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Thyroid gland diseases

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IntroductionThyroid hormone is essential for the growth and maturation of many target tissues, including the brain and skeleton.As a result, abnormalities of thyroid gland function in infancy and childhood is a

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Слайд 1Thyroid gland diseases
Karazin Kharkiv National University
Department of Pediatrics
Assistant

Tatyana Golovko

Thyroid gland diseasesKarazin Kharkiv National University Department of Pediatrics Assistant Tatyana Golovko

Слайд 3Introduction
Thyroid hormone is essential for the growth and maturation of

many target tissues, including the brain and skeleton.

As a result,

abnormalities of thyroid gland function in infancy and childhood is a result not only in the metabolic consequences of thyroid dysfunction seen in adult patients, but in unique effects on the growth and /or maturation of these thyroid hormone-dependent tissues as well.
IntroductionThyroid hormone is essential for the growth and maturation of many target tissues, including the brain and

Слайд 4Location: Located close to thyroid cartilage. Has two lateral lobes

connected by thyroid isthmus medially. Weight range from 12 to

30g

Development: Develops from endodermal floor of early pharynx
Location: Located close to thyroid cartilage. Has two lateral lobes connected by thyroid isthmus medially. Weight range

Слайд 7Thyroid Physiology
 

Thyroid Physiology 

Слайд 8Pathways of thyroid
Hormone metabolism

Pathways of thyroid Hormone metabolism

Слайд 9Feedback regulation Of TSH

Feedback regulation Of TSH

Слайд 10Thyroid physiology, continuation
 

Thyroid physiology, continuation 

Слайд 11Production of Thyroid Hormones
NIS (Na+/I- Sympoter)
TPO

Production of Thyroid HormonesNIS (Na+/I- Sympoter)TPO

Слайд 12Thyroid Hormone
Majority of circulating hormone is T4 (98,5% T4, 1,5%

T3 )

Total Hormone load is influenced by serum binding

proteins:
Albumin 15%;
Thyroid Binding Globulin 70%;
Transthyretin 10%.

Regulation is based on the free component of thyroid hormone.

Thyroid HormoneMajority of circulating hormone is T4 (98,5% T4, 1,5% T3 ) Total Hormone load is influenced

Слайд 13Effects of thyroid hormones
Fetal brain and skeletal maturation;
Increase in basal

metabolic rate;
Inotropic and chronotropic effects on heart;
Stimulates gut motility;
Increase bone

growth;
Increase in serum glucose, decrease in serum cholesterol;
Play role in thermal regulation.


Effects of thyroid hormonesFetal brain and skeletal maturation;Increase in basal metabolic rate;Inotropic and chronotropic effects on heart;Stimulates

Слайд 14Thyroid hormones
 
 

Thyroid hormones  

Слайд 15Comparative analysis of thyroid hormones

Comparative analysis of thyroid hormones

Слайд 16
THYROTOXICOSIS (Hyperthyroidism)
Overproduction of thyroid hormones;

HYPOTHYROIDISM (Gland destruction)
Underproduction of thyroid hormones;

NEOPLASTIC

PROCESSES
Benign;
Malignant.
THYROID GLAND DISORDERS DIVIDED INTO:

THYROTOXICOSIS (Hyperthyroidism)Overproduction of thyroid hormones;HYPOTHYROIDISM (Gland destruction)Underproduction of thyroid hormones;NEOPLASTIC PROCESSESBenign;Malignant.THYROID GLAND DISORDERS DIVIDED INTO:

Слайд 17Diagnostic of Thyroid gland disease
 

Diagnostic of Thyroid gland disease 

Слайд 18LABORATORY EVALUATION TSH (thyroid-stimulating hormone) normal, practically excludes abnormality
 

LABORATORY EVALUATION TSH (thyroid-stimulating hormone) normal, practically excludes abnormality 

Слайд 19High TSH usually means Hypothyroidism

Rare causes:
TSH-secreting pituitary tumor;
Thyroid hormone resistance;
Assay

artifact.

Low TSH usually indicates Thyrotoxicosis

Other causes:
First trimester of pregnancy;
After treatment

of hyperthyroidism;
Some medications (Esteroids-dopamine).




High TSH usually means HypothyroidismRare causes:	TSH-secreting pituitary tumor;Thyroid hormone resistance;Assay artifact.Low TSH usually indicates ThyrotoxicosisOther causes:First trimester

Слайд 21RAIU (Radioactive iodine uptake )
Scintillation counter measures radioactivity after I123

or I131 administration (per os or IV). Radioactivity of TG

measures between 4 h to 24 h. In children is limited in use.

Uptake varies greatly by iodine status:
Indigenous diet (normal uptake 10% vs. 90%);
Amiodarone, Contrast study, Topical betadine.
High RAIU with hyperthyroid symptoms
Graves’;
Toxic goitre.
Low RAIU with hyperthyroid symptoms:
Thyroiditis (Subacute, Active Hashimoto’s);
Hormone ingestion (Thyrotoxicosis factitia, Hamburger Thyrotoxicosis);
Excess I- intake in Graves’ (Jod-Basedow effect);
Ectopic thyroid carcinoma (Struma ovarii).
RAIU (Radioactive iodine uptake )Scintillation counter measures radioactivity after I123 or I131 administration (per os or IV).

Слайд 22Iodine states
Normal Thyroid



Inactive Thyroid



Hyperactive Thyroid

Iodine statesNormal ThyroidInactive ThyroidHyperactive Thyroid

Слайд 23
Thyrotoxicosis
Primary;
Secondary;
Without Hyperthyroidism;
Exogenous or factitious.

Hypothyroidism
Primary;
Secondary;
Peripheral.

Thyrotoxicosis Primary;Secondary;Without Hyperthyroidism;Exogenous or factitious.HypothyroidismPrimary;Secondary;Peripheral.

Слайд 24HYPERTHYROIDISM or THYROTOXICOSIS:
- is the result of excessive thyroid

gland function because is defined as the state of thyroid

hormone excess.

GOITRE
- is a chronic enlargement of the thyroid gland, that is not due to malignant neoplasm.



HYPERTHYROIDISM or THYROTOXICOSIS: - is the result of excessive thyroid gland function because is defined as the

Слайд 25Primary Hyperthyroidism:
Graves’;
Toxic Multinodular Goitre;
Toxic adenoma;
Functioning thyroid carcinoma metastases;
Activating mutation of

TSH receptor;
Struma ovary;
Drugs: Iodine excess.
Causes of Thyrotoxicosis:

Primary Hyperthyroidism:Graves’;Toxic Multinodular Goitre;Toxic adenoma;Functioning thyroid carcinoma metastases;Activating mutation of TSH receptor;Struma ovary;Drugs: Iodine excess.Causes of Thyrotoxicosis:

Слайд 26Causes of Thyrotoxicosis:
Thyrotoxicosis without hyperthyroidism:
Subacute thyroiditis;
Silent thyroiditis;
Other causes of thyroid

destruction:
Amiodarone, radiation, infarction of an adenoma;
Exogenous/Factitious.

Secondary Hyperthyroidism:
TSH-secreting pituitary adenoma;
Thyroid hormone

resistance syndrome;
Chorionic Gonadotropin-secreting tumor;
Gestational thyrotoxicosis.
Causes of Thyrotoxicosis:Thyrotoxicosis without hyperthyroidism:Subacute thyroiditis;Silent thyroiditis;Other causes of thyroid destruction:Amiodarone, radiation, infarction of an adenoma;Exogenous/Factitious.Secondary Hyperthyroidism:TSH-secreting

Слайд 27Symptoms of Hyperthyroidism
Heat intolerance, dislike of hot weather;
Hyperactivity, irritability, nervousness,

fatigue;
Weight loss (normal to increased appetite);
Diarrhea;
Tremor, palpitations;
Diaphoresis (sweating);
Lid retraction, thyroid

stare;
Pretibial myxedema and Graves ophthalmopathy (chemosis, diplopia, and exophthalmos);
Menstrual irregularity;
Goitre;
Tachycardia;
Females are more commonly affected( F:M = 5:1).
Symptoms of HyperthyroidismHeat intolerance, dislike of hot weather;Hyperactivity, irritability, nervousness, fatigue;Weight loss (normal to increased appetite);Diarrhea;Tremor, palpitations;Diaphoresis

Слайд 28Causes of Transient Neonatal Hyperthyroidism
Neonatal hyperthyroidism is almost always transient

and results from the transplacental passage of maternal TSH, receptor

stimulating antibodies.
Hyperthyroidism develops only in babies born to mothers with the most potent stimulatory activity in serum.
This corresponds to 1-2% of mothers with Graves ‘ disease, or 1 in 50,000 newborns.
Causes of Transient Neonatal HyperthyroidismNeonatal hyperthyroidism is almost always transient and results from the transplacental passage of

Слайд 29Situations That Should Prompt Consideration of Neonatal
Hyperthyroidism:

● Unexplained tachycardia, goitre

or stare;
● Unexplained petechiae, hyperbilirubinemia, or hepatosplenomegaly;
● There is a

persistently high TSH receptor antibody titer in mother during pregnancy in history;
● There is a persistently high requirement for antithyroid medication in mother during pregnancy in history;
● There is a thyroid ablation for hyperthyroidism in mother in history;
● There are previously affected sibling in history.
Situations That Should Prompt Consideration of NeonatalHyperthyroidism:● Unexplained tachycardia, goitre or stare;● Unexplained petechiae, hyperbilirubinemia, or hepatosplenomegaly;●

Слайд 30Congenital thyrotoxic goiter of and infant born to a mother

with thyrotoxicosis

Congenital thyrotoxic goiter of and infant born to a mother with thyrotoxicosis

Слайд 31Therapy of Transient neonatal hyperthyroidism
Treatment is accomplished by maternal administration

of antithyroid medication in fetus.
Till nowadays propylthiouracil (PTU) was

the preferred drug for pregnant women in North America, but current recommendations suggest the use of mercazolilum rather than PTU after the first trimester because of concerns about potential PTU-induced hepatotoxicity.
The goals of therapy are to utilize the minimal dosage which is necessary to normalize the fetal heart rate and render the mother euthyroid or slightly hyperthyroid.
Therapy of Transient neonatal hyperthyroidismTreatment is accomplished by maternal administration of antithyroid medication in fetus. Till nowadays

Слайд 32Therapy of Transient neonatal hyperthyroidism
In the neonate, treatment is the

follows: either PTU
(5 to10 mg/kg/day) or mercazolilum

(0.5 to 0.7 mg/kg/day) has been used initially in 3 divided doses.

If the hyperthyroidism is severe, a strong iodine solution (Lugol’s solution or SSKI, 1 drop every 8 hours) is added to block the release of thyroid hormone immediately.

Often the effect of PTU and mercazolilum is not as delayed in infants as it is in older children or adults.
Therapy of Transient neonatal hyperthyroidismIn the neonate, treatment is the follows: either PTU   (5 to10

Слайд 33Therapy of Transient neonatal hyperthyroidism
Propranolol (2 mg/kg/day in 2 or

3 divided doses) is added if sympathetic overstimulation is severe,

particularly in the presence of pronounced tachycardia.
If cardiac failure develops, treatment with digoxin should be initiated, and propranolol should be discontinued.
Rarely, prednisone (2 mg/kg/day) is added for immediate inhibition of thyroid hormone secretion.
Measurement of TSH receptor antibodies in treated babies may be helpful in predicting when antithyroid medication can be safely discontinued.
Lactating mothers on antithyroid medication must continue nursing as long as the dosage of PTU or mercazolilum does not exceed 400 mg or 40 mg respectively.
Therapy of Transient neonatal  hyperthyroidismPropranolol (2 mg/kg/day in 2 or 3 divided doses) is added if

Слайд 34Permanent neonatal hyperthyroidism
Rarely, neonatal hyperthyroidism is inconvertible and is due

to a germline mutation in the TSH receptor resulting in

its constitutive activation.
Function mutation of the TSH receptor should be suspected if persistent neonatal hyperthyroidism occurs in the absence of detectable TSH receptor antibodies in the maternal circulation.
An autosomal dominant inheritance has been noted in many of these infants. Other cases have been sporadic, arising from new mutation.


Permanent neonatal hyperthyroidismRarely, neonatal hyperthyroidism is inconvertible and is due to a germline mutation in the TSH

Слайд 35Permanent neonatal hyperthyroidism
Early recognition is important because the thyroid function

of affected infants is frequently difficult to manage medically, and,

when diagnosis and therapy is delayed, irreversible sequelae, such as cranial synostosis and developmental delay may result.

For this reason early, aggressive therapy with either thyroidectomy or even radioablation has been recommended.
Permanent neonatal hyperthyroidismEarly recognition is important because the thyroid function of affected infants is frequently difficult to

Слайд 37Goitre
Endemic goitre:
Areas where > 5% of children 6-12 years old

have goiter
Common in China and central Africa
Sporadic goitre:
Areas where

< 5% of children 6-12 years old have goiter
Multinodular goiter in sporadic areas often denotes the presence of multiple nodules rather than gross gland enlargement
Familial.

GoitreEndemic goitre:Areas where > 5% of children 6-12 years old have goiterCommon in China and central AfricaSporadic

Слайд 38Goitre
Etiology
Hashimoto’s thyroiditis:
Early stages only, late stages show atrophic changes;
May present

with hypo, hyper or euthyroid states;
Graves’:
Due to chronic stimulation of

TSH receptor;
Diet: vegetarian with mainly usage of various types cabbage;
Chronic iodine excess:
iodine excess leads to increased colloid formation and can prevent hormone release;
If a patient does not develop iodine leak, excess iodine can lead to goiter;
Medications:
Lithium prevents release of hormone, causes goiter in 6% of chronic users;
Neoplasm.
GoitreEtiologyHashimoto’s thyroiditis:Early stages only, late stages show atrophic changes;May present with hypo, hyper or euthyroid states;Graves’:Due to

Слайд 39Goitre
 

Goitre 

Слайд 40Classification of Goitre WHO (1994)
0 – goitre is absent;
I

– goitre isn’t visualized, but it’s size less than distal

phalanx of thumb;
II – goitre is palpated and visualized.
Classification of Goitre  WHO (1994)0 – goitre is absent;I – goitre isn’t visualized, but it’s size

Слайд 41Functional condition of Thyroid influence may be as

Euthyroidism;
Hypothyroidism;
Hyperthyroidism.

Functional condition of Thyroid influence may be asEuthyroidism;Hypothyroidism;Hyperthyroidism.

Слайд 42Non-Toxic Goitre
Cancer screening in non-toxic MNG (Multinodular goitre )
Longstanding MNG

has a risk of malignancy of solitary nodules (

nodules < 1.5 cm may be followed clinically;
MNG with non-functioning nodules > 4cm should be excised:
No FNA needed due to poor sensitivity;
Incidence of cancer (up to 40%);
Fine-needle aspiration (FNA) in MNG:
Sensitivity 85% - 95%;
Specificity 95%;
Negative FNA can be followed with annual US (ultrasound);
Insufficient FNA’s should be repeated;
While FNA hyperfunctioning nodules may mimic follicular neoplasm.
Non-Toxic GoitreCancer screening in non-toxic MNG (Multinodular goitre )Longstanding MNG has a risk of malignancy of solitary

Слайд 43Non-Toxic Goitre
Treatment options (no compressive symptoms):

Use follow-up to monitor for

progression;

Thyroid suppression therapy:
May be used for progressive growth;
May reduce gland

volume up to 50%;
Goitre regrowth occurs rapidly following therapy cessation.

Surgery indications:
Suspicious neck lymphadenopathy;
There is a radiation to the cervical region in history;
Rapid enlargement of nodules;
Papillary histology;
Microfollicular histology.
Non-Toxic GoitreTreatment options (no compressive symptoms):Use follow-up to monitor for progression;Thyroid suppression therapy:May be used for progressive

Слайд 44Non-Toxic Goitre
Treatment options (compressive symptoms):

Radioactive iodine (RAI) ablation:
Volume reduction 33%

- 66% in 80% of patients
Improvement of dysphagia or dyspnea

in 70% - 90%
Post RAI hypothyroidism 60% of patients during 8 years
Post RAI Graves’ disease 10% of patients
Post RAI lifetime cancer risk 1.6% of patients

Surgery treatment apply rare:
Most commonly recommended treatment if conservative treatment noneffective.

Non-Toxic GoitreTreatment options (compressive symptoms):Radioactive iodine (RAI) ablation:Volume reduction 33% - 66% in 80% of patientsImprovement of

Слайд 45Toxic Goitre
Treatment for Toxic MNG:
Thionamide medications:
Not indicated for long-term use

due to complications;
May be used for symptomatic individuals until definitive

treatment.
Radioiodine:
Primary treatment for toxic MNG;
Large I131 dose required due to gland size;
Goitre size reduction by 40% within 1 year;
Risk of hypothyroidism 11% - 24%;
May require second dose.
Surgery:
Used for compressive symptoms;
Hypothyroidism occurs in up to 70% of subtotal thyroidectomy patients;
Pre-surgical stabilization with thionamide medications;
Avoid SSKI (Saturated Solution Of Potassium Iodine) due to risk for acute toxic symptoms.


Toxic GoitreTreatment for Toxic MNG:Thionamide medications:Not indicated for long-term use due to complications;May be used for symptomatic

Слайд 46Graves’ Disease
Diffuse toxic goitre is an autoimmune pathology with prolonged

elevation T3 and T4 and enlagment of thyroid gland. In

70% cases with ophthalmopathy.
Most common cause of thyrotoxicosis is in the industrialized world.
Autoimmune condition with anti-TSHreceptor antibodies.
Onset of disease may be related to severe stress which changes the immune response.
Diagnosis
TSH, T4, T3 to establish toxicosis;
Radioactive iodine uptake (RAIU) scan to differentiate toxic conditions;
Anti-TPO, Anti-TSAb, fT3 as certain markers.
Graves’ DiseaseDiffuse toxic goitre is an autoimmune pathology with prolonged elevation T3 and T4 and enlagment of

Слайд 48Differentiating Causes of Hyperthyroidism

Differentiating Causes of Hyperthyroidism

Слайд 49Pathophysiology of ophthalmopathy

Pathophysiology of ophthalmopathy

Слайд 50Graves disease Ophthalmopathy
A feeling of "sandpaper" in the eyes and

discomfort in the eyes;
Retrobulbar pressure or pain;
Eyelid retraction;
Periorbital edema, chemosis,

scleral injection;
Proptosis of eyebulb;
Extraocular muscle dysfunction;
Exposure keratitis;
Optic neuropathy.


Graves disease OphthalmopathyA feeling of

Слайд 51Graves Disease: Treatment
• Medications:
– Beta-blockers for symptoms – can be

discontinued as thyroid function tests normalize;
– Methimazole (mercazolilum): block and

replace the thyroid hormones;
• Surgery;
• Radioactive iodine administer in patients on the shady side of forty;
Concurrent treatment of eye disease.
Graves Disease: Treatment• Medications:– Beta-blockers for symptoms – can be discontinued as thyroid function tests normalize;– Methimazole

Слайд 52Нypothyroidism
Hypothyroidism - syndrome with particular or total deficiency of T3,

T4 or their acts to target cells.


НypothyroidismHypothyroidism - syndrome with particular or total deficiency of T3, T4 or their acts to target cells.

Слайд 53Classification of hypothyroidism
PRIMARY - defects of biosynthesis of T3, T4

due
to pathology of thyroid gland.

SECONDARY - decreasing T3, T4

level due to
deficiency of TSH (pituitary) or TRH (hypothalamus)
or resistance of receptors for T3, T4 .
Classification of hypothyroidismPRIMARY - defects of biosynthesis of T3, T4 dueto pathology of thyroid gland. SECONDARY -

Слайд 54Primary:

Autoimmune (Hashimoto´s);
Iatrogenic Surgery or 131I administration;
Drugs: amiodarone, lithium;
Congenital (1 in

3000 to 4000);
Iodine defficiency;
Infiltrative disorders.


Primary:Autoimmune (Hashimoto´s);Iatrogenic Surgery or 131I administration;Drugs: amiodarone, lithium;Congenital (1 in 3000 to 4000);Iodine defficiency;Infiltrative disorders.

Слайд 55
Secondary:
Pituitary gland destruction;
Isolated TSH deficiency;
Bexarotene treatment;
Hypothalamic disorders.

Peripheral:
Rare, familial tendency.

Secondary:Pituitary gland destruction;Isolated TSH deficiency;Bexarotene treatment;Hypothalamic disorders.Peripheral:Rare, familial tendency.

Слайд 56Ethyology of congenital hypothyroidism

Ethyology of congenital hypothyroidism

Слайд 57Expected Findings in Congenital Hypothyroidism

Expected Findings in Congenital Hypothyroidism

Слайд 58Expected Findings in Congenital Hypothyroidism

Expected Findings in Congenital Hypothyroidism

Слайд 59Congenital hypothyroidism
Agenesis (no goiter) or dysgenesis ( aplasia, hypoplasia, ectopic

gland) are the most common causes 85%.
Dyshormonogenesis (10%) and a

goiter will be present. Pendred syndrome with sensorineural deafness is the most common ( often euthyroid).
Transplacental maternal TSH receptor blocking Abs (TRBAb) in 5% of cases.
Pituitary failure and maternal administration of toxic substitute for thyroid gland.
Congenital hypothyroidismAgenesis (no goiter) or dysgenesis ( aplasia, hypoplasia, ectopic gland) are the most common causes 85%.Dyshormonogenesis

Слайд 60Congenital hypothyroidism Clinical features
Coarse facial features, dry skin, prolonged jaundice, large

fontanelles, posterior fontanell > 1cm, cutis marmorata, bradycardia, hypothermia, hoarse

cry, cold extremities, short stature, possible deafness.
Hypotonia, lethargy, poor feeding, constipation, macroglossia, umbilical hernia and edema.
The brain is extremely sensitive to the presence of thyroid hormones from end of pregnancy until the 1st week of life, and if left untreated may result in irreversible mental retardation.

Congenital hypothyroidism Clinical featuresCoarse facial features, dry skin, prolonged jaundice, large fontanelles, posterior fontanell > 1cm, cutis

Слайд 63Hypothyroidism Screening in the Newborn
More often the heel stick dried

blood spot on 4th day in term and on 7th

day in preterm is used to examine the T4 level and TSH.

Because of the rapid changes in T4 and TSH in the first few days of life, it is important to take into account when the sample is obtained. Some programs check in follow up in 2-4 weeks.

Different criteria must be employed for LBW babies.


Hypothyroidism Screening in the NewbornMore often the heel stick dried blood spot on 4th day in term

Слайд 66DIAGNOSTIC STUDIES IN HYPOTHYROIDISM
Thyroid scan – 99Tc or I123 uptake;


Bone age;
TSH level!!!
Free T4 level – if hypothalamic-pituitary hypothyroidism
suspected;
TBG (Thyroid

Binding Globulin) – if TBG deficiency is
suspected;
Anti-thyroid antibodies – if there is thyroiditis in
maternal history.
DIAGNOSTIC STUDIES IN HYPOTHYROIDISMThyroid scan – 99Tc or I123 uptake; Bone age;TSH level!!!Free T4 level – if

Слайд 67Biochemical markers of CH
Low serum T4 level and T3 level

with evaluated TSH (primary) level;
T3 –normal, T4 ↓- severe or

longstanding;
T4 –normal but TSH is elevated – compensative CH, transient or subclinical hyperthyroidism;
T4 ↓ but TSH normal- congenital TBG-deficiency or hypothalamic-pituitary hypothyroidism.
Biochemical markers of CHLow serum T4 level and T3 level with evaluated TSH (primary) level;T3 –normal, T4

Слайд 68Biochemical markers of CH
Other:
Elevated serum cholesterol;
Elevated creatinphosphokinase;
Hyponatriemia.

Biochemical markers of CHOther:Elevated serum cholesterol;Elevated creatinphosphokinase;Hyponatriemia.

Слайд 69Instrumental data
Slightly decrease heart rate and amplitude of R wave

(ECG);
Increased left ventricular wall thickness, decrease LV chamber size and

decrease cardiac output (EchoCG);
Low-amplitude diffuse slowing (EEG).
Instrumental dataSlightly decrease heart rate and amplitude of R wave (ECG);Increased left ventricular wall thickness, decrease LV

Слайд 70A. Delayed epiphyseal appearance

B. Epiphyseal dysgenic

A. Delayed epiphyseal appearance         B. Epiphyseal dysgenic

Слайд 71High TSH and Low T4
Management
Primary Congenital Hypothyroidism
Thyroxine
Tablets
25-50-75 ug
Crush it,

add to
5-10 ml of water
or milk
Normal T4
In 2 wks
(upper

½ of N)

Normal TSH
In one month
(lower ½ of N)

Form

Goals

Treatment prevents bone loss, cardiomyopathy, myxedema

High TSH and Low T4Management Primary Congenital HypothyroidismThyroxineTablets25-50-75 ugCrush it, add to5-10 ml of wateror milkNormal T4

Слайд 72Myxedema coma
Reduced level of consciousness, seizures;
Hypotension/shock;
Hypothermia;
Hyponatremia.

Myxedema comaReduced level of consciousness, seizures;Hypotension/shock;Hypothermia;Hyponatremia.

Слайд 73Treatment L-thyroxin (Levothyroxine)

Treatment L-thyroxin (Levothyroxine)

Слайд 74PROGNOSIS
If treatment is delayed, physical development can be hurt slightly.

Early treatment is crucial to prevent mental and intellectual retardation.
Early

treatment of pregnant woman with thyroiditis may prevent mental subnormality in her child.
PROGNOSISIf treatment is delayed, physical development can be hurt slightly. Early treatment is crucial to prevent mental

Слайд 75Juvenile hypothyroidism
A child with growth retardation, constipation, becomes less sociable,

gain weight; his school performance is deteriorating and he is

intolerant to cold. He may also has goiter.
Typical face with dry pale skin and periorbital edema.
Typically no effect on intellect.

Juvenile hypothyroidismA child with growth retardation, constipation, becomes less sociable, gain weight; his school performance is deteriorating

Слайд 76Causes of juvenile hypothyroidism
Hashimoto thyroiditis. More common in girls who

may have initial thyrotoxicosis or be euthyroid or hypothyroid.
Hashimoto may

be associated with Down, Turner and Klinefelter syndromes as well as SLE (systemic lupus erythematosus) and other autoimmune disorders.
A goiter may be present initially with no clinical features of disturbed thyroid function.
Other causes of JH include administration of goitrogens, iodine deficiency, hypothalamic/pituitary disorders and post thyroidectomy.
Causes of juvenile hypothyroidismHashimoto thyroiditis. More common in girls who may have initial thyrotoxicosis or be euthyroid

Слайд 77JH investigations
Antithyroglobulin and antimicrosomal antibodies are found.
Serum T4 is

low (earlier than T3).
Bone age is delayed.
Treatment is with thyroxine.

JH investigations Antithyroglobulin and antimicrosomal antibodies are found.Serum T4 is low (earlier than T3).Bone age is delayed.Treatment

Слайд 78ETIOLOGY OF ACQUIRED HYPOTHYROIDISM
Chronic lymphocytic (Hashimoto`s) thyroiditis (CLT);
Subacute thyroiditis (De

Quervain`s);
Goitrogens (iodide, thiouracil, etc.);
Thyroidectomy or ablation following radioactive iodine;
Infiltrative disease

(e.g., cystinosis, histiocytosis X);
Systemic disease.
Hypothalamic or pituitary disease;
Congenital thyroid disorders, e.g., ectopia, may not decompensate until later childhood and thus may appear acquired;
Peripheral resistance to thyroid hormones, including receptor defects;
Jatrogenic (propylthiouracil, methimazole, iodides, lithium,amiodarone);
Hemangiomas of the liver.
ETIOLOGY OF ACQUIRED HYPOTHYROIDISMChronic lymphocytic (Hashimoto`s) thyroiditis (CLT);Subacute thyroiditis (De Quervain`s);Goitrogens (iodide, thiouracil, etc.);Thyroidectomy or ablation following

Слайд 79SYMPTOMS OF ACQUIRED HYPOTHYROIDISM
Slow growth;
Edema;
Decreased appetite;
Constipation;
Swollen thyroid gland;
Lethargy;
Drop in

school performance;
Cold Intolerance;
Short stature;

Delayed dentition;
Myxedema or mildly overweight;
Goiter;
Galactorrhea;
Menometrorrhagia.

SYMPTOMS OF ACQUIRED HYPOTHYROIDISMSlow growth;Edema; Decreased appetite;Constipation;Swollen thyroid gland;Lethargy;Drop in school performance;Cold Intolerance;Short stature;Delayed dentition;Myxedema or mildly

Слайд 80SIGNS OF ACQUIRED HYPOTHYROIDISM
Delayed reflex return;
Mental depression;
Pale, thick,

or cool skin;
Muscle pseudohypertrophy;
Delayed puberty or precocious puberty;
Treatment – same

CH.

SIGNS OF ACQUIRED HYPOTHYROIDISM Delayed reflex return; Mental depression;Pale, thick, or cool skin;Muscle pseudohypertrophy;Delayed puberty or precocious

Слайд 81Chronic thyroiditis Hashimoto disease
Clinical presentation:
Painless diffuse goiter;
Goiter with euthyroidism;


Toxic thyroiditis;
Hypothyroidism with or without thyromegaly;
Dysphagia, pain or

pressure sensation in the neck, cough and headache.
Chronic thyroiditis Hashimoto diseaseClinical presentation:Painless diffuse goiter; Goiter with euthyroidism;   Toxic thyroiditis;Hypothyroidism with or without

Слайд 82Autoimmune hypothyroidism

Autoimmune hypothyroidism

Слайд 83Diagnosis Hashimoto disease

T4 total and free, serum TSH;
Biopsy;
Antibodies test: antithyroglobulin

antibodies to thyroperoxidase, antimicrosomal test.

Diagnosis Hashimoto diseaseT4 total and free, serum TSH;Biopsy;Antibodies test: antithyroglobulin antibodies to thyroperoxidase, antimicrosomal test.

Слайд 84Treatment
Levothyroxine if hypothyroid;
Triiodothyronine (for myxedema coma);
Thyroid suppression (levothyroxine) to decrease

goiter size;
Surgery treatment if compression or pain take place.

TreatmentLevothyroxine if hypothyroid;Triiodothyronine (for myxedema coma);Thyroid suppression (levothyroxine) to decrease goiter size;Surgery treatment if compression or pain

Слайд 85Subacute Thyroiditis DeQuervain’s, Granulomatous
Most common cause of painful thyroiditis.
Often follows upper

respiratory infection.
FNA may reveal multinuleated giant cells or granulomatous change.
Disease

running:
Pain and thyrotoxicosis (3-6 weeks);
Asymptomatic euthyroidism;
Hypothyroid period (weeks to months);
Recovery (complete in 95% after 4-6 months).
Subacute Thyroiditis DeQuervain’s, GranulomatousMost common cause of painful thyroiditis.Often follows upper respiratory infection.FNA may reveal multinuleated giant

Слайд 86Subacute Thyroiditis DeQuervain’s, Granulomatous
 

Subacute Thyroiditis DeQuervain’s, Granulomatous 

Слайд 87Acute Thyroiditis
Causes:
68% Bacterial (S. aureus, S. pyogenes);
15% Fungal;
9% Mycobacterial.

May occur

secondary to:
Pyriform sinus fistulae;
Pharyngeal space infections;
Persistent Thyroglossal Duct Cyst;
Thyroid

surgery wound infections (rare).

More common in HIV.
Acute ThyroiditisCauses:68% Bacterial (S. aureus, S. pyogenes);15% Fungal;9% Mycobacterial.May occur secondary to:Pyriform sinus fistulae;Pharyngeal space infections;Persistent Thyroglossal

Слайд 88Acute Thyroiditis
Diagnosis:
Warm, painful, enlarged thyroid;
FNA to drain abscess;
RAIU normal (versus

decreased in DeQuervain’s);
CT or US if infected Thyroglossal Duct Cyst

suspected.

Treatment:
High mortality without prompt treatment;
Antibiotics intravenous:
Nafcillin / Gentamycin or Rocephin for empiric therapy;
Search for pyriform fistulae (X-ray examination with barium meal, endoscopy);
Recovery is usually complete.


Acute ThyroiditisDiagnosis:Warm, painful, enlarged thyroid;FNA to drain abscess;RAIU normal (versus decreased in DeQuervain’s);CT or US if infected

Слайд 89Thank you for listening!!!

Thank you for listening!!!

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