St.

Louis Review Center

Iligan City

Name:

Endocrine Disorders
Prepared by: Roquee Hospicio H. Paragoso, RN

I. The Endocrine System

a. Second great controlling system of the body
b. Small and unimpressive organs yet with a very impressive function: to
maintain body homeostasis
c. Both the nervous and immune systems interact closely with this
system
d. Hormones (from Greek word meaning “to arouse”) – chemical
substances, secreted by cells into the extracellular fluids, that regulate
the metabolic activity of other cells in the body.

II. Classification and Action of Hormones

e. Steroid – penetrates the cell membranes and interact with intracellular
receptors
f. Amino acid-based – interact with receptor sites on the cell surface

III. Control of Hormone Release

g. Negative Feedback Mechanisms
i. Hormonal Stimulus
- most common
- endocrine organs are prodded into action by other
hormones
- “One goes up the other goes down”

ii. Humoral Stimulus

- Changing blood levels of certain ions and nutrients serve
as stimuli for hormone release

iii. Neural Stimulus

- Stimulation by nerve fibers

IV. Major Endocrine Organs

1. Pituitary gland
- Anterior pituitary
a. Growth hormone (GH) – promotes total body growth
b. Prolactin (PRL) – production of breast milk
c. Adrenocorticotropic hormone (ACTH) – stimulates adrenal
cortex to release its hormones
d. Thyroid-stimulating hormone (TSH) – stimulates thyroid gland
to release its hormones
e. Gonadotropic hormones
 i. Follicle-stimulating hormone (FSH) – stimulates follicle
development and estrogen production in females; sperm
production in males
ii. Luteinizing hormone (LH) – stimulates ovulation, converts
follicle to corpus luteum and causes eventual production of
progesterone; stimulates male’s testes to produce
testosterone

- Posterior pituitary
a. Oxytocin – stimulates powerful uterine contraction
and causes milk ejection
b. Antidiuretic hormone (ADH) – causes kidney tubules
to reabsorb and conserve body water and
increase BP by constricting blood vessels
2. Thyroid gland
a. Thyroid hormones (Thyroxine [T4] and triiodothyronine [T3])
– body’s metabolic hormones
b. Calcitonin – released as a response to high serum calcium
levels; causes calcium reabsorption of the bones

3. Parathyroid gland
a. Parathyroid hormone (PTH) – released as a response to low
serum calcium levels; causes liberation of calcium from the
bones into the blood

4. Adrenal gland
- Adrenal cortex
a. Mineralocorticoids – primarily aldosterone; regulate Na
and K ion reabsorption by the kidneys
b. Glucocorticoids – enables body to resist long-term
stress by increasing blood glucose levels and depressing
inflammatory response
c. Sex hormones – (mainly male sex hormones) are
produced in small amounts throughout life

- Adrenal medulla
a. Catecholamines (epinephrine and norepinephrine) –
released in response to SNS stimulation enhancing or
prolonging the effects of the fight-or-flight response to short-
term stress

5. Pancreatic islets
a. Insulin – released by the B-cells of the Islets of Langerhans as
a response to high serum glucose levels increasing the rate
of glucose uptake and metabolism by body cells
b. Glucagon – released by the A-cells of the Islets of Langerhans
as a response to low serum glucose levels stimulating the
liver to release glucose to blood
 6. Pineal gland – releases melatonin which affects biological rhythms and
reproductive behavior

7. Thymus gland – its hormone, thymosin, promotes maturation of T

lymphocytes, important in body defense

8. Gonads
- Ovaries
a. Estrogens – influenced by FSH, they stimulate maturation of the
female reproductive organs and development of secondary
sex characteristics of the female.
b. Progesterone – influenced by LH, released from the corpus
luteum and works with estrogen to establish the menstrual
cycle

- Testes
a. Testosterone – influenced by LH, promotes maturation of the
male reproductive organs, male secondary sex
characteristics and production of sperm by the testes

V. Common Diseases of the Endocrine System

HYPERTHYROIDISM
- Also known as Grave’s Disorder, Parry’s Disorder,
Exopthalmic Goiter, Toxic Diffuse Goiter, Thyrotoxicosis
- Commonly occurs in women below 40 years of age, after
severe emotional stress and as a result of an autoimmune disorder
(Hashimoto’s disease)

Simple Pathophysiology Hyperactivity of the thyroid gland would cause

an increased production of the thyroid hormones thus increasing metabolic
rate (T3), increasing body temperature (T4) and causing hypocalcemia
(calcitonin).

Assessment Findings
a. Heat intolerance
b. Tachycardia
c. Hypertension
d. Weight loss
e. Increased appetite
f. Diarrhea
g. Diaphoresis
h. Restlessness, nervousness, irritability, agitation
i. Amenorrhea
j. Fine tremors
k. Fine silky hair
l. Opthalmopathy
• Exopthalmos – due to the accumulation of fluids at the
fatpads behind the eyeballs, pushing the eyeballs forward
 • Lid Lag (Von Graefe’s Sign) – Long and deep palpebral
fissure is still evident when one looks down
• Jeffrey’s Sign – Forehead remains smooth when one looks
up
• Thyroid Stare (Dalyrimple’s Sign) – bright-eyed stare,
infrequent blinking

Diagnostics
a. Palpation and Auscultation of the Thyroid Gland
- The isthmus is the only portion of the thyroid that is normally palpable
unless the patient is very thin
- Auscultation (to check for bruit) follows when the thyroid is enlarged
upon palpation
b. Thyroid-Stimulating Hormone
- Single, best screening test of thyroid function in outpatients because of
its high sensitivity
- Values above 0.4-6.15 μU/ml: primary hypothyroidism; below the normal:
hyperthyroidism
c. T3 and T4 levels (if both are increased, hyperthyroidism; if both are
decreased, hypothyroidism)
d. PBI (protein-bound iodine)
- No foods, drugs, test dyes containing iodine 7-10 days prior the test

Partial List of Medications That May Alter Thyroid

Test Results:
Estrogens Chloral Hydrate
Propylthiouracil
Sulfonylureas X-ray contrast agents
Corticosteroids Opiates
Iodine Androgens
Propranolol Clofibrate
Cimetidine Furosemide
5-Fluorouracil Diazepam
Phenytoin Danazol
Heparin Dopamine antagonists

e. Radioactive Iodine Uptake

- oral intake of a tracer dose of I131
- Exposure to scintillation camera for 2°, 6° and 24°
- No foods, drugs, and test dyes with iodine, as well as oral contraceptive
pills 7-10 days prior to the test
- Increased uptake, hyperthyroidism; Decreased uptake, hypothyroidism
f. Thyroid Scan
- Patient is given an radioisotope per IV and then exposed to a scintillation
camera
g. Fine Needle Biopsy
- assesses malignant growth in the thyroid gland
h. Basal Metabolic Rate
- measures O2 consumption at the lowest cellular activity
 - Procedures:
 NPO 10-12° before the procedure
 Get a good night’s sleep of 8-10°
 Do not get up from bed the following morning until
the test is finished
 A device with a noseclip and a mouthpiece is used;
the client is then asked to perform deep breathing exercises
 Normal: ± 20% (euthyroid state)

Nursing Management
To address manifestations:
a. Provide a non-stimulating cool environment to promote rest
b. ↑ calorie, protein, vitamin and mineral supplements
c. ↓ fibers if diarrhea is present and avoid stimulants
d. Promote safety
e. Protect the eyes – give artificial tears at regular intervals and
encourage to wear sunglasses when going out under the sun.
f. Replace fluid-electrolyte losses as ordered.

Medical Management
a. Medications
• Beta-blockers (Inderal) – to control tachycardia and hypertension
• Potassium Iodide Saturated Solution (KISS or Lugol’s Solution) –
to inhibit release of thyroid hormone
- Mix with icy fruit juice or cold glass of water to improve taste
- Use drinking straw to prevent permanent staining of teeth
- Monitor for allergic reactions, increased salivation and coryza
• Propylthiouracil (PTU) and Tapazole (Methimazole) – inhibit
synthesis of thyroid hormone by interfering with the iodination of
thyrosine and the coupling of iodothyrosines
- Monitor for fever, sore throat and rashes (S/S of
Agranulocytosis and Neutropenia)
• Calcium-channel blockers
• Thyroid hormones (Levothyroxine sodium [Synthroid] and
Thyroglobulin [Proloid]) – puts the thyroid gland at rest. These are
slow-acting drugs and usually take about 10 days to take effect.
b. Radiation Therapy
- Radiation with I131
- DTS still applies. Isolation for few days; Body secretions are
radioactive.
- Do not use in pregnant women because of its teratogenic effects.
Delay pregnancy for 6 months post-therapy
c. Surgery
 Subtotal Thyroidectomy
- 5/6 of the thyroid gland is removed
- reserved for special circumstances: pregnant women allergic to
antithyroid medications, patients with large goiters or patients
unable to take antithyroid agents
- performed soon after achievement of euthyroid state within 4-
6 weeks of therapy

PREOP CARE
1. Promote euthyroid state
2. Administer iodides as ordered – reduces the size and
vascularity of the thyroid gland thereby preventing post-
op hemorrhage and consequent thyroid crisis
3. Monitor ECG – prolonged hypertension and tachycardia
often results to heart failure or cardiac damage

POSTOP CARE
1. Semi-Fowler’s position with head, neck and
shoulder erect.
2. Prevent hemorrhage – place ice collar over
neck. ALWAYS CHECK BACK OF NECK for blood.
3. Keep tracheostomy set available for the first
48° postoperatively – hypocalcemia as a result of
parathyroid damage causes laryngospasm and
consequent airway obstruction
4. Encourage to speak every hour upon return
of consciousness – to assess for laryngeal nerve damage
5. Ca gluconate at bedside – calcium
replacement when hypocalcemia develops
6. Monitor body temperature – hyperthermia is
an initial sign of thyroid storm
7. Check BP in upper arm – assesses for
Trousseau’s sign (carpopedal spasm is induced by
occluding the blood flow to the arm for 3 minutes with a
BP cuff)
8. Steam Inhalation to soothe irritated airways
9. Observe for signs and symptoms of potential
complications
- Hemorrhage
- Airway obstruction
- Tetany
- Recurrent laryngeal nerve damage
- Thyroid crisis/storm/thyrotoxicosis
- Myxedema (accumulation of mucopolysaccharides
in subcutaneous and other insterstitial tissues
secondary to hypothyroidism)
10. Client Teaching
• Encourage ROM exercises of the neck 3-4 times a day
after discharge
• Apply cocoa butter lotion over incision site to minimize
scarring
• Teach about monitoring S/S of THYROID STORM:
a. Causes – stress, infection, unprepared thyroid
surgery
b. Manifestations:
 - Hyperthermia (initial sign!)
- ↑ BP, HR and RR with dysrhythmias
- Tremors, apprehension, restlessness
- Delirium, psychosis and coma
c. Management:
- Monitor temp, I/O, neurologic and cardiovascular
status q hour
- Provide hypothermic blankets, ice packs and a cool
environment to reduce hyperthermia
- Administer hydrocortisone to treat shock or adrenal
insufficiency
- Administer O2 to improve tissue oxygenation and to
meet the high metabolic demands
- Administer IVF containing dextrose to replace liver
glycogen stores that have been decreased
- Administer PTU or methimazole to impede
formation of thyroid hormone
- Administer iodine to decrease T4 output from the
thyroid gland
- Administer propanolol combined with digitalis to
reduce severe cardiac symptoms.

ADDISON’S DISEASE
(Adrenocortical Insufficiency)
- Results when adrenal cortex function is
inadequate to meet the patient’s need for cortical hormones
- Hyposecretion of adrenal cortex hormones
(i.e., sugar, salt, sex)

Causes
1. Autoimmune or idiopathic atrophy of the adrenal glands (80%)
2. Surgical removal of both adrenal glands
3. Infection of the adrenal glands (Tuberculosis and histoplasmosis)
4. Inadequate secretion of ACTH from the pituitary gland
5. Therapeutic use of corticosteroids

Manifestations
a. Muscle weakness
b. Anorexia
c. Gastrointestinal symptoms
d. Fatigue
e. Emaciation
f. Dark pigmentation of the skin, knuckles, knees, elbows and mucous
membranes
g. Hypotension
h. Hypoglycemia, hyponatremia, hyperkalemia
i. Mental status changes – 60-80% of patients
j. Severe, chronic dehydration – severe cases of sodium and potassium
disturbances
Addisonian Crisis
- Develops as a result of disease progression
and acute hypertension characterized by cyanosis and the classic signs of
circulatory shock
- May be triggered the stress of surgery or
dehydration resulting from preparation for diagnostic tests or surgery
- Manifestations:
a. Pallor
b. Apprehension
c. Rapid and weak pulse
d. Rapid respirations
e. Low BP
f. Headache
g. Nausea
h. Abdominal pain
i. Diarrhea
j. Confusion and restlessness

Diagnostics
1. ACTH Stimulation Test
- This is the most specific test
- Short-acting
- Synthetic ACTH is given by IV and blood and
urine cortisol levels are measured and repeated 30-60 minutes
after
- Normal values: ↑ blood and urine cortisol
levels
- Hypofunction of adrenal cortex: ↓ blood and
urine cortisol levels

2. CRH Stimulation Test

- Performed when ACTH test is abnormal
- Synthetic CRH is injected intravenously and
blood cortisol is measured before and 30, 60, 90, and 120 minutes
after the injection
- ↑ ACTH but no cortisol: pituitary defect
- ↓ ACTH with deficient cortisol: hypothalamic
defect

Medical and Nursing Interventions

1. Replace deficient adrenal cortex hormones
a. Hydrocortisone – synthetic glucocorticoid; taken ONCE or TWICE daily
(2/3 [20mg] of dose in the morning, 1/3 [10mg] of dose in the afternoon);
don’t give evening doses because this may cause INSOMNIA
b. Fludrocortisone – synthetic mineralocorticoid; restoration of normal
renin level – best indicator of adequate treatment
c. Addisonian Crisis:
- D5NSS + 100mg Hydrocortisone over 2 hours initially to
correct hypoglycemia
- NSS to treat dehydration and hyponatremia
 - Vasopressors to treat hypotension
- Antibiotics to treat infection if it caused the crisis
- Oral intake is resumed as soon as tolerated (↓ IV fluids)
2. Diet: High-caloric, high-protein to treat
dehydration and high-sodium to replace sodium losses in GI disturbances
and very hot weather
3. Monitor BP and I/O

CUSHING’S SYNDROME
- Results from excessive adrenocortical
activity
- Triggered by excessive administration of
corticosteroids or ACTH or from hyperplasia of the adrenal cortex
- ↑ salt, sugar, sex hormones

Manifestations
- Alteration of the functions of cortisol:
 helps maintain blood pressure and
cardiovascular function
 helps slow the immune system's
inflammatory response
 helps balance the effects of insulin in
breaking down sugar for energy
 helps regulate the metabolism of proteins,
carbohydrates, and fats
 helps maintain proper arousal and sense of
well-being

a. ↑ mineralocorticoids – edema, moon-face, hypertension, heart failure

b. ↑ glucocorticoids – truncal obesity, central obesity, buffalo hump,
susceptibility to infection, hyperglycemia or overt diabetes
c. ↑ androgens – hirsutism, atrophy of breasts, clitoral enlargement,
deepening of voice, cessation of menses, decreased libido in both men
and women
d. muscle wasting and osteoporosis - ↑ protein catabolism

Diagnostics
a. Dexamethasone suppression test
- Widely used screening test
- 1 mg dexamethasone is give p.o. at 11 PM and plasma cortisol level is
taken 8 AM the next morning
- If ↑: Cushing’s Disorder

Medical Management
a. Adrenalectomy
- Treatment of choice in patients with primary adrenal hypertrophy
- Adrenal insufficiency appears 12-48 hours post-op: treated with
hydrocortisone for several months
 - For bilateral adrenalectomy: lifetime replacement of adrenal cortex
hormones

b. Transsphenoidal hypophysectomy
- Treatment of choice for secondary disease i.e., caused by pituitary
tumors instead of tumors of the adrenal cortex
- 90% success rate

c. Adrenal enzyme inhibitors

- reduce hyperadrenalism if the disease is caused by ACTH oversecretion
by a tumor that cannot be eradicated
1. Aminogluthethemine - ↓ cholesterol (source of steroids)
2. Ketoconazole - ↓ glucocorticoid synthesis (side-effect used as
therapeutic effect)
3. Mitotane – direct suppression of adrenal cortex
4. Metyrapone – blocks cortisol synthesis (similar to mitotane but more on
diagnostics than cure)

Nursing Management
1. Provide safety – prevent falls, fractures and other injuries to bones and
soft tissues
2. Diet: High in protein, calcium and vitamin D to minimize muscle
wasting and osteoporosis
3. Avoid infection – due to ↓ anti-inflammatory effects
4. Encourage rest and activity.
5. Provide meticulous skin care.
6. Provide emotional and psychological support.

DIABETES MELLITUS
- Group of metabolic diseases characterized
by elevated levels of glucose in the blood (hyperglycemia) resulting
from defects in insulin secretion, insulin action, or both.
- “Starvation in the midst of plenty"

Insulin
- Secreted by the beta cells of the Islets of Langerhans in the pancreas
- Anabolic, or storage, hormone
- Functions:
a. Transports and metabolizes glucose for energy
b. Stimulates storage of glucose in the liver and muscle (in the form of
glycogen)
c. Signals the liver to stop the release of glucose
d. Enhances storage of dietary fat in the adipose tissue
e. Accelerates transport of amino acids into cells
f. Inhibits the breakdown of stored glucose, protein and fat
- Works together with glucagon to maintain constant level of glucose in
the blood

Simple Pathophysiology
 Hyperglycemia

Cell hunger Osmotic diuretic effect of excess glucose

Hypothalamus Polyuria

Hunger Intracellular dehydration

Polyphagia Thirst mechanism activated

Polydipsia

Cell looks for other non-CHO sources

(Gluconeogenesis)

CHON depletion Fats

(CHON breakdown) (Lipolysis)

Weight loss, muscle wasting Fatty Acids

Hyperlipidemia

↑ Ketone bodies
Atherosclerosis

↓ pH
Macroangiopathy,
Microangiopathy,
Metabolic acidosis
Neuropathy

Risk Factors
a. Family history of diabetes
b. Obesity (≥ 20% over desired body weight) – adipose tissues are
resistant to insulin, therefore glucose uptake by the cells is poor
c. Age ≥ 45 years
d. Previously identified impaired fasting glucose or impaired glucose
tolerance
e. History of gestational diabetes or delivery of babies over 9 lbs
f. Viral Infection – increased risk to autoimmune disorders

Classification of Diabetes
1. Type 1 Diabetes
2. Type 2 Diabetes
3. Gestational Diabetes
4. Diabetes Mellitus associated with other
conditions

Gestational DM r/t other

Criteria Type 1 Type 2
DM conditions
Previous Juvenile Adult-onset Gestational Secondary
 diabetes,
diabetes,
Ketosis-resistant
Juvenile onset,
diabetes, Non-
Ketosis-prone
insulin-
Names DM Insulin- diabetes diabetes
dependent
dependent
diabetes
diabetes
mellitus
mellitus (IDDM)
(NIDDM)
During
Usually young;
Usually over 30 pregnancy,
Age at Onset less than 30 Any age
years usually in the 2nd
years
or 3rd trimester
Pancreatic
Human
diseases,
Beta cell Insulin placental
Cause hormonal
desruction resistance lactogen
abnormalities,
secretion
medications
Inhibited action
Decreased due to the
Insulin Absent or very insulin or placental Age at
Production little insulin increased insulin hormone, pregnancy
resistance human placental
lactogen
Depending on
Rare, except in
the ability of the
Ketoacidosis Present stress or Absent
pancreas to
infection
secrete insulin
Hyperglycemic, Same as with
Diabetic hyperosmolar, other types
Progression to
Complication ketoacidosis nonketotic depending on
Type 2 DM
(DKA) syndrome the insulin
(HHNKS) production
Weight loss,
exercise, dietary
Depends; oral
Insulin to modification, Diet, and if
Management antidiabetic
preserve life oral antidiabetic needed, insulin
agents or insulin
agents, insulin
in some cases

Criteria for the Diagnosis of Diabetes Mellitus (any of these)

1. Symptoms of diabetes + random blood sugar ≥ 200 mg/dL
“random” – any time of day without regard to time since last meal
“symptoms” – polyuria, polydipsia, polyphagia and unexplained weight loss
2. Fasting blood sugar ≥ 126 mg/dL
“fasting” – no caloric intake for at least 8 hours
3. 2-hour postprandial blood sugar ≥ 200 mg/dL
uses a glucose load containing the equivalent of 75 g anhydrous glucose
dissolved in water as in an oral glucose tolerance test

Note: In absence of symptoms, these criteria should be confirmed by repeat

testing on a different day.
 Impaired fasting glycemia - fasting glucose levels between 100 and
125 mg/dL
Impaired glucose tolerance - plasma glucose at or above 140 mg/dL 2
hours after a 75 g oral glucose load; major risk factor for progression to full-
blown diabetes mellitus as well as cardiovascular disease.

Other Diagnostic Tests

1. Oral Glucose Tolerance Test
- The patient should have fasted for at least 8 hours
- Test done in the morning (glucose tolerance is better in the morning)
- Given glucose solution P.O. (1.75 g/kg of weight to a maximum of 75 g)
- Blood specimen is collected after 30 minutes, 1°, 2° (glucose should return
to normal), 3°, 4° or 5° as required

2. Glycosylated Hemoglobin
- A form of hemoglobin used primarily to identify the average plasma glucose
concentration over prolonged periods of time
- Usually done to assess effectiveness of therapy
- In the normal 120-day life span of the RBC, excess glucose bind with
hemoglobin forming glycated hemoglobin; if ↑, poorly controlled diabetes

3. Urine Exam (Benedict’s Test)

- Renal threshold is 180-200 mg/dL
- Color changes:
Blue Green –----------- Trace glucose
Green ------------------- +1
Yellow Green --------- +2
Yellow Orange ------- +3
Orange/Brick Red -- +4

Diabetes Management

Nutrition
- Control of total caloric intake to attain or
maintain a reasonable body weight and control of blood glucose levels:
most important objective
- Diet is highly individualized and should
consider the patient’s food preferences, lifestyle, usual eating times, and
ethnic and cultural background
- Ordinary Caloric Requirements/day: 30
cal/kg/day
- Diabetic diet:
Carbohydrates 50 – 60%
Fats 20 – 30%
Protein 10 – 20%
- ↑ Fiber intake: soluble fiber is related to
the formation of a gel in the GI tract that slows stomach movement thus
decreasing glucose absorption. Insoluble fiber increases stool bulk and
preventing constipation.
Exercise
- Lowers the blood glucose levels by
increasing muscular uptake of glucose and improving insulin utilization
- Don’t exercise until urine tests negative for
ketones and serum glucose is closer to normal! → aggravates
hyperglycemia
- Encourage regular daily exercise rather than
sporadic exercise
- Usually done 1-2 hours after a meal to cut
the need for a pre-exercise snack
- Monitor blood glucose before and after
exercise
- Snacks before (fruit exchange) and after
exercise in some cases

Medications
1. Oral Hypoglycemic Agents
- Effective for patients who have Type 2
diabetes that cannot be treated by diet and exercise alone
a. Sulfonylureas – directly stimulates pancreas to secrete insulin
- Take before meals
- Avoid alcohol intake when in therapy (produces a disulfiram type of
reaction)
- e.g. Glipizide
b. Biguanides – facilitates insulin’s action on peripheral receptor sites
- Metformin (Glucophage)
- Monitor for lactic acidosis and renal dysfunction
- Enhanced function when combined with sulfonylureas
c. Alpha-Glucosidase Inhibitors – delays the absorption of glucose in
the intestinal system
- Acarbose (Precose)
- Taken immediately before a meal because it affects food absorption
d. Thiazolinediones – enhances insulin action at the receptor sites
without increasing secretion from the pancreas
- Can cause resumption of ovulation in perimenopausal anovulatory
women making pregnancy a possibility
- Rosiglitazone (Avandia)
e. Meglitinides – lowers the blood glucose levels by stimulating insulin
release
- Taken before each meal

2. Insulin
a. Short-Acting
- Regular: clear insulin (Humulin R, Semilente)
- Onset: 30 minutes - 1 hour
- Peak: 2 - 4 hours
- Duration: 6 - 8 hours
- Hypoglycemia occurs: before lunch (+4 hours) if administered at 7
AM
b. Intermediate-Acting
- NPH/Neutral Protamine Hagedorn (Humulin N, Lente)
- Onset: 1 – 2 hours
- Peak: 6 - 8 hours
- Duration: 18 - 24 hours
- Hypoglycemia occurs: before supper (+12 hours) if administered at
7 AM

c. Long-Acting
- Ultralente
- Onset: 3 – 4 hours
- Peak: 16 - 20 hours
- Duration: 30 – 36 hours
- Hypoglycemia occurs: before breakfast (the following day if
administered at 7 AM

Nursing Responsibilities in Insulin Therapy:

1. Route: Subcutaneous
- Less painful route
- In cases of DKA, insulin is given per IV
- Do not massage the site of injection

2. Administer at ROOM TEMPERATURE

- Prevents the development of cold lipodystrophy

3. Rotate the site of injection

- Prevents lipodystrophy which could inhibit insulin absorption
- Do not inject into the limb that will be exercised because it will
be absorbed faster resulting to hypoglycemia

4. Store vial of insulin in current use at ROOM TEMPERATURE

- Ready for injection; unopened vials should be refrigerated
- Used vials should not be stored for more than 1 month

5. Gently roll vial in between the palms to redistribute insulin

particles
- Prevents bubble formation that may make it difficult to
aspirate exact amount

6. Observe for side effects

a. Localized
Induration or redness, swelling and tenderness –
appears at the injection site 1-2 hours after the insulin
administration but disappears with continued use; give
antihistamine 1 hour before the injection as prescribed by
doc

Lipodystrophy – delays absorption of insulin; don’t

administer in these areas, rotate injection sites to prevent
 this, injections to the site may be resumed once the
hypertrophy disappears

b. Systemic
Morning Hyperglycemia:
- Dawn Phenomenon: relatively normal blood glucose until
3 AM when the levels begin to rise; due to nocturnal surges
of growth hormone that create a greater need for insulin;
change time of injection of evening intermediate-acting
insulin from dinnertime to bedtime as treatment
- Insulin Waning: progressive rise in blood glucose from
bedtime to morning; increase evening dose of intermediate
or long acting insulin as treatment
- Somogyi Effect: normal or elevated blood glucose at
bedtime, a decrease at 2-3 AM to hypoglycemic levels, and a
subsequent increase caused by production of
counterregulatory hormones; decrease evening dose of
intermediate acting insulin or increase bedtime snack

Hypoglycemia:
Causes: skipping of meals, overexercise, overdosage of
insulin
Manifestations: Cold, clammy skin, diaphoresis, tremors
and tachycardia, irritability, dizziness, blurred vision, altered
LOC (“Cold and clammy needs candy”)
Interventions:
- Allow patient to eat
- Give simple sugars P.O.:
3 –4 commercially prepared glucose tablets
4 – 6 oz of fruit juice or regular soda
6 – 10 Life Savers or other hard candies
2 – 3 teaspoons of sugar or honey
- If unconscious: D50W 25 - 50 mL IV
- Monitor blood sugar

Hyperglycemia
Type 1: Diabetic Ketoacidosis
Causes: absence or markedly inadequate amount of
insulin causing an increased conversion of fatty acids into
ketone bodies
Triggers: decreased or missed dose of insulin, illness or
infection, undiagnosed and untreated diabetes
Onset: Rapid (<24 hours)
Blood Glucose Levels: >250 mg/dL
Mortality: <5%
Manifestations: Hyperglycemia, dehydration and electrolyte
loss and acidosis
Management:
a. Rehydration
- NSS IV fast drip (0.5-1 L/hour for 2-3 hours)
 - D5W when blood glucose reaches 300 mg/dL
- Monitor signs of fluid overload
- Plasma expanders to correct severe
hypotension that do not respond to IV
therapy
b. Restoring Electrolytes
- Potassium replacement begins once
potassium levels drop to normal following
rehydration and insulin treatment. Withhold
when the patient is not urinating.
c. Reversing Acidosis
- NSS + insulin IV (drip)
- Must be continued even if blood glucose levels
are dropping to prevent reaccumulation of ketone
bodies

Type 2: Hyperglycemic Hyperosmolar Nonketotic

Syndrome
Causes: caused by lack effective insulin
Trigger: Physiologic stress (infection, surgery, CVA, MI)
Onset: Slower (over several days)
Blood Glucose Levels: Usually >600 mg/dL
Mortality Rate: 10-40%
Manifestations: hypotension, profound dehydration,
tachycardia, variable neurologic signs
Management:
a. Fluid and electrolyte replacement
- Plain NSS or 0.45 NS depending on the
sodium level
- Insulin at a continuous low rate to treat
hyperglycemia
b. Follow up laboratory results
c. Close monitoring of vital signs

Education
Instruct about FOOT CARE:
a. Take care of your diabetes.
b. Inspect your feet every day (look for wounds and feel for changes in
temperature)
c. Wash your feet every day with warm water. Do not soak. Do not feel
temperature with your feet.
d. Pat dry your feet – do not rub.
e. Keep the skin soft and smooth by applying lotion over tops and bottoms of
feet but not between toes.
f. Smooth corns and calluses gently.
g. Trim your toenails each week or when needed. Straight across and file the
edges.
h. Wear properly fitting and comfortable shoes and socks at all times
i. Protect your feet from hot and cold.
j. Keep the blood flowing to your feet. Put your feet up when sitting. Do not
cross your legs for long periods of time. Do not smoke.
k. Check with your doctor if you found out foot problems. Do not self
medicate!