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Physiology Block 3- Endocrine Physiology > L5 - Parathyroid Gland, Calcitonin, and Ca++ Regulation > Flashcards

L5 - Parathyroid Gland, Calcitonin, and Ca++ Regulation Flashcards

1
Q

How is the release of parathyroid hormone regulated?

A

Decreased plasma calcium levels and increased inorganic phosphate stimulates the release of PTH. Vitamin D and high Ca++ levels inhibit its release

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2
Q

What are the effects of PTH on the kidney? On bone?

A

Increased Vitamin D activation, increased Ca++ reabsorption, decreased inorganic phosphate reabsorption; Increases bone resorption

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3
Q

How does the parathyroid cell sense calcium level changes?

A

Ca++-sensing receptors– GqPCR; high calcium levels activate the receptor which stimulates PLA2 leading to leukotriene synthesis- the leukotrienes stimulate degradation of the PTH

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4
Q

How does vitamin D suppress PTH secretion?

A

Vitamin D binds to its cytosolic receptor, it translocates into the nucleus and suppresses PTH expression

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5
Q

How does PTH circulate in the blood? What is its half-life

A

Circulates free; half-life is 4-10 minutes

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6
Q

What PTH metabolites circulate in the blood? What is the best method for measuring PTH?

A

PTH (10%) is degraded to active amino terminus fragments (10%) and carboxy terminus fragments (80%); determination of the intact molecule is only reliable index of PTH levels

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7
Q

What is the main physiologic response elicited by PTH?

A

Increase plasma Ca++ by increasing Ca++ renal reabsorption, Ca++ mobilization from bone, and intestinal absorption

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8
Q

To what kind of receptor does PTH bind? In what tissues? Which responsible for the major physiologic effects?

A

PTHR1 in bone and kidney (major); PTHR2 in brain, placenta, and pancreas; PTHR3– mostly acts as a GsPCR

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9
Q

How does PTH binding affect epithelial cells within the distal tubules of the kidneys?

A

The main effect is to stimulate the insertion and opening of the Ca++ channel, allowing for influx through the apical membrane

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10
Q

What happens to Ca++ that has entered the apical membrane of a epithelial cell of the distal tubule?

A

It binds to calbindin-D28K and is transported to the basolateral membrane and is transported out of the cell into the interstitial space via a Na+/Ca++ exchanges and Ca++-ATPase

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11
Q

How does PTH affect the epithelial cells of the proximal tubule in the kidney?

A

PTH increases inorganic phosphate excretion by sequestering type II Na+/phosphate cotransporter followed by degradation, which decreases reabsorption

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12
Q

Where is most of the calcium in the body located? Phosphate?

A

In the skeleton

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13
Q

How is calcium transported through the plasma?

A

50% ionized, 40% protein bound (80-90% albumin, 10-20% globulins), 10% citrate and phosphate complex

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14
Q

How does pH affect the binding of Ca++ to albumin?

A

Acidosis decreases binding and increases ionized calcium; alkalosis increases binding and decreases ionized calcium

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15
Q

How is phosphate circulated in the blood?

A

50% ionized; 35% complexed, and 15% protein bound

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16
Q

On which cells of bone tissue are PTH receptors expressed? What is the effect of PTH binding to these cells?

A

Osteoblasts; PTH binding triggers the synthesis and expression of RANKL (ODF)

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17
Q

What is RANK?

A

Receptor activator of nuclear factor-kappa B– a receptor expressed on osteoclast precursor cells that binds to RANKL

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18
Q

What happens subsequent to RANKL binding to RANK?

A

Increases expression of specific genes leading to differentiation of the osteoclast precursor into a fully mature, bone-resorbing osteoclast; Additionally, it stimulate expression of collagenase, IL-6, and IGF-1

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19
Q

What is osteoprotegerin? How does it work? How is it hormonally regulated

A

Protein member of TNF receptor superfamily that is secreted by osteoblasts and acts as an antagonist of RANKL; functions as an osteoclastogenesis inhibitory factor; synthesis is stimulated by estrogen and suppressed by glucocorticoids (chronic stress)

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20
Q

How do osteoclasts break down bone?

A

Osteoclasts seal onto bone, acidic vesicles fuse onto the ruffled border of the bone and pump H+ into the bone via H+-ATPases, which facilitates the solubility of hydoxyapetite; Ca++ and phosphate are endocytosed, transcytosed and are released from the other side of the osteoclast to enter circulation

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21
Q

What is the name of the active form of vitamin D?

A

Calcitriol

-1,25-OH vitamin D

22
Q

What are the mechanisms by which vitamin D is produced?

A

Provitamin D (7-dehydrocholesterol) is converted to cholecalciferol (D3) by UV-radiation and isomerization. Vitamin D2 is taken from the diet. D3 and D2 circulate bound to D-binding protein and reach the liver to undergo hydroxylation to produce 25-OH vitamin D. Renal 1 alpha hydroxylase hydoxylates 25-hydroxyvitamin D resulting in active 1,25 (OH2) (calcitriol)

23
Q

What is the major circulating form of vitamin D? What form of vitamin D is most commonly measured?

A

25-hydroxyvitamin D

24
Q

How does PTH affect vitamin D synthesis? How do vitamin D and calcium levels affect vitamin D synthesis?

A

PTH stimulates the activity of 1-alpha-hydroxylase, favoring an increase in the synthesis of vitamin D; vitamin D and high calcium levels inhibit 1alpha-hydroxylase activity

25
Q

In what tissues are Vitamin D receptors expressed? What is the cellular location of these receptors?

A

Main effects in intestines, parathyroid, and in bone; also found in skin, lymphocytes, skeletal muscle and cardiac muscle

26
Q

What are the primary effects of Vitamin D? What is the overall goal?

A

Increased bone turnover, calcium absorption, calcium reabsorption, decreased PTH synthesis; overall goal of maintaining plasma calcium levels

27
Q

What is the half-life of calcitonin?

A

5 minutes

28
Q

What cells produce calcitonin? What is the stimulus for its release?

A

Thyroid parafollicular C cells; Released in response to high calcium levels

29
Q

In what tissues are calcitonin receptors found? What kind of receptor?

A

Bone and kidney; GPCR

30
Q

What are the physiologic effects elicited by calcitonin?

A

Decreased plasma Ca++ and phosphate concentrations by decreasing bone resorption and increasing urinary calcium excretion

31
Q

How can calcitonin be used therapeutically?

A

Calcitonin can be used to treat malignant calcinemia

32
Q

What are other negative regulators of Ca++ metabolism?

A

Excess TH increases bone resorption, glucocorticoids will increase bone resorption and suppress bone synthesis, and inflammatory cytokines will increase osteoclasts activity and differentiation

33
Q

What are other positive regulators of Ca++ metabolism?

A

Sex steroids will decrease bone resorption, and GH/IGF-1 increase bone protein synthesis, bisphosphonates inhibit osteoclast function

34
Q

What are the causes of excess PTH/ hyperparathyroidism? What are the effects

A

Primary- parathyroid gland adenoma- increased osteoclast activity, hypercalcemia–> nephrolithiasis, dereased phosphate reabsorption; Secondary- chronic renal failure- kidney can’t activate vitamin D, increases plasma phosphate, and decreased calcium sensor function

35
Q

How does hyperphosphatemia affect calcium metabolism/homeostasis?

A

Hyperphosphatemia stimulates the release of fibroblast growth factor 23 from osteoblasts, which suppresses the activity of 1-alpha hydroxylase, inhibiting formation of vitamin D. There is increased PTH release due to decreased inhibition– this results in increased bone resorption and decreased renal function

36
Q

How is hyperphosphatemia treated?

A

Calcium and Vitamin D supplements and dietary phosphate restriction

37
Q

How does chronic renal failure affect Ca-induced suppression of PTH?

A

Chronic renal failure can result in loosing sensitivity of the calcium receptors to varying levels of plasma calcium – calcium has to be higher to achieve same level of suppression

38
Q

What are the potential causes of hypoparathyroidism? How does it present?

A

Endocrine disorders, neoplasias, or surgical removal of parathyroids; Hypocalcemic tetany (Chvostek’s sign)

39
Q

What causes pseudohypoparathyroidism?

A

An abnormal response to PTH bc of a congenital defect in the G protein associated with the PTHR1

40
Q

What is the pathophysiology of vitamin D deficiency? How is it clinically manifested in children? In adults?

A

Decreased intestinal Ca++ absorption, decreased renal PTH-mediated Ca++ reabsorption; Children- rickets, adults- loss of bone mineral osteomalacia

41
Q

What can cause a vitamin D deficiency?

A

Decreased intake or lack of sunlight exposure (including using SPF-8), inactivation of 1-alpha-hydroxylase, resistance to vitamin D action in tissues

42
Q

What other nonskeletal consequences of vitamin D deficiency?

A

Cancer, heart disease, autoimmune disease, influenca, type 2 diabetes, depression

43
Q

(L5) TRUE/FALSE

PTH release is under hypothalamic regulation.

A

False; PTH releases in response to substance (Ca2+)

44
Q

(L5) Vitamin D deficiency

a) is more frequent during the summer
b) is infrequent in the elderly
c) responds to UV light therapy
d) is not seen in dark skinned individuals

A

c) responds to UV light

45
Q

(L5 back of book) 43yo male admitted to ER for severe pain in his left flank, radiating to the groin.
Pain is intermittent and initiated after running a marathon on a hot summer day.
blood detected in the urine
Lab results
ca2+ 12 mg/dl [8.5-10.5]
PTH 130 pg/ml [10-65]

Which of the following findings would be predictable in this patient?

a) increased serum Pi
b) increased serum alkaline phosphatase
c) increased intestinal ca loss
d) decreased urinary ca excretion

A

b) increased serum alkaline phosphatase

high calcium, high PTH; blood detected in urine (kidney stones - dehydration)
a - high PTH inhibits Pi

alkaline phosphatase increased in individuals with bone damage or high bone turnover (high bone resorption)

46
Q

(L5 back of book) 43yo male admitted to ER for severe pain in his left flank, radiating to the groin.
Pain is intermittent and initiated after running a marathon on a hot summer day.
blood detected in the urine
Lab results
ca2+ 12 mg/dl [8.5-10.5]
PTH 130 pg/ml [10-65]

The mechanism underlying the abnormalities observed is:

a) increased calcitonin release
b) decreased 25-hydroxylase activity
c) increased osteoclast apoptosis
d) loss of negative feedback regulation of PTH release

A

d) loss of negative feedback regulation of PTH release

high calcium, high PTH.

a - no; problem is increased ca2+
b - 25-hydroxylase turns vitamin d inactive: would want this to happen to decrease ca levels
c - osteoclast apoptosis would stop the calcium levels from rising (but no reason for that as diagnosis was dehydration)

47
Q

(L5 back of book) 73yo sever vomiting and generalized weakness.
initial lab values reveal elevated Ca2+ levels.
breast cancer and metastasized to bone.

Which of the following laboratory values would be compatible with this clinical scenario?

PTH [10-65]
phosphate [3-4.5]
alkaline phosphatase [30-120]

a) PTH 5, phosphate 6, alp 600
b) PTH 90, pi 6, alp 30
c) PTH 5, pi 2, alp 20
d) PTH 3, pi 2, alp 100

A

a) PTH 5, phosphate 6, alp 600

old age: low calcium due to high bone resorption natural
hypercalcemia from malignancy;

  • alp would be high due to high bone resorption
  • PTH low because high Ca2+ inhibiting
  • phosphate elevated because pi released during bone resorption
48
Q

(L5 back of book) 73yo sever vomiting and generalized weakness.
initial lab values reveal elevated Ca2+ levels.
breast cancer and metastasized to bone.

The most likely cause of hypercalcemia (from malignancy) in the patient is:

a) increased PTH production
b) increased responsiveness of the PTH receptor 1
c) increased PTHrP production
d) increased calcitonin release

A

c) increased PThrP production

malignant hypercalcemia
old age: high Ca2+ due to high bone resorption; high alkaline phosphatase due to high bone resorption

49
Q

(L5 back of book) leading stars of soap operas are prone to enter fits of hysteria associated with hyperventilation.
in real life, usually leads to muscle cramping (tetanic contractions).

What is the physiologic concept that explains what happens in that situation?

a) decreased protein-bound calcium
b) hypercalcemia secondary to PTH-mediated bone resorption
c) increased dissociation of protein-bound calcium
d) decreased ionized plasma calcium levels
e) increased renal calcium excretion

A

c) decreased ionized plasma calcium levels

hyperventilation - respiratory alkalosis (low H+)

  • acidosis: releases free ionized Calcium
  • alkalosis: increases bound calcium
50
Q

(L5 back of book) The physiologic mechanisms affected by medical strategies for the management of osteoporosis include:

a) decreased apoptosis of osteoclasts by biphosphonates
b) increased activation of osteoclast activity by calcitonin
c) increased osteoblast differentation by selected estrogen receptor modulators
d) decreased instestinal ca2+ secretion by vitamin d

A

c) increased osteoblast differentiation by selected estrogen receptor modulators

a-no; want there to be more apoptosis of osteoclasts for more ca2+ free
b-calcitonin decreases ca2+
d-no vitamin d stimulates ca absorption

Physiology Block 3- Endocrine Physiology (10 decks)

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