Endocrine SystemThyroid 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 cellsthat 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 targetorgan or are secreted locally to produce an effect.

Transportation of the hormones Bounded to plasma proteins such thyroid andsteroid (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 hormonesare of three basic types: Steroid/products of cholesterol breakdown such as glucorticoids and mineral corticoids. Monoacids analogderivated 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 detectchanges in the hormonal levels.

Hormones are adjusted to maintainnormal body levels.

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

When the hormonal levels rise abovenormal, the sensors cause a decreased in hormonal production.

Hormonal control Hormones are released by yourhypothalamus 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 fivebroad 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. Disorder of the transport mainly related to lack of protein to bind the hormones. Results in increase free level of the hormone

Abnormality of hormonal transport or metabolism.

Thyroid gland A small gland shaped like a butterflylocated below the larynx; it weights 1520g.

Needs iodine to produce hormones It produces these two hormone thyroxineand triiodothyronine.

Thyroid hormones The glands containtwo types of cells Follicular cells which produce T3 and T4 Parafocicullar cells which secrete thyrocalcitonin

T3=9% of thehormone secreted is in active form.

T4=90% of thehormone 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

Drugs such as propylthoracic (PTU)

Radiologic contrast Malnutrition Trauma Increased age

dye

Dexamethasone Propranolol andamiodarone

Functions of thyroid hormones. They act on most body systems usually stimulating them Metabolism=Controls and increased the basicmetabolic 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 fattissue and free fatty acid oxidation.

Protein metabolism=stimulate protein synthesis Growth=accelerates body growth

and degradation; stimulate turn over of proteins.

Body Weight=usually decreases due to increase inBMR

Functions of thyroid hormones. Cardiovascular=Vasodilatation related to acceleratedmetabolism 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 ofdepth 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 tothe extremities.

Cardiovascular= decreased blood pressure, heartrate, 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 Hashimotos thyroid Autoimmune disorder that destroy thyroid tissue and replace it with fibrous tissue

Etiology of hypothyroidism Radioactive iodine ablation hypothyroidism Other drugs Lithium Dopamine inhibitreleased TSH from the pituitary gland.

Secondary dysfunctionrelated related to pituitary dysfunction. Hypophysectomy pituitary tumor or infection

carbonate=inhibits hormone release

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 butdisorientation, 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 Assesscardiovascular system

Avoid coldenvironment

Paced activities

Decrease CO in hypothyroidism TH deficit causes a reduction of HR andstroke volume, resulting in decreased cardiac output.

In addition it might be fluid accumulationaround the pericardial sac that will further compromise the cardiac function.

Decrease CO in hypothyroidism Assess heart rate andrhythm

Monitor cardiacfunction. Fluid overload heart failure

Hypothermia Hypothermia: lack of heatgeneration 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 bodyprocess.

The body tries to compensate for thedecreased metabolic rate by: peripheral vasoconstriction, decreased HR, BP, CO, and contractility.

Myxedema coma signs and symptoms Hypothermia Hypoglycemia Hyponatremia Hypotension Cardiovascularcollapse

Shock Coma

Physical assessment of myxedema coma CV: Bradycardia, pericardial effusions ,hypotension.

Respiratory:Hypoventilation andrespiratory 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 Graves 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

Propylthiouracil (PTU)

Drug therapy for hyperthyroidism

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 thepatient 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 bodyrequire

Decreased CO r/t hyperthyroidism Assess for BP, pulse rate and rhythm,respiratory rate, and breath sounds. Increased TH increases HR, stroke volume andtissue 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 characterizedby accelerated signs of hyperthyroidism

Excessive production of thyroid hormoneT3 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 2040 years. Adrenergic(cathecolomines ) 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 resistanceand 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 beaffected 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.

Clinical manifestations thyroid storm Neurological functions restlessness nervousness tremors hyperreflexia proximal muscle weakness

Clinical manifestations thyroid storm Hepatic hepatomegaly Elevated ALT (alaninetransaminase)

Bilirubin Alkaline phosphate

AST(aspartametransaminase)

Bilirubin

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 ofpropanolol (beta adrenergic blocking agent) It decreases effects ofcathecholamines decreasing heart rate and tremors.

Administer thyroidinhibiting 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 thyroidinhibiting drugs Lithium Carbonate-itblocks the release of TH from the gland; use in patients that are intolerant to PTU or Tapazole.

Lugol solution (SSKI orsaturated 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 locatedabove 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

Headache

Palpitationstachycardia

Feelings of anxiety

Treatments for pheochromocytoma Surgery=(will need to replace corticalhormones) Radiation therapy

Beta-blockers Alpha adrenergic blockers

Nursing interventions Prepare the patient for surgical intervention. Administer adrenergic blocking agents usually 2weeks before surgery (Prazosin)

Administer drugs to inhibit cathecholaminesynthesis (Meyrosine)

Educate patient and family Possible triggers ofattacks includes: constipation Heavy lifting Sudden changes in temperature

Drugs that couldpotentiate catecholemine Tricyclic Glucagon Histamine Opiates OTC cold medications /decongestants.

Adrenal cortex functions. Adrenal steroid hormones Glucortocosteroids Mineralcorticosteroids Androgens

Disorders of the adrenal cortex. Cushings Syndrome Caused by excess of cortisol production or byexcessive use of cortisol or other similar steroid (glucorticoid)

Addisons Disease Addisons disease is a severe or total deficiency ofthe 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 beforeACTH 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 aldosteroneand 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)

Endogenous or exogenous.

Etiology of Cushings Syndrome

Tumors: oat cell carcinomas, renal, ovarian,lungs, thymus, pancreas or other organs Chronic administration of glucocorticoids or ACTH or iotrogenic cause.

Etiology of Cushings Syndrome A pituitary tumor producing ACTHstimulating the adrenals to growth (hyperplasia) and to produce too much cortisol. It is the most common type and is called Cushings disease. It is the cause of 70% of spontaneous Cushings syndrome.

Signs and Symptoms of Cushings Syndrome Hypertension Hypervolemia Hyperglycemia Hypokalemia Ketosis Immunosupression Osteoporosis Emotional liability

Buffalo hump and moon face

Advance Cushing's

Signs and Symptoms of Cushings Syndrome Changes in bodyappearance:

Striae/stretch marks. Bruising Hirsutism Viralization

truncal obesity moon face muscle wasting

Patient with Cushing's syndrome before and after surgery

Signs and Symptoms of Cushings Syndrome Symptoms : Weakness Fatigue Lack of menstrual periods Mood swings Increased thirst and urination

Treatment for Cushings disease Medications Radiation Surgery

Medications for TX, Cushings 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 toadrenals. Cyprohetadine inhibits ACTH secretions.

Radiation as a treatment Radiation therapy may be useful inpatients with primary Cushings syndrome.

In secondary Cushings syndromeisotopes 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 ofpituitary tumor usually with a Transsphenoid resection (behind the nose) usually done by a neurosurgeon)

Keep the HOB 30degrees all the time.

Mouth care q4hrs Avoid brushing teeth for10 days

Avoid vigorous

coughing, sneezing.

Sent any drainage tolab r/o CSF

Analgesia

Nursing care Fluid Volume excess Risk for injury Risk for infection

Fluid volume excess Excess cortisol secretion cause sodiumand water reabsorption the result is fluid volume excess.

Patient will have hypertension, weight gainand edema.

Fluid volume excess Weight the patient at the same time everyday 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 Cushings 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.

Addisons 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.

Addisons disease etiology Secondary adrenal insufficiency results from deficient pituitary ACTH secretion from dysfunction or destruction of hypothalamus or the anterior pituitary gland.

Addisons 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 reactionin which the body immune system erroneously makes antibodies against the cells of the adrenal cortex and slowly destroys it.

This process can takemonths to years.

Other rare infectionscan causes Addison s disease examples: TB, CMV, fungal infections, and adrenal cancer.

Signs and symptons of addisons 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 isdecreased

Adrenal scans CT scans EKG = t peak waves,wide QRS, and an increased PR interval

Blood glucose isdecreased

Increased potassium

Treatments Hormone replacement therapy. Patient education

Major adrenocortical Meds Cortisone acetate(Cortelan)

Fludrocortisoneacetate (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 andConfusion, lethargy that rapidly progress to comma.

Signs and symptoms of Addisonian crisis GI: Nausea/ vomiting/ anorexia, weightloss, abdominal pain.

SKIN: Hyperpigmentation (dark color skin)

Laboratory findings for primary or secondary adrenal insufficiency Hypoglycemia Hyperkalemia Hypercalcemia Increased serumosmolality

Increased BUN andcreatine ratio

Decrease cortisolmetabolites 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 electrolytesbalance to prevent Hyponatremia Level q4hrs. Assess for hyperreplexia Hyperkalemia Assess N/V, abdominal cramps dehydration or fatigue

Treatment of addisonian crisis. Administer steroidreplacement ICU.

Pt. Need to be put in the Bolus ofhydrocortisone 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 patients 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 steroidreplacement 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 otherphysiological stressors may require increase in cortisol replacement doses.

Advised patient/family to notify health care providerof such events.

The end