Parathyroid diseases Flashcards by Michael Gedestad

the inferior parathyroid glands arise from which branchial pouches?

3rd

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the superior parathyroid glands arise from which branchial pouches?

4th

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what is the predominant epithelial cell of the parathyroid gland, histologically?

chief cell

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which parathyroid gland cell has an eosinophilic granular cytoplasm?

oxyphil cell

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what are the cells of the parathyroid gland? which contain(s) PTH?

chief cell
oxyphil cell

both have PTH

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the gene for PTH production is located on which chromosome?

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what is the half life of PTH?

2-4 minutes

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what calcium receptor is what type of receptor?

GPCR

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what are the 3 target organs of PTH?

bone
intestinal mucosa
kidney

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how does PTH affect osteoclasts?

increases osteoclastic bone resporption of calcium and phosphate

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what is the effect of PTH on the kidney?

increases distal convoluted tubular calcium reabsorption and decreases proximal tubular phosphate reabsorption

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what is the net effect of PTH?

increased serum calcium

decreased serum phosphate

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PTH is responsible for fine tuning of calcium absorption in what part of the nephron?

distal nephron

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in which part of the nephron does PTH inhibit phosphate reabsorption?

proximal tubule

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in hyper PTH states, what is the effect on bicarb? why?

bicarb reabsorption is also impaired (inhibition of sodium / proton antiporter activity)

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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