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NE3 > Regulation of Calcium and Phosphate Metabolism > Flashcards

Regulation of Calcium and Phosphate Metabolism Flashcards

1
Q

Where is most calcium stored?

A

In bones and teeth

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2
Q

The extracellular calcium concentration has a dramatic effect on the ? of cells

A

Excitability (particularly nerve fibers)

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3
Q

What are symptoms of hypocalcemia?

A

Hyperreflexia, spontaneous twitching, muscle cramps, tingling, numbness

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4
Q

What is Chvostek sign?

A

Twitching of facial muscles elicited by tapping on facial nerve when patient is hypocalcemic

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5
Q

What is Trousseau sign?

A

Carpopedal spasm upon inflation of BP cuff

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6
Q

What are symptoms of hypercalcemia?

A

Decreased QT interval, constipation, decreased appetite, polyuria (excess dilute urine), polydipsia (thirst), muscles weakness, hyporeflexia, lethargy, coma

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7
Q

What causes hypocalcemic tetany?

A

Hypocalcemia reduces activation threshold for Na+ channels = increased membrane excitability = easier to evoke APs (aka spontaneous APs occur)

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8
Q

How do acidemia and alkalemia alter ionized Ca2+ concentration?

A

Acidemia = more H+ bound to albumin (-) so less Ca2+ bound = more free Ca2+
Alkalemia - more Ca2+ bound to albumin (-), decreased free Ca2+ concentration (usually accompanied by hypocalcemia)

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9
Q

To maintain Ca2+ balance, kidneys must excrete ___ Ca2+ that is absorbed by the GI tract

A

The same amount

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10
Q

What is the relationship between Ca2+ and phosphate?

A

Inverse relationship

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11
Q

Extracellular [Pi] is regulated by?

A

The same hormones that regulate [Ca2+]

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12
Q

What is the normal range of extracellular Pi?

A

2.5-4.5 mg/dL

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13
Q

Where is most Pi located?

A

Bone (85%) and ICF (15%). <1% in plasma

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14
Q

Explain the regulation of PTH gene expression and secretion

A

High levels of Ca2+ bind to calcium sensing receptors (CaSR) which are Gi GPCRs in parathyroid cell membranes. The downstream effects of these GPCRs = inhibition of PTH gene in parathyroid cells and inhibition of PTH secretion

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15
Q

What does chronic hypercalcemia cause?

A

Decreased synthesis/storage of PTH (chief cells) and increased breakdown of stored PTH

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16
Q

What does chronic hypocalcemia cause?

A

Increased synthesis/storage of PTH and hyperplasia of parathyroid glands (secondary hyperparathyroidism)

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17
Q

What does hypomagnesemia cause?

A

Inhibition of PTH synthesis, storage, and secretion

seen in…. you guessed it….ALCOHOLISM (aka: what med school is slowly driving us to)

18
Q

The PTH in humans can be pretty long, how much of a molecule is actually involved in it’s activity?

A

the first 34 amino acids

-apparently the rest is just for shits and gigs

19
Q

What are some of the main actions PTH likes to do when plasma [Ca2+] is low?

A
  • Increase bone resorption (bone)
  • Decrease Pi reabsorption, Increase Ca2+ reabsorption, and increase urinary cAMP (kidney)
  • Increase Ca2+ absorption indirectly via vitamin D…1,25-dihydroxycholecalciferol (Intestine)

all just to increase the [Ca2+] in plasma
(more than Natalie will ever do for me) ):

20
Q

How good is Vitamin D?

A

Good enough to raise both Ca2+ and Pi plasma concentrations—> which promotes mineralization of new bone

Is regulated by Neg feedback (aka: “dr. that’s too rough”)

21
Q

What is the main form of vit D in circulation?

and what is the active form?

A

25-OH-cholecalciferol = main circulating, low activity

1,25-(OH)2-cholecalciferol (active)
–converted by the 1alpha-hyroxylase (CYP1a) enzyme in proximal renal tubule

22
Q

What are the short and long-term effects of PTH on bone?

A

Short term: Bone formation (direct osteoblast action)- basis for osteoporosis treatment (synthetic PTH administration)

Long-term: Increased bone resorption (via indirect action of osteoblast cytokines on osteoclasts)

23
Q

What is M-CSF role in bone formation/resorption?

A

induces stem cells–>osteoclast precursors….all the way to matured osteoclasts

24
Q

What are RANKL’s roles?

A

RANKL: (receptor activator for NF-kappaB)

  • produced by osteoblasts
  • primary mediator of osteoclast formation
  • binds to RANK receptor on osteoclast precursors
25
Q

What is the role of OPG (osteoprotegerin)?

A

Released by osteoblasts: plays as decoy receptor for the RANKL to inhibit the interaction btw RANKL and RANK for osteoclast maturation

26
Q

What are the actions of PTH and Vit D on bone resorption and formation?

A

PTH: increases RANKL decreases OPG (increased osteoclast formation = bone resorption)
Vit D: increases RANKL

27
Q

What is the mechanism of action of PTH on the kidney?

A

Inhibits Na+/Pi transporter to decrease reabsorption of Pi and increase Pi excretion in urine
(also acts on distal tubule to increase Ca2+ reabsorption

28
Q

How does vitamin D act in the intestine to increase Ca2+ absorption?

A

Vitamin D stimulates synthesis of calcium transporters (like TRPV6) and calbindin protein (buffer) to move Ca2+ from intestinal lumen into the blood

29
Q

How does vitamin D act in the intestine to increase Pi uptake?

A

Activates Na+/Pi transporter

30
Q

What are the actions of calcitonin?

A

Decreases blood Ca2+ and Pi concentrations by inhibiting bone resorption (decreases activity/number of osteoclasts)

31
Q

What effect does estradiol-17B have in terms of Ca2+?

A

Stimulates intestinal calcium absorption and renal tubular calcium reabsorption

Form of estrogen: women don’t want to be big boned, but estrogen says screw it and makes damn sure bones are being formed properly (by promoting osteoblast survival and the apoptosis of osteoclasts)

32
Q

What does estrogen do to osteoblasts and osteoclasts?

A

Promotes survival of osteoblasts and apoptosis of osteoclasts for bone formation

33
Q

What effects do adrenal glucocorticoids have on bone?

A

Promote bone resorption and renal calcium wasting, inhibit intestinal calcium absorption

34
Q

What is primary hyperparathyroidism?

A

Adenoma of parathyroid gland secretes elevated PTH = stones, bones, groans
Stones - hypercalciuria (excessive excretion of calcium)
Bones - increased calcium resorption
Groans - constipation (decreased gut motility)

35
Q

What is secondary hyperparathyroidism?

A

Low calcium in blood (due to renal failure or vit D deficiency) causes increase in PTH levels

  • high Pi in renal failure due to retention
  • low Pi in vit D deficiency due to excretion
36
Q

What is hypoparathyroidism?

A

Low PTH secretion due to thyroid/parathyroid surgery, autoimmune, or congenital causes. Symptoms similar to those of hypocalcemia.
-high Pi due to decreased secretion in kidney

37
Q

What is Albright hereditary osteodystrophy?

A

Pseudohypoparathyroidism type 1a
-inherited, no activation of adenylyl cyclase when PTH binds PTH receptor. Hypocalcemia and hyperphosphatemia develop, high PTH levels.

38
Q

What is humoral hypercalcemia of malignancy?

A

PTH-related peptide (PTHrp) produced by tumor, binds and activates PTH receptor. Low PTH levels coming from parathyroid gland. Causes hypercalcemia and hypophosphatemia

39
Q

What is familial hypocalciuric hypercalcemia (FHH)?

A

Mutation in CaSR in parathyroid cells = decreased calcium excretion and increased serum calcium

40
Q

What can impaired vitamin D metabolism cause?

A

Rickets (children) and osteomalacia (adults)

41
Q

What is the difference in causes between vitamin D-dependent rickets type I and II?

A

I - decrease in 1alpha-hydroxylase

II - decrease in vitamin D receptor

42
Q

What is osteomalacia caused by?

A

GI disorder (gastric bypass, Crohn’s, etc) or suboptimal nutrition and inadequate sun exposure

NE3 (17 decks)

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