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Endocrine Physiology > CH5 Parathyroid Gland & Ca++ & PO4- Regulation > Flashcards

CH5 Parathyroid Gland & Ca++ & PO4- Regulation Flashcards

1
Q

What is the broad effect of Parathyroid Hormone PTH?

A

increase serum concentration of Ca++

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2
Q

What thyroid hormone counteracts parathyroid hormone?

A

calcitonin

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3
Q

Where does calcitonin come from? How does it effect blood Calcium level? What is its mechanism?

A

produced by Parafollicular “C” Cells of the Thyroid; decrease serum concentration of Ca++ & PO4– by inhibiting Osteoclasts in bone & stimulating renal excretion of Ca++

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4
Q

How does Parathyroid Hormone effect bone? [general]

A

stimulates bone resorption (release of Ca++) (indirectly through stimulation of osteoblast activity) – releases Ca++ & PO4–

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5
Q

How does Parathyroid Hormone effect the kidney? [general]

A

promotes Ca++ resorption and EXCRETION of inorganic phosphate in urine

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6
Q

What is the active form of vitamin D? How is it formed?

A

calcitriol; PTH stimulates the hydroxylation of 25-hydroxyvitamin D via 1-alpha Hydroxylase in the Kidney

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7
Q

How does Vitamin D effect the Kidney?

A

Vitamin D enhances calcium reabsorption by stimulating the synthesis of Vitamin D dependent Calbindin to form Calbindin-D for the diffusion of Ca++ from apical (influx) to basolateral membrane (efflux); also stimulates activity of Ca++-ATPase

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8
Q

How does Vitamin D effect the gut?

A

increases intestinal absorption of dietary Ca++

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9
Q

How does Vitamin D effect bone?

A

increases bone resorption (release Ca++)

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10
Q

How does Calcitonin effect bone?

A

inhibits bone resorption by osteoclasts

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11
Q

How does Calcitonin effect the Kidney?

A

increases renal Ca++ EXCRETION

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12
Q

What stimulates PTH release?

A

decrease in concentration of Ca++ OR increase in concentration of Pi; catecholamines, PTH

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13
Q

What inhibits PTH release?

A

high concentration of Ca++ & Vitamin D (negative feedback inhibition); severe hypomagnesemia

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14
Q

What cells secrete PTH?

A

Chief Cells of the Parathyroid Gland

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15
Q

How is Parathyroid Hormone Synthesized & Released & Degraded?

A

synthesized as a pre-pro-hormone –> pro-PTH –> mature PTH. Synthesis and release is continuous. PTH is degraded by the kidney and liver.

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16
Q

What occurs during hypocalcemia?

A

1) preformed PTH is released, 2) reduction in intracellular degradation of PTH, 3) increase in PTH release

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17
Q

What does active Vitamin D do at the molecular level?

A

decrease PTH gene transcription

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18
Q

What is the broad effect of increased Phosphate concentration in serum?

A

stimulate PTH release

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19
Q

What is the effect of slightly decreased & severely decreased Magnesium?

A

slight decrease stimulatse PTH release (increase Ca++ serum conc) if magnesium is slightly low, it’ll let calcium go up; severe decrease inhibits PTH release (severe hypomagnesemia is linked to hypocalcemia) – if magnesium is super low, it won’t let calcium go up without it.

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20
Q

What ion is Magnesium closely linked to?

A

Ca++ (magnesium depletion or deficiency is frequently associated with hypocalcemia)

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21
Q

How do Catecholamines affect PTH concentration in serum?

A

stimulate PTH release

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22
Q

What type of receptor is the Ca++ sensor? Where is it found?

A

Gq (when Ca++ bound) & Gi (when unbound); parathyroid chief cells, thyroid parafollicular C cells, kidney tubule cells

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23
Q

When Ca++ is bound to Ca++ sensor, what happens?

A

Ca++ release activates phospholipase C, D, & A2. Phospholipase A2 activates arachidonic acid cascade, which increases leukotriene synthesis. Leukotriene inhibits PTH secretion. (degrades pre-formed PTH, so if released, it will be in inactive form).

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24
Q

How does Ca++ sensor react during hypocalcemia?

A

Ca++ sensor is unbound, relaxed, & does not activate (no PTH degredation)

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25
What is the broad effect of decreased Phosphate concentration in serum?
decrease PTH release
26
How does Phosphate increase or decrease PTH release at the molecular level?
Phosphate, at high conc., decreases Phospholipase A2 activity (degradation pathway) - to stimulate PTH release; also decrease plasma Ca++ & vitamin D activation
27
How does severe hypomagnesemia effect bone?
prevents responsiveness of bone to PTH-mediated bone resorption (cannot take Ca++ from bone to increase serum Ca++ conc.)
28
Where does PTH exert its effects? What receptor do these cells display? What kind of receptor is it? What does it bind?
mainly kidney & bone osteoblasts (indirectly intestinal absorption through Vitamin D); Parathryroid Receptor 1 PTHR1; G-protein coupled (Gs & Gq); Binds PTH & PTHrP
29
What is PTHrP? What is it clinically responsible for? What does it bind to? Where is it expressed?
Parathyroid Hormone-related Protein. Clinically responsible for hypercalcemia of malignancy. Binds to PTHR1. Expressed in multiple tissues, therefore it acts locally (paracrine, autocrine)
30
What kind of receptor is PTHR1? What does it do?
Gprotein-coupled (Gs & Gq). PKA results in induction of gene transcription; IP3 results in increase in cytosolic Ca++ (RECALL: this is occurring in bone and kidney)
31
Track how PTH increases Ca++ reabsorption in the Kidney starting with binding of PTH to PTHR1.
PTH enters kidney and binds to PTHR1 of the DISTAL TUBULES, stimulating insertion and opening of apical Ca++ channels. Ca++ enters cell. Ca++ binds to Calbindin-D and diffuses to basolateral membrane. Here, Ca++ is exported in one of two ways: Na+/Ca++ exchanger (3:1) OR Ca++-ATPase
32
What is transcellular vs paracellular routes for Ca++ reabsorption? Which is important to PTH and why?
transcellular is active, paracellular is passive; PTH regulates the active, transcellular component (esp. in distal tubules); passive paracellular Ca++ absorption is dependent on sodium absorption.
33
What is Calbindin? What does it do?
calbindin is a Vitamin-D dependent Ca++-binding protein. It facilitates the cytosolic diffusion of Ca++ from apical (influx) to basolateral (efflux) as Calbindin-D
34
How do thiazide diuretics influence Ca++ concentration?
Thiazide Diuretics are calcium-sparing drugs. Act like PTH and increase Ca++ reabsorption
35
How does PTH suppress PO4-- reabsorption in the Kidney and Intestine?
decreases expression of Type II Na+/PO4-- Cotransporter by stimulating irreversible internalization (degraded) within the kidney (type IIa) & intestine (type IIb)
36
Track how PTH increases Ca++ release in bone starting with PTH binding to PTHR1.
PTH binds to PTHR1 on OsteoBLASTS. This causes synthesis and activation of Osteoclast-Differentiating Factor ODF (also known as receptor activator of nuclear factor-kB ligand RANKL) (also known as Osteoprotegerin Ligand). Result is activation of osteoblasts and recruitment of osteoclasts, which release Ca++ from bone matrix.
37
Why is PTH used to stimulate bone formation when it causes bone resorption?
Chronic elevations of PTH result in bone resorption. Intermittent administration of PTH stimulates bone formation over bone resorption.
38
What are the other names for Osteoclast-Differentiating Factor ODF?
Receptor activator of nuclear factor-kb ligand (RANKL) & Osteoprotegerin Ligand
39
What is Osteoprotegerin? How does it work? What stimulates/inhibits it?
antagonist protein secreted by osteoblasts that binds to RANKL to inhibit RANKL-RANK mediated differentiation of osteoclasts; stimulated by estrogens, inhibited by PTH and glucocorticoids
40
How do Osteoclasts work?
Osteoclast differentiation is stimulated by RANKL-RANK interaction. To dissolve bone, osteoclasts attach to bone surface via beta-integrins (microenvironment), generate H+ ions via Carbonic Anhydrase II, & release H+ ions via H+-ATPases (pH~4). This dissolves HYDROXYAPATITE. Osteoclast then releases lysosomal proteases (collagenase, cathepsins). Products are endocytosed and released via transcytosis (Ca++, PO4--, & alkaline phosphatases).
41
What molecule in bone serves as a reservoir for Ca++? What other ion is sequestered there?
hydroxyapatite; phosphate is also released when degraded
42
How does pH effect free blood calcium levels?
Majority of protein-bound calcium is bound to albumin, which is sensitive to pH changes. Acidosis decreases binding (increase free Ca++); Alkalosis increases binding (decreases free Ca++)
43
What are the sources for Vitamin D precursors? How is Vitamin D synthesized?
2 sources (cholecalciferol D3 & ergocalciferol D2) are bound to Vitamin D-Binding Protein in circulation and go to Liver. In liver, they are hydroxylated at C-25 --> 25(OH)D (25-hydroxyvitamin D). Travels to kidney bound to Vitamin D-Binding Protein. In Kidney PROXIMAL tubules, 1-alpha-Hydroxylase works at C1 --> 1,25(OH)2D (calcitriol/active Vitamin D). Calcitriol is released and functions as an endocrine hormone.
44
What is the Vitamin D reserve in the body?
25-hydroxyvitamin D bound to Vitamin D-binding Protein; this is the principle storage form of Vitamin D & the major circulating form of Vitamin D. half life of 15 days
45
How is Vitamin D concentration regulated?
PTH stimulates 1-alpha-hydroxylase; high Ca++ levels and Vitamin D (negative feedback) suppress 1-alpha-hydroxylase (forms inactive 24,25(OH)2D instead)
46
What type of hormone is Vitamin D?
steroid (derived from cholesterol, lipid-soluble)
47
What are problems caused by Vitamin D excess?
Calcinosis (calcification of soft tissues), deposition of Ca++ & PO4 in kidney, & increased Ca++ levels (can lead to cardiac arrhythmia)
48
How do patients with Vitamin D deficiency present? What are possible causes?
bone deformities (rickets in children), decreased bone mass (osteomalacia in adults), weakness, bowing of weight bearing msucles, dental defects, hypocalcemia; possible causes are mutation in 1-alpha-hydroxylase or resistance to vitamin D via Vitamin D Receptor mutation
49
What is Paget Disease?
abnormal bone remodeling with increased bone resorption accompanied by hypercalcemia
50
What factors regulate Ca++ & bone metabolism? How?
Sex Steroids (increase 1-alpha-hydroxylase activity, increase osteoprotegerin synthesis, net decrease of bone loss "get Ca++ from anywhere but bone"), Growth Hormone/IGF-1 (stimulate bone synthesis and growth), Glucocorticoids (increase bone resorption, decrease bone synthesis), Inflammatory Cytokines [Tumor Necrosis Factor, Interleukin 1, Interleukin 6] (increase bone resorption via osteoclast proliferation and differentiation)
51
In a state of hypocalcemia (simple calcium deficiency), what occurs?
[ex. of secondary hyperparathyroidism] stimulation of PTH release --> increase bone resorption, increase of Vitamin D, excretion of PO4--, Ca++ isn't resorbed because it's deficient --> excretion of PO4-- (hypophosphatemia) prevents mineralization of new bone, Vitamin D stimulates also increases bone resorption --> overall loss of bone mass
52
How does Vitamin D deficiency differ from simple calcium deficiency (hypocalcemia)?
Vitamin D Deficiency reduces the mineral content of the bony tissue itself and leads to abnormal bone composition, but begins with calcium malabsorption (simple calcium deficiency) -- Recall: Vitamin D stimulates bone resorption, but more importantly, Calbindin is Vitamin D dependent.
53
What does bone density determine? How is it measured?
bone density determines degree of osteoporosis (bone loss) and fracture risk; measured using Dual-Energy X-Ray Absorptiometry (DEXA) scan. Two scores given: T score (comparison to avg. peak bone density) & Z score (comparison to avg. bone density of similar stats)
54
What hormones & abnormalities are often seen with elevated ionized calcium levels in serum?
elevated PTH, elevated Vitamin D, elevated bone resorption
55
What hormones and abnormalities are often seen with elevated plasma phosphate?
renal failure (can't filter it out), hypoparathyroidism (no PTH to degrade phosphate resorption channels), vitamin D intoxication (increases bone resorption which causes increases in Ca++, PO4--, & alkaline phosphatase)
56
What hormones and abnormalities are often seen with decreased levels of plasma phosphate?
hyperparathyroidism (lots of PTH to degrade phosphate resorption channels), vitamin D deficiency (lack of bone resorptino, so no release of Ca++, PO4--, or alkaline phosphatase)
57
What hormones and abnormalities are often seen with elevated levels of plasma alkaline phosphatase?
increased osteoblastic activity
58
In a patient with Primary Hyperparathyroidism, what clinical manifestations are seen?
elevated intact PTH levels, hypercalcemia, hypercalciuria (increased urinary calcium excretion) - which may lead to urolithiasis (kidney stones); decreased plasma phosphate levels
59
What is the principle example of Secondary Hyperparathyroidism? What symptoms are seen?
Chronic Renal Failure. First, a decrease in plasma Vitamin D and free Ca++ is seen --> results in increased PTH release. As chronic renal failure progresses, Parathyroid decreases expression of Vitamin D & Ca++ receptors (becomes very resistant to negative feedback), so regardless of Vitamin D/Ca++ levels, PTH is continuously released. Will also notice hyperphosphatemia (elevated plasma phosphate) due to inability to filter & bone resorption.
60
What is the Chvostek Sign?
Nerve Hyperexcitability (tetany): (seen in hypoparathyroidism/hypocalcemia) twitching or contraction of facial muscles in response to tapping a facial nerve.
61
What is Pseudohypoparathyroidism? How does it present?
defect with PTHR1. 2 types: Ia (resistance to hormones, short stature, skeletal anomalies) & Ib (renal resistance to PTH, normal appearance). Patients present with low plasma Ca++, high phosphate levels, elevated PTH

Endocrine Physiology (15 decks)

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