«confirm» on methodical meeting of endocrinology department a chief of endocrinology department, prof. Vlasenko M. V. “ 31 ” august 2012 y methodological recommendations icon

«confirm» on methodical meeting of endocrinology department a chief of endocrinology department, prof. Vlasenko M. V. “ 31 ” august 2012 y methodological recommendations




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MINISTRY OF HEALTH PROTECTION OF UKRAINE

Vynnitsa national medical university named after M.I.Pyrogov





«CONFIRM»

on methodical meeting of endocrinology department

A chief of endocrinology department, prof. Vlasenko M.V.


_________________

“_31_”_august___ 2012 y



METHODOLOGICAL RECOMMENDATIONS

for independent work of students

by preparation for practical classes



Scientific discipline

Internal medicine

Мodule № 1

^ Basis of Internal medicine

substantial module №1

Diagnostic, treatment and prophylactic basis of main endocrinology diseases”


Topic

^ Topic №10: Thyroididtis. Classification. Clinics. Diagnostics. Differential diagnosis. Treatment.

Course

4

Faculty

Medical № 1



Vynnitsa – 2012


^ METHODOLOGICAL RECOMMENDATIONS

for the students of 4-th course of medical faculty for preparation to the practical classes from endocrinology


1.Тopic №10: Thyroididtis. Classification. Clinics. Diagnostics. Differential diagnosis. Treatment.


2. Relevance of topic: 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 follicle occurs, yet each disorder has distinctive histologic characteristics. Thyroiditis are accompanied by unpleasant subjective feelings almost always, except the atrophy form of autoimmune thyroiditis. There is a goi­ter, sometimes nodular formation. That is why problems of diagnostics and treatment of thyroiditis are extraordinarily actual, their decision help in de­creasing of frequency of complications of this pathology.


^ 3. Aim of lesson:

- to learn etiology, pathogenesis, diagnostic criteria of thyroiditis

- to be able to fnd out the symptoms of hypothyroidism and thyroiditis from anamnestic data and information of objective inspection.

- to prescribe an adequate pathogenetic and symptomatic treatment thyroiditis, to estimate its effciency.

- to defne the working capacity of patient, tactic of clinical supervision.

- to formulate deontologyc principles of work with patients with thyroiditis.

- to develop understanding of infuencing of environmental factors on de­velopment of thyroiditis.


4. References

4.1. 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.

4.2. Additional literature

  1. 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.

  2. Thyroid Disordes (Aclevelend Clinic Guide) by Mario Skugor, Jesse Bryant Wilder Clevelend Press,2006. – 224p.



Basic Level.

1. Anatomy and physiology of thyroid gland.

2. Regulation of thyroid gland function.

3. Influence of thyroid hormones on different tissues and organs.


Students’ Independent Study Program

You should prepare for the practical class using the existing text books and lectures. Special attention should be paid to the following:

  1. Classification of thyroiditis.

  2. Thyroiditis (acute, subacute and autoimmune): etiology and pathogenesis.

  3. Acute thyroiditis: diagnostic criteria, treatment.

  4. Subacute thyroiditis: diagnostic criteria, treatment.

  5. Chronic (autoimmune) thyroiditis: diagnostic criteria, treatment.

  6. Clinic of acute, subacute and autoimmune thyroiditis.

  7. Differential diagnostics of thyroiditis with acute clinical course.

  8. Etiologic and pathogenetic treatment of thyroiditis.

  9. Modern diagnostic criteria of autoimmune thyroiditis.

  10. Prognosis and estimation of working capacity of patients with hypothy-roidism and thyroiditis.

Short content of theme



Type of thyroiditis

Etio-pathogenetic factors

Thyroiditis acute

Bacteria, fungal, parasite

Thyroiditis subacute

Viruses

Thyroiditis chronic: thyroiditis of Hashimoto; post-natal thyroiditis; lymphocytic thyroiditis of teenagers; chronic fbrotic thyroiditis (Ridel)

Autoimmune origin of illness

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.

  1. Chronic thyroiditis:

  • Hashimoto thyroiditis;

  • Ridel struma.

  1. Specific thyroiditis.

  2. 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.)


^ Differential diagnostics of acute and subacute thyroiditis

Description Thyroiditis acute Thyroiditis subacute



Etiology

Bacterial (more frequent Streptococcus pyogenus, Staphylococcus aureus, Streptococcus pneumoniae)

Viral

Anamnesis

Connection with a bacterial infection Trauma Vices of development of thy­roid-tongue duct

Connection with a previous viral infection

Thyroid gland

Rapid, more frequent asym­metric thyroid gland enlarge­ment.

Induration and pain in the projection of thyroid gland, especially at palpation An irradiation of pain in an ear, occiput, lower jaw. A skin above is red and hot; fuctua-tion can be determined

Enlarged (more frequent asym­metric), sickly, dense

Thyroid gland function

Usually not broken

Characteristic stage course: frst 1–4 weeks easy thyreotoxicosis can be, then easy hypothyroidism can be, then euthyroidism

Clinical blood test

Leukocytosis with a shift to Leukocytosis is normal.

the left. Lymphcytosis can be.

ESR is moderately promoted ESR is signifcantly increased

Ultrasonogra-phy of thyroid gland

Areas of abscess formation

A cloud-like area with reduced echogenic without a clear cap­sule, which occupies usually no less than 1/3 particles of thyroid gland, which changes sizes and localization during a supervision

Autoantibodies

Absent

Can appear on 3-d week of disease and saved during 6–12 months

Treatment

– Antibiotics parenteral – Opening of abscess and drainage

– At the exposure of vices of thyroid-tongue duct develop­ment – to remove their

– Glucocorticoid – Nonsteroid antiinfamatory preparations at easy course – At thyrotoxicosis – β-adreno-blockers

Result

Complications are possible: involuntary opening of ab­scess, neck thrombophlebitis; relapsing course at the unre-moved anatomic defects

As a rule, complete convales­cence



^ 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 so-called 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.

Diagnostic criteria of autoimmune thyroiditis

  1. The diagnosis of autoimmune thyroiditis (АІТ) can not be set only on the basis of information of palpation of thyroid gland, or also increase or decrease of its volume by the results of ultrasonography.

  2. Basic diagnostic signs, combination of which gives a possibility to set the diagnosis of АІТ, is:

– increasing volume of thyroid gland;

– a presence of increased titer of antibodies to thyroid gland tissue and

ultrasonic signs of autoimmune pathology; – primary hypothyroidism (manifestal or subclinical).

  1. In the case when hypothyroidism is determined (subclinical or mani-festal) diagnostics of АІТ gives a possibility to set nature of thyroid gland functional decline, but practically not refected on tactic of vicarious thyroid hormones treatment.

  2. Punctional thyroid gland biopsy for confrming diagnosis of АІТ is not indicated.

  3. Dynamic research of antibodies level to thyroid gland with the pur­pose to estimate development and progress of АІТ has not diagnostic and prognostive value.


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.




  1. Tests and Assignments for Self-assessment.

Multiple Choice.

Choose the correct answer/statement:

1. At patient of 37 years old, the asymmetric increase of thyroid gland of the ІІІ stage is exposed, a gland is painful at palpation, pain irradi­ates in a lower jaw. Temperature of the body 38 °С. A week ago carried a quinsy. In the general analysis of blood - ESR increased. Most reliable that patient has:

    1. Subacute thyroiditis

    2. Fibrotic thyroiditis

    3. Diffuse toxic goiter

  1. Toxic adenoma of thyroid gland

  2. Autoimmune thyroiditis

2. Patient К., 52 years, complains of the increase of body mass, weakness, constipations, worsening of memory. The indicated symptoms slowly grew during last 1.5 year. Objectively: dryness of skin, moderate edema of face and extremities, heart bounds are extended, tones are muffed, pulse - 66/min., BP is 110/70 mmHg, thyroid gland is not palpated. In a blood the exposed antibodies to thyroglobulin (+) and microsomal antigen (+++); level of thyreostimulate hormone - 15.2 mU/l. USI of thyroid gland: gland of the diminished sizes, heterogeneous structure. Set a diagnosis:

  1. Autoimmune thyroiditis, hypothyroidism

  2. Diffuse nontoxic goiter

  3. Autoimmune thyroiditis without violation of the thyroid gland function

  4. Endemic goiter

  5. Subacute thyroiditis

Answer: 1 – A. 2- A.

Real-life situations to be solved:


Patient L., 40 years old, complaints on acute pain in the region of anterior part of the neck, which irradiates into ears and mandibular, fever. During examination was found increased and painful thyroid gland, the skin is red, lymphatic nodes are increased. In blood there is leucosytosis and increase ESR. Put diagnosis and make the plan of treatment.

Answer: Acute thyroiditis. Patient have to be treated in surgical department by antibiotics. If it is necessary by surgical treatment.


Students Practical Activities.


Work 1 : Students’ group is divided into 2 sub-groups, that work near the patients’ bed: ask the patients on organs and systems, take anamnesis of the disease , anamnesis of life, make objective exam. With the teacher’s presence. In the class-room they discuss the patients, learn data of laboratory and instrumental exam. of these patients.

1.To group the symptoms into the syndromes.

2.To find out the leading syndrome and make differential diagnosis.

3.To formulate the diagnosis.

4.To make a plan of treatment.


Methodological recommendation prepared assistant, c.m.s. Chernobrova O.I.

It is discussed and confirm on endocrinology department meeting

" 31 " august 2012 y. Protocol № 1.

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