Regulation of Calcium and Phosphate Metabolism

Question 1

Free, ionized Ca2+ is the biologically ___ form.

Answer 1

active

Question 2

____ symptoms include hyperreflexia, spontaneous twitching, muscle cramping, tingling, and numbness.

Answer 2

Hypocalcemia

Question 3

____ sign is twitching of the facial muscles elicited by tapping on the facial nerve and indicates _____.

Answer 3

Chvostek; hypocalcemia

Question 4

____ sign is carpopedal spasm upon inflation of a BP cuff and indicates ____.

Answer 4

Trousseau; hypocalcemia

Question 5

____ symptoms include decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, and coma.

Answer 5

Hypercalcemia

Question 6

Hypocalcemia reduces the activation threshold for Na+ channels, so it is ___ to evoke an AP, which results in membrane excitability.

Answer 6

easier

Question 7

Generation of spontaneous APs is the physical basis for hypocalcemic ____ and produces tingling, numbness, and spontaneous muscle twitches.

Answer 7

tetany

Question 8

Hypercalcemia causes ____ membrane excitability, so the nervous system becomes depressed and reflex responses are slowed.

Answer 8

decreased

Question 9

An increase in plasma protein concentration ____ total Ca2+ concentration.

Answer 9

increases

Question 10

An increase in Ca2+ complexed with anions will ____ ionized Ca2+ concentration.

Answer 10

decrease

Question 11

Acid-base abnormalities will alter the ionized concentration of Ca2+ by changing the fraction of Ca2+ bound to ____.

Answer 11

albumin

Question 12

Acidemia ____ free ionized Ca2+ concentration because ___ Ca2+ is bound to albumin.

Answer 12

increases; less

Question 13

Alkalemia _____ free ionized Ca2+ concentration because ___ Ca2+ is bound to albumin.

Answer 13

decreases; more

Question 14

Alkalemia is often accompanied by _____.

Answer 14

hypocalcemia

Question 15

Extracellular concentration of Pi is ___ related to that of Ca2+.

Answer 15

inversely

Question 16

The chief cells of the parathyroid glands synthesize and secrete ___.

Answer 16

PTH

Question 17

PTH is stimulated to be secreted when there are ___ levels of plasma Ca2+.

Answer 17

low

Question 18

High extracellular Ca2+ concentration ____ PTH synthesis and secretion.

Answer 18

inhibits

Question 19

Chronic hypercalcemia causes ___ synthesis and storage of PTH, ___ breakdown of stored PTH, and release of inactive PTH fragments into circulation.

Answer 19

decreased; increased

Question 20

Chronic hypocalcemia causes ___ synthesis and storage of PTH and hyperplasia of parathyroid glands (secondary hyperparathyroidism).

Answer 20

increased

Question 21

Severe hypomagnesemia (ie alcoholism) ____ PTH synthesis, storage, and secretion.

Answer 21

inhibits

Question 22

PTH acts as a ___.

Answer 22

GPCR

Question 23

Decreased plasma Ca2+ concentration leads to ___ PTH secretion. This leads to ___ bone resorption; ___ Pi reabsorption, ___ Ca2+ reabsorption, and ___ urinary cAMP by the kidneys; and ___ Ca2+ absorption (indirect via VitD) by the intestine.

Answer 23

increased; increased; decreased; increased; increased; increased

Question 24

____ __ promotes mineralization of new bone through its coordinated actions in the regulation of both Ca2+ and Pi plasma concentrations.

Answer 24

Vitamin D

Question 25

Vitamin D ___ both Ca2+ and Pi plasma concentrations.

Answer 25

increases

Question 26

PTH receptors are located on ____.

Answer 26

osteoblasts

Question 27

Short-term actions of PTH include bone ____ via direct action on osteoblasts.

Answer 27

formation

Question 28

Long-term actions of PTH include increased bone ___ via indirect action of osteoclasts mediated by cytokines released from osteoblasts.

Answer 28

resorption

Question 29

Vitamin D acts synergistically with PTH to stimulate ____ activity and bone ____.

Answer 29

osteoclast; resorption

Question 30

____ induces stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts, and finally, mature, multinucleated osteoclasts.

Answer 30

M-CSF

Question 31

____ is a cell surface protein produced by osteoblasts, bone lining cells, and apoptotic osteocytes. This is the primary mediator of osteoclast formation.

Answer 31

RANKL

Question 32

____ is a cell surface protein receptor on osteoclasts and osteoclast progenitors.

Answer 32

RANK

Question 33

___ is a soluble protein produced by osteoblasts, is a decoy receptor for RANKL, and inhibits RANKL/RANK interaction.

Answer 33

OPG (osteoprotegerin)

Question 34

PTH ___ RANKL and ___ OPG.

Answer 34

increases; decreases

Question 35

Vitamin D ___ RANKL.

Answer 35

increases

Question 36

Inhibition of Na+-P transporter by PTH causes ____.

Answer 36

phosphaturia

Question 37

___ in PTH causes urinary cAMP.

Answer 37

increase

Question 38

PTH ____ 1-alpha-hydroxylase activity in the kidney.

Answer 38

stimulates

Question 39

PTH stimulates osteoblastic ___ and ___.

Answer 39

growth; survival

Question 40

Sustained elevated levels of PTH shift the balance to a relative increase in osteoclast activity, thereby ___ bone turnover and ____ bone density.

Answer 40

increasing; reducing

Question 41

PTH stimulates Ca2+ ____ in the kidney.

Answer 41

reabsorption

Question 42

Vitamin D ___ Ca2+ and Pi absorption in the small intestine.

Answer 42

increases

Question 43

Vitamin D sensitizes osteoblasts to ___ in the bone.

Answer 43

PTH

Question 44

____ regulates osteoid production and calcification.

Answer 44

Vitamin D

Question 45

Vitamin D promotes Pi _____ by proximal nephrons in the kidney.

Answer 45

reabsorption

Question 46

Vitamin D has ____ actions on Ca2+ in the kidney.

Answer 46

minimal

Question 47

Vitamin D directly ___ PTH gene expression in the parathyroid gland.

Answer 47

inhibits

Question 48

Vitamin D directly ___ CaSR gene expression in the thyroid gland.

Answer 48

stimulates

Question 49

____ is a G-protein coupled receptor which senses extracellular levels of calcium ion.

Answer 49

CaSR

Question 50

____ decreases blood Ca2+ and Pi concentrations by inhibiting bone resorption.

Answer 50

Calcitonin

Question 51

Calcitonin receptors are expressed on ___.

Answer 51

osteoclasts

Question 52

____ plasma Ca2+ concentration stimulates calcitonin to be released.

Answer 52

Increased

Question 53

Calcitonin ___ have a role in chronic regulation of plasma Ca2+ concentration.

Answer 53

doesn't

Question 54

_____ stimulates intestinal Ca2+ absorption and renal tubular Ca2+ reabsorption.

Answer 54

Estradiol-17-beta

Question 55

Estrogen promotes ____ of osteoblasts and ____ of osteoclasts, favoring bone ____ over ____.

Answer 55

survival; apoptosis; formation; resorption

Question 56

Adrenal glucocorticoids (ie cortisol) ____ bone resorption and renal Ca2+ wasting, and ____ intestinal Ca2+ absorption.

Answer 56

promote; inhibit

Question 57

Primary hyperparathyroidism has ___ PTH, ___ Ca2+, ___ Pi, and ___ VitD.

Answer 57

high; high; low; high

Question 58

____ hyperparathyroidism causes high PTH levels secondary to low Ca2+ concentration in blood.

Answer 58

Secondary

Question 59

Secondary hyperparathyroidism caused by renal failure has ___ PTH, ___ Ca2+, ___ Pi, and ___ VitD.

Answer 59

high; low; high; low

Question 60

Secondary hyperparathyroidism caused by VitD deficiency has ___ PTH, ___ Ca2+, ___ Pi, and ___ VitD.

Answer 60

high; low; low; low

Question 61

___ presents with symptoms of low Ca2+ and is treated with oral Ca2+ supplement and an active form of VitD.

Answer 61

Hypoparathyroidism

Question 62

Hypoparathyroidism has ___ PTH, ___ Ca2+, ___ Pi, and ___ VitD.

Answer 62

low; low; high; low

Question 63

Albright hereditary osteodystrophy (pseudohypoparathyroidism type 1a) has ___ PTH, ___ Ca2+, ___ Pi, and ___ VitD.

Answer 63

high; low; high; low

Question 64

Pseudohypoparathyroidism type 1a has high PTH levels. Administration of exogenous PTH produces __ phosphaturic response and __ increase in urinary cAMP.

Answer 64

no; no

Question 65

Patients with _____ ___ ___ present with short stature, short neck, obesity, subQ calcification, and shortened metatarsals and metacarpals.

Answer 65

Pseudohypoparathyroidism type 1a

Question 66

Humoral hypercalcemia of malignancy has __ PTH, __ Ca2+, __ Pi, and __ VitD.

Answer 66

low; high; low; low

Question 67

Familial hypocalciuric hypercalcemia (FHH) has ___ PTH, ___ serum Ca2+, ___ urine Ca2+, ___ Pi, and ___ VitD.

Answer 67

normal/high; high; low; normal; normal

Question 68

___ is causes by mutations that inactivate CaSR in parathyroid glands and parallel Ca2+ receptors in the ascending limb of the kidney. This results in hypocalciuria and hypercalcemia.

Answer 68

FHH

Question 69

____ is caused by impaired vitamin D metabolism.

Answer 69

Rickets-Osteomalacia

Question 70

Vitamin D-dependent rickets type 1 is caused by low _____.

Answer 70

1-alpha-hydroxylase

Question 71

Vitamin D-dependent rickets type 2 is caused by low ____.

Answer 71

vitamin D receptor

Question 72

____ ____ can originate from either a GI disorder, suboptimal nutrition, or inadequate sun exposure.

Answer 72

Nutritional osteomalacia

Question 73

Vitamin D deficiency presents with ___ PTH, ___ serum Ca2+, ___ serum Pi, ___ urine Pi, ___ urine cAMP, and ___ vitamin D.

Answer 73

high (secondary); normal/low; low; high; high; very low