deficient fluid volume.
Long Term:
After 1 week of
nursing interventions
the client will be able
to maintain fluid
volume at a functional
level as evidenced by
individually adequate
urinary output with
normal and stable vital
signs, moist mucous
membranes, good
skin turgor.

Nursing Interventios

Rationale

1.Establish rapport

1. To gain the trust of

the patient

2.Monitor vital signs

2. To monitor for
occurance of
hypovolemia, can be
manifested by
hypotension and
tachycardia

3. Assess peripheral
pulses, capillary refill,
skin turgor, and
mucous membranes.

3. This is an indicator
of the level of
dehydration, or an
adequate circulating
volume.

4. Monitor urine output

4. To provide
estimates of the need
for fluid replacement,
renal function, and
effectiveness of the
therapy given.
5. Indicates sufficient
dehydration to cause
poor cerebral

Evaluation
Short term:
The client shall have
demonstrate dan
behaviors to monitor
and prevent the
development of
deficient fluid volume.

Long Term:
The client shall have
maintained fluid
volume at a
functional level as
evidenced by
individually adequate
urinary output with
normal and stable
vital signs, moist
mucous membranes,
good skin turgor.

5. Note Change
Level
consciousness.

in
of

perfusion or can
reflect electrolyte
imbalance.
6. To provide the best
assessment of fluid
status of ongoing and
further to provide a
replacement fluid.

6. Measure weight
every day.

7. Change position
frequently.

7. To reduce
pressure oon fragile
skin and tissues.
8. To prevent injury
from dryness.

8.Provide frequent oral

as well as eye care .

 IMBALANCED NUTRITION: LESS THAN BODY REQUIREMENTS

Assessment
S:

O:
Loss of weight
with adequate
fluid intake
Weakness of
muscles required
for mastication or
swallowing; poor
muscle tone
Pale mucous
membrane
With the ff.
signs:
T: 36.5
P: 71
R: 16
Bp: 120/80

vital

Nursing
Diagnosis
Imbalanced
Nutrition: less
than body
requirements
related to
insufficiency of
insulin,
decreased oral
input as
evidenced by
loss of weight
with adequate
fluid intake.

Objectives
Short term:
After 4 hours of
nursing
interventions the
patient will be
able to
demonstrate
behaviors,
lifestyle changes
to regain and/or
maintain
appropriate
weight.
Long term:
After 1 week of
nursing
interventions the
client will be able
to demontrate
progressive

Nursing Interventios
1.Establish Rapport.

Rationale
1.To gain the trust
of the patient.

2.Determine clients
ability to chew,
swallow, and taste
food. Evaluate teeth
and gums for poor
oral health, and note
denture fit, as
indicated.

2. These factors
can affect ingestion
and/or digestion of
nutrients.

3.Ascertain
understanding of the
clients
nutrional
needs.

3. To determine
informational needs
of client/SO.

4. Weigh per day or

as indicated.

Evaluation
Short term:
The patient shall
have demonstrated
behaviors, lifestyle
changes to regain
and/or maintain
appropriate weight.
Long term:

4. Assessing an
adequate food
intake (including
absorption and
utilization).
5. If the patient's

The client shall have

demontrated
progressive weight
gain toward goal.

weight gain
toward goal.

5. Identification of
preferred food /
desired include the
needs of ethnic /
cultural.

6. Review usual
activities and exercise
program noting
repetitive activities
(e.g., constant pacing)
or inappropriate
exercise (e.g.,
prolonged jogging).
7. Evaluate total daily
food intake. Obtain
diary of calorie intake,
patterns, and times of
eating.

food preferences
can be included in
meal planning, this
cooperation can be
pursued after
discharge.

6. May reveal
obsessive nature of
weight-control
measures.

7. To reveal
possible cause of
malnutrition and
changes that could
be made in clients
intake.

POTENTIAL PROBLEM:
RISK FOR INFECTION
Assessment
S:

O:
Vital signs:
T: 36.5
P: 71
R: 16
Bp: 120/80

Nursing
Diagnosis
Risk for
Infection
related to
hyperglycemia

Objectives
Short Term:
After 6 hours of
nursing
interventions
the client will
be able to
demonstrate
techniques,
lifestyle
changes to
promote safe
environment.

Long Term:

Nursing
Interventios
1. Observe signs of
infection and
inflammation.

Rationale
1. Patients may be
entered with an
infection that usually
has sparked a state
of ketoacidosis or
may have
nosocomial
infections.

Evaluation
Short Term:
The client shall have
demonstrated
techniques,
lifestyle
changes to promote
safe environment.

2. Promote good
hand washing by
staff and client.

2. Reduces risk of
crosscontamination.

Long Term:

3. Maintain aseptic
technique in
invasive
procedures.

3. High glucose
levels in blood
would be the best

The
client
shall
achieved
timely
wound healing; be
free
of
purulent

After 3 days of
nursing
interventions th
client will be
able to achieve
timely wound
healing; be free
of purulent
drainage or
erythema; be
afebrile.

medium for the

growth of germs.
4. Give your skin
with regular care
and earnest.

5. Improve efforts to
prevention by good
hand washing for all
people in contact
with patients
including the
patients
themselves.
6. Make changes to
the position,
effective coughing
and encourage
deep breathing.

4. The peripheral
circulation may be
disturbed that puts
patients at
increased risk of
damage to the skin /
skin irritation and
infection.

5. Prevents
infection.

cross

6. Assist in all areas

and
mobilize
pulmonary
secretions.

drainage or erythema;
be afebrile.

REFERENCES:
Harmel, A. P., Mathur, R., & Davidson, M. B. (2004). Davidson's diabetes mellitus: Diagnosis and treatment. Philadelphia,
PA: W.B. Saunders.
Wong, D. L., Hockenberry, M. J., & Wilson, D. (2007). Wong's nursing care of infants and children. St. Louis, MO:
Mosby/Elsevier.
Online sources:

http://www.webmd.com/diabetes/guide/types-of-diabetes-mellitus?page=3
http://care.diabetesjournals.org/content/27/suppl_1/s5.full
https://www.southerncross.co.nz/AboutTheGroup/HealthResources/MedicalLibrary/tabid/178/vw/1/ItemID/185/Diabete

s-Symptoms-Diagnosis-Treatment.aspx
https://www.ucsfhealth.org/conditions/diabetes_mellitus/treatment.html

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/diabetes-mellitus-treatment/#
http://www.drugs.com/diabetes-treatment.html