1. Hypothyroidism is caused by thyroid hormone deficiency and can occur due to problems with the thyroid gland itself or with the pituitary or hypothalamus. Common causes include Hashimoto's thyroiditis, surgery or radiation treatment of the thyroid, and iodine deficiency. 2. Symptoms of hypothyroidism are wide-ranging and affect nearly every organ system. They include fatigue, dry skin, joint pain, constipation, weight gain, depression, and increased cholesterol levels. 3. Treatment involves lifelong thyroid hormone replacement therapy, typically with levothyroxine to replace T4, with dosages tailored to the individual to relieve symptoms and lower elevated TSH levels into the normal

1. Medical information and significance about Hypothyroidism,
thyroiditis and Cancer of the Thyroid gland
It is the characteristic reaction to thyroid hormone deficiency. The spectrum of hormone ranges
from a few non - specific symptoms to overt hormone, to myxedema coma. Hypothyroidism occurs in
3 to 6 for the adult population, but is symptomatic only in a minor of them. It occurs 8 to 10 times
more often in woman than in men and usually develops after the age of 30.
Classification
1.Congetial.
2. Acquired:Â Â Â Â Â Â Â Â Â Â 1. Primary (thyroid gland disturbances).
2. Secondary (due to pituitary disease).
3.Tertiary (due to hypothalamic disease).
4.Peripheral.
Etiology
A cause  is usually evident from the history and physical examination.
1.Primary (thyroidal) hypothyroidism.
1)Â Â Â Â Â surgical removal, total
thyroidectomy of thyroid carcinoma, subtotal
thyroidectomy (hypothyroidism occurs from 25
to 75 of patients in different series);
2)Â Â Â Â Â irradiation (hypothyroidism results
from external neck irradiation therapy in doses
2000 rads or more such as are used in the
treatment of malignant lymphoma and
laryngeal carcinoma); I131 therapy for
hyperthyroidism (it results in hyperthyroidism
in 20 % to 60 % of patients within the first year after therapy and in 1 % to2 % each year there
after);
3)Â Â Â Â Â during or after therapy with propylthyouracil, methimazole, iodides or beta-blockers;
4)Â Â Â Â Â autoimmune processes (hypothyroidism usually occurring as a sequel to Hashimoto's
thyroiditis and results in shrunken fibroid thyroid gland with a little or no function and infiltrative
diseases (tuberculosis, actynomycosis);

2. 5)Â Â Â Â Â trauma;
6)Â Â Â Â Â iodine deficiency.
2.Secondary and tertiary hypothyroidism
It occurs due to either deficient secretion of TSH from the pituitary or lack of secretion of TRH from
the hypothalamus.
-Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Tumor;
-Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Infarction;
-Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Infiltrative process;
-Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Trauma;
-Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Â Drugs (reserpin, parlodel).
3. Peripheral hypothyroidism:
-Â Â Â Â Â Â Â Â Â peripheral tissue resistance to thyroid hormones;
-Â Â Â Â Â Â Â Â Â decreasing of T4 peripheral transformation into T3 (in liver or in kidneys) ;
-Â Â Â Â Â Â Â Â Â production of antibodies to thyroid hormones.
Congenital:
-Â Â Â Â Â Â Â Â Â Maldevelopment -hypoplasia or aplasia;
-Â Â Â Â Â Â Â Â Â Inborn deficiencies of biosynthesis or action of thyroid hormone;
-Â Â Â Â Â Â Â Â Â Atypical localization of thyroid gland;
Classification. (cont.)
B.     1. Laboratory (subclinical) hypothyroidism.
2. Clinical hypothyroidism, which can be divided on stages of severity: mild, moderate, severe.
C.     1. Compensation.
2. Subcompensation.
3. Decomposition.
D.     1. Without complications.
2. With complications (myopathy, polyneuroparhy, encephalopathy, coma).

3. Clinical features
The major symptoms and signs of hypothyroidism reflect showing of physiologic function. Virtually
every organ system can be affected. The onset of symptoms may be rapid or gradual, severity varies
considerably and correlates poorly with biochemical changes. Because many manifestations of
hypothyroidism are non-specific, the diagnosis is particularly likely to be overlooked in patients with
other chronic illnesses and elderly.
Nervous system
 Most of hypothyroid patients complain of fatigue, loss of energy, lethargy, forgetfulness, reduced
memory. Their level of physical activity decreases, and they may speak and move slowly. Mental
activity declines and there is inattentiveness, decreased intellectual function, and sometimes may be
depression.
Neurological symptoms include also hearing loss, parasthesias, objective neuropathy, particularly
the carpal tunnel syndrome, ataxia.
Tendon reflex shows slowed or hung-up relaxation.
Skin and hair.
Hypothyroidism results in dry, thick and silk skin, which is often cool and pale.
Glycosoamynoglicanes, mainly hyaluronic acid accumulate in skin and subcutaneous tissues
retaining sodium and water. So, there is nonpitting edema of the hands, feet and periorbital regions
(myxedema). Pitting edema also may be present. The faces are puffy and features are coarse. Skin
may be orange due to accumulation of carotene. Hair may become course and brittle, hair growth
slows and hair loss may occur. Lateral eyebrows thin out and body hair is scanty.
Cardiovascular system.
There may be bradycardia, reduced cardiac output, quiet heart sounds, a flabby myocardium,
pericardial effusion, cardiac wall is thick, it is increased by interstitial edema. (These findings, along
with peripheral edema, may simulate congestive heart failure). Increased peripheral resistance may
result in hypertension. The ECG may show low voltage and/or non-specific ST segment and T wave
changes. Hypercholesterolaemia is common. Whether or not these is an increased prevalence of
ischemic heart disease is controversial. Angina symptoms, when present, characteristically occur
less often after the onset of hypothyroidism, probably because of decreased activity.
Gastrointestinal system.
Hypothyroidism does not cause obesity, but modest weight gain from fluid retention and fat
deposition often occurs. Gastrointestinal motility is decreased loading to constipation and abdominal
distension. Abdominal distension may be caused by ascities as well. Ascitic fluid, like other serous
effusions in myxedema, has high protein content. Achlorhydria occurs, often associated with
pernicious anemia.
Renal system.
Reduced excretion of a water load may be associated with hyponatriemia. Renal blood flow and
glomerular filtration rate are reduced, but serum creatinine is normal. May be mild proteinuria and

4. infections of urinary tract.
Respiratory system.
Dyspnea of effort is common. This complaint may be caused by enlargement of the tongue and
larynx, causing upper airway obstruction, or by respiratory muscle weakness, interstitial edema of
the lungs, and for plural effusions which have high protein content. Hoarseness from vocal curt
enlargement often occurs.
Musculoskeletal system.
Muscle and joint aches, pains and stiffness are common. Objective myopathy and joint swelling or
effusions are less often present. The relaxation phase of the tendon reflexes is prolonged. Serum
creatine phosphokinase and alanine aminotransferase activities are often increased, probably as
much to slowed enzyme degradation as to increased release from muscle.
Hemopoetic system.
Anemia, usually normocytic, caused by decreased red blood cell production, may occur. It is
probably from decreased need of peripheral oxygen delivery rather than hematopoetic defect.
Megaloblastic anemia suggests coexistent pernicious anemia. Most patients have no evidence iron,
folic acid or cyancobalamin deficiency.
Endocrine system.
There may be menorrhagia (from anovulatory cycles), secondary amenorrhea, infertility and rarely
galactorrhea. Hyperprolactinemia occurs because of the absence of the inhibitory effect of thyroid
hormone on prolactine secretion (and causes galactorrhea and amenorrhea or Van - Vik - Cheness -
Ross's syndrome).
Pituitary-adrenal function is usually normal. Pituitary enlargement from hyperplasia of the
thyrotropes occurs rarely in patients with primary hypothyroidism -such enlargement also may be
caused by a primary pituitary tumor, which resulting TSH deficiency.
Enlargement of thyroid gland in young children with hypothyroidism suggests a biosynthetic defect.
Hypothyroidism in adults is caused by Hashimoto thyroiditis.
Secretion of growth hormone is deficient because thyroid hormone is necessary for synthesis of
growth hormone. Growth and development of children are retarded. Epiphyses remain open.
Metabolic system.
Hypothermia is common. Hyperlipidemia with increase of serum cholesterol and trigliceride occurs
because of reduced lipoprotein lipase activity.
Subclinical (laboratory) hypothyroidism.
It is a state in which we cant find clinical features of hypothyroidism and euthyroidism is reached by
compensatory increasing of TSH secretion and that's why synthesis and secretion of such level of
thyroid hormone that will be enough for organism. It is an asymptomatic state in which serum T4
and free T4Â Â are normal, but serum TSH is elevated. The therapy may provide the patient with

5. more energy, a feeling of well being, desirable weight reduction, improved bowel function or other
signs of better health even though the patient is not aware of these symptoms before therapy.
Peculiaritis of congenital hypothyroidism
o         Children are born with increased weight
o         Subcutaneous edema
o         Hypotermia
o         Prolonged jaundice
o         Physical (dwarfism) and mental retardation (cretinism
Diagnostic of hypothyroidism is based on:
1)Â Â Â Â Â history;
2)Â Â Â Â Â clinical features;
3)Â Â Â Â Â blood analysis: anemia; hypercholesterolemia;
4)Â Â Â Â Â levels of thyroid hormone: both serum T4Â Â and T3Â Â are decreased (but in 25% of
patients with primary hypothyroidism may be normal circulating levels of T3);
5)Â Â Â Â Â ECG;
6)Â Â Â Â Â examination of tendon reflexes;
7)Â Â Â Â Â ultrasonic examination;
Differential diagnosis of primary and secondary hypothyroidism:
1)Â Â Â Â Â clinical features:
Secondary hypothyroidism is not common, but it often involves other endocrine organs affected by
the hypothalamic - pituitary axis. The clue to secondary hypothyroidism is a history of amenorrhea
rather than menorrhagia in a woman with known hypothyroidism.
 In secondary hypothyroidism, the skin and hair are dry but not as coarse; skin depigmentation is
often noted; macroglossia is not prominent; breasts are atrophic; the heart is small without
accumulation of the serous effusions in the pericardial sac; blood pressure is low, and hypoglycemia
is often found because of concomitant adrenal insufficiency or growth hormone deficiency.
2)Â Â Â Â Â laboratory evaluation:
shows a low level of circulating TSH in secondary hypothyroidism, whereas in primary
hypothyroidism there is no feedback inhibition of the intact pituitary and serum levels of TSH are
very high. The serum TSH is the most simple and sensitive test for the diagnosis of pituitary
hypothyroidism.

6. Serum cholesterol is generally low in secondary hypothyroidism, but high in pituitary
hypothyroidism.
Other pituitary hormones and their corresponding target tissue hormones may be low in secondary
hypothyroidism.
The TSH test is useful in distinguishing between secondary and tertiary hypothyroidism in the
former; TSH is not released in response to TRH; whereas in the later, TSH is released. Â
Treatment of hypothyroidism.
1.   Diet No10.
2.   Regimen is not restricted.
3. 1) replacement therapy:
-Â Â Â Â Â Â Â Â Â desiccated animal thyroid (this is an extract of pig and cattle thyroid glands,
which standardized based on its iodine content but they are too variable in potency to be reliable
and should be avoided);
-Â Â Â Â Â Â Â Â Â synthetic preparations of :
T4 (l-thyroxine)
-Â Â Â Â Â Â Â Â Â T4 is preparation of choice, because it produces stable serum levels of both T4
and T3.
-Â Â Â Â Â Â Â Â Â Absorption is fairly constant 90 to 95% of the dose. T3Â Â is generated from
T4Â Â by the liver.
-Â Â Â Â Â Â Â Â Â The initial dosage can be 1.6 mkg/kg of ideal weight or 12.5-25 mkg in older
patients and 25-50 mkg in young adult.
-Â Â Â Â Â Â Â Â Â The dosage can be increased in 25-50 mkg increments at 4 to 6 week intervals
until clinical and biochemical euthyroidism is achieved. In older patients more gradual increments
are indicated. Cautious replacement is particularly warranted in patients with ischemic heart
disease, because angina pectoris or cardiac arrhythmia may be precipitated by T4 therapy.
-Â Â Â Â Â Â Â Â Â The average maintenance dosage is 100 to 150 mkg/day orally, only rarely is a
larger dosage required. In general, the maintenance dose may decrease in the elderly and may
increase in pregnancy.
-Â Â Â Â Â Â Â Â Â The dosage should be minimum that restores TSH levels to normal (though this
criterion cannot be used in patients with secondary hypothyroidism).
-Â Â Â Â Â Â Â Â Â Patient takes the whole dose of T4 once a day (in the morning), in the summer the
dose may be decreased and in the winter should be increased.
T3 (liothyronine sodium)Â should not be used alone for long-term replacement because its rapid
turnover requires that it be taken. T3 is occasionally used mainly in starting therapy because the

7. rapid excretion is useful in the initial titration of a patient with longstanding hypothyroidism in
whom cardiac arrhythmia may occur early in replacement therapy. The risk of jatrogenic
hyperthyroidism is therefore greater in patients receiving these preparations.
 In addition, administering standard replacement amounts of T3 (25 to 50 mkg/day) results in
rapidly increasing serum T3 levels to between 300 and 1000 mkg within 2 to 4 h, these levels return
to normal by 24 h. Therefore, when assessing serum T3 levels in patients on this particular regimen,
it is important for the physician to be aware of the time of prior administration of the hormone.
Additionally, patients receiving T3 are chemically hyperthyroid for at least several hours a day and
thus are exposed to greater cardiac risks. Similar patterns of serum T3Â Â concentrations are seen
when mixtures of T3 and  T4 are taken orally, although the peak levels of T3  are somewhat
lower. Replacement regimes with synthetic preparations of T4Â Â reflect a different pattern of
serum T3Â response increases in serum T3 occur gradually over weeks, finally reaching a normal
value about 8 wk. after starting therapy.
 Synthetic T3 and T4 combinations (liotrix, thyreocomb). These preparations were developed
before it was appreciated that T4 is converted to T3 outside of the thyroid. These preparations
should not be used.
      2) Symptomatic therapy:
-Â Â Â Â Â Â Â Â Â beta-blockers (should be used in patients with tachycardia and hypertension) in
the dose of 20 - 40 - 60 mg/day;
-Â Â Â Â Â Â Â Â Â hypolypidemic agents;
-Â Â Â Â Â Â Â Â Â vitamins (A, B, E);
-Â Â Â Â Â Â Â Â Â diuretics and others.
Subclinical hypothyroidism
Many endocrinologists would treat such patients with T4, especially if hypercholesterolemia were
present. Even in the absence of hyperlipidemia, a trial of therapy might be varianted to determine if
the patient experiences improvement presumably the normal serum T4 concentrations before
therapy did not reflect adequate tissue effects of thyroid hormones in such patients. Unfortunately, it
is also reasonable to follow these patients without T4 therapy by surveying thyroid function at 4-to 6
months intervals to determine whether thyroid failure has occurred, as indicated by the serum T4
falling to subnormal levels along with a greater increase in serum TSH and the appearance of clear
symptoms.