Lori McCoy, DO

Hypothyroidism and Hyperthyroidism

and the features, causes, workup and treatment of each

HYPOTHALAMIC-PITUITARY-THYROID AXISNEGATIVE FEEDBACK MECHANISM

HYPOTHYROIDISM

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

HYPOTHYROIDISMIn 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

TSH T4 T3

Hypothyroidism High Low Low

Hyperthyroidism Low High High

BUT WHAT IF:

TSH = HIGH

FREE T3 AND T4 = NORMAL

…..this is considered mild or subclinicalhypothyroidism

Do assays for autoimmune/antibodies to thyroidperoxidase (TPO) and thyroglobulin (TG): If these arepositive, 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

inpatients who are hypo-, eu-, or hyperthyroid).

About 5-15% of solitary nodules will be malignant.  

Benign nodule

Suspicious nodule with calcifications

TREATMENT OF H

YPOTHYROIDISM

HYPOTHYROIDISM TREATMENT

Levothyroxine (Synthroid) is the treatment of choice for the routine management of hypothyroidism.

Adults: Usual starting dose is 25 mcg/dChildren up to 4.0 mcg/kg of body weight/dElderly <1.0 mcg/kg of body weight/d

Clinical and biochemical evaluations at 6-8 week intervals until theserum 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/mL TSH <0.5 IU/mL

Initial Levothyroxine Dose

IncreaseLevothyroxine

Dose by12.5 to 25 mcg/d

Repeat TSH Test

6-8 Weeks

TSH 0.5- 2.0 IU/mLSymptoms Resolved

Measure TSH at 6 Months, Then Annually or

When Symptomatic

Continue Dose DecreaseLevothyroxine

Dose by12.5 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 T4 to T3 Clearance

Amiodarone Selenium deficiency

Others Lovastatin and Sertraline

FACTORS THAT MAY REDUCE LEVOTHYROXINE EFFECTIVENESS

HYPERTHYROIDISM

HYPERTHYROIDISM

Typical symptoms include:nervousness and irritability palpitations heat intolerance and increased sweatingtremors weight loss with increase in appetitefrequent bowel movementsPretibial myxedema irregular menses insomnia Changes in vision, eye irritation or exophthalmos

 

“Typical” Thyroid Hormone Levels in Thyroid Disease

TSH T4 T3

Hypothyroidism High Low Low

Hyperthyroidism Low High High

HYPERTHYROIDISM Thyrotoxicosis will show suppressed TSH and elevatedT3 and T4.   Subclinical hyperthyroidism has low TSHand 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 ofthyroperoxidase (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.

SUBCLINIC

AL

HYPERTHYROIDISM

DEFINITION OF SUBCLINICAL HYPERTHYROIDISM

Decreased TSH level

Normal total or free serum T4 and T3 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 Depends on the individual circumstances and presentation of the patient:presentation of the patient:

Usually will treat if TSH < 0.1If 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

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 (the 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 STORMAKA thyroid or thyrotoxic crisis…acute, life-threatening,hypermetabolic state induced by excessive release of thyroidhormones in patients with thyrotoxicosis.

Usually 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 befollowed by CHF that is associated with hypotension and shock.

THYROID STORM

OSTEOPATHIC PRINCIPLESCan use OMT to treat somatic components of thyroiddysfunction: 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