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CRRAB II (Elaina) > Renal Phys > Flashcards

Renal Phys Flashcards

1
Q

powerhouse of reabsorption

A

proximal tubule

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2
Q

what is reabsorbed in PT

A

100% glucose
65% h2O (iso-osmotic)
65% Na
80% HCO3

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3
Q

where does Vit D conversion & gluconeogenesis happen

A

Proximal tubule

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4
Q

what is always on basolateral side?

A

3Na/2K ATPase & K+ leak channels

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5
Q

Na+ transport in Proximal Tubule

A

Na/K ATPase on basolateral –> creates Na gradient that allows Na to be drawn in from lumenal side and powers other transporters (secondary) such as glucose, secrete H, AA, PO4

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6
Q

What increases action of Na/H pump in PT?

A

Want to INCREASE Na reabsorption <== SNS, AGII

Want to INCREASE H+ secretion <== low pH, Inc. CO2

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7
Q

How are amino acids transported in PT

A

w/ Na as it travels down its gradient (created by Na/K atpase)

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8
Q

how is H+ handled in PT?

A

Secreted in exchange for Na traveling down its gradient (created by Na/K atpase)

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9
Q

How is glucose handled in PT

A

w/ Na as it travels down its gradient (created by Na/K atpase)
SGLT 1 and 2

Then facilitated diffusion into PT capillaries

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10
Q

How is PO4 handled in PT

A

w/ Na as it travels down its gradient (created by Na/K atpase)
Then facilitated diffusion out of cell into PT capillaries

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11
Q

saturation point of Na/Glucose transporters

A 
transport maximum (Tm)
If reach, cannot reabsorb additional glucose --> urine (at 15 mM glucose)
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12
Q

How is chloride handled in PT

A

Transported in exchange for Formate which can make HF and diffuse in for recycling
H in lumen from Na/H antiporter
Cl leaves cell to PT capillaries via Cl or Cl/K+ fac. diffusion

ALSO PARACELLULAR

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13
Q

how is HCO3 handled in PT

A

reclamation
Diffuse in as CO2
CA –> HCO3 –> leave via Na/3HCO3 fac diffusion

H+HCO3 –> H2CO3 –> CO2 + H2O
H+ from Na/H antiporter

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14
Q

three reasons we need H in lumen from Na/H antiporter

A 
secrete H (low pH or high CO2)
need H+ and Formate --> HF to diffuse into cell for Cl- reabsorption in exchange for formate (recycling)
need H+ +HCO3 to let CO2 into cell --> HCO3 reclamed
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15
Q

how is water handled in PT

A

ISO-OSMOTIC

reabsorbed to follow solute via aquaporins and tight junctions (1/3)

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16
Q

how are WOA/WOB handled in PT

A

only in PT usually
Most you cannot lose, some you can - most freely filtered

neutral/negative enter w/ Na
cations enter uniporters driven by negative membrane potential
some secreted (specific transporter on basolateral side)

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17
Q

polar substances in PT

A

Cannot diffuse in w/ water despite concentration gradient –> excrete

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18
Q

non-polar in PT

A

diffuse in w/ increasing gradient as water is reabsorbed

can make non-polar –> polar so we excrete them (drugs) = biotransformation in liver

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19
Q

Thick ascending LOH absorbs ____ % of filtered sodium

A

25%

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20
Q

Main transporter in thick ascending limb

A

NKCC2 (loop transporter)
Brings in K, Na, 2 Cl
K recycles via RomK

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21
Q

basolateral thick ascending limb LOH

A

KCl symporter
Cl (Barttin)
K leak channels
NaK ATPase

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22
Q

Paracellular transport TAL LOH

A

Ca, Mg, Na

23
Q

Regulation of NKCC2

A

Upregulated by AGII and ADH (not ever downregulated)

24
Q

Bartter syndome

A

Genetic mutation in any of transporters in TAL LOH (NKCC2, RomK, Barttin Cl)
Growth/mental Retardation, volume depletion w/ low blood pressure, hypokalemia, metabolic alkalosis, normal or elevated calciuria

25
Drugs in TAL LOH
Lasix blocks NKCC2
26
DCT main transporter
NCC (NaCl)
27
DCT basolateral side
Cl, KCl, K leak, NaK ATPase, Na/Ca antiporter
28
Ca handling in DCT
TRPV5 --> calbindin --> Na/Ca antiporter | 7-10% reabsorption
29
Gitleman Syndrome
Defect in NCC (NaCl) channel in DCT | Normal blood pressure, metabolic alkalosis, hypocalciuria, hypomagnesiumia, hypokalemia
30
drugs in DCT
thiazide diuretics inhibit NCC channel in DCT
31
two primary types of cells in connecting segment and collecting duct
principal - salt, chloride reabsorption and potasisum excretion intercalated - H and HCO3- excretion and K reabsorption
32
% sodium reabsorption in CD
0-5% (Variable due to regulation of ENaC!)
33
Main transporter in CD
ENaC (Na in --> electrogenic forces push K+ out of RomK)
34
Regulation of ENaC
Aldosterone binds SRE --> inc. genetic expression --> inc. ENaC activity triggered by low Na, high K
35
Little syndrome
Inc. ENaC --> high Na --> HTN and low K (K wasting)
36
Type 1 Pseudohypoaldosteronism
Dec. ENaC --> high aldosterone but low ENaC --> lose Na
37
SNS effect in renal sodium handling
Stimulate Na Uptake in PT (inc. NaK ATPase, inc. Na/H antiporter) Control AA/EA tone to reduce renal blood flow and GFR triggered by hypovolemia, AGII
38
Renin effect in renal sodium handling
Renin --> AGI --> AGII --> Aldosterone Aldosterone inc. ENaC AGII many effects triggered by SNS (NE), decreased stretch in AA, decreased Cl to Macula densa
39
AGII actions
``` systemic vasoconstrictor stimulate PT reabsorption (NaK atpase and NaH antiporter) inc. ENaC (via aldosterone?) Stimulate salt, thirst Stimulate aldosterone inc. SNS activity ```
40
macula densa detects _____ and _____
flow and chloride
41
macula densa if increased flow
inc. GFR - increased filtration and more chloride delivery - reduce renin release
42
macula densa if decreased flow
decreased flow, decreased chloride delivery = not enough sodium or GFR too low --> 1) Prostaglandin release 2) Renin release triggering RAAS
43
Factors that regulate the Na/K pump
insulin, catecholamines, aldosterone | plasma K, exercise, cell breakdown, chronic disease
44
tx for hyperkalemia
insulin + glucose B2 agonist shift K into cells
45
How does aldosterone work with High K
Inc. ROMK, inc. BK (mass secretion of K) but no increase in ENaC (so not huge Na reabsorption)
46
How does aldosterone/AGII work with normal K but very low Na/volume
inc. ENaC but AGII blocks RomK so don't lose a lot of K
47
where and how is K reabsorbed
Type A/B intercalated cell reabsorbed via H+/K+-ATPase (antiporter) upregulated in metabolic acidosis! reabsorbing K+ requires secrete H, reabsorb HCO3
48
Ca++ reabsorption in PCT
passive, paracellular mostly
49
Ca++ reabsorption in TAL LOH
Paracellular (w/ Na, Ca, Mg) | Regulation: Calcium sensing receptor (iCa++) --l claudins --> less Ca gets across
50
Ca reabsoprtion in DCT/CD
TRPV5 -- Calbindin PTH receptor --> inc. uptake and extrusion Ca ATPase to cross basolateral side, also Na/Ca antiporter
51
PTH on bone
``` stimulate release of Ca from stores bone resorption (also get PO4) ```
52
PTH on gut
ca and po4 absorption | mediated by increased 1,25 vit D (inc. production in kidneys)
53
PTH on kidney
inc. Ca resorption, inc. phosphorus exretion | inc. 1,25 vit D production (--> inc. gut absorption)

CRRAB II (Elaina) (7 decks)

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