DIABETES

BY: ROSE MARIE LEE

OBJECTIVES

WHAT IS DIABETES?
TYPES OF DIABETES
ETIOLOGY
INSULIN AND ITS FUNCTIONS
NORMAL GLUCOSE METABOLISM
GLUCOSE METABOLISM IN DIABETES
SYMPTOMS OF DIABETES
COMPLICATIONS OF DIABETES
DIABETIC KETOACIDOSIS AND HYPEROSMOLAR
COMA
THE DIABETIC FOOT
DIAGNOSIS OF DIABETES
MEDICAL MANAGEMENT
NURSING MANAGEMENT

WHAT IS DIABETES?
Diabetes mellitus (DM) is impaired insulin secretion
and variable degrees of peripheral insulin
resistance leading to hyperglycemia. Early
symptoms are related to hyperglycemia and
include polydipsia, polyphagia, polyuria, and
blurred vision. Later complications include vascular
disease, peripheral neuropathy, nephropathy, and
predisposition to infection. Diagnosis is by
measuring plasma glucose. Treatment is diet,
exercise, and drugs that reduce glucose levels,
including insulin and oral antihyperglycemic drugs.
Complications can be delayed or prevented with
adequate glycemic control; heart disease remains
the leading cause of mortality in DM- Merck Manual
(2014).

What is Diabetes?
8.5% of the US population have diabetes - 25.8 million
children and adults.
Researchers from the Jefferson School of Population
Health (Philadelphia, PA) published a study which
estimates that by 2025 there could be 53.1 million
people with the disease.
18.8 million people have been diagnosed with diabetes
About 7 million people with diabetes have not been
diagnosed.

 About 79 million people have pre-diabetes

1.9 million people aged 20 years or more were newly
diagnosed with diabetes in 2010
215,000 (0.26%) people younger than 20 years have
diabetes
Approximately 1 in every 400 kids and teenagers has
diabetes
11.3% of people aged 20+ years have diabetes; a total of
25.6 million individuals
26.9% of people aged 65+ years have diabetes; a total
of 10.9 million people
11.8% of men have diabetes; a total of 13 million people
10.8% of women have diabetes; a total of 12.6 million
people

Age-adjusted* percentage of people aged 20 years or

older with diagnosed diabetes, by race/ethnicity,
United States, 20102012

TYPES OF DIABETES

Pre-diabetes
Pre-diabetes- The vast majority of patients with type 2
diabetes initially had pre-diabetes. Their blood glucose
levels where higher than normal, but not high enough to
merit a diabetes diagnosis. The cells in the body are
becoming resistant to insulin.
Studies have indicated that even at the pre-diabetes
stage, some damage to the circulatory system and the
heart may already have occurred.

Insulin-dependent diabetes mellitus (IDDM)

TYPE 1 DIABETES

 The body does not produce insulin. Some people may

refer to this type as insulin-dependent diabetes, juvenile
diabetes, or early-onset diabetes. People usually
develop type 1 diabetes before their 40th year, often in
early adulthood or teenage years.
Type 1 diabetes is nowhere near as common as type 2
diabetes. Approximately 10% of all diabetes cases are
type 1.
This is an auto-immune destruction of pancreatic betacells that produce insulin.
Susceptibility genes include those within the major
histocompatibility complex (MHC)especially HLADR3,DQB1*0201 and HLA-DR4,DQB1*0302, which are
present in > 90% of patients with type 1 DM

 Several viruses (including coxsackievirus, rubella virus,

cytomegalovirus, Epstein-Barr virus, and retroviruses)
have been linked to the onset of type 1 DM. Viruses may
directly infect and destroy cells, or they may cause cell destruction indirectly by exposing autoantigens,
activating autoreactive lymphocytes, mimicking
molecular sequences of autoantigens that stimulate an
immune response (molecular mimicry), or other
mechanisms.
Diet may also be a factor. Exposure of infants to dairy
products (especially cow's milk and the milk protein
casein), high nitrates in drinking water, and low vitamin D
consumption have been linked to increased risk of type 1
DM. Early (< 4 mo) or late (> 7 mo) exposure to gluten
and cereals increases islet cell autoantibody production.
Mechanisms for these associations are unclear.

Non- Insulin dependent Diabetes Mellitus (NIDDM)

TYPE 2 DIABETES

 The body does not produce enough insulin for

proper function, or the cells in the body do not
react to insulin (insulin resistance).
Approximately 90% of all cases of diabetes
worldwide are of this type.
Obesity and weight gain are important
determinants of insulin resistance in type 2 DM.
They have some genetic determinants but also
reflect diet, exercise, and lifestyle. An inability to
suppress lipolysis in adipose tissue increases
plasma levels of free fatty acids that may impair
insulin-stimulated glucose transport and muscle
glycogen synthase activity.

 Adipose tissue also appears to function as

an endocrine organ, releasing multiple
factors (adipocytokines) that favorably
(adiponectin) and adversely (tumor
necrosis factor-, IL-6, leptin, resistin)
influence glucose metabolism.
Intrauterine growth restriction and low birth
weight have also been associated with
insulin resistance in later life and may
reflect adverse prenatal environmental
influences on glucose metabolism

Gestational diabetes

TYPE 3 DIABETES

 At least 5% of pregnant women develop

diabetes during pregnancy. This disorder is
called gestational diabetes. Gestational diabetes
is more common among obese women, women
with a family history of diabetes, and certain
ethnic groups, particularly Native Americans,
Pacific Islanders, and women of Mexican,
Indian, or Asian descent.
If diabetes is poorly controlled early in the
pregnancy, the risk of an early miscarriage and
significant birth defects is increased. Babies
born to women with diabetes tend to be larger
than those born to women without diabetes.

 If diabetes is poorly controlled, babies may be

particularly large. A large fetus is less likely to
pass easily through the vagina and is more likely
to be injured during vaginal delivery.
Consequently, cesarean delivery may be
necessary. Also, the fetus's lungs tend to mature
slowly.
The risk of preeclampsia (a type of high blood
pressure that occurs during pregnancy) is also
increased for women with diabetes, as is the risk
of stillbirth.
Newborns of women with diabetes are at
increased risk of having low sugar, low calcium,
and high bilirubin levels in the blood

 Miscellaneous types: Miscellaneous causes of

DM that account for a small proportion of cases
include genetic defects affecting -cell function,
insulin action, and mitochondrial DNA (eg,
maturity-onset diabetes of youth);
pancreatic diseases (eg, cystic fibrosis,
pancreatitis, hemochromatosis);
endocrinopathies (eg, Cushing syndrome,
acromegaly);
toxins (eg, the rodenticide pyriminyl [Vacor]);
and
drug-induced diabetes, most notably from
glucocorticoids, -blockers, protease inhibitors,
and therapeutic doses of niacin.

Regulating blood glucose

INSULIN AND ITS ACTIONS

 Insulin helps control blood glucose levels

by signaling the liver and muscle and fat
cells to take in glucose from the blood.
Insulin therefore helps cells to take in
glucose to be used for energy. If the body
has sufficient energy, insulin signals the
liver to take up glucose and store it as
glycogen.

 Insulin is a hormone that is exclusively produced by

pancreatic beta cells. Beta cells are located in the
pancreas in clusters known as the islets of Langerhans.
Type 2 glucose transporters (GLUT2) mediate the entry
of glucose into beta cells.
As the raw fuel for glycolysis, the universal energyproducing pathway, glucose is phosphorylated by the
rate-limiting enzyme glucokinase. This modified glucose
becomes effectively trapped within the beta cells and is
further metabolized to create ATP, the central energy
molecule.
The ATP transmits open calcium channels releases
Insulin from its vesicles in the beta-cells.

 Insulin release is a biphasic process. The initial amount

of insulin released upon glucose absorption is dependent
on the amounts available in storage. Once depleted, a
second phase of insulin release is initiated. This latter
release is prolonged since insulin has to be synthesized,
processed, and secreted for the duration of the increase
of blood glucose.
Insulin molecules circulate throughout the blood stream
until they bind to their associated (insulin) receptors. The
insulin receptors promote the uptake of glucose into
various tissues that contain type 4 glucose transporters
(GLUT4). Such tissues include skeletal muscles (which
burn glucose for energy) and fat tissues (which convert
glucose to triglycerides for storage).

WHAT GOES WRONG IN DIABETES?

Either the insulin is not secreted to regular
levels (as in type 1DM) or the insulin
receptors are desensitized.

WHAT DOES THIS CAUSE?

TYPE 1 DM
These patients (33.33%) first present with diabetic
ketoacidosis (discussed later).
Symptoms develop quickly in type 1 diabetes, usually
over 2 to 3 weeks or less, and tend to be quite obvious.
High blood sugar levels cause the child to urinate
excessively. This fluid loss causes an increase in thirst
and the consumption of fluids. Some children become
dehydrated, resulting in weakness, weight loss, lethargy,
and a rapid pulse. Vision may become blurred.

Type 2 DM
People with type 2 diabetes may not have any
symptoms for years or decades before they are
diagnosed. Symptoms may be subtle. Increased
urination and thirst are mild at first and gradually worsen
over weeks or months. Eventually, people feel extremely
fatigued, are likely to develop blurred vision, and may
become dehydrated.
Sometimes during the early stages of diabetes, the blood
glucose level is abnormally low at times, a condition
called hypoglycemia.
Because people with type 2 diabetes produce some
insulin, ketoacidosis does not usually develop even when
type 2 diabetes is untreated for a long time.

COMPLICATIONS OF
DIABETES

Blood vessels
Fatty material (atherosclerotic plaque) builds up
and blocks large or medium-sized arteries in the
heart, brain, legs, and penis.
The walls of small blood vessels are damaged
so that the vessels do not transfer oxygen to
tissues normally, and the vessels may leak.
Poor circulation causes wounds to heal poorly
and can lead to heart attacks, strokes, gangrene
of the feet and hands, erectile dysfunction
(impotence), and infections.

Eyes
The small blood vessels of the retina are
damaged, leading to formation of new fragile
blood vessels that tend to bleed.
Vision decreases, and ultimately, blindness
occurs.
Diabetic retinopathy is the most common cause
of adult blindness in the US

Kidneys
Blood vessels in the kidneys thicken.
Protein leaks into urine.
Blood is not filtered normally.
The kidneys malfunction, and
ultimately, kidney failure occurs.
Diabetic nephropathy is a leading
cause of chronic kidney disease in
the US.

Nerves
Nerves are damaged because glucose is not used normally and
because the blood supply is inadequate
Legs suddenly or gradually weaken.
People have reduced sensation, tingling, and pain in their hands
and feet.
Diabetic neuropathy is the result of nerve ischemia due to
microvascular disease, direct effects of hyperglycemia on neurons,
and intracellular metabolic changes that impair nerve function.
There are multiple types, including :

Symmetric polyneuropathy (with small- and large-fiber variants)

Autonomic neuropathy
Radiculopathy
Cranial neuropathy
Mononeuropathy

Autonomic nervous system

The nerves that control blood pressure
and digestive processes are damaged
Swings in blood pressure occur.
Swallowing becomes difficult.
Digestive function is altered, and
sometimes nausea or bouts of diarrhea
occur.
Erectile dysfunction develops.

Skin
Blood flow to the skin is reduced, and
sensation is decreased, resulting in
repeated injury
Sores and deep infections (diabetic
ulcers) develop.
Healing is poor.

Blood
White blood cell function is
impaired.
People become more susceptible
to infections, especially of the
urinary tract and skin.

DIABETIC KETOACIDOSIS
Diabetic ketoacidosis develops when your body
is unable to produce enough insulin. Insulin
normally plays a key role in helping sugar
(glucose) a major source of energy for your
muscles and other tissues enter your cells.
Without enough insulin, your body begins to
break down fat as an alternate fuel. This process
produces a buildup of toxic acids in the
bloodstream called ketones, eventually leading
to diabetic ketoacidosis if untreated.

 Diabetic ketoacidosis signs and symptoms often

develop quickly, sometimes within 24 hours:
Excessive thirst
Frequent urination
Nausea and vomiting
Abdominal pain
Weakness or fatigue
Shortness of breath
Fruity-scented breath
Confusion
High blood sugar level (hyperglycemia)
High ketone levels in urine

HYPEROSMOLAR HYPERGLYCEMIC
NON-KETONIC COMA
HHC is characterized by hyperglycemia,
hyperosmolarity, and dehydration without significant
ketoacidosis. Most patients present with severe
dehydration and focal or global neurologic deficits.
Plasma glucose level of 600 mg/dL or greater
Effective serum osmolality of 320 mOsm/kg or greater
Profound dehydration, up to an average of 9L
Serum pH greater than 7.30
Bicarbonate concentration greater than 15 mEq/L
Small ketonuria and absent-to-low ketonemia
Some alteration in consciousness

DIABETIC FOOT
A diabetic foot is a foot that exhibits any pathology that
results from diabetes mellitus.
Features:
Cellulitis
Ulcers
Abcess
Osteomyelitis
Gangrene
Neuropathic Arthropathy

DIAGNOSIS OF DIABETES

 Fasting plasma glucose (FPG)

levels
HbA1c 6.5% = DM
HbA1c 5.7 to 6.4% =
prediabetes or at risk of DM
Glycosylated Hb (HbA1c)
Sometimes oral glucose
tolerance testing

 Screening for disease: Screening for DM

should be conducted for people at risk of the
disease.
People at high risk of type 1 DM (eg, siblings
and children of people with type 1 DM) can be
tested for the presence of islet cell or antiglutamic acid decarboxylase antibodies, which
precede onset of clinical disease.
Risk factors for type 2 DM include age > 45;
overweight or obesity; sedentary lifestyle; family
history of DM; history of impaired glucose
regulation; gestational DM or delivery of a baby
> 4.1 kg; history of hypertension or dyslipidemia;
polycystic ovary syndrome; and black, Hispanic,
Asian American, or American Indian ethnicity.

 Screening for complications:

All patients with type 1 DM should begin
screening for diabetic complications 5 yr after
diagnosis. For patients with type 2 DM,
screening begins at diagnosis. Typical screening
for complications includes
Foot examination
Funduscopic examination
Urine testing for proteinuria and
microalbuminuria
Measurement of serum creatinine and lipid
profile