Download Thyroid gland diseases

Thyroid gland diseases. The diagnosis, the differential diagnosis,
preventive maintenance and craw treatment.
The thyroid is a firm vascular organ lying in the neck, caudal to cricoid cartilage. It is
composed of two nearly equal lobes connected by a thin isthmus and weights approximately 20 gr.
Rests of thyroid tissue are occasionally presents in sublingual or retrosternal areas.
Thyroid secrets: T3, T4,thyrocalcitonin. The thyroid hormones, thyroxine (T4) and
triiodothyronine (T3) are secreted under the stimulatory influence of pituitary thyrotropin (thyroidstimulating hormone or TSH). TSH secretion is primary regulated by a dual mechanism:
-
thyrotropin-releasing hormone (TRH);
thyroid hormone.
Thyroid hormones exits in circulation in both free and bound forma. The thyroid gland is the
sole source of T4 and only 20% of T3 is secreted in the thyroid. Approximately 80% of T3 in blood
is derived from peripheral tissue (mainly hepatic or renal) deiodinatoin of T4 to T3.
Iodide, ingested in food or water, is actively concentrated by the thyroid gland, converted
organic iodine by peroxidase, and incorporated (by the thyroid gland) into tyrosine in intrafollicular
thyroglobulin. The thyrosines are iodinated at either one (monoiodotyrosine, MIT) or two
(diodotyrosine, DIT) sites and then coupled to form the active hormones (diiodotyrosine +
diiodotyrosine → tetraiodothyronine (thyroxine, T4); diiodotyrosine + monoiodotyrosine →
triiodotyronine (T3).
Thyroglobuline, a glycoprotein, containing T3 and T4 within its matrix, is taken up from the
follicle as colloid droplets by the thyroid cells. Lysosomes containing proteases cleave T3 and T4
from thyroglobulin, resulting in release of free T3 and T4. The iodotyrosines (MIT and DIT) are also
released from thyroglobulin but do not normally reach the bloodstream. They are deiodinated by
intracellular deiodinases, and their iodine is neutralized by the thyroid gland.
Although some of free T3 and T4 is deiodinated in the thyroid gland with the iodine
reentering the thyroid iodine pool, most diffuses into the bloodstream where it is bound to certain
serum proteins for transport. The major thyroid transport protein is thyroxine binding globulin
(TBG), which normally accounts for about 80% of the bound thyroid hormones. Other thyroid
binding proteins, including thyroxine-binding prealbumin (TBPA) and albumin, account for the
remainder of the bound serum thyroid hormone (20 %). About 0,05 % of the total serum T4 and 0,5
% of the total serum T3 remain free but in equilibrium with the bound hormone.
About 15 - 20 % of the circulating T3 is produced by the thyroid. The remainder is produced
by monodeiodination of the auter ring of T4, mainly in the liver. Monodeiodination of the inner
ring of T4 also occurs in hepatic and extrahepatic sites, including kidney, to yield 3,3/, 5/-T3 (reverse
T3 or rT3). This compound has minimal metabolic activity but is present in normal human serum or
globulin.
Observations pertaining to rT3 metabolism in fetal life are of great importance. Total amniotic T4
and T3 are low, in contrast to levels in maternal serum. Fetal rT3 levels in amniotic fluid are much
higher than the corresponding values in maternal serum throughout pregnancy (15 to 42 wk). These
data imply that rT3 derives primarily from the fetus and that it may be possible to diagnose fetal
hypothyroidism as early as 15 wk of pregnancy, utilizing radioimmunoassay for rT3. These levels
appear to decrease after 30 wk gestation and may be serve as a useful index of pregnancies of < 30
wk duration.
Physiologic effects of thyroid hormones .
Thyroid hormones have a major physiologic effects:
1) they increase protein synthesis in virtually every body tissue
2) they increase O2 consumption by increasing the activity of Na+ H+ ATPase (Na pump),
primarily in tissues responsible for basal O2 consumption (i.e., liver, kidney, heart and
skeletal muscle).)
Hyperthyroidism (thyrotoxicosis) Toxic diffuse goiter. Grave’s diseaseis the condition resulting from the effect of excessive amounts of thyroid hormones on body tissues.
Thyrotoxicosis is a main syndrome. Sometimes the term hyperthyroidism can be used in a
narrower sense to denote this state when the thyroid gland is producing too much thyroid hormones
in contrast with excessive ingestion of thyroid hormone medication. At one time or another,
approximately 0,5 % of the population suffers from hyperthyroidism. Graves disease is the most
common cause of hyperthyroidism and is fairly common in the population. It is responsible for over
80 % of hyperthyroid cases. It occurs most often in young women, but it may occur in men and at
any age.
Cause:
Autoimmune disorders, which can be provoked by:
- insolation;
- acute infections;
- hormone disbalance (pregnancy and others).
Pathogenesis.
Insufficiency of T suppressors  excessive level of T helpers  increasing function of B
lymphocyte  secretion of thyroid – stimulating immunoglobulin (TSI)  blood  the thyroid.
TSI works as an antibody to the thyrotropin receptor on the thyroid follicular all resulting in
stimulation of this receptor  secretion of T4, T3.
Pathogenesis
Insufficiency of T suppressors
Increasing function of B lymphocyte
Toxic influence of lymfocytes
Secretion of thyroid – stimulating
immunoglobulin (TSI)
The thyroid
Secretion of T4, T3
Thyrotoxicosis
Pathologic changes in different organs and systems
Clinical manifestations
The clinical presentation may be dramatic or subtle.
Cardiovascular system
Dysfunction of the cardiovascular system is common, and in some instances, the only manifestation
of hyperthyroidism. Heart rate and cardiac output are increased, and peripheral resistance is
decreased. These changes result in:
- permanent palpitation;
-sinus tachycardia or atrial fibrillation;
-heart failure.
Examination reveals:
- tachycardia;
- widened pulse pressure;
- a prominent apical impulse;
- bounding arterial pulsation;
- accentuated heart sounds;
- systolic ejection murmurs;
- occasionally cardiac enlargement..
Other than arrhythmia, electrocardiographic changes are limited to nonspecific ST and T wave
abnormalities.
Psychological symptoms:
- nervousness;
- physical hyperactivity;
- emotional lability;
- anxiety;
- distractibility;
- insomnia.
These changes occur commonly and often result in impairment of work or school performance and
disturbances in home and family life.
Neuromuscular symptoms:
- a fine tremor is often evident in the hands and fingers;
- performance of skills requiring fine coordination becomes difficult;
- deep tendon reflexes are hyperactive;
- some evidence of myopathy is common;
- weakness lit usually develops gradually, is progressive, and may be accompanied by muscle
wasting.
Skin.
The skin is warm, fine, moist and its texture is smooth or velvety erythema and pruritus may be
present. Increased sweating is common complaint . Hair may become thin and fine, and alopecia
occurs. Infiltrative dermopathy, also known as pretibial mixedema (a confusing term, since
mixedeme suggests hypothyroidism), is characterized by nonpitting infiltration of proteinaceous
ground substance, usually in the pretibial area. The lesion is very pruritic and erythematous in its
early stages and subsequently becomes browny it may appear years before or after the
hyperthyroidism. TSIS are invariably present. The dermopathy usually remits spontaneously after
months or years.
Eyes. Eye sings include:
- stare (Schtelvag’s symptom);
- lid lag;
- lid retraction (symptoms of Dalrympl; Greffe; Koher),
which results in “apparent” proptosis, but not eye and is often accompanied by symptoms of:
- conjunctival irritation.
These eye signs are largely due to excessive adrenergic stimulation and zemit promptly after
upon successful treatment of thyrotoxicosis
- infiltrative ophthalmopathy is present in 20 to 40% of patients with Graves’ disease. It is
characterized by increased retro-orbital tissue, producing exophthalmos and by lymphocyte
infiltration of the extraocular muscles, producing a spectrum of ocular muscle weakness
frequently leading to blurred and double vision. The pathogenesis of infiltrative ophthalmopatny
is poorly understood.
It may occur before the onset of hyperthyroidism or as 15 to 20 years afterward and frequently
worseness or improves independent of the clinical course of hyperthyroidism. Infiltrative
ophthalmopathy results from immunoglobulins directed to the extraocular muscles and specific
antibodies that cause retro – orbital inflammation and subsequent edema (it is not because of TSH
or LATS). The antibodies are distinct from those initiating Graves’ type hyperthyroidism.
The symptoms include:
- pain in the eyes;
- lacrimation;
- photophobia;
- diplopia;
- blurring or loss of vision.
The major signs are:
- proptosis (exophthalmos);
- periorbital and conjunctival congestion and edema (chemosis);
- limitation of ocular mobility.
Thyroid gland
Enlargement of thyroid gland is very common. Both thyroid lobes are usually moderately
symmetrically enlarged, but thyroid enlargement may be absent.
Degrees of thyroid gland enlargement.
0- we can’t see or palpate thyroid gland;
I- we can palpate but can’t see;
II – we can palpate and see thyroid gland in any position of the head.
Respiratory function
Abnormalities of respiration include:
- decreased vital capacity;
- decreased pulmonary compliance.
They result in dyspnea and hyperventilation during exercise and sometimes rest.
Gastrointestinal system
Increased caloric utilization is almost always present. It results in increased appetite and
food intake, but compensation is usually inadequate, and modest loss occurs.
Increased gastrointestinal motility may result in increased frequency of bowel movements
and even frank diarrhea.
Minor abnormalities in hepatic function are often found.
Hematopoetic system
Some patients have a modest anemia, caused by mild deficiency in one or more
hematopoetic nutrients or increased plasma volume. Mild granulocytopenia and thrombocytopenia
may be present.
Energy and intermediary metabolism because of increased energy expenditure, energy
production must be augmented, this is accompanied by increased oxygen consumption and heat
production. In patients with diabetes mellitus, requirement for exogenous insulin catabolism.
Endocrine system
In women, hypomenorrhea or amenorrhea may occur, although no changes are noted.
In men, there may be loss of libido and impotence hypercalcemia is found occasionally; it is
caused by increased bone resorption, but clinical osteopenia is rare.
In patients mild adrenal insufficiency may occur. It is present by low diastolic blood
pressure and darkness of upper lid (Elynecks symptom).
Degrees of severity
I. mild degree: work capacity is normal;
heart beat – is under 100/min;
weight loss is less than 10 %.
II. moderate degree: work capacity is decreased;
heart beat – is 100 to 120/min;
weight loss is 10 to 20 %.
III. severe degree: patients cant work;
heart beat – is over 120/min and arrhythmia is present;
weight loss is more than 20%.
Diagnosis of toxic diffuse goiter.
I.
Clinical manifestations (were discussed).
II.
Laboratory findings.
(The diagnosis of hyperthyroidism is usually
straightforward and depends on careful clinical history and physical examination, a high index of
suspection, and routine thyroid hormone determination).
1. In most patients serum total T3 and T4 concentrations, are increased (however, these changes,
also can be caused by increased thyroxine – binding globulin production, e.g. as a result of
estrogen therapy).
2. Elevation of T3 - resin uptake.
(T3 - resin uptake is not a measurement of circulating T3. In normal patients, 25 to 35% of TBG
binding sites are occupied by thyroid hormone. When 131I-T3 is added to the patients serum, in
vitro, a portion binds to unoccupied TBG sites. After equilibration, a resin is added that binds
the remaining unbound 125/-T3).
Thus in hyperthyroidism, characterized by increased levels of circulating thyroid hormone,
there are more occupied and less unoccupied TBG binding sites. Less 131I-T3 is bound to TBG,
resulting in more uptake of 131I-T3 by the resin.
3. TSN (serum thyroid stimulating hormone) may be decreased, but it is not very sensitive assay in
the assessment of thyroid hyperfunction.
4. If the diagnosis of hyperthyroidism remains unclear after these initial tests, more expensive,
sophisticated and time – consuming tests may be required, e.g. A TRH test (thyrotropin releasing hormone).
Serum TSN is determined before and after an i/v injection of 500 mkg of synthetic TRH. Normally,
there is a rapid rise in TSH of 5 to25 mkU/ml, reaching a peak in 30 min and returning to normal by
120 min.
In patients with hyperthyroidism TSH release remains suppressed, even in response to
injected TRH, because of the inhibitory effects of the elevated free T4 and T3 on the pituitary
thyrotroph cells.
The diagnosis of infiltrative ophthalmopathy when hyperthyroidism is or recently was
present is not difficult. The diagnosis is less certain if the patient is not or never was hyperthyroid
orbital ultrasonography or computed tomography is the best procedure to confirm the diagnosis of
ophtalmopathy such as orbital pseudotumor and orbital tumors.
Other forms of hyperthyroidism.
Toxic adenoma and toxic multinodular goiter (Plummer’s disease)
One or more thyroid nodules occasionally hyperfunction autonomously for unknown reasons.
The excess T3 and T4 inhibit the hypothalamic – pituitary axis, stopping TSH production and
decreasing production of hormone in the rest of the thyroid. RAI uptake in the hyperfunctioning
nodule is increased while in the rest of the gland, it is decreased. Multinodular goiter with or
without hyperthyroidism is more common in older people. Neither toxic multinodular goiter nor
toxic adenoma is associated with LATS, exophthalmos, or the pretibial myxedema found in Grave’s
disease. Since nodules often produce selective increases in T3 levels, determination of the serum
total T3 should be included in the thyroid function tests selected for evaluation of nodular goiter.
Toxic adenoma and multinodular goiter are treated surgically or with radioiodine.
T3 toxicosis. Both T3 and T4 are regularly increased in patients with hyperthyroidism.
Increases in serum T3 are usually somewhat greater proportionally compared to T4, probably
because of both increased thyroidal secretion of T3 and increased peripheral conversion of T4 to
T3. In some thyrotoxic patients, only T3 is elevated; this condition is called “T3 toxicosis”. It is
difficult to diagnose because T3 is not measured by the ordinary thyroid function tests, but requires
a specific RIA. The criteria to establish the diagnosis are:
1) symptoms and signs of hyperthyroidism;
2) normalT4 and 131I uptake;
3) nonsuppressible 131I uptake;
4) failure to release TSH in response to TRH;
5) elevated serum T3.
T3 toxicosis may be seen in any of the natural disorders producing hyperthyroidism, including
Graves’ disease, multinodular goiter, and the autonomously functioning solitary thyroid nodule. If
T3 toxicosis continues untreated, the patient eventually develops the typical laboratory
abnormalities of hyperthyroidism; i.e., elevated T4 and 131I uptake. This suggests that T3 toxicosis
is an early manifestation of ordinary hyperthyroidism and should be treated as such.
Thyrotoxicosis fastitia.
This syndrome of hyperthyroidism results from self-administration of thyroid hormone;
patients (commonly medical or paramedical personnel) may be surreptitiously taking T4 or T3.
Laboratory evaluation will vary accoringly. If the disorder is caused by ingestion of preparations
containing T4, the serum T4 will be elevated. When ingestion of T3 is the cause, serum T4 will be
below normal. In either case, serum T3 levels will be increased, particularly when preparations
containing T3 are the causative agnts; there will be no goiter.
Excess TSH produced by a pituitary tumor can cause secondary hyperthyroidism through
overproduction of thyroid hormone. Hyperthyroidism secondary to metastatic embryonal carcinoma
or choriocarcinoma is due to the TSH-like properties of human chorionic gonadotropin (HCG).
Struma ovarii is generally benign ovarian teratoma containing predominantly thyroid tissue.
Approximately 5 % of the patients with struma ovarii develop hyperthyroidism. Treatment involves
removal of teratoma.
Treatment.
I.
1. Antithyroid drugs.
2. Drugs to ameliorate thiroid hormone effects .
131
II.
I- therapy
III.
Surgery.
I.
1. Antithyroid drugs
Propylthiouracil (PTU) and methimazole (MML) are effective inhibitors of thyroid hormone
biosynthesis. PTU also inhibits extrathyroidal conversation of T4 to T3.
The usual starting dosage is 100 to 150 mg orally g 8h and for MML 10 to 15 mg when the
patient becomes eythyroid the dosage is decreased to the lowest effective amount, usually 100 to
150 mg PPU in 2 or 3 divided doses or 10 to 15 mg MML daily. In general control can be achieved
within 6 wk to 3 month. More rapid control can be achieved by increasing the dose of PPU to 400
to 600 mg /day , the risk of increasing the incidence of side effects, maintenance doses can be
continued for one year or many years depending on the clinical circumstances.
Carbinazole (merkazolile ) is rapidly converts in vivo to MML. The usual starting dosage is
10 to 15 mg orally q 8h, maintenance dosage is 10 to 15 mg/ daily. The incidence of
agranulocytosis appears to be higher for carbimazole than for eighter PPU or MML.
Adverse effects include:
- allergic reactions;
- nausea;
- loss of weight;
- fever;
- arthritis, hepatitis;
- anemia, thrombocytopenia;
- agranulocytosis (in < 1% of patients).
If the patient allergic to one agent, it is acceptable to go to other, but there is a chance of cross
sensitivity. In case of agranulocytosis, it is unacceptable to go to another agent, and more definitive
therapy should be invoked, such as radioiodine or surgery.
2. Some manifestations of hyperthyroidism are ameliorated by adrenergic antagonists - β –
adrenergic blocking drugs.
Propranolol has had the greatest use phenomena that can be improved: tachycardia, tremor,
mental symptoms, heat intolerance and sweating (occasional), diarrhea (occasional), proximal
myopathy (occasional).
II.
Radioactive sodium iodine (131I)
It can be used in patients > 40 yr. of age, because 131I might cause thyroidal or other neoplasm or
gonadal damage.
There are only two important untoward effects of 131I therapy: persistent hyperthyroidism and
hypothyroidism.
III.
Surgery is used: - in patient <21 yr. who should not receive radioiodine;
- in persons who can not tolerate other agents because of hypersensitivity or other problems;
- in patient with very large goiters (100 to 400 gm) (normal thyroid weights 20gm);
- in some patients with toxic adenoma and multinodular goiter;
- hyperthyroidism during pregnancy;
- recurrent hyperthyroidism after course of antithyroid treatment.
Precautions:
- patient must be euthyroid before operation.
Results of the surgery:
- normalization of thyroid gland function;
- postoperative recurrences (2-9 %);
- hypothyroidism (in about 3 % of patient the first years and in about 2 % with each succeeding
year);
- vocal cord paralysis;
- hypoparathyroidism.
Iodine is used in preparing the patient for surgery. Surgical procedures are more difficult in patients
who previously have undergone thyroidectomy or radioiodine therapy.
Treatment endocrine ophthalmopathy include:
- steroid therapy: prednisolone 20 – 40 mg daily;
- electrophoresis with glucocorticoids or KI;
- aloe, FIBS;
- dehydration therapy;
- cavinton, piracetam;
- lateral tarsorrhaphy: when there is corneal ulcer due to inability to close the lids;
- extra – ocular muscle surgery: to correct persistent diplopia.
Thyroid storm.
Thyroid storm is a life- threatening emergency requiring prompt and specific treatment.
In is characterized by abrupt onset of more severe symptoms of thyrotoxicosis, with some
exacerbated symptoms and signs atypical of uncomplicated Graves disease:
- fever;
- marked weakness and muscle wasting;
- extreme restlessness with wide emotional swings;
- confusion;
- psychosis or even coma;
- hepatomegaly with mild jaundice;
- the patient may present with cardiovascular collapse or shock.
Thyroid storm results from:- untreated or inadequately treated thyrotoxicosis
It may be precipitated by:
- infection;
- trauma
- surgery;
- embolism;
- diabetic acidosis;
- fright;
- toxemia of pregnancy;
- labor;
- discontinuance of antithyroid medication;
- radiation thyroiditis.
Treatment of thyroid storm;
Iodine-30 drops Lugol’s solution/day orally in 30g 4 divided doses; or 1 to 2 gr. sodium iodide
slowly by i/v drip.
Propylthiouracil (merkazolil) - 900 to 1200 mg/day orally or by gastric tube.
Propranolol - 160mg/day orally in 4 divided doses; or 1mg slowly i/v g 4h under careful
monitoring; a rate of administration should not exceed 1mg/min; a repeat 1mg dose may be given
after 2 min i/v glucose solutions .
Correction of dehydration and electrolyte imbalance cooling blanket for hypertermia.
Digitalis if necessary.
Treatment of underlying disease such as infection.
Corticosteroids-100 to 300mg hydrocortisone/day i/v.
Iodine in pharmacological doses inhibits the release of T3 to T4 within hours and inhibits the
organification of iodine, a transitory effect lasting from a few days to a week (”escape
phenomenon”.)
Indications (it is used for)
- the emergency management of thyroid storm;
- thyrotoxic patients undergoing emergency surgery;
- preoperative preparation of thyrotoxic patients selected for subtotal thyroidectomy /since it also
decreases the vascularity of the thyroid gland.
It is not used for routine treatment of hyperthyroidism. The usual dosage is 2 to 3 drops of satured
potassium iodide solution orally tid or dig 1300 to 600 mg/day; or 0,5gr sodium iodide in 0,9%
sodium chloride solution given i/v slowly g 12h.
Complication of iodine therapy include:
- inflammation of the salivary glands;
- conjunctivitis;
- skin rashes;
- a transient hyperthyroidism (iod-BASEDOW phenomenon) (it can be observed in patients with
nontoxic goiters after administration of iodine-contrast agents).
Antithyroid drugs
Doses of PPU of 450-600 mg/day or greater 800 to 1200mg/day are generally reserved for the
patient with thyroid storm, because such doses block the peripheral conversation of T4 to T3.
β-adrenergic blocking drugs. Propranolol rapidly decreases heart rate, usually within 2 to 3 h when
given orally and within minutes when given i/v.
Hypothyroidism (myxedema)
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:
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) surgical removal, total thyroidectomy of thyroid carcinoma, subtotal thyroidectomy
(hypothyroidism occurs from 25 to 75 of patients in different series);
2) 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) during or after therapy with propylthyouracil, methimazole, iodides or beta-blockers;
4) 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);
5) trauma;
6) 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.
Tumor;
Infarction;
Infiltrative process;
Trauma;
Drugs (reserpin, parlodel).
3. Peripheral hypothyroidism:
- peripheral tissue resistance to thyroid hormones;
- decreasing of T4 peripheral transformation into T3 (in liver or in kidneys) ;
- production of antibodies to thyroid hormones.
Congenital:
- Maldevelopment –hypoplasia or aplasia;
- Inborn deficiencies of biosynthesis or action of thyroid hormone;
- 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, polyneuropathy, encephalopathy, coma).
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 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 T4 are normal, but serum TSH is elevated. The therapy may provide the
patient with 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.
Diagnostic of hypothyroidism is based on:
1) history;
2) clinical features;
3) blood analysis: anemia; hypercholesterolemia;
4) levels of thyroid hormone: both serum T4 and T3 are decreased (but in 25% of patients with
primary hypothyroidism may be normal circulating levels of T3);
5) ECG;
6) examination of tendon reflexes;
7) ultrasonic examination;
Differential diagnosis of primary and secondary hypothyroidism:
1) 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) 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.
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.
Treatment of hypothyroidism
Diet №10.
Regimen is not restricted
etiologic
Therapy of
the cause
Pathogenetic
replacement therapy
Thyroid
hormones
symptomatic
Treatment
of complications
1. Diet №10.
2. Regimen is not restricted.
3. 1) replacement therapy:
- 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);
- synthetic preparations of :
T4 (l-thyroxine)
-
T4 is preparation of choice, because it produces stable serum levels of both T4 and T3.
Absorption is fairly constant 90 to 95% of the dose. T3 is generated from T4 by the liver.
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.
- 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.
- 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.
- The dosage should be minimum that restores TSH levels to normal (though this criterion
cannot be used in patients with secondary hypothyroidism).
- 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) 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
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 T3 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 T4 reflect a different pattern of serum T3
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:
- beta-blockers (should be used in patients with tachycardia and hypertension) in the dose of
20 – 40 - 60 mg/day;
- hypolypidemic agents;
- vitamins (A, B, E);
- 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.
Myxedema coma.
It is a life-threatening complication of hypothyroidism, which is extremely rare in warm climates
but not uncommon in cold areas.
Precipitating factors include:
- exposure to cold;
- infection;
- trauma;
- drugs that suppress the CNS.
Myxedema coma characteristics include a background of long-standing hypothyroidism with
extreme hypothermia (temperatures 24 to 32), areflexia, seizures, CO2 retention, and respiratory
depression caused by decreased cerebral blood flow. Severe hypothermia may be missed unless
special low reading thermometers are used. Rapid diagnosis (based on clinical judgement, history,
and physical examination) is imperative because early death is likely.
Treatment of myxedema coma.
It is treated with large doses of T4 (250-500 mkg I/v bolus 3 – 4 times a day) or T3 if
available (40 – 100 mkg I/v bolus 3 times a day), because TBG must be saturated before any free
hormone is available for response. The maintenance dose for T4 is 50 mkg/day I/v and for T3 10 20
mkg/day I/v until the hormone can be given orally.
The patient should not be rewarmed rapidly because of the threat of cardiac arrhythmia.
Hypoxemia is common, so PaO2 should be measured at the outset of treatment. If alveolar
ventilation is compromised, immediate mechanical ventilatory assistance is required.
Thyroiditis
The various types of thyroiditis encompass a heterogeneous group of inflammatory disorders of
diverse etiologies and clinical features. With all forms of thyroiditis, destruction of the normal
architecture of the thyroid follicular occurs, yet each disorder has distinctive histologic
characteristics. For the purposes of understanding the clinical manifestations, thyroiditis is
classified according to either the severity or duration of illness using the following scheme:
1.
Acute thyroiditis.
2.
Subacute thyroiditis:
- subacute granulamatous thyroiditis;
- subacute lymphocytous thyroiditis.
3.
Chronic thyroiditis:
- Hashimoto thyroiditis;
- Ridel struma.
4.
Specific thyroiditis.
5.
Thyroiditis caused by mechanical or physical factors.
Acute thyroiditis
Etiology
Acute thyroiditis it is an acute bacterial inflammation due to a bacterial pathogen, most
commonly staphylococcus aureus, streptococcus hemolytica,streptococcus pneumonie, of anaerobic
streptococcal organisms. Infection due to other bacterial pathogens, such as salmonella and
escherichia coli have been reported, as well as fungal infections such as coccidiodomycosis.
Infection occurs either secondary to hematogenous or lymphatic spread, or as a result of direct
introduction of an infective agent by trauma. Persistent thyroglossal duct abnormalities have also
been associated with acute thyroiditis.
Clinical features
Fever, chills and other systemic signs or symptoms of abscess formation are present. Anterior
neck pain and swelling are usual, with pain occasionally radiating to the ear or mandible.
The physical examination suggests the presence of an abscess, with erythema of the skin,
marked tenderness to palpation, and at times fluctuance.
Laboratory tests
Leucocytosis with a left shift, increased ESR are usually present. Thyroid hormone
concentrations in blood are normal, although hyperthyroxinemia has been reported.
Treatment
Patient should be treated at surgical department. Parental antibiotics should be administered
according to the specific pathogen identified. If fluctuance is present, incision and drainage might
be required. Bacterial thyroiditis must be treated early and aggressively, since abscess formation
can occasionally dissect downward into the mediastinum. Recurrences of the disorder are very rare.
(Duration of the treatment must be nearly 1,5-2 month).
Subacute thyroiditis
It is an acute inflammatory disease of the thyroid probably caused by a virus.
Subacute granulomatous thyroiditis (giant cell thyroiditis) SAT.
Etiology
SAT is most likely viral in origin .The specific agent responsible for the disorders is not
known, although coxsackie virus, adenovirus and the mumps, echovirus, influenza and Epstein-Barr
viruses have been implicated in the etiology.
A genetic predisposition is likely because of the association of HLA-BW 35
histocompatibility antigens.
Clinical features
The most common symptom is unilateral anterior neck pain, often associated with unilateral
radiation of pain to the ear or mandible. Pain is often proceeded by a few weeks prodrome of
myalgias, low-grade fever, malaise and sore throat. Dysphagia is also common. Symptoms of
hyperthyroidism (such as tachycardia, weight loss, nervousness, and diaphoresis occur in up to 50%
of patients as the disorder processes, pain can migrate to the contralateral side.
Physical examination discloses an exquisitely tender, very hard, nodular enlargement, which
is most often unilateral. Tenderness is often so extreme that palpation is limited. Bilateral
tenderness and goiter can occur as well. Tachycardia, a widened pulse pressure, warm skin and
diaphoresis are also observed when hyperthyroidism is present.
Laboratory findings.
Early in the disease we can find an increase in T4, a decrease in RAI uptake (often 0),
leucocytosis and a high ESR. After a several weeks, the T4, is decreased and the RAI uptake
remains low. Full recovery is the rule; rarely, patients may become hypothyroid.
Treatment
An acute phase lasts from 4-8 weeks, during which treatment is symptomatic (aspirin 600 mg
q 3-4 h, prednisolone 10-20 mg orally tid; after 1 week prednisolone can be tapered by 5 mg every
2-3 days; thus glucocorticoids are usually not required for longer than several weeks. Symptoms of
hyperthyroidism are effectively controlled by the use of beta-blockers).
Following the acute phase euthyroidism is restored, and the thyroid becomes depleted of
stored hormone. Patients can either remain euthyroid or progress to hypothyroid phase. It rarely
lasts longer than 2-3 months, and during this phase thyroid hormone replacement in the form of
levothyroxine 0,10-0,15 mg/day should be given. After several months of treatment T4 can be
discontinued.
Following the hypothyroid phase recovery occurs, and the normal histologic features and
secretory capacity of the thyroid are restored.
Subacute lymphocytic thyroiditis (silent thyroiditis)
A subacute disorder occurring most commonly in women , often in the postpartum period,
characterized by a variable, but mild degree of thyroid enlargement, absence of thyroid tenderness,
and self-limited hyperthyroid phase of several weeks to several months, often followed by transient
hypothyroidism but with eventual recovery to the euthyroid state.
Etiology
Recent evidence suggests on:
1) autoimmune component (because of autoantibodies observed);
2) genetic predisposition (this is a significant prevalence of HLA-DRW3 and HLA-DRW5
histocompatibility agents);
3) viral etiology (viral antibody titers are rarely elevated);
Clinical features.
Hyperthyroid symptoms are frequent and vary from mild to normal. (Postpartum thyroiditis
occur 6 weeks to 3 months after delivery).
Physical examination usually discloses a mildly enlarged, diffuse, firm, nontender goiter it has
been reported that up to 50 % of patients do not have goiter.
Laboratory findings
Serum total and free T4 and T3 are elevated. Biopsies reveal lymphocytic infiltration as seen
in Hashimotos thyroiditis.
Thyroid autoantibodies are positive in greater than 50 % of patients.
Treatment
Hyperthyroid phase lasts from 6 weeks to 3 month. Treatment is conservative, usually
requiring only B-adrenergic blockers with propranolol.
Euthyroid interval lasts for 3-6 weeks.
During hypothyroid period (it usually lasts no longer than 2-3 months thyroid hormone
supplementation with T4 0,10-0,15 mg/day may be required. Following the hypothyroid phase
patients usually remain clinically euthyroid.)
Chronic thyroiditis.
Hashimoto thyroiditis (chronic lymphocytic thyroiditis) HT
Etiology
HT is an organ - specific autoimmune disorder, a chronic inflammation of the thyroid with
lymphocytic infiltration of the gland generally though to be caused by autoimmune factors.
It is mire prevalent (8:1) in woman than men and is most frequent between the ages of 30 and
50 . A family history of thyroid disorders is common, and incidence is increased in patients with
chromosomal disorders, including Turners, Down and Klinefelters syndromes. Histologic studies
reveal extensive infiltration of lymphocytes in the thyroid.
The basic defect underlying this disease suggests an abnormality in suppressor T lymphocytes
that allows helper T lymphocytes to interact with specific antigens directed against the thyroid cell.
A genetic predisposition is suggested because of the frequent occurrence of the HLA- DR5
histocompatibility antigen in patients with HT.
Clinical features
HT is characterized by a wide spectrum of clinical features, ranging from no symptoms and
the presence of small goiter to frank myxedema.
Occasionally patients complain of a vague sensation of tightness in the area of the anterior
neck or mild dysphagia. In general, however, thyroid enlargement is insidious and asymptomatic.
Symptoms of hypothyroidism may or may not be present, depending on the presence or absence of
biochemical hypothyroidism.
Physical examination usually discloses a symmetrically enlarged, very firm goiter, a smooth
or knobby consistency is common. Occasionally patients present with a single thyroid nodule.
A small group of patients have a form of HT termed primary idiopathic hypothyroidism,
goiter is usually absent in this group.(atrophic form of HT).
Yet a small subset of patients(probably 2-4%) present with hyperthyroidism and have socalled hashitoxicosis (hypertrophy from of HT).
Laboratory findings
1) early in the disease a normal T and high titers of antithyroid (antimicrosomal) antibodies can
be detected. Late in the disease, the patient develops hypothyroidism with a decreased in T and
antibodies in this stage are usually no longer detectable;
2) the thyroid scan typically shows a irregular pattern of iodine uptake;
3) fine-needle biopsy of the nodule or enlarging area should be done to rule out a coexistent
neoplasm.
Treatment
1) treatment of HT requires lifelong replacement with thyroid hormone to correct and prevent
hypothyroidism. The average oral replacement dose with l-thyroxine is 100 to 150 mkg/day;
2) glucocorticoids have been reported to be effective in HT when true is a rapidly enlarging goiter
associating with pressure symptoms;
3) symptomatic therapy
Ridel thyroiditis
Etiology
This extremely rare inflammatory disorder is of uncertain etiology, and earlier suggestions
that it might be a fibroid variant of HT have not been substained.
Clinical features
Clinically, Ridel thyroiditis presents with pressure symptoms, and on examination an
extremely hard , immobile thyroid gland is palpated The thyroid can be uniformly enlarged, or only
one lobe might be affected. The disorder can be associated with other focal sclerosing symptoms,
including retroperitoneal and mediastenal fibrosis and ascending cholecystitis.
Laboratory findings
1. Thyroid function tests show hypothyroidism in approximately 25 % of patients.
2. Thyroid antibodies are usually negative.
3. The thyroid scan shows decreased uptake in involved areas.
Treatment
- is surgical for those patients in whom symptoms of obstruction occur.
- Thyroid hormone is required for treatment of hypothyroidism, but thyroid hormone alone
will not result in goiter shrinkage.
Iodine-defcit disease of thyroid gland:
– a diffuse euthyroidic (nontoxic) goiter is the diffuse enlargement ofthyroid gland without its
disfunction;
– nodular euthyroid (colloid) goiter;
– functional autonomy of thyroid gland and thyrotoxic adenoma; – iodine-defcit hypothyrodism (at
the sharply expressed iodine defcit).
Day’s necessity in an iodine (WHO, 2005)
Age group or physiological state
Necessity in iodine, mkg per
day
Neonates (from 0 to 1 year)
50
Children of young age (from 1 to 5 years)
90
Children of school age (from 6 to 12 years)
120
Adults
150
Pregnant and breast-feeding women
200
A goiter is the pathological enlargement of thyroid gland without clari-fcation of its functional
state. The size of thyroid gland is determined by its examining, palpation and measuring a volume
by ultrasonic investigation (USI). By international norms, in the case of using of USI in adults (over
18 years) a goiter is diagnosed, if volume of gland is more than 18 ml in women, and more than 25
ml in men.
Classifcation of goiter (WHO, 2001)
0 There is no goiter (the sizes of parts do not exceed the sizes of distal phalanx of large fnger of the
inspected person)
1 A goiter is palpated, but is not visible at normal head position. Nodular formations which do not cause
the enlargement of the gland belong to this class
2 A goiter is palpated and is visible at normal head position
Formula for the calculation of thyroid gland volume by the data of USI
Volume = [(Tl × Wl × Ll) + (Td × Wd × Ld)] × 0,479 The volume of every part is
counted up by multiplying of thickness (Т), width (W) and length (L) with the coeffcient of
correction on the ellipse structure of part (0,479). The volume of all gland consists of volumes of its
parts; the volume of the isthmus is disregarded usually.
The normal thyroid gland volume in children and teenagers (97-percentil; from data of
USI) [WHO, 2001]
ABS (m2) 0,8
Girl
3,4
Boys
3,3
0,9
4,2
3,8
1,0
5,0
4,2
1,1
5,9
5,0
1,2
6,7
5,7
1,3
7,6
6,6
1,4
8,4
7,6
1,5
9,3
8,6
1,6 1,7
10,2 11,1
9,9 11,2
ABS is the area of body surface which is calculated by the nomogram or by a formula (M is
body mass in kilograms, H is height in centimetres):
ABS = М0,425 × H0,725 × 71,84 × 10 - 4
Epidemiological criteria of estimation (assessment) of iodine-defcit degree
Criteria
Population
Easy
Frequency of goiter
(%) by the data of
palpation
Frequency of goiter
(%) increase of
volume of gland from
data of USI
Concentration of iodine
in urine (median,
mkg/l)
Frequency of the
TSH level > 5
mIU/ml at neonatal
screenning
Level of
thyroglobulinum in a
blood (median, ng/ml)
Degree of iodine-defcit
Middle
Heavy
schoolboys
5,0–19,9 %
20,0–29,9 %
> 30,0 %
schoolboys
5,0–19,9 %
20,0–29,9 %
> 30,0 %
schoolboys
50–99
20–49
< 20
babies
3,0–19,9 %
20,0–39,9 %
> 40,0 %
children
adult
10,0–19,9
20,0–39,9 %
> 40,0
Spectrum of iodine-deficiency pathology (WHO, 2001)
Age periods
Inwardly-uterine
period
New-born
Children and
teenagers
Adults
For any age
Iodine-defcit pathology
• Abortions
• Stillborn
• Innate anomalies
• Increasing of perynatal death rate
• Increasing of child’s death rate
• Neurological cretinism:
mental backwardness
deaf-and-dumb
squint
• Mixedemic cretinism:
mental backwardness undersized (low height)
hypothyroidism
• hypothyroidism
neonatal
psycho-motor violations
• Violation of mental and physical development
• Goiter and its complication
• Iodine-inducted thyrotoxicosis
• Goiter
• hypothyroidism
• Cognitive function disorders
• Increase of absorption of radio-active iodine at
nuclear catastrophes
Methods of prophylaxis of iodine-defcit diseases
– a mass iodine prophylaxis is a prophylaxis in the scale of population; it is carried out by
addition of iodine in the most widespread food stuff (kitchen salt);
– a group iodine prophylaxis is a prophylaxis in the scale of certain groups of the high risk of
the IDD development: children, teenagers, pregnant and breast-feeding women. It is carried out by
the regular prolonged reception of medicaments which contain the physiological doses of iodine;
– an individual iodine prophylaxis is the prophylaxis of individuals by the prolonged reception
of medicaments which contain the physiological doses of iodine.
Histological classifcation of thyroid gland tumors (WHO, 1988)
1. Epithelial tumors 1.1. Benign tumors
1.1.1 Follicular adenoma:
• normofollicullar
• macrofollicular
• microfollicullar
• trabecullar solid
1.1.2 Others
1.2 Malignant
1.2.1 Follicular carcinoma:
• minimum invasive
• wide invasive
oxyfphilic cellular variant light cellular variant
1.2.2. Papillary carcinoma: papillar microcarcinoma
encapsulated variant follicular variant diffusesclerosis variant oxyphilic cellular variant
1.2.3. Medullary carcinoma:
mixed medullar-follicular carcinoma
1.2.4. Undifferentiated (anaplastic) carcinoma
1.2.5. Other carcinomas
2. Unepithelial tumors:
thyroid sarcoma
malignant hemangiothelioma
3. Malignant lymphoma
4. Mixed tumors
5. Secondary tumors
6. Unclassifed tumors
List of diseases with the single nodules of thyroid gland
which is necessary to differentiate
Primary thyroid gland damage
Adenoma
Carcinoma
Cyst
Thyroiditis autoimmune
Lymphoma
Previous hemithyroidectomy
Cyst of thyroid-tongue duct
Thyroid hemiagenesy
Non thyroidic damage
Lymphadenopathy
Adenoma or prothyreoid cyst
Cyst-like hygroma
Carotid aneurism
Metastases
Clinical classifcation of thyroid gland cancer
TNM – classifcation of differentiated thyroid gland cancer
(actual since 01.01.2003)
T – primary tumor
Тх – conclusion about a primary tumor is impossible;
T0- primary tumor is not found;
Т1 – tumor size is to 2 cm, localized in a gland;
Т2 – tumor size is more than 2 cm and to 4 cm, limited by the gland capsule;
Т3 – tumor size over 4 cm, localized only in a thyroid gland, or tumor of any size with minimum
extrathyroid spreading (by an invasion in M. sternohyoіdales or in parathyroid muscles and
cellular tissue);
Т4а – tumor spreads outside the thyroid gland capsule with the invasion in one or a few of such
anatomic structures: hypodermic cellular tissue, trachea, throat, gullet, recurrence nerve
T4b – tumor infltrate paravertebral fascia, vessels of mediastinum and surrounds a carotid artery
* multifocal tumors not depending on their histological analysis must be marked by the letter of
“m”, thus the gradation “Т” is determined by the tumor of most size.
N – regional lymphatic nodules (lymphatic nodules of neck and mediastinum) (LN)
Nх – conclusion about the regional LN damage is impossible;
N0 – metastases in regional LN is not found;
N1 – metastases in regional LN;
N1а – damage of pretracheal, paratracheal, laryngeal LN;
N1b – damage of other neck LN uni- or bilateral, contralateral on both sides or only on opposite
and/or superior LN of mediastinum.
** pT, pN, pM categories which specify on morphological confrmation of the Т, N, M factors.
*** pN0 – is proposed after conducting of selective lymphadenectomy and histological investigation
usually from 6 LN and more. In case if in investigated LN is not determined metastatic process,
but their amount does not arrive at 6, pN0-stage have to be appropriated.
М – distant metastases
Мх – conclusion about distant metastases is impossible;
М0 – distant metastases are not determined;
М1 – there are distant metastases.
Ultrasonic signs of nodular formation in thyroid gland
True cyst
Clear limited, spherical, echo-negative, non-echogenic formation of regular shape
with even and thin walls, with homogeneous incorporations, has a capsule
Nodes with focal There is a node in thyroid lobule with presence of hypoecho-cystic changes
genic areas, in which blood fow is absent at coloured echodo-plerography. Has a clear capsule
Colloid node Nodes formation in thyroid gland with expressed hypoecho-genic, has a clear
capsule, on periphery hydrophillic halo-rim can be determined (rim is low
echogenic, width 1–2 mm, located around the formation)
Adenoma
Nodes formation of round form with clear contours, encapsulated, of decreased
echogenic
Adenocarcino Thyroid gland formation with unclear contours, dense structure, of decreased
ma
echogenic with the presence of microcal-cinats in formation and (or) absence or
unclear capsule. A suspicious node does not change during pressure on it by an
ultrasonic sensor. Enlarged regional lymphatic nodes as hypoechogenic formations
of round or oval form are often determined
References
Main literature
1. Endocrinology. Textbook/Study Guide for the Practical Classes. Ed. By Petro M. Bodnar: Vinnytsya: Nova Knyha Publishers, 2008.-496 p.
2. Basіc & Clіnіcal Endocrіnology. Seventh edіtіon. Edіted by Francіs S. Greenspan, Davіd G.
Gardner. – Mc Grew – Hіll Companіes, USA, 2004. – 976p.
3. Harrison‘s Endocrinology. Edited J.Larry Jameson. Mc Grew – Hill, USA,2006. – 563p.
4. Endocrinology. 6th edition by Mac Hadley, Jon E. Levine Benjamin Cummings.2006. –
608p.
5. Oxford Handbook of Endocrinology and Diabetes. Edited by Helen E. Turner, John A. H.
Wass. Oxford, University press,2006. – 1005p.
Additional literature
6. Endocrinology (A Logical Approach for Clinicians (Second Edition)). William Jubiz.-New
York: WC Graw-Hill Book, 1985. - P. 232-236. Pediatric Endocrinology. 5th edition. –
2006. – 536p.
7. Thyroid Disordes (Aclevelend Clinic Guide) by Mario Skugor, Jesse Bryant Wilder
Clevelend Press,2006. – 224p.
Lecture prepared assistant, c.m.s. Chernobrova O.I.
It is discussed and confirm on endocrinology department meeting
" 31 " august 2012 y. Protocol № 1.