Psl2 - Exam 4 - Part 2

Front 1

Urinary excretion of substance x =

Back 1

Urinary excretion of substance x =

concentration of x * urinary flow rate

Front 2

urinary filtration rate of glucose =

Back 2

urinary filtration rate of glucose =

plasma glucose concentration * rate of flow

Front 3

units of filtration and excretion

Back 3

mg/min

Front 4

Rate of reabsorption =

Back 4

Rate of reabsorption =

rate of filtration - rate of excretion

for a given substance

Front 5

rate of secretion =

Back 5

rate of secretion =

rate of excretion - rate of filtraton

for a given substance

Front 6

GFR

Back 6

glomerular filtration rate

Front 7

clearance

Back 7

how efficiently a substance is removed by a particular organ or process

Front 8

clearance =

Back 8

clearance = VOLUME of plasma cleared/time

Front 9

renal arterial input =

Back 9

renal arterial input =

renal venous output + urinary output

Front 10

mass balance

Back 10

what goes in equals what comes out

Front 11

renal clearance equals =

Back 11

renal clearance equals the excretion rate of a given substance divided by the plasma concentration

Front 12

Cx =

Back 12

Cx = (Ux * V)/Px

excretion rate/plasma concentration
for given substance

Front 13

If a particular substance is neither reabsorbed nor secreted in the nephron, then

Back 13

Cx = GFRx

for that substance

Front 14

GFR is filtration of _____, not filtration of ____

Back 14

GFR is filtration of A SUBSTANCE,

not filtration of FLUID

Front 15

2 substances for which Cx = GFRx

Back 15

insulin

creatinine

Front 16

substance that has significant secretion rate in kidney

Back 16

PAH

Front 17

for substances that are actively secreted, Cx =

Back 17

for substances that are actively secreted,

Cx = renal plasma flow

Front 18

renal plasma flow =

Back 18

RPF = (Ux * V)/Px

where Ux = urine concentration
V = rate of urine flow
Px = plasma concentration

Front 19

how is renal blood flow related to Hct?

Back 19

RBF = Cx/(1-Hct)

where x is a substance that is actively secreted in the kidney

Front 20

Do problems on R15

Back 20

Do problems on R15

Front 21

plasma creatinine concentration vs. GFR is what type of mathematical relationship?

Back 21

inverse

Front 22

2 caveats for using plasma creatinine to estimate GFR

Back 22

relationship not sensitive when changes in plasma creatinine are small (either end of inverse curve)

functional nephrons hypertrophy and compensate for nonfunctional nephrons in kidney disease

Front 23

filtered load =

Back 23

filtered load =

plasma concentration x GFR

for given substance

Front 24

renal threshold of glucose

Back 24

plasma glucose concentration at which you start to see glucose in the urine

Front 25

concentrations of which two substances are elevated in the efferent arterioles compared to the afferent?

Back 25

albumin

RBCs

Front 26

concentrations of what substances are decreased in Bowman's space compared to afferent arterioles?

Back 26

albumin

RBCs

Front 27

8 plasma concentrations that increase as a result of kidney failure

Back 27

PO4
BUN
Creatinine
uric acid
Na+
organic ions
K+
H+

Front 28

What ion concentration goes DOWN in plasma and why?

Back 28

Ca2+ goes down

b/c PO4- goes up

Front 29

As a result of renal failure, what vitamin level is decreased in the GI tract? What is the result?

Back 29

D3 is decreased in the GI tract

leading to decreased Ca2+ absorption

Front 30

Subsequent to renal function loss, arterial BP rises because...

Back 30

Na+ concentration rises
so extracellular fluid volume rises
so arterial BP rises

Front 31

2 direct causes of increased arterial BP due to renal function loss

Back 31

increased renin-angiotensin

increased plasma sodium & ECVF

Front 32

What blood count goes down as a result of renal function loss? Why?

Back 32

Hct

b/c of decreased erythropoietin production by the kidney

Front 33

What drug is used to increase Hct in renal failure pts?

Back 33

Epo

Front 34

Kf refers to what two factors?

Back 34

how permeable is glomerular membrane?

how much area of membrane is available?

Front 35

filtration pressure equilibrium in glomerulus

Back 35

point at which protein becomes equally concentrated on both sides of glomerular membrane

therefore, despite glomerular membrane being present, no gradient to promote filtration

Front 36

Kf is (higher/lower) than filtration constants of systemic capillaries

Back 36

much HIGHER

Front 37

where are there sharp decreases in pressure in renal blood flow?

where are there virtually no changes in pressure?

Back 37

sharp decreases - afferent and efferent arterioles

no change - glomerular capillary

Front 38

vasoconstrictors have what effect on pressure in glomerular capillary

Back 38

more resistance in arterioles --> lower the pressure in glomerular capillary

Front 39

vasodilators have what effect on pressure in glomerular capillary

Back 39

less resistance in arterioles --> increase the pressure in glomerular capillary

Front 40

effect of vasoconstriction on renal plasma flow?

Back 40

decrease!

with constriction, less plasma moving through arterioles!

Front 41

autoregulatory range of mean arterial BP

Back 41

70 - 160 mmHg

Front 42

despite changes in arterial BP, ___ & ____ are held almost constant

Back 42

GFR

RBF

Front 43

myogenic feedback

Back 43

as smooth muscle is stretched, it reflexively contracts

"stretch depolarization"

Front 44

tubuloglomerular feedback

Back 44

increased GFR -->
increased filtration -->
increased NaCl delivery to Henle's loop -->
-->increased Na+ at macula densa --> signal to constrict afferent arteriole
--> decrease GFR

Front 45

SNS effects on Pgc, GFR and RBF

where Pgc = pressure in glomerular capillaries

GFR = glomerular filtration rate
RBF = renal blood flow

Back 45

vasoconstriction of afferent arteriole -->

decreased GFR
decreased RBF

Front 46

how does increased production Angiotensin II affect Pgc, GFR and RBF

where Pgc = pressure in glomerular capillaries

GFR = glomerular filtration rate
RBF = renal blood flow

Back 46

vasoconstriction of efferent arteriole

decreased RBF
increased Pgc
increased GFR

Front 47

how do ACE inhibitors affect Pgc, GFR and RBF

where Pgc = pressure in glomerular capillaries

GFR = glomerular filtration rate
RBF = renal blood flow

Back 47

relax efferent arteriole

increase RBF
decreased Pgc
decreased GFR

Front 48

effects of NO on Pgc, GFR and RBF

where Pgc = pressure in glomerular capillaries

GFR = glomerular filtration rate
RBF = renal blood flow

Back 48

relaxes afferent arterioles

increased Pgc
increased GFR
increased RBF

Front 49

relative concentration in glomerular filtrate =

Back 49

ultrafiltrate concentration/plasma concentration

of a given substance

Front 50

If relative concentration in glomerular filtrate is less than 1, ...

Back 50

plasma concentration is greater

Front 51

where does colloid osmotic pressure stop increasing?

why?

Back 51

at efferent arteriole

b/c filtration stops after glomerular capillaries

Front 52

what pressure decreases starting at efferent arteriole?

Back 52

osmotic

b/c filtration has stopped

Front 53

glomerulotubular balance

Back 53

more filtration -->

more concentrated ultrafiltrate -->

more reabsorption

Front 54

effect of urinary tract obstruction on pressures. which pressure affected and how? end result?

Back 54

increase bowman's space hydrostatic pressure.

opposes filtration (decreased GFR)

Front 55

effect on hypotension on pressures.

which pressure affected? end result?

Back 55

lower Pgc

decrease GFR

Front 56

what filtration-related is affected by DM nephropathy?

Back 56

Kf

decreased GFR

Front 57

effect on GFR from hyperalbuminemia

Back 57

increased colloid osmotic pressure

decreased GFR

Front 58

average, normal GFR

Back 58

180 L/day

Front 59

average, normal plasma sodium concentration

Back 59

142 mmol

Front 60

What carries Cl- into proximal tubule cells?

Back 60

formate oxalate

Front 61

2 anions that accompany Na+

Back 61

Cl-

HCO3-

Front 62

important mechanism for acidifying urine

Back 62

HCO3- cycle

Carbonic anhydrase (CA)
HCO3- --> H20 + CO2 outside the cell

H2O + CO2 --> HCO3 inside the cell

Front 63

CA inhibitors are what type of drug?

Back 63

diuretics

inhibits resorption of HCO3-
ergo, reduce resorption of Na+
ergo, reduce resorption of water
ergo, MORE URINE

Front 64

main mechanism of eliminating drugs from blood stream

Back 64

organic ion secretion in nephron

Front 65

penicillin is brought into proximal tubule cells in exchange with what?

Back 65

alpha-KG

Front 66

penicillin is brought into tubule urine from proximal tubule cells in exchange with what?

Back 66

anion, usu. Cl-

Front 67

T/F: creatinine is zwitterionic

Back 67

TRUE: creatinine is a zwitterion at physiologic pH

Front 68

What blocks the NCCK transporter?

Back 68

furosamide (diuretic)

Front 69

what blocks Na/Cl- cotransporters?

Back 69

thiazides (diuretics)

Front 70

ENAC

Back 70

epithelial Na+ channels

Front 71

# of ENAC on apical side of DC cells regulated by...

Back 71

aldosterone

Front 72

CA inhibitor diuretics work in what type of cells?

Back 72

proximal tubule cells

Front 73

thiazide and furosomide diuretics work in what type of cells

Back 73

DC cells in distal tubule

Front 74

obligatory output

Back 74

regardless of how limited water intake is, still must produce a certain amount of urine to get rid of excess solutes

Front 75

ADH is released from the ______ and travels to the ______

Back 75

ADH is released from the POSTERIOR PITUITARY

and travels to the DISTAL COLLECTING TUBULE

Front 76

2 main stimulators of ADH secretion

Back 76

hyperosmolality (high solute concentration in plasma)

hypovolemia/hypotension

Front 77

6 stimulators of ADH secretion

Back 77

hyperosmolality

hypovolemia

Angiotensin II

pain

stress

anethesia

Front 78

2 inhibitors of ADH secretion

Back 78

EtOH

ANP

Front 79

central (neurogenic) diabetes insipidus (DI)

Back 79

lacking production/release of ADH

b/c no ADH, produce large amount of very dilute urine

responds to injected ADH

Front 80

nephrogenic diabetes insipidus

Back 80

normal release of ADH, but ADH not affect kidney properly

same symptoms as central CI, but
unresponsive to injected ADH

Front 81

function of ADH

Back 81

makes collecting duct water permeable

Front 82

fluid in descending tubule is ____ tonic

fluid in the loop of Henle is ____ tonic

fluid in the ascending tubule is ____ tonic

Back 82

ISO -

HYPER-

HYPO-

Front 83

DOES FURASAMIDE BLOCK THE ABILITY TO CONCENTRATE OR DILUTE URINE?

Back 83

both

blocks creation of gradient

Front 84

ADH receptor

Back 84

V2R - Gprotein coupled

Front 85

action of ADH

Back 85

--> insertion of aquaporin-2 channels in DC cells

--> increased synthesis of aquaporin-2

Front 86

2 vascular structures with low pressure sensors

Back 86

cardiac atria

pulmonary vasculature

Front 87

3 vasculature structures with high pressure sensors

Back 87

carotid sinus

aortic arch

jugulomedullary apparatus

Front 88

angiotensinogen is released by the ____

renin is released by the ______

Back 88

angiotensinogen is released by the LIVER

renin is released by the JGA

Front 89

enzyme that converts angiotensin I to angiotensin II

Back 89

ACE

Front 90

3 functions of angiotensin II

Back 90

--> hypothalamus --> thirst & ADH

--> adrenals --> aldosterone secretion

--> decrease reabsorption of sodium and water

Front 91

5 vascular measurements that tend to all change in unison

Back 91

sodium resorption
effective circulating volume (ECV)
cardiac output
stroke volume
arterial BP

Front 92

where does the discrepancy occur in the 4 unison measurements in heart failure

Back 92

discrepancy between ECF volume & stroke volume

and cardiac output & arterial BP

ergo, EFFECTIVE circulating volume down, but ECF volume up

Front 93

majority of K+ elimination is done by the ____

Back 93

kidneys

Front 94

most K+ in filtered load presented to nephron is ____, but some is _____

Back 94

reabsorbed, but some is secreted

Front 95

major causes of K+ imbalance stem from the _____

Back 95

kidneys

Front 96

insulin promotes K+ _____ and lowers ______

Back 96

insulin promotes K+ uptake and lowers plasma K+ concentration

used to stablize hyperkalemia

Front 97

mechanism of action of insulin on K+ uptake

Back 97

leads to activation of Na+/K+ ATPase pumps

Front 98

lack of insulin, as in DM I, can lead to _____ (wrt K+)

Back 98

hyperkalemia

Front 99

3 hormones that stimulate K+ uptake

Back 99

insulin

epinephrine

aldosterone

Front 100

Addison's disease includes an inadequate production of ____

Back 100

aldosterone

Front 101

low plasma pH has what effect on K+ in body?

Back 101

low plasma pH = high [H+]

high [H+] increases drive of H+ into cells

increase rate of H+/K+ exchange, driving K+ out of cells

Front 102

where does significant secretion of K+ occur at normal to high K+ intake levels?

Back 102

principle cells

Front 103

2 aays elevation of plasma K+ increases K+ secretion by principle cells

Back 103

directly affects principal cells to cause secretion

increases aldosterone secretion from adrenals

aldosterone affects principal cells to stimulate Na+/K+ ATPase, driving K+ out of cells