THYROIDITIS HYPOTHYROIDISM - SRM University and... · THYROIDITIS & HYPOTHYROIDISM A PRESENTATION ON. CONTENTS OF ... Struma lymphomatosa –a

THYROIDITIS &

HYPOTHYROIDISM

A PRESENTATION ON

CONTENTS OF PRESENTATION

I.THYROIDITIS

• ACUTE SUPPURATIVE THYROIDITIS• SUBACUTE THYROIDITIS

‐ Subacute granulomatous‐ Subacute lymphomatous

• CHRONIC THYROIDITIS‐ Hashimoto’s thyroiditis‐ Riedel’s thyroiditis

II.HYPOTHYROIDISM

CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s thyroiditis)

• Struma lymphomatosa – a transformation of thyroid tissue to lymphoid tissue

• First described autoimmune disease

• Commonest form of thyroiditis

Hashimoto’s thyroiditis is named after Hakaru Hashimoto (May 5, 1881 –January 9, 1934) , who described it first in 1912

CHRONIC LYMPHOCYTIC THYROIDITIS (Hashimoto‘s

thyroiditis)

ACTIVATION OF CD4+T HELPER CELLS SPECIFIC FOR THYROID ANTIGENS

CD 8+ CYTOTOTOXIC CELLS ARE RECRUITED

AUTO ANTIBODIES AGAINST THYROID ANTIGENS

COMPLEMENT FIXATION AND KILLING BY NATURAL KILLER CELLS

DESTRUCTION OF THYROCYTES

MECHANISM OF DISEASE DEVELOPMENT


thyroiditis)

RISK FACTORS• Genetic predisposition

• Chromosomal abnormalities (eg. Turner’s, Down’s)

• HLA B8, DR5, DR3


thyroiditis)

PRESENTATION• Common in 30 – 50 yr old women

• Moderately enlarged, firm, nodular gland

• Symptoms of transient hyperthyroidism (HASHITOXICOSIS)

• Hypothyroidism

• Papillary carcinoma and malignant lymphoma ( non hodgkins type) are occasionally associated


thyroiditis)DIAGNOSIS

• Elevated TSH ( transiently reduced during Hashitoxicosis)

• Thyroid auto antibodies – antibodies against

‐Thyroid peroxidase

‐Thyroglobulin

‐TSH receptor

• USG – nodular enlarged thyroid

• FNAC


thyroiditis)

PATHOLOGY

• Diffuse parenchymal infiltration by lymphocytes (plasma Bcells) leading to germinal centre formation

• Atrophied colloid bodies lined by Hurthle cells or askanazy cells This high power microscopic

view of the thyroid with Hashimoto's thyroiditis demonstrates the pink Hürthle cells at the center and right. The lymphoid follicle is at the left.


thyroiditis)TREATMENT• Thyroid hormone replacement

• Maintenance of normal TSH LEVELS

• INDICATIONS FOR SURGERY

‐ Compressive symptoms

‐ Cosmetic deformity

RIEDEL’S THYROIDITIS(Riedel's struma )

• Chronic form of Autoimmune thyroiditis

• Replacement of the normal thyroid parenchyma by a dense fibrosis

• Invades adjacent structures of the neck and extends beyond the thyroid capsule.

• Associated with other focal sclerosing syndromes


PRESENTATION• Common in women 30 – 60 ys old• Painless , hard, enlarged thyroid gland• Compressive symptoms are common• Hypothyroidism and hypo parathyroidism

DIAGNOSIS• Pathological examination of tissue obtained from wedge biopsy of

isthmus• FNAC is not useful


TREATMENT• Tracheal decompression by wedge biopsy of isthmus

• Thyroid hormone replacement

• Corticosteroids

• Tamoxifen ( in steroid resistant cases)

ACUTE SUPPURATIVE THYROIDITIS

• Very rare, accounting for about 0.1‐0.7% of all thyroiditis

• More common among children

• Modes of infection

‐ Hematogenous spread‐ Lymphatic spread‐ Congenital pyriform sinus fistula‐ Penetrating trauma


PATIENT PRESENTATION• Severe pain

• High grade fever with chills

• Odynophagia / dysphonia

INVESTIGATIONS• Leucocytosis

• USG – unilateral thyroid swelling

• FNAC – for gram stain / culture / cytology

• CT SCAN – extent of infection


• Common organisms involved

‐ Staph. aureus

‐ Strep. pyogenes

‐ Strep. pneumoniae

• Confirmation of a persistent pyriform sinus fistula

‐ Laryngioscopy

‐ Barium swallow

‐ CT scan

BARIUM SWALLOW SHOWING A PYRIFORM SINUS FISTULA


TREATMENT • Appropriate parenteral antibiotics

• Surgical drainage of the abscess

• Resection of the sinus tract , including area of thyroid where the tract terminates


COMPLICATIONS• Tracheal or esophageal rupture

• Systemic sepsis

• Jugular vein thrombosis

• Laryngeal chondritis

• Sympathetic trunk paralysis

SUBACUTE THYROIDITIS

SUBTYPES

I. Subacute granulomatous thyroiditis (painfull type)

II. Subacute lymphocytic thyroiditis (painless type)

SUBACUTE GRANULOMATOUS THYROIDITIS(Painfull thyroiditis)

• Also known as DE QUERVAIN’S THYROIDITIS

• Associated with post viral inflammatory response , leading to auto immune destruction of thyroid follicles

PRESENTATION• 30 – 40 yr old female with preceding history of viral illness

• Sudden / gradual onset neck pain

• Enlarged, tender, firm thyroid gland

• Painful dysphagia

SUBACUTE GRANULOMATOUS THYROIDITIS(Painfull thyroiditis)

COURSE OF DISEASE

Thyroid follicle damage and release of colloids into the circulation

HYPER THYROID PHASE

Pitutary reduces the release of TSH

EUTHYROID PHASE

Inappropriately released colloids are depleted from circulation

HYPOTHYROID PHASE

RESOLUTION TO EUTHYROID PHASE

SUBACUTE GRANULOMATOUS THYROIDITIS(Painfull

thyroiditis)INVESTIGATIONS• TFT

• Radio iodine uptake scan

‐ Reduced iodine uptake

( increased iodine uptake is a feature of GRAVE’S DISEASE)

• Thyroid antibodies

• Raised ESR

• HPE – granuloma, with multinucleated giant cells

A granuloma in subacute thyroiditis.

SUBACUTE GRANULOMATOUS THYROIDITIS(Painfull

thyroiditis)TREATMENT• Self limiting disease course

• NSAIDS

• Beta blockers for symptomatic releif

• Short term thyroid replacement

• Thyroidectomy – indicated only in prolonged , unresponsive disease

SUB ACUTE LYMPHOCYTIC THYROIDITIS(PAINLESS THYROIDITIS)

• Auto immune etiology

• Can occur in

‐ SPORADIC FORM

‐ POSTPARTUM FORM

• POSTPARTUM THYROIDITIS – caused due to immune system changes that occur during pregnancy

SUB ACUTE LYMPHOCYTIC

THYROIDITIS(PAINLESS THYROIDITIS)PRESENTATION

• Common in 30 – 60 yr old females• Normal or slightly enlarged, firm painless

thyroid gland• TSH , Tg fluctuations similar to PAINFULL

THYROIDITIS

INVESTIGATIONS• TFT• Normal ESR• RAIU – reduced• Thyroid antibodies

SUB ACUTE LYMPHOCYTIC

THYROIDITIS(PAINLESS THYROIDITIS)

TREATMENT• NSAIDS

• Beta blockers for symptomatic releif

• Thyroidectomy is reserved only for recurrent disabling disease

POST PARTUM THYROIDITIS

• Beta blockers in symptomatic hyperthyroid phase

• Short course of L – thyroxine in case of severe hypothyroidism

• Treatment usually upto one year postpartum

HYPOTHYROIDISM

DISCUSSION INCLUDES

I. ADULT HYPOTHYROIDISM

II. CRETINISM

ADULT HYPOTHYROIDISM

CLASSIFICATIONPrimary Primary defect in the function of thyroid gland

• Iodine deficiency • Hashimoto's thyroiditis,• Radioiodine therapy for hyperthyroidism• Subacute thyroiditis• Temporary hypothyroidism due to the Wolff‐

Chaikoff effect• Amiodarone ,lithium‐based mood stabilizers, usually

used to treat bipolar disorder interferon alpha, interleukin‐2, and thalidomide

ADULT HYPOTHYROIDISM

CLASSIFICATIONSecondary• Occurs if the pituitary gland does not

create enough thyroid‐stimulating hormone (TSH) to induce the thyroid gland to produce enough thyroxine and triiodothyronine.

Tertiary• Results when the hypothalamus fails

to produce sufficient thyrotropin‐releasing hormone (TRH).

Signs and symptoms

• CNS – impaired memory, impaired cognitive function, increased need to sleep, sluggish reflexes

• ANS – low basal body temperature, cold intolerance, decreased sweating

• PSYCHOLOGICAL – mood istability, irritability, depression

• CVS – bradycardia, conduction defects

• GIT – weight gain, constipation

• MUSCULOSKELETAL – muscle hypotonia, muscle cramps,joint pain

Signs and symptoms

• SENSORY – deafness, anosmia

• DERMATALOGICAL – dry itchy skin, brittle nails, yellowish discolouration of skin, loss of hair, thinning of lateral one thirds of eye brow(sign of Hertoghe)

• HEMATOLOGICAL – anemia

• HORMONAL – menstural abnormality, female infertility, loss of libido in male, gynecomastia

• OTHERS – hoarseness of voice, caused by Reinke's Edema.

MYXEDEMA

MYXEDEMA is used to describe the clinical syndrome secondary to severe

hypothyroidism.

SYMPTOMS• Supraclavicular puffiness, • Malar flush, • Yellow tinge to the skin • Depression , • Mental slowness, • Weakness , • Bradycardia , • Fatigue ,• Hypothermia ,• Alopecia

MYXEDEMA COMA

MYXEDEMA COMA• Represents the severest form of hypothyroidism and has an associated

mortality rate of 30 percent to 40 percent.

• It can occur due to ‐ long‐standing, untreated hypothyroidism, ‐ Precipitating factors ‐ eg .Acute infection, myocardial infarction, congestive heart failure, cerebral vascular accident, trauma,

• FEATURES ‐ Altered mental status , hypothermia. Hypoglycemia, hypotension, hyponatremia, bradycardia, and hypoventilation

INVESTIGATIONS

Thyroid function tests• High levels of TSH• Free triiodothyronine (fT3)• Free thyroxine (fT4)• Free T3 from 24‐hour urine catch

OTHER INVESTIGATIONS• Investigations to rule out THYROIDITIS• Testing for anemia • Serum cholesterol —may be elevated • Prolactin — test of pituitary function

TREATMENT

• Hypothyroidism is treated with the levorotatory forms of thyroxine (levothyroxine) (L‐T4) and triiodothyronine (liothyronine) (L‐T3).

• T4 only ‐ currently the standard treatment in mainstream medicine.

Myxoedema coma• Large intravenous bolus of levothyroxine should be administered (200 to

400 mcg), followed by daily doses of 50 to 100 mcg,

• combination of both T3 and T4.

CRETINISM

CAUSES• Endemic cretinism caused by iodine deficiency• Dysgenesis of the thyroid gland ‐ agenesis and ectopy • Inborn errors of thyroid hormone metabolism – eg.

‐ Dyshormonogenesis .‐ Thyroid‐stimulating hormone (TSH) unresponsiveness ‐ Impaired ability to uptake iodide‐ Peroxidase, or organification, defect ‐ Thyroid hormone resistance‐ TSH or thyrotropin‐releasing hormone (TRH) deficiencies

• Maternal autoimmune disease• Radioactive iodine therapy of pregnant women

CRETINISM

CLINICAL FEATURES• Coarse facial features

• Macroglossia

• Large fontanelles

• Umbilical hernia

• Mottled, cool, and dry skin

• Developmental delay

• Pallor

• Myxedema

• Goiter

• ASD / VSDCONGENITAL HYPOTHYROIDISM WITH MACROGLOSSIA

CRETINISM

DIAGNOSIS

• Diagnosis of primary hypothyroidism is confirmed by demonstrating decreased levels of serum thyroid hormone (total or free T4) and elevated levels of thyroid‐stimulating hormone (TSH).

• If maternal antibody–mediated hypothyroidism is suspected, maternal and neonatal antithyroid antibodies may confirm the diagnosis

TREATMENT

• The mainstay in the treatment of congenital hypothyroidism is early

diagnosis and thyroid hormone replacement.

Thank you for the patient listening…PRESENTED BY

R. VISHNU SUNDAR

POST GRADUATE

DEPARTMENT OF GENERAL SURGERY

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THYROIDITIS HYPOTHYROIDISM - SRM University and... · THYROIDITIS & HYPOTHYROIDISM A PRESENTATION ON. CONTENTS OF ... Struma lymphomatosa –a