Parathyroid diseases Flashcards
the inferior parathyroid glands arise from which branchial pouches?
3rd
the superior parathyroid glands arise from which branchial pouches?
4th
what is the predominant epithelial cell of the parathyroid gland, histologically?
chief cell
which parathyroid gland cell has an eosinophilic granular cytoplasm?
oxyphil cell
what are the cells of the parathyroid gland? which contain(s) PTH?
chief cell
oxyphil cell
both have PTH
the gene for PTH production is located on which chromosome?
11
what is the half life of PTH?
2-4 minutes
what calcium receptor is what type of receptor?
GPCR
what are the 3 target organs of PTH?
bone
intestinal mucosa
kidney
how does PTH affect osteoclasts?
increases osteoclastic bone resporption of calcium and phosphate
what is the effect of PTH on the kidney?
increases distal convoluted tubular calcium reabsorption and decreases proximal tubular phosphate reabsorption
what is the net effect of PTH?
increased serum calcium
decreased serum phosphate
PTH is responsible for fine tuning of calcium absorption in what part of the nephron?
distal nephron
in which part of the nephron does PTH inhibit phosphate reabsorption?
proximal tubule
in hyper PTH states, what is the effect on bicarb? why?
bicarb reabsorption is also impaired (inhibition of sodium / proton antiporter activity)
what is the most common cause of hypercalcemia in ambulatory patients?
hyperparathyroidism
what is the most common cause of hypercalcemia in hospitalized patients?
malignancy
what is the first line test in hypercalcemic patients?
PTH levels
what are the clinical features of primary hyper PTH disease?
BONES (long bone pain)
STONES (kidneys and polyuria, polydipsia)
GROANS (gastric ulcers)
MOANS (psychiatric - depression)
what are the labs seen in primary hyper PTH disease?
- increased calcium
- decreased or normal serum phosphate
- increased or normal iPTH - INAPPROPRIATELY normal
- increased urine calcium
primary hyper PTH tends to affect what type of bone? what is seen on X ray?
cortical bone
- “salt and pepper” skull
- osteitis fibrosa cystica (fibrous replacement of resorbed bone - bone pain, tenderness, deformity, fracture)
what is the cure for primary hyper PTH disease? what does it require?
surgery
requires subtotal parathyroidectomy
what is hungry bones syndrome?
surgical complication of primary hyper PTH disease
in patients with preexisting parathyroid bone disease the bones mop up calcium as the parathyroid drive ceases - causes acute hypocalcemia within 48 hours
what is the medical therapy for primary PTH disease?
- avoid diuretics
- adequate hydration
- estrogen
- bisphosphonates
- calcimimetics
- monitor serum calcium
what are the variants of hyperparathyroidism and their causes?
secondary (COMMON) - vitamin D deficiency, renal failure
tertiary - end stage renal disease, continuous parathyroid stimulation in secondary hyperparathyroidism as in renal failure leads to autonomous parathyroid glands
what is the cause for familial hypocalciuric hypercalcemia (FHH)? what do the labs look like?
- inactivating mutation in calcium sensor / receptor (parathyroids and kidneys)
- labs: mild hypercalcemia and normal or elevated iPTH
what are the causes of hypo PTH - decreased PTH production?
- surgical excision
- infiltrative process - wilsons, hemochromatosis
- autoimmune destruction
- congenital - DiGeorge, defective branchial arch formation
- decreased magnesium - impairs PTH secretion and action
- familial
symptoms of hypo PTH
- paresthesiae, carpopedal spasm, tetany, laryngeal stridor, convulsions, apathy, depression
- calcification of basal ganglia on brain CT and benign intracranial hypertension
- GI: nausea, vomiting, abdominal pain, malabsorption
- cardiac: prolonged QT interval on ECG
- cataracts, alopecia
- mucocutaneous candidiases in DiGeorge
effects of hypoparathyroidism
- low mobilization of calcium from bone
- low renal distal tubular calcium reabsorption
- low renal phosphate excretion
- low renal production of 1,25 diOH vitamin D
- low calcium and high phosphate
- low PTH or inappropriately normal
in diagnosing hypocalcemia what is important to remember in order to confirm true low calcium?
correct for serum albumin
treatment for hypocalcemia
- IV calcium gluconate or PO calcium carbonate
- vitamin D3 (calcitriol or similar) PO twice daily
what is NATPARA? what are its benefits?
synthetic PTH analog
- decreases risk for kidney stone formation
- decreases risk for bone demineralization
- decreases pill burden on patients with hypoparathyroidism
what is the pseudo hypoparathyroidism? what are the clinical features / labs?
end organ resistance to PTH due to receptor or post receptor defect
hypocalcemia, hyperphosphatemia, HIGH PTH
