NCLEX® Review

The endocrine system is a complex pathway that plays a role in the function of a variety of organ and blood systems. Its headquarters located in the brain where the hypothalamus and pituitary gland release a variety of hormones that can lead to profound effects systemically. Through signaling pathways the endocrine system can alter body fluid levels, bone and muscle strength, blood sugar levels, temperature, heart rate, and much more.

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For this reason, the endocrine system proves to be a critical one to understand when preparing for the NCLEX® exam as disorders within it can lead to serious medical conditions described below.

Addison’s vs. Cushing Diseases

One of the primary effects the endocrine system has involves hormones that ultimately impacts the production of endogenous steroids. The pathway begins with the hypothalamus which secretes CRH triggering the release of ACTH from the pituitary. The signal eventually reaches the adrenal cortex which can alter the production of endogenous steroids such as cortisol. Two famous disorders involving this pathway are called Addison’s disease and Cushing’s disease.

Addison’s Disease:

Addison’s is a debilitating disease that can generally be thought of as the under production of endogenous steroids. To remember this, you can think of the treatment of Addison’s which involves adding steroids. Addison’s can be triggered by autoimmune destruction of adrenal or pituitary cells, cancer or infection of these hormones, or due to trauma (e.g. hemorrhage) of the adrenal glands.

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Signs and Symptoms – Addison’s

There are a variety of signs and symptoms that can be observed in Addison’s patients including reduced blood sugar, reduced salt and therefore water retention, decreased sexual appetite, hair loss (alopecia), low blood pressure, and more. Patients may report reduced tolerance to temperature, symptoms of depression, and slow and irregular menstrual cycles in female populations. One of the standout symptoms observed in Addison’s patients is a strange pigmentation on their skin sometimes regarded as a “bronze pigment”.

Key clinical manifestations to watch out for in Addison’s includes sodium loss or hyponatremia (Na+ < 135 mEq/L) and water loss as a result. Patients may be subject to significant weight loss which should be monitored as excess water gets excreted from the body. Additionally, patients may experience potassium retention leading to hyperkalemia (K+ > 5 mEq/L) potentially causing irregular heartbeat (arrythmia).

Pharmacology and Nursing Interventions – Addison’s

Corticosteroids prove to be the staple treatment for patients with Addison’s as it treats the underlying steroid deficit. Examples of steroids that may be used in these patients are prednisone and hydrocortisone with dosages that may vary based on the patient’s weight and the severity of the condition.

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It is critical to note that since these patients may be treated chronically with steroids, they will be at increased risk of Addisonian crisis from acute steroid insufficiency. Abrupt discontinuation of steroids may lead to critical conditions, primarily severe hypotension which can potentially be fatal for the patient. For this reason, patients that are on chronic steroids who should be educated to never suddenly discontinue their regimen – instead they should be instructed to taper the dose down.

In the event of Addisonian crisis the key intervention other than restarting steroids are to increase the patient’s blood pressure. Patients with severe hypotension should be treated with fluids – either normal saline or D5W.

Generally, the approach to Addison’s treatment involves replacing whatever deficiencies are creating the problem. Patients may need to be treated with hormones that are chronically suppressed as a result of the condition (e.g. testosterone, estrogen, etc.) Other treatments may include sodium supplementation with saline solutions or sugar containing solutions for low blood sugar. Monitoring the electrolyte, hormone, and vital sign imbalances are essential when treating patients with Addison’s serving as a key intervention for all patients with this disease.

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Cushing’s Disease:

Cushing’s disease can be considered effectively the opposite of Addison’s regarding its signs, symptoms, and treatment approaches. Cushing’s disease involves the overproduction or secretion of steroids in the body leading to a variety of systemic effects. It can be caused by both exogenous factors such as steroid overuse or endogenous factors such as a tumor on the adrenal or pituitary gland. Notably patients with small cell lung cancer may be at an increased risk of developing Cushing’s disease.

Signs and Symptoms – Cushing’s

The signs and symptoms related to Cushing’s can be very apparent and debilitating for the patient. It presents in almost the exact opposite way as Addison’s ranging from weight gain (due to water and salt retention) which can lead to purple striae or stretch marks as a result of substantial abdominal or facial growth. Patients with progressed disease may show an enlarged face which is often regarded as a “moon face” and a large fat pad that looks like a “buffalo hump” on their upper back. They may also grow excessive amounts of hair known as hirsutism.

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Clinically these patients may demonstrate elevated blood pressure (systolic > 140 mmHg), elevated blood glucose and increased sodium retention (hypernatremia). Patients may also be at increased risk of infection with white blood cell suppression as a result of excessive steroid production. These clinical manifestations should be closely monitored in patients as they can lead to a variety of serious consequences.

Pharmacology and Nursing Interventions – Cushing’s

The goal when treating Cushing’s disease is to attack the underlying cause whether it be exogenous or endogenous. A key exogenous factor to be aware of is steroid overuse – therefore the key treatment is to taper these patients off steroids slowly. Patients who may be prone to this event include those with chronic inflammatory conditions for example patients with rheumatoid arthritis.

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Cushing’s patients with endogenous factors such as a tumor on the pituitary or adrenal gland may need to be surgically removed. As a result, removal of endocrine glands may require supplementation of the affected hormones or steroids that the patient may be deprived of after the procedure.

Excessive levels of steroids in the system can lead to a variety of other clinical manifestations that require intervention. A key one is that steroids can lead to increased blood sugar leading to hyperglycemia. Patients with acute hyperglycemia should be treated with insulin when clinically appropriate. Other considerations include water and salt retention. Water retention can be monitored by measuring the patient’s body weight. Increases in weight by 1 lbs/day or 2-3 lbs in a few days will require pharmacologic intervention.

Patients with Cushing’s should be screened for bone weakness or osteoporosis as increased steroids can reduce bone mineral density – therefore requiring osteoporosis treatment such as calcium and vitamin D supplementation. Cushing’s victims may also be at an increased risk of developing a cataract which requires a referral to an optometrist.

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SIADH vs. Diabetes Insipidus

Antidiuretic hormone (ADH) – which is secreted by the posterior pituitary gland – plays a crucial role in the body in fluid retention and excretion. The key function of ADH is to reduce the frequency of diuresis or urine output ultimately leading to fluid retention in the body. When ADH becomes inhibited urine output increases and therefore patients fail to retain water and become dehydrated. SIADH or Syndrome of Inappropriate Anti-Diuretic Hormone is the condition where ADH production increases leading to reduced urine output – the opposite condition is known as Diabetes Insipidus where urinary output is too high and excess water becomes secreted.


Signs and Symptoms – SIADH

SIADH is caused primarily by physical augmentation of the pituitary gland which may be the result of increased intracranial pressure (ICP) or a tumor on the pituitary gland. Increased ICP can be the result of brain trauma or serious septic infections (e.g. meningitis) while tumors may derive from diseases like small cell lung cancer or carcinomas. Overproduction of ADH ultimately results in the excessive retention of water. Patients with SIADH will therefore exhibit increased weight gain and blood pressure. Other signs and symptoms relate to these effects such as reports of headaches due in part to high blood pressure and part to low concentrations of sodium in the blood.

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A key clinical feature of SIADH revolves around the excess levels of water in the body which ultimately causes low concentrations of electrolytes like sodium. Whenever the ratio of water to electrolytes becomes skewed it can affect various organs in the body such as the brain. Low serum sodium or hyponatremia (Na+ < 135 mEq/L) can increase a patient’s risk of having a seizure which could further exacerbate their condition. Another key manifestation involves the specific gravity of the urine (1.030+) which suggests that the urine has become too thick.

Nursing Interventions and Pharmacology – SIADH

Patients with SIADH should always be treated for the underlying cause of the condition when possible – for example patients with meningitis should be treated with potent antibiotics. Regardless of whether the SIADH can be cured the primary concern should always be the acute conditions manifesting in the patient which can put them at greater risk.

Hyponatremia is a key problem for SIADH patients as it can ultimately increase the patient’s risk of having a seizure which can exacerbate the issue. Therefore, these patients will simply need to be treated with hypertonic saline solutions (e.g. 3% IV sodium) and increase dietary salt intake when appropriate. Providing sodium to these patients will not only act against the hyponatremia but also may help draw water out of the tissues to be excreted – thus treating edema.

Key monitoring for these patients are to take daily weights as it will inform providers of their fluid levels. Edema may be a chief complaint noted by the patient which may indicate the use of diuretics such as furosemide to excrete water and reduce their weight. Additionally, their blood pressure should be monitored as increased volumes of water can significantly increase BP. Intervention may be necessary if their blood pressure exceeds dangerous levels leading to hypertensive crisis (BP > 180 systolic).

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Diabetes Insipidus:

Signs and Symptoms – DI

Diabetes insipidus (DI) presents as essentially the opposite condition in patients compared to SIADH. Like SIADH – DI may be derived from brain tumors, infection, or physical trauma to the brain. It is not however associated with small cell lung cancer or carcinomas unlike SIADH.

Patients with DI essentially drain their body too quickly of fluid via increased urine output. These patients will present with various signs of dehydration ranging from dry skin and mucosa and increased thirst. Other signs may be weight loss as well as hypotension since patients are excreting large volumes of water.

Clinically these patients will present with hyperosmolar conditions where there is too little water compared to their electrolyte concentrations. Hypernatremia is a key feature where serum sodium exceeds 145 mEq/L. Additionally the specific gravity of their urine will be much lower than in SIADH patients with values around 1.005 – which can be described as more dilute urine.

Nursing Interventions and Pharmacology – DI

Patients with DI should be treated in a similar manner to SIADH in the sense that the underlying cause should be cured when possible. Managing their acute condition is the priority as the physiological effects of the disease can be serious and potentially life threatening. Treatment of DI may vary based on the specific subset that they are exhibiting (e.g. central diabetes insipidus vs. gestational DI vs. nephrogenic DI). A core treatment for the disease is to manage the patient’s blood pressure which can become dangerously low – which can cause organ damage and death.

Vasopressors may be used in these patients to help increase their blood pressure as well as decrease urine output. Vasopressors work like ADH by increasing fluid retention and by causing vasoconstriction. Examples of vasopressors includes vasopressin and desmopressin. The patient may not respond effectively to these treatments which may suggest an issue with the kidneys requiring other treatment modalities. Caution should be used when giving vasopressors as they can cause hyponatremia like ADH leading to increased seizure risk.

Patients may also exhibit severe hypernatremia which should be managed with sodium restriction when clinically appropriate. Monitoring their weight will be key to assess their fluid management. In addition to vasopressors they may require IV fluids to aid in blood pressure restoration as well as maintaining hydration status.

Hyperthyroidism vs. Hypothyroidism

The thyroid gland plays key role in the endocrine system as it manages a variety of pathways was significant clinical implications. Generally, the thyroid gland and the hormones involved are associated with the regulation of metabolism. Hyperthyroidism can be attributed with an increased metabolism while the opposite is true for hypothyroidism.

The pathway originates in the hypothalamus where it secretes thyroid releasing hormone (TRH) – thereby triggering thyroid stimulating hormone (TSH) – ultimately leading to the production of two hormones. T4 is the first hormone produced and T3 is the second one which is also known as the active thyroid hormone. TSH also stimulates the release of calcitonin which causes the removal of calcium from the blood into the bones. It is also important to note that iodine is a key component in thyroid hormone production.


Signs and Symptoms – Hyperthyroidism

Hyperthyroidism can be caused by several factors including excessive iodine intake via diet, Graves’ disease, and potentially thyroid replacement overdose (levothyroxine overdose). Hyperthyroidism can be attributed largely to characteristics that reflect increased metabolism suggesting increased energy. A clinical manifestation of hyperthyroidism is called a thyroid storm where too much thyroid hormone is released into the system. A patient with thyroids storm will present with marked agitation, confusion, and restlessness.

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In addition, these patients may experience increased temperature, tachycardia (HR > 100 bpm), heart palpitations, and hypertension. Physically patients suffering from hyperthyroidism may exhibit grape eyes (exophthalmos) where the eyes appear to bulge outwards. They may also develop a goiter which is an abnormal enlargement of the thyroid gland. Other manifestations may be weight loss as the patient’s metabolism becomes ramped up as well as diarrhea as the digestive tract becomes sped up.

Nursing Interventions and Pharmacology – Hyperthyroidism

There are a variety of interventions that can be made on the behalf of patients experiencing hyperthyroidism. A key one to make is to eliminate the cause whether it is reducing the dose of thyroid replacement therapy or dietary iodine reduction. As a result of increased metabolism these patients may require increased caloric intake high in proteins and carbs depending on their baseline weight. They may need to consume frequent meals and snacks up to 6-8 times per day. Due to other effects such as diarrhea in these patients it is advised that they avoid caffeine, high fiber foods, and spicy foods as well.

There are several pharmacological interventions that patients with hyperthyroidism may benefit from. A commonly prescribed medication for this condition is methimazole. Methimazole works by inhibiting the synthesis of thyroid hormone. It is important to know that methimazole is not safe for pregnant women where other treatments may be. PTU or propylthiouracil also works to inhibit the production of thyroid hormone like methimazole but through different mechanisms. This medication is safe for pregnancy but may cause side effects such as fever or sore throat.

Patients may be required to remove the thyroid gland which can be achieved by two different modalities. The first begins by providing patients potassium iodide which acts to shrink the thyroid gland in preparation for thyroidectomy (surgical removal of the gland). Potassium iodide may stain the patient’s teeth and should not be taken with methimazole or PTU. During the removal of the thyroid gland the hormones may dump into the patient’s system which can cause a thyroid storm, so monitoring is a key intervention for these patients.

It is also important to note that abrupt discontinuation of thyroid hormone production can cause a Myxedema coma which can be life threatening. An endotracheal tube should be at the patient’s bedside to intervene in the presence of severe respiratory depression. Calcium levels should also be monitored in the event of hypocalcemia (Ca++ < 8.6 mEq/L). Hypocalcemia may present with Chvostek's sign which is the twitching of facial muscles or Trousseau's sign which are carpopedal spasms which occurs after inflating a blood pressure cuff for 3 minutes.

Another thyroid removal method involves the destruction of the thyroid gland by administering radioactive iodine also known as radioactive iodine uptake (RAIU). RAIU destroys the thyroid gland in the same way radiation would. This should only be used in patients who are not pregnant so women should have a negative result before starting. These patients should not be given sedatives or anesthesia and should not be wearing jewelry around the neck or dentures. They should hold antithyroid medications 5-7 days prior to the procedure to prevent acute hypothyroidism. Lastly, these patients should avoid other people especially pregnant women as the isotope can damage their thyroid gland as well. They may even be advised to use separate restrooms and flush multiple times to prevent any further issues.

The last consideration to keep in mind for treatment of hyperthyroid patients is that their heart rate may be dangerously elevated. They can be treated with a beta blocker to reduce their heart rate. Examples of beta blockers includes atenolol, propranolol, and metoprolol. All beta blockers end with the suffix “prolol” which can aid in memorization of the various treatments.


Signs and Symptoms

Hypothyroidism is a much more prevalent disorder which can be caused by low dietary iodine, Hashimoto’s disease, a pituitary tumor, and naturally due to the removal of the thyroid gland. Another potential cause is abrupt discontinuation of thyroid replacement therapy (e.g. levothyroxine). Some classic signs and symptoms includes reduced energy, weight gain, slowed mental status and depression. Weight gain is due to both water retention and reduced energy output since the patient’s metabolism is low. Other symptoms can include hair loss (alopecia), constipation, dry skin turgor, reduced sexual appetite and irregular and slowed menstrual cycles (amenorrhea).

Clinically these patients may exhibit bradycardia (HR < 60 bpm), reduced blood pressure, reduced temperature and cold intolerance, and a reduced respiratory rate. A key manifestation of this respiratory depression is known as a Myxedema coma where the patient’s breathing becomes drastically inhibited potentially leading to death.

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Nursing Interventions and Pharmacology

Patients with hypothyroidism may need to be managed according to their reduced metabolic rate. The implication is that they should reduce their caloric load as well as cholesterol and saturated fats. They should be advised to rest frequently as well as avoid CNS depressants (e.g. opioids, benzos, muscle relaxants, EtOH).

Pharmacological intervention for hypothyroidism are relatively straight forward as the hormone simply need to get replaced. The most common medication used for this condition is levothyroxine which is simply a synthetic form of T4. Another thyroid supplement is armor thyroid which replaces both T3 and T4. Patients on these medications should be counseled on taking it in the early morning on an empty stomach (30-60 minutes before breakfast). Levothyroxine takes several weeks (3-4 weeks) to achieve relief in patients. Patients will have to be on thyroid replacement chronically for the rest of their lives – which may take time for the physician to determine the optimal dosage. Levothyroxine and other replacement hormones should not be stopped abruptly which could lead to events like a Myxedema coma.


The endocrine system is a complex web of pathways that has been the target of numerous interventions over the last few decades. There are many debilitating diseases that can affect patients ranging from steroid production to metabolic efficiency. The physical and clinical manifestations of these disorders are numerous yet often easy to distinguish. For this reason, it is imperative to understand these diseases well when preparing for the NCLEX® exam.