Ch40 Endocrine disorders

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wvuong
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Ch40 Endocrine disorders
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2015-03-14 22:08:01
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week 6
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  1. Classification of endocrine disorders 
    [primary]
    [secondary]
    Primary: intrinsic malfunction of the hormone producing target gland

    Secondary: malfunction of the hypothalamus pituitary cells that control the hormone -producing target gland
  2. Growth hormone 
    [primary target]
    [functions]
    Primary target is the liver 

    -Increase lean body mass, reduce fat mass, and induces the liver to release glucose under conditions of hypoglycemia
  3. Growth hormone deficiency is classified as?
    • -Decrease GH secretion 
    • -defective GH action 
    • -defective IGF-1 (somatomedin) generation
  4. GH deficiency associated with 
    [relevant in children]
    • birth history of labor or breech delivery 
    • midline craniocerebral defects 
    • congenital malformation/chromosomal anomaly 
    • mystagmus, retinal abnormalities, midline of midfacial abnormalities (cleft lip/palate)
  5. GH deficiency 
    [presentation adults]
    • diminished lean body mass 
    • hypercholesterolemia 
    • decreased bone density 
    • treatment w/ individualized therapy
  6. GH excess 
    [etiology/pathogenesis]
    • uncontrolled production by a tumor in the pituitary (somatotropic tumor) 
    • stimulates liver to produce IGF-1
    • together cause up-regulated growth of soft and bony tissue
  7. Pituitary giantism
    • occurs in childhood before skeletal epiphyses are closed 
    • Acromegaly: occurs in adults
  8. Acromegaly
    GH excess that occurs in adults
  9. acromegaly 
    [treatment]
    • surgical removal of tumor 
    • counteracting effects of GH (octreotide, synthetic somatostatin)
    • may be radiation
  10. What regulates thyroid hormones, triiodothyronine and thyroxine?
    • TSH that are secreted from the anterior pituitary
    • regulators of metabolism
  11. Hypothyroidism 
    [etiology]
    • congenital/acquired 
    • majority are primary due to intrinsic dysfunction of the thyroid gland 
    • congenital hypothyroidism (cretinism) due to thyroid dysgenesis
  12. Secondary hypothyroidism
    • defects in TSH production 
    • results from: head trauma, cranial neoplasms, brain infections, cranial irradiation, neurosurgical procedures
  13. Hypothyroidism
    [clinical manifestations in infants]
    • dull appearance, thick, protuberant tongue, thick lips (=feeding difficulties)
    • prolonged neonatal jaundice
    • poor muscle tone 
    • bradycardia, mottled extremities 
    • umbilical hernia 
    • hoarse cray
  14. Hypothyroidism 
    [clinical manifestations in children/adults]
    • weakness, lethargy, cold intolerance, decreased appetite 
    • bradycardia, mild/moderate wt gain 
    • elevated serum cholestrol and triglycerides 
    • enlarged thyroid, dry skin, constipation 
    • depression, difficulties with concentration/memory 
    • menstrual irreg.
  15. Primary hypothyroidism
    • will manifest as elevated TSH 
    • hypothalamic-pituitary dysfunction results in low levels of TSH and T4
  16. Hypothyroidism
    [treatment]
    • levothyroxine 
    • intravenous levothyroxine used for myxedema coma
  17. Hyperthyroidism 
    [etiology/pathogenesis]
    • increased T4 and T3 (Graves disease) 
    • thyroid follicular cell destruction with release of preformed T4 and T3 (Hashimoto thyroiditis)
    • ingestion of excessive thyroid hormone/iodide preparation
  18. Primary hyperthyroidism
    autonomous
  19. Secondary hyperthyroidism
    mediated thru stimulation of TSH receptors by substances such as TSH 

    Autoimmune - related to S=TSH receptor antibodies
  20. Hyperthyroidism
    [etiologies]
    • pituitary adenoma
    • thyroid carcinoma
    • inflammation of thyroid follicular cells 
    • ingestion of thyroid hormone preparations/excessive iodides 
    • toxic goiter 
    • common in women
  21. Primary hyperthyroidism
    will manifest as undetectable TSH levels and serum T4 and T3
  22. Thyroid storm
    • from hyperthyroidism 
    • -a form of life-threatening thyrotoxicosis that occurs when excessive amts of thyroid hormones are acutely released into circulation
  23. Hyperthyroidism 
    [treatments]
    • B-blockers 
    • antithyroid drugs, thioamides
    • radioactive iodine treatment 
    • surgical removal of thyroid gland (for tumors)
    • pituitary adenoma surgically removed
  24. Thyroid storm 
    [treatment]
    • achieve metabolic balance 
    • antithyroid drugs, follow by iodine adm.
    • B-blockers for symptoms and control blood pressure 
    • antipyretic therapy
    • fluid replacement
    • glucocorticoids
  25. What does the adrenal cortex do?
    synthesizes glucocortiocoids, mineralocorticoids, and androgens 

    cortisol is primary glucocorticoid and negative feedback suppresses ACTH release
  26. Adrenocortical insufficiency 
    [etiology]
    • primary: hyposecretion due to disease of adrenal cortex (Addison disease) 
    • Seconardy: inadequate secretion of ACTH from anterior pituitary
    • Tertiary: lack of CRH secretion from hypothalamus due to hypothalamic malfunction or injury
  27. Primary adrenal insufficiency
    caused be destruction of adrenal gland
  28. Secondary adrenal insufficiency
    • hypothalamic-pituitary dysfunction 
    • related to corticosteroid therapy, which suppresses ACTH, CRH
  29. Addisonian crisis/acute adrenal insufficiency
    life threatening condition caused by inadequate levels of glucocorticoids and mineralocorticoids in circulation
  30. Adrenocortical insufficiency 
    [treatment]
    replace absent/deficient hormones - to mimics natural production
  31. Adrenal crisis 
    [treatment]
    • intraenous glucocorticoids 
    • volume replacement
  32. Adrenogenital syndrome
    • congenital adrenal hyperplasia 
    • enzyme needed for cortisol production lacking due to gene defect
  33. Adrenogenital syndrome 
    [treatment]
    glucocorticoids
  34. Hypercortisolism 
    [etiology/pathogenesis]
    • primary adrenocortical hyperfunction (due to adrenal adenoma) 
    • secondary: cause by hyperfunction of anterior pituitary ACTH secreting cells 
    • Tertiary: by injury
  35. Cushing syndrome
    • type of hypercortisolism 
    • -used to describe the clinical features of hypercortisolism, regardless of cause
  36. Cushing disease
    diagnosis reserved for pituitary dependent conditions of hypercortisolism
  37. Hypercortisolism 
    [etiologies]
    • excessive production of pituitary ACTH
    • exogenous steroid - common cause of Cushing syndrome
  38. Hypercortisolism
    [clinical manifestations]
    • round face w/ flushed cheeks, 'moon facies'
    • wt gain w/ excess total body fat (esp in abdomen)
    • decreased muscle mass, muscle weakness
    • glucose intolerance, hyperglycemia
    • hypertension 
    • osteoporosis
    • ^ androgen production = excessive hair prod., acne, menstrual irreg.
  39. Hypercortsolism
    [diagnosis]
    • ACTH measurement: 
    • --primary = low ACTH 
    • --seconardy = high ACTH 
    • urinary free cortisol levels 
    • dexamethasone suppression test
  40. Hypercortisolism 
    [treatment]
    treat based on etiology
  41. Hyperaldosteronism 
    [primary  & secondary]
    primary - Conn syndrome; usually due to aldosterone-secreting tumors 

    Secondary - associated with poor kidney perfusion that stimulates the RAAS cascade (heart failure, reduced kidney perfusion, liver cirrhosis)
  42. Hyperaldosteronism
    • salt and water retention 
    • low K+ level
  43. Hyperaldosteronism 
    [treatment]
    • spironolactone to increase sodium excretion and potassium retention 
    • sodium restriction and K+ replacement may be
  44. Pheochromocytoma 
    [etiology]
    • part of the adrenal medulla 
    • secretes catecholamines, norepinephrine and epinephrine 
    • a tumor of chromaffin tissue - excessive production and release of catecholamines
  45. pheochromocytoma 
    [clinical manifestations]
    • hypertension 
    • headache, tachycardia, diaphoresis
    • tremor nervousness, 
    • hypermetabolic state with fever, wt loss, polyuria, and polydipsia
  46. Pheochromocytoma 
    [treatment]
    • sympathetic blocking meds to manage bp 
    • surgical removal of tumor 
    • meds to block catecholamine prod
  47. regulation and actions of parathyroid hormone
    • detect [Ca+] and help maintain constant levels thru regulation of Ca+ absorption and resorption from bone
    • absorption of Ca+ from intestine and renal tubules is vitamin D dependent and may be impaired in conditions in which vitamin D is deficient (renal failure)

    • serum Ca+ levels provide the feedback to regulate PTH
    • decrease in Ca+ causes PTH release 
    • elevated Ca+ levels lead to suppression of PTH secretion

    PTH increases osteoclastic activity, and increases renal Ca+ reabsorption
  48. Calcitonin
    • produced by thyroid parafollicular cells of parathyroid hormone 
    • controls calcium content of blood by increasing bone formation by osteoblasts and inhibit bone breakdown by osteoclasts 
    • decrease blood Ca+ levels and promotes conservation of hard bone matrix
  49. Hyperparathyroidism
    [etiology]
    • despite ^ Ca+ level, PTH cont. to be secreted 
    • -genetic origin
    • -parathyroid adenoma
    • -hyperplasmia of parathyroid glands
  50. Chronic renal failure
    can result from reduced production of active Vita D (impairs Ca absorption)
  51. Hyperparathyroidism 
    [clinical manifestations]
    • kidney stones 
    • osteoporosis
    • polyuria and dehydration 
    • anorexia, nausea, vomit, constipaton 
    • bradycardia, heart block ,and cardiac arrest
  52. Primary hypothyroidism
    serum Ca+ levels are elevated wtih low to normal phosphorus levels
  53. Hyperparathyroidism 
    [treatment]
    surgically remove parathyroid gland
  54. Lab works of hypoparathyroidism
    • serum Ca+: low 5-7 mg/dl 
    • Phosphorus Lvl: high 7-12 mg/dl 
    • levels of antibodies to parathyroid glands are high if autoimmune mechanism is present
  55. Hypoparathyroidism 
    [treatment]
    oral calcium supplement with Vita D
  56. ADH
    • are vasopressin secreted by posterior pituitary gland - response to blood osmolality 
    • acts directly on renal collecting ducts and distal tubules, ^ membrane permeability to and reabsorption of H2O
  57. Diabetes insipidus 
    [etiology]
    disorder of insufficient ADH activity = excessive loss of water in urine
  58. Syndrome of inappropriate Antidiuretic hormone (SIADH) 
    [etiology]
    • excessive ADH due to tumors, tb
    • results in hyponatremia
  59. SIADH
    [clinical manifestations]
    • hyponatremia
    • high urine osmolality
    • low serum osmolality
    • weakness, muscle cramps,
  60. SIADH
    [treatment]
    • free water restriction 
    • if severe, IV adm of saline with diuretics 
    • hyponatremia corrected slowly to avoid rapid changes in brain cell volume

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