Endocrine System -...

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:

– Steroid/products of

cholesterol

breakdown such as

glucorticoids and

mineral corticoids.

– Monoacids analog-

derivated from amino

acid tyrosine (T3 and

T4)

– 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 thyroid-

stimulating 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 15-20g.

• 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

• Fasting

• Malnutrition

• Trauma

• Increased age

• Drugs such as propyl-

thoracic (PTU)

• Radiologic contrast dye

• Dexamethasone

• 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.


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


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)


• Iodine deficiency

– Iodine is necessary for TH synthesis and

secretion.

– Causes: Drugs that block TH synthesis or

goitrogenic compounds in food.


• Hashimoto’s thyroid

– Autoimmune disorder that destroy thyroid

tissue and replace it with fibrous tissue


– Radioactive iodine ablation hypothyroidism

– Other drugs• Lithium

carbonate=inhibits hormone release

• Dilantin (Phenytoin) decreases conversion of T4 to T3

• Dopamine inhibit

released TSH from the

pituitary gland.

• Secondary dysfunction

related related to

pituitary dysfunction.

– 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.


hypothyroidism

– Respiratory=hypoventilation , respiratory

failure.

– Gastrointestinal =weight gain with decreased

appetite, constipation

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

intolerance.


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

• Hypoglycemia

• Hyponatremia

• Hypotension

• Cardiovascular

collapse

• Shock

• Coma

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.

– Peak incident is ages 20-40

years.

– Adrenergic(cathecolomine

s) directly related to

increased levels of TH.

– Likely to occur in

association with an

autoimmune disease.

– Thyroid storm last 8 to 10

days due to the half life of

TH (22hrs for T3 and 6 days

for T4)

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

– CV-Atrial fibrillations,

palpitations, S3 gallop.

– Increased stroke volume,

myocardial demands

– Oxygen consumption,

blood pressure and

widen pulse pressure.

– Pulmonary edema and

congestive heart

failure.


storm• Neurological

functions

– restlessness

– nervousness

– tremors

– hyperreflexia

– proximal muscle

weakness


storm

• Hepatic

– hepatomegaly

• Elevated ALT (alanine

transaminase)

• AST(aspartame

transaminase)

• Bilirubin

• Bilirubin

• Alkaline phosphate


storm

• Gastrointestinal

– Increased gastric

motility (diarrhea)

– Nausea/ Vomiting

– Increased appetite

with weight loss

– Abdominal pain


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 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

• 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 hormonesAdrenal steroid hormonesAdrenal steroid hormonesAdrenal 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

• Hypervolemia

• Hyperglycemia

• Hypokalemia

• Ketosis

• Immunosupression

• Osteoporosis

• Emotional liability

Buffalo hump and moon face

Advance Cushing's



• Changes in body

appearance:

• truncal obesity

• moon face

• muscle wasting

• Striae/stretch marks.

• Bruising

• Hirsutism

• Viralization

Patient with Cushing's syndrome

before and after surgery



• Symptoms :

– Weakness

– Fatigue

– Mood swings

– Increased thirst and

urination

– 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 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

in which the body

immune system

erroneously makes

antibodies against the

cells of the adrenal

cortex and slowly

destroys it.

• This process can take

months to years.

• Other rare infections

can causes Addison ‘s

disease examples: TB,

CMV, fungal

infections, and

adrenal cancer.

Signs and symptons of addison’s

• Chronic fatigue

• Muscle weakness

• Loss of appetite

• Weight loss

• Nausea/vomiting.

• Low blood Pressure

• Hyperpigmentation

• Irritability/depression

Hyper pigmentation

Diagnostic findings in Addison

disease

• Primary disease

– Increased ACTH

– Decrease cortisol

– Abnormal ACTH

stimulation test

• Secondary disease

– Decrease ACTH

– Decreased Cortisol

– Normal ACTH

stimulation test

Diagnostic and lab findings in

Addison disease

• Serum sodium is

decreased

• Blood glucose is

decreased

• Increased potassium

• Adrenal scans

• CT scans

• EKG = t peak waves,

wide QRS, and an

increased PR interval

Treatments

• Hormone replacement therapy.

• Patient education

Major adrenocortical Meds

• Cortisone acetate

(Cortelan)

• Hydrocortisone

(Sulucortef)

• Prednisone

(Methylprednisone)

• Fludrocortisone

acetate (Florinef)

• Deoxycorticosterone

(Cortate)

• 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

• Hyperkalemia

• Hypercalcemia

• Increased serum

osmolality

• Increased BUN and

creatine ratio

• 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


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


crisis.

– Monitor glucose levels q2hrs.

– Conserve patient’s energy by assisting with all

aspects of care.

– Initiated self care education to prevent

recurring crisis.


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;


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

Endocrine System -...

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