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NE (Neuroendocrine) Exam 3 > Lecture 50: Calcium and Phosphate Homeostasis > Flashcards

Lecture 50: Calcium and Phosphate Homeostasis Flashcards

1
Q

Distribution of Calcium in the Body

A
  • 99% of calcium found in Bones and Teeth
  • free, ionized Calcium is the biologically active form
  • 50% is ionized, 40% is protein bound, 10% to anions
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2
Q

Calcium Homeostasis and aging

A
  • aging = dec. in amount of calcium absorbed from dietary intake
  • existing bone cells are Reabsorbed faster than new bone can be made = osteopenia/osteoporosis
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3
Q

Hypocalcemia characteristics

A
  • dec. plasma calcium concentration
  • hyperreflexia, spontaneous twitch, tingling/numbness
  • reduce activation threshold = easier AP generation

Chovstek sign: facial muscles via tap on facial nerve
Trousseau sign: carpopedal spasm w/blood pressure cuff inflation

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4
Q

Hypercalcemia characteristics

A
  • inc. plasma calcium concentration
  • inc. activation threshold = harder AP generation (dec. membrane excitability)
  • dec. QT interval, constipation, no appetite, muscle weakness, hyporeflexia, lethargy, coma
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5
Q

Changes in Calcium Concentration

  1. Change Plasma Protein Concentration
  2. Change Anion Concentration
  3. Acid-Base Abnormalities
A
  1. move in same direction (inc. plasma protein = inc. total calcium concentration; no ionized calcium conc. change)
  2. change calcium complexed w/anions (inc. phosphate = dec. ionized calcium)
  3. alter ionized concentration by changing fraction of calcium bound to albumin
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6
Q

Acidemia vs Alkalemia

A

Acidemia = inc. ionized calcium

  • LESS calcium bound to albumin
  • more hydrogen bound to albumin

Alkalemia = dec. ionized calcium

  • MORE calcium bound to albumin
  • less hydrogen bound to albumin
  • accompanied by hypocalcemia
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7
Q

Relationship of Calcium and Phosphate

A
  • extracellular Phosphate concentration INVERSELY related to Calcium
  • extracellular Phosphate concentrations regulated by SAME HORMONES that regulate Calcium concentration
  • 85% of Phosphate found in bone (84% of plasma conc. (< 1%) is ionized, 10% protein bound)
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8
Q

Where does PTH (Parathyroid Hormone) come from? What are PTH’s characteristics?

A
  • Chief cells of the parathyroid gland synthesize and secrete
  • peptide hormone (1-34 AA molecules are biologically active (near N terminal) of the 84 total) –> packaged in secretory granules
  • regulates plasma calcium concentration (low Ca conc. STIMULATES inc. PTH synthesis and secretion)
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9
Q

Chronic Hypercalcemia vs Chronic Hypocalcemia

A

Hyper: dec. synth/storage of PTH, inc. PTH breakdown

Hypo: inc. synth/storage of PTH, hyperplasia of parathyroid glands (secondary hyperparathyroidism)

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10
Q

Severe Hypomagnesemia

A
  • chronic Magnesium depletion (Alcoholism)

- inhibition of PTH synthesis, storage, and secretion

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11
Q

Vitamin D characteristics

A
  • inc. both Ca and Phosphate plasma concentrations
  • inc. Ca x P product = mineralization of new bone
  • must be successfully hydroxylated to be an active metabolite
  • STEROID HORMONE –> receptors are in nucleus
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12
Q

Vitamin D Synthesis

A
  1. Cholecalciferol from Diet and UV light
    • liver (25-hydroxylase) converts to 25-OH-cholecal.
    • main circulatory form, low activity
  2. Transported to Kidney
    • 1a-hydroxylase = 1,25 dihydroxycholcalciferol
    • 24-hydrozylase = 24,25 dihydroxycholcalciferol
  3. Active Vitamin D stimulated by low Ca/Pi conc. and high PTH conc.
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13
Q

Regulation of 1a-Hydroxylase

A

(+) = increased PTH –> CYP1a gene

(-) = increased Ca, 1,25 dihydroxycholecalciferol

  • 1,25 activates CYP24 gene = 24-hydroxylase
  • makes more 24,25 (INACTIVE form of Vitamin D)
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14
Q

PTH and Osteoblasts/Osteoclasts

A
  • PTH receptors on Osteoblasts ONLY (no osteoclasts)

Short Term: bone formation –> inc. calcium/phosphate from osteoblast to form bone

Long Term: inc. bone resorption (mediated by cytokines released from osteoblasts)

  • Vitamin D works synergistically to stimulate osteoclast activity and bone resorption
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15
Q

Osteoclast Formation

A
  • PTH and Vitamin D act on Osteoblasts, which release M-CSF (stem cells), RANKL and IL-6 (bind to osteoclast precursors)
  • becomes preosteoclast, then differentiates into a mature osteoclast (multinucleated) = BONE RESORPTION
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16
Q

RANKL, RANK, and OPG on Osteoclast formation

A

RANKL: from osteoblast, prime mediator of osteoclast formation

RANK: receptor on osteoclasts/osteoclast precursors

OPG (osteoprotegerin): osteoblast produced, decoy RANKL receptor = inhibit RANKL/RANK interaction

17
Q

PTH action on Kidney (2 –> calcium and phosphate)

A
  • activates GCPR –> activates Adenyl Cyclase –> gen. cAMP –> protein kinase (Proximal Nephrons)
  • protein kinase phosphorylates Sodium/Phosphate Symporter = phosphaturia (inc. excretion of phosphate in urine)
  • stim Calcium reabsorption (Thick Ascending Henle’s Loop Limb and Distal Convoluted Tubule)
18
Q

Vitamin D action on Kidney (phosphate)

A
  • promotes phosphate reabsorption by proximal nephrons

- stimulates NPT2a expression (Sodium/Phosphate Transporter)

19
Q

Vitamin D action on Kidney (calcium) –> protein synthesis

A
  • TRPV6 allows calcium into intestinal epithelial cells (Transcellular)
  • Calbindin binds incoming calcium and takes to transporters that will shuttle them to interstitial space
  • Calbindin acts as a buffer to help keep Calcium Conc. gradient normal
20
Q

Calcitonin Actions

A
  • released from Thyroid Gland; acts on bones/kidneys (dec. blood calcium/phosphate lvls) –> inhibit bone resorption
  • receptors on osteoclasts (dec. activity and number)
  • stimulus = inc. plasma calcium (no effect on chronic regulation of plasma calcium)
21
Q

Estradiol and Adrenal Glucocorticoid effects on Calcium metabolism

A

Estradiol-17B - intestinal calcium absorption/renal tubular calcium reabsorption

  • potent regulator of osteoblast/osteoclast function
  • favors bone formation (osteoclast apoptosis)

Cortisol - bone resorption, renal calcium wasting/inhibit intestinal calcium absorption
- patients treated w/high lvls = OSTEOPOROSIS

22
Q

Primary Hyperparathyroidism

A
  • “stones, bones, and groans” –> ADENOMA
  • inc. lvls of PTH, Calcium, Vitamin D/dec. lvls phosphate
  • hypercalciuria (stones), inc. bone resorption (bones), constipation (groans)
  • Hypercalcemia/Hypophosphatemia
23
Q

Secondary Hyperparathyroidism

A
  • inc. PTH SECONDARY to low blood calcium
  • Renal Failure (high PTH/Phosphate & low Ca/Vit D)
  • Vit D Deficient (high PTH & low Ca/Vit D/Phosphate)
24
Q

Hypoparathyroidism

A
  • most symptoms associated with dec. Calcium conc.
  • decreased PTH production, decreased Phosphate excretion = Hypocalcemia/Hyperphosphatemia
  • dec. PTH/Ca/Vit D & inc. Phosphate
25
Q

Albright Hereditary Osteodystrophy (Pseudohypoparathyroidism type 1a)

A
  • Gs for PTH receptor in bone/kidney defective
  • hypocalcemia/hyperphosphatemia develop
  • inc. lvls of PTH
  • short stature/neck, obesity, calcification, short metatarsals and metacarpals
26
Q

Humoral Hypercalcemia of Malignancy

A
  • PTH-related peptide (PTHrP) from tumors bind and activate same receptor as PTH
  • similar profile to primary hyperthyroidism (hypercalcemia, hypophosphatemia)
  • has low PTH lvls
27
Q

Familial Hypocalciuric Hypercalcemia (FHH)

A
  • mutation inactivates CaSR in parathyroid glands and parallel calcium receptors in ascending limb of kidney
  • hypocalciuria and hypercalcemia
  • inc/normal PTH, inc. serum Ca, dec. urine Ca, normal phosphate/Vit D
28
Q

Rickets Type 1 vs Rickets Type 2

A
  • insufficient amount of calcium/phosphate to mineralize growing bone (growth failure/skeletal deformities)

Type 1: dec. 1a-hydroxylase
Type 2: dec. vitamin D receptor

29
Q

Osteomalacia

A
  • new bone fails to mineralize (bending/softening of weight-bearing bones)
  • gastrointestinal disorder or suboptimal nutrition/inadequate sun exposure
  • muscle spasms, cramps, (+) Chvostek’s, tingling/numbness, fracture, bone tenderness/pain

NE (Neuroendocrine) Exam 3 (16 decks)

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