RN.

coms Assessment Series: Focused Endocrine Assessment

Presented by: RN.com 12400 High Bluff Drive San Diego, CA 92130

This course has been approved for one (1) contact hour. This course expires on September 28, 2006.
Copyright 2004 by RN.com. All Rights Reserved. Reproduction and distribution of these materials are prohibited without the express written authorization of RN.com.

First Published: September 28, 2004

Acknowledgements________________________________________________________________________ 2 Purpose & Objectives _____________________________________________________________________ 3 Introduction _____________________________________________________________________________ 4 Assessing Common Endocrine Abnormalities__________________________________________________ 5 Pituitary Disorders______________________________________________________________________ 6 Thyroid Disorders ______________________________________________________________________ 7 Adrenal Disorders ______________________________________________________________________ 9 Pancreatic Disorders ___________________________________________________________________ 11 Conclusion______________________________________________________________________________ 14 References ______________________________________________________________________________ 15 Post Test Viewing Instructions _____________________________________________________________ 16

ACKNOWLEDGEMENTS
RN.com acknowledges the valuable contributions of
Lori Constantine MSN, RN, C-FNP, author of Focused Endocrine Assessment. Lori has been a nurse for nine years and has a broad range of clinical experience. She has worked as a staff nurse, charge nurse, and nurse preceptor on many different medical surgical units including vascular, neurology, neurosurgery, urology, gynecology, ENT, general medicine, geriatrics, oncology, and blood and marrow transplantation. She received her Bachelors in Nursing in 1994 and a Masters in Nursing in 1998, both from West Virginia University. Additionally, in 1998, she was certified as a Family Nurse Practitioner. She has worked in staff development as a Nurse Clinician and Education Specialist since 1999 at West Virginia University Hospitals, Morgantown, WV.

PURPOSE & OBJECTIVES

The purpose of this article is to familiarize you with conducting a focused endocrine assessment. This will allow you to hone in on your patients endocrine signs and symptoms and intervene effectively. Ultimately, the hormones secreted by your endocrine organs execute their effects on specific cells and tissues to maintain homeostasis within the body. If there is an overproduction or underproduction of these hormones, the patient usually presents with symptoms. It is your duty as the patients nurse to recognize these symptoms and to act upon them as needed. After successful completion of this course, you will be able to: 1. Identify assessment findings in common endocrine abnormalities. 2. Briefly discuss the role specific hormones play in selected disease processes.

INTRODUCTION
Every cell in our body is under the influence of our endocrine system. The endocrine system acts to maintain homeostasis at the cellular level and is a vital link in proper body operations. When there is an upset to this system, illness or death can result. Treatment usually requires management of the deviant hormone by either reducing or increasing its production or secretion from its associated endocrine gland. Therefore, a thorough understanding of the endocrine system and how it functions is necessary in accurately assessing and treating endocrine disorders.

Hypothalamus Pituitary Thyroid

Adrenal

Pancreas

ASSESSING COMMON ENDOCRINE ABNORMALITIES

When conducting a focused endocrine assessment on your patient, begin with a thorough history of their chief complaints. You will need to elicit information about any experienced signs or symptoms of endocrine disease or disorders. Endocrine disorders and diseases usually manifest according to which endocrine hormone is being overproduced and secreted or underproduced and secreted. The key to discovering the nature of the symptoms lies in your understanding of the functions of the endocrine hormones. When assessing the endocrine system you most likely will perform a problem-focused assessment. The problem-focused endocrine assessment is necessary after a comprehensive assessment indicates a potential endocrine abnormality. This assessment may also be necessary when an interval or abbreviated assessment shows a change in status from your last assessment or report you received. When a new symptom emerges or the patient develops some distress also consider a focused endocrine assessment. The advantage of this assessment is that it allows you to ask about symptoms and move quickly to conducting a focused physical exam. Physical exam techniques used in your focused endocrine assessment are the same techniques used in your general exam; inspection, auscultation, percussion, and palpation. During inspection, you are looking for things you can observe with your eyes, ears or nose. Examples of what to inspect related to endocrine abnormalities are skin color, location of lesions, bruises or rashes, symmetry, size of body parts, and abnormal sounds or odors. Auscultation is used in your focused endocrine assessment before percussion or palpation. Examples of exam findings you will auscultate during your focused endocrine assessment include: Murmurs. Cardiac irregularities. Adventitious breath sounds. Alterations in bowel sounds.

Palpation is another physical exam technique you will use in your focused endocrine assessment. During light palpation, you press the skin about inch to 3/4 inch with the pads of your fingers. When using deep palpation, use your finger pads and compress the skin about 1 inches to 2 inches. Palpation allows you to assess for texture, tenderness, temperature, moisture, pulsations, masses, and internal organs (Shaw, 1998). Finally, percussion is used in your focused endocrine assessment to allow you to elicit tenderness or sounds that point to underlying problems. When percussing directly over suspected areas of tenderness, monitor the patient for signs of discomfort. Examples of endocrine abnormalities you may percuss are an enlarged pancreas, a pleural effusion associated with specific endocrine abnormalities, or a hormone-secreting tumor. Assessing endocrine abnormalities requires strong history and physical exam skills. Depending upon your patients chief complaint, specific parts of each body system will be assessed. It requires skill and knowledge on your behalf to focus your assessment and hone in on the suspected endocrine abnormality. Therefore, it is useful to review the possible endocrine disorders and their associated pathology, signs, and symptoms. If you understand these, you will be able to rapidly focus your assessment to pinpoint the endocrine disease or disorder affecting your patient.

Pituitary Disorders
The pituitary gland, also known as the hypophysis, is located at the base of the brain. It is actually two very different glands; the anterior pituitary and the posterior pituitary. Each gland has a unique link to the hypothalamus. Antidiuretic hormone (ADH), or vasopressin, is the major hormone secreted by the posterior pituitary. The anterior pituitarys major hormones are growth hormone (GR), thyroid stimulating hormone (TSH), and adrenocorticotropin (ACTH) (Sherwood, 1997). The hypothalamus, also known as the master gland, produces and releases hormones that stimulate the pituitary gland, namely growth hormone releasing hormone (GRH), thyrotropic-releasing hormone (TRH), and corticotropin releasing hormone (CRH) (Sherwood, 1997). The following table summarizes key assessment findings and their associated disorder or disease, aberrant hormone, potential causes of the disorder or disease, and key subjective and objective assessment findings.

Pituitary Gland

Hypothalamus

Syndrome of Inappropriate ADH (SIADH)- Above normal ADH release Possible Cause of Abnormality ADH secreting tumor Chemotherapy Oat cell carcinoma Key Assessment Findings Subjective Anorexia Nausea Headache Fatigue Irritability Key Assessment Findings - Objective

Weight gain Vomiting Muscle weakness Muscle spasms or cramps Possible coma Hallucinations Decreased LOC Confusion Low serum sodium Low serum osmolarity High urine osmolarity Normal urine sodium excretion Low edema (Pathophysiology: A 2-in-1 reference, 2004)

Diabetes Insipidus (DI)- Below normal ADH release Possible Cause of Abnormality Key Assessment Findings Key Assessment Findings Subjective Objective Fluid intake 5-20 liters/day Abrupt onset of polydipsia CVA and polyuria Urine output of 2-20 liters/day Hypothalamic-pituitary tumors Nocturia of dilute urine Cranial trauma or surgeries Urine specific gravity < 1.006 Sleep disturbances related Hereditary to nocturia Fever Drugs (lithium and phenytoin Fatigue Changes in LOC [Dilantin]) Headache Hypotension Alcohol (transient DI) Visual disturbances Tachycardia (American Association of Critical Care Nurses, 1998; Pathophysiology: A 2-in-1 reference, 2004) 6

Thyroid Disorders
The thyroid gland lies in the anterior portion of the neck and straddles the trachea. It secretes two hormones that play a major role in the bodys metabolism, thyroxine (T4) & triiodothyronine (T3). Absence of these hormones may decrease the bodys basal metabolic rate by 60% and excess of these hormones may increase the bodys basal metabolic rate by 100% (American Association of Critical Care Nurses, 1998). The following tables summarize key assessment findings and their associated disorder or disease, aberrant hormone, potential causes of the disorder or disease, and key subjective and objective assessment findings. Hypothyroidism - Chronic deficiency of T4 & T3 Possible Cause of Abnormality Thyroid gland dysfunction Inadequate release of TRH or TSH from the hypothalamicpituitary axis (hypophysectomy or pituitary radiation) Surgical removal or radioiodine ablation with hyperthyroidism Hashimotos thyroiditis (chronic inflammation of the thyroid) Key Assessment Findings - Subjective Diminished hearing Cold intolerance Fatigue Lethargy Complaints of constipation Key Assessment Findings - Objective

Thyroid

Bradycardia Decreased LOC Hypothermia Hypoventilation Hypoactive bowel sounds Weight gain Elevated TSH Free T4 decreased Elevated CK-MB T3, T4 decreased pCO2 increased pO2 decreased pH decreased Hypoglycemia (American Association of Critical Care Nurses, 1998; Pathophysiology: A 2-in-1 reference, 2004)

Myxedema Coma - Acute deficiency of T4 & T3 Possible Cause of Abnormality Insufficient thyroid supplementation Increased stressors in patients with hypothyroidism (trauma, cold, anesthesia, infection) Key Assessment Findings - Subjective Subjective findings associated with hypothyroidism Key Assessment Findings - Objective

Similar S/S of hypothyroidism but even more pronounced, anasarca, hoarseness, pericardial & pleural effusions, diminished hearing, paralytic ileus, unresponsiveness, decreased breathing, low blood pressure, low blood sugar, and below normal temperature ACUTE SITUATION (American Association of Critical Care Nurses, 1998; Nurse's Assessment video series: Endocrine signs and symptoms, 2002)

Hyperthyroidism - Chronic increase in T4 & T3 Possible Cause of Abnormality Adenoma Thyroiditis Overtreatment of hypothyroidism Discontinuation of thyroid supplements Stress Iodine load with preexisting hyperthyroid state Pituitary tumor Key Assessment Findings - Subjective Irritability Restlessness Heat intolerance Complaints of diarrhea Insomnia Key Assessment Findings - Objective

Tachycardia Atrial arrhythmias PVCs PACs Dyspnea Palpitations Weight loss Hyperthermia Elevated T4 & T3, Decreased TSH Increased TSH if from a TSH secreting tumor (in pituitary) (+) Test for thyroid antibodies (Graves Disease) Hyperglycemia Diaphoresis (American Association of Critical Care Nurses, 1998; Nurse's Assessment video series: Endocrine signs and symptoms, 2002; Pathophysiology: A 2-in-1 reference, 2004)

Thyrotoxicosis or Thyroid Storm - Acute increase in T4 & T3 Possible Cause of Abnormality Decompensation of pre-existing hyperthyroid state after stressor (surgery, anesthesia, infection, trauma) Key Assessment Findings - Subjective Restlessness Agitation changes in LOC Key Assessment Findings - Objective

Same as for hyperthyroidism but more pronounced: tachycardia, diaphoresis, fever, diarrhea, confusion, signs and symptoms associated with CHF and pulmonary edema CRITICAL SITUATION (American Association of Critical Care Nurses, 1998; Nurse's Assessment video series: Endocrine signs and symptoms, 2002) Sick Euthyroid Syndrome - Underproduction of TSH from the anterior pituitary, which stimulates the production and release of T4 & T3. Possible Cause of Abnormality Common in acutely ill Key Assessment Findings - Subjective May be absent Key Assessment Findings - Objective

Normal or low TSH Abnormal T4 (low or high) Abnormalities in thyroid T3 may be low function occur in patients with Absence of thyroid symptoms serious illness not caused by The degree of reduction in thyroid primary thyroid or pituitary hormone levels appears to be dysfunction. correlated with the severity of nonthyroidal illness (American Association of Critical Care Nurses, 1998) 8

Adrenal Disorders
The adrenal glands are two organs located atop of each kidney. They are responsible for the secretion of mineralocorticoids, glucocorticoids and the corticosteriods, epinephrine and norepinephrine. Aldosterone accounts for 95% of all mineralocorticoids produced and secreted by the adrenal cortex. Cortisol is the primary glucocorticoid secreted by the adrenal cortex. Epinephrine and norepinephrine are hormones secreted from the adrenal medulla (Sherwood, 1997). The following table summarizes key assessment findings and their associated disorder or disease, aberrant hormone, potential causes of the disorder or disease, and key subjective and objective assessment findings.
Adrenal Glands

Primary Adrenal Insufficiency or Addisons Disease - Chronic deficiency or secretion of cortisol (from adrenal cortex) (Aldosterone is usually unaffected) Secondary Adrenal Insufficiency - Chronic deficiency of ACTH (from the anterior pituitary), which stimulates cortisol release from the adrenal cortex

Hyperpigmentation (only in primary adrenal insufficiency) Orthostatic hypotension Decreased cardiac size and output Weak & irregular pulse X-rays may show adrenal calcification (only in primary adrenal insufficiency) Decreased cortisol levels Elevated plasma ACTH levels (in primary adrenal insufficiency due to disorder of the adrenal gland) Decreased plasma ACTH (when dysfunction is a result of the hypothalamic-pituitary axis) Other endocrine abnormalities (in secondary adrenal insufficiency due to pituitary abnormality) (American Association of Critical Care Nurses, 1998; Nurse's Assessment video series: Endocrine signs and symptoms, 2002; Pathophysiology: A 2-in-1 reference, 2004.)

Possible Cause of Abnormality Autoimmune destruction of the adrenal gland Adrenal destruction from surgery, trauma, sepsis, suppression of gland related to drugs (ketoconazole [Nizoral], rifampin [Rifadin], phenytoin [Dilantin]), infection, Tuberculosis, hemorrhage, or bilateral adrenelectomy Pituitary hypofunction (surgery, trauma, ischemia)

Key Assessment Findings - Subjective Nausea Abdominal pain Fatigue Malaise Weakness

Key Assessment Findings - Objective

Adrenal Crisis - Acute decrease in aldosterone and cortisol (from adrenal cortex) OR acute deficiency of ACTH (from the anterior pituitary) which stimulates cortisol release from the adrenal cortex Possible Cause of Abnormality Decompensation in a patient with chronic adrenal insufficiency Abrupt cessation of chronic steroid administration Key Assessment Findings - Subjective Nausea Abdominal pain Fatigue Malaise Weakness Key Assessment Findings - Objective

Hypoglycemia Hyponatremia Hypovolemia, Hypotension Tachycardia Hyperkalemia Hypercalcemia Vomiting Decreased cortisol levels Elevated plasma ACTH levels Increased BUN Metabolic acidosis (in primary adrenal insufficiency due to disorder of the adrenal gland) Decreased plasma ACTH (when dysfunction is a result of the hypothalamic-pituitary axis) X-rays may show adrenal calcification (American Association of Critical Care Nurses, 1998; Pathophysiology: A 2-in-1 reference, 2004, Shaw 1998) Cushings Syndrome - Overproduction or oversecretion of cortisol (from adrenal cortex) Cushings Disease - Overproduction or secretion of ACTH (from anterior pituitary), which stimulates cortisol release from the adrenal cortex Possible Cause of Abnormality Cortisol secreting tumor (20% of cases) such as oat cell carcinoma of the lung Adrenal carcinoma Cortisol secreting adrenal tumor (usually benign) Key Assessment Findings Subjective Weakness Increased appetite Irritability Emotional lability Headache Complaints of easy bruising Reports symptoms associated with decreased stress and immunologic response Key Assessment Findings - Objective

Pathologic fractures Purple striae Facial edema Acne Buffalo hump Poor wound healing Peptic ulcers Hypertension Left ventricular hypertrophy Dyslipidemia Renal calculi (from bone demineralization) Urinary free cortisol levels > 150 micrograms in 24 hours, hyperglycemia Hypernatremia Hypokalemia Hypocalcemia Metabolic alkalosis Increased lymphocytes (American Association of Critical Care Nurses, 1998; Pathophysiology: A 2-in-1 reference, 2004)

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Pheochromocytoma (Adrenal Neoplasm) - Increase epinephrine & norepinephrine (from adrenal medulla) Possible Cause of Abnormality Tumor of the adrenal medulla Key Assessment Findings Subjective Headache Palpitations Dizziness Complaints of constipation Anxiety Key Assessment Findings Objective Hypertension Hyperglycemia Dyslipidemia Irregular heart rate Diaphoresis Syncope

(Pathophysiology: A 2-in-1 reference, 2004).

Primary Aldosteronism - Increase in production and secretion of aldosterone (from adrenal cortex) Possible Cause of Abnormality Key Assessment Findings Objective Hypernatremia Most cases of primary hyperaldosteronism result Hypervolemia from a benign tumor of the Hypertension adrenal gland and occur in Hypokalemia people between 30 and 50 Elevated plasma & elevated years old. urinary aldosteronism (Pathophysiology: A 2-in-1 reference, 2004) Key Assessment Findings Subjective Headache Muscle weakness Fatigue Numbness

Pancreatic Disorders
The endocrine pancreas produces and secretes insulin, glucagon, and somatostatin. All three of these hormones play a significant role in carbohydrate, fat, and protein metabolism (American Association of Critical Care Nurses, 1998). The following table summarizes key assessment findings and their associated disorder or disease, aberrant hormone, potential causes of the disorder or disease, and key subjective and objective assessment findings.
Pancreas

Diabetes Mellitus - Absolute decreased production of insulin (Type I) OR resistance of cells to circulating insulin (Type II) Key Assessment Findings Key Assessment Findings - Objective Subjective Hyperglycemia Headaches Polyuria Fatigue Polydipsia Lethargy Polyphagia Reduced energy levels Anorexia Irritability Muscle cramps Emotional lability Type I presents usually emergently Vision changes Type II presents insidiously Numbness Tingling (Diabetes mellitus: pathophysiology for nurses video series, 2000; Pathophysiology: A 2-in-1 reference, 2004) Possible Cause of Abnormality Type I: Genetics, autoimmune disease, viral infections Type II: Genetic factors, obesity Gestational: Pregnancy induced

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Pancreatic Neoplasms Insulin production and secretion may be impaired Possible Cause of Abnormality Benign or malignant tumor of the pancreas Key Assessment Findings Subjective Anorexia Nausea Malaise Abdominal or back pain Key Assessment Findings - Objective

Jaundice Clay-colored stool Vomiting Weight loss Blood in stool Hypoglycemia or hyperglycemia (Pathophysiology: A 2-in-1 reference, 2004)

Pancreatitis Insulin production and secreting may be impaired. Inflammation of the pancreas occurs due to edema, hemorrhage, or necrosis. Possible Cause of Abnormality Key Assessment Findings Objective Mottled skin Alcoholism Tachycardia Trauma Dehydration Peptic ulcer disease Hypovolemia Biliary tract disease Hemodynamic instability Pancreatic cysts or tumors Abdominal distention Drugs (sulfonomides, thiazides, birth control pills, NSAIDs) Crackles in lung bases Kidney failure Pleural effusions Organ transplantation Increased serum amylase, lipase, and glucose Endoscopic exam of the biliary tree (Pathophysiology: A 2-in-1 reference, 2004) Key Assessment Findings Subjective Severe, knife-like midepigastric abdominal pain, which can radiate to the back

Hypoglycemia - Increased insulin production, secretion, and/or administration Possible Cause of Abnormality Overproduction, secretion or administration of insulin Key Assessment Findings - Subjective Dizziness Weakness Nervousness Agitation Headache Mental dullness Key Assessment Findings - Objective Pallor Cool, clammy skin Diaphoretic Polyphagia Tachycardia Palpitations Confusion Blurred vision Paresthesias Seizures Coma Decreased blood glucose level (<60-80 mg/dL)

(Diabetes mellitus: pathophysiology for nurses video series, 2000; Pathophysiology: A 2-in-1 reference, 2004).

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Diabetic Ketoacidosis (DKA) - Decreased insulin administration in Type I Diabetics Possible Cause of Abnormality Lack of circulating insulin in Type I Diabetics leading to a hyperosmolar and hyperglycemic state with ketone production New onset diabetes Inadequate insulin use in a known diabetic patient Stress (MI, CVA, trauma, surgery, emotional upset) in a known Type I diabetic Medications (steroids, beta blockers, thiazide diuretics) Alcohol use Key Assessment Findings Subjective Myalgias Flu-like signs and symptoms Lethargy Nausea Decreased level of consciousness Coma Key Assessment Findings Objective Warm, dry skin Increased blood glucose levels (approximately 300700mg/dL) Polydipsia Polyuria (due to osmotic diuresis) Dehydration Increased BUN, HCT, HGB, acetone breath (exhalation of ketones) (+) Urine & serum ketones Metabolic acidosis Kussmauls respirations Increased serum osmolarity

(Diabetes mellitus: pathophysiology for nurses video series, 2000; Pathophysiology: A 2-in-1 reference, 2004; Shaw, 1998) Hyperosmolar, Hyperglycemic, Non-ketotic Syndrome (HHNKS) - - Increased blood glucose levels in Type II Diabetics Possible Cause of Abnormality Lack of circulating insulin in Type II Diabetics leading to a hyperosmolar and hyperglycemic state without ketone production Key Assessment Findings - Subjective Myalgias Flu-like signs and symptoms Lethargy Nausea Decreased level of consciousness Coma Key Assessment Findings - Objective Warm, dry skin Increased blood glucose levels (approximately 400-2,000mg/dL) Polydipsia, polyuria (due to osmotic diuresis) Severe dehydration Increased BUN, HCT, HGB (-) Urine & serum ketones Absence of acetone breath (no ketones, no acidosis) Increased serum osmolarity (> 315 mOsm/kg) Wider variety of mental status changes including hallucinations, seizures, aphasia

(Diabetes mellitus: pathophysiology for nurses video series, 2000; Pathophysiology: A 2-in-1 reference, 2004; Shaw, 1998)

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CONCLUSION
Integrating the health history and physical exam in a focused endocrine assessment takes experience, and more importantly, practice. It is not enough to simply ask the right questions and perform the physical exam. As the nurse, you must critically analyze all of the data you obtain, synthesize the data into a relevant problem focus, and then identify a plan of care for your patient based upon this synthesis. As the plan of care is being carried out, reassessments must occur on a periodic basis. How often these reassessments occur is unique to each patient, based upon their specific endocrine disorder.

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REFERENCES
American Association of Critical Care Nurses (1998). The Endocrine System. In J. Alspach (Ed.), Core curriculum for critical care nursing (5th ed., Rev., pp. 565-577). Philadelphia: Saunders. Diabetes mellitus: pathophysiology for nurses video series. (2000). Blanchard & Loeb. Nurse's Assessment video series: Endocrine signs and symptoms. (2002). Blanchard & Loeb. Pathophysiology: A 2-in-1 reference. (2004). Philadelphia: Lippincott, Williams & Wilkins. Shaw, M. (Ed.). (1998). Pathophysiology Made Incredibly Easy. Springhouse, PA: Springhouse. Sherwood, L. (Ed.). (1997). Human physiology: From cells to systems (3rd ed.). Belmont, California: Wadsworth.

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POST TEST VIEWING INSTRUCTIONS

In order to view the post test you may need to minimize this window and click TAKE TEST. You can then restore the window in order to review the course material if needed.

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