thyroiditis by dr shahjada selim
TRANSCRIPT
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Thyroiditis
Dr Shahjada SelimAssistant Professor
Department of EndocrinologyBangabandhu Sheikh Mujib Medical University, Dhaka
Email: [email protected]
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THYROIDITIS
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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Classification of Tyroiditis:
1. Acute thyroiditisInfectious Non-infectious
2. Subacute thyroiditis
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Classification of Thyroiditis:
3. Autoimmune thyroiditisa.Chronic autoimmune thyroiditis:
o Hashimoto’s thyroiditis
o Atrophic thyroiditis
o Focal thyroiditis o Juvenile thyroiditis
b. Silent thyroiditis
c. Postpartum thyroiditis
4. Riedel’s 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 perfusionefficient lymphatic drainagecapsulation of the thyroidhigh concentration of iodine …. Even then infection can occur..
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Etiologic agents:Streptococcus pyogenes Streptococcus pneumoniae Escherichia coliPseudomonas aeruginosa Salmonella typhianaerobes 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 seedingfrom distant foci
extension from adjacent infected structures
direct trauma
through a persistent
thyroglossal duct
Infection to the thyroid occurs by::
How thyroid becomes infected
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Clinical Picture of 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 Picture of 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 Picture of 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 Thyroidtis
• 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 131I THERAPY
(for 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 Neck Trauma (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 QUERVAIN’S 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 infections;There are some evidence:Often preceded by an upper respiratory tract viral infection
Prodromal viral symptomsSeasonal 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, which 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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Laboratory Findings of Subacute Thyroiditis
elevated erythrocyte sedimentation rate (>55mm/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 <5% (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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a goitrous form
(Hashimoto thyroiditis)
an atrophic form (atrophic thyroiditis
or primary myxedema)
AUTOIMMUNE THYROIDITIS
Chronic Autoimmune Thyroiditis Presents with 2 Clinical Entities:
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Treatment with immunosuppressive agents (corticosteroids) is not recommended in autoimmune thyroiditis.
Lifelong substitution therapy with L-thyroxine is indicated in hypothyroid patients.
AUTOIMMUNE THYROIDITIS
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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.
AUTOIMMUNE THYROIDITIS
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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.
AUTOIMMUNE THYROIDITIS
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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.
AUTOIMMUNE THYROIDITISETIOLOGY
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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)
AUTOIMMUNE THYROIDITISETIOLOGY
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ANTITHYROID ANTIBODIES: thyroid peroxidase antibodies
(TPOAb), thyroglobulin antibodies
(TgAb), TSH-blocking antibodies
AUTOIMMUNE THYROIDITISETIOLOGY
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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.
AUTOIMMUNE THYROIDITISETIOLOGY
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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.
AUTOIMMUNE THYROIDITISETIOLOGY
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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.
AUTOIMMUNE THYROIDITISClinical Feature
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On physical examination most Hashimoto’s 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;
AUTOIMMUNE THYROIDITISClinical Feature
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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.
AUTOIMMUNE THYROIDITISClinical Feature
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Thyrotoxicosis (Hashitoxicosis) rarely occurs, due to a combination of Hashimoto’s thyroiditis with Graves’ disease in the same patient or to the transient discharge of performed thyroid hormones as a result of the inflammatory process.
AUTOIMMUNE THYROIDITISClinical Feature
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AUTOIMMUNE THYROIDITISDIAGNOSTIC PROCEDURES
TSH, FT4 and FT3 serum levels
HASH
ITOXICO
SIH
ASHITO
XICOSI
SS
FTFT44 FT FT33
TSHTSH
HYPO
THYRO
IDIS
HYPO
THYRO
IDIS
MM
FTFT44 FT FT33
TSH TSH
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AUTOIMMUNE THYROIDITIS
DIAGNOSTIC PROCEDURESAntithyroid antibodies are positive:• TPOAb 95% patients• TgAb 60-80% patients
In a few patients antithyroid antibodies are in low or undetectable titers (seronegative Hashimoto’s 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 Hashimoto’s 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:
Addison’s 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 recommendedSubstitution 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 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.
SILENT (PAINLESS) THYROIDITIS
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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 ~ 2:1;
SILENT (PAINLESS) THYROIDITIS
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SILENT THYROIDITISCLINICAL PICTURE
Silent thyroiditis presents with a relatively abrupt onset of symptoms of mild thyrotoxicosis:
tachycardiaheat intoleranceSweatingnervousnessweight 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 severeduration of thyrotoxicosis < 3 months,
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SILENT THYROIDITISCLINICAL PICTURE
thyroid bruit, ophthalmopathy and dermopathy absent,
T3/T4 ratio < 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: β-adrenergic blocking agents
In hypothyroid phase: L-T4 replacement therapy
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During pregnancy all autoimmune reactions are inhibited by a number of physiologic factors, and followingdelivery there is a reversal of these alterations with rebound of autoimmune phenomena.
POSTPARTUM THYROIDITIS (PPT)
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The incidence of PPT ranges from 1% to 16% of women during the first year after delivery.
POSTPARTUM THYROIDITIS (PPT)
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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.
POSTPARTUM THYROIDITIS (PPT)
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The clinical course and treatment are the same as described above for
silent thyroiditis
POSTPARTUM THYROIDITIS (PPT)
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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 elderlywomen.
RIEDEL’S THYROIDITIS (SCLEROSING THYROIDITIS, INVASIVE FIBROUS
THYROIDITIS)
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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
RIEDEL’S THYROIDITIS CLINICAL PICTURE
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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.
RIEDEL’S THYROIDITIS CLINICAL PICTURE
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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.
RIEDEL’S THYROIDITIS CLINICAL PICTURE
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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.
RIEDEL’S THYROIDITIS CLINICAL PICTURE
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Thanks