Fall, 2009
Hypothyroidism is an endocrine disorder in which there is abnormal excretion of the thyroid hormones from the thyroid gland, this abnormality results in an array of clinical symptoms that the patient presents with, which in certain cases are treatable however sometimes these disorders are identified so late that they become untreatable. Thyroid hormone binds to receptors that regulate its expression. Thyroid hormone produces an increase in oxygen consumption; it also causes thermogenesis, and accelerates LDL cholesterol degradation. In the heart, T3 increases the contraction and relaxation of the myocyte by the action of sarcoplasmic reticulum adenosine triphosphatase (ATPase). In the conduction system of the heart, T3 increases the heart rate by altering sinoatrial node depolarization and repolarization. Other physiologic effects of thyroid hormone include increased mental alertness, increased gastrointestinal motility, and bone turnover. In utero, it affects the fetal development, by critically controlling the brain development and skeletal maturation. (Ladenson, P. Kim, M. 2004).
Primary hypothyroidism is due to hormone deficiency, the cause is usually an internal dysfunction of the thyroid gland as seen in myexedema, which disturbs the formation, regulation and secretion of its hormones T4 and T3. However in case of overt hypothyroidism there is an elevated TSH level, associated with a low level of free T4 than normal. (Ladenson, P. Kim, M. 2004).
Primary hypothyroidism occurs in cases where there is insufficient thyroid tissue that can function properly; this is seen in partial or complete congenital absence of the thyroid gland, autoimmune disease Hashimoto’s thyroiditis, this can be classified into goitrous and atrophic thyroiditis, surgical removal of thyroid tissue, radioactive iodide uptake, and infiltrative destruction as seen in hemochromatosis, scleroderma, and amyloidosis. Primary hypothyroidism is also caused because of an impairment of thyroid tissue to produce thyroid hormone; this is seen in iodide deficiency, congenital defects, and inhibition of thyroid gland because of drugs like thionamides and lithium. (Ladenson, P. Kim, M. 2004).
Sonographic evaluation of some hypothyroid conditions
A 12-14 MHz linear transducer is used to evaluate thyroid. Patient is prepped with pillow under shoulders and extended neck, very sick patients however may not be able to lay flat as health conditions may not allow it.
The thyroid gland may be visibly large in hypothyroidism due to compensatory hypertrophy of the gland.
 Fig-1 normal thyroid gland

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 Fig-2, machine
Fig-3, position of patient

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Fig-4scanning position

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Fig-5-6    Agenesis of the thyroid 

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Fig-7-8 Hashimoto’s thyroiditis
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  Hypoechoic, coarse echo texture with fine echoes/ fibrosis, and increased vascularity of thyroid gland on Doppler are considered diagnostic for Hashimoto’s thyroiditis.
 Fig-9 Ultrasound and color Doppler imaging of multinodular goiter

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Figure-10 Ultrasound and color Doppler imaging of multinodular goiter 
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Fig-11-Congenital Hypothyroidism
Fig-11-Congenital Hypothyroidism 

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Secondary hypothyroidism is due to hypothalamic disorders like neoplasm-lymphoma, germinoma, glioma, inflammation and irradiation, and pituitary leisions seen due to neoplasms, surgery, radiation and hemorrhagic apoplexy, and lymphocytic hypophysitis. (Ladenson, P. Kim, M. 2004).
Figure-12- Hypothalamus and Pituitary affect thyroid 
Signs and Symptoms 
Patient with hypothyroidism feels fatigued and lethargic all the time, these people will gain weight even though they have a poor appetite, they  have intolerance to cold due to reduced basal metabolic rate, hoarseness of voice, reduced peristalsis causes constipation, weakness, myalgias, arthralgias, paresthesias, dry skin, and hair loss. Female patients may develop precocious puberty if they are still young and menstrual problems like menorrhagia, amenorrhea, and galactorrhea.  Patients feel depressed and socially challenged. They have a variety of cognitive deficits from some episodes of forgetfulness to delirium, dementia, seizures, and coma. (Ladenson, P. Kim, M. 2004).
The physical findings of hypothyroidism depend upon the age at which hypothyroidism develops, and the severity of the disease. Younger age group presents with delay in height and continued weight gain, precocious or delayed puberty where girls become physically mature earlier than normal, they develop breasts and begin to menstruate as early as five years of age. (Ladenson, P. Kim, M. 2004).
Boys have earlier signs like hoarseness of voice and smelly sweat.  They look big because there is pseudohypertrophy of muscle. Adults present myexedema, with a low heart rate bradycardia, hypertension, and mild hypothermia. Thinning of scalp hair and eyebrows is seen. The skin becomes coarse, dry and yellow; it feels cool due to hypothermia and peripheral vasoconstriction. The nails become brittle and chip off easily. On chest examination murmurs can be heard. There is nonpitting edema caused by the deposition of glycosaminoglycans in lower dependant limbs. Neurologically they have slow dysarthric speech and slow deep tendon reflexes at the terminal relaxation phase. (Ladenson, P. Kim, M. 2004).
Inscisional scars are seen on the neck in case of previous thyroid surgery; on examination a normal sized or diffusely enlarged thyroid may be seen. It may be atrophic and non palpable. It may be soft and smooth with a lobular texture or firm and irregular with a heterogeneous nodular texture. (Ladenson, P. Kim, M. 2004).
There is development of myxedema in older patients and cretinism in children. Myxedema has specific facial features; there is loss of eyelashes, the areas of vitiligo around the mouth, the region around the eyes, and the scalp, puffiness around the eyes and loss of or thinning of scalp hair. Cretinism seen in children has specific features, these include; severe mental retardation, impairment of physical growth and retardation of bone development, dwarfism, large tongue and protruded big abdomen. (Schneider, A. Szanto, P. 2006).
 Figure- 13 cretinism

As seen in figure-14 the Myxedemic patient has many facial features of low thyroid activity and disappearance few weeks after therapy. 
 Figure-14- two cases of hypothyroidism
Figure-14- two cases of hypothyroidism, patient before (A and C) and after (B and D) after full replacement with thyroid hormone recovered from hypothyroidism. In fig A, Notice the loss of eyelashes, the areas of vitiligo around the mouth, the region around the eyes, and the scalp. In figure-C, Notice the lethargic expression and the periorbital puffiness disappears with therapy (D).
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Laboratory values
The measure of thyroid hormones is compulsory to make the diagnosis of hypothyroidism. There is an elevated TSH level from its normal range. Measurement of free T4 is characteristic if it is low with a high TSH, this shows overt or secondary hypothyroidism. However, in case of low-normal T4 and high TSH shows primary causes. In case of Hashimotos thyroiditis there are t-cells and antithyroid antibodies are seen. The pituitary cause’s will have a sellar (sella turcica) mass, history of surgical removal or irradiation of pituitary is present. In such cases a low –normal T4 is diagnostic. The TSH level may be low, normal or high. (Ladenson, P. Kim, M. 2004).
There is an increase in cholesterol in serum with the decreased free serum T4 and increased serum TSH. There is also decrease in total T4. T3resin uptake also called thyroid hormone binding ratio (THBR), is now becoming obsolete. (Schneider, A. Szanto, P. 2006).
Diagnosis is usually made on a complete picture with clinical manifestations laboratory values and history of patient and ultrasound images. A considerable differential for hypothyroidism is multinodular goiter and thyroid carcinoma, in which case antibodies are also present. An ultrasound can be done for looking at thyroid texture to determine if thyroid disease is heterogeneous enlargement as seen in Hashimotos thyroiditis or if there is a solitary nodule or multinodular goiter. (Ladenson, P. Kim, M. 2004).
The primary goal of treatment is to replace the hormones that are produced by the thyroid gland, so that avoid the symptoms of hypothyroidism and to treat the complications of the disease. Levothyroxine sodium is the drug of choice in hypothyroidism, in both primary and secondary hypothyroid cases. Levothyroxine has a seven day half life that makes it release a daily dose of medicine for a week. Thyroxine is also used for the treatment however slight variation of dosage can produce clinical consequences. The dosage also depends upon the weight and height of the patient. Also patients with post surgical removal will require higher doses than Hashimotos thyroiditis since some normal tissue may be left in the latter. (Ladenson, P. Kim, M. 2004).
Medications, mineral supplements, and foods hamper thyroxine absorption; these include ferrous sulfate, calcium carbonate, aluminum hydroxide, sucralfate, cholestyramine, and soy-containing foods therefore thyroxine doses should be separated by at least four or more hours. The over dosage of the drug can cause complications like bone loss, atrial fibrillation, myocardial ischemia and hair loss. (Ladenson, P. Kim, M. 2004).
Complications of hypothyroidism 
Myxedemic coma is a complication of severe hypothyroidism; this is a severe life threatening condition in which there is hypothermia, bradycardia, hypotension, altered mental status, and multisystem organ failure. This condition is most often seen in patients who are old and have a low level of health care. They may also have underlying disease of many organs. Treatment with thyroxine and triiodothyronine is done. (Ladenson, P. Kim, M. 2004).
Case study -1
A 60 year old female presents with severe burning of feet for three months. Physical examination showed loss of tendon reflexes and the nerve conduction study results suggested sensory neuropathy. Laboratory findings included decreased value of thyroid hormones. The patient was treated with thyroid hormone replacement, and in a few months thyroid function returned and the patient reported of a huge decrease in the neurologic symptoms. About 6-12 months later nerve conduction studies became normal, skin biopsy showed a complete recovery of innervations of epidermis.( Paola, P.  Raffaella,  L. Francesca, C. Claudia, C. Giuseppe, L. 2009)
Case study-2
A fisherman finds it hard to row his boat, his thyroid dysfunction has caused myotonia and rowing movements of his arms are difficult especially extension after flexion and opening his grip on the rows is hard due to myotonia. The replacement of thyroid hormone relieves his myotonia and thus relieving his symptoms. (Abhijit, D. Ajith, C. Thomas, C.2009).

Case study -3
A case of sub clinical hypothyroidism in a 65 yr old female, with breast cancer on therapy with third generation aromatase inhibitor, presents with fatigue and weakness after the therapy began. Her thyroid function tests before the drug administration were normal, with no history in the family of thyroid disease, she was diagnosed with hypothyroidism. This was confirmed with lab findings of an elevated TSH only. Thyroid gland was normal on ultrasound. 
Figure-15 normal thyroid 

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The patient was administered with Levothyroxine sodium 50 micrograms and the third generation aromatase was stopped. The thyroid dysfunction was restored at a 1-yr follow up. This was the first reported case in literature for drug induced hypothyroidism and proves that it is treatable. (Mazokopakis, E. Karefilakis, C. Tsartsalis, A. Milkas, A. Starakis, I. 2008).
The treatment options for hypothyroidism are excellent therefore the prognosis of the disease is good. In case of underlying disease and older age of patient the prognosis not as good however many times the quality of life can be improved.
Hypothyroidism is a curable disease since the medication thyroxine has many qualities, it has a 7-day half life which allows daily dosing of the medicine, it is well absorbed and it is more active than T3. Thyroxine also cures most of the symptoms and signs of the disease. (Ladenson, P. Kim, M. 2004).
Abhijit, D. Ajith, C. Thomas, C. (2009). A Fisherman could not Row. 
Hypothyroidism. January 1st 2009. VOL-373, pp432-432. Retrieved April 10th 2009 from Academic Search Premier. NC live.
Ladenson, P. Kim, M. (2004.).Thyroid. In L. Goldman & D. Ausiello (Eds.). 
Cecil Text book of Medicine. (23nd ed., pp1700-1713).  Philadelphia: W.B.Sauders. Retrieved April 9th 2009 from Merck Medicus.com-Cecil Textbook of Medicine. 
Mazokopakis, E. Karefilakis, C. Tsartsalis, A. Milkas, A. Starakis, I. (2008).
Exemestane-Induced Subclinical Hypothyroidism: A Case Report. Hypothyroidism. 2008.(28th vol, pp-669). Retrieved April 10th 2009 from Academic Search Premier. NC Live.
Paola, P.  Raffaella, L. Francesca, C. Claudia, C. Giuseppe, L. (2009). 
Painful Neuropathy in Subclinical Hypothyroidism: Clinical and Neuropathological recovery after Hormone Replacement Therapy. Neurological sciences. (30th vol, pp-149-151). April, 2009. Retrieved April 9th 2009 from Academic Search Premier. NC Live.
Schneider, A. Szanto,P. (2005-2006). Hypothyroidism. Endocrine System.
Neiginski, E. (Eds). Board Review Series, Pathology. (2ND edition p.343-344). Philadephia. PA. Lippincott Williams & Wilkins.