the endocrine system for dental students dr ibrahim hassan alzahrani frcpath -uk chairman of...
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The Endocrine system The Endocrine system for dental studentsfor dental students
DR IBRAHIM HASSAN DR IBRAHIM HASSAN ALZAHRANI FRCPath -UKALZAHRANI FRCPath -UK Chairman of Pathology Chairman of Pathology
DepartementDepartementFaculty of Medicine Faculty of Medicine
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CONTENTS:CONTENTS:• Pituitary gland
– Hypopituitarism– Hyperpituitarism– Posteroir pituitary syndromes
• Thyroid galnd– Hypothyrodism– Hyperthyrodism– Goiter– Thyrodidtis– Tumors
• Parathyroid glands– Hyperparathyroidism – Hypoparathyroidism
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• Adrenal gland – Cortex
– Medulla . Tumors
• Multiple endocrine neoplasia • Endocrine pancreas (D.M )
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THYROID GLANDTHYROID GLAND
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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:Hypothyroidism:
• Causes:– structural or functional– 95% are due to:
• Surgical or radiation ablation• Hashimoto’s thyroiditis• Primary idiopathic hypothyroidism
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CretinismCretinism
• 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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MyxedemaMyxedema• 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 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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ThyrotoxicosisThyrotoxicosis
Upper, thyrotoxicosis
Lower, after treatment
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GoiterGoiter
• Goiter simply means enlarged thyroid
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Diffuse GoiterDiffuse 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 GoiterMultinodular 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 noduleSolitary 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 noduleSolitary 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 DISEASEGRAVE’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 ♀ 3rd & 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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MorphologyMorphology
• Gross: diffuse symmetrical enlargement of thyroid
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THYROIDITISTHYROIDITIS
• Hashimoto’s thyroiditis• Subacute
(granulomatous,DeQuervian) thyroiditis
• Chronic lymphocytic (painless) thyroiditis
• Riedel’s fibrous thyroiditis
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Hashimoto’s thyroiditisHashimoto’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 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 CourseClinical Course
• Euthyroid--- hypothyroid• Moderate goiter• Hashitoxicosis(hyperthyroidism)
occasionally• 5% - B cell lymphoma or rarely
papillary carcinoma of thyroid
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THYROID TUMOURSTHYROID 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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ADENOMAADENOMA
• 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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ADENOMAADENOMA
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ADENOMAADENOMA
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CARCINOMA OF CARCINOMA OF THYROIDTHYROID
• Causes:– Ionizing radiation– Hashimoto’s thyroiditis– Grave’s disease?
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Papillary CarcinomaPapillary Carcinoma 60-70%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 CarcinomaPapillary Carcinoma
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Follicular CarcinomaFollicular 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 CarcinomaFollicular 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 Medullary Carcinoma of
thyroid <5%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 Medullary Carcinoma
amyloid
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Medullary CarcinomaMedullary 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%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 GLANDPARATHYROID GLAND
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PARATHYROID GLANDPARATHYROID GLAND
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HyperparathyroidismHyperparathyroidism - 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 featuresClinical 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 adenomaParathyroid 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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Parathyroid carcinomaParathyroid carcinoma
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MULTIPLE ENDOCRINE MULTIPLE ENDOCRINE NEOPLASIANEOPLASIA
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MULTIPLE ENDOCRINE MULTIPLE ENDOCRINE NEOPLASIA (NEOPLASIA (MEN)MEN)
• MEN are syndromes characterized by hyperplasic or neoplastic involvement of at least two endocrine glands and sometimes associated with non-endocrine lesions.
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• MEN I: Wermer ’ s Syndrome– Parathyroid adenom/hyperplasia .– Pituitary adenoma .– Pancreatic lesions (hyperplasia
adenoma , carcinoma )– Mutant gene(MEN1) locus at 11q13– Autosomal dominnant
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• MEN II (IIa):Sipple Syndrome– Medullary carcinoma of thyroid– Pheochromocytoma .– Occasionally parathyroid lesion
(30%) – Mutant gene locus at 10q11.2
(RET proto-oncogen)– Autosomal dominant
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• MEN III (IIb): William syndrome:
similar to MEN II plus – Marfanoid bodily habitus– Multiple mucocutanenous
ganglioneuromas– Parathyroid involvement :
(none/rare).