DM TYPE 1
May be part of metabolic syndrome
> the number of people older than 20 years
newly diagnosed with diabetes increases by
1.7 million per year (Centers of Disease
Control and Prevention [CDC], 2014).
> In 2014, the worldwide estimate of the
prevalence of diabetes was 422 million
people, and by 2-4-, this is expected to
increase to more than 642 million (World
Health Organization)
Classifications of DM
Type 1
➢ Is an autoimmune disorder in which beta
cells of the pancreas are destroyed in a
generally susceptible person and no
insulin is produced
Type 1 diabetes:
a. Is abrupt in onset.
b. Requires insulin injections to prevent
hyperglycemia and ketosis and to
sustain health – don’t do oral
hypoglycemic just insulin
c. Represents fewer than 10% of all
people who have diabetes
d. Occurs primarily in childhood and
adolescence but can occur at any age
e. Causes patient to be thin and
underweight
f. May follow viral infection; viral
infection can trigger autoimmune
destructive actions.
Type 2
➢ Is a problem resulting from a reduction
int eh ability of most cells to respond to
insulin (insulin resistance), poor control
of liver glucose output, and decreased
beta cell function,
Type 2 diabetes:
A. Is generally slow in onset and may be
present for years before it is
diagnosed.
B. May require oral antidiabetic drug
therapy or insulin to correct
hyperglycemia
C. Is usually found in the middle-aged
and older adults but may occur in
younger people
D.
or obesity
E. Is usually not associated with
ketoacidosis.
F. Represents about 90% of all people
who have diabetes.
Pathophysiology:
Functions of Insulin – hormone secreted by
beta cells in the pancreas; anabolic or storage
hormone.
1. Transports and metabolizes glucose
for energy.
2. Stimulate storage of glucose in the
liver and muscle (in the form of
glycogen)
3. Signals the liver to stop the release
of glucose
4. Enhances storage of dietary fat in
the adipose tissue
5. Accelerates transport of amino acids
(derived from dietary protein) into
cells.
6. Inhibits the breakdown of stored
glucose, protein and fat.
DM 1 – it is characterized by the destruction
of the pancreatic beta cells (Grossman &
Porth ,2014)
➢ Genetic Factors – genetic susceptibility
➢ Immunologic – autoantibodies against
islet cells and against endogenous
(internal) insulin have been detected in
people at the time of diagnosis and even
several years before the development of
clinical signs of type 1 diabetes.
➢ Environmental Factors – such as viruses
or toxins that may initiate destruction of
the beta cell continue to be investigated.
 PATHOPHYSIOLOGY
1. Destruction of beta cells – because
beta cell produce insulin it causes
2. No/ Little insulin production – and
because insulin is responsible for the
transport of glucose,
3. Glucose cannot be used by the body
*Hyperglycemia – no glucose inside
the cells but a lot in the blood stream.
* Glucose derived from food cannot
be stored in the liver.
4. Glucose in the blood exceeds renal
threshold – glucose may not be abel
to reabsorb filtered glucose, this is
why the glucose will appear un urine.
5. Glycosuria –
6. Osmotic Diuresis - when excess
glucose is excreted in the urine, it is
accompanied by excessive loss of
fluids and electrolytes
7. Glycogenolysis and Gluconeogenesis
8. Further hyperglycemia
9. Fat breakdown occurs resulting in
increased production of ketone
bodies.
10. Diabetes ketoacidosis – occurs most
commonly on pt with DM1
Clinical Manifestations (3 P’s)
1. Polyuria – increased urination (attempt
of the body to remove excess glucose in
the body)
2. Polydipsia – increased thirst’ occur as a
result of the excess loss of fluid
associated with osmotic diuresis.
3. Polyphagia – (increased appetite) that
results from the catabolic state induced
by insulin deficiency and the breakdown
of proteins and fats.
Other Symptoms
➢ Include fatigue and weakness, sudden
vision changes tingling or numbness in
hands or feet, dry skin, skin lesions or
wounds that are slow to heal and
recurrent infections
Onset of type 1 DM
➢ May also be associated with sudden
weight loss or nausea, vomiting, or
abdominal pains, if DKA has developed.
Criteria for the Diagnosis of Diabetes
1. Symptoms of diabetes plus casual plasma
glucose concentration equal or greater
than 200mg/dL (11.1 mmol/L).
2. Fasting plasma glucose greater than or
equal to 126 mg/dL (7.0 mmol/L)
3. Two-hour post load glucose equal to or
greater than 200 mg/dL (11.1 mmol/L)
during an oral glucose tolerance test.
4. A1C is equal to 6.5% (48 mmol/mol)
Acute Complications
1. Diabetic Ketoacidosis.
a. DKA occurs in people with type 1 DM
and is most often precipitated by
illness, especially infection.
b. B Patients have acidosis and severe
dehydration.
c. Laboratory diagnosis is based on
serum glucose level equal to or
greater than 300 mg/dL (16.7
 mmol/L), arterial pH less than 15 • Neuroglycopenic Symptoms
mEq/L, blood urea nitrogen level of Hypoglycemia:
greater than 20 mg/dL, creatinine 1. Headache
nitrogen level greater than 20 mg/dL, 2. Confusion
creatinine level greater than 1.5 3. Slurred speech
mg/dL, and ketonuria. 4. Behavioral changes
5. Coma
CLINICAL KETOACIDOSIS (DKA) Clinical
Manifestations Chronic Complications of DM
➢ Decreased skin turgor 1. Macrovascular – affects large blood
➢ Dry mucous membranes vessels of the body.
➢ Hypotension • Coronary artery disease
➢ Tachycardia includes angina, MR and
➢ Tachypnea heart failure.
➢ Kussmaul respirations • Cerebrovascular disease
➢ Abdominal pain includes stroke and worse
➢ Nausea and vomiting outcomes following stroke
➢ CNS depression results in changes in (e.g., greater disability and
consciousness varying from lethargy to mortality)
coma. – high int mortality in older • Peripheral vascular diseases
patients with stroke, MI, muscular include venous leg ulcers and
thrombosis, infections, intestinal arterial insufficiency leading
obstructions or Pneumonia. to amputation.
• Nephropathy (kidney
2. Hyperglycemic -hyperosmolar state dysfunction)
(HHS): • Neuropathy (nerve
a. HHS differs from KDA by the relative dysfunction)
absence of ketosis and much higher • Retinopathy (vision
blood glucose levels (may exceed 600 problems)
mg/dL) and osmolarity levels (greater • Male ED (ejaculatory
than 320 m0sm/L) disorders)
b. Dehydration is the most common • Dementia
cause of HHS and becomes worse
with the disorder. Medical – Nursing Management
c. HHS occurs almost exclusively in ➢ Insulin Therapy – most important
patients with Type 2 DM. management of DM type 1
3. Hypoglycemia - Insulin is available in rapid-, short-,
a. Hypoglycemia is a blood glucose level intermediate, and long-acting forms,
lower than 70 mg/dL which may be injected separately,
b. It can be caused by excessive insulin, and some can be mixed in the same
insufficient food intake, and syringe (We have to know the peaks
increased physical activity. and onset of this insulins so that we
• Neurogenic Symptoms of can predict as to when pt is going to
hypoglycemia: be hypoglycemic).
1. Hunger - Insulin regimens try to duplicate the
2. Diaphoresis normal release pattern of insulin
3. Weakness from the pancreas, including single
4. Nervousness
 daily injections, two-dose protocol,
three-dose protocol, four-dose
protocol, combination therapy and
intensifies insulin regimens.
- Teach patient that insulin type,
injection techniques, site of
injections and individual response
can all affect absorption, onset,
degree, and duration of insulin
activity and reinforce that changing
insulin may affect blood glucose
control.
Complications of Insulin Therapy
a. Hypoglycemia
b. Dawn phenomenon, a fasting
hyperglycemia thought to result
from the nocturnal release of
growth hormone secretion that
may cause blood glucose
elevations around 5:00 to 6:00
AM- Dawn Phenomenon can be
prevented or managed by
providing insulin in the
overnight period.
c. Somogyi’s phenomenon, a
morning hyperglycemia
resulting from an effective
counterregulatory response to
nighttime hypoglycemia. –
Somogyi can be managed by
providing adequate dietary
intake at bedtime.
d. Hypertrophic lipodystrophy, a
spongy swelling on injection
sites
e. Lipoatrophy, a loss of
subcutaneous fat in areas of
repeated injection that is
treated by injection of human
insulin at the edges of the
atrophied area.
f. Lipohypertrophy , an increased
swelling of fat that occurs at the
site of repeated injections and
is prevented by rotating
injections sites.
Nursing Responsibility
➢ Teach the pt about storage, does
preparation, injection procedures and
complications associated with drug
therapy.
➢ Instruct the pt to always but the same
type of syringes and use the same gauge
and needle length., short needles are not
used for obese patients.
➢ The patient needs to know how to
perform all aspects of self-monitoring of
blood glucose (SMBG)
➢ Teach the pt how to clean the
equipment to prevent infection.
Nutrition Therapy
1. Collaborate with the patient, physician
and dietician to formulate an
individualized meal plan for the patient.
2. Day-to-day consistency in the timing and
amount of food eaten helps control
blood glucose. Pt taking insulin need to
eat at consistent times that are
coordinated with the timed action of
insulin.
3. Base the meal plan on blood glucose
monitoring results, total blood lipid
levels and weight management goals.
Dietary guidelines are based on the individual
needs of the pt.
a. Carbohydrate intake should be 50-6-% of
daily calories, with a minimum of 130
g/day.
b. A protein intake of 15% to 20% of total
daily calories is appropriate for patients
with normal kidney function. In patients
with microalbuminuria or chronic kidney
disease, reduction of protein may slow
progression of kidney failure.
c. Limit total fat intake to 20% to 30% of
daily calorie intake with less than 200mg
of dietary cholesterol daily. Choose
mono- and poly-unsaturated fats over
unsaturated and trans fats.
d. Fiber intake improves carbohydrate
metabolism and lowers cholesterol levels.
Advise a goal of 25 g of fiber daily for
 women and 38 g for men. Suggest that
adding high fiber foods to the diet
gradually can help prevent cramping.
Loose, stools and flatulence.

Nutrition Therapy
➢ Reinforce dietary teaching such as how
to follow the exchange system for meal
planning and how to perform
carbohydrate counting.
➢ Reinforce reading of nutritional labels.
➢ Support and reinforce information
provided by the dietician regarding how
to make adjustments in nutritional
intake during illness, planned exercises
and social occasions.
Exercise:
➢ Collaborate with the pt and
rehabilitation specialist to develop an
exercise program.
➢ Instruct patient to have a complete
physical examination before starting an
exercise program at home
➢ Instruct pt to wear proper footwear and
good traction and cushioning and to
examine the feet after exercise.
➢ Discourage exercise in extreme heat or
cold or cold during period of poor
glucose control.
➢ Advise the pt to stay hydrated
➢ Pt with type 1 DM should perform
vigorous exercise only fi blood glucose
levels are between 80 and 250 mg/dL
and no ketones are present in the urine.
➢ Teach the opt about the risks and
complications related to exercise, such
as prolonged alterations in blood glucose
levels vitreous hemorrhage, retinal
detachment in pts with proliferative
retinopathy, and increased proteinuria.