Lecturer- assistant professor of Department of

Internal medicine #2 Panevskaya Galina

 Location - neck, anterior to the trachea, between the
cricoid cartilage and the suprasternal notch ⁄ 5th -6th
rings of trachea .
 Consists of two lobes that are connected by an isthmus.
 Normal weight in newborns 1-2 g, in adults - from 20
to 30 g.
 Highly vascular, and soft in consistency.
 Innervations: sympathetic and parasympathetic nerves

.  Lobular consists of 20-30 follicles  Follicle walls are covered one layer of epithelial cells ( thyrocytes. THYROID GLAND  Structural. А. aminopeptidase are able to produce Н2О2 for biosynthesis of thyroid hormones .functional unit of thyroid gland is follicle/ ( 20- 300мкм). Thyrocyte′s base is located on a membrane  Main function of thyrocytes is biosynthesis of thyroid hormones.  Thyropeptidase.  Basal part of thyrocyte contains receptors to thyrotropine.cells)  Apex of cell is directed to follicle cavity.

Function of thyroid gland Biosynthesis and production of two hormones .  2) organification of iodine ( with participation of TPO and H2O2). triiodothyronine (T3) .  3)condensation of iodine with tyrosine → → thyroxine (T4).  4)secretion of thyroid hormones is controlled by thyrostimulating hormone ( TSH) according principle of feed back mechanism . triiodothyronine (T3) 4 stages of biosynthesis of thyroid hormones :  1)absorption of iodides by thyroid gland and oxidation of iodides to molecular iodine.thyroxine (T4).

REGULATION OF THE THYROID FUNCTION Hypothalamic thyrotropin- releasing hormone (TRH) stimulates pituitary production of thyroid-stimulating hormone (TSH) TSH stimulates thyroid hormone synthesis and secretion. .

ENDOCRINE FEEDBACK LOOP  Thyroid hormones inhibit TRH and TSH production  Reduced levels of thyroid hormone increase basal TSH production and enhance TRH-mediated stimulation of TSH  High thyroid hormone levels suppress TSH and inhibit TRH- mediated stimulation of TSH .

formerly known as thyroxine-binding prealbumin. THYROID HORMONES TRANSPORT T3 and T4 circulate bound to plasma proteins:  thyroxine-binding globulin (TBG)  transthyretin (TTR. or TBPA)  albumin .

FUNCTIONS OF SERUM-BINDING PROTEINS  increase the pool of circulating hormones  delay hormone clearance  modulate hormone delivery to selected tissue sites .

THYROID HORMONES METABOLISM T4 is a precursor for the more (4- 5times) potent T3 and is being secreted from the thyroid gland in 20-fold excess over T3. 20% Т3 is synthesized in thyroid gland. 80% T4 is converted to T3 by the deiodinase enzymes .

brain. and thyroid gland. has a relatively low affinity for T4. has a higher affinity for T4. liver. and kidney. DEIODINASES  Type I deiodinase is located primarily in thyroid.  Type III deiodinase inactivates T4 and T3 and is the most important source of reverse T3 (rT3) . brown fat. It allows to regulate T3 concentrations locally.  Type II deiodinase is located primarily in the pituitary gland.

but their relative levels of expression vary among organs. which explains its increased hormonal potency.  After binding to thyroid hormone receptors (TRs).  Thyroid hormones bind with similar affinities to TRα and TRβ . . THYROID HORMONES ACTION  Thyroid hormones act by binding to nuclear receptors. termed thyroid hormone receptors (TRs) α and β.  T3 is bound to both receptors with 10 to 15 times greater affinity than T4. thyroid hormone induces conformational changes in the receptors that modify its interactions with accessory transcription factors. Both TRα and TRβ are expressed in most tissues.

depletion of ATP)  Activation of oxidative phosphorylation  Stimulation of glycogenolysis  Stimulation of lipolysis  Stimulation of proteins synthesis and catabolism . THYROID HORMONES PHYSIOLOGIC EFFECTS  Activation of sympathetic nervous system  Increase of metabolic rate  Increase of oxygen consumption (hypoxia.

85 nmol/l  Т3 free – 4.0-7.54-3.Normal values of laboratory methods of investigation of thyroid function  Т3 total – 1.6 nmol/l  Т4 free – 11.17 – 4.5 мЕ/ml  Кальцитонин – 0-28 nmol/l .8-24.5 – 441.8 nmol/l  Т4 total – 51.6 nmol/l  ТSH – 0.

CLASSIFICATION OF THE DISORDERS OF THYROID GLAND I. Congenital a) aplasia and hypoplasia (with hypothyrosis) b) aberrant thyroid gland c) persistent thyroglossal ductus .

CLASSIFICATION OF THE DISORDERS OF THYROID GLAND II. I. hypothyrosis with cretinism. II b) Forms: diffuse. Iodine deficiency diseases Endemic goiter a) Degree of enlargement. 0. hyperthyrosis . nodular. mixed c) Thyroid function: euthyrosis.

forms. Toxic adenoma ( solitary. multinodular) V Diffuse toxic goiter a) mild b) moderate c) severe .CLASSIFICATION OF THE DISORDERS OF THYROID GLAND III. Sporadic goiter (degree of enlargement. thyroid function) IV.


syphilis. Inflammatory thyroid diseases a) Immune inflammation  acute thyroiditis (suppurative and non-suppurative)  subacute thyroiditis (de Quervain's thyroiditis. or viral thyroiditis)  chronic thyroiditis (Hashimoto's thyroiditis and Riedel's thyroiditis) b) Infectious inflammation (tuberculosis.CLASSIFICATION OF THE DISORDERS OF THYROID GLAND VII . actinomycosis) . granulomatous thyroiditis.


postpartum)  Struma ovarii  Functioning thyroid carcinoma metastases  Ingestion of excess thyroid hormone . CAUSES OF HYPERTHYROIDISM  Diffuse toxic goiter  Toxic multinodular goiter  Toxic solitary adenoma ( Plummer′s disease)  TSH-secreting pituitary adenoma  Thyroid hormone resistance  Toxicosis of pregnancy  Thyroiditis ( subacute.

 Thyrotoxycosis is a clinical syndrome caused by negative influence of persistent excess of thyroid hormones to organism. .

Robert Graves  1840 – Karl Basedow .  1835 . Diffuse toxic goiter (GRAVES' DISEASE)  This is the most common cause of hyperthyroidism and is due to autoimmune process.

. Diffuse toxic goiter (GRAVES' DISEASE) Epidemiology  accounts for 60 to 80% of thyrotoxycosis.  occurs in up to 2% of women and in 0.  rarely begins before adolescence and typically occurs between 20 and 50 years of age.2% of men. may also occurs in the elderly.

It′s manifested by diffuse goiter and clinical syndrome of thyrotoxicosis. Diffuse toxic goiter (Graves ′disease )  Systemic autoimmune disease due to production of serum IgG – antibodies to the thyroid TSH receptor stimulating thyroid hormone production behaving like TSH.  .

 Provoking factors are stresses. and DR2 and 50% concordance is seen among monozygotic twins with 5% concordance in dizygotic twins. insolation. tobacco smoking. Etiology of Graves ′disease There is an association with HLA. infections. -DR3.В8 . .

fibrosis becomes prominent.ophthalmopathy and dermopathy are due to immunologically mediated activation of fibroblasts in the extraocular muscles and skin. Later. Diffuse toxic goiter Pathogenesis The extrathyroidal manifestations of Graves' disease . with accumulation of glycosaminoglycans. leading to the trapping of water and edema. The fibroblast activation is caused by cytokines derived from locally infiltrating T cells and macrophages. .

Diffuse toxic goiter Clinical manifestations Main complains:  Hyperactivity. irritability. dysphoria  Palpitation  Weight loss with increased appetite  Proptosis  Tremor  Diarrhea  Sweating  Fatigue and weakness .

proximal myopathy  Lid retraction or lag  Thyroid gland: diffusely enlarged. soft or slightly firmed.detectable on palpation. visible . moist skin  Hairs are fine. Diffuse toxic goiter Clinical manifestations Physical examination  Goiter  Warm. and a diffuse alopecia occurs in up to 40% of patients  Muscle weakness. systolic murmur on auscultation Enlargement of thyroid:  0 – normal size  I – larger than distal phalanx of patient’s thumb on palpation. painless on palpation . not visible  II .

Methods of thyroid gland palpation .




tearfulness. psychosis. nervousness. hyperkinesis  Tremor of fingers  Tremor of all body  Hyperreflexia  Muscle wasting  Proximal myopathy without fasciculation . Diffuse toxic goiter Clinical manifestations Neurologic  Irritability. logorrhea.

atrial fibrillation. supraventricular tachycardia)  high cardiac output (produces a bounding pulse. Diffuse toxic goiter Clinical manifestations Cardiovascular  tachycardia (sinus tachycardia. widened pulse pressure. loud cardiac sounds and systolic murmur on auscultation)  thyrotoxic cardiac myopathy – enlargement of the heart and symptoms and signs of heart failure  hypertension (by increase of systolic and drop of diastolic blood pressure) .

non-specific changes of ST segment and T wave. shortening of PR interval. sinus tachycardia advanced stage – reduction of voltage. prolongation of QRS complex. Diffuse toxic goiter ECG early stage .high voltage. atrial fibrillation .

Diffuse toxic goiter Clinical manifestations Gastrointestinal  increased motility  decreased secretion  abdominal pain  nausea and vomiting  increased stool frequency. often with diarrhea and occasionally mild steatorrhea .

permanent loss of vision) . Clinical manifestations Ophthalmopathy  Exophtalmus in 50% patients  sensation of grittiness  eye discomfort  excess tearing  proptosis (sclera between the lower border of the iris and the lower eyelid. with the eyes in the primary position. positive Mebius. peripheral field defects. Cocher and Greafae symptoms )  periorbital edema  scleral injection  diplopia  compression of the optic nerve (leading to papilloedema.



osteoporosis . Syndrome of hypermetabolism  Weight loss. increased appetite  Heat intolerance  Increase of skin temperature  Subfebrile temperature  Muscle weakness  Osteopenia.

Syndrome of Dermopathy  Pretibial myxoedema( pretibial areas are swelling.brownish in colour)  Palmar erythema  Vitiligo  Hyperpigmentation on lids  Nails and hair are brittle .


amenorrhea  Carbohydrate intolerance.  Diabetes mellitus . Affection of endocrine glands  Adrenal insufficiency  Dysmenorrhea.

weight loss to 20%. < 120 per minute . mild weakness  Moderate degree: Pulse rate > 100. Pulse rate < 100 per minute. Clinical classification  Mild form: Neurologic symptoms and signs . decrease of ability to work . ↓ diastolic BP. ↑ systolic BP. < 100 1 . weight loss to 10%.

Clinical classification  Severe form:  Pulse rate > 120 per minute  Atrial fibrillation is characteristic  Cardiac failure is prominent ( II-III degree)  Pulse pressure ↑ to 80-100 mm Hg  Weight loss is over 30%  High risk of thyrotoxic crisis .

Diffuse toxic goiter

Laboratory evaluation

 T4 and T3 are increased
 TSH is low
 Determination of TSH-R-stimulating
 Determination of thyroid peroxidase
(TPO) antibodies

Diffuse toxic goiter

The thyroid gland selectively transports
radioisotopes of iodine (123I, 125I, 131I) and
99mTc pertechnetate, allowing thyroid
imaging and quantitation of radioactive
tracer fractional uptake.

Graves' disease is characterized by an
enlarged gland and increased tracer
uptake that is distributed

Diffuse toxic goiter


Ultrasonography is used to assist in the
diagnosis of nodular thyroid disease.
In addition to detecting thyroid nodules,
ultrasound is useful for monitoring
nodule size, for guiding biopsies, and for
the aspiration of cystic lesions.

Diffuse toxic goiter Diagnosis  Biochemically confirmed thyrotoxicosis  Diffuse goiter on palpation  Ophthalmopathy  Positive thyroid peroxidase (TPO) antibodies  Positive TSH-R-stimulating immunoglobulins .

Diffuse toxic goiter Differential Diagnosis Diseases. that mimic thyrotoxicosis  Panic attacks  Mania  Pheochromocytoma  Weight loss associated with malignancy .

that cause thyrotoxicosis Nodular thyroid disease (palpation. and the finding of a pituitary tumor on computed tomography (CT) or magnetic resonance imaging (MRI) scan). radionuclide or ultrasound scan) Ectopic thyroid tissue (palpation. radionuclide or ultrasound scan) Destructive thyroiditis (palpation. radionuclide or ultrasound scan) Pituitary tumor secreting TSH (nonsuppressed TSH level. . Diffuse toxic goiter Differential Diagnosis Diseases.

BP. Diagnostics. examination of lymph nodes. Plan of examination  Interrogation (complaints). BMI. cardiovascular system etc  Inspection and palpation of thyroid gland  Ophthalmologic examination . family history (presence of autoimmune pathology in closed relatives )  Physical examination: height. weight. skin examination . present history. heart rate. pulse rate.

stimulating immunoglobulins . Diffuse toxic goiter Diagnosis  Biochemically confirmed thyrotoxicosis  Diffuse goiter on palpation and USI  Autoimmune ophthalmopathy  Positive thyroid peroxidase (TPO) antibodies  Positive TSH-R.

Diffuse toxic goiter Differential Diagnosis Diseases. that mimic thyrotoxicosis  Panic attacks  Mania  Pheochromocytoma  weight loss associated with malignancy .

radionuclide or ultrasound scan) Pituitary tumor secreting TSH (nonsuppressed TSH level. and the finding of a pituitary tumor on computed tomography (CT) or magnetic resonance imaging (MRI) scan. radionuclide or ultrasound scan) Ectopic thyroid tissue .(palpation. radionuclide or ultrasound scan) Destructive thyroiditis (palpation. . Diffuse toxic goiter Differential Diagnosis Diseases. that cause thyrotoxicosis Nodular thyroid disease (palpation.

stage of medicamental subcompensation. Endocrine ophtalmopathy of II degree. severe form . Heart failure II. Clinical diagnosis  Diffuse toxic goiter II degree. . tachysystolic form. Thyrotoxic heart. Atrial fibrillation .

thyrostatics)  Reducing the amount of thyroid tissue (subtotal thyroidectomy or radioiodine ( 131I) treatment) . Diffuse toxic goiter TREATMENT  Reducing thyroid hormone synthesis (antithyroid drugs.

After euthyroidism is restored daily dose is 50-100 mg. Once-daily dosing is possible after euthyroidism is restored (usually 2. Carbimazole or methimazole (mercazolil) is usually 10 to 20 mg every 8 or 12 h for 3-6 weeks.5-10 mg daily) (leucocytes count should be checked once a month because of possible development of leucopenia ) Duration of treatment – up to 1. Diffuse toxic goiter TREATMENT (antithyroid drugs) Propylthiouracil is given at a dose of 100 to 200 mg every 6 to 8 h for 3-6 weeks.5-2 years Combined treatment with thyrostatics and L-thyroxin ( 50 mкg) – “Block and replace” . Divided doses are usually given throughout the course.

Diffuse toxic goiter TREATMENT (antithyroid drugs) Potassium iodide Short period of effectiveness (usually up to 10 days). Is used for pre-operative treatment to suppress secretion of T3 and T4 Dose – 250 mg twice-daily. Duration of treatment – 2-4 weeks. . Glucocorticosteroids In cases of severe thyrotoxicosis or adrenocortical deficiency Dose – 20-30 mg daily (for prednisolone).

blockers Propranolol (10-20 mg to 40 mg every 6 h) or longer acting beta blockers. Diffuse toxic goiter TREATMENT  ß. such as atenolol (50 mg once a day or twice a day) or metoprolol (50 mg once a day or twice a day)  Sedatives .

counterindicating for thyroidectomy  Relapse after thyroidectomy  No patient’s consent for surgery Contraindications  Nodular goiter  Children and adolescents  Pregnancy and breast feeding . complicated thyrotoxicosis  Concomitant diseases. Diffuse toxic goiter TREATMENT Radioiodine (131I) Causes progressive destruction of thyroid cells. Indications  Severe.

particularly with atrial fibrillation  Relapse after treatment with antithyroid drugs . Diffuse toxic goiter TREATMENT Subtotal thyroidectomy Indications  Ineffectiveness of antithyroid drugs after 2 months of treatment  Very large goiter  Severe thyrotoxicosis.

Treatment – thyroid hormone + corticosteroids  Relapse of thyrotoxicosis. Treatment – thyroid hormone  Long-term hypothyroidism (autoimmune mechanisms). Diffuse toxic goiter TREATMENT subtotal thyroidectomy Possible complications of thyroidectomy  Short-term hypothyroidism (superfluous excision of thyroid tissue). Treatment – compensation of thyroid status with antithyroid drugs or radioiodine (131I) and another surgery  Worsening of ophthalmopathy  Tetany  Paresis of the recurrent laryngeal nerves  Thyrotoxic crisis .

delivery  Withdrawal of antithyroid drugs  Sympathomimetics treatment  Radioiodine (131I) treatment . Diffuse toxic goiter Thyrotoxic crisis Precipitating factors  Thyroid surgery  Infectious or inflammatory disease  Psychological stress  Intensive palpation of the thyroid  Trauma  Non-thyroid surgery  Diabetic ketoacidosis  Toxicosis of pregnancy.

accompanied by fever (up to 40°C). coma. delirium. Diffuse toxic goiter Thyrotoxic crisis Clinical manifestations Life-threatening exacerbation of hyperthyroidism. . arrhythmia. heart failure. diarrhea. seizures. tachycardia (up to 180-200 bpm). and jaundice. vomiting.

25 g intravenously every 6 h)  Propranolol (40 to 60 mg orally every 4 h.2-4 mg intravenously every 4 h)  Glucocorticosteroids (I ⁄ v Hydrocortisone 100mg 3-4 times ⁄24h. albumin. Diffuse toxic goiter Thyrotoxic crisis TREATMENT  Methimazole (mercazolil) 20-40 mg every 8 h or propylthiouracil (600 mg loading dose and 200 to 300 mg every 6 h orally)  Potassium iodide (5 drops every 6 h)  Sodium iodide (0. Prednisolone 200-300 mg within 24 h or Dexamethasone 2 mg every 6 h)  Cooling  Intravenous fluids (5% glucose. or 1. polyglucin)  Antibiotics (if infection is present) .

mostly among elderly women.  Depression of thyroid function due to different diseases  Distribution is about 12% . . Hypothyroidism  Hypothyroidism is a clinical syndrome caused by persistent decrease of influence of thyroid hormones to target tissues.

 excess of vasopressin and  deficiency of ADH . Pathogenesis of hypothyroidism  Depression of metabolic rate  Decrease of demands in oxygen  Myxoedema due to accumulation of glycosaminoglycanes.

Classification of hypothyroidism  According pathogenesis :  Primary ( due innate or acquired disorders of thyroid function )  Secondary ( because diseases of anterior hypophysis)  Tertiary (because diseases of hypothalamus)  Tissue (peripheral. transport) .

and diiodothyronine to triiodothyronine and thyroxine • defects of deiodinases function . CLASSIFICATION (CAUSES) PRIMARY Congenital  Hypoplasia or aplasia  Genetic defects of thyroid hormones synthesis • TSH-R mutation • defects of thyroid iodine uptake • defects of conversion of inorganic iodine to organic iodine • defects of conversion of mono.

amiodarone  infiltrative disorders . α-interferon. CLASSIFICATION (CAUSES) PRIMARY Acquired  chronic autoimmune Hashimoto’s thyroiditis  iodine deficiency  hypothyroid stage of subacute thyroiditis  decrease of the functioning thyroid tissue after 131 I treatment or subtotal thyroidectomy  overdosage of antithyroid drugs  p-aminosalicylic acid.

CLASSIFICATION (CAUSES) SECONDARY Hypopituitarism  tumors  ischemia or infarction  hemorrhage  pituitary surgery or irradiation  trauma  genetic forms of combined pituitary hormone deficiencies  isolated TSH deficiency or inactivity  infiltrative disorders .

CLASSIFICATION (CAUSES) TERTIARY Hypothalamic diseases  dysgenesis  tumors  trauma  encephalitis  infiltrative disorders .

. T4 or TSH. CLASSIFICATION (CAUSES) PERYPHERAL  Resistance to thyroid hormone (mutations in the TRβ gene)  Inactivation of circulating T3.

Clinical Manifestations Complaints  Tiredness. poor memory  Constipation  Weight gain with poor appetite  Dyspnea  Hoarse voice  Menorrhagia (later oligomenorrhea or amenorrhea)  Paresthesias  Impaired hearing . weakness  Dry skin  Feeling cold  Hair loss  Difficulty concentration.


Clinical Manifestations Nervous system Inhibited thinking and emotional reactions. difficult concentration. poor memory. drowsiness. retarded movements. .

Puffy face.dry and coarse. Accumulation of gialuronic acid in the skin lead to subcutaneous accumulation of water. Nail growth is retarded. often with a yellow tinge due to carotene accumulation. and falls out easily. Hair is dry. There is pallor. hands and feet (myxoedema). Peripheral edema. Clinical Manifestations Skin and mucous . difficult to manage. brittle. .

Clinical Manifestations Metabolic rate is reduced – weight gain despite poor appetite. absence of sweating . cool peripheral extremities. hypothermia.

Clinical Manifestations Cardiovascular system – dull pain in cardiac region. bradycardia. hypotension or hypertension. pericardial effusion . enlarged heart. development and progression of atherosclerosis and all atherosclerosis- associated diseases. weak sounds on auscultation.

ECG signs ECG – low voltage. especially of P. long PR interval (AV conduction disorders) and other conduction abnormalities .waves.and T.

Clinical manifestations Respiratory system  Night apnoe  Hypoxia  Hypercapnia .

Clinical Manifestations Gastrointestinal tract Suppressed appetite Enlarged tongue Constipation and meteorism (abdominal distension) due to bowel hypokinesia .

Clinical manifestations  Genito-urinary system  Dysmenorrhea. amenorrhea  Decreased libido  Galactorrhea due to hyperprolactinemia  Polycystosis of ovarii .

usually irregular and firm in consistency.goiter may be of the normal size or slightly enlarged.  Congenital dysgenesis – size is reduced or the gland is absent.  Hashimoto's thyroiditis . painless. soft. Clinical Manifestations State of thyroid gland depends of the cause of hypothyroidism  Iodine deficiency – diffusely enlarged. may be slightly painful .

as it will not detect subclinical or mild hypothyroidism.  T4 is inferior to TSH when used as a screening test. .  If TSH is elevated.  T3 measurements are not indicated. Laboratory Evaluation DIAGNOSIS OF HYPOTHYROIDISM  TSH is normal or low – pathology of pituitary or hypothalamus  normal TSH level excludes primary hypothyroidism. a free T4 level is needed to confirm the presence of clinical hypothyroidism.  presence of TPO antibodies indicates to autoimmune hypothyroidism.

Laboratory Evaluation OTHER ABNORMAL FINDINGS  Increased creatine phosphokinase  Elevated cholesterol and triglycerides  Anemia (usually normocytic or macrocytic) .

Subclinical Hypothyroidism Biochemical evidence of thyroid hormone deficiency (high TSH and normal T4) in patients who have few or no apparent clinical features of hypothyroidism .

Elderly age . L. Middle age – 1. TREATMENT Clinical Hypothyroidism Replacement of thyroid hormone.25-50 μg daily. .thyroxine combined with triiodothyronine may also be used. If patient has concomitant coronary artery disease – 25-50 μg daily. If not effective – dose increase in 25 μg every month. Most common is Levothyroxine (T4). Young age – 2-2.5-25 μg every 2-4 weeks.5 μg/kg daily. If not effective – dose increase in 12.5-2 μg/kg daily. If not effective – dose increase in 25 μg every month.

Clinical Hypothyroidism Dose adjustment and monitoring Primary hypothyroidism – the dose is adjusted on the basis of TSH levels.4 mU ⁄ l . ТSH level normally is 0. TSH responses should be measured about 2 months after instituting treatment or after any subsequent change in levothyroxine dosage. . optimal level is -0.  Other causes of hypothyroidism .5 mU ⁄ l) Clinical effects of levothyroxine replacement are often slow to appear.the dose is adjusted on the basis of T4 evaluation. ideally in the lower half of the reference range.4. Patients may not experience full relief from symptoms until 3 to 6 months after normal TSH levels are restored.5-1. with the goal of treatment being a normal TSH.

TREATMENT and MONITORING Subclinical Hypothyroidism  Monitoring of TSH and T4 (assessment every 4-6 month).  If the trend to increase of TSH and decrease of T4 is revealed. treatment is administered by starting with a low dose of levothyroxine (25 to 50 μg/d) with the goal of normalizing TSH .

which can reach 23°C  Severe bradycardia  Hypotension. . sometimes associated with seizures  Severe features of hypothyroidism  Hypothermia. Myxoedema coma Clinical manifestations  Reduced level of consciousness.

. Myxedema coma Laboratory findings  hyponatremia  hypochloridemia  hyperkaliemia  hyperuremia  acidosis.

anesthetics. antidepressants). such as drugs (especially sedatives. gastrointestinal bleeding.  Trauma  Surgery  Infections  Cooling . pneumonia. or cerebrovascular accidents. congestive heart failure. myocardial infarction. Myxoedema coma Causes Almost always occurs in the elderly  Non-treated hypothyroidism or treated hypothyroidism with poor compliance  Factors that impair respiration.

It is usually continued at a dose of 50 μg/d. Myxoedema coma TREATMENT Replacement of thyroid hormone  Levothyroxine .loading dose .  An alternative is to give L-iodothyronine (T3) intravenously or via nasogastric tube. in doses ranging from 10 to 25 μg every 4 to 12 h. .  .intravenous bolus of 500 μ g in 4 injections . It is usually continued at a dose of 75 to 100 μg/d.  Another option is to combine levothyroxine (200 ug) and liothyronine (25 μg) as a single intravenous bolus followed by daily treatment with levothyroxine (50 to 100 μg/d) and liothyronine (10 μg every 8 h).

intravenous glucose .50 mg every 6 h External warming .if the temperature is less than 30°C Ventilatory support with regular blood gas analysis is usually needed during the first 48 h Prevention of hyponatremia . Myxoedema coma TREATMENT Prevention of adrenocortical insufficiency  hydrocortisone .intravenous hypertonic saline Prevention of hypoglycemia .

nonsuppurative  Subacute (viral) thyroiditis de Quervain  Chronic thyroiditis . Thyroidites are inflammatory diseases of thyroid gland  Classification:  Acute thyriodites: purulent.

septicomycotic  Ridel’s fibrous thyroiditis (as a symptom of some systemic diseases) . Chronic thyroiditis  Autoimmune hypertrophic thyroiditis (Hashimoto’s goiter)  Autoimmune atrophic thyroiditis  Asymptomatic thyroiditis  Painless thyroiditis  Postnatal  Specific: tuberculous. syphilitic.

. Staph. more frequently caused by Str. aureus.  Unsuppurative thyroiditis is caused by ionizing radiation (radiation thyroiditis ). Usually only one lobe is affected. Acute thyroiditis  Etiology: bacterial infection.  Pathogenesis: the ways of infection are lymphogenic or hematogenic. pyogenes.

rigor.  Complications:  Abscess formation: symptom of fluctuatuion.  TG is expanded. body temperature is above 38-39°С. Hyperemia of skin over the lesion focus. phlegmon of a neck. . tachycardia. Clinical features of acute purulent thyroiditis  Acute onset. Pain irradiate to an ear and a mandible. algetic.  Fistulae may open to the front surface of a neck or to mediastinum (mediastinitis).

 Thyrotoxicosis signs: tachycardia. .  Palpatory tenderness in TG regio. Clinical features of acute nonsuppurative thyroiditis. disposition to sweating etc.

inoculation for revealing the causative agent. Addition methods of investigation  Clinical blood count (leukocytosis with shift to the left)  US of TG. .  Fine-needle biopsy.

Treatment of acute
 Hospitalization to surgical department.
 Antibacterial therapy with broad spectrum antibiotics.
Lancing and draining of abscess.
 ß-adrenoceptor blockers ( propranolol 20-40 mg 3
times a day till full liquidation of clinical
manifestations will be obtained).
 Analgesic.

Subacute thyroiditis
 Granulematous, viral, de Quervain, giantcell.
 Etiology: Coxsackie viruses, adenoviruses, mumps
viruses, flu viruses, Epstein-Barr viruses.
 Pathogenesis: Viral penetration → destruction of TG
→ Т3,Т4 releasing into blood, transient
 On the tissue level - focal granulomatous infiltration
by neutrophils and histiocytes.

Clinical features of
subacute thyroiditis
 ↑ body temperature to 38-39° С after 2-3 weeks from
ARD (viral etiology).
 Pain at the affected side of a front surface of a neck.
Pain extends to an ear or to a mandible from the same
side. Pain increases during swallowing or head
 Sometimes palpation of TG is impossible due to
strong pain.

then ↓Т3. . abrupt increasing of ESR. ↑ Т4 .  US of TG: hypoechoic focal areas.  TG Scanning (if needed) – area of inflammation (« cold» area).Additional methods of investigation  Clinical blood count: lymphocytosis.  ↑ content of fibrinogen  ↑ Т3. ↓Т4  Autoantibodies to thyroglobulin and TPO.  Hyper-γ-globulinemia.

o.  Antiinflammatory therapy:  NSAID (acetylsalicylic acid p.  SAID ( 10-14 days):  Prednisolon 30-60 mg p. . after meals in dosage 600 mg each 4 hours till disappearance of pain syndrome and decreasing of body temperature. Treatment of subacute thyroiditis  Hospitalization into an endocrinological department. after meals 1 time a day till liquidation of clinical manifestations.o.

supressors → → Т. Chronic autoimmune thyroiditis  The most common form of thyroiditis  Etiology: association with HLA antigenes: HLA DR3 and DR5 .  Lymphoid infiltration of TG. It combines with other autoimmune diseases. ↓ Т.helpers interact with native antigenes of TG cells. . F: M – 10-15:1.  Pathogenesis:  AT –autoimmune inflammation of TG.

 TG is enlarged on palpation. heterogeneous. . its structure is solid. Clinical manifestations of chronic autoimmune thyroiditis  Function of TG: gradual changes from thyrotoxicosis at the onset and consequent euthyroidism to hypothyroidism.  Frequent combination with other autoimmune or TG diseases.

 Indication of antibodies to TG tissues. TPO. .  US of TG (hypoechogenity). Addition methods of investigation  Thyroid hormones’ rate evaluation.  Fine-needle biopsy is needed for differential diagnostics with nodular goiter.

6 μg⁄kg or 100-150 μg daily. Treatment of autoimmune thyroiditis  Conservative:  Treatment of TG functional status disturbances.  Levothyroxine natrii 1.  Hyperthyroid phase: ß-adrenoceptor blockers  Hypothyroid phase: adequate replacement therapy. .