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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
Q

Drugs in TAL LOH

A

Lasix blocks NKCC2

26
Q

DCT main transporter

A

NCC (NaCl)

27
Q

DCT basolateral side

A

Cl, KCl, K leak, NaK ATPase, Na/Ca antiporter

28
Q

Ca handling in DCT

A

TRPV5 –> calbindin –> Na/Ca antiporter

7-10% reabsorption

29
Q

Gitleman Syndrome

A

Defect in NCC (NaCl) channel in DCT

Normal blood pressure, metabolic alkalosis, hypocalciuria, hypomagnesiumia, hypokalemia

30
Q

drugs in DCT

A

thiazide diuretics inhibit NCC channel in DCT

31
Q

two primary types of cells in connecting segment and collecting duct

A

principal - salt, chloride reabsorption and potasisum excretion
intercalated - H and HCO3- excretion and K reabsorption

32
Q

% sodium reabsorption in CD

A

0-5% (Variable due to regulation of ENaC!)

33
Q

Main transporter in CD

A

ENaC (Na in –> electrogenic forces push K+ out of RomK)

34
Q

Regulation of ENaC

A

Aldosterone binds SRE –> inc. genetic expression –> inc. ENaC activity

triggered by low Na, high K

35
Q

Little syndrome

A

Inc. ENaC –> high Na –> HTN and low K (K wasting)

36
Q

Type 1 Pseudohypoaldosteronism

A

Dec. ENaC –> high aldosterone but low ENaC –> lose Na

37
Q

SNS effect in renal sodium handling

A

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
Q

Renin effect in renal sodium handling

A

Renin –> AGI –> AGII –> Aldosterone

Aldosterone inc. ENaC
AGII many effects

triggered by SNS (NE), decreased stretch in AA, decreased Cl to Macula densa

39
Q

AGII actions

A 
systemic vasoconstrictor
stimulate PT reabsorption (NaK atpase and NaH antiporter)
inc. ENaC (via aldosterone?)
Stimulate salt, thirst
Stimulate aldosterone
inc. SNS activity
40
Q

macula densa detects _____ and _____

A

flow and chloride

41
Q

macula densa if increased flow

A

inc. GFR - increased filtration and more chloride delivery - reduce renin release

42
Q

macula densa if decreased flow

A

decreased flow, decreased chloride delivery = not enough sodium or GFR too low –>

1) Prostaglandin release
2) Renin release triggering RAAS

43
Q

Factors that regulate the Na/K pump

A

insulin, catecholamines, aldosterone

plasma K, exercise, cell breakdown, chronic disease

44
Q

tx for hyperkalemia

A

insulin + glucose
B2 agonist

shift K into cells

45
Q

How does aldosterone work with High K

A

Inc. ROMK, inc. BK (mass secretion of K) but no increase in ENaC (so not huge Na reabsorption)

46
Q

How does aldosterone/AGII work with normal K but very low Na/volume

A

inc. ENaC but AGII blocks RomK so don’t lose a lot of K

47
Q

where and how is K reabsorbed

A

Type A/B intercalated cell

reabsorbed via H+/K+-ATPase (antiporter)
upregulated in metabolic acidosis!

reabsorbing K+ requires secrete H, reabsorb HCO3

48
Q

Ca++ reabsorption in PCT

A

passive, paracellular mostly

49
Q

Ca++ reabsorption in TAL LOH

A

Paracellular (w/ Na, Ca, Mg)

Regulation: Calcium sensing receptor (iCa++) –l claudins –> less Ca gets across

50
Q

Ca reabsoprtion in DCT/CD

A

TRPV5 – Calbindin

PTH receptor –> inc. uptake and extrusion

Ca ATPase to cross basolateral side, also Na/Ca antiporter

51
Q

PTH on bone

A 
stimulate release of Ca from stores
bone resorption (also get PO4)
52
Q

PTH on gut

A

ca and po4 absorption

mediated by increased 1,25 vit D (inc. production in kidneys)

53
Q

PTH on kidney

A

inc. Ca resorption, inc. phosphorus exretion

inc. 1,25 vit D production (–> inc. gut absorption)

CRRAB II (Elaina) (7 decks)

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