ASSESSMENT OF ENDOCRINE SYSTEM

HISTORY TAKING:

During the health history interview, help the client sequence the recalled experiences and
manifestations. History taking may include the following:

 Biographical and Demographic Data: it includes client’s age, gender, ethnic background
and geographical residence.
 Current health includes chief complaints: it includes asking the client to indicate when
the problem began; the onset, duration, intensity, and the characteristics of the problem.
 Clinical Manifestations: it includes asking the client about pain and its description are
often helpful in diagnosing the origin of the problem.
 Review of systems: inquire about clinical manifestations that are related to the metabolic
and endocrine disorders that could contribute to the current chief complaints.
 Past Medical history and recent hospitalization
 Surgical history
 Allergies
 Medications
 Dietary habits
 Social history
 Family health history
History Taking of Thyroid gland abnormality
 Subjective Data includes:
        Hypothyroidism
1.      Family or personal history of thyroid disease.
2.      Goitre or history of goitre.
3.      Prior or current thyroid use.
4.      History of other autoimmune disease.
        Hyperthyroidism
1. Family or personal history of thyroid disease
2.     Goitre or history of goitre.
3.     Prior or current thyroid use.
4.     History of other autoimmune disease.
5.     Recent iodine exposure.
 
 Objective Data
Hypothyroidism: Clients with hypothyroidism may be asymptomatic or may experience vague
manifestations that escape detection such as cold, lethargy, dry skin, forgetfulness, depression
and some weight gain. Undiagnosed or untreated hypothyroidism that may cause Myxedema.
Hyperthyroidism: Clients with excessive thyroid hormones experience Fatigue,Weight loss
without change in appetite, Heat intolerance, Depression or nervousness, irritablility,anxiety or
agitation, Menstural irregularities (oligomenorrhea) , Weakness,Tremor, Palpitations, Exertional
dyspena,Hyperdefecation, Anterior neck pain, Insomnia (Grave’s disease). The three main
complications of Grave’s disease are exophthalmos, heart disease and thyroid storm (thyroid
crisis, thyrotoxicosis).

History taking of Parathyroid gland abnormality

 Subjective Data includes
Hypoparathyroidism:
       Insufficient amount of parathormone after Thyroid surgery or Radiation therapy of
neck (idiopathic hypoparathyroidism is rare)
        As level of parathormone drops, serum calcium level also drops causing Tetany
        Concomitant rise in serum phosphate level occurs.
Hyperparathyroidism:
 Apathy,
 fatigue,
 muscle weakness,
 nausea, vomiting,
 constipation,
 hypertension,
 cardiac dysrhythmias may occur; all are attributable to the increased concentration of
calcium in the blood.
 
 Objective Data includes
Hypoparathyroidism:
        Trousseau Sign; Carpopedal spasm within 3 minutes after a BP cuff is inflated 20 mm
Hg above patient’ssystolic pressure.
        Chovestek Sign: Spasm of the facial muscles in response to tapping near the angle of
the jaw.
        Decreased serum calcium and Parathormone Levels;
elevated serum phosphate level.
        Stridor and Wheezing from Laryngeal spasm; tremors; seizures.
        Cardiac dysrhythmias, alkalosis, cataracts if disease is chronic.
Hyperparathroidism:
        Bone cysts, Pathogenic Fractures
        Renal damage, pyelonephritis, polyuria, Renal calculi composed of calcium.
        Vomiting, Constipation
        Cardiac dysrhythmias
         Increased serum calcium and parathormone levels; decreased serum phosphorus level.
 
History Taking of Adrenal gland abnormality
 Subjective Data includes
Hypoaldosteronism:
        Weakness   
        Fatigue
        Anorexia
        Nausea
        Lethargy
Hyperaldosteronism:
        Muscle weakness and cramping
        Polydepsia
        Polyuria
        Paresthesia
 
 Objective Data includes
Hypoaldosteronism:
        Increased bronze pigmentation of skin.
        Vomiting, diarrhea
        Impaired protein anabolism resulting in emaciation and fatigue
        Hypotension
        Decreased levels of serum cortisol, 17-ketosteroids, and 17-hydroxysteroids,
increased plasma ACTH level.
        Electrolyte imbalances
        Hyponatremia
        Hypoglycemia
        Hyperkalemia
Hyperaldosteronism:
       Obese trunk, thin trunk thin arms and legs, moon face, buffalo hump, acne,
hirsutism, ecchymotic areas, purple striae on breasts and abdomen, amenorrhea,
increased susceptibility to infections.
        Hypertension
        Hyperglycemia, hypokalemia elevated plasma cortisol level.
        Elevated levels of 17-hydroxysteroids and 17-ketosteroids in urine.
        Osteoporosis, fractures, kyphosis.
        Protein wasting, which causes muscle wasting and weakness.
        Hypernatremia caused by sodium and water retention, resulting in edema and
hypertension.

History Taking of Pitutary gland abnormality

  Hypopitutarism:
Subjective Data includes:
        Lethargy
        loss of strength and libido
        decreased tolerance for cold
Objective data includes:
        Decreased temperature
        Postural hypotension
        Hypoglycemia
        Decreased levels of GH, ACTH, TSH, FSH,  and LH
        Sterility; loss of secondary sexual characteristics
        Visual disturbances if tumor impinges on optic nerve
 Hyperpitutarism:
Subjective Data includes
        Headaches,
        Depression,
        Weakness
Objective data includes
        Increased soft tissue and bone thickness
        Facial features become coarse and heavy, with enlargement of lower jaw, lips, and
tongue
        Enlarged hands and feet
        Increased GH, ACTH, or PRL X-ray examination of long bones, skull (sella turcica
area), and jaw demonstrates change in structure
        Amenorrhea
        Clinical findings of increased intracranial pressure (e.g., vomiting, papilledema, focal
neurologic  deficits)
        Diabetes and hyperthyroidism may result

History Taking of Pancreas abnormality

 Hyposecretion of Insulin causes:
Subjective Data:
        Polydipsia
        Polyphagia
        Fatigue
        Blurred vision (retinopathy; osmotic changes)
        Peripheral neuropathy.
ObjectiveData:
        Polyuria
        Weight loss
        Glycosuria
         Peripheral vascular changes
        Ulcers
        Delayed wound healing
        Infection
        Gangrene
 Hypersecretion of Insulin causes:
Subjective Data:
        Mental confusion
        Blurred vision
        Diplopia
        Slurred speech
        Fatigue
        Seizures
        Nervousness
        Weakness,
        Pallor
        Diaphoresis
        Tremor
        Tachycardia
        Hunger
 Objective Data:
       Hyperglycemia: detected by casual plasma glucose measurement of 200 mg/dL or
higher, fasting plasma glucose level of 126 mg/dL or higher, and 2-hour postload glucose
level of 200 mg/dL or higher.
Monitored by hemoglobin A1c (Hb A1c, glycosylated hemoglobin) measurement, which reflects
average glucose level over preceding 2 to 3 months and should not exceed 7%.

PHYSICAL EXAMINATION

Physical examination of endocrine gland dysfunction involves careful examination of entire

body and is integrated throughout the interaction with client. It includes examination of all body
systems in a systematic manner from head to toe using inspection, auscultation, percussion and
palpation; provides details related to the physical assessment of the endocrine system.
Physical assessment includes:
 Inspection
 Auscultation
 Percussion
 Palpation
Physical assessment findings in the Healthy Adult in respect to Thyroid gland:

Inspection: The thyroid gland is not normally seen on inspection.

Palpation: The gland rises and falls with swallowing. Isthmus at midline. Right lobe slightly
larger than the left lobe. Texture rubbery without nodules.
Auscultation: No bruits heard over either lobe.

Physical assessment findings in Thyroid gland dysfunction:

Inspection:

      Observe the patient for mood and affect (emotional tone) throughout the physical
assessment. Inspect the neck for thyroid enlargement.
      Look for eyes that bulge (exophthalmos).
      Note posture, body fat, and presence of tremor.
     Observe skin and hair texture and moisture. Note the presence of a moonlike face or
“buffalo hump” on the upper back.
      Observe the lower extremities for skin and color changes that might indicate
circulatory impairment.

Palpation :

        The thyroid gland is the only palpable endocrine gland. The licensed practical
nurse/licensed vocational nurse (LPN/ LVN) may assist a physician or nurse practitioner
to palpate the thyroid gland.
        The practitioner stands behind or in front of the seated patient and palpates the gland
while the patient swallows a sip of water. You can assist with positioning the patient,
providing water, and instructing the patient to take a sip of water and hold it in his or her
mouth until told to swallow.
        The thyroid gland should never be palpated in a patient with uncontrolled
hyperthyroidism because this can stimulate secretion of additional thyroid hormone.
        Palpate all peripheral pulses. The posterior tibial and dorsalis pedis pulses may be
diminished in patients with circulatory impairment. Palpate skin turgor by gently
pinching  a small piece of skin.
        If a “tent” remains, the patient may be dehydrated as a result of water loss, as in ADH
deficiency.

Auscultation and Percussion: Auscultation and percussion are not usually part of an endocrine
assessment.

Physical Examination of Parathyroid gland dysfunction:

Hypoparathyroidism:
        History of muscle spasms, numbness or tingling of extremities, visual disturbances, or
seizures.
        Neuromuscular irritability.
        Status of respiratory functioning.
        Heart rate and rhythm.
        Serum calcium and phosphate levels.
Hyperparathyroidism:
        GI disturbance or bone pain.
        History of renal calculi or fractures.
        Clinical findings of renal calculi(e.g. Hematuria, Flank pain).
        Use of thiazides diuretics or vitamin D, which can increase serum calcium level.
        Serum calcium and phosphorus levels.
        Baseline vital signs, particularly heart rate and rhythm.

Physical Examination of Adrenal gland dysfunction:

Hyperaldosteronism
A)    Excess Glucocorticoids
        Weight gain or obesity (see Figure 24-4).
        Heavy trunk; thin extremities.
        “Buffalo hump” (fat pad) in neck and supraclavicular area.
        Rounded face (moon face); plethoric, oily.
        Fragile and thin skin, striae and ecchymosis, acne.
        Muscles wasted because of excessive catabolism.
        Osteoporosis—characteristic kyphosis, backache.
        Mental disturbances—mood changes, psychosis.
        Increased susceptibility to infections.
B)     Excess Mineralocorticoids
        Hypertension.
        Hypernatremia
         Hypokalemia.
        Weight gain.
        Expanded blood volume.
        Edema.
C)     Excess Androgens
        Women experience virilism (masculinization).
        Hirsutism—excessive growth of hair on the face and midline of trunk.
        Breasts—atrophy.
        Clitoris—enlargement.
        Voice—masculine.
         Loss of libido.
        If exposed in utero—possible hermaphrodite.
        Males—loss of libido. 
Hypoaldosteronism:
        Hyponatremia and hyperkalemia.
        Water loss, dehydration, and hypovolemia.
        Muscular weakness, fatigue, weight loss.
        GI problems—anorexia, nausea, vomiting, diarrhea, constipation, abdominal pain.
        Hypotension, hypoglycemia, low basal metabolic rate, increased insulin sensitivity.
        Mental changes—depression, irritability, anxiety, apprehension caused by
hypoglycemia and hypovolemia.
        Normal responses to stress lacking.
         Hyperpigmentation.

Physical Examination of Pitutary gland dysfunction:

Hypopitutarism:
        Baseline vital signs
        Sexuality (e.g., loss of libido; painful intercourse; inability to maintain an erection).
        Past and present menstrual patterns.
        Visual acuity.
        Loss of secondary sexual characteristics. Activity
 tolerance.
Hyperpitutarism:
        Changes in energy level, sexual function, and menstrual patterns; signs of increased
intracranial pressure.
        Face, hands, and feet for thickening, enlargement; changes in the size of hat, gloves,
rings, or shoes.
        Dysphagia or voice changes.
        Presence of hypogonadism as a result of hyperprolactinemia.
        Reaction to changes in physical appearance and sexual function.

Physical Examination of pancreas dysfunction:

Hyposecretion:
        Mild hypoglycemia: The client remains fully awake but displays adrenergic
symptoms; the blood glucose level is lower than 70 mg/dL (4.0 mmol/L).
         Moderate hypoglycemia: The client displays symptoms of worsening hypoglycemia; the
blood glucose level is usually lower than 40 mg/dL (2.2 mmol/L).
        Severe hypoglycemia: The client displays severe neuroglycopenic symptoms; theblood
glucose level is usually lower than 20 mg/dL (1.1 mmol/L).
Hypersecretion:
        A change in vision is caused by the rupture of small microaneurysms in retinal blood
vessels.
        Blurred vision results from macular edema.
        Sudden loss of vision results from retinal detachment.
        Cataracts result from lens opacity.

DIAGNOSTIC TESTS:

Noninvasive endocrine Function tests for Thyroid Gland :

A. Radioactive iodine uptake

.      This thyroid function test measures the absorption of an iodine isotope to determine
how the thyroid gland is functioning.
2.      A small dose of radioactive iodine is given by mouth or intravenously; the amount
of radioactivity is measured in 2 to 4 hours and again at 24 hours.
3.      Normal values are 3% to 10% at 2 to 4 hours, and 5% to 30% in 24 hours.
4.      Elevated values indicate hyperthyroidism, decreased iodine intake, or increased
iodine excretion.
5.      Decreased values indicate a low T4 level, the use of antithyroid medications,
thyroiditis, myxedema, or hypothyroidism.
6.      The test is contraindicated in pregnancy. C. T3 and T4 resin uptake test. Normal
values (normal findings vary between laboratory settings)
 a. Triiodothyronine, total T3: 70–205 ng/dL (1.2–3.4 nmol/L)
 b. Thyroxine, total T4: 5–12 mcg/dL (64–154 nmol/L)
 c. Thyroxine, free (FT4): 0.8–2.8 ng/dL (10–36 pmol).
d. The T4 level is elevated in hyperthyroidism and decreased in hypothyroidism.

B. Thyroid scan 
1.      A thyroid scan is performed to identify nodules or    growths in the thyroid gland.
2.      A radioisotope of iodine or technetium is administered before scanning the thyroid
gland.
3.      Reassure the client that the level of radioactive medication is not dangerous to self
or others.
4.      Determine whether the client has received radiographic contrast agents within the
past 3 months, because these may invalidate the scan.
 5.      Check with the health care provider (HCP) regarding discontinuing medications
containing iodine for 14 days before the test and the need to discontinue thyroid
medication before the test.
6.      Instruct the client to maintain NPO (nothing by mouth) status after midnight on the
day before the test; if iodine is used, the client will fast for an additional 45 minutes
after ingestion of the oral isotope and the scan will be performed in 24 hours.
7.      If technetium is used, it is administered by the intravenous(IV) route 30minutes
before the can.
8.      The test is contraindicated in pregnancy.

Invasive endocrine Function tests for Thyroid Gland:

A. Stimulation and suppression tests

        Stimulation tests

1.      In the client with suspected underactivity of an endocrine gland, a stimulus may be
provided to determine whether the gland is capable of normal hormone production.
2.      Measured amounts of selected hormones or substances are administered to
stimulate the target gland to produce its hormone.
3.      Hormone levels produced by the target gland are measured.
4.      Failure of the hormone level to increase with stimulation indicates hypofunction.

        Suppression tests

1.      Suppression tests are used when hormone levels are high or in the upper range of
normal.
2.      Agents that normally induce a suppressed response are administered to determine
whether normal negative feedback is intact.
3.      Failure of hormone production to be suppressed during standardized testing
indicates hyperfunction.

B. Overnight dexamethasone suppression test

1.      Used to distinguish between Cushing’s syndrome and Cushing’s disease.

2.      In Cushing’s disease the source of excess cortisol is the pituitary gland rather than
the adrenal cortex or exogenous corticosteroid administration.
3.      Dexamethasone, a potent long-acting corticosteroid given at bedtime, should
suppress the morning cortisol in clients without Cushing’s disease by suppressing
adrenocorticotropic hormone (ACTH) production; in the client with Cushing’s
disease, this suppression will not occur.

C. Thyroid-stimulating hormone  

            1. Blood testisused to differentiate the diagnosis of     primary hypothyroidism.

            2. Normal value is 2–10 mcU/L (2–10 mU/L).

            3. Elevated values indicate primary hypothyroidism.

            4. Decreased values indicate hyperthyroidism or secondary hypothyroidism.

D. Needle aspiration of thyroid tissue     

1.      Aspiration of thyroid tissue is done for cytological examination.

2.      No client preparation is necessary; NPO status may or may not be prescribed.
3.      Light pressure is applied to the aspiration site after the procedure.

          G. 24-hour urine collection for vanillylmandelic acid (VMA)

1.      Diagnostic tests for pheochromocytoma include a 24-hour urine collection for VMA,
a product of catecholamine metabolism, metanephrine, and catecholamines, all of
which are elevated in the presence of pheochromocytoma.
2.      The normal range of urinary catecholamines:
a.     Epinephrine:<20 mcg/day (<109 nmol/day).
b.     Norepinephrine: 15–80 mcg/day (89–473 nmol/day).

Diagnostic tests for Parathyroid gland abnormality:

Hypoparathyroidism:
        Phosphorus level in blood is elevated.
        Decrease in serum calcium level to a low level (7.5 mg/ 100 mL or less).
        PTH levels are low in most cases; may be normal or elevated in
pseudohypoparathyroidism.
        In chronic hypoparathyroidism, bone density may be increased as seen on
radiography.
Hyperparathyroidism:

        Persistently elevated serum calcium (11 mg/100 mL); test is performed on at least
two occasions to determine consistency of results.
       Exclusion of other causes of hypercalcemia—malignancy (usually bone or breast),
vitamin D excess, multiple myeloma, sarcoidosis, milk-alkali syndrome, such drugs as
thiazides, Cushing’s disease, hyperthyroidism.
        PTH levels are increased.
       Serum calcium and alkaline phosphatase levels are elevated and serum phosphorus
levels are decreased.
        Skeletal changes are revealed by X-ray.
         Early diagnosis typically is difficult. (Complications may occur before this condition
is diagnosed.)
        Cine computed tomography (CT) will disclose parathyroid tumors more readily than
X-ray.
        Sestamibi scan is used to evaluate location of the tumor prior to surgery.

Diagnostic tests for Adrenal Gland abnormality:

Hyperaldosteronism:
        Excessive plasma cortisol levels.
        An increase in blood glucose levels and glucose intolerance.
        Decreased serum potassium level.
        Reduced eosinophils.
       Elevated urinary 17-hydroxycorticoids and 17-ketogenic steroids.
        Elevation of plasma ACTH in patients with pituitary tumors.
        Low plasma ACTH levels with adrenal tumor.
        Loss of diurnal variation of cortisol secretion.
        X-rays of the skull may detect erosion of the sella turcica by a pituitary tumor.
        Overnight DST or 48-hour low-dose DST, possibly with cortisol urinary excretion
measurement.
a. Unsuppressed cortisol level in Cushing’s syndrome caused by adrenal tumors.
b. Suppressed cortisol levels in Cushing’s disease caused by pituitary tumor.
        Elevated levels of cortisol measured in saliva are significant.
        CT scan and ultrasonography detect location of tumor.
Hypoaldosteronism:
        Blood chemistry—decreased glucose and sodium; increased potassium, calcium, and
BUN levels.
        Increased lymphocytes on complete blood count.
        Low fasting plasma cortisol levels; low aldosterone levels.
        24-hour urine studies—decreased 17-ketosteroids, 17hydroxycorticoids, and 17-
ketogenic steroids.
        ACTH stimulation test—no rise or minimal rise in plasma cortisol and urinary 17-
ketosteroids.

Diagnostic tests for Pitutary gland abnormality:

Hypopitutarism: 
        Polyuria (5 to 25 L/24 hr); polydipsia
        Dilute urine; specific gravity 1.001 to 1.005 or less; osmolality 50 to 200 mOsm/kg.
        Increased serum sodium level and plasma osmolality.
         Clinical findings of dehydration (e.g., poor skin turgor, dry mucous membranes,
elevated temperature, hypotension) because of excessive water loss.
Hyperpitutarism:
        Increased soft tissue and bone thickness.
        Facial features become coarse and heavy, with enlargement of lower jaw, lips, and
tongue.
        Enlarged hands and feet d. Increased GH, ACTH, or PRL.
        X-ray examination of long bones, skull (sella turcica area), and jaw demonstrates
change in structure.
        Amenorrhea.
       Clinical findings of increased intracranial pressure (e.g., vomiting, papilledema, focal
neurologic  deficits). Diabetes and hyperthyroidism may result.

 Diagnostic tests for Pancreas abnormality:

 FASTING PLASMA GLUCOSE-Diagnosis of diabetes mellitus is based on plasma

glucose levels measured by a laboratory. According to the American Diabetes
Association,3 a normal plasma glucose level is less than 100 mg/dL, although different
laboratories may have slightly different normal values. When the fasting plasma glucose
(drawn after at least 8 hours without eating) is 126 mg/dL, diabetes is diagnosed. A
second test may be required if the first test is not clearly diagnostic. If the fasting plasma
glucose is between 100 and 125 mg/dL, the patient has impaired fasting glucose (IFG).

    CASUAL PLASMA GLUCOSE. Sometimes it is not feasible to check a fasting

plasma glucose. A casual plasma glucose (CPG) is checked without regard to the last
meal. Diabetes is diagnosed if the CPG is 200 mg/dL, with symptoms of diabetes.

    GLYCOHEMOGLOBIN. The glycohemoglobin test (also called glycosylated

hemoglobin, or HbA1c) is used to gather baseline data and to monitor progress of
diabetes control (not to diagnose diabetes). Glucose in the blood attaches to hemoglobin
in the red blood cells. Red blood cells live about 3 months in the body. When the glucose
that is attached to the hemoglobin is measured, it reflects the average blood glucose level
for the previous 2 to 3 months. A normal HbA1c is 4% to 6%. This is a helpful
measurement when blood glucose levels fluctuate and a single measurement would be
misleading. It also assists in determining the degree of effectiveness of a patient’s
treatment plan. Newer methods allow this test to be done in a physician’s office while the
patient waits. Glycohemoglobin testing might be inaccurate in some people, such as those
with anemia. These individuals may have a glycated serum protein test, which is asimilar
test that indicates glucose levels over a period of 1 to 2weeks instead of 3 months.
 BIBLIOGRAPHY:

 Joyce M. Black, Jane Hokanson Hawks, “Medical Surgical Nursing”, Volume-1,

published by Elsevier.
 Linda S. Williams, Paula D. Hopper, “ Understanding Medical surgical Nursing”, Third
edition, published by F.A. Davis Company.
 Lippincott ,“ Manual Of Nursing practice”, Ninth Edition, published by Lippincott
Williams and Wilkins.
 Brunner & Suddarth’s “Textbook of Medical-Surgical Nursing”,  tenth edition