Renal--Physiology--Organic Anions/cations/glucose/phosphate/calcium/excretion Of Waste Products

Front 1

How do anions and cations enter the renal tubule

Back 1

They are actively secreted in the proximal tubule

Front 2

Why is excretion by filtration ineffective for organic anions/cations

Back 2

because they are protein bound and not freely filtered, need secretory mechanisms

Front 3

What creates a potential for drug/drug pharmockinetic interactions in organic anion/cation secretion?

Back 3

Organic ions compete for the same family of transporters, there is no individual transporter for each separate ion.

Front 4

True/False: Both secretion and reabsorption are energy consuming?

Back 4

True

Front 5

How does the filtered amount of PAH increase with plasma PAH concentration

Back 5

linearly forever

Front 6

How does the secreted amount of PAH change in response to increasing plasma PAH

Back 6

approaches a transport maximum at which point the transporters are saturated-- increasing PAH in plasma does not increase amount secreted

Front 7

How does the excreted amount of PAH vary with increasing plasma PAH

Back 7

PAH excreted rises sharply with increase in plasma PAH uptill the transport maximum for secretion is reached. At this point, the slope of the excreted curve is less steep.

Front 8

How are non-ionized forms of compounds dealt with in the tubule?

Back 8

Passive re-absorption or passive secretion also may occur

Front 9

What THREE factors affect passive handling (ie passive reabsorption/passive secretion)?

Back 9

1) urinary pH (determines amount of substance in ionized vs non-ionized forms)
2) pK of the substance
3) high urine flow rate=keeps gradient

Front 10

What is the typical chemical characteristics of drugs?

Back 10

weak organic acids or bases

Front 11

How much of the filtered load of glucose is reabsorbed?

Back 11

100%

Front 12

When is glucose excreted in urine?

Back 12

When the transport maximum of glucose has been exceeded

Front 13

What two conditions are a result of uncontrolled sugar in diabetics?

Back 13

1) glucosuria (glucose in urine)
2) increased urine flow rate

Front 14

What does SGLT2 do (transport type, substance, location)?

Back 14

-secondary active
-glucose reabosrption
-early PCT on luminal membrane

Front 15

What does GLUT2 do (transport type, localization)

Back 15

-facilitated diffusion
-glucose reabsorption
-basolateral membrane

Front 16

What happens to the filtered, absorbed, and excreted amount of glucose when transport maximum reached?

Back 16

1) filtered- keeps increasing linearly
2) absorbed- levels off
3) excreted- used to be 0, now starts increasing

Front 17

Where is the major body store of phosphate and calcium?

Back 17

bone

Front 18

Where is the excretion of phosphate/calcium regulated? Where specifical is calcium regulated

Back 18

kidney, calcium is specifically regulated in the distal tubule

Front 19

Is the secretion of Ca/PO4/Mg greater, less than or equal to intake

Back 19

equal, a steady state is achieved w/ everything going on

Front 20

what is mineral bone made out of?

Back 20

hydroxyapatite- mix of calcium, phosphate, and OH

Front 21

What two important roles does phosphate play?

Back 21

1) high circulation of phosphate promotes deposition of Calcium and phosphate in bone
2) acts as a urinary pH bufffer

Front 22

How much phosphate is filtered, what is the rest up to?

Back 22

90-95%, rest is protein bound

Front 23

Where is phosphate reabsorbed, using what transporter?

Back 23

- PCT, and proximal straight tubule via Na/phosphate co-transporter on apical side, antiported on basolateral

Front 24

About how much phosphate is excreted?

Back 24

roughly 15% of filtered

Front 25

What is the effect of PTH, in terms of the phosphate and discuss specific biochem/cell bio mechanisms?

Back 25

- inhibits phosphate reabsorption by inhibitting the Na/Pi transporter

Front 26

What is the effect of hypocalcemia

Back 26

muscle tetany, spastic muscle contractions

Front 27

What is the effect of hypercalcemia?

Back 27

cardiac arrhythmias, depressed neuromuscular excitability

Front 28

What factor impacts the relative amount of calcium bound versus free?

Back 28

plasma pH

Front 29

True/False: plasma calcium levels are tightly regulated?

Back 29

true

Front 30

What percent of plasma calcium is typically in ionized form?

Back 30

50%

Front 31

What is the primary means of controlling total body calcium?

Back 31

GI modulation of Ca2+ absorption

Front 32

What does calcium homeostasis consist of?

Back 32

the distribution of Ca between bone and ECF

Front 33

What regulates PTH secretion?

Back 33

plasma Ca and plasma phosphate concentrations

Front 34

What percent of calcium is freely filterable? Why?

Back 34

50% b/c the other 50 is protein bound

Front 35

What is the effect of PTH on calcium reabsorptoin and where in the kidney does it take place?

Back 35

promotes reabsorption in distal tubule

Front 36

Is calcium secreted by renal tubule?

Back 36

no

Front 37

What is the primary means of regulating plasma calcium

Back 37

GI

Front 38

What is the mechanism of prox tubule Ca reabsoprtion?

Back 38

intracellular calcium low due to sequestering. Ca moves through channel into cell, then transported out via Na/Ca transporter into plasma

Front 39

What is the effect of PTH, how does it do it?

Back 39

EFFECT: increase plasma Ca
-increase bone breakdown
-decrease renal excretion

Front 40

What is calcitriol?

Back 40

1,25 dihydroxy vitamin D3

Front 41

What is the effect of calcitriol

Back 41

1)increases plasma Ca via increased GI absorption
2) increased phosphate reabsorption
3) increased renal phosphate reabsorption

Front 42

What is the effect of PTH on bone?

Back 42

increases Ca and Pi mobilization from the bone

Front 43

What is the interaction of PTH and vitamin D3

Back 43

stimulates activation of vitamin D3

Front 44

What is the effect of high plasma calcium on PTH

Back 44

low plasma PTH

Front 45

What are the steps in the activation of vitamin D3, where do they occur, and when is it most active

Back 45

1) Vitamin D3-->25-hydoxy Vitamin D3 activation in liver, not very potent
2) 25-OH Vitamin D3-->1,25 dihydroxy Vitamin D3 activation BY PTH in kidney, very potent

Front 46

What are the three effects of calcitrol?

Back 46

1) increase renal phosphate absorption
2) increase GI phosphate absorption
3) increase intestinal calcium absorption

Front 47

Name all four effects of PTH

Back 47

Kidneys:
1) decrease phosphate reab
2) increase calcium reab
3) increase Vitamin D3 formation
Bone
1) increase bone resorption (breakdown)

Front 48

What is the danger of so much water reabsorption in the tubule?

Back 48

This really concentrates the urine of solute, if some of the solutes are drugs that are toxic at high concentration, then exposes tubule to toxicity

Front 49

What is a negative effect of concentration gradients in terms of waste product excretion?

Back 49

The concentration in tubule is high, so the gradients promote absoprtion and make the excretion of waste products inefficient

Front 50

What type of molecules are most likely to be reabsorbed

Back 50

non-polar ie lipid soluble

Front 51

How much of filtered urea is passively reabsorbed in the proximal tubule?

Back 51

40-50%

Front 52

why is urea an ineffective osmole?

Back 52

because it is highly permeable and contributes little to tubular osmolarity

Front 53

What parts of the tubule are impermeable to urea?

Back 53

distal tubule and early collecting duct

Front 54

how does urea recycling work?

Back 54

water reabsorption in collecting duct concentrates a urea creating a gradient for diffusion so urea diffuses out and concentrates the medullary space