CLIENTS WITH PROBLEMS IN ENDOCRINE SYSTEM

ENDOCRINE SYSTEM
By; ROMMEL LUIS C. ISRAEL III
By: ROMMEL LUIS C. ISRAEL III 1

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

WHAT DOES THE
HYPOTHALAMUS DO?
The hypothalamus is a small area in the
center of the brain. It helps produce
hormones that regulate heart rate, body
temperature, hunger, and the sleep-
wake cycle.
The hypothalamus’ main role is to keep
the body in HOMEOSTASIS (a healthy
and balanced internal state) as much as
possible.

WHAT DOES THE
HYPOTHALAMUS DO?
The hypothalamus works between the
endocrine and nervous systems.
As different systems and parts of the
body send signals to the brain, they can
alert the hypothalamus to any
unbalanced factors that need
addressing. The hypothalamus
responds by stimulating relevant
endocrine activity to address this
balance. By: ROMMEL LUIS C. ISRAEL III 10

WHAT DOES THE
HYPOTHALAMUS DO?
For example, if the hypothalamus
receives a signal that the internal
temperature is too high, it will tell the
body to sweat.
If it receives the signal that the
temperature is too cold, the body will
create its own heat by shivering.

WHAT DOES THE
HYPOTHALAMUS DO?
It also plays a role in:
• Growth
• thirst
• appetite
• weight control
• emotions
• sleep-wake cycles
• sex drive
• childbirth
• breast milk production

WHAT DOES THE
HYPOTHALAMUS DO?
To maintain homeostasis, in conjunction with
the pituitary gland, the hypothalamus secretes
the following hormones:
Antidiuretic hormone (ADH)
Corticotropin-releasing hormone (CRH)
Gonadotropin-releasing hormone
Oxytocin
Prolactin-controlling hormones
Thyrotropin-releasing hormone

WHAT DOES THE
HYPOTHALAMUS DO?
The hypothalamus also directly influences
growth hormones. It commands the pituitary
gland to either increase or decrease levels in
the body, which is essential for both growing
children and fully developed adults.

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
Somatotro
pin
Stimulates
growth of
body
tissues and
bones

Growth hormone
Increases
breakdown of fatty
acid in adipose
tissue
Increases blood
sugar

ACTH
Adrenocorticotropic hormone
(ACTH) is a tropic hormone
produced by the anterior pituitary.
Stimulates the adrenal cortex to
produce and release
adrenocorticoids, esp. Cortisol, as
well as growth of adrenal glands
ACTH has little effect on
aldosterone

How is adrenocorticotropic
hormone controlled?
Secretion of ACTH is controlled by three inter-
communicating regions of the body,
the hypothalamus, the pituitary gland and the adrenal
glands. This is called the hypothalamic–pituitary–
adrenal (HPA) axis.
When cortisol levels in the blood are low, a group of
cells in the hypothalamus release a hormone
called corticotrophin-releasing hormone (CRH) which
stimulates the pituitary gland to secrete
adrenocorticotropic hormone into the bloodstream.

hormone controlled?
High levels of ACTH are detected by the adrenal
gland receptors which stimulate the secretion of
cortisol, causing blood levels of cortisol to rise.
As the cortisol levels rise, they start to slow down the
release of corticotrophin-releasing hormone from the
hypothalamus (long loop inhibition) and
adrenocorticotropic hormone from the pituitary gland
(short loop inhibition).
As a result, the ACTH levels start to fall and
consequently cortisol. This is called a negative
feedback loop.

hormone controlled?
Stress, both physical and psychological,
also stimulates ACTH production and
hence increases cortisol levels.
Cortisol plays an important role in the
stress response. Maintaining an
adequate balance of cortisol is essential
for health.

TSH and Thyroid gland
Stimulates growth of thyroid gland
and release of thyroid hormones

Thyroid Stimulating Hormone
(TSH) is produced and released
into the bloodstream by the pituitary
gland.
It stimulates the production of the
thyroid hormones: thyroxine (T4)
and triiodothyronine (T3), by the
thyroid gland by binding to its
receptors in the thyroid gland.

Thyroxine (T4) and triiodothyronine
(T3) are essential for maintaining
the body’s metabolic rate, heart
and digestive functions, muscle
control, brain development and
bone activity.

FSH, LH  Gonads

FSH-LH
Luteinizing hormone (LH) and follicle-
stimulating hormone (FSH) are
called gonadotropins because
stimulate the gonads - in males, the
testes, and in females, the ovaries.
They are not necessary for life, but are
essential for reproduction.
These two hormones are secreted from
cells in the anterior pituitary
called gonadotrophs. Most

FSH-LH
These two hormones are secreted from
cells in the anterior pituitary
called gonadotrophs.
Most gonadotrophs secrete only LH or
FSH, but some appear to secrete both
hormones.

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

CONTROL OF GONADOTROPHINE
SECRETION
The principle regulator of LH and FSH
secretion is gonadotropin-releasing
hormone (GnRH, also known as LH-
releasing hormone).
GnRH is a ten amino acid peptide that
is synthesized and secreted from
hypothalamic neurons and binds to
receptors on gonadotrophs.

SECRETION
The GnRH
stimulates
secretion of LH,
which in turn
stimulates
gonadal secretion
of the sex
steroids
testosterone,
estrogen and
progesterone.

SECRETION
In a classical
Negative
Feedback Loop,
sex steroids
inhibit secretion
of GnRH and
also appear to
have direct
negative effects
on gonadotrophs.

Melanocyte Stimulating Hormone
ALTERNATIVE NAMES:
MSH; α-melanocyte-stimulating
hormone;
alpha-MSH; α-MSH;
alpha-melanotropin;
alpha-melanocortin;
alpha-intermedin;
melanophore-stimulating hormone

Melanocyte-stimulating hormone is a
collective name for a group of peptide
hormones produced by the skin,
pituitary gland and hypothalamus.
In response to ultraviolet (UV)
Radiation, its production by the skin and
pituitary is enhanced, and this plays a
key role in producing colored
pigmentation found in the skin, hair and
eyes. By: ROMMEL LUIS C. ISRAEL III 39

induces specialized skin cells called
melanocytes to produce a pigment
called melanin;
melanin protects cells from DNA-
(1)'>DNA damage, which can lead to
skin cancer (melanoma).

Melanocyte can also suppress
appetite by acting on receptors
in the hypothalamus in the
brain.
This effect is enhanced by
leptin, a hormone released from
fat cells.

Melanocyte-stimulating hormone
also has anti-inflammatory effects
It can influence the release of the
hormone aldosterone, which
controls salt and water balance in
the body,
and also has an effect on sexual
behaviour.

How is melanocyte-stimulating
hormone controlled?
• Melanocyte-stimulating hormone
secretion from the pituitary is
increased by exposure to UV light.
• Unlike most hormones,
melanocyte-stimulating hormone
release is not thought to be
controlled by a direct feedback
mechanism.

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

Oxytocin
Stimulates uterine contractions during
delivery and the release of milk in lactation
Oxytocin is a nonapeptide hormone released
from the posterior pituitary and multiple
organs (uterus, placenta, amnion, corpus
luteum, testes, and heart) in response to
social bonding, interactions, and the
emotional context of social relationships
(Shamay-Tsoory and Abu-Akel, 2016).

Oxytocin
It is released in large amounts during labor,
and after stimulation of the nipples.
It is a facilitator for childbirth and
breastfeeding.
One of the oldest applications of oxytocin as
a proper drug is as a therapeutic agent during
labor and delivery.

Oxytocin
Oxytocin is also present in men, playing a
role in sperm transport and production of
testosterone by the testes.
In the brain, oxytocin acts as a chemical
messenger and has an important role in
many human behaviours including sexual
arousal, recognition, trust, romantic
attachment and mother–infant bonding.

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

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

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

Estrogen
– Development of secondary sex
characteristics in the female
– Maturation of sex organs
– sexual functioning
Progesterone
– maintenance of pregnancy

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

DISEASES OF THE
ENDOCRINE SYSTEM

Disorders of the
Pituitary Gland
Hypopituitarism
Hyperpituitarism
SIADH
Diabetes Insipidus

Hypopituitarism
Hypopituitarism is a rare condition in which
the pituitary gland doesn't make one or more
hormones or doesn't make enough
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
Tumor: bitemporal hemianopia on visual
confrontation (describes the ocular defect
that leads to impaired peripheral vision in
the outer temporal halves of the visual field
of each eye.)

Signs and Symptoms
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, undescended
testes (cryptorchidism)

Signs and Symptoms
–Acquired
•Loss of body hair
•Infertility, decreased libido,
impotence in males,
amenorrhea in females
•muscle atrophy

Signs and Symptoms
- Osteopenia
is a condition where the
density of the bone mineral
decreases, making bones weaker
and more susceptible to
fractures.

Signs and Symptoms
Thyroid-stimulating (TSH)
deficiency
–Causes hypothyroidism with
manifestations such as
fatigue, weakness, weight
change, and hyperlipidemia

Signs and Symptoms
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
hypersecretion prior
to closure of
epiphyses;
proportional growth
Acromegaly: GH
hypersecretion after
closure of
epiphyses;
disproportional
growth

Growth Hormone Hypersecretion
ACROMEGALY: abnormal growth of the hands, feet,
and face, caused by overproduction of growth hormone
by the pituitary gland.

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
(Obstructive Sleep Apnea)

Signs and symptoms
Hypertension, cardiomegaly, heart failure
Insulin resistance DM
Visual field defects: bitemporal
hemianopsiacomplete blindess
Bitemporal hemianopsia is a condition where
you can't see the outer halves of your visual
field in both eyes

Signs and symptoms
Headaches
Arthritis
Hypogonadism
People experience hypogonadism when their
sex glands, or gonads, produce insufficient
levels of sex hormones. In adult women, the
ovaries don’t secrete enough estrogen,
leading to hot flashes, changes in mood and
energy levels, and irregular or stopped
menstruation.

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
an effective
neurosurgical
technique for
removing
pituitary tumors,
and other
intrasellar
tumors,

Transsphenoidal hypophysectomy
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.
*WOF (Watch Out For)

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

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.

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

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 sodium 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.

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.

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.

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.

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)

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.

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.

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)

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

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

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

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

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

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.

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

– 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.

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.

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

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

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

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 By: ROMMEL LUIS C. ISRAEL III 166

Hypothyroidism: Signs and
symptoms
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
Congenital
Hypothyroidism

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).

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

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

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
Cortisol
Absent or low
Adrenal Gland
Destruction of
the adrenal cortex
Aldosterone
Absent or Low
Liver
Decrease in hepatic
Glucose output
Heart
Arrhythmias and
Decrease CO
Kidney
Na and H2O loss with
K retention
Stomach
Decrease in Digestive
Enzyme
Hypoglycemia
Hypovolemia
And
Hypotension
Vomiting, Cramps
And Diarrhea
Shock
Brain
Coma and Death
Profound
Hypoglycemia

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).

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.

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.

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

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.

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).

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

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.

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.

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.

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.

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.

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.

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.

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
glucose
tolerance
Impaired
glucose
tolerance
Diabetes
Mellitus
Fasting
Plasma
Glucose
<110
mg/dl
110-125
mg/dl
> 126
mg/dl
2 hours
after
glucose
< 140
mg/dl
> 140 but
< 200
> 200
mg/dl

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
Acting
Insulin analog
(Humalog)
10 - 15 min 1 hour 3 hours
SAI
(Humulin regular)
½-1 hr 2-4 hrs 4-6 hours
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 hours
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 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.

References:
Oxytocin | You and Your Hormones from the Society for Endocrinology. (n.d.).
Www.yourhormones.info.
https://www.yourhormones.info/hormones/oxytocin/#:~:text=by%20the%20nipple.-
US EPA, O. (2015, July 6). Overview of the Endocrine System. Www.epa.gov.
https://www.epa.gov/endocrine-disruption/overview-endocrine-
system#:~:text=The%20endocrine%20system%2C%20made%20up
Hypothalamus: Function, hormones, and disorders. (n.d.). Www.medicalnewstoday.com.
https://www.medicalnewstoday.com/articles/312628#disorders
Biology LibreTexts. (2016). 13.27: Hormone Regulation. [online] Available at:
https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Introductory_Biology_(
CK-
12)/13%3A_Human_Biology/13.27%3A_Hormone_Regulation#:~:text=Most%20hormones%20are
%20controlled%20by.
Better Health (2017). Growth hormone. [online] Vic.gov.au. Available at:
https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/growth-hormone.
Allen, M.J. and Sharma, S. (2021). Physiology, Adrenocorticotropic Hormone (ACTH). [online] PubMed. Available at:
https://www.ncbi.nlm.nih.gov/books/NBK500031/#:~:text=Adrenocorticotropic%20hormone%20(ACTH)%20is%20a.

References:
Shomon, M. (2004). High and Low TSH Levels: What They Mean. [online] Verywell Health. Available
at: https://www.verywellhealth.com/understanding-thyroid-blood-tests-low-or-high-tsh-3233198.
Luteinizing and Follicle Stimulating Hormones. (n.d.). Www.vivo.colostate.edu.
http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/lhfsh.html#:~:text=Luteinizin
g%20hormone%20%28LH%29%20and%20follicle-stimulating%20hormone%20%28FSH%29%20are
Yourhormones.info. (2018). Melanocyte-stimulating hormone | You and Your Hormones from the
Society for Endocrinology. [online] Available at:
https://www.yourhormones.info/hormones/melanocyte-stimulating-hormone/.
Melanocyte-stimulating hormone | You and Your Hormones from the Society for Endocrinology.
(2018). Yourhormones.info. https://www.yourhormones.info/hormones/melanocyte-stimulating-
hormone/
Verywell Health. (n.d.). A Quick Rundown of the Symptoms of Hypogonadism. [online] Available at:
https://www.verywellhealth.com/hypogonadism-signs-symptoms-and-complications-5191935.
Bing. (n.d.). Transsphenoidal hypophysectomy. [online] Available at:
https://www.bing.com/search?q=Transsphenoidal+hypophysectomy&cvid=349c865c86eb4249a78
60659ce931476&aqs=edge..69i57j0l8.1337j0j4&FORM=ANAB01&PC=NMTS [Accessed 13 Aug.
2023].

References:
• Mayo Clinic (2021). Diabetes insipidus - Symptoms and causes. [online] Mayo
Clinic. Available at: https://www.mayoclinic.org/diseases-conditions/diabetes-
insipidus/symptoms-causes/syc-20351269.
• Vallie, S. (n.d.). What Is SIADH? [online] WebMD. Available at:
https://www.webmd.com/a-to-z-guides/what-is-siadh.
• Society for Endocrinology (2019). Adrenocorticotropic hormone | You and
Your Hormones from the Society for Endocrinology. [online]
Yourhormones.info. Available at:
https://www.yourhormones.info/hormones/adrenocorticotropic-hormone/.
• Australia, H. (2020). The role of cortisol in the body. [online]
www.healthdirect.gov.au. Available at: https://www.healthdirect.gov.au/the-
role-of-cortisol-in-the-
body#:~:text=Cortisol%20is%20a%20hormone%20produced.

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