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Endocrine & Liver Diseases

Q. L. Endocrine & Liver Diseases. The Pathological Basis of Disease - Graduate Studies Course CMM 5001. Qiao Li, MD, PhD Dept of Pathology & Laboratory Medicine Faculty of Medicine University of Ottawa qiaoli@uottawa.ca Ext. 8491. Q. L. Outline. Adrenal Gland

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Endocrine & Liver Diseases

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  1. Q L Endocrine & Liver Diseases The Pathological Basis of Disease - Graduate Studies Course CMM 5001 Qiao Li, MD, PhD Dept of Pathology & Laboratory Medicine Faculty of Medicine University of Ottawa qiaoli@uottawa.ca Ext. 8491

  2. Q L Outline • Adrenal Gland • Anatomy Histology & Function • Steroid Hormones • Cushing Syndrome • Clinical Case Presentation • Liver • Anatomy, Histology & Function • Metabolic & Toxic Conditions • Cirrhosis • Tumors • Clinical Case Presentation

  3. Q L Adrenal Gland • Anatomy, Histology & Function • Steroid Hormones • Cushing’s Syndrome • Clinical Case Presentation

  4. Adrenal Gland - Anatomy

  5. Adrenal Gland - Anatomy

  6. Adrenal Gland – Gross

  7. Adrenal Gland – Cut Surface

  8. Adrenal Gland – Low Power Medulla Zona fasciculata Capsule Zona reticularis Zona glomerulosa Periadrenal fat

  9. Q L Adrenal Gland • Anatomy, Histology & Function • Steroid Hormones • Cushing’s Syndrome • Clinical Case Presentation

  10. Q L Adrenal Cortex Steroids Zone Class Representative Physiologic Effects glomerulosaMineralocorticoids Aldosterone salt and water homeostasis fasiculataGlucocorticoids Cortisol carbohydrate metabolism reticularisSex Steroids Androgens minimal effects

  11. Histone acetylation p300/CBP TAFII250 GR GR TBP RNA Pol II Q L Glucocorticoids & the Receptor • Cortisol, the majority of glucocorticoid activity in most mammals, also known as hydrocortisone. • About 90% of circulating cortisol binds to plasma proteins, corticosteroid-binding globulin (transcortin), decreasing the rate of metabolic clearance and the concentration fluctuation (the transcortin bound cortisol is biologically inactive). • Nobel Prize, Edward Kendall, Tadeus Reichstein & Philip Showalter Hench

  12. CRH Q L Control of Cortisol Secretion HPA Axis Hypothalamus Pituitary ACTH Cortisol Adrenal Cortex Dr. Gary Farr

  13. Q L Adrenal Gland • Anatomy, Histology & Function • Steroid Hormones • Cushing’s Syndrome • Clinical Case Presentation

  14. CRH ACTH Cortisol Q L Cushing’s Syndrome • Excessive Endogenous Cortisol • - ACTH independent: cortical tumor • - ACTH dependent: pituitary adenoma • small cell carcinoma • Administration of Glucocorticoids • - The most common cause • Clinical Manifestations • weight gain, truncal obesity and moon face • - muscle weakness, thin arms and legs • hypertension and osteoprosis • moodiness, irritability, or depression Harvey Cushing 1912

  15. Adrenal Gland - Comparison

  16. Q L Adrenal Gland • Anatomy, Histology & Function • Steroid Hormones • Cushing’s Syndrome • Clinical Case Presentation

  17. Striae- Clinical Presentation

  18. History • A 35-year-old female with weakness, mainly of the shoulders and thighs, increasing thirst, headache, easy bruisibility and depression. • Physical examination: moon face, truncal obesity, purple striae on the lateral aspects of abdomen, reduced strength in the proximal muscles of both shoulders and hips. • Blood pressure: 180/110 • The patient was then admitted to the hospital and underwent various laboratory test.

  19. Laboratory Test Plasma glucose: 300 mg/dL (normal 70-110 mg/dL) Overnight DEX suppression plasma cortisol: 10 µg/dL next 9 am (normal < 5 µg/dL) Plasma cortisol: 28 µg/dL at 9 am (normal 10-25) 25 µg/dL at 6 pm (normal < 10 µg/dL) 24-hour urine free cortisol: 200 µg/day (normal < 50 µg/day) Plasma ACTH: 125 pg/mL (normal 20-100 pg/mL) Low-dose DEX suppression (0.5 mg/6 hours for 48 hours, 2 mg/day): urinary 17-hydroxycorticosteroids, 12 mg/day (normal < 4 mg/day) High-dose DEX suppression (2 mg/6 hours for 48 hours, 8 mg/day): urinary 17-hydroxycorticosteroids, 3.6 mg/day (suppressed by 70%) Proceed to MRI & CT scanning of the brain and adrenal glands Hall mark: loss of circadian hormone rhythm

  20. Adrenal Glands – Gr / CS Nodular Cortical Hyperplasia Confluent Nodules

  21. Adrenal Glands – Gr / CS Nodular Cortical Hyperplasia Confluent Nodules

  22. Adrenal Glands – Low Power Nodular Cortical Hyperplasia Nodule

  23. Adrenal Glands – Low Power Nodular Cortical Hyperplasia Nodule

  24. Adrenal Glands – High Power Nodular Cortical Hyperplasia

  25. Q L Diagnosis Cushing’s Syndrome

  26. Q L Liver • Anatomy, Histology & Function • Metabolic & Toxic Conditions • Cirrhosis • Tumors • Clinical Case Presentation

  27. Liver - Anatomy Columbia University Howard J. Worman, M. D.

  28. Liver - Gross Columbia University Howard J. Worman, M. D.

  29. Liver - Cut Surface Portal vein Hepatic vein Columbia University Howard J. Worman, M. D.

  30. Q L Function of the Liver, hepatocyte Metabolism - Dietary carbohydrates, protein and fat Synthesis - Albumin, clotting factors & complement proteins Storage - Glycogen, triglycerides, vitamins & minerals Detoxification - Endogenous substances & foreign compounds Production - Bile for fat digestion & waste elimination

  31. Liver – Histology Portal triads Zoning by oxygen supply Central vein Columbia University Howard J. Worman, M. D.

  32. Q L Liver • Anatomy, Histology & Function • Metabolic & Toxic Conditions • Cirrhosis • Tumors • Clinical Case Presentation

  33. Q L Pathophysiology Alcohol: absorbed from the stomach and small intestine metabolized through oxidation in liver Acetaldehyde by alcohol dehydrogenase & cytochrome P‑450 2E1 Acetate by mitochondrial acetaldehyde dehydrogenase.

  34. Q L Alcoholic Liver Disease • Excess alcohol ingestion • the most common cause of liver disease • Risk for severe hepatic injury • daily intake > 40 or 80 g alcohol for 10 years • Individual susceptibility • females > males • body mass • genetic background

  35. Pathology

  36. Liver, Alcoholic Hepatic Steatosis (Fatty Liver) – Gr / CS Columbia University Howard J. Worman, M. D.

  37. Liver, Alcoholic Hepatic Steatosis (Fatty Liver) - Histology Columbia University Howard J. Worman, M. D.

  38. Liver, Alcoholic Hepatic Steatosis (Fatty Liver) – High Power Columbia University Howard J. Worman, M. D.

  39. Liver, Alcoholic Hepatitis - LP Trichrome stain

  40. Liver, Alcoholic Hepatitis - LP Trichrome stain

  41. Liver, Alcoholic Hepatitis - MP Mallory bodies Hepatocytes

  42. Liver, Alcoholic Hepatitis - MP Mallory bodies

  43. Liver, Alcoholic Hepatitis - MP Hepatocytes

  44. Liver, Alcoholic Cirrhosis – Gross Columbia University Howard J. Worman, M. D.

  45. Liver, Alcoholic Cirrhosis – MRI Enlarged spleen Columbia University Howard J. Worman, M. D.

  46. Liver, Alcoholic Cirrhosis – MRI Enlarged spleen Columbia University Howard J. Worman, M. D.

  47. Liver, Alcoholic Cirrhosis – Gross Columbia University Howard J. Worman, M. D.

  48. Liver, Alcoholic Cirrhosis – CT Enlarged spleen Columbia University Howard J. Worman, M. D.

  49. Liver, Alcoholic Cirrhosis – CT Enlarged spleen Columbia University Howard J. Worman, M. D.

  50. Liver, Alcoholic Cirrhosis - CS Regenerative Nodules

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