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Parathyroid adrenal pancreas dr faeza
- 1.
- 2. PTH • Hypocalcemia ismain stimulus (9-10.5 mg/dl) • Antagonize Calcitonin 35-50 mg
- 4. Parathyroid Gland –note small dark staining chief cells and larger, eosinophilic oxyphil cells
- 5. PARATHYROID DISORDERS • PrimaryHyperparathyroidism – Adenoma: 85% to 95% – Primary hyperplasia (diffuse or nodular): 5% to 10% – Parathyroid carcinoma: 1%∼ • Secondary Hyperparathyroidism - (LOW CA++ of Renal Failure) • Hypoparath-: Surgical, congenital, familial, idiopathic • Pseudo - hypoparath. – (end organ resistance)
- 6. Parathyroid adenoma. A,Solitary chief cell parathyroid adenoma revealing clear delineation from the residual gland below. B, High-power detail of a chief cell parathyroid adenoma. some slight tendency to follicular formation
- 7. HYPER-PARATHYROIDISM – Bone pain,fractures – Nephrolithiasis – Constipation, ulcers, gallstones – Depression, lethargy – Weakness, fatigue – Calcifications, esp. Lung, VALVES
- 8. HYPO-PARATHYROIDISM – Neuromuscular irritability –Mental status change – Parkinsonism like effects – Widened QT interval – Defective, carious, teeth
- 9. MEN-1, Wermer Syndrome (3P’s( • HYPERPARATHYROIDISM, chiefly hyperplasia • Pancreatic endocrine tumors • Pituitary adenoma, usually prolactinoma
- 10. MEN-2 • MEN-2A (SIPPLE):Pheochromo, Medullary Thyroid CA., Parathyroid hyperplasia • MEN-2B: NO hyperparathyroidism, but neuromas present • Familial Medullary Thyroid CA
- 11. ADRENAL CORTEX • Glomerulosa(Salt), mineralocorticoids – ALDOSTERONE • Fasciculata (Sugar), glucocorticoids – CORTISOL • Reticularis (Sex), gonadocorticoids – ANDROGENS, ESTROGENS
- 12.
- 14. Adrenal Cortex Zona Glomerulosa (clumps,cords, and follicle like structures Zona Fasciculata (cords of spongiocytes)
- 15.
- 16. HYPERADRENALISM • HYPERALDOSTERONISM (G). •CUSHING SYNDROME (CORTISOL) (F). • ADRENOGENITAL (VIRILIZING) SYNDROME (R).
- 17. CUSHING SYNDROME • Exogenoussteroid (90%)*** • ACTH-DEPENDENT ** - pituitary adenoma; - Ectopic corticotropin syndrome (ACTH-secreting pulmonary small-cell carcinoma, bronchial carcinoid) • Adrenal adenoma • Adrenal Carcinoma • Hyperplasia.
- 18. CUSHING SYNDROME • CENTRAL OBESITY •MOON FACIES • WEAKNESS • HYPERTENSION • DIABETES • OSTEOPOROSIS • HIRSUTISM • STRIAE
- 19.
- 20.
- 21. Cushing syndrome • Dependingon the cause of the hypercortisolism the adrenals have one of the following abnormalities: • (1) cortical atrophy, • (2) diffuse hyperplasia, • (3) macronodular or micronodular hyperplasia, • (4) an adenoma or carcinoma.
- 22. Diffuse hyperplasia of theadrenal contrasted with normal adrenal gland
- 23. Cushing syndrome Dx: •(1) Increased the 24-hour urine free-cortisol concentration. • (2) loss of normal diurnal pattern of cortisol secretion.
- 24. Cushing syndrome • Dxthe cause of Cushing syndrome depends on; • Serum ACTH and • Dexamethasone suppression test; Measurement of urinary steroid excretion after administration of dexamethasone.
- 25. PRIMARY HYPERALDOSTERONISM (Conn’s Syndrome( •Na+ RETENTION • K+ EXCRETION • HYPERTENSION
- 27. Secondary hyperaldosteronism • Activationof the renin-angiotensin system, (increased plasma renin) • In the following conditions: • Decreased renal perfusion (arteriolar nephrosclerosis, renal artery stenosis) • Arterial hypovolemia and edema (CHF, cirrhosis, nephrotic syndrome) • Pregnancy (due to estrogen-induced increases in plasma renin substrate)
- 28. SECONDARY HYPERALDOSTERONISM • DECREASEDRENAL PERFUSION • EDEMA (HEART, LIVER, KIDNEY) • PREGNANCY
- 29. ADRENOGENITAL SYNDROME • VIRILIZATION/feminization •CORTICAL NEOPLASM • CORTICAL HYPERPLASIA • 21-Hydroxylase Deficiency
- 31. ADRENAL INSUFFICIENCY • PRIMARYACUTE (ADRENAL CRISIS) • PRIMARY CHRONIC (auto-immune ADDISON DISEASE) • SECONDARY (PITUITARY) • hyperkalemia, hyponatremia, volume depletion, and hypotension
- 32. PRIMARY ACUTE • Rapidwithdrawal of steroid • Massive adrenal hemorrhage - Newborns with difficult delivery - Anticoagulant RX - Postsurgical DIC patient - MASSIVE ADRENAL HEMORRHAGE (WATERHOUSE-FRIDERICHSEN, if it follows infection and shock)
- 33.
- 34. PRIMARY CHRONIC • Mostof Addison disease is auto-immune adrenalitis • INFECTIONS (Tuberculosis, fungal) • METASTASES (adrenals are preferred site for early lung carcinoma metastases) • AIDS • Acute hemorrhagic necrosis (Waterhouse- Friderichsen syndrome) • Amyloidosis, sarcoidosis, hemochromatosis, lymphoma. • GENETIC DISORDERS
- 35.
- 36. NEOPLASMS • ADENOMAS ofADRENAL CORTEX • CARCINOMAS of ADRENAL CORTEX
- 37. Adrenocortical adenomas; awell-circumscribed, nodular lesion up to 2.5 cm expands the adrenal. Most are clinically silent
- 38.
- 39.
- 40. Carcinoma of theadrenal cortex
- 41. Carcinoma of theadrenal cortex
- 42. Low magnification ofthe Adrenal Gland Medulla Cortex
- 43.
- 44. ADRENAL MEDULLA • PHEOCHROMOCYTOMAS,“rule of 10s”. Primary tumors of adrenal medulla – 10% arise in an MEN setting – 10% are EXTRA-adrenal – 10% are bilateral – 10% are malignant – 10% are not associated with hypertension, (hypertension in 90%). – 10% are in childhood – can only call them malignant if they metastasize.
- 45.
- 46. TWO crucially importantpoints specific for endocrine tumors: • 1. FUNCTIONING carcinomas are very RARE in ANY endocrine gland. • 2. Benign adenomas may have extremely bizarre nuclei, but are most usually BENIGN!!!
- 47. MEN-1, Wermer Syndrome (3P’s( • HYPERPARATHYROIDISM, chiefly hyperplasia • Pancreatic endocrine tumors • Pituitary adenoma, usually prolactinoma
- 48. MEN-2 • MEN-2A (SIPPLE):Pheochromo, Medullary Thyroid CA., Parathyroid hyperplasia • MEN-2B: Pheochromo, Medullary Thyroid CA., neuromas, NO hyperparathyroidism.
- 49.
- 50. High mag ofan Islet – note Beta cells and more eosinophilic Alpha2 cells Acini Alpha Cells
- 51. Exocrine Endocrine Islets Alpha Cells Beta Cells DeltaCells (suppress insulin and glucagon) Pancreatic Polypeptide (PP) cells Epsilon Cells make gherlin, which causes hunger
- 52. Glucagon Insulin Immunohistochemistry ofa pancrearic Islet of Langerhans
- 53. • β cellproduces insulin, • α cell secretes glucagon, • δ cells contain somatostatin, which suppresses both insulin and glucagon • PP cells contain pancreatic polypeptide that exerts secretion of GIT enzymes and inhibits its motility. • D1 cells elaborate vasoactive intestinal polypeptide (VIP), that induces glycogenolysis and hyperglycemia; • Enterochromaffin cells synthesize serotonin and are the source of pancreatic tumors that cause the carcinoid syndrome Pancrearic Islet of Langerhans
- 54. DIABETES MELLITUS • 16Million in the USA • 1 Million/yr
- 55. How to DiagnoseDm: • Glucose >200 • Or……………. • Fasting glucose >126 trice • Or……………. • Post-prandial glucose > 200, 2 hrs AFTER standard OGTT (Oral Glucose Tolerance Test)
- 56. Classification of DiabetesMellitus American Diabetes Association 1. Type 1 diabetes (β-cell destruction, usually leading to absolute insulin deficiency) Immune – mediated Idiopathic 2. Type 2 diabetes (combination of insulin resistance and β-cell dysfunction) 3. Genetic defects of β-cell function; Maturity-onset diabetes of the young (MODY) 4. Exocrine pancreatic defects 5. Endocrinopathies 6. Genetic defects in insulin action 7. Infections 8. Drugs 9. Gestational diabetes mellitus 10.Genetic syndromes associated with diabetes
- 57. TWO* Types ofDM •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
- 58. Type 1 DiabetesMellitus Type 2 Diabetes Mellitus CLINICAL Onset: usually childhood and adolescence Onset: usually adult; increasing incidence in childhood and adolescence Normal weight or weight loss preceding diagnosis Vast majority are obese (80%( Progressive decrease in insulin levels Increased blood insulin (early); normal or moderate decrease in insulin (late( Circulating islet autoantibodies (anti-insulin, anti-GAD, anti- ICA512( No islet auto-antibodies Diabetic ketoacidosis in absence of insulin therapy Nonketotic hyperosmolar coma more common
- 59. GENETICS Major linkage toMHC class I and II genes; also linked to polymorphisms in CTLA4 and PTPN22, and insulin gene VNTRs No HLA linkage; linkage to candidate diabetogenic and obesity-related genes (TCF7L2, PPARG, FTO, etc.( PATHOGENESIS Dysfunction in regulatory T cells (Tregs) leading to breakdown in self-tolerance to islet auto-antigens Insulin resistance in peripheral tissues, failure of compensation by β- cells Multiple obesity-associated factors (circulating nonesterified fatty acids, inflammatory mediators, adipocytokines) linked to pathogenesis of insulin resistance
- 60. PATHOLOGY Insulitis (inflammatory infiltrate ofT cells and macrophages( No insulitis; amyloid deposition in islets β-cell depletion, islet atrophy Mild β-cell depletion
- 61.
- 62. Metabolic actions ofinsulin
- 63. PATHOGENESIS • 1 • T-Lymphocytes reactingagainst 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”
- 64. MODY (Maturity OnsetDiabetes of the Young( • Multiple types • 2-5% of diabetics • Primary beta cell defects • Multiple genetic mechanisms, especially GLUCOKINASE mutations
- 65.
- 66.
- 67. COMPLICATIONS MORPHOLOGY • (MACRO-vascular) Atherosclerosis •MICRO-vascular – Retinopathy – Nephropathy- glomerular, vascular, KW – Neuropathy (most common cause of neuropathy) • Infections
- 68.
- 69.
- 70. Diabetic Nephropathy • Renalfailure is second only to MI as a cause of death from DM. • Three lesions are encountered: (1) Glomerular lesions; capillary BM thickening, diffuse mesangial sclerosis, and nodular glomerulosclerosis (2) vascular lesions, arteriolosclerosis; (3) PN, including necrotizing papillitis.
- 71.
- 72.
- 73. Diffuse and nodulardiabetic glomerulosclerosis (PAS stain). Note the diffuse increase in mesangial matrix and characteristic acellular PAS-positive nodules.
- 74. Severe renal hyalinearteriolosclerosis
- 75.
- 76. RETINOPATHY in Dm Showsmicroaneurysms, areas of hemorrhage, cotton wool spots, hard exudates, venous beading, neovascularization, retinal detachment, vitreous detachment, pre retinal hemorrhage
- 78. INFECTIONS in Dm •SKIN • TUBERCULOSIS • PNEUMONIA • PYELONEPHRITIS • CANDIDA
- 79. NEOPLASMS of theEndocrine 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
- 80.
- 81. Pineal Body The Seatof the Soul The Third Eye
- 82. PINEAL “GLAND” • PINEALOMAS –PINEOBLASTOMAS – PINEOCYTOMAS
- 84. Pineal Gland N –neuroglia P –pinealocytes S – Brain Sand
Editor's Notes
- #3 PTH stimulates osteoclasts to chew up bone and transfer calcium from the bone to the serum “compartments”.
- #8 Hyperparathyroidism symptoms are the same as hypercalcemia symptoms, and vice versa.
- #9 Hypoparathyroidism symptoms are the same as hypocalcemia symptoms, and vice versa.
- #10 MEN-1 is the three “P”s
- #11 Madullary thyroid carcinoma is present in ALL three types of MEN-2
- #13 Is this a right or a left adrenal gland?
- #21 What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)
- #23 Diffuse hyperplasia of the adrenal contrasted with normal adrenal gland. In cross-section the adrenal cortex is yellow and thickened, and a subtle nodularity is seen (contrast with Figure 24-46 ). Both adrenal glands were diffusely hyperplastic in this patient with ACTH-dependent Cushing syndrome.
- #27 The major causes of primary hyperaldosteronism and its principal effects on the kidney.
- #29 Once again, the amazing reninangiotensinaldosterone axis
- #30 Congenital adrenal hyperplasia is generally synonymous with adrenogenital syndrome.
- #31 Note that the COLOR and CONSISTENCY of the tumor is the same as that of the CORTEX. What is the normal thickness of a bright yellow adrenal cortex? Ans: about 1 mm
- #34 Waterhouse-Friderichsen Syndrome septicemia , shock, DIC, adrenocortical insufficiency with bilateral adrenal hemorrhage
- #37 Adenomas and carcinomas are about equally common in adults; in children, carcinomas predominate
- #38 Note that the COLOR and CONSISTENCY of the tumor is the same as that of the CORTEX. That is precisely WHY you know this is a tumor of the adrenal cortex. Most adrenocortical adenomas are clinically silent and are usually incidental findings at autopsy or during abdominal imaging for an unrelated cause
- #39 Adenoma
- #40 Adenoma
- #42 Carcinoma of the adrenal cortex.
- #46 Note that the COLOR and CONSISTENCY of the tumor is the same as that of the MEDULLA.
- #48 MEN-1 is the three “P”s
- #49 Madullary thyroid carcinoma is present in ALL three types of MEN-2
- #52 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?
- #58 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.
- #62 Fill in the blanks, or better yet, get a tattoo!
- #63 Metabolic actions of insulin in striated muscle, adipose tissue, and liver. Insulin is the most potent anabolic hormone known, with multiple synthetic and growth-promoting effects
- #66 Like just about ANY auto-immune disorder we see inflammatory changes against tissue with NO known external pathogen, in this case LYMPHOCYTES (T-Cells) attacking islets. Could this be called an isletitis or islitis? YES
- #67 Hyalinization in the islets of Langerhans is a common finding in type 2 diabetes. Often, the “hyaline” is amyloid.
- #70 In pathology, you almost assume if you get an amputation specimen, it is from a diabetic.
- #73 In “nodular” glomerulosclerosis, aka, K-W kidneys, “nodules” of PAS positive matrix trapping mesangial cells, are found at the periphery of glomeruli.
- #75 Severe renal hyaline arteriolosclerosis. Note a markedly thickened, tortuous afferent arteriole. The amorphous nature of the thickened vascular wall is evident. (PAS stain).
- #76 Nephrosclerosis in a patient with long-standing diabetes. The kidney has been bisected to demonstrate both diffuse granular transformation of the surface (left) and marked thinning of the cortical tissue (right). Additional features include some irregular depressions, the result of pyelonephritis, and an incidental cortical cyst (far right).
- #83 Younger looking cells “BLASTomas” are primarilly in kids, more mature looking cells CYTomas are in adults. BOTH are quite rare.