Management of patients with

thyroid diseases at
ambulance
Docent G. N. Panevskaya
Tasks of out- patient department
 Consultations/clinical examination of patients
 Laboratory and instrumental investigation to
confirm diagnosis
 Assessment of indications for hospitalization
(planned or on emergency)
 Treatment
 Education of patients, medical workers
 Dispensary observation
 ANATOMY
OF THE THYROID GLAND
 Location - neck, anterior to the trachea,
between the cricoid cartilage and the
suprasternal notch ⁄ 5th -6th rings of trachea .
 Consists of two lobes those 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
 THYROID GLAND
 Structural- functional unit of thyroid gland is follicle/ ( 20-
300мкм).
 Lobule consists of 20-30 follicles
 Follicle walls are covered by one layer of epithelial cells
( thyrocytes, А- cells)
 Apex of cell is directed to follicle cavity. Thyrocyte′s base is
located on a membrane
 Main function of thyrocytes is biosynthesis of thyroid
hormones.
 Thyropeptidase, aminopeptidase are able to produce Н2О2
for biosynthesis of thyroid hormones .
 Basal part of thyrocyte contains receptors to thyrotropine.
 Function of thyroid gland
Biosynthesis and production of two hormones - thyroxine
(T4), triiodothyronine (T3)
4 stages of biosynthesis of thyroid hormones :
 1)absorption of iodides by thyroid gland and oxidation of
iodides to molecular iodine;
 2) organification of iodine ( with participation of TPO and
H2O2);
 3)condensation of iodine with tyrosine → → thyroxine (T4),
triiodothyronine (T3) ;
 4)secretion of thyroid hormones is controlled by
thyrostimulating hormone ( TSH) according a principle of feed
back mechanism
 REGULATION OF THE THYROID
FUNCTION

Hypothalamic thyrotropine-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
 THYROID HORMONES
TRANSPORT
T3 and T4 circulate bound to plasma
proteins:
 thyroxine-binding globulin (TBG)
 transthyretin (TTR, formerly known
as thyroxine-binding prealbumin, 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% T3 is converted fromT4 by the deiodinase
enzymes
 DEIODINASES
 Type I deiodinase is located primarily in
thyroid, liver, and kidney, has a relatively low
affinity for T4.
 Type II deiodinase is located primarily in the
pituitary gland, brain, brown fat, and thyroid
gland, has a higher affinity for T4. It allows to
regulate T3 concentrations locally.
 Type III deiodinase inactivates T4 and T3 and
is the most important source of reverse T3
(rT3)
 THYROID HORMONES ACTION
 Thyroid hormones act by binding to nuclear receptors,
termed thyroid hormone receptors (TRs) α and β. Both
TRα and TRβ are expressed in most tissues, but their
relative levels of expression vary among organs;
 Thyroid hormones bind with similar affinities to TRα and
TRβ .
 T3 is bound to both receptors with 10 to 15 times greater
affinity than T4, which explains its increased hormonal
potency.
 After binding to thyroid hormone receptors (TRs),
thyroid hormone induces conformational changes in the
receptors that modify its interactions with accessory
transcription factors.
 THYROID HORMONES
PHYSIOLOGICAL EFFECTS
 Activation of sympathetic nervous system
 Increase of metabolic rate
 Increase of oxygen consumption (hypoxia, depletion
of ATP)
 Activation of oxidative phosphorylation

 Stimulation of glycogenolysis

 Stimulation of lipolysis

 Stimulation of proteins synthesis and catabolism

Normal values of laboratory methods of
investigation of thyroid function

 Т3 total – 1,54-3,85 nmol/l

 Т3 free – 4,0-7,8 nmol/l
 Т4 total – 51,5 – 441,6 nmol/l
 Т4 free – 11,8-24,6 nmol/l
 ТSH – 0,17 – 4,5 IU/ml
 Calcitonin – 0-28 nmol/l
 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. Iodine deficiency diseases
Endemic goiter

a) Degree of enlargement; 0; I; II
b) Forms: diffuse; nodular; mixed
c) Thyroid function: euthyrosis; hypothyrosis
with cretinism; hyperthyrosis
CLASSIFICATION OF THE DISORDERS
OF THYROID GLAND
III. Sporadic goiter (degree of enlargement,
forms, thyroid function)
IV. Toxic adenoma ( solitary,
multinodular)
V Diffuse toxic goiter
a) mild
b) moderate
c) severe
CLASSIFICATION OF THE DISORDERS
OF THYROID GLAND

VI . HYPOTHYROIDISM

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

VIII. Trauma of thyroid gland

IX. Thyroid carcinoma
 Thyroid carcinoma
▪Papillary (60-70% of all thyroid cancers)
▪Follicular (15%)
▪Medullary (solid)
▪Anaplastic (10%)
▪in MEN (multiple endocrine neoplasia)
syndromes
 Thyroid carcinoma
 Papillary carcinoma: females are affected two or three
times more often than males
 It is more frequent in the young, but is more
malignant in the elderly
 It is more common in patients with a history of
radiation exposure and spreads via the lymphatic
system
 Well- differentiated cancer may develop in goiters
secondary to Hashimoto‘s thyroiditis and to be TSH-
dependent
 Thyroid carcinoma
Treatment surgical (total thyroidectomy) with
postoperative radioiodine scans and
subsequent ablation of residual thyroid tissue
with appropriately large dose of 131 I
administered when the patient is hypothyroid.
TSH suppressive doses of L thyroxine
To detect serum thyroglobulin to determine
recurrent or persistent disease
 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, postpartum)
 Struma ovarii
 Functioning thyroid carcinoma metastases
 Ingestion of excess thyroid hormone
 Thyrotoxycosis is a clinical
syndrome caused by negative
influence of persistent excess of
thyroid hormones to organism.
 Diffuse toxic goiter
(GRAVES' DISEASE)
 This is the most common cause of
hyperthyroidism and is due to
autoimmune process.

 1835 - Robert Graves

 1840 – Karl Basedow
 Diffuse toxic goiter
(GRAVES' DISEASE)

Epidemiology

 accounts for 60 to 80% of thyrotoxycosis.

 occurs in up to 2% of women and in 0,2% of men.
 rarely begins before adolescence and typically
occurs between 20 and 50 years of age, may also
occurs in the elderly.
 Diffuse toxic goiter
(Graves ′disease )
 Systemic autoimmune disease due to
production of serum Ig G – antibodies to
the TSH receptors stimulating thyroid
hormone production behaving like TSH.
It's manifested by diffuse goiter and
clinical syndrome of thyrotoxicosis.

 Etiology of Graves ′disease
There is an association with HLA- В8 , -
DR3, and DR2 and 50% concordance is
seen among monozygotic twins with
5% concordance in dizygotic twins.
 Provoking factors are stresses,
infections, tobacco smoking, insolation.
 Diffuse toxic goiter
Pathogenesis

The extrathyroidal manifestations of Graves'

disease - ophthalmopathy and dermopathy are due
to immunologically mediated activation of
fibroblasts in the extraocular muscles and skin, with
accumulation of glycosaminoglycans, leading to the
trapping of water and edema. Later, fibrosis
becomes prominent. 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
 Diffuse toxic goiter
Clinical manifestations
Physical examination
 Goiter
 Warm, moist skin
 Hairs are fine, and a diffuse alopecia occurs in up to 40% of
patients
 Muscle weakness, proximal myopathy
 Lid retraction or lag
 Thyroid gland: diffusely enlarged, soft or slightly firmed,
painless on palpation , systolic murmur on auscultation

Enlargement of thyroid:
 0 – normal size
 I – larger than distal phalanx of patient’s thumb on palpation,
not visible
 II - detectable on palpation, visible
Methods of thyroid gland palpation
 Diffuse toxic goiter
Clinical manifestations
Neurologic
 Irritability, nervousness, tearfulness, psychosis,
logorrhea, hyperkinesis
 Tremor of fingers
 Tremor of all body
 Hyperreflexia
 Muscle wasting
 Proximal myopathy without fasciculation
 Diffuse toxic goiter
Clinical manifestations
Cardiovascular
 tachycardia (sinus tachycardia, atrial fibrillation,
supraventricular tachycardia)
 high cardiac output (produces a bounding pulse, 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)
 Diffuse toxic goiter
ECG

early stage - high voltage, shortening of PR

interval; sinus tachycardia
advanced stage – reduction of voltage,
prolongation of QRS complex, non-specific
changes of ST segment and T wave, 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
 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, Cocher and Greafae symptoms )
 periorbital edema
 scleral injection
 diplopia
 compression of the optic nerve (leading to papilloedema,
peripheral field defects, permanent loss of vision)
 Syndrome of hypermetabolism

 Weight loss, increased appetite

 Heat intolerance
 Increase of skin temperature
 Subfebrile temperature

 Muscle weakness
 Osteopenia, osteoporosis
 Syndrome of Dermopathy

 Pretibial myxoedema (pretibial areas are

swelling, brownish in colour)
 Palmary erythema
 Vitiligo
 Hyperpigmentation on lids
 Nails and hair are brittle
 Affection of endocrine glands
 Adrenal insufficiency
 Dysmenorrhea, amenorrhea
 Carbohydrate intolerance,
 Diabetes mellitus
 Clinical classification
 Mild form: Neurological symptoms and signs ,
Pulse rate < 100 per minute, weight loss to
10%, mild weakness
 Moderate degree: Pulse rate > 100, < 120 per
minute , weight loss to 20%, ↑ systolic BP, ↓
diastolic BP, decrease of ability to work
 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
immunoglobulins
 Determination of thyroid peroxidase (TPO)
antibodies
 Diffuse toxic goiter
THYROID SCANNING

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 homogeneously.
 Diffuse toxic goiter

THYROID ULTRASOUND

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
 Diffuse toxic goiter
Differential Diagnosis
Diseases, that cause thyrotoxicosis

Nodular thyroid disease (palpation, radionuclide or

ultrasound scan)
Destructive thyroiditis (palpation, radionuclide or
ultrasound scan)
Ectopic thyroid tissue (palpation, 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).
 Diagnostics. Plan of examination
 Interrogation (complaints), present history,
family history (presence of autoimmune
pathology in closed relatives )
 Physical examination: height, weight, BMI,
BP, heart rate, pulse rate, skin examination,
examination of lymph nodes, cardiovascular
system etc
 Inspection and palpation of thyroid gland
 Ophthalmologic examination
 Diffuse toxic goiter
Diagnosis

 Biochemically confirmed thyrotoxicosis

 Diffuse goiter on palpation and USI
 Autoimmune 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
 Diffuse toxic goiter
Differential Diagnosis
Diseases, that cause thyrotoxicosis

Nodular thyroid disease (palpation, radionuclide or

ultrasound scan)
Destructive thyroiditis (palpation, radionuclide or
ultrasound scan)
Ectopic thyroid tissue - (palpation, 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.
 Clinical diagnosis
 Diffuse toxic goiter II degree, severe
form , stage of medicamental
subcompensation. Thyrotoxic heart,
Atrial fibrillation , tachysystolic form.
Heart failure II;
Endocrine ophtalmopathy of II degree.
 Diffuse toxic goiter
TREATMENT

 Reducing thyroid hormone synthesis

(antithyroid drugs, thyrostatics)

 Reducing the amount of thyroid tissue

(subtotal thyroidectomy or radioiodine (131I)
treatment)
 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. After euthyroidism is
restored daily dose is 50-100 mg. Divided doses are
usually given throughout the course.
Carbimazole or methimazole (mercazolil) is usually 10
to 20 mg every 8 or 12 h for 3-6 weeks. Once-daily
dosing is possible after euthyroidism is restored
(usually 2,5-10 mg daily) (leucocytes count should be
checked once a month because of possible development
of leucopenia)
Duration of treatment – up to 1,5-2 years
Combined treatment with thyrostatics and
L-thyroxin ( 50 mкg) – “Block and replace”
 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.
Glucocorticosteroids
In cases of severe thyrotoxicosis or adrenocortical
deficiency
Dose – 20-30 mg daily (for prednisolone).
Duration of treatment – 2-4 weeks.
 Diffuse toxic goiter
TREATMENT
 ß- blockers
Propranolol (10-20 mg to 40 mg every 6 h) or
longer acting beta blockers, such as atenolol (50
mg once a day or twice a day) or metoprolol
(50 mg once a day or twice a day)

 Sedatives
 Diffuse toxic goiter
TREATMENT
Radioiodine (131I)
Causes progressive destruction of thyroid cells.
Indications
 Severe, complicated thyrotoxicosis
 Concomitant diseases, counterindicating for
thyroidectomy
 Relapse after thyroidectomy
 No patient’s consent for surgery

Contraindications
 Nodular goiter
 Children and adolescents
 Pregnancy and breast feeding
 Diffuse toxic goiter
TREATMENT
Subtotal thyroidectomy
Indications
 Ineffectiveness of antithyroid drugs after 2
months of treatment
 Very large goiter
 Severe thyrotoxicosis, particularly with
atrial fibrillation
 Relapse after treatment with antithyroid
drugs
 Diffuse toxic goiter
TREATMENT
subtotal thyroidectomy

Possible complications of thyroidectomy

 Short-term hypothyroidism (superfluous excision of
thyroid tissue). Treatment – thyroid hormone
 Long-term hypothyroidism (autoimmune mechanisms).
Treatment – thyroid hormone + corticosteroids
 Relapse of thyrotoxicosis. 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
 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, delivery
 Withdrawal of antithyroid drugs
 Sympathomimetics treatment
 Radioiodine (131I) treatment
 Diffuse toxic goiter
Thyrotoxic crisis
Clinical manifestations

Life-threatening exacerbation of hyperthyroidism,

accompanied by fever (up to 40°C), delirium,
seizures, tachycardia (up to 180-200 bpm),
arrhythmia, heart failure, coma, vomiting,
diarrhea, and jaundice.
 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 (0,25 g intravenously every 6 h)
 Propranolol (40 to 60 mg orally every 4 h; or 1- 2-4 mg
intravenously every 4 h)
 Glucocorticosteroids (I ⁄ v Hydrocortisone 100mg 3-4 times ⁄24h,
Prednisolone 200-300 mg within 24 h or Dexamethasone 2 mg
every 6 h)
 Cooling
 Intravenous fluids (5% glucose, albumin, polyglucin)
 Antibiotics (if infection is present)
 Hypothyroidism
 Hypothyroidism is a clinical syndrome
caused by persistent decrease of influence
of thyroid hormones to target tissues.
 Depression of thyroid function due to
different diseases
 Distribution is about 12% , mostly among

elderly women.
Pathogenesis of hypothyroidism
 Depression of metabolic rate
 Decrease of demands in oxygen
 Myxoedema due to accumulation of
glycosaminoglycanes,
 excess of vasopressin and
 deficiency of ADH
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)
 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- and diiodothyronine to
triiodothyronine and thyroxine
• defects of deiodinases function
 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, α-interferon, amiodarone
 infiltrative disorders
 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
 CLASSIFICATION (CAUSES)

PERYPHERAL

 Resistance to thyroid hormone

(mutations in the TRβ gene)

 Inactivation of circulating T3, T4 or

TSH.
 Clinical Manifestations
Complaints

 Tiredness, weakness
 Dry skin
 Feeling cold
 Hair loss
 Difficulty concentration, poor memory
 Constipation
 Weight gain with poor appetite
 Dyspnea
 Hoarse voice
 Menorrhagia (later oligomenorrhea or amenorrhea)
 Paresthesias
 Impaired hearing
 Clinical Manifestations
Nervous system
Inhibited thinking and emotional
reactions,
retarded movements,
difficult concentration,
poor memory, drowsiness.
 Clinical Manifestations
Skin and mucous - dry and coarse.
Accumulation of gialuronic acid in the skin
lead to subcutaneous accumulation of water.
Puffy face, hands and feet (myxoedema).
Peripheral edema. There is pallor, often with a
yellow tinge due to carotene accumulation.
Nail growth is retarded. Hair is dry, brittle,
difficult to manage, and falls out easily.
 Clinical Manifestations
Metabolic rate is reduced –
weight gain despite poor appetite,
cool peripheral extremities,
hypothermia,
absence of sweating
 Clinical Manifestations
Cardiovascular system –
dull pain in cardiac region,
bradycardia,
enlarged heart,
weak sounds on auscultation,
hypotension or hypertension,
development and progression of
atherosclerosis and all atherosclerosis-
associated diseases, pericardial effusion
 ECG signs

ECG – low voltage, especially of P-

and T- waves; long PR interval (AV
conduction disorders) and other
conduction abnormalities
 Clinical manifestations
Respiratory system

 Nightapnoe
 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
 Clinical Manifestations
State of thyroid gland depends of the cause of
hypothyroidism

 Iodine deficiency – diffusely enlarged, soft,

painless.
 Congenital dysgenesis – size is reduced or the
gland is absent.
 Hashimoto's thyroiditis - goiter may be of the
normal size or slightly enlarged, usually irregular
and firm in consistency, may be slightly painful
 Laboratory Evaluation
DIAGNOSIS OF HYPOTHYROIDISM

 TSH is normal or low – pathology of pituitary or

hypothalamus
 normal TSH level excludes primary hypothyroidism.
 If TSH is elevated, a free T4 level is needed to confirm
the presence of clinical hypothyroidism.
 T4 is inferior to TSH when used as a screening test, as it
will not detect subclinical or mild hypothyroidism.
 T3 measurements are not indicated.
 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
 TREATMENT
Clinical Hypothyroidism

Replacement of thyroid hormone. Most

common is Levothyroxine (T4).
L- thyroxine combined with triiodothyronine
may also be used.
Young age – 2-2,5 μg/kg daily. If not effective – dose
increase in 12,5-25 μg every 2-4 weeks.
Middle age – 1,5-2 μg/kg daily. If patient has
concomitant coronary artery disease – 25-50 μg daily. If
not effective – dose increase in 25 μg every month.
Elderly age - 25-50 μg 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, with the goal of treatment being a
normal TSH, ideally in the lower half of the reference
range.
 Other causes of hypothyroidism - the dose is
adjusted on the basis of T4 evaluation.
TSH responses should be measured about 2 months
after instituting treatment or after any subsequent
change in levothyroxine dosage. ТSH level normally is
0,4- 4 IU ⁄ l , optimal level is -0,5-1,5 IU ⁄ l)
Clinical effects of levothyroxine replacement are often
slow to appear. Patients may not experience full relief
from symptoms until 3 to 6 months after normal TSH
levels are restored.
 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
 Myxoedema coma
Clinical manifestations

 Reduced level of consciousness,

sometimes associated with seizures
 Severe features of hypothyroidism
 Hypothermia, which can reach 23°C
 Severe bradycardia
 Hypotension.
 Myxedema coma

Laboratory findings

 hyponatremia
 hypochloridemia
 hyperkaliemia
 hyperuremia
 acidosis.
 Myxoedema coma
Causes
Almost always occurs in the elderly
 Non-treated hypothyroidism or treated hypothyroidism
with poor compliance
 Factors that impair respiration, such as drugs
(especially sedatives, anesthetics, antidepressants),
pneumonia, congestive heart failure, myocardial
infarction, gastrointestinal bleeding, or cerebrovascular
accidents.
 Trauma
 Surgery
 Infections
 Cooling
 Myxoedema coma
TREATMENT
Replacement of thyroid hormone
 Levothyroxine - intravenous bolus of 500 μ g in 4
injections - loading dose . It is usually continued at a
dose of 75 to 100 μg/d.
 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. It is usually
continued at a dose of 50 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). .

 Myxoedema coma
TREATMENT

Prevention of adrenocortical insufficiency

 hydrocortisone - 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 - intravenous hypertonic
saline
Prevention of hypoglycemia - intravenous glucose
 Thyroidites are inflammatory diseases of
thyroid gland
 Classification:
 Acute thyriodities: suppurative,
nonsuppurative
 Subacute (viral) thyroiditis (de Quervain
thyroiditis)

 Chronic thyroiditis
 Chronic thyroiditis
 Autoimmune hypertrophic thyroiditis (Hashimoto’s
goiter)
 Autoimmune atrophic thyroiditis
 Asymptomatic thyroiditis
 Painless thyroiditis
 Postnatal
 Specific: tuberculous, syphilitic, septicomycotic
 Ridel’s fibrous thyroiditis (as a symptom of some
systemic diseases)
 Acute thyroiditis
 Etiology: bacterial infection, more frequently
caused by Str. pyogenes, Staph. aureus.
 Pathogenesis: the ways of infection are
lymphogenic or haematogenic.
Usually only one lobe is affected.
 Unsuppurative thyroiditis is caused by
ionizing radiation (radiation thyroiditis).
 Clinical features of acute purulent
thyroiditis
 Acute onset, body temperature is above 38-39°С,
rigor, tachycardia.
 TG is expanded, algetic. Pain irradiates to an ear and
a mandible.
 Complications:
 Abscess formation: symptom of fluctuation.
Hyperemia of skin over the lesion focus.
 Fistulae may open to the front surface of a neck or to
mediastinum (mediastinitis), phlegmon of a neck.
Clinical features of acute nonsuppurative
thyroiditis.
 On palpation - tenderness in TG
region.
 Thyrotoxicosis signs:
tachycardia, disposition to
sweating etc.
Additional methods of investigation
 Clinical blood count (leukocytosis with
shift to the left)
 US of TG.
 Fine-needle biopsy, inoculation for
revealing the causative agent.
 Treatment of acute thyroiditis
 Hospitalization to surgical department.
 Antibacterial therapy with broad spectrum antibiotics.
Lancing and draining of abscess.
 ß-adrenoreceptor blockers ( propranolol 20-40 mg 3
times a day till full liquidation of clinical
manifestations will be obtained).
 Analgesics.
 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
thyrothoxicosis.
 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 is on 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
rotation.
 Sometimes palpation of TG is impossible due to
severe pain.
 There are 4 stages: TRANSIENT THYROTOXICOSIS
(4-6 WEEKS) , EUTHYROIDISM, HYPOTHYROIDISM
(2-3 MONTH), CONVALISCENCE.
Additional methods of investigation
 Clinical blood count: lymphocytosis, abrupt
increasing of ESR.
 Hyper-γ-globulinemia.
 ↑ content of fibrinogen
 ↑ Т3, ↑ Т4 , then ↓Т3, ↓Т4
 Autoantibodies to thyroglobulin and TPO.
 US of TG: hypoechoic focal areas.
 TG Scanning (if needed) – area of
inflammation (« cold» area).
 Treatment of subacute thyroiditis
 Hospitalization into an endocrinological department.
 Antiinflammatory therapy:
 NSAID (acetylsalicylic acid p.o. after meals in
dosage 600 mg each 4 hours till disappearance of
pain syndrome and decreasing of body temperature.
 SAID ( 10-14 days):
 Prednisolon 30-60 mg p.o. after meals 1 time a day
till liquidation of clinical manifestations.
 Chronic autoimmune thyroiditis
 The most common form of thyroiditis
 Etiology: association with HLA antigenes: HLA DR3
and DR5 . F: M – 10-15:1.
 Pathogenesis:

 AT –autoimmune inflammation of TG.

↓ Т- supressors → → Т- helpers interact with native

antigenes of TG cells. It combines with other
autoimmune diseases.
 Lymphoid infiltration of TG.
 Clinical manifestations of chronic
autoimmune thyroiditis
 Function of TG: gradual changes from
thyrotoxicosis at the onset and consequent
euthyroidism to hypothyroidism.
 TG is enlarged on palpation, its structure is
solid, heterogeneous.
 Frequent combination with other autoimmune
or TG diseases.
 Addition methods of investigation
 Thyroid hormones’ rate evaluation.
 Indication of antibodies to TG tissues, TPO.
 US of TG (hypoechogenity).
 Fine-needle biopsy is needed for differential
diagnostics with nodular goiter.
 Treatment of autoimmune
thyroiditis
 Conservative:
 Treatment of TG functional status
disturbances.
 Hyperthyroid phase: ß-adrenoreceptor
blockers
 Hypothyroid phase: adequate replacement
therapy.
 Levothyroxine natrii 1,6 μg⁄kg or 100-150 μg
daily.
 Thyroid diseases without it‘s
function disorder
 Iododeficiency diseases
 Nodular euthyroid goiter
 Thyroid carcinoma
 Acute suppurative and invasive fibrous
thyroidities
 Iododeficiency diseases
 Diffuse nontoxic goiter
 Nodular or multinodular goiter
 Iododeficiency hypothyroidism with cognitive
disorders
 Functional autonomy of thyroid
 Diffuse enlargement of thyroid ( goiter), euthyroidism
 Enlargement of thyroid ( goiter), with a node or
nodes, euthyroidism
 Enlargement of thyroid ( goiter), hypothyroidism
 Thyrotoxicosis
 Endemic and sporadic goiter
 Endemic goiter is a disease manifested by
progressing enlargement of thyroid gland and
associated with Iodine deficiency in external area
with involvement of the majority of population in
concrete geography conditions
 Sporadic goiter is a disease manifested by
progressing enlargement of thyroid gland in some
individuals those live out regions of goiter endemia
with enough Iodine consumption
 Epidemiology
 Real Iodine consumption in Russia 40 – 80
mkg/24 hrs
 In Russia goiter was detected in 2% children
younger 1 year, in 20- 30% of 7-10-th year
children, in 30 – 50% of adolescents
 Testing of children in different regions of
Russia (2005) revealed IQ decrease for 11-
18%
 Daily Iodine consumption
 Age Iodine Consumption

 Children ≤1 year 50 mkg

 Cnildren of 2-6 years 90
 Children of 7-12 years 110 - 130
 Adolescents 130 -150
 Adults 150 – 200
 Pregnants 250 – 300
 Lactation 250 - 300
 Ethiology and pathogenesis iodine
deficiency diseases
 Iodine is a microelement that is necessary for
synthesis of thyroid hormones
 The sources of Iodine are fish, seafood, meat,
milk, chicken eggs, oak flakes, salad leaves,
spinach, bitter root, grape, iodized salt,
enriched with Iodine milk and bread,
medicamental preparations
Lecturer- associated professor of
Department of Internal medicine #2
Panevskaya Galina Nikolayevna
 ANATOMY
OF THE PARATHYROID GLANDS
 ANATOMY
OF THE PARATHYROID GLANDS
 An endocrine organ usually associated with the thyroid
gland
 There are normally 4 (can be from 3-6 )parathyroid
glands.
 They are small epithelial bodies with the weight to 0,5 g
 Location – posterior to the thyroid and or within its tissue.
In 25% of cases it‘s atypical, i.e. behind the esophagus,
trachea or sternum
 Parenchyma consists of parathyrocytes that produce
parathyroid hormone ( PTH)
 Highly vascular ( branches of thyroid artery).
 Innervations: sympathetic and parasympathetic nerves
 PARATHYROID HORMONE
 Parathormone ( PTH) is an 84-amino-acid hormone
derived from a 115-residue prehormone
 PTH is secreted from the chief cells of the four
parathyroid glands
 Secretion is the most intensive at nighttime.
 It‘s regulated through feedback, i.e. by a level of
Ca++ in blood . PTH levels rise as serum ionized
Ca++ falls due to Ca-sensing receptors on the
plasma membrane of the parathyroid cells
 Maintenance of stable level of Ca++ in blood ,
ranging from 2,2 to 2,6 mmol /l
 Parathyroid hormone functions
●Increasing osteoclastic resobrtion of bone and
Calcium delivery from it into blood (occurring
rapidly)
●Increasing intestinal absorption of calcium
(a slow response)
●Increasing synthesis of 1,25- (OH)2D3
●Increasing renal tubular reabsorption of Calcium
● Increasing excretion of phosphate

At cellular level PTH acts through adenylate

cyclase system, augmenting AMP formation
REGULATION OF CALCIUM METABOLISM

Daily Calcium consumption is about

1 g ( 25 mmol).
Acidic food, proteins, pregnancy stipulate
↑of intestinal Ca absorption.
Alkaline food, use of glucocorticoids,
excess of phosphates @ oxalates lead to
it's ↓
 Calcium Metabolism
 99% of total body calcium resides in bone
 Remainder:
 40% bound to serum proteins
 13% complexed with anions
 47% free ionized calcium – physiologically

active form, regulated by vitamin D and

PTH
 Calcium Metabolism
 Decreased serum calcium
stimulates PTH secretion
within seconds
 PTH ½ life in serum is about 4
minutes
 REGULATION OF CALCIUM and
PHOSPHORUS METABOLISM
 Parathormone ( PH)
 Vitamin D3 (cholecalciferol) is received
partially with food and is partially produced
in skin from vitamin D2(ergocalciferol).
After hydroxylation in liver with 25-
hydroxyvitamin- D3 (an inactive form) production
of 1,25- dihydroxyvitamin - D3 (calcitriol) is
formed in kidneys
 REGULATION OF CALCIUM and
PHOSPHORUS METABOLISM

 Calcitonin produced by
parafollicular thyroid cells is
antagonist of PTH.
 It inhibits the resorbtion of bone and
↓ Ca and P metabolism in blood,
↑excretion of Ca and P with urine
and inhibits intestinal Ca absorption.
 Hyperparathyroidsm

Recklinghausen's disease,
(generalized fibrous-cystic
osteodystrophy) is resulted in
hyperfunction of parathyroid
glands due to tumor of
parathyroid gland or their
hyperplasia
 Hyperparathyroidsm
Incidence of primary hyperparathyroidism
is 25-39 per 100 000 population.
Morbidity is from 0,1 to 2% of
the population.
It occurs mostly in elderly females and
very rarely in children
 Hyperparathyroidsm
Etiology

 Primary hyperparathyroidism
develops due to single or multiple
parathyroid Adenoma ( 80-90%), or
 Hyperplasia of all four PTG (0,1-
2%), or
 Carcinoma of PTG ( 1-5%)
 Hyperparathyroidsm.
Etiology
Forms of hyperparathyroidism:
 Sporadic form
 Familial form is usually combined with
genetic MEN 1 ( multiple endocrine
neoplasia) syndrome or MEN 2
 Familial form without MEN is detected
in children
 Hyperparathyroidsm
Etiology
 Etiology of adenoma, carcinoma and
hyperplasia of PTG is not completely
clear.
 Risk factors: infectious and
autoimmune diseases, radiation of a
head and a neck, usage of some
medications
 Hyperparathyroidsm
Pathogenesis
 Chronic hypersecretion of PTH
 Decrease of renal excretion of Calcium
 Increase of Phosphate clearance
 Increase of hydroxycholecalciferol (active form of
vitamin D) synthesis that stimulates intestinal
absorption of Ca and Ca mobilization from bones
 Hypercalcaemia is the main pathobiochemical and
diagnostic factor in hyperparathyroidism
Hyperparathyroidism
 Hyperparathyroidsm
Etiology
 Secondary hyperparathyroidism is a
result of hypocalcaemia due to kidneys or
liver diseases, or deficiency of vitamin D
 Tertiary hyperparathyroidism
occurs on a background of existing
secondary hyperparathyroidism
 Hyperparathyroidsm
Clinical manifestations

Clinical symptoms and signs of

Hyperparathyroidism develop slowly

It can be manifested only by

asymptomatic hypercalcaemia
 Hyperparathyroidsm
Clinical manifestations
General features:
 Tiredness, general weakness, fatigue
 Muscle hypotrophy, muscular weakness
 Joint pain
 Dehydration
 Depression
 Poor appetite, weight loss
 Hyperparathyroidsm
Clinical manifestations
Involvement of skeleton and other bones due
to osteoporosis, osteoarthrosis, osteitis:
 slow and/or shaken gait (walking),
 intensive stable bone pain,
 frequent fractures,
 deformation of bones,
 change of configuration of skull, thorax,
curvature of backbone,
 reduction of height
 Clinical Symptoms/Signs
Involvement of kidneys:
 Hyposthenuria
 Decreased GFR
 Alkaline reaction of urine
 Nephrolithiasis
 Nephrocalcinosis
 Polyuria/polydipsia
 Hyperparathyroidsm
Clinical manifestations
CVS changes:
Arterial hypertension
Shortening of interval ST
on ECG
 Hyperparathyroidsm
Clinical manifestations
Involvement of GIS:
 Anorexia, nausea, vomiting,
constipation, weight loss,
stomachaches
 Chronic pancreatits due pancreatic
calcification,
 Peptic gastroduodenal ulcer
Mental /psychiatric changes of CNS

Irritability, tearfulness
Fatigue, apathy
Drowsiness at daytime
Anxiety/ or Depression
Psychosis
Coma/ diffuse EEG changes
 Hyperparathyroidism.
Symptoms / Signs
Ocular
Band keratopathy
Conjunctivitis
Conjunctival calcifications
 Hyperparathyroidsm
Diagnostics
The most typical signs:
■ Hypercalcaemia > 2,0 – 2,55 mmol/l
■ Hypophosphatemia< 0.69-1,25 mmol/l
■ PTH >14,0-62,0 pg/mmol
■ Excretion of Ca is normal or ↑
■ Hyperphosphaturia
■ ↑Activity of alkaline phosphatase
■ ↑pH
 Hyperparathyroidsm
Diagnostics
CBC:
Anemia
Eosinophilia
Neutrophilia
Hyperparathyroidsm
Diagnostics
Urinalysis:
Isohypostenuria
Albuminuria
 Hyperparathyroidsm
Diagnostics. Instrumental methods

■ Ultrasonography (with biopsy) of

parathyroid glands
■ X-ray (tomography) of retrosternal space
with contrast agents
■ Scanning of parathyroid glands
■ Selective arteriography with contrast
agents
■ Magnetic –resonance imaging (MRI)
 Hyperparathyroidsm
Diagnostics. Instrumental methods
X-ray gram of skeleton:
Signs of osteoporosis and multiple
cysts
Decrease of vertebral corpora height
(fish-like deformation)
 Hyperparathyroidsm
Diagnostics. Instrumental methods

X-ray gram of skull:

Miliary granularity with rarefication
Thinning of cortical layer of tubular bones
Widening of marrow channel
Subperiostal resorbtion of distant hand
phalanxes
Hyperparathyroidsm. Diagnostic tests
 With Insulin- induced hypoglycaemia:
Insulin in a dose of 0,05 IU/kg IV
induces during 15 minutes ↑PH level up
to 130% compared to a basal one
 With Adrenaline:

In a dose of 2,5-10μg/min it ↑ the PH

level
Hyperparathyroidsm. Diagnostic tests
 With Secretin:
Level PH sharply raises in healthy
people
 With Calcitonin:
Level of Somatotropin ↑
Ca level↓ in healthy people
 Differential diagnosis of Primary
Hyperparathyroidism
■ Metastatic Carcinoma in primary
bronchial, kidney, prostate, thyroid and
mammary cancer, lymphoma is the most
common in hospitalized patients
■ Multiple Myeloma:
myelomatous nodes, specific nephrosis
with proteinura, paraproteinemia, defects
of various sizes (“convolutional
markings”) on X-ray films of flat bones,
skull, ribs, hipbones
 Differential diagnosis of Primary
Hyperparathyroidism
 Hyperthyroidism
 Hypervitaminosis D (or A)
 Immobilization
 Sarcoidosis
 Addisonian crisis
 Paget‘s disease (arthrosis, bone pain,
cysts on the X-ray films, normal level
of Ca, P, ↑alkaline phosphatase activity,
thickening of cortical layer of tubular
bones, narrowing of the marrow channel)
 Differential diagnosis of Primary
Hyperparathyroidism
 Osteoporosis (postmenopausal,
senile, idiopathic) is accompanied by
abnormalities of backbone, hipbones,
skull, ribs is manifested bone pain,
fractures in typical places .
 Presence of cysts, bone deformation,
biochemical abnormalities
Vertebrae changes in
osteoporosis
 Differential diagnosis of Primary
Hyperparathyroidism
 Rachitic signs occurs even in the first
months of life.
 Deformation of bones,
 Changes of nervous system, internal
organs, muscular hypotonia
 Normal content of Ca, P

 Hyperparathyroidism in children is

extremely rare
 Differential diagnosis of Primary
Hyperparathyroidism

Ewing´s sarcoma:
■Affection marrow of tubular bone (shin- bone,
splint-bone, humerus, ulna and/or femur
■Secondary changes of bones with metastases in
other organs of hemopoetic system (lymphatic
nodes, spleen, liver)
■Characteristic diffuse lesions of bones are absent
■Hypercalcemia is absent
 Hyperparathyroidism
Treatment
 Surgery
 Diet fortified with Ca
 Calcium medications
 Vitamin D3

 Anabolic steroids
 Calcitonin
 Physiotherapy
Removing of parathyroid adenoma
 Hypoparathyroidism

 Hypoparathyroidism is the
disease caused by
insufficiency of parathormone
(PH) and is shown by tetany
and reduction of serum calcium
content
 Hypoparathyroidism Etiology
Pathogenesis

 Idiopathic
 a) Congenital hypoplasia or aplasia of
parathyroid gland
 b) Autoimmune pathogenesis sometimes
accompanied by hypocorticism, and
candidiasis
 Hypoparathyroidism Etiology
Pathogenesis
 Postoperative:
 thyroidectomy / thyroid gland
resection
 Traumatic damage
 Other etiology factors:
 Radiation,vascular, infectious
damage, haemochromatosis
 Pseudohypoparathyroidism
■ Hereditary disease ( Albright-McCune- Stenberg
osteodystrophy)
■ Kidneys and bones are tolerant to action of the
PH that leads to biochemical and clinical pattern
of hypoparathyroidism
■Reaction to exogenous PH is not available
Calcium metabolism is not disorderd
■Abnormality of mental and physical
development:
small stature, short neck, brachydactyly
 Pseudohypoparathyroidism
 Tissue tolerance to PH depends on decrease in activity of the
specific protein (guanine-nucleotide- connecting regulatory
protein-GN-protein) that provides interaction between a
receptor and membrane adenylate cyclase and participates in
realization of functions of this enzyme
 Pseudohypoparathyroidism type1: the activity of GN-protein
is decreased by 40-50%
 Pseudohypoparathyroidism type II: the receptor sensitivity to
PH is not violated. Activity of GN –protein is normal, whereas
PH can stimulate adenylate cyclase. The ability of Ca and P
transport system to react on normally formed cyclic adenosine
monophosphate is supposed
 Hypoparathyroidism
Symptoms and signs
Increase of excitability of the nervous- muscular
system
 Fits, tetany or predisposition to them
 Painful tonic muscular spasms
 Symmetric groups of flexors of upper and lower
extremities are involved : during an attack hands are
bent in joints, a hand is fixed in the form of
“obstetrician hand", a foot is in a state of a sharp
plantar bending with bent fingers ( “tip foot”
 Spasm of smooth muscles of facial muscles cause the
“sardonic” form of a mouth, i. e. a “fish” mouth,
there comes a spasm of chewing muscles- trismus
 Hypoparathyroidism
Symptoms and signs
 Spasm of smooth muscles of internal
organs can stimulate an “ acute
abdomen”, a renal colic, a heart
attack
 Contraction of intercostal muscles,
diaphragm, laryngospasm and
bronchospasm can lead to asphyxia
 Hypoparathyroidism
Symptoms and signs
 Chvostek’s sign is the
contraction of face muscles
under percussion in a place of an
exit of nervus facialis ahead of
external acoustical pass
 Hypoparathyroidism
Symptoms and signs

 Trousseau’s sign is a spasm in

extensor in the area of a hand
through 2-3 minutes after pulling
a shoulder by a plait or cuff of a
device for blood pressure
measurement
 Hypoparathyroidism
Symptoms and signs
 Schlesinger’s symptom is
spasms in extensor muscles of a
hip and foot at fast passive
bending a leg in a hip joint at the
straightened knee joint
 Hypoparathyroidism
Symptoms and signs
 Trophic abnormalities in ectodermal
structures:
 Defects of dental enamel, caries, earlier
turning grey hair, atrophy, fragility of
nails, dryness of a skin, eczema,
dermatosis, candidiasis are typical for
hypoparathyroidism
 Cataract, papillary swelling
 Hypoparathyroidism
Symptoms and signs
 GIS: spastic pains in a stomach,
pylorospasm with vomiting, diarrhea.
 CVS: hypotonia, tachycardia, arythmia,
spastic cardialgia, elongation of QT and ST
intervals without change of wave T and
resistance to cardiac glycoside
 Hypoparathyroidism
Symptoms and signs

CVS: hypotension, tachycardia,

arrhythmia, spastic cardialgia, elongation
of QT and ST intervals without change
of wave T and resistance to cardiac
glycoside
 GIS: spastic pains in a stomach,
pylorospasm with vomiting, diarrhea.
 Diagnosis of Hypoparathyroidism:
 Surgical intervention on a thyroid gland in
anamnesis
 Hypocalcemia and Hyperphosphatemia
 ↓Parathyroid hormone in blood
 Hypocalciuria and Hypophosphaturia
 ↓Excretion of cAMP
 Osteosclerosis and Periostosis of long tubular
bones
 Premature calcification of rib cartilages
 Calcification of kidneys, muscles and basal
 Differential diagnosis

 All diseases and conditions (epilepsy, hypoglycemia,

tetanus, poisoning with strychnine, hydrophobia, long-
term vomiting, alkalosis, syndrome of malabsorbtion ,
hysteria, lack of magnesium, etc) accompanied by a
convulsive syndrome
 All diseases and conditions accompanied by a cataract
 Hypocalcemia due to insufficient absorption of vitamin
D ( a rickets, spasmophilia in children)
 Hypocalcemia in the disease of Albright-McCune –
Sternberg (pseudohypoparathyroidism)
 Hypocalcemia in pregnant and breastfeeding women
 Treatment of Hypoparathyroidism
1. Daily need of Calcium 1-2 g is provided by
Administration of Calcium in salts:
 Calcium carbonate – 400 mg/1g of salt
 Calcium phosphate tribasic - 400 mg/1g of salt
 Calcium phosphate dibasic anhydride - 290 mg/1g
of salt
 Calcium chloride - 270 mg/1g of salt
 Calcium citrate - 211 mg/1g of salt
 Calcium lactate – 130 mg/1g of salt
 Calcium gluconate – 90 mg/1g of salt
2. Administration of Vitamin D
 Treatment of Hypoparathyroidism
Daily need of Calcium 1-2 g
Content of Calcium in salts:
 Calcium carbonate – 400 mg/1g of salt
 Calcium phosphate tribasic - 400 mg/1g of salt
 Calcium phosphate dibasic anhydride - 290 mg/1g
of salt
 Calcium chloride - 270 mg/1g of salt
 Calcium citrate - 211 mg/1g of salt
 Calcium lactate – 130 mg/1g of salt
 Calcium gluconate – 90 mg/1g of salt
 Treatment of Hypoparathyroidism
 Administration of Calcium in salts:
 Calcium gluconate – 90mg/1 tab
TID/QID
 Calcium lactate – 50mg/1 tab TID/QID

 Control of Calcaemia level each 3-6 months!

 Treatment of Hypoparathyroidism

Metabolites of vitamin D (D3):

 A dose 50 000-100 000 units
 Initial dose 250 000-400 000
units
 Treatment of Hypoparathyroidism
 Calcitriol, 1,25(OH)2D3 – Rocaltrol
 Alfacalcidol ( Alpha D3 –Teva) –a
synthetic analogue of cholecalciferol
 Tahystyn - a synthetic analogue of
dihydrotahysterol
 Treatment of Hypoparathyroidism

 Parathormone preparations are used

rarely
 Surgical methods: replanting of
conserved bonelets for formation of
depot of Calcium
 Autotransplantation of parathyroid
gland
Treatment of Hypoparathyroidism
Acute attack of tetany is
supervised by IV infusion
of 20-60 ml
of 10% of Calcium gluconate or
Calcium chloride solutions