Gland Hormone Functions

Hypothalamus Corticotropin – releasing Stimulates ACTH secretion

Hormone (CRH)
Gonadotropin-releasing Stimulates secretion of FSH
Hormone (GnRH) and LH
Prolactin Inhibiting Inhibits Prolactin Secretion
Hormone
Somatostatin Inhibits secretion of Growth
Hormone
Thyrotropin-releasing Stimulates secretion of TSH
hormone (TRH)
Growth Hormone – Stimulates Growth Hormone
releasing hormone (GHRH) secretion

Oxytocin – stored in the posterior pituitary

Antidiuretic Hormone (ADH) – stored in the posterior

pituitary
 Gland Hormone Functions
Pituitary
Anterior Somatotropin Growth of bones, muscles &
Lobe ( Growth Hormone ) other organs

TSH Growth & secretory activity of

Thyroid gland

Growth & secretory activity of

ACTH
Adrenal Cortex

FSH Estrogen secretion

Oogenesis / Spermatogenesis

LH Ovulation, secretion of
progesterone

Prolactin Secretion / production of milk

Melanocyte Stimulating Hormone Pigmentation

 Gland Hormone Functions
Pituitary
Posterior Lobe ADH Reabsorption of H2O
- from the ( Vasopressin) Blood Pressure
hypothalamus
Oxytocin Milk expression
Uterine contraction
Pineal Gland Melatonin Sexual Maturation
Day-night cycle (“sleep trigger”)
Memory

Thyroid Thyroxine (T4) Metabolic Rate, growth and

Glands Triiodothyronine (T3) development

Calcitonin Inhibits bone resorption

Lowers blood Ca level
Parathyroid
Parathormone (PTH) Promotes bone resorption
Glands
Raises blood Ca level
Increases Ca absorption
 Gland Hormone Functions
Adrenal Glands Mineralocorticoids Reabsorption of Sodium
Cortex ( aldosterone ) Elimination of potassium
Blood Pressure

Glucocorticoids Increase blood glucose levels by

( Cotisol and increasing glycogenolyis
Corticosterone) Increase protein catabolism
Increase mobilization of fatty acids
Anti-inflammatory effect
Response to stress

Secondary Sex Hormones Secondary sex characteristics

(androgens : Estrogen and Preadolescent growth spurt
Progesterone)

Adrenal Glands Epinephrine Functions in acute stress, same as

Medulla Norepinephrine SNS: increase HR, BP, dilate
bronchioles, convert glycogen to
glucose as needed for energy
 Gland Hormone Functions
Pancreas Insulin • Allows glucose to diffuse across the
cell membrane
• Convert glucose to glycogen
• Lowers blood glucose level

Glucagon Increases blood glucose, glycogenolysis

Testes Testosterone Maturation of sex organs, sexual

functioning, development of secondary
sex characteristics

Ovaries Estrogen
• Maturation of sex organs, sexual
Progesterone functioning, development of secondary
sex characteristics
• Maintenance of Pregnancy & Growth
of uterine lining
• Maintenance of Calcium in the bones
(estrogen)

Thymus Thymosin Programs maturation of T cells

 Gland Hormone Functions
Heart Atrial Natriuretic Promotes Sodium excretion,
Hormone (ANP) inhibits Renin release
Inhibit Aldosterone secretion
Kidneys Erythropoietin Stimulates RBC production
Stomach Gastrin Stimulates HCl secretion

Small Intestine Secretin Inhibits gastric motility and stimulate

Cholecystokinin bile and pancreatic juice secretion
(CKK)
Skin 1,25 Stimulates intestines to absorb
Dihydrovitamin Calcium
D³
Placenta Human Stimulates corpus luteum to produce
Chorionic estrogen and progesterone
Gonadotropin
(hCG)
Human Placental Prepares the breasts for lactation
Lactogen
Relaxes pelvic ligaments and symphysis
Relaxin pubis, making them flexible to ease the
birth passage
*hyposecretion of growth hormone by the anterior
pituitary gland - Dwarfism

*S/Sx: retarded physical growth, premature aging, low

intellectual development, poor development of secondary
sex characteristics

*Given human growth hormone & offer emotional support

to client & family
*hypersecretion of GH by anterior pituitary gland which
results in Gigantism or Acromegaly
* Initial symptom of Acromegaly – coarsening of facial
features and progressive increase in shoe size
*gigantism occurs in childhood before the closure of
epiphyses of the long bones vs. acromegaly which occurs
after the closure of epiphyses of the long bones
*S/Sx: large hands & feet, thickening & protrusion of jaw,
arthritic changes, visual disturbances, diaphoresis, oily &
rough skin, organomegaly, hypertension, dysphagia,
deepening of voice
*Emotional support; frequent skin care; pharmacologic &
non- pharmacologic interventions for joint pains
*Prepare for radiation of pituitary gland or hypophysectomy
*removal of pituitary gland
*post-operative care:
-monitor V/S, neurological status & LOC
-Elevate head of bed
-Monitor for increased intracranial pressure & any
postnasal drip which might be CSF
-Avoid sneezing, coughing & blowing nose
-Monitor for temporary diabetes insipidus
-Monitor I & O & water intoxication
-Administer antibiotics, analgesics, antipyretics,
hormones & glucocorticoids if entire gland is
removed
*hyposecretion of ADH / deficiency of vasopressin
*S/Sx: polyuria of 4-24 liters/day; polydipsia, dehydration,
decreased skin turgor, dry mucus membranes, inability to
concentrate urine, low urine specific gravity of 1.006 or
less; fatigue, postural hypotension, headache.
*Provision of safe environment especially with decreasing
LOC, monitoring I & O with specific gravity, wear Medic-
Alert bracelet
*Meds: vasopressin tannate (Pitressin Tannate)
desmopressin acetate (DDAVP, Stimate)
lypressin (Diapid)
Enhances reabsorption of water in the kidnyes
promoting antidiuretic effect & regulates fluid balance
A/R: hypertension; nasal congestion
*continuous release of ADH, initial manifestation is Mental
Confusion
*S/Sx: Signs of fluid overload; changes in LOC & mental
status; weight gain, hypertension, tachycardia, hyponatremia

*Monitor I & O and daily weight; monitor fluid & electrolyte

balance; restrict fluids as prescribed; administer diuretics &
monitor IV fluids carefully

*Meds: demeclocycline (Declomycin) inhibits ADH-induced

water reabsorption & produces water diuresis
Hypothyroidism

• Cretinism
• Myxedema
 Hypothyroidism
• Primary : Inability of the gland to
secrete sufficient amount of T4 & T3
• Secondary : failure of pituitary gland to
secrete an adequate TSH
• Cretinism : severe form resulting from
deficiency of thyroid function during fetal
life shortly after birth
• Normal T3 ( Triiodothyronine: 75 - 220
ng/dL )
• Normal T4 ( Thyroxine: 4 – 11 ng/dL)
 Etiology
Iodine deficiency
Thyroidectomy
Use of radioactive iodine
Over-treatment with antithyroid drugs
Idiopathic
Chronic immunologic dysfunction
Hashimoto’s thyroiditis – autoimmune
disorder wherein antibodies are produced
that destroy thyroid tissue
 Pathophysiology

Inadequate secretion of thyroid hormones:

• slowing of physical & mental process
• depression of cellular enzymes
• decrease metabolic activity
• reduced O2 consumption
• reduced oxidation of nutrients for
energy
• produced less body heat
 Assessment Findings :
• Fatigue and Facial Edema
– initial manifestation • Menstrual irregularities
• Slowed mental process • Non-pitting edema
• Dull look • Bradycardia
• Slow, clumsy movements • CAD, MI, Angina, CHF
• Anorexia, Weight gain • Hypersensitivity to
• Constipation
sedatives, narcotics and
• Intolerance to cold
anesthetics
• Dry, scaly skin • Exaggeration of these
• Dry, sparse hair
findings :
• Brittle nails
• Mood swings
MYXEDEMA COMA
• Cretin – often hypoactive
( initial manifestation ),
described as a well
-behaved child
 Medical Management :
Drug Therapy
• Levothyroxine ( Synthroid )
• Thyroglobulin
• Liothyronin

Myxedema Coma
• IV thyroid hormones
• Correction of hypothermia
• Maintenance of vital functions
• Treatment of precipitating causes
*Monitor HR including rhythm

*Instruct patient re: thyroid replacement therapy

*Instruct on low-calorie, low-cholesterol, low-

saturated fat diet

*Assess for constipation & provide roughage

*Provide for warm environment

*Monitor for overdose of thyroid meds

 Nursing Interventions
• V/S
• I&O
• Daily weights
• Observe for edema
• Administer thyroid replacement hormones
a. observe for thyrotoxicosis ( tachycardia,
palpitations, n&v, diarrhea, sweating, tremors,
agitation, dyspnea )
b. increase dosage gradually, esp. in clients
with cardiac complications
 Nursing Interventions
• Provide a comfortable and warm environment
• Avoid sedatives, and reduce dose to half
• Institute measures to prevent skin breakdown
• Prevent constipation ( fluids, fiber foods), stool
softeners as ordered

Patient Teaching:
• Take daily dose of meds in the morning to prevent
insomnia
• Self-monitor for thyrotoxicosis
• Regular follow-up care
• Additional protection during cold weather
• Measures to prevent constipation
 Hyperthyroidism
Excessive activity of thyroid glands
Incidence : more common in women
Types : Graves’ s disease
Toxic nodular goiter
Etiology : Unknown , immunologic origin
Thyroid stimulating antibody
Genetic predisposition, female sex
Emotional stress, shock, infection
 Pathophysiology
Hypertrophy & hyperplasia of the gland
Autoimmune reaction which the antibody
mimics the action of the TSH
Increase body heat production
Increase sympathetic effect
Hypermetabolic conditions
Cardiovascular & neuromuscular activity
 Grave’s Disease / Thyrotoxicosis
• Excessive secretion of thyroid hormones in the blood
and causes an increase in metabolic processes.
• Overactivity & changes in the thyroid gland may be present
• Cause : unknown
Assessment Findings :

rritability, agitation, restlessness Exopthalmos & goiter

Hyperactive movements
Warm, smooth skin
Tremors, sweating, insomnia
Fine, soft hair
ncreased appetite, weight loss
Diarrhea Tachycardia, BP

ntolerance to heat palpitations

Medical Management :

Drug Therapy
• Antithyroid drugs (propylthiouracil / methimazole )
• These block synthesis of thyroid hormones
• Adrenergic blocking agents (Inderal – propanolol ) to
decrease SNS and alleviate symptoms like tachycardia

Radioactive Iodine Therapy

• Radioactive isotope of iodine given to destroy the
thyroid gland thus decreasing production of thyroid
hormone
• Used in patients resistant to or have developed toxicity
to drugs
• Hypothyroidism is a potential complication

Surgery
• thyroidectomy
 Nursing Interventions
• V/S
• I&O
• Daily weight measurement
• Administer anti - thyroid Medications
as ordered
• Provide for periods of uninterrupted rest
• Assign a private room away from excessive activity
• Administer medications to promote sleep as ordered
• Provide a cool environment
• Minimize stress in the environment
• Encourage quiet, relaxing diversional activities
• Diet : high carbohydrates, proteins, calories, vitamins and
minerals
• Supplemental feedings between meals and at bedtime
• Observe for complications : Exopthalmos / Proptosis –
protect eyes with dark glasses and artificial tears
*Provide adequate rest & administer sedatives as px

*Provide cool & quiet environment

*Obtain daily weight & give high-calorie food

**Administer anti - thyroid meds & avoid giving stimulants

*Prepare the patient for the following:

- iodine preparations to inhibit release of thyroid hormones
- propanolol (Inderal) for tachycardia
- radioactive iodine to destroy thyroid cells
- for thyroidectomy as px
Also called Thyroid crisis
• Uncontrolled and potentially life - threatening
hyperthyroidism caused by a sudden and excessive
release of thyroid hormones into the bloodstream.
• Precipitating factors :
1. Stress
2. Infection
3. Unprepared thyroid surgery
4. Abrupt withdrawal of medications
Assessment Findings :
Apprehension, restlessness Tachycardia
Extremely high temperature CHF
Delirium Coma
Respiratory distress
Nursing Interventions
• Maintain a patent airway and adequate ventilation

• Administer O2 as ordered

• Administer IV therapy

• Administer medications as ordered

• Antithyroid drugs
• Corticosteroids
• Sedatives
• Cardiac drugs

*Administer cooling blankets & nonsalicylate antipyretics

*Given antithyroids, iodines, beta - blockers and

glucocorticoids
 Thyroidectomy
*Removal of thyroid gland & performed for persistent
hyperthyroidism
*PRE - OPERATIVE CARE:
- Assess V/S, weight, electrolyte & glucose level
- Teach DBE & coughing as well as how to support neck in
post - op period when coughing & moving
- Administer antithyroid meds to prevent thyroid storm
*POST-OP CARE:
- Monitor for respiratory distress & have tracheostomy set,
O2 & suction machine at bed side
- Maintain semi-Fowler’s position
- Check surgical site for edema & bleeding
- Limit client talking & assess for hoarseness
- Assess for laryngeal nerve damage…high-pitched voice,
stridor, dysphagia, dysphonia & restlessness
- Monitor for signs of hypocalcemia & tetany & have calcium
gluconate at bed side
 Thyroidectomy
Preparation for surgery :
Must be euthyroid at time of surgery
Antithyroid drugs to control hyperthyroidism
Iodine is given to reduce vascularity &
increase firmness of the thyroid gland
Pre-operative teaching :
O2 is given & patient is instructed to
minimize speaking after surgery
Teach deep breathing, coughing and position
after surgery
 Postoperative care
Administer humidified air
Move patient carefully, provide adequate
support to the head so that no tension
is placed on the suture
Place the patient in semi-Fowler’s
position with the head elevated and
supported by pillows, avoid flexion
 Complications
• Tracheostomy set & suction set at bedside
• Damage to the laryngeal nerve : Hoarseness
• Hemorrhages: between 12 to 24 hours after the
surgery
• Observe for blood at side & back of the neck
– Throat clearing
– Frequent swallowing
– irregular breathing and swelling
• Note & report sign of hypotension, tachycardia
Tetany : accidental removal of parathyroid glands
Signs of hypocalcemia :
• Tingling sensation of toes, fingers & perioral
area
• Chvostek’s sign
• Trousseau’s sign
• paresthesia
• muscle weakness
• Bronchospasm / stridor
• seizure
Intravenous replacement of Calcium
Seizure precautions
Levothyroxine (Synthroid, Levothroid, Levoxyl)
Thyroglobulin (Proloid)

*Controls the metabolic rate of tissues & accelerates heat

production & oxygen consumption
*For hypothyroidism, myxedema & cretinism
*A/R: cramps, diarrhea, nervousness, tremors, hypertension,
tachycardia, insomnia, seating & heat intolerance

*Taken same time every day preferably in the a.m. with food
*Teach client to how to take HR
*Avoid foods that will inhibit thyroid secretions such as:
strawberries, peaches, pears, cabbage, turnips, spinach,
Brussels sprouts, cauliflower, peas & radishes
*Wear Medic-Alert bracelet
iodine solution (Lugol Solution, potassium iodide solution)
methimazole (Tapazole) , Propylthiouracil (PTU)

*Inhibits the synthesis of thyroid hormones

*Used for Hyperthyroidism or Grave’s Disease

*A/R: Agranulocytosis & Iodism (vomiting, abdominal pain,

metallic taste in the mouth, rash & sore salivary gland

*Take meds with food

*Call MD if fever or sore throat develops
*Abruptly stopping meds will cause thyroid storm (fever,
flushed skin, tachycardia, confusion & behavioral changes)
*Monitor for iodism
• Enlargement of the thyroid gland not caused by
inflammation or neoplasm
Types
1. Endemic
• Nutritional iodine deficiency
• Usually, adolescence and pregnancy
2. Sporadic
• Ingestion of large amounts of goitrogenic foods
(decreases Thyroxine production) like cabbage,
soybeans, peanuts, peaches peas, peaches, strwberries,
spinach, radishes
• Use of goitrogenic drugs : propylthiouracil, large doses of
iodine, Phenylbutazone, salicylic acid, cobalt, lithium
• Genetic defects
• Low levels of thyroid hormone stimulate increase secretion
of TSH :
Thyroid increases in size to compensate and produce more
thyroid hormones.
 Medical Management :
Drug Therapy
• Hormone replacement
• Small doses of iodine ( Lugol’s solution ) for goiter
due to iodine deficiency.

Avoidance of goitrogenic foods and drugs

Surgery

Nursing Interventions
• Administer replacement therapy as ordered

• Client teaching :
1. Use iodized salt
2. Thyroid hormone replacement
 Hashimotos Thyroiditis
• Also known as Lymphocytic Thyroiditis
• A chronic progressive disease of the gland
caused by the infiltration of lymphocytes
• Results in progresive destruction of the
parenchyma and hypothyroidism if untreated
• Cause is unknown
• Believed to be an autoimmune disease;
genetically transmitted and perhaps related to
Grave’s disease
• 95% of cases: women (40s or 50s)
• Possibly the most common cause of adult
hypothyroidism
 Hashimotos Thyroiditis
• Manifestations:

– Marked by slowly developing, firm

enlargement of the thyroid gland
– Usually no gross nodules
– BMR is usually low
– Periods of hyperthyroidism from large
amounts of T4 and T3 released into the
bloodstream
 Hashimotos Thyroiditis

• Diagnostic Evaluation:

– T3 and T4: normal to subnormal

– TSH level: elevated
– Antithyrogobulin antibodies and
antimicrosomal antibodies: present
– Normal or high concentration of thyroglobulin-
binding protein
 Hashimotos Thyroiditis
• Management:
– Thyroid medications to maintain a normal
level of circulating thyroid hormone; to
suppress the production of TSH; prevent the
enlargement of the gland and maintain a
euthyroid state
– Surgical resection of goiter if tracheal
compression, cough or hoarseness occur
– Careful follow-up to detect and treat
hypothyroidism
 Hashimotos Thyroiditis
• Complications:
– Progressive hypthyroidism to myxedema

• Nursing Assessment:
– Anxiety related to the enlargement of the neck
• Nursing Intervention:
– Relieve anxiety
 Hashimotos Thyroiditis
• Patient Education:
– Teach signs of tracheal compression that
should be reported to health care providers
– Explain outcome of hypothyroidism and
necessity of taking thyroid hormones every
day for life
– Explain need for a regular follow up check up
to monitor thyroid and TSH level

• Outcome-based Evaluation
• Verbalizes reduced anxiety, more relaxed,
sleeps better
• HYPOPARATHYROIDISM

• HYPERPARATHYROIDISM
*Positive Chvostek’s Sign
*Positive Trousseau’s Sign
*Wheezing and dyspnea (bronchospasm,
laryngospasm)
*Numbness & tingling of face & extremities
*Carpopedal spasm
*Visual disturbances (photophobia)
*Muscle & abdominal cramps
*Cardiac dysrhythmias
*Seizures
*Monitor for hypocalcemia & institute seizure precautions

*Place a tracheostomy set, O2 & suction machine at bed

side

*Prepare for calcium gluconate/chloride IV

*Provide high-calcium/low-phosphorus diet

*Give vitamin D to enhance calcium absorption at the GIT

*Given phosphate binders

*Wear medic-alert bracelet

 Hypoparathyroidism
Deficiency of parathyroid hormone & is
characterized by hypocalcemia &
neuromuscular hyperexcitability

Etiology : most common is accidental removal

during thyroidectomy & radical neck dissection
for malignancy

Decrease in gland function – idiopathic,

autoimmune or familial origin

Malignancy or metastatic cancer of the gland

Resistance to parathyroid hormone
 Pathophysiology
Decreased resorption of calcium from the
renal tubules and bones
Decreased absorption of calcium from the
gastrointestinal tract
Blood calcium level falls, causing symptoms of
muscular hyperirritability, uncontrolled
spasm & tetany
Rise in the serum phosphates & decreased
phosphates renal excretion
Acute onset result to acute airway obstruction
& cardiac failure
 Clinical manifestation &
Diagnostic evaluation
Elevated phosphorus & decreased
calcium
Tetany : Chvostek’s sign, Trousseau’s
sign carpopedal spasm, tremors,
laryngeal spasm, paresthesia
Anxiety
Renal colic : pre - existing stone loosen
& migrate into the ureter
Nursing Interventions

• A syringe & Calcium ampule at

bedside at all time
• Calcium administration – infusion
every 10 minutes for rapid relieve of
tetany ; monitor for cardiac failure
• Slow drip of Calcium containing fluid
until tetany is control - IM – Oral form
of Calcium
• Vitamin D added to calcium intake
• Sedate patient
 Hyperparathyroidism
Overactivity of the gland
Caused by overgrowth or hypertrophy of the
parathyroid gland
- primary disorder : adenoma & hyperplasia
- secondary condition : renal failure as a
result of phosphorus retention &
hypocalcemia
Malignacy in the gland or secretion of
parathyroid hormone by an ectopic tissue
*Hypersecretion of parathyroid hormones
*S/Sx:
• hypercalcemia & hypophosphophatemia
• fatigue & muscle weakness
• skeletal pain & tenderness
• bone deformities resulting from pathologic
fractures
• weight loss
• constipation
• hypertension
• cardiac dysrhythmias
• renal stones
 Clinical manifestations
• Decalcification of stone : skeletal pain,
backache, pain on weight bearing, pathologic
fractures, deformities & bone marrow problems
• Hypercalcemia
• Depression of neuromuscular function :
general fatigue, weakness, loss of memory,
emotional instability, changes in LOC, stupor &
coma
• Signs of renal failure, nephrolithiasis
• Cardiac dysrhythmias & hypertention
• Constipations, Pancreatitis, UGIB
 Diagnostic evaluations
Persistently elevated serum Calcium level
Serum alkaline phosphatase are increased
Serum phosphorus are decreased
Parathyroid levels are increased with
hyperactivity of the parathyroid glands
Skeletal changes are revealed in the X rays
 Other causes of hypercalcemia
• Malignacy
• Vitamin D excess
• Multiple myeloma
• Drugs : thiazides
• Sarcoidosis
• Cushing’s disease
• Hyperthyroidism
 Management
• Hydration & diuretics (furosemide)
• Oral phosphate
• Dietary Calcium restriction :
– Vitamin D
– Milk & dairy products
– Salmon
• Parathyroidectomy
Nursing Interventions

*Encourage fluids & administer furosemide

(Lasix) & IV saline as prescribed
*Move patient slowly & carefully
*Administer phosphates as prescribed
*Administer calcitonin (Calcimar) as
prescribed to decrease skeletal calcium
release & increase renal calcium clearance
& monitor for hypocalcemia & report to MD
*Prepare for parathyroidectomy
*Removal of 1 or more parathyroid gland
*PRE-OPERATIVE CARE:
- monitor calcium, phosphate & magnesium level
- ensure that calcium is near normal
- explain to patient that talking may be painful 2 days
post-op
*POST-OPERATIVE CARE:
- monitor for respiratory distress &have a tracheostomy
set, O2 & suction machine at bed side
- Semi-Fowler’s position & Check for bleeding
- Check for hypocalcemic crisis, Trousseau’s or
Chvostek’s sign
- Assess changes in voice pattern & for laryngeal nerve
damage
- Administer calcium & vitamin D supplements as px
CALCIUM SUPPLEMENTS
calcium carbonate (Tums)
calcium gluconate
calcium lactate

VITAMIN D SUPPLEMENTS
calcifediol (Calderol)

CALCIUM REGULATORS
calcitonin human (Cibacalcin)

ANTIHYPERCALCEMICS
edetate disodium (Disotate)
*Parathyroid hormone regulates serum calcium
levels

*Low serum calcium level stimulate parathyroid

hormone release

*Hyperparathyroidism…give antihypercalcemics

*Hypoparathyroidism…give calcium & Vit. D

ADRENAL CORTEX
Addison’s disease
Cushing’s syndrome
Aldosteronism (Conn’s Syndrome)

ADRENAL MEDULLA
Pheochromocytoma
Adrenocortical Insufficienncy
Inadequate secretion of the hormones of
the adrenal cortex
Primarily the glucocorticoids &
mineralocorticoids
Primary : Addison’s disease –
destruction & hypofunction of adrenal
cortex
Secondary : a result of Pituitary ACTH
deficiency, use of exogeneous steroid
 Pathophysiology
The chief hormone affected is aldosterone
and cortisol, few symptoms are related to
sex androgen deficiency
Inadequate aldosterone lead to disturbance
of sodium, potassium & water metadolism
Cortisol deficiency produces abnormal fat,
protein & carbohydrates metabolism
Absence of cortisol during stress lead to
adrenal crisis and death if treatment is
inadequate
 Assessment findings :
• Fatigue, muscle weakness

• Anorexia, n & v

• Abdominal pain, weight loss

• Hypotension, weak pulse

• Bronzelike pigmentation of skin

• Decreased capacity to handle stress

• Hyponatremia, hyperkalemia and

hypoglycemia
 Nursing Interventions
1. Monitor Hormone Replacement Therapy as ordered :
• Glucocorticoids ( cortisone, hydrocortisone )
• Mineralocorticoids ( florinef )
2. V/S
3. Decrease stress in the environment
4. Prevent infection exposure
5. Provide rest periods
6. Monitor I & O

7. Weigh daily

8. Small frequent feedings

9. Diet : high carbohydrates, sodium and protein

 Cushing’s syndrome
• Hyperfunction of the adrenal cortex

• Excessive secretion of corticosteroids

• Primary : caused by tumors or neoplasms

• Secondary : pituitary or neoplasm secreting too

much ACTH

• Iatrogenic : prolonged use of corticosteroids

 Cushing’s Syndrome
Condition in which plasma cortisol levels are
elevated
Etiology : Cushing’s disease – overstimulation
of adrenal cortex by ACTH
Adenoma or carcinoma in the adrenal cortex
Ectopic - tumors elsewhere in the body
producing excess ACTH
Exogeneous intake of Steroids
 Pathophysiology
Manifestations of Cushing’s syndrome
are the result of excess hormones
(glucocorticoids, mineralocorticoids &
sex hormones )
Predominant hormone secreted in
excess determines the predominant
symptom
Glucocorticoids
 Assessment findings :
• Muscle weakness, fatigue

• Obese trunk with thin arms and legs

• Irritability, depression, mood swings

• Moon face, buffalo hump, pendulous abdomen

• Purple striae on trunk

• Signs of masculinization in women

• Menstrual dysfunction, decreased libido

• Osteoporosis, decreased resistance to infection

• Hypertension, edema
 Clinical manifestations due to
excess glucocorticoids
• Weight gain, central type obesity
• Heavy trunk, thin extremities, wasted muscles
• Buffalo hump in the neck & supraclavicular area
• Rounded face
• Skin-fragile & thin, striae & ecchymosis
• Osteoporosis
• Mood changes & psychosis
• Increase susceptibility to infection
• Hyperglycemia
 Clinical manifestations due to
excess Mineralocorticoids

• Hypertension
• Hypernatremia
• Hypokalemia
• Increase weight gain
• Expanded blood volume
• Edema
 Clinical manifestations due to
excess Sex Androgen
Female :
Virilism or masculinization
Hirsutism
Breast atrophy
Enlarged clitoris
Musculine voice
Loss of libido
In Utero : pseudohermaphrodite
Male : loss of libido
 Surgical Management &
Hormonal replacement
Surgical removal of the causative factor :
Transsphenoidal hypophysectomy &
pituitary irradiation – Cushing’disease
Adrenalectomy – bilateral hyperplasia &
adrenal adenoma
Replacement of hormones :
Adrenalectomy : Glucocotrticoids &
Mineralocortocords
Hypophysectomy and irradiation :
hydrocortisone, thyroid hormones &
gonadal hormone
 Medical management
In patient unable to undergo surgery
because of contraindications
Mitotane : toxic to adrenal cortex,
medical adrenalectomy
Metyrapone : control the steroid
hypersecretion in patient who do not
respond to Mitotane therapy
 Nursing Interventions
1. Maintain Muscle tone
ROM exercises Assist with ambulation
2. Prevent accidents or falls and provide adequate rest
3. Protect client from exposure to infection
4. Maintain skin integrity – meticulous skin care
5. Minimize stress in the environment
6. Monitor V / S
7. Monitor I & O, daily weights
8. Diet : low in calories, sodium and high in protein,
potassium, calcium and vitamin D.
9. Prepare for hypophysectomy or radiation if condition
is caused by a tumor
10. Prepare for adrenalectomy if caused by adrenal
tumor or neoplasia.
*Hypersecretion of aldosterone from the adrenal cortex of the
adrenal gland commonly caused by adenoma

*S/Sx: hypertension, hypokalemia, HA, polydipsia & polyuria,

hypernatremia, low urine specific gravity

*Monitor I & O & administer spironolactone (Aldactone) &

potassium
supplements & maintain Na restriction

*Administer antihypertensives as px

*Wear Medic-Alert bracelet

*Usually will be undergoing adrenalectomy; administer

glucocorticoids pre & post-op
 Aldosteronism
Excessive secretion of aldosterone by
the adrenal cortex
Primary : caused by a adrenal adenoma
Conn’s syndrome
Secondary : in conjunction with heart
failure, renal dysfunction or cirrhosis of
the liver
 Clinical manifestations
• Hypokalemia & alkalosis : muscle
weakness, arrhythmias, polyuria,
tetany, paresthesia
• Hypernatremia : increase serum
osmolality, polydipsia, arterial
hypertension
• Hypertension
• Complication of HPN : Heart failure,
stroke, retinopathy, Myocardial
Infarction
 Diagnostic evaluation &
Management
• Primary aldosteronism : hypertension
with hypokalemia, CT scan to localize
the cortical adenoma, treatment
adrenalectomy
• Secondary aldosteronism :
Treatment of the underlying disorder,
Spironolactone (Aldactone) – effective
in controlling hypertension and
hypokalemia
*Catecholamine - producing tumor usually found in the
adrenal gland but also found in the abdomen; usually
excised
*Causes hypersecretion of epinephrine & norepinephrine by
the adrenal medulla
*Cx: hypertensive retinopathy, CVA & CHF
*S/Sx: HPN, severe HA, palpitations, pain in chest or
abdomen, hyperglycemia & glucosuria
*Monitor for hypertensive crisis & avoid stimuli which
triggers it such as : increased abdominal pressure, vigorous
abdominal palpation & micturation
*Instruct patient not to smoke, drink cola, coffee or tea
 Pheochromocytoma
• Cathecholamine - secreting neoplasm
associated with hyperfunction of the
adrenal medulla
• Most are benign; 10% are malignant
• Occur at any age but most commom
between the ages of 30 – 60 years
• Increase secretion of Epinephrine &
Norepinephrine
 Pathophysiology & Clinical
manifestations
• Excessive secretion of catecholamines :
• Paroxysmal or persistent hypertension
• Hypermetabolism produce : tachycardia,
excessive perspiration, tremors, pallor or
facial flushing, nervousness
• Hyperglycemia produce : polyuria, N & V,
diarrhea, abdominal pain & paresthesia
• Symptoms are triggered : allergy,
emotional stress and physical exertion,
unknown
 Diagnostic evaluation
• CT scan & MRI – locate the tumor
• Clonidine suppression test :
differentiate the essential HPN
from Pheochromocytoma
– will suppress the catecholamine in
essential HPN but not in
Pheochromocytoma
 Management
• Diagnose the condition accurately
• Control blood pressure : Alpha - adrenergic
blocking agents like phentolamine or
phenoxybenzamine to inhibit the effect of
catecholamines
• Metyrosine – catecholamine synthesis
inhibitor
• Propanolol – helpful in controlling cardiac
dysrhythmia & tachycardia
• Remove tumors or the Adrenal glands
bethamethasone (Celestone), cortisone (Cortone)
dexamethasone (Decadron), prednisone (Orasone)
*Stimulate the adrenal cortex to secrete cortisol
*Produces an antiinflammatory effect for multiple sclerosis
*A/R: Increased appetite, mood swings, water & Na
retention,
hypocalcemia & hypocalcemia
*Check I & O, weight and for edema (decrease Na intake)
*Monitor for infection
*Monitor electrolyte & calcium levels
*Monitor for poor wound healing, menstrual irregularities,
decrease in growth & edema
*Dose must be tapered & not stopped abruptly
*Advise to wear Medic-Alert bracelet
*Produce metabolic effects; alters normal immune
response & suppress inflammation; promote Na & H2O
excretion & K+ excretion
*Produce antiinflammatory , antiallergic & anti-stress
effects; replacement for adrenocortical insufficiency
*A/R: hyperglycemia, hypokalemia, edema & masks signs
& symptoms of infection
*C/I: DM, increases effect of anticoagulants & oral
antidiabetic agents; increases potency of aspirins &
NSAIDS & K-sparing diuretics
*Check for overdose or signs of Cushing’s syndrome;
check with MD before receiving vaccines; additional
doses during stress / surgery
fludrocortisone (Florinef)
*Steroid hormones that enhance the reabsorption of NaCl
& promote K+ excretion & hydrogen at the renal tubule
promoting fluid & electrolyte balance
*Used in primary & secondary Addison’s disease

*A/R: Na/H2O retention, hypokalemia, hypocalcemia,

delayed wound healing, increased susceptibility to
infection, mood swings, weight gain

*Take with food or milk; high-K+ diet

*Wear Medic-Alert bracelet

Glucose absorbed from the gastrointestinal (GI) tract
into the blood is used to supply cells throughout the
body
The cells require a regular supply of glucose that must
be maintained between mealtimes when no further
glucose is being supplied to the body.

Blood glucose levels are kept between relatively narrow

limits by a hormonal control system
If the supply of glucose exceeds the energy
requirements of the cells, the excess is converted to
glycogen and fat for storage.

On the other hand, if blood glucose levels begin to

fall, glucose is released from glycogen and fat stores
Failure of this control system can lead to blood glucose
levels moving outside the 'normal' range, with serious
implications for the health of the person affected.

The tasks of glucose metabolism are…

• to supply the cells of the body with a source of
energy
• to maintain a constant supply of glucose
• to act through a system of hormonal controls.
The body uses glucose in a number of ways. Depending on
the current energy requirements of the body, glucose may
be:
• used as an energy source to drive cellular processes
• converted to glycogen for storage
• converted to lipids for storage
• used to synthesize amino acids
• eliminated in the urine
Glucose is normally reabsorbed completely
from the urine by the kidneys.

However, as blood glucose levels rise above

normal, the capacity of the kidneys to
reabsorb glucose may be exceeded and
glucose is excreted in the urine
(glycosuria).

Diabetes is often first detected when a

routine test indicates that glucose is
present in the urine.
Hormonal control of blood glucose
Pancreatic hormones are produced by
small clusters of cells within the pancreas,
called the islets of Langerhans. These
clusters consist of a number of specialized
cell types, including:

• ß-cells: these secrete insulin, which acts

to lower blood glucose levels
• A-cells: these secrete glucagon, an
insulin antagonist, which increases blood
glucose levels by inhibiting the action of
insulin.
Failure of this hormonal control system has serious
consequences, the most significant of which is the
development of diabetes
In diabetes, there is a breakdown of glycemic control due
to either:
1. reduced insulin secretion: not enough insulin is
secreted by the ß - cells to produce the required
reduction in blood glucose levels
2. insulin resistance: when a given amount of
insulin produces less of a blood glucose-lowering
effect (e.g. less uptake of glucose by skeletal muscle
cells) than would normally be expected.
Where a state of insulin resistance exists, tissues that
would normally respond to insulin are less responsive
and are described as insulin resistant.
 Negative Feedback Control of Glucose
Blood Glucose Blood Glucose
Levels Increase Levels Decrease

Pancreatic Pancreatic
A - cells B - cells

Glucagon is Insulin
secreted Is secreted

Enhanced Glucose Increased use

Release from & storage of
Glycogen & fat stores Glucose
 Diabetes Mellitus
• a disorder in which blood levels of glucose
are abnormally high because the body does not
release or use insulin adequately.
• comes from Greek words for "flow" and
"honey", referring to the excess urinary flow
that occurs when diabetes is untreated, and to
the sugar in that urine
• characterized by hyperglycemia resulting
from defects of insulin secretion or insulin
insensitivity of the cells or both.
• a disorder in which blood levels of glucose
are abnormally high because the body does not
release or use insulin adequately.
CLASSIFICATIONS :

1. Type 1 ( insulin - dependent diabetes mellitus )

2. Type 2 ( non – insulin - dependent diabetes

mellitus )

3. Gestational diabetes mellitus

4. Diabetes Mellitus associated with other

conditions like pancreatic disease, cushing’s
syndrome and due to medications.
 Classification of
Diabetes Mellitus
Insulin- dependent DM Non- Insulin dependent DM

Unable to produce Defect in insulin release or

endogenous insulin resistance to insulin

They need insulin to Don’t need insulin to

prevent ketoacidosis & survive
survive
Autoimmune or viral Hereditary
factors
Insulin - Dependent Non-Insulin
Dependent
Commonly seen in
young Older 40 & above
Thin individuals
Obese individuals
Sudden onset of
polyuria, Late onset & can
polydipsia & prevent &
polyphagia postponed

Type I or juvenile
Type 1 Diabetes Mellitus

• the pancreas produce little or no insulin at all

• The onset of type 1 diabetes is typically early in life,

with 50% of all cases diagnosed before 20 years of age
and usually develops before the age of 30

• this is characterized by a destruction of the pancreatic

beta cells due either thru viral, nutritional or
immunologic factors.
• more than 90% of the beta cells are permanently
destroyed

• resulting insulin deficiency is so severe, regular insulin

injections are required for survival.
Because insulin normally inhibits glycogenolysis
(breakdown of stored glucose ) and gluconeogenesis
(production of new glucose), these processes occur
unrestrained in people with insulin deficiency and
contribute to hyperglycemia.
Fat breakdown occurs, and KETONE Bodies ( byproduct of
fat breakdown ) builds up.
ALERT : ketone bodies are acids, when they accumulate in
large amounts, they result to Diabetic Ketoacidosis (DKA):
• abdominal pain
• nausea and vomiting
• hyperventilation
• fruity odor of the breath

If left untreated : altered LOC

Coma
Death
Type 2 Diabetes Mellitus

• 2 main problems :
1. Impaired insulin secretion
2. Insulin resistance

• When insulin resistance develops, insulin -

mediated effects - such as increased glucose
uptake, glycogen synthesis and conversion of
glucose to fat - are reduced and blood glucose
levels tend to rise.
• Insulin resistance refers to a decreased sensitivity
of tissues to insulin, thus rendering insulin less
effective at stimulating glucose uptake by the tissues.
 1. Increased Insulin Resistance
Insulin secretion
compensates for Down regulation of Reduced Insulin
increased insulin Insulin receptors Sensitivity
resistance
Increased Insulin
Secretion

2. Insulin -secreting Eventually, the B-cells

capacity of the B- cannot compensate for
cells exceeded the insulin resistance

Increased levels of glucose

3. Insulin secretion in the blood
declines as blood
glucose continues
to rise
Reduced insulin secretion
Despite impaired insulin secretion, there is still enough
insulin to prevent breakdown of fat and accumulation of
Ketone bodies , thus no DKA .
Risk Factors

• Obesity
• Age greater than 45 years
• Some ethnic groups (particularly African-Americans/
Hispanics)
• Gestational diabetes or delivering a baby weighing
more than 9 lbs
• High blood pressure
• High blood levels of triglycerides (a type of fat
molecule)
• High blood cholesterol level
 Clinical Manifestations :
The three “P’s” of diabetes Results from excess fluid loss
1. Polyuria associated with osmotic diuresis.
2. Polydipsia
Due to catabolic state induced
3. Polyphagia by Insulin deficiency and
breakdown of fats and proteins.

Fatigue and weakness

Sudden vision changes
Tingling or numbness in the hands and feet

Dry skin
Sores / wounds that are slow to heal

Recurrent infections
Diagnostic Tests :
Fasting Blood sugar

A urine analysis may be used to look for

glucose and ketones from the breakdown
of fat. However, a urine test alone does not
diagnose diabetes`

Oral glucose tolerance test

Random (non-fasting) blood glucose level

 Diagnostic evaluation
In a presence of classic symptoms:
• a random blood glucose value > 200mg/dl
• Fasting blood glucose of > 126mg/dl on
two occasions
• 110-126 mg/dl ; impaired glucose
tolerance
• 75mg Oral glucose tolerance test : 2 hour
plasma glucose value > 200mg/dl
 Blood Sugar levels and their interpretation
mmol/l mg/dl interpretation
2.0 35 extremely low, danger of
unconciousness
3.0 55 low, marginal insulin reaction
4.0 75 slightly low, first symptoms of
lethargy etc.
5.5 100 optimum
5-6 90-110 normal preprandial in nondiabetics
8.0 150 normal postprandial in nondiabetics
10.0 180 maximum postprandial in nondiabetics
11.0 200
15.0 270 a little high to very high depending
16.5 on patient
300
 Blood Sugar levels and their interpretation

mmol/l mg/dl interpretation

20.0 360 very high

22 400 max mg/dl for some meters and
strips
33 600 high danger of severe
electrolyte imbalance

Preprandial = before meal

Postprandial = after meal

There is no cure for diabetes
The immediate goals are to stabilize your blood sugar and
eliminate the symptoms of high blood sugar. The long -
term goals of treatment are to prolong life, relieve
symptoms, and prevent complications.

5 Components of Diabetes Management :

1. Nutrition management

2. Exercise

3. Monitoring

4. Pharmacologic therapy

5. Education
D - Diet: 50-60% CHO, 20-30% FATS
and 10-20% CHON
I - Insulin
A - Antidiabetic agents:
Sulfunylureas / Metformin
B - Blood sugar monitoring
E - Exercise
T - Transplant of the pancreas
E - Ensure adequate food intake
S - Scrupulous foot care
 Dietary management and
Exercise
Diet : Complex rather than simple
carbohydrates, fiber & polyunsaturated fat,
less added saturated fat, low cholesterol &
low sodium intake.
Exercise : promotes utilization of
carbohydrates & enhance the action of
Insulin
Uncontrolled DM should not go into exercise
unless blood glucose levels are normal
Obese – weight reduction & diet
Nutrition
Diet and weight control constitute the foundation
of diabetes management.
Weight loss is important since it decreases
insulin resistance.
High fiber, low fat diet is recommended.
Reduce alcohol intake
Exercise
Lowers blood glucose levels and improves insulin
utilization
Improves circulation and muscle tone
Reduces cardiovascular risk factors.
Monitoring Glucose and Ketones
Frequent monitoring of blood glucose levels enables
people to adjust the treatment regimen to obtain optimal
blood glucose control.
Pharmacologic Treatment
Type 1
*Insulin increases glucose transport into cells & promotes
conversion of glucose to glycogen, decreasing serum
glucose levels
*Primarily acts in the liver, muscle, adipose tissue by
attaching to receptors on cellular membranes & facilitating
transport of glucose, potassium & magnesium

*Hormone secreted by the alpha cells of the islets of

Langerhans in the pancreas
*Increase blood glucose by stimulating glycogenolysis in
the liver
*given SC, IM or IV routes
*Used to treat insulin-induced hypoglycemia when
semiconscious / unconscious
Insulin & hypoglycemic drugs
Insulin : lower the blood glucose by
decreasing the release of glucose from the
liver & increasing the utilization in the
muscles & adipose tissue

Who needs Insulin?: Type I DM & Type II

DM with acute illness, stress, infection,
surgery or pregnancy
 Type of insulin
1. Short acting : clear , onset 0.25 - 1 hr, peak 2 -
4 hrs, duration 5 - 7 hrs
Regular, Humulin R, actrapid

2. Intermediate : turbid, onset 1- 4 hrs, peak 2 -

15 hrs, duration 12 - 28 hrs
Lente, Humulin N, NPH

3. Long acting : turbid, onset 4 - 6 hrs, peak 10 -

30 hrs, duration 36+ hours
Ultralente, PZI, Ultratard
 Insulin reactions

Hypoglycemia : < 50mg/dl

Too much insulin, not enough food,

excessive physical activity

Commonly seen before meals, but can

happen anytime

Be familiar with the peak & duration of

insulin
 1. Short acting : used in treating ketoacidosis,
during surgery, infection, trauma and to
supplement longer - acting insulins

2. Intermediate acting : used for maintenance

therapy

3. Long acting : used for maintenance in clients

who experience hyperglycemia during the
night with intermediate – acting insulin.

4. Insulin pumps
TYPE ONSET PEAK DURATION
RAPID-ACTING INSULIN
Aspart (NovoLog) Immediate 5 min. 30 min.
Lispro (Humalog) 10-15 mins 1 hour 3 hours

SHORT-ACTING INSULIN
Humulin Regular 0.5-1 hour 2-3 hours 4-6 hours

INTERMEDIATE-ACTING INSULIN
Humulin NPH 3-4 hours 4-12 hours 16-20 hours
Humulin Lente 3-4 hours 4-12 hours 16-20 hours

LONG-ACTING INSULIN
Humulin Ultralente 6-8 hours 12-16 hours 20-30 hours

PREMIXED INSULIN 0.5-1 hour 2-12 hours 18-24 hours

70% NPH-30% Regular
• To mix insulin suspension, swirl vial gently or rotate
between palms or between palm and thigh.
• Don't shake vigorously - this causes bubbling and air in
syringe.
• When mixing regular insulin with intermediate or long-
acting insulin, always draw up regular insulin into syringe
first.
• When NPH or lente is mixed with regular insulin in the
same syringe, give immediately to avoid loss of potency.
• NovoLog should be given 5 to 10 minutes before the start
of a meal. Because of drug's rapid onset and short
duration of action, patients may need longer acting
insulins to prevent hyperglycemia before meals
• Advise patient not to smoke within 30 minutes after
insulin injection. Cigarette smoking decreases the
absorption of insulin injected s/c
• Inform patient that marijuana use may increase insulin
requirements.
COMPLICATIONS OF INSULIN THERAPY

*LOCAL ALLERGIC REACTION

*INSULIN LIPODYSTROPHY

*INSULIN RESISTANCE

*DAWN PHENOMENON

*SOMOGYI’S EFFECT

*INSULIN WANING - Insufficient or waning insulin is

simple. If the effective duration of intermediate or long
acting insulin ends sometime during the night, the
relative level of circulating insulin will be too low, and
your blood sugars will rise.
DAWN PHENOMENON
• A sudden rise in blood glucose levels in the early
morning hours.
• Unlike the Somogyi effect, it is not a result of an insulin
reaction.
• People who have high levels of blood glucose in the
mornings before eating may need to monitor their blood
glucose during the night.
• If blood glucose levels are rising, adjustments in evening
snacks or insulin dosages may be recommended
Dawn Phenomenon is associated with:
1. Poor Control
2. Short duration of diabetes
3. Adequate counter - regulatory hormones (glucagon,
epinephrine, norepinephrine, growth hormone, and
cortisol )
4. High insulin needs
Somogyi’s Effect
• Compensatory rebound hyperglycemia
that last 12 - 72 hour following
hypoglycemia caused by excessive dose
of insulin
• Gradual reduction of Insulin dose &
increase of the diet at the time of
hypoglycemia
• Insulin lipodystrophy : at site of insulin
injection, affects the effect of insulin,
rotate the injection site

• Insulin absorption : deltoid / anterior

thighs / abdomen / buttocks

• Instruct : maintain regular diet, bring

simple sugars, between meal & bedtime
snack

• Frequent blood test is necessary

Type 2 Diabetes Mellitus
Oral hypoglycemic agents
Sulfunylureas – stimulates the pancreas to secrete insulin
Biguanides ( metformin ) – facilitate insulin’s action on
receptor sites
Oral alpha glucosidase inhibitors ( acarbose ) – delays
absorption of glucose in the GIT, resulting to lower blood
glucose level.
Thiazolidinediones ( Rosiglitazone - Avandia ) – enhance
insulin action at the receptor sites w/o increasing insulin
secretion from the beta cells of the pancreas.
Meglitinides ( prandin ) – stimulates insulin release from
the beta cells.
 Oral hypoglycemics
Effective for older, Non-Insulin
dependent DM, non-ketotic patients
Sulfonylureas : stimulates the
pancreas to secrete endogenous
insulin
Tolbutamide
Chlorpropamide
Tolazamide
Glyburide
Glipizide
Glibenclamide
FIRST-GENERATION SULFONYLUREAS
Short-Acting
Tolbutamide (Orinase)
Intermediate Acting
Acetohexamide (Dymelor)
Long-Acting
Chlorpropamide (Diabenese)

SECOND-GENERATION SULFONYLUREAS
Glyburide (Micronase)
NONSULFONYLUREAS
Metformin (Glucophage)
*Prescribed for clients with Type 2 DM
*Sulfonylureas: stimulate beta cells to produce more
insulin do not give with ROH
Nonsulfonylureas: affect hepatic & GI production of
glucose; may be combined with sulfonylureas
*Insulin may be needed for surgery, stress or infection
*Compliance is a must & wear Medic-Alert bracelet
Education
Teach about the pathogenesis of the disease,
it’s treatments, diet, exercise and drug
modalities.

Teach patient how to monitor blood glucose

Teach foot care.

Emphasize importance of regular eating habits,

never skip meals
Nursing Interventions:
1. Administer insulin or oral hypoglycemic agents as
ordered, monitor for hypoglycemia, especially during
period of the drug’s peak action.
2. Provide special diet as ordered
Ensure that the client is eating all meals
If all food is not ingested, provide measured amount
of orange juice to substitute for leftover food
Provide snack later in the day
3. Monitor urine and sugar and acetone.

4. Perform finger sticks to monitor blood glucose levels

as ordered ( more accurate than urine tests.

5. Observe for signs of hypoglycemia

 6. Provide meticulous skin care and prevent injury.

7. Maintain I & O, weigh daily.

8. Provide emotional support

General Care
• Perform good oral hygiene
• Have regular eye exams
• Care for “ SICK DAYS “
Do not omit insulin or oral hypoglycemics
since infection causes increased blood
sugar
• Notify physician
• Monitor urine and blood glucose and urine
ketones frequently
• If nausea and vomiting occurs, sip on clear
liquids with simple sugars.
9. Provide client teaching and discharge planning
concerning :
• Disease process
• Diet
• Insulin
1. How to draw up into syringe
• use insulin at room temperature
• gently roll vial between palms of hands
• draw up insulin using sterile technique
• if mixing insulins, draw up clear insulin before
cloudy insulin
2. Injection technique
• systematically rotate sites to prevent lipodystrophy
• insert needle at 45 or 90 degree angle depending on
amount of adipose tissue
3. May store current vial at room temperature,
refrigerate extra supplies.
4) Provide many opportunities for return demonstration

• Oral hypoglycemic agents

a. Stress importance of taking the drug regularly
b. Avoid alcohol intake while on medication

• Urine testing ( Type 2 )

a. Perform tests before meals and at bedtime
b. Use freshly voided urine
c. Be consistent in brand of urine test used

• Blood Glucose Monitoring ( Type 1 )

a. Instruct client in finger-stick technique
b. Use monitor device
• Foot Care
1. Wash feet with mild soap and water,
pat dry
2. Apply lanolin to prevent drying and
cracking
3. Cut toenails straight across
4. Avoid constricting garments
5. Wear clean, absorbent socks
6. Buy properly - fitting shoes
7. Never go barefoot
8. Inspect feet daily
• Exercise
1.Regular exercise
2.Increase food intake before exercise
3.Best performed after meals when blood
sugar is high

• During hypoglycemic attacks:

1. eat hard candy
2.Take glucose tablets
3.Fruit juice or regular soda
4. 2 – 3 teaspoons of sugar or honey
 1. Hypoglycemia
• Sweating
• Tremors
• Tachycardia
• Palpitations
• Nervousness
• hunger

2. Atherosclerosis : leads to CAD, MI, CVA and peripheral

vascular disease

3. Ocular Disorders
• Cataracts
• Diabetic retinopathy

4. Peripheral neuropathy
*HYPOGLYCEMIA
*DIABETIC KETOACIDOSIS (DKA)

*HYPERGLYCEMIC HYPEROSMOLAR
NONKETOTIC SYNDROME (HHNS)
*sweating
*tremor
*tachycardia
*palpitations
*nervousness
*hunger
• 3 or 4 commercially prepared glucose tablets
• CHILD: 2 - 3 GLUCOSE TABS
• 4 - 6 ounces of fruit juice or regular soda
• CHILD: ½ CUP OR 120 ML OF ORANGE
JUICE OR SUGAR-SWEETENED JUICE
• 6 - 10 Life Savers or hard candy
• CHILD: 3 - 4 HARD CANDIES OR 1 CANDY
BAR
• 2 - 3 teaspoons of sugar or honey
• CHILD: 1 SMALL BOX OF RAISINS
 Signs & symptoms of
hypoglycemia

Release of adrenalin from CNS –

sweating, pallor, tachycardia,
palpatation, tremors, nervousness
CNS depression – headaches, confusion,
emotional changes, memory lapse,
drowsiness, lack of coordination,
staggering gait, convulsions,
comatose
Management of Hypoglycemia
Patient is conscious and can swallow
give simple sugars like : oranges juices,
candy, glucose tablet , lump of sugar
Semi-conscious and can’t take oral sugar
Subcutaneous or IM Glucagon
If doesn’t respond to above measure : 50 ml of
50% glucose IV or 1000ml of 5-10% glucose
in water
Diabetic Ketoacidosis (DKA)
Acute complication of diabetes : hyperglycemia
and accumulation of ketones in the body
resulting to acidosis. KUSSMAUL BREATHING
• is the rapid, deep, and
Type 1 diabetes labored breathing of people
• whopolyuria
Polydipsia, polyphagia, have ketoacidosis or
• who are in a diabetic coma.
Kussmaul’s respiration
• Also called "air hunger."
• Acetone breath – fruity odor of the breath
• N & V, abdominal pain
• Warm, flushed dry skin
• Hypotension, tachycardia
• Increased serum glucose and ketones
• Metabolic acidosis
Assessment:

*3 Ps
*Blurred Vision
*Weakness
*Headache
*Hypotension
*Weak, rapid pulse
*Anorexia, nausea, vomiting & abdominal pain
*Acetone breath (fruity odor)
*Kussmaul respirations
*Mental status changes
Management
Maintain patent airway
Maintain fluid and electrolyte balance.
Provide insulin
Keep client warm
Protect from coma
Test blood sugar every 2 hours

A- Airway
F - Fluids
I - Insulin
 Hyperglycemic Hyperosmolar
Nonketotic Coma

Acute complication of diabetes :

hyperglycemia without accumulation of
ketones.

Type 2 DM

Similar to DKA, but without the ketones

*Prevent moisture from accumulating between toes
*Wear loose socks & well-fitting (not tight) shoes &
instruct client not to go barefoot
*Change into clean cotton socks daily
*Wear socks to keep feet warm
*Do not wear the same shoes 2 days in a row
*Do not wear open toed shoes or shoes with strap that
goes between toes
*Check shoes for tears or cracks in lining & for foreign
objects before putting them on
*Break in new shoes gradually
*Cut toenails straight across & smooth nails with an
emery board
*Do not smoke
*Meticulous skin care & proper foot care
*Inspect feet daily & monitor feet for redness, swelling or
break in skin integrity
*Avoid thermal injuries from hot water, heating pads &
baths
*Wash feet with warm (not hot) water and dry thoroughly
(avoid foot soaks)
*Do not soak feet
*Do not cross legs or wear tight garments that may
constrict blood flow
*Apply moisturizing lotion to feet but not between toes
*Take insulin or oral hypoglycemic agents as prescribed
*Test blood glucose & test the urine for ketones every 3 - 4
hours
*If meal plan cannot be followed, substitute with soft food
6 - 8 x per day
*If vomiting, diarrhea or fever occurs, consume liquids
every ½ to 1 hour to prevent dehydration & to provide
calories
*Notify doctor if vomiting, diarrhea, or fever persists, if
blood glucose levels are greater than 250 to 300 mg/dL,
when ketonuria is present for more than 24 hours, when
unable to take food or fluids for a period of 4 hours, when
illness persists for more than 2 days
 Herbal Alert
1. BITTER MELON
• for diabetes
• potentiates effects of sulfonylureas, insulin & other
antidiabetic meds
2. GINSENG (PANAX)
• combats physical effects of stress
• Helps treat impotence and infertility in men, boosts
energy
• used to stimulate the adrenal gland, and thereby
increase energy
• beneficial effect on reducing blood sugar .in patients
with diabetes mellitus
• Monitor glucose level.
3. Basil, Bay, Bee pollen, Burdock & Sage
• Affect glycemic control. Monitor glucose level
closely.