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Facts Flashcards

1
Q

renal cortex

A

90% of renal blood

glomeruli, PCT and DCT

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2
Q

renal medulla

A

10% of renal blood: prevents washing out hypertonic medulla

tubules and vasa recta

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3
Q

cortical nephrons

A

85% of nephrons
small; short LoH
lower arterial perfusion and filtration rate
reserve capacity

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4
Q

juxtamedullary nephrons

A

15%
large; long LoH
higher arterial perfusion and filtration rate
operate at full capacity
concentration of urine: conserve water and Na conservation to produce hypertonic medulla

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5
Q

mesangium

A

support capillary loops
can alter capillary SA (actin and myosin)
ingest and remove circulating immune complexes (only fenestrated endothelial cells between it and blood; no BM)

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6
Q

podocytes

A

visceral epithelial cells

heavy proteinuria: podocyte problem

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7
Q

macula densa

A

cortical thick ascending limb
senses Cl and syn. and releases renin (systemic) and Na-K-2Cl cotransporter releases ATP or Ca for smooth muscle contraction (auto regulation)
low delivery: vasodilate afferent
high delivery: constrict afferent

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8
Q

proximal tubule

A

cortex (PST descends to corticomedullary junction)
bulk reabsorption (2/3 of filtrate): iso-osmotic
reabsorption:
50-55%: Na (active) and H2O
90% (active): HCO3
100% (active): glucose, amino acids
PO4, urate, organic anions
urea, K (passive)
production: NH3
secretion (mostly active cotransporters): organic acids and bases (cations, anions)
passive Cl paracellular reabsorption (Na reabsorption creates a neg. lumen driving Cl and HCO3 reabsorption; maintains electroneutrality)

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9
Q

Na/K- ATPase

A 
all cells
primary active transport
basolateral: interstitial
3 Na out of cell (into capillary)
2 K into cell
creates Na electrochemical potential gradient
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10
Q

Na/X cotransport

A

proximal tubule
luminal
active: coupled to Na electrochemical potential gradient
X: glucose or amino acids or PO4

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11
Q

Cl-/anion exchanger

A 
proximal tubule
passive
luminal
Cl- into cell
anion into tubule lumen
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12
Q

Na/H exchanger

A

proximal tubule
luminal
Na into cell
H into tubule lumen

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13
Q

HCO3 reabsorption

A

proximal tubule

active: driven by H secretion
1. H in lumen (due to Na/H exchanger) binds filtered HCO3
2. lumen: CA converts carbonic acid to CO2 + H2O that move into cell
3. cell: CA converts CO2 + H2O to H + HCO3
4. HCO3 moves into interstitium (HCO3/Na cotransporter) creating a negative charge on interstitial side of cell
5. negative charge drives paracellular reabsorption of Na, Ca, Mg

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14
Q

Thin descending limb

A 
cortex to outer medulla
passive: osmotic gradient
reabsorption: H2O, urea
impermeable: Na
concentrates tubular fluid
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15
Q

Thin ascending limb

A

passive: osmotic gradient
reabsorption: NaCl
impermeable: H2O, urea
decrease tubular fluid osmolarity

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16
Q

Thick ascending limb

A

between medulla and cortex
active
reabsorption: NaCl (20-25%), Ca, Mg
impermeable: H2O, urea
recycle: NH4
requires O2 to operate N/K-ATPase that maintains ion gradient for Na/K/2Cl
other: basolateral Cl (into interstitium), basolateral K/Cl cotransporter (into interstitium), apical K channel (into tubular fluid)

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17
Q

Na/K/2Cl transporter

A

thick ascending limb
luminal
Na/K/2Cl into cell from tubular lumen
driven by: electrochemical gradient

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18
Q

ROMK

A

thick ascending limb
K from cell into tubular lumen that makes it more positive
drives Mg, Ca into interstitium (paracellular)

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19
Q

active Na reabsorption in thick ascending limb

A

DCT and CD

  1. Na/K ATPase creates concentration gradient by pumping Na out of the cell into the interstitium
  2. Na/K/2Cl transporter needs all ions to work
  3. K must be supplied to tubule by ROMK for Na/K/2Cl to work
  4. Cl leaves cell via basolateral Cl channels
  5. K in tubular lumen causes paracellular reabsorption of Na, Ca, Mg
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20
Q

affarent arteriole

A

baroreceptor

myogenic sensor: release renin from JG cells in response to low flow or inhibit renin release in high flow (systemic)

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21
Q

distal convoluted tubule

A 
cortex
reabsorption: Na (5-8%), Cl
impermeable: H2O, urea
major site of Ca reabsorption/regulation
dilution of tubular fluid
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22
Q

Na/Cl cotransporter (NCCT)

A

DCT
luminal
electroneutral
Na and Cl into cell

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23
Q

Ca dependent protein (TRPV5)

A

DCT: responds to PTH
luminal
Ca into cell

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24
Q

Ca/Na countertransporter

A

DCT
basolateral
3 Na into cell
1 Ca into interstitium

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25
collecting duct
6-8 DT form 1 CD cortex through medulla reabsorption: Na (2-3%), Cl secretion: K (ONLY place) impermeable: H2O, urea more Na reabsorption than K secretion: Cl reabsorbed *water deprivation: ADH causes high water permeability: reabsorb water
26
principal cells
cortical CD and inner medullary CD reabsorption: Na/H2O secretion: K
27
alpha-intercalated cells
``` cortical CD and outer medullary CD active normal pH: secretion: H alkalosis: reabsorb H H-ATPase or H-K ATPase ```
28
beta-intercalated cells
CD normal pH: reabsorb HCO3 secrete: HCO3 under alkalosis Cl-HCO3 exchanger
29
epithelial sodium channel (ENac)
CD luminal Na into cell due to negative cell interior created by ATPase now negatively charged lumen favors secretion of K
30
cortical collecting duct
concentrates urine
31
medullary collecting duct
urea concentration in urine increases
32
What does the kidney do during fasting?
gluconeogenesis
33
ECF
1/3 TBW Na, Cl, HCO3 slightly more Na and less Cl in plasma (Gibbs Donnan: Pr-)
34
plasma
1/4 ECF | Pr
35
interstitial fluid
3/4 ECF
36
ICF
2/3 TBW K, Mg, PO4, Pr NO Ca
37
TBW
60% body weight in males 50% females inversely related to fat
38
mMol/L vs. mOsm/L
Osm counts each particle that a molecule can ionize into | Mol counts each molecule
39
low PNa, high urea
iso-osmotic: hypoosmotic NaCl with added urea to make iso-osmotic cell swells: urea gets into ICF and ECF becomes hypo-osmotic
40
normal PNa, elevated urea
hyperosmotic | no change in cell volume
41
low PNa, high glycerol
shrink initially, then swell
42
driving force for Na reabsorption
``` active through length of nephron driving forces: decrease in intracellular Na increase in membrane potential ```
43
HCO3/Na cotransporter
PT luminal 3 HCO3 and 1 Na into interstitium from cell
44
water reabsorption
PT facilitated by mass solute reabsorption in PT osmotic gradient drives water reabsorption by leaky epithelium with high hydraulic conductivity (high Kf)
45
protein and peptide reabsorption
PCT large proteins not filtered peptides have greater filtration and are reabsorbed by transporters
46
PO4 reabsorption
PCT Na/PO4 cotransporter low threshold (poised at plasma concentration), partially excreted in urine PTH: decreases transport maximum
47
Cl reabsorption
PCT passive driven by: concentration gradient created by water reabsorption, Na electrochemical potential gradient less reabsorbed because of HCO3 active transport
48
K reabsorption
PCT | passive transport along concentration gradient though claudins
49
reabsorption of urea
PCT passive: slow only 50% reabsorbed increase in urine flow increase urea clearance
50
mannitol
poorly permeant freely filtered, not reabsorbed: increase osmolarity and cause diuresis Tx: cerebral edema; reduce intracranial and intraocular pressure, promote excretion of toxins, edema
51
Na channels
PT luminal passive
52
What maintains net filtration in glomerular capillary bed 50-100x greater than other capillary beds?
glomerular capillary bed is separated by the afferent and efferent arterioles (resistance arterioles) that cause arterio-venous pressure drops that occur in two steps maintaining high hydrostatic pressure
53
What happens to plasma hydrostatic pressure and oncotic pressure from afferent to efferent arteriole? How does this effect the peritubular capillary?
hydrostatic pressure drops in afferent and efferent arteriole: increase in oncotic pressure from afferent to efferent arteriole resulting in a low hydrostatic pressure in peritubular capillary and an increase in peritubular oncotic pressure allowing for reabsorption
54
B1 adrenergic nerves
SNS response stimulates renin release from JG cells (systemic)
55
renin-angiotensin system
decrease BP or perfusion decreases ECFV 1. increased SNS firing 2. JG cells release renin 3. renin converts alpha2 globulin to angiotensin I 4. angiotensin converting enzyme converts angiotensin I to angiotensin II 5. angiotensin II importent regulatory system in intact system NOT part of kidney autoregulation
56
SNS activation effects on kidney
constrict afferent and efferent arterioles causing reduced RPF and PG and therefore GFR stimulates renin secretion and increase Na reabsorption ONLY important under severe ECFV loss: overrides auto regulation decrease Kf by stimulating mesangial cells
57
determinants of GFR
Kf and net filtration pressure: hydraulic conductivity, glomerular SA, capillary hydrostatic pressure, capillary oncotic pressure, bowman's space hydrostatic pressure
58
duct of Bellini
CDs join in medulla | drain into minor calyx
59
K secretion
CD driven: high intracellular K and negative lumen regulated by: increase: increase Na delivery of Na to CD: change in lumen-negative voltage: aldosterone, vomiting, diuretics, Barrter's, Gitelman's decreased: renal failure, distal tubular disfunction, decreased distal tubular flow, hypoaldosteronism
60
H-ATPase
``` DCT and CD luminal active H secretion alkalosis: basolateral: H into interstitium ```
61
HCO3-Cl exchanger
``` DCT and CD? basolateral HCO3 into interstitium Cl into cell alkalosis: luminal: HCO3 into lumen, Cl into cell ```
62
H/K- ATPase
electroneutral transport | expressed under high acidosis condition
63
HCO3 secretion
*under alkalosis condition H-ATPase and HCO3-Cl exchanger switches direction activate alpha and B intercalated cells
64
bicarbonate buffer system
CO2 + H2O .... H2CO3.... H + HCO3
65
What is going on if Na concentration stays constant but Cl concentration changes?
acid-base disorder
66
How do acid base disorders affect serum K?
alkalosis: hypokalemia acidosis: hyperkalemia
67
How does plasma tonicity affect K serum?
solvent drag: K moves in direction of water hyperosmolarity: hyperkalemia hypoosmolarity: hypokalemia
68
How do cell lysis and cell proliferation affect K?
lysis: hyperkalemia proliferation: take up K: hypokalemia
69
osmoreceptor
hypothalamus: senses changes in osmolarity 1. supraoptic and paraventricular nuclei stimulates posterior pituitary: increase intracellular Ca causes fusion of AVP vesicles at nerve terminal and secretion of AVP 2. lateral preoptic nucleus: regulate thirst
70
positive CH2O
Uosm less than Posm | dilute urine: increase plasma osmolarity
71
negative CH2O
Uosm greater than Posm | concentrate urine: decrease plasma osmolarity
72
factors responsible for medullary hyperosmolarity
1. arrangement of loop of Henlee and vasa recta 2. active transport of Na and co transport of K and Cl out of TALH into medullary ISF 3. active transport of Na out of CD into ISF 4. passive diffusion of urea from inner medially CD into medullary ISF 5. only small amount of water from medullary tissues into medullary interstitium 6. low medullary blood flow
73
components of GBM
perlecan, entactin, laminin, type IV collagen
74
When do ECV and ECFV not move in the same direction?
Liver disease, CHF, nephrotic syndrome, pregnancy and anaphylaxis ECV decreased ECFV increased ECV decrease is due to either decreased CO or arterial vasodilation causing secondary ECFV increase

SS- Renal (11 decks)

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