Endocrine Flashcards

1
Q

Diagnostic Procedures for the Endocrine System

A

-blood, urine, or saliva; determine an excess or lack of a particular hormone
-Some of these tests stimulate a reaction in the body that will facilitate diagnosis of a particular disorder.

-Stimulation testing involves giving hormones to stimulate the target gland to determine if the gland is capable of normal hormone production.

-Suppression testing involves giving medications or substances to evaluate the body’s ability to suppress excessive hormone production.

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2
Q

Pituitary Disorders: Caused by

A

-Disease of the pituitary gland or the hypothalamus
-Trauma
-Tumor
-Vascular lesion

-Over secretion of ACTH from the anterior pituitary gland results in Cushing’s disease.
-Over secretion of GH results in gigantism in children and acromegaly in adults.
-Under secretion of GH in children results in dwarfism.

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3
Q

Acromegaly

A

(Pituitary disorder)
-Medications
–Octreotide (Sandostatin)-synthetic GH
–Parlodel (Permax)- dopamine agonist
-Therapeutic Measures
–Surgical removal of pituitary gland; surgery is generally the first treatment option.
–Replacement therapy will be needed following removal of the pituitary gland and may need needed following radiation therapy
—Corticosteroids
—Thyroid hormones
-Radiation therapy

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4
Q

Giantism

A

(Pituitary Disorder)
-Hypersecretion of GH with follow-up appointments prior to closure of growth plates.
–Proportional overgrowth in all body tissue
Diagnostic
–Procedures/Collaborative Care: same as acromegaly

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5
Q

Dwarfism

A

(Pituitary Disorder)
-Hypersecretion of GH during fetal development or childhood that results in limited growth congenital or result from damage to the pituitary gland.
–Manifestations
—Head and extremities are disproportionate to torso
Face may appear younger
—Short stature, slow or flat growth rate
—Progressive bowed legs and lordosis
–Delayed adolescence or puberty

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6
Q

Dwarfism Diagnostic Procedures

A

-Comparison of height/weight against growth charts, slowed growth rate will be noted
-Serum growth hormone level
–Most providers will also evaluate other hormonal levels to ensure that no secondary deficiencies exist
–MRI of the head (to assess pituitary gland)

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7
Q

Diabetes Insipidus

A

-Caused from a deficiency of ADH
–Reduces the ability of the distal renal tubules in the kidneys to collect and concentrate urine.
-Results in:
–Excessive diluted urination
–Excessive thirst
–Electrolyte imbalance
–Excessive fluid intake

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8
Q

Risk Factors of Diabetes Insipidus

A

-Head injury
-Tumor or lesion
-Surgery or irradiation near or around the pituitary gland
-Infection
-Meningitis
-Encephalitis
-Patients who are taking lithium carbonate or demeclocycline

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9
Q

DI: Clinical Findings

A

Polyuria
-abrupt onset of excessive urination
-urinary output of 4 to 30 L/day of dilute urine
-failure of the renal tubules to collect and reabsorb water
Polydipsia
-excessive thirst
-consumption of 2 to 20 L/day

-Nocturia
-Sunken eyes
-Tachycardia
-Hypotension
-Loss or absence of skin turgor
-Dry mucous membranes
Weak, poor peripheral pulses
-Weight loss, muscle weakness
-Headache, Dizziness, -Fatigue
-Constipation

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10
Q

DI: Lab Tests

A

-Electrolyte imbalances: such as increased sodium
-Urine chemistry: Think DILUTE.
Decreased urine specific gravity (less than 1.005)
Decreased urine osmolality (less than 200 mOsm/L)
Decreased urine pH
Decreased urine sodium
Decreased urine potassium
-As urine volume increases, urine osmolality decreases.

-Serum chemistry: Think CONCENTRATED

Increased serum osmolality (greater than 300 mOsm/L)
Increased serum sodium
Increased serum potassium

-As serum volume decreases, the serum osmolality increases.

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11
Q

Diagnostic Tests for Posterior Pituitary Gland

A

-The water deprivation test
Monitor body weight, hourly urine output.
-ADH
-Serum and urine electrolytes and osmolality
-Urine specific gravity
-MRI of hypothalamus and pituitary
-24-hour urine

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12
Q

Water Deprivation Test

A

-The expected reference range for osmolality is 285 to 295 mOsm/kg H2O.

-Osmolality increases with dehydration and decreases with over hydration, so it provides important information about fluid and electrolyte balance.

-Contraindications for this test include:
Renal insufficiency
Uncontrolled diabetes mellitus
Hypovolemia
Adrenal or thyroid hormone deficiency

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13
Q

Vasopressin Test

A

-This is an easy and reliable diagnostic test.
-Dehydration is induced by withholding fluids.
-A subcutaneous injection of vasopressin produces urine output with an increased specific gravity and osmolality.
-The test is positive for DI if the kidneys are unable to concentrate urine despite increased plasma osmolarity.

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14
Q

DI Medications

A

-Desmopressin acetate (DDAVP)
-Vasopressin (Pitressin)
-If DI is nephrogenic in origin, thiazide diuretics will be prescribed.
-Patient Education:
–Lifetime vasopressin replacement therapy
–Report weight gain or loss, polyuria, or polydipsia to the provider
–Monitor fluid intake and urine output
–Avoid foods with diuretic action

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15
Q

SIADH: Syndrome of Inappropriate Antidiuretic Hormone

A

-Excessive release of ADH, also known as vasopressin, secreted by the pituitary gland.
-Results in the inability to excrete an appropriate amount of urine thus developing fluid retention and dilutional hyponatremia.
-Leads to renal reabsorption of water causing renal excretion of sodium leading to:
–water intoxication
–cellular edema
–dilutional hyponatremia

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16
Q

SIADH Risk Factors

A

-Malignant tumors
-Increased intrathoracic pressure
-Head injury
-Meningitis
-Stroke
-Tuberculosis
-Medications
chemotherapy agents
SSRIs
Opioids
antibiotics

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17
Q

SIADH Early Manifestations

A

-Headache
-Weakness
-Anorexia
-Muscle cramps
-Weight gain

18
Q

SIADH Physical Assessment Findings

A

Confusion
Lethargy
Cheyne-Stokes respirations

19
Q

SIADH Manifestations of FVE

A

Tachycardia
Bounding pulses
Possible hypertension
Crackles in lungs
Distended neck veins
Taut skin
Intake is greater than output

20
Q

SIADH Lab Tests

A

-Urine chemistry: Think CONCENTRATED
Increased urine sodium
Increased urine osmolarity
As urine volume decreases, urine osmolarity increases

-Blood chemistry: Think DILUTE
Decreased serum sodium (dilutional hyponatremia)
Decreased serum osmolarity (less than 270 mEq/L)
As serum volume increases, serum osmolarity decreases

21
Q

SIADH Nursing Care

A

-Restrict oral fluids to 500 to 1,000 mL/day to prevent further hemodilution (first priority)
-During fluid restriction, provide comfort measures for thirst
-Flush all enteral and gastric tubes with 0.9% sodium chloride, instead of water, to replace sodium and prevent further hemodilution
-Monitor I&O
-Report decreased urine output
-Monitor vital signs for increased blood pressure, tachycardia, and hypothermia
-Auscultate lung sounds to monitor for pulmonary edema (can develop rapidly and is a medical emergency)
-Monitor for decreased serum sodium/osmolarity and elevated urine sodium/osmolarity
-Weigh the patient daily
-A weight gain of 1 kg (2.2 lb) indicates a gain of 1 L of fluid. Report this to
the provider
-Report altered mental status
-Reduce environmental stimuli and position as needed
-Provide a safe environment
-Maintain seizure precautions
-Monitor for indications of heart failure, which can occur from fluid overload.
-Use of a loop diuretic can be indicated.

22
Q

SIADH Medications

A

-Tetracycline derivative (demeclocycline)
-Unlabeled use to correct fluid and electrolyte imbalances by stimulating urine flow
-Contraindicated in impaired kidney function.

Instruct the client to avoid taking demeclocycline at the same time as calcium, iron, magnesium supplements, antacids containing aluminum, or milk products.
● Advise the client to monitor for indications of a yeast infection, such as a white, cheese-like film inside
the mouth.
● Advise the client to avoid prolonged exposure to sunlight. Protective clothing and sunscreen should be used.
● Instruct the client to notify the provider if diarrhea develops.

23
Q

SIADH Patient Education

A

-Advise the patient to report difficulty breathing or shortness of breath
Include information about medications with discharge instructions
-Advise the patient to monitor for indications of hypervolemia and any neurological changes, which can lead to seizures.
-Advise the patient to notify the provider of indications of hyponatremia
-Advise the patient to avoid consumption of alcohol.

24
Q

Addison’s Disease

A

Adrenal insufficiency: The hyposecretion of adrenal cortex hormones
Caused by:
Autoimmune disease
TB histoplasmosis
adrenalectomy
tumors
HIV
Can be induced by the abrupt cessation of steroid medications.

With Addison’s, you need to ADD cortisol

25
Q

Addison’s Disease Clinical Manifestations

A

Weakness and fatigue
Nausea and vomiting
Hyperpigmentation
Hypotension
Increased heart rate
Hypoglycemia
Hyponatremia
Hyperkalemia
Hypercalcemia

26
Q

Cushing’s Disease/Syndrome

A

Cushing’s disease (hypercortisolism) and Cushing’s syndrome are caused by an oversecretion of the hormones the adrenal cortex produces.

Cushing’s disease can be the result of a tumor in the pituitary gland resulting in release of the hormone ACTH.

Cushing’s syndrome results from long‑term use of glucocorticoids to treat other conditions, such as asthma or rheumatoid arthritis.

27
Q

Cushing’s Disease Risk Factors

A

Women between the ages of 20 and 40 years

CAUSES OF INCREASED CORTISOL
-Adrenal hyperplasia
-Adrenocortical carcinoma
-Pituitary carcinoma that secretes adrenocorticotropic hormone (ACTH)
-Carcinomas of the lung, gastrointestinal (GI) tract, or pancreas (these tumors can secrete ACTH)
-Therapeutic use of glucocorticoids for the following.
Organ transplant
Chemotherapy
Autoimmune diseases
Asthma
Allergies
Chronic inflammatory diseases

28
Q

Cushing’s Disease Expected Findings

A

-Weakness, fatigue, sleep disturbances
-Back and joint pain
-Altered emotional state (irritability, depression)
-Decreased libido

PHYSICAL ASSESSMENT FINDINGS
-Evidence of decreased immune function and decreased inflammatory response (infections without fever, swelling, drainage, redness)
-Thin, fragile skin
-Bruising and petechiae (fragile blood vessels)
-Hypertension (sodium and water retention)
-Tachycardia
-Gastric ulcers due to oversecretion of hydrochloric acid
-Weight gain and increased appetite
-Irregular menses
-Dependent edema: Changes in fat distribution, including the characteristic fat distribution of moon face, truncal obesity, and fat collection on the back of the neck (buffalo hump)
-Fractures (osteoporosis)
-Bone pain and fractures with an increased risk for falls
-Muscle wasting (particularly in the extremities)
-Impaired glucose tolerance
-Frequent infections, poor wound healing
-Hirsutism
-Acne
-Red cheeks
-Striae (reddened lines on the abdomen, upper arms, thighs)
-Clitoral hypertrophy
-Thinning, balding hair
-Hyperglycemia
-Emotional lability

29
Q

Cushing’s Disease Diagnostic Procedures

A

Dexamethasone suppression tests: Tests vary in length and amount of dexamethasone to administer.
24-hr urine collections show suppression of cortisol excretion in clients who do not have Cushing’s disease.

DIAGNOSTIC PROCEDURES
X-ray, magnetic resonance imaging, and CT scans identify lesions of the pituitary gland, adrenal gland, lung, GI tract, and pancreas.
Radiological imaging determines the source of adrenal insufficiency (tumor, adrenal atrophy).

30
Q

Hyperthyroidism

A

-Hyperthyroidism is a clinical syndrome caused by excessive circulating thyroid hormones.
-Because thyroid activity affects all body systems, excessive thyroid hormone exaggerates normal body functions and produces a hypermetabolic state.

31
Q

Cause of Hyperthyroidism

A

-Graves’ disease is the most common cause
-Autoimmune antibodies result in hypersecretion of thyroid hormones.
-Autosomal recessive trait passed to females
-Toxic nodular goiter
-Caused by overproduction of thyroid hormone due to the presence of thyroid nodules
-Exogenous hyperthyroidism is caused by excessive dosages of thyroid hormone.

32
Q

Hyperthyroidism Clinical Findings

A

Nervousness
Irritability
Hyperactivity
Emotional lability
Decreased attention span
Cries or laughs without cause
Change in mental or emotional status
Weakness, easy fatigability, exercise intolerance
Muscle weakness
Heat intolerance
Weight change (usually loss) and increased appetite
Insomnia and interrupted sleep
Frequent stools and diarrhea
Menstrual irregularities (amenorrhea or decreased menstrual flow)
Decreased fertility
Libido initially increased in both men and women, followed by a decrease as the condition progresses
Warm, sweaty, flushed skin with velvety-smooth texture
Hair thins, and develops a fine, soft, silky texture
Tremor, hyperkinesia, hyperreflexia
Exophthalmos (Graves’ disease only) due to edema in the extraocular muscles and increased fatty tissue behind the eye
Blurred or double vision and tiring of eyes due to pressure on the optic nerve
Photophobia (sensitivity to light)
Excessive tearing and bloodshot appearance of eyes
Vision changes
Eyelid retraction (lag): movement of the eyelid is delayed when the eye moves downward
Globe (eyeball) lag: upper eyelid pulls back faster than the eyeball when the client gazes upward
Hair thinning or loss
Goiter
Bruit over the thyroid gland
Elevated systolic blood pressure and widened pulse pressure
Tachycardia, palpitations, and dysrhythmias
Dyspnea
Findings in older adult clients are often more subtle than those in younger clients.

33
Q

Hyperthyroidism Diagnostic Procedures

A

-Ultrasound:
Used to produce images of the thyroid gland and surrounding tissue

-Electrocardiogram:
Used to evaluate the effects of excessive thyroid hormone on the heart (tachycardia, dysrhythmias).
ECG changes include atrial fibrillation, and changes in the P and T waveforms.

-Radioactive iodine uptake: Nuclear medicine test
Clarifies size and function of the gland.
Contraindicated in pregnant women.
An assessment for an allergy to iodine or shellfish should be completed prior to this test.
The uptake of radioactive iodine, administered orally 24 hr prior to the test, is measured.
An elevated uptake is indicative of hyperthyroidism.

34
Q

Hyperthyroidism Nursing Care

A

Minimize energy expenditure by assisting with activities and by encouraging alternate periods of rest with activity.
Promote a calm environment.
Assess mental status and decision-making ability.
Monitor nutritional status.
Monitor I&O
Monitor patient’s weight.
Provide eye protection (patches, eye lubricant, tape to close eyelids) for a patient who has exophthalmos.

Monitor vital signs and hemodynamic parameters.
Reduce room temperature.
Provide cool shower/sponge bath to promote comfort.
Provide linen changes as necessary.
Report a temperature increase of 1° F or more to the provider immediately, because this is indicative of an impending thyroid crisis.
Monitor ECG for dysrhythmias.
Avoid excessive palpation of the thyroid gland.
Administer antithyroid medications.
Prepare the patient for a total/subtotal thyroidectomy if unresponsive to antithyroid medications or has an airway-obstructing goiter.

35
Q

Hypothyroidism

A

-Suboptimal levels of thyroid hormone resulting in decreased metabolism.
-Occurs most frequently in older women
Fatigue
Increased sensitivity to cold
Constipation
Dry skin, brittle hair and nails
Weight gain
Deepened, hoarse voice
Joint pain
Hyperlipidemia and anemia
Depression
Menstrual disturbances

36
Q

Myxedema

A

Myxedema coma is a life-threatening condition that occurs when hypothyroidism is untreated or when a stressor (e.g., acute illness, surgery, chemotherapy, discontinuing thyroid replacement therapy, or use of sedatives/opioids) affects a client who has hypothyroidism.

37
Q

Myxedema Manifestations

A

Respiratory failure
Hypotension
Hypothermia
Bradycardia, dysrhythmia
Hyponatremia
Hypoglycemia
Coma

38
Q

Myxedema Nursing Considerations

A

-Maintain airway patency with ventilatory support if necessary.
-Provide continuous ECG monitoring.
-Monitor ABGs to detect hypoxia, hypercapnia, respiratory acidosis.
-Monitor mental status.
-Cover the client with warm blankets.
-Monitor body temperature hourly until stable.
-Replace fluid with 0.9% sodium chloride IV.
-Replace thyroid hormone by administering large doses of levothyroxine IV bolus.
-Monitor vital signs because rapid correction of hypothyroidism can cause adverse cardiac effects.
-Monitor I&O and daily weights.
-With treatment, urine output should increase, and body weight should decrease. Failure to do so should be reported to
the provider.
-Treat hypoglycemia with glucose.
-Administer corticosteroids.
-Initiate aspiration precautions
-Check for possible sources of infection

39
Q

Hypoparathyroidism

A

-The hyposecretion of parathyroid hormone (PTH), resulting in hypocalcemia and hyperphosphatemia
-Usually caused by surgical removal of the parathyroid gland disuse during
Parathyroidectomy
Thyroidectomy
Radical Neck Dissection

40
Q

Hypoparathyroidism Clinical Manifestations

A

from Hypocalcemia

-Paresthesia
-Muscle cramps and tetany
-Chvostek’s sign
-Trousseau’s sign
-Circumoral paraesthesia with numbmess and tingling of the fingers
-Severe tetany may lead to bronchospasm, laryngeal spasm, carpopedal spasm, dysphagia, cardiac dysrhythmias, and seizures

41
Q

Hypoparathyroidism Nursing Interventions

A

-Monitor ECG
-Assess for neuromuscular irritability
-Provide high calcium, low phos diet
-Institute seizure precautions

Medications
-Acute: IV calcium gluconate
-Chronic: Oral calcium salts, Vitamin D