Endocrine Diseases

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 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 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  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 ablation hypothyroidism

 Dopamine inhibit

 Other drugs  Lithium

 Secondary dysfunction

carbonate=inhibits hormone release

 Dilantin (Phenytoin)

decreases conversion of T4 to T3

released TSH from the pituitary gland.

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.

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  Hyponatremia  Hypotension

 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 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 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.

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)

 Administer thyroid inhibiting drugs

 Propylthiouracil

(PTU)can inhibit conversion T4 to T3.

 It decreases effects of cathecholamines decreasing heart rate and tremors.

 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

 Drugs that could

attacks includes:

potentiate catecholemine

 constipation  Heavy lifting  Sudden changes in temperature

    

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

 Striae/stretch marks.

appearance:

 truncal obesity  moon face  muscle wasting

 Bruising  Hirsutism  Viralization

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 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

 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

 Adrenal scans

decreased

 Blood glucose is decreased

 Increased potassium

 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



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