E: Renal Filtration / Tubular Transport /Body Fluids Flashcards
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A: Ultrafiltration (driven by Starling Forces) is the 1st part of creating Urine and Ultrafiltrate usually has NO proteins or [cellular elements]. Salt & Organic compound makeup is similar here as it is in plasma. GFR and RPF are held in their physiologic ranges by autoregulation
B: [Glomerular filtration barrier] determines makeup of Ultrafiltrate – based on size & electrical charge.
ºCATion/Neutral molecules smaller than [20 Å] = GOOD FILTRATION
ºMolecules between [20 - 42 Å] = {variable based on chrge} –> ( [ANionic serum albumin] weighs 35Å but filters poorly. The little that’s filtered is ReAbsorbed by PCT and some goes to urine)
ºANions DON’T FILTER WELL BECAUSE [NEGATIVE GLYCOPROTEINS] EXIST ON THE [Glomerular filtration barrier] surface and Repels them away!
C: CATions FILTER BETTER than Neutral molecules
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A:NEGATIVELY CHARGED [Glomerular Capillaries] have low resistance and HIGH filtration coefficient —> {Kf= [PermeabilityGC] • [AreaGC] }
B: The 2 major plasma proteins are [Albumin] and [Immunoglobulins IgG] –> Because [IgG are BIGGER than 42Å they are NOT Filtered!
C: Starling Forces Drive Glomerular Filtration. There are 4 types that [Favor/+] and [impede/-]
- Forces tht [Favor/+] [Glomerular Filtration]:
º[Glomerular capillary HYDROSTATIC pressure]= {+PGC}
º[Bowman space Oncotic pressure (which equals 0 anyways)] = {+©BS}
C2: Net Ultrafiltration pressure = [©BS + (PGC - ©gc - pbs) ]
[P= HYDROSTAIC PRESSURE]
[©: OnCotic Pressure]
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C: Starling Forces Drive Glomerular Filtration. There are 4 types that [Favor/+] and [impede/-]
- forces that [impede/-] [glomerular filtration]
•[glomerular capillary oncotic pressure] = [-©gc}
•[bowman space hydrostatic pressure] = {-pbs}
C2: Net Ultrafiltration pressure = [©BS + (PGC - ©gc - pbs) ]
C3: GFR ={ Kf x [©BS + (PGC - ©gc - pbs) ] }
A: Changes in Forces along glomerular capillaries:
1) small DEC in PGC since we have low resistance capillaries
2) LARGE INC in {©gc} since these are a concentration of proteins that do NOT filter and impede filtration
3) No change in {pbs} (this is a constant force that propels urine through tubules)
4) DEC in net ultrafiltration pressure
5) Glomerular Flow = [(Hydraulic Conductance) • (net pressure gradient) ]
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A: [Glomerular capillaries] have a PGC that’s TWICE as large than systemic capillaries and [Kf that’s 100x larger]! GFR can be altered by changing Kf or any of the [Starling Forces].
A2: Normal people regulate GFR by manipulating afferent/Efferent arteriolar resistance—>changes PGC
3 BIDIRECTIONAL rules for changing PGC
1) DEC EFFERENT arteriolar resistance—>DEC PGC
2) DEC afferent arteriolar resistance —> INC PGC
B: Renal Dz
ºGlomerulonephritis –> {early stages=DEC {©gc}–>INC GFR} BUT {LATE STAGES= INC {pbs]–>DEC GFR}
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ºRenal Stones = INC {pbs}–>DEC GFR
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º[nephritic syndrome]= INC Kf –> Proteinuria :-(
Kf = permeability of glomerular capillaries
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A: TOTAL RENAL BLOOD FLOW = 1200 mL blood/min and [4 mL blood/min PER gram of tissue]. Although blood-flow distribution is NOT FIXED all over the Kidneys…
1st: RENAL CORTEX has HIGHEST vascularization (90% RBF)
2nd: Outer Medulla has Little vascularization (8% RBF)
3rd: inner medulla has lowest vascularization (2% RBF)
B: There is a 7:1 ratio of [CORTICAL:juxtamedullary] nephrons–>MUCH more CORTICAL nephrons. Glomerular & Peritubular capillaries are confined to the RENAL CORTEX.
C: [Hydrostatic Pressure] overall DEC from Renal Artery
–>renal vein BUT DECREASES MOST in [afferent & EFFERENT arterioles] due to their high resistance.
D:
º[Oncotic Pressure ©] INC in glomerular capillaries due to concentration of plasma proteins during filtration
º[oncotic pressure ©] decreases in peritubular capillaries due to dilution and lost of those plasma proteins from ReAbsorption
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A: Glomerular Autoregulatory mechanisms work Only within arterial pressures between 100-180 mmHg.
- If BP is GREATER than 180 —> [GFR/RBF] INC
- *if bp is lower than 100—> [gfr/rbf] will decrease
A2: xxxRenal Shutdown occurs when arterial pressure falls lower than 70 mmHg! xxx–>Kidneys are still perfused but No urine is made. RENAL DEATH OCCURS WHEN BP is lower than 0 mmHg.
B: Glomerular Autoregulatory mechanisms include:
- Smooth m. myogenic theory
- [Tubuloglomerular feedback theory]
- Intrinsic factors such as Prostaglandins / NO / dopamine / Kinins / (endothelin)
- Extrinsic Regulation
C: [Tubuloglomerular feedback theory] =
INC GFR–>INC NaCl in tubule fluid of [loop of Henle]
—>sensed by [macula densa] –>INC Afferent arteriole resistance —> DEC GFR!
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A: During Extrinsic Regulation of Glomerular Autoregulation ºsympathetic innervation to afferent & EFFERENT arterioles, ºblood borne/endogenous substances (Angiotensin II / ADH / ATP / ACE) and
ºstress factors like hemorrhage, dehydration and severe hypoxia all DEC [GFR & RBF]
B: Hemorrhaging stimulates [Renal Sympathetic nerves] and [afferent intrarenal receptors] to produce (Angiotensin II Constrictor) via [Renin-Angiotenin pathway]!
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A: Urine formation involves 3 processes
- ultrafiltration of plasma by glomerulus
- ReAbsorption of water/solutes from that ultrafiltrate
- Secretion of selected solutes into tubular fluid
B: Less than 1% of filtered [water and NaCl] is actually excreted in urine. MOST OF [Water and NaCl] IS REABSORBED!
[50% of Filtered Urea is Excreted OUT in Urine]
C: By Using transport proteins on nephron membranes the Kidneys can ReAbsorb & Secrete to modulate Urine composition/volume –> precisely controls composition/volume, pH and osmolality of [extracellular/intracellular fluid compartments]
C2: Genetic/Acquired defects to these transport proteins on nephron membranes are the cause of many kidney Dz
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There are 4 [Renal Membrane Transport] mechanisms:
1. [Passive Simple Diffusion] (UnLimited vs. [facilitated limited])
2. Primary Active Transport
3. Secondary Active Transport
4. [Transepithelial Solute & Water Transport————————————————————————————–
1. [Passive Simple Diffusion]
A: UnLimited = ions move passively downhill from High –>Low Electrochemical Gradients & [water moves passively from low–>high osmotic gradients (AKA OSMOSIS)]
vs.
B: [facilitated limited] = INC rate of passive transfer of species complexed with membrane entities/uniporter proteins (i.e. in RBC)
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There are 4 [Renal Membrane Transport] mechanisms:
- [Passive Simple Diffusion] (UnLimited vs. [facilitated limited])
- Primary Active Transport
- Secondary Active Transport
- [Transepithelial Solute & Water Transport
- ————————————————————————————- - Primary Active Transport= Transport substances UpHill AGAINST electrochemical gradient requiring [DIRECT energy/hydrolysis of ATP].
ºEFFECTS of the pump can be saturated but NOT the pump itself = [Gradient-time limited]
ºEnodcytosis of proteins is ATP dependent an example of [Primary Active Transport]
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There are 4 [Renal Membrane Transport] mechanisms:
- [Passive Simple Diffusion] (UnLimited vs. [facilitated limited])
- Primary Active Transport
- Secondary Active Transport
- [Transepithelial Solute & Water Transport]
- ————————————————————————————- - Secondary Active Transport= Transport substances UpHill AGAINST electrochemical gradient requiring [inDirect energy/ion gradient]
ºTHE PUMP ITSELF CAN BE OVERSATURATED = [Tm limited]
ex: =
ºsymporter pumps for [Na/[Amino Acid]] and [Na/Glucose] exchange
OR
ºAntiPorter pumps for [Na+/H+] TRADE OUT
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There are 4 [Renal Membrane Transport] mechanisms:
1. [Passive Simple Diffusion] (UnLimited vs. [facilitated limited])
2. Primary Active Transport
3. Secondary Active Transport
4. [Transepithelial Solute & Water Transport]
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4. [Transepithelial Solute & Water Transport]
A: transceullar pathway = Na+ runs across cells using [Na/K ATPase pump]
vs.
B: PARAcellular pathway = Ca/Mg/K moves between cells by [solvent drag bulky transport] which occurs when a solvent literally drags ions along with it when osmosing
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A: When Solute/Water moves across the apical membrane of the PCT CELL some of it reenters tubule fluid but MOST Enters interstitial space which then flows into [Body blood capillaries] for ReAbsorption.
A2: Starling forces across capillary wall determines how much fluid will chose either pathway.
A3: [Renal Membrane Transport mechanisms] determine amount
of solute and water that INITIALLY enters PCT cell
B: Fick principle in Kidneys = DEC O2 supply —> DEC O2 demand from the kidneys. If blood flow is restricted to Kidneys—>KIDNEYS WILL EXTRACT LESS OXYGEN to help the situation!
(vs. Sk. muscle which extracts more O2 when perfusion is decreased due to CONSTANT O2 demand–>restricts perfusion)
B2: [Renal O2 consumption] ≈ [Na+ ReAbsorbed] ≈ [Na+ Filtered] ≈ [GFR] ≈ [RPF] ≈ [RBF]
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A: {Tm} = [Tubular Transport Max} and is measured in units of LOAd = mg/min. You can only EVER calculate Tm when it is exceeded! —>
ex: Tm for Active ReAbsorption Processes. { [Tm of Z] =
([Pa] x GFR) - ([urine concentration] x [Urine flow rate]) }
B: Splay disallows direct correspondence between Tm & RPT = If splay is present: INC plasma concentrations of substance Z will [INC RPT of Z] BEFORE [Tm is maximized]
B2: There are different Tm values among nephrons
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A: {RPT} = [Renal Plasma Threshold] and is measured in units of concentration = mg/ML blood. It is the point at which glucose FIRST appears in the urine (ReAbsorption).
OR
point where secretion slope of PAH FIRST DECREASES (Secretion)
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B: Splay disallows direct correspondence between Tm & RPT = If splay is present: INC plasma concentrations of substance Z will [INC RPT of Z] BEFORE [Tm is maximized]
