Endocrine Lecture 2 Pituitary

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Endocrine Lecture 2 Pituitary
2013-09-17 20:11:43
BC CRNA PV3 Endocrine

Endocrine Lecture 2 Pituitary (9/16/13)
Show Answers:

  1. Where is the pituitary located?
    Sella turcia: Bony cavity in the base of the brain
  2. Physiologically the pituitary gland has two parts, what are they?
    • anterior pituitary = adenohypophysis
    • posterior pituitary = neurohypophysis.
  3. Pituitary is __cm in diameter and weighs about __-__g.
    1cm; 0.5-1g
  4. How is the pituitary is connected to the hypothalamus?
    hypophysial (or pituitary) stalk
  5. What is the Pars intermedia?
    • Relatively avascular area between the anterior and posterior pituitary.
    • Almost absent in humans
  6. The way the hypothalamus controls this is through the interaction w/the pituitary gland. There’s two ways it does this depending on whether we’re talking anterior or posterior pituitary. Describe these two ways.
    Posterior: hormones that get released and then get transported directly to posterior pituitary by that hypophyseal stalk or tract. Anterior: release of hormones that will mediate the anterior pituitary hormones release (into blood) the tropic hormones
  7. What are the peptide hormones of the anterior pituitary? (There are SIX)
    • ACTH
    • TSH
    • GH
    • LH
    • FSH
    • Prolactin
  8. What is another name for Growth Hormone?
    Somatotropin (somatotropic hormone)
  9. Growth Hormone is a small protein (___ amino acids) with a molecular weight of ______
    191; with a molecular weight of 22,005
  10. Growth hormone causes growth of ALL tissues, how?
    • ↑ cell size
    • ↑ rate of mitosis
  11. What are the metabolic effects of Growth Hormone?
    • ↑ rate of protein synthesis in most cells (enhances body protein)
    • ↑ mobilization of fatty acids (↑ utilization of fat stores)
    • ↓ rate of glucose utilization (Conserves carbohydrates)
  12. Growth Hormone exerts it's metabolic effects on protein synthesis/deposition in tissues though the following mechanisms...
    • Enhanced amino acid transport thru cell membrane (↑ Intracellular amino acid concentration (in the cells)
    • Enhanced RNA translation → ↑ protein synthesis
    • ↑ Transcription of nuclear DNA causing ↑ RNA formation → ↑ protein synthesis → growth
    • ↓ Catabolism of protein & amino acids (Fatty acids are mobilized & used for energy so “protein-sparing”)
  13. Growth Hormone exerts it's metabolic effects on fat utilization for energy by these mechanisms...
    • GH causes release of fatty acids from adipose
    • GH enhances conversion of fatty acids → acetyl- CoA → used for energy
    • “Ketogenic” effect (Acetoacetic acid formed by the liver → ketosis & Fatty liver may result)
  14. How do we get an increase in lean body mass with the Growth Hormone?
    • By the use of fat and the synthesis of protein we get an increase in lean body mass.
    • Mobilization of fat takes longer (several hours) than the enhancement of protein synthesis which can occur in minutes
  15. Growth hormone exerts it's metabolic effects  on CHO by....
    • CHO utilization decreases → GH-induced insulin resistance
    • ↓ glucose uptake in skeletal muscle & fat
    • ↑ glucose production by the liver
    • ↑ insulin secretion
  16. Growth Hormone only causes growth if what two things are present?
    • There is adequate insulin
    • There is adequate CHO in the diet
    • ** partly due to the need for energy for metabolism of growth (and insulin enhances transport of AA into cells)
  17. True or False. GH essentially opposes the effect of insulin and will increase the BS level. Therefore GH is referred to as being diabetogenic (produces essentially a type 2 diabetes)
    • TRUE
    • GH induced “insulin resistance” which attenuates insulin’s action to stimulate the uptake & utilization of glucose in skeletal muscle and adipose tissue and to inhibit gluconeogenesis by the liver.
    • This leads to increased blood glucose concentration and a compensatory increase in insulin secretion.
  18. GH effects cartilage and bone by ___Deposits of protein by chondrocytic & osteogenic cells → bone growth & ___ Rate of reproduction of these cells. There is deposition of new bone 2° conversion of chrondrocytes to osteogenic cells.
    Deposits of protein by chondrocytic & osteogenic cells → bone growth & Rate of reproduction of these cells
  19. GH secretion decreases after adolescence, in very old age, secretion of GH is about __% of what it was
  20. What is the pulsatile secretion of GH related to?
    Nutritional statusLevel of stress
  21. GH secretion is stimulated by what SEVEN things?
    • Starvation, esp. protein deficiency
    • Hypoglycemia
    • ↓ fatty acid concentration
    • Exercise
    • Excitement
    • Trauma
    • First two hours of deep sleep
  22. GH secretion is inhibited by what seven things?
    • Hyperglycemia
    • ↑ fatty acid levels
    • Aging
    • Obesity
    • Somatostatin (GH inhibitory hormone)
    • Exogenous GH
    • Insulin-like growth factors
  23. TRUE or FALSE. Under acute conditions low  protein is more potent stimulator of GH than low BS
    • FALSE!!
    • Under acute conditions low BS is more potent stimulator of GH than low protein
    • But if we’re talking chronic conditions the situation is reversed
  24. Under severe conditions of protein malnutrition, are adequate calories alone enough to correct the excess production of GH?
    • NO!! Under severe conditions of protein malnutrition, adequate calories alone are not enough to correct an excess production of growth hormone.
    • The protein deficiency must also be corrected before the GH level will return to normal.
  25. In relation to the hypothalamus, regulation of GH secretion is by what two things?
    • GHRH (Secreted by ventromedial nucleus of hypothalamus, Major effect to increase secretion of GH)
    • GHIH (somatostatin)
  26. Other hormones secreted by hypothalamus also increase rate of GH secretion include what three things?
    • Catecholamines
    • Dopamine
    • Serotonin
  27. Even though GHRH and GHIH are both released to hypothalamus, most of the control is d/t the ....
    releasing hormone and not to the inhibitory hormone
  28. Is GH secretion regulated by positive or negative feedback
    negative feedback
  29. What is the syndrome of GH deficiency?
    • Panhypopituitarism
    • ↓ secretion of all anterior pituitary hormones (not just GH)
    • Congenital (dwarfism) vs Acquired (usually 2° pituitary tumors that destroy the gland)
    • Endocrine features vary depending on patient age but all anterior pituitary hormones are affected
  30. What kinds of things could cause panhypopituitarism and the deficiency of GH?
    • Craniopharyngioma or Chromophobe tumor. Both of these as they get enlarged will cause the anterior pituitary cells to be destroyed so the GH can’t be produced.
    • Thrombosis of pituitary blood vessels, destroy pituitary gland and prevent GH from being manufactured and released
    • Radiation therapy or surgical hypophysectomy
  31. TRUE or FALSE Anterior pituitary, is only gland where there can be destruction by compressing against a body cavity, in this case the sella turcia.
  32. For Panhypopituitarism, endocrine features vary depending on patient age but all anterior pituitary hormones are affected. What else might we see because of this?
    • Expect patient to also exhibit hypothyroidism, depressed glucocorticoid/cortisol production, and depressed gonadotropin production.
    • Because of that the early manifestations could be impotence (Male) and amenorrhea (female).
  33. If there is excess GH, why does it matter if it's before or after epiphyses fuse?
    • Gigantism: if excess GH secretion before epiphyses fuse
    • Acromegaly: if excess GH secretion after epiphyses fuse
  34. If you have excess GH (giantism), what can happen to your blood sugar
    Hyperglycemia → beta cell hyperactivity → beta cell degeneration → DM in 10% of patients
  35. How can excess GH (giantism) cause Panhypopituitarism
    • Panhypopituitarism if untreated 2° pituitary tumor
    • Treatment: radiation or surgery
  36. Describe the clinical manifestations of Acromegaly
    • Enlargement is seen in hands/feet/vertebrae ( could potentially cause kyphosis), frequently the cranium and the lower jaw.
    • *overgrowth of soft tissues in the upper airway, like the tongue and the epiglottis*
    • Can actually be vocal cord abnormalities because of the enlargement of tissues of larynx, the cartilage and the structures the patient may be hoarse.
    • And other soft tissues (kidney and liver) can become enlarged as well.
  37. What are the signs and symptoms of excessive GH?
    • Overgrowth of tissue
    • Peripheral neuropathy
    • Glucose intolerance
    • Increased incidence of HTN, ischemic heart disease, osteoarthritis & osteoporosis, lung volumes are increased and can be V/Q mismatching
  38. Anesthetic implications of acromegaly?
    • Difficult airway!!!!(Mask & ETT)
    • Presence of hoarseness or stridor suggests laryngeal involvement (thickened vocal cords or paralysis of the recurrent laryngeal nerve because of stretching) 
    • Plan for FOI, smaller ETT (Large on outside but the glottis may be small d/t overgrowth of tissue)
    • Skeletal muscle weakness may be present (Monitor neuromuscular blockade)
    • Monitor blood glucose
  39. According to Barash, there is a a __-__% incidence of difficult intubation
  40. Vasopressin is secreted from where exactly (in the hypothalamus)?
    Secreted in supraoptic (5/6) & paraventricular (1/5) nuclei of hypothalamus then transported to the POSTERIOR pituitary
  41. Vasopressin (ADH) is secreted in response to what?
    • Secreted in response to osmotic stimulus (osmoreceptors in hypothalamus)
    • ↑ plasma osmolarity & ↓ blood volume
  42. So what happens when ADH is secreted?
    • results in insertion of aquaporins in cell membrane & ↑ permeability of collecting ducts & tubules to water
    • increased permeability of water so more water absorbed back into the circulation.
    • And actually in absence of vasopressin, the collecting ducts in kidneys are almost impermeable to water, so if don’t have vasopressin we’ll just excrete a large dilute urine.
  43. What is the mechanism for release of ADH (in response to increased osmolarity)?
    • Loss of intracellular water from osmoreceptors in the hypothalamus during dehydration → shrinkage of cells & release of ADH
    • Occurs before the sensation of thirst
    • Very sensitive mechanism so that a change of 1% in plasma osmolarity produces altered secretion
  44. Besides increased osmolarity, what are the other mechanisms for release of ADH?
    • Stretch receptors in LAand possibly also the pulmonary veins (sensitive to a ↓ blood volume)
    • Barash: The need to fix blood volume can override the osmotic inhibition of ADH release.
    • Also,  positive pressure ventilation, beta adrenergic stimulation and histamine release. (as well as stress, anxiety, and hyperthermia)
  45. __% of body weight is water in males, __% in females
    60; 50
  46. Describe the fluid compartments (%)
    • ICF (40% body weight)
    • ECF (20% of body weight)
    • --Intravascular (5 % of body weight)
    • --Interstitial (15% of body weight)
  47. Defeine: Molarity, Osmolarity, & Osmolality
    • Molarity: concentration measured by the number of moles of solute per liter of solution
    • Osmolarity:the # of osmotically active particles/L of solvent
    • Osmolality: the # of osmotically active particles/kg
  48. What is the normal serum osmolality?
    Normal serum osmolality is ~285mOsm/L.
  49. What is the equation for serum osmolality?
    Osmolality= (Na x2) + (glucose/18) + (BUN/2.3)
  50. What are the two types of diabetes insipidus?
    • Central (neurogenic): not enough ADH
    • Nephrogenic: kidneys don't respond to ADH
  51. What are the causes of central DI?
    • Destruction of posterior pituitary
    • After head trauma or neurosurgery (transient in those cases)
  52. What causes nephrogenic DI?
    • Congenital
    • Acquired : Chronic renal disease, Hypokalemia & hypocalcemia, & Sickle cell disease
  53. What is the treatment of DI?
    • Central : ADH as DDAVP
    • Nephrogenic: fluid replacement & Rx underlying cause
  54. What are the symptoms of DI?
    Polyuria & polydipsia in absence of hyperglycemia
  55. What are the causes of SIADH?
    • Intracranial tumors
    • Hypothyroidism
    • Porphyria
    • Carcinoma of the lung (esp. undifferentiated small cell)
    • After major surgery
  56. Drugs that can  cause increase in ADH release...
    morphine, barbiturates, and beta agonists
  57. What are the s/s of SIADH?
    • Dilutional hyponatremia
    • ↑ urine Na & urine osmolarity
    • Weight gain from water reabsorption
    • Skeletal muscle weakness
    • Mental status changes (confusion, convulsions)
    • Prognosis is dependent on ID and treating the underlying cause.
  58. What is the treatment for SIADH?
    • Fluid restriction (500 ml/day)
    • IV NaCl (hypertonic if neuro sx but not too fast!)
    • Demeclocycline
  59. If you have neuro symptoms from SIADH and want to give hypertonic NaCl, how fast can you give it?
    • 12mEq/L/24hrs.
    • If the correction is too fast a disorder called central pontine myelinolysis can occur (fatal neurologic disorder).
  60. Describe the vasoconstriction of vasopressin
    • ↑ BP d/t constriction of arterioles at high levels of ADH
    • ↓ blood volume (15-25%) → ↑ ADH secretion up to 50 X normal
    • Stimulation of atria stretch receptors d/t overfilling ↓ Inhibition of ADH
    • ** reverse occurs with hypovolemia →↑ ADH & ↑ bl vol