Endocrine Disorders Nio C. Noveno, RN, MAN, MSN 8/13/2009

ENDOCRINE DISORDERS 8/13/2009
Nio C. Noveno, RN, MAN, MSN
1 ENDOCRINE DISORDERS nionoveno@yahoo.com
ENDOCRINE GLANDS
Pituitary gland
Adrenal glands
Pancreatic islets
Thyroid glands
Parathyroid glands
Gonads
NLE Review, 2009 1

ENDOCRINE SYSTEM
ENDOCRINE GLANDS
Secrete their products directly into the bloodstream
Different from exocrine glands
Exocrine glands: secrete through ducts onto epithelial surfaces
or into the gastrointestinal tract
HORMONES
Chemical substances secreted by endocrine glands
Can travel moderate to long distances or very short
distances
Act only on cells or tissues that have receptors specific
for them
Target organ: the cell or tissue that responds to a
particular hormone
HYPOTHALAMUS AND
PITUITARY GLAND
NLE Review, 2009 2

REGULATION OF HORMONES:
NEGATIVE FEEDBACK MECHANISM
If the client is healthy, the concentration or hormones is
maintained at a constant level.
When the hormone concentration rises, further

production of that hormone is inhibited.
When the hormone concentration falls, the rate of

production of that hormone increases.
Diseases of the Endocrine System
“Primary” disease
problem in target gland; autonomous
“Secondary” disease
problem outside the target gland; most often due to a
problem in the pituitary gland
Disorders of the
Anterior Pituitary
HYPOPITUITARISM
HYPERPITUITARISM
NLE Review, 2009 3

HYPOPITUITARISM
Caused by low levels of one or more anterior pituitary

hormones
Lack of the hormone leads to loss of function in the gland

or organ that it controls.
Causes of Primary Hypopituitarism

Pituitary tumors
Inadequate blood supply to pituitary gland
Sheehan syndrome
Infections and/or inflammatory diseases
Sarcoidosis
Amyloidosis
Radiation therapy
Surgical removal of pituitary tissue
Autoimmune diseases
Congenital absence
Causes of secondary hypopituitarism

(affecting the hypothalamus):
Tumors of the hypothalamus
Inflammatory disease
Head injuries
Surgical damage to the pituitary and/or blood vessels or

nerves leading to it
NLE Review, 2009 4

Signs and Symptoms

Tumor: bitemporal
hemianopsia on visual
confrontation
Varying signs of hormonal

disturbances depending on
which hormones are being
under secreted
Signs and Symptoms

Gonadotropin deficiency
Congenital onset
Delayed or absent secondary sexual characteristics
May have micropenis, cryptorchidism
Acquired
Loss of body hair
Infertility, decreased libido, impotence in males, amenorrhea in females
Osteopenia, muscle atrophy
Prolactin deficiency
Failure to lactate
Signs and Symptoms

Thyroid-stimulating (TSH) deficiency
Causes hypothyroidism with manifestations such as fatigue,
weakness, weight change, and hyperlipidemia
Adrenocorticotropic hormone (ACTH) deficiency

Results in diminished cortisol secretion
Symptoms include weakness, fatigue, weight loss, and
hypotension
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Signs and Symptoms

Growth hormone (GH)
deficiency
In childhood; failure to
grow
In adulthood; mild to
moderate central obesity,
increased systolic blood
pressure, and increases in
LDL cholesterol
Diagnostics
X-ray, MRI or CT scan:
pituitary tumor
Plasma hormone levels:

decreased
Treatment
Surgery for tumors: transsphenoidal hypophysectomy
Radiation therapy for tumors
Hormonal substitution: maybe for life
Corticosteroids
Levothyroxine
Androgen for males
Estrogen for females
Growth hormone
NLE Review, 2009 6

HYPERPITUITARISM
Hyperfunction of the anterior pituitary gland →
oversecretion of one or more of the anterior pituitary
hormones
Usually caused by a benign pituitary adenoma
Most common hormones affected:
Prolactin
Growth hormone
PROLACTINOMA
Female: galactorrhea,
menstrual disturbances,
infertility, signs of estrogen
deficit (vaginal mucosal
atrophy, decreased vaginal
lubrication and libido)
Male: decreased libido and

possible impotence,
reduced sperm count and
infertility, gynecomastia
Growth Hormone Hypersecretion

Gigantism
GH hypersecretion prior to closure of the epiphyses;
proportional growth
Acromegaly
GH hypersecretion after closure of epiphyses; disproportional
growth
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Gigantism vs. Acromegaly
Gigantism vs. Acromegaly
Growth Hormone Hypersecretion:

Signs and Symptoms
Enlarged hand and feet; carpal tunnel syndrome common
Coarsening of features esp. in acromegaly; prominent
mandible, tooth spacing widens
Macroglossia
Hypertension, cardiomegaly, heart failure
Insulin resistance → DM
Visual fields defect: bitemporal hemianopsia → complete
blindness
Headaches
Arthritis
Hypogonadism
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Clinical Manifestations
Arthritis
Chest is barrel-shaped
Rough facial features
Odd sensations in the hands and feet
Muscle weakness & fatigue
Enlargement of organs
Growth of coarse hair
Amenorrhea; breast milk production
Loss of vision; headaches
Impotence; increased perspiration
Snoring
Treatment
Medication
Bromocriptine and cabergoline (dopamine agonist) for
prolactinoma and GH hypersecretion
Ocreotide (somatostatin) for GH hypersecretion
Surgery
Transsphenoidal hypophysectomy
Radiation therapy for large tumors
Diet
NURSING INTERVENTIONS
Provide emotional support → striking body change can
cause psychological stress
Perform or assist with range of motion exercises to

promote maximum joint mobility and prevent injury
Evaluate muscle weakness
NLE Review, 2009 9

NURSING INTERVENTIONS
Keep the skin dry
Be aware that pituitary tumor may cause visual problems.
Warn relatives that hyperpituitarism can cause inexplicable

mood changes
If the patient is a child, explain to the parents that surgery

prevents permanent soft-tissue deformities but won’t correct
bone changes that have already occurred.
Emphasize the importance of continuing hormonal

replacement therapy.
Disorders of the
Posterior Pituitary
Diabetes Insipidus
SIADH
Vasopressin or Antidiuretic Hormone

Regulate water
metabolism
Released during stress or

in response to an increase
in plasma osmolality to
stimulate reabsorption of
water and decreased urine
output
NLE Review, 2009 10

Diabetes Insipidus
Disorder characterized by
massive polyuria due to
either lack of ADH or
kidney’s insensitivity to it
Types:
Central DI
Nephrogenic DI
Diabetes Insipidus
Central diabetes insipidus: Deficiency of vasopressin
Primary diabetes insipidus

Maybe familial, occurring as a dominant trait, or sporadic (“idiopathic”)
Secondary diabetes insipidus

Due to damage to the hypothalamus or pituitary stalk by tumor,
surgical or accidental trauma, infection
Diabetes Insipidus
“Nephrogenic” DI
Due to defect in the kidney
tubules that interferes with
water absorption
Polyuria is unresponsive to
vasopressin
Patients have normal
secretion of vasopressin
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ADH
Diabetes Insipidus
SIGNS AND SYMPTOMS
Polyuria
Polydipsia
Dehydration
Inadequate water replacement
hyperosmolality
hypovolemia
Diabetes Insipidus
DIAGNOSTICS
Fluid deprivation test
Administration of desmopressin
24 hour urine collection for volume, glucose, and creatinine
Serum for glucose, urea nitrogen, calcium, uric acid, potassium,
sodium
NLE Review, 2009 12

Diabetes Insipidus
MEDICATIONS
For Central DI
Desmopressin; intranasal
Lypressin; intranasal
Vasopressin tannate in oil; IM
For Nephrogenic DI
Indomethacin-hydrochlorothiazide
Indomethacin-desmopressin
Indomethacin-amiloride
Clofibrate, chlorpropamide
Psychotherapy
Diabetes Insipidus:
Nursing Management
Maintain fluid and sodium balance
Record I and O. Weigh patient daily.
Maintain fluid intake to prevent severe dehydration
WOF: dehydration and shock
Keep the side rails up and assist with walking if the patient is
dizzy or has muscle weakness
Monitor urine specific gravity between doses. Watch for
decreased specific gravity with increased urine output.
Add more bulk food and fruit juices to diet
Diabetes Insipidus:
Nursing Management
Provide meticulous skin and mouth care, an apply a lubricant to
cracked or sore lips
Diet: low in sodium
Carry out drug therapy
Caution with vasopressin if coronary disease is present →
vasoconstriction
Assist in searching for the underlying pathology
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Syndrome of Inappropriate Antidiuretic Hormone

(SIADH)
Disorder due to excessive ADH release

Signs and symptoms:
Persistent excretion of concentrated urine
Signs of fluid overload
Change in level of consciousness
Hyponatremia
No edema
Causes of SIADH
Tumors Pulmonary
Bronchogenic CA TB
Lymphoma Pneumonia
Pancreatic cancer Lung abscess
Mesothelioma COPD
Pneumothorax
P. carinii pneumonia
Causes of SIADH
CNS Drugs
Meningitis Vincristine
Subdural hematoma Phenothiazines
Subarachnoid hemorrhage Tricyclic antidepressants
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(SIADH): Diagnostic Tests
Low serum sodium < 135 meq/LO
Low serum osmolality
High urine osmolality ( >100 mOsmol/kg)
High urine sodium excretion ( >20 mmol/L)
Normal renal function (low BUN <10 mg/dL)

(SIADH): Management
Maintain fluid balance
Restriction of water intake
If the patient has evidence of fluid overload – loop diuretics

(Furosemide) is added.
Chronic treatment: Lithium or demeclocycline
Monitoring of body weight

(SIADH): Management
Maintain sodium balance
Increase sodium intake
If the serum sodium is below 120 or if the patient is seizing,
emergency treatment of 3% NaCl followed by furosemide
Excessive rapid correction of hyponatremia may cause central
pontine myelinolysis
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Hypernatremia
Skin flushed
Agitation
Low-grade fever
Thirst
Disorders of the
Thyroid Gland
Hyperthyroidism
Hypothyroidism
The Thyroid Gland

A butterfly-shaped organ
located anterior to trachea
Consists of two lateral lobes
connected by an isthmus
About 5 cm long, 3 cm wide
and weighs about 30 grams
Produces three hormones
Thyroxine (T4)
Triiodothyronine (T3)
Calcitonin
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Function of Thyroid Hormones

T4 and T3
Control the cellular
metabolic activity
T4 maintains body
metabolism in a steady state
T3, 5x more potent than T4,
has more rapid metabolic
action
Influence cell replication and
are important in brain
development
Regulated by TSH
Function of Thyroid Hormones

Calcitonin
Produced by parafollicular
cells of the thyroid gland
Reduces plasma Ca2+
levels by increasing its
deposition in bones
(mineralization)
Tests of Thyroid Function

Thyroid-Stimulating Hormone
Single best screening test because of high sensitivity
Normal levels: 0.38 and 6.15 mcU/mL
If TSH normal – free thyroxine (FT4) is normal
Used for monitoring thyroid hormone replacement
therapy
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Serum Free Thyroxine
Used to confirm an abnormal TSH
A direct measurement of free thyroxine, the only
metabolic fraction of T4
Normal levels:
0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L)

Total Serum T3 and T4
Normal range for total serum T4:
4.5 to 11.5 ug/dl (58.5 to 150 nmol/L)
T3 level appears to be a more accurate indicator of
hyperthyroidism.
Normal range for total serum T3:
70 to 220 ng/dl (1.15 to 3.10 nmol/L)

Thyroid scan, Radioscan, or Scintiscan
A scintillation detector or gamma camera moves back
and forth across the area to be studied and a visual image
is made of the distribution of radioactivity in the area
being scanned
Isotopes used
¹²³I – most commonly used isotope
Technetium-99m pertechnetate, thallium, americium
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Radioactive Iodine Uptake (RAIU)
Measures the rate of iodine uptake by the thyroid gland
The patient is administered a tracer dose of iodine-123
Measures the proportion of the administered dose
present in the thyroid gland at a specific time after
administration
Hyperthyroidism → high uptake of ¹²³I
Hypothyroidism → very low uptake
Fine Needle Aspiration

Biopsy
Sampling thyroid tissue to

detect malignancy
Initial test for evaluation

of thyroid masses

Nursing Implications of Thyroid Tests
It is necessary to determine whether the patient has
taken medications or agents that contain iodine because
these alter the results of some of the scheduled tests.
Assess for allergy to iodine or shellfish.
For the scans, tell patient that radiation is minimal.
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Hyperthyroidism
Increased metabolic rate
Causes:
Grave’s disease
Initial manifestation of thyroiditis
Toxic adenoma
TSH screening pituitary tumor
Factitious thyrotoxicosis
Amiodarone induced
Hyperthyroidism:
Signs and Symptoms
Enlarged thyroid gland Nervousness and fine
Tachycardia tremors of hands
Hypertension Hyperactive reflexes, body
Heat intolerance, weakness
diaphoresis Personality changes, mood
Smooth, soft, warm skin swings
Fine soft hair Clubbing and swelling of
fingers (Plummer’s nails)
Diarrhea, weight loss
inspite of increased Menstrual disturbances,
appetite decreased infertility
Osteoporosis
Signs and Symptoms of Grave’s Disease

All S/S of thyrotoxicosis
Exophthalmos → vision loss, diplopia
Nonpitting pretibial and pedal edema
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Thyroid Storm
A medical emergency: high mortality
Marked delirium, severe tachycardia, vomiting, diarrhea,
dehydration, high fever
Occurs in patients with existing but unrecognizable
thyrotoxicosis, stressful illness, thyroid surgery, RAI
Increased systemic adrenergic activity – epinephrine
overproduction and severe hypermetabolism
Hyperthyroidism: Diagnostics
Radioimmunoassay test shows elevated T4 and T3
Thyroid scan reveals increased radioactive iodine (¹²³I)
uptake
↓ TSH in primary hyperthyroidism
↑ TSH in secondary hyperthyroidism
Orbital sonography and computed scan confirm
subclinical ophthalmopathy
Hyperthyroidism: Management
Antithyroid drug therapy
Propylthiouracil (PTU) and methimazole
Used for pregnant women and patient who refused surgery or
RAI treatment
During pregnancy PTU – preferred therapy
A few (1%) of the infants born to mothers receiving antithyroid
medication will be hypothyroid
Mechanism of action: blocks thyroid hormone synthesis
WOF agranulocytosis
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Radioactive iodine (¹³¹I), potassium or sodium iodide,
strong iodine solution (Lugol’s solution)
Adjunct with other antithyroid drugs in preparation for
thyroidectomy
Treatment for thyrotoxic crisis
Mechanism of action
Inhibits the release and synthesis of thyroid hormones
Decreases vascularity of the thyroid gland (KI)
Decreases thyroidal uptake of RAI
Hyperthyroidism:
Nursing Management
Potassium or sodium iodide, strong iodine solution
Dilute oral doses in water or fruit juice and give with
meals to prevent gastric irritation, to hydrate the patient,
and to mask the very salty taste
Warn the patient that sudden withdrawal may precipitate
thyrotoxicosis.
Store in light resistant container.
Give iodides through a straw to avoid teeth discoloration.
Force fluids to prevent fluid volume deficit.
Hyperthyroidism: Nursing Management of RAI

treatment
Food may delay absorption.The patient should fast
overnight before administration.
After dose for hyperthyroidism, the patients urine and
saliva are slightly radioactive for 24 hours; vomitus is
highly radioactive for 6 to 8 hours.
Institute full radiation precautions during this time.
Instruct the patient to use appropriate disposal methods
when coughing and expectorating.
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treatment
After dose for thyroid cancer, isolate the patient and
observe the following precautions:
Pregnant personnel shouldn’t take care of the patient
Disposable eating utensils and linens should be used
Instruct the patient to save all urine in lead containers for 24
to 48 hours so amount of radioactive material excreted can be
determined
Or flush the toilet twice after urination

treatment
The patient should drink as much fluid as possible for 48
hours after drug administration to facilitate excretion
Limit contact with the patient to 30 minutes per shift per
person the 1st day; may increase time to 1 hour on 2nd
day and longer on 3rd day

treatment
If the patient is discharged less than 7 days after ¹³¹I dose
for thyroid cancer, warn patient
To avoid close, prolonged contact with small children
Not to sleep in the same room with his spouse for 7 days after
treatment → increase risk of thyroid cancer in persons
exposed to ¹³¹I.
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B-blockers, Digoxin, anticoagulation
Prednisone for ophthalmopathy
Treatment for thyroid storm
PTU
I.V. propranolol (Inderal) to block sympathetic effects
Corticosteroids to replace depleted cortisol levels
Iodide to block release of thyroid hormone
Surgery: thyroidectomy
Preop: give Lugol’s iodide to prevent thyroid storm
Care of post-thyroidectomy client
Monitor for respiratory distress
Have tracheotomy set, oxygen, and suction at bedside
Semi-fowlers position
Monitor for laryngeal nerve damage
Monitor for signs of hypocalcemia and tetany
Monitor for thyroid storm
Hyperthyroidism:
Nursing Management
Record vital signs and weight
Monitor serum electrolyte levels, and check periodically
for hyperglycemia and glycosuria
Monitor cardiac function
Check levels of consciousness and urine output
If patient is in her 1st trimester of pregnancy: report for
signs of spontaneous abortion
Diet
High protein, high calorie, vitamin supplements
Low sodium diet for patients with edema
No stimulants like coffee, tea
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Hyperthyroidism:
Nursing Management
For exophthalmos
Suggest sunglasses or eye patches to protect eyes from light
Moisten the conjunctivae with artificial tears
Warm the patient with severe lid retraction to avoid sudden
physical movement that might cause the lid to slip behind the
eyeball
Elevate the head of the bed to reduce periorbital edema
Stress the importance of regular medical follow-up after
discharge because hypothyroidism may develop
Drug therapy and RAI therapy require careful monitoring
and comprehensive teaching
Hypothyroidism
Hypothyroidism
A state of low serum thyroid hormone levels or cellular
resistance to thyroid hormone
Causes:
May result from thyroidectomy
Radiation therapy
Chronic autoimmune thyroiditis
Inflammatory conditions
Pituitary failure to produce TSH
Hypothalamic failure to produce thyrotropin-releasing hormone
(TRH)
Inborn errors of thyroid hormone synthesis
Antithyroid medications such as PTU
Inability to synthesize thyroid hormone because of iodine deficiency
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Hypothyroidism:
Signs and Symptoms
Weakness
Fatigue
Forgetfulness
Cold intolerance
Unexplained weight gain
Constipation
Goiter
Slow speech
Decreasing mental stability
Cool, dry, coarse, flaky,
inelastic skin
Hypothyroidism:
Signs and Symptoms
Puffy face, hands, feet
Dry, sparse hair
Thick, brittle nails
Slow pulse rate
Anorexia
Abdominal distention
Menorrhagia
Decreased libido
Infertility
Ataxia, Intention tremor
Congenital hypothyroidism
Myxedema Coma
Manifests as hypotension, bradycardia, hypothermia,
hyponatremia, hypoglycemia, respiratory failure, coma
Can be precipitated by acute illness, rapid withdrawal if
thyroid medication, anesthesia, surgery, hypothermia, use
of opioids
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Hypothyroidism: Diagnostics
Radioimmunoassay tests: ↓ T3 T4
↑ TSH level with primary hypothyroidism
↓ TSH level with secondary hypothyroidism
Serum cholesterol and triglyceride levels are increased
In myxedema coma
Low serum sodium levels
Respiratory acidosis because of hypoventilation
Hypothyroidism: Management
Prevention: prophylactic iodine supplements to decrease
the incidence of iodine deficient goiter
Symptomatic cases:
Hormonal replacement: synthroid (synthetic hormone
(Levothyroxine))
Dosage is increased q 2-3 weeks esp. if the patient is an elderly
Nursing Management
of replacement therapy
Different brands of levothyroxine may not be
bioequivalent
Warn the patient to tell the doctor if
Chest pain, palpitations, sweating, nervousness, or their signs or
symptoms of overdosage
Signs and symptoms of aggravated cardiovascular disease
(chest pain, dyspnea, tachycardia)
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Nursing Management
Instruct the patient to take thyroid hormones at the same
time each day to maintain constant hormone levels
Suggest a morning dosage to prevent insomnia
Monitor apical pulse and blood pressure. If pulse is >100,
withhold the drug. Assess for tachyarrhytmias and chest
pain.
Nursing Management
Thyroid hormones alter thyroid function test results
For ¹²³I uptake studies
D/C levothyroxine 4 wks before the test
D/C liothyronine 7 to 10 days before the test
Monitor prothrombin time
WOF: unusual bleeding and bruising
Hypothyroidism:
Nursing Interventions
Diet: high-bulk, low calorie diet
Encourage activity
Maintain warm environment
Administer cathartics and stool softeners
To prevent myxedema coma, tell the patient to continue
course of thyroid medication event if symptoms subside
Maintain patent airway
Administer medications – synthroid, glucose, corticosteroids
IV fluid replacement
Wrap patient in blanket
Treat infection or any underlying illness
NLE Review, 2009 28

Disorders of the
Parathyroid Glands
Hyperparathyroidism
Hypoparathyroidism
Parathyroid glands
Hyperparathyroidism
Characterized by excess
activity or one or more of
the four parathyroid
glands, resulting in
excessive secretion of
parathyroid hormone
(PTH)
May be primary or
secondary
NLE Review, 2009 29

Hyperparathyroidism: Causes
Primary hyperparathyroidism:
Single adenoma, genetic disorders, or multiple endocrine
neoplasias
Secondary hyperparathyroidism:
Rickets, vitamin D deficiency, chronic renal failure, or phenytoin
or laxative abuse
Hyperparathyroidism
Effect of PTH secretion: ↑ calcium
Through increased bone resorption, increased GI and renal
absorption of calcium
Complications
Renal calculi → renal failure
Osteoporosis
Pancreatitis
Peptic ulcer
Hyperparathyroidism: Signs and Symptoms

Think of Hypercalcemia:
CNS; psychomotor and personality disturbances, loss of
memory for recent event, depression, overt psychosis, stupor
and, possibly coma
GI: anorexia, nausea, vomiting, dyspepsia, and constipation
Neuromuscular: fatigue, marked muscle weakness and atrophy,
particularly in the legs
NLE Review, 2009 30

Hyperparathyroidism: Signs and Symptoms

Renal: symptoms of recurring nephrolithiasis → renal
insufficiency
Skeletal and articular: chronic lower back pain and easy
fracturing from bone degeneration, bone tenderness, joint pain
Others: skin pruritus, vision impairment from cataracts,
subcutaneous calcification
Hyperparathyroidism: Diagnostics
↑ serum PTH levels
↑ serum calcium and ↓ phosphorus levels
X-rays may show diffuse demineralization of bones
Elevated alkaline phosphatase
Hyperparathyroidism: Treatment
Surgery to remove adenoma
Force fluids: limiting dietary calcium intake
For life threatening hypercalcemia: promote sodium and
calcium excretion, using normal saline solution,
furosemide; and administering oral sodium or potassium
phosphate, calcitonin
Postmenopausal women: estrogen supplements
NLE Review, 2009 31

Hypoparathyroidism
A deficiency of parathyroid hormone (PTH)
PTH primarily regulates calcium balance;
hypoparathyroidism leads to hypocalcemia and produces
neuromuscular symptoms ranging from paresthesia to
tetany
Hypoparathyroidism: Causes
Congenital absence or malfunction of the parathyroid
glands
Autoimmune destruction
Removal or injury to one or more parathyroid glands
during neck surgery
Massive thyroid radiation therapy
Ischemic infarction of the parathyroids during surgery
Hypoparathyroidism:
Signs and Symptoms
Neuromuscular irritability
Increased deep tendon reflexes
Dysphagia
Paresthesia
Tetany seizures
Psychosis
NLE Review, 2009 32

Hypoparathyroidism:
Signs and Symptoms
Arrhythmias
Abdominal pain
Dry, lusterless hair
Brittle fingernails
Dry and scaly skin
Weakened tooth enamel
Hypoparathyroidism:
Diagnostic tests
↓ PTH and serum calcium levels
↑ serum phosphorus levels
X-rays reveal increased bone density
ECG: prolonged QTi, QRS-complex and ST-elevation
changes
Hypoparathyroidism: Treatment
Vitamin D with supplemental calcium
Lifelong therapy, except for patient with the reversible
form of the disease
Acute life-threatening tetany calls for immediate IV
administration of calcium
Sedatives and anticonvulsants are given to control spasms
until calcium levels rise
Seizure precautions
NLE Review, 2009 33

Disorders of the
Pancreas
Diabetes Mellitus
The Pancreas
Hormones of the Pancreas

Insulin
Decreases blood sugar by:
Stimulating active transport of glucose into muscle and adipose tissue
Promoting the conversion of glucose to glycogen for storage
Promoting conversion of fatty acids into fat
Stimulating protein synthesis
Secreted in response to high blood sugar
Found in β cells of the Islets of Langerhans
NLE Review, 2009 34

Hormones of the Pancreas

Glucagon
Increases blood glucose by stimulating hepatic gluconeogenesis
and glycogenolysis
Secreted in response to low blood sugar
Found in the α-cells of the Islets of

Langerhans
Diabetes Mellitus
Chronic disease characterized by hyperglycemia
Either due to total or partial insulin deficiency or due to

insensitivity of the cells to insulin
Characterized by disorders in the metabolism of CHO,

fats, and CHON
NLE Review, 2009 35

Types of Diabetes Mellitus

Type 1
Usually occurs in children or in non-obese adults
Type 2
Usually occurs in obese adults or over age 40
Gestational DM
Secondary DM
Induced by trauma, surgery, pancreatic disease or medications
Can be treated as either type 1 or type 2
Pathophysiology
Lack of insulin causes hyperglycemia (insulin is necessary
for the transport of glucose across the membrane)
Body excretes excess glucose through kidneys →

osmotic diuresis → polyuria → dehydration → polydipsia
Cellular starvation → polyphagia
The body turns to fats and proteins for energy; but in the
absence of glucose in the cell, the fats cannot be
completely metabolized and ketones are produced
NLE Review, 2009 36

Chronic Complications
Microangiopathy:
Retinopathy
Nephropathy
Macroangiopathy
peripheral vascular disease
atherosclerosis
CAD
Neuropathy
Instruction in the Care of the Feet

Hygiene of the feet
Wash feet daily with mild soap and lukewarm water. Dry
thoroughly between the toes by pressure. Do not rub
vigorously, as this is apt to break the delicate skin.
Rub well with vegetable oil to keep them soft, prevent excess
friction, remove scales, and prevent dryness.
If the feet become too soft and tender, rub them with alcohol
about once week.

Hygiene of the feet
When rubbing the feet, always rub upward from the tips of the toes.
If varicose veins are present, massage the feet very gently; never
massage the legs.
If the toenails are brittle and dry, soften them by soaking for 1 ½
hour each night in lukewarm water containing 1 tbsp of powdered
sodium borate (borax) per quart.
Clean around the nails with an orangewood stick. If the nails become
too long, file them with an Amery board. File them straight across
and no shorter than the underlying soft tissue of the toes. Never cut
the corner of the nails.
NLE Review, 2009 37


Wear low heeled shoes of soft leather that fit the shape
of the feet correctly.
Wide toes that will cause no pressure, fit close in the arch, and
grip the heels snugly.
Wear new shoes one-half hour only on the first day and
increase by 1 hour each following day.
Wear thick, warm, loose stockings.

Treatment of corns and calluses
Corns and calluses are due to friction and pressure, most often
from improperly fitted shoes and stockings. Wear shoes that fit
properly and cause no friction or pressure.
To remove excess calluses or corns, soak the feet in lukewarm

water, using a mild soap, for about 10 minutes and then rub off
the excess tissue with a towel or file. Do not tear it off.
No to skin irritation

Treatment of corns and calluses
Do not cut corns or calluses. If they need attention it is safer
to see a podiatrist.
Prevent callus formation under the ball of the foot:

by exercise, such as curling and stretching the toes several times a day;
by finishing each step on the toes and not on the ball of the foot; and
by wearing shoes that are not too short and that do not have high
heels.
NLE Review, 2009 38

Diagnostics: FBS and OGTT

Normal Impaired
glucose Diabetes
glucose
mellitus
tolerance tolerance
Fasting
<110 110-125 ≥ 126
Plasma
Glucose mg/dl mg/dl mg/dl
2 hours < 140 ≥ 140 but < ≥ 200

after
mg/dl 200 mg/dl mg/dl
glucose
Diagnostics:
Glycosylated hemoglobin
Reflects effectiveness of management

of hyperglycemia
< 7.5% (good control)
7.6% - 8.9% (fair control)
> 9% (poor control)
Therapeutic Interventions
Life-style changes
Weight control and exercises
Planned diet
50 – 60% of calories are complex carbohydrates, high fiber
12 – 20% daily calories is CHON
Fat intake not to exceed 30% of daily calories, more of
monounsaturated fats
Basic tools: food exchange groups
Self-monitoring of blood glucose
NLE Review, 2009 39

Therapeutic Interventions
Insulin administration
Type 1 IDDM and type 2 DM when diet and weight control
therapy failed
Aspirin, alcohol, oral anticoagulants, oral hypoglycemics, beta

blockers, tricyclic antidepressants, tetracycline, MAOIs increase
the hypoglycemic effects of insulin
Glucocorticoids, thiazide diuretics, thyroid agents, oral

contraceptives increase blood glucose levels
Illness, infection, and stress increase the need for insulin
Insulin Administration
Insulin Onset Peak Duration
Ultra rapid acting insulin analog (Humalog) 10-15 min 1 hour 3 hours
SAI (Humulin regular) ½ - 1 hour 2-4 hrs 4-6 hrs
IAI (Humulin lente, Humulin NPH) 3-4 hrs 4-12 hrs 16-20 hrs
LAI (Protamine zinc, Humulin ultralente) 6-8 hrs 12-16 hrs 20-30 hrs
Premixed insulin (70% NPH, 30% regular) ½-1 hour 2-12 hrs 18-24 hrs
Complications of Insulin Therapy

Local allergic reaction, lipodystrophy, insulin resistance
Dawn phenomenon
Increase in blood sugar because of release of growth hormone
at around 3AM
Tx: Give at 10PM, intermediate-acting insulin
Somogyi effect
Rebound hyperglycemia at 7 AM after a bout of hypoglycemia
at around 2-3AM
Tx: Decrease evening dose of intermediate-acting insulin
NLE Review, 2009 40

Complications of Insulin Therapy

Hypoglycemia
If awake, give 10-15 g of fast-acting simple juice carbohydrate
(glucose tablets, fruit juice, and soda)
If unconscious, glucagon SQ or IM
If in the hospital, 25-50 cc of D50%
Oral Hypoglycemic Agents

For NIDDM (type 2)
May have to be shifted to insulin when sick, under stress,

during surgery
Necessary to shift to insulin when pregnant
Oral Hypoglycemic Agents

Sulfonylureas
Promotes increase insulin secretion from pancreatic beta cells
through direct stimulation
First Generation Agents:
Tolbutamide, Acetohexamide, Tolzamide, Chlorpropamide
Second Generation Agents
Glipizide, Glyburide
NLE Review, 2009 41

Oral Hypoglycemics
Biguanides
Reduces hepatic production of glucose by inhibiting
glycogenolysis
Decrease the intestinal absorption of glucose and improving
lipid profile
Agents:
Phenformin, Metformin, Buformin
Oral Hypoglycemics
Alpha-glucosidase inhibitors
Inhibits alpha-glucosidase enzymes in the small intestine and
alpha amylase in the pancreas
Decreases rate of complex carbohydrate metabolism resulting
to a reduced rate postprandially
Agents:
Acarbose (precose), Miglitol (glyset)
Oral Hypoglycemics
Thiazolidinediones
Enhances insulin action at the cell and post-receptor site and
decreasing insulin resistance
Agents:
Pioglitazone (Actos)
Rosiglitazone (Avandia)
NLE Review, 2009 42

The client is TIRED!

remors
T achycardia
Hypoglycemia is blood
Irritability glucose level <50 mg/dL or a
sudden drop of blood
Restlessness glucose level
E xcessive hunger
xcitability
Diaphoresis Causes:
Overtreated hyperglycemia
Increased exercise
β-blockers
Gastric paresis
Alcohol intake
Erratic insulin absorption
Clinical management for hypoglycemia

Mild:
Shakiness 10-15 gm carbohydrate
Tremors
Excessive hunger 4 oz. orange juice
Paresthesias 6 oz. regular soda
Pallor 6-8 oz 2% skim milk
Diaphoresis 1 small (2 oz.) tube of cake
icing

Moderate:
Drowsiness
Impaired judgment 20-30 gm carbohydrate
Double or blurred vision
Glucagon 1 mg SQ/IM
Headache
Inability to concentrate
Mood swings
Irritability
Slurred speech
NLE Review, 2009 43


Severe:
Seizures
Unconsciousness 25 gm D50 dextrose IV
Disorientation
Glucagon 1 mg IM/IV
Acute Complication: DKA

Characterized by hyperglycemia and accumulation of
ketones in the body causing metabolic acidosis
Occurs in insulin-dependent diabetic client
Precipitating factors: undiagnosed diabetes, neglect of

treatment, infection, other physical or emotional stress
Onset slow, maybe hours to days
DKA: Signs and Symptoms

Polydipsia, polyphagia and polyuria
Nausea and vomiting, abdominal pain
Skin warm, dry and flushed
Dry mucous membrane
Kussmaul’s respirations or hyperventilation; acetone
breath
Alterations in LOC
Hypotension
Tachycardia
NLE Review, 2009 44

Hyperglycemic Hyperosmolar Nonketotic Coma

(HHNK)
Characterized by hyperglycemia and a hyperosmolar state
without ketosis
Occurs in NIDDM or non-diabetic persons (typically

elderly persons)
Precipitating factors: undiagnosed diabetes, infection, or

other stress; certain medications, dialysis,
hyperalimentation, major burns
Diabetic KetoAcidosis [DM Type-1]

Ketoacidosis To correct:
Urinary changes Regular insulin drip
Sunken eyeballs 0.9% or 0.45% NSS
Skin is warm & flushed 1:1
100 units: 100 cc
Membranes are dry
Nursing care:
Arrhythmias
Check glucose
Upset GI system
250-300 mg/dL [q30-
Low BP 60mins]
Saline solution 250 mg/dL
DC the drip
Hyperglygemic hyperosmolar
nonketotic come (HHNK) [DM Type-II]
NON
Ketosis is absent
Electrolyte imbalance [K+ decrease]
Thirst
Obtundation
Treat with regular insulin drip
Inform client of diet
Correct hyperglycemia
NLE Review, 2009 45

Nephropathy
Normal creatinine?
Erythrocyte sedimentation rate [ESR: 0-20 mm/hr]
Poor glycemic control
Hemodialysis
Restrict: Na+, CHON, K+, weight
Output & input (MIO)
No symptoms; initially
Retinopathy
Reduced O2 in the eye
Elevated sugar & BP
Tension in the retina is high
Increased lens opacity
NO eyesight
Annual eye examination [every 6-12 months]
Neuropathy
Sensorimotor: paresthesia [foot care]
Focal nerve compression: weakness or loss of sensation: CN
palsy; CTS [2-12 months recovery; surgery]
Autonomic:
GI: gastroparesis & diarrhea [metoclopramide: 10 mg PO ac
& hs for 2-8 wk PRN; high fiber; NO milk]
GU: incontinence [bladder training]; impotence/retrograde
ejaculation [implants & medications]; dyspareunia
[lubricants]
CARDIAC: low BP; increased HR [fludrocortisone, salt]
NLE Review, 2009 46

Emergency Management:
For both DKA and HHNK, treat dehydration first with
0.9% or 0.45% saline solution
Shift to D5W when glucose level is down to 250-300mg/dl
WOF rapid correction, it can cause rapid fluid shifts (brain
edema and increased ICP, ARDS)
IV regular insulin 0.1 unit/kg bolus then 0.1 unit/kg/h drip
Correcting electrolyte imbalance:
WOF hypokalemia as a result of treatment
Disorders of the Adrenal Glands
Cushing’s Syndrome
Hyperaldosteronism
Adrenal Insufficiency
Pheochromocytoma
Adrenal Glands
NLE Review, 2009 47

Adrenal Medulla
Release cathecholamines
Epinephrine
Norephinephrine
Released during “fight or

flight” situations
(sympathetic effect)
Adrenal Cortex Hormones

Glucocorticoids
Cortisol, corticosterone
Increase blood glucose levels by increasing rate of
gluconeogenesis
Increase protein catabolism
Increase mobilization of fatty acids
Promote sodium and water retention
Anti-inflammatory effect
Aid the body in coping with stress

Mineralocorticoids
Aldosterone, Corticosterone, Deoxycorticosterone
Regulate fluid and electrolyte balance
Stimulate reabsorption of sodium, chloride and water
Stimulate potassium excretion
Under the control of Renin-Angiotensin-Aldosterone
system (RAAS)
NLE Review, 2009 48


Sex hormones
Androgens, Estrogens
Influences the development of sexual characteristics
Hypercortisolism
(Cushing’s Syndrome)
Cluster of physical abnormalities due to excessive
cortisol release
Cortisol excess may be due to:

Autonomous steroid release from adrenals
Increased ACTH release from pituitary
Complication from exogenous steroid tx
NLE Review, 2009 49

Hypercortisolism
(Cushing’s Syndrome)
Altered metabolism
Na and H2O retention
CHO: hyperglycemia
Hypokalemia, hypocalcemia
CHON: muscle wasting,
thin, fragile skin, impaired Acne, hirsutism, menstrual
wound healing changes, decreased libido
Fats: central obesity, moon

face, buffalo hump
Hypercortisolism (Cushing’s Syndrome)
NLE Review, 2009 50

Complications
Osteoporosis
Peptic ulcer
Immune and inflammatory response is also compromised
Other complications include HPN, and sexual and
psychological complications
BUFFALO HUMP
Buffalo hump
Unusual behavior (depression,
personality changes,
fatigability)
Hypertension, hyperglycemia,
Facial features (moonface, hypernatremia
hirsutism in women)
Urinary cortisol elevated
Fat (obesity)
Menstrual irregularities
ACTH and cortisol in blood
elevated;ACTH and Porosity of bones
dexamethasone test (osteoporosis)
abnormalities
Loss of muscle mass
Overextended skin (abdominal
striae with easy bruisability)
Cushing’s Syndrome: Diagnostics

ACTH level determines whether the syndrome is ACTH-
dependent.
24-hr urine collection for cortisol, midnight serum
cortisol
Dexamethsone suppression test:
1 mg dexamethasone is given at 11 pm and serum cortisol
taken at 8 AM the next day
Radiologic evaluation
NLE Review, 2009 51

Cushing’s Syndrome: Management

Transsphenoidal resection of pituitary tumor
Medications:
Aminogluthetimide: adrenal enzyme inhibitor
Metyrapone and ketokonazole: suppress hypercortisolism in
unresectable adrenal tumor
Antihypertensives
Adrenalectomy as needed
Cushing’s Syndrome:
Nursing Considerations
Monitor VS, WOF for HPN
Safety precaution:
Maintain muscle tone
Prevent accidents or falls and provide adequate rest
Protect client from exposure to infection, monitor WBC
Maintain skin integrity
Minimize stress
Provide diet low in calories, sodium, and high in protein,
potassium, calcium and Vitamin D
Monitor for urine glucose and acetone, administer insulin if
necessary
Prepare client for adrenalectomy if needed
Hyperaldosteronism
Hypersecretion of aldosterone from the adrenal cortex
Two types:
Primary disease of the adrenal cortex
Secondary condition due to increased plasma renin activity
Causes:
Excessive reabsorption of sodium and water
Excessive renal excretion of potassium
NLE Review, 2009 52

Hyperaldosteronism: Causes
Primary aldosteronism: autonomous secretion of
aldosterone from adrenals
Benign adrenal adenoma (Conn’s syndrome)
Bilateral adrenocortical hyperplasia
Hyperaldosteronism: Causes
Secondary hyperaldosteronism: high renin state →
stimulating aldosterone release
Renal artery stenosis
Wilm’s tumor
Pregnancy
Oral contraceptive use
Nephritic syndrome
Cirrhosis with ascites
Idiopathic edema
Heart failure
Extrarenal sodium loss
Hyperaldosteronism: Signs and Symptoms

Hypertension
Headache and visual disturbance
Hypokalemia
Muscle weakness and fatigue
Paresthesia and arrhythmias
Polyuria and polydipsia
Tetany from alkalosis
Hypernatremia
NLE Review, 2009 53

Hyperaldosteronism: Diagnostics
Hypokalemia (<3.5 meq/L)
Hypernatremia (>145 meq/L)
Elevated serum bicarbonate and pH
Hypomagnesemia
Elevated plasma and urinary aldosterone
↓ Renin in primary hyperaldosteronism
↑ Renin in secondary hyperaldosteronism
Low specific gravity urine (diluted urine)
Hyperaldosteronism: Treatment
Primary aldosteronism:
Unilateral adrenalectomy
Potassium-sparing diuretic
Antihypertensives
Aminogluthemide
Diet: sodium restriction, increase potassium
Treatment of secondary hyperaldosteronism
Adrenal Insufficiency
Addison’s disease- the most common form of adrenal
hypofunction
Autoimmune process, circulating antibodies react

specifically against the adrenal tissue
Acute adrenal insufficiency, or adrenal crisis (Addisonian

crisis) is a medical emergency requiring immediate,
vigorous treatment
NLE Review, 2009 54

Adrenal Insufficiency: Causes

Autoimmune destruction of the adrenal gland,
tuberculosis, bilateral adrenalectomy, hemorrhage into the
adrenal gland, neoplasm, fungal infection
Secondary adrenal hypofunction

Hypopituitarism
Abrupt withdrawal of long-term corticosteroid therapy
Adrenal Insufficiency:
Signs and Symptoms
Weakness, fatigue
Weight loss, nausea and vomiting, anorexia
Chronic constipation or diarrhea
Cardiovascular abnormalities
Postural hypotension, decreased heart size and cardiac output
Weak, irregular pulse
Decreased tolerance for minor stress
NLE Review, 2009 55

Signs and Symptoms
Conspicuous bronze skin coloration
Poor coordination
Fasting hypoglycemia: and craving for salty food
Amenorrhea
Adrenal crisis
Diagnostic tests
Decreased plasma cortisol and serum sodium levels
Increased ACTH (in Addison’s), serum potassium, and

blood urea nitrogen level
Adrenal Insufficiency : Treatment

Corticosteroid replacement
Fludrocortisone acetate – acts as mineralocorticoid to

prevent dehydration and hypotension
Adrenal crisis: prompt IV bolus of corticosteroids, 3 to 5

L of IV fluids, dextrose
NLE Review, 2009 56

Nursing Management
WOF adrenal crisis
Hypotension and signs of shock
Decreased level of consciousness and urine output
WOF hyperkalemia before treatment and for hypokalemia
after treatment (from excessive mineralocorticoid effect)
If patient has diabetes, check blood glucose levels

periodically because replacement may necessitate
changing the insulin dosage
Nursing Management
Diet: maintain sodium and potassium balance, high
protein, and carbohydrates
If the patient is anorexic, suggest six small meals per day
to increase calorie intake
Observe the patient receiving steroids for cushingoid
signs, such as fluid retention around the eyes and face
Adrenal insufficiency:
Nursing Management
Instruct on lifelong cortisone replacement therapy. “Do
not omit medications”. Give 2/3 of dose in AM and 1/3 in
PM
Instruct the patient that he’ll need to increase the dosage
during times of stress
Warn that infection, injury, profuse sweating may
precipitate crisis
NLE Review, 2009 57

Pheochromocytoma
Rare disorder, a chromaffin-cell tumor of the sympathetic
nervous system, usually in the adrenal medulla, secretes
an excess of the catecholamine epinephrine and
norepinephrine
Causes episodes of hypertension and symptoms of
catecholamine excess
Usually benign but may be malignant
Pheochromocytoma
Pheochromocytoma:
Signs and Symptoms
Think sympathetic!
Persistent or paroxysmal hypertension
Palpitations, tachycardia, headache, visual disturbance,

diaphoresis, pallor, warmth or flushing, paresthesia, tremor,
excitation
Anxiety, fright, nervousness, feelings of impending doom,

abdominal or chest pain, tachypnea, nausea and vomiting,
fatigue, weight loss, constipation
NLE Review, 2009 58

Pheochromocytoma:
Diagnostics
Increased plasma levels of catecholamines, elevated blood

sugar, glucosuria
Elevated urinary catecholamines and urinary

vanillylmandelic acid levels
Avoid coffee, nuts, chocolates, banana
Tumor on CT scan
Pheochromocytoma: Treatment
Surgical removal of the tumor with sparing of normal
adrenals
WOF: hypo or hypertension post-op
Antihypertensives
Alpha-adrenergic blocker
Beta-adrenergic blocker
Calcium channel blockers
Metyrosine may be used to block catecholamine synthesis
Adrenalectomy
Resection or removal of one or both adrenal glands
The treatment of choice:

For adrenal hyperfunction and hyperaldosteronism
Adrenal tumors, such as adenomas and pheochromocytomas
NLE Review, 2009 59

Adrenalectomy: Pre-op
Correct electrolyte imbalance
Potassium
Sodium
Calcium
Manage hypertension
Adrenalectomy: Post-op
Monitor vital signs
WOF: shock from hemorrhage
Keep in mind that post-op hypertension is common
because of handling of the adrenal glands stimulate
catecholamine release
WOF: adrenal crisis – hypotension, hyponatremia,
hyperkalemia
Adrenalectomy:
Nursing Interventions
Instruct the patient to take prescribed medication as
directed
If patient had unilateral adrenalectomy, explain that he

may be able to taper his medication in a few months
Inform patient that sudden withdrawal of steroids can

precipitate adrenal crisis
NLE Review, 2009 60

Endocrine Disorders Nio C. Noveno, RN, MAN, MSN 8/13/2009

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ENDOCRINE DISORDERS 8/13/2009

Nio C. Noveno, RN, MAN, MSN

1 ENDOCRINE DISORDERS nionoveno@yahoo.com

2 ENDOCRINE DISORDERS nionoveno@yahoo.com

3 ENDOCRINE DISORDERS nionoveno@yahoo.com

NLE Review, 2009 1

4 ENDOCRINE DISORDERS nionoveno@yahoo.com

5 ENDOCRINE DISORDERS nionoveno@yahoo.com

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NLE Review, 2009 2

When the hormone concentration rises, further

When the hormone concentration falls, the rate of

7 ENDOCRINE DISORDERS nionoveno@yahoo.com

Diseases of the Endocrine System

8 ENDOCRINE DISORDERS nionoveno@yahoo.com

9 ENDOCRINE DISORDERS nionoveno@yahoo.com

NLE Review, 2009 3

Caused by low levels of one or more anterior pituitary

Lack of the hormone leads to loss of function in the gland

10 ENDOCRINE DISORDERS nionoveno@yahoo.com

Causes of Primary Hypopituitarism

11 ENDOCRINE DISORDERS nionoveno@yahoo.com

Causes of secondary hypopituitarism

Surgical damage to the pituitary and/or blood vessels or

12 ENDOCRINE DISORDERS nionoveno@yahoo.com

NLE Review, 2009 4

Signs and Symptoms

Varying signs of hormonal

13 ENDOCRINE DISORDERS nionoveno@yahoo.com

Signs and Symptoms

14 ENDOCRINE DISORDERS nionoveno@yahoo.com

Signs and Symptoms

Adrenocorticotropic hormone (ACTH) deficiency

15 ENDOCRINE DISORDERS nionoveno@yahoo.com

NLE Review, 2009 5

Signs and Symptoms

16 ENDOCRINE DISORDERS nionoveno@yahoo.com

Plasma hormone levels:

17 ENDOCRINE DISORDERS nionoveno@yahoo.com

18 ENDOCRINE DISORDERS nionoveno@yahoo.com

NLE Review, 2009 6

19 ENDOCRINE DISORDERS nionoveno@yahoo.com

Male: decreased libido and

20 ENDOCRINE DISORDERS nionoveno@yahoo.com

Growth Hormone Hypersecretion

21 ENDOCRINE DISORDERS nionoveno@yahoo.com

NLE Review, 2009 7

Gigantism vs. Acromegaly

22 ENDOCRINE DISORDERS nionoveno@yahoo.com

Gigantism vs. Acromegaly

23 ENDOCRINE DISORDERS nionoveno@yahoo.com

Growth Hormone Hypersecretion:

24 ENDOCRINE DISORDERS nionoveno@yahoo.com

NLE Review, 2009 8

25 ENDOCRINE DISORDERS nionoveno@yahoo.com

26 ENDOCRINE DISORDERS nionoveno@yahoo.com

Perform or assist with range of motion exercises to

Evaluate muscle weakness

27 ENDOCRINE DISORDERS nionoveno@yahoo.com

NLE Review, 2009 9

Be aware that pituitary tumor may cause visual problems.

Warn relatives that hyperpituitarism can cause inexplicable