Calcium & Phosphorous Homeostasis Flashcards by Kyra Porter

calcium - roles

*myocardial & smooth muscle contraction
*blood coagulation
*intracellular messaging
*structural

How well did you know this?

Not at all

Perfectly

phosphate - roles

*energy production
*protein production
*skeletal/structural

How well did you know this?

Not at all

Perfectly

calcium distribution

99% in bone
1% intracellular
0.10% extracellular

How well did you know this?

Not at all

Perfectly

renal calcium reabsorption

1) proximal tubule: calcium reabsorption is passive, linked to sodium reabsorption
2) sodium absorbed in thick ascending loop of henle by furosemide-sensitive NKCC transporter with backleak of K+ → leads to increased paracellular calcium reabsorption
3) DCT: transcellular calcium reabsorption in the presence of PTH and calcitriol

How well did you know this?

Not at all

Perfectly

effects of thiazide diuretics on calcium

*cause sodium-wasting distally that is compensated for by proximal sodium uptake
*leads to INCREASED CALCIUM REABSORPTION and HYPOCALCIURIA (decreased calcium excretion), and rarely hypercalcemia

How well did you know this?

Not at all

Perfectly

effects of furosemide (loop diuretics) on calcium

*Loops LOSE calcium
*block the NKCC transporter & results in loss of electrochemical gradient
*results in DECREASED CALCIUM REABSORPTION and HYPERCALCIURIA (increased excretion of calcium); hypocalcemia

How well did you know this?

Not at all

Perfectly

furosemide (loop diuretics) - effects on urine calcium and serum calcium

*urine calcium: INCREASED
*serum calcium: decreased
*used to be used as a treatment for hypercalcemia (i.e. lowers serum calcium)

How well did you know this?

Not at all

Perfectly

thiazide diuretics - effects on urine calcium and serum calcium

*serum calcium: increased
*urine calcium: decreased
*may cause hypercalcemia (i.e. raises serum calcium)

How well did you know this?

Not at all

Perfectly

phosphate distribution

86% in bone
14% intracellular
.03% extracellular

How well did you know this?

Not at all

Perfectly

total serum calcium =

= protein-bound calcium + ionized calcium + complexed calcium

50% ionized
40% protein-bound
10% complexed

note - we are really interested in the ionized calcium

How well did you know this?

Not at all

Perfectly

factors affecting serum calcium

*albumin binding
*other protein binding
*pH

How well did you know this?

Not at all

Perfectly

total serum calcium vs. ionized calcium

*total serum calcium:
-part of basic metabolic panel
-inexpensive to test
-includes ionized calcium, complexed calcium, bound calcium
-low serum albumin affects total calcium but not ionized calcium

*ionized calcium:
-separate test
-collected in a different tube
-more expensive
-the “important” calcium level

How well did you know this?

Not at all

Perfectly

corrected serum calcium =

[(4 - serum albumin) x 0.8] + serum calcium

How well did you know this?

Not at all

Perfectly

hypocalcemia - clinical manifestations

*INCREASED neuromuscular excitability / tetany
1. Chvostek’s sign - tapping on the facial nerve results in contraction of ipsilateral facial muscles
2. tetany - diffuse involuntary muscle contractions
3. Trousseau’s sign - carpal-pedal spasm occurring with inflation of blood pressure cuff
4. PROLONGED QT interval

How well did you know this?

Not at all

Perfectly

hypercalcemia - clinical manifestations

“stones, bones, moans, and groans”:
*nephrolithiasis
*bone pain
*lethargy/anorexia
*constipation

How well did you know this?

Not at all

Perfectly

vitamin D metabolism

sunlight converts 7-dehydrocholesterol → cholecalciferol (vitamin D3)
liver converts cholecalciferol → 25-hydroxyvitamin D3 (this is what we MEASURE)
kidney converts 25-hydroxyvitamin D3 → 1,25-dihydroxyvitamin D3 (ACTIVE FORM)

dietary sources of vitamin D

*concentrated source: liver of cold water fishes (trout, salmon)
*supplementation in milk (vitamin D3)

active form of vitamin D

active form = 1,25-dihydroxy Vitamin D

made by conversion in the proximal tubules in the kidneys

roles of 1,25-dihydroxy Vitamin D

*increased intestinal calcium & phosphate absorption
*increases calcium & phosphate resorption from bone
*overall: INCREASED SERUM Ca2+ and INCREASED SERUM phosphate

rickets - overview

*caused by decreased 1,25 dihydroxy vitamin D
*results in decreased calcium absorption
*decreased calcium available for skeletal growth
*presents at 3-18 months of age

rickets - causes

*breast feeding without vitamin D supplementation
*skin that is less able to let UV light penetrate in an environment with decreased sun
*celiac disease
*genetic causes

7-dehydrocholesterol

*precursor to vitamin D
*converted in skin by sun to vitamin D3

vitamin D3

*aka cholecalciferol
*made in humans (conversion from 7-dehydrocholesterol) or given as a vitamin D supplement in milk

25 hydroxy vitamin D

*made from 25-hydroxylation of vitamin D3 (cholecalciferol) in the LIVER
*NOT the most active form
*we measure levels of this in most people to determine vitamin D status

1,25 dihydroxy vitamin D

***made in the kidney *ACTIVE FORM OF VITAMIN D** *if you have kidney failure, you cannot make this *also called **calcitriol** *can be given as vitamin to patients with kidney failure

vitamin D2

*aka ergocalciferol *not produced in humans *has same efficacy as vitamin D3 as a supplement

parathyroid hormone - overview

*released from parathyroid glands in response to hypocalcemia *effect: **increases serum calcium levels** by: 1. **stimulating osteoclast activity: promotes bone resorption** → release of calcium & phosphate into blood 2. **increases urinary excretion of phosphate** *overall: **increased serum calcium, slightly decreases serum phosphate**

parathyroid hormone (PTH) - roles

***osteoBLASTS have PTH receptors → stimulate osteoCLAST resorption** *renal effects occur in distal tubule: -**stimulate calcium reabsorption** → inreased serum calcium -**stimulates phosphate excretion** → decreased serum phosphate *result: INCREASED SERUM CALCIUM; NORMAL to LOW PHOSPHATE

hyperparathyroidism - results

*hypercalcemia (high serum calcium) *normal or low serum phosphate *hypercalciuria: -kidney stones in some individuals -osteoporosis

fibroblast growth factor 23 - overview

*produced by osteocytes in response to high serum phosphate levels *effect = **decreases serum phosphate levels** *decreased proximal tubular phosphate reabsorption → INCREASED EXCRETION OF PHOSPHATE IN URINE ***decreases 1,25 hydroxy vitamin D (calcitriol) production *decreases PTH secretion**

calcitonin - overview

*hormone produced by the parafollicular cells of the thyroid ***"tones down" calcium: decreases serum calcium & serum phosphate** *opposes the effect of PTH *inhibits osteoclast activity in bone *inhibits tubular reabsorption of calcium & phosphate

major problems in chronic kidney failure

1. **decreased urinary phosphate excretion** (decreased phosphate filtration) -results in **increased FGF-23 production** -occurs in stage 3 CKD 2. **decreased calcitriol production** (due to increased FGF-23 and increase serum phosphate) -less calcitriol → increased PTH 3. **increased PTH production** (due to decreased 1,25 dihydroxy vitamin D & increased serum phosphate) -causes bone resorption 4. dysregulation of calcium/phosphate metabolism; results in: -decreased bone mineralization (from increased PTH) -accelerated vascular calcification (from increased serum phosphate)

chronic kidney failure - overview of problems

*decreased phosphate excretion / **increased serum phosphate** *increased FGF-23 *decreased 1,25 OH Vit D (calcitriol) / **decreased serum calcium** *increased PTH *increased vascular calcification *decreased bone mineralization ***increased alkaline phosphatase (bone enzyme)**

treating chronic kidney failure

1. decrease phosphate in diet 2. remove phosphate with dialysis 3. use phosphate binders with meals