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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
chemical messengers
secreted by endocrine
organs and
transported
throughout the body
where they exert their
action on specific
cells called target
cells.
– Hormones do not
cause reactions but
rather they are
regulator of tissue
responses.
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
are of three basic
types:
– Monoacids analogderivated from amino
acid tyrosine (T3 and
T4)
– Steroid/products of
cholesterol
breakdown such as
glucorticoids and
mineral corticoids.
– Peptides either a large
proteins or a chain of
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 thyroidstimulating hormones (TSH).
– (TSH). triggers your thyroid gland to make
hormones thyroxine (T4) and
triiodothyronine (T3).
Endocrine dysfunctions
• Can be divided into five
broad categories
– Subnormal hormonal
production, resulting from
malformation, or absent of
the endocrine glands, or
the gland could be
diseased, or destroyed or
secretions are block.
– Hormonal excess
tends to caused
severe disease.
– Production of
abnormal hormone
cause by a gene
mutation.
Endocrine dysfunction
– Disorder of hormonal
receptors.
– Abnormality of
hormonal transport or
metabolism.
– Disorder of the
transport mainly
related to lack of
protein to bind the
hormones.
– Results in increase
free level of the
hormone
Thyroid gland
• A small gland shaped like a butterfly
located below the larynx; it weights 1520g.
• Needs iodine to produce hormones
• It produces these two hormone
thyroxine and triiodothyronine.
Thyroid hormones
• The glands contain
two types of cells
– Follicular cells which
produce T3 and T4
– Parafocicullar cells
which secrete
thyrocalcitonin
• T3=9% of the hormone
secreted is in active
form.
• T4=90% of the
hormone secreted is
bounded to protein as
a storage form; this
form is inactive until
converted to T3.
Inhibition of the conversion of T4
to T3
• Several illness
• Drugs such as propylthoracic (PTU)
• Fasting
• Radiologic contrast dye
• Malnutrition
• Dexamethasone
• Trauma
• Increased age
• Propranolol and
amiodarone
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
ablation
hypothyroidism
• Dopamine inhibit
released TSH from the
pituitary gland.
– Other drugs
• Secondary dysfunction
related related to
pituitary dysfunction.
• Lithium
carbonate=inhibits
hormone release
• Dilantin (Phenytoin)
decreases conversion
of T4 to T3
– Hypophysectomy
– pituitary tumor or
infection
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
(measure T3
remaining after
unbounded sites have
been filled.)
– Cardiomegaly
– Hypoglycemia
– Increased cholesterol:
the liver is unable to
excrete cholesterol in
the bile so it
accumulate and leads
to arteriosclerosis and
leads to PVD, and CAD
– EKG= bradycardia and
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
generation related to
decreased metabolism.
– Monitor temperature
– Rewarm patient gradually
and passively (plain
blanket and warm room)
– Avoid electrical
warming blanket
because it can lead to
vasodilatation and
vascular collapse.
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
Difficulty sleeping
Hand tremors
Weight loss despite
increase appetite
• Skin =warm, moist,
smooth,flushed
• Amenorrhea
•
•
•
•
Hoarseness
Dyspnea
Tachycardia
Increase blood
volume
• increased CO
• Palpitations
• 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
(nine times greater ) than
in men.
– Likely to occur in
association with an
autoimmune disease.
– Peak incident is ages 20-40
years.
– Thyroid storm last 8 to 10
days due to the half life of
TH (22hrs for T3 and 6 days
for T4)
– Adrenergic(cathecolomine
s) directly related to
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
Tachycardia
Systolic Hypertension
Abdominal symptons
– diarrhea
– vomiting
• Agitation
• Tremors
• Confusion
Clinical manifestations thyroid
storm
• All body system can be
affected by increased
levels of T3
– Oxygen consumption,
blood pressure and
widen pulse pressure.
– CV-Atrial fibrillations,
palpitations, S3 gallop.
– Pulmonary edema and
congestive heart
failure.
– Increased stroke volume,
myocardial demands
Clinical manifestations thyroid
storm
• Neurological
functions
– restlessness
– nervousness
– tremors
– hyperreflexia
– proximal muscle
weakness
Clinical manifestations thyroid
storm
• Hepatic
– hepatomegaly
• Elevated ALT (alanine
transaminase)
• AST(aspartame
transaminase)
• Bilirubin
• Bilirubin
• Alkaline phosphate
Clinical manifestations thyroid
storm
• Gastrointestinal
– Increased gastric
motility (diarrhea)
– Nausea/ Vomiting
– Increased appetite
with weight loss
– Abdominal pain
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
inhibiting drugs
• Lithium Carbonate-it
blocks the release of TH
from the gland; use in
patients that are
intolerant to PTU or
Tapazole.
• Lugol solution (SSKI or
saturated solution of
potassium iodine)
blocks the release of
thyroid hormone.
Other medications effects on
thyroid storm
– Radioactive iodine is
taken up by the gland
and it is destroyed in
the follicles.
– Administer pain
medication as needed
avoid acetylsalicylic
acid (ASA) as it
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 norepinephrine 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
• Shakiness,
diaphoresis
• Palpitations
tachycardia
• Feelings of anxiety
• Headache
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
attacks includes:
– constipation
– Heavy lifting
– Sudden changes in
temperature
• Drugs that could
potentiate
catecholemine
–
–
–
–
–
Tricyclic
Glucagon
Histamine
Opiates
OTC cold medications
/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
appearance:
• Striae/stretch marks.
• 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 :
– Weakness
– Mood swings
– 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
high in proteins low
in sodium and high
in potassium.
– Monitor blood values
– Glucose and
electrolytes levels
– Used aseptic
technique
– Teach cough and
deep breathing
techniques.
Surgery Care
• Post-op nursing care
– Monitor V.S.
– Monitor lab values.
– Monitor intake and
output.
– Used aseptic
technique
– pain control
– Watch signs and
symptoms of adrenal
insufficiency
Adrenalectomy surgery
• Adrenalectomy
– Removal of the tumor with
an abdominal or flank site
incision.
– Tumors are usually
unilateral. The other
adrenal gland is left in. it
will grow to a normal size
and function.
– Watch for signs and
symptoms of adrenal
insuffiency
– After the surgery
replacement steroid
hormone are given and
slowly tapered over few
months .
Hypophysectomy surgery
• Surgical removal of
pituitary tumor usually
with a Transsphenoid
resection (behind the
nose) usually done by a
neurosurgeon)
• Avoid vigorous
coughing, sneezing.
• Sent any drainage to
lab r/o CSF
• Keep the HOB 30
degrees all the time.
• Mouth care q4hrs
• Avoid brushing teeth
for 10 days
• Analgesia
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 ‘s
cells of the adrenal
disease examples: TB,
cortex and slowly
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
stimulation test
– Normal ACTH
stimulation test
Diagnostic and lab findings in
Addison disease
• Serum sodium is
decreased
• Adrenal scans
• CT scans
• Blood glucose is
decreased
• Increased potassium
• EKG = t peak waves,
wide QRS, and an
increased PR interval
Treatments
• Hormone replacement therapy.
• Patient education
Major adrenocortical Meds
• Cortisone acetate
(Cortelan)
• Fludrocortisone
acetate (Florinef)
• Hydrocortisone
(Sulucortef)
• Deoxycorticosterone
(Cortate)
• Prednisone
(Methylprednisone)
• Dexamethasone
(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
creatine ratio
• Hyperkalemia
• Hypercalcemia
• Increased serum
osmolality
• Decrease cortisol
metabolites in 24
hour urine collection
.
Treatment of addisonian
crisis.
• Oxygen therapy
• Vascular support
– Restore fluid
balance/resuscitated
immediately with
NS/LR
– Maintain accurate I&O
• Restore electrolytes
balance to prevent
– Hyponatremia
• Level q4hrs.
• Assess for
hyperreplexia
– Hyperkalemia
• Assess N/V,
abdominal
cramps
dehydration or
fatigue
Treatment of addisonian
crisis.
• Administer steroid
replacement
• Pt. Need to be put in
the ICU.
• Bolus of
hydrocortisone
follows by a continues
infusion.
– Or administer 100mg
of hydrocortisone IV
every q6hrs; then
decrease to 50mg
over next 24hrs;
dose can be tapered
and be changed to
an oral form.
– Mineral corticoids
• 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