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

CONTENTS:CONTENTS:• Pituitary gland

– Hypopituitarism– Hyperpituitarism– Posteroir pituitary syndromes

• Thyroid galnd– Hypothyrodism– Hyperthyrodism– Goiter– Thyrodidtis– Tumors

• Parathyroid glands– Hyperparathyroidism – Hypoparathyroidism

• Adrenal gland – Cortex

– Medulla . Tumors

• Multiple endocrine neoplasia • Endocrine pancreas (D.M )

THYROID GLANDTHYROID GLAND

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

Normal thyroid seen microscopically consists of follicles lined

by a cuboidal epithelium and filled with pink, homogenous colloid

Hypothyroidism:Hypothyroidism:

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

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

CretinismCretinism

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

Myxedma, cretenismMyxedma, cretenism

• Neurologic & myxedematous patterns

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

protruding tongue– muscle weakness and umbilical hernia

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)

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

•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

• 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

ThyrotoxicosisThyrotoxicosis

Upper, thyrotoxicosis

Lower, after treatment

GoiterGoiter

• Goiter simply means enlarged thyroid

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 ).

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

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

Solitary thyroid noduleSolitary thyroid nodule

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

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

•Pathogenesis• B-cells secrete autoantibodies

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

MorphologyMorphology

• Gross: diffuse symmetrical enlargement of thyroid

THYROIDITISTHYROIDITIS

• Hashimoto’s thyroiditis• Subacute

(granulomatous,DeQuervian) thyroiditis

• Chronic lymphocytic (painless) thyroiditis

• Riedel’s fibrous thyroiditis

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.

Pathogenesis Pathogenesis

• B cells autoantibodies against microsomes and thyroglobulin.

• Cell-mediated destruction of the gland

• ♀ : ♂ = 10 : 1 middle-aged • Higher incidence of autoimmune

disease

Clinical CourseClinical Course

• Euthyroid--- hypothyroid• Moderate goiter• Hashitoxicosis(hyperthyroidism)

occasionally• 5% - B cell lymphoma or rarely

papillary carcinoma of thyroid

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)

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.

ADENOMAADENOMA

ADENOMAADENOMA

CARCINOMA OF CARCINOMA OF THYROIDTHYROID

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

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)

•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

Papillary CarcinomaPapillary Carcinoma

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).

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.

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

Medullary Carcinoma Medullary Carcinoma

amyloid

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

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

PARATHYROID GLANDPARATHYROID GLAND

PARATHYROID GLANDPARATHYROID GLAND

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

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

Parathyroid adenomaParathyroid adenoma

adenoma

normal

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.

Parathyroid carcinomaParathyroid carcinoma

MULTIPLE ENDOCRINE MULTIPLE ENDOCRINE NEOPLASIANEOPLASIA

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.

• MEN I: Wermer ’ s Syndrome– Parathyroid adenom/hyperplasia .– Pituitary adenoma .– Pancreatic lesions (hyperplasia

adenoma , carcinoma )– Mutant gene(MEN1) locus at 11q13– Autosomal dominnant

• 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

• MEN III (IIb): William syndrome:

similar to MEN II plus – Marfanoid bodily habitus– Multiple mucocutanenous

ganglioneuromas– Parathyroid involvement :

(none/rare).