parathyroid Flashcards

1
Q

parathyroid cell types

A

chief cells

oxyphil cells

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2
Q

chief cells

A

predominate
water-clear appearcne due to cytoplasmic glycogen
secretory granules with PTH

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3
Q

oxyphil cells

A

lots of mito

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4
Q

PTH fnx

A

increases renal tubular Ca absorption
increased activation of Vit D
increased urinary excretion of phosphate
augments GI Ca absorption

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5
Q

primary hyperparathyroidism

A

one of most common endocrine disorders and it is an important cause of hypercalcemia

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6
Q

causes of primary hyperparathryoidsim

A

adenoma (85-95%)
primary hyperplasia
parathyroid carcinoma

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7
Q

sporadic mutations in parathyroid adenomas

A

Cyclin D1 gene inversion

MEN1 mutations

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8
Q

familial mutations in parathyroid adenomas

A

MEN1 and 2
RET
familial hypocalciuric hypercalcemia (rare) -> loss of fnx of CASR

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9
Q

parathyroid adenomas

A

almost always solitary
can be in thyroid or ectopic
usually mostly chief cells

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10
Q

primary hyperplasia of parathyrodi

A

sporadic or in MEN

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11
Q

parathyroid carcinomas

A

may be circumscribed and difficult to distinguish from adenomas or may be obviously invasive
usually enclosed by dense fibrous capsule

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12
Q

Dx of parathyroid carcinomas

A

only way to know is if it invades

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13
Q

skeletal abnomralities of hyperparathyroidism

A

osteoporosis -> dissecting osteitis
brown tumors
osteitis fibrosa cystic

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14
Q

osteitis fibrosa cystica

A

aka con Recklinghausen disease

combo of osteoclast activity, paratrabecular fibrosis, and brown tumors

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15
Q

urinary tract in hyperparathyroidism

A

stones

calcification of renal interstitium and tubules (nephrocalcinosis)

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16
Q

asymptomatic hypercalcemia

A

most commonly caused by primary hyperparathyroidism

17
Q

symptomatic primary hyperparathyroidism

A

usually malignancy

painful bones, renal stones, abdominal groan, and psychic moans

18
Q

GI issues in primary hyperparathyroidism

A

constipation, nausea, peptic ulcers, pancreatitis, gallstones

19
Q

CNS and primary hyperparathyroidism

A

depression, lethargy, seizures, weakness, fatigue

20
Q

secondary hyperparathyroidism

A

renal failure most common cause

other causes: Ca deficiency, steatorrhea, vit D deficiency

21
Q

chronic renal insufficiency

A

decreased phosphate excretion -> hyperphosphatemia -> depress serum Ca -> increase PTH
also decrease Vit D activation

22
Q

clinical secondary hyperparathyroidism

A

usually milder skeletal abnormalities then primary
calciphylaxis
often responds to vit D supplementation

23
Q

calciphylaxis

A

vascular calcification leading to significant ischemic damage to skin and organs

24
Q

causes of hypoparathyroidism

A
sugically induces
autoimmune polyendocrine syndrome type 1
autosomal dominant hypoparathyroidism
familial isolated hypoparathyroidism
congenital absence
25
Q

autoimmune polyendocrine syndrome type 1

A

hypoparathyroidism
chronic candidiasis
primary adrenal insufficiency
mutations in AIRE gene

26
Q

autosomal dominant hypoparathyroidism

A

gain of fnx in CASR

27
Q

familial isolated hypoparathyroidism (FIH)

A

rare
autosomal dominant- mutation in PTH precursor
autosomal recessive- mutation in GGM2

28
Q

congenital absence

A

associated with thymic hyperplasia and CV defects or part of DiGeorge syndrome

29
Q

symptoms of hypocalcemia

A
tetany
paresthesia
capopodal spasm
seizures
mental status changes
calcification of basal ganglia -> parkinsonian like disorders
long OT
30
Q

signs of hypocalcemia

A

Chvostek (facial mm contractions on mechanical stimulation)

Trousseau (carpal spasms if blood flow occluded by bp cuff)

31
Q

pseudohypoparathyroidism

A

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