Hypothyroidism. Iodine deficiency disorders.
Department of Internal Medicine N2
as.-prof. Svystun I. I.
Anatomy of thyroid gland
The thyroid is a firm vascular organ lying in the neck, caudal to cricoid cartilage.
It is composed of two nearly equal lobes connected by a thin isthmus and weights approximately 20 – 30 g.
Rests of thyroid tissue are occasionally presents in sublingual or retrosternal areas.
Thyroid secrets: T3, T4, calcitonin.
Hyoid Bone
Cricothyroid Ligament
Thyroid Cartilage
Cricoid Cartilage
Trachea
Thyroid GlandPyramidal Lobe
Right LobeIsthmus
Left Lobe
A follicle is structural and functional unit of the thyroid gland
• The follicle contains colloid (which consists of thyroglobuline, a glycoprotein, containing T3 and T4 within its matrix)
• Epithelial cells• Parafollicle cells (C-cells)
(synthesized calcitonine)
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The thyroid hormones, thyroxine (T4) and triiodothyronine (T3)
are secreted under the stimulatory influence of pituitary thyrotropin (thyroid-stimulating hormone or TSH). TSH secretion is primary regulated by a dual mechanism:
• thyrotropin-releasing hormone (TRH);
• thyroid hormone.
Thyroid hormone exits in circulation in both free and bound formas. The thyroid gland is the sole source of T4 and only 20% of T3 is secreted in the thyroid. Approximately 80% of T3 in blood is derived from peripheral tissue (mainly hepatic or renal) deiodinatoin of T4 to T3.
Hypothalamus
TRH stimulation
inhibition
Pituitary
TSH stimulation
Thyroid
T4
T3Liver
ThyroidBindingproteins
Free hormone Bound hormone
Major deiodinative and non-deiodinative pathways of thyroid hormones metabolism.
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Physiologic effects of thyroid hormones
1. Increasing of protein metabolism in virtually every body tissue
2. Increasing of O2 consumption by increasing the activity of Na+ H+ ATPase (Na pump), primarily in tissues responsible for basal O2 consumption (i.e., liver, kidney, heart and skeletal muscle).)
3. Stimulation of erythropoesis
4. Positive chrono- inotropic effects on myocardium
5. Achievement of formation of nervous system and skeleton in perinatal period
Goitre• is an enlargement of the thyroid gland.
Degrees of thyroid gland enlargement(WHO, 1994)
0 –goiter is absent
1- we can palpate but can’t see
2 – thyroid gland can be palpated and seen
Hypothyroidism (myxedema)
is the characteristic reaction to thyroid hormone deficiency.
The spectrum of hormone ranges from a few non – specific symptoms to overt hormone, to myxedema coma.
Historical perspective
• The first full clinical description of the hypothyroidism and mixedema was made in 1874 by Gull (by the cretinoid state supervening in adult life in women)
• Term “myxedeme” first used by Ord in 1978
Epidemiology
- Hypothyroidism occurs in 3 to 6 % for the adult population, but is symptomatic only in a minor of them.
- Usually develops after the age of 30
- It occurs 8 to 10 times more often in women than in men
Classification
I. CongenitalII. Acquired
1. Laboratory (subclinical) hypothyroidism
2. Clinical hypothyroidism
1. Primary (thyroid gland disturbances).
2. Secondary (due to pituitary disease).
3.Tertiary (due to hypothalamic disease).
4.Peripheral.
Etiology of primary hypothyroidism• Congenital- Maldevelopment –hypoplasia or aplasia- Inborn deficiencies of biosynthesis or action of thyroid hormone- Atypical localization of thyroid gland- Severe iodine deficiency• Acquired- iodine deficiency- autoimmune processes (Hashimoto’s thyroiditis): MAE 1 & 2- surgical subtotal removal or total thyroidectomy- irradiation therapy (organs of the neck)- I131 therapy- during or after therapy with propylthyouracil, methimazole, iodides
for hyperthyroidism- infiltrative diseases (tuberculosis, actynomycosis)- trauma- medications such as amiodarone, interferon alpha, thalidomide
Etiology of secondary and tertiary hypothyroidism
• Congenital
- Congenital pituitary or hypothalamus disorders (anatomical or physiological)
• Acquired- Tumors or metastasis• hemorrhagic necrosis (Sheehan’s syndrome)- Inflammatory disorders (infection, infiltrative process)- Trauma- surgical and radiation treatment for pituitary or hypothalamic
disease- Chemical and pharmacological intoxications (reserpin,
bromocriptine).
Etiology of peripheral hypothyroidism
• peripheral tissue resistance to thyroid hormones
• decreasing of T4 peripheral transformation into T3 (in liver or in kidneys)
• production of antibodies to thyroid hormones
Skin and hair
- Skin is dry, thick and silk, is often cool and pale.
- Nonpitting edema of the hands, feet and periorbital regions (myxedema). Pitting edema also may be present.
- The faces are puffy and features are coarse.
the loss of the lateral aspect of the eyebrow, sometimes termed Queen Anne's sign
Skin and hair
- Skin may be orange due to accumulation of carotene.
- Hair may become course and brittle, hair growth slows and hair loss may occur. Lateral eyebrows thin out and body hair is scanty.
- Hypothyroidism does not cause obesity, but modest weight gain from fluid retention and fat deposition often occurs
Nervous system
Patients complain on fatigue, loss of energy, lethargy, forgetfulness, reduced memory.
- Their level of physical activity decreases, and they may speak and move slowly. Mental activity declines and there is inattentiveness, decreased intellectual function, and sometimes may be depression.
- Neurological symptoms include also hearing loss, parasthesias, objective neuropathy, particularly the carpal tunnel syndrome, ataxia.
- Tendon reflex shows slowed or hung-up relaxation.
Cardiovascular system
Complains on: dyspnea, pain in the region of the heart
Objective examination:
• Increased peripheral resistance
• Hypertension
• Bradycardia
• LV hypertrophy with decreased contractility, reduced cardiac output
• Pericardial effusion
• Congestive heart failure- The ECG may show low voltage
and/or non-specific ST segment and T wave changes.
- Hypercholesterolemia
Gastrointestinal system- Gastrointestinal motility is
decreased loading to constipation
and abdominal distension,
pseudoobstruction of intestines,
paralytic ileus.
- Abdominal distension may be
caused by ascities as well. Ascitic
fluid, like other serous effusions in
myxedema, has high protein
content.
- Achlorhydria occurs, often
associated with pernicious anemia.
Renal system- Reduced excretion of a water load may be associated
with hyponatriemia Renal blood flow and glomerular filtration rate are
reduced, but serum creatinine is normal May be mild proteinuria and infections of urinary tract
-Dyspnea of effort is common. This complaint may be caused by enlargement of the
tongue and larynx, causing upper airway obstruction, or by respiratory muscle weakness, interstitial edema of the lungs, and for plural effusions which have high protein content
-Hoarseness from vocal curt enlargement often occurs
Respiratory system
Musculoskeletal system
- Muscle and joint aches, pains and stiffness are common
- Objective myopathy and joint swelling or effusions are less often present
- The relaxation phase of the tendon reflexes is prolonged
- Serum creatine phosphokinase and alanine aminotransferase activities are often increased, probably as much to slowed enzyme degradation as to increased release from muscle
Blood disorders
- Anemia, usually normocytic,
caused by decreased red blood
cell production, may occur.
It is probably from decreased need of peripheral oxygen delivery rather than hematopoetic defect
- Megaloblastic anemia suggests coexistent pernicious anemia
- Most patients have no evidence iron, folic acid or cyancobalamin deficiency
Endocrine system- Thyroid gland: nonpalpable or enlargement. - Adrenal glands: hypofunction
- Pituitary system: secretion of growth
hormone is deficient because thyroid hormone
is necessary for synthesis of growth
hormone. Growth and development of
children are retarded. Epiphyses remain open. - Gonadal glands: menorrhagia (from
anovulatory cycles), secondary amenorrhea,
infertility and galactorrhea; decreased potention in men
Metabolic system
- Hypothermia is common
- Hyperlipidemia with increase of serum cholesterol and trigliceride occurs because of reduced lipoprotein lipase activity
Clinical features
• Hypothyroidism can be presented in many different ways and can mimic other disorders
• Because many manifestations of hypothyroidism
are non-specific,
the diagnosis is particularly likely to be overlooked
in patients with other chronic illnesses and elderly
and can lead to significant morbidity and even mortality
Subclinical (laboratory) hypothyroidism
It is a state in which we can’t find clinical features of
hypothyroidism and euthyroidism is reached by compensatory increasing of TSH secretion and that’s why synthesis and secretion of such level of thyroid hormone that will be enough for organism.
It is an asymptomatic state in which serum T4 and free T4 are normal, but serum TSH is elevated. This designation is only applicable when thyroid function has been stable for weeks or more, the hypothalamic-pituitary-thyroid axis is normal, and there is no recent or ongoing severe illness.
Diagnosing and Managing Thyroid Disease in the Nursing Home . JAMDA. Volume 9, Issue 1 , Pages 9-17, January 2008
Recommendations of Six Organizations Regarding Screening of Asymptomatic Adults for Thyroid Dysfunction
ORGANIZATION SCREENING
RECOMMENDATIONS
American Thyroid Association Women and men >35 years of age
should be screened every 5 years.
American Association of Clinical
Endocrinologists
Older patients, especially women,
should be screened.
American Academy of Family
Physicians
Patients ≥60 years of age should be
screened.
American College of Physicians Women ≥50 years of age with an
incidental finding suggestive
of symptomatic thyroid disease should
be evaluated.
U.S. Preventive Services Task Force Insufficient evidence for or against
screening
Royal College of Physicians of London Screening of the healthy adult
population unjustified
Treatment of hypothyroidism
Replacement therapy
• Synthetic preparations – T4 (l-thyroxine)– T3 (liothyronine sodium)
• Combined:- Thyrocomb- Thyrotom- Thyroidin- Novothyral
Side effects- Allergic reactions- Angina pectoris- Cardiac arrhythmia
Congenital hypothyroidism• Children are born with increased weight• Subcutaneous edema• Hypotermia• Prolonged jaundice• Physical (dwarfism) and mental retardation
(cretinism)
Peculiarities of treatment
< 3 month – 25 mcg/day
3 -12 month – 37,5 mcg/day
1 – 5 years – 75 mcg/day
5 – 7 years – 75 – 100 mcg/day
> 7 years – 100 mcg/day
Precipitating factors include• exposure to cold• infection• Trauma• Surgery• Myocardial infarction• Bleeding • Stress situation• Drugs that suppress the CNS
Myxedema coma - is a life-threatening complication of hypothyroidism
- Slow development (weakness, somnolence, coma)- extreme hypothermia (temperatures 24 to 32)- Areflexia- Seizures- Bradycardia, hypotension- Polyserositis - CO2 retention, and respiratory depression caused by
decreased cerebral blood flow, nonreversible brain changes
- Rapid diagnosis (based on clinical judgment, history, and physical examination) is imperative because early death is likely.
Clinical signs of myxedema coma
Treatment of myxedema coma- large doses of T4 (200-500
mcg i/v bolus 3 – 4 times a day) or T3 if available (40 – 100 mcg i/v bolus 3 times a day), because TBG must be saturated before any free hormone is available for response.
- The maintenance dose for T4 is 50 mkg/day i/v and for T3 10 -20 mcg/day i/v until the hormone can be given orally.
Treatment of myxedema coma- Corticosteroid therapy
(hydrocortisone 200 – 400 – 600 mg/day i/v).
- The patient should not be rewarmed rapidly because of the threat of cardiac arrhythmia.
- Hypoxemia is common, so PaO2 should be measured at the outset of treatment. If alveolar ventilation is compromised, immediate mechanical ventilatory assistance is required.
Thyroiditis
The various types of thyroiditis encompass a heterogeneous group of inflammatory disorders of diverse etiologies and clinical features.
With all forms of thyroiditis, destruction of the normal architecture of the thyroid follicular occurs, yet each disorder has distinctive histologic characteristics.
1. Acute thyroiditis.2. Subacute thyroiditis:• subacute granulamatous thyroiditis;• subacute lymphocytous thyroiditis.3. Chronic thyroiditis:• Hashimoto thyroiditis;• Ridel struma.4. Specific thyroiditis. 5. Thyroiditis caused by mechanical or
physical factors.
Classification
Acute thyroiditis is an acute bacterial inflammation
Etiology: a bacterial pathogen:
- St. aureus, - Str. hemolyticus, - Str. pneumonie, - anaerobic
organisms, - E. coli, - coccidiodomycosis. Infection occurs either - secondary to
hematogenous or lymphatic spread,
- or direct introduction of an infective agent by trauma.
Clinical signs: fever, chills and other signs of abscess formation.
Anterior neck swelling and pain radiating to the ear or mandible.
The physical examination suggests the presence of an abscess, with erythema of the skin, marked tenderness to palpation, and at times fluctuance.
Laboratory: Leucocytosis with a left shift, increased ESR. Thyroid hormone concentrations in
blood are normal, although hyperthyroxinemia has been reported
Treatment
- Patient should be treated at surgical department. - Parental antibiotics should be administered according
to the specific pathogen identified. - If fluctuance is present, incision and drainage might be
required. - Bacterial thyroiditis must be treated early and
aggressively, since abscess formation can occasionally dissect downward into the mediastinum. Recurrences of the disorder are very rare.
- (Duration of the treatment must be nearly 1,5-2 month).
Subacute thyroiditis –an acute inflammatory disease of the
thyroid probably caused by a virus with destruction of thyrocytes
• subacute granulamatous thyroiditis;
• subacute lymphocytous thyroiditis
Subacute thyroiditisEtiology- Coxsackie virus- Adenovirus- Mumps- Echovirus- Influenza- Epstein-Barr virusesA genetic
predisposition is likely because of the association of HLA-BW 35 histocompatibility antigens.
Clinical signs - unilateral anterior neck pain, often
associated with unilateral radiation of pain to the ear or mandible.
- Pain is often proceeded by a few weeks prodrome of myalgias, low-grade fever, malaise and sore throat.
- Dysphagia- Symptoms of hyperthyroidism
Physical examination: an exquisitely tender, very hard, nodular enlargement, which is most often unilateral.
- Tenderness is often so extreme that palpation is limited.
- Tachycardia, a widened pulse pressure, warm skin and diaphoresis are also observed when hyperthyroidism is present.
Subacute thyroiditis• Laboratory findings- Early in the disease we can find an increase in T4, a decrease
in RAI uptake (often 0), leucocytosis and a high ESR. - After a several weeks, the T4, is decreased and the RAI uptake
remains low. - Full recovery is the rule; rarely, patients may become
hypothyroid.• Treatment- An acute phase lasts from 4-8 weeks, during which treatment is
symptomatic (aspirin 600 mg q 3-4 h, prednisolone 10-20 mg orally tid; after 1 week prednisolone can be tapered by 5 mg every 2-3 days; thus glucocorticoids are usually not required for longer than several weeks.
- Symptomatic therapy due to the phase (hyperthyroid – anrithyroid drugs, beta-blockers, hypothyroid – thyroid hormone replacement (levothyroxine 100-150 mkg/day).
• Following the hypothyroid phase recovery occurs, and the normal histologic features and secretory capacity of the thyroid are restored.
Ultrasound of the right lobe of the thyroid demonstrates an ill-defined irregular region of heterogeneous hypoechogenicity without elevation of flow on Colour Doppler examination.
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Chronic thyroiditis.Hashimoto thyroiditis (chronic
lymphocytic thyroiditis) HT• HT is an organ - specific autoimmune
disorder, a chronic inflammation of
the thyroid with lymphocytic infiltration
of the gland generally though to be
caused by autoimmune factors.
It is more prevalent (8:1) in woman than men and is most frequent between the ages of 30 and 50 .
A family history of thyroid disorders is common, and incidence is increased in patients with chromosomal disorders, including Turners, Down and Klinefelters syndromes.
Histologic studies reveal extensive infiltration of lymphocytes in the thyroid.
Clinical features
HT is characterized by a wide spectrum of clinical features, ranging from no symptoms and the presence of small goiter to frank myxedema.
- sensation of tightness in the area of the anterior neck - mild dysphagia. Physical examination usually discloses a
symmetrically enlarged, very firm goiter, a smooth or knobby consistency. Occasionally patients present with a single thyroid nodule.
A small group of patients have a form of HT termed primary idiopathic hypothyroidism, goiter is usually absent in this group (atrophic form of HT).
Yet a small subset of patients(probably 2-4%) present with hyperthyroidism and have so-called hashitoxicosis (hypertrophy from of HT).
Laboratory findings
1. early in the disease - high titers of antithyroid (antimicrosomal) antibodies. Late in the disease, the patient develops hypothyroidism with a decreased in T4,T3 and antibodies in this stage are usually no longer detectable;
2. the thyroid scan typically shows a irregular pattern of iodine uptake;
3. fine-needle biopsy of the nodule or enlarging areashould be done to rule out a coexistent neoplasm.
Ultrasound of thyroid glandUltrasound reveals - hypoechoic thyroid gland with coarse or "micronodular" echotexture of the gland - color doppler imaging reveals augmentation of the vascularity of the gland
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Treatment
- treatment of HT requires lifelong replacement with thyroid hormone to correct and prevent hypothyroidism. The average oral replacement dose with L-thyroxine is 100 to 150 mkg/day;
- glucocorticoids have been reported to be effective in HT when true is a rapidly enlarging goiter associating with pressure symptoms;
- symptomatic therapy
National iodine status in 2013
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• The resulting low level of thyroid hormones in the blood (hypothyroidism) is the principal factor responsible for damage to the developing brain and other harmful effects known collectively as “iodine deficiency disorders” . The adoption of this term emphasizes that the problem extends far beyond simply goitre and cretinism.
Recommended iodine intakeUNICEF, ICCIDD, and WHO recommend that the
daily intake of iodine should be as follows: • • 90 μg for preschool children (0 to 59 months);• • 120 μg for schoolchildren (6 to 12 years);• • 150 μg for adolescents (above 12 years) and
adults; • • 250 μg for pregnant and lactating women.
Diagnostic procedures
Diagnostic procedures
Diagnostic procedures
Blood constituents• TSH
• Thyroglobulin (The thyroid hyperplasia and goitre characteristic of iodine deficiency increases serum Tg levels, and in this setting serum Tg reflects iodine nutrition over a period of months or years)
• thyroxin (T4) and triiodothyronine (T3), is usually not recommended for monitoring iodine nutrition (the serum T4 is typically lower and the serum T3 higher than in normal populations)
Treatment • Iodine Replacement (In an adult, 150 mcg/day)• Universal salt iodization (USI)• Iodine supplementation
• Levothyroxine
• Surgery (standard of care for large goiter associated with obstructive symptoms such as dough, stridor, and dysphagia is thyroidectomy, if the goiter extends into the anterior mediastinum)
THYROID NODULESBenign nodular goiter
Chronic lymphocytic thyroiditis
Simple or hemorrhagic cysts
Follicular adenomas
Subacute thyroiditis
Papillary carcinoma
Follicular carcinoma
Hürthle cell carcinoma
Poorly differentiated carcinoma
Medullary carcinoma
Anaplastic carcinoma
Primary thyroid lymphoma
Sarcoma, teratoma, and miscellaneous tumors
Metastatic tumors
Indications for US of thyroid gland:
–Patients at risk for thyroid malignancy
–Patients with palpable thyroid nodules or MNGs
–Patients with lymphadenopathy suggestive of a malignant lesion
Indications for FNA• Of diameter larger than 1.0 cm that is solid and hypoechoic on
US• Of any size with US findings suggestive of extracapsular growth
or metastatic cervical lymph nodes• Of any size with patient history of neck irradiation in childhood
or adolescence; PTC, MTC, or MEN 2 in first-degree relatives;• Of any size with patient history of previous thyroid surgery for
cancer;• Of any size with patient history of increased calcitonin levels in
the absence of interfering factors;• Of diameter smaller than 10 mm along with US findings
associated with malignancy ;• the coexistence of 2 or more risk of thyroid cancer• Nodules that are hot on scintigraphy should be excluded from
FNA biopsy
Suspicion of malignancy
Suspicion of malignancy
FNA Results and Recommendations
FNA Result Recommendation
Benign Observation
Nondiagnostic Repeat ultrasonography-guided FNA
Papillary thyroid cancer Surgery with preoperative ultrasonography
Suspicious for papillary thyroid cancer
Surgery with preoperative ultrasonography
Indeterminate Hürthle cell neoplasm: Surgery
Bethesda SystemCategory Risk of Malignancy Recommended
Therapy
Nondiagnostic or unsatisfactory
1%-4% Ultrasonography-guided FNA
Benign 0%-3% Observation
Atypia or follicular lesion of undetermined significance
5%-15% Repeat FNA
Follicular neoplasm or suspicious for follicular neoplasm
15%-30% Thyroid lobectomy
Suspicious for malignancy
60%-75% Near total thyroidectomy or lobectomy
Malignant 97%-99% Near total thyroidectomy
An alternative method of reporting thyroid cytopathology is the Bethesda System. In The Bethesda System for Reporting Thyroid Cytopathology (TBSRTC), it is recommended that every report begin with 1 of 6 diagnostic categories. Clinicians can use the diagnostic category and the implied risk of malignancy to guide treatment planning.
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