Endocrine Lecture 3 Parathyroid

  1. Where are the parathyroids located?
    • 2 imbedded in superior part of thyroid and two in the inferior part of the thyroid.
    • There is wide variation in the # and location of the PTH glands. Sometimes they’re in the mediastinum.
  2. Are the parathyroids vascular?
    VERY vascular
  3. How many cell types are there in the parathyroid? What are they?
    • TWO
    • Chief cells (majority of cells) those are the ones that make and secrete PTH hormone. The other cell types are called oxyphil cells. Not known what they do some think they’re just degenerated chief cells.
  4. Is the PTH a peptide or protein hormone?
    Polypeptide with 84 amino acids
  5. What are the two primary targets of the PTH?
    Bone and Kidneys
  6. What effect does PTH have on bone?
    • Bone reabsorption of calcium
    • Acts directly on bone to increase bone reabsorption & mobilize calcium
  7. What effect does PTH have on the kidneys?
    Kidney ↑’s reabsorption of calcium (distal tubules) & ↓ reabsorption of phosphate
  8. What effect does PTH have on the intestine?
    intestinal absorption (of Ca+) indirectly by vitamin D activation
  9. What does PTH do to electrolyte levels?
    Secretion causes ↑ plasma calcium levels & ↓ plasma phosphate levels along with ↑ excretion of phosphate in the urine
  10. What is the main physiologic effect of the PTH?
    to maintain calcium homeostasis by tight feedback system according to plasma calcium levels
  11. TRUE or FALSE. There is a Calcium sensing receptor on the parathyroid cells and for a given calcium level there is an optimal PTH level which may be altered by disease
  12. PTH release is stimulated by what three things?
    • Hypocalcemia
    • Hyperphosphatemia
    • Catecholamines
  13. PTH release is suppressed by what three things?
    • Hypercalcemia
    • Vitamin D
    • Severe hypomagnesemia
  14. Calcitonin is a _____ hormone with ____ amino acids and MW = ____
    • Peptide hormone
    • 32 AA
    • MW = 3400
  15. Where is calcitonin secreted from?
    Secreted by parafollicular cells (C cells) of thyroid (0.1% of thyroid gland)
  16. What does Calcitonin do?
    ↓’s plasma calcium
  17. Which has a more quantitative role in calcium homeostasis, PTH or calcitonin?
    Calcitonin has ess of a quantitative role in calcium homeostasis than PTH
  18. What % of plasma calcium is ionized? What is the normal value?
    • 50%
    • 1.2 mmol/L
  19. What % of plasma calcium is protein bound? What is the normal value?
    • 41%
    • 1 mmol/L
  20. What % of Calcium is complexed to anions? What is it's normal value?
    • 9%
    • 0.2 mmol/L
  21. How many grams of Ca+ do we have in our body? Where is most of it located?
    Our bodies have 1100g of Ca+ most are in the bones and the teeth. (99%)
  22. What is the physiologically active form of Ca+?
    • the ionized form
    • It doesn’t easily pass through the lipid membrane but it does go through Ca+ channels so it is diffusible.
  23. What is the total calcium value (plasma)?
    9-10 mg/dL
  24. What is the iCa reported in (units)
    • mEq/L
    • so if it's 1/2 of total calcium, and normal is 10mg/dL, then normal iCa is 5mg/dL
  25. What is the role of Vitamin D?
    • it will increase intestinal absorption of dietary Ca+ and renal reabsorption of any Ca+ that gets filtered at the glomerulus
    • (Vitamin D is activated in the kidney's by PTH)
  26. Will both Calcitonin and PTH will decrease plasma phosphate levels?
  27. What is the etiology of hypoparathyroidism?
    • Impaired production of PTH
    • May be associated with other endocrine disorders & neoplasias
    • Result from surgical removal of the parathyroids (usual cause)
    • Pseudohypoparathyroidism
  28. What is Pseudohypoparathyroidism?
    • Congenital disorder where kidneys can’t respond to PTH
    • Patients will have mental retardation, calcification of basal ganglia, obesity, & structural abnormalities
  29. What are the clinical manifestations of hypoparathyroidism?
    • Hypocalcemia
    • Chvostek’s sign (tap on facial nerve)
    • Trousseau’s sign (the BP cuff)
    • Paresthesias
    • Convulsions Irritability & psychosis
    • Muscle cramps
    • Decreased myocardial contractility, first degree AV block
    • Intestinal malabsorption
  30. What is very important to use regarding the clinical manifestations of hypoparathyroidism?
    spasms involve the larynx, laryngospasm can result
  31. What is the treatment for hypoparathyroidism?
    • High calcium diet with vitamin D
    • Thiazide diuretics to decrease renal clearance of calcium
    • Acute hypocalcemia treated with 10 ml of 10% calcium gluconate IV
  32. What lab values would you expect with hypoparathyroidism?
    decreased serum Ca and increased serum phosphate (usual phosphate level is 3-4mg/dL)
  33. What are the anesthesia implications for hypoparathyroidism?
    • Avoid hyperventilation as alkalosis will further ↓ calcium levels as it causes ↑ binding to protein & ↓ in free, ionized calcium
    • Careful with blood administration if preserved with ACD
    • Monitoring neuromuscular blockade
    • Avoid 5% albumin as will bind to calcium and lower levels of ionized
  34. What are blood transfusions problematic in hypoparathyroidism?
    • w/rapid transfusion 500ml of 5-10min.
    • Or couldn’t be metabolized because the pt has liver disease, hypothermia, or kidney disease. Antyhing that interferes w/metabolism of the citrate.
  35. Most common cause of hypercalcemia in the general population is...
    primary hyperparathyroidism
  36. What are the causes of primary hyperthyroidism?
    • Benign parathyroid adenoma (90%) *
    • Carcinoma (5%)
    • Hyperplasia *
    • * most common presenting symptom of multiple endocrine neoplasia (MENS) type I
  37. What is the cause of secondary hyperparathyroidism?
    Response of parathyroid to secrete excess PTH to counteract hypocalcemia caused by some other disease process (i.e. renal disease)
  38. Does hypercalcemia usually occur in secondary hyperparathyroidism?
    NO, Hypercalcemia usually doesn’t occur as hypersecretion (of PTH) is 2° hypocalcemia
  39. What is the treatment for hyperparathyroidism?
    Treatment is to control underlying disease
  40. What is the hallmark of hyperparathyroidism?
    • serum Ca+ (Total calcium) of greater than 5.5mEq/L
    • Or an ionized Ca+ of greater than 2.5mEq/L
  41. For primary hyperparathyroidism, how can you tell if it is likely to be caused by something benign or malignant?
    • Benign: serum Ca is less than 11mEq/L
    • Malignant: serum Ca greater than 14mEq/L
  42. Besides primary and secondary hyperparathyroidism, there can be Ectopic hyperparathyroidism  (pseudohyperparathyroidism). What is this?
    • Secretion of PTH by tissues other than the parathyroid
    • Occurs in CA of lung, breast, pancreas, or kidney and in lymphoproliferative diseases
  43. What are the s/s of (primary) hyperparathyroidism?
    • Sx related to the high ionized calcium 
    • ↓ neuromuscular excitability
    • Muscle weakness, decreased muscle tone
    • Fatigue
    • Mental confusion, depression, coma (with levels > 15 mg/dl
  44. What is the temporary treatment for hyperparathyroidism?
    • Hydration with IV saline
    • Loop diuretics to inhibit calcium reabsorption in Loop of Henle
  45. What is the definitive treatment for hyperparathyroidism?
    • Surgical
    • Following removal of abnormal or diseased gland, calcium levels normalize in 3-4 days
  46. What are the anesthesia implications for hyperparathyroidism?
    • Maintain adequate hydration & urine output
    • Care with sedation & avoid ketamine 2° mental status changes & somnolence
    • Consider possibility of co-existing renal disease with drug selection
    • Monitor TOF, EKG, BP
Card Set
Endocrine Lecture 3 Parathyroid
Parathyroid Endocrine Lecture 3