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52 Cards in this Set
- Front
- Back
Calcium homeostasis depends
on a balance between |
between the
amount of total body calcium (bone) and distribution of Calcium to the ECF |
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Secreted by chief cells of
the parathyroid gland to hypocalcemia and promotes bone resorption and diminishes excretion |
PTH
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Calcitrio
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: Vitamin D metabolite
secreted by proximal tubules by hypocalcemia; promotes GI uptake and bone resorption, and inhibits excretion |
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Calcitonin
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Secreted by thyroid
Parafollicular cells, secreted to hypercalcemia and promotes bone formation |
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Calcitronin metabolism
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UV light converts 7-dehydrocholesterol into cholecalciferol, this is metabolized in the lover into 25-OH-chole..and goes on to kidney, function of proximal tubules cells to convert active form of VitD
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enzyme in the proximal tubule that activates Vit D
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1 ALPHA Hydroxylase
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1 alpha hydroxylase is activated by
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decrease in [Ca2+]
Increase in PTH Decrease in Phosphate |
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1-25OH...active form of Vit D carried in blood by
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VDBP and exerts actions in
target tissues by binding to nuclear receptor, VDR, activating transcription of target genes. |
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Filtered Load of Ca2+ equation
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=[P]ca (GFR)(0.6)
0.6 because 0.4 of Ca2+ bond to protein |
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Proximal Tubule absorption of Ca2+
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20% Transcellular; 80% paracelluar
via solvent drag and the positive transluminal electrical gradient in the late proximal tubule |
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Ca2+ REAB in thick ascending limb
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Trans- and paracellular
transport similar to PT; however, since there is no H2O permeability in this segment, all paracellular transport depends on transluminal electrical gradient. |
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Ca+2 reab in distal tubule
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Reabsorption is entirely transcellular
and active. Dependent on the TRPV5/6 Ca++ luminal channel, calbindin, and active extrusion by pumps on the basolateral membrane. This is a PTH sensitive mechanism dependent on PTH binding to a basolateral receptor, triggering adenylate cyclase and cAMP |
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Transluminal Electrical gradient dependent on
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the NKCC2 pump
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Main site of regulation of Ca2+ reabsorption
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is on distal tubule because it is sensitve to PTH.
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PTH stimulates Ca++ reabsorption in distal tubules via
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a cAMP dependent mechanism
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In proximal tubule: interstitial Ca2+ is reduced by hypoCa2+, causing
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plasma and interstitial fluid equilibrate leading to increased paracellular transport
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Low levels of Ca2+(hypcalcemia) stimulates NKCC2 which results in
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Stimulation of NKCC2 pump in TAL induced
via CaSR on the basolateral membrane, thus enhancing the transluminal electrical gradient for calcium uptake via paracellular pathways |
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Hypocalcemia triggers in the distal tubule PTH binding to PTHR which is a coupled Gs which causes an
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increases cAMP in distal convoluted tubule, Ca2+ goes up into celll…intraceullular free levels are low because it is bound to calbinding and buffers Ca2+, then Ca2+ is pumped across basolateral membrane via Ca2+ pump (1ary), or Na/Ca2+ exchanger (secondary)
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Hypocalcemia will cause CaSR to influence distal tubule and thick ascencing limb to
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decrease Ca excretion
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Hypocalcemia will cause CaSR to influence chief cells to
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increase PTH secretion
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Hypocalcemia will cause CaSR to influence proximal tubule to
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increase calcitriol which will elevate GI Ca++ absorption
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Hypocalcemia will cause CaSR to influence parafollicular cells to
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decrease calcitonin secretion
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PTH effect on Calcitrol, Ca excretion from distal and TAL
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increase
decrease |
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Total plasma Ca++ =
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Total plasma Ca++ = 2.2 – 2.6 mmol/L
Ionized plasma Ca++ = 1.1 – 1.3 mmol/L |
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Dieases that can cause hypocalcemia
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Hypoparathyroidism
Vit D defficiency Pseudohypoparathyroidism Renal Failure |
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Hypoparathyroidism:
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PTH deficiency produces hypocalcemia
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Vitamin D deficiency
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Low calcitriol levels and deficient calcium absorption
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Pseudohypoparathyroidsim
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Usually a defect in Gs ; PTH normal to hig
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Renal Failure
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Deficient levels of calcitriol; Vitamin D hydroxylation defect
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diseases that can cause hypercalcemia
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Prmary Hyperparathyroidism
Familial Hypocalciuric Hypercalcemia |
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Primary Hyperparathyroidism
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Parathyroid gland tumor
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Familial Hypocalciuric Hypercalcemia
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Mutation in the CaSR
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Phosphate homeostasis depends
on a balance between |
the
amount of total body Pi and distribution to the ECF. |
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Phosphate balance maintained by
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by matching
dietary intake with excretion. Regulated by the kidney. |
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GI phosphate uptake stimulated by
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calcitriol
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Pi
mobilization from bone stimulated by |
PTH and calcitriol
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Pi deposition in bone stimulated by
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calcitonin
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Calcitriol stimulates absorption of Phosphate from intestine as well as resorption from bone but it would inhibit
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excretion of phosphate all these increases amount of Phosphate for bone formation. Action of Calcitriol is to break down old bone and have more free Ca2+ to use it for new bone formation
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PTH maintains plasma pool of Ca2+. It stimulates of excretion of phosphate (phosphoturic activity) which leads to
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reduction of free phosphate in plasma. And free Ca2+ increases ‘cause its no longer complexed to Phosphate
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PTH main site of action with respect to phosphate reabsorption is PT. PTH causes phosphate excretion by
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causing endocytic removal of Na/Phosphate transporters in the apical membrane of PT (npt2). NPT2 is secondary transport. Na that enters through this transporter goes across basolateral membrare via NA/K pump, and phosphate crosses in an electroneutral way via antiport system with an anion
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distrubution of water in body
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ICF = 2/3 = 28 L
ECF = 1/3 = 14 L |
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ECF composed of
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Plasma = 1/4 ECF = 3.5 L
Intersitial Fluid = 10.5 L |
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Total solutes equation
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Total solutes=Total body water (Osmolality=285)
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Although the osmolality is equilibrated across the compartments, the ion and cation contents are
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different across the ECF and ICF
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Diarrhea or isosmotic ECF volume contraction referes to
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luid loss in diarrhea lost in diarrhea has the same osmolality as the fluid in the body. Whenever theres volume contraction or expansion those are changes in ECF. Vascular detection to regulate volume only detects ECF changes
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if 15% volume loss in ECF due to diarrhea (isosmotic), whats the water loss and mosmoles loss in ECF?
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Example 15% volume loss
.15 X 14 = 2.1 L .15 X 3990 = 599 mosmoles Total Solute Decreases to 11371 mosmoles |
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Diarrhea Isosmotic volume contraction
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Fluid lost removed from ECF..no change in ICF, no change in total body osmolality change because change was isoosmotic..this is in the case of volume contraction
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Saline IV infusion (Isosmotic Volume Expansion)
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Volume isoosmotic expansion, giving a patient saline IV with same osmolality as body fluid. Volume added to ECF, since ECF osmolality is not changed, ICF doesn’t change
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Water restriction, burns, perfuse sweating (hyperosmotic volume contraction)
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Hyperosmotic volume contraction..dehydration, perfussed sweating, loosing more water than solute. If burns, blisters filled up with fluid more dilute than body fluid so more water than solute loss. Osmolality of ECF increases due to water loss, water leaves ICF and goes into ECF
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High Na+ Intake (Hyperosmotic Volume Expansion)
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Eating a pound of salt osmolality of ECF goes up, fluid from ICF goes into ECF and ECF volume goes up and ICF volume goes down.
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Adrenal Insufficiency; Salt Wasting nephritis (Hyposmotic Volume Contraction)
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Failure to secrete aldosterno, Na lost in urine. ECF becomes hypoosmolar, ECF water goes to ICF and ICF becomes higher
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Excessive H20 Intake or SIADH (Hyposmotic Volume Expansion)
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SIADHS: too much ADH and water retention. Osmolality of ECF goes down, ECF water goes to ICF.
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