Transcript hypothyroidism

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
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 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
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
Initial Levothyroxine Dose
6-8 Weeks
TSH >3.0 IU/mL
Repeat TSH Test
TSH <0.5 IU/mL
TSH 0.5- 2.0 IU/mL
Symptoms Resolved
Increase
Levothyroxine
Dose by
12.5 to 25 mcg/d
Continue Dose
Measure TSH at 6 Months,
Then Annually or
When Symptomatic
Decrease
Levothyroxine
Dose by
12.5 to 25 mcg/d
FACTORS THAT MAY REDUCE
LEVOTHYROXINE EFFECTIVENESS
Malabsorption Syndromes
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Gastric bypass surgery
Short bowel syndrome
Celiac disease
Reduced Absorption
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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
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
TSH
T4
T3
Hypothyroidism
High
Low
Low
Hyperthyroidism
Low
High
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.
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
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 (the enterohepatic circulation
of thyroid hormones is increased in thyrotoxicosis. Bilesalt 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.
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 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