Thyroid Disorders
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Transcript of Thyroid Disorders
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Lori McCoy, DO
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Hypothyroidism and Hyperthyroidism
and the features, causes, workup and treatment of each
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HYPOTHALAMIC-PITUITARY-THYROID AXISNEGATIVE FEEDBACK MECHANISM
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HYPOTHYROIDISM
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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
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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
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HYPOTHYROIDISM
Typical causes include:
Autoimmune (Hashimoto’s) Treatment for hyperthyroidism Status post thyroid surgery or radiation Medication-induced Congenital disease Pituitary disorder
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“Typical” Thyroid Hormone Levels in Thyroid Disease
TSH T4 T3
Hypothyroidism High Low Low
Hyperthyroidism Low High High
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BUT WHAT IF:
TSH = HIGH
FREE T3 AND T4 = NORMAL
…..this is considered mild or subclinicalhypothyroidism
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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).
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May also consider….
CBC, BMP, and FLP….which may show anemia,hyponatremia, hyperlipidemia and reversible increases in serum Cr.
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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.
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Benign nodule
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Suspicious nodule with calcifications
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TREATMENT OF H
YPOTHYROIDISM
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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
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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
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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
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HYPERTHYROIDISM
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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
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“Typical” Thyroid Hormone Levels in Thyroid Disease
TSH T4 T3
Hypothyroidism High Low Low
Hyperthyroidism Low High High
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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
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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.
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SUBCLINIC
AL
HYPERTHYROIDISM
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DEFINITION OF SUBCLINICAL HYPERTHYROIDISM
Decreased TSH level
Normal total or free serum T4 and T3 levels
Few or no signs or symptoms of hyperthyroidism
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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!
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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)
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TREATMENT OF
HYPERTHYROIDISM
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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.
.
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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
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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
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WHICH TREATMENT TO CHOOSE?
Depends on:
Patient preference Severity of hyperthyroidism Evidence of complications of hyperthyroidism Pregnancy The cause of hyperthyroidism
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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.
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THYROID STORM
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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
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QUESTIONS?
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REFERENCES
UpToDate Journal of Endocrinology and Metabolism Clinical Endocrinology Thyroid.org