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endo II exam1 > parathyroid > Flashcards

parathyroid Flashcards

1
Q

avg weight 1 parathyroid gland

A

25-50 mg

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2
Q

color of normal parathyroid

A

yellow

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3
Q

red brown parathryoid gland

A

adenoma

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4
Q

2 cell types in parathyroid gland

A

chief cells and oxyphil cells

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5
Q

why are oxyphil cells pink

A

lots of mitochondria

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6
Q

function of parathyroid gland

A

regulate calcium homeostasis

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7
Q

how do PTH glands regulate Ca

A

icnrease renal tubular resorption of Ca
increase conversion of Vit D to active form in kidneys
increase urinary PO4 lowering serum PO4
change GI Ca absorption

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8
Q

what is primary hyperPTH

A

autonomous overproduction of PTH usually resulting from adenoma or hyperplasia of PTH tissue

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9
Q

what is secondary hyper PTH

A

compensatory hypersecretion of OTH in response to prolonged hypoCa, usually from chronic renal failure

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10
Q

what is tertiary hyper PTH

A

persistent hypersecretion of PTH even after the cause of prolonged hypoCa is corrected
(e.g after renal transplant)

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11
Q

3 most common causes of primary hyper PTH

A

pituitary adenoma
primary hyperplasia (diffuse or nodular)
PTH carcinoma

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12
Q

microscopic PTH adenoma

A

uniform polygonal chief cells with small central nuclei

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13
Q

what type of PTH adenoma resemble hurthle cell changes

A

oxyphil adenomas

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14
Q

what is endocrine atypia

A

pleomorphic nuclei in adenomas

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15
Q

histo of PTH adenoma

A

no fat, thin rim of normal PTH (has fat globules)

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16
Q

most common cause primary hyeprPTH

A

solitary PTH adenoma arising sporadically

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17
Q

how is hyper PTH detected usually

A

first incidental finding of hyeprCa

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18
Q

genetic syndromes assoc with familial PTH adenomas

A

MEN 1 and 2

germline mutations in MEN1 and RET

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19
Q

bone Sx of hyperPTH

A

osteoporosis, brown tumors, osteitis fibrosa cystica

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20
Q

osteoclasts in hyperPTH affect what bone type more than medullary bone

A

cortical (subperiosteal and endosteal surfaces)

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21
Q

what is dissecting osteitis

A

when osteoclasts in medullary bone dissect centrally along the trabeculae creating appearance of railroad tracks

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22
Q

What is osteitis fibrosa cystica

A

von Recklinghausen disease of bone

increased osteoclast activty, peritrabecular fibrosis and cystic brownt tumors

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23
Q

what is a cystic brown tumor in bone from

A

loss of bone causes microfractures, hemorrhage and influx of macrophages that cause reparative fibrous tissue and reactive tissue i.e. brown tumor

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24
Q

how does hyper PTH affect renal system

A

nephrolithiasis and nephrocalcinosis

met calcification can occur in stomach lungs myocardium and blood from hyperCa

25
Q

most common cause asymptomatic hyper Ca

A

primary hyperPTH

26
Q

cause of symptomatic hyperCa in adults

A

malignancy: solid tumors like lung, breast, head and neck and renal cancers
multiple myeloma

27
Q

mech in which osteolytic tumors induce hyperCa

A

secretion of PTH related peptide PTHrP

28
Q

Causes of hyper Ca with decreased PTH levels too

A 
hyperCa of malignancy
Vit D toxicity
immobilization
thiazide diuretics
granulomatous disease (sarcoidosis)
29
Q

painful bones, renal stones, abdominal groans and psychic moans

A

primary hyperPTH

30
Q

Abdominal Sx from primary hyper PTH

A

nausea, vomiting, constipation, indigestion

31
Q

effects of hyperPTH on nervous system

A

lethargy, fatigue, memory loss, psychosis, depression

32
Q

most common cause secondary hyper PTH

A

renal failure

33
Q

what occurs in secondary hyper PTH

A

chronic hypocalcemia that leads to compensatory overactivity of the PTH glands

34
Q

kimmelstein wilson glomeruli

A

DM and nodular glomerulosclerosis

35
Q

what other diseases can cause secondary hyper PTH

A

inadequate dietary intake of Ca, steatorrhea, vit D deficiency

36
Q

morphology of PTH glands d/t secondary hyperPTH

A

all 4 glands enlarged
hyperplastic with increased chief cells and abundant clear cytoplasm
fat cells are decreased in number

37
Q

secondary hyperPTH has met calcificaitons where

A

lungs, heart stomach and blood vessels

38
Q

what is calicphylaxis

A

vascular calcification assoc with secondary hyper PTH from ischemic damage to skin and other organs

39
Q

what do you Tx patients with secondary hyperPTH

A

dietary vit D supp

phosphate binders which dec the hyperphosphatemia

40
Q

what is tertiary hyperPTH

A

autonomous and excessive with resultant hyperCa

41
Q

Tx tertiary hyperPTH

A

parathyroidectomy

42
Q

acquire hypoPTH is usually a consequence of

A

surgery

43
Q

PTH glands are mistaken for what

A

lymph nodes

44
Q

what is autoimmune hypoPTH

A

chronic mucocutaneous candidiasis and primary adrenal insufficiency
autoimmune polyendocrine syndrome type 1

45
Q

what mutations cause autoimmune polyendocrine syndrome type 1

A

autoimmune regulator gene

46
Q

how does autoimmune hypoPTH present

A

candidiasis in childhoos followed by hypoPTH and adrenal insufficiency in adolescence

47
Q

what is autosomal dominant hypoPTH caused by

A

gain of function mutations in Ca sensing R gene

results in hypocalcemia and hypercaliuria

48
Q

What is familial isolated hypoPTH

A

FIH rare condition with auto dom or auto recessive patterns

49
Q

What causes auto dom FIH (familial isolated hypoPTH)

A

mutation in gene encoding PTH precursor peptide which impairs its processing to the mature hormone

50
Q

What causes auto recessive FIH(familial isolated hypoPTH)

A

loss of function mutations in transcription factor gene glial-cells-missing-2 GCM2 which is needed for development of parathyroid

51
Q

what can cause congenital absence of PTH glands

A

thymic aplasia, CV defects

22q11 deletion syndrome(digeorge)

52
Q

hallmark clinical features hypoPTH

A

tetany with neuromuscular irritability (Decreased serum Ca levels)
circumoral numbness, parasthesias of distal extremities and carpopedal spasm to life threatening laryngospasm and generalized seizures

53
Q

What is a Chvostek sign

A

tap along facial nerve to induce contractions of the muscles of the eye mouth or nose

54
Q

What is a Trousseau sign

A

carpal spasms produced by occlusion of the circulation to the forearm and hand with a bp cuff for several minutes

55
Q

other clinical features to hypoPTH

A

mental status changes like emotional instability and anxiety
intracranial manifestations like calcifications of basal ganglia
ocular- calcification of lens and cataract
CV manifestations- long QT
dental- dental hypoplasia, failure eruption, defective enamel and root formation

56
Q

what causes the intracranial manifestations of hypoPTH

A

increased phosphate levels resulting in tissue deposits with Ca that exists in local extracellular milieu

57
Q

what causes pseudohypoPTH

A

end-organ Resistance to the actions of PTH

58
Q

how does pseudohypoPTH present

A

hypoCa, hyperphosphatemia, elevated circulating PTH

59
Q

signs of pseudohypoPTH

A

+chvosteks and trousseaus
short stature and short fingers
increased PTH
mental retardation

endo II exam1 (14 decks)

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