THYROID GLAND

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THYROID GLAND

• THYROIDITIS

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THYROIDITIS

• It is a heterogeneous group of inflammatory
  disorders involving the thyroid gland, of which
  the etiologies range from autoimmune to
  infectious origins.
• The clinical course may be
• acute, subacute, or chronic.

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A classification of thyroiditis

• Autoimmune thyroiditis
• Chronic autoimmune thyroiditis
• Hashimotos thyroiditis
• Atrophic thyroiditis
• Focal thyroiditis
• Juvenile thyroiditis
• Silent thyroiditis
• Postpartum thyroiditis

• Acute thyroiditis
• infectious
• non-infectious
• Subacute thyroiditis

• IV. Riedels thyroiditis

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ACUTE INFECTIOUS THYROIDITIS

• Rare, serious, bacterial inflammatory disease of
  the thyroid.

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Protective mechanisms of the thyroid gland

• very good perfusion
• efficient lymphatic drainage
• capsulation of the thyroid
• high concentration of iodine

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Etiologic agents

• Streptococcus pyogenes,
• Streptococcus pneumoniae,
• Escherichia coli,
• Pseudomonas aeruginosa,
• Salmonella typhi,
• anaerobes of the oropharyngeal cavity.

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RARE FORMS OF INFECTIOUS THYROIDITIS

• the thyroid is rarely the seat of tuberculosis,
  syphilis, fungal infections (Aspergillus
  species), or parasites
• Pneumocystis carinii infection of the thyroid has
  been reported in patients with AIDS.

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• hematogenous seeding
• from distant foci

Infection to the thyroid occurs by

• direct
• trauma

through a persistent thyroglossal duct
extension from adjacent infected structures
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CLINICAL PICTUREOF ACUTE INFECTIOUS THYROIDITIS

• severe anterior neck pain of abrupt onset, pain
  may radiate to the ear, mandible, or occiput
  dysphagia, dysphonia, fever, rigor, diaphoresis
• palpation shows a unilateral or less-frequently
  bilateral tender swelling of the thyroid which is
  associated with cervical lymphadenopathy

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CLINICAL PICTUREOF ACUTE INFECTIOUS THYROIDITIS

• the skin over the infected area is erythematous
  and warm
• the white cell count and erythrocyte
  sedimentation rate are elevated
• thyroid antibodies are absent
• serum T4 and T3 levels are usually normal as well
  as thyroid RAIU

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CLINICAL PICTUREOF ACUTE INFECTIOUS THYROIDITIS

• the isotope scans reveal a cold defect in the
  involved lobe
• ultrasonography shows an enlarged irregular mass
  of mixed echogenicity
• the presence at fine-needle aspiration of
  purulent material is confirmatory of suppurative
  thyroiditis and allows for the identification of
  the causative agent

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Ultrasonography of acute bacterial thyroiditis
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Ultrasonography of acute bacterial thyroiditis
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TREATMENT OF INFECTIOUS THYROIDITIS

• this type of thyroiditis requires the
  administration of appropriate antibiotics based
  on the findings of the culture from a fine-needle
  aspirate, and surgical drainage (or excision) of
  any area of fluctuance or abscess.

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• Before the results of the culture
• a combined regimen of nafcilin and gentamicin or
  a third generation cephalosporin would be
  appropriate treatment.

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NON-INFECTIOUS THYROIDITIS

• clinical picture depends on causative agents

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NON-INFECTIOUS THYROIDITIS

• AFTER 131J THERAPY
• (hyperthyroidism, thyroid cancer)
• tender swelling of the thyroid,
• itching of the skin over thyroid,
• subfebrile body temperature

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NON-INFECTIOUS THYROIDITIS

• AFTER RADIOTHERAPY
• (external radiotherapy of the thyroid cancer,
  complementary external radiotherapy in patients
  with breast cancer)
• asymptomatic or oligosymptomatic course, leading
  into hypothyroidism

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NON-INFECTIOUS THYROIDITIS

• AFTER TRAUMA OF THE NECK
• (bleeding to thyroid parenchyma
• or thyroid cyst)
• severe anterior neck pain of abrupt onset,
• swelling of the thyroid,
• fluctuation

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NON-INFECTIOUS THYROIDITISTREATMENT

• In milder cases disappear spontaneously
• In some cases
• salicylates or
• non steroidal anti-inflammatory drugs
• (Polopiryni S 2-3 g/day,
• Paracetamol 1.5-2.0g/day)
• Exceptionally
• corticosteroids
• (Prednisone 20-30mg/day)

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SUBACUTE (GRANULOMATOUS) THYROIDITIS (DE
QUERVAINS DISEASE)

• A spontaneously remitting, painful, inflammatory
  disease of the thyroid, probably of viral origin.
  
• It is the most frequent cause of anterior neck
  pain.
• Most prevalent in the temperate zone.
• Afflicts more frequently women between the third
  and sixth decades of life.

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SUBACUTE THYROIDITIS ETIOLOGY

• PROBABLY VIRAL,
• THERE ARE SOME EVIDENCES
• Often preceded by an upper respiratory tract
  viral infection
• Prodromal viral symptoms
• Seasonal distribution (summer and fall)

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SUBACUTE THYROIDITIS ETIOLOGY

• Occurs in coincidence with outbreaks of viral
  diseases (mumps, measles, influenza)
• Elevated titers of viral antibodies
  (coxsackievirus, adenovirus, mumps) have been
  found in convalescent sera of patients with
  subacute thyroiditis

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SUBACUTE THYROIDITIS HISTOPATHOLOGICAL CHANGES

• infiltration with neutrophils and mononuclear
  cells,
• disruption of follicles,
• typical lesion characterized by a central core of
  colloid surrounded by a large number of
  individual histiocytes
• (giant multinucleated cells).

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SUBACUTE THYROIDITIS CLINICAL PICTURE

• There is usually a viral prodrome with
• myalgias,
• low-grade fever,
• sore-throat
• dysphagia

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SUBACUTE THYROIDITIS CLINICAL PICTURE

• Anterior neck pain occurs abruptly, is sometimes
  unilateral, and may radiate to the ear, mandible
  or occiput, pain may shift to the contralateral
  lobe
• (creeping thyroiditis)
• moving the head, swallowing, or coughing
  aggravate the pain.

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SUBACUTE THYROIDITIS CLINICAL PICTURE

• Symptoms of thyrotoxicosis
• may occur
• ?
• the release of performed thyroid hormones from
  disrupted follicles

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SUBACUTE THYROIDITIS CLINICAL PICTURE

• On palpation
• the thyroid is slightly to moderately enlarged,
• sometimes asymmetrical or even nodular,
• firm,
• tender
• and painful

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SUBACUTE THYROIDITIS LABORATORY FINDINGS

• elevated erythrocyte sedimentation rate
  (gt55mm/h),
• normal or slightly elevated leukocyte counts,
• increased serum IL-6 and Tg concentrations during
  the thyrotoxic phase,
• thyroid antibodies are transiently detectable at
  low titers in a minority of patients

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THE PHASES OF SUBACUTE THYROIDITIS

• THYROTOXIC
• high T4 and/or T3 level,
• low TSH level,
• RAIU value lt5
• (isotope scans show a cold area in the involved
  section of the gland or no uptake at all)

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THE PHASES OF SUBACUTE THYROIDITIS

• HYPOTHYROID
• low T4,
• high TSH level,
• normal RAIU value

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THE PHASES OF SUBACUTE THYROIDITIS

• RECOVERY
• normal T4 and T3 level,
• normal TSH level,
• normal RAIU value

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SUBACUTE THYROIDITIS

• The course of the disease may last 2 to 6 months
  without treatment.
• Recurrences of the subacute thyroiditis are
  reported in about one-fifth of the patients.
• Permanent hypothyroidism is rare
• (1-5).
• The disease may evolve into chronic autoimmune
  thyroiditis.

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SUBACUTE THYROIDITISTREATMENT

• In milder cases
• salicylates or non steroidal anti-inflammatory
  drugs provide some relief of pain and tendernees.

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SUBACUTE THYROIDITISTREATMENT

• In more severe cases
• corticosteroids
• (prednisone 40-60mg/day)
• have a more dramatic and rapid effect
• the corticosteroid is slowly tapered over the
  next 6 to 8 weeks and then discontinued.

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SUBACUTE THYROIDITISTREATMENT

• Symptoms of thyrotoxicosis should be managed
  with B-adrenergic blocking agents
• (Propranolol 20-40mg,
• 3 to 4 times daily)
• In patients with hypothyroidism L-T4 replacement
  is needed.

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AUTOIMMUNE THYROIDITIS

• CHRONIC AUTOIMMUNE THYROIDITIS PRESENTS WITH TWO
  CLINICAL ENTITIES

a goitrous form (Hashimoto thyroiditis)
an atrophic form (atrophic thyroiditis or primary
myxedema)
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AUTOIMMUNE THYROIDITIS

• Treatment with immunosuppressive agents
  (corticosteroids) is not recommended in
  autoimmune thyroiditis.
• Lifelong substitution therapy with L-thyroxine is
  indicated in hypothyroid patients.

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AUTOIMMUNE THYROIDITIS

• Among children living in areas of iodine
  sufficiency, juvenile lymphocytic thyroiditis is
  the cause of euthyroid goiter in about one-half
  to two-thirds of patients.
• Silent thyroiditis is characterized by transient
  thyrotoxicosis with low thyroid radioiodone
  uptake and a small, painless, nontender goiter.

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AUTOIMMUNE THYROIDITIS

• The postpartum rebound of immunity may be
  accompanied by destructive thyroiditis
  (postpartum thyroiditis), resulting in transient
  thyrotoxicosis evolving to hypothyroidism, or
  hypothyroidism alone, followed by gradual
  recovery.

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AUTOIMMUNE THYROIDITISETIOLOGY

• Organ-specific autoimmunity is the cause of the
  disease,
• the thyroid is infiltrated by lymphocytes,
• thyroid antibodies are present in serum,
• and there is a clinical or immunological overlap
  with other autoimmune diseases.

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AUTOIMMUNE THYROIDITISETIOLOGY

• Activated, autoreactive T-helper recruit in the
  thyroid
• cytotoxic T cells
• (T cells may kill directly thyroid cells or also
  cause tissue injury by release of cytokines)
• and B cells
• (are transformed into plasmacytes which produce
  antithyroid antibodies)

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AUTOIMMUNE THYROIDITISETIOLOGY

• ANTITHYROID ANTIBODIES
• thyroid peroxidase antibodies (TPOAb),
• thyroglobulin antibodies (TgAb),
• TSH-blocking antibodies

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AUTOIMMUNE THYROIDITISETIOLOGY

• Environmental factors
• (infectious agents, therapeutically administered
  interferon alpha, physical and emotional stress,
  and increased iodine intake)
• may be important for the development of
  autoimmune thyroiditis.

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AUTOIMMUNE THYROIDITISEPIDEMIOLOGY

• the disease is most often diagnosed between the
  ages of 50 - 60 years,
• 5 to 7 times more frequently in women than in
  men
• the prevalence of thyroid antibodies
• (which correlates with autoimmune thyroiditis)
• is higher in communities with sufficient iodine
  intake and increases from 6 to 27 in the second
  to sixth decades of life in women.

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AUTOIMMUNE THYROIDITISCLINICAL PICTURE

• Patients may present a goiter with or without
  hypothyroidism.
• A feeling of tightnees in the neck may occur, but
  compression of the trachea is uncommon.

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AUTOIMMUNE THYROIDITISCLINICAL PICTURE

• On physical examination
• most Hashimotos glands are diffusely enlarged,
• but one lobe may be larger than the other,
• and the pyramidal lobe may be palpable
• the goiter is generally moderate in size, though
  massive enlargements may occur

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AUTOIMMUNE THYROIDITISCLINICAL PICTURE

• On physical examination
• the gland is nontender, firm or rubbery in
  consistency, with a bosselated surface
• the thyroid gland is reduced in size in atrophic
  thyroiditis.

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AUTOIMMUNE THYROIDITISCLINICAL PICTURE

• Thyrotoxicosis (Hashitoxicosis) rarely occurs,
  due to a combination of Hashimotos thyroiditis
  with Graves disease in the same patient or to
  the transient discharge of performed thyroid
  hormones as a result of the inflammatory process.

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AUTOIMMUNE THYROIDITISDIAGNOSTIC PROCEDURES

• TSH, FT4 and FT3 serum levels

HYPOTHYROIDISM
HASHITOXICOSIS
FT4? FT3? TSH?
FT4? FT3? ? ? TSH ?
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AUTOIMMUNE THYROIDITISDIAGNOSTIC PROCEDURES

• Antithyroid antibodies are positive
• TPOAb ?95 patients
• TgAb ?60-80 patients
• In a few patients antithyroid antibodies are in
  low or undetectable titers
• (seronegative Hashimotos thyroiditis)

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AUTOIMMUNE THYROIDITISDIAGNOSTIC PROCEDURES

• Thyroid radionuclide scan and radioactive iodine
  uptake (RAIU) are not crucial to the diagnosis
• (normal, low, or high).
• An ultrasound pattern of the thyroid
• ?
• diffusely reduced echogenicity

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AUTOIMMUNE THYROIDITISDIAGNOSTIC PROCEDURES

• FNAB- cytological smears of Hashimotos
  thyroiditis are rich in lymphocytes and oxyphil
  cells
• (it is advisable in patients with suspicious
  nodules or a rapidly enlarging goiter in order to
  rule out malignancy).

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• Chronic autoimmune thyroiditis is a component of
  type 2 autoimmune polyglandular syndrome, a
  condition characterized by a coexistence of two
  or more of the following disorders
• Addisons disease, autoimmune thyroiditis,
  insulin dependent diabetes mellitus, atrophic
  gastritis with or without pernicious anemia,
  vitiligo, alopecia, myasthenia gravis, and
  hypophysitis.

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AUTOIMMUNE THYROIDITISTREATMENT

• Corticosteroids are not recommended
• Substitution therapy with L-T4 at a dose that
  normalizes serum TSH levels
• the average daily replacement dose of L-T4 in
  adults is 1.6ug/kg body weight
• 75-100ug/day in women and 100-150ug/day in men.

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SILENT (PAINLESS) THYROIDITIS

• it is characterized by transient thyrotoxicosis
  with low RAIU, and a small, painless, nondender
  goiter.
• Thyrotoxicosis results from damage of follicular
  cells by the inflammatory process, with leakage
  of performed thyroid hormones in the bloodstream.

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SILENT (PAINLESS) THYROIDITIS

• The overall prevalence of silent thyroiditis as a
  cause of thyrotoxicosis ranges from 4 to 15
• greater prevalence in previously iodine-deficient
  areas, but recently exposed to sufficient iodine
  
• the female/male ratio is 21

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SILENT THYROIDITISCLINICAL PICTURE

• Silent thyroiditis presents with a relatively
  abrupt onset of symptoms of mild thyrotoxicosis
• tachycardia, ?heat intolerance,
• sweating, ?nervousness,
• weight loss.
• Serum Tg and urinary iodine concentrations are
  increased

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SILENT THYROIDITISCLINICAL PICTURE

• THERE ARE 3 PHASES
• thyrotoxicosis,
• hypothyroidism,
• recovery.
• Persistent hypothyroidism may also develop in
  about 5.

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SILENT THYROIDITISCLINICAL PICTURE

• Differentiation from Graves hyperthyroidism is
  important.
• In silent thyroiditis
• abrupt onset,
• thyrotoxicosis less severe,
• duration of thyrotoxicosis lt 3 months,
• thyroid bruit, ophthalmopathy and dermopathy
  absent,
• T3/T4 ratio lt 20/1,
• RAIU low,
• TSH-R antibodies usually negative,
• thyrotoxicosis transient.

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SILENT THYROIDITISTREATMENT

• Anti-thyroid drugs or radioiodine are
  inappropriate for treatment of silent
  thyroiditis.
• In thyrotoxic phase
• ß-adrenergic blocking agents
• In hypothyroid phase
• L-T4 replacement therapy

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POSTPARTUM THYROIDITIS

• During pregnancy all autoimmune reactions are
  inhibited by a number of physiologic factors,
  and following delivery there is a reversal of
  these alterations with rebound of autoimmune
  phenomena.

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POSTPARTUM THYROIDITIS

• The incidence of PPT
• ranges from 1 to 16 of women
• during the first year after delivery.

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POSTPARTUM THYROIDITIS

• Risk factors for the development of PPT include
• positive TPOAb in the first trimester of
  pregnancy,
• type 1 diabetes mellitus,
• a history of chronic autoimmune thyroiditis or
  Graves disease, or a previous episode of PPT
  during a preceding pregnancy.

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POSTPARTUM THYROIDITIS

• The clinical course and treatment are the same as
  described above for silent thyroiditis

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RIEDELS THYROIDITIS (SCLEROSING THYROIDITIS,
INVASIVE FIBROUS THYROIDITIS)

• It is a rare, chronic inflammatory disorder of
  unknown etiology, characterized by dense fibrosis
  involving the thyroid and adjacent tissues, and
  extracervical areas
• (fibrous mediastinitis, retroperitoneal fibrosis,
  retro-orbital fibrosis, sclerosing cholangitis,
  and pancreatitis).
• It occurs mainly in middle-age or elderly women.

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RIEDELS THYROIDITIS CLINICAL PICTURE

• A patient will present with a long history of a
  painless, progressively increasing anterior neck
  mass.
• Pressure symptoms
• dysphagia, cough, hoarseness, stridor, attacks of
  suffocation)
• may appear.
• Most patients are euthyroid

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RIEDELS THYROIDITIS CLINICAL PICTURE

• On physical examination
• ?
• a stony-hard or woody thyroid mass that varies in
  size from small to very large, may involve one or
  both lobes, and is fixed to surrounding
  structures.

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RIEDELS THYROIDITIS CLINICAL PICTURE

• Thyroid antibodies are present in up to 45 of
  patients.
• Serum calcium may be low due to parathyroid
  invasion.
• Differentiation from thyroid carcinoma or
  lymphoma of the thyroid requires open biopsy,
  since FNAB may be difficult to interpret.

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RIEDELS THYROIDITIS CLINICAL PICTURE

• Surgical treatment is necessary to relieve
  pressure on the trachea and to establish
  diagnosis.
• Corticosteroids are of little or no value.
• The course of the lesion may be slowly
  progressive, may stabilize, or remit.
• Extrathyroidal fibrotic lesions may complicate
  the prognosis.