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Endocrine - MSI Spring > Regulation of Ca and PO4 Metabolism > Flashcards

Regulation of Ca and PO4 Metabolism Flashcards

1
Q

Describe the distribution of Ca in the body

A

ECF - .1%
Plasma - .5% or less
ICF - 1%
Bones and teeth - 99%

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2
Q

What is the biologically active form of Ca? What percentage does this Ca make of the total amount of Ca in the body?

A

Free, ionized Ca - 50%

Protein-bound - 40%
Complexed to anions - 10%

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3
Q

What is the normal Ca levels for adult pts?

A

in the 9’s mg/dl

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4
Q

What are the symptoms and signs for hypocalcemia?

A

Symptoms: hyperreflexia, spontaneous twitching, muscle cramp, tingling and numbness

Chvostek sign: twitching of facial mm when facial n tapped
Trousseau sign: carpopedal spasm upton inflation of blood pressure cuff

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5
Q

What are the symptoms of hypercalcemia?

A

Decreased QT intervals, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, coma

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6
Q

How does hypocalcemia influence membrane excitability?

A 
Reduces activation threshold for Na channels-> easier to evoke AP
Increase membrane excitability 
Spontaneous AP: hypocalcemia tetany 
Tingling and numbness on sensory neurons
Mm twitches on motorneurons and m
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7
Q

How does hypercalcemia influence membrane excitability?

A

Nervous system becomes depressed and reflex responses are slowed
Decrease excitability

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8
Q

How can the forms of Ca in the plasma be altered?

A
  1. change plasma protein concentration: Increase protein = increase total Ca concentration (no change in Ca ionized)
  2. Changes in [anion]: Increase PO4, decrease ionized [Ca]
  3. acid-base abnormalities: more H+, increase free ionized [Ca]
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9
Q

How does acidemia cause increase in free ionized Ca?

A

H+ outcompetes for spots on albumin, thus less Ca is bound to albumin

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10
Q

What levels of Ca often accompanies alkalemia?

A

hypocalcemia

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11
Q

Calcium homeostasis is tightly regulated and involves the coordinated actions of what?

A

3 organ systems: bone, kidney and intestine

3 hormones: PTH, Calcitonin, Vit D

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12
Q

During homeostasis, describe bone remodeling

A

no net gain or loss of Ca
new bone is formed (deposited)
old bone is resorbed

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13
Q

To maintain Ca balance, how much Ca must the kidneys excrete?

A

same amount of Ca that is absorbed by GI tract

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14
Q

What hormones promote increase in extracellular Ca levels? Where do they act?

A

Vit D: in intestines to absorb
Vit D and PTH: on bone to resorb
PTH: on kidneys to reabsorb

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15
Q

Describe the relationship of Phosphate with Ca

A

Critical for biological processes
Component of ATP, second messenger molecules, DNA, RNA, and Phospholipids
Intracellular anion
Involved in activation and deactivation of enzymes
Buffer in bone, serum, and urine

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16
Q

Describe the distribution of Pi in the body

A

Bone - 85%
plasma - less than 1% (85%: ionized, 10% protein bound, 6% complexed to cations)
ICF - 15%

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17
Q

What is extracellular concentration of Pi regulated by?

A

same hormones that regulate Ca concentration

*Extracellular [Pi] inversely related to that of Ca

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18
Q

What secretes PTH?

A

Chief cells of parathyroid glands that are posterior on the thyroid

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19
Q

What happens to levels of Ca stored as the body ages?

A

There are decreases in amount of Ca absorbed from dietary intake, and in dietary intake of Ca
Existing bone cells reabsorbed by the body faster than new bone is made
Aging contributes to osteopenia or osteoporosis

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20
Q

describe the structure and synthesis of PTH

A

Peptide hormone - single-chain with 84 a.a.
Synthesized on ribosomes as preproPTH: 115 aa
cleaved to proPTH: 90 aa
Transported to golgi and cleaved to form PTH
Packaged

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21
Q

What is the stimulus for PTH secretion?

A

low plasma Ca

*increase in EC [Ca] inhibits PTH synthesis and secretion thru Gq and Gi pathways

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22
Q

What does chronic hypercalcemia cause?

A

Decrease in synthesis and storage of PTH

Increase breakdown of stored PTH and release of inactive PTH fragment into circulation

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23
Q

What does chronic hypocalemia cause?

A

increase in synthesis and storage of PTH, hyperplasia of parathyroid glands (secondary hyperparathyroidism)

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24
Q

What role does Mg have on PTH?

A

parallel but less significant effects on PTH secretion

In alcoholism, hypoMg inhibits PTH synthesis, storage and secretion

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25
What are the actions of PTH on bone, kidney and intestine?
Bone resorption Kidney: decrease reabsorption of Pi, increase Ca reabsorption, Increase urinary cAMP Intestine: Ca absorption via vit D
26
How does Vit D promote mineralization of new bone?
Increase both Ca and Pi plasma concentrations | Increase Ca x Pi product to promote mineralization
27
What is the main circulating form of Vit D?
25-OH-cholecalciferol
28
Describe the Vit D synthesis process
7-dehydrocholesterol -> cholecalciferol with UV light Cholecalciferol from diet ->25-OH cholecalciferol in liver via 25-hydroxylase Activated in renal proximal tubule via 1a-hydroxylase if [Ca] and [PO4] is low and PTH is high (Gs pathway for enzyme activation)
29
What is the active form of Vit D?
1,25 -(OH) cholecalciferol
30
What is the gene for 1a-hydroxylase?
CYP1a gene
31
Vit D is modified to what inactive form in the kidney? by what enzyme and its gene?
24,25 - (OH) cholecalciferol by 24 hydroxylase | Gene: CYP24 *promoted by increase levels of active Vit D
32
Where is the PTH receptor located in bone?
on osteoblasts | NOT osteoclasts
33
What are the short term actions of PTH on bone?
bone formation: via direct action on osteoblast *basis for intermittent synthetic PTH administration in osteoporosis tx
34
What are the long-term actions of PTH on bone?
bone resorption: indirect action on osteoclasts mediated by cytokines released from osteoblast
35
What is M-CSF role in bone?
induce stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts, and mature multinucleated osteoclasts
36
What is RANKL?
cell surface protein produced by osteoblasts, bone lining cells, and apoptotic osteocytes Primary mediator of osteoclast formation
37
What is RANK?
cell surface protein receptor on osteoclasts and osteoclast precursors
38
What is OPG (Osteoprotegerin)?
soluble protein produced by osteoblasts; decoy receptor for RNAKL; inhibits RANKL/RANK interactions
39
PTH causes an _____ in RANKL, ______ OPG
increase | Decrease
40
Vit D causes an ____ in RANKL
increase
41
What are the actions of PTH on distal convoluted tubule?
complements increase in plasma [Ca] Acts through Gs to form cAMP (urinary cAMP) Protein kinase Phosphorylates and Inhibits Na/PO4 cotransporter (phosphaturia)
42
What are the actions of Vit D on the kidney?
Ca and Pi reabsorbtion
43
How does Vit D in the intestine promote absorption of Ca?
Promotes transcription of calbindin | Calbindin takes free Ca in cell and helps transport it via Ca ATPase and Ca/Na antiporter
44
What is the role of PTH on Ca and Pi homeostasis in the kidney?
stimulates 1a-hydroxylase activity Stimulates Ca reabsorption by thick ascending limb of henle's loop and distal tubule Inhibits Pi reabsoption by proximal nephrons (NPT2a)
45
What is Vit D role in bone?
sensitizes osteoblasts to PTH | Regulates osteoid production and calcification
46
What is Vit D role in the kidney?
promotes Pi reabsorption by proximal nephrons | Minimal actions of Ca
47
What is Vit D role in parathyroid gland?
Directly inhibits PTH gene expression | Directly stimulates CaSR gene expression
48
Describe calcitonin's actions on bone. What is the major stimulus ?
Inhibits bone resorption Thus decreases blood Ca and Pi concentrations *effect occurs ONLY at high circulating levels of the hormone Decreases activity and # of osteoclasts via calcitonin receptors on osteoclasts Major stimulus: increase in plasma [Ca]
49
What role does Calcitonin have on chronic (minute-to-minute) regulation of plasma [Ca}?
No role Thyroidectomy: decreased calcitonin but no effect in Ca metabolism Thyroid tumors: increase calcitonin but no effect in Ca metabolism
50
Does calcitonin have a role in the kidneys?
yes, reduces Ca uptake in kidneys
51
What does Estradiol-17 beta stimulate?
intestinal Ca absorption and renal tubular Ca reabsorption
52
What effect does estradiol-17b have on osteoblasts and osteoclasts function?
one of most potent regulators Promotes survival of osteoblasts and apoptosis of osteoclasts favors bone formation over resorption
53
What effect do adrenal glucocorticoids like cortisol, have on Ca levels?
promote bone resorption Renal Ca wasting Inhibit intestinal Ca absorption all this = glucocorticoid-induced osteoporosis in pt taking it for anti-inflammatory and immunosuppressive symptoms
54
What occurs with primary hyperparathryoidism?
Adenoma of the parathyroid: increase PTH secretion High Ca, high Vit D Patients excrete excessive amounts of Pi, cAMP, and Ca (Ca-oxalate stones) Stones, bones, and groans (hypercalciuria, increase bone resoprtion, constipation)
55
What is the usual treatment for primary hyperparathyroidism?
Parathyroidectomy
56
What is secondary hyperparathyroidism?
Increase in PTH levels is secondary to low [Ca] in blood due to renal failure, vit D deficiency
57
What are the levels of PTH, Ca, Pi and Vit in renal failure pts? And in Vit D deficient pt?
Renal: High PTH, Low Ca, High Pi, Low Vit D | Vit D: High PTH, Low Ca, Low Pi, Low Vit D
58
What are the causes of hypoparathyroidism?
thyroid surgery, parathyroid surgery, autoimmune or congenital (less common)
59
What are most symptoms of hypoparathyroidism associated with?
decrease Ca Muscle spasm or cramping Numbness, tingling, or burning (esp around mouth and fingers) Seizures Kids: poor teeth development and mental deficiency
60
What is the treatment for hypoparathyroidism?
oral Ca supplement and active form of Vit D
61
What are the levels of PTH, Ca, Pi, and Vit D in pt with hypoparathyroidism?
PTH low, Ca low, Pi high, Vit D low
62
What is Albright hereditary osteodystrophy (pseudohypoparathyroidism type 1a)?
Autosomal dominant disorder Gs for PTH in bone and kidney defective Hypocalcemia and hyperphosphatemia develop Increase PTH levels *Administration of exogenous PTH = no Phosphaturic response and no increase urinary cAMP
63
What is the phenotype of Pseudo Hypoparathyroidism?
PTH high, Ca Low, Pi high, Vit D low Short, short neck, obesity, subcutaneous calcification, short metatarsals and carpals
64
What are the symptoms of hyperparathyroidism?
Kidney stones Osteoporosis GI disturbances, peptic ulcers, nausea, constipation Muscle weakness, decreased m tone Depression, lethargy, fatigue, mental confusion Polyuria High serum Ca concentration; low serum PO4 concentration in most cases
65
What are the symptoms of hypoparathyroidism?
Tetany, convulsions, paresthesias, muscle cramps Decreased myocardial contractility First-degree heart block CNS problems - irritability and psychosis Intestinal malabsorption Low serum Ca; high serum PO4
66
How is hypercalcemic syndrome associated with malignancy?
The tumor cells (with TGFb stimulus) produce PTHrP PTHrP is aa peptide with close homology in N-terminal to PTH Binds to Type 1 PTH receptors to stimulate reabsorption of Ca, resorption of Ca and Pi excretion
67
How is malignancy/hypercalcemia similar to primary hyperparathyroidism?
Increase levels of: urinary Ca, Urinary Pi, Urinary cAMP, blood Ca Decreased levels of blood Pi
68
How is humoral hypercalcemia of malignancy different from primary hyperparathryoidism?
Decreased bone formation Decreased PTH levels Decreased Vit D (in cancer, vit D levels normally suppressed)
69
What is the treatment for malignancy/hypercalcemia ?
Tx: furosemide (inhibits renal Ca reabsorption and increases Ca excretion) Etidronate (inhibits bone resorption)
70
What is the pathophysiology of PTH in Familial hypocalciuric hypercalcemia?
Autosomal Dominant Mutations that inactivate CaSR in parathyroid glands Ca receptors in ascending limb of kidney Results: decrease urinary Ca excretion, increase serum Ca
71
What is CaSR?
Ca receptor in the parathyroid that is connected to Gq and Gi that both inhbit PTH gene transcription and PTH secretion In the kidney it uses the same pathway to inhibit transcription of CYP1a gene into 1a-hydroxylase
72
What are the levels of PTH, Ca, Pi and Vit D in FHH?
``` PTH: N/increase Serum Ca: increase Urine Ca: decrease Pi: N Vit D: N ```
73
What can impair Vit D metabolisM
Dietary deficiency | Vit D resistance: Absence of 1a-hydroxylase, mutations affecting vit D receptor
74
Describe Rickets
Congenital disorder Pseudovitamin D-deficient rickets or vitamin D-dependent rickets type 1 (decrease in 1a-hydroxylase) Vitamin D-dependent rickets type II - Decrease in vitamin D receptor Insufficient amount of Ca and Pi available to mineralize growing bone Growth failure and skeletal deformities
75
What is the treatment for rickets-osteomalacia?
Vit D2 (ergocalciferol) or D3 (cholecaciferol) Ca Sunlight 1,25-(OH)2 - D3: calcitriol
76
What is osteomalacia?
Happens in adults New bone fails to mineralize Bending and softening of weight-bearing bones
77
What is the treatment of osteoporosis - bones become brittle and fragile ?
Antiresorptive therapy with bisphosphonates, estrogen, SERMs (raloxifene, tamoxifen), Calcitonin, RANKL inhibitors (Denosumab) Anabolic therapy: PTH

Endocrine - MSI Spring (15 decks)

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