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Neuro Exam 3 > Lecture 13: Regulation of Calcium and Phosphate Metabolism > Flashcards

Lecture 13: Regulation of Calcium and Phosphate Metabolism Flashcards

1
Q

Where is calcium stored?

A

Bones and Teeth

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2
Q

What is the biologically active form of calcium?

A

Free, ionized Ca2+

About 50% of calcium in body

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3
Q

What are symptoms of hypocalcemia

A
  • Hyperreflexia
  • Spontaneous twitching
  • Muscle cramps
  • Numbness and tingling
  • Tetany
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4
Q

What is Chvostek sign?

A

Twitching of the facial muscles elicited by tapping on facial nerve

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5
Q

What are two indicators of hypocalcemia?

A

Chvostek sign

Trousseau sign: Carpopedal spasm upon inflation of blood pressure cuff

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6
Q

What are symptoms of hypercalcemia?

A
  • Decreased QT interval
  • Constipation
  • Lack of appetite
  • Polyuria
  • Polydipsia
  • Muscle weakness
  • Hyporeflexia
  • Lethargy
  • Coma
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7
Q

How does hypocalcemia affect membrane excitability?

Low extracellular calcium

A
  • Reduces activation threshold for Na+ channels
    • Easier to evoke action potentials
  • Increased membrane excitability
    • Spontaneous action potentials
    • Hypocalcemic tetany (spontaneous muscle contractions)
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8
Q

How does hypercalcemia affect membrane excitability?

High extracellular calcium

A
  • Increases activation threshold for Na+ channels
    • Harder to evoke action potentials
  • Decreased membrane excitability
    • Less action potentials
    • Nervous system depressed and reflex responses are slowed
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9
Q

How can calcium concentration be altered?

A
  • Changes in plasma protein concentration
    • Increase in plasma protein means increase in total Ca2+ concentration and vice versa
    • No change in Ca2+ ionized (protein changes are usually more chronic issues)
  • Changing anion concentration
    • Increase in Pi concentration will decrease Ca2+ ionized concentration
  • Acid-Base Abnormalities
    • Alters ionized concentration by changing the fraction of Ca2+ bound to albumin
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10
Q

What happens to calcium levels in acidemia?

A
  • Increase in free ionized Ca2+ since less calcium is bound to albumin
  • Instead, H+ is taking up Ca2+ binding spots
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11
Q

What happens to calcium levels in alkalemia?

A
  • Decrease in free ionized Ca2+ because more is bound to albumin
  • Less H+ bound to albumin
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12
Q

What three organs are important in maintaining Ca2+ homeostasis?

A
  • Bone
  • Kidney
  • Intestine
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13
Q

What three hormones are important in maintainin Ca2+ homeostasis?

A
  • PTH
  • Vitamin D
  • Calcitonin
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14
Q

What is the role of the kidneys to maintain calcium homeostasis?

A

Kidneys must excrete same amount of calcium absorbed by GI tract?

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15
Q

What is the relationship between calcium and phosphate concentration in the ECF?

A
  • Inversely proportional to one another
    • High Ca2+ means low Pi
  • Both are regulated by the same hormones
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16
Q

What is the normal range for phoshate?

How is phoshpate distributed?

A
  • 2.5-4.5 mg/dL
  • Distribution of phosphate:
    • 84% ionized
    • 15% ICF
    • 1% plasma
      • mostly ionized
      • some protein bound
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17
Q

What secretes PTH?

What stimulates the secretion of PTH?

A

Chiefe cells of parathyroid gland

Low calcium levels

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18
Q

How is PTH regulated?

A
  • CaSR sense increasing calcium plasma levels
    • Gq and Gi send inhibitory signals to PTH gene
  • 1,25 Vitamin D also inhibits PTH gene
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19
Q

How does chronic hypercalcemia affect the regulation of PTH gene expression and secretion?

A
  • Decrease synthesis and storage of PTH
  • Breakdown of stored PTH
  • Inactive PTH is released
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20
Q

How does chronic hypocalcemia affect the regulation of PTH gene expression and secretion?

A

Increased synthesis and storage of PTH

  • Hyperplasia of parathyroid glands

=2nd hyperparathyroidism

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21
Q

How does magnesium affect the regulation of PTH gene expression and secretion?

A

Severe hypomangesium can inhibit PTH synthesis, storage, and secretion

Maybe from alcoholism

22
Q

PTH acts on the bone and kidney tubule via which type of receptor?

A
  • GPCR (Gs)
  • Increased cAMP
    • Pathological increases in activity of PTH will show concomitant increase in urinary cAMP
23
Q

How does PTH act on the bone, kidney, and intestine?

A
  • Bone: Increased bone resorption
  • Kidney:
    • Increased reabsorption of Ca2+
    • Increased excretion cAMP and Pi in the urine
  • Intestine: Indirectly increases absorption of Ca2+ via Vitamin D
24
Q

What is the function of Vitamin D?

A
  • Increases both Ca2+ and Pi plasma concentrations
  • Promotes mineralization of new bone
25
Q

What enzyme converts 25-OH-cholecalciferol to its active form of 1,25 dihydroxycholecalciferol?

Where is this enzyme located?

What stimulates this enzyme?

A
  • Enzyme: 1 α-hydroxylase
  • Location: Proximal tubule of the kidney
  • Stimulus: Low calcium and phosphate levels & high PTH
26
Q

How is 1 α-hydoxylase regulated?

A
  • Inhibits:
    • Calcium
    • 1,25 dihydroxycholecalciferol
  • Promotes:
    • PTH
27
Q

Where are PTH receptors located in bones?

What are its actions?

A
  • PTH receptors are located on osteoblasts
  • Short term: PTH promotes bone formation
  • Long term: Increase bone resorption (indirectly through the release of cytokines from osteoblasts acting on osteoclasts)
28
Q

What are the steps of the bone resorption?

A
  1. PTH & Vit D stimulates osteoblasts
  2. Osteoblasts release M-CSF, RANKL & IL-6
    1. M-CSF stimulate Stem cells form into osteoclast precursors
    2. RANKL bind RANK & IL-6 bings IL-6R stimulate osteoclast precursor
  3. precursor –> mononuclear osteoclasts
  4. Mononuclear –> multinucleated
  5. Multinucleated –> bone resorption
29
Q

What is the function of M-CSF?

A

Induces stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts, and mature multinucleated osteoclasts

30
Q

What is the function of RANKL?

A
  • Receptor for NF-kB ligand
  • Cell surface protein produced by osteoblasts, bone lining cells, and apoptotic osteocytes
  • Primary mediator of osteoclast formation
31
Q

What is the function of RANK?

A
  • Cell surface protein receptor on osteoclasts and osteoclast precursors
32
Q

What is the function of OPG?

A
  • Produced by osteoblasts
  • Decoy receptor for RANKL
  • Inhibits RANKL/RANK interaction
33
Q

How does PTH work on the agents in bone formation/reabsorption?

A
  • Increase RANKL
  • Decrease OPG
34
Q

How does vitamin D work on the agents in bone formation/reabsorption?

A
  • Increase RANKL
35
Q

How does PTH work on the kidney?

A
  • PTH binds GPCR on basolateral surface of cell in proximal tubule of kidney
  • Activates Gs and cAMP/PKA
  • PKA phosphorylates Na+/Pi cotransporter on apical surface, preventing Pi reabsorption
  • cAMP is excreted w/ Pi
36
Q

How does Vitamin D promote Ca2+ absorption in the intestine?

A
  • Increases transcription of :
    • Ca2+ transporter (TRPV6) on apical membrane
    • Ca2+/3 Na+ exchanger on basolateral membrane
    • Calbindin
37
Q

What are the actions of calcitonin?

A
  • Responds to increase in blood Ca2+
  • Decreases blood Ca2+ and Pi by inhibiting bone resorption
    • Calcitonin receptors on osteoclasts
  • Decrease activity and number of osteoclasts
  • No role in chronic regulation of plasma Ca2+
38
Q

How do thyroidectomies and thyroid tumors affect regulation of calcitonin?

A
  • Affect calcitonin levels but have no effect on Ca2+ metabolism
    • Thyroidectomy: reduce calcitonin
    • Thyroid tumors: increase calcitonin
39
Q

What is the function of estradiol-17B?

A
  • Stimulates intestinal Ca2+ absorption and renal tubular Ca2+ absorption
  • Promotes survival of osteoblasts and apoptosis of osteoclasts
    • Favors bone formation over resorption
40
Q

How do adrenal glucocorticoids (e.g. cortisol) affect bones?

A
  • Promotes bone resorption
  • Promotes renal Ca2+ wasting
  • Inhbits Ca2+ absorption in the SI

Chronic use of glucorticoids can lead to osteoporosis

41
Q

What is seen in patients with primary hyperparathyroidism?

A

Blood levels:

  • PTH levels increase
  • Ca2+ levels increase
  • Pi levels decrease
  • Vitamin D levels increase

Symptoms: Stones, Bones, and Groans

  • Hypercalciuria (stones)
  • Increased bone resorption (bones)
  • Constipation (groans)

Treatment: Parathyroidectomy

42
Q

What is seen in patients with secondary hyperparathyroidism?

A
  • Increase in PTH levels secondary to low blood Ca2+
  • Low blood Ca2+ causes:
    • Renal failure
    • Vitamin D deficiency
  • Blood Levels:
    • PTH increased
    • Low Ca2+
    • Low Vitamin D
43
Q

How does renal failure differ from Vitamin D deficieny?

A
  • Renal failure: Pi increases
  • Vitamin D: Pi decreases
44
Q

What causes hypoparathyroidism?

What is a treatment?

A

Causes

  • Thyroid/parathyroid surgery
  • Autoimmune or congenital disorder

Treatment

  • Oral Ca2+ supplement and active form of Vitamin D
45
Q

What do you see with patients that have hypoparathyroidism?

A

Symptoms

  • Muscle spasm or cramping
  • Numbness/tingling or burning around mouth and fingers
  • Seizures
  • Kids: poor teeth development and mental deficiences

Blood Levels:

  • Decreased PTH
  • Decreased Ca2+
  • Increased Pi
  • Decreased Vitamin D
46
Q

What is Albright hereditary osteodystrophy (Pseudohypoparathyroidism type 1a)?

What symptoms do you see?

A
  • Autosomal dominant disorder
    • Gs for PTH in bone and kidney is defective
  • Hypocalcemia and hyperphosphatemia develop
    • Increase in PTH levels
  • Symptoms
    • Short stature and short neck
    • Obesity
    • Subcutaneous calcification
    • Shortened metatarsals and metacarpals
  • Levels:
    • ​PTH increased
    • Ca2+ decreased
    • Pi increased
    • Vitamin D decreased
47
Q

What is humoral hypercalcemia of malignancy?

A
  1. PTHrP produced by tumor cells
  2. Binds and activates the same receptor as PTH
  3. Decreased PTH levels
  4. Decreased Vitamin D
  5. Increased urinary Ca2+
  6. Increased urinary Pi and cAMP
  7. Increased blood Ca2+
  8. Decreased blood Pi
48
Q

What is familial hypocalciuric hypecalcemia (FHH)?

A
  • Autosomal dominant disorder
    • Mutations that inactivate CaSR in parathyroid glands and parallel Ca2+ receptors in ascending limb of the kidney
  • PTH levels are normal or increased
  • Serum Ca2+ elevated
  • Urine Ca2+ low
  • Pi normal
  • Vitamin D normal
49
Q

What is the physiology behind rickets and osteomalacia?

A
  • Impaired Vitamin D metabolism
  • GI disorders
  • Chronic renal failure
  • Pi depletion
50
Q

What is seen with patients who have rickets?

A
  • Insufficient amount of calcium and phosphate to mineralize growing bone
  • Characterized by growth failure and skeletal deformities
  • Blood Levels
    • Increased PTH
    • Normal or decreased Ca2+
    • Decreased Pi
    • Increased phosphate and cAMP in urine
    • Decreased Vitamind D
51
Q

What is osteomalacia?

A
  • New bones fail to mineralize
  • Bending and softening of weight bearing bones
52
Q

What is the treatment for osteoporosis?

A
  • Anabolic Therapy
    • PTH
  • Antiresorptive therapy
    • Bisphosphates
    • Estrogen
    • Selective estrogen receptor modulators (SERMS: Raloxifene, Tamoxifen)
    • Calcitonin
    • RANKL inhibitors (Denosumab)

Neuro Exam 3 (16 decks)

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