Thyroid and Parathyroid Disorders Notes

Thyroid Disorders

Learning Objectives

• Understand the function of the thyroid and parathyroid glands.

• Discuss the etiology of thyroid and parathyroid dysfunction, especially when related to autoimmune disease.

• Identify signs and symptoms of hyper/hypothyroidism and hyper/hypoparathyroidism.

• Anticipate medication therapy for thyroid and parathyroid abnormalities.

• Plan nursing care for patients with acute and subacute thyroid and parathyroid conditions.

Key Terms

• Calcitonin

• Chvostek’s sign

• Exophthalmos

• Goiter

• Goitrogens

• Grave’s Disease

• Hashimoto’s Thyroiditis

• Hyperthyroidism

• Hyperparathyroidism

• Hypothyroidism

• Hypoparathyroidism

• Myxedema

• Parathyroid Hormone (PTH)

• Tetany

• Thyrotoxicosis

• Thyroxine

• TRH

• Triiodothyronine

• Trousseau’s sign

• TSH

Thyroid & Parathyroid Glands

• The thyroid gland is located in the anterior neck, below the larynx.

• Parathyroid glands are located on the posterior side of the thyroid gland.

• Thyroid cells only cells that utilize iodine.

Hypothalamus, Pituitary Gland & Thyroid Hormones

• Hypothalamus releases Thyrotropin-Releasing Hormone (TRH).

• TRH causes the anterior pituitary to release Thyroid-Stimulating Hormone (TSH).

• TSH stimulates the thyroid to release Thyroxine (T4), Triiodothyronine (T3), and calcitonin.

• Summary: Hypothalamus → TRH → anterior pituitary → TSH → (T4) Thyroxine, T3 (Triiodothyronine), and calcitonin.

• T4 and T3 exert negative feedback on the hypothalamus and pituitary gland.

Calcitonin and Parathyroid Hormone (PTH)

• Calcitonin is released by the thyroid gland in response to high blood calcium levels; it lowers serum calcium.

• Parathyroid Hormone (PTH) is released in response to low blood calcium levels; it increases serum calcium.

Thyroid Gland: Normal Feedback Mechanism

• Three hormones produced and secreted by the thyroid gland:

  • Thyroxine (T4): Accounts for 90% of thyroid hormone.

  • Triiodothyronine (T3): More potent with greater metabolic effects.

  • Calcitonin: Inhibits transfer of calcium from bone to blood (increases calcium storage in the bone and renal excretion of calcium and phosphorus to lower serum calcium levels).

    • Produced by thyroid gland in response to high blood calcium.

• T4 and T3 affect:

  • Metabolic rate

  • Caloric requirements

  • Oxygen consumption

  • Carbohydrate and lipid metabolism

  • Growth and development

  • Brain function, and other nervous system activities

• When circulating T3/T4 levels are low:

  • Hypothalamus releases thyrotropin-releasing hormone (TRH).

  • TRH causes the anterior pituitary to release TSH (increases).

• When circulating T3/T4 levels are high:

  • TSH decreases.

• TSH and TRH release become sluggish as we get older. Pituitary sensitivity to T4 decreases as well.

Goiter

• Goiter = enlarged thyroid gland.

  • A clinical manifestation when something is possibly wrong with the thyroid.

• Etiology:

  • Overactive thyroid.

  • Underactive thyroid.

  • Lack of iodine in diet; most common cause worldwide.

  • Goitrogens (disrupts production of hormone in thyroid) Drugs = Sulfa, PTU/methimazole, toxic iodine levels, amiodarone, lithium.

  • Goitrogens (disrupts production of hormone in thyroid) Foods = Broccoli, Brussel Sprouts, Cauliflower, Kale, Turnips, Peanuts, Strawberries, Mustard.

  • Thyroid needs iodine to produce T3 and T4 but goitrogens block iodine uptake.

• Nontoxic = diffuse thyroid enlargement with normal hormone levels.

• Nodular Goiters = nodules secrete thyroid hormones.

• Toxic = Nodular goiters that secrete enough thyroid hormone to cause hyperthyroidism; common in Graves disease; often age >40y.

• Goiter is not always caused by hypo/hyperthyroidism.

• Assessment:

  • Finds out cause: hyper, hypo, euthyroid.

  • Labs → TSH, T4, Thyroid antibodies.

    • Hyper = T3 and T4 elevated.

    • Hypo = T3 and T4 low.

  • Assess for inflammation/thyroiditis.

    • Pts thyroids may get inflamed and develop a hyper or hypothyroidism that is transient (meaning once their thyroiditis has gone away, their symptoms of hyper/hypothyroidism should resolve as well).

Continuum of Thyroid Dysfunction

• Hyperthyroidism (elevated T3, T4)

  • Thyrotoxicosis

• Euthyroid (Between/Middle) → Ideal

• Hypothyroidism (low levels T3, T4)

  • Myxedema Coma

Hyperthyroidism

• Hyperactivity of the thyroid gland.

  • Sustained increase of thyroid hormones by thyroid gland.

• More common in women than men (5:1 ratio) and prevalence increases with older women.

• Highest frequency in people 20-40 years of age.

• More common in smokers.

  • Due to vasoconstriction (thyroid is very vascular) and the thyroid must work overtime due to the decrease in blood flow.

• Etiology:

  • Most common form is Graves Disease (autoimmune).

  • Other causes: toxic nodular goiter, thyroiditis (inflamed or infected thyroid), excess iodine intake, pituitary tumors especially on the anterior pituitary (increases TSH → increases T3 T4), thyroid cancer.

Graves Disease

• Most Common Cause of hyperthyroidism (75% of cases).

• Autoimmune disease.

  • Diffuse thyroid enlargement.

  • Excessive thyroid hormone secretion (T3, T4, calcitonin).

• Precipitating factors interact with genetic factors.

  • Infection, stress, lack of iodine.

• Cigarette smoking increases risk.

  • Vasoconstriction

• Most often in younger women (late 20s, early 30s)

  • 5x more likely in women than men.

Graves Disease: Pathophysiology

• Antibodies to TSH receptors.

  • Attach to receptors and stimulate release of T3, T4, or both.

    • Excess circulating hormones increase metabolic processes (metabolism, heart rate, blood pressure, SNS, thought processes).

• Characterized by remissions and exacerbations.

• May progress to destruction of thyroid tissue, eventually resulting in hypothyroidism.

• Often cooccurs with other autoimmune disorders: RA, SLE, Addison’s disease, and celiac disease.

Clinical Manifestations of Hyperthyroidism

• Increased sympathetic nervous system stimulation.

  • Hypertension, tachycardia, tachypnea, dysrhythmias.

• Palpable goiter (>50% of cases).

• Exophthalmos

  • Protrusion of eyeballs from orbit due to fat deposits & fluid in orbital tissues & ocular muscles.

  • Can lead to diplopia, corneal ulcers, and vision loss.

• GI Symptoms.

  • Weight loss, increased appetite/thirst, diarrhea.

• Nervous System:

  • Nervousness, tremor, insomnia, rapid speech, irritability/lability, heat intolerance.

• Integument:

  • Warm, diaphoretic, hair loss, thin/brittle nails.

  • Acropachy = thickening of the extremities; advanced disease.

• Reproductive:

  • ↓ libido, ↓ fertility, menstrual irregularities or amenorrhea (no menstrual period), gynecomastia (male breast enlarged).

Diagnostics of Hyperthyroidism

• ↓ TSH (<0.4 mU/L).

• Normal or ↑ free thyroxine (free T4).

  • Subclinical hyperthyroidism = normal T4.

  • Overt hyperthyroidism = elevated T4.

• Total T3 and T4.

• Radioactive iodine uptake (RAIU).

  • Differentiates Graves’ disease from other forms of thyroid disease.

    • Graves disease = uptake of 35%-95%.

    • Other types of hyperthyroidism = uptake of <2%.

Complications: Thyrotoxicosis

• Also referred to as “thyrotoxic crisis” or “thyroid storm”.

• An acute, life-threatening, and rare condition.

• Occurs when excessive amounts of thyroid hormones are released into the circulation.

• Etiology → stressors such as infection, trauma, or surgery in a pt w/ pre-existing hyperthyroidism; potential complication immediately post-thyroidectomy.

• Symptoms: dysrhythmias, heart failure, hyperthermia, shock, delirium, seizures.

• Necessitates aggressive treatment.

• Medications to block thyroid hormone production and SNS stimulation.

• Treatment Goals

  • Block adverse effects of thyroid hormones.

  • Suppress hormone over secretion.

  • Prevent complications.

Interprofessional Care - Hyperthyroidism

• First treatment option:

  • Medications: given to stabilize hormone levels before radiation or surgery, or during thyrotoxicosis. Some patients may experience spontaneous remission (20-40%).

    • Anti-thyroid medications

      • Propylthiouracil (PTU) and Methimazole (Tapazole).

      • MOA Inhibit 1st step in the synthesis of thyroid hormone & suppresses peripheral conversion of T4 to T3.

    • Iodine

      • MOA large doses inhibit synthesis of T3, T4. Not effective for long-term use.

      • Drink with a straw (teeth staining); monitor for toxicity.

    • β-Adrenergic blockers (propranolol or atenolol)

      • MOA decrease sympathetic stimulation by blocking B1B2 receptors. Used during thyrotoxicosis.

Interprofessional Care – Hyperthyroidism

• Second treatment option:

  • Radioactive iodine therapy (RAI)

    • Treatment of choice in non-pregnant adults.

    • Isotope that destroys thyroid tissue.

    • Delayed response of 2 to 3 months.

    • Treated with anti-thyroid drugs and β-blocker before and during first 3 months.

    • 80% will develop post-treatment hypothyroidism.

  • Potential side effects: thyroiditis and parotitis.

    • Nursing care – ice chips, salt and baking soda gargle, “magic mouthwash” (antacid/lido/benadryl).

Interprofessional Care - Hyperthyroidism

• Third treatment option:

  • Surgery

    • Subtotal thyroidectomy = preferred surgical procedure.

    • Involves removal of 90% of thyroid, can be done endoscopically or robotically.

    • Indications:

      • Large goiter compressing the trachea.

      • Lack of response to methimazole or PTU.

      • Thyroid Cancer.

Thyroidectomy, Post-op Care

• Assess vital signs frequently (monitor for thyrotoxicosis).

• Monitor airway and respiratory status.

  • Assess for signs of hemorrhage or tracheal compression from goiter.

  • Have suction equipment and a tracheostomy kit available for immediate use.

• Assess the ability to speak aloud, noting voice quality, tone, and any problems speaking. Notify the HCP of any permanent hoarseness or loss of vocal volume.

• Monitor calcium levels

  • Assess for signs of hypocalcemia.

  • Keep IV calcium (calcium gluconate, calcium chloride) available for immediate use.

• Keep the patient in a semi-Fowler position. Support the head and neck with pillows. Avoid neck flexion to prevent tension on the suture line.

Hypocalcemia Signs

• Trousseau's Sign: Involuntary carpal spasm induced by inflating a BP cuff above systolic pressure for a few minutes.

• Chvostek's Sign: contraction of facial muscles in response to a light tap over the facial nerve in front of the ear.

Interprofessional Care - Hyperthyroidism Nutrition Education

• Increased metabolic rate → high risk for tissue breakdown and weight loss.

• May initially need high-calorie diet (4000-5000 cal/day).

• Protein intake of 1-2 g/kg ideal body weight.

• Avoid caffeine products and high-fiber foods.

Hypothyroidism

• Deficiency of thyroid hormone causing a general slowing of the metabolic rate.

• More common in women than men.

• 4% of the population have mild hypothyroidism.

• Iodine deficiency most common cause worldwide.

• Atrophy of thyroid gland most common cause in US.

  • As we age, our thyroid shrinks (atrophy).

Hypothyroidism – Etiology/Pathophysiology

• Primary (Problem with the thyroid gland itself/primary gland)

  • Destruction of thyroid gland

    • Atrophy r/t autoimmune disease or getting older

    • Radiation or surgical removal

      • Especially radiation to neck area

  • Defective synthesis of hormones

    • Iodine deficiency, lithium toxicity

• Secondary (problem with anterior pituitary)

  • Pituitary disease

    • Decreased TSH secretion (this means it doesn’t act on the thyroid, therefore doesn’t release hormones → hypothyroidism)

  • Often caused by infarction or a bleed in that area.

• Tertiary

  • Hypothalamic dysfunction

    • Decreased TRH secretion (this means it doesn’t act on the anterior pituitary to release TSH to act on the thyroid)

  • Often caused by infarction or a bleed in that area.

Hashimoto’s Thyroiditis

• Most common type of hypothyroidism

• Chronic autoimmune thyroiditis

• Frequent cause of goiter/hallmark

• Older white females with positive family history

• Destruction of thyroid tissues by anti-thyroid antibodies

• Diagnostics

  • TSH increased

    • Primary hypothyroidism, meaning it’s acting on the thyroid itself and destroying tissues.

  • T4 T3 decreased

  • Antithyroid antibodies present

• Treatment

  • Thyroid replacement → levithyroxine

Hypothyroidism - Clinical Manifestations

• Systemic Effects

  • Decreased cardiac output, exercise intolerance, DOE

  • Fatigue, Lethargy

  • Impaired memory, decreased initiative, appear depressed

  • Slowed speech

  • Weight gain

  • Anemia

    • Low EPO levels; Vit B12, folic acid, iron deficiencies

  • Cold intolerance, cool & dry skin, hair loss, thick brittle nails

  • Constipation

  • Decreased libido, fertility, and changes to menstrual cycle

Hypothyroidism - Diagnostics

• Labs → Check TSH, T4, Thyroid antibodies

• Determine cause

  • High TSH when defect is in the thyroid itself

  • Low TSH when defect is in pituitary or hypothalamus

  • Positive antibodies indicate autoimmune disease

• Free T4

  • Low in either case

  • Exception: subclinical hypothyroidism (high TSH, normal T4)

• Other labs to review to manage SEs: lipid panel, CBC

Complications of Hypothyroidism

• Myxedema

  • Severe long-standing hypothyroidism

  • Alters physical appearance

  • Puffiness of subcutaneous tissues

  • Facial & periorbital edema

  • Masklike effect

• Myxedema Coma

  • Medical emergency precipitated by infection, drugs, exposure to cold, trauma

  • Subnormal temperature, hypotension, hypoventilation, lactic acidosis, cardiovascular collapse

  • Treated with IV thyroid hormone replacement and supportive care

Collaborative Care - Medication for Hypothyroidism

• Goal = Restoration of euthyroid state

• Levothyroxine (Synthroid)

  • Synthetic T4 identical to endogenous thyroid hormone

  • MOA = increases metabolic rate

    • O2 consumption, respirations, heart rate

    • Fat, protein & carbohydrate metabolism

• Other thyroid meds: Liothyronine (Cytomel), Armour Thyroid

• 1 -3 weeks of treatment may be required to produce a therapeutic effect.

• 50-80% of absorption takes place in the GI tract

• Calcium, iron & antacids can decrease absorption

• Lifelong therapy usually required.

Interprofessional Care - Hypothyroidism

• Low calorie diet to reduce weight gain

• Educate on medication compliance

  • Do not stop taking

  • Do not double doses (may be desirable for weight loss)

  • Monitor for s/s of hyperthyroidism

  • Do no switch brands of thyroid medicine w/o consulting HCP

• Prevent skin breakdown

• Treat and prevent constipation

Parathyroid Disorders

• The parathyroid glands are 4 glands embedded on posterior thyroid → superior and inferior glands.

  • These glands regulate serum calcium and phosphate levels, through secretion of parathyroid hormone (PTH)

• PTH Function:

  • Reabsorb calcium from bones

  • Reabsorb calcium from renal tubules

  • Activation of Vitamin D

• The PTH raises blood calcium levels as needed.

Maintaining Blood Calcium Levels (Thyroid Gland & Parathyroid Glands)

• If calcium in the blood is high → thyroid gland releases calcitonin → blood calcium decreases.

• If calcium in the blood is low → parathyroid glands release PTH → blood calcium increases.

Serum Calcium and Phosphorus Relationship

• Normal Serum Calcium: 9.0 - 11.0 \frac{mg}{dl}

• Normal Serum Phosphorus: 3.0-4.5 \frac{mg}{dl}

• Calcium and Phosphorus have an inverse relationship (downward trend of one, upward trend of the other).

Hyperparathyroidism

• Increased secretion of Parathyroid Hormone (PTH)

  • Elevated serum calcium levels

• Primary

  • Over secretion of PTH r/t adenoma (a benign tumor on one parathyroid gland) or hyperplasia of the parathyroid glands (enlargement of all 4 glands).

    • The gland itself over-secretes PTH → increases calcium.

  • More common in women than men; peak incidence age 40-50s

  • Etiology: often a benign tumor (adenoma) in parathyroid gland

  • Risk Factors: head and neck radiation; lithium therapy (ex. treatment medications for bipolar disorder).

• Secondary

  • Compensatory PTH release r/t hypocalcemia (low calcium in blood)

  • Etiology: Vitamin D deficiency, CKD (because of high phosphates from inability to activate vitamin D and filter out), hyperphosphatemia

    • Vitamin D is required to absorb calcium.

• Tertiary

  • Hyperplasia of parathyroid r/t prolonged secondary hyperparathyroidism (all 4 parathyroid glands get stuck in overdrive to increase calcium no matter its level in the blood).

    • The parathyroid glands become permanently overactive despite the original problem being fixed.

  • Etiology: CKD or renal transplant with long history of dialysis

Hyperparathyroidism – Clinical Manifestations

• Starts out asymptomatic and is caught on routine labs.

• Main Diagnostics:

  • Increased PTH levels

  • Hypercalcemia (\uparrow Ca^{+2} )

    • Can lead to anorexia, fatigue, n/v, irritability, impaired memory, constipation, muscle weakness/atrophy, paresthesia, decreased reflexes.

  • Hypophosphatemia (\downarrow Phos)

  • Urinalysis - Hypercalciuria (calcium in urine)

• Complications:

  • Osteoporosis (decreased bone density), bone fractures (pathologic or compression)

    • Pathologic fracture = fracture related to osteoporosis.

  • Renal Failure, Kidney Stones

  • Pancreatitis

  • Cardiac changes (angina, dysrhythmias)

Interprofessional Care for Hyperparathyroidism

• Additional Diagnostics:

  • Alkaline Phosphatase (Alk Phos) – elevated in presence of bone disease

    • Higher indicator of pt having osteoporosis.

  • Bone Density - DEXA scan

    • Low bone density → might be able to catch on DEXA scan.

  • Ultrasound (start), CT, or MRI to look for adenoma if primary hyperparathyroidism suspected

    • Start with ultrasound (least invasive)

• Surgical Options:

  • Most effective treatment for primary or secondary causes

  • Partial or complete removal of parathyroid glands

    • Outpatient via endoscopy

    • Helps decrease complications later on

  • Autotransplantation

    • Parathyroid tissue implantation

    • Option if multiple glands removed and PTH levels are too low

      • They will remove the glands place them elsewhere (graft) and help with release.

Parathyroidectomy and Autotransplantation

• Parathyroidectomy: removal of parathyroid glands.

• Autotransplantation: implantation of parathyroid tissue in another location.

Interprofessional Care for Hyperparathyroidism

• Increase fluid intake → helps prevent kidney stones

• Severe hypercalcemia

  • IV Fluids

  • IV Loop Diuretics

    • Used if too much calcium is in the blood stream and not enough is coming out in the urine.

  • IV Bisphosphonates (“-dronates”), ex. alendronate (Fosamax)

• Mild/Ongoing hypercalcemia

  • PO Phosphate (renal function must be normal otherwise leads to hyperphosphatemia)

  • Calcimimetic agents, ex. cinacalcet (Sensipar)

    • Increase sensitivity of calcium receptors, leading to ↓ PTH

Interprofessional Care for Hyperparathyroidism

• Post-op Care

  • Similar to thyroidectomy care

  • Monitor for bleeding, fluid and electrolyte abnormalities

    • Pt may have sudden drop of hormone when removed → electrolyte abnormalities (especially calcium).

  • Tetany = neuromuscular hyperexcitability r/t hypocalcemia (from hormone drop)

    • Early signs → paresthesia of hands and mouth

    • Late signs → muscle spasms, laryngospasms (concerned for airway).

    • Chvostek and Trousseau signs

  • Encourage mobility and strength training to maintain bone density

  • Dietician referral

Hypoparathyroidism

• Inadequate circulating parathyroid hormone (PTH)

  • Decreased serum Ca^{+2} levels

• Etiology:

  • Iatrogenic (most common)

    • Medical cause

  • Severe hypomagnesemia

  • Tumor

  • Heavy metal poisoning

  • PTH resistance (pseudohypoparathyroidism) – genetic defect

    • Parathyroid doesn’t recognize that it needs to release PTH

Hypoparathyroidism – Clinical Manifestations

• Signs and Symptoms of Hypocalcemia:

  • Dysrhythmias, hypotension

  • Abdominal cramps

  • Weakness, fatigue

  • Hyperreflexia, muscle cramps, tremor

  • Irritability, Depression

  • Sudden decrease → Tetany (lip tingling, stiff extremities, sudden involuntary muscle movements, dysphagia, laryngospasm, seizures, arrythmias)

    • Laryngospasm can affect breathing

• Laboratory Findings:

  • ↓ Ca^{2+} , ↓ PTH

  • ↑ Phos

Hypocalcemia Signs

• Trousseau's sign: carpal spasm induced by inflating a BP cuff above systolic pressure for a few minutes.

• Chvostek's sign: contraction of facial muscles in response to a light tap over the facial nerve in front of the ear.

Interprofessional Care for Hypoparathyroidism

• Tetany = sudden, severe hypocalcemia = EMERGENCY!!!!

  • IV calcium gluconate

    • Must be given slowly

    • Must be on cardiac monitor (monitor for ↓BP, dysrhythmia, cardiac arrest)

  • Encourage rebreathing

    • ↑ CO_2 lowers serum pH (acidosis) which ↑ ionized (free) calcium in the blood.

      • Ex. Paper bag, holding breath, or ventilator at deceased rate to hold onto CO2.

• Chronic Medication Therapy

  • PO calcium, magnesium, and vitamin D (helps calcium be more readily absorbed).

• Nutrition Therapy

  • High calcium diet

    • Dark green, leafy vegetables, soybeans, tofu → Avoid warfarin.

  • AVOID foods with oxalic acid (inhibits calcium absorption)

    • Ex. spinach, rhubarb