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Endocrine > Regulation of Ca and Phosphate Metabolism > Flashcards

Regulation of Ca and Phosphate Metabolism Flashcards

1
Q

calcium homeostasis

A

a. Almost every cell in the body uses Ca
i. Extracellular Ca conc has a dramatic effect on the excitability of cells—particularly nerve fibers
b. Ca is stored in bones
c. Ca homeostasis is tightly regulated
d. During aging, there are decreases in the amount of Ca absorbed from dietary intake and in dietary intake of Ca
i. Existing bone cells are reabsorbed by the body faster than new bone is made
ii. Aging contributes to osteopenia or osteoporosis

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2
Q

distribution of Ca in the body

A

Most of it found in bones and teeth followed by ICF

50% of total Ca is in ionized form

Free ionized Ca is biologically active form

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3
Q

amt of Ca in the blood is kept within a narrow range

A

a. ages 0-9: 8.7-10.2
b. ages 10-25: 9.2-10.7
c. ages 26-?: 8.7-10
i. adults are “in the 9’s”

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4
Q

hypocalcemia*

A

a. dec plasma Ca conc

i. symptoms: hyperreflexia, spontaneous twitching, muscle cramp, tingling, numbness

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5
Q

Chvostek sign*

A

indicator of hypocalcemia

-twitching of the facial muscles elicited by tapping on the facial nerve

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6
Q

Trousseau sign*

A

indicator of hypocalcemia

-carpopedal spasm upon inflation of a blood pressure cuff

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7
Q

hypercalcemia*

A

a. inc plasma Ca conc
i. Symptoms: decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, coma

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8
Q

low extracellular Ca

A

a. hypocalcemia
i. reduces the activation threshold for Na channelseasier to evoke AP (less or no stimulus required to trigger AP)
ii. results in inc in membrane excitability (spontaneous APs)
iii. generation of spontaneous AP is the physical basis for hypocalcemic tetany—spontaneous muscle contractions due to low extracellular Ca
iv. produces tingling and numbness (on sensory neurons) and spontaneous muscle twitches (on motorneurons and muscle)

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9
Q

high extracellular Ca

A

i. opposite of hypocalcemia mechanism—dec membrane excitability
ii. NS becomes depressed and reflex responses are slowed

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10
Q

how can the conc of Ca be changed in the blood?

A
  • changes in plasma protein concentration
  • changes in anion concentration
  • acid base abnormalities
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11
Q

changes in plasma Ca conc and how Ca concentration in the blood changes

A
  1. Alter total Ca concentration in the same direction (ie. Inc plasma protein conc, inc total Ca conc)
  2. No change in Ca ionized
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12
Q

changes in anion concentration and how Ca concentration in the blood changes

A
  1. Change the fraction of Ca complexed with anions

2. Ie. If inc phosphate conc, dec ionized Ca concentration

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13
Q

acid base abnormalities and how Ca concentration in the blood changes

A
  1. Alter the ionized conc by changing the fraction of Ca bound to albumin
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14
Q

acidemia*

A
  1. free ionized Ca concentration increases, b/c less is bound to albuminmore H+ binds to albumin because the H+ conc inc with the decreasing pH, so more Ca is pushed off and is free
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15
Q

alkalemia*

A
  1. free ionized Ca conc dec, b/c pH is higher, so less H+ to push the Ca off albumin, and more Ca is bound to albumin
    a. Often accompanied by hypocalcemia
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16
Q

what is involved in the coordinated action of Ca?

A
  1. 3 organ systems: bone, kidney, intestine

2. 3 Hs: parathyroid H, calcitonin, and vitamin D

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17
Q

vitamin D and Ca

A
  1. if we ingest 1000 mg of Ca, vitamin D stimulates absorption of 350 mg to the ECF from the GI tract
    a. 150 mg is secreted from the ECF to the GI tract
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18
Q

bone and Ca

A

a. from the extracellular fluid, Ca is deposited as bone
b. bone resorption is stimulated by PTH and vitamin D and is inhibited by calcitonin
c. bone remodeling:
i. no net gain or loss of Ca
ii. new bone is formed—deposited
iii. old bone is resorbed

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19
Q

kidney and Ca

A

a. Ca is filtered from the ECF to the kidneys

b. Reabsorption of Ca from the kidneys is stimulated by PTH

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20
Q

Ca excretion thru feces and urine

A

a. To maintain Ca balance, kidneys must excrete the same amount of Ca that is absorbed by the GI tract

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21
Q

what is phosphate used for in biological processes?

A
  1. Component of ATP, second messenger mcs, DNA, RNA, and phospholipids
  2. Intracellular anion
  3. Involved in activation and deactivation of enzymes
  4. Buffer in bone, serum, and urine
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22
Q

extracellular concentration of phosphate and the relation to Ca

A

i. Extracellular concentration of phosphate is inversely related to that of Ca
1. Extracellular conc of Pi is regulated by the same Hs that regulate Ca concentration
2. Normal range of extracellular is 2.5-4.5 mg/dL

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23
Q

where is PTH secreted from?

A

a. PTH is synthesized in and secreted from the parathyroid glands
i. 4 parathyroid glands—2 superior and 2 inferior
ii. sit posterior on the thyroid
iii. chief cells of the parathyroid glands synthesize and secrete PTH

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24
Q 
PTH 
what type of 
H?
process of synthesis?
where packaged?
what is the stimuli for secretion?
A

i. Peptide H
ii. Synthesized on ribosomes as preproparathyroid H then it is cleaved to form proparathyroid H, followed by transportation to golgi to further cleavage to form PTH
iii. Packaged in secretory granules
iv. Stimuli for PTH secretion
1. Dec plasma Ca—at low plasma Ca con, PTH secretion is at its highest

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25
Q

how does inc extracellular Ca affect the PTH secretion?

A

i. Inc extracellular Ca concentration inhibits PTH synthesis and secretion

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26
Q

chronic hypercalcemia*

A
  1. Long term inc Ca plasma conc
  2. Causes dec synthesis and storage of PTH, inc breakdown of stored PTH, and release of inactive PTH fragment into circulation
27
Q

chronic hypocalcemia*

A
  1. Long term dec Ca plasma conc

2. Causes inc synthesis and storage of PTH, and hyperplasia of parathyroid glands—secondary hyperparathyroidism

28
Q

magnesium

A
  1. Parallel but less significant effects on PTH secretion
  2. However, an exception:
    a. Severe hypomagnesemia—result of chronic Mg depletion as in alcoholism
    i. Inhibits PTH synthesis, storage, and secretion
29
Q

PTH and G protein receptor

A

i. PTH binds to R which activates G protein

ii. This in turn activates adenylyl cyclase and stimulates production of cAMP

30
Q

actions of PTH on bone, kidney, intestine

A

i. Dec plasma Cainc PTH secretion
1. Bone:
a. Inc bone resorption
2. Kidney:
a. Dec phosphate resorption (phosphaturia)
b. Inc Ca reabsorption
c. Inc urinary cAMP
3. Intestine
a. inc Ca absorption (via vitamin D)
ii. all result in inc plasma Ca concentration toward normal

31
Q

vitamin D

  • what does it do?
  • what kind of H?
  • 2 sources?
A

a. promotes mineralization of new bone through its coordinated actions in the regulation of both Ca and phosphate plasma concentrations
i. inc both Ca and phosphate plasma concentrations
ii. inc Ca and Phosphate product to promote mineralization of new bone
iii. like PTH, has actions in intestine, kidney, bone
iv. vitamin D=cholecalciferol
v. is a prohormone
1. itself is physiologically inactive
2. must be successively hydroxylated to an active metabolite—regulated by negative feedback mechanisms
vi. 2 sources:
1. ingested in diet
2. synthesized in skin from 7-dehydrocholesterol in the presence of UV light

32
Q

vitamin –what type of H and what kind of Rs?

A

a. binds to Rs inside the cell and then moves to nucleus to stimulate or suppress gene transcription

33
Q

regulation of vitamin D synthesis in the liver?

A

i. 7 dehydrocholesterol is converted by UV light to cholecalciferol
1. cholecalciferol is also brought in by the diet
ii. in the liver, 25 hydroxylase converts cholecalciferol to 25-OH-cholecalciferol which is the main circulating form but has very low activity

34
Q

regulation of vitamin D synthesis in the kidney?

A

i. 7 dehydrocholesterol is converted by UV light to cholecalciferol
1. cholecalciferol is also brought in by the diet
ii. in the kidney:
1. 1 alpha hydroxylase (CYP1 alpha) in the renal proximal tubule converts the 25 OH cholecalciferol to 1,25 OH2 cholecalciferol—active steroid H
a. stimulated by: dec in Ca, inc in PTH, and dec in phosphate
2. 24 hydroxylase converts 25 OH cholecalciferol to 24, 25 OH2 cholecalciferol—inactive form
a. 1 alpha hydroxylase is tightly regulated at the transcriptional level in the kidney

35
Q

PTH and bone

A
  1. PTH receptors located on osteoblasts not osteocalsts
  2. Short term: bone formation via direct action on osteoblast
    a. Basis for the use of intermittent synthetic PTH administration in osteoporosis treatment
  3. Long term: inc bone resorption via indirect action on the osteoclasts mediated by cytokines released from osteoblasts
  4. Increases RANKL and dec OPG
36
Q

vitamin D and bone

A
  1. Acts synergistically with PTH to stimulate osteoclast activity and bone resorption
  2. Increases RANKL
37
Q

M-CSF

A
  1. (macrophage colony stimulating factor)—induce stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts, and then, mature, multinucleated osteoclasts
38
Q

RANKL

A
  1. (receptor activator for NF-kappaB ligand)
    a. Cell surface protein produced by osteoblasts, bone lining cells, and apoptotic osteocytes
    b. Primary mediator of osteoclast formation
39
Q

RANK

A

cell surface protein R on osteoclasts and osteoclasts precursors

40
Q

OPG–osteoprotegrin

A

(Osteoprotegrin)—soluble protein produced by osteoblasts; decoy R for RANKL; inhibits RANKL/RANK interaction so inhibits osteoclastogenesis

41
Q

MOA of PTH on kidney

A

i. PTH binds to a R and activates Gs protein
ii. Adenylyl cyclase is activated and produces cAMP which is excreted in the urine
iii. cAMP works thru the protein kinase and then undergoes phosphorylation to bring in Na and phosphate into the cell thru the symporter
1. inhibition of NPT (Na/P symporter) by PTH causes phosphaturia which increases excretion of phosphate in the urine
2. PTH acts on DCT and complements the increase in plasma Ca that resulted from the combination of bone resorption and phosphaturia

42
Q

actions of vitamin D on the kidney

A

Stimulates both Ca and P reabsorption

43
Q

MOA of vitamin D on the intestine

A

i. Vitamin D is brought into the cell and goes to the nucleus to modulate protein synthesis
1. Proteins act on the Na/Ca exchanger on the basolateral blood membrane to push Ca out of the cell and pull Na in
2. Proteins work on the NaP/Na symporter on the side of the intestinal lumen and pulls both into the cell
3. Proteins work to pull Ca into the cell
a. The Ca binds to calbindin which was formed by protein synthesis and then calbindin is removed and Ca is pushed out into the blood

44
Q

PTH on the small intestine

A

i. No direct action

45
Q

PTH on bone

A

i. Promotes osteoblastic growth and survival
ii. Regulates M-CSF, RANKL, and OPG production by osteoblast
iii. Sustained elevated levels of PTH shift the balance to a relative increase in osteoclast activity, thereby increasing bone turnover and reducing bone density

46
Q

PTH on kidney

A

i. Stimulates 1 alpha hydroxylase activity
ii. Stimulates Ca reabsorption the the thick ascending LOH and the DCT
iii. Inhibits P reabsorption by proximal nephrons—represses NPT2a expression

47
Q

PTH on parathyroid gland

A

no direct action

48
Q

vitamin D on the small intestine

A

i. Inc Ca and P absorption by increasing calbindin expression

49
Q

vitamin D on bone

A

i. Sensitizes osteoblasts to PTH

ii. Regulates osteoid production and calcification

50
Q

vitamin D on parathyroid gland

A

i. Directly inhibits PTH gene expression

ii. Directly stimulates CaSR gene expression

51
Q

actions of calcitonin

A

a. Primary actions on bone and kidney
b. Dec blood Ca and P concentrations by inhibiting bone resorption—effects only occur at high circulating levels of the H
i. Dec activity and number of osteoclasts
ii. Calcitonin Rs expressed on osteoclasts
iii. Major stimulus: inc plasma Ca
c. No role in chronic (min to min) regulation of plasma Ca
i. Thyroidectomy
1. Dec calcitonin but no effect in Ca metabolism
ii. Thyroid tumors
1. Inc calcitonin but no effect in Ca metabolism

52
Q

estradiol 17 beta

A

a. Estradiol 17beta—stimulates intestinal Ca absorption and renal tubular Ca reabsorption
i. also one of the most potent regulators of osteoblast and osteoclast function
1. estrogen promotes survival of osteoblasts and apoptosis of osteoclasts; favoring bone formation over reabsorption

53
Q

adrenal glucocorticoids

A
  • cortisol
    a. promotes bone resorption and renal Ca wasting and inhibit intestinal Ca absorption
    i. pts treated with high levels of glucocorticoid (such as an anti-inflammatory and immunosuppressive drug) can develop glucocorticoid induced osteoporosis
54
Q

primary hyperparathyroidism*

A
  1. Patients excrete excessive amounts of P, cAMP, and C
    a. Ca oxalate stones
  2. “stone,” “bones,” “groans”
    a. hypercalciuria—stones
    b. inc bone resorption—bones
    c. constipation—groans
  3. treatment usually requires parathyroidectomy
  4. inc PTH, inc Ca, dec P, inc vitamin D
55
Q

secondary hyperparathyroidism*

A
  1. inc in PTH levels is secondary to low Ca in the blood
  2. causes for low Ca include:
    a. renal failure
    i. inc PTH, dec Ca, inc P, dec vitamin D
    b. vitamin D deficiency
    i. inc PTH, dec Ca, dec P, dec vitamin D
56
Q

hypoparathyroidism*

A
  1. causes:
    a. thyroid surgery
    b. parathyroid surgery
    c. autoimmune or congenital—less common
  2. most symptoms are associated with dec Ca
    a. muscle spasm or cramping
    b. numbness, tingling, or burning especially around the mouth and fingers
    c. seizures
    d. in kids, poor teeth development, mental deficiency
  3. treatment: oral Ca supplement and active form of vitamin D
  4. dec PTH, dec Ca, inc P, dec vitamin D
57
Q

Albright Hereditary Osteodystrophy—pseudohypoparathyroidism type 1a*

A
  1. Inherited autosomal dominant disorder—Gs for PTH in bone and kidney is defective
  2. Hypocalcemia and hyperphosphatemia develop
  3. Inc PTH levels
    a. Administration of exogenous PTH produces no phosphaturic response and no inc in urinary cAMP
  4. Inc PTH, dec Ca, inc P, dec vitamin D
  5. Phenotype:
    a. Short stature, short neck, obesity, subcutaneous calcification, shortened metatarsals and metacarpals
58
Q

symptoms of hyperparathyroidism*

A
  1. Kidney stones
  2. Osteoporosis
  3. GI disturbances, peptic ulcers, nausea, constipation
  4. Muscle weakness, decreased muscle tone
  5. Depression, lethargy, fatigue, mental confusion
  6. Polyuria
  7. High serum Ca concentration; low serum phosphate conc
59
Q

symptoms of hypoparathyroidism*

A
  1. Tetany, convulsions, paresthesias, muscle cramps
  2. Decreased myocardial contractility
  3. First degree heart block
  4. CNS problems, including irritability and psychosis
  5. Intestinal malabsorption
  6. Low serum Ca conc; high serum phosphate conc
60
Q

Humoral hypercalcemia of malignancy*

A
  1. Hypercalcemic syndrome associated with malignancy
  2. PTH related peptide (PTHrP) is a peptide produced by tumors with close homology in the N terminal to PTH (product of gene duplication of PTH)
    a. Binds and activates same R as PTH—type 1 PTH R
  3. Inc PTHrP levels
  4. Produces similar profile to primary hyperparathyroidism
    a. Inc urinary Ca, inc urinary P, inc cAMP
    b. Inc blood Ca (hypercalcemia), dec blood P (hypophosphatemia)
  5. Different from primary hyperparathyroidism
    a. Dec bone formation
    b. Dec PTH levels
    c. Dec vitamin D—in cancer, vitamin D levels are normally suppressed
  6. Tx:
    a. Furosemide—inhibits renal Ca reabsorption and inc Ca excretion
    b. Etidronate—inhibitor of bone resorption
  7. Dec PTH, inc Ca, dec P, dec vitamin D
61
Q

Familial hypocalciuric hypercalcemia (FHH)*

A
  1. Autosomal dominant disorder
  2. Cause: mutations that inactivate CaSR in parathyroid glands and parallel Ca Rs in the ascending limb of the kidney
  3. Results in: dec in urinary Ca excretion (hypocalcicuria) and inc serum Ca (hypercalcemia)
  4. Normal to inc PTH, inc serum Ca, dec urine Ca, normal P, normal vitamin D
62
Q

rickets-osteomalacia*

A
  1. Impaired vitamin D metabolism
    a. Dietary deficiency of vitamin D
    b. Vitamin D resistance
    i. Deficit in synthesis of active vitamin D—absence of 1alpha hydroxylase
    ii. Mutations affecting vitamin D receptor
  2. GI disorders, chronic renal failure, P depletion can lead to pathophysiological changes in vitamin D metabolism
  3. Rickets—children
    a. Insufficient amount of Ca and P are available to mineralize growing bone
    b. Characterized by growth failure and skeletal deformities
  4. Osteomalacia—adults
    a. New bone fails to mineralize
    b. Characterized by bending and softening of weight bearing bones
  5. Congenital disorders
    a. Pseudovitamin D deficient rickets or vitamin D dependent rickets type 1—dec 1 alpha hydroxylase
    b. Pseudovitamin D deficient rickets or vitamin D dependent rickets type II—dec vitamin D receptor
  6. Inc PTH (secondary), normal to dec Ca, dec P, inc P and cAMP in the urine, dec vitamin D, osteomalacia—inc resorption
  7. Tx:
    a. Vitamin D2—ergocalciferol—or D3—cholecalciferol
    b. Ca
    c. Sunlight
    d. 1,25 OH2-D3—calcitriol
63
Q

osteoporosis*

A
  1. bone mass/Ca inc for both sexes until about 25-30 yo
  2. for females, bone mass/Ca dec steadily until about 50 yo, then takes a sharp drop, then dec steadily again
  3. for males, bone mass/Ca dec steadily from 30 on
  4. tx:
    a. antiresorptive therapy
    i. bisphosphonates
    ii. estrogen
    iii. selective estrogen receptor modulators (SERMs)—raloxifene, tamoxifen
    iv. calcitonin
    v. RANKL inhibitors—denosumab
    b. Anabolic therapy—PTH

Endocrine (15 decks)

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