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Thyroid Disorders

Oct 03, 202411 min read

A butterfly-shaped organ, the thyroid gland is located anterior to the trachea, and inferior to the larynx. Its central area is the isthmus flanked by the wing-like left and right lobes. Each lobe is embedded with a parathyroid gland (primarily on the posterior surface). Thyroid tissue is composed primarily of thyroid follicles, a central cavity surrounded by epithelial follicle cells. The central cavity is filled with colloid, where hormone synthesis primarily occurs.

Thyroid Hormone Synthesis and Secretion

Iodine, an essential and unique component of thyroid hormones, attaches to a glycoprotein, produced by follicle cells, within the colloid.

  1. TSH binds to its receptors in the follicle cells, stimulating the active transport of iodide ions across their cell membranes, resulting in the concentration of iodide ions within the follicular cells.
  2. Iodide ions move to the lumen of the follicle bordering the colloid, where oxidation (removal of negative charge) occurs. Oxidation of two iodide ions (I-) results in iodine (I2) formation.
  3. In the colloid, peroxidase enzymes link iodine and tyrosine amine acids in thyroglobulin to produce two intermediaries:
    • Tyrosine attached to one iodine
    • Tyrosine attached to two iodine
  4. Linkage of either of these intermediaries through covalent bonds result in the formation of thyroid hormones:
    • Two tyrosine with three total iodine: Triiodothyronine (T3). It is more potent than T4, and many cells even convert T4 to T3 through the removal of an iodine atom.
    • Two tyrosine with four total iodine (more common): Tetraiodothyronine (T4) also known as Thyroxine
  5. These compounds remain in the colloid center until endocytosis occurs from TSH stimulation. Lysosomal enzymes break apart the thyroglobulin colloid, releasing free T3 and T4 that diffuse across the follicle cell membrane, entering the bloodstream.
  6. Less than 1% of circulating thyroid hormones remain unbound and can cross the lipid bilayer of cell membranes. The remaining 99%+ of thyroid hormones are bound to specialized transport proteins called thyroxine-binding globulins (TBGs), to albumin, or other plasma proteins. This allows for a buffer for when thyroid hormone levels decrease, and bound thyroid hormones are unbound.
  7. Regulation of these processes are done by the TSH released by the anterior pituitary gland, which is in turn regulated by the thyrotropin-releasing hormone (TRH) from the hypothalamus.
    • A negative feedback system is employed for all of these hormones (T3, T4, TSH, TRH) as increasing levels of thyroid hormones in the blood stream decrease their production.
    • TRH is released when plasma levels of T3, and T4 (and subsequently metabolic processes) are decreased.

Thyroid Hormone Functions

  1. Metabolism: these hormones are also commonly known as “metabolic hormones” because of their influence on the body’s basal metabolic rate. While the processes stimulated by these hormones do produce ATP, it is often in an inefficient manner. As a result, an abnormally increased level of heat is released (body heat) as byproducts from the reactions termed as the calorigenic effect.
    • Mitochondria, the powerhouse of the cell, have receptors which thyroid hormones bind to. This leads to an increase in nutrient breakdown and the use of oxygen to produce ATP.
    • The hormones also initiate the transcription of genes involved in glucose oxidation.
  2. Thyroid hormones also play a part in protein synthesis and fetal and childhood tissue development and growth, especially critical for the normal development of the nervous system. They continue to support neurological function into adulthood.
  3. Thyroid hormones have a complex interrelationship with reproductive hormones. Deficiency may influence libido, fertility, and other aspects of reproductive function.
  4. Catecholamine sensitivity is affected by upregulation of receptors in the blood vessels. Increases in thyroid hormones result in increases in the beta1-adrenergic receptors for norepinephrine and epinephrine, resulting in a stronger response (increased heart rate, heart contraction, and blood pressure)

Hyperthyroidism

A hyperthyroid state resulting from hypersecretion of the thyroid hormones (triiodothyronine and thyroxine). It may be caused by:

  • Graves’ Disease: autoimmune derivation; circulating anti-TSH autoantibodies that displace TSH from and activate the thyroid receptors.
    • Associated with Hashimoto’s Disease a state of chronic inflammation of the thyroid gland that usually causes hypothyroidism.
  • Thyrotoxicosis (excessive thyroid hormones) may result from autoimmune diseases, functional thyroid adenomas, and infection.

Complications

  1. Thyrotoxicosis, or a Thyroid Crisis/Thyroid Storm is a sudden exacerbation of symptoms of hyperthyroidism that often occur with infection or stress. Immediate hospitalization is required.
    • Fever
    • Decreased Mental Alertness
    • Abdominal Pain
  2. Heart-related Complications: tachycardia, CHF, atrial fibrillation
  3. Increased risk for osteoporosis in long-lasting hyperthyroidism.
  4. Complications secondary to surgical management:
    • Scarring of the neck
    • Vocal hoarseness due to nerve damage to the voice box.
    • Hypocalcemia due to parathyroid damage.
  5. Complications secondary to other managements: radioactive iodine, and hormone replacement therapy also have other potential complications.

Assessment Findings

  1. Enlarged Thyroid Gland (Goiter) e.g. in Graves’ disease, autoimmune disorders
  2. Palpitations, Cardiac Dysrhythmias (tachycardia or even atrial fibrillation in severe cases), Hypertension, increased cardiac output: increased thyroid hormones stimulate the heart.
  3. Exophthalmos (bulging eyes) may be present, particularly in those with Graves’ disease. This results from swelling of the tissues around the eyes.
  4. Heat Intolerance: increased body heat results in being less tolerance even to warm environments.
  5. Diaphoresis: heightened metabolic activity and body temperature.
  6. Weight Loss: heightened metabolic activity results in increased energy expenditure despite an increase in appetite.
  7. Diarrhea: gastrointestinal motility may be enhanced by hyperthyroidism.
  8. Smooth and soft skin and hair: thyroid hormones stimulate skin cell regeneration and hair keratin production (integumentary effects).
  9. Nervousness, Fine Tremors of the Hands: nervous system stimulation by the thyroid hormones.
  10. Personality Changes, Mood Swings, Irritability, and Agitation: neurotransmitters in the brain and the nervous interact with thyroid hormones.
  11. Oligomenorrhea (irregular menstrual periods) as thyroid hormones are involved in the regulation of the menstrual cycle.

Diagnostic Examination

  • Primary Nursing Diagnosis: Activity intolerance related to exhaustion and fatigue
  • TSH Assay reveals decreased levels (normally 0.5 to 1.5 mU/L) of TSH as the body attempts to regulate elevated thyroid hormones.
  • T3 and T4 radioimmunoassay show elevations reflecting overproduction. These values are also used to monitor effect of therapy.
    • Triiodothyronine levels are normally 80 to 230 ng/dL. These levels are lower than T4 as T3 has a greater effect on the body.
    • Thyroxine levels are normally 5.0 to 12.0 μg/dL.
  • 24 hour Radioactive Iodine Uptake
  • Thyroid Autoantibody Testing
  • Antithyroglobulin
  • Electrocardiogram

Medical Management

(a) Reduction of thyroid hyperactivity for symptomatic relief and (b) removing the cause of complications

  1. Irradiation via radioactive Iodine (131I or 123I) of overactive thyroid cells. This is the most common form of treatment for the elderly, but is contraindicated in pregnancy and nursing mothers. Iodine may cross the placenta and is secreted in breast milk.
  2. Pharmacotherapy: Antithyroid medications that inhibit hormone synthesis/release or reduce the amount of thyroid tissue.
    • Propylthiouracil; PTU (Propacil) and Methimazole (Tapazole) are the most common, used until thyroid hormones are normal. Both of these drugs inhibits the ability of the thyroid to utilize iodine. A maintenance dose is established followed by a gradual withdrawal for several months. Contraindicated for late pregnancy due to risk for goiter and cretinism in the fetus.
  3. Surgery: removal of most of the thyroid gland; no longer the preferred choice of therapy for Graves’ disease, but is still used for patients who cannot tolerate antithyroid drugs, have significant ophthalmopathy, have large goiters, or cannot undergo radioiodine therapy.

Adjunctive Therapy

  1. Potassium Iodide, Lugol’s Solution, and Saturated Solution of Potassium Iodide (SSKI) may also be added to induce the Wolff-Chaikoff Effect, a protective mechanism as a result of elevated iodine levels, where thyroid peroxidase (used for synthesis of hormones) downregulation occurs to prevent excessive production from iodine saturation.
  2. Beta-Adrenergic Agents (Propanolol) may be used to reduce effects of hyperthyroidism on the sympathetic nervous system e.g. nervousness, tachycardia, tremors, anxiety, and heat intolerance.

Nursing Interventions

  1. Provide adequate rest (activity intolerance)
  2. Administer sedatives as prescribed.
  3. Provide a cool and quiet environment
  4. Obtain daily weight.
  5. Provide a high-calorie diet (increased metabolism)
  6. Administer antithyroid medications, iodine preparations, or propanolol as prescribed.
  7. Prepare for radioactive iodine therapy as ordered.
  8. Prepare for thyroidectomy as ordered.

Documentation

  • Physical Findings: cardiovascular status (resting pulse, blood pressure, presence of angina or palpitations), bowel activity, edema, condition of skin, activity tolerance, hypermetabolism, eye status, heat intolerance.
  • Medication Response, skin care regimen, nutrition, body weight, comfort level
  • Psychosocial Response to changes in bodily function, mental acuity, behavioral patterns, emotional stability.

Discharge Education

  • Disease Process: the role of the thyroid gland, disease, treatment plan, and its side effects.
  • Medications: thorough explanation of all medications (dosage, route, action, adverse effects, monitoring).
    • Take PTU or Methimazole with meals to limit gastric irritation.
    • Mix iodine solutions with milk or juice to limit gastric irritation. Use a straw to minimize risk for teeth discoloration.
  • Complications: have the patient report any manifestations of thyrotoxicosis (tachycardia, palpitations, shakiness, tremors, DOB, N&V), neck swelling, dysphagia, or weight loss immediately.

Hypothyroidism

Suboptimal levels of thyroid hormones in the body results in hypothyroidism.

  • This commonly occurs in patients with overcorrection of previous hyperthyroidism treated with radioiodine, antithyroid medications, or thyroidectomy.
  • It more often occurs in older women, and also by virtue of thyroid cancer experienced by men who have undergone radiation therapy for head and neck cancer.
  • Myxedema, a dermatologic condition found in severe hypothyroidism, is a state where an accumulation of mucopolysaccharides in subcutaneous and other interstitial tissues occur (generalized edema). (Myxedema is also sometimes used interchangeably with severe hypothyroidism)

Classifications

  • Primary/Thyroidal Hypothyroidism: failure of the thyroid to produce adequate thyroid hormones. This is found in ~95% of patients with hypothyroidism.
  • Central Hypothyroidism: failure of the pituitary gland and/or the hypothalamus to stimulate the production of thyroid hormones.
  • Secondary/Pituitary Hypothyroidism: an entirely pituitary disorder, leading to decreased TSH secretion, and subsequent decreased T3 and T4 production.
  • Tertiary/Hypothalamic Hypothyroidism: a hypothalamic disorder wherein thyrotropin-releasing hormone (TRH) is not produced, and the release of TSH is inhibited, resulting in decreased T3 and T4 production.

Causes

  • The most common (general) cause is thyroid inflammation, damaging the gland’s cells.
  • Autoimmune diseases is the most common cause of hypothyroidism in adults (autoimmune thyroiditis) or Hashimoto’s Disease.
  • Thyroid Atrophy occurs naturally when aging.
  • Hyperthyroidism Therapy may result in hypothyroidism, such as in radioiodine therapy, and thyroidectomy.
  • Medications such as lithium, iodine compounds, and antithyroid medications decrease TSH production.
  • Iodine Deficiency: iodine is an essential component of thyroid hormones.
  • Iodine Excess: iodine saturation results in suppression of thyroid hormone production (inhibition of thyroid peroxidase) as a protective mechanism against hyperthyroidism (Wolff-Chaikoff Effect).

Complications

  • Myxedema Coma: a decompensated state of severe hypothyroidism in which the patient becomes hypothermic and unconscious.

Assessment Findings

  1. Extreme Fatigue: due to hypometabolism
  2. Menstrual Disturbances (Menorrhagia, Amenorrhea): thyroid hormones have complex interrelationships with reproductive hormones and function.
  3. Weight Gain: due to hypometabolism
  4. Cold Intolerance: decreased body heat results in intolerance to cold environments.
  5. Thick Skin: generalized accumulation of mucopolysaccharides in subcutaneous tissue results in the thickening of the skin.
  6. Irregular Thyroid Gland: palpation of they thyroid gland is routine. Enlargement or atrophy should be noted.

Diagnostic Examination

  1. Physical Examination: palpation of the thyroid gland in all patients.
  2. Serum TSH Test: the single-best screening test for thyroid function due to its high sensitivity. Normal TSH levels are 0.5 to 1.5 mU/L.
  3. Serum Thyroid Hormones Tests include both protein-bound and free hormone levels in response to TSH secretion.
  4. Thyroid Antibody Testing: immunoassay techniques look for antithyroid antibodies which are active in all case of Hashimoto’s Thyroiditis.

Medical Management

The primary objective is to restore normal metabolic status through hormone replacement. Prevention of complications and supportive therapy are included.

  1. Pharmacologic therapy: Synthetic Levothyroxine is the preferred preparation for hypothyroidism and suppression of non-toxic goiters.
  2. Prevention of Cardiac Dysfunction: subnormal metabolism result in decreased oxygen requirements. Reductions in blood supply may be tolerated without overt symptoms, but coronary artery disease may become evident once metabolism is restored to normal status.
  3. Supportive Therapy: oxygen saturation is monitored, fluids are administered cautiously (due to fluid retention), external heat application should be avoided, and oral thyroid hormone therapy should be continuous.

Nursing Interventions

Assessment

  • Palpation from an anterior and posterior position, assessing for any abnormalities, firmness (Hashimoto’s) or tenderness (thyroiditis)
  • Auscultation of the thyroid gland if any abnormalities are palpated.

Diagnoses and Interventions

  • Activity Intolerance related to decreased physiological and psychological energy
    • Promote rest and self-care activities.
  • Risk for impaired thermoregulation
    • Provide thermoregulation precautions: blankets, no external heat sources, temperature monitoring, avoiding exposure to drafts, etc.
  • Constipation related to decreased gastrointestinal peristalsis
    • Encourage fluid and dietary fiber intake. Mobility should be encouraged within tolerable limits, and use of laxatives or enemas should be used sparingly. Monitor bowel activity.
  • Impaired breathing associated with depressed ventilation.
    • Assess respiratory parameters (depth, rate, pattern, oximetry, ABG)
    • Encourage deep breathing, coughing, and incentive spirometry.
    • Verify any hypnotics or sedatives being ordered. If necessary, monitor for adverse side effects.
    • If necessary, suctioning and mechanical ventilation may be done.
  • Acute confusion associated with altered cardiovascular and respiratory status and depression.
    • Orient the patient to the four spheres: person, place, time, situation

Discharge Education

  1. Medication Compliance: emphasis of compliance with life-long therapy.
  2. Thermoregulatory Precautions: avoid extreme cold until condition is stable.
  3. Follow-up Care: state the importance of follow-up care.
  4. Weight Reduction Strategies and Prevention of Constipation: identify strategies with the patient e.g. a high-fiber, low-calorie and adequate fluid diet.

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