parathyroid Flashcards
primary targets for PTH
bones, kidney and GI
how does PTH impact bone
mobilizes calcium from bone - increases bon resorption (calcium from bone to blood)
how does parathyroid detect lowering calcium
calcium sensing receptors (CSRs)
impact of PTH on kidney (3 general)
- increases reabsorption of renal tubular calcium
- increases phosphate excretion
- enhance 1-hydroxylation of 25 hydroxy vitamin D
name the active metabolite of vitamin D
1,25-dihydroxyvitamin D (calcitriol)
action of 1,25-dihydroxyvitamin D (calcitriol)
active absorption of calcium in small intestine
describe general vitamin D
- steroid hormone from cholesterol
- two forms D3 and D2
vitamin D3
- cholecalciferol
- dietary source
- more potent than D2
vitamin D2
- ergocalciferol
- rare
name the natural ligand of vitamin D receptor
1,25(OH)2D
list the vitamin D conversion steps that take place in the skin
7-dehydrocholesterol –(UVB radiation)–> vitamin D3
describe the steps of vitamin D conversion that take place in the liver
vitamin D3–(25-hydroxylase)–>25(OH)vitamin D
list the vitamin D conversion steps that take place in the kidney
25(OH)Vitamin D –(1-hydroxylase)-> 1,25(OH)2 vitamin D active metabolite
in what organ order does the vitamin D activation pathway follow
skin - vitamin D3
liver - 25(OH)vitamin D
kidney - 1,25(OH)vitamin D
vitamin D impact on phosphate
increases absorption (higher passive)
body response to high blood calcium
- decrease bone resorption
- increase urinary loss
- decrease active vitamin D production = decrease GI absorption
renal failure patients calcium impact
- disturbed calcium and phosphate metabolism
- can’t convert 25 to 1,25
- failure to excrete phosphate in urine = hyperphosphatemia
What does hyperphosphatemia cause
- PTH and fibroblast growth factor 23 (FGF23)
- FGF23 causes low active Vit D levels
- hypocalcemia
PTH levels in chronic renal failure
elevated
describe bone turnover
coupled process of bone formation and breakdown for balanced formation
define resorption
bone breakdown to release calcium
bone formation markers
- ALP
- osteocalcin
- procollagen N terminal
bone resorption markers
- hydroxyproline
- N-teopeptide/C-telopeptide
- pryridinium crosslink
- TRAP
describe cortical bone and trabecular bone
- cortical -shaft
- trabecular bone - honeycomb top
describe primary hyperparathyroidism (PHPT)
- hypercalcemia most common cause
- key feature: autonomous overproduction of PTH from single gland
diagnosis criteria for PHPT
elevated serum calcium and elevated PTH relateive to serum calcium
biochemical findings in PHPT
- hypercalcemia
- hypophosphatemia
- low-normal 25 and high-normal 1,25
- elevated urinary calcium
- metabolic hypercholeremia acidosis
- elevated ALP
common PTH assessments
- sandwich ELISA
- electrochemiluminescent
PHPT important points
- gradual progression
- kidney stones (20-30%)
- bone loss (cortical>trabecular)
- surgery = treatment
- single gland tumor is common
secondary hyperparathyroidism
- elevated PTH in response to hypocalcemia
- transient PTH elevation
biochemical findings in secondary hyperparathyroidism
- low: blood Ca and P
- increased: ALP
- Vit D deficiancy or lack of Vit D effect
name the difference between secondary and tertiary hyperparathyroidism
sustained hypercalcemia
Tertiary: sustained hyper
Secondary: transient
familial hypocalciruis hypercalcemia
germline mutation causing benign hypercalcemia
- multiple family members impacted
- no end organ damage
- mild elevation of magnesium
parathyroid hormone related protein (PTHrP)
- structurally similar to PTH
- leads to hypercalcemia since it acts as PTH
difference between PTH and PTHrP
PTHrP can’t facilitate renal hydroxylation of 25-hydroxyvitamin D to active vitamin D
rickets
osteomalacia in children
- abnormal mineralization of bone
- diagnosed by PTH measurement
- genetic defect in Vit D metabolism (usually)
osteomalacia
abnormal mineralization of bone
vitamin D deficiency
osteoporosis
product of bone malformation or excessive resorption
