parathyroid Flashcards
parathyroid cell types
chief cells
oxyphil cells
chief cells
predominate
water-clear appearcne due to cytoplasmic glycogen
secretory granules with PTH
oxyphil cells
lots of mito
PTH fnx
increases renal tubular Ca absorption
increased activation of Vit D
increased urinary excretion of phosphate
augments GI Ca absorption
primary hyperparathyroidism
one of most common endocrine disorders and it is an important cause of hypercalcemia
causes of primary hyperparathryoidsim
adenoma (85-95%)
primary hyperplasia
parathyroid carcinoma
sporadic mutations in parathyroid adenomas
Cyclin D1 gene inversion
MEN1 mutations
familial mutations in parathyroid adenomas
MEN1 and 2
RET
familial hypocalciuric hypercalcemia (rare) -> loss of fnx of CASR
parathyroid adenomas
almost always solitary
can be in thyroid or ectopic
usually mostly chief cells
primary hyperplasia of parathyrodi
sporadic or in MEN
parathyroid carcinomas
may be circumscribed and difficult to distinguish from adenomas or may be obviously invasive
usually enclosed by dense fibrous capsule
Dx of parathyroid carcinomas
only way to know is if it invades
skeletal abnomralities of hyperparathyroidism
osteoporosis -> dissecting osteitis
brown tumors
osteitis fibrosa cystic
osteitis fibrosa cystica
aka con Recklinghausen disease
combo of osteoclast activity, paratrabecular fibrosis, and brown tumors
urinary tract in hyperparathyroidism
stones
calcification of renal interstitium and tubules (nephrocalcinosis)
asymptomatic hypercalcemia
most commonly caused by primary hyperparathyroidism
symptomatic primary hyperparathyroidism
usually malignancy
painful bones, renal stones, abdominal groan, and psychic moans
GI issues in primary hyperparathyroidism
constipation, nausea, peptic ulcers, pancreatitis, gallstones
CNS and primary hyperparathyroidism
depression, lethargy, seizures, weakness, fatigue
secondary hyperparathyroidism
renal failure most common cause
other causes: Ca deficiency, steatorrhea, vit D deficiency
chronic renal insufficiency
decreased phosphate excretion -> hyperphosphatemia -> depress serum Ca -> increase PTH
also decrease Vit D activation
clinical secondary hyperparathyroidism
usually milder skeletal abnormalities then primary
calciphylaxis
often responds to vit D supplementation
calciphylaxis
vascular calcification leading to significant ischemic damage to skin and organs
causes of hypoparathyroidism
sugically induces autoimmune polyendocrine syndrome type 1 autosomal dominant hypoparathyroidism familial isolated hypoparathyroidism congenital absence
autoimmune polyendocrine syndrome type 1
hypoparathyroidism
chronic candidiasis
primary adrenal insufficiency
mutations in AIRE gene
autosomal dominant hypoparathyroidism
gain of fnx in CASR
familial isolated hypoparathyroidism (FIH)
rare
autosomal dominant- mutation in PTH precursor
autosomal recessive- mutation in GGM2
congenital absence
associated with thymic hyperplasia and CV defects or part of DiGeorge syndrome
symptoms of hypocalcemia
tetany paresthesia capopodal spasm seizures mental status changes calcification of basal ganglia -> parkinsonian like disorders long OT
signs of hypocalcemia
Chvostek (facial mm contractions on mechanical stimulation)
Trousseau (carpal spasms if blood flow occluded by bp cuff)
pseudohypoparathyroidism
end-organ resistance to actions of PTH
serum PTH levels are normal or elevated
sometimes can have resistance to THS, FSH, and LH
all are GPCRs
