Diabetes Mellitus

A group of metabolic diseases characterized by elevated levels of glucose in

the blood resulting from defects in insulin secretion, insulin action, insulin
receptors or any combination of conditions.
A chronic disorder of impaired glucose, protein and fat metabolism
BASIC PATHOLOGY: Insulin problem
( either deficiency or impaired action)
Insulin is a hormone secreted by the BETA cells of the pancreas
Stimulus of insulin- HYPERGLYCEMIA
Action of insulin:
it promotes entry of glucose into the body cells by binding to the insulin
receptor in the cell membrane
INSULIN: Physiology
Insulin Metabolic Functions:
1. Transports and metabolizes GLUCOSE
2. Promotes GLYCOGENESIS
3. Promotes GLYCOLYSIS
4. Enhances LIPOGENESIS
5. Accelerates PROTEIN SYNTHESIS
RISK FACTORS for Diabetes Mellitus
1. Family History of diabetes
2. Obesity
3. Race/Ethnicity
4. Age of more than 45
5. Hypertension
7. Hyperlipidemia
8. History of Gestational Diabetes Mellitus
CLASSIFICATION OF DM
1. Type 1 DM
Insulin dependent Diabetes Mellitus
This type of DM is characterized by the destruction of the pancreatic beta
cells
No INSULIN production
Etiology:
1. Genetic susceptibility- HLA DR3 and DR4
2. Autoimmune response
3. Toxins, unidentified viruses and environmental factors
PATHOPHYSIOLOGY
Destruction of BETA cells
decreased insulin production
uncontrolled glucose production by the liver hyperglycemia  signs and
symptoms
CLASSIC P’s
Polyuria due to osmotic diuresis
Polydipsia to compensate polyuria
Polyphagia due to cellular starvation

2. Type 2 DM
Non-insulin dependent Diabetes Mellitus
A type of DM characterized by insulin resistance and impaired insulin
production

Etiology:
1. Unknown
2. Probably genetic and obesity
PATHOPHYSIOLOGY
Decreased sensitivity of insulin receptor to insulin
less uptake of glucose
HYPERGLYCEMIA
Decreased insulin production
diminished insulin action
hyperglycemia and signs and symptoms
BUT (+) insulin in small amount
prevent breakdown of fats
DKA is unusual

3. Gestational DM
Diabetes Mellitus diagnosed during pregnancy
Blood glucose returns to normal after delivery of the infant
NEVER administer ORAL HYPOGLYCEMIC AGENTS to PREGNANT
MOTHERS!

4. DM associated with other conditions or syndromes

ASSESSMENT FINDINGS
1. Classic 3 P’s
2. Fatigue
3. Body weakness
4. Visual changes
5. Slow wound healing
6. Recurrent skin and mucus membrane infections

DIAGNOSTIC TESTS
1. FBS- > 126
2. RBS- >200
3. OGTT- > 200
4. HgbA1- for monitoring!!
5. Urine glucose
6. Urine ketones
DIAGNOSTIC CRITERIA
1. FBS equal to or greater than 126 mg/dL (7.0mmol/L)
(Normal 8 hour FBS- 80-109 mg/dL)
2. OGTT value 1 and 2 hours post-prandial equal to or greater than 200
mg/dL
Normal OGTT 1 and 2 hours post-prandial- is 140 mg/dL
3. RBS of equal to or greater than 200 mg/dL PLUS the 3 P’s
NURSING MANAGEMENT OF DM
The main goal is to NORMALIZE insulin activity and blood glucose level
by:
1. Nutritional modification
2. Regular Exercise
3. Regular Glucose Monitoring
4. Drug therapy
5. Client Education
HISTORY
Symptoms and characteristics
PHYSICAL EXAMINATION
VS, BMI, Fundoscopy, and Neuro assessment
Diabetes Mellitus
The Patient with DM
LABORATORY EXAMINATION
FBS, RBS, HgbA1c, lipid profile, ECG, and Urinalysis
REFERRALS
Ophthalmologist, Podiatrist, Dietician, etc..

NUTRITIONAL MANAGEMENT
1. Review the patient’s diet history to identify eating habits and lifestyle
2. Coordinate with the dietician in meal planning for weight loss
3. Plan for the caloric intake distributed as follows- CHO 50-60%; Fats 20-
30%; and Proteins 10-20%
4. Advise moderation in alcohol intake
5. Using artificial sweeteners is acceptable
EXERCISE Management
1. Teach that exercise can lower the blood glucose level
2. Diabetics must first control the glucose level before initiating exercise
programs.
3. Offer extra food /calories before engaging in exercise
4. Offer snacks at the end of the exercise period if patient is on insulin
treatment.
5. Advise that exercise should be done at the same time every day, preferably
when blood glucose levels are at their peak
6. Regular exercise, not sporadic exercise, should be encouraged.
7. For most patient, WALKING is the safe and beneficial form of exercise
GLUCOSE MONITORING
Self-monitoring of blood glucose (SMBG) enables the patient to adjust the
treatment regimen to obtain optimal glucose control
Diabetes Mellitus
Most common method involves obtaining a drop of capillary blood applied
to a test strip.
The usual recommended frequency is TWO-FOUR times a day.
When is it done?
At the peak action time of the medication to evaluate the need for
adjustments.
To evaluate BASAL insulin  test before meals
Diabetes Mellitus Monitoring therapy
Testing the glycosylated hemoglobin (HbA1c)
This glycosylated hemoglobin refers to the blood test that reflects the
average blood glucose over a period of TWO to THREE months.
Normal value is 4 to 6 %
No patient preparation is needed for this testing
Done to monitor therapy
Urine testing for glucose
Benedict’s test
Urine testing for ketones
Ketones are by-products of fat breakdown
This is performed whenever TYPE 1 DM have glucosuria or persistent
elevation of blood glucose, during illness, and in gestational diabetes
DRUG THERAPY and MANAGEMENT
Usually, this type of management is employed if diet modification and
exercise cannot control the blood glucose level.
Because the patient with TYPE 1 DM cannot produce insulin, exogenous
insulin must be administered for life.
TYPE 2 DM may have decreased insulin production, ORAL agents that
stimulate insulin production are usually employed
PHARMACOLOGIC INSULIN
This may be grouped into several categories according to:
1. Source- Human, pig, or cow
2. Onset of action- rapid-acting, short-acting, intermediate-acting,
long-acting and very long acting
This may be grouped into several categories according to:
3. Pure or mixed concentration
4. Manufacturer of drug
GENERALITIES
1. Human insulin preparations have a shorter duration of action than animal
source
2. Animal sources of insulin have animal proteins that may trigger allergic
reaction and they may stimulate antibody production that may bind the
insulin, slowing the action
3. ONLY Regular insulin can be used INTRAVENOUSLY!
4. Insulin are measured in INTERNATIONAL UNITS or “iu”
5. There is a specified insulin injection calibrated in units
RAPID ACTING INSULIN
Lispro (Humalog) and Insulin Aspart (Novolog)
Produces a more rapid effect and with a shorter duration than any other
insulin preparation
ONSET- 5-15 minutes
PEAK- 1 hour
DURATION- 3 hours
Instruct patient to eat within 5 to 15 minutes after injection
REGULAR INSULIN
Also called Short-acting insulin
“R”
Usually Clear solution administered 30 minutes before a meal
ONSET- 30 minutes to 1 hour
PEAK- 2 to 3 hours
DURATION- 4 to 6 hours
INTERMEDIATE ACTING INSULIN
Called “NPH” or “LENTE”
Appears white and cloudy
ONSET- 2-4 hours
PEAK- 4 to 6 hours
DURATION- 16-20 hours
LONG- ACTING INSULIN
“UltraLENTE”
Referred to as “peakless” insulin
ONSET- 6-8 hours
PEAK- 12-16 hours
DURATION- 20-30 hours
PEAK A BOO
Rapid Acting Peak is 1 hour
Short acting Regular insulin Peak is 2 hours
Intermediate acting Lente, Semi- Peak is 4 hours to 6 hours
lente, NPH
HEALTH TEACHING
Regarding Insulin SELF- Administration
1. Insulin is administered at home subcutaneously
2. Cloudy insulin should be thoroughly mixed by gently inverting the vial or
ROLLING between the hands
3. Insulin NOT IN USE should be stored in the refrigerator, BUT avoid
freezing/extreme temperature
4. Insulin IN USE should be kept at room temperature to reduce local
irritation at the injection site
5. INSULIN may be kept at room temperature up to 1 month
6. Select syringes that match the insulin concentration.
U-100 means 100 units per mL
7. Instruct the client to draw up the REGULAR (clear) Insulin FIRST before
drawing the intermediate acting (cloudy) insulin
8. Pre-filled syringes can be prepared and should be kept in the refrigerator
with the needle in the UPRIGHT position to avoid clogging the needle
9. The four main areas for insulin injection are- ABDOMEN, UPPER
ARMS, THIGHS and HIPS
Insulin is absorbed fastest in the abdomen and slowest in the hips
Instruct the client to rotate the areas of injection, but exhaust all available
sites in one area first before moving into another area.
10. Alcohol may not be use to cleanse the skin
11. Utilize the subcutaneous injection technique- commonly, a 45-90 degree
angle.
12. No need to instruct for aspirating the needle
13. Properly discard the syringe after use.
T-I-E
Test blood Inject insulin  Eat food

COMPLICATIONS OF INSULIN THERAPY

1. Local allergic reactions
Redness, swelling, tenderness and induration appearing 1-2 hours after
injection
Usually occurs in the beginning stage of therapy
Disappears with continued use
Antihistamine can be given 1 hour before injection time
Porcine and bovine insulin preparations have a higher tendency to produce
this reaction
2. SYSTEMIC ALLERGIC REACTIONS
Very rare
Generalized urticaria is the manifestation
Treatment is desensitization

3. INSULIN DYSTROPHY
A localized reaction in the form of lipoatrophy or lipohypertrophy
Lipoatrophy- loss of subcutaneous fat usually caused by the utilization of
animal insulin
Lipohypertrophy- development of fibrofatty masses, usually caused by
repeated use of injection site

4. INSULIN RESISTANCE
Most commonly caused by OBESITY
Defined as daily insulin requirement of more than 200 units
Management- Steroids and use of more concentrated insulin
5. MORNING HYPERGLYCEMIA
Elevated blood sugar upon arising in the morning
Caused by insufficient level of insulin
DAWN phenomenon
Relatively normal blood glucose until about 3 am, when the glucose level
begins to RISE
Results from the nightly surges of GROWTH HORMONE secretion
Management: Bedtime injection of NPH
SOMOGYI effect
Nocturnal hypoglycemia followed by rebound hyperglycemia
Due to the production of counter regulatory hormones- glucagon. cortisol
and epinephrine
Management- decrease evening dose of NPH or increase bedtime snack
INSULIN WANING
Progressive rise in blood glucose from bedtime to morning
Seen when the NPH evening dose is administered before dinner
Management: Move the insulin injection to bedtime

ORAL HYPOGLYCEMIC AGENTS

These may be effective when used in TYPE 2 DM that cannot be treated
with diet and exercise
These are NEVER used in pregnancy!
There are several agents:
Sulfonylureas
MOA- stimulates the beta cells of the pancreas to secrete insulin
Classified as to generations- first and second generations
FIRST GENERATION- Acetoheximide, Chlorpropamide, Tolazamide and
Tolbutamide
SECOND GENERATION- Glipizide, Glyburide, Glibenclamide,
Glimepiride
Diabetes Mellitus: Sulfonylureas
The most common side –effects of these medications are Gastro-intestinal
upset and dermatologic reactions.
HYPOGLYCEMIA is also a very important side-effect
Chlorpropamide has a very long duration of action. This also produces a
disulfiram-like reaction when taken with alcohol
Second generation drugs have shorter duration with metabolism in the
kidney and liver and are the choice for elderly patients
Biguanides
MOA- Facilitate the action of insulin on the peripheral receptors
These can only be used in the presence of insulin
BIGUANIDES= “formin”
They have no effect on the beta cells of the pancreas
Metformin (Glucophage) and Phenformin are examples
The most important side effect is LACTIC ACIDOSIS!
These are not given to patient with renal impairment
These drugs are usually given with a sulfonylurea to enhance the glucose-
lowering effect more than the use of each drug individually
Alpha-glucosidase inhibitors
MOA- Delay the absorption of glucose in the GIT
Result is a lower post-prandial blood glucose level
They do not affect insulin secretion or action!
Side-effect: DIARRHEA and FLATULENCE
Examples of AGI are Acarbose and Miglitol
They are not absorbed systemically and are very safe
They can be used alone or in combination with other OHA
Side-effect if used with other drug is HYPOGLYCEMIA
Note that sucrose absorption is impaired and IV glucose is the therapy for
the hypoglycemia
Thiazolidinediones
MOA- Enhance insulin action at the receptor site
They do not stimulate insulin secretion
Examples- Rosiglitazone, Pioglitazone
These drugs affect LIVER FUNCTION
Can cause resumption of OVULATION in peri-menopausal anovulatory
women

Meglitinides
MOA- Stimulate the secretion of insulin by the beta cells
Examples- Repaglinide and Nateglinide
They have a shorter duration and fast action
Should be taken BEFORE meals to stimulate the release of insulin from the
pancreas
Principal side-effect of meglitinides- hypoglycemia
Can be used alone or in combination
OHA Action
Sulfonylureas Stimulate Beta cells to produce insulin
Meglitinides Stimulate Beta cells to produce insulin
Biguanides Enhance action of insulin in the receptors
Thiazolidinediones Enhance action of insulin in the receptors
ACUTE COMPLICATIONS OF DM
Hypoglycemia
Diabetic ketoacidosis
Hyperglycemic hyperosmolar non-ketotic syndrome (HHNS)
CHRONIC COMPLICATIONS OF DM
Macrovascular complications- MI, Stroke, Atherosclerosis, CAD, and
Peripheral vascular disease
Microvascular complications- micro-angiopathy, retinopathy, nephropathy
Peripheral neuropathy
HYPOGLYCEMIA
S/S:
Shaking
Sweating
Anxious
Dizziness
Hunger
fast heartbeat
impaired vision
weakness/ fatigue
headache
irritable
Blood glucose level less than 50 to 60 mg/dL
Causes: Too much insulin/OHA, too little food and excessive physical
activity
Mild- 40-60
Moderate- 20-40
Severe- less than 20
ASSESSMENT FINDINGS
1. Sympathetic manifestations- sweating, tremors, palpitations, nervousness,
tachycardia and hunger
HYPOGLYCEMIA
2. CNS manifestations- inability to concentrate, headache, lightheadedness,
confusion, memory lapses, slurred speech, impaired coordination, behavioral
changes, double vision and drowsiness
DIAGNOSTIC FINDINGS
RBS- less than 50-60 mg/dL level
Nursing Interventions
1. Immediate treatment with the use of foods with simple sugar- glucose
tablets, fruit juice, table sugar, honey or hard candies
2. For unconscious patients- glucagon injection 1 mg IM/SQ; or IV 25 to 50
mL of D50/50
3. re-test glucose level in 15 minutes and re-treat if less than 75 mg/dL
4. Teach patient to refrain from eating high-calorie, high-fat desserts
5. Advise in-between snacks, especially when physical activity is increased
6. Teach the importance of compliance to medications
Diabetic Ketoacidosis (DKA)
This is cause by the absence of insulin leading to fat breakdown and
production of ketone bodies
Three main clinical features:
1. HYPERGLYCEMIA
2. DEHYDRATION & electrolyte loss
3. ACIDOSIS
PATHOPHYSIOLOGY (DKA)
No insulin reduced glucose breakdown and increased liver glucose
production  Hyperglycemia
Hyperglycemia kidney attempts to excrete glucose  increased osmotic
load  diuresis  Dehydration
No glucose in the cell fat is broken down for energy  ketone bodies are
produced Ketoacidosis
Risk factors(DKA)
1. infection or illness- common
2. stress
3. undiagnosed DM
4. inadequate insulin, missed dose of insulin
ASSESSMENT FINDINGS (DKA)
1. 3 P’s
2. Headache, blurred vision and weakness
3. Orthostatic hypotension
4. Nausea, vomiting and abdominal pain
5. Acetone (fruity) breath
6. Hyperventilation or KUSSMAUL’s breathing
HYPERGLYCEMIA
S/S:
Extreme thirst
Frequent urination
Dry skin
Hunger
Blurred vision
Drowsiness
nausea
LABORATORY FINDINGS(DKA)
1. Blood glucose level of 300-800 mg/dL
2. Urinary ketones
3. ABG result of metabolic acidosis- LOW pH, LOW pCO2 as
compensation, LOW bicarbonate
4. Electrolyte imbalances- potassium levels may be HIGH due to acidosis
and dehydration
NURSING INTERVENTIONS (DKA)
1. Assist in the correction of dehydration
Up to 6 liters of fluid may be ordered for infusion, initially NSS then D5W
Monitor hydration status
Monitor I and O
Monitor for volume overload
2. Assist in restoring Electrolytes
Kidney function is FIRST determined before giving potassium supplements!
3. Reverse the Acidosis
REGULAR insulin injection is ordered IV bolus 5-10 units
The insulin is followed by drip infusion in units per hour
BICARBONATE is not used!

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS)

A serious condition in which hyperosmolarity and extreme hyperglycemia

predominate
Ketosis is minimal
PATHOPHYSIOLOGY
Lack of insulin action or Insulin resistance  hyperglycemia
Hyperglycemia osmotic diuresis  loss of water and electrolytes
Insulin is too low to prevent hyperglycemia but enough to prevent fat
breakdown
Occurs most commonly in type 2 DM, ages 50-70
Precipitating factors
1. Infection
2. Stress
3. Surgery
4. Medication like thiazides
5. Treatment like dialysis
ASSESSMENT FINDINGS
1. Profound dehydration
2. Hypotension
3. Tachycardia
4. Altered sensorium
5. Seizures and hemiparesis
DIAGNOSTIC TESTS
1. Blood glucose- 600 to 1,200 mg/dL
2. Blood osmolality- 350 mOsm/L
3. Electrolyte abnormalities
NURSING INTERVENTIONS
Approach is similar to the DKA
1. Correction of Dehydration by IVF
2. Correction of electrolyte imbalance by replacement therapy
3. Administration of insulin injection and drips
4. Continuous monitoring of urine output

MACROVASCULAR CX
Nursing management
1. Diet modification
2. Exercise
3. Prevention and treatment of underlying conditions such as MI, CAD and
stroke
4. Administration of prescribed medications for hypertension,
hyperlipidemia and obesity

Retinopathy- a painless deterioration of the small blood vessels in the

retina, may be classified as to background retinopathy, pre-proliferative and
proliferative retinopathy
Permanent vision changes and blindness can occur
Retinopathy-ASSESSMENT FINDINGS
Blurry vision
Spotty vision
Asymptomatic
Retinopathy: Diagnostic findings
1. Fundoscopy
2. Fluorescein angiography
Painless procedure
Side-effects- discoloration of the skin and urine for 12 hours, some allergic
reactions, nausea
Flash of camera may be slightly uncomfortable
MICROVASCULAR CX
NURSING INTERVENTIONS
1. Assist in diagnostic procedure
Advice YEARLY eye examination
2. Assist in the preparation for surgery- laser photocoagulation
3. Health teaching regarding prevention of retinopathy by regular
ophthalmic examinations, good glucose control and self-management of eye
care regimens
4. Maintain client safety
MICROVASCULAR CX
DIABETIC NEPHROPATHY
Progressive deterioration of kidney function
HYPERGLYCEMIA causes the kidney filtration mechanism to be
stressed  blood proteins leak into the urine
Pressure in the kidney blood vessels increases stimulate the development
of nephropathy
MICROVASCULAR CX
ASSESSMENT findings for diabetic nephropathy
1. Albuminuria
2. Anemia
3. Acidosis
4. Fluid volume overload
5. Oliguria
6. Hypertension
7. UTI
NURSING MANAGEMENT

1. Assist in the control of hypertension- use of ACE inhibitor

2. Provide a low sodium and low protein diet
3. Administer prescribed medication for UTI
4. Assist in dialysis
5. Prepare patient for renal transplantation, if indicated
Diabetic Neuropathy
A group of disorders that affect all type of nerves including the peripheral,
autonomic and spinal nerves
Two most common types of Diabetic Neuropathy are sensori-motor
polyneuropathy and autonomic neuropathy

MICROVASCULAR CX
Peripheral neuropathy- ASSESSMENT findings
1. paresthesias- prickling, tingling or heightened sensation
2. Decreased proprioception
3. Decreased sensation of light touch
4. Unsteady gait
5. Decreased tendon reflexes
MICROVASCULAR CX
Peripheral neuropathy- Nursing Management
1. Provide teaching that good glucose control is very important to prevent its
development
2. Manage the pain by analgesics, antidepressants and nerve stimulation
Autonomic Neuropathy- ASSESSMENT findings
1. Silent, painless ischemia
2. delayed gastric emptying
3. orthostatic hypotension
4. N/V and bloating sensation
5. urinary retention
6. sexual dysfunction
Autonomic Neuropathy-Nursing management
1. Educate about the avoidance of strenuous physical activity
2. Stress the importance of good glucose control to delay the development
3. Provide LOW-fat, small frequent feedings
4. Administer bulk-forming laxatives for diabetic diarrhea
5. Provide HIGH-fiber diet for diabetic constipation
MICROVASCULAR CX
MANAGEMENT OF FOOT AND LEG PROBLEMS

Soft tissue injury in the foot/leg formation of fissures and callus  poor
wound healing  foot/leg ulcer
RISK FACTORS for the development of foot and leg ulcers
1. More than 10 years diabetic
2. Age of more than 40
3. Smoking
4. Anatomic deformities
5. History of previous leg ulcers or amputation
MANAGEMENT of Foot Ulcers
Teach patient proper care of the foot
Daily assessment of the foot
Use of mirror to inspect the bottom
Inspect the surface of shoes for any rough spots or foreign objects
Properly dry the feet
Instruct to wear closed-toe shoes that fit well, recommend use of low-heeled
shoes
MICROVASCULAR CX
MANAGEMENT
Instruct patient NEVER to walk barefoot, never to use heating pads, open-
toed shoes and soaking feet
Trim toenails STRAIGHT ACROSS and file sharp corners
Instruct to avoid smoking and over-the counter medications and home
remedies for foot problems