Endocrine System Part 1. Endocrine System The endocrine system is the “other” control system of…
Endocrine Tutorial
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Hyperthyroidism
• Clinical features– CVS: tachycardia, palpitations, atrial fib– CNS: tremor, anxiety, lability, insomnia– Heat intolerance; warm, moist, flushed skin– Weight loss with increased appetite
Hyperthyroidism
• Clinical features– CVS: tachycardia, palpitations, atrial fib– CNS: tremor, anxiety, lability, insomnia– Heat intolerance; warm, moist, flushed skin– Weight loss with increased appetite
• Causes
Hyperthyroidism
• Clinical features– CVS: tachycardia, palpitations, atrial fib– CNS: tremor, anxiety, lability, insomnia– Heat intolerance; warm, moist, flushed skin– Weight loss with increased appetite
• Causes– Graves disease– Exogenous thyroid hormone– Functioning multinodular goitre/thyroid adenoma– Thyroiditis– Secondary (hypothal/pituitary dysfunction)
Hypothyroidism
• Clinical features– CVS: bradycardia, cardiomegaly, pericardial effusion– CNS: slowed mental activity, apathy, fatigue, cretinism– Cold intolerance; cool skin; myxedema; hair loss– Weight gain with decreased appetite– Coarsening of features
Hypothyroidism
• Clinical features– CVS: bradycardia, cardiomegaly, pericardial effusion– CNS: slowed mental activity, apathy, fatigue, cretinism– Cold intolerance; cool skin; myxedema; hair loss– Weight gain with decreased appetite– Coarsening of features
• Causes
Hypothyroidism
• Clinical features– CVS: bradycardia, cardiomegaly, pericardial effusion– CNS: slowed mental activity, apathy, fatigue, cretinism– Cold intolerance; cool skin; myxedema; hair loss– Weight gain with decreased appetite– Coarsening of features
• Causes– Hashimoto thyroiditis– Surgery / Radiation / Drug-induced– Infiltration by tumour– Secondary (hypothal/pituitary dysfunction)
Graves disease
• Epidemiology – Women, 20-40 yrs, (M:F = 1:7)
• Pathogenesis– Autoimmune disorder– Activation of thyroid by thyroid autoantibodies
• Anti-TSH R, anti-thyroglobulin, anti-T3/T4
– Associated with certain HLA types– Associated with other AI disorders
• Hashimoto thyroiditis, pernicious anaemia, rheumatoid arthritis
Graves disease
• Gross findings
– Mild symmetrical thyroid enlargement
– Eyes: exophthalmos, lid retraction, lid lag
– Skin: pretibial myxedema
Hashimoto Thyroiditis
• Epidemiology– Women, 45-65 yrs, (M:F = 1:10 to 20)
• Pathogenesis– Autoimmune disorder– Destruction of thyroid by thyroid autoantibodies
• Anti-TSH R, anti-thyroglobulin
– Associated with certain HLA types– Associated with other AI disorders
• SLE, pernicious anaemia, rh. Arthritis, Sjogrens, IDDM, Graves
– May cause transient hyperthyroidism in early stages– Gradual destruction and fibrosis hypothyroidism
Hashimoto Thyroiditis
• Gross findings
– Enlarged pale thyroid initially
– Atrophic thyroid eventually
Thyroiditis
• Painful– Infectious
• Adjacent sinusitis, mycobacteria, fungi
– Subacute (granulomatous)• Post viral
• Painless– Hashimoto’s– Fibrous
• Fibrosis, atrophy, hypothyroidism
Goitre
• What is it?– Enlarged thyroid– Due to impaired thyroid hormone synthesis
• Causes– Iodine deficiency– Goitrogens– Inherited disorders
Goitre
• Pathogenesis– Hyperplasia of follicular epithelium– Increased thyroid hormone release (decreased colloid)– Involution of follicles when enough thyroid hormone
released– Accumulation of colloid
• Two forms:– Diffuse– Multinodular
Goitre• Microscopic findings
– Diffuse (initial hyperplastic stage):• Hyperplastic and hypertrophied follicles• Decreased colloid
– Diffuse (involution stage)• Dilated follicles, atrophic epithelium• Abundant colloid
Goitre• Microscopic findings
– Multinodular goitre:
– Recurrent episodes of stimulation and involution• Hyperplastic and hypertrophied follicles with decreased
colloid
• Dilated follicles with atrophic epithelium and abundant colloid
• Haemorrhage, fibrosis, calcification, cyst formation
Thyroid neoplasms
• Risk factors– M:F = 1:4– Radiation therapy– Hashimoto’s– Multinodular goitre
• Types– Follicular adenoma– Carcinoma
• Papillary• Follicular• Anaplastic• Medullary
Follicular carcinoma
• Morphology:
– Same as follicular adenoma!
BUT– Vascular / capsular invasion– Haematogenous mets
Hyperadrenalism
• Presentation– Cushing’s syndrome– Conn’s syndrome
• Causes– Primary
• Hyperplasia, adenoma, carcinoma
– Secondary• Hypothalamic/pituitary disorders• Ectopic ACTH secretion• Activation of renin-angiotensin system