Finla presentation on pitutary&aderenal gland

DEBRE MARKOS UNIVERSITY
COLLEGE OF HEALTH SCIENCE
BY:
GETNET DESSIE(BSc,MSc in Adult health nursing)
DMU
may,2018
Pituitary gland disorder

By the end of this lecture, students should be able to:
• Discuss the anatomy ,and functions of pituitary
• Describe pituitary gland dysfunction, and pathophysiology.
• Describe clinical manifestations of pituitary tumours,
assessment and diagnostic findings, and an overview of
medical management.
• Define diabetes insipidus, describe its manifestations,
diagnostic evaluation, medical and nursing management.
Objectives

• Introduction
• Pituitary anatomy & Physiology
• Pituitary tumors,
• Hypopituitarism
• common hormone producing tumors:
– Acromegaly
– Cushing disease
outline

• Anatomic and Physiologic Overview
• The pituitary gland, or hypophysis, is a round
structure about 1.27 cm (½ inch) in diameter
• located on the inferior aspect of the brain.
Introduction

 The pituitary often referred to as master gland
because together with the hypothalamus,, it
orchestrates the complex regulatory functions of
multiple endocrine glands
 consists of anterior and posterior lobe..
 Pituitary hormones are produced in Pulsatile
manner.
Anatomic and Physiologic Overview……..

Anatomic and Physiologic Overview……..

9
Endocrine glands in the human head and neck and their hormones

• Growth
• Blood pressure
• Uterine contractions during childbirth
• Breast milk production
• Sex organ functions
• Thyroid gland function
• Water and osmolality regulation in the body
• Temperature regulation
Function of the Pituitary

• Rule of "Too's“
• Too-mor (tumor)
Too much
Too little
When things go wrong

• pituitary tumor is calld “pituitary adenoma” —
adeno means gland, oma means tumor.
• Most pituitary adenomas develop in the front
two-thirds of the pituitary gland.
• That area is called the adenohypophysis, or
the anterior pituitary
(American brain tumor association 2015)
Pituitary Tumors

• Almost all pituitary tumors are benign (non-
cancerous)
• These tumors don’t spread to other parts of
the body, like cancers can do
• but their location and effects on hormone
production by target organs can cause life-
threatening effects.
Pituitary Tumors

• About 10,000 pituitary tumors are diagnosed each
year in the United States.
• When examining people who have died or who have
had imaging tests (like MRI scans) of their brain for
other health problems, it is found that as many as 1
out of 4 people have a pituitary adenoma without
knowing it.
(American cancer society,2014)
key statistics about pituitary tumors

• Pituitary tumors account for 12 -19% of all primary brain
tumors, making them the third most common primary brain
tumor in adults, following meningioma and the gliomas.
• 20 – 25% of the general population have small, symptomless
pituitary tumors or cysts.
• 10% have an abnormality big enough to see on magnetic
resonance imaging (MRI).
key statistics about pituitary tumors…..
..

• Pituitary tumors can be found in every age group, but
their incidence tends to increase with age
• Women are more often than men.
• On systemic review prevalence of pituitary
adenomas of 16.7% (14.4% in autopsy studies and
22.5% in radiologic studies)(Shereen Ezzat,2004).
..

• Pituitary tumors can occur at any age
(including in children), but they are most
often found in older adults.
• Almost all of these tumors are benign
pituitary adenomas.
(American cancer society,2014)
..

• based on size:Microadenoma versus
macroadenoma
1.Microadenomas(smaller than 1 cm).
• rarely damage the rest of the pituitary or nearby
tissues.
• they can cause symptoms if they make too much of
a certain hormone.
• Many people actually have small adenomas that are
never detected because they never grow large
enough or secrete enough hormones to cause a
problem.
Pituitary Tumors classification

2.Macroadenomas are tumors 1 cm across or larger.
• Affect a person’s health in 2 ways.
• First, they can cause symptoms if they make too
much of a certain hormone.
• Second, they can cause symptoms by pressing on
normal parts of the pituitary or on nearby nerves,
such as the optic nerves.
Pituitary Tumors classification …………

 25% of the pituitary adenomas.
 Null cell adenomas,
 oncocytomas,
 silent corticotroph adenomas and
 silent gonadotroph and
 thyroph adenomas fall into this group.
These tumors grow slowly and generally cause
minimal symptoms.
non-functioning pituitary tumors

• When they expand outside the sella turcica, they may
press on the nearby optic nerves causing vision loss
and headache.
• Such tumors can also compress the pituitary gland
cause hypopituitarism, this symptom is associated
with general weakness and fatigue, a pale
complexion, loss of sexual function and apathy.
non-functioning pituitary tumors

• anything that changes a person’s chance of
getting a disease.
For example;
• smoking is a risk factor for cancer of the lung
and many other cancers.
• Family history
What are the risk factors for pituitary tumors?

Genetic syndromes
• Multiple endocrine neoplasia, type I (MEN1):
This is a hereditary condition in which people
have a very high risk of developing tumors of
3 glands: the pituitary, parathyroid, and
pancreas.
Can be Transmit to children

• Multiple endocrine neoplasia, type IV (MEN4):
MEN4 is caused by inherited changes in a gene
called CDKN1B.
• McCune-Albright syndrome: This syndrome is
caused by changes in a gene called GNAS1,that
aren’t inherited but occur before birth.
• Carney complex: This is a rare syndrome in which
people can have heart, skin, and adrenal problems.

• These benign tumors do not spread outside the
skull.
• They usually remain confined to the sella turcica
• Sometimes they grow into the walls of the sella
turcica and surrounding blood vessels, nerves, and
coverings of the brain.
• They don’t grow very large, but they can have a big
impact on a person’s health.
Pathophysiology of Pituitary Tumors

• There is very little room for tumors to grow in this
part of the skull.
• Therefore, if the tumor becomes larger than
about a centimeter across, it may grow upward,
• can compress and damage nearby parts of the
brain and the nerves that arise from it.
• This can lead to symptoms such as vision changes
or headaches (Signs and symptoms of pituitary
tumors).
Pathophysiology of Pituitary Tumors

 excess hormone secretion
 local effects of a tumor
 the result of inadequate production of
hormone by the remaining normal pituitary,
i.e. hypopituitarism.
Effects of tumor on pituitary gland

Three principal types of pituitary tumors represent an
overgrowth of
(1) eosinophilic cells,
(2) basophilic cells, or
(3) chromophobic cells (neither of two)
Pituitary Tumors

Eosinophilic
–If it is early in life result in gigantism.
–If the disorder begins during adult ,
acromegaly.
– However, enlargement involves all tissues and
organs of the body.
– Many of these patients suffer from severe
headaches and visual disturbances because
the tumors exert pressure on the optic nerves
(Porth, 2005).
Clinical Manifestations

–loss of color discrimination,
–diplopia (double vision), or blindness in a
portion of a field of vision.
–Decalcification of the skeleton, muscular
weakness, and endocrine disturbances,
similar to those occurring in patients with
hyperthyroidism.
Clinical Manifestations of Eosinophilic ………..

– Basophilic tumors give rise to Cushing's syndrome
with features largely attributable to
hyperadrenalism, including
– masculinization and
– amenorrhea in females,
– truncal obesity,
– hypertension, osteoporosis, and polycythemia.
Clinical Manifestations of Basophilic tumors

– Chromophobic tumors represent 90% of pituitary
tumors.
– These tumors usually produce no hormones but
destroy the rest of the pituitary gland, causing
hypopituitarism.
– People with this disease are often obese and
somnolent and exhibit fine, scanty hair; dray, soft
skin; a pasty complexion; and small bones.
Clinical Manifestations of Chromophobic tumors

–headaches,
–loss of libido,
–visual defects progressing to blindness.
–polyuria, polyphagia,
–a lowering of the basal metabolic rate,
and a subnormal body temperature.
Clinical Manifestations of Chromophobic tumors ……….

• careful history and physical examination, including
assessment of visual acuity and visual fields.
• Computed tomography (CT) and magnetic
resonance imaging (MRI)
• Serum levels of pituitary hormones plus hormones
of target organs (eg, thyroid, adrenal) to assist in
diagnosis if other information is inconclusive.
Assessment and Diagnostic Findings

• bromocriptine To decrease GH levels.
• Radiation :Stereotactic or conventional radiation
therapy.
• Surgical removal of the pituitary gland through a
transsphenoidal approach is the usual treatment.
• Hypophysectomy
– is the treatment of choice in patients with
Cushing’s syndrome
Medical &Surgical Management of pituitary Tumors

Medical &Surgical Management of pituitary Tumors

• Pre op hypophysectomy
Anxiety r/t
fear of unknown
brain involvement
Nursing Management &Nursing Diagnosis

• Sensory-perceptual alteration r/t :
visual field cuts
 diplopia
 secondary to pressure on optic nerve.
• Alteration in comfort (headache) r/t tumor
growth/edema

• Knowledge deficit r/t no post-op teaching
• Teach the person about
pain control
ambulation
hormone replacement
activity

• Incisional disruption after transsphenoidal
hypophysectomy
– Avoid bending and straining X 2 months post
transsphenoidal hypophysectomy,
– Use stool softeners
– Avoid coughing
– Saline mouth rinses
– No toothbrushes for 7-10 days

• Assess for any clear rhinorrhea
–Notify physician
–HOB 30 degrees
–Bed rest
Prevent Post-op complications

• Periocular edema/ecchymosis
• Headaches
• Visual field cuts/diplopia
• Post operative care
• hormone deficiency: Have no enough ADH
• Decrease ACTH will require cortisone replacement
due to decrease glucocorticoid production.
Post-op complications…………………

• Decrease in sex hormones can lead to infertility due
to decreased production of ova & sperm
Post-op complications…………………

• Results in excess production and
secretion of one or more hormones such
as GH, PRL, ACTH.
• Prolactin and GH are the hormones most
commonly over-produced by adenomas
• Most common cause is a benign
adenoma.
1.Too much

• It may be primary or secondary defect
• Primary: the defect is in the gland itself
which releases that particular hormone
that is too much or too little.
• Secondary: defect is somewhere outside
of gland i.e. GHRH from hypothalamus
»TRH from hypothalamus
Anterior hyper pituitary Disorders

Some General Facts
• 3 people in 1 million have pituitary gigantism in the
world
• 100 cases to day in United States
• 2 – 3 times higher mortality rate in comparison to
general population
• No racial predilection
• Males and females affected equally
• Not a genetic disorder
( American brain ca socity,2010)

Robert Pershing Wadlow
• Robert Wadlow – “The Alton
Giant”
• Tallest man ever at 8’11”,
suffered from the disorder
• Born normal weight and size
but 30 lbs at 6 months of
age
• Died at 22

The Alton Giant
• No treatment in 1920’s for overactive pituitary
• Maintained normal lifestyle,
• participated as a boy scout, collected stamps and
enjoyed photography
• Shoes cost $100 (specially made)
• Worked for international shoe company as an
attraction, went on nationwide tour in U.S. in
exchange for free shoes for life

Cause and pathophysiology
• The main cause of too much growth
hormone released is from a non-cancerous
tumor of the pituitary gland.
• is the result of GH hypersecretion before
the closure of the epiphyseal plates
(childhood).
– Abnormally tall but body proportions are normal

Clinical presentation
 Excessive growth
 The child is large for their age
 Delayed puberty
 Double vision or difficulty with peripheral vision,
Headaches
 Increased sweating
 Large hands and feet
 Thickening of facial features

Diagnostic Procedures
 CT or MRI of head
 There will be high prolactin levels
 Increased insulin growth factor levels

Treatment
 Surgery to remove the tumor
 Medication that will reduce how much growth
hormone is released
 Radiation Therapy

complication
• Life span is generally reduced and disturbed due
to :
• osteoarthritis, cardiovascular diseases, benign
tumor growth, diabetes, varying levels of obesity
and sleep apnea,
• Tumor in pituitary can cause chronic headache
and visual impairment due to proximity of gland to
optic chiasm

Nursing consideration
• Gigantism and acromegaly generally have
outward negative effects that can be treated
medically, i.e. sleep disturbances, joint pain,
cardiovascular issues, etc.
• Teach the patient to protect these
complications
• gigantism very traumatic emotionally

• Acromegaly is over secretion of GH in
adulthood at age of greater than 17 years
– Continued growth of boney, connective tissue
leads to disproportionate enlargement of tissue..
– Rare condition – develops between ages 30-50
2. Acromegaly

In Iceland national survey from 1955-2013:
o 32 men with diseases
o Average age 44.5
o 9 patient died
o Symptoms for more than 3 years
o 25 (48%) develop HTN
o 63 % cured after surgery
(Gudrun thuridu hoskuldsdottir et.al,2015 etal)
General facts about Acromegaly

• Acromegaly most often occurs as a result of a
benign pituitary tumor (adenoma).
• The excessive secretion of GH results in an
overgrowth of soft tissues and bones in the hands,
feet, and face.
• Because the problem develops after epiphyseal
closure, the bones of the arms and legs do not
grow longer.
Etiology and Pathophysiology

• The changes can occur over a number of
years and may go unnoticed by family and
friends.
• Patients experience enlargement of hands
and feet with joint pain that can range from
mild to crippling.
• Carpal tunnel syndrome
• Thickening and enlargement of the bony
and soft tissues on the face, feet, and head
occur
Clinical manifestation

• speech difficulties,
• the voice deepens because of hypertrophy
of the vocal cords.
• Sleep apnea may occur because of upper
airway narrowing
• The skin becomes thick, leathery, and oily.
• peripheral neuropathy and proximal
muscle weakness.
• Visual disturbance Headaches
• hyperglycemia,

Clinical manifestation Acromegaly………

• glucose intolerance and manifestations of
diabetes mellitus may occur, including
polydipsia and polyuria
• increases free fatty acid levels in the blood
Clinical manifestation Acromegaly………

 History & physical exam
 plasma insulin-like growth factor 1 (IGF-1)
 OGTT :Two baseline GH levels are obtained
before ingestion of 75 or 100 g of oral glucose, and
additional GH measurements are made at 30, 60,
90, and 120 minutes.
 Normally, GH concentration falls during an OGTT.
 In acromegaly GH levels do not fall, and in some
cases GH concentration rises.
Assessment and diagnosis

• Serum GH
– Men: <4 ng/mL (<4.0 mcg/L)
– Women: <18 ng/mL (<18 mcg/L)
– Values >50 ng/mL (>50 mcg/L) suggest
acromegaly.
• MRI and CT scan to detect pituitary tumor
diagnosis

Treatment
• Surgery (hypophysectomy is the primary
choice)
• Radiotherapy
• Drug treatment – when surgery is not
feasible
• Combinations of above

• Dopamine agonists: Dopamine agonists work on the
surface of the tumor to inhibit GH release from the
tumour (Parlodel).
• Somatostatin: GH receptor antagonist decreases the
action of GH on target tissues. (octreocide acetate)
• Dopamine agonists are taken by mouth but in general
are less effective than somatostatin analogues, which
have to be injected.
Drug treatment of Acromegaly

NURSING ASSESSMENT
• Assess the patient for signs and symptoms
of abnormal tissue growth and evaluate
changes in physical size.
• It is important to question patients about
increases in hat, glove, and shoe sizes

NURSING IMPLEMENTATION
• elevating the head of the patient’s at 30-degree angle to
avoids pressure on the sella turcica and decreases
headaches
• Monitor the pupillary response, speech patterns
• Perform mouth care every 4 hours to keep the surgical area
clean and free of debris
• Observe the patient for any signs of bleeding, since
hemorrhage may be a complication, particularly when larger
tumors are removed

NURSING IMPLEMENTATION
• Instruct the patient to avoid vigorous coughing, sneezing,
Valsalva maneuver to prevent CSF leakage.
• Notify the surgeon, and send any clear nasal drainage to the
laboratory to be tested for glucose.
• A glucose level greater than 30 mg/dL (1.67 mmol/L) indicates
CSF leakage from an open connection to the brain.
• If this happens, the patient is at increased risk for meningitis.
• Observe for sign of DI

SIADH: syndrome of Inappropriate Anti-Diuretic Hormone
• Too much ADH produced or secreted.
• SIADH commonly results from malignancies, CHF, &
CVA - resulting in damage to the hypothalamus or
pituitary which causes failure of the feedback loop
that regulates ADH.
• Client retains water causing dilutional hyponaetremia
& decreased osmolality.
Hyper – Posterior Pituitary

– in the Europe Hyponatremia is the most
common electrolyte didturbance btween
2.5% and 30% pt withn SIDH
– The most common causes of SIADH are
malignancy,
– pulmonary disorders, CNS disorders and
medication;
– (M J Hannon and C J Thompson,2010)
Facts about SIADH

CAUSES OF SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
Malignant Tumors
• Small cell lung cancer
• Pancreatic cancer
• Lymphoid cancers
(Hodgkin’s
lymphoma, non-
Hodgkin’s lymphoma,
• Lymphocytic
leukemia)
European endocrinology society, 2010
• Drug Therapy
• carbamazepine (Tegretol)
• chlorpropamide
• General anesthesia
agents
• Opioids
• oxytocin
• Thiazide diuretics
• SSRI antidepressants
• Tricyclic antidepressants

CAUSES OF SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
• CNS Disorders
• Head injury
• subdural hematoma,
• Subarachnoid hemorrhage
• Stroke
• Brain tumors
• encephalitis,meningitis
• Cerebral atrophy
• Guillain-Barré syndrome
Miscellaneous Conditions
• Hypothyroidism
• Lung infection (pneumonia,
• tuberculosis, lung abscess)
• Chronic obstructive
• pulmonary disease
• Positive pressure mechanical
• ventilation
• HIV
• Adrenal insufficienc
European endocrinology society, 2010

Pathophysiology of SIADH
FIG. Pathophysiology of syndrome of inappropriate antidiuretic hormone
(SIADH).

• low urine output and increased body weight
• Lethargy & weakness
• Confusion or changes in neurological status
• Cerebral edema
• Muscle cramps
• Decreased urine output
• Weight gain without edema
• Hypertension
(Note: b/c of the low Na, edema will not accompany
the FVE)
Signs and Symptoms

• simultaneous measurements of urine and
serum osmolality(, serum osmolality less than
280 mOsm/kg
• Urine osmolality disproportionately elevated
in relation to the serum osmolality
• Urine specific gravity elevated >1.025
• Plasma ADH elevated
• Serum sodium low(serum sodium less than
134 mEq/L)
Assessment and diagnosis

1. Hypo-osmolality; plasma osmolality <280
mosmol/kg, or plasma sodium concentration <134
mmol/l
2. Inappropriate urinary concentration (Uosm >100
mosmol/kg) for hyponatraemia
3. Patient is clinically euvolaemic
4. Elevated urinary sodium (>40 mmol/l), with
normal dietary salt and water intake
5. Exclusion of hypothyroidism, diuretics and
glucocorticoid deficiency – particularly in patients
with neurosurgical conditions
diagnostic criteria for the diagnosis of SIADH.
European endocrinology socity (2010)

 Treat underlying cause
 Hypertonic or isotonic IV solution
 Monitor for signs of fluid and electrolyte
imbalance
 Monitor for neurological effects
 Monitor in and out, Weight
 Restrict fluid intake
 Lithium inhibits action of ADH
Treatment of SIADH

• If symptoms are mild and serum sodium is
greater than 125 mEq/L the only treatment may
be a fluid restriction of 800 to 1000 mL/day.
• Position the head of the bed flat or elevated no
more than 10 degrees to enhance venous return
to the heart and increase left atrial filling
pressure reducing the release of ADH
Nursing management

• Lasix may given only if the serum sodium
is at least 125 mEq/L (125 mmol/L)
• Because furosemide increases potassium,
calcium, and magnesium losses,
supplements is needed
Nursing management

• Frequent turning, positioning, and range-of-motion
exercise (if patient is bedridden)
• Protect the patient from injury (LOC).
• Implement seizure precautions.
• Provide the patient with frequent oral care and
distractions to decrease discomfort related to thirst
from the fluid restrictions.
Nursing management

• It is Hormone deficiency caused by the
inadequate secretion of one or more of the
hormones normally secreted by the
pituitary,
• It may be caused by compression of the
normal tissue by a developing tumor,
surgery, or radiotherapy.
HYPOPITUITARISM-ANTERIOR LOBE

• Dwarfism, condition of being undersized, or
less than 127 cm (50 in) in height.
• Some dwarfs have been less than 64 cm (24
in) tall when fully grown.
• The term midget is usually applied to
physically well-proportioned dwarfs.
• The term pygmy is applied to people whose
shortness of stature is a racial trait and not
caused by disease.
Decreased GH in child: Dwarfism

• cause
– Cretinism
– Down syndrome,
– Achondroplasia
– spinal tuberculosis; and deficiency of the
secretions of the pituitary gland or of the ovary.
Decreased GH in child: Dwarfism

• GH binds to receptors on liver cells and they release
insulin- like growth factor- 1 (IGF-1).
• This hormone causes body cells to grow and stimulates
protein synthesis within cartilage, bones, and muscle.
• This hormone increases the growth rate of bones and
muscles during childhood.
• GH stimulates the rate at which amino acids enter cells
and protein synthesis occurs.
• GH stimulates fat and carbohydrate metabolism.

Hyposecretion (underproduction)
of the Growth Hormone during
growing years causes slow bone
growth and the epiphyseal plates
close before normal height is
reached.
DX,
 clinically
 serum GH level
Treatment: hormonal replacement
What Causes this Disorder?

• Complete lack of GH is not fatal in adults
as would be the case with some
hormones,
• but it can have major detrimental effects
that may cause disease some years
earlier than might otherwise have been the
case.
Hypopituitarism (Adult)- GH

• Lack of GH causes changes in blood
cholesterol concentrations
• GH deficient adults have been shown to
suffer from excessive tiredness, anxiety,
depression and generally feeling unwell, as
well as having feelings of social isolation
and a tendency to be easily upset.
Hypopituitarism (Adult)- GH……….

–Increased CV disease
–Excessive tiredness
–Anxiety
–Depression
–Reduced “quality of life”
–Possible premature death
Generally Lack of GH leads to:

Hypofunction – Posterior pituitary
Normal urine production

• Diabetes insipidus (DI) literally means the
passage of copious volumes of urine
'lacking taste', in contrast to the 'sweet
tasting' urine typical of diabetes mellitus.
• DI is characterized by the production of
large volumes of dilute urine (more than 3
liters per day) and constant thirst.
Diabetes Insipidus

• DI is usually insidious but can occur with
damage to the hypothalamus or the pituitary
(neurogenic DI)
• May be a result of defect in renal tubules, do not
respond to ADH (nephrogenic DI)
• Decreased production or release of ADH results
in massive water loss
• Leads to hypovolemic & dehydration
Diabetes Insipitus (DI)

1.Primary/Idiopathic: account for approximately 50 % of
the cases of diabetes insipidus.
2. Injury to the hypothalamus –pituitary area: may
result from head trauma, neurosurgical procedures such
as hypophysectomy.
3. Less common causes: neoplasms, histiocytosis,
granulomas, vascular lesions, infections
(encephalitis)
causes of Diabetes Insipidus

TYPES &ETIOLOGY OF DIABETES INSIPIDUS

facts about Diabetes Insipidus
 in USA, 3 cases per 100,000 population
 No significant sex-related differences in central or
nephrogenic DI exist, with male and female prevalence
being equal.
 no significant differences in prevalence among ethnic groups
have been found.
 With both central and nephrogenic DI, inherited causes
account for approximately 1-2% of all cases.
 An incidence of about 1 in 20 million births for nephrogenic
DI caused by AQP2 mutations (Romesh Khardori,2013)

• different types of receptor for vasopressin.
• The V1 receptor present in the endothelial cells
leads to a pressor effect by the activation of Ca++
pathway whereas
• V2R is the one responsible for water reabsorption
by activating cyclic adenosine monophosphate
(cAMP) in the kidneys and opening of the
aquaporin
pathophysiology of Diabetes Insipidus

• balance is normally achieved by three
mechanisms:
1.adequate vasopressin secretion
2.thirst appreciation and drinking
3.vasopressin-responsive kidneys

• The onset of central DI is usually acute and
accompanied by excessive fluid loss.
• if it is secondary two brain surgery central DI has a
triphasic pattern:
abrupt onset of polyuria,
urine volume normalizes,
central DI is permanent.
The third phase occurs within 10 to 14 days postoperatively.

• Polyuria: with urine volume f 3-15 L daily,
Nocturia is almost always present, which may
disturb sleep and cause mild day time fatigue
or somnolence.
• Thirst (polydipsia): A conscious patient with
normal thirst mechanism and free access to
water will maintain hydration.

• If oral fluid intake cannot keep up with urinary
losses, severe dehydration results especially in
unconscious patients or infants.
• In addition, the patient may show central nervous
system (CNS) manifestation ranging from
irritability and mental dullness to coma, related to
increasing serum osmolality and hypernatremia.

 Polyuria of more than 3 litres per 24
hours in adults (may be up to 20!)
 Urine specific gravity low <1.005
 urine osmolality of less than 100 mOsm/kg
(100 mmol/kg).
 Serum osmolality is elevated (usually
greater than 295 mOsm/kg
Diagnostic Tests

• plasma osmolality in untreated patients
helps to distinguish the cause of polyuria.
• In DI, the loss of free water leads to high
osmolality (up to 310 mOsm/kg).
• In psychogenic polydipsia excess fluid
intake is primary and serum osmolality is
low (255 -280 mOsm/kg )
Diagnostic Tests

• Used to differentiate causes of diabetes insipidus .
• After The patient is deprived of water for 8 to 12
hours osmolality is measured !
• Five (5 U) of aqueous vasopressin or 2 μg of
desmopression is injected SC. Urine osmolality after
1 hr .Patients with central DI exhibit a dramatic
increase in urine osmolality, from 100 to 600
mOsm/kg, In nephrogenic DI not increase.
Water deprivation test

Interpretations of Water deprivation test

• Another test to differentiate central DI from
nephrogenic DI is to measure the level of ADH
after an analog of ADH (e.g., desmopressin) is
given.
• If the cause is central DI, the kidneys will
respond to the hormone by concentrating urine.
• If the kidneys do not respond in this way, then
the cause is nephrogenic.
Diagnostic Tests

Medical management includes
Rehydration IV fluids (hypotonic)
Symptom management
Hormonal therapy
For nephrogenic DI: thiazide diuretics,
mild salt depletion, prostaglandin
inhibitors (i.e. ibuprophen)
Management

• Aqueous vasopressin SC or IM in doses of 5-10 U.
Since effect lasts 6 h or less, use in chronic
treatment is limited.
• Desmopresin (synthetic vasopressin) in a dose of
0.05-0.2ml applied to the upper respiratory
mucous membrane twice daily by nasal cannula
or nasal spray.
• The effect lasts 12-24 h, can be given SC or IV
• Has preparation of choice for both adults and
children.
Management

• Chlorpropamide :in patients who have partial
ADH deficiency : 250-500 mg PO
• Thiazide diuretics: Thiazides are only partially
effective, decreasing the urine volume by
30%-50 %.
• Restricting salt intake may be helpful.
• Prostaglandin inhibitors such as indomethacin
(1.5-3 mg/kg/d PO in divided doses) may be
effective.
• Treatment of underlying causes of DI
Management

–Carbamazepine
–In vivo studies showed carbamazepine
decreased the urinary volume and increased the
urinary osmolality by increasing that aquaporin
2 expression in the inner medullary collecting
duct
–Indapamide : for mild form of CDI as it increases
urinary osmolality and decrease serum
osmolality
(J. D. Cook, Y. H. Caplan.et.al,2013)
Evidences on Treatment of DI

– Chlorpropamide : It potentiates the antidiuretic
action of circulating arginine vasopressin and leads
to a reduction of urinary output by 15%.
– But it has side effect .i.e.hypoglycemia,
hyponatremia, hyperlipidemia, hyperuricemia,
hypercalcemia,hypokalemia, metabolic alkalosis,
and myopathy.
(J. D. Cook, Y. H. Caplan.et.al,2013)
Treatment

–Lithum-induced NDI can be managed to a
large extent by simply increasing water
intake.
–Amiloride at doses 2.5–10 mg/dL
decreases the lithium entry into principal
cells
(Chadi Saifan, Rabih Nasr,2013)
Treatment

– Thiazides induce hypovolemia and increase the
proximal tubular water reabsorption and thus
reduce polyuria.
– NSAIDS on the other hand can reduce the
negative effect of intrarenal prostaglandins on
urinary concentrating mechanism and help manage
NDI.
(Chadi Saifan, Rabih Nasr,2013)
Treatment

 assess for signs of fluid and electrolyte
imbalance
 Monitor patient level of consciousness
 Assess serum and urine values
 Assess level of drayness
Nursing assessment

• Fluid Volume Deficit
• Risk for Injury r/t altered LOC
• Sleep Pattern Disturbance r/t urinary frequency
or anxiety
• Altered Urinary Elimination r/t excess urinary
output
• Body Image disturbance related to frequent
urination
POSSIBLE NURSING DIAGNOSIS

 Monitor for signs of fluid and electrolyte
imbalance
 Monitor in and out
 Daily weight
 Monitor for excessive thirst or output
 Assess serum and urine values (decreased SG,
decreased urine osmolality, high serum
osmolality are early indicators of the problem
Nursing intervention

– almost all of the pituitary related problems are directly or
indirectly relted with tumor
– Most of the time tumors are asymptomatic
– Pituitary disorders are due to either increase or decrease
hormonal secration
– Anterior pituitary disorders
• Excess:giantizem,acromegaly,cushing diseases
• Hyposecretion,dawarfizem in childrens
– Postirior:excess;SIADH,if Hypo:DI
summery

After completion of the lecture the student able to ;
• Understand the normal anatomic and physiological over
view of adrenal gland
• Describe major adrenal gland disorder.i.e
pheochromocytoma,cushing syndrome, and primary
aldostrolizem
• Discuses etiology of adrenal gland disorders
• Explain the pathophysiology and clinical presentation of
those disorders
• Identify the appropriate medical and nursing management
Disorder of The Adrenal gland

Anatomic and Physiologic Overview

• The adrenal gland lies just above the kidneys
• Divided into two main sub-organs
Adrenal cortex
–Secretes the steroid hormones
• Glucocorticoid
• Mineralocorticoid
• Androgens

Adrenal medulla
Stimulation of preganglionic sympathetic
nerve fibers, which travel directly to the cells
of the adrenal medulla, causes release of the
catecholamine hormones epinephrine and
norepinephrine

–The hypothalamus secretes corticotropin-
releasing hormone (CRH),
–stimulates the pituitary gland to secrete
ACTH, which stimulates the adrenal cortex to
secrete glucocorticoid hormone (cortisol).
–Increased levels of the adrenal hormone then
inhibit the production or secretion of CRH
and ACTH.

• Glucocorticoids
• Glucocorticoids are secreted from the adrenal
cortex in response to the release of ACTH from the
anterior lobe of the pituitary gland
• The glucocorticoids are so named because they
have an important influence on glucose metabolism:
• increased hydrocortisone
secretion results in elevated blood glucose levels.
Major hormones secreted from adrenal
gland

• Mineralocorticoids: aldosterone
• Mineralocorticoids exert their major effects on electrolyte
metabolism.
• They act principally on the renal tubular and gastrointestinal
epithelium to cause increased sodium ion absorption in
exchange for excretion of potassium or hydrogen ions.
• It is primarily secreted in response to the presence of
angiotensin II in the bloodstream.
gland

• Adrenal Sex Hormones (Androgens)
• exert effects similar to those of male sex
hormones.
• The adrenal gland may also secrete small
amounts of some estrogens, or female sex
hormones.
• ACTH controls the secretion of adrenal
androgens.
gland

Pheochromocytoma
• Pheochromocytoma is a tumor that is usually
benign and originates from the chromaffin cells of
the adrenal medulla.
• In 90% of patients the tumor arises in the medulla;
• in the remaining patients, it occurs in the extra-
adrenal chromaffin tissue located in or near the
aorta, ovaries, spleen, or other organs.
Specific Disorders of the Adrenal Glands

• It may occur at any age, but its peak incidence is
between 40 and 50 years of age
• It affects men and women equally.
• Ten percent of the tumors are bilateral, and 10% are
malignant.
• Because of the high incidence in family members of
affected people, the patient's family members should
be alerted and screened for this tumor.
Pheochromocytoma…………………………..

• Pheochromocytoma is the cause of high blood
pressure in 0.1% of patients with hypertension
(Bravo & Tagle, 2003).
• Although it is uncommon, it is one form of
hypertension that is usually cured by surgery
• without detection and treatment, it is usually
fatal.

Rule of Tens: Ten percent of
pheochromocytomas are:
–bilateral ,malignant ,extra-adrenal, familial ,in
children
–Pheochromocytomas occur in people of all
races, although they are diagnosed less
frequently in blacks. (Michael A Blake,2015)

Pheochromocytomas may occur in persons of any
age, but the peak incidence is from the third to the
fifth decades of life.
Fifty percent of pheochromocytomas in children are
solitary intra-adrenal lesions, 25% are present
bilaterally, and 25% are extra-adrenal.
(Michael A Blake,2015)

– Multiple endocrine neoplasia, type II (MEN II) is a
disorder resulting in tumors in more than one part of
the body's hormone-producing (endocrine) system
i.e.thyroid, parathyroid, lips, tongue and
gastrointestinal tract.
– Von Hippel-Lindau disease can result in tumors at
multiple sites, including the central nervous system,
endocrine system, pancreas and kidneys.
Etiology: Genetic factors

–Neurofibromatosis 1 (NF1) results in multiple
tumors in the skin (neurofibromas),
pigmented skin spots and tumors of the optic
nerve.
–Hereditary paraganglioma syndromes are
inherited disorders that result in either
pheochromocytomas or paragangliomas.
Etiology

–Pheochromocytomas are chromaffin cell
tumor that synthesize and release
catecholamines.
–Norepinephrine is usually the most abundant
with smaller doses of epinephrine.
–All sign and symptoms is related with
excessive catecholamines secretion
Pathophysiology of Pheochromocytoma

• The nature and severity of symptoms depend
on the relative proportions of epinephrine and
norepinephrine secretion.
• The typical triad of symptoms is headache,
diaphoresis, and palpitations in the patient
with hypertension
• 8% of patients are completely asymptomatic.

• The hypertension may be intermittent or persistent.
• However, only half of patients with
pheochromocytoma have sustained or persistent
hypertension.
• If the hypertension is sustained, it may be difficult
to distinguish from other causes of hypertension.
Clinical Manifestations………..

• tremor,
• headache,
• flushing, and anxiety.
• Hyperglycemia may result from conversion
of liver and muscle glycogen to glucose
due to epinephrine secretion;
Clinical Manifestations………..

– characterized by acute, unpredictable attacks
lasting seconds or several hours.
– Symptoms usually begin abruptly and subside
slowly.
– During these attacks, the patient is extremely
anxious, tremulous, and weak.
– Blood pressures exceeding 250/150 mm Hg have
been recorded.
clinical picture in the paroxysmal form of
pheochromocytoma

– polyuria, nausea, vomiting, diarrhea, abdominal
pain, and a feeling of impending doom.
– Associated with blood pressure :dysrhythmias,
dissecting aneurysm, stroke, and acute renal failure.
– Postural hypotension, (lightheadedness, dizziness
on standing) occurs in 70% of patients with
untreated pheochromocytoma.
clinical picture in the paroxysmal form of
pheochromocytoma

– Physical exertion, Anxiety or stress
– Changes in body position, Bowel movement, Labor
and delivery
– Foods high in tyramine, a substance that affects
blood pressure, also can trigger a spell.
– Tyramine is common in foods that are fermented,
aged, pickled, cured, overripe or spoiled.
factors that exacerbate acute attack:

– These foods may include: Some cheeses, beers
and wines, Dried or smoked meats ,Avocados,
bananas and fava beans, Pickled fish
– Certain medications:Decongestants,Monoamine
oxidase inhibitors (MAOIs), such as phenelzine
(Nardil), tranylcypromine (Parnate) and
isocarboxazid (Marplan),Stimulants, such as
amphetamines or cocaine
factors that exacerbate acute attack………

Clinically: “five Hs”: hypertension, headache,
hyperhidrosis ,hypermetabolism, and
hyperglycemia.
–The presence of these signs has a 93.8%
specificity and a 90.9% sensitivity for
pheochromocytoma (Brunner 11th
,edition,American ca society ,2014).

–urine and plasma levels of catecholamines
and metanephrine (MN),
–a catecholamine metabolite, are the most
direct and conclusive tests for over activity of
the adrenal medulla.
–A negative test result virtually excludes
pheochromocytoma.
– However, increased levels of at least one
catecholamine or MN can occur in 10% of
patients with essential hypertension.
Assessment and Diagnostic Findings…………….

–A 24-hour specimen of urine is collected
for determination of free
catecholamines, MN, and VMA; the use
of combined tests increases the
diagnostic accuracy of testing.
–Levels can be as high as two times the
normal limit.

Reference interval :
• Vanillyl mandelic acid (VMA) : 1.4-6.5
mg/24 hr (7-33 μmol/day)
• Keep 24-hr urine collection at pH <3.0 with
HCl acid as preservative.
• Metanephrine 92-934 mcg/day

• A number of medications and foods, such as coffee
and tea (including decaffeinated varieties), bananas,
chocolate, vanilla, and aspirin, may alter the results
of these tests;
• Urine collected over a 2- or 3-hour period after an
attack of hypertension can be assayed for
catecholamine content.
• Avoid physical stress :Supine position and at rest for 30 minutes

• amphetamines, nose drops or sprays,
decongestant agents, bronchodilators) may
increase
• Normal plasma values of epinephrine are
100 pg/mL (590 pmol/L); norepinephrine
less than 100 to 550 pg/mL (590 to 3240
pmol/L).

• Values of epinephrine greater than 400 pg/mL
(2180 pmol/L) or norepinephrine values greater
than 2000 pg/mL (11,800 pmol/L) are considered
diagnostic of pheochromocytoma.
• Values that fall between normal levels and those
diagnostic of pheochromocytoma indicate the need
for further testing.

A clonidine suppression test normally
decrease
–In pheochromocytoma, increased
catecholamine levels result from the
diffusion of excess catecholamines into the
circulation, bypassing normal storage and
release mechanisms.

–Imaging studies, such as CT, MRI, and
ultrasonography,
–evaluating the function of other endocrine
glands because of the association of
pheochromocytoma in some patients with
other endocrine tumors.

• Alcohol withdrawal
• Labile essential hypertension
• Hyperventilation
• Multiple pharmacologic agents: Monoamine oxidase
inhibitors (MAOIs), decongestants, and
sympathomimetics Illegal drug use
• Migraine headache
• Autonomic neuropathy
Differentials diagnosis

Non pharmacological
–During an episode or attack of
hypertension, tachycardia :bed rest with the
head of the bed elevated to promote an
orthostatic decrease in blood pressure.
Medical Management

• alpha-adrenergic blocking agents (eg,
phentolamine [Regitine]) or
• smooth muscle relaxants (eg, sodium
nitroprusside [Nipride]) to lower the blood
pressure quickly.
• Phenoxybenzamine (Dibenzyline), a long-
acting alpha-blocker, may be used after the
blood pressure is stable to prepare the patient
for surgery.
Pharmacologic Therapy

–Calcium channel blockers such as nifedipine
–They are also useful for prevention of
cardiovascular complications, because they
prevent catecholamine-induced coronary
vasospasm and myocarditis
–propranolol (Inderal) may be used in
patients with cardiac dysrhythmias and in
those not responsive to alpha-blockers.

–Alpha-adrenergic and beta-adrenergic
blocking agents must be used with caution,
because patients with pheochromocytoma
may have increased sensitivity to them.
–preoperatively catecholamine synthesis
inhibitors, such as alpha-methyl-p-tyrosine
(metyrosine) May be used

• The definitive treatment of
pheochromocytoma is surgical removal of the
tumor, usually with adrenalectomy.
• Bilateral adrenalectomy may be necessary if
tumors are present in both adrenal glands.
Surgical Management

• Manipulation of the tumor during surgical excision
may cause release of stored epinephrine and
norepinephrine, with marked increases in blood
pressure and changes in heart rate.
• Therefore, use of sodium nitroprusside (Nipride) and
alpha-adrenergic blocking agents may be required
during and after surgery
Surgical Management…….

• Corticosteroid replacement is required if bilateral
adrenalectomy or for the first few days or weeks
after removal of a single adrenal gland.
• IV administration of corticosteroids
(methylprednisolone sodium succinate begin on the
evening before surgery and continue during the
early postoperative period to prevent adrenal
insufficiency.

• Oral preparations of corticosteroids (prednisone) are
prescribed after the acute stress of surgery
diminishes.
• Hypotension and hypoglycemia may occur because
of the sudden withdrawal of excessive amounts of
catecholamines.
• Therefore, careful attention is directed toward
monitoring and treating these changes.

• Blood pressure is expected to return to normal
with treatment; one third of patients continue to be
hypertensive after surgery if
 not all pheochromocytoma tissue was removed,
 pheochromocytoma recurs, or
 if the blood vessels were damaged by severe and
prolonged hypertension.

–Several days after surgery, urine and
plasma levels of catecholamines and their
metabolites are measured to determine
whether the surgery was successful.

Cardiac: CHF, MI, arrhythmias, orthostasis
from volume contraction
Metabolic: Increased metabolic rate, weight
loss
Endocrine: Hyperglycemia from suppression of
insulin production by the excessive
catecholamines
Complications of Pheochromocytoma

Assessment
vital signs
• Blood pressure
– Hypertension (before and during surgery)
– Hypotension (after surgery)
• Blood sugar
• Hypoglycemia (after surgery)
• Hyperglycemia (before and during surgery)
Nursing processes

hemodynamic parameters
 fluid and electrolyte status—
including intake and urinary output
and urine catecholamine levels.
 Assess the patient for bleeding and
infection
Assess the patient for pain
Nursing asst…….

• Anxiety related to potential seriousness
and Sudden onset sign and symptoms of
the problem.
• Ineffective renal tissue perfusion related to
adverse effects of high blood pressure in
renal vascular system.
• Risk for injury related to potential for
hypertensive crisis.
Possible Nursing DX

preoperative
• Patient preparation includes control of
blood pressure and blood volumes; usually
this is carried out over 4 to 7 days.
• Nifedipine and nicardipine may be used
safely without causing undue hypotension.
Nursing Management

–the nurse informs the patient about the
importance of follow-up monitoring to
ensure that pheochromocytoma does not
recur undetected
–Several IV lines are inserted for administration
of fluids and medications.
preoperative……..

–The patient is monitored for several days in
the intensive care unit with special attention
given to ECG changes, arterial pressures,
fluid and electrolyte balance, and blood
glucose levels.
postoperative phase nursing care

• Teaching Patients Self-Care
• After adrenalectomy, use of corticosteroids
may be needed.
• Therefore, the nurse instructs the patient
about their purpose, the medication
schedule, and the risks of skipping doses or
stopping their administration abruptly.
postoperative phase nursing care……..

• It is important to teach the patient and family how
to measure the patient's blood pressure and when
to notify the health care provider about changes in
blood pressure.
• provides verbal and written instructions about the
procedure for collecting 24-hour urine specimens
to monitor urine catecholamine levels.

• Continuing Care
• A follow-up visit from a home care nurse may
be indicated to assess the patient's
postoperative recovery, surgical incision, and
compliance with the medication schedule.
• This may help reinforce previous teaching
about management and monitoring.

• nurse also obtains BP measurements and assists the
patient in preventing problems that comes from long-
term use of corticosteroids.
• Because of the risk for recurrence of hypertension,
periodic checkups are required, for young patients
and families history of pheochromocytoma.
• The patient should have appointments to observe
urine levels of catecholamine.

1) Pheochromocytomas are causes of hypertension.
2) Diagnosis is usually made by increased 24 hour
urine catecholamine metabolites.
3) Surgery is the treatment of choice but it
considered as high risk due to hemodynamic
instability.
4) Pre-operative treatment includes use of alpha
blockers, beta blockers, and metyrasine.
Key Points about Pheochromocytomas

• Addison's disease, or adrenocortical insufficiency,
occurs when adrenal cortex function is inadequate
to meet the patient's need for cortical hormones.
• Inadequate secretion of ACTH from the pituitary
gland also results in adrenal insufficiency because
of decreased stimulation of the adrenal cortex.
Adrenocortical Insufficiency (Addison's Disease)

• Autoimmune or idiopathic atrophy of the adrenal
glands is responsible for 80% to 90% of cases
• surgical removal of both adrenal glands and
infection of the adrenal glands.
• Tuberculosis and histoplasmosis are the most
common infections that destroy adrenal gland
tissue.
Etiology &Pathophysiology

• Therapeutic use of corticosteroids is the most
common cause of adrenocortical insufficiency
• sudden cessation of exogenous
adrenocortical hormonal therapy, which
suppresses the body's normal response to
stress and interferes with normal feedback
mechanisms.

• primary cause (Addison’s disease) Adrenocortical
insufficiency (hypofunction of the adrenal cortex)
• secondary cause (lack of pituitary ACTH secretion).
• In Addison’s disease, all adrenal corticosteroids
(glucocorticoids,mineralocorticoids, and androgens)
are reduced but in secondary adrenocortical
insufficiency, corticosteroids and androgens are
deficient others are almost not decrease.

• In Iceland from secondary data 26 weman,27 men from
100,000 has Addison diseases (Anderi snaer,2016)
• In Germany between 100 and 129 per million and showed
an annual increase of 6.7 % on average. The prevalence
was lower in men (73-90 per million with an annual increase
of 5.5 % on average) than in women (129-169 per million
with an annual increase of 7.1 % on average) (Meyer G
.et.al,2014)
General fact about Addison's

• dark pigmentation of the mucous membranes
and the skin, especially of the knuckles, knees,
and elbows; (1st sign)
• muscle weakness; anorexia; gastrointestinal
symptoms; fatigue; emaciation;
• hypotension; and low blood glucose, low serum
sodium, and high serum potassium levels.

• Mental status changes such as depression,
emotional lability, apathy, and confusion are
present in 60% to 80% of patients.
• In severe cases, the disturbance of sodium
and potassium metabolism may be marked by
depletion of sodium and water and severe,
chronic dehydration.

• Addisonian crisis :With disease progression
and acute hypotension, addisonian crisis
develops
causes
 dehydration resulting from preparation for
diagnostic tests
 surgery
Clinical Manifestations…..

• characterized by cyanosis and the classic
signs of circulatory shock:
• pallor, apprehension, rapid and weak pulse,
rapid respirations, and low blood pressure.
Clinical Manifestations Addisonian crisis

• In addition, the patient may complain of headache,
nausea, abdominal pain, and diarrhea and may show
signs of confusion and restlessness.
• Even slight overexertion, exposure to cold, acute
infection, or a decrease in salt intake may lead to
circulatory collapse, shock, and death
if untreated.
Clinical Manifestations Addisonian crisis…….

• clinical manifestations presented appear specific,
but it may presented with nonspecific symptoms.
• The diagnosis is confirmed Combined
measurements of early-morning serum cortisol
and plasma ACTH are performed to differentiate
patients with primary adrenal insufficiency from
those with secondary adrenal insufficiency

• Patients with primary insufficiency have a
greatly increased plasma ACTH level (more
than 22.0 pmol/L) and a serum cortisol
concentration lower than the normal range
(less than 165 nmol/L) or
• Other findings hypoglycemia , hyponatremia,
hyperkalemia, and leukocytosis.
Assessment and Diagnostic Findings……….

• If the adrenal cortex is destroyed,ACTH
administration fails to cause the normal increase in
plasma cortisol and urinary 17
hydroxycorticosteroids.
• If the problem is on pituitary, a normal response to
repeated doses of exogenous ACTH is seen, but no
response occurs after the administration of
metyrapone, which stimulates endogenous ACTH.
Assessment and Diagnostic Findings……….

• In acute case First Rx circulatory shock: 5%
dextrose in normal saline.
• monitoring vital signs, and placing the patient in a
recumbent position with the legs elevated.
• Hydrocortisone, IV, 200 mg stat, followed by 100
mg, IV, 6 hourly until condition is stable
• Vasopressor amines may be required if
hypotension persists.
Medical Management

• Maintenance
• Prednisolone, oral, 5 mg morning and 2.5 mg
evening each day - Patients SHOULD NOT stop
treatment if they become ill. Rather double the
regular doses of corticosteroids where required.
• Revert to hydrocortisone, IV for even minor surgical
procedures including labor and delivery
Pharmacologic mgt

• Antibiotics may be administered if infection has
precipitated adrenal crisis
• Oral intake may be initiated as soon as tolerated.
• IV fluids are gradually decreased after oral fluid
intake is adequate to prevent hypovolemia.
• supplement dietary intake with added salt during
gastrointestinal losses of fluids through vomiting and
diarrhea.
Medical Management…………………………

• Assess for symptoms of fluid imbalance
• blood pressure and pulse rate as the patient moves
from a lying to a standing position.
• skin color and turgor for hypovolemia.
• assessments weight changes, muscle weakness,
and fatigue and
• any illness or stress that may have precipitated the
acute crisis
Nursing Management

• Monitoring and Managing Addisonian Crisis
• The patient at risk is monitored for signs and
symptoms indicative of addisonian crisis.
• The patient with addisonian crisis requires immediate
treatment with IV administration of fluid, glucose, and
electrolytes, especially sodium; replacement of
missing steroid hormones; and vasopressors.
Nursing Management…………….

• anticipates the patient's needs and takes measures
to meet them to avoid exertion which exacerbate
addisonian crisis .
• Assess vital signs, weight, and fluid and electrolyte
status which indicates patient's progress.
• efforts are made to identify and reduce the factors
that may have led to the crisis.

• Restoring Fluid Balance
• assesses the patient's for fluid imbalance ,
• instructing the patient to report increased thirst, which
may indicate impending fluid imbalance.
• Lying, sitting, and standing BP provide information
about fluid status.
• A decrease in systolic pressure (20 mm Hg or more)
may indicate depletion of fluid volume

• Improving Activity Tolerance
• Until the patient's is stabilized, avoid unnecessary
exertion to decrease hypotenesion
• Efforts are made to detect signs of infection or the
presence of other stressors.
• Explaining all procedures to the patient and family
reduces their anxiety.

• During the acute crisis, the nurse maintains a
quiet, non stressful environment and
performs all activities (eg, bathing, turning)
for the patient.
• Explaining the rationale for minimizing stress
during the acute crisis assists the patient to
increase activity gradually.

• Teaching Patients Self-Care
• patient and family members receive explicit verbal
and written instructions about replacement
therapy,how to modify the medication dosage and
increase salt intake in times of illness, very hot
weather, and other stressful situations.
• About diet and fluid intake to help maintain fluid and
electrolyte balance.

• Teach about preloaded, single-injection syringes of
corticosteroid for use in emergencies.
• Specific instructions about how and when to use the
injection are also provided.
• Precautions (wear a medical alert bracelet) to
administer corticosteroids.
• Inform about signs of excessive or insufficient
hormone replacement.

–If the patient requires surgery, careful
administration of fluids and corticosteroids is
necessary before, during, and after surgery to
prevent addisonian crisis.

• Continuing Care
• In some patients they might have concurrent
illnesses or incomplete recovery
• home care to assess the patient's recovery, monitor
hormone replacement, and evaluate stress in the
home.
• The nurse assesses the patient's and family's
knowledge about medication and dietary
modifications.

• Cushing's is a disorder in which the adrenal
glands are producing too much cortisol
(hypercotisolism).
• If the source of the problem is the pituitary gland,
then the correct name is Cushing's Disease
• if it originates anywhere else (adrenal tumors,
long term steroid administration) then the correct
name is Cushing's Syndrome.
Cushing's Syndrome

 Men had a 3x greater incidence of the ectopic
ACTH syndrome,
 Women are 3-8x more likely than men to
develop Cushing's disease, 4-5x more likely to
have Cushing's syndrome
 Age-related incidence: increasing rapidly after
age 50 years
 Cushing's disease occurs mainly in women aged
25 to 45 years
(European endocrinology society report ,2011)
Facts about Cushing syndrome

• 40 cases per million population .
• 2-5% of patients are with poorly controlled
diabetes and hypertension.
• Female preponderance is generally
assumed to be close to 3:1
 Frederic Castinetti et.al.2012
Facts about Cushing syndrome

• Iatrogenic hypercortisolism resulting from
medical intervention is most common cause
of Cushing Syndrome.i.e. long term
glucocorticoid treatment for asthma, arthritis,
and other conditions.
• Pituitary hyper secretion and pituitary tumors
account for 70% of Cushing’s Disease.
Etiology - Hypercortisolism

• Adrenal tumors account for 30%.
• Ectopic secretion of ACTH by tumors located
outside the pituitary gland are rare cause of
the syndrome and associated with increased
morbidity/mortality (American CA socity
2014).

Frederic Castinetti et.al.2012

• Regardless of the cause, the normal feedback
mechanisms that control the function of the adrenal
cortex become ineffective, and the usual diurnal
pattern of cortisol is lost.
• The signs and symptoms of Cushing's syndrome are
primarily a result of oversecretion of glucocorticoids
and androgens (sex hormones), although
mineralocorticoid secretion also may be affected.
pathogenesis

• moon face - particularly filling in of the temporal
fossa
• weight gain - central obesity
• muscle wasting and proximal myopathy (patients
have difficulty standing from a seated position
without use of arms), muscle wasting, osteoporosis,
truncal obesity

• “buffalo hump” ( cervical fat pad ) and
supraclavicular fat pads contribute to the
Cushingiod appearance
• Symptoms of androgen excess (e.g.
oligomenorrhea, hirsutism, and acne)
• Poor wound healing: due to impaired immune
function.
• Growth retardation in children may be severe.

• Neurological: Psychosis, emotional labiality,
loss of memory, depression
• Integumentary: ecchymosis, purple striae on
abdomen, poor wound healing, skin
infections, thin skin, acne.

Clinical manifestation………………..

• CV: HTN
• GI: peptic ulcers
• Metabolic: hyppokalemia, hypernatremia,
edema, moon face, weight gain.
• Classic symptoms of Cushing’s: moon face,
buffalo hump, purple straie, truncal obesity.
Clinical manifestation………………..

• 24 hr urine cortisol levels
• Serum sodium levels
• Serum potassium levels
• Serum glucose level
• Serum ACTH in Cushing Disease
• ACTH suppression test to identify cause
• Dexamethasone supression test: cause
pituitary or adrenal
• Radiological exam to reveal pituitary or
adrenal tumor
Assessment and Diagnosis

• Plasema (ACTH) (corticotropin) level
• Measures plasma level of ACTH.
• Reference interval:
• Morning: <120 pg/mL (<26 pmol/L)
• Evening: <85 pg/mL (<19 pmol/L)
• Patient should be NPO after midnight before
morning
• blood draw between 6-8 AM.

ACTH measurement : may help to differentiate the cause
of Cushing’s syndrome
a. High normal or slightly elevated ACTH in Cushing’s
diseases
b. Markedly elevated ACTH in Ectopic ACTH production
c. Extremely low ACTH level in automatically functioning
adrenal tumor is the source of excess cortisol.
• Pituitary secretion of ACTH is suppressed due to the
excess cortisol

ACTH stimulation with cosyntropin
• Used to evaluate adrenal function.
• After baseline cortisol sample is drawn, give
cosyntropin (synthetic ACTH) by IV bolus.
• Cortisol samples are drawn 30 and 60 min after
bolus.
• Plasma cortisol at 60 min should increase by >7
mcg/dL from baseline.

• Overnight Dexamethasone suppression test
• Dexamethasone (Decadron) 1 mg (low dose) or 4 mg (high
dose) is given at 11 PM to suppress secretion of corticotropin-
releasing hormone. Plasma cortisol sample is drawn at 8 AM.
• Reference interval: Cortisol level <3 mcg/dL (<0.08 μmol/L) for
low dose and <50% of baseline in high dose indicates normal
adrenal response.
• Ensure that patient has fasted, not take med increase ACTH

Standard Dexamethasone Suppression Test

Response for standard Dexamethasone Suppression Test

• Cortisol (free) Measures free (unbound) cortisol.
Preferred test to evaluate hypercortisolism.
• Reference interval: 20-90 mcg/24 hr (55-248
nmol/day)
• Instruct patient about 24-hr urine collection and
avoidance of stressful situations and excessive
physical exercise.

•At least two first-line tests should be abnormal to
establish the diagnosis of Cushing's syndrome
• Late night salivary cortisol, urinary cortisol, and the
low-dose dexamethasone suppression tests are
first-line tests
• Urinary and salivary cortisol measurements should
be obtained at least twice
2008 Endocrine Society Clinical Guidelines to dx
cushing syndrom

1. Adrenal adenoma : complete surgical resection
of the adenoma cures the disease , but
• patients may need cortisol replacement post
operatively for several months
2. Ectopic ACTH syndrome: can be cured by
treating or removal of the tumor that is producing
the ectopic ACTH.
Medical and surgical management

3. Cushing’s Disease
a. Pituitary radiation : is effective in children but it
cures fewer than 1/3 of adult patients
b. Bilateral adrenalectomy cures Cushing’s
syndrome. Has Disadvantages:
• Patients will develop Addison’s disease
• Nelson’s syndrome: in which pituitary adenomas
undergo rapid growth,
Medical and surgical management

3.Transphenoidal surgery: if due to a pituitary tumor
• Where surgery is contraindicated or fails to reduce
cortisol levels, adrenalectomy and/or pituitary
radiation may be necessary.
• Adrenocortical Inhibitors: (metapyrone,
aminogluthimide, effective short-term.
• Diet: low calorie, carbohydrate & salt. High
potassium.
treatment

• Fluid volume excess
• Risk for infection
• Risk for injury
• Activity intolerance
• Anxiety
• Knowledge deficit
• Risk for impaired tissue integrity
Priority Nursing Diagnoses

• Diet
• Medications
• Medic alert bracelet
• Hormone levels and stress
• Signs of excessive or deficient adrenal
hormones
Patient Teaching

• Post op care for cranial surgery (CSF leak,
ICP etc.)
• Hydrocortisone therapy, some on a long-
term basis
• If surgery results in hypopituitarism, long-
term hormone replacement therapy will be
required
• Moods swings and depression may be a
serious problem that may take months to
treat
Post op Care following Transphenoidal
Surgery

• It is due to Excessive production of
aldosterone causes a distinctive pattern of
biochemical changes and a corresponding set
of clinical manifestations
• Causes
functioning tumors of the adrenal gland
Primary Aldosteronism

• Hypokalemia, decrease hydrogen ions
(alkalosis),
• increase in pH and serum bicarbonate
concentration.
• The serum sodium level is normal or elevated,
depending on the amount of water
reabsorbed with the sodium.
• Hypertension is the most prominent and
almost universal
Pathophysiology and Clinical Manifestations

• muscle weakness, cramping, and fatigue
(Hypokalemia),
• kidneys fail to acidify or concentrate the urine.
• Diluted polyuria.
• Serum, by contrast, becomes abnormally
concentrated (polydipsia) and arterial
hypertension.

• aldosterone action on nerve receptors,
such as the carotid sinus, result in
hypertension.
• sign of hypocalcemia,due to alkalosis
• Glucose intolerance may occur, because
hypokalemia interferes with insulin
secretion from the pancreas.

• high serum aldosterone and low serum renin
levels.
• aldosterone excretion rate after salt loading
• The renin–aldosterone suppresion test can
differentiating the cause of primary aldosteronism.
• Antihypertensive medication may be discontinued
up to 2 weeks before testing.

• Used to assess for hyperaldosteronism.
• Reference interval:
• Upright posture: 7-30 ng/dL (0.19-0.83
nmol/L)
• Supine position: 3-16 ng/dL (0.08-0.44
nmol/L)
Aldostrone level

• Adrenalectomy.
• Spironolactone may be prescribed to control
hypertension.
• Patient is risk for fluctuations in adrenocortical
hormones and requires administration of
corticosteroids, fluids, and other agents to
maintain blood pressure and prevent acute
complications.
Medical Management

• If the adrenalectomy is bilateral, replacement of
corticosteroids will be lifelong;
• if one adrenal gland is removed, replacement
therapy may be temporarily necessary because of
suppression by high levels of adrenal hormones.
• A normal serum glucose level is maintained with
insulin, appropriate IV fluids, and dietary
modifications.
Medical Management

• frequent assessment of vital signs to detect
early signs and symptoms of adrenal
insufficiency and crisis or hemorrhage.
• Explaining all treatments and procedures,
providing comfort measures, and providing
rest periods can reduce the patient's stress
and anxiety level.
Nursing Management

1. Disease of the adrenal cortex
a) Resulting from excess production of hormones
• Cushing’s syndrome : excess cortisol production
• Primary hyperaldosteronism : excess production
of aldosteron
• b) Inadequate production ;Addison’s diseases :
inadequate production of cortisol and aldosteron
Summery of Common Adrenal gland diseases

2. Disease of the adrenal medulla
• Pheochromocytoma: excess production of
catecholamine
• In general adrenal gland problem are
associated with either excess or Inadequate
production of catecholamine, and hormones.
Summery of Common Adrenal gland diseases

• American Cancer Society. (2014). Cancer facts
and figures. Atlanta: Author.
• Brunner & Suddarth's Textbook of Medical-Surgical
Nursing, 11th edition.
• Brunner & Suddarth’s Textbook of Medical-surgical
Nursing. 2010, 12th Ed.
• Medical-Surgical Nursing: Patient-Centered
Collaborative Care, 2013, 7th edition
References

 Lewis Direkson ,Heitkemper Bucher,medical
surgical nursing assessment,9th edition
 Sharon L. Lewis, Shannon Ruff Dirksen, Et Al
.Medical-surgical Nursing: Assessment And
Management Of Clinical Problems, 2014,
Elsevier Inc. Ninth Edition
 Wolters Kluwer,Incrideble medical surgical
nursing practice,2012
References

• Kumar and klark’s.clinical medicine,
2009, Elsevier Limited. 7th edition.
• Porth’s pathophysiology. Concepts of Altered
Health States, 2014 ,9th edition.
• Patricia Gonce Morton, critical care nursing A holistic
approach, 2013, 10th edition.
References

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