DIABETES

MELLITUS

BY: WENDIE DO & BECKY SHIM

 What is Insulin?
-A hormone produced by the cells of the pancreas
-It helps muscle, liver and fat cells absorb glucose & lower the blood
sugar level

The Metabolic Effects of Insulin

-Enhance protein synthesis
-Inhibit gluconeogenesis (the production of glucose from amino
acids and other simpler molecules)
-Enhance fat deposition
-Inhibit lipolysis (process of fat breakdown to generate energy)
-Stimulate cellular growth
REGULATION OF GLUCOSE METABOLISM
Hormonal Regulation:
-The only hormone known to lower blood glucose levels is insulin
-The hormones that raise blood glucose levels include: glucagon, growth hormone,
glucocorticoid hormones, epinephrine, norepinephrine, & thyroid hormone
-Insulin is formed from its precursor proinsulin
-After eating a meal, insulin levels in the blood rise within minutes, peak in 30 min, &
plateau in 3 hours
-Between meals, stored glucose is used for cellular energy requirements

Neural Regulation:
-Once food is placed in the mouth, the parasympathetic NS is stimulated
-The brain has many glucose-sensitive cells that become activated when glucose levels
fall or rise
-The pancreatic cells are stimulated to release insulin
REGULATION OF GLUCOSE METABOLISM
Exercise:
- Exercise has complex effects on glucose metabolism.
- The decrease in production of insulin and the increase in secretion of
glucagon and catecholamines lead to elevated blood glucose levels.
- However, exercising muscle has increased insulin sensitivity, which
facilitates glucose uptake.

Stress:
- A number of hormones released during stress increase blood glucose
levels and compete against the effects of insulin.
- Catecholamines, glucocorticoids, and glucagon may cause stress
hyperglycemia.
 PRE-DIABETES
Impaired glucose tolerance (IGT) &
Impaired fasting glucose tolerance (IFG)

-Intermediate stages between normal glucose metabolism and the onset

of diabetes
-IGT or IFG type depends on what test was used to detect
-IFG: Patient doesnt eat anything for 8 hours prior to a blood test. Blood
glucose level of 100-125 mg/dl indicate prediabetes.
-IGT: Patient drinks 75-gm of a glucose solution and has blood glucose
level tested after 2 hours. Blood glucose level of 140-199 mg/dl indicates
prediabetes.
The lowest fasting plasma glucose level suggestive
of a diagnosis of DM is:

A. 90 mg/dl
B. 115 mg/dl
C. 126 mg/dl
D. 180 mg/dl
 PRE-DIABETES
Etiology:
-Risk factors: Being
overweight/obese, sedentary
lifestyle, family history of
diabetes, women who have
had gestational diabetes
-When your body cannot use
insulin the right way, the
glucose stays in the blood
-Buildup of glucose causes
prediabetes
 PRE-DIABETES
Pathophysiology
- When glucose levels remain high, the fat free tissues such as muscle
become supersaturated with glucose and start to down regulate the
glucose transporters, accelerating systemic insulin resistance.

-Elevated glucose level and the development of insulin resistance.

-Insulin resistance- body produces insulin, but does not use it effectively
-Glucose builds up in the blood instead of being absorbed by the cells.
 PRE-DIABETES
Incidence/
Prevalence
-86 million American Adults-
More than 1 out of 3 have
prediabetes

- 9 out of 10 people with

diabetes do not know they
have it

(CDC National Diabetes Statistics Report, 2014)

 PRE-DIABETES

Signs and Symptoms:

-Many people with prediabetes may show no signs and symptoms

-Signs and Symptoms can be increased thirst, excessive hunger,

fatigue, frequent urination, and weight gain
PRE-DIABETES Treatment

-Losing weight by
eating healthy and
being more active

-Without weight loss

and moderate
physical activity 15
to 30 percent of
people will develop
type 2 diabetes
within 5 years

(CDC National Diabetes Statistics Report, 2014)

 PRE-DIABETES: Nursing
Interventions
- Educate patients that with lifestyle changes and weight loss, it is
possible to bring blood glucose level back to normal.

- Encourage patient to quit smoking cigarettes

 DIABETES MELLITUS TYPE 1
-Characterized by destruction of cells of the pancreas
-Peaks at the ages of 2, 4-6, and 10-14 years of age
-Cannot be prevented
Etiology
Type 1A (Immune-mediated diabetes):
-More common between the 2 types
-The result of an autoimmune attack on the pancreas
-Strong genetic component; mutations in several genes likely contribute
-Viral infection or exposure to toxins may be the environmental factors that trigger the
autoimmune process in individuals with the genes
Type 1B (Idiopathic):
-Etiology is unknown
-Associated with -cell destruction without autoimmune markers
DIABETES MELLITUS TYPE 1
Pathophysiology
- Type1 A : Your immune system/
specifically the WBC mistaken
pancreatic Beta cells for foreign
invaders
- and sends autoantibodies to
destroy your own Beta cells
- T-lymphocytes infiltrate the islets
and destroy the Beta cells through
the secretion of cytokines(CD4) and
direct cytotoxic action (CD8 Cells)
- As a result the pancreas produce
little to no insulin
- Glucose level builds up in blood
resulting Hyperglycemia
- Cells cannot use glucose for energy
it needs
 DIABETES MELLITUS TYPE 1
Incidence/ Prevalence
-1.25 million Americans are living with T1D
(200,000 are under age 20 and over 1 million are over age 20)
-40,000 people are diagnosed each year
-Estimated healthcare cost associated with T1D is $14,000,000,000
-By 2050, 5 million Americans are expected to have T1D
-Between 2001-2009, the prevalence of T1D in people under age 20
increased by 21%

(CDC National Diabetes Statistics Report, 2014)

 DIABETES MELLITUS TYPE 1
Signs and Symptoms
classic symptoms of
diabetes: (3Ps)
- increased thirst
(polydipsia)
- increased urination
(polyuria)
- increased hunger
(polyphagia)
- weight loss
- blurred vision
- nausea
- fatigue
 DIABETES MELLITUS TYPE 1
Treatment
-Goals: Achieve metabolic control of blood glucose levels and prevent acute and
chronic complications
-Oral sulfonylureas (glipizide, glyburide, glimepiride) do not work for people with T1D
-Insulin therapy is required in all people diagnosed with T1D
-A min. of two or more daily injections of rapid-acting and long-acting insulins are
usually used
-Exercise can lower insulin requirements because exercise increases sensitivity to
insulin. Teach patients to balance/adjust insulin doses according to what they eat
and what activities they plan on doing because they are at a high risk for
hypoglycemia and ketoacidosis.
-Nutrition: ADA recommends 25% protein, 25% grains & starchy foods, and 50%
non-starchy vegetables
-Stress management
 DIABETES MELLITUS TYPE 1
Nursing Interventions
- monitor for signs and symptoms of hypo/hyperglycemia
such as: headache, dizziness, hunger, shaking, diaphoresis,
weakness,decreased consciousness, pallor, and tremor (hypoglycemia)
- perform fingerstick glucose testing
- teach patient about diabetes
- teach patient signs and symptoms of hypo/hyperglycemia
- teach patient how to check blood glucose at home
- teach skin and foot care: wear non-constricting shoes and avoid
walking around barefoot
- teach patient how to inject insulin: subcutaneous/ rotate sites
- teach patient how to monitor carbohydrate intake
Type 1 Diabetes can be caused by:
1.
A. Environmental and genetic factors
B. Environmental factors only
C. Genetic factors only
 DIABETES MELLITUS TYPE 2
Etiology
-Body becomes resistant to the action of insulin on peripheral tissues
-At first, the pancreas makes extra insulin to make up for it. Over time it
isn't able to keep up and can't make enough insulin to keep blood glucose
at normal levels.
-Risk factors: #1 is obesity. Having a lot of abdominal fat puts people at
higher risk of DM.
-Aging, a sedentary lifestyle, family history, or being a female can also
contribute
-Research shows strong genetic component but no specific gene has
been identified (in identical twins, if one is affected the prevalence of the
other being affected is close to 100%)
-Can be prevented!!
 DIABETES MELLITUS TYPE 2
- Is a progressive disease characterized by
development of insulin resistance, at first
Pathophysiology compensated by increased insulin
production and hyperinsulinemia (excess
level of insulin circulating in the blood).
- Decompensation occurs as the impaired
Beta cells are unable to produce sufficient
insulin to come over insulin resistance.
- Insulin levels, however, remain elevated
above normal until later in progression of the
disease.
- Relatively decreased insulin levels,
continued insulin resistance, and
hyperglucagonemia result in the
hyperglycemia of diabetes.
- Hyperglycemia itself may then increase
insulin resistance and further diminish insulin
secretion.
 DIABETES MELLITUS TYPE 2
Incidence/Prevalence
-In adults, Type 2 Diabetes accounts for 90-95% of all diagnosed cases of
diabetes
-About 24 million Americans have T2D
-Close to 26.9% of Americans over the age of 65 have diabetes
-Prevalence of diabetes is 7.1% in the non-Hispanic white population,
12.6% in non-Hispanic blacks, and 11.8% in Hispanic/Latino-Americans.
-Greatest at-risk population is adolescent Native Americans

(Copstead & Banasik, 2013)

 DIABETES MELLITUS TYPE 2
Signs and Symptoms
-increased thirst -weight loss
-increased hunger -blurred vision
-increased urination -sores that do not heal
-fatigue -nausea
 DIABETES MELLITUS TYPE 2
Treatment
-Nutrition: Nutrition and weight management are key!
-Keep BMI between 18.5-24.9
-Exercise: CDC recommends moderate intensity exercises 5 days a week for at
least 30 minutes, or vigorous intensity exercises 3 days a week for 20 minutes.
-Exercise can eliminate the need for pharmacologic agents in T2D.
-Stress management

Sulfonylureas:
-Glipizide, glyburide, glimepiride
-Work by increasing the amount of insulin
made by the pancreas & reducing the
hepatic production of glucose
-Side effects: hypoglycemia, nausea,
dizziness, headache, allergic reactions
Biguanides:
-Metformin
-Work by suppressing gluconeogenesis and
enhancing glucose uptake by peripheral
tissues without causing hypoglycemia
-Associated with improvement in dyslipidemia
& weight loss
-Side effects: nausea & diarrhea
 DIABETES MELLITUS TYPE 2
Treatment Continued...
Insulin:
-Required in 35% of people with T2D
-Can be required intermittently in times of stress (illness, surgery, inactivity, weight gain)
-Once the stress is resolved, patient may be able to discontinue insulin use
-Usually used in combination with oral antidiabetics
-Long-acting insulin (Lantus, Levemir) can only be used to improve fasting glycemia
-Rapid-acting (Humalog, NovoLog) or short-acting insulins (Regular insulin) can only be used to
improve postprandial glycemia
-Fasting glucose is normally targeted first
-If HbA1c goals are not met, other insulins are introduced to meet prandial needs
-Action of insulin is affected by: climate, alteration in blood flow, tobacco use, & injection site
-Absorbed most rapidly from abdomen, less rapidly from the arm, most slowly from legs & buttocks
-Absorbed more rapidly from areas that are massaged after injection
-Side effects: hypoglycemia (pallor, diaphoresis, anxiety, palpitation, tremor), lipodystrophy, insulin
resistance (exacerbated by obesity)
 DIABETES MELLITUS TYPE 2
Nursing Interventions
- Advise patient on the importance of an individualized meal plan in
meeting weight-loss goals
- Explain the importance in maintaining/reducing body weight
- Teach patient the importance of accuracy in insulin and meal timing to
avoid hypoglycemia
- Assess patient for cognitive or physical impairments that may interfere
with ability to administer insulin correctly
- Encourage patient to carry a portable treatment for hypoglycemia at all
times (E.g. glucose tab, food, or drink)
Rotating injection sites when administering insulin
prevents which of the following complications?

A. Insulin edema
B. Insulin lipodystrophy
C. Insulin resistance
D. Systemic allergic reactions
DIAGNOSIS OF DIABETES
SCREENING FOR DIABETES
ADA RECOMMENDATION FOR
NUTRITIONAL THERAPY
 The end!!!
Thanks for listening :)

https://www.youtube.com/watch?v=OXAe3eOjqCk Great Video!

 References
Centers for Disease Control and Prevention. (2014). National diabetes statistics report:

Estimates of diabetes and its burden in the united states. Retrieved from

https://medlineplus.gov/ency/article/001652.htm

Copstead, L. C., & Banasik, J. L. (2013). Pathophysiology (5th ed.). St. Louis, MO: Elsevier.