ppt on thyroid gland

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THYROID GLAND

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Page 1: Ppt on Thyroid Gland

THYROID GLAND

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CONTENTS:• Thyroid gland

– Hypothyrodism– Hyperthyrodism– Goiter– Thyrodidtis– Tumors

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• This is the normal appearance of the thyroid gland on the anterior trachea of the neck..

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Normal thyroid seen microscopically consists of follicles lined

by a cuboidal epithelium and filled with pink, homogenous colloid

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Hypothyroidism:

• Causes:– structural or functional– 95% are due to:

• Surgical or radiation ablation• Hashimoto’s thyroiditis• Primary idiopathic hypothyroidism

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Cretinism

• This is uncommon disease of childhood due to failure of thyroid to synthesize thyroid hormones hypothyroidism

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Myxedma, CretenismMyxedma, Cretenism

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• Neurologic & myxedematous patterns • Clinically:

– mental retardation– growth retardation (short stature)– coarse facial features with dry skin and

protruding tongue– muscle weakness and umbilical hernia

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Myxedema• Hypothyroidism in adult.• - Clinically:

– appear insidiously & subtle– lethargy & weakness with slow speech– cold intolerance with cool & rough skin– menstrual problems & psychosis– cardiac changes: cardiac output, hypertrophy,

(myxedema heart), pericardial effusion– deposition of mucopolysaccharides in connective tissue– atherosclerosis ( cholesterol)

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Hyperthyroidism

• Excess thyroid hormone (Thyrotoxicosis)• Causes:

– primary diffuse toxic hyperplasia (Grave’s disease) > 95%

– toxic multinodular goiter– toxic adenoma– certain form of thyroiditis– secondary to pituitary or hypothalamic lesion

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• Clinical features:

• nervousness and emotional instability• menstrual changes• fine tremors of the hands• heat intolerance with warm skin and sweating• weight loss despite a good appetite

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• Eye changes: (exopthalmos, widened palpebral fissures, staring gaze)

• Cardiac changes: (tachycardia, palpitations, atrial fibrillation and thyrotoxic cardiomyopathy----- cardiac failure)

• skeletal muscle atrophy and fatty infiltration• lymphadenopathy• fatty change of the liver• Osteoporosis

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ThyrotoxicosisThyrotoxicosisUpper, thyrotoxicosis

Lower, after treatment

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Goiter

• Goiter simply means enlarged thyroid

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Diffuse Goiter

• Characterized by diffuse symmetrical enlargement of thyroid (200 - 300 gm) with normal thyroid function.

• Hypofunction may occur early in the course .• Usually occurs in: Endemic areas (

iodine & goiterogens) or• Sporadic (physiological ,autoimmune ,

familial ).

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Multinodular Goiter

• Characterized by nodular asymmetrical enlargement of thyroid (up to 1000 gm)

• Slowly evolves from diffuse goiter.It can be toxic or non-toxic

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Solitary thyroid nodule

• Size (symptoms)• Possible hyperfunction• Usually colloid nodule >70%• Adenoma 20-30%• Carcinoma <5%• - Radioactive iodine (Hot & cold nodule)• FNA & biopsy• Thyroid function

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Solitary thyroid nodule

• Invisigations: • thyroid hormons: (T3,T4,TSH)• radiological examinations : * ultrasound (cystic/solid) * radioactive iodine (cold/hot)• Fine needle aspiration cytology

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GRAVE’S DISEASE• Primary Diffuse Toxic Hyperplasia• The most common cause of thyrotoxicosis• It is an autoimmune disease• Classically shows:

– 1-Exopthalmos (proptosis)– 2-Dermopathy (pretibial myxedema)– 3-Hyperthyroidism

• Common in 3♀ rd & 4th decade• ♀ : = 10 : 1♂• HLA – DR3 & Familial predisposition• Other autoimmune diseases may occur

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• Pathogenesis• B-cells secrete autoantibodies against

mainly TSH – Receptors (Abs. against microsomes, thyroglobulin, T3 & T4 can be seen)

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Morphology

• Gross: diffuse symmetrical enlargement of thyroid

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THYROIDITIS

• Hashimoto’s thyroiditis• Subacute (granulomatous,DeQuervian)

thyroiditis• Chronic lymphocytic (painless) thyroiditis• Riedel’s fibrous thyroiditis

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Hashimoto’s thyroiditis

• This is an autoimmune most common type of thyroiditis characterized by symmetrical modesty enlarged thyroid responsible for most cases of primary goiterous hypothyroidism.

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Pathogenesis

• B cells autoantibodies against microsomes and thyroglobulin.

• Cell-mediated destruction of the gland • ♀ : = 10 : 1 middle-aged ♂• Higher incidence of autoimmune disease

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Clinical Course

• Euthyroid--- hypothyroid• Moderate goiter• Hashitoxicosis(hyperthyroidism) occasionally• 5% - B cell lymphoma or rarely papillary

carcinoma of thyroid

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THYROID TUMOURS

1-BENIGN: Follicular adenoma

2-MALIGNANT:• Carcinoma of thyroid

– Papillary carcinoma– Follicular carcinoma– Medullary carcinoma– Anablastic carcinoma –Lymphoma Others –

rare (sq. ca, sarcomas, metastasis)

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ADENOMA

• Always follicular adenoma• No papillary adenoma of thyroid.• Solitary & encapsulated.• No capsular invasion.• Histology: Follicles –> macro (colloid), micro (fetal), normal

size (simple), trabecular (embryonal).• Sometimes composed of Hürthl cells (oncocytic)

Hurthle cell adenoma.

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ADENOMA

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ADENOMA

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CARCINOMA OF THYROID

• Causes:– Ionizing radiation– Hashimoto’s thyroiditis– Grave’s disease?

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Papillary Carcinoma 60-70%

• The most common type• Young age 20-50y , F:M=3:1• Forming papillae and psammoma bodies• Cells typically show ground-glass appearance with clear

grooved nuclei “Orphan Annie” and intranuclear inclusion

• 50% at presentation Cervical LN metastasis• Haematogenous spread is rare (not common)

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• Follicular variant of papillary carcinoma : No papillary formation . The nuclei shows typical nuclear ground glass appearance of papilary crcinoma.

• Grow slowly with indolent course• Occult microscopic variant

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Papillary Carcinoma

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Follicular Carcinoma• Macroscopically often encapsulated similar to

adenoma • Histologically : composed of follicles

with no papillary formation and no groundglass nuclear changes.

• sometimes the cells are oncocytic (Hurthle cell carcinoma).

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Follicular Carcinoma• Haematogenous spread (lung, bone, liver. . )• Poorer in prognosis than papillary carcinoma.• Represent approximatly 15%• Most patients are >40y • TYPES: 1- minimally

invasive FC. 2- widely invasive FC.

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Medullary Carcinoma of thyroid <5%

• Derived from calcitonin – secreting C-cells• Characterized by formation of amyloid

material from calcitonin, surrounded by small to medium sized cells with round to spindle shaped nuclei forming sheets, nests or cords

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Medullary Carcinoma

amyloid

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Medullary Carcinoma

• It has slow but progressive growth • Both lymphatic and hematogenous

metastasis occurs• 10-20% are familial, multicenteric in young

age, associated with MEN 2&3 • Immuno: +ve calcitonin• 80-90% sporadic, solitary, old age

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Anablastic carcinoma 5-10%

0ccurs in patient > 60 y• Poorly differentiated, highly malignant tumour usually forms

bulky necrotic mass often disseminate extensively through blood

• death occurs within 1-2 years (<10% survive for 10y)

• Histological variants:

• Giant cells, spindle cells(sarcomatoid), squamoid cells

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PARATHYROID GLAND

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PARATHYROID GLAND

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Hyperparathyroidism - Primary Hyperparathyroidism: Increase PTH due to parathyroid lesion

(Adenoma/hyperplasia) Hypercalcaemia

PTH Hypercalcaemia :– osteoclast to mobilize Ca++ from bone– Ca++ reabsorption in the kidney– Ca++ absorption in Git .through vit .D.– excretion of phosphate in urine .

• Part of MEN I & II• F : M = 3 : 1 > 40y

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Clinical features

• Asymptomatic (lethargy&weakness)• Bone pain (osteomalacia, osteoporosis & osteitis

fibrosa cystica/brown tumor)• Renal stones (nephrolithiasis)• Nephrocalcinosis• Metastatic calcification (blood vessels, soft tissue & &

joints)• Abdominal pain (peptic ulcer,pancreatitis) and mental

change

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Parathyroid adenoma

adenoma

normal

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Adenoma & Hyperplasia In adenoma one gland, Hyperplasia >one gland

• Frozen section (intraoperative consultation) required to confirm presence of parathyroid tissue.

Carcinoma of parathyroid: * Rare – Invasion and metastasis– Bands of collagen in the stroma– High mitotic figures.

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Reporters:Jinky G. GomezMay Garcia P T C Sec B7:30-9:30amChild & Development