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

Addison’s Disease vs Cushing’s

One of the primary effects the endocrine system has involves hormones that ultimately impact the production of endogenous steroids. The pathway begins with the hypothalamus which secretes corticotropin-releasing hormones (CRH), triggering the release of adrenocorticotropic hormone (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 underproduction 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.

Symptoms of Addison’s Disease

There are a variety of signs and symptoms that can be observed in Addison’s clients including reduced blood sugar, reduced salt and therefore water retention, decreased sexual appetite, hair loss (alopecia), low blood pressure, and more.

Clients 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 clients 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. Clients may be subject to significant weight loss which should be monitored as excess water gets excreted from the body. Additionally, clients may experience potassium retention leading to hyperkalemia (K+ > 5 mEq/L) potentially causing an irregular heartbeat (arrythmia).

Addison’s Disease Nursing Interventions and Pharmacology

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

It’s critical to note that since these clients 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 client. For this reason, clients that are on chronic steroids 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 is to increase the client’s blood pressure. Clients with severe hypotension should be treated with normal saline or D5W fluids.

Generally, the approach to Addison’s treatment involves replacing whatever deficiencies are creating the problem. Clients 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 is essential when treating clients with Addison’s serving as a key intervention for all clients with this disease.

Clinically, these clients may demonstrate elevated blood pressure (systolic > 140 mmHg), elevated blood glucose, and increased sodium retention (hypernatremia). Clients 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 clients as they can lead to a variety of serious consequences.

Cushing’s Disease Nursing Interventions and Pharmacology

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 clients off steroids slowly. Clients who may be prone to this event include those with chronic inflammatory conditions for example clients with rheumatoid arthritis.

Cushing’s clients 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 client 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. Clients 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 client’s body weight. Increases in weight by 1 lbs/day or 2-3 lbs in a few days will require pharmacologic intervention.

Clients 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.

Diabetes Insipidus vs. SIADH

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 clients 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 (DI) where urinary output is too high, and excess water becomes secreted.

Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH):

Symptoms of 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. Clients with SIADH will therefore exhibit increased weight gain and blood pressure. Other signs and symptoms related 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.

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 client’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.

SIADH Nursing Interventions and Pharmacology

Clients with SIADH should always be treated for the underlying cause of the condition when possible. For example, clients 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 client which can put them at greater risk.

Hyponatremia is a key problem for SIADH clients as it can ultimately increase the client’s risk of having a seizure which can exacerbate the issue. Therefore, these clients 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 clients 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 clients is to take daily weights as it will inform their health care provider (HCP) of their fluid levels. Edema may be a chief complaint noted by the client, indicating the use of diuretics such as furosemide to excrete water and reduce weight.

Additionally, their blood pressure (BP) 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).

Diabetes Insipidus (DI):

Diabetes Insipidus Symptoms

Diabetes insipidus (DI) presents as essentially the opposite condition in clients 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.

Clients with DI essentially drain their body too quickly of fluid via increased urine output. These clients 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 clients are excreting large volumes of water.

Clinically, these clients 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 clients with values around 1.005 – which can be described as more dilute urine.

Diabetes Insipidus Nursing Interventions and Pharmacology

Clients 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 client’s blood pressure which can become dangerously low, and can cause organ damage and death.

Vasopressors may be used in these clients 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 include vasopressin and desmopressin.

The client may not respond effectively to these treatments, suggesting 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.

Clients 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). This triggers 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.

Hyperthyroidism:

Symptoms of 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 client with thyroids storm will present with marked agitation, confusion, and restlessness.

In addition, these clients may experience increased temperature, tachycardia (HR > 100 bpm), heart palpitations, and hypertension. Physically clients 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 client’s metabolism becomes ramped up as well as diarrhea as the digestive tract becomes sped up.

Hyperthyroidism Nursing Interventions and Pharmacology

There are a variety of interventions that can be made on the behalf of clients 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 clients 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 clients, it’s advised that they avoid caffeine, high-fiber foods, and spicy foods as well.

There are several pharmacological interventions that clients with hyperthyroidism may benefit from. A commonly prescribed medication for this condition is methimazole.

Methimazole works by inhibiting the synthesis of thyroid hormone. It’s 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.

Clients may be required to remove the thyroid gland which can be achieved by two different modalities. The first begins by providing clients potassium iodide which acts to shrink the thyroid gland in preparation for thyroidectomy (surgical removal of the gland).

Potassium iodide may stain the client’s teeth and should not be taken with methimazole or PTU. During the removal of the thyroid gland the hormones may dump into the client’s system which can cause a thyroid storm, so monitoring is a key intervention for these clients.

It’s 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 client’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, carpopedal spasms which occurs after inflating a blood pressure cuff for three 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 clients who are not pregnant so women should have a negative result before starting.

These clients 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 clients should avoid other people (especially pregnant women) as the isotope can also damage their thyroid gland. 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 clients 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.

Hypothyroidism:

Symptoms of Hypothyroidism

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 client’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 clients 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 client’s breathing becomes drastically inhibited potentially leading to death.

Hypothyroidism Nursing Interventions and Pharmacology

Clients 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.

Clients 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 clients. Clients 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.

Parathyroidism

The parathyroid glands are mainly responsible for controlling the regulation of blood calcium. Parathyroidism is a condition that causes the parathyroid glands to produce too much or too little parathyroid hormone (PTH). 

Hyperparathyroidism Pathophysiology 

Hyperparathyroidism is a result of the increased production of PTH. PTH makes bones weak by taking calcium from its storage. This also results in high calcium, also known as hypercalcemia (over 10.5).

Hypoparathyroidism Pathophysiology

Hypoparathyroidism is a result of decreased production or resistance to PTH. This also results in low calcium, also known as hypocalcemia (under 9.0) 

Signs include: 

• Trousseau’s Sign:
  •  T – Twerk with BP cuff
• Chvostek’s Sign
  •  C – Cheeky smile when stroking the face
• 3. Diarrhea

Hyperparathyroidism Causes

• Tumor
  •  • Adenoma – NOT cancerous
  •  • Malignant – Cancerous
• Vitamin D deficiency (since it helps Ca absorb)
• GI issues = Malabsorption of calcium
• Renal failure

Hypoparathyroidism Causes

• Thyroidectomy
• Low Mag+ (Hypomagnesemia)
• Autoimmune – body attacks the parathyroids
• Radiation Treatment – damages the thyroid

Hyperparathyroidism Treatment

• Lower the high blood calcium
  • IV furosemide & saline to flush out Ca
  • IV phosphate to lower Ca
• Parathyroidectomy – cut the tumor out

Hypoparathyroidism Treatment

• Increase the low blood calcium
  • IV Calcium gluconate
  • Vitamin D (helps the absorption of Ca)
• Seizure precautions and phenobarbital to decrease neuronal excitability

Endocrine System Conclusion

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 clients 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.