Diseases of thyroid gland
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Transcript Diseases of thyroid gland
Chair of pediatrics with medical genetics
THEME OF LECTION:
“Diseases of thyroid gland”
Actuality
Diseases of thyroid gland occupy 2nd place after
saccharine diabetes.
Thyroid gland (TG) – one of major organs of
incretion. Alage of TG takes place on 4th week of
gestation. Thyroid tissue appears on 2th month. On
16th week TG is differentiated. There are 2 periods
of stormy growth of TG (5-7 and 12-15 years).
Hormones of TG are: thyroxin (T4) and triiodothyronine (T3). T4 has 65 % iodine. Initial product
of biosynthesis of thyroid hormones is AA –
tyrosine and iodine.
Physiology of hormones of TG
Main factor of regulation of function of TG
is TTH. Regulation takes place on principle
of feedback between hypophysis and TG.
Secretion
of
thyrotropin
of
adenohypophysis takes place under
influence a hypothalamus (thyrotropinreleasing factor).
Physiological action of thyroid hormones:
influence
on all types of metabolism;
important role in development of fetus, processes of
growth and differentiation of tissues (especially brain);
assist normal physical and mental development of
child;
strengthen lypolysis and metabolisn of
carbonhydratess, decrease maintenance of glycogen in
liver;
actively influence on a mineral and water
metabolism;
in ordinary doses have an anabolic effect, in high –
catastatic.
Hypothyroidism
Hypothyroidism – endocrine-metabolitic disease in
origin of which there is a decline or nonfunction of
thyroid gland.
Classification:
I. By the time of origin:
-congenital
-acquired
ІІ. By form:
-primary
-secondary
-tertiary
ІІІ. By degree of severity:
-easy
-intermedius
-severe
Hypothyroidism
– it is arisen up as a result of primary
defeat of thyroid gland.
Secondary – at the defeat of hypophysis (as a
result of hypopituitarism, isolated lack of TTH or
secretion of nonactive TTH). More frequent meets
at the tumours of hypophysis.
Tertiary – related to the defeat a hypothalamus
and synthesis of thyroliberine.
Primary
Hypothyroidism
I. Congenital hypothyroidism.
Etiology:
-90 % - defeat the precusor of thyroid gland on 4-9 week of
gestation (dysgenesis and ectopia);
-thyrostatic medicinal therapy (mercasolil, iodine, bromide, salts
of lithium, tranquilizers);
-autoimmune thyroiditis at mother;
-influence of different chemical substances, irradiation on fetus;
-intrauterine infections.
In 10 % of cases Congenital hypothyroidism arises up because of
genetical deficit of synthesis of thyroid hormones.
ІІ. Acquired.
Etiology:
-after ectomia of thyroid gland, as a result of autoimmune viral,
bacterial or radioimmune thyroiditis.
Pathogenesis of congenital hypothyroidism
In basis of pathogenesis is violation of
metabolism of albumens, fats and carbonhydrates.
Through the decline of synthesis of hormones of TG
there is diminishing of amount of neurons, violation
of differentiation of brain, suppression of function
of CNS. Decline of metabolic processes causes
delay of growth and forming of skeleton, processes
of metabolism are violated (hyperketonemia and
lipidemia).
For congenital hypothyroidism very important
is early diagnostics of disease (pathological changes
of CNS are reverse only to 4th week).
Clinical symtoms of congenital hypothyroidism:
In new-born:
mass of body at birth more than 4 kg;
postmaturity;
bad increase of weight;
languor, somnolence, oppression, muscular hypotonia;
trophic disorders of skin (pallor, dryness, cold on touch);
late falling off of umbilical cord;
protracted icterus, mucinous edemas;
increase of stomach, constipation;
umbilical hernia;
large language;
low pitched voice;
stridor;
amimia;
bradycardia, deafness of cardiac tones, cardiomegalia
Clinical symptoms of congenital hypothyroidism
At late diagnostic:
-delay of psychomotoric development (cretinism);
-considerable delay of growth (bone age);
-violation of sexual development;
-severe anaemia.
Easy forms of innate thyroprivia
Can be manifestated in 2-5 years or even
during sexual development. Is characterized by
the delay of growth and sexual development,
decline of intellect, the symptoms of myocardial
dystrophy, constipations, xerosis.
Diagnostic criterias of congenital hypothyroidism
-decreased concentarion of T4 in blood (N=110-225
nmole/l) and Т3 (N=2-4 nmole/l);
-increased concentration of TTH (N=1,5-20 MCED/ml);
-delay of bone age;
-scannography of TG (agenesia, ectopia, enzyme
disorders.)
Acquired hypothyroidism
Is manifestated after 1 year of life. More frequent
meets at girls.
Clinical symptoms:
-slow growth;
-delay of sexual development;
-intolerance to overcooling;
-bad appetite;
-somnolence;
-constipation;
-at examination: edema of face, rough lines, flattened
bridge of the nose, xerosis, dry and fragile hair.
Laboratory diagnostics of acquired
hypothyroidism
-decreasing of concentration of T3 and T4;
-increasing of TTH;
-expressed delay of bone age;
-determining of antithyroid antibodies;
-scanography of TG.
Treatment of hypothyroidism
L-tyroxine (thyreocomb). Initial dose – 3-5
mcg/kg, with a gradual increase each 3-5 days on 10-15
mcg to 10 mcg/kg. Treatment of congenital
hypothroidism continues to 1-3 years.
Criteria of adequacy of choice of endocrinotherapy
dose:
-pulse
-AP
-weight
-activity of child
-level of TTH, T3 and T4
-estimation of growth and bone age
Euthyroid goiter
Euthyrosis (diffuse non-toxic goitre) is euthyroid
hyperplasy of TG, which is manifestated as its
enlargement without parafunction. Enlargement of
TG is scray reaction which is directed on providing of
synthesis of enough quantity of thyroid hormones in
the conditions of iodic deficit.
Theories of origin:
inherited defects of delight and organization of
iodine;
disbalance of oligoelementss (surplus of Cu and Co);
influence of small doses of radionuclides;
hasty growth of organism.
Classification of euthyrosis
I. Endemic goitre – it is arisen up as a result of
deficit of endogen iodides and other
oligoelementss in soil.
ІІ. Sporadic goitre – arises up in endemic
districts, is provoked by the protracted use of
goitriferous preparations and influence of
ecological situation.
ІІІ. Juvenile hyperplasy of TG – provoked by
increased requirement in iodine and thyroid
hormones during sexual development.
Diagnostic criterias of severity of euthyrosis by WHO
І. On spreading of goiter (results of palpation).
ІІ. On sizes of TG (results of US).
ІІІ. On concentration of TTH.
ІV. On concentration of thyreoglobulin.
V. On mediana of iodineuria.
Epidemiological criterias of estimation of severity of
euthyrosis on frequency of determining in population
Degree of severity
Frequency of determining
No deficit
<5 %
Easy deficit
5-19,9 %
Intermedius severity
20-29,9 %
Severe deficit
>30 %
Clinical symptoms
I. Palpatory increase of TG.
ІІ. Visual increase of TG.
ІІІ. Palpatory and visual increase of TG, but it is inside m.
sternocleidomastoideus.
IV. It is outside m. sternocleidomastoideus.
V. Giant goitre.
Sizes of goitre after WHO
0 degree – a goitre is absent, size of each lobe is not bigger
than size of distal phalanx of pollex of hand of examinated
patient.
I degree –gland is palpated, but it is absent visual increase.
ІІ degree - visual increase of TG at normal position of neck.
Estimation of degree of severity of euthyrosis by
concentration of J in urine
Mediana of concentration
of J іn urine, mcg/l
100-200
50-99
20-49
<20
Наявність дефіциту J
no deficit
easy deficit
intermedius deficit
severe deficit
Plan of research at presence of goiter
Palpation of TG.
US.
Determining of level of thyroid hormones in blood.
Determining of antibodies to tissue of thyroid gland.
Determining of level of day iodineuria.
By prescriptions - punctional biopsy.
Prophylaxis of iodine-deficit
1.
2.
3.
Mass – substances with iodine are artificially
plugged in feed (salt, bread, dairy products).
Group - preparations which contain
physiological dose of iodine are used the origin
in the groups of iodine deficit risk (to put,
teenagers, pregnant).
Individual - use of products with increased
maintenance of iodine (seafood, oarweed) and
use of medications (antistrumin, potassium
iodide 200).
Requirement in J in different age
Adults – 150 mcg/day
Pregant – 200 mcg/day
Mature newborns – 15 mcg/kg/day
Premature newborns – 30 mcg/kg/day
First year children – 50 mcg/day
Children of 1-6 years – 90 mcg/day
Children of 7-12 years – 120 mcg/day
(WHO)
Treatment of euthyrosis
Always begins with prescribing of iodinated
preparations: KJ - 100 mcg/day. If on
background of treatment with preparations of
iodine there is not normalization of sizes of TG
during 6 month –L-тироксин (initial dose – 3
mcg/day, in future chosing of dose takes place
under control of determination of TTH in blood
of patient) is prescribed.
Hyperthyroidism
Diffuse toxic goitre (thyrotoxicosis, Basedow’s disease,
Graves disease) – endocrine-exchange disease in basis of
which there are hyperproduction of hormones of TG. On
the modern stage a toxic goitre is determined as
autoimmune disease at which LATS-factor is increased
(longitude action stimulator of synthesis of thyroid
hormones).
Etiology:
infections;
stresses;
psychical and physical traumas;
overheat in the sunshine
Clinical manifestations of hyperthyroidism
enlargement
of TG;
violation of activity of CNS (crossness, fussiness, enhanceable
motive activity, rapid fatigueability, emotional lability, sleep
disturbance, headache, tremor of extremities);
violation of activity of CVS (tachycardia, arhythmia, systolic
murmur, increased voltage of indents on ECG);
cachexia;
eye symptoms (exophthalmus; Graves oculopathy - lymphoid
infiltration of conjunctiva, its hyperemia and edema; Dalrimil’s
symptom - wide opening eye crack; Ellinec’s - strengthening of
pigmentation of eyelids; Zinger’s - an edema of eyelids;
Rosenbach's symptom – tremor of eyelids; Kraus’ symptom increased brilliance of eyes; Stellwag’s is the infrequent blinking
and retraction of overhead eyelid; Möbius's symptom - violation
of convergence; Graefe's sign - lag of overhead eyelid at a look
downward.
Laboratory changes at hyperthyroidism
-increasing of concentration Т3, Т4;
-decreasing of concentration of ТТH;
-bone age prevails factical on 2-5 years;
-decreasing of cholesterol in blood serum;
-CBA: leucopenia, lymphocytosis, increasing of ESR.
Features of DTG at children
-girls are more frequently ill (95 %);
-family anamnesis;
-manifestation of disease in pubertal period;
-course on background of chronic disease of
nasopharynx;
-in anamnesis – psychical trauma.
Treatment of hyperthyroidism
Mercasolil
- 30-40 mg/day during 10-15 days,
with the gradual (5 mg/week) decreasing to the
minimal maintaining dose (5 mg/day).
Propiltiouracil - initial dose – 150-300 мг/м2,
with a gradual decline to maintaining– 100 мг/м2
Duration of treatment in maintaining doses is
from 2 to 6 years.
Thyroiditis
Chronic lymphocytic, autoimmune thyroiditis
(Hashimoto’s disease).
Organospecific autoimmune disease, which is
accompanied by formation of autoantibodies
to tissue of TG. More frequent meets at
children and juvenile age. Girls are ill twice
more frequent boys.
Is characterised by lymphocytic infiltration of
TG, there can be only hyperplasia of TG on
the early stages. Disease is inherited with the
system HLA.
Clinical manifestations of Hashimoto’s disease
disease
begins during 3 first years of life, after 6
frequency is increased (max – in teens);
goitre develops gradually and without symptoms
(diffuse enlargement of TG, a surface is uneven by
touch, in course of time becomes solid with nodes);
children are irritable, easily excitative, hiperhydrosis,
hyperactive (it is possible to suspect hyperthyroidism,
but not confirmed laboratory);
clinical course is various (spontaneous diminishing and
disappearance or remain without changes during many
years);
stages of disease: hyperthyroidism (transitory stage) –
euthyrosis –hypothyroidism.
Diagnostics of Hashimoto’s disease
high titer of autoantibodies in blood serum
(more frequent AB to thyroglobuline 1:100 and
AG of microsomes >1:32);
level of T4 and TTH in blood is normal, or
increased concentration of TTH at normal level
of T4 (“compensated” hypothyroidism), or
decline of level of T4 at increased concentration
of TTH (hypothyroidism);
unclear and rough contours of TG at US;
scanning of TG is prescribed at suspicion on
forming of nodes;
biopsy – lymphoid infiltration is expressed (for
children is conducted very rarely).
Treatment of Hashimoto’s disease
Medicinal treatment depends on stage of disease
Prescriptions to surgical treatment of thyroiditis:
-symptoms of compressing and stenosis of trachea
and esophagus;
-progressive growth of goiter (in spite of
medicinal therapy);
-suspicion on malignant neoplasm.
Subacute thyroiditis
Disease of TG of inflammatory character
(for certain viral etiology), meets rarely.
Clinical signs:
sore throat and pain in the area of TG (it can
arise up also in the area of ear and jaw, can
become acute at motions of neck);
fever, weakness;
at examination – algetic and swollen TG.
Subacute thyroiditis
Diagnostics:
on early stages – concentration of T4 in blood is
moderately increased, level of TTH is decreased;
decreased absorption by TG of radionuclides;
poorly expressed and not needing correction
symptoms of hypothyroidism;
presence of symptoms of general intoxication
leucocytosis and increase of ESR;
on the late stages (2-6 months) - symptoms of
hypothyroidism.
Treatment:
Symptomatic (anaesthetic preparations – at
easy cases, steroid hormones – at severe cases)
Acute thyroiditis
Develops at acute (purulent and non-purulent)
infections of TG (more frequent staphylococcus
aureus,
β-hemolytic
streptococcus,
pneumococcus).
Clinical symptoms:
acute toxic fever;
expressed pain in the area of TG, which
increases at tension of neck;
expressed pain of TG at palpation;
hyperemia and local increase of temperature in
the area of TG;
Acute thyroiditis
Diagnostics:
-clinical picture;
-leukocytosis with prevailing of young forms;
-increasing of ESR;
-normal level of Т4 та ТТH;
-normal absorption of radioactive J;
-US of TG (determining of abscess);
-punction of TG with aspiration of content (by
prescriptions).
Treatment.
Is begun immediately. Parenteral injection of big doses of
broad spectrum antibiotics. Surgical drainage of abscess
of TG.
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