Thyroid. Structure and functions. Thyroid thyroid hormones presentation Presentation of thyroid hormones
Date: 10/11/16
The thyroid gland and its hormonal functions. Diseases in violation of the function of the thyroid gland. Measures for the prevention of thyroid diseases in the Republic of Kazakhstan.
The thyroid gland (glandula thyroidea
The thyroid gland (glandula thyroidea) is an endocrine gland that synthesizes a number of hormones necessary to maintain homeostasis.
PATHOLOGY
Clinical manifestations thyroid diseases are caused either by excessive or insufficient production of thyroid hormones, or by excessive production of calcitonin and prostaglandins (for example, with medullary carcinoma - a calcitonin-producing tumor), as well as symptoms of compression of the tissues and organs of the neck of an enlarged thyroid gland without impaired hormone production (euthyroidism).
Five degrees of enlargement of the thyroid gland:
About degree- the gland is not visible during examination and is not determined by palpation;
I degree- when swallowing, the isthmus is visible, which is determined by palpation, or one of the lobes of the thyroid gland and the isthmus are palpated;
II degree- both lobes are palpable, but on examination, the contours of the neck are not changed;
III degree- the thyroid gland is enlarged due to both lobes and the isthmus, visible when viewed as a thickening on the anterior surface of the neck (thick neck);
IV degree- goiter large sizes, slightly asymmetric, with signs of compression of nearby tissues and organs of the neck;
V degree- extremely large goiter.
CAUSE OF THYROID DISEASES
- stress
- increased level of solar activity
- hereditary predisposition
- iodine deficiency
- premature or late puberty,
- violations menstrual cycle,
- anovulation,
- infertility,
- not carrying a pregnancy,
- pathology of the fetus and newborn.
Thyroid function disorders in the form of hypo- and hyperthyroidism are observed with its various pathologies:
- Graves' disease;
- nodular toxic goiter;
- multinodular toxic goiter;
- subacute thyroiditis;
- asymptomatic thyroiditis;
- iodine-induced thyrotoxicosis.
Thyrotoxicosis (hyperthyroidism)
increased levels of thyroid hormones.
Most often, thyrotoxicosis syndrome develops with diffuse toxic goiter (disease
Graves-Basedow),
multinodular toxic goiter,
subacute thyroiditis,
with an overdose of thyroid hormone preparations, etc.
Clinical manifestations of thyrotoxicosis syndrome include damage to various organs and systems .
Heart rhythm disturbances (tachycardia, extrasystole, paroxysmal atrial fibrillation)
Arterial hypertension
Increased excitability, tearfulness
sleep disorder
Tremor of outstretched fingers, tremor of the whole body
Unsteady stool, abdominal pain
Weight loss
Subfebrile body temperature (temperature rise up to 37-38°C)
Hot skin, sweating
increased appetite
muscle weakness
Impaired glucose tolerance
Exophthalmos (protrusion of the eyeball)
diffuse alopecia
Diffuse toxic goiter (Graves-Basedow disease)
Graves' disease is a systemic autoimmune disease characterized by a persistent pathological increase in the production of thyroid hormones, usually in combination with a diffuse enlargement of the thyroid gland and extrathyroid disorders (endocrine ophthalmopathy).
Endocrine ophthalmopathy - manifested by the expansion of the palpebral fissure, patients rarely blink,
pretibial myxedema manifested by hyperemia of the skin of the anterior surface of the lower leg, in this area are formed edema and tissue compaction.
In most cases, this symptomatology is accompanied by itching in the anterior surface of the lower leg.
Characteristic for acropathies is a thickening of the phalanges of the fingers due to swelling of the dense tissues of the phalanges and periosteal bone formations.
At x-ray examination periosteal formations of bone tissue (phalanges of the fingers, bones of the wrist) resemble bubbles of soap suds
Hypothyroidism
Hypothyroidism Syndrome- decreased hormone production
Most common causes hypothyroidism- chronic autoimmune thyroiditis. due to thyroid surgery
irradiation,
lack of iodine
taking certain medications.
Puffiness of the face
Swollen tongue, with imprints of teeth along the edges
Alopecia (hair loss on the head), thinning of the eyebrows, eyelashes
chilliness
Pastosity of the legs
Fat metabolism disorders (increased levels of triglycerides, LDL)
Menstrual irregularity
There are primary, secondary and tertiary hypothyroidism.
If the decrease in thyroid function occurs due to a lack or absence of the stimulating effect of thyroid-stimulating hormone (TSH) or releasing hormone (TSH-RG), then we are talking about secondary and tertiary hypothyroidism pituitary or hypothalamic genesis, respectively (at present, these forms are often combined into one - secondary hypothyroidism).
In the primary form the process leading to the development of hypothyroidism is localized directly in the thyroid gland (a congenital defect in the development of the thyroid gland, a decrease in the volume of its functioning tissue after surgery / inflammation, destruction by radioactive iodine or a tumor, etc.).
nodular goiter
Nodules in the thyroid gland occur as a result of iodine deficiency. They are distinguished by their autonomy, since the hormones of the pituitary and hypothalamus do not act on them. Often, such autonomous nodes synthesize hormones with increased activity, then symptoms similar to Graves' disease develop. If the nodule is very small, conservative treatment is prescribed. In severe cases, carry out surgical intervention or treatment with radioactive iodine.
Diagnostics
- General blood analysis
- Blood chemistry
- Hormonal blood test (TSH, T4 free, T3 free, etc.)
- Immunological blood test (AT to TPO, AT to TG, AT to TSH receptors, etc.)
- ECG, Cardiovisor, Cardiocode, 24-hour ECG and blood pressure monitoring
- Thyroid ultrasound
- Elastography thyroid gland - a new method of soft tissue imaging based on differences
characteristics of elasticity, allows you to more clearly differentiate malignant tumors and
other educations.
- Thyroid scintigraphy can show - the whole organ has an increased function
- or in the gland there is a node with increased function (one or more hyperfunctioning nodes).
HYPOTHALAMO-ADENOGYPOPHISAL-THYREOID OSTIREOLIBERIN
HYPOTHALAMUS
thyrotropin
adenohypophysis
THYROID
TARGET ORGANS
T3 and T4
STAGES OF THYROID HORMONE SYNTHESIS AND SECRETION
1. Capture of iodide from blood plasma by thyrocytes2. Iodization of thyroglobulin with the formation
mono- and diiodotyrosines
3. Formation of tri - and tetraiodothyronines
5. Accumulation of thyronins in colloid
6. Endocytosis of thyroglobulin colloid through
apical membrane of thyrocytes
7. Gyrolysis of thyroglobulin by thyrocyte protease
8. Secretion of iodothyronines into the blood
THYROID HORMONES
1. Iodine-containing:thyroxine
Triiodothyronine
2. Iodine Free:
Thyrocalcitonin
Participate in the regulation of all types of metabolism,
processes of growth and differentiation of tissues, organs
Increase the intensity of oxidative processes,
energy expenditure of the body
Stimulate the development and function of the reproductive system
Participate in the regulation of development nervous system and her
excitability
Increase heat generation in tissues and temperature
body
PHYSIOLOGICAL EFFECTS OF IODINE-CONTAINING HORMONES
Hypofunction in childhood - cretinism(mental and physical retardation), myxedema
((mucous edema)
Hyperfunction - thyrotoxicosis (Graves' disease),
symptoms: bulging eyes, irritability, emaciation,
increased appetite, irritability, tremor, etc.
The lack of iodine in water, soil, products leads to
decrease in thyroid function, with its growth
tissues - the so-called endemic goiter.
METABOLIC EFFECTS OF THYROID HORMONES
CARBOHYDRATE METABOLISMACTIVATION OF GLUCOSE ABSORPTION IN THE INTESTINE
- ACTIVATION OF GLYCOGENOLYSIS AND GLYCOLISIS IN THE LIVER
- POTENTIZATION OF THE EFFECTS OF INSULIN
- ACTIVATION OF UTILIZATION OF GLUCOSE IN MUSCLE AND FAT TISSUE
FAT METABOLISM
- FAT MOBILIZATION (LIPOLYSIS) FROM ADIPOSE TISSUE, ITS REDUCTION
MASSES
- ACTIVATION OF SYNTHESIS, TRIGLYCERIDE CONCENTRATION
-ACTIVATION OF CHOLESTEROL SYNTHESIS AND OXIDATION
- REDUCED SERUM CHOLESTEROL
PROTEIN METABOLISM
- ACTIVATION OF PROTEIN SYNTHESIS IN MYOCARDIA AND SKELETAL MUSCLES
- ACTIVATION OF PROTEOLYSIS IN OTHER TISSUES Cretinism
18 year old
young woman MYXEDEM
OR
HYPOTHYROISIS Very big
goiter
with congenital
hypothyroidism exophthalmos
(bulging eyes)
at
hyperthyroidism SICK
BAZEDOVA
DISEASE,
operated
Five times “Evolution simply could not
refrain from not
loading calcium in one role
after another"
MAIN FUNCTIONS OF CALCIUM
Is the main integral part bones andteeth, providing their rigidity;
Ensures membrane integrity and
maintaining their normal permeability, because
calcium ions promote tight packing
membrane proteins;
Is one of the secondary intermediaries
regulatory influences on cells;
Provides a process for the release of mediators in
synaptic cleft;
MAIN FUNCTIONS OF CALCIUM
Starts the process of muscle contraction;Participates in the conduction of nerve impulses;
Participates in the regulation of ion channels
cells, regulation of excitability and cellular
electrogenesis;
Participates in the regulation of the activities of a number of
enzymes, being a cofactor;
Necessary for the normal functioning of the cell genome;
It is an important factor in hemocoagulation;
MAIN FUNCTIONS OF CALCIUM
Involved in the regulation of the secretion of manyhormones (parathyrin, calcitonin, insulin,
catecholamines, pituitary hormones);
Activates with insulin intake
glucose into cells
Participates in the process of fertilization;
Involved in the regulation of acid-base balance
balance;
Participates in the maintenance of osmotic
balance;
MAIN FUNCTIONS OF CALCIUM
Provides mast cell stabilizationinhibits the release of histamine
manifestations of inflammation, allergic reactions and
pain;
Participates in the formation of the immune response;
Reduces blood cholesterol;
Participates in the regulation of thoracic secretion
milk;
Participates in phagocytosis, cell migration, their
association with the extracellular matrix.
THREE CALCIUM REGULATORY HORMONES
–Parathyroid hormone parathyrin
(parathyroid hormone)
–
Thyroid hormone - calcitonin
(thyreocalcitonin)
–
The kidney hormone calcitriol
vitamin D)
Parathyroid glands (according to Guyton, 2006)
Parathyroid glandson a surface
thyroid gland
PARATIRIN (84 a.c.)
CHROMOGRAIN A
chief cells
acidophilic cells
PARATHYRIN LIKE
PROTEIN (141 a.a.)
The main effects of parathyroid hormone
1. Activation of osteoclasts and leaching of calcium frombones
2. Increased absorption of calcium in the intestine and
kidneys
3. Stimulation of synthesis in the kidneys of calcitriol
4. Hypercalcemia
Other effects of parathyrin
Pronounced inotropic effect. Parathyrinstimulates heart contractions;
The hormone raises blood pressure;
Parathyrin increases glomerular filtration;
The hormone has a weak contra-insular effect on
carbohydrate metabolism;
Stimulates secretion of hydrochloric acid and pepsin in
stomach
In almost all cells, parathyrin increases the removal
calcium from the cytoplasm to the extracellular environment or
intracellular depot;
With excessive secretion, it inhibits spermatogenesis, leading to
hyperlipoproteinemia
MAIN EFFECTS OF CALCITONIN
BLOOD>Ca2+
CALCITONIN
R, Sa
BONE
P, Ca, Mg
Intestines
Ca
Bud
Effects of Calcitonin
1.Suppression of osteoclast activity andbone resorption;
2. Stimulation of osteoblast activity,
bone matrix synthesis, uptake
calcium and phosphate by bone tissue;
3. Decreased calcium and
phosphate in the blood;
Effects of Calcitonin
4. Suppression of calcium reabsorption in the kidneysand phosphate, sodium and water. diuretic,
natriuretic, calcium and
phosphaturic effects;
5. Decreased secretion of gastrin and hydrochloric
acids in the stomach;
6. Decreased secretion of trypsin and amylase
pancreas;
Effects of Calcitonin
7. Reducing the secretion of calcium in the intestine,increased secretion of water, sodium, potassium and
chloride;
8. Analgesic effect;
9. Dipsogenic effect;
10. Suppression of prolactin secretion
11. Stimulation of the synthesis of calcitriol in the kidneys
12. Inhibition of macrophage migration
13. Vasodilating effect
SUMMARY
main physiological rolecalcitonin is normal
ensuring the formation of the structure
skeleton during growth, pregnancy
and lactation, when the need for tissues
increases sharply in calcium Albrecht Dürer
(1512, Germany)
Madonna and Child Lucas Cranach the Elder
(Germany, 1525)
Madonna and Child Dirk Boats
(1450, Netherlands)
Madonna and Child and
Saints Peter and Paul Jean Fouquet
(1460, France)
Madonna and Child in
surrounded by angels Correggio
(1501, Italy)
Madonna with saints P. Batoni
(1740, Italy)
Madonna and Child
MAIN MILESTONES IN THE HISTORY OF CALCITRIOL STUDIES
1650 - Glisson - description of the development of rickets (English b-n)1920 - Mellanby - anti-rachitic effect of fish oil
due to a fat-soluble vitamin;
1924 - Steenbock and Nelson - UV rays hinder development
rickets;
1925-1930 - McCollum et al. - anti-rachitic properties
inherent in vitamin D3;
1926 - Windaus et al. – UV rays act on ergosterol,
which is converted to vitamin D3;
1935 - Windaus et al. – release of vitamin D3
1970 - Fraser and Kodicek - active is synthesized in the kidneys
vitamin D3 metabolite
FORMATION OF CALCITRIOL
UV - INSOLATION7-dehydrocholesterol in
SKIN
LIVER
VITAMIN - D3 - cholecalciferol
Vitamin D
contact
plasma protein
BUD
25(OH)D3
1.25 (OH)2 D3
or CALCITRIOL
24, 25 (OH)2 D3
→ calcitroic acid
REGULATION OF CALCITRIOL FORMATION
PTGHYPOPHOSPHATEMIA
PARATHYRIN
25 (OH)D3
Calcitonin
Insulin,
estrogen,
prolactin,
Somatotropin
Mechanism of action of calcitriol
Sa2+
Calcitriol
Membrane
receptor
Secondary
intermediaries
Membrane
conveyor
Ca2+
+
calcium binding
protein
Nucleus
Ca2+
calcium
pump
MAIN EFFECTS OF CALCITRIOL
BloodCa++
PARATHYRIN
CALCITRIOL
Bone
Bud
Ca++
R
Ca++
R
Intestines
Ca++
Р, Mg2+
EFFECTS OF CALCITRIOL
1. Activation of calcium absorption andphosphate in the small intestine (duodenum)
2. Stimulation of protein stroma synthesis
bones, mineralization, remodeling
bone tissue
3. Stimulation of calcium reabsorption and
phosphate in the tubules of the kidneys
4. Suppression of the synthesis of parathyrin in
parathyroid glands
EFFECTS OF CALCITRIOL
5. Support metabolism and contractilitymuscles
6. Stimulation of the transformation of monocytes into
macrophages
7. Stimulation of proliferation and differentiation
lymphocytes
8. Promote reproductive function and
lactation
9. Neuroprotective action
slide 2
Macroanatomy of the thyroid gland
slide 3
Fascia of the neck. Blood supply to the thyroid gland.
slide 4
Hormones synthesized by thyrocytes.
1) hormones - tetraiodothyronine (thyroxine, T4); triiodothyronine (T3), reverse triiodothyronine (p-T3), diiodothyrosine (DIT) and monoiodothyrosine (MIT); 2) protein compounds - thyroglobulins. The precursor of T3 and T4 is the amino acid L-tyrosine.
slide 5
Chemical structure of thyroid hormones
slide 6
Function of iodine-containing hormones:
1. Activate the processes of energy production, accelerate the catabolism of proteins, fats and carbohydrates (basal metabolism and consumption of O2 increase, protein synthesis and activity of Na *, K *, ATPase are stimulated) 2. Increase glycogenolysis (increase in blood sugar levels) (heart rate and cardiac output increase, nervousness, irritability, muscle tremor appear and muscle hypotrophy occurs)
Slide 7
The mechanism of regulation of the synthesis of thyroid hormones
Slide 8
The main symptoms that characterize the hypofunction of the thyroid gland.
Apathy and drowsiness Decreased memory Chilliness and poor tolerance to cold Weight gain with reduced appetite Pain in the muscles Swelling of the face and extremities Hair loss, brittle nails
Slide 9
The main symptoms that characterize the hyperfunction of the thyroid gland.
Tearfulness and irritability Feeling of heat and poor heat tolerance Weight loss with increased appetite Sweating, palpitations, diarrhea. Tachycardia, tremor, eye symptoms and goiter.
Slide 10
Diagnosis of thyroid diseases
Inspection and palpation
slide 11
Radioisotope scanning (thyroid scintigraphy) (iodine-131, preferably iodine-123 and technetium-99)
slide 12
Radioisotope study of the thyroid gland
slide 13
Ultrasound examination (size, volume of lobes, echostructure) X-ray examination - soft tissue radiography and CT scan of the cervical trachea. (displacement, narrowing of the trachea and esophagus, retrosternal goiter) Biopsy of the thyroid gland (fine-needle, trepan-biopsy) under ultrasound control.
Slide 14
Thyroid ultrasound
slide 15
Study of the functional activity of the thyroid gland
Main markers: total and free thyroxine (T4) total and free triiodothyronine (T3) pituitary thyroid stimulating hormone (TSH) In latent diseases, special functions. tests (stimulating test with thyroliberin, suppression test using triiodothyronine) Achievement of recent years - more sensitive non-isotope technologies of hormonal immunoassay (systems "Amerleit", "Delphia")
slide 16
Classification
I. Congenital anomalies: a) aplasia and hypoplasia (with hypothyroidism or myxidema); b) ectopia of the gland tissue (abberant forms of goiter) c) non-closure of the lingual-thyroid duct (median cysts and fistulas of the neck) II. Endemic goiter: a) 0, I, II st. enlargement of the gland b) in form: diffuse, nodular, mixed c) in terms of functional manifestations: euthyroid, hyperthyroid, hypothyroid III. Sporadic goiter categorized according to the same parameters as endemic goiter
Slide 18
Goiter
Goiter is called an increase in the thyroid gland due to the growth of its tissue, not associated with inflammation, hemorrhage or malignant growth. The occurrence of goiter is a compensatory - adaptive reaction of the body to specific features environment.
Slide 19
Classification of thyroid enlargement
WHO (1992) About Art. - no goiter I st. - dimensions are larger than the distal phalanx of the thumb, the goiter is palpable, but not visible II st. - the goiter is palpable and visible by ultrasound: the volume of the thyroid gland in women is more than 18 ml, and in men it is more than 25 ml - goiter is diagnosed
Slide 20
endemic goiter
According to WHO, about 1 billion live in endemic areas. About 7% of the world's population suffers from endemic goiter. Endemic areas in Russia: central part, Ural, North Caucasus, Siberia, Far East
slide 21
Etiology and pathogenesis
The main reason is iodine deficiency Consumption of less than 150-300 micrograms per day leads to a decrease in the production of thyroid hormones The feedback principle causes an increase in TSH secretion Proliferation of the thyroid epithelium is stimulated (to ensure required level secretion of thyroid hormones) Compensatory increases in thyroid mass
slide 22
MorphologyThree forms of endemic goiter: diffuse, nodular (adenomatous) and mixed Histologically - diffuse micro - or macrofollicular goiter Colloidal Vascular
slide 23
Clinic
It is determined by: The functional state of the thyroid gland The size of the goiter Localization (There is no correlation between the size of the goiter and the degree of functional changes)
slide 24
With a significant iodine deficiency, hypothyroidism appears (the disease develops gradually)
Complaints: Lethargy, drowsiness, apathy, sluggishness, chilliness, memory loss, constipation On examination: "Puffiness" of the face with poor facial expressions Edema on the body and extremities Bradycardia, decreased blood pressure Inhibition of nonspecific defense factors (Hypothyroidism in early childhood can lead to a decrease in mental development up to cretinism)
Slide 25
Diagnostics
Living or living in areas of iodine deficiency In primary hypothyroidism, the level of TSH is increased The content of T3 and T4 is reduced The test with thyroliberin is positive.
slide 26
Treatment
Methods of treatment depend on the size, morphological changes and functional state of the thyroid gland Diffuse goiter - conservative treatment (thyroidin, triiodothyronine) Surgical treatment: Nodular and mixed goiter (large size, impaired function of neighboring organs) - hemithyroidectomy Multinodular or mixed goiter - subtotal resection of the thyroid gland
Slide 27
sporadic goiter
The etiology has not been finally established (the separation of sporadic and endemic is conditional) It is assumed: 1. A number of genetic factors lead to a deficiency of triglycerides 2. Food rich in strumogens-thiocyanates (cabbage, turnips, soybeans, etc.) contributes - the content of iodine and the synthesis of triglycerides decreases The lack of triglycerides includes the same mechanism for the development of thyroid hyperplasia as in endemic goiter.
Slide 28
Diagnostics
Enlarged thyroid gland (presence of a node) Palpation data Puncture with nodular goiter Additionally Functional state(T3, T4, TSH) If it is not possible to detect the location of the thyroid gland in a typical place during p / n or its unusual growth is noted - ultrasound, CT, isotope study
Slide 29
Treatment
The principles of treatment of sporadic goiter do not differ from the principles of treatment of endemic goiter. As much as possible, unchanged thyroid tissue is preserved.
slide 30
thyrotoxicosis syndrome
The term thyrotoxicosis refers to persistent hyperfunction of the thyroid gland associated with hyperproduction of thyroid hormones (T4 and T3) and endogenous intoxication Causes of thyrotoxicosis 1. Diffuse toxic goiter, as one of the manifestations of Greevs' disease (Graves' goiter) (1835 - the disease was described by Greevs; 1821 . - Peri, 1840 - Karl Basedow) 2. Toxic adenoma of the thyroid gland - Plummer's disease. 3. Multinodular toxic goiter (Greevs' disease) is a multisystem, autoimmune disease that proceeds according to the type of delayed-type hypersensitivity.
Slide 31
Diffuse toxic goiter
Occurs ubiquitously Affects predominantly females (female to male ratio 10:1) Age 20 to 50 years Autoimmune disease (occurs in individuals with a congenital defect in immune control - an inherited special recessive gene) The basis of the disease is a defect in T-suppressors Causes: infection, insolation, severe emotional stress
slide 32
T-helpers stimulate B-cells, thyroid-stimulating antibodies (TSaB) are produced. With an excess of cortisol, the control of T-suppressors is impaired
TSaB “sit” on receptors, the gland becomes under the control of antibodies Growth of the gland is stimulated More T3 and T4 are produced
Slide 33
Clinic.
The clinical picture of diffuse toxic goiter is diverse. It is determined by the severity of thyrotoxicosis. Classic Graves' triad: exophthalmos, tachycardia, goiter
slide 34
The severity of thyrotoxicosis
Mild form: moderate weight loss (by 10-15% of body weight) Nervous excitability Pulse no more than 100 beats per minute without disturbing the rhythm and function of other organs and systems Basic metabolism does not exceed + 30% Some decrease in working capacity
Slide 35
Thyrotoxicosis of moderate severity
More significant weight loss Increased nervous excitability (mild irritability, tearfulness) Tachycardia up to 100-120 beats per minute Short-term rhythm disturbances Increased systolic blood pressure, Hc I Changes in carbohydrate metabolism Gastrointestinal disorders (frequent loose stools) Basic metabolism increased to +60 %. Significant performance degradation
slide 36
Severe (visceropathic) form of thyrotoxicosis
Sharply increased nervous excitability Significant loss of body weight up to cachexia Tachycardia over 120 beats. 1 min, atrial fibrillation Heart failure, Hc-II-III Basal metabolic rate exceeded up to + 60%. Manifest changes in the cardiovascular and nervous systems Complete loss of working capacity
Slide 37
The main clinical manifestations of thyrotoxicosis
Complaints about: a feeling of heat (a lot of thermal energy is formed) Sweating, skin is hot, moist Feeling of internal trembling, trembling of hands (a small tremor of outstretched arms, eyelids with closed eyes is typical) Fussiness, anxiety, quick speech, irritability, touchiness, tearfulness, bad dream
Slide 38
Changes in the cardiovascular system:
Tachycardia An increase in systolic and a decrease in diastolic blood pressure Left ventricular hypertrophy Atrial fibrillation Eye symptoms: exophthalmos, Stelvag, Dalrymple, Kraus, Graefe, Kocher, Mobius (damage to retrobolbubar tissue)
Slide 39
Criteria for the diagnosis of "diffuse toxic goiter":
1. High level of thyroid hormones and normal or reduced levels of thyrotropin in the blood 2. Presence of thyroid-stimulating antibodies and antibodies to thyroglobulin and microsomal fraction of the thyroid gland in the blood 3. Diffuse enlargement of the thyroid gland, determined by palpation 4. Increase in volume and diffuse decrease in the echogenicity of the thyroid tissue glands on ultrasound
Slide 40
Treatment (conservative therapy is a preparation for surgery)
Emotional and physical rest Thyrostatic drugs: a) methylmazol derivatives (mercasolil, metatilin, methylmazol) b) thiuracil derivatives (propylthiuracil) Radioactive iodine (I131) after 35-40 years Inorganic iodine (Lugol's solution) Beta-blockers
Slide 41
Indications for surgical treatment
1. Failure of conservative treatment 2. Large goiter that disrupts the function of neighboring organs 3. Young age of patients 4. Intolerance to antithyroid drugs 5. Retrosternal forms of toxic goiter 6. Toxic adenoma (nodular toxic goiter)
Slide 42
Surgical treatment of thyrotoxic goiter
The amount of thyroid tissue left after resection should be individual With the removal of most of the hyperfunctioning follicular cells, the mass of the antigen decreases. The mass of the thyroid residue ranges from 3-4 to 7-8 g. The more severe thyrotoxicosis, the more glandular tissue is removed
slide 43
Operation of choice - subtotal subfascial strumectomy according to Nikolaev
Slide 44
Complications
Rare: asphyxia in tracheomalacia; air embolism; pneumothorax; infectious complications Typical: damage to the laryngeal nerves; recurrent nerve (vocal cord paresis, impaired phonation and breathing) Hypoparathyroidism Bleeding Thyrotoxic crisis
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Clinical manifestations of thyroid diseases are due either to excessive or insufficient production of thyroid hormones, or excessive production of calcitonin and prostaglandins (for example, in medullary carcinoma of a calcitonin-producing tumor), as well as symptoms of compression of the tissues and organs of the neck of an enlarged thyroid gland without impaired hormone production (euthyroidism). PATHOLOGY
About the degree of iron is not visible during examination and is not determined by palpation; I degree when swallowing, the isthmus is visible, which is determined by palpation, or one of the lobes of the thyroid gland and the isthmus are palpated; II degree, both lobes are palpated, but on examination, the contours of the neck are not changed; III degree the thyroid gland is enlarged due to both lobes and the isthmus, visible when viewed as a thickening on the anterior surface of the neck (thick neck); Grade IV goiter of large size, not sharply asymmetric, with signs of compression of nearby tissues and organs of the neck; V degree goiter is extremely large. Five degrees of enlargement of the thyroid gland:
The cause of thyroid diseases is stress, an increased level of solar activity, hereditary predisposition, iodine deficiency, premature or late puberty, menstrual disorders, anovulation, infertility, miscarriage, pathology of the fetus and newborn.
Clinical manifestations of thyrotoxicosis syndrome include damage to various organs and systems. - Heart rhythm disturbances (tachycardia, extrasystole, - paroxysmal atrial fibrillation) - Arterial hypertension - Increased excitability, tearfulness - Sleep disorder - Tremor of the fingers of outstretched hands, tremor of the whole body - Unstable stool, abdominal pain - Weight loss - Subfebrile body temperature (increase temperatures up to °C) - Hot skin, sweating - Increased appetite - Muscle weakness - Violation of the menstrual cycle - Impaired glucose tolerance - Exophthalmos (protrusion of the eyeball) - Diffuse alopecia Thyrotoxicosis (hyperthyroidism)
Diffuse toxic goiter (Graves-Basedow's disease) Graves' disease is a systemic autoimmune disease characterized by a persistent pathological increase in the production of thyroid hormones, usually in combination with diffuse enlargement of the thyroid gland and extrathyroid disorders (endocrine ophthalmopathy).
Clinical picture -Puffiness of the face -Edematous tongue, with imprints of teeth along the edges -Alopecia (hair loss on the head), thinning of the eyebrows, -eyelashes -Childness -Puffiness of the legs -Disturbances in fat metabolism (increased levels of triglycerides, LDL) -Irregular menstruation -Constipation Hypothyroidism Syndrome - Reduced Hormone Production The most common cause of hypothyroidism is chronic autoimmune thyroiditis. a consequence of operations on the thyroid gland, radiation, lack of iodine, taking certain medications. Hypothyroidism
Thyroid nodules result from iodine deficiency. They are distinguished by their autonomy, since the hormones of the pituitary and hypothalamus do not act on them. Often, such autonomous nodes synthesize hormones with increased activity, then symptoms similar to Graves' disease develop. If the nodule is very small, conservative treatment is prescribed. In severe cases, surgery or radioactive iodine treatment is performed. nodular goiter