Renal II Flashcards

1
Q

difference between osmolarity and osmolality?

A
R= osmol/L
L= osmol/kg
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2
Q

what is antidiuresis?

A

normal land-dweller state: when you have high ADH in the blood, urine excretion is low, high reabsorption of urea

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3
Q

what contributes to the hyperosmotic gradient from cortex to medulla?

A

urea- 50%- 600 osmol
Na- 25%- 300 osmol
Cl- 25%- 300 osmol

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4
Q

3 mechanisms that generate hyperosmotic gradient from from cotex to medulla?

A
  1. countercurrent multiplier- permeability differences for Na and H20
  2. urea cycle- leaking out in collecting duct & only participating in right loop
  3. countercurrent exchanger- slow vasa recta flow (permeable to everything) allows time for Na to move in and H20 to move out
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5
Q

5 requirements for hyperosmolarity

A

1) long loops of Henle
2) blood & urine flowing in opposite direction
3) active salt pumping (in basolateral membrane of cells near TAL/DT/CD)
4) differential permeabilities
5) destruction takes days to re-establish

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6
Q

equation for osmolar clearance (Cosm)

A

Cosm= V * Uosm/Posm

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7
Q

what is Ch20? what is -Ch20 also called? what is the equation for Ch20?

A
Ch20= the amount of pure water kidney adds to urine
-Ch20= TcH20

Ch20= V-Cosm

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8
Q

do alterations in Na change the volume or Na concentration of the ECF?

A

only the volume!!

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9
Q

what is the ECV?

A

effective circulating volume- the portion of the ECF that is effectively perfusing the tissues (normally direction proportional to ECF)

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10
Q

what are the 4 ways of regulating renal salt excretion via afferent sensors?

A

a- venous (increased atrial stretch, increased ANP, natriuresis)
b- arterial (increased barros, decreased symp, decreased ADH)
c- hepatic sensors (increased liver p, decreased symp)
d- CNS sensors (increased Na in CSF, decreased symp)

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11
Q

what is natriuresis?

A

increased sodium secretion in urine, followed by water

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12
Q

what is the sympathetic pathway

A

increased sympathetics decreases GFR by constricting afferent arteriole, which increases renin (RAAS) and increases Na reabsorption

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13
Q

what are the affects of angiotensin II and aldosterone?

A

angiotensin II- Na is reabsorbed proximally, causes secretion of ADH
aldosterone- increases NA reabsorption in TAL, DT, CD

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14
Q

how do ANP, BNP, and urodilatin work?

A

decrease aldosterone, decrease renin (decreases Na reabsorption), (decrease sympathetics- increase GFR- increase Na in tube- increase Na excretion)

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15
Q

what are the 3 things that stimulate renin secretion?

A

1) perfusion pressure sensed by baroreceptors in afferent arteriole
2) sympathetic nerves that innervate afferent arterioles
2) tubuloglomerular feedback senses decreased NaCl in macula densa

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16
Q

when is ANP released from atria?

A

1) increase in extracellular fluid volume
2) increase in arterial pressure (increase in LV pressure)
3) increase in venous pressure (increase in right atrial pressure)

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17
Q

what does reabsorption depend on in 3 parts of kidney?

A

1- proximal- filtered load
2- TAL- Na delivery rate
3- DT/CD- Na load remaining

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18
Q

during euvolemia, you have a _______; what percent of Na is filered?

A

net zero Na balance

-99% is filtered

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19
Q

what happens to GFR during volume expansion?

A

GFR increases, decrease reabsorption in proximal tubule and collecting duct
- see decrease sympathetics, increased urodilatin, increased ANP and BNP

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20
Q

what happens during edema? how can it be fixed?

A
  • see decrease in ECV and plasma volumes

- fixed by giving diuretics to decrease Pc and increase PIc

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21
Q

what are 3 things that cause K+ release from the cell?

A

1) epinephrine acting on alpha receptors
2) cell lysis (burns, surgery)
3) hyperosmolarity

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22
Q

what are 5 things that cause K+ uptake by the cell?

A

1) epinephrine activating B2 receptors, especially during exercise
2) increased extracellular K+ stimulating the Na/K ATPase
3) insulin (especially following a meal)
4) aldosterone
5) hyposmolarity

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23
Q

what percent of K+ in kidneys is reabsorbed? what percent is excreted?

A

85-95% is reabsorbed (decreases with more in diet)

15-80% is excreted (increased with more in diet)

24
Q

what 3 factors regulate K+ secretion in the DT & collecting duct

A

1) Na-K atp pump
2) cell-lumen -40 electrochemical gradient
3) K+ permeability of apical membrane

25
Q

5 factors altering K+ secretion

A

1) hormones (aldosterone, GCs ADH)
2) tubular fluid flow
3) dietary intake
4) metabolic acidosis
5) diuretics

26
Q

3 hormones that control distribution of Ca2+ between bone and ECF

A

1) parathyroid hormone
2) calcitriol
3) calcitonin

27
Q

what does parathyroid hormone do?

A
  • released with low Ca2+
  • increase Ca & Pi in plasma by increasing kidney reabsorption, decreases Ca excretion, increases Pi excretion
  • stimulates bone resorption
  • stimulates calcitrol
28
Q

what does calcitriol do?

A
  • made in proximal tubule of kidney
  • stimulates the reabsoption of Ca2+ and Pi by the kidney
  • inhibits the excretion of Ca2+ and Pi
    • stimulates bone resorption
29
Q

what does calcitonin do?

A
  • protects against high Ca2+
  • stimulates bone formation (decreases plasma concentration of Ca2+) & the excretion of Ca2
  • has same effect on Ca2+ and Pi
30
Q

when do you see the spillover effect for phosphate?

A

when you have excess plasma Pi- plasma concentration at rest is super close to RPT, so any extra is filtered/excreted

31
Q

glomerulotubular balance vs. tubuloglomerular feedback

A

GT balance- 67% of what’s put in is reabsorbed
vs
TG feedback- Na sensed by macula densa controls afferent arteriole and GFR

32
Q

what is a non-volatile acid? what is a volatile acid?

A
  • not derived from CO2 (H2CO3 is the ONLY volatile acid- can be excreted as gas by lungs)
33
Q

what is a titratable acid and what is an example?

A
  • any acid that will lose a proton at physologic pH (e.g. H2PO4-)- HPO4- combines with H+ in tubule
34
Q

where is the majority of bicarb reabsorbed? how?

A

proximal tubule as H20 + CO2 when H+ is secreted

35
Q

which buffer is able to adjust it’s quantity based on acidosis?

A
  • ammonium- NH4
36
Q

what happens in the distal tubule?

A

have no CA & most of bicarb has been reabsorbed so mostly have secretion of H+ via H+ K ATPase and H+ ATPase inserted with ISF is acidified

37
Q

what is the difference between type 1 and type 2 RTA?

A

type 1- distal nephron doesn’t secrete H+, H+ goes back into blood
type 2- proximal tubule creates acidosis because low CA inhibits H+ recycling, HCO3- isn’t reabsorbed

38
Q

how is bicarb regulated near RPT?

A

have HCO3-/Cl- antiporter in collecting duct

39
Q

7 factors that regulate HCO3 reabsorption

A
1 GFR
2 Na balance
3 systemic acid-base balance
4 aldosterone
5 arterial K+
6 arterial Cl- 
7 ECV
40
Q

3 forms of protons in urine

A

1 free hydrogen ions
2 titratable acids with HPO4-
3 diffusion trapped with NH4+

41
Q

2 ways in which NH4 is secreted into collecting duct

A

1 non-ionic diffusion and trapping- NH3 follows H+ getting pumped into lumen
2 NH4- H+ antiporters in basolateral & apical membranes

42
Q

how does hypokalemia influence pH?

A
  • low K+ stimulates H+ secretion into tubule
  • have H+/K+ antiporter on basolateral membrane, if K+ isn’t coming into cell, H+ won’t be put back into blood, will be extruded into tube instead
43
Q

3 major systems that maintain plasma H+? which is fastest?)

A

1) chemical buffering
2) renal system (slow)
3) respiratory system (fast)

44
Q

what is the henderson-hasselbach equation adjusted for renal?

A

pH= pKa + log (kidney- bicarb)/(lung- PCO2*0.03)

45
Q

where is phosphate a weak buffer, and where is it stronger?

A

weak- blood

stronger- kidney

46
Q

what is the assumed pKa of blood?

A

6.1

47
Q

what is the difference between an open and closed buffer system?

A
  • open- can easily get rid of acids (Co2 expiration, H+ excretion)
  • closed- total concentration is fixed, just juggle between associated and dissociated forms (Hb, phosphate)
48
Q

what happens to open system buffering power as pH decreases?

A

it increases exponentially, because pCO2 rises and that facilitates removal (closed system peaks where pH= pKa)

49
Q

what is the isohydric principle?

A

when a solution contains more than 1 buffer, all buffer pairs are at equilibrium with the same proton concentration

50
Q

normal pH

A

7.35-7.45

51
Q

normal PaCO2

A

35-45

52
Q

normal bicarb

A

22-28 mM

53
Q

normal H+

A

35-45 nM

54
Q

what is the compensation for metabolic acidosis?

A
  • dec pH
  • dec Co2
    COMP: decrease CO2 more
55
Q

what is the compensation for respiratory alkalosis?

A
  • inc pH
  • dec Co2
    COMP: decrease HCO3