DIABETES MELLITUS

DIABETES MELLITUS
An endocrine disorder in which there
is insufficient amount or lack of
insulin secretion to metabolize
carbohydrates.
It is characterized by hyperglycemia,
glycosuria and ketonuria.

Normal glucose absorption

Insulin binds to
receptors on the cell
membrane, much as a
key fits into a lock,
signal glucose
transporters

Glucose
transporters move
to the cell
membrane and bind
to glucose.

Dr. Sunita Gupta

Glucose enters the

cell.

When the system fails

to absorb glucose.
Type 1 Diabetes

An

Type 2 Diabetes

immune
system Cells develop a
attack severely limits
resistance to insulin.
the ability of the
Glucose builds up in
pancreas to produce
the bloodstream.
insulin Glucose cannot
enter the cells.
Dr. Sunita Gupta

When the insulin is high/ low

Higher insulin levels increase certain
processes, like
cell growth and duplication,
protein synthesis, and
fat storage.

If the amount of insulin available is

insufficient due to
insulin insensitivity or resistance - poor
response of the cells
defective insulin, then glucose will
neither be absorbed properly by those body
cells that require it
nor will it be stored appropriately in the
liver and muscles.

The net effect

persistent high levels of blood glucose,
poor protein synthesis, and
other metabolic derangements, such as
acidosis.
Dr. Sunita Gupta

When the body begins to

malfunction
The defective food
processing cycle

Glucose, after food is

absorbed from the intestines
and distributed to all the body
cells through the bloodstream.

The glucose concentration in

the blood
body keeps constant and
avoids extra glucose right
after every meal
and starves the body between
the meals and overnight.
Dr. Sunita Gupta

Diabetes Mellitus
Pathophysiology
The beta cells of the Islets of
Langerhan of the Pancreas gland are
responsible for secreting the
hormone insulin for the carbohydrate
metabolism.
Remember the concept - sugar into
the cells.

Diabetes Mellitus
Types
Type 1 - IDDM
little to no insulin
produced
20-30% hereditary
Ketoacidosis

Gestational
overweight; risk for
Type 2

Type 2 - NIDDM
some insulin
produced
90% hereditary

Other types include

Secondary Diabetes :
Genetic defect beta cell
or insulin
Disease of exocrine
pancreas
Drug or chemical
induced
Infections-pancreatitits
Others-steroids,

INSULIN
Insulin is a protein made of 2 chainsalpha and beta
Preproinsulin is produced initially
Precursor molecule that is inactive
Must be made smaller before becoming active

Proinsulin
Precursor that includes alpha and beta chains
Also has a C-peptide chain
C-peptide levels are used to measure rate
that beta cells secrete insulin

INSULIN
Insulin allows glucose to move into cells to make energy
Liver is first major organ to be reached
Promotes production and storage of glycogen
(glycogenisis)
Inhibits glycogen breakdown into glucose
(glycogenolysis)
Increases protein and lipid synthesis
Inhibits tissue breakdown by inhibiting liver
glycogenolysis (ketogenesis- converts fats to acids) &
gluconeogenisis (conversion of proteins to glucose)
In muscle, promotes protein and glycogen synthesis
In fat cells, promotes triglyceride storage

INSULIN
Pancreas secretes 40-50 units of
insulin daily in two steps:
Secreted at low levels during fasting
( basal insulin secretion
Increased levels after eating (prandial)
An early burst of insulin occurs within 10
minutes of eating
Then proceeds with increasing release
as long as hyperglycemia is present

GLUCOSE HOMEOSTASIS
Glucose is main fuel for CNS
Brain cannot make or store, therefore
needs continuous supply
Fatty acids can be used when glucose
is not available ( triglycerides)
Need 68-105 mg/dL to support brain
Decreased levels of glucose, insulin
release is stopped with glucagon
released

GLUCOSE
Glucagon causes release of glucose
from liver
Liver glucose is made thru glycogenolysis
(glucogen to glucose) &
Gluconeogenesis

When liver glucose is not available,

lypolysis occures ( breakdown of fat)
OR
Proteinlysis (breakdown of amino
acids)

ABSENCE OF INSULIN
Insulin needed to move glucose
into cells
Without insulin, body enters a
state of breaking down fats and
proteins
Glucose levels increase
(hyperglycemia)

Absence of Insulin

Hyperglycemia
Polyuria
Polydipsia
Polyphagia
Hemoconcentration, hypervolemia,
hyperviscosity, hypoperfusion, and
hypoxia
Acidosis, Kussmaul respiration
Hypokalemia, hyperkalemia, or
normal serum potassium levels

Assessment
History
Blood tests
Fasting blood glucose test: two tests >
126 mg/dL
Oral glucose tolerance test: blood
glucose > 200 mg/dL at 120 minutes
Glycosylated hemoglobin
(Glycohemoglobin test) assays
Glucosylated serum proteins and albumin

FSBS (finger stick) monitoring blood

sugar

Urine Tests
Urine testing for ketones
Urine testing for renal function
Urine testing for glucose

Diabetes Mellitus
Clinical Manifestation
Hyperglycemia
Three Ps Polyuria
Polyphagia
Polydispsia

Gradual Onset

Hypoglycemia
Weak, diaphoretic,
sweat, pallor,
tremors, nervous,
hungry, diplopia,
confusion, aphasia,
vertigo, convulsions
Treatment - OJ with
sugar, or IV glucose

Sudden onset

Hyperglycemia - Clinical
Manifestations
Three Ps
polyuria,
polydypsia,
polyphagia
Glycosuria
Dehydration
Hypotension
Mental Changes

Fever
Hypokalemia
Hyponatremia
Seizure
Coma

Life Threatening!!!

Risk for Injury Related to

Hyperglycemia
Interventions include:
Dietary interventions, blood
glucose monitoring, medications
Oral Drugs Therapy
(Continued)

Risk for Injury Related to

Hyperglycemia (Continued)
Oral therapy

Sulfonylurea agents
Meglitinide analogues
Biguanides
Alpha-glucosidase inhibitors
Thiazolinedione antidiabetic agents

Oral Hypoglcemias
Key Points
Monitor serum glucose levels
Teach patient signs and symptoms of
hyper/hypoglycemia
Altered liver, renal function will affect
medication action
Avoid OTC meds without MD approval
Assess for GI distress and sensitivity
Know appropriate time to administer med

Diet Therapy
Goals of diet therapy
Principles of nutrition in diabetes
Protein, fats and carbohydrates,
fiber, sweeteners, fat replacers
Alcohol
Food labeling
Exchange system, carbohydrate
counting
Special considerations for type 1
and type 2 diabetes

Diabetes Mellitus
Diet
American Diabetic
Association
Food groups/
exchanges
Carbohydrates 60%
Fats - 30%
Protein - 12-20%

Diabetes - Monitoring
Glucose Levels
Urine - Ketones
FSBS

Wear ID Bracelet

Diabetes - Treatment
Exercise
Purpose - controls
blood glucose and
lowers blood
glucose
Purpose - reduce
the amount of
insulin needed

Exercise Therapy
Benefits of exercise
Risks related to exercise
Screening before starting
exercise program
Guidelines for exercise
Exercise promotion

Drug Therapy
Drug administration
Drug selection
Insulin therapy:
Insulin analogue
Short-acting insulin
Concentrated insulin
Intermediate
(Continued)

Drug Therapy (Continued)

Fixed-combination
Long-acting
Buffered insulins

Insulin Regimens

Single daily injection protocol

Two-dose protocol
Three-dose protocol
Four-dose protocol
Combination therapy
Intensified therapy regimens

Pharmacokinetics of
Insulin

Injection site
Absorption rate
Injection depth
Time of injection
Mixing insulins

Complications of Insulin
Therapy

Hypoglycemia
Lipoatrophy
Dawn phenomenon
Somagyi's phenomenon

Alternative Methods of
Insulin Administration
Continuous subcutaneous
infusion of insulin
Implanted insulin pumps
Injection devices
New technology includes:
Inhaled insulin
Transdermal patch (being tested)

Client Education

Storage and dose preparation

Syringes
Blood glucose monitoring
Interpretation of results
Frequency of testing
Blood glucose therapy goals

Diabetic Education Preventive Medicine

Proper skin and
foot care

Diabetic Neuropathy

Proper Eye Exam

Diabetic
Retinopathy

Proper diet and

fluids

Diabetic
Nephropathy
Diabetic
gastroparesis

Diabetes Mellitus
Complications
Hyperglycemia
Hypoglycemia
Diabetic Ketoacidosis
Hyperosmolar Hyperglycemic
Nonketotic Syndrome

Acute Complications of
Diabetes
Diabetic ketoacidosis
Hyperglycemic-hyperosmolarnonketotic syndrome
Hypoglycemia from too much
insulin or too little glucose

Diabetic Ketoacidosis

Potential for Diabetic

Ketoacidosis
Interventions include:
Monitoring for manifestations
Assessment of airway, level of
consciousness, hydration status,
blood glucose level
Management of fluid and
electrolytes
(Continued)

Potential for Diabetic

Ketoacidosis (Continued)
Drug therapy goal: to lower serum
glucose by 75 to 150 mg/dL/hr
Management of acidosis
Client education and prevention

Complication Ketoacidosis
Treatment

Patent airway
Suctioning
Cardiac monitoring
Vital Signs
Central venous
pressure
Blood work ABG,
BS, chemistry
panel

Administration of
Na Bicarb
Foley monitor
urinary output
I&O
Frequent
Repositioning

Complication HHNC
Hyperosmolar
Hyperglycemic
Non-Ketotic Coma
Fluid moves from
inside to outside cell
vausing diuresis and
loss of Na+ and K+
Treatment - Give
insulin and correct
fluid and electrolytes
imbalance

Signs and Symptoms

Hypotension
Mental changes
Dehydration
Hypokalemia
Hyponatremia

Life Threatening!!!

Chronic Complications of
Diabetes

Cardiovascular disease
Cerebrovascular disease
Retinopathy (vision) problems
Diabetic neuropathy
Diabetic nephropathy
Male erectile dysfunction

Diabetes Mellitus
Nursing Process
Assessment Medicines, Allergies, Symptoms,
Family Hx
Nursing Diagnosis- Anxiety and Fear, Altered
Nutrition, Pain, Fluid Volume Deficit
Planning Address the nursing diagnosis
Implementation Prevent complications, monitor
blood sugars, administer meds and diet, teach
diet and meds, Asess , Assess, Assess
Evaluation- Goals, EOCs

Whole-Pancreas
Transplantation

Operative procedure
Rejection management
Long-term effects
Complications
Islet cell transplantation
hindered by limited supply of
beta cells and problems caused
by antirejection drugs

Risk for Delayed Surgical

Recovery
Interventions include:
Preoperative care
Intraoperative care
Postoperative care and monitoring
includes care of:
Cardiovascular
Renal
Nutritional

Risk for Injury Related to

Sensory Alterations
Interventions and foot care
practices:
Cleanse and inspect the feet daily.
Wear properly fitting shoes.
Avoid walking barefoot.
Trim toenails properly.
Report nonhealing breaks in the
skin.

Wound Care
Wound environment
Debridement
Elimination of pressure on
infected area
Growth factors applied to
wounds

Chronic Pain
Interventions include:
Maintenance of normal blood
glucose levels
Anticonvulsants
Antidepressants
Capsaicin cream

Risk for Injury Related to

Disturbed Sensory Perception:
Visual
Interventions include:
Blood glucose control
Environmental management

Incandescent lamp
Coding objects
Syringes with magnifiers
Use of adaptive devices

Ineffective Tissue
Perfusion: Renal
Interventions include:
Control of blood glucose levels
Yearly evaluation of kidney
function
Control of blood pressure levels
Prompt treatment of UTIs
Avoidance of nephrotoxic drugs
Diet therapy
Fluid and electrolyte management

Potential for
Hypoglycemia

Blood glucose level < 70 mg/dL

Diet therapy: carbohydrate
replacement
Drug therapy: glucagon, 50%
dextrose, diazoxide, octreotide
Prevention strategies for:
Insulin excess
Deficient food intake
Exercise
Alcohol

Potential for Hyperglycemic-Hyperosmolar

Nonketotic Syndrome and Coma

Interventions include:
Monitoring
Fluid therapy: to rehydrate the client
and restore normal blood glucose
levels within 36 to 72 hr
Continuing therapy with IV regular
insulin at 10 units/hr often needed to
reduce blood glucose levels

Health Teaching
Assessing learning needs
Assessing physical, cognitive, and
emotional limitations
Explaining survival skills
Counseling
Psychosocial preparation
Home care management
Health care resources

Diabetes Mellitus
Summary

Treatable, but not curable.

Preventable in obesity, adult client.
Diagnostic Tests
Signs and symptoms of hypoglycemia and
hyperglycemia.
Treatment of hypoglycemia and
hyperglycemia diet and oral
hypoglycemics.
Nursing implications monitoring,
teaching and assessing for complications.

DIABETES SELF CARE STAR

MEALS

MONITORING
* PLASMA
*FEET

MANAGEMENT
*SICK DAY
*HYPOGLYCEMIA
* HYPERGYCEMIA

MEDICATIONS
*INSULIN
*ORAL
AGENTS

MOTION