ENDOCRINE SYSTEM

ENDOCRINE SYSTEM
The endocrine system
integrates body functions
by the synthesis and
release of hormones.
The functions of the
endocrine and the nervous
system are interrelated.
Hypothalamus: link
between the nervous
system and the
endocrine system.
ENDOCRINE GLANDS
Pituitary Gland
Adrenal Glands
Pancreas
Thyroid Glands
Parathyroid
Glands
Gonads
Endocrine System
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
are chemical substances that are
secreted by the endocrine glands.
can travel moderate to long distances or
very short distances.
acts only on cells or tissues that have
receptors for the specific hormone.
Target Organ: The cell or tissue that
responds to a particular hormone
Hypothalamus and
Pituitary Gland
Pituitary gland: “Master Gland”
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.
The Hormones of the
Anterior Pituitary
(Adenohypophysis)
Growth Hormone
Growth hormone
aka Somatotropin
Stimulates growth of
body tissues and
bones
Increases
breakdown of fatty
acid in adipose
tissue
Increases blood
sugar
ACTH and Adrenals
ACTH
Stimulates the adrenal cortex to
produce and release
adrenocorticoids, esp. Cortisol, as
well as growth of adrenal glands
ACTH has little effect on
aldosterone
TSH and Thyroid gland

Stimulates growth of thyroid gland

and release of thyroid hormones
FSH, LH  Gonads
 FSH, LH  Gonads
FSH: Stimulates growth, maturation, and
function of primary and secondary sex organs
including production of estrogen and
testosterone
LH: Works with FSH in final maturation of
follicles; promotes ovulation and
progesterone secretion; maintains corpus
luteum and progesterone secretion
Melanocyte Stimulating Hormone

Controls the degree of pigmentation by

acting on the melanocytes on the skin
Prolactin
Stimulates breastmilk
production
 Hormones of the
Posterior Pituitary
(Neurohypophysis)
Vasopressin or Antidiuretic
Hormone
Regulates water
metabolism
Released during stress
or in response to an
increase in plasma
osmolality to stimulate
reabsorption of water
and decreased urine
output
Summary: Effect of ADH
 Oxytocin

Stimulates uterine contractions during

delivery and the release of milk in lactation
Hormones of the
Adrenal Glands
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
Adrenal Cortex Hormones
Mineralocorticoids
– Aldosterone, Corticosterone, Deoxycorticosterone
– Regulate fluid and electrolyte balance
– Stimulate reabsorption of sodium, chloride and
water
– Stimulate potassium excretion
Under the control of the Renin-Angiotensin-
Aldosterone system
Adrenal Cortex Hormones
Sex Hormones
– Androgens, Estrogens
– Influences the development of sexual
characteristics
Summary: Adrenal Cortex
Hormones
Sugar
Salt
Sex
Adrenal Medulla
Releases
catecholamines
– Epinephrine
– Norepinephrine
Released during
“fight or flight”
situations 
SYMPATHETIC
effect
Hormones of the
Thyroid Gland
Hormones of the Thyroid Gland
T3(Triiodothyronine)
T4 (Thyroxine)
– Regulate metabolic rate
– Regulate Carbohydrate, Fat and Protein
metabolism
– Aid in regulating physical and mental
growth and development
Under the direct control of TSH
Hormones of the Thyroid Gland
Thyrocalcitonin
– Lowers serum calcium by increasing bone
deposition
Controlled by calcium level
 Hormone of the
Parathyroid Glands
Hormone of the Parathyroid
Glands
PTH
– Regulates serum calcium and phosphate
levels
– Increases serum calcium level by bone
resorption, increased GI absorption, and
increased renal reabsorption of calcium
– Secretion is controlled by serum calcium
level
Hormones of 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
Hormones of the Pancreas
Glucagon
– Increases blood glucose by
• causing gluconeogenesis and glycogenolysis
in the liver
– Secreted in response to low blood sugar
– Found in the α-cells of the Islets of
Langerhans
The Gonadal Hormones
The Gonadal Hormones
Estrogen
– Development of secondary sex
characteristics in the female
– Maturation of sex organs
– sexual functioning
Progesterone
– maintenance of pregnancy
The Gonadal Hormones
Testosterone
– Development of secondary sex
characteristics in the male
– Maturation of sex organs
– Sexual functioning
Diseases of the Endocrine
System
Primary” Disease  problem in target
organ; autonomous

“Secondary” disease  most often due

to a problem in pituitary gland
Disorders of the
Pituitary Gland

Hypopituitarism
Hyperpituitarism
SIADH
Diabetes Insipidus
Hypopituitarism

Caused by low levels of one or more anterior

pituitary hormones.
May result from destruction of the anterior
lobe of the pituitary gland.
Panhypopituitarism (Sheehan syndrome or
Simmonds’ disease) is total absence of all
pituitary secretion and is rare.
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
– e.g. Sheehan syndrome
infections and/or inflammatory diseases
– sarcoidosis
– amyloidosis
radiation therapy
surgical removal of pituitary tissue
autoimmune diseases
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
Signs and Symptoms
The visual tract
Tumor: bitemporal
hemianopia 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
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.
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
Signs and Symptoms
Panhypopituitarism
– Absence of all anterior pituitary hormones
– Patients with long-standing hypopituitarism
tend to have dry, pale, finely textured skin.
– Face has fine wrinkles and an apathetic
countenance
Diagnostics
X-ray, MRI or CT
scan: pituitary tumor
Plasma hormone
levels: decreased
Treatment
Hormonal Substitution: may be for life
– Corticosteroids
– Levothyroxine
– Androgen for males
– Estrogen for females
– Growth hormone
Radiation therapy for tumors
Surgery for tumors: Transsphenoidal
hypophysectomy
Nursing Intervention
Provide care for the client undergoing
hypophysectomy or radiation therapy if
indicated
Provide client teaching and discharge
planning concerning hormone
replacement therapy and importance of
follow up care
Hyperpituitarism
Hyperfunction of the anterior pituitary
gland  oversecretion of one or more
of the anterior pituitary hormones
Usually caused by a benign pituitary
adenoma
2 most common hormones affected:
– Prolactin
– Growth hormone
Pituitary Tumor:

Prolactinoma Somatotropinoma
Prolactinoma
Female: menstrual
disturbances, infertility,
galactorrhea, ovarian steroid
deficit manifestations
( 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 Acromegaly: GH
hypersecretion prior hypersecretion after
to closure of closure of
epiphyses; epiphyses;
proportional growth disproportional
growth
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  OSA
Hypertension, cardiomegaly, heart failure
Insulin resistance DM
Visual field defects: bitemporal
hemianopsiacomplete blindess
Headaches
Arthritis
Hypogonadism
Treatment
Medication
– Bromocriptine and cabergoline (dopamine agonist) for
prolactinoma and GH hypersecretion
– Octreotide (somatostatin) for GH hypersecretion
Surgery
– Surgical remission is achieved in about 70% of patients
followed over 3 years.
– Growth hormone levels fall immediately; diaphoresis and
carpal tunnel syndrome often improve within a day after
surgery.
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, especially in the patient
with late-stage acromegaly.
Keep the skin dry. Avoid using an oily lotion because
the skin is already oily.
Be aware that pituitary tumor may cause visual
problems. If there is hemianopia, stand where he can
see you.
Nursing Interventions
Hyperpituitarism can cause inexplicable mood changes.
Reassure that family that these mood changes result
from the disease and can be modified with treatment.
Before surgery, reinforce what the surgeon has told the
patient and try to allay the patient’s fear with a clear and
honest explanation of the scheduled operation.
If the patient is a child, explain to the parents that such
surgery prevents permanent soft-tissue deformities but
won’t correct bone changes that have already occurred.
Before discharge, emphasize the importance of
continuing hormone replacement therapy.
Transsphenoidal hypophysectomy
Transsphenoidal hypophysectomy
Endoscopic, transnasal, transsphenoidal pituitary
microsurgery removal of adenoma while preserving
anterior pituitary function in most patients.
Transsphenoidal surgery is usually well tolerated,
but complication occur in about 10% (infection,
CSF leak, and hypopituitarism)
Hyponatremia can occur 4-13 days postoperatively
and is manifested by nausea, vomiting, headache,
malaise, or seizure.
Diabetes insipidus may occur
Postoperative Care
Keep the patient on bed rest for 24 hours after
surgery and encourage ambulation
Keep the head of bed elevated to avoid placing
tension or pressure on the suture line.
Instruct patient not to sneeze, cough, blow his
nose, or bend over for several days to avoid
disturbing the suture line.
Mild analgesics for headache cause by CSF
loss during surgery or for paranasal pain.
Paranasal pain typically subsides when the
catheters and packing are removed, usually 24
to 72 hours after surgery. Provide oral care.
Postoperative Care
Anticipate that the patient may develop
transient diabetes insipidus, usually 24 to 48
hours after surgery.
Be alert for increased thirst and increased
urine volume with a low specific gravity.
If diabetes insipidus occurs, replace fluids
and administer aqueous vasopressin, or give
sublingual desmopressin acetate, as ordered.
Diabetes insipidus may resolve within 72
hours.
Postoperative Care
WOF: Hyponatremia 4-13 days post-op.
Dietary salt supplements for 2 weeks
postoperatively may prevent this complication.
WOF: CSF leak, infection, hemorrhage
Arrange for visual field testing as soon as
possible because visual defects can indicate
hemorrhage.
Advise the patient not to brush his teeth for 2
weeks to avoid suture line disruption.
Patient may need hormonal replacement
therapy due to decreased pituitary secretion
of tropic hormones.
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 (without an
identifiable organic lesion noted on MRI of the
pituitary and hypothalamus)
• May be familial, occurring as a dominant trait, or
sporadic (“idiopathic”).
– Secondary diabetes insipidus
• Due to damage to the hypothalamus or pituitary stalk by
tumor, anoxic encephalopathy, surgical or accidental
trauma, infection (encephalitis, tuberculosis, syphilis),
sarcoidosis, or multifocal Langerhans cell (eosinophilic)
granulomatosis (“histiocytosis X”).
DIABETES INSIPIDUS
– Vasopressin-induced diabetes insipidus
• May be seen in the last trimester of pregnancy and in
puerperium
• Associated with oigohydramnios, preeclampsia, or
hepatic dysfunction.
“Nephrogenic” Diabetes Insipidus
– Due to defect in the kidney tubules that interferes
with water reabsorption.
– Polyuria is unresponsive to vasopressin.
– Patients have normal secretion of vasopressin
DIABETES INSIPIDUS
Signs and Symptoms
Polyuria  enormous daily output of very dilute, water-
like urine with a specific gravity of 1.001 to 1.005
Intense thirst (patient tends to drink 4 to 40 liters of fluid
daily), especially with a craving for ice water,
Dehydration  weight loss, poor tissue turgor, dry
mucous membranes, constipation, muscle weakness,
dizziness.
Inadequate water replacement results in
– Hyperosmolality (irritability, mental dullness, coma,
hyperthermia) because of dehydration and
hypernatremia
– Hypovolemia (hypotension, tachycardia, and shock
eventually)
DIABETES INSIPIDUS
Diagnostics
Fluid deprivation test  to differentiate
between psychogenic polydipsia and DI
Administration of desmopressin  to
differentiate between central DI and
nephrogenic DI
24-hour urine collection for volume, glucose,
and creatinine
serum for glucose, urea nitrogen, calcium,
uric acid, potassium and sodium.
DIABETES INSIPIDUS
Management Objectives
– to replace vasopressin ( long-term
therapeutic program)
– to ensure adequate fluid replacement
– to search for and correct the underlying
intracranial pathology
DIABETES INSIPIDUS
Medications
For central DI
– Desmopressin (DDAVP): intranasal
– Lypressin: intranasal
– Vasopressin tannate in oil: IM
For nephrogenic DI:
– Indomethacin-hydrochlorothiazide (with potassium
supplementation)
– indomethacin-desmopressin
– indomethacin-amiloride
Clofibrate, chlorpropamide and thiazide diuretics
(mild DI)
Psychotherapy
DIABETES INSIPIDUS: Nursing
Management
Record I and O. Weight patient daily.
Maintain fluid intake to prevent severe dehydration.
WOF: signs of hypovolemic shock, and monitor blood
pressure and heart and respiratory rates regularly,
especially during the water deprivation test.
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  need for the next dose or a dosage increase.
Add more bulk foods and fruit juices to the diet  to
prevent constipation. Laxative (milk of magnesia) prn.
DIABETES INSIPIDUS: Nursing
Management
Provide meticulous skin and mouth care, and
apply a lubricant to cracked or sore lips.
Make sure caloric intake is adequate and the
meal plan is low in sodium.
Support to patient and family, especially those
undergoing studies for a possible cranial lesion.
Instruct about follow-up care and emergency
measures.
Wear a medical identification bracelet and to
carry medication and information about this
disorder at all times.
Caution must be used with administration of
vasopressin if coronary artery disease is present
 causes vasoconstriction.
Syndrome of Inappropriate
Antidiuretic Hormone (SIADH)
Disorder due to excessive ADH release
Patients with this disorder cannot excrete dilute urine.
They retain fluid and develop a sodium deficiency
(dilutional hyponatremia).

Signs and symptoms:

– Persistent excretion of concentrated urine
– Signs of fluid overload
– Change in level of consciousness
– NO EDEMA
– HYPONATREMIA
Syndrome of Inappropriate Antidiuretic
Hormone (SIADH): Causes of SIADH
Tumors: bronchogenic carcinoma, lymphoma,
pancreatic cancer, mesothelioma
Pulmonary: TB, pneumonia, lung abscess, COPD,
pneumothorax, HIV infection
CNS: meningitis, head injury, subdural hematoma,
subarachnoid hemorrhage, neurosurgery
Drugs: Some medications (vincristine,
phenothiazines, tricyclic antidepressants, thiazide
diuretics, and others) and nicotine have been
implicated in SIADH; they either directly stimulate the
pituitary gland or increase the sensitivity of renal
tubules to circulating ADH
Syndrome of Inappropriate
Antidiuretic Hormone (SIADH):
Diagnostic Tests
low serum sodium (<135 meq/L0
low serum osmolality
high urine osmolality (urine osmolality >100
mosmol/kg)
high urine sodium excretion (>20 mmol/L)
Normal renal function (low BUN <10 mg/dL),
absence of hypothyroidism and glucocorticoid
deficiency and recent diuretic therapy.
Syndrome of Inappropriate Antidiuretic
Hormone (SIADH): Medical
Management
Restriction of water intake (500 ml/day).
If the patient has evidence of fluid
overloading, a history of CHF, or is
resistant to treatment, loop diuretics
(Furosemide) may be added as well. 
Chronic treatment: lithium or
demeclocycline which inhibit ADH
action.
Monitoring of body weight
Syndrome of Inappropriate
Antidiuretic Hormone (SIADH):
Medical Management
If the serum sodium is below 120 or if the patient
is seizing, emergency treatment is
administration of 3%
sodium chloride solution to raise the serum sodiu
m to 125
. May be followed by furosemide.
Excessively rapid correction of hyponatremia may
cause central pontine myelinolysis.
– Central pontine myelinolysis (CPM) is a rare
demyelinating condition of the pons
– Patients with a plasma sodium concentration
greater than 125 mmol/l rarely need specific
therapy for hyponatremia.
Syndrome of Inappropriate
Antidiuretic Hormone (SIADH):
Nursing Management
Close monitoring of fluid intake and output,
daily weight, urine and blood chemistries, and
neurologic status is indicated for the patient
at risk for SIADH.
Educate her about the need for fluid
restriction (< 1 liter/day) Fluid restriction takes
3 to 10 days to start working
Assess her neurologic status to monitor for
improvement, deterioration, or new problems.
Syndrome of Inappropriate Antidiuretic
Hormone (SIADH): Nursing Management

Administer medications as ordered.

– Antineoplastic therapy helps manage SIADH by
destroying the SCLC cells that produce ectopic
antidiuretic hormone (ADH).
Demeclocycline, 600 to 1,200 mg/day,
with or without fluid restriction for
moderate SIADH (serum sodium 115 to
125 mEq/liter).
– Adverse reactions: infection, photosensitivity,
nausea, hepatotoxicity, and a reversible, dose-
related diabetes insipidus syndrome.
Syndrome of Inappropriate Antidiuretic
Hormone (SIADH): Nursing Management
Severely decreased sodium levels (less
than 115 mEq/liter) can cause severe, even
life-threatening signs and symptoms.
– The patient requires intensive nursing
care, diuresis, and intravenous (I.V.)
therapy with hypertonic (3% to 5%)
sodium chloride solution, and
chemotherapy.
Institute seizure precautions and teach your
patient's family how to respond to seizures
Disorders of the Thyroid
Gland

Hyperthyroidism
Hypothyroidism
The Thyroid Gland
Thyroid gland is a butterfly-shaped organ located in
the lower neck anterior to the trachea.

•It consists of two lateral

lobes connected by an
isthmus.
•The gland is about 5 cm
long and 3 cm wide and
weighs about 30 g.
•It produces three
hormones: thyroxine (T4)
and triiodothyronine
(T3), and calcitonin.
Function of Thyroid Hormones
T4 and T3
Control the cellular metabolic activity.
T4, a relatively weak hormone, maintains body metabolism in a
steady state.
T3, is about five times as potent as T4 and has a more rapid
metabolic action.
Accelerates metabolic processes.
Influence cell replication and are important in brain development.
Necessary for normal growth.

Calcitonin
Or thyrocalcitonin, secreted in response to high plasma levels of
calcium and it reduces the plasma level of calcium by increasing
its deposition in bone.
Tests of Thyroid Function
Thyroid-Stimulating Hormone
Single best screening test of thyroid function because
of its high sensitivity.
Values above the normal range of 0.38 to 6.15
uU/mL are indicative of primary hypothyroidism, and
low values indicate hyperthyroidism
If TSH is normal, there is a 98% chance that the free
thyroxine (FT4) is also normal.
Used for monitoring thyroid hormone replacement
therapy and for differentiating between disorders of
the thyroid gland and disorders of the pituitary or
hypothalamus.
Tests of Thyroid Function
Serum Free Thyroxine
Test used to confirm an abnormal TSH is FT4.
FT4 is a direct measurement of free (unbound) thyroxine, the only
metabolically active fraction of T4.
The range of FT4 in serum is normally between 0.9 and 1.7 ng/L
(11.5 to 21.8 pmol/L).

Serum T3 and T4
Normal range for T4 is between 4.5 and 11.5 ug/dL (58.5 to 150
nmol/L).
Although serum T3 and T4 levels generally increase or decrease
together, the T3 level appears to be a more accurate indicator of
hyperthyroidism, which causes a greater rise in T3 than T4 levels.
Normal range for serum T3 is 70 to 220 ng/dL (1.15 to 3.10 nmol/L)
Tests of Thyroid Function
Radioactive Iodine Uptake
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 its
administration.
Affected by the patient’s intake of iodide or thyroid
hormone; therefore, a careful preliminary clinical
history is essential in evaluating results.
hyperthyroidism  high uptake of the 123 I
hypothyroidism  very low uptake.
Tests of Thyroid Function
Thyroid scan, Radioscan, or Scintiscan
In a thyroid scan, 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, and
americium
Scans are helpful in determining location, size,
shape, and anatomic function of the thyroid gland,
particularly when thyroid tissue is substernal or large.
Identifying areas of increased function (“hot” areas)
or decreased function (“cold” areas) can assist in
diagnosis.
Tests of Thyroid Function
Fine-Needle Aspiration
Biopsy
Sampling thyroid tissue
to: detect malignancy.
Initial test for evaluation
of thyroid masses.
Results are reported as
(1) negative (benign),
(2) positive (malignant),
(3) indeterminant
(suspicious), and (4)
inadequate
(nondiagnostic)
Tests of Thyroid Function
Other Diagnostic Tests
Achilles tendon reflex time: measures period
of contraction and relaxation of Achilles
tendon reflex)
Serum cholesterol levels
Electrocardiogram (ECG)
Muscle enzyme studies (ALT, LDH, CK)
Ultrasound
CT scanning
MRI
Tests of Thyroid Function
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
Hyperthyroidism
Or Thyrotoxicosis
Increased metabolic rate
Causes:
– Grave’s disease
– Initial manifestations of thyroiditis
(Hashimoto’s and subacute thyroiditis)
– Toxic Adenoma
– TSH-secreting pituitary tumor
– Factitious thyrotoxicosis
– Jodbasedow disease
– Amiodarone-induced
Hyperthyroidism: Signs and
symptoms
Enlarged thyroid gland
Tachycardia  atrial fibrillation, heart failure
Hypertension
Heat intolerance, diaphoresis
Smooth, soft, warm skin
Fine, soft hair
Diarrhea, weight loss inspite of increased appetite
Nervousness and fine tremors of hands
Hyperactive reflexes, body weakness
Personality changes, mood swings
Osteoporosis
Clubbing and swelling of fingers, Plummer’s nails
Menstrual disturbances, decreased infertility
Signs and symptoms of Grave’s
Disease
All s/s of
thyrotoxicosis
Grave’s
exophthalmos 
vision loss,
diplopia
Pretibial
myxedema
Thyroid Storm
A medical emergency : high mortality
Marked delirium, severe tachycardia,
vomiting, diarrhea, dehydration, high
fever
Occurs in patients with existing but
unrecognized thyrotoxicosis, stressful
illness, thyroid surgery, RAI
administration
increased systemic adrenergic activity 
epinephrine overproduction and severe
hypermetabolism
Hyperthyroidism: Diagnostics
Radioimmunoassay test shows
elevated T4 and T3.
Thyroid scan reveals increased
radioactive iodine (123 I) 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 refuse
surgery or 131I treatment.
During pregnancy PTU, is the preferred therapy
A few (1%) of the infants born to mothers
receiving antithyroid medication will be
hypothyroid.
Mechanism of action
– Blocks thyroid hormone synthesis
Hyperthyroidism: Management
Nursing considerations
Give the drug with meals to reduce GI effects
Watch for signs of hypothyroidism (mental
depression, cold intolerance, hard, nonpitting
edema)
WOF: Agranulocytosis
– Warn the patient to immediately report
fever, sore throat, or mouth sores
– Agranulocytosis can develop too rapidly
to be detected by periodic blood cell
counts
Hyperthyroidism: Management
Instruct patient to report for skin eruptions
(sign of hypersensitivity)
The drug should be stopped if severe rash
develops or cervical lymph nodes become
enlarged
Advise patient to avoid foods high in iodine
(seafood, iodized salt, cabbage, kale, turnips)
or potassium
Warn the patient against the use of the over-
the-counter medication; many contain iodine
Store the drug in a light-resistant container
Hyperthyroidism: Management
Radioactive iodine (sodium iodide)131 I, potassium
or sodium iodide (potassium iodide SSKI), 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 the vascularity of the thyroid gland
– Decreases thyroidal uptake of radioactive iodine following
radiation emergencies or administration of radioactive
isotopes of iodine
Hyperthyroidism: Nursing
Management
Potassium or sodium iodide, (potassium iodide
solution, SSKI), strong iodine solution (Lugol’s
solution) Category D
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 a light-resistant container
Give iodides through a straw to avoid tooth
discoloration
Force fluids to prevent fluid volume deficit
Hyperthyroidism: Nursing
Management of RAI treatment
Radioactive iodine (sodium iodide or 131I )
– Category X
Food may delay absorption. The patient should fast
overnight before administration
After dose for hyperthyroidism, the patient’s 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.
Hyperthyroidism: Nursing
Management of RAI 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
Hyperthyroidism: Nursing
Management of RAI 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.
Hyperthyroidism: Nursing
Management of RAI treatment
If the patient is discharged less than 7
days after 131 I 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 
increased risk of thyroid cancer in persons
exposed to 131 I.
Hyperthyroidism: Management
B-blockers, Digoxin, anticoagulation
Prednisone for ophthalmopathy
Treatment for thyroid storm:
– PTU
– I.V. propranolol to block sympathetic effects
– Corticosteroids to replace depleted cortisol
levels
– Iodide to block release of thyroid hormone
Hyperthyroidism: Management
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-Fowler’s position
– Monitor for laryngeal nerve damage (respiratory
obstruction, dysphonia, high-pitched voice, stridor,
dysphagia, restlessness)
– Monitor for signs of hypocalcemia and tetany
• Prepare to administer calcium gluconate or calcium
chloride as prescribed for 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 level of consciousness and urine output
If patient is in her first trimester of pregnancy, report
signs of spontaneous abortion (spotting and occasional
mild cramps) to the doctor immediately.
Diet
– high protein, high calorie diet, with six meals per day and
vitamin supplements.
– Low sodium diet for the patients with edema.
– No stimulants like coffee, tea
Hyperthyroidism: Nursing
Management
For exophthalmos
– suggest sunglasses or eye patches to protect his eyes from
light
– Moisten the conjunctivae often with artificial tears
– Warn 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
from 2 to 4 weeks postoperatively.
Drug therapy and 131 I therapy require careful
monitoring and comprehensive teaching.
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 (Hashimoto’s disease)
inflammatory conditions such as amyloidosis and
sarcoidosis
pituitary failure to produce TSH
hypothalamic failure to produce thyrotropin-releasing
hormone (TRH).
Inborn errors of thyroid hormone synthesis
an inability to synthesize thyroid hormone because of
iodine deficiency
use of antithyroid medications such as propylthiouracil.
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
Nystagmus
Hypothyroidism: Signs and
Congenital
symptoms Hypothyroidism
Puffy face, hands and feet
Periorbital edema
Dry, sparse hair
Thick, brittle nails
Slow pulse rate
Anorexia
Abdominal distention
Menorrhagia
Decreased libido
Infertility
Ataxia
Intention tremor
 Myxedema Coma
Manifests as hypotension, bradycardia,
hypothermia, hyponatremia,
hypoglycemia, respiratory failure, coma
Can be precipitated by acute illness, rapid
withdrawal of thyroid medication,
anesthesia, surgery, hypothermia, use of
opioids
Hypothyroidism: Diagnostics
Radioimmunoassay tests: ↓ T3, T4
↑TSH level with primary hypothyroidism
↓ TSH in secondary hypothyroidism
↓TRH in hypothalamic insufficiency
Serum cholesterol and triglyceride levels are
increased
In myxedema coma
– low serum sodium levels
– respiratory acidosis because of hypoventilation
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.
– After the patient’s condition has been stabilized on one
brand, warn patient not to switch to another, as this may
affect drug bioavailability. Avoid generic levothyroxine.
Warn the patient (especially the elderly) to tell the
doctor if with
– chest pain, palpitations, sweating, nervousness,
or other signs or symptoms of overdosage
– signs and symptoms of aggravated
cardiovascular disease (chest pain, dyspnea, and
tachycardia).
Nursing Management of
replacement therapy
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 bpm, withhold the drug. Assess
for tachyarrhythmias and chest pain.
Prepare I.V. dose immediately before
injection
Nursing Management of
replacement therapy
Thyroid hormones alter thyroid function test
results.
– A patient taking levothyroxine who needs to have
123I uptake studies must discontinue the drug 4
weeks before the test.
– A patient taking liothyronine who needs to have 123I
uptake studies must discontinue the drug 7 to 10
days before the test.
Monitor prothrombin time; a patient taking
these hormones usually requires less
anticoagulant.
– WOF: unusual bleeding and bruising
Nursing Management of
replacement therapy
Liothyronine sodium: not indicated to relieve vague
symptoms, such as physical and mental sluggishness,
irritability, depression, nervousness, and ill-defined
aches and pains; to treat obesity in euthyroid persons;
to treat metabolic insufficiency; or to treat menstrual
disorders or male infertility, unless associated with
hypothyroidism.
Thyroid USP (desiccated): thyroid hormone
replacement requirements are about 25% lower in
patients over age 60 than in young adults. Use
carefully in patients with myxedema, they’re unusually
sensitive to thyroid hormone.
Hypothyroidism: Nursing
Interventions
Diet: high-bulk, low-calorie diet
Encourage activity
Maintain warm environment
Administer cathartics and stool softeners, as needed.
To prevent myxedema coma, tell the patient to continue his
course of antithyroid medication even if his symptoms
subside.
– maintain patent airway
– administer medications – Synthroid, glucose,
corticosteroids
– IV fluid replacement
– Wrap patient in blanket
– Treat infection or any underlying illness
Disorders of the Adrenal
Glands

Adrenal Insufficiency
Cushing’s Syndrome
Hyperaldosteronism
Pheochromocytoma
Adrenal Insufficiency
Addison’s disease, the most common form of adrenal
hypofunction  occurs when more than 90% of the
adrenal gland is destroyed.
Autoimmune process, circulating antibodies react
specifically against the adrenal tissue  decreased
secretion of androgen, glucocorticoids, and
mineralocorticoids.
It may also be caused by a disorder outside the
gland, in which case aldosterone secretion frequently
continues.
Acute adrenal insufficiency, or adrenal crisis
(Addisonian crisis), is a medical emergency
requiring immediate, vigorous treatment.
Adrenal Insufficiency: Causes
Tuberculosis, bilateral adrenalectomy, hemorrhage
into the adrenal gland, neoplasms, or fungal
infections
Secondary adrenal hypofunction is caused by
– Hypopituitarism
– abrupt withdrawal of long-term corticosteroid
therapy
In a patient with adrenal hypofunction, adrenal crisis
occurs when the body’s stores of glucocorticoids are
exhausted by trauma, infection, surgery, or other
physiologic stressors.
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 even minor
stress
Adrenal Insufficiency: Signs and
Symptoms
conspicuous bronze skin coloration, especially in
hand creases and over the metacarpophalangeal
joints, elbows, and knees
poor coordination
fasting hypoglycemia; and craving for salty food.
Amenorrhea
Adrenal crisis
– profound weakness and fatigue, shock, severe
nausea and vomiting, hypotension, dehydration
and high fever.
POMC: the “Big Momma”
MSH is produced when ACTH production is
increased hyperpigmentation
 Adrenal Crisis
Liver
Decrease in hepatic Hypoglycemia Profound
Glucose output Hypoglycemia

Cortisol
Stomach
Absent or low Vomiting, Cramps
Decrease in Digestive
And Diarrhea
Enzyme

Brain
Coma and Death
Adrenal Gland
Destruction of
the adrenal cortex

Kidney
Na and H2O loss with
K retention
Aldosterone Hypovolemia
Shock
Absent or Low And
Hypotension
Heart
Arrhythmias and
Decrease CO
Adrenal Insufficiency: Diagnostic
tests
Decreased plasma cortisol and serum sodium
levels
Increased corticotropin, serum potassium,
and blood urea nitrogen levels
Corticotropin stimulation test  provocative
studies that determine whether adrenal
hypofunction is primary or secondary
Adrenal Insufficiency: Treatment
Corticosteroid replacement, usually with
cortisone or hydrocortisone  primary
lifelong treatment
Fludrocortisone acetate: acts as a
mineralocorticoid to prevent dehydration
and hypotension.
Adrenal crisis : prompt I.V. bolus of
corticosteroids, 3 to 5 L of I.V.fluids,
dextrose
Adrenal Insufficiency: Nursing
Management
In an adrenal crisis, monitor signs of
hypotension, volume depletion, and
signs of shock (decreased level of
consciousness and urine output).
Watch for hyperkalemia before
treatment and for hypokalemia after
treatment (from excessive
mineralocorticoid effect).
Adrenal Insufficiency: Nursing
Management
If patient has diabetes, check blood
glucose levels periodically because
steroid replacement may necessitate
changing the insulin dosage.
Force fluids to replace excessive fluid
loss until the onset of mineralocorticoid
effects.
Adrenal Insufficiency: 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, or profuse
sweating in hot weather may precipitate a
crisis.
Hypercortisolism (Cushing’s
Syndrome)
 Cluster of physical
abnormalities due to excessive
cortisol release
 Cortisol excess is due either to:
 autonomous steroid release from
adrenals
 Increased ACTH release from
pituitary
 complication of exogenous
steroid therapy
Hypercortisolism (Cushing’s
Syndrome)
Altered metabolism of
CHO: hyperglycemia
CHON: muscle wasting, thin, fragile
skin, impaired wound healing
Fats: central obesity, moon face,
buffalo hump
Na and water retention
Hypokalemia, hypocalcemia
Acne, hirsutism, menstrual changes,
decreased libido
Weakness, emotional lability
Complications
Osteoporosis
Peptic Ulcer (from steroid intake)
Immune and inflammatory response is also
compromised
Other complications include HPN, and sexual
and psychological complications
Cushing’s Syndrome: Diagnostics
ACTH Levels  determine whether the syndrome is
ACTH dependent
24-hr urine collection for cortisol, midnight serum cortisol
Dexamethasone Suppression Test  1 mg
dexamethasone given at 11 pm and serum cortisol
taken at 8 AM the next day
• Cortisol level <5ug/dl excludes Cushing’s
syndrome with 98% certainty
Radiologic evaluation
– tumor in the pituitary or adrenal gland
Cushing’s Syndrome: Management

Transsphenoidal resection of pituitary tumor

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
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
Renin-angiotensin-aldosterone
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 and excessive renal excretion of
potassium
Hyperaldosteronism : Causes
Primary hyperaldosteronism: Autonomous secretion of
aldosterone from adrenals
Benign adrenal adenoma (Conn’s syndrome)
Bilateral adrenortical hyperplasia
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
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 hyperaldosteronism:
– unilateral adrenalectomy
• After adrenalectomy, observe for weakness,
hyponatremia, rising serum potassium levels, and
signs of adrenal insufficiency such as hypotension.
potassium-sparing diuretic (such as spironolactone or
amiloride)
antihypertensives
sodium restriction
Treatment may include calcium channel blockers and
aminogluthetimide which inhibits synthesis of aldosterone.
Treatment of secondary hyperaldosteronism: include
correction of the underlying cause.
Hyperaldosteronism:
Nursing interventions
Monitor and record urine output, BP , weight, and serum
potassium levels.
Watch for signs of tetany (muscle twitching, positive
Chvostek’s sign) and for hypokalemia-induced cardiac
arrhythmias, paresthesia, or weakness.
Give potassium replacements as ordered
Ask the dietician to provide a low-sodium, high-potassium
diet.
If the patient is taking spironolactone, advise him to watch for
signs of hyperkalemia.
– Long term use may result to libido, impotence, and
gynecomastia.
Instruct female patients about the possibility of menstrual
irregularities.
Pheochromocytoma
Rare disorder, a chromaffin-cell tumor of the
sympathetic nervous system, usually in the
adrenal medulla, secretes an excess of the
catecholamines epinephrine and
norepinephrine.
This causes episodes of hypertension and
symptoms of catecholamine excess.
The tumor is usually benign but may be
malignant in as many as 10% of patient.
Pheochromocytoma
Pheochromocytoma:
Signs and symptoms
persistent or paroxysmal hypertension
palpitations, tachycardia, headache, visual
disturbances, diaphoresis, pallor, warmth or
flushing, paresthesia, tremor, and excitation
anxiety, fright, nervousness, feelings of
impending doom, abdominal or chest pain,
tachypnea, nausea and vomiting, fatigue,
weight loss, constipation, postural
hypotension, paradoxical response to
antihypertensives (common), glycosuria,
hyperglycemia, and hypermetabolism.
Pheochromocytoma:
Diagnostic tests:
– Increased plasma levels of
catecholamines, elevated blood sugar,
glucosuria
– Elevated urinary catecholamines and
urinary vanilylmandelic acid (VMA) levels
– Tumor on CT scan
Pheochromocytoma: Treatment
Surgical removal of the tumor with
sparing of normal adrenals, if possible
Antihypertensives:
– Alpha-adrenergic blocker
(phentolamine, prazosin, or
phenoxybenzamine)
– A beta-adrenergic blocker
(propranolol)
– Calcium channel blockers
Metyrosine may be used to block
catecholamine synthesis
Pheochromocytoma: Treatment
Postoperatively, I.V. fluids, plasma
volume expanders, vasopressors,
and transfusions may be required if
marked hypotension occurs.
The first 24 to 48 hours
immediately after surgery are the
most critical because blood
pressure can drop drastically.
Pheochromocytoma: Treatment
Hypertensive crisis:
– nifedipine 10 mg SL
– I.V. administration of phentolamine
(push or drip) or nitroprusside
• Prolonged nitroprusside administration
can cause cyanide toxicity.
Tachyarrhythmia is treated with IV
atenolol, esmolol, or lidocaine
Pheochromocytoma: Nursing
interventions
To ensure the reliability of urine
catecholamine measurement, make
sure the patient avoids foods high in
vanillin (such as coffee, nuts, chocolate,
and bananas) for 2 days before urine
collection for VMA measurements.
Instruct patients on drugs that may
interfere with the accurate determination
of VMA levels (such as guaifenesin and
salicylates).
Pheochromocytoma: Nursing
interventions
Collect the urine in a special container
prepared by the laboratory containing
hydrochloric acid.
Post-op: If the patient receives vasopressors
I.V., check blood pressure every 3 to 5
minutes and regulate the drip to maintain a
safe pressure.
Arterial pressure lines facilitate constant
monitoring
Pheochromocytoma: Nursing
interventions
WOF: Postoperative hypertension
WOF: post-op profuse sweating keep the
room cool and change the patient’s clothing
and bedding often.
If the patient is receiving phentolamine,
monitor blood pressure several times per day
with the patient in supine and in standing
positions.
– WOF: and record adverse effects, such as
dizziness, hypotension, and tachycardia.
Pheochromocytoma: Nursing
interventions
Post-op:
Watch for abdominal distention and return of
bowel sounds.
Check dressings and vital signs for indications
of hemorrhage
Give analgesics for pain, as ordered, but
monitor BP  analgesics, especially
meperidine, can cause hypotension.
Obtain blood pressure readings often because
transient hypertensive attacks are possible.
Pheochromocytoma: Nursing
interventions
Tell the patient to report headaches, palpitations,
nervousness, or other acute attack symptoms.
If hypertensive crisis develops, monitor blood
pressure and heart rate every 2 to 5 minutes
until blood pressure stabilizes.
Check blood for glucose, and watch for weight
loss from hypermetabolism.
If autosomal dominant transmission of
pheochromocytoma is suspected, the patient’s
family should also be evaluated for this
condition.
ADRENALECTOMY
Resection or removal of one or both
adrenal glands.
The treatment of choice for adrenal
hyperfunction and hyperaldosteronism.
Used to treat adrenal tumors, such as
adenomas and pheochromocytomas,
Adrenalectomy: Pre-op
Correct electrolyte imbalance
– Potassium, sodium, calcium
Manage hypertension
Adrenalectomy: Postoperative
Care
Monitor vital signs
WOF: shock from hemorrhage.
Keep in mind that postoperative hypertension is
common because handling of the adrenal glands
stimulates catecholamine release.
WOF: adrenal crisis  hypotension, hyponatremia,
hyperkalemia
Remember, glucocorticoids from the adrenal
cortex are essential to life and must be replaced
to prevent adrenal crisis until the hypothalamic,
pituitary, and adrenal axis resumes functioning.
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
Adrenalectomy: Nursing
interventions
Instruct patient that he needs continued
medical follow-up to adjust his steroid dosage
appropriately during stress or illness.
Notify physician if adverse reactions such as
weight gain, acne, headaches, fatigue, and
increase urinary frequency, which can
indicate steroid overdosage.
Take steroid with meals or antacids to
minimize gastric irritation.
Hyperaparathyroidism
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.
Hyperaparathyroidism
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
Hyperaparathyroidism: 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.
Hyperaparathyroidism:
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.
Hyperaparathyroidism:
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.
Hyperaparathyroidism:
Diagnostics
↑serum PTH levels
Increased serum calcium and
decreased phosphorus levels
X-rays may show diffuse
demineralization of bones
Elevated Alkaline phosphatase
Hyperaparathyroidism: Treatment
Surgery to remove the adenoma
Force fluids; limiting dietary calcium intake;
For life threatening hypercalcemia: promote sodium and
calcium excretion, using normal saline solution (up to 6 L
in life-threatening situations), furosemide; and
administering oral sodium or potassium phosphate,
Calcitonin
Postmenopausal women: estrogen supplements
I.V. administration of magnesium and phosphate or
sodium phosphate solution given by mouth or by
retention enema.
Hyperaparathyroidism: Treatment

Supplemental calcium also may be needed during

the first 4 to 5 days after surgery, when serum
calcium falls to low-normal levels.
Vitamin D or calcitriol may also be used to raise
the serum calcium level
Secondary hyperparathyroidism must correct the
underlying cause of parathyroid hypertrophy.
Vitamin D therapy or aluminum hydroxide for
hyperphosphatemia in the patient with renal
disease.
Hyperaparathyroidism:Nursing
interventions

Monitor intake and output as the patient

receives hydration to reduce serum calcium
levels.
Strain urine to check for stones.
Monitor sodium, potassium, and magnesium
levels frequently.
Auscultate for breath sounds often, and be
alert for pulmonary edema in the patient
receiving large amounts of I.V. saline solution
Prevent injury, patient prone to fractures.
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 of or injury to one or more parathyroid
glands during neck surgery
rarely, from massive thyroid radiation therapy.
Ischemic infarction of the parathyroids during surgery
diseases, such as amyloidosis or neoplasms
suppression of normal gland function caused by
hypercalcemia (reversible)
hypomagnesemia-induced impairment of hormone
secretion (reversible).
Hypoparathyroidism: Signs
and symptoms
Neuromuscular irritability
Increased deep tendon reflexes, positive Chvostek’s and Trousseau’s
signs
Dysphagia
Paresthesia
Psychosis
Mental deficiency in children
Tetany seizures
Arrhythmias
Abdominal pain
Dry, lusterless hair, spontaneous hair loss
Brittle fingernails that develop ridges or fall out.
Dry and scaly skin
Weakened tooth enamel may cause teeth to stain, crack, and decay
easily
Hypoparathyroidism:
Diagnostic tests

Decreased PTH and serum calcium

levels
Elevated 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-threatenting tetany calls for
immediate I.V. administration of calcium
to raise serum calcium levels.
Sedatives and anticonvulsants are
given to control spasms until calcium
levels rise.
Hypoparathyroidism: Nursing
interventions
Maintain patent I.V. line and keep 10%
calcium gluconate solution available
Institute seizure precautions
Keep tracheostomy tray and endotracheal
tube at the bedside, because laryngospasm
may result from hypocalcemia.
For patient with tetany, administer 10%
calcium gluconate by slow I.V. infusion and
maintain a patent airway.
Hypoparathyroidism: Nursing
interventions
When caring for the patient with
hypothyroidism, particularly a child, stay alert
for minor muscle twitching ad for signs of
laryngospasm (respiratory stridor or
dysphagia). These effects may signal the
onset of tetany.
Watch out for heart block and signs of
decreased cardiac output.
Watch for signs and symptoms of digoxin
toxicity (arrhythmias, nausea, fatigue and
changes in vision)
Diabetes Mellitus
Chronic disease characterized by
hyperglycemia
It is due to total or partial insulin deficiency
or insensitivity of the cells to insulin
Characterized by disorders in the
metabolism of CHO, FAT and CHON as
well as changes in the structure and
function of blood vessels
Types of DM
Type 1 or IDDM
– Usually occurs in children or in non-obese adults
Type 2 or NIDDM
– Usually occurs in obese adults over age 40
Gestational DM
Secondary DM
– Induced by trauma, surgery, pancreatic disease or
medications
– Can be treated as either type 1or 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
Cont. Pathophysiology

The body turns to fats and protein for

energy; but in the absence of glucose in
the cell, fats cannot be completely
metabolized and ketones are produced
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 a week.
Instruction in the Care of the Feet
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 11/2 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 emery board. File
them straight across and no shorter than
the underlying soft tissue of the toes.
Never cut the corners of the nails.
Instruction in the Care of the Feet

Wear low-heeled shoes of soft leather that fit

the shape of the feet correctly. The shoes
should have 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 day following. 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.
Instruction in the Care of the Feet
To remove excess calluses or corns, soak the feet in
lukewarm (not hot) 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. Under no
circumstances must the skin become irritated.
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 (a)
by exercise, such as curling and stretching the toes
several times a day; (b) by finishing each step on the
toes and not on the ball of the foot; and (c) by
wearing shoes that are not too short and that do not
have high heels.
Diagnostics: FBS and OGTT
Normal Impaired Diabetes
glucose glucose Mellitus
tolerance tolerance
Fasting <110 110-125 > 126
Plasma mg/dl mg/dl mg/dl
Glucose
2 hours < 140 > 140 but > 200
after mg/dl < 200 mg/dl
glucose
Diagnostics: Glycosylated
hemoglobin
NV= 7.5% or less, good control
7.6% -- 8.9% fair control
9% or greater, poor control
 Therapeutic interventions:
 Life-style changes
– Weight control and Exercises
– Planned diet
• 50 – 60 % of calories are complex carbohydrates, high
fiber
• 12 -20 % of daily calories is protein, 60 – 85 g/day
• Fat intake not to exceed 30% of daily calories, more of
polyunsaturated/monounsaturated fats
• Basic tools: food exchange groups, using the
exchange system of dietary control, food composition
tables
– Self-monitoring of blood glucose
 Cont. Therapeutic
interventions:
Insulin Administration
– For 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 effect of insulin
– Glucocorticoids, thiazide diuretics, thyroid
agents, oral contraceptives increase blood
glucose level
– Illness, infection, and stress increase the need for
insulin
Insulin Onset Peak Duration
Ultra rapid 10 - 15 min 1 hour 3 hours
Acting
Insulin analog
(Humalog)
SAI ½-1 hr 2-4 hrs 4-6 hours
(Humulin regular)

IAI 3-4 hrs 4-12 hrs 16-20 hrs

(Humulin lente,
Humulin NPH)
LAI 6-8 hrs 12-16 hrs 20-30 hours
(Protamine Zinc,
Humulin
Ultralente)
Premixed Insulin ½-1 hour 2-12 hrs 18-24 hrs
(70% NPH, 30%
Regular)
 Complications of insulin
therapy
Local allergic reaction, lipodystrophy, Insulin
resistance
Dawn phenomenon
– increase in blood sugar because of release of
growth hormone at around 3 AM;
– Tx: give at 10 pm, intermediate-acting insulin
Somogy effect
– rebound hyperglycemia at 7 am after a bout of
hypoglycemia at around 2-3 AM.
Tx: decrease the evening dose of intermediate-
acting insulin
Complications of insulin
therapy
Hypoglycemia
 If awake, give 10-15 g of fast-acting simple
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 DM type 2
May have to be shifted to insulin when
sick, under stress, during surgery.
Necessary to shift to insulin when
pregnant.
ORAL HYPOGLYCEMICS

Sulfonylureas
– promotes inc. insulin secretion from
pancreatic beta cells through direct
stimulation (requires at least 30 % normally
functioning beta cells)
– First-Generation Agents:
• Tolbutamide, Acetohexamide, Tolazamide,
Chlorpropamide
– Second-Generation Agents
• Glypizide, Glyburide
 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
– Decrease 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)
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
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
Emergency Management:
For both DKA and HHNK, treat dehydration first
with 0.9% or 0.45% saline.
– Shift to D5W when glucose level is down to 250-
300 mg/dl.
– WOF too rapid correction, it can cause rapid fluid
shifts (brain edema and increased ICP, ARDS)
IV Regular Insulin 0.1 unit/kg bolus and then 0.1
u/k/h drip
Correcting electrolyte imbalance. Watch out for
hypokalemia as a result of treatment. For severe
acidosis (pH < 7.1), DKA patients may have to
be given NaHCO3.