Endocrine System

Thyroid Gland
Adrenal Glands
Functions of endocrine
system
 Response to stress and injury.

 Growth and development.

 Reproduction.

 Homeostasis

 Energy metabolism.
 Endocrine glands
 Endocrine glands are specialized cluster of cells
that secrete hormones.

 Secreted hormones go directly into the blood stream

(ductless gland ) in respond to the nervous system
stimulation.

 Endocrine glands include :

 The pituitary gland, thyroid gland,parathyroid glands,
adrenals glands, ovaries and testes.
 Endocrine system
 Hormones are  Hormones do not
chemical messengers cause reactions but
secreted by endocrine rather they are
organs and regulator of tissue
transported throughout responses.
the body where they
exert their action on
specific cells called
target cells.
 Hormones
 Secreted in minimum amount in respond to need.

 Either travel through the blood stream to the target

organ or are secreted locally to produce an effect.

 Transportation of the hormones

 Bounded to plasma proteins such thyroid and
steroid (they serve as a reserve for acute changes)
 Some are transported free in the blood only free
hormones are biological active.
Hormone structure and function
 Chemically hormones  Monoacids analog-
are of three basic derivated from amino
acid tyrosine (T3 and
types:
T4)

 Steroid/products of
cholesterol breakdown  Peptides either a large
such as glucorticoids proteins or a chain of
and mineral corticoids. proteins such ACTH,
TSH or ADH.
 Hormones
 Maintain homeostatic balance utilizing a
feedback mechanism that involves other
hormones, blood or chemicals,and the
nervous system.
 Feedback loop mechanism.
 Sensors in the endocrine system detect
changes in the hormonal levels.

 Hormones are adjusted to maintain

normal body levels.
 Feedback loop mechanism.
 When the sensor detect a decreased in
hormone levels. They began to act to
cause at increased in hormonal level.

 When the hormonal levels rise above

normal, the sensors cause a decreased in
hormonal production.
 Hormonal control
 Hormones are released by your
hypothalamus signals:

 Anterior pituitary gland makes thyroid-

stimulating hormones (TSH).

 (TSH). triggers your thyroid gland to make

hormones thyroxine (T4) and
triiodothyronine (T3).
 Endocrine dysfunctions
 Can be divided into five  Hormonal excess
broad categories tends to caused
severe disease.
 Subnormal hormonal
production, resulting from
malformation, or absent of
the endocrine glands, or  Production of
the gland could be
diseased, or destroyed or
abnormal hormone
secretions are block. cause by a gene
mutation.
 Endocrine dysfunction
 Disorder of hormonal  Disorder of the
receptors. transport mainly
related to lack of
protein to bind the
hormones.
 Abnormality of
hormonal transport or
 Results in increase
metabolism.
free level of the
hormone
 Thyroid gland
 A small gland shaped like a butterfly
located below the larynx; it weights 15-
20g.

 Needs iodine to produce hormones

 It produces these two hormone thyroxine

and triiodothyronine.
 Thyroid hormones
 The glands contain  T3=9% of the
two types of cells hormone secreted is
 Follicular cells which in active form.
produce T3 and T4

 T4=90% of the
 Parafocicullar cells hormone secreted is
which secrete
bounded to protein as
thyrocalcitonin
a storage form; this
form is inactive until
converted to T3.
 Inhibition of the conversion of
T4 to T3
 Several illness  Drugs such as propyl-
thoracic (PTU)
 Fasting
 Radiologic contrast
 Malnutrition dye

 Trauma  Dexamethasone

 Increased age  Propranolol and

amiodarone
 Functions of thyroid
hormones.
 They act on most body systems usually
stimulating them

 Metabolism=Controls and increased the basic

metabolic rate (BMR) increasing oxygen
consumption and heat production.

 Carbohydrate metabolism= stimulates cellular

glucose uptake, glycolysis,gluconeogenesis, GI
absorption and insulin secretion.
 Functions of thyroid
hormones.
 Fat metabolism=enhance lipid metabolism from fat
tissue and free fatty acid oxidation.

 Protein metabolism=stimulate protein synthesis

and degradation; stimulate turn over of proteins.

 Growth=accelerates body growth

 Body Weight=usually decreases due to increase in

BMR
 Functions of thyroid
hormones.
 Cardiovascular=Vasodilatation related to accelerated
metabolism and heat production; increased cardiac output,
increase stroke volume and heart rate.

 GI=increased appetite, food absorption, and GI tract motility.

 Pulmonary=increased oxygen demand leads to increased of

depth and rate of ventilation.

 CNS=nervousness, agitation, restlessness.

 Laboratory thyroid tests

 TSH -level (serum)

 Level T4
 Level T3
Thyroid Function Tests: TSH, T3, and T4
 Diagnostic thyroid test

 RAI uptake test

 A radioactive iodine RAI uptakes test
measure the absorption of I -131 or I -123 by
the thyroid gland. A calculated dose of
radioactive iodine is given P.O or IV 24 hours
later the thyroid is scan. If the uptake of iodine
is increased hyperthyroidism is suspected.
The side and shape of gland can be found.
Thyroid scan
 Hypothyroidism
 The result of decreased thyroid hormone.

 Classified as primary and secondary

 Age of onset is usually over 40 years

 Incident higher in women 5-10:1

 Pathophysiology of
hypothyroidism
 Lack of thyroid hormone lead to decrease in
all body processes, progressing to coma

 The body try to compensate by:

 Peripheral vasoconstriction decrease blood flow to
the extremities.

 Cardiovascular= decreased blood pressure, heart

rate, contractibility, cardiac output and slowed
conductivity.
 Pathophysiology of
hypothyroidism
 Interstitial accumulation of
mucopolysaccharide substance (greatly
increased quantities hyaluronic acid
chondroitin sulfate binds with a protein to form
excessive tissue gel in the interstitial spaces)

 As a result, water accumulated in the

interstitial spaces, which leads to nonprinting
edema.
 Etiology of hypothyroidism
 Primary dysfunction of the thyroid accounts
for 95% of all cases and be associated with
the followings.
 Increased dysfunction after trauma

 Withdrawal of thyroid replacement therapy

 Exposure to cold

 Administrations of tranquilizers, barbiturates or narcotics.

 Removal thyroid gland (thyroidectomy)
 Etiology of hypothyroidism
 Iodine deficiency

 Iodine is necessary for TH synthesis and

secretion.

 Causes: Drugs that block TH synthesis or

goitrogenic compounds in food.
 Etiology of hypothyroidism

 Hashimoto’s thyroid

 Autoimmune disorder that destroy thyroid

tissue and replace it with fibrous tissue
 Etiology of hypothyroidism
 Radioactive iodine  Dopamine inhibit
ablation released TSH from the
hypothyroidism pituitary gland.

 Other drugs  Secondary dysfunction

related related to
 Lithium pituitary dysfunction.
carbonate=inhibits
hormone release  Hypophysectomy
 pituitary tumor or
infection
 Dilantin (Phenytoin)
decreases conversion
of T4 to T3
 Clinical Manifestations of
Hypothyroidism

 Exhaustion

 Depression

 Dry coarse skin

 Manifestations or signs and
symptoms(continue)
 Cold intolerance

 Constipation

 weight gain
Hypothyroidism patients
 Clinical manifestation of
hypothyroidism
 Cardiovascular=Bradycardia, hypotension ,
decreased contractility and cardiac output.

 Neurological =Decreased LOC, lethargy,

memory impairment, slow speech seizure and
coma.

 Most patient do not present with coma but

disorientation, lethargy and confusion.
 Clinical manifestation of
hypothyroidism
 Respiratory=hypoventilation , respiratory
failure.

 Gastrointestinal =weight gain with decreased

appetite, constipation

 Thermal : hypothermia less 35C (95F) cold

intolerance.
 Clinical manifestation of
hypothyroidism
 Edema and deposit of mucopolyssacharide
substance:

 skin facial= edema and enlarged tongue,

 Vocal cords=hoarse
 Middle ear=decreased hearing
 Heart=pericardial effusion
 Lungs= Pleura effusion
 Bowels=paralytic ileus
 Lab and diagnostic for Primary
Hypothyroidism
 TSH is usual increase

 T3 decrease

 T4 decrease
 Diagnostic studies
 Decreased T3 uptake  Increased cholesterol:
(measure T3 the liver is unable to
remaining after excrete cholesterol in
unbounded sites have the bile so it
accumulate and leads
been filled.) to arteriosclerosis and
leads to PVD, and
 Cardiomegaly CAD

 EKG= bradycardia and

 Hypoglycemia prolonged QT , low
voltage
Treatment of hypothyroidism.

 Pharmacological Treatments

 Levothyroxine sodium (T4)

 Liothyroid (T3)

 Liotrix(T4 &T3)
 Nursing responsibility
 Give I hour before meals or 2 hours after a
meal.

 Watch closely patients on anticoagulants,

insulin, and digitalis medications.

 Assess for coronary insufficiency, CP,

increased HR and dispend.
 Nursing Diagnosis.
 Decreased cardiac output

 Alteration in bowel elimination

 Alteration in Skin integrity

 Decreased CO r/t
hypothyroidism
 Assess
cardiovascular
system

 Avoid cold
environment

 Paced activities
Decrease CO in hypothyroidism
 TH deficit causes a reduction of HR and
stroke volume, resulting in decreased
cardiac output.

 In addition it might be fluid accumulation

around the pericardial sac that will further
compromise the cardiac function.
Decrease CO in hypothyroidism
 Assess heart rate and
rhythm

 Monitor cardiac
function.

 Fluid overload

 heart failure
 Hypothermia
 Hypothermia: lack of heat  Avoid electrical
generation related to warming blanket
decreased metabolism. because it can lead to
vasodilatation and
 Monitor temperature vascular collapse.
 Rewarm patient gradually
and passively (plain
blanket and warm room)
Alteration in Bowel elimination

 Encourage patient to keep PO intake of

2000ml per day

 Maintain high fiber diet

 Encourage activities as tolerated

 Myxedema coma

 Characterized by extreme hypothyroidism

 Inadequate circulation of thyroid hormones

 It is a medical and a nursing emergency

Etiology for myxedema coma

 It can be caused by:

 Trauma
 infection
 Emotional stress
 Exposure to cold
 Interruption of medicine

 Pathophysiology
 Lack of TH leads to a decrease in all body
process.

 The body tries to compensate for the

decreased metabolic rate by:
 peripheral vasoconstriction, decreased HR,
BP, CO, and contractility.
 Myxedema coma signs and
symptoms
 Hypothermia  Cardiovascular
collapse
 Hypoglycemia
 Shock
 Hyponatremia
 Coma
 Hypotension
 Physical assessment of
myxedema coma
 CV: Bradycardia, pericardial effusions ,
hypotension.

 Respiratory:Hypoventilation and
respiratory failure

 Thermoregulation: hypothermia
 Physical assessment of
myxedema coma

 Neuromuscular: decrease LOC,

psychosis, and coma.

 GI: weight gain, constipation, and ileus

 Laboratory findings in
myxedema coma
 Decreased T3 and T4 levels

 Hypokalemia

 Elevated cholesterol and lipid

 Hypoglycemia
 Hyperthyroidism
 Define: As an excess of TH in the body

 Cause an increased in Metabolic rate

 Cardiac rate and stroke volume

 Peripheral blood flow
 Oxygen consumption
 Body temperature
 Causes of hyperthyroidism

 Grave’s Disease

 Toxic multinodular goiter

 Excessive thyroid intake

 Excess TSH stimulation

 Lab and Diagnostics
/hyperthyroidism
 TSH-Low in primary disease

 T4 -increase

 T3-radio immunoassay (T3RIA) elevated

 Signs and symptoms

 Fatigue  Hoarseness
 Difficulty sleeping  Dyspnea
 Hand tremors  Tachycardia
 Weight loss despite  Increase blood
increase appetite volume
 Skin =warm, moist,  increased CO
smooth,flushed  Palpitations
 Amenorrhea  Exophthalmos
Patients with hyperthyroidism
Treatments for hyperthyroidism
 Pharmacology

 Radioactive Iodine

 Surgery
 Drug therapy for
hyperthyroidism
 Propylthiouracil (PTU)

 Methimazole(Tapazole)

 Propranolol
 Drug therapy for
hyperthyroidism
 Antithyroid drugs inhibit TH production.
they do not affect the release or activity of
hormone that is already formed.

 Several weeks may elapse before the

patient experience therapeutic effects.
 Drug therapy for
hyperthyroidism
 Iodine Solutions
 Large doses of iodine inhibits TH synthesis
and release. Iodine also make the
hyperplastic thyroid prior to surgery less
vascular and hasten the ability of other thyroid
drug to reduce natural hormones output.

 Sodium Iodine
 SSKI-Potassium iodine
 Radioactive iodine
 Thyroid gland takes iodine in any form,
radioactive iodine I-131 concentrates in
thyroid gland and damage or destroy thyroid
cell so that less TH is produced.

 Radioactive iodine is given P.O ; It takes 6 to

8 weeks to work.
 Thyroid Surgery

 Pre-op-care
 Antithyroid drugs

 Iodine preparation

 Answer questions

 Discuss concern

 Teach pt. to place both hands posteriorly

 Thyroid Surgery

 Post-op -care
 keep HOB 45 degrees

 Support neck and head with pillows.

 Keep suction, oxygen and tracheostomy tray

in the patient room

 Keep an ampulla of CaCl or Calcium

Gluconate in the room
 Nursing
Diagnosis/hyperthyroidism
 Decreased cardiac output

 Sensory Perceptual/Visual

 Alteration in Nutrition less than body

require
 Decreased CO r/t
hyperthyroidism
 Assess for BP, pulse rate and rhythm,
respiratory rate, and breath sounds.

 Increased TH increases HR, stroke volume and

tissue demand for oxygen, causing stress on the
heart this lead to hypertension, cardiac arrhymias
tachycardia and CHF.

 Assess for peripheral edema, jugular vein

distention, activity intolerance.
 Decreased CO r/t
hyperthyroidism

 Provide an environment that is cool and free

of distractions.

 Balance activity with rest periods.

 Decreased stress by explaining procedures

and treatments.
 Sensory perceptual visual R/T
Hyperthyroidism
 Monitor visual acuity,
photophobia,integrity
of the cornea and lid
closure.

 Sleep HOB elevated.

Sensory perceptual visual R/T
Hyperthyroidism
 Report any changes or
pain in vision

 Teach measures for

protecting the eye.

 Apply artificial tear to

moisten eyes

 Use tinted glasses

 Thyroid Crisis/thyroid storm
 Life threatening emergency characterized
by accelerated signs of hyperthyroidism

 Excessive production of thyroid hormone

T3 and T4 result in a persistence
hypermetabolic state.
 Thyroid Crisis/thyroid storm
 More common in women  Likely to occur in
(nine times greater ) than association with an
in men.
autoimmune disease.

 Peak incident is ages 20-

40 years.  Thyroid storm last 8 to
10 days due to the half
 Adrenergic(cathecolomines life of TH (22hrs for T3
) directly related to and 6 days for T4)
increased levels of TH.
 Etiology of thyroid storm
 Causes:
 Stress,infection and trauma

 untreated DM (DKA) thyroid hormone needed

to maintain hypermetabolic rate.

 Manipulation of thyroid gland

 Etiology of thyroid storm
 Graves disease-the most common caused of
thyroid storm.

 Toxic nodular goiter-multiple nodules secrete

T3; most common in the elderly.

 Toxic adenoma

 Excess thyroid hormone intake

 Diagnostic findings for thyroid
crisis
 Enlarge thyroid

 Elevated serum and free T3 and T4

 Elevated T3 resin uptake( > metabolism)

 Hyperglycemia(due to insulin resistance

and breakdown of store glucose)
Diagnostic findings for thyroid
crisis
 Increased sodium and Calcium,
transaminases, creatine kinase (due to
increased tissue breakdown)
 Thyroid crisis signs and
symptoms
 Hyperthermia  Agitation
 Tachycardia  Tremors
 Systolic Hypertension  Confusion
 Abdominal symptons
 diarrhea
 vomiting
 Clinical manifestations thyroid
storm
 All body system can be  Oxygen consumption,
affected by increased blood pressure and
levels of T3 widen pulse pressure.

 CV-Atrial fibrillations,  Pulmonary edema and

palpitations, S3 gallop. congestive heart
failure.
 Increased stroke volume,
myocardial demands
 Clinical manifestations thyroid
storm
 Neurological functions  proximal muscle
weakness
 restlessness

 nervousness

 tremors

 hyperreflexia
 Clinical manifestations thyroid
storm
 Hepatic  Bilirubin
 hepatomegaly
 Alkaline phosphate

 Elevated ALT (alanine

transaminase)

 AST(aspartame
transaminase)

 Bilirubin
 Clinical manifestations thyroid
storm
 Gastrointestinal  Abdominal pain

 Increased gastric
motility (diarrhea)

 Nausea/ Vomiting

 Increased appetite
with weight loss
 Clinical manifestations thyroid
storm
 Thermal
 heat intolerance

 temperature may rise

above 40.6 C(105 F)

 profound fluid losses

from diaphoresis /up to
4 L a day
 Treatment for thyroid crisis
 Stabilizing cardiovascular functions

 Support any body system

 Reducing TH function and secretion

 Medications for thyroid storm
 Administration of
propanolol (beta
adrenergic blocking
agent)
 It decreases effects of
cathecholamines
decreasing heart rate
and tremors.
 Administer thyroid
inhibiting drugs
 Propylthiouracil
(PTU)can inhibit
conversion T4 to T3.
 Methimazole
(Tapazole) inhibit
thyroid
peroxides(enzyme for
oxidation of iodine)
which is used for TH
formation
 Medications for thyroid storm
 Administer thyroid
 Lugol solution (SSKI or
inhibiting drugs saturated solution of
potassium iodine)
 Lithium Carbonate-it blocks the release of
blocks the release of thyroid hormone.
TH from the gland; use
in patients that are
intolerant to PTU or
Tapazole.
Other medications effects on
thyroid storm
 Administer pain
 Radioactive iodine is medication as needed
taken up by the gland avoid acetylsalicylic
and it is destroyed in acid (ASA) as it
the follicles. displaces T3 from
protein , making
available for metabolic
activity.
Compare patients with thyroid
disorders
 The adrenal glands
 The adrenal glands are bilaterally located
above each kidney and consist of two
tissues in one gland:

 Cortex -outer layer

 Medulla-inner portion
 Adrenal medulla produces
 Medulla
 Makes up 15% of the gland
 mimic sympathetic nervous system stimulation.
 Catecholamines

 Epinephrine

 Norepinephrine
Disorder of the adrenal medulla
 Pheochromocytoma a benign tumor of the
adrenal medulla leading to hyper production
of epinephrine and nonepinephrin.

 Ectopic cells in the abdomen or along the

ganglia

 Excess of adrenal medulla hormones

 Adrenal medulla
Labs
 Cathecholamines: epinephrine and nor-
epinephrine can be measured in 24hrs
urine collection;by measuring their
metabolites

 Vanillymandelic Acid (VMA)

 Metanephie
 Adrenal medulla
Labs and diagnostic

 Cathecholamine increases in the blood

 X ray or radiology studies

 Signs and symptons of
pheochromocytoma
 Hypertension  Headache

 Shakiness,
diaphoresis

 Palpitations
tachycardia

 Feelings of anxiety
 Treatments for
pheochromocytoma
 Surgery=(will need to replace cortical
hormones)
 Radiation therapy

 Beta-blockers

 Alpha adrenergic blockers

 Nursing interventions
 Prepare the patient for surgical intervention.

 Administer adrenergic blocking agents usually 2

weeks before surgery (Prazosin)

 Administer drugs to inhibit cathecholamine

synthesis (Meyrosine)
 Educate patient and family
 Possible triggers of  Drugs that could
attacks includes: potentiate
catecholemine
 constipation  Tricyclic
 Glucagon
 Heavy lifting  Histamine
 Opiates
 Sudden changes in  OTC cold medications
temperature /decongestants.
 Adrenal cortex functions.

 Adrenal steroid hormones

 Glucortocosteroids

 Mineralcorticosteroids

 Androgens
Disorders of the adrenal cortex.
 Cushing’s Syndrome
 Caused by excess of cortisol production or by
excessive use of cortisol or other similar steroid
(glucorticoid)

 Addison’s Disease
 Addison’s disease is a severe or total deficiency of
the hormones made in the adrenal cortex, cause
by a destruction of the adrenal cortex.
Adrenal glands
 Adrenal diagnostic Lab values
 Adrenal Cortex

 Serum cortisol
 correlates with sleep awake cycle
 Level should be checked at 8:00am and at 4:00pm
 The 4:00PM level should be one third the 8:00am level
 measurement ACTH /higher 7:00am-10:00am/
lower7:00pm-10:00pm
 Adrenal cortex Lab
values(cont…)
 ACTH stimulation
 Obtain a base line cortisol level 30 minutes before
ACTH is given.

 Administer an IV injection (cosyntropin)

 measure cortisol level 1/2 hr. to 1 hr.

 Adrenal cortex Lab
values(cont…)
 Mineral corticoid suppression test
 Draw baseline of aldosterone level
 Give IV saline; draw periodic serum aldosterone
and should see a decrease from baseline.

 Serum Aldosterone level

 Primary mineral corticoid
 Adrenal diagnostic Lab values
 Cortisol levels urine
 can be assess
 Metabolites of cortisol in 24hrs urine
 17-ketogenic glucorticoids(17-KGs)

 17-Hydroxy corticosteroid(17ohcs)

 17-ketosteroids(17KS)
 Etiology of Cushing’s
Syndrome
 Endogenous or exogenous.
 Tumors: oat cell carcinomas, renal,
ovarian,lungs, thymus, pancreas or other
organs

 Chronic administration of glucocorticoids or

ACTH or iotrogenic cause.
Etiology of Cushing’s Syndrome
 A pituitary tumor producing ACTH
stimulating the adrenals to growth
(hyperplasia) and to produce too much
cortisol.

 It is the most common type and is called

Cushing’s disease. It is the cause of 70% of
spontaneous Cushing’s syndrome.
 Signs and Symptoms of
Cushing’s Syndrome
 Hypertension  Ketosis

 Hypervolemia  Immunosupression

 Hyperglycemia  Osteoporosis

 Hypokalemia  Emotional liability

Buffalo hump and moon face
Advance Cushing's
 Signs and Symptoms of
Cushing’s Syndrome
 Changes in body  Striae/stretch marks.
appearance:
 Bruising
 truncal obesity
 Hirsutism
 moon face
 Viralization
 muscle wasting
 Patient with Cushing's
syndrome before and after
surgery
 Signs and Symptoms of
Cushing’s Syndrome
 Symptoms :  Mood swings

 Weakness  Increased thirst and

urination
 Fatigue
 Lack of menstrual
periods
 Treatment for Cushing’s
disease
 Medications

 Radiation

 Surgery
 Medications for TX, Cushing’s
syndrome
 Pharmacological treatment is used :

 Pts. With pituitary tumor used it as adjunct

therapy to surgery and radiation.

 Pts. With inoperable pituitary or adrenal

malignancies .
 Drugs to inhibit cortisol
 Elipten (aminoglutethimide, Cytraden)

 Metyrapone (Metopirone)
 Mitotane (O, p1DDD)+cytotoxic to
adrenals.
 Cyprohetadine inhibits ACTH secretions.
 Radiation as a treatment
 Radiation therapy may be useful in
patients with primary Cushing’s syndrome.

 In secondary Cushing’s syndrome

isotopes or pituitary irradiation are used to
destroy the pituitary gland.
 Treatment

 Surgery

 Adrenalectomy

 Hypophysectomy
 Surgery Care

 Pre-op Nursing Care

 Teach pt. about diets  Used aseptic
high in proteins low in technique
sodium and high in
potassium.
 Teach cough and
 Monitor blood values deep breathing
techniques.
 Glucose and
electrolytes levels
 Surgery Care

 Post-op nursing care  Used aseptic

technique

 Monitor V.S.
 pain control

 Monitor lab values.

 Watch signs and
symptoms of adrenal
 Monitor intake and insufficiency
output.
 Adrenalectomy surgery
 Adrenalectomy
 Watch for signs and
 Removal of the tumor with symptoms of adrenal
an abdominal or flank site insuffiency
incision.
 After the surgery
 Tumors are usually
unilateral. The other replacement steroid
adrenal gland is left in. it hormone are given and
will grow to a normal size slowly tapered over few
and function. months .
Hypophysectomy surgery
 Surgical removal of
pituitary tumor usually  Keep the HOB 30
with a Transsphenoid
resection (behind the degrees all the time.
nose) usually done by a
neurosurgeon)  Mouth care q4hrs

 Avoid brushing teeth for

 Avoid vigorous 10 days
coughing, sneezing.

 Sent any drainage to  Analgesia

lab r/o CSF
 Nursing care
 Fluid Volume excess

 Risk for injury

 Risk for infection

 Fluid volume excess
 Excess cortisol secretion cause sodium
and water reabsorption the result is fluid
volume excess.

 Patient will have hypertension, weight gain

and edema.
 Fluid volume excess

 Weight the patient at the same time every

day and record results. (1L fluid=2lbs.)

 Maintain accurate I&O

 Monitor V.S closely

 Fluid volume excess
 Assess signs of fluid overload

 breath sounds, peripheral edema and jugular

vein distention

 Teach the patient &family the reason for fluid

restriction.
 Risk for injury
 Excess cortisol causes:
 Increase absorption of calcium from the
bones

 Demineralization of the bones

 Osteoporosis

 pathologic fractures
 Risk for injury
 Maintain a safe environment by

 keeping unnecessary clutter and equipment out of the

way and off the floor.

 Ensure adequate lighting, especially at night

 Encourage the patient to use assistive devices for

ambulation or ask help if needed
 Risk for injury
 Put glasses on if needed

 Encourage nonskid shoes

 Body image disturbances
 The patient with Cushing’s syndrome has
obviously physical changes and appearance

 The abnormal fat distribution

 moon face
 buffalo hump
 acne, facial hair
 Striae
 Body image disturbance
 Encourage the patient to express feeling and
to ask questions of the disease

 Encourage significant others and family to get

involve

 Ask patient to describe self strength and past

used coping mechanism
 Body image disturbance
 Discuss signs of progress in controlling
symptoms.
Addison’s Disease etiology
 Classified as primary or secondary.

 Primary adrenal insufficiency is caused by

gradual destruction of the outer layer of
the adrenal glands by the body own
immune system.
 Lack or decreased glucocorticoid and
mineral corticoid.
 Addison’s disease etiology

 Secondary adrenal insufficiency results from

deficient pituitary ACTH secretion from
dysfunction or destruction of hypothalamus or
the anterior pituitary gland.
 Addison’s Disease
 It is a hypofunction of the adrenal cortex.

 Adrenal glands do not produce enough of the

adrenal cortisol.

 Rare disorder can occur at any age; most

common among adult white women
 What causes Addison ‘s
disease?
 Autoimmune reaction  This process can take
in which the body months to years.
immune system
erroneously makes  Other rare infections
antibodies against the can causes Addison
cells of the adrenal ‘s disease examples:
cortex and slowly TB, CMV, fungal
destroys it. infections, and
adrenal cancer.
 Signs and symptons of
addison’s
 Chronic fatigue  Nausea/vomiting.

 Muscle weakness  Low blood Pressure

 Loss of appetite  Hyperpigmentation

 Weight loss  Irritability/depression

Hyper pigmentation
 Diagnostic findings in Addison
disease
 Primary disease  Secondary disease

 Increased ACTH  Decrease ACTH

 Decrease cortisol  Decreased Cortisol

 Abnormal ACTH
 Normal ACTH
stimulation test
stimulation test
 Diagnostic and lab findings in
Addison disease
 Serum sodium is  Adrenal scans
decreased
 CT scans
 Blood glucose is
decreased  EKG = t peak waves,
wide QRS, and an
 Increased potassium increased PR interval
 Treatments
 Hormone replacement therapy.

 Patient education
 Major adrenocortical Meds
 Cortisone acetate  Fludrocortisone
(Cortelan) acetate (Florinef)

 Hydrocortisone  Deoxycorticosterone
(Sulucortef) (Cortate)

 Prednisone  Dexamethasone
(Methylprednisone) (Decadron
 Nursing Care

 Fluid volume deficit

 Knowledge deficit
 Acute adrenal crisis
 It is a medical and a nursing emergency.
 Treatment must be given immediately.

 It can happen suddenly with a, severe lack of

cortisol, which can also be accompanied by a
sudden severe deficiency of Aldosterone. It is
usually caused by stress.
 Acute adrenal crisis
 Result from a decreased secretion of both mineral
corticoid and glucocorticoid

 most common in adult white women

 Chronic insufficiency can be controlled; however an

acute exacerbation must be treated immediate
attention to treat severe hypo tension, hypoglycemia,
and hyperkalemia.
 Signs and symptoms of
Addisonian crisis
 CV: Severe hypotension, hypovolemia,
decreased cardiac output, tachycardia,
and EKG with tall peak T waves.

 Neurologic: fatigue weakness and

Confusion, lethargy that rapidly progress
to comma.
 Signs and symptoms of
Addisonian crisis
 GI: Nausea/ vomiting/ anorexia, weight
loss, abdominal pain.

 SKIN: Hyperpigmentation (dark color skin)

 Laboratory findings for primary
or secondary adrenal
insufficiency
 Hypoglycemia
 Increased BUN and
 Hyperkalemia creatine ratio

 Hypercalcemia  Decrease cortisol

metabolites in 24
 Increased serum hour urine collection
osmolality .
 Treatment of addisonian
crisis.
 Oxygen therapy  Restore electrolytes
 Vascular support balance to prevent
 Restore fluid  Hyponatremia
balance/resuscitated  Level q4hrs.
immediately with  Assess for
NS/LR hyperreplexia
 Maintain accurate I&O  Hyperkalemia
 Assess N/V,
abdominal
cramps
dehydration or
fatigue
 Treatment of addisonian
 Administer steroid
crisis.
replacement  Or administer 100mg
of hydrocortisone IV
every q6hrs; then
 Pt. Need to be put in the decrease to 50mg
ICU. over next 24hrs;
dose can be tapered
and be changed to
 Bolus of an oral form.
hydrocortisone follows
 Mineral corticoids
by a continues infusion.
 Fludrocrotisone
(florinef)0.1mg po
qd
 Treatment of addisonian
crisis.
 Monitor glucose levels q2hrs.

 Conserve patient’s energy by assisting with all

aspects of care.

 Initiated self care education to prevent

recurring crisis.
 Treatment of addisonian
crisis/education.
 Review disease process

 Review the importance of life long steroid

replacement and the dangers of abrupt
withdrawal.

 Emphasize that stressful events (acute illness

with increased temperature and metabolic rate)
may bring on an addisonian crisis;
 Treatment of addisonian
crisis/education.
 Injury, trauma, surgery, burns, and other
physiological stressors may require increase in
cortisol replacement doses.

 Advised patient/family to notify health care provider

of such events.
The end