Focused Endocrine Assessment2004

8/13/2019 Focused Endocrine Assessment2004

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Presented by:RN.com

12400 High Bluff DriveSan 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 distributionof these materials are prohibited without the

express written authorization of RN.com.

First Published: September 28, 2004

RN.coms Assessment Series: Focused Endocrine Assessment


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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


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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 nineyears 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 receivedher 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 asa Nurse Clinician and Education Specialist since 1999 at West Virginia University Hospitals, Morgantown, WV.


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PURPOSE & OBJECTIVES

The purpose of this article is to familiarize you with conducting a focused endocrine assessment. This willallow you to hone in on your patients endocrine signs and symptoms and intervene effectively. Ultimately, thehormones secreted by your endocrine organs execute their effects on specific cells and tissues to maintainhomeostasis 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 actupon 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.


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ASSESSING COMMON ENDOCRINE ABNORMALITIES

When conducting a focused endocrine assessment on your patient, begin with a thorough history of their chiefcomplaints. You will need to elicit information about any experienced signs or symptoms of endocrine diseaseor disorders. Endocrine disorders and diseases usually manifest according to which endocrine hormone is beingoverproduced 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 potentialendocrine abnormality. This assessment may also be necessary when an interval or abbreviated assessmentshows a change in status from your last assessment or report you received. When a new symptom emerges orthe patient develops some distress also consider a focused endocrine assessment. The advantage of thisassessment is that it allows you to ask about symptoms and move quickly to conducting a focused physicalexam.

Physical exam techniques used in your focused endocrine assessment are the same techniques used in yourgeneral 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 abnormalitiesare skin color, location of lesions, bruises or rashes, symmetry, size of body parts, and abnormal sounds orodors.

Auscultation is used in your focused endocrine assessment before percussion or palpation. Examples of examfindings 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 fortexture, 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 patientfor 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 knowledgeon your behalf to focus your assessment and hone in on the suspected endocrine abnormality. Therefore, it isuseful to review the possible endocrine disorders and their associated pathology, signs, and symptoms. If youunderstand these, you will be able to rapidly focus your assessment to pinpoint the endocrine disease or disorderaffecting your patient.


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Pituitary Disorders

The pituitary gland, also known as the hypophysis, is located atthe base of the brain. It is actually two very different glands; theanterior pituitary and the posterior pituitary. Each gland has aunique link to the hypothalamus. Antidiuretic hormone (ADH),or vasopressin, is the major hormone secreted by the posterior

pituitary. The anterior pituitarys major hormones are growthhormone (GR), thyroid stimulating hormone (TSH), andadrenocorticotropin (ACTH) (Sherwood, 1997).

The hypothalamus, also known as the master gland, producesand releases hormones that stimulate the pituitary gland, namelygrowth hormone releasing hormone (GRH), thyrotropic-releasinghormone (TRH), and corticotropin releasing hormone (CRH)(Sherwood, 1997). The following table summarizes keyassessment findings and their associated disorder or disease,aberrant hormone, potential causes of the disorder or disease, andkey subjective and objective assessment findings.

Syndrome of Inappropriate ADH (SIADH) - Above normal ADH release

Possible Cause ofAbnormality

Key Assessment Findings -Subjective Key Assessment Findings - Objective

ADH secreting tumor Chemotherapy Oat cell carcinoma

Anorexia Nausea Headache Fatigue Irritability

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 AbnormalityKey Assessment Findings -

SubjectiveKey Assessment Findings -

Objective CVA Hypothalamic-pituitary tumors Cranial trauma or surgeries Hereditary Drugs (lithium and phenytoin

[Dilantin]) Alcohol (transient DI)

Abrupt onset of polydipsiaand polyuria

Nocturia Sleep disturbances related

to nocturia Fatigue Headache Visual disturbances

Fluid intake 5-20 liters/day Urine output of 2-20 liters/day

of dilute urine Urine specific gravity < 1.006 Fever Changes in LOC Hypotension Tachycardia

(American Association of Critical Care Nurses, 1998; Pathophysiology: A 2-in-1 reference, 2004)

PituitaryGland Hypothalamus


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Thyroid Disorders

The thyroid gland lies in the anterior portion of the neck andstraddles the trachea. It secretes two hormones that play amajor role in the bodys metabolism, thyroxine (T4) &triiodothyronine (T3). Absence of these hormones maydecrease the bodys basal metabolic rate by 60% and excess ofthese hormones may increase the bodys basal metabolic rate

by 100% (American Association of Critical Care Nurses,1998 ). The following tables summarize key assessmentfindings and their associated disorder or disease, aberranthormone, potential causes of the disorder or disease, and keysubjective and objective assessment findings.

Hypothyroidism - Chronic deficiency of T4 & T3

Possible Cause of Abnormality Key AssessmentFindings - Subjective

Key Assessment Findings - Objective

Thyroid gland dysfunction Inadequate release of TRH or

TSH from the hypothalamic- pituitary axis(hypophysectomy or pituitaryradiation)

Surgical removal orradioiodine ablation withhyperthyroidism

Hashimotos thyroiditis(chronic inflammation of thethyroid)

Diminished hearing Cold intolerance Fatigue Lethargy Complaints of

constipation

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



Insufficient thyroid

supplementation Increased stressors in patientswith hypothyroidism (trauma,cold, anesthesia, infection)

Subjective findings

associated withhypothyroidism

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 andsymptoms, 2002)

Thyroid


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Hyperthyroidism - Chronic increase in T4 & T3


Key AssessmentFindings - Subjective Key Assessment Findings - Objective

Adenoma Thyroiditis Overtreatment of

hypothyroidism Discontinuation of

thyroid supplements Stress Iodine load with pre-

existing hyperthyroidstate

Pituitary tumor

Irritability Restlessness Heat intolerance Complaints of

diarrhea Insomnia

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 andsymptoms, 2002; Pathophysiology: A 2-in-1 reference, 2004)

Thyrotoxicosis or Thyroid Storm - Acute increase in T4 & T3

Possible Cause of AbnormalityKey Assessment

Findings - SubjectiveKey Assessment Findings - Objective

Decompensation of pre-existinghyperthyroid state after stressor

(surgery, anesthesia, infection,trauma)

Restlessness Agitation changes in LOC

Same as for hyperthyroidism but more pronounced: tachycardia, diaphoresis,

fever, diarrhea, confusion, signs andsymptoms associated with CHF and

pulmonary edemaCRITICAL SITUATION

(American Association of Critical Care Nurses, 1998; Nurse's Assessment video series: Endocrine signs andsymptoms, 2002)

Sick Euthyroid Syndrome - Underproduction of TSH from the anterior pituitary, which stimulates the production and release of T4 & T3.



Common in acutely ill Abnormalities in thyroid

function occur in patients withserious illness not caused by

primary thyroid or pituitarydysfunction.

May be absent Normal or low TSH Abnormal T4 (low or high) T3 may be low Absence of thyroid symptoms The degree of reduction in thyroid

hormone levels appears to becorrelated with the severity ofnonthyroidal illness

(American Association of Critical Care Nurses, 1998)


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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 andnorepinephrine. Aldosterone accounts for 95% of allmineralocorticoids produced and secreted by the adrenal cortex.Cortisol is the primary glucocorticoid secreted by the adrenalcortex. Epinephrine and norepinephrine are hormones secretedfrom the adrenal medulla (Sherwood, 1997). The following tablesummarizes key assessment findings and their associated disorderor disease, aberrant hormone, potential causes of the disorder ordisease, and key subjective and objective assessment findings.

Primary Adrenal Insufficiency or Addisons Disease - Chronic deficiency or secretion of cortisol (fromadrenal cortex) (Aldosterone is usually unaffected)

Secondary Adrenal Insufficiency - Chronic deficiency of ACTH (from the anterior pituitary), which stimulatescortisol release from the adrenal cortex


Key Assessment Findings- Subjective


Autoimmune destructionof the adrenal gland

Adrenal destructionfrom surgery, trauma,sepsis, suppression ofgland related to drugs(ketoconazole [Nizoral],rifampin [Rifadin],

phenytoin [Dilantin]),infection, Tuberculosis,hemorrhage, or bilateraladrenelectomy

Pituitary hypofunction(surgery, trauma,ischemia)

Nausea Abdominal pain Fatigue Malaise Weakness

Hyperpigmentation (only in primaryadrenal 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 ofthe adrenal gland)

Decreased plasma ACTH (whendysfunction is a result of thehypothalamic-pituitary axis)

Other endocrine abnormalities (insecondary adrenal insufficiency due to

pituitary abnormality)(American Association of Critical Care Nurses, 1998; Nurse's Assessment video series: Endocrine signs andsymptoms, 2002; Pathophysiology: A 2-in-1 reference, 2004.)

AdrenalGlands


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Pheochromocytoma (Adrenal Neoplasm) - Increase epinephrine & norepinephrine (from adrenal medulla)

Possible Cause of AbnormalityKey Assessment Findings

SubjectiveKey Assessment Findings -

Objective

Tumor of the adrenal medulla Headache Palpitations Dizziness Complaints of constipation Anxiety

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 Subjective

Key Assessment Findings -Objective

Most cases of primary

hyperaldosteronism resultfrom a benign tumor of theadrenal gland and occur in

people between 30 and 50years old.

Headache

Muscle weakness Fatigue Numbness

Hypernatremia

Hypervolemia Hypertension Hypokalemia Elevated plasma & elevated

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

Pancreatic DisordersThe endocrine pancreas produces and secretes insulin, glucagon,and somatostatin. All three of these hormones play a significantrole in carbohydrate, fat, and protein metabolism (American

Association of Critical Care Nurses, 1998). The following tablesummarizes key assessment findings and their associated disorderor disease, aberrant hormone, potential causes of the disorder ordisease, and key subjective and objective assessment findings.

Diabetes Mellitus - Absolute decreased production of insulin (Type I) OR resistance of cells to circulatinginsulin (Type II)


Key Assessment Findings -Subjective


Type I: Genetics,autoimmune disease,

viral infections Type II: Genetic factors,

obesity Gestational: Pregnancy

induced

Headaches Fatigue Lethargy Reduced energy levels Irritability Emotional lability Vision changes Numbness Tingling

Hyperglycemia Polyuria Polydipsia Polyphagia Anorexia Muscle cramps Type I presents usually emergently Type II presents insidiously

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

Pancreas


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Pancreatic Neoplasms Insulin production and secretion may be impaired


Key Assessment Findings -Subjective Key Assessment Findings - Objective

Benign or malignant tumorof the pancreas

Anorexia Nausea Malaise Abdominal or back pain

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 toedema, hemorrhage, or necrosis.



Alcoholism

Trauma Peptic ulcer disease Biliary tract disease Pancreatic cysts or tumors Drugs (sulfonomides, thiazides,

birth control pills, NSAIDs) Kidney failure Organ transplantation Endoscopic exam of the biliary tree

Severe, knife-like mid-

epigastric abdominal pain, which can radiateto the back

Mottled skin

Tachycardia Dehydration Hypovolemia Hemodynamic instability Abdominal distention Crackles in lung bases Pleural effusions Increased serum amylase,

lipase, and glucose(Pathophysiology: A 2-in-1 reference, 2004)

Hypoglycemia - Increased insulin production, secretion, and/or administration




Overproduction,secretion oradministration ofinsulin

Dizziness Weakness Nervousness Agitation Headache Mental dullness

Pallor Cool, clammy skin Diaphoretic Polyphagia Tachycardia Palpitations Confusion Blurred vision

Paresthesias Seizures Coma Decreased blood glucose level (


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Diabetic Ketoacidosis (DKA) - Decreased insulin administration in Type I Diabetics



Lack of circulating insulin in Type IDiabetics leading to a hyperosmolarand 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 Idiabetic

Medications (steroids, beta blockers,thiazide diuretics)

Alcohol use

Myalgias Flu-like signs and

symptoms Lethargy Nausea Decreased level of

consciousness Coma

Warm, dry skin Increased blood glucose

levels (approximately 300-700mg/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 TypeII Diabetics




Lack of circulating insulinin Type II Diabetics

leading to a hyperosmolarand hyperglycemic statewithout ketone production

Myalgias Flu-like signs and

symptoms Lethargy Nausea Decreased level of

consciousness Coma

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 moreimportantly, practice. It is not enough to simply ask the right questions and perform the physical exam. As thenurse, 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 forcritical 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

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Focused Endocrine Assessment2004

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