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endocrine term 2 quiz 2 - julia's notes > regulation of ca and PO4 metabolism - chapter 9 > Flashcards

regulation of ca and PO4 metabolism - chapter 9 Flashcards

1
Q

normal total ca concentration in blood

A

about 10 mg/mL
40% bound to plasma proteins
60% not protein-bound - ultrafilterable
- some complexed to anions but most free - 50% free - only form that’s biologically active

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2
Q

hypocalcemia symptoms

A 
spontaneous twitching
muscle cramps
tingling
numbness
chvostek sign and trousseau sign
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3
Q

chvostek sign

A

twitching of the facial muscles elicited by tapping on the facial nerve
used to diagnose hypocalcemia

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4
Q

trousseau sign

A

carpopedal spasm upon inflation of a blood pressure cuff

used to detect hypocalcemia

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5
Q

low extracellular ca causes:

A

1: increased excitability of excitable cells => lower threshold potential, less inward current needed to depolarize => tingling and numbness and spontaneous muscle twitches

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6
Q

hypercalcemia symptoms

A 
constipation
polyuria
polydipsia
neurologic signs of hyporeflexia
lethargy
coma 
death
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7
Q

changes in anion concentration on ca concentration

A

change the fraction of ca complexed with anions
if plasma phosphate concentration increases => fraction of ca that is complexed increases => decreased ionized ca concentration

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8
Q

acidemia

A

excess H+ in blood => more H+ bound to albumin => fewer sites for Ca => increase in free ca

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9
Q

alkalemia

A

deficit of H+ in blood => less H+ bound to albumin => more sites for Ca to bind => hypocalcemia

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10
Q

vitamin D,1,25-dihydroxycholecalciferol

A

stimulates absorption of Ca in GI tract

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11
Q

chief cells of parathyroid gland

A

synthesize and secrete PTH

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12
Q

PTH

A

secreted by chief cells of parathyroid gland
single-chain with 84 AA
biologic activity resides in N-terminal 34 AA

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13
Q

synthesis of PTH

A

1: synthesized as preproPTH on ribosomes (115 AA)
2: 25 AA signal sequence cleaved off => 90 AA pro-PTH
3: pro-PTH transported to golgi
4: 6 AA cleaved => PTH
5: packaged into secretory granules for release

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14
Q

short-term regulation of PTH secretion

A

by plasma ionized ca concentration
secreted at basal level when ca levels normal
reaches maximal rates when ca levels at 7.5
response within seconds
mg levels also regulate

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15
Q

mechanism of PTH secretion

A

1: parathyroid cell membrane has Ca sensing receptors linked via Gq to phospholipase C
2: extracellular ca concentration increased
3: Ca binds to receptor
4: phospholipase C activated
5: increased levels of IP3/Ca2+
6: inhibits PTH secretion

if amounts of ca binding receptor decrease, inhibition of PTH secretion is decreased so more PTH secreted

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16
Q

long-term regulation of PTH secretion

A

chronic changes in plasma Ca concentration alter transcription of gene for preproPTH, synthesis and storage of PTH, and growth of parathyroid glands
therefore, chronic hypocalcemia => secondary hyperparathyroidism => increased synthesis and storage of pTH and hyperplasia of parathyroid glands
chronic hypercalcemia => decreased synthesis and storage of PTH, increased breakdown of PTH, and release of inactive PTH fragments

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17
Q

secondary hyperparathyroidism

A

due to chronic hypocalcemia
increased synthesis and storage of PTH
hyperplasia of parathyroid glands

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18
Q

Mg on PTH secretion

A

hypomagnesia stimulates PTH
hypermagnesia inhibits
except with severe hypomagnesia associated with chronic Mg depletion (alcoholism) => inhibition of PTH synthesis, storage, secretion

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19
Q

mechanisms of action of PTH

A

on bone and kidney, direct, mediated by cAMP

on intestine, indirect via activation of vitamin d

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20
Q

mechanism of PTH action on kidney

A

1: PTH binds receptor
2: receptor coupled to adenylyl cyclase via Gs protein
3: adenylyl cyclase catalyzes conversion of ATP to cAMP
4: cAMP activates protein kinases
5: protein kinases phosphorylate intracellular proteins
6: these proteins inhibit Na/phosphate cotransport at luminal membrane

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21
Q

PTH on bone

A

increased bone resorption
1: PTH receptors on osteoblasts, not osteoclasts - direct action on osteoblasts initially creates increase in bone formation
2: long-term, causes increase in bone resorption via indirect action on osteoclasts mediated by cytokines released by osteoblasts => release of both Ca and P to ECF - also release of hydroxyproline, which is excreted in urine
not enough to explain entire increase in ca due to PTH, though - other mechanisms

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22
Q

PTH on kidney

A

decreased phosphate reabsorption (phosphaturia)
increased ca reabsorption
increased urinary cAMP
1: inhibits phosphate reabsorption by inhibiting Na-phosphate cotransport in PCT => phosphaturia - prevents phosphate released along with ca by resorption of bone from complexing with ca in ECF
cAMP generated in PT cells also excreted in urine
2: stimulates Ca reabsorption - on DCT

23
Q

actions of PTH of intestine

A

increase ca absorption (indirectly via 1,25-dihydroxycholechalciferol)
stimulates renal 1alpha-hydroxylase => conversion of 25-hydroxycholecalciferol to active form = 1,25-dihyroxycholecaliferol => stimulates intestinal ca absorption

24
Q

hyperparathyroidism

A

rater of bone resorption elevated => increased serum Ca concentration

25
1alpha-hydroxylase
renal enxyme that is stimulated by PTH converts 25-hydroxycholecalciferol to active form 1,25-dihydroxycholecalciferl (activates vitamin D) therefore stimulates intestinal ca absorption
26
primary hyperparathyroidism (table)
increased PTH increased 1,25-dihydroxyholecalciferol (because of PTH's effect on 1alpha-hydroxylase) increased bone resorption increase urine phosphate concentration adn ca increase urine cAMP increased serum ca decreased serum phos
27
surgical hypoparathyroidsm (table)
``` decreased PTH decreased 1,25-dihydroxyholecalciferol (because of PTH's effect on 1alpha-hydroxylase) decreased bone resorption decrease urine phosphate concentration decreased urine cAMP decreased serum ca increased serum phos ```
28
pseudohypoparathyroidism (table)
``` increased PTH decreased 1,25-dihydroxyholecalciferol (because of PTH's effect on 1alpha-hydroxylase) decreased bone resorption (defective Gs) decrease urine phosphate concentration decrease urine cAMP decreased serum ca increased serum phos ```
29
humoral hypercalcemia of malignancy (increase PTH-rp) (table)
``` decrease PTH increases 1,25-dihydroxyholecalciferol increase bone resoprtion increase urine posphate increase urine ca because of high filtered load increase urine cAMP increase serum ca decrease serum phos ```
30
chronic renal failure (table)
increase PTH (secondary) decrease 1,25-dihydroxyholecalciferol osteomalacia due to decreased 1,25-dihydroxyholecalciferol increased bone resorption due to increased PTH decreased urine phosphate due to decreased GFR decreased serum ca due to decreased 1,25-dihydroxyholecalciferol decreased serum phos due to decreased urine phos
31
primary hyperparathyroidism
most commonly caused by parathyroid adenomas => secretion of excessive amounts of PTH increased PTH hypercalcemia due to increased bone resorption, increased renal ca reabsorption and increased intestinal ca absorption hypophosphatemia due to decreased renal phosphate reabsorption and phosphaturia get "stones, bones, and groans" = stones from hypercalcemia, bones from increased bone resorption, groans from constipation treat with parathyroidectomy
32
secondary hyperparathyroidism
parathyroid glands are normal but are stimulated to secrete excess PTH secondary to hypocalcemia - can be due to vitamin D deficiency or chronic renal failure blood levels of ca low or normal but never high circulating PTH levels elevated
33
hypoparathyroidism
inadvertent consequence of thyroid surgery or parathyroid surgery can also be autoimmune or congenital low circulating pTH, hopcalcemia due to decreased bone resorption, decreased renal Ca reabsorption and decreased intestinal ca absorption hyperphosphatemia due to increased phosphate reabsorption treat with oral ca supplement and active form of vitamin D
34
pseudohypoparathyroidism - albright's hereditary osteodystrophy
hypocalcemia, hyperphosphatemia, short stature, short neck, obesity, subcuateneous calcification, shortened fourth metatarsals and metacarpals administration of endogenous PTH produces no phosphaturic response and no increase in cAMP inherited autosomal dominant disorder in which Gs protein for PTH in kidney and bone is defective
35
humoral hypercalcemia of malignancy
when malignant tumors (lung, breast) secrete PTH-related peptide (PTH-rp) = structurally homogenous to PTH - has all actions of PTH => hypercalcemia and hypophosphatemia despite low circulating levels of PTH treat with furosemide and etridronate
36
furosemide
used to treat humoral hypercalcemia of malignancy | inhibits renal ca reabsorption and increases ca excretion
37
etidronate
used to treat humoral hypercalcemia of malignancy | inhibits bone resorption
38
familial hypocalciuric hypercalcemia (FHH)
autosomal dominiant decreased urinary ca excretion increased serum ca concentration due to inactivation mutations of the ca sensing receptors in parathyroid glands adn parallele recptors in the thick AL of kidney defective renal receptors => high serum ca concentration incorrectly sensed as normal so PTH secretion not inhibited as it should be
39
clinical presentation of primary hyperthyroidism
``` generalized weakness easy fatigability loss of appetite occasional vomiting higher urine output unusually thirsty lab tests show: hypercalcemia and hypophosphatemia and phosphaturia, elevated PTH ```
40
calcitonin
secreted by parafollicular cells of thyroid gland | straight-chain peptide with 32 AA
41
stimuli for calcitonin release
increased plasma Ca
42
actions of calcitonin
inhibits osteoclastic bone resorption => decreased plasma ca concentration doesn't participate in minute-to-minute regulation
43
vitamin D versus PTH
PTH maintains plasma ca concentration - actions coordinated to increase ionized ca concentration toward normal vitamin D - promotes mineralization of new bone - actions coordinate to increase both ca and phosphate concentrations in plasma so they can be used in bone
44
synthesis of vitamin D
1a: 7-dehydrocholesterol is converted in the skin by UV light to cholecalciferol 1b: cholecalciferol is acquired through dietary intake 2: liver converts cholecalcifero to 25-OH-cholecalciferol - in ER, requires NADPH, O2, Mg2+ but not cytochrome P450 3: bound to an alpha-globulin in plasma 4a: 25-OH-cholecalciferol is converted in kidney to 1,25-(OH)2-cholecalciferol by 1alpha-hydroxylase 4b: 25-OH-cholecalciferol is converted to 24,25-(OH2-cholecalciferol (inactive)
45
1alpha-hydroxylase
in kidney mitochondria requires NADPH, O2, Mg, and cytochrome P450 converts 25-OH-cholecalciferol to active form = 1,25-(OH)2-cholecalciferol activated by: 1: decreased ca 2: increased PTH 3: decreased phosphate
46
regulation of vitamin D synthesis
can go to step 4a or 4b depending on status of ca in body - when sufficient, 4b
47
actions of vitamin D on intestine
increases both ca and phosphate absorption | induces synthesis of vitamin-d dependent ca binding protein = calbindin D-28 D
48
calbindin D-28 K
cytosolic protein in intestine synthesis stimulated by vitamin D binds four ca ions exact role uncertain
49
mechanism of intestinal ca absorption
1: ca diffuses from the lumen into the cell, down its electrochemical gradient 2: ca is bound to calbindin D-28K 3: ca is pumped across the basolateral membrane by ca atpase
50
actions of vitamin D in kidney
parallel to actions on intestine stimulates ca and p reabsorption (PTH stimulates ca reabsorption but INHIBITS p reabsorption)
51
actions of vitamin D in bone
acts synergistically with PTH to stimulate osteoclast activity and bone resorption allows for mineralized old bone to be resorbed to provide more ca and p to ecf so that new bone can be made
52
rickets
due to vitamin d deficiency in children not enough ca and p to mineralize bone growth failure and skeletal deformities
53
osteomalacia
due to vitamin d deficiency in adults | new bone fails to mineralize, resulting in bending and softening of weight-bearing bones
54
vitamin d resistance
when kidney unable to produce ative metabolite (1,25...) | can be due to congenital absence of 1alpha-hydroxylase or chronic renal failure

endocrine term 2 quiz 2 - julia's notes (16 decks)

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