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
Мodule № 1
substantial module №1
Topic
Course
Faculty
Internal medicine
Basis of Internal medicine
“Diagnostic, treatment and prophylactic basis of
main endocrinology diseases”
Topic №10: Thyroididtis. Classification. Clinics. Diagnostics.
Differential diagnosis. Treatment.
4
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
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.
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
Thyroiditis acute
Thyroiditis subacute
Thyroiditis chronic: thyroiditis of
Hashimoto;
post-natal
thyroiditis;
lymphocytic
thyroiditis of teenagers; chronic
fbrotic thyroiditis (Ridel)
Etio-pathogenetic factors
Bacteria, fungal, parasite
Viruses
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.
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.)
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
Thyroid
gland
function
Clinical
blood test
Rapid, more frequent asymmetric thyroid gland
enlargement.
Induration and pain in the projection of thyroid Enlarged (more frequent asymgland, especially at palpation An irradiation of pain
metric), sickly, dense
in an ear, occiput, lower jaw. A skin above is red
and hot; fuctua-tion can be determined
Usually not broken
Leukocytosis with a shift to Leukocytosis is normal.
the left.
Lymphcytosis can be.
ESR is moderately promoted ESR is signifcantly increased
Ultrasonogr
a-phy of
thyroid
gland
Areas of abscess formation
Autoantibodi
es
Absent
Treatment
Result
Characteristic stage course: frst
1–4 weeks easy thyreotoxicosis
can be, then easy
hypothyroidism can be, then
euthyroidism
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
Can appear on 3-d week of
disease and saved during 6–12
months
– Antibiotics parenteral – Opening of abscess and – Glucocorticoid – Nonsteroid
drainage
antiinfamatory preparations at
– At the exposure of vices of thyroid-tongue duct easy course – At thyrotoxicosis
development – to remove their
– β-adreno-blockers
Complications are possible: involuntary opening
convalesof abscess, neck thrombophlebitis; relapsing course As a rule, complete
cence
at the unre-moved anatomic defects
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).
3. 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.
4. Punctional thyroid gland biopsy for confrming diagnosis of АІТ is not indicated.
5. 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.
I.
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:
A. Subacute thyroiditis
B. Fibrotic thyroiditis
C. Diffuse toxic goiter
D. Toxic adenoma of thyroid gland
E. 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:
A. Autoimmune thyroiditis, hypothyroidism
B. Diffuse nontoxic goiter
C. Autoimmune thyroiditis without violation of the thyroid gland function
D. Endemic goiter
E. 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.