Calcium and Vitamin D Disorders Flashcards
45% of serum calcium is bound to…
protein, primarily albumin. Albumin levels will alter serum calcium levels
If the pH were in a state of alkalosis what would happen to the binding of albumin?
increased binding to albumin
If the pH were in a state of Acidosis what would happen to the binding of albumin?
decreased binding to albumin
What is Calcium regulated by?
PTH, vit D via effects on bone , kidney and GI tract
Negative inhibition by acting on Ca Sensing receptor (CaSR)
At level of PTH gland-inhibits release of PTH
Kidney: inc excretion of calcium, dec calcium reabsorption
Primary hyperparathyroidism is most commonly cause by what?
85% single adenoma
Where does most of the loss of BMD in PHPTH occur?
lumbar spine
What are the guidelines for surgical management of Asymptomatic HPTH?
Plasma calcium >1.0 mg/dL of the ULN
Calculated Cr C <50 years
Monitoring:
Yearly serum Ca++
Yearly Plasma Cr
BMD every 1-2 years
Preoperative localization for PHTPH
Done once a diagnosis is made and pt to have surgery
Sestamibi scan
US neck
CT neck
What are the treatment guidelines for hypercalcemia?
Ca< 12-14 mg/dL: may be tolerated chronically and may not require immediate therapy
Calcium >14 mg/dL requires therapy, regardless of symptoms
How do we treat hypercalcemia?
IV hydration:
Saline 200-300 ml/hr
Adjust to keep urine output 100-150mL/h
Diuresis with lasix only if signs of fluid overload
Calcitonin/Bisphosphonates
Use of Calcimimetics (inhibit PTH release)
Dialysis in some cases
Glucocorticoids when indicated
Identify/Treat underlying cause
Calcitonin
Osteoclast inhibitor/inc renal excretion
4IU/kg, IV or SC, Q12 hours
can be increased to 6-8 IU/kg Q6 hr
Nasal form not efficacious
Rapid reduction in calcium (within 4-6 hours)
Short lived effect-limited to initial 48 hrs
tachyphylaxis (poss receptor down-regulation)
Bisphosphonates
Pamidronate
Zolendronate
Osteoclast inhibitors
IV route
Expect reduction in serum calcium 24-36 hours
Duration of effects is variable
Cinacalcet
Calcimimetic- inc the sensitivity of the CaSR to extracellular calcium
Inhibits PTH release
Indications:
parathyroid cancer
secondary HPTH
non surgical primary HPTH with severe hypercalcemia
Pseudohypoparathyroidism
Resistance to PTH action
2/2 to defective signaling of PTH action via cell membrane receptor (G- protein)
Elevated PTH level, elevated phosphorus and low calcium
Also affects TSH, LH, FSH, GH signaling
Autosomal Dominant gene mutation of GNAS1 ( alpha subunit of G protein):
G protein is unable to activate downstream signaling and end organ response to PTH
GNAS1 is imprinted in humans so what is expressed depends on how an allele was transmitted:
Maternal transmission (type 1 A): -biochemical abnormalities + phenotypic features
paternal transmission (pseudo-pseudo): -phenotypic features only
Albright’s hereditary osteodystrophy
Most common type of pseudo-hypoparathyroidism (type 1 A)
Labs: Inc PTH, Inc phos and low Calcium and resistance to other G protein coupled hormones Constellation of symptoms: Short stature Obesity Round face Developmental delay Short metacarpals 4 and 5, dimples instead of knuckle