25 endocrine
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This document provides an overview of endocrine system pathology. It discusses various endocrine glands including the pituitary gland, thyroid gland, parathyroid glands, pancreas, and adrenal glands. For each gland it covers normal function, pathologies such as tumors and inflammatory conditions, and associated clinical features. It also briefly mentions the pineal gland and discusses feedback systems that regulate hormone production and secretion.
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25 endocrine
- 1. ENDOCRINE
- 2. JOHN MINARCIK, MD • minarcik@gmail.com • http://snurl.com/pathology • OPTIONAL – youtube.com “histopathology” – youtube.com “shotgun histology”
- 3. CLASSICAL ALGORHYTHM • PITUITARY –ANTERIOR –POSTERIOR • THYROID • PARATHYROID • PANCREAS (endo.) • ADRENAL –CORTEX –MEDULLA • DEGENERATION (aka, “involution”) • INFLAMMATION • NEOPLASM –BENIGN –MALIGNANT
- 4. BETTER ALGORHYTHM • NON-NEOPLASTIC – HYPER-function – HYPO-function • NEOPLASTIC – FUNCTIONAL – NON-FUNCTIONAL – Functional endocrine malignancies are RARE. Why? • PITUITARY – ANTERIOR – POSTERIOR • THYROID • PARATHYROID • PANCREAS (endo.) • ADRENAL – CORTEX – MEDULLA
- 5. FEEDBACK SYSTEMS • HYPOTHALAMUS • ANTERIOR PITUITARY • ENDOCRINE GLAND • END ORGAN • HYPOTHALAMUS
- 8. HORMONES •POLYPEPTIDE (2nd MESSENGER) •STEROID (DIRECT on NUCLEUS)
- 9. ACIDOPHILS BASOPHILS CHROMOPHOBES AXONS AXONS and “PITUI-”cytes A I P
- 11. ANTERIOR PITUITARY • ACIDOPHILS –GROWTH HORMONE –PROLACTIN • BASOPHILS –TSH –ACTH –LH, FSH
- 13. POSTERIOR PITUITARY • OXYTOCIN (contracts uterine smooth muscle) • VASOPRESSIN (ADH) (vasoconstriction, gluconeogenesis, platelet aggregation, release of Factor-VIII and vWb factor, concentrates urine, main effects on kidney and brain)
- 14. PITUITARY PATHOLOGY • CLINICAL FEATURES, mimic the endocrine effects or mass effects) • FUNCTIONING ADENOMAS • HYPO-PITUITARISM • POSTERIOR PITUITARY SYNDROMES • HYPOTHALAMIC (SUPRASELLAR) TUMORS
- 15. CLINICAL FEATURES • HYPER: growth, lactation, thyroid, adrenal cortex • HYPO: growth, thyroid, adrenal cortex • MASS EFFECT: visual fields, brain
- 17. G A L A C T O R R H E A
- 18. GIGANTISM (excess somatotropin [GH] BEFORE epiphyseal closure)
- 19. ACROMEGALY: (excess somatotropin [GH] AFTER epiphyseal closure)
- 20. MOON FACIES BUFFALO HUMP STRIAE
- 25. HYPO-pituitarism • Pituitary tumors, functional or not. • NON-pituitary tumors, primary or metastatic • Pituitary surgery, of course • Radiation, of course • “Apoplexy”, i.e., sudden hemorrhage • Sheehan’s syndrome (Post-partum ischemic necrosis) • Cysts (Rathke’s cleft) • Empty sella syndrome, (is NOT a disease) • Genetic defects (pit-1 gene mutations)
- 26. POSTERIOR pituitary •DIABETES INSIPIDUS •SIADH (Syndrome of Inappropriate Andi- Diuretic Hormone)
- 27. DIABETES INSIPIDUS • ADH deficiency • Head trauma, tumors, inflam. hypothal/pit • Hyperdiureses with LOW sp.gr.
- 28. Inappropriate ADH • ADH EXCESS –Hyponatremia, cerebral edema, neurologic symptoms –Neoplasms, esp. Small Cell CA. –NON-neoplastic lung diseases –Posterior pituitary injury
- 30. 15-25 grams
- 32. HYPER-THYROIDISM • aka, thyrotoxicosis • Diffuse • Nodular • Adenoma • Carcinoma • Neonatal • Secondary to TSH pituitary adenoma
- 33. HYPER-THYROIDISM • HYPERMETABOLISM • Tachycardia, palpitations • Increased T3, T4 • Goiter • Exophthalmos • Tremor • GI hypermotility • Thyroid “storm”, life threatening
- 35. HYPO-THYROIDISM • 1° Developmental • 1° Surgery, I-131, external radiation • 1° Auto-immune (i.e., Hashimoto’s) • 1° Iodine deficiency • 1° Li+, iodides, p-aminosalicylates • 2° (pituitary) • 3° (hypothalamic, rare)
- 36. HYPO-THYROIDISM • Cretinism – Severe retardation – CNS/Musc-skel – Short stature – Protruding tongue – Umbilical hernia • Myxedema (coma) – Sluggishness – Cool skin
- 37. THYROIDITIS • Hashimoto (Auto-Immune) (Lymphoid follicles with germinal centers), MOST COMMON cause of acquired hypothyroidism in USA • Subacute Granulomatous (DeQuervain) • Subacute Lymphocytic (just like Hashimoto’s but NO fibrosis and no germinal centers), often post-partum
- 41. GRAVES DISEASE (aka, diffuse toxic goiter) • HYPERTHYROIDISM • EXOPHTHALMOS • PRE-TIBIAL MYXEDEMA • Autoimmune, auto-antibodies to TSH
- 43. SCALLOPING
- 45. GRAVES DISEASE (aka, diffuse toxic goiter) PLUMMER DISEASE (aka, nodular toxic goiter) HARDER TO TREAT Surg PTU (Propyl Thio Uracil) I-131
- 46. GOITERS (aka, thyromegaly, diffuse or nodular) • IODINE deficiency • Increased TSH • Goitrogens, e.g., cabbage, Brussels sprouts, cauliflower, turnips, cassava) • Associated with HYPO thyroidism eventually, NOT hyperthyroidism
- 48. G O I T E R
- 49. Thyroid Neoplasms • “Nodules” vs. true neoplasms • Adenomas vs. Carcinomas
- 50. “NODULES” • Solitary vs. Multiple • Younger vs. Older • Male vs. Female • Hx. neck radiation vs. NO Rx. • “Cold” vs. HOT (really NOT-cold)
- 52. NEOPLASMS • ADENOMAS –FOLLICULAR –HÜRTHLE (oxyphilic) • CARCINOMAS –FOLLICULAR –PAPILLARY –MEDULLARY (AMYLOID) –ANAPLASTIC (worst)
- 55. HÜRTHLE CELL ADENOMA, note “atypia”
- 60. ORPHAN ANNIE CELLS in PAPILLARY CARCINOMA
- 61. MEDULLARY CARCINOMA of the thyroid with “HYALINIZATION”, i.e., AMYLOID!!!
- 62. HYALINIZATION showing APPLE GREEN birefringence in CONGO RED stain, i.e., AMYLOID
- 63. BIOLOGIC BEHAVIOR • Papillary CA lymph nodes • Follicular CA blood vessels, bone
- 64. 35-40 mg
- 65. PTH • HYPOCALCEMIA is MAIN STIMULUS (9-10.5 mg/dl) • ANTAGONIZES CALCITONIN
- 66. PARATHYROID DISORDERS • HYPER- –PRIMARY (usually adenomas) –SECONDARY (LOW CA++ of Renal Failure) • HYPO-: Surgical, congenital, familial, idiopathic • PSEUDO-HYPO- –(end organ resistance)
- 67. HYPER-PARATHYROIDISM • Bone pain, fractures • Nephrolithiasis • Constipation, ulcers, gallstones • Depression, lethargy • Weakness, fatigue • Valve calcifications
- 68. HYPO-PARATHYROIDISM • Neuromuscular irritability • Mental status change • Parkinsonism like effects • Lens calcification* (paradox) • Widened QT interval • Defective, carious, teeth
- 69. ADRENAL CORTEX • Glomerulosa (Salt), mineralocorticoids – ALDOSTERONE • Fasciculata (Sugar), glucocorticoids – CORTISOL • Reticularis (Sex), gonadocorticoids – ANDROGENS, ESTROGENS
- 71. 4 g.
- 72. SALT SUGAR SEX STRESS
- 73. HYPERADRENALISM • HYPERALDOSTERONISM • CUSHING SYNDROME (CORTISOL) • ADRENOGENITAL (VIRILIZING) SYNDROME
- 74. CUSHING SYNDROME • CENTRAL OBESITY • MOON FACIES • WEAKNESS • HIRSUTISM • HYPERTENSION • DIABETES • OSTEOPOROSIS • STRIAE
- 75. MOON FACIES BUFFALO HUMP STRIAE
- 76. CUSHING SYNDROME • PITUITARY ACTH INCREASE • TUMOR ACTH INCREASE • HYPERPLASIA OF CORTEX • ADENOMA OF CORTEX • CARCINOMA OF CORTEX •EXOGENOUS STEROIDS (90%)
- 77. PRIMARY HYPERALDOSTERONISM (Conn’s Syndrome) • Na+ RETENTION • K+ EXCRETION • HYPERTENSION
- 78. PRIMARY HYPERALDOSTERONISM • CORTICAL NEOPLASM • CORTICAL HYPERPLASIA • FAMILIAL (rare)
- 79. SECONDARY HYPERALDOSTERONISM • DECREASED RENAL PERFUSION • EDEMA (HEART, LIVER, KIDNEY) • PREGNANCY
- 80. ADRENOGENITAL SYNDROME • VIRILIZATION/feminization • CORTICAL NEOPLASM • CORTICAL HYPERPLASIA • 21-Hydroxylase Deficiency
- 82. ADRENAL INSUFFICIENCY • PRIMARY ACUTE (ADRENAL CRISIS) • PRIMARY CHRONIC (ADDISON DISEASE) • SECONDARY (PITUITARY)
- 83. PRIMARY ACUTE • RAPID WITHDRAWAL OF STEROIDS • MASSIVE ADRENAL HOMORRHAGE (WATERHOUSE-FRIDERICHSEN, if it follows infection and shock) –Newborns with DIFFICULT DELIVERY –ANTICOAGULANT RX –POSTSURGICAL DIC PATIENTS
- 84. PRIMARY CHRONIC • Most of Addison disease is auto-immune adrenalitis • INFECTIONS • METASTASES • GENETIC DISORDERS
- 85. NEOPLASMS • ADENOMAS of ADRENAL CORTEX • CARCINOMAS of ADRENAL CORTEX
- 90. ADRENAL MEDULLA • PHEOCHROMOCYTOMAS, aka, primary tumors of the adrenal medulla – 10% arise in an MEN setting –10% are EXTRA-adrenal – 10% are bilateral – 10% are malignant –10% are in childhood – You can only call them malignant if they metastasize
- 91. PHEO
- 92. TWO crucially important points specific for endocrine tumors: • 1. FUNCTIONING carcinomas are very RARE in ANY endocrine gland. Why? (KEY principle of oncology) • 2. Benign adenomas may have extremely bizarre nuclei, but are most usually BENIGN!!!
- 93. MEN-1, aka, Wermer Syndrome (3 P’s) • HYPERPARATHYROIDISM, chiefly hyperplasia •Pancreatic endocrine tumors •Pituitary adenoma, usually prolactinoma
- 94. MEN-2 • MEN-2A (SIPPLE): Pheo, Medullary CA., Parathyroid hyperplasia • MEN-2B: NO hyperparathyroidism, but neuromas present • Familial Medullary Thyroid CA
- 95. PINEAL “GLAND” •PINEALOMAS –PINEOBLASTOMAS –PINEOCYTOMAS
- 99. Exocrine Endocrine Islets Alpha Cells Beta Cells Delta Cells (suppress insulin and glucagon) Pancreatic Polypeptide (PP) cells Epsilon Cells make gherlin
- 100. DIABETES MELLITUS • 16 Million in the USA • 1 Million/yr • 50K people die of it per year in the USA
- 101. How to Diagnose Dm: • Glucose >200 • Or……………. • Fasting glucose >126 trice • Or……………. • Post-prandial glucose > 200, 2 hrs AFTER standard OGTT (Oral Glucose Tolerance Test)
- 102. * MODY might be regarded as the third type TWO* Types of DM •1 • Genetic • Autoimmune • Childhood (juvenile) onset • Antibodies to beta cells • Beta cell depletion • NON-OBESE patients •2 • Genetic, but diff. from Type 1 • NOT autoimmune • Adult, or maturity onset, e.g., 40’s, 50’s • Insulin may be low, BUT, peripheral resistance to insulin is the main factor • OBESE patients
- 103. Dm •POLY- •POLY- •POLY-
- 104. INSULIN • FAT – IN-creased glucose uptake – IN-creased lipogenesis – DE-creased lipolysis • MUSCLE – IN-creased glucose uptake – IN-creased glycogen synthesis – IN-creased protein synthesis • LIVER – DE-creased gluconeogenesis – IN-creased glycogen synthesis – IN-creased lipogenesis
- 105. PATHOGENESIS • 1 • T-Lymphocytes reacting against poorly defined beta cell antigens • Inflammatory inflitrate, chronic, i.e., “INSULITIS” • 2 • Diet • Life Style • Obesity • INSULIN RESISTANCE • Beta cells UN-able to adapt to the “long term demands of insulin resistance”
- 106. MODY (Maturity Onset Diabetes of the Young) • Multiple types • 2-5% of diabetics • Primary beta cell defects • Multiple genetic mechanisms, especially GLUCOKINASE mutations
- 107. PANCREAS in Dm
- 108. PANCREAS in Dm
- 109. COMPLICATIONS • MACRO-VASCULAR disease, i.e., ASCVD • MICRO-VASCULAR disease, kidneys, retina, nerves • IMMUNE related problems, INFECTIONS, e.g., TB, pneumonia, pyelonephritis, candida, etc.
- 110. COMPLICATIONS • ADVANCED GLYCATION – collagen, laminin, polypeptides, GBM (glomerular basement membrane) • ACTIVATION of PROTEIN KINASE C, VEGF, endothelin-1, increased ECM, decreased fibrinolysis, inflam. cytokines • INTRACELLULAR HYPERGLYCEMIA
- 111. COMPLICATIONS MORPHOLOGY • (MACRO-vascular) Atherosclerosis • MICRO-vascular – Retinopathy – Nephropathy- glomerular, vascular, KW – Neuropathy • Infections
- 112. ATHEROSCLEROSIS
- 113. ATHEROSCLEROSIS
- 114. RETINOPATHY in Dm Shows microaneurysms, areas of hemorrhage, cotton wool spots, hard exudates, venous beading, neovascularization, retinal detachment, vitreous detachment, pre retinal hemorrhage
- 116. NEPHROPATHY Kimmelstiel- Wilson (KW) Kidneys Is………… “Nodular” glomerulosclerosis
- 119. NEPHROPATHY Diffuse Mesangial Sclerosis
- 120. INFECTIONS in Dm • SKIN • TUBERCULOSIS • PNEUMONIA • PYELONEPHRITIS • CANDIDA
- 121. NEOPLASMS of the Endocrine Pancreas • Islet cell tumors – Beta cells INSULINOMAS (NOT rare) – Alpha cells GLUCAGONOMAS (rare) – Delta cells SOMATOSTATINOMAS (rare) –GASTRINOMAS, producing ZOLLINGER-ELLISON SYNDROME, consisting of increased acid and ulcers