parathyroid Flashcards
Number of PTH glands
Normal: 4
5%: 3
4% 5
Primary targets for PTH (Parathyroid hormone)
Bone and Kidneys
PTH effect on bones
Mobilize Ca
PTH effect on kidneys
Increase absorption of Ca
Increase phosphate excretion
Enhance 1a-hydroxilation of 25 hydroxy vit D
Vitamin D
Steroid hormone
D3 and D2 forms
Synthesized from sunlight
1,25 (OH) VD natual ligand for receptor (functional form)
Vit D3
Rare in nature
More potent than D2
from liver and seafood
Vit D2
Less potent than D3
From edible mushrooms
Vit D pathway
7-Dehydrocholesterol + UVB -> Vit D3 -> (liver) Vit D3 +25 hydroxylase -> 25 (OH) Vit D -> (kidney) 25 (OH) Vit D +1a hydroxylase -> 1,25 (OH)2 Vit D
Vitamin D Effects
Active absorption of Ca
Absorption of phosphate (less dependent)
Stimulate osteoclast precursors
PTH effects on the GI tract
Required for normal function
absorption of Vit D and Ca
Disease states: short bowel syndrome, gastric bypass, intestinal mucosal disease, genetic defects, bowel fistula
Bone physiology
Osteoblasts build bone
Osteoclasts break bone down
Coupled response - ensures bone is built and broken at the same time
Bone turnover markers are monitored for therapies
Bone turn over markers
ALP
Osteocalcin
Procollagen N- terminal peptides
Bone resorption markers
Hydroxyproline
Telopeptide
pyridinium crosslinks
TRAP
Bone Types
Cordical Bone: Shafts. Predominant type. Strong and lightweight
Trabecular: Vertebrae. honeycomb, weightbearing
Hypercalcemia
Elevated blood Ca
Lethargy, stupod, coma, intellectual weariness, nausea, anorexia, etc
PHPT most common cause
Primary Hyperthyroidism (PHPT)
Autonomous overproduction of PTH
3x more likely in women
diagnosis made w/ elevated blood Ca and inappropriately or normal PTH
Biochem marker for PHPT
Hypercalcemia
Hypophosphatemia
elevated PTH relative to serum
Abnormal 1,25 OH vit D
Detected through sandwich ELISA and Electrochemiluminecense
Treated through parathyroidectomy - cure
PHPT important points
Insidious onset and gradual prog
20-30% have kidney stones
bone loss from Cortical > Trabecular
single glad tumor common at 85%
Secondary Hyperparathyroidism
Hypocalcemia
Rise in PTH in response to outside factors
Secondary Hyperparathyroidism effects
Low blood Ca and phosphate
elevated ALP
Hypocalciuria and phosphaturia
Vit D deficiency or disfunction
Chronic Kidney Disease (CKD)
Failure to adequately create functional Vit D or excrete phosphate
Secondary hyperparathyroidism
Familial Hypocalciuric Hypercalcemia (FHH)
Low urine Ca
No end organ damag
Multiple family members effected
elevated Mg
Surgery ineffective
Parathyroid Hormone related protein (PTHrP)
secreted by cancers
Similar to N terminal on PTH
Does not cause the PTH feedback loop (continued bone reabsorption when at suppression of PTH)
Causes of hypoparathyroidism
Thyroidectomy
Accidental removal of glads
damage to glads during surgery
Autoimmune destruction (addison’s, Hashimoto’s, Type 1 diabetes)