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Physiology Unit 6 > Parathyroid Hormone > Flashcards

Parathyroid Hormone Flashcards

1
Q

calcium in plasma

A
  • total 9-10.6 mg/dl, typically measured (false high if albumin is high)
  • ionized 4.5-5.2- tightly regulated portion
  • acidosis blocks Ca binding to albumin and increases free ionized
  • total broken into bound (40%) and ultrafilterable (60%)
  • ultrafilterable is 50% ionized and 10% complexed to anions
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2
Q

calcium in body

A
  • 1 kg, 99% in skeleton

- 1 % in ECF and muscles

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3
Q

high calcium

A
  • greater than 12 mg/dl
  • fatigue, apathy, anorexia, delirium, coma
  • headache, inctracranial pressure, muscle weakness
  • increases membrane polarization and reduces neural responses
  • bradycardia, short QT interval
  • polydipsia, polyuria, hypertension, calculi
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4
Q

low calcium

A
  • due to poor diet/malabsorption, lactation
  • learning retardation, apnea
  • tetany, reduces membrane polarization and increases hypersensitivity (more excitable)
  • long QT interval, cardiac output reduced
  • Ca/PO4 deficiency, weak bone development- rickets or osteomalacia
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5
Q

normal balance of calcium

A
  • gut, ECF, bone, kidney
  • over 80% of ingested daily calcium is excreted in the feces
  • kidneys filter 10x average daily intake and recapture all by 175 mg or so
  • bone is an active repository and buffer of calcium with daily turnover of 280 mg
  • if dietary intake is low, kidneys can compensate by increasing reabsorption of filtered Ca, in long run bone reservoir will bear brunt by increasing resportion, loss of bone mass and density
  • PTH and vitamin D
  • phosphate
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6
Q

calcitonin

A
  • thyroid gland
  • stronger role in early development
  • potent inhibitor of bone resporption
  • used to be used as treatment (from salmon)
  • role in adult unclear
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7
Q

PTH

A
  • peptide hormone
  • high when Ca low
  • target 1-kidney- increases absorption in distal tubule decreases re absorption of P in proximal tubule, and increases second step syn of Vit D
  • target 2 is bone cells
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8
Q

target 2

A
  • bone cells
  • osteoclastic resorption via receptors on osteoblasts (RankL)
  • increases Ca and Po in ECF and plasma
  • increases osteocytic osteolysis
  • (pulse PTH can enhance bone formation)
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9
Q

PTH secretion

A
  • parathyroid chief cells
  • secrete more PTH when Ca is below set point
  • sensor is G protein coupled with signaling cascade that involves Ca binding/releasing to ER that controls PTH
  • when calcium drops, PTH increases fast
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10
Q

familial hypercalcemic hypocaluria (FHH)

A
  • curve shifted right, urine Ca is low
  • ppl are symptom free even though they have high calcium
  • genetic defect in Ca sensors
  • increased Ca reabsorption
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11
Q

Ca transport in kidney

A
  • increase in PTH causes increased Ca reabsorption in the distal tubule
  • reduces P re-absorption in proximal tubule (increases P in urine)
  • 60% of daily calcium reabsorption occurs in proximal tubule (active transport) and 9% in distal (active transport, what is controlled)
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12
Q

Ca transport in kidney 2

A
  • PTH increases reabsorption in distal tubule

- Vit D helps by increasing amount of calbindin to increase Ca transport and efflux at the basal side

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13
Q

vitamin D

A
  • target 1- intestine- increases Ca and P absorption
  • bone is second target- increases osteoclastic resorption by receptors on osteoblasts
  • parathyroid gland suppresses PTH in negative feedback
  • kidney distal tubule- aids in increased Ca and P transport
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14
Q

vitamin D 2

A

-synthesized from cholecalciferol to 25-OH-D3 in liver, then 1,25-diOH-D3 in kidney
-cacidiol can be stored and released slowly
-25-hydroxylase and 1a-hydroxylase
-PTH increases 1a-hydroxylase
-

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15
Q

calcium in the intestine

A

-Vitamin D increases passive and active transport of Ca and P int o the blood by increasing synthesis of calbindin

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16
Q

rickets

A
  • chronic deficiency in Vitamin D and/or deficiency of dietary calcium or phosphorous
  • disturbance of developing bone formation
  • poor mineralization due to lack of Ca
  • weakened and mechanically distorted long bones
  • large and abnormal growth plates
  • adults get osteolamacia-poor quality bone formed during remodeling
17
Q

primary hyperparathyroidism

A
  • high calcium
  • high serum PTH
  • low P
  • alkaline P and urinary C elevated
  • would expect high PTH when calcium is low
  • adenoma on parathyroid releasing PTH
  • bone resportion releasing Ca into ECF increased alkaline phosphatase
  • urine high in Ca because chronically high serum will eventually increase Ca excretion despite PTH
  • surgical removal of offending nodule, leaving 3 normal
  • adenoma
18
Q

humoral hpercalcemia of malignancy

A
  • serum Ca high, P low, PTH low, alkaline P very elevated
  • serum Ca high due to release of PTH-related peptide from lung tumor
  • activates same actions as PTH, caused Ca to increase by increasing reabsorption, absorption in kidney, resorption of bone, decreasing reabsorption of P
  • PTH was decreased because the negative feedback was still working
  • normal albumin- high total not due to Ca bound to excess, really due to ionized
19
Q

secondary hyperparathyroidism

A
  • hypocalcemia is primary, causes the excess PTH

- low D, renal failure, diet

20
Q

hypoparathyroidism

A
  • hypocalcemia

- surgical damage to gland or genetic

21
Q

pseudohypoparathyroidism

A
  • hypocalcemia

- genetic defect in G protein in PTH receptor in kidney

22
Q

phosphorous

A
  • plasma 2.5-2.5 mg/dl
  • inorganic portion
  • 10-20% Pi is protein bound
  • Pi not rigidly maintained, plus/minus 30% per diurnal variations
  • PTH influences reabsorption in proximal tubule
  • PTH increases P absorption form small intestine, but decreases reabsorption from proximal tubule and excretes more
23
Q

chronic kidney failure

A

-P excretion is reduced and hyperphosphatemia results

24
Q

collagen matrix synthesis and mineralization

A

-pre collagen triple helix molecules are synthesized by osteoblast and then polymerized extracellularly, forming fibrils and osteoid matrix that eventually mineralizes

25
Q

osteoblasts

A
  • line the bone surfaces
  • become rounder and contain extra ER
  • precursors synthesized here then exported by telopeptides
  • osteoid is b/n osteoblasts and matrix
  • do most of the signaling-osteoblasts
  • osteocyte also important
  • osteoblasts have receptors for Vitamin D, PTH, estrogen, paracrine and GFs
26
Q

bone mineralization

A
  • microcrystalline HA mineral deposition in collagen matrix
  • seeding on collagen-via phosphoproteins starts in gaps and then keeps going
  • bone mineral is 65% of weigh
  • rest is collagen (22%), fluid (10%) and 1-2% non collagenous proteins and cells
27
Q

microcrystalline hydroxylapatite

A
  • bone mineral
  • Ca10(OH)2(PO4)6 with Mg, Co3 and other trace constituents
  • once seeded, crystals coalesce and accumulate within and around the collagen fibrils until the area is fully mineralized with 65% by weight of mineral
28
Q

bone remodeling

A
  • rate can accelerate or decline in response to plasma calcium, injury, immobilization and metabolic and hormonal changes
  • varies by location and age
  • spinal vertebrae and other trabecular areas can rapidly lose or gain bone, cortex in tibia more stable
  • SA:V much bigger in trabecular bone
  • osteoclast, secretes acidic molecules to dissolve mineral, and proteases to digest and phagocytize the collagen matrix
  • mature osteoclasts do not divide but must develop from mono-nuclear precursors
  • they don’t last longer than a few days
29
Q

bone remodeling 2

A
  • RANKL (RANKL/OPG system) from osteoblasts activates osteoclasts and precursors, increases osteoclast number and bone resorption and turnover
  • RANKL release from blasts stimulated by endocrine factors, PTH, calcitriol, other systemic hormones and GFs
  • osteoblastic cells can also produce OPG, which binds to RANKL-sites and inhibits binding of RANKL and production and activation of osteoclasts -slows resorption
30
Q

estrogen

A
  • reduces resorption (receptors on blasts)

- mode of action unclear

31
Q

calcitonin

A

-transient inhibitor of clasts

32
Q

glucocorticoids

A

-primarily inhibits intestinal Ca absorption

33
Q

GH

A

-stimulate bone formation

34
Q

mechanical loading

A

-locally promotes bone accrual and maintenance

35
Q

mechanical loading

A
  • osteocyte and canaliculae network are highly sensitive to fluid shear
  • express Sclerostin- inhibits bone formation, increased with subnormal loading (not enough mechanical force, bone doesn’t form)
  • increased loading stimulates bone formation and repair
36
Q

osteoporosis

A
  • loss of bone mass associated with fracture
  • trabecular and cortical sites (and/or)
  • can be local or systemic
  • related to disease or aging (idiopathic)
  • inappropriate or excess remodeling
  • trabecular first/more common, walls become thinner and less numerous
  • cortical bone thinner and more porous
  • excess resorption- lack of Ca, D, or excess PTH
  • immobilization and lack of suitable loading
  • poor kidney function, long term glucocorticoids
  • slight annual loss with aging
  • treatment-replacing nutrients, loading exercise, drugs to stop clasts or stimulate blasts

Physiology Unit 6 (12 decks)

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