The metabolism can become unbalanced, and the control of many bodily functions can change as a result of an underactive or hyperactive thyroid gland. Today, exogenous thyroid hormone can be used to treat hypothyroidism after a simple blood test to diagnose the condition.

Differences Between Hypothyroidism and Hyperthyroidism

Hypothyroidism is a common condition where the thyroid doesn’t create and release enough thyroid hormone into the bloodstream. This makes the metabolism slow down.

Also called underactive thyroid, hypothyroidism can make a client experience fatigue, constipation, depression, weight gain, and intolerance to cold temperatures.

Hyperthyroidism (overactive thyroid) occurs when the thyroid gland produces too much of the hormone thyroxine.

Hyperthyroidism can accelerate the body’s metabolism, causing unintentional weight loss, sleeplessness, flushing, intolerance to heat, and a rapid or irregular heartbeat. Several treatments are available for hyperthyroidism.

Let’s dive into these differences in symptoms, pathophysiology, nursing interventions, and pharmacology.

Hypothyroidism vs. Hyperthyroidism Symptoms

Hypothyroidism Symptoms

• Fatigue
• Depression
• Weight gain
• Face swelling
• Goiter
• Difficulty breathing or swallowing
• Thinning hair
• Dry skin
• Intolerance to cold
• Aching in muscles and joints
• Constipation
• Reduced sweating
• Irregular or heavy menstrual cycles
• Infertility
• Decreased heart rate

Hyperthyroidism Symptoms

• Anxiety
• Pounding or racing heartbeat (or palpitations)
• Restlessness
• Fatigue
• Difficulty concentrating
• Hand tremor
• Frequent bowel movements
• Goiter (visibly enlarged thyroid gland)
• Enlarged thyroid nodules
• Hair loss
• Nail thickening or flaking
• Irregular menstrual periods
• Heat intolerance
• Increased appetite
• Increased sweating
• Weight loss
• Weight gain (in few cases)

Hypothyroidism Pathophysiology

The thyroid gland’s inability to produce enough thyroid hormone is the most frequent cause of hypothyroidism.

Though less frequent, thyroid dysfunction can also be caused by the hypothalamus and pituitary. Thyrotropin-releasing hormone (TRH), which is secreted by the hypothalamus, stimulates the pituitary gland to create thyroid-stimulating hormone (TSH).

Thyroxine (T4) has a half-life of 7 to 10 days, and finally, T4 is peripherally converted to triiodothyronine (T3) through 5′-deiodination. T3 and T4 levels, particularly T3, negatively affect the synthesis of TRH and TSH.

Hypothyroidism has several causes, including:

• Hashimoto’s disease
• Thyroiditis, or inflammation of the thyroid
• Congenital hypothyroidism, or hypothyroidism that is present at birth
• Surgical removal of part or all of the thyroid
• Radiation treatment of the thyroid
• Some medications

Less often, hypothyroidism is caused by too much or too little iodine in the diet.

Hashimoto’s disease

Hashimoto’s disease, an autoimmune disorder, is the most common cause of hypothyroidism. With this disease, the immune system attacks the thyroid. As a result, the thyroid becomes inflamed and can’t make enough thyroid hormones.

Hyperthyroidism Pathophysiology

The pathophysiology of the condition determines the specific hyperthyroidism variation. Hyperthyroidism in the form of painless thyroiditis is typically detected in the postpartum period.

In lymphocytic thyroiditis, it is determined by looking at the clinical history and palpating the thyroid gland. Lymphocytic thyroiditis is an autoimmune disorder where immune cells attack the thyroid gland and affect thyroid hormone production.

There is initially a phase of increased thyroid hormone (hyperthyroidism or thyrotoxicosis) followed by a hypothyroidism phase – which may be acute or chronic.

Usually, iatrogenic, iodine-induced hyperthyroidism (Jod-Basedow phenomenon) is brought on by the use of iodine-containing drugs such as amiodarone or contrast media. The history, diagnostic results, and treatment all differ between the two kinds.

In contrast, clients with type 2 amiodarone-induced thyrotoxicosis might not have had a history of thyroid disease in the past. Contrary to the causes of hyperthyroidism previously stated, this etiology of hyperthyroidism is remarkably uncommon.

Thyroiditis

Thyroiditis, an inflammation of the thyroid gland, causes stored thyroid hormone to leak out of the thyroid gland. The leakage increases the blood’s hormone levels, leading to thyrotoxicosis, a condition in which thyroid hormone levels are too high.

After that, the thyroid may become underactive and require thyroid hormone replacement.

Three types of thyroiditis can cause thyrotoxicosis, followed by hypothyroidism:

• Subacute thyroiditis involves a painfully inflamed and enlarged thyroid.
• Postpartum thyroiditis develops after a woman gives birth.
• Silent thyroiditis is painless, even though the thyroid may be enlarged (thought to be an autoimmune condition).

Hypothyroidism Nursing Interventions

• Analyze the client’s appetite and weight.
• Encourage the client to increase fiber and take laxatives (to counter constipation).
• If the client’s skin is dry, suggest that they use moisturizer.
• Client education regarding thyroid hormone therapy compliance.
• Encourage exercise.
• Check the thyroid hormone levels in the lab.
• Watch fluid intake.
• Encourage the client to continue working with a mental health care provider (since depression is common in hypothyroidism).
• Monitor warning signals and side effects of levothyroxine overuse.
• Overtreatment warning signals include those that resemble hyperthyroidism such as: tachycardia, palpitations, anxiety, heat intolerance, fever, excessive perspiration, appetite changes, and weight loss.

Hyperthyroidism Nursing Interventions

• Keep an eye on clients’ vitals, especially heart rate and blood pressure (both increase in hyperthyroidism).
• Find out if the client has any chest pain (due to increased heart work).
• Check for heart murmurs.
• Get an ECG (atrial arrhythmias may occur in hyperthyroidism).
• Educate the client to unwind.
• Administer drugs (including antithyroids and beta-blockers) as directed.
• Examine intake and outflow (diarrhea is a common feature in hyperthyroidism).
• Regularly weigh the client.
• Client education regarding thyroid surgery.
• Inform the client about the dangers of radioactive iodine and how it can cause thyroid cancer.
• If the saturation is less than 94%, give oxygen.
• Give the client a cooling blanket if they have a fever.
• Look at thyroid function tests.

Hypothyroidism Pharmacology

Suppression of pituitary TSH in treating or preventing various types of euthyroid goiters.

In order to treat or prevent various types of euthyroid goiters, including Hashimoto’s goiter, cleints with hypothyroidism may receive replacement therapy or a dietary supplement.

Suppression tests may use these treatments to distinguish between thyroid gland autonomy and suspected mild hyperthyroidism.

Liothyronine & Triiodothyronine (T3)

Liothyronine is a thyroid hormone T3 that the thyroid gland typically produces in a 4:1 ratio when compared to T4: T3. The active form of thyroxine is liothyronine, which has tyrosine with bonded iodine as part of its fundamental chemical structure.

Triiodothyronine reaches the nucleus in living organisms, interacting with nuclear thyroid hormone receptors, which then bind to thyroid response elements (TREs) found in target genes.

When combined with enlisted coactivators, Triiodothyronine’s receptor binding causes maximum transcriptional activation following binding to TREs.

Levothyroxine & Thyroxine (T4)

Levothyroxine is a synthetic levoisomer of thyroxine (T4) that resembles thyroid gland hormones. In the tissues of the periphery, thyroxine is de-iodinated to produce triiodothyronine (T3).

T3 enters the cell and binds to nuclear thyroid hormone receptors, which in turn activates gene expression and creates proteins necessary for the control of cellular respiration, thermogenesis, cellular development and differentiation, and the metabolism of proteins, carbohydrates, and lipids.

Actions: T4 converts to T3 (the active form) inside one of two distinct deiodinase cells (depending on the tissue). In the nucleus of a wide spectrum of body tissues, T3 binds to specific nuclear receptor proteins (alpha & beta). This results in altered gene expression and increased formation of RNA and protein.

Side effects:

• Nervousness
• Anxiety
• Tremor
• Heat intolerance
• Weight loss
• Increased appetite
• Arrhythmias (palpitations)

Hyperthyroidism Pharmacology

One complication of hyperthyroidism is Graves’ disease. A life-threatening complication of Graves’ disease is thyroid storm, also known as accelerated hyperthyroidism (or thyrotoxic crisis). It’s more likely when severe hyperthyroidism is untreated or treated inadequately.

Thyrotoxicosis is a common endocrine condition that may be secondary to a number of underlying processes. Thyroid storm (also known as thyroid or thyrotoxic crisis) represents the severe end of the spectrum of thyrotoxicosis and is characterized by compromised organ function.

The sudden and drastic increase in thyroid hormones can produce many effects, including fever, sweating, vomiting, diarrhea, delirium, severe weakness, seizures, irregular heartbeat, yellow skin and eyes (jaundice), severe low blood pressure, and coma. Therefore, thyroid storm requires immediate emergency care.

Let’s take a look at the various medications that can be given for complications of thyroid crisis.

Propylthiouracil (PTU)

Actions: Suppresses the thyroid peroxidase (TPO)-catalyzed interactions between iodine and tyrosine, which precludes the formation of thyroid hormones at the iodine organification stage (see Figure 1 in methimazole).

It prevents iodotyrosine joining to generate T3 and T4 (see methimazole), and hinders T4 to T3 deiodination in the periphery (deiodinase D1).

Side effects:

• Rash
• Edema
• Agranulocytosis (occurs in 0.1-0.5% of patients, and is usually reversible upon drug withdrawal)
• Hepatitis
• Cholestatic jaundice

Methimazole

Actions: Hinders the production of thyroid hormone. The thyroid enzyme thyroid peroxidase, commonly known as iodide peroxidase or thyroperoxidase, is inhibited by methimazole (TPO)

Side effects:

• Maculopapular rash (4-6% of patients), sometimes associated with fever
• Agranulocytosis – dangerous but only occurs in 0.1-0.5% of patients
• Hepatitis
• Cholestatic jaundice (potentially fatal)
• Nausea
• GI distress
• Altered taste or smell

Potassium Iodide

Actions: Iodide inhibits thyroid hormone release as one of its main effects.
Inhibits thyroidal peroxidase, which prevents the thyroid gland from producing thyroid hormones. As a result, less thyroid hormone is produced.

Side effects:

• Acne-like rash
• Metallic taste in the mouth
• Fever
• Swollen salivary glands
• Ulcerations of mucous membranes
• Conjunctivitis
• Rhinorrhea

Cholestyramine

Actions: The liver converts cholesterol into bile acids by an oxidation process.
These medications inhibit the normal reabsorption of bile acids by binding to them in the intestinal lumen. The GI tract does not absorb the resin (cholestyramine) itself.

Side effects: Constipation

Hyperthyroidism vs Hypothyroidism Conclusion

The thyroid gland is a bilobed organ found in the front of the trachea, between the suprasternal notch and the cricoid cartilage. It receives nourishment from the inferior thyroid artery, a branch of the thyrocervical trunk, and the superior thyroid artery (which arises from the external carotid artery).

The organic precursor to thyroid hormones, thyroglobulin, needs iodide to become a thyroid hormone. Organification is the largely self-regulated process; iodide is integrated into monoiodotyrosine (MIT) or diiodotyrosine (DIT) molecules.

Thyroid-stimulating hormone (TSH), which is secreted by the anterior pituitary, is stimulated by TRH, which in turn stimulates thyroid gland T4 release. One common misunderstanding is that the terms thyrotoxicosis and hyperthyroidism are interchangeable.

Low thyroid hormone levels cause hypothyroidism, which has a variety of causes and symptoms. Hypothyroidism that is left untreated raises mortality and morbidity.

The most frequent cause of hypothyroidism in the United States is autoimmune thyroid disease (Hashimoto thyroiditis). But the most frequent cause worldwide is a lack of iodine in the diet. Asymptomatic disease and myxedema coma are just a few examples.

Sources

https://blogs.bcm.edu/2022/01/10/hyperthyroidism-versus-hypothyroidism/
https://www.mountsinai.org/health-library/diseases-conditions/hyperthyroidism
https://medlineplus.gov/hypothyroidism.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7233645/
https://tmedweb.tulane.edu/pharmwiki/doku.php/thyroid_drugs
https://tmedweb.tulane.edu/pharmwiki/doku.php/antithyroid_drugs
https://www.ncbi.nlm.nih.gov/books/NBK568782/
https://www.ncbi.nlm.nih.gov/books/NBK568746/
https://www.ncbi.nlm.nih.gov/books/NBK537053/
https://www.ncbi.nlm.nih.gov/books/NBK519536/
https://health.clevelandclinic.org/whats-the-difference-between-hypothyroidism-and-hyperthyroidism/
https://pubchem.ncbi.nlm.nih.gov/compound/Liothyronine