020215 parathyroid gland Flashcards
effects of PTH
kidney: increases calcium reabsorption, decreases phosphate reabsorption, converts 25-hydroxyvit D to 1,25-dihydroxyvit D
intestine: increases calcium and phosphate absorption through 1,25D
bone: increases calcium and phosphate resorption
calcium sensing receptor on parathyroid cell can have what kinds of mutations
loss of fxn familial hypocalcinuric hypercalcemia (FHH)
gain of fxn autosomal dominant hypocalcemia (ADH)
calcimimetic (cinacalcet)
can be used to tx severe hyperparathyroidism
symptoms of hypercalcemia
most ambulatory pts-no clear symptoms
fatigue, weakness nausea, vomiting, constipation anorexia polyuria, polydipsia dehydration memory impairment drowsiness, confusion, coma
vicious cycle of hypercalcemia
hypercalcemia leads to renal salt and water loss, which leads to ECF volume contraction, which leads to decreased Ca excretion, which aggravates hypercalcemia (can’t excrete Ca)
hypercalcemia is caused by
increase in PTH secretion (primary hyperparathyroidism-usually a parathyroid adenoma)
causes of hypercalcemia- PTH dependent
primary hyperparathyroidism:
- -sporadic (single and multiple gland disease, carcinoma)
- -multiple endocrine neoplasias
- -hyperparathyroidism jaw tumor syndrome
physiological findings for primary hyperparathyrdoidism
decreased sensitivity of PTH-secreting cells to inhibition by plasma Ca
increased or inappropriately not suppressed serum PTH
hypercalcemia
hypophosphatemia
some pts: hypercalciuric
genetics of familial hypocalciuric hypercalcemia (FHH)
FHH1-most families-Ca sensing receptor mutation that causes parathyroid cell to not sense Ca and the kidney tubule cell to not sense Ca so that more Ca is reabsorbed
tx of FHH and primary hyperparathyroidism
FHH-don’t do surgery
primary hyperparathyroidism-surgery
bone fibrosis
severe primary hyperparahthyrodism
most common cause of PTH-independent hypercalcemia
malignancy (bone metastases, PTH-related protein, osteoclast activating factors, unregulated calcitriol production, true ectopic PTH)
calcitriol-mediated (granulomatous, inflammatory). calcitriol is 1,25(OH)2D
hyperthyroidism (increases bone resorption)
milk-alkali syndrome or calcium alkali syndrome (pt consumes huge amts of Ca carbonate)
immobilization (bone resorption)
PTHrP
parathyroid hormone related peptide
can be secreted by tumor cells (breast, lung, kidney, squamous)
how does calcitriol-mediated hypercalcemia come about?
non-renal or unregulated expression of 1-hydroxylase by:
sarcoid
lymphoma
hypercalcemia can be divided into what two causes
PTH dependent
PTH independent
if it’s PTH dependent hyperparathyroidism, what tests can you do to determine cause
24 hr urine calcium and creatinine to determine if it’s primary hyperparathyroidism or FHH
tx of hypercalcemia
normal saline IV fluid (pts are dehydrated often)
loop diuretics (furosemide)–augment Ca excretion
calcitonin
BISPHOSPHONATES (inhibit osteoclastic bone resorption)
signs and symptoms of hypocalcemia
neuromuscular irritability (paresthesias, muscle cramps, tetany) lowered seizure threshold mental status changes cardiac-prolonged QT, arrhytmias, CHF basal ganglia calcification cataracts positive Chvostek's, Trousseau's signs
basal ganglia calcification
hypoparathyroidism
Chvostek sign
tapping of facial nerve causes muscle spasm
positive in hypocalcemia
Trousseau sign
filling of blood pressure cuff causes muscle spasm
positive in hypocalcemia
causes of hypoparathyroidism
genetic disorders
autoimmune
infiltrative
pseudohypoparathyroidism (PTH resistance)–type 1a has GNAS mutation and Albrights hereditary osteodystrophy
signs of pseudohypoparathyroidism
short stature
short 4th and 5th fingers
round face
diagnosing hypercalcemia
see slide 22
