Endocrine Lecture 2 Adrenal

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cmatthews
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Endocrine Lecture 2 Adrenal
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2013-09-18 17:15:02
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BC CRNA Endocrine Adrenal
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Endocrine Lecture 2 (9/16/13)
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  1. What is the functional anatomy of the adrenal glands?
    • 2 adrenal glands
    • 4 grams each
    • Located at superior pole of kidney
  2. What are the 3 parts of the adrenal cortex?
    • Zona glomerulosa
    • Zona fasciulata
    • Zona reticularis
  3. Name the two parts of the adrenal glands and the respective percentages
    • Adrenal medulla (inner 20%)
    • Adrenal cortex (outer 80%)
  4. TRUE or FALSE. Adrenal medulla is functionally a SNS ganglion.
    FALSE
  5. Describe the Zona glomerulosa
    • Outermost 15% of the cortex
    • Secretes aldosterone
  6. Describe the Zona fasciulata
    • Middle & largest layer (75% of cortex)
    • Secretes glucocorticoids cortisol & corticosterone & small amount of androgens & estrogens
    • ACTH stimulates secretion
  7. Describe the Zona reticularis
    • Deepest layer
    • Secretes androgens (DHEA), small amounts of estrogens & glucocorticoids via ACTH
  8. What does the zones of the adrenal cortex have to do with the way aldosterone and cortisol are regulated?
    Because of the way the adrenal cortex is zoned, aldosterone and cortisol secretion are independently regulated so that Angiotensin II will only stimulate the zone of glomerulosa. ACTH has no effect on that zone (does effect Zona fasciulata and Zona reticularis)
  9. What are the mineralcorticoids of the adrenal cortex? (there are six)
    • Aldosterone (90%)
    • Desoxycoticosterone
    • Corticosterone9
    • α Fluorocortisol (synthetic)
    • Cortisol
    • Cortisone (synthetic)
  10. What are steroid hormones derived from?
    • Cholesterol.
    • 80% of cholesterol comes form the low density lipoprotein in the plasma.
    • Aldosterone is major one.
  11. What does Aldosterone (a mineralcorticoid) do?
    • It will increase Na reabsorption and K+ secretion by the renal tubules.
    • Holds onto Na and passively also holds onto water.
    • The mineralo- refers to effect on Na and K.
  12. What happens when there is excess aldosterone?
    • ↑ ECF volume → ↑ BP → pressure natriuresis & pressure diuresis → ↑ renal excretion of sodium & water = aldosterone escape
    • ↓Potassium
    • ↑hydrogen ion secretion by renal tubules → mild alkalosis
  13. How much does BP have to increase before we get pressure naturiesis and diuresis?
    • 15-25mmHg
    • So when aldosterone increases ECF and BP, we get excretion of the Na and water it was holding onto
  14. How low can K+ go with excessive aldosterone secretion?
    • hypokalemia down to a level of 2mEq/L can occur
    • (Cardiac irritability, muscle weakness, etc).
  15. What are the two most important stimuli for the synthesis and release of aldosterone?
    • ↑ ECF potassium → ↑ aldosterone
    • ↑ renin-angiotensin activity → ↑ aldosterone
  16. Besides the two important stimuli, what else can regulate the synthesis and release of aldosterone?
    • ↑ ECF sodium → sl ↓ aldosterone
    • ACTH is necessary for aldosterone secretion but doesn’t control rate of secretion
  17. Describe the HPA axis and the effects on the  adrenal cortex
    • Refers to the fact that corticotropic releasing factor (produced and released by hypothalamus) will stimulate release of ACTH from the anterior pituitary.
    • Then ACTH from anterior pituitary will stimulate synthesis of glucocorticoids by the adrenal cortex.
    • The glucocorticoids from adrenal cortex will provide negative feedback for both ACTH and the corticotropic releasing factor.
  18. How will glucocorticoids will affect metabolism?
    stimulate proteolysis and gluconeogenesis, and they’ll increase fatty acid mobilization
  19. List all the glucocorticoids from the adrenal cortex? (there are six)
    • Cortisol (95%) 20 mg secreted daily
    • Corticosterone (4%)
    • Prednisone (synthetic, 4 X as potent as cortisol)
    • Cortisone (synthetic, almost as potent as cortisol)
    • Methylprednisone (synthetic, 5 X as potent as cortisol)
    • Dexamethasone (synthetic, 30 times as potent as cortisol)
  20. Describe the rhythmic release of cortisol
    • Release of cortisol is pulsatile and under direct stimulation of ACTH.
    • It follows the circadian rhythm, sensitive to light, sleep, stress, and disease.
    • We secrete the most cortisol in early waking hours and the levels decline as the day progresses
  21. There are four synthetic types of glucocorticoids, list them in order of least to most potency when compared to cortisol
    • Cortisone (synthetic, almost as potent as cortisol)
    • Prednisone (synthetic, 4 X as potent as cortisol)
    • Methylprednisone (synthetic, 5 X as potent as cortisol)
    • Dexamethasone (synthetic, 30 times as potent as cortisol)
  22. What causes the slow elimination of cortisol from the plasma?
    • Most of cortisol is bound to plasma protein.
    • So that slows the elimination from the plasma
  23. What is the effect of cortisol on CHO metabolism?
    • Stimulation of gluconeogenesis
    • ↓ utilization of glucose by cells
    • Hyperglycemia & ↑ insulin levels
    • Cause insulin resistance, develops diabetes
  24. What is the effect of cortisol on protein metabolism?
    • Reduction in cellular protein → muscle weakness (Decreased synthesis & Increased breakdown)
    • Increased liver & plasma proteins
    • Increased amino acids & transport to hepatic cells
  25. What is the effect of cortisol on the fat metabolism?
    • Mobilization of fatty acids
    • Obesity
    • Centripedal obesity, moon face, etc
  26. Describe Cortisol and the stress response
    • Stress causes ↑ ACTH by the anterior pituitary
    • ACTH → ↑ cortisol by adrenal cortex
    • Proteins are mobilized & broken down to make amino acids available to synthesize substances needed to sustain life
    • Anti-inflammatory effects
  27. Describe the two mechanisms of the anti-inflammatory response and cortisol
    • Blocks early stages of inflammatory response
    • Causes rapid resolution of inflammation
  28. How does cortisol block the early stages of inflammatory response?
    • Stabilizes lysosomal membranes
    • Decreases capillary permeability
    • Decreases WBC migration & phagocytosis
    • Suppresses immune system
    • Attenuates fever 2° ↓ interleukin-1 from WBCs
  29. Primary aldosteronism (aka Conn’s syndrome, hyperaldostoerone syndrome) causes mineralcorticoid excess. What are the causes of this?
    • Unilateral adenoma
    • Bilateral hyperplasia
    • Carcinoma of adrenal gland
  30. What is the cause of secondary aldosteronism?
    • Stimulation of aldosterone secretion by affecting renin-angiotensin system
    • stimulus of RAAS could be congestive heart failure or decreased blood volume, cirrhosis, renal artery hypertension where there is increased renin activity.
  31. What are the s/s of mineralcorticoid excess?
    • HTN
    • Hypervolemia
    • Hypokalemia
    • Muscle weakness(common w/endocrine)
    • Metabolic alkalosis
    • Polyuria (common w/endocrine)
    • Decreased ionized calcium → tetany
    • Patients are commonly obese.
    • Hyperglycemia occurs in about 50% of patients
  32. What are the anesthesia implications for mineralcorticoid excess?
    • Correct fluid & electrolyte disturbances (hypernatremia, hypokalemia, as well as elevated blood sugar)
    • Patient may also have a decrease in gastric pH, H2 blocker may be beneficial pre-op.
    • A-line may be helpful, possibly a CVP.
    • Hypokalemia so may have a potentiation of the neuromuscular blockade.
    • D/t elec. disturbances they could have a prolonged emergence from anesthesia.
    • Already have metabolic alkalosis, avoid hyperventilating them.
  33. What could cause mineralcorticoid deficiency?
    • Atrophy or destruction of adrenals
    • Unilateral adrenalectomy
    • Diabetes mellitus
    • Heparin therapy
  34. What are the s/s of mineralcorticoid deficiency?
    • Hyperkalemia
    • Acidosis
    • hypotension
  35. What are the anesthesia implications of mineralcorticoid deficiency?
    give exogenous hormone (fludrocortisone)
  36. Hyperadrenalism is mostly due to excess...
    • glucocorticoid (Cortisol)
    • CUSHING'S SYNDROME
  37. Cushing's syndrome can have dependent or independent causes. What are the dependent causes?
    • Means it’s dependent on excess ACTH or potentially corticotropic releasing hormones 
    • Abnormality of hypothalamus (excess CRH)
    • Pituitary tumor (excess ACTH) = Cushing’s disease
    • Ectopic tumors (excess ACTH
  38. Cushing's syndrome can have corticotropin dependent or independent causes. What are the independent causes?
    • independent of ACTH levels. This is d/t some abnormality of adrenal cortical tissue itself.
    • Adenomas of adrenal cortex
    • Exogenous glucocorticoid administration
  39. TRUE or FALSE. Pituitary tumor w/excess ACTH Cushing’s disease is the least common form of Cushing’s syndrome
    FALSE. It is the MOST COMMON FORM
  40. What are the anesthetic implications of hyperadrenalism (glucocorticoid excess)?
    Consider physiologic changes with ↑ cortisol
  41. Glucocorticoid deficiency can be d/t primary or secondary adrenal insuficiency. If it is a primary adrenal insufficiency, it is Addison's. Describe this.
    • Rare
    • Deficiency of glucocorticoids, mineralocorticoids, & androgens
    • From destruction of adrenal (autoimmune)
    • May be an autoimmune situation (80% of cases is autoimmune)
    • Could also be cancer destroying the tissue.
  42. What is considered a primary adrenal insufficiency? (cortisol level less than...)
    Baseline cortisol level of less than 20mcg/dL.
  43. In adrenal insufficiency,  ___% of the adrenals has to be involved for it to cause adrenal insufficiency.
    90%
  44. What are the s/s of primary adrenal insufficiency (Addison's)?
    • N/V, anorexia, weakness, fatigue, skin hyperpigmentation, hypovolemia, hyponatremia, hypotension, and hyperkalemia.
    • Here there is often a deficiency of cortisol and aldosterone
  45. Can a person die from primary adrenal insufficiency?
    YES, if there is total destruction of adrenal cortex pt will die due to circulatory collapse.
  46. What causes secondary adrenal insufficiency?
    • From ↓ secretion of CRH or ACTH
    • Effectively suppression of the HPA axis.
    • This may be d/t radiation, pituitary surgery, or most commonly, because of chronic steroid administration
  47. If a patient has been on steroids chronically, what should we think about?
    • Consider if they are at risk for suppression of HPA axis (Stress of surgery needs more cortisol)
    • If suppression pt may not be able to release excess cortisol so may need to give exogenous steroids.
  48. What are the anesthetic concerns for a patient w/Addison's?
    • Pt would be hyperkalemic, acidotic and saliva may be acidotic, may have dental decay and loose teeth so be careful w/airway assessment.
    • Need to correct volume and any electrolyte abnormalities ( likely to be increase K, decreased sodium, and decreased glucose) and monitor for arrhythmias because of electrolyte abnormalities.
  49. We produce __mg of cortisol daily. Under the stress of surgery, don’t produce any more than about ___mg/day
    20; 150
  50. How much the HPA axis is stimulated is dependent upon...
    • nature of the surgery & the magnitude the duration
    • ACTH will usually stay elevated, will increase w/incision and stay elevated, the peak occurring at the time of muscle relaxant reversal and extubation.
    • Constantly peaking throughout the surgery
  51. Regarding steroid administration in the OR, most agree to supplement for those who have been on steroids for ___ weeks in the last_____M.
    1-2 weeks in the last 6-12M.
  52. What does Stoelting recommend regarding steroid supplementation?
    • Superficial surgery; dental; biopsy (None)
    • Minor surgery; inguinal hernia (25 mg IV)
    • Moderate surgery; cholecystectomy (50-75 mg IV, taper 1-2 days)
    • Severe surgery; cardiovascular (100-150 mg IV, taper 1-2 days)
    • ICU; sepsis, shock (50-100 mg q 6-8 hr for 2 days – 1 week, taper)
  53. If there is HPA axis suppression, why do we give cortisol supplementation but not aldosterone?
    giving NaCl so don’t’ need to give aldosterone
  54. Why is Etomidate contraindicated in adrenal insufficiency?
    It inhibits the synthesis of cortisol transiently
  55. What three hormones are released by the adrenal medulla?
    • Epinephrine – 80% (Can increase metabolic rate of body by as much as 100% above normal & Longer duration of action)
    • Norepinephrine – 20%
    • Dopamine
  56. Epi increase the metabolic rate of body by how much ?
    as much as 100% above normal
  57. Also the effect of adrenal medulla stimulation is identical to SNS stimulation except ......
    it has a longer duration of action (5-10x longer).
  58. What is a pheochromocytoma?
    Catecholamine secreting tumor (epi, norepi)
  59. What % of pheochromocytomas are malignant?
    10-15% are malignant
  60. What % of pheochromocytomas are bilateral or extra adrenal?
    10-15% are bilateral or extra-adrenal
  61. What % of pheochromocytoma are in the adrenal medulla?
    90% are in adrenal medulla (More than 95% are intraabdominal---90% in the adrenal medulla)
  62. What is the age of presentation of a pheochromocytoma?
    Age at presentation 30-50
  63. What are the s/s of pheochromocytoma?
    • HTN, diaphoresis, headache, palpitations, weight loss (triad = diaphoresis, tachycardia, headache in the hypertensive patient)
    • If triad isn’t there, pheo is unlikely
    • Hypovolemia
  64. What is the triad in a pheochromocytoma?
    • triad = diaphoresis, tachycardia, headache in the hypertensive patient
    • If it's not there, pheochromocytoma is unlikely
  65. How do we diagnose a pheochromocytoma?
    • by a 24hr urine for free (unconjugated) epi and norepi as well as metabolites & vanilylmandelic acid.
    • Clonidine suppression test, clonidine will suppress catecholamine levels in essential HTN and not in pheochromocytoma
  66. What is a REALLY important thing about pheochromocytoma pre-op?
    One of the things that is REALLY important is the patient be alpha blocked pre-op
  67. Tell me about Phenoxybenzamine in regards to pheochromocytoma
    • Use phenoxybenzamine 10-20mg BID for 10-14 days pre-op.
    • Causes that irreversible alpha blockade.
  68. When do we beta block our patient w/a pheochromocytoma
    • Can only establish beta blockade after alpha blockade has been established
    • The need to block alpha receptors 1st is so we can essentially vasodilate and correct the volume situation 1st
    • If we beta block 1st, the betablock myocardium the may not be able to eject against the high SVR
  69. What do we want to avoid with a pheochromocytoma?
    • Avoid SNS stimulating drugs
    • Avoid volatiles that sensitize the myocardium to epi
  70. What can happen with the patient who had a pheochromocytoma during the post-op period?
    • patient can be hypotensive.
    • May develop CHF.
    • Can actually have psych changes because of the decreased catecholes.
  71. What should you have available for a pheochromocytoma?
    Have sodium nitroprusside (Nipride) and dopamine available but might be exaggerated responses to those drugs
  72. What is Multiple endocrine neoplasia?
    • Autosomal dominant multiglandular disorder
    • Patient were to present thyroid surgery for medullary thyroid cancer, want to think do they have underlying pheo.
    • Or if the patient has a parathyroid adenoma, think pheo.
    • Those kinds of things can be associated w/pheochromocytoma.
    • Bear in mind if pt is coming in for some sort of endo disorder do they also have something more dangerous (undiagnosed pheo)

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