Diseases of adrenal gland

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Diseases of adrenal gland

  1. 1. ADRENAL GLANDS <ul><ul><ul><ul><ul><li>ANATOMY: 2 GLANDS WITH A TOTAL WEIGHT OF 6 TO 10 GRS. </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>CORTEX (80-90%) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Glomerulosa (Mineralocorticoid) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Fasciculata( Gluco>Sex) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Reticularis ( Sex>Gluco) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>MEDULLA(10-20%) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Epinephrine </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Glucocorticoids: Cortisol and corticosterone </li></ul></ul></ul></ul></ul>www.freelivedoctor.com
  2. 2. CONTROL OF SECRETION: ACTH LEVELS <ul><li>ACTH HAS A COMPLEX CONTROL REGULATION: </li></ul><ul><ul><li>C.R.F. </li></ul></ul><ul><ul><li>CIRCADIAN RYTHM (Highest 8:00 a.m.-Lowest 12:00 p.m.) </li></ul></ul><ul><ul><li>PULSES </li></ul></ul><ul><ul><li>NEGATIVE FEED-BACK </li></ul></ul><ul><ul><li>RESPONSES TO INTERNAL /EXTERNAL STIMULI </li></ul></ul>www.freelivedoctor.com
  3. 3. ACTH ACTIONS: <ul><li>HYPERTROPHY OF ADRENAL GLANDS CELLS </li></ul><ul><ul><ul><li>INCREASE IN CHOLESTEROL UPTAKE </li></ul></ul></ul><ul><ul><ul><li>INCREASE IN DESMOLASE ACTIVITY </li></ul></ul></ul><ul><ul><ul><li>INCREASE IN STEROID SYNTHESIS </li></ul></ul></ul><ul><ul><ul><li>RELEASE OF STORAGE AND NEW STEROIDS </li></ul></ul></ul><ul><ul><ul><li>INCREASE LIPOLYSIS( FATTY ACIDS MOVILIZATION) </li></ul></ul></ul><ul><ul><ul><li>INCREASE INSULIN RELEASE </li></ul></ul></ul><ul><ul><ul><li>INCREASE SKIN PIGMENTATION </li></ul></ul></ul>www.freelivedoctor.com
  4. 4. GLUCOCORTICOID HORMONES <ul><li>ARE “ESSENTIAL” FOR LIFE </li></ul><ul><li>ARE “CATABOLIC” HORMONES </li></ul><ul><li>ARE “PERMISSIVE”HORMONES </li></ul>www.freelivedoctor.com
  5. 5. GLUCOCORTICOID HORMONES AFFECTS: <ul><li>CARBOHIDRATES METABOLISM </li></ul><ul><li>PROTEIN METABOLISM </li></ul><ul><li>LIPID METABOLISM </li></ul><ul><li>ELECTROLYTE / WATER BALANCE </li></ul><ul><li>STRESS OR EMERGENCY SITUATIONS </li></ul><ul><li>CARDIOVASC. SYSTEM FUNCTION </li></ul><ul><li>RENAL FUNCTION , SKELETAL MUSCLE </li></ul><ul><li>C.N.S., HEMATOPOIETIC SYSTEM </li></ul><ul><li>IMMUNE SYSTEM, GASTRIC ACID SECRETION, SKIN, CONECTIVE TISSUE </li></ul><ul><li>GROWTH RATE AND DEVELOPMENT </li></ul>www.freelivedoctor.com
  6. 6. CORTISOL <ul><li>CARBOHYDRATE METABOLISM </li></ul><ul><ul><li>INCREASE GLUCONEOGENESIS </li></ul></ul><ul><ul><li>INCREASE HEPATIC GLYCOGENOLYSIS </li></ul></ul><ul><ul><li>DECREASE PERIPHERAL GLUCOSE UPTAKE </li></ul></ul><ul><ul><li>NET EFFECT: INCREASE IN GLUCOSE LEVELS TO AVOID HYPOGLICEMIA </li></ul></ul><ul><ul><li>ANTIINSULINIC ACTION </li></ul></ul>www.freelivedoctor.com
  7. 7. PROTEIN METABOLISM <ul><li>INCREASE PROTEIN BREAKDOWN (GLUCONEOGENESIS) </li></ul><ul><li>DECREASE PROTEIN SYNTHESIS </li></ul><ul><li>NET EFFECT: CATABOLISM AND ANTIANABOLISM STATE WITH NEGATIVE NITROGEN BALANCE </li></ul>www.freelivedoctor.com
  8. 8. LIPID METABOLISM: <ul><li>SLIGHT DIRECT LIPOLYTIC EFFECT </li></ul><ul><li>ENHANCE THE LIPOLYTIC EFFECT OF EPINEPHRINE, GROWTH HORMONE. </li></ul><ul><li>INCREASE LIPOGENESIS IN OTHERS </li></ul><ul><li>NET EFFECT: OBESITY WITH CHARACTERISTIC DISTRIBUTION </li></ul>www.freelivedoctor.com
  9. 9. HYDROELECTROLYTE BALANCE <ul><li>MINERALOCORTICOID EFFECT </li></ul><ul><li>SODIUM RETENTION </li></ul><ul><li>POTASSIUM SECRETION </li></ul><ul><li>HYDROGEN SECRETION </li></ul><ul><li>WATER RETENTION </li></ul><ul><li>NET EFFECTS: HYPOKALEMIC METABOLIC ALCALOSIS WITH HYPERVOLEMIA </li></ul>www.freelivedoctor.com
  10. 10. CARDIOVASCULAR SYSTEM: <ul><li>PERMISSIVE ACTION TO: </li></ul><ul><ul><li>CATECHOLAMINES VASOCONSTRICTION </li></ul></ul><ul><ul><li>DECREASE IN VASCULAR PERMEABILITY </li></ul></ul><ul><ul><li>NET EFFECT: INCREASE IN BLOOD PRESSURE </li></ul></ul><ul><ul><li>STRESS OR EMERGENCY SITUATIONS </li></ul></ul><ul><ul><li>PREVENTS “HYPOGLICEMIA, SHOCK AND DEATH) </li></ul></ul>www.freelivedoctor.com
  11. 11. SKELETAL MUSCLE SYSTEM <ul><li>BONE FORMATION </li></ul><ul><ul><li>DECREASE COLLAGEN SYSTEM </li></ul></ul><ul><ul><li>DECREASE OSTEOBLAST ACTIVATION </li></ul></ul><ul><ul><li>ANTAGONIZE VIT. D ACTIVATION </li></ul></ul><ul><ul><li>INCREASE RENAL CALCIUM EXCRETION </li></ul></ul><ul><ul><li>NET EFFECT: OSTEOPOROSIS, DECREASE IN OSEUS MATRIX, AND DECREASE IN BONE REABSORPTION </li></ul></ul>www.freelivedoctor.com
  12. 12. MUSCULAR SYSTEM <ul><li>DECREASE CONTRACTILITY AND STRENGTH </li></ul><ul><li>MUSCLE ATROPHY (PROTEIN CATABOLISM) </li></ul>www.freelivedoctor.com
  13. 13. CENTRAL NERVOUS SYSTEM: <ul><li>DECREASE SEIZURE THRESHOLD </li></ul><ul><li>PSIQUIATRIC DISORDERS </li></ul>www.freelivedoctor.com
  14. 14. HEMATOPOIETIC SYSTEM: <ul><li>INCREASE LIFE SPAN OF RED BLOOD CELLS </li></ul><ul><li>INCREASE PLATELETS NUMBER </li></ul><ul><li>INCREASE NEUTROPHILS NUMBER </li></ul><ul><li>DECREASE MONOCYTES, LYMPHOCITES </li></ul><ul><li>DECREASE EOSINOPHYLS AND BASOPHILS </li></ul>www.freelivedoctor.com
  15. 15. CONECTIVE TISSUE: <ul><li>DECREASE COLLAGEN SYNTHESIS </li></ul><ul><ul><li>SKIN ATROPHY </li></ul></ul><ul><ul><li>CAPILLARY FRAGILITY </li></ul></ul>www.freelivedoctor.com
  16. 16. GROWTH AND DEVELOPMENT: <ul><li>DECREASE GROWTH </li></ul><ul><ul><li>DECREASE PROTEIN SYNTHESIS </li></ul></ul><ul><ul><li>DECREASE BONE FORMATION </li></ul></ul><ul><ul><li>DECREASE FIBROBLASTIC ACTIVITY </li></ul></ul>www.freelivedoctor.com
  17. 17. IMMUNE SYSTEM: <ul><li>DECREASE MACROPHAGE RESPONSES TO M. I. F. </li></ul><ul><li>DECREASE RECEPTORS NUMBER TO I gE </li></ul>www.freelivedoctor.com
  18. 18. ANTI-INFLAMMATORY EFFECTS:DECREASE <ul><li>CAPILLARY PERMEABILITY </li></ul><ul><li>LEUCOCYTE MIGRATION </li></ul><ul><li>FIBRIN SYNTHESIS </li></ul><ul><li>LYSOSOMAL STABILIZATION </li></ul><ul><li>PG AND Tx SYNTHESIS </li></ul><ul><li>FIBROBLAST PROLIFERATION </li></ul>www.freelivedoctor.com
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  20. 20. CAUSES OF CUSHING´S SYNDROME <ul><li>I.-ADRENAL HYPERPLASIA </li></ul><ul><ul><li>A) Secondary to pituitary ACTH overproduction </li></ul></ul><ul><ul><ul><li>1.-Pituitary –hypothalamic dysfunction </li></ul></ul></ul><ul><ul><ul><li>2.-Pituitary ACTH –producing micro or macroadenomas </li></ul></ul></ul><ul><ul><ul><li>B) Secondary to ACTH or CRH-producing nonendocrine tumors (bronchogenic carcinoma, carcinoid of the thymus, pancreatic carcinoma, Bronchial adenoma) </li></ul></ul></ul>www.freelivedoctor.com
  21. 21. CAUSES OF CUSHING´S SYNDROME <ul><li>II.-ADRENAL NODULAR HYPERPLASIA </li></ul><ul><li>III.-ADRENAL NEOPLASIA </li></ul><ul><ul><li>A) Adenoma </li></ul></ul><ul><ul><li>B) carcinoma </li></ul></ul><ul><ul><li>IV.-EXOGENOUS, IATROGENIC CAUSES </li></ul></ul><ul><ul><ul><li>A) Prolonged use of glucocorticoids </li></ul></ul></ul><ul><ul><ul><li>B) Prolonged use of ACTH </li></ul></ul></ul>www.freelivedoctor.com
  22. 22. <ul><li>ADRENALS </li></ul><ul><li>Adrenal Cortex </li></ul><ul><li>  Adrenocortical Hyperfunction (hyperadrenalism) </li></ul><ul><li>Adrenal secretes 3 major groups of steroid </li></ul><ul><li>hormones a) glucocorticoids (cortisol) – Cushing </li></ul><ul><li> Syndrome b) mineralocorticoids (aldosterone) – </li></ul><ul><li>hyperaldosteronism c) androgens – virilizing syndromes </li></ul>www.freelivedoctor.com
  23. 23. 1. Cushing Syndrome a) any factor that causes  cortisol (i.e., glucocorticoids) i) mainly due to administration of glucocorticoids (iatrogenic) ii) hypersecretion of ACTH iii) hyperplasia or neoplasia iv) ectopic secretion of ACTH www.freelivedoctor.com
  24. 24. <ul><li>In hypersecreting ACTH ( ii above)  “Cushing </li></ul><ul><li>Disease” a) more often in women b) 20-30 yrs c)   in most patients, pituitary usually has </li></ul><ul><li> small ACTH secreting adenoma i) less sensitive to (-) feedback control on ACTH release d) anterior pituitary has areas of corticotroph-cell hyperplasia without adenoma </li></ul>www.freelivedoctor.com
  25. 25. <ul><li>e)  CRH from hypothalamus f) neoplasia/hyperplasia  ~30% of cases of Cushing syndrome g) most other case caused by  ectopic sites of ACTH secretion (usually small carcinoma of lung) i) other sites have included pancreas, thyroid </li></ul><ul><li>Clinical a) patients who have exogenous glucocorticoids (i.e., cortisol) i) adrenals are atrophied due to  ACTH release b) endogenous ACTH  adrenal hyperplasia </li></ul>www.freelivedoctor.com
  26. 26. c) known affects of glucocorticoids i) hypertension ii) weight gain (“moon face” “buffalo hump”) iii) atrophy of fast (type II) twitch myofibers  muscle atrophy and limb weakness iv) hyperglycemia and glucosuria v) proteolysis and bone resorption (osteoporosis) vi) suppresses immune system   risk for infections vii) hirsuitism viii) CNS  mood changes www.freelivedoctor.com
  27. 27. www.freelivedoctor.com
  28. 28. <ul><li>Hyperaldosteronism </li></ul><ul><li>Excessive levels of aldosterone a)  sodium retention b )  potassium excretion  c) which results in  BP and hypokalemia </li></ul><ul><li>Primary or Secondary a) primary i) autonomous overproduction of aldosterone   renin-angiotensin system ii) caused by adrenocortical adenoma or by hyperplasia   </li></ul>www.freelivedoctor.com
  29. 29. <ul><li>iii) primary aldosterone secreting adenoma (in >80%) – “Conn syndrome” </li></ul><ul><li>iv) carcinomas are rare v) no ACTH (-) feedback; therefore other regions of adrenals are not atrophic </li></ul><ul><li>vii) Conn syndrome more often in adults whereas hyperplasia occur more often in children </li></ul><ul><li>Adrenogenital Syndrome </li></ul><ul><li>Caused by variety of diseases </li></ul><ul><li>a) primary gonadal disorders and  </li></ul><ul><li>  </li></ul>www.freelivedoctor.com
  30. 30. <ul><li>b) primary adrenal disorders </li></ul><ul><li>Adrenal cortex </li></ul><ul><li>a) secretes </li></ul><ul><li>i) dehydroepiandrosterone </li></ul><ul><li>ii) androstenedione </li></ul><ul><li>b) both require conversion to testosterone in peripheral tissues </li></ul><ul><li>c) these adrenal androgen formation requires ACTH </li></ul><ul><li>i) secretion can occur de novo or through  </li></ul><ul><li>ii) excess ACTH secretion (e.g., Cushing Syndrome) </li></ul>www.freelivedoctor.com
  31. 31. d) adrenal causes of  androgens i) neoplasms (more likely to be carcinomas) ii) adrenal hyperplasia - group of autosomal recessive disorders causing  cortisol production with feedback  in ACTH with resultant adrenal hyperplasia (e.g., congenital) - the most common enzymatic defect in congenital adrenal hyperplasia is 21-hydroxylase deficiency which accounts for ~95% of cases. www.freelivedoctor.com
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  33. 33. www.freelivedoctor.com
  34. 34. <ul><li>Clinical: </li></ul><ul><li>a) congenital adrenal hyperplasia </li></ul><ul><li>i) bilateral adrenal hyperplasia </li></ul><ul><li>- driven by  ACTH </li></ul><ul><li>b) hyperplasia of ACTH producing cells is present in anterior pituitary c) clinical manifestation determined by specific enzyme deficiency i) androgens ii) sodium homeostasis iii) depending on severity of diseases, </li></ul><ul><li> S & S usually present during infancy and early childhood and less commonly during childhood. </li></ul>www.freelivedoctor.com
  35. 35. d) 21-hydroxylase deficiency causes excessive androgenic activity i) masculinization in females - hirsutism - oligomenorrhea ii) in males, enlargement of external genitalia e) some rare forms of congenital adrenal hyperplasia i) 17-  -hydroxylase deficiency ii) in other forms of congenital adrenal hyperplasia (e.g., 11  -hydroxylase deficiency) www.freelivedoctor.com
  36. 36. - accumulated intermediates steroids have sodium retention properties and subsequent hypertension f) congenital adrenal hyperplasia should be suspected in neonate with ambiguous genitalia i) severe enzyme deficiency in infancy can be life threatening - vomiting - diarrhea - sodium loss (dehydration) ii) in all cases, an androgen producing neoplasm in the ovary must be R/O www.freelivedoctor.com
  37. 37. <ul><li>Adrenal Insufficiency (adrenocortical hypofunction) </li></ul><ul><li>May reflect either primary adrenal disease (i.e., </li></ul><ul><li>primary hypoadrenalism) or secondary via </li></ul><ul><li>decreased stimulation of the adrenals caused by </li></ul><ul><li>ACTH deficiency (e.g., Sheehan syndrome, </li></ul><ul><li>nonfunctioning pituitary adenomas and/or </li></ul><ul><li>lesions of hypothalamus, etc.) </li></ul><ul><li>Further divided (primary adrenocortical </li></ul><ul><li>insufficiency) a) chronic primary adrenocortical insufficiency (Addison Disease) or b) acute primary adrenocortical insufficiency </li></ul>www.freelivedoctor.com
  38. 38. <ul><li>1. Addisons Disease (chronic) </li></ul><ul><li>Progressive destruction of adrenal cortex a) S & S usually do not appear until ~90% of adrenal gland has been compromised </li></ul><ul><li>Causes: a) autoimmune adrenalitis i) ~75-90% of all cases of Addison disease in developed countries ii) sporadically or familial component iii) In ~50% of patients, autoimmune cause affects only the adrenal glands whereas the remaining patients also exhibit other autoimmune disorders </li></ul>www.freelivedoctor.com
  39. 39. - Hashimoto - Pernicious anemia - Type I diabetes - idiopathic Hypoparathyroidism iv) Type I and II polyglandular syndrome - Type I : - autosomal recessive; mutations located on chromosome 21q - Type II : - strong link to histocompatibility antigens (HLA-B8, HLA- DR3 and HLA-DQ5) www.freelivedoctor.com
  40. 40. v) circulating antibodies to several steroidal enzymes (e.g., 21 and 17  -hydroxylase) have been found in all types of autoimmune adrenalitis b) Infections i) TB (accounted for ~90% of primary chronic adrenocortical insufficiency) antituberculosis drugs have  the incidence of Addisons disease ii) Fungi (Histoplasma capsulatum and coccidioides immitis) iii) AIDS, due to contracting a variety of infections www.freelivedoctor.com
  41. 41. c) Metastatic neoplasms i) common site of metastatic disseminated carcinomas ii) carcinomas of breast and lung are source of majority of metastases in the adrenals iii) other neoplasms from GI, melanomas and hematopoietic neoplasms may also metastasize to the adrenals www.freelivedoctor.com
  42. 42. <ul><li>  Clinical a) insidious onset with progressive weakness and easy fatigability b) GI disturbances are common complaint i) anorexia, vomiting, nausea, weight loss and diarrhea c) In patients with primary disease, melanocytes are stimulated with hyperpigmentation (via  ACTH precursor hormone stimulation) </li></ul><ul><li>i) face, axilla,nipples, areola, perineum ii) hyperpigmentation is not seen in primary pituitary or hypothalamic disease </li></ul>www.freelivedoctor.com
  43. 43. d) Primary adrenal insufficiency i)  aldosterone   Na + loss;  K + retention; volume depletion  hypotension ii) heart smaller than normal (? Chronic hypovolemia) iii) hypoglycemia (via glucocorticoid deficiency) and impaired gluconeogenesis iv) acute stress in the patients (e.g., infections, surgical procedures, trauma) may initiate an “ acute adrenal crisis ” www.freelivedoctor.com
  44. 44. <ul><li>- intractable vomiting - abdominal pain - hypotension, vascular collapse, - coma - death unless corticosteroids are replaced immediately. </li></ul><ul><li>2. Acute Adrenocortical Insufficiency </li></ul><ul><li>Rapid withdrawal of steroids (from previous </li></ul><ul><li>treatment) </li></ul><ul><li>Massive adrenal hemorrhage a) destroy adrenal cortex i) may occur in patients maintained on chronic anticoagulant therapy ii) pregnancy </li></ul>www.freelivedoctor.com
  45. 45. iii) DIC iv) overwhelming sepsis (i.e., Waterhouse-Friderichsen syndrome) - classically associated with Nisseria meningitides septicemia - also can be caused by pneumococci, Haemophilus influenza and pseudomonas sp. - pathogenesis unclear (may involve ETX induced vascular damage?) - DIC, shock, skin purpura - more common in children - massive adrenal clots   www.freelivedoctor.com
  46. 46. www.freelivedoctor.com
  47. 47. <ul><li>Adrenocortical Neoplasms </li></ul><ul><li>May be responsible for a variety of </li></ul><ul><li>hyperadrenalisms a) functional adenomas most commonly associated with hyperaldosteronism and Cushing syndrome </li></ul><ul><li>A virilizing neoplasm  high incidence to be </li></ul><ul><li>carcinogenic </li></ul><ul><li>Functional and non-functional adrenocortical </li></ul><ul><li>neoplasms cannot be differentiated solely on </li></ul><ul><li>basis of morphology a) hormone measurements b) most adrenocortical adenomas do not cause hyperfunction </li></ul>www.freelivedoctor.com
  48. 48. <ul><li>Adrenocortical carcinomas are rare a) two rare inherited adrenal cortical carcinomas i) Li-Fraumeni syndrome </li></ul><ul><ul><ul><li>- autosomal dominant </li></ul></ul></ul><ul><ul><ul><li>- predisposition to develop other cancers due to mutations in p53 ii) Beckwith-Wiedemann syndrome </li></ul></ul></ul><ul><li>Generally, adrenal adenomas are small (1-2cm) </li></ul><ul><li>whereas adrenal carcinomas are large, invasive </li></ul><ul><li>lesions a) adrenal carcinomas metastasize via lymphatics and inferior vena cava i) mean survival is ~2 yrs. </li></ul>www.freelivedoctor.com
  49. 49. <ul><li>Adrenal Medulla </li></ul><ul><li>Most important diseases of adrenal </li></ul><ul><li>medulla are the neoplasms a) neuronal i) neuroblastoma ii) mature ganglionic cell tumors </li></ul><ul><li>b) chromaffin cells i) pheochromocytoma </li></ul><ul><li>Pheochromocytoma a) neoplasm composed of chromaffin cells i) synthesize and release catecholamines b) familial syndromes (~10%) </li></ul>www.freelivedoctor.com
  50. 50. www.freelivedoctor.com
  51. 51. i) MEN2A and MEN2B ii) type I neurofibromatosis iii) Von Hippel-Lindau disease iv) Sturge-Weber syndrome c) Extra-adrenal source (~10%) i) carotid body ii) organ of Zuckerkandl d) are bilateral (~10%) i) may be as high as 50% in familial cases e) malignant (~10%) i) more common when arise in extra- adrenal sites www.freelivedoctor.com
  52. 52. f) clinical i) hypertension! - chronic, elevated BP (~70% of cases) ii) other hormones can be secreted - ACTH - somatostatin iii) dx   urinary excretion of catecholamines and metabolites - vanillylmandelic acid - metanephrines iv) isolated pheochromocytomas treated surgically - multifocal  medically treated www.freelivedoctor.com
  53. 53. <ul><li>Multiple Endrocrine Neoplasia Syndromes (MEN) </li></ul><ul><li>Group of inherited diseases a) hyperplasias, adenomas and carcinomas of multiple endocrine organs i) occur at younger age vs. cancers ii) arise in multiple endocrine organs iii) even in one organ, they are multifocal iv) tumors preceded by hyperplasia v) more aggressive and recur more frequently vs. sporadic tumors </li></ul>www.freelivedoctor.com
  54. 54. <ul><li>MEN-1 a) inherited as autosomal dominant b) is a tumor suppressor gene i) loss of MEN-1 therefore causes tumor genesis - parathyroid (95% involved) - pancreas (>40%) - pituitary (>30%) </li></ul><ul><li>Parathyroid gland a) primary hyperparathyroidism arising from hyperplasia is a common feature of MEN-1 </li></ul>www.freelivedoctor.com
  55. 55. <ul><li>Pancreas a) leading cause of death in MEN-1 b) aggressive c) often functional tumors i) gastrinomas (Zollenger-Ellison syndrome) ii) insulinomas and resultant hypoglycemia </li></ul><ul><li>Pituitary a) most common in MEN-1 is prolactinoma   </li></ul>www.freelivedoctor.com
  56. 56. <ul><li>MEN-2b (William syndrome) a) involve also the thyroid b) adrenal (medulla) c) major differences between MEN-2a and MEN-2b is i) do not develop primary hyperparathyroidism (MEN-2b) ii) develop at extra endocrine sites - lips - tongue - GI tract </li></ul><ul><li>MEN-2 carry RET Protooncogene a) persons are advised to have prophylactic thyroidectomy to prevent carcinoma. </li></ul>www.freelivedoctor.com

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