Lori McCoy, DO

Hypothyroidism and Hyperthyroidism and the features, causes, workup and treatment of each

HYPOTHALAMIC-PITUITARY-THYROID AXIS NEGATIVE FEEDBACK MECHANISM

HYPOTHYROIDISM

 In the U.S. and other areas of the world with adequate iodine intake, the most common cause is autoimmune thyroid disease (Hashimoto’s).  Occurs when the thyroid gland produces less than the normal amount of thyroid hormone  May be temporary but usually is a permanent condition  The frequency of hypothyroidism, goiters and thyroid nodules increases with age

HYPOTHYROIDISM In its earliest stage, it may cause very few symptoms…but as thyroid hormone decreases and metabolism slows, patients may complain of: fatigue forgetfulness brittle hair/nails dry skin constipation sore muscles weight gain heavy/irregular menses

HYPOTHYROIDISM Typical causes include:  Autoimmune (Hashimoto’s)  Treatment for hyperthyroidism  Status post thyroid surgery or radiation  Medication-induced  Congenital disease  Pituitary disorder

“Typical” Thyroid Hormone Levels in Thyroid Disease TSHT4 T3 Hypothyroidism HighLow Low Hyperthyroidism LowHigh High

BUT WHAT IF: TSH = HIGH FREE T3 AND T4 = NORMAL …..this is considered mild or subclinical hypothyroidism

Do assays for autoimmune/antibodies to thyroid peroxidase (TPO) and thyroglobulin (TG): If these are positive, this is Hashimoto’s Disease. (About 1 out of 10 people who have mild/subclinical disease will go on to have hypothyroidism within 3 years).

May also consider…. CBC, BMP, and FLP….which may show anemia, hyponatremia, hyperlipidemia and reversible increases in serum Cr.

As well as ordering… Thyroid US....then Fine Needle Aspiration if any suspicious nodules are found (remember thyroid nodules can be found in patients who are hypo-, eu-, or hyperthyroid). About 5-15% of solitary nodules will be malignant.

Benign nodule

Suspicious nodule with calcifications

TREATMENT OF HYPOTHYROIDISM

HYPOTHYROIDISM TREATMENT Levothyroxine (Synthroid) is the treatment of choice for the routine management of hypothyroidism.  Adults: Usual starting dose is 25 mcg/d  Children up to 4.0 mcg/kg of body weight/d  Elderly <1.0 mcg/kg of body weight/d Clinical and biochemical evaluations at 6-8 week intervals until the serum TSH concentration returns to normal Take with full glass of water 30 minutes to 1 hour before breakfast, on an empty stomach

PRIMARY HYPOTHYROIDISM TREATMENT ALGORITHM TSH >3.0  IU/mLTSH <0.5  IU/mL Initial Levothyroxine Dose Increase Levothyroxine Dose by 12.5 to 25 mcg/d Repeat TSH Test 6-8 Weeks TSH  IU/mL Symptoms Resolved Measure TSH at 6 Months, Then Annually or When Symptomatic Continue Dose Decrease Levothyroxine Dose by 12.5 to 25 mcg/d

Malabsorption Syndromes  Gastric bypass surgery  Short bowel syndrome  Celiac disease Reduced Absorption  Colestipol hydrochloride  Sucralfate  Ferrous sulfate  Food (eg, soybean formula)  Aluminum hydroxide  Cholestyramine Drugs That Increase Clearance  Rifampin  Carbamazepine  Phenytoin Factors That Reduce T 4 to T 3 Clearance  Amiodarone  Selenium deficiency Others  Lovastatin and Sertraline FACTORS THAT MAY REDUCE LEVOTHYROXINE EFFECTIVENESS

HYPERTHYROIDISM

Typical symptoms include: nervousness and irritability palpitations heat intolerance and increased sweating tremors weight loss with increase in appetite frequent bowel movements Pretibial myxedema irregular menses insomnia Changes in vision, eye irritation or exophthalmos

“Typical” Thyroid Hormone Levels in Thyroid Disease TSHT4 T3 Hypothyroidism HighLow Low Hyperthyroidism LowHigh High

HYPERTHYROIDISM Thyrotoxicosis will show suppressed TSH and elevated T3 and T4. Subclinical hyperthyroidism has low TSH and normal T3 and T4. Some causes of hyperthyroidism:  Most common are toxic diffuse goiter (Graves disease), toxic multinodular goiter (Plummer disease), and toxic adenoma.  Painful subacute thyroiditis  Silent thyroiditis  Iodine and iodine-containing drugs and radiographic contrast agents  Exogenous thyroid hormone ingestion

Further tests… Check thyroid autoimmune/antibodies of thyroperoxidase (TPO), thyroglobulin (TG), and thyroid-stimulating immunoglobulin (TSI). Graves Disease will reveal very elevated TPO and TSI. Toxic multinodular goiter or Toxic adenoma will reveal low or absent TPO.

SUBCLINICAL HYPERTHYROIDISM

DEFINITION OF SUBCLINICAL HYPERTHYROIDISM  Decreased TSH level  Normal total or free serum T 4 and T 3 levels  Few or no signs or symptoms of hyperthyroidism

POTENTIAL CONSEQUENCES OF SUBCLINICAL HYPERTHYROIDISM  Decreased bone density with increase risk of osteopenia or osteoporosis  Increased risk of cardiac arrhythmias, especially in the elderly  Increased risk of miscarriage in pregnancy  May or may not have obvious symptoms!

SHOULD SUBCLINICAL HYPERTHYROIDISM BE TREATED? Depends on the individual circumstances and presentation of the patient: Usually will treat if TSH < 0.1 If TSH between 0.1 and 0.5:  May initially observe only and follow for development of overt hyperthyroidism (especially if young and otherwise healthy patient)  Should consider treatment if evidence of potential complications of hyperthyroidism (especially if osteopenia/osteoporosis or a-fib is present)

TREATMENT OF HYPERTHYROIDISM

 Methimazole (Tapazole) and Propylthiouracil (PTU) are meds of choice.  Titrate dose every 6 weeks until thyroid levels normalize and the patient stabilizes.  Goal is to inhibit the synthesis of T3 and T4..

TREATMENT OF HYPERTHYROIDISM Radioactive iodine therapy  Iodine-131 taken up by functioning thyroid tissue to decrease thyroid hormone production, then fibrosis and destruction of the thyroid occurs over weeks to many months. Dose is intended to render the patient hypothyroid. Again, monitor thyroid levels q 6 weeks until levels are normalized. Surgical resection  Remove hyperplastic and adenomatous tissues  Restore normal thyroid function and, consequently, pituitary function

ADJUNCTIVE THERAPY OF HYPERTHYROIDISM  Beta blockers  Corticosteroid therapy  Bile acid sequestrants (t he enterohepatic circulation of thyroid hormones is increased in thyrotoxicosis. Bile- salt sequestrants bind thyroid hormones in the intestine and thereby increase their fecal excretion).  Iodide

WHICH TREATMENT TO CHOOSE? Depends on:  Patient preference  Severity of hyperthyroidism  Evidence of complications of hyperthyroidism  Pregnancy  The cause of hyperthyroidism

THYROID STORM AKA thyroid or thyrotoxic crisis…acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones in patients with thyrotoxicosis. U sually occurs in patients with untreated or partially treated thyrotoxicosis who experience a precipitating event like surgery, infection or trauma. The clinical presentation includes fever, tachycardia, hypertension, neurological and GI abnormalities. HTN may be followed by CHF that is associated with hypotension and shock.

THYROID STORM

OSTEOPATHIC PRINCIPLES Can use OMT to treat somatic components of thyroid dysfunction:  Upper thoracic HVLA  Thoracic inlet release  Ribs 1 and 2  C4-6 myofascial release  Occipito-Atlantal myofascial release

QUESTIONS?

REFERENCES  UpToDate  Journal of Endocrinology and Metabolism  Clinical Endocrinology  Thyroid.org