PTH Flashcards
Why does primary hyperthyroidism occur?
Autonomous PTH secretion secondary to glandular hyperplasia
Parathryroid adenomas
Parathyroid carcinoma (rare)
What are the clinical manifestation of hyperparathyroidism caused by?
Hypercalcemia
T/F removal of hyperfunctioning parathyroid gland is usually curative for hyperparathyroidism
True, 90% cure rate
Where do the parathyroid glands originate from embryonically?
Upper glands- from 4th brachial pouch Lower glands (and thymus)- from 3rd brachial pouch
Where are the parathyroid glands located?
Upper glands are behind thyroid, close to the inf thyroid artery
Lower glands w/in 2 cm of lower thyroid pole
What is the arterial supply to the parathyroid glands
All 4 are supplied by the inferior thyroid artery.
Where are aberrant glands usually located?
Upper abberant- intrathyroid or posterior mediastinal
Lower abberant- intrathymic or anterior mediastinal
What are the effects of primary hyperthyroidism on calcium and phosphate?
Excess PTH means calcium is taken out of bones, and there is also stimulation of renal tubular absorption of calcium. So, there is hypercalcemia.
Excess PTH inhibits renal phosphate reabsorption, so it’s peed out and there is hypophosphatemia.
Overall, total body calcium and phosphate wasting occur –> osteoporosis and bony mineral loss.
What associated conditions can develop as a result of hyperparathyroidism’s metabolic imbalances?
pancreatits nephrolithiasis nephrocalcinosis gout pseudogout HTN peptic ulcer dz
What is secondary hyperparathyroidism?
Usu in pts w renal dz.
Hyperphosphatemia causes Hypocalcemia, which stim’s PTH production.
The PTH glands are usu hyperplastic since there is chronic hypocalcemia.
(Note that this is the OPPOSITE of the Ca and Phosphate levels in primary hyperparathyroidism!)
What is tertiary hyperthyroidism?
Usu in dialysis-dep pts w ESRD
Caused by long-standing secondary hyperparathyroidism- persistent hypocalcemia causes devt of autonomous hyperplastic gland fn. Since gland is autonomous, it can produce as much PTH as it wants.
What is Pseudohyperparathyroidism?
Like primary- hypercalcemia, hypophosphatemia
But dt oat cell cancer or squamous cell cancer of the lung, head/neck, kidney, or ovary.
These cancers make PTHrP, which causes hypercalcemia.
T/F the majority of cases of hyperparathyroidism are dt a single hyperfunctioning adenoma
True.
Most cases are sporadic.
What are the genetic origins of hyperparathyroidism?
MEN I or IIa
What is MEN I?
Wermer’s 3 p’s:
parathyroid
pituitary
pancreas
What is MEN IIa?
Sipple:
hyperparathyroidism
pheochromocytoma
MTC
T/F Pts with MEN I or II require removal of all 4 parathyroid glands.
True.
Usu have diffuse 4-gland hyperplasia, so require bilateral neck exploration for removal of all glands.
Risk factors for developing hyperparathyroidsim
Childhood radiation therapy to head/neck
Fam hx of MEN
T/F pts w hyperparathyroidism are generally asx at px
True- dx is usu made after discovering hypercalcemia on routine screening.
In the past, pts px’d w ESRD d/t staghorn caliculi and obstructive uropathy; also with pathologic fractuers.
Sx of hyperparathyroidism
Bones Stones Abd groans Psychic moans Fatigue overtones
Bone sx in hyperparathyroidism
aches, arthralgias from structural chgs in bony architecture (dt hypercalcemia, no calcium in bones)
Pseudogout (chondrocalcinosis) causes severe joint pain when articular cartilage becomes calcified.
“Stones” sx in hyperparathyroidism
Renal caliculi from hypercalcemia can cause renal colic sx
Calculi can also cause obstructive uropathy –> UTIs, renal failure
can also have nephrocalcinosis- calcification of renal parenchyma
“Abd groans” sx in hyperparathyroidism
Filtration of high serum calcium loads –> dehydration, constipation
Pancreatitis
Can stimulate gastin production –> elevated gastric acid secretion
Peptic ulcer dz
“Psychic moans” and “fatigue overtones” in hyperparathyroidism
Hypercalc –> anorexia, naus/vom.
High mineral lvls in kidney –> polyuria –> thirst, polydipsia
Behavioral chg- mood swings, organic psychosis, dementia
Lassitude, muscular fatigue
Phys Ex for hyperparathyroidism
Usu nothing.
Occasional palpable neck mass
Rarely, focal bone swelling- dt brown tumors of osteoclasts
Most common cause of hypercalcemia?
Mets to bone. (osseous metastatic dz)
Dx eval for hyperparathyroidism
Persistent hypercalcemia
Elevated serum PTH
Elevated alk phos if bony dz
Elevated creatinine if renal dz
XR- subperosteal reabs of phalanges, osteopenia, osteoclastomas, mets calcifications
Bone density scan for osteopenia
Abd XR for renal calculi or nephrocalcinosis
Rx for hyperthyroidism
Remove hyperfng glands.
Pre-op localization of tumor w sestamibi scan
also intra-op rapid PTH immunoassay
What are the sx of hypercalcemic crisis? what is the rx?
Coma delerium anorexia vom abd pain Rx: IV hydration and forced calciuresis w furosemide. After stabilized, surgery.
T/F once the tumor is removed, PTH levels should decrease siginificantly
True,
should decrease to <25% of baseline.
Operation for primary hyperthyroidism
Curvilinear necklace incision
Most tumors are attached to posterior capsule of thyroid, on top of recurrent laryngeal n. and next to inf thyroid artery.
Remove only the problematic gland, but find all 4 in case of multiple adenomas.
Operation for parathyroid hyperplasia
All glands are diseased, so remove all except one.
Subtotal excision of one gland prevents hypocalcemia.
Rx for secondary and tertiary hyperparathyroidism
secondary- it’s dt renal dz and low Ca2+, so treat medically
tertiary- it’s dt autonomous gland hyperplasia, so it sometimes requires surgery.
What happens after parathyroid surgery?
Hypocalcemia (secondary to reduced PTH lvls) Osseous remineralization (hungry bones)
Sx of hypocalcema
periorbital numbness parasthesia carpopedal spasm seizures Chovstek's sign of hypocalcemia- tap facial nerve in cheek and cause muscle spasm
Rx for hypocalcemia
Mild- give oral Ca2+ supplements and high calcium diet
If spasm/seizure- immed IV calcium gluconate or calcium chloride
T/F Recurrent hyperparathyroidism after gland removal is possible.
True, happens in 5% of single adenoma removal
do re-exploration w sestamibi and PTH assay.
