Diseases of endocrinal glands


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  • Classical endocrine glands and classical disease categories
  • Classical endocrine glands and BETTER (i.e., more appropriate) disease categories.
  • Positive and negative feedback systems are the principles of of the endocrine system and there effects upon each other and target organs.
  • Generally, “releasing” hormones are between the hypothalamus and adenohypophysis, and “stimulating” hormones are between the pituitary and other major endocrine glands. Build up of a and hormone tells the hypothalamus and pituitary to “slow down” production. It is important to understand the difference between POSITIVE and NEGATIVE feedback.
  • Anterior pituitary lobe = adenohypophysis = Rathke’s pouch = pars distalis. Hormones released here are also made here. Posterior pituitary lobe = neurohypophysis = infundibulum = pars nervosa. Hormones released here are made in the hypothalamus.
  • Overall cellular mechanisms of action of the two major classes of hormones, polypeptide and steroid.
  • All three lobes of the pituitary: Anterior, intermediate, and posterior lobes. Note that the pituitary also has a “portal” circulation, i.e., artery  capillaries  veins  capillaries, rather than just a  c  v. Why? Ans: to create a “secondary” circulation between the pituitary and the hypothalamis releasing factors!
  • The differentiation between acidophils and basophils is usually not too difficult unless the stain is really lousy. Chromophobes are uncommon, and have minimal cytoplasm and no granules. Chromophobe cytoplasm stains close to basophil cytoplasm in color, but is less granular and has is a minimal cytoplasm.
  • Hormones from basophils go to other endocrine glands, thyroid, adrenal cortex, ovary, testis. Cells from acidophils do NOT.
  • The posterior pituitary (aka, pars nervosa or neurohypophysis) looks like typical brain tissue. Why? Ans: It IS typical brain tissue. The pituicytes are glial cells. Herring bodies are massively dilated terminal axons from the hypothalamus.
  • The posterior pituitary does not make these hormones, it just releases them. The hypothalamus actually makes the hormones and transfers it down the stalk to the neurohypophysis.
  • Note the extreme proximity of the pituitary stalk (infundibulum) to the optic chiasm
  • Galactorrhea in a young woman (non pregnant of course) is often the expression of an acidophil tumor of the adenohypophysis.
  • Recognize this famous pituitary giant? What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)
  • What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)
  • What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)
  • Normal pituitary.
  • Find the pituitary adenoma.
  • Usually the bitemporal hemianopsia is NOT perfectly symmeetrical. Why? Because tumors are under no law to grow perfectly symmetrically.
  • The usual differential of hypopituitarism
  • Recall the basic thyroid blood supply, from subclavian (inferior posterior) and carotid (superior anterior)
  • The normal weight of the thyroid , in grams, is also the same as its 24 hour radioactive iodine uptake percentage. Why? Ans: Because it take up 1% per gram.
  • Find the colloid, follicular cells, and para-follicular cells (also known as C cells or light cells)
  • If there was such a thing as a hypothalamic adenoma producing excessive TRF (thyroid releasing factor), would this be tertiary hyperthyroidism? Ans: Yes. Would an adenoma or a carcinoma more likely produce hyperthyroidism? Ans: Adenoma Why?
  • The diagnosis of Hashimoto thyroiditis requires not only lymphoid follicles in the thyroid, but SECONDARY (i.e., germinal centers) follicles should be present.
  • NO scalloping
  • Scalloping
  • Podiatric case of the week.
  • Decreased Iodine leads to decreased thyroid hormone, which leads to increased TSH which leads to increased growth of follicles. That’s how an iodine deficiency leads to a goiter.
  • Many vegetables are goiterogens, fruits are NOT.
  • Most goiters worldwide are due to iodine deficiency. Why? Ans: The thyroid enlarges to try to trap more iodine, when serum levels are low. This is a adaptive response.
  • Every type of thyroid disorder known is more common in females than males? Why? Ans: unknown What is the difference between a cold and a not-cold nodule isotopically?
  • Did you ever know anybody who died from thyroid cancer? Why not?
  • EXTREMELY well encapsulated tumor. Benign.
  • EXTREMELY well encapsulated tumor. Benign.
  • Note the resemblance of H ü rthle cells to oncocytes, oxyphil cells, gastric parietal cells and apocrine cells, i.e., very bright red and abundant cytoplasm. In general however, please remember that “ATYPIA” in benign endocrine neoplasms is VERY COMMON, and, in contrast with other organ systems of the body, ususlly does NOT imply malignancy or PRE-malignancy!
  • EXTREMELY NON well encapsulated tumor. Malignant. Thyroid tissue can look perfectly normal, but come out of bone or liver? In contrast with marked atypia seen in BENIGN endocrine neoplasms, often NO ATYPIA is seen with malignant endocrine neoplasms, and invasion or metastases is often the only evidence that endocrine tissue is malignant.
  • Papillary neoplasms do NOT usually look uniform on cut surface.
  • To make things simple, let’s just say you can regard ALL papillary thyroid neoplasms as benign.
  • Orphan Annie cells are papillary carcinoma of the thyroid cells in which considerably cytoplasm has invaginated into the nucleus.
  • Is amyloid a type of “Hyaline”? What are some other types? What is hyaline?
  • This is just a generality, not a law.
  • Find the chief cells, find the oxyphil cells, find the fat.
  • PTH stimulates osteoclasts to chew up bone and transfer calcium from the bone to the serum “compartments”.
  • Hyperparathyroidism symptoms are the same as hypercalcemia symptoms, and vice versa.
  • Hypoparathyroidism symptoms are the same as hypocalcemia symptoms, and vice versa.
  • Is this a right or a left adrenal gland? Ans: LEFT Why: Right is usually flatter and much less triangular. Think of the liver as squishing it.
  • Congenital adrenal hyperplasia is generally synonymous with adrenogenital syndrome.
  • Note that the COLOR and CONSISTENCY of the tumor is the same as that of the CORTEX.
  • Note that the COLOR and CONSISTENCY of the tumor is the same as that of the CORTEX.
  • Note that the COLOR and CONSISTENCY of the tumor is the same as that of the MEDULLA.
  • MEN-1 is the three “P”s
  • Madullary thyroid carcinoma is present in ALL three types of MEN-2
  • Younger looking cells “BLASTomas” are primarilly in kids, more mature looking cells CYTomas are in adults. BOTH are quite rare.
  • 4 hormones of the islets: glucagon, insulin, somatostatin. and pancreatic polypeptide from alpha, beta, delta, and PP cells, respectively. Can you tell from routine H&E microscopy which cell is which? Why not? Can immunoperoxidase help?
  • Even though there are TWO types of diabetes the complications from both are identical, although, of course, the effects of type-1 may have been present longer in a persons life.
  • Hyalinization in the islets of Langerhans is a common finding in type 2 diabetes. Often, the “hyaline” is amyloid.
  • In “nodular” glomerulosclerosis, aka, K-W kidneys, “nodules” of PAS positive matrix trapping mesangial cells, are found at the periphery of glomeruli.
  • Diffuse mesangial sclerosis. Note the “sclerotic” part, or fibrosis, is stained blue by the trichrome stain.
  • Diseases of endocrinal glands

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