Parathyroid diseases Flashcards

1
Q

the inferior parathyroid glands arise from which branchial pouches?

A

3rd

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2
Q

the superior parathyroid glands arise from which branchial pouches?

A

4th

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3
Q

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

A

chief cell

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4
Q

which parathyroid gland cell has an eosinophilic granular cytoplasm?

A

oxyphil cell

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5
Q

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

A

chief cell
oxyphil cell

both have PTH

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6
Q

the gene for PTH production is located on which chromosome?

A

11

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7
Q

what is the half life of PTH?

A

2-4 minutes

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8
Q

what calcium receptor is what type of receptor?

A

GPCR

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9
Q

what are the 3 target organs of PTH?

A

bone
intestinal mucosa
kidney

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10
Q

how does PTH affect osteoclasts?

A

increases osteoclastic bone resporption of calcium and phosphate

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11
Q

what is the effect of PTH on the kidney?

A

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

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12
Q

what is the net effect of PTH?

A

increased serum calcium

decreased serum phosphate

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13
Q

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

A

distal nephron

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14
Q

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

A

proximal tubule

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15
Q

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

A

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

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16
Q

what is the most common cause of hypercalcemia in ambulatory patients?

A

hyperparathyroidism

17
Q

what is the most common cause of hypercalcemia in hospitalized patients?

A

malignancy

18
Q

what is the first line test in hypercalcemic patients?

A

PTH levels

19
Q

what are the clinical features of primary hyper PTH disease?

A

BONES (long bone pain)
STONES (kidneys and polyuria, polydipsia)
GROANS (gastric ulcers)
MOANS (psychiatric - depression)

20
Q

what are the labs seen in primary hyper PTH disease?

A
  • increased calcium
  • decreased or normal serum phosphate
  • increased or normal iPTH - INAPPROPRIATELY normal
  • increased urine calcium
21
Q

primary hyper PTH tends to affect what type of bone? what is seen on X ray?

A

cortical bone

  • “salt and pepper” skull
  • osteitis fibrosa cystica (fibrous replacement of resorbed bone - bone pain, tenderness, deformity, fracture)
22
Q

what is the cure for primary hyper PTH disease? what does it require?

A

surgery

requires subtotal parathyroidectomy

23
Q

what is hungry bones syndrome?

A

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

24
Q

what is the medical therapy for primary PTH disease?

A
  • avoid diuretics
  • adequate hydration
  • estrogen
  • bisphosphonates
  • calcimimetics
  • monitor serum calcium
25
Q

what are the variants of hyperparathyroidism and their causes?

A

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

26
Q

what is the cause for familial hypocalciuric hypercalcemia (FHH)? what do the labs look like?

A
  • inactivating mutation in calcium sensor / receptor (parathyroids and kidneys)
  • labs: mild hypercalcemia and normal or elevated iPTH
27
Q

what are the causes of hypo PTH - decreased PTH production?

A
  • surgical excision
  • infiltrative process - wilsons, hemochromatosis
  • autoimmune destruction
  • congenital - DiGeorge, defective branchial arch formation
  • decreased magnesium - impairs PTH secretion and action
  • familial
28
Q

symptoms of hypo PTH

A
  • 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
29
Q

effects of hypoparathyroidism

A
  • 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
30
Q

in diagnosing hypocalcemia what is important to remember in order to confirm true low calcium?

A

correct for serum albumin

31
Q

treatment for hypocalcemia

A
  • IV calcium gluconate or PO calcium carbonate

- vitamin D3 (calcitriol or similar) PO twice daily

32
Q

what is NATPARA? what are its benefits?

A

synthetic PTH analog

  • decreases risk for kidney stone formation
  • decreases risk for bone demineralization
  • decreases pill burden on patients with hypoparathyroidism
33
Q

what is the pseudo hypoparathyroidism? what are the clinical features / labs?

A

end organ resistance to PTH due to receptor or post receptor defect

hypocalcemia, hyperphosphatemia, HIGH PTH