Physio Exam 3 Renal 5

Front 1

Calcium homeostasis depends
on a balance between

Back 1

between the
amount of total body calcium
(bone) and distribution of
Calcium to the ECF

Front 2

Secreted by chief cells of
the parathyroid gland to
hypocalcemia and promotes
bone resorption and diminishes
excretion

Back 2

PTH

Front 3

Calcitrio

Back 3

: Vitamin D metabolite
secreted by proximal tubules
by hypocalcemia; promotes GI
uptake and bone resorption, and
inhibits excretion

Front 4

Calcitonin

Back 4

Secreted by thyroid
Parafollicular cells, secreted
to hypercalcemia and promotes
bone formation

Front 5

Calcitronin metabolism

Back 5

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

Front 6

enzyme in the proximal tubule that activates Vit D

Back 6

1 ALPHA Hydroxylase

Front 7

1 alpha hydroxylase is activated by

Back 7

decrease in [Ca2+]
Increase in PTH
Decrease in Phosphate

Front 8

1-25OH...active form of Vit D carried in blood by

Back 8

VDBP and exerts actions in
target tissues by binding to nuclear receptor, VDR, activating
transcription of target genes.

Front 9

Filtered Load of Ca2+ equation

Back 9

=[P]ca (GFR)(0.6)
0.6 because 0.4 of Ca2+ bond to protein

Front 10

Proximal Tubule absorption of Ca2+

Back 10

20% Transcellular; 80% paracelluar
via solvent drag and the positive transluminal electrical
gradient in the late proximal tubule

Front 11

Ca2+ REAB in thick ascending limb

Back 11

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.

Front 12

Ca+2 reab in distal tubule

Back 12

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

Front 13

Transluminal Electrical gradient dependent on

Back 13

the NKCC2 pump

Front 14

Main site of regulation of Ca2+ reabsorption

Back 14

is on distal tubule because it is sensitve to PTH.

Front 15

PTH stimulates Ca++ reabsorption in distal tubules via

Back 15

a cAMP dependent mechanism

Front 16

In proximal tubule: interstitial Ca2+ is reduced by hypoCa2+, causing

Back 16

plasma and interstitial fluid equilibrate leading to increased paracellular transport

Front 17

Low levels of Ca2+(hypcalcemia) stimulates NKCC2 which results in

Back 17

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

Front 18

Hypocalcemia triggers in the distal tubule PTH binding to PTHR which is a coupled Gs which causes an

Back 18

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)

Front 19

Hypocalcemia will cause CaSR to influence distal tubule and thick ascencing limb to

Back 19

decrease Ca excretion

Front 20

Hypocalcemia will cause CaSR to influence chief cells to

Back 20

increase PTH secretion

Front 21

Hypocalcemia will cause CaSR to influence proximal tubule to

Back 21

increase calcitriol which will elevate GI Ca++ absorption

Front 22

Hypocalcemia will cause CaSR to influence parafollicular cells to

Back 22

decrease calcitonin secretion

Front 23

PTH effect on Calcitrol, Ca excretion from distal and TAL

Back 23

increase
decrease

Front 24

Total plasma Ca++ =

Back 24

Total plasma Ca++ = 2.2 – 2.6 mmol/L
Ionized plasma Ca++ = 1.1 – 1.3 mmol/L

Front 25

Dieases that can cause hypocalcemia

Back 25

Hypoparathyroidism
Vit D defficiency
Pseudohypoparathyroidism
Renal Failure

Front 26

Hypoparathyroidism:

Back 26

PTH deficiency produces hypocalcemia

Front 27

Vitamin D deficiency

Back 27

Low calcitriol levels and deficient calcium absorption

Front 28

Pseudohypoparathyroidsim

Back 28

Usually a defect in Gs ; PTH normal to hig

Front 29

Renal Failure

Back 29

Deficient levels of calcitriol; Vitamin D hydroxylation defect

Front 30

diseases that can cause hypercalcemia

Back 30

Prmary Hyperparathyroidism
Familial Hypocalciuric Hypercalcemia

Front 31

Primary Hyperparathyroidism

Back 31

Parathyroid gland tumor

Front 32

Familial Hypocalciuric Hypercalcemia

Back 32

Mutation in the CaSR

Front 33

Phosphate homeostasis depends
on a balance between

Back 33

the
amount of total body Pi
and distribution to the ECF.

Front 34

Phosphate balance maintained by

Back 34

by matching
dietary intake with excretion.
Regulated by the kidney.

Front 35

GI phosphate uptake stimulated by

Back 35

calcitriol

Front 36

Pi
mobilization from bone stimulated by

Back 36

PTH and calcitriol

Front 37

Pi deposition in bone stimulated by

Back 37

calcitonin

Front 38

Calcitriol stimulates absorption of Phosphate from intestine as well as resorption from bone but it would inhibit

Back 38

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

Front 39

PTH maintains plasma pool of Ca2+. It stimulates of excretion of phosphate (phosphoturic activity) which leads to

Back 39

reduction of free phosphate in plasma. And free Ca2+ increases ‘cause its no longer complexed to Phosphate

Front 40

PTH main site of action with respect to phosphate reabsorption is PT. PTH causes phosphate excretion by

Back 40

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

Front 41

distrubution of water in body

Back 41

ICF = 2/3 = 28 L

ECF = 1/3 = 14 L

Front 42

ECF composed of

Back 42

Plasma = 1/4 ECF = 3.5 L
Intersitial Fluid = 10.5 L

Front 43

Total solutes equation

Back 43

Total solutes=Total body water (Osmolality=285)

Front 44

Although the osmolality is equilibrated across the compartments, the ion and cation contents are

Back 44

different across the ECF and ICF

Front 45

Diarrhea or isosmotic ECF volume contraction referes to

Back 45

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

Front 46

if 15% volume loss in ECF due to diarrhea (isosmotic), whats the water loss and mosmoles loss in ECF?

Back 46

Example 15% volume loss
.15 X 14 = 2.1 L

.15 X 3990 = 599 mosmoles Total Solute Decreases to 11371 mosmoles

Front 47

Diarrhea Isosmotic volume contraction

Back 47

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

Front 48

Saline IV infusion (Isosmotic Volume Expansion)

Back 48

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

Front 49

Water restriction, burns, perfuse sweating (hyperosmotic volume contraction)

Back 49

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

Front 50

High Na+ Intake (Hyperosmotic Volume Expansion)

Back 50

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.

Front 51

Adrenal Insufficiency; Salt Wasting nephritis (Hyposmotic Volume Contraction)

Back 51

Failure to secrete aldosterno, Na lost in urine. ECF becomes hypoosmolar, ECF water goes to ICF and ICF becomes higher

Front 52

Excessive H20 Intake or SIADH (Hyposmotic Volume Expansion)

Back 52

SIADHS: too much ADH and water retention. Osmolality of ECF goes down, ECF water goes to ICF.