Transcript THyroid_gland1

Thyroid gland diseases.
Ethiology. Pathogenesis.
Diagnostics. Clinical pattern.
Complications. Principles of
treatment. The role of a doctordentist in early diagnostics and
prophylaxis
N. Bilkevych
Structure and location of thyroid
gland
Physiological actions of thyroid
hormones
Protein metabolism – stimulation of protein synthesis;
Carbohydrate metabolism – acceleration of their resorption from
intestine and consumption by a liver;
Fat metabolism - acceleration of lipolysis, cholsterol synthesis and
metobolism;
Liquid exchange - intensification of water evacuation by kidneys
Mineral homeostasis – regulation of Са, К, Р, Сl metabolism.
Increased oxygen consumption with all tissues (except of brain
tissue, spleen and testes);
Increased heat production;
Increased amount of catecholamine receptors in myocardium;
Regulation of respiratory centre;
Stimulation of erythropoiesis;
Stimulation of bone tissue formation and resorption.
Influence of thyroid
hormones on an
organism:
Nervous system and psychic
Cardiovascular system
Digestive system
Reproductive system
Skin and intertguments
Musculosceletal apparatus
Endemic goitre
This is a disease manifested
with thyroid gland enlargement.
It develops in certain
biogeochemical regions
characterized by iodine
deficiency in the environment
Ethiology
• Iodine deficiency is the main obvious factor
• Additional factors:
• deficiency of microelements cobalt, copper, fluorine,
zinc, molybdenum (participate in iodine metabolism);
Influence of strumogens – substances which decelerate
biosynthesis of thyroid hormones
Hypersecretion of thyrotrophic hormone (TTH) by
hypophysis
• Diseases of digestive tract, a liver with disordered iodine
absorption.
Palpation may be
performed, if a doctor
stands behind or
before the patient,
his arms are put at
the zone of projection
of the gland
Classification of thyroid gland
enlargement (WHPO, 2001)
Degree of enlargement – 0
Goitre is absent (sizes of both lobules
don’t exceed medial phalange of human’s
thumb
Degree of enlargement - І
Thyroid gland is palpable but is not
visible in normal position of patient’s
neck: nodal formations which don’t cause
thyroid gland enlargement
Degree of enlargement - ІІ
Thyroid gland is visible in any position of
the patient
Diagnostics
•
1. Anamnesis – residence in endemic region
• 2. Palpation of thyroid gland – thyroid gland
is enlarged, painless, homogenous, mildelastic
• 3. Level of thyroid hormones: Т4,Т3 normal, ТТH normal or increased
3. Ultrasound examination of thyroid gland
Nodal goitre
Treatment
• 1. Thyroid hormones – L-thyroxin - 50-100
мcg/d;
2. Iodinum preparations – 100-200 мcg/d
• Prophylaxis of iodine defficiensy
• Iodinum-containing products (salt, bred, milk);
2. Iodinum preparations:
iodide potassium, lipiodol
100-200 мcg/d.
Diffuse toxic goitre (DTG)
Epidemiology
Spreading of thyrotoxicosis is about 0,5 %
DTG often develops in the age 20-50 years
Females develop this disease in 5-7 times
more often than males
Ethiology and provoking factors
stress;
Infectious diseases;
insolation;
smocking;
Inflammatory processes in thyroid
gland
Hormonal disbalance
heredity
Pathogenesis
• Deficiency of T-supressors
• CD4+, CD8+
• T- and B-lymphocytes recognizing thyroid
gland antigens
• antigenspecific stimulation of Blymphocytes
• Production of stimulating antibodies to
TTH receptors
Clinical pattern
Complaints
• Nervous system –tearfulness, depression, deranged
sleep, irritability, oversweating
Cardiovascular system – Permanent palpitation, periodical
intermissions, dyspnea
• Metabolism – poor tolerance to heat, low body weight
while appetite is increased, muscular weakness
Digestive tract - increased appetite; abdominal pain;
periodical diarrhoea
Ophthalmopathy – feeling of protrusion of eyes,
dacryagogue; photophobia
Interguments – brittle hair, loosing hair.
Objective examination
 Red dermographism.
 Cardiovascular system – tachicardia, extrasystoly, atrial
fibrillation;
 Intensification of І heart sound, systolic murmur,
 Heart failure;
 Systolic arterial hypertension
 Sex glands – Disorders of menstrual function and
problems with pregnancy in females, impotence in males
 Nervous system – Emotional lability, irritability;
 Tremor of the body (symptom of «telegraph post»)
especially nails of hands (Mary symptom).
• Metabolism – subfebrile body temperature,
skin is warm
Low body weight.
Ostheoporosis.
Skin is warm and moist, mild, velvet-like;
Pretibial myxedema
• Thyroid gland is enlarged, of solid-elastic
consistency, systolic murmur above it
• Sex glands – mastopathy, gynecomastia
Ophthalmopathy
• Exophthalmos
* Dalrimpl’s sign (wide eye slits)
* Graefe’s sign (white space above cornea if a patient changes point
of view from up to down)
* Mebius sign (convergention disorders)
* Elinek’s sign (eyelids hyperpigmentation)
* Stellwag’s sign (rare blinking)
* Rosenbach’s sign (tremor of closed eyelids)
* Kocher’s sign – exposure of the sclera between the lower edge of
the upper eyelid and the upper edge of the iris when the eyes are fixed on
the upwardly moved object
Laboratory and instrumental
examination
• ECG: synus tachicardia, extrasystoly,
paroxysmal tachycardia, atrial fibrillation;
Ultrasound examination of a heart: high heart
output;
Rogr - cardiomegaly
• Metabolism – Increased serum Ca, excretion
of Ca with urine
• Digestive tract – Changes of indexes of liver
function
Ocular symptoms
Grefe’s sign
Degrees of severity of thyrotoxicosis
Mild
 Heart rate - less than 100 b/min
 Body mass defficiensy - less than 10 %
 Work capacity - preserved or slightly limited
Moderate




Heart rate - 100 - 120 b/min
Body mass defficiensy - 10 - 20 %
Changes of other organs and systems - ophthalmopathy
Work capacity - decreased
Severe
 Heart rate - more than 120 b/min, atrial fibrillation
 Body mass defficiensy - more than 20 %
 Changes of other organs and systems - ophthalmopathy;
dystrophy of parenchimal organs
 Work capacity - lost.
Diagnostics of DTG
Anamnesis
Provoking factors
Clinical pattern
Signs of thyrotoxicosis and diffuse enlargement of thyroid
gland
Laboratory tests
1) Common and free Т3 і Т4 are increased;
2) Increased level of common Т3 and normal Т4 (Т3 –
thyrotoxicosis)
3) Decreased level of thyrotrophic hormone (TTH)
4) Increased consumption of radioactive iodinum J131 with
thyroid gland
5) High level of antibodies to TTH receptors
Instrumental diagnostics
1) Ultrasound examination of thyroid gland
(enlargement and diffuse
decreased density);
2) Scintigraphy (insuspiction on retrosternal
goitre and in nodal goitre)
3) Puncture biopsy of thyroid gland is
executed for diagnostics of all nodal
formations in the gland
Laboratory and instrumental
examination
• ECG: synus tachicardia, extrasystoly,
paroxysmal tachycardia, atrial fibrillation;
Ultrasound examination of a heart: high heart
output;
Rogr - cardiomegaly
• Metabolism – Increased serum Ca, excretion
of Ca with urine
• Digestive tract – Changes of indexes of liver
function
Ultrsound examination of thyroid
gland
Radioisotopic scanogrm of thyrid
gland
Puncture biopsy of thyroid gland
Treatment
Antithyroid preparations
(propilthiouracil, tiamazol (merkasolil)
within 1-2 years
Mercasolil (5 mg) – 30-60 mg per os,
gradually decrease dosage till 5-15
mg.
Beta-adrenobloquers (metoprolol 50200 mg/d, bisoprolol 5-10 mg/d,
propranolol 80-120 mg/d
Thyrotoxic crisis
Clinical manifestation
 Acute beginning;
 Nervous excitation or psychosis, fear of death;
 Skin is hot and moist, chande of profound sweating on
skin dryness, face is hyperemud, cianosis of limbs,
tongue and lips are dry.
 Muscular weakness, adynamia, pareses;
 Tachicardia, atrial fibrillation, elevation of BP with its
following sudden dropacute left entricular failure;
 Nausea, vomiting, diarrhoea
 Lab tests
Anemia, leukocitosis, decreased hematocrit; elevated Т3
and Т4
Treatment
 Inhibition of production and secretion of thyreoid hormpones;
 Inhibition of nervous system irritation;
 Restoration of adrenal glands function;
 Correction of cardiovascular disorders;
 Normalization of voter and salt metabolism acid-alkaline
balance;
 Treatment of hypoxia, hypertermia
Hypothyreosis
A disease caused by prolobged
permanent thyroid hormones
deficiency with following
decrease of metabolism and
functional disorders in
different organs and systems
Face in hypothyreosis
Hypothyreosis in bnewborns
Pretibial myxoedema
Pretibial myxedema
Clinical pattern
Complaints
• Metabolism – body mass gain
• Skin – dryness, induration and change of color (“waxlike”), rugged face features, enlargement of foots,
speech is not clear, decreased hearing.
 Nervous system - somnolence, indisposition, depression,
decreased memory and intellect, frequent headaches,
dizziness; sensitiveness to cold, parestesias, deranged
vision.
 Musculoskeletal system – musculaer pains and crumps,
weakness.
• Cardiovascular system – pain in heart
region, dyspnea in physical load.
• Digestive system – constipation,
decrease appetite, nausea
• Respiratory system – frequent
bronchitis exacerbations, pneumonias
(body temperature is normal).
• Urogenital system – decreased
diuresis, pyelonephritis, decreased
potention in males, menstrual-ovarial
cycle disorders in females.
Objective examination
• Metabolism - hypothermia, overweight
Skin – dry, cold, yellow, it is nit possible to
make skin fold, symptom of dirty elbows
and колін; dryness and brittlessness of
hair, psilosis, loosing of external parts od
eyebroves; nails are sick, with streaks; face
is pastous, enlarged lips and a tongue with
teeth pattern, hoarse voice
Myxedematous edema (myxaedema)–
accumulation of gucosaminoglacals
(hialuronic and chondroitinsulfate acids), with
accumulation of liquid and sodium in tissues
(skin, subcutaneous fat, vocal slits, mucous
memvranes.
Nervous system – disordered coordination,
poor vision.
Digestive system –tonque enlqrgement with
teeth patter on its sides, hepatomegaly,
dyskinesia of bile dicts and intestine, ascites.
Cardiovascular system - bradicardia,
extrasystoly
Apex beat is low, relative cardiac dullness
borders are displaced, weak heart sounds,
systolic murmur at the apex, signs of
heart failure. BP low or normal.
Respiratory system – superficial breathing,
pleuricy.
Thyroid gland – is of normal size or
slightly enlarged,mild or of moderat
density, painless.
Laboratory and instrumental
diagnostics
• Blood – hyperlipoproteidemia, increased level of
cholesterol and triglicerides. Anemia (normochromic,
hypochromic iron-deffiicency or В12- irondeffiicency)
Nervous system - Eectroencephalography: decreased
amplitude of waves, narroving of vision fields,
increased intraocular pressure.
Musculoskeletal system – osteoporosis, sinovial fluid.
Cardiovascular system - ECG: low voltage, sinus
bradicardia, disordered conduction ( P-Q
prolongation), extrasystoly.

Ultrasound of a heart – pericardial effusion, left
ventricular wall sickness.
Digestive system – achlorhydria and authimmune
gastritis.
Urogenital system - decreased diuresis, renal blood
flow and glomerular filtration, moderate proteinuria.
Dry hear
Falling of external
eyebroves hair
Periorbital edema
Edematous face
dry skin
Diagnostics
Changes of Т3, Т4, ТТH.
Subclinical hypothyreosis – increased TTH,
normal Т4.
Primary hypothyreosis – increased TTH,
decreased Т4.
Secondary hypothyreosis – decreased TTH,
decreased Т4 thyroliberin test is negative
Tertiary hypothyreosis – decreased TTH,
decreased Т4 thyroliberin test is positive
Treatment
Ethiological
treatment of the cause
Pathogenetic
thyroid hormones
1) poor Т4 (levothyroxin, L-thyroxin, euthirox)
– for prolonged замісної treatment;
2) poor Т3 (thriiodtironin) – is used for
diagnostics;
3) Combined preparations (tireocomb,
tireotom, novotirol) – is difficult to choose
proper dosage.
Hypothyroid coma
Causes : unproper treatment of hypothyreosis
Provoking factors: overcooling, infections, physical trauna,
operations, myocardial infarction, stress, bleeding, usage of
tranquillisers
Clinical manifestation: gradual beginning; affection of
nervous system (weaklness, somnolence, inhivited
conscioussness), hypothermia, cardiovascular disorders
(marked bradicardia, weak heart sounds, hypotension),
respiratoryt disorders (bradypnoe, hypercapnia), ishuria,
dynamic intestinal obsruction.
- 3) lab tests: anemia, increasd ESR, low serum level of Т3 and
Т4, hyperpotassiemia, acidosis, hypoxia.
Treatment
1.
Corticosteroids – for prevention of adrenal insufficiency
(hydrocortison 100-150 mg or prednisolon 30-50 mg i/v.
2.
200 мcг of thyroxin, glucous 40% - 60 ml, ISS 500 мл, 5%
ascorbic acid 5 0 i/v.
3.
Oxygen. Artificial lung ventilation.
4.
In edema and high BP – diuretics (lasix 2 ml i/m), in hypotesion
- mesaton 1% - 0,5-1,0 ml i/v, corglivon 0,06% - 1,0.
5.
Antibiotics.
•Thank you!