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Pathoma LAH > Endocrine: 15.5: Parathyroid > Flashcards

Endocrine: 15.5: Parathyroid Flashcards

1
Q

Decreased serum free Ca++ stimulates _____.

A

the parathyroid glands –> increased PTH

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2
Q

Why does hypercalcemia cause acute pancreatitis?

A

Ca++ is an enzyme activator

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3
Q

What is pseudohypoparathyroidism?

A
  • end-organ resistance to PTH (no response)
    • defective Gs protein
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4
Q

How does someone get pseudohypoparathyroidism?

A

it’s auto. dominant

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5
Q

What are the consequences of hypercalcemia?

A
  • nephrolithiasis
  • nephrocalcinosis (Ca++ deposited into the tubules)
  • CNS disturbances (depression, sz)
  • constipation
  • acute pancreatitis
  • PUD
  • osteitis fibrosa cystica
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6
Q

What will the PTH level be in primary hyperparathyroidism? Why?

A
  • increased
  • the adenoma is secreting it
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7
Q

What will the serum PTH level be in secondary hyperparathyroidism? Why?

A
  • increased
  • from increased secretion of PTH
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8
Q

What will the serum PO4- level be in secondary hyperparathyroidism? Why?

A
  • increased
  • increased absorption from the kidneys
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9
Q

What will the serum PO4- level be in primary hyperparathyroidism? Why?

A
  • decreased
  • decreased renal absorption
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10
Q

What will the serum alk. phos. level be in secondary hyperparathyroidism? Why?

A
  • increased
  • PTH is causing increased osteoblast activity in the bones
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11
Q

What is the key cell in the parathyroid gland?

A

Chief cells

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12
Q

What is the effect of PTH in the GI tract?

A

activates vitamin D –> increases absorption of Ca++ and PO4- in the small intestine

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13
Q

What is the most common cause of primary hyperparathyroidism?

A

parathyroid adenoma

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14
Q

What is parathyroid adenoma?

A

a benign neoplasm that produces excess PTH –> hypercalcemia

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15
Q

What will the lab findings be in pseudohypoparathyroidism?

A
  • hypocalcemia
  • increased PTH
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16
Q

What is the tx for primary hyperparathyroidism?

A

surgical removal of gland

17
Q

An alkaline environment is necessary to activate _____ and ______ calcium on bone.

A
  • osteoblasts
  • lay down
18
Q

What is the effect of PTH in the bones?

A

activates osteoblasts –> increased osteoclast activity –> resorb bone –> release Ca++ and PO4- into the blood

19
Q

What will the serum Ca++ level be in secondary hyperparathyroidism? Why?

A
  • decreased
  • high phosphate decreases serum Ca++
20
Q

What is osteitis fibrosa cystica?

A

Loss of Ca++ from bones –> fibrosis, cysts

21
Q

What physical exam findings are assoc. with pseudohypoparathyroidism?

A
  • short stature
  • short 4th and 5th digits
22
Q

What lab findings are seen in hypoparathyroidism?

A
  • decreased PTH
  • decreased serum Ca++
23
Q

What affect does DiGeorge Syndrome have on the parathyroid gland?

A

agenesis –> decreased PTH (hypoparathyroidism)

24
Q

What will the urinary cAMP level be in primary hyperparathyroidism? Why?

A
  • increased PTH
  • activates Gs –> adenylate cyclase –> increased cAMP
25
Q

What does phosphate bind?

A

free Ca++

26
Q

Renal failure causes _____ hyperparathyroidism.

A

secondary

27
Q

What is the effect of PTH in the kidneys?

A
  • increases calcium reabsorption
  • decreases PO4- reabsorption
28
Q

What is secondary hyperparathyroidism?

A

extrinsic increased PTH (not from the parathyroid gland itself)

29
Q

This is the loss of Ca++ from bones –> fibrosis, cysts.

A

osteitis fibrosa cystica

30
Q

What will the serum alk. phos. level be in primary hyperparathyroidism? Why?

A
  • increased
  • increased osteoblast activity in bone
31
Q

What is a marker for increased osteoblast activity?

A

increased serum alk. phos.

32
Q

What is primary hyperparathyroidism?

A

excess PTH due to a disorder of the parathyroid gland itself

33
Q

What is hypoparathyroidism?

A

low PTH due to a problem with the parathyroid glands

34
Q

What will the serum Ca++ level be in primary hyperparathyroidism? Why?

A
  • high
  • increased GI, bone, and kidney resorption
35
Q

What are the systemic affects of hypoparathyroidism?

A
  • numbness and tingling (esp. perioral)
  • tetany/muscle spasms (esp. on facial nerve tapping, upon BP cuff inflation)
36
Q

What kind of receptor is PTH coupled to? What are the downstream affects?

A

Gs –> adenylate cyclase –> cAMP

Pathoma LAH (77 decks)

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