• Thyroid disease is common, affecting approximately

5% to 15% of the general population.

• Females are three to four times more likely than
males to develop any type of thyroid disease.
• The typical thyroid disorders are
 Hypothyroidism
 Hyperthyroidism
 Nodular disease
 Thyroid cancer
• Triiodothyronine (T3) and thyroxine (T4) are the two
biologically active thyroid hormones produced by the
thyroid gland in response to hormones released by
the pituitary and hypothalamus.
• Thyroid hormones affect the function of virtually
every organ system
 Hypothyroidism
• Hypothyroidism is a clinical syndrome that
results from a deficiency of thyroid hormone.

• The prevalence of hypothyroidism is 1.4% to

2% in females and 0.1% to 0.2% in males.

• The incidence increases in persons older than

60 years to 6% of women and 2.5% of men
• Classification a. Hashimoto disease: Most common
hypothyroid disorder in areas with iodine sufficiency i.
Autoimmune-induced thyroid injury resulting in decreased
thyroid secretion ii. Disproportionately affects women
• b. Iatrogenic: Thyroid resection or radioiodine ablative
therapy for hyperthyroidism
• c. Iodine deficiency most common cause worldwide
• d. Secondary causes.I Pituitary insufficiency (failure to
produce adequate TSH secretion, called by some a central
or secondary hypothyroidism) ii. Drug induced (e.g.,
amiodarone, lithium)
 Hashimoto's disease
• Hashimoto's disease, an autoimmune
disorder, caused by destruction of thyroid
cells by circulating thyroid antibodies
produces an underlying defect or block in the
intrathyroidal, organo-binding of iodide.
 Symptoms

• General: weakness, tiredness, lethargy, fatigue

• Cold intolerance
• Headache
• Loss of taste/smell .
• Deafness
• Hoarseness
• Modest weight gain Muscle cramps, aches, pains
• Dyspnea
• Slow speech
• Constipation
• Menorrhagia
 Diagnosis
• Low free T4 serum concentrations b. Elevated
TSH concentrations, typically seen as first
laboratory abnormality, usually greater than
10 mIU/L (normal or low if central
hypothyroidism is the cause
 Treatment of Hypothyroidism
• Levothyroxine (L-thyroxine) is the preferred thyroid
replacement preparation.
• ) Initial (1) In otherwise healthy adults, 1.6 mcg/kg (use ideal
body weight) per day (2) In patients age 50–60, consider 50
mcg/day. (3) In those with existing cardiovascular disease,
consider 12.5–25 mcg/day.
• Adverse effects (a) Hyperthyroidism (b) Cardiac
abnormalities (tachyarrhythmias, angina, myocardial
infarction) (c) Linked to risk of fractures (usually at higher
dosages or over-supplementation) v. Efficacy: If levothyroxine
is properly dosed, most patients will maintain TSH and free T
• In myxedema coma, intravenous (IV) therapy
with large initial doses of L-thyroxine (e.g., 400
mcg) is necessary to increase the active free
hormone level by saturating the empty
thyroid-binding sites and to prevent the 60%
to 70% mortality rate.
• In subclinical hypothyroidism, it is
controversial whether T4 replacement therapy
is benefi
• Once a euthyroid state is attained, laboratory
tests can be monitored every 3 to 6 months for
the first year and then yearly thereafter.
• Medications that interfere with T4 absorption
(e.g., iron, aluminum-containing products,
some calcium preparations, cholesterol resin
and phosphate binders, raloxifene) should not
be
coadministered with T4.
 HYPERTHYROIDISM
• Classification
• a. Toxic diffuse goiter (Graves disease): Most common
hyperthyroid disorder i. Autoimmune disorder ii. Thyroid-
stimulating antibodies directed at thyrotropin receptors mimic
TSH and stimulate triiodothyronine (T3 ) and T4 production.
• b. Pituitary adenomas: Produce excessive TSH secretion that
does not respond to normal T3 negative feedback
• c. Toxic adenoma: Nodule in thyroid, autonomous of pituitary,
and TSH
• d. Toxic multinodular goiter (Plummer disease): Several
autonomous follicles that, if large enough, cause excessive
thyroid hormone secretion
• Drug induced (e.g., excessive exogenous
thyroid hormone dosages, amiodarone
therapy.
• . Diagnosis
• a. Elevated free T4 serum concentrations
• b. Suppressed TSH concentration
 Clinical presentation
• a. Weight loss or increased appetite
• b. Lid lag c
• . Heat intolerance
• d. Goiter
• e. Fine hair
• f. Heart palpitations or tachycardia g. Nervousness,
anxiety, insomnia h
• . Menstrual disturbances (lighter or more infrequent
menstruation, amenorrhea) caused by hypermetabolism
of estrogen i. Sweating or warm, moist ski
 Therapy goals
• a. Minimize or eliminate symptoms, improve
quality of life b. Minimize long-term damage
to organs (heart disease, arrhythmias, sudden
cardiac death, bone demineralization, and
fractures)
• Thioureas (i.e., propylthiouracil, methimazole) i.
Mechanism of action: Inhibits iodination and synthesis
of thyroid hormones; propylthiouracil can block T4 /T3
conversion in the periphery as well at high doses ii.
Dosing (a) Propylthiouracil (1) Initial: 50–150 mg by
mouth three times daily (2) Once euthyroid, can
reduce to 50 mg two or three times daily (3)
Recommended over methimazole in the first trimester
of pregnancy because of the risk of embryopathy; can
change to methimazole in second trimester
• Methimazole (1) Preferred agent for Graves
disease according to the American Association
of Clinical Endocrinologists (AACE) and the
American Thyroid Association for most
patients (2) Initial: 10–30 mg by mouth once
daily (use higher dose in those with higher
baseline free T4 concentrations) (3) Once
euthyroid, may reduce to 5–10 mg/day
 Adverse effects
• Hepatotoxicity risk (boxed warning for PTU): Consider
baseline liver function tests Routine evaluation of liver
function while receiving antithyroid agents has not been
shown to prevent severe hepatotoxicity.
• (b) Rash (, lupus-like symptoms
• (d) Fever
• (e) Agranulocytosis early in therapy (usually within 3
months): Guidelines recommend a baseline complete
blood cell count; no routine monitoring recommended.
Can repeat if patient becomes febrile or develops
pharyng
• Nonselective β-blockers (primarily propranolol;
sometimes nadolol)
• . Mechanism of action: Blocks many
hyperthyroidism manifestations mediated by β-
adrenergic receptors; also may block (less active)
T4 conversion to (more active) T3 when used at
high doses
• ii. Propranolol dosing (a) Initial: 20–40 mg by
mouth three or four times daily (b) Maximal: 240–
480 mg/day.
• Iodines and iodides (e.g., Lugol’s solution, saturated solution of
potassium iodide) i. Mechanism of action: Inhibits the release
of stored thyroid hormone. Minimal effect on hormone
synthesis. Helps decrease vascularity and size of gland before
surgery ii. Dosing (a) Lugol’s solution (6.3–8 mg of iodide per
drop) (b) Saturated solution of potassium iodide (38–50 mg of
iodide per drop) (c) Potassium iodide tablets: 130-mg tablets
contain 100 mg of iodide. (d) Usual daily dose: 120–400 mg
mixed with juice or water, split three times daily iii. Adverse
effects (a) Hypersensitivity (b) Metallic taste (c) Soreness or
burning in mouth or tongue (d) Do not use in the days before
ablative iodine therapy (may reduce uptake of radioactive