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42 Cards in this Set

  • Front
  • Back
list the 3 components of the Juxtaglomerular apparatus
1.Renin-producing Granular cells.

2.Macula Densa.

3.Extraglomerular matrix (mesangial cells).
Where is MOST of the Na and H2O reabsrobed in the nephron?
Proximal Tubule
Which part of the loop of henley is HIGHLY permeable to Water? NaCl?
1.Water: Thin descending limb (creates hyperosmolar urine).

2.NaCl: Thin Ascending limb & Actively in the THICK Ascending limb (create Hypoosmolar urine).
What kind of urine presents to the Distal Convoluted tubule?
DILUTE!!
What is the target of Loop Diuretics? Where is it located?
The Tri-Transporter (Na/2Cl/K) in the Thick Ascending limb of the loop of Henley.
What affect to does ADH have on the reabsorption of Water?
It INCREASES the number of aquaporin channels in the collecting ducts whihc will INCREASE reabsorption of H2O
What structure is the juxtaglomerular apparatus in close proximity to?
Renal Corpuscle
What cells serve as INTRA-renal baroreceptors
Renin-producing granular cells.

**They also produce and store the Renin
What does the Macula Densa monitor? what 3 things does it influence? ***TEST
MD detects NaCl concentrations.

**Influences:
1.RBF.
2.GFR.
3.Release of Renin.
What does GFR actually measure/represent? ***TEST
The VOLUME of filtrate formed per unit TIME.

***Vol/Time (180L/day)
Equation for GFR
GFR = Kf x NFP.

**Kf: filtration coefficient, NFP: net filtration pressure
Equation for NFP
NFP = (PGC + πBC) – (PBC + πGC).

**πBC is negligable, so it is NFP = (PGC - PBC - πGC)
What does πGC stand for?
Glomerular capillary oncotic pressure
List the 4 main direct determinants of GFR ***
1.Kf.

2.PGC.

3.PBC.

4.πGC
What happens if Kf Inc? Dec?
1.Inc Kf: Inc GFR due to Inc glomerular SA (relaxation of mesangial cells).

2.Dec Kf: Dec GFR due to Dec glomerular SA
What happens if PGC INC? Dec?
1.Inc PGC: Inc GFR due to Inc renal artery pressure AND efferent VC with afferent VD.

2.Dec PGC: Dec GFR
What happens if PBC Inc? Dec
1.Inc PBC: Dec GFR due to INC intratubular pressure from an obstruction of a downstream tubule.

2.Dec PBC: Inc GFR
What happens if πGC INC? Dec?
1.Inc πGC: Dec GFR b/c there are stronger forces pulling water back into the GC from BC.

2.Dec πGC: Inc GFR
Effect on GFR with afferent VC
Dec GFR via Dec PGC & RBF
Effect on GFR with efferent VC
Inc GFR via Inc PGC
Effect on GFR with BOTH afferent and efferent VC due to a large sympathetic outflow
MAINTAINS GFR despite the DEC in RBF
Is the filtration equilibrium reached faster with slow of fast glomerular plasma flow?
SLOW (low) **You will filter our MORE fluid and πGC will increase much faster
Does Low of High glomerular plasma flow have more wasted capillary space?
Low.

**reaches equilibriuim faster!!
____ Glomerular Plasma Flow has greater NFP and more glomerulus available for filtration at ANY one point
High
Does RBF or plasma flow have an independent affect on GFR outside of vessel VC and VD?
Yes, were you even paying attention to the last 2 note cards? Is anyone even listening to me?
What is the equation for Filtration fraction (FF)? is it greater at higher or lower plasma flows?
FF = GFR/RBF (vol of filtrate from a given volume of plasma entering the glomeruli).

**It is Greater at LOWER renal plasma flows
Why exactly does GFR decrease with afferent VC?
b/c both PGC and RBF fall
Describe the effects of PGC and RPF on GFR when the efferent arteriole is VC
At lower efferent arteriolar VC, GFR will INCREASE due to Inc PGC. However, at higher efferent VC, GFR will DECREASE due to falling RBF
What is Angiotensin II (AngII) affect on GFR
It maintains VC of efferent arterioles more so than on afferent arterioles, this will INCREASE GFR
Therefore if AngII is blocked, by and ACEI or ARB, what happens to GFR?
It will not be maintained at lower artery pressure like it normally would. It will Dec much sooner with a fall in pressure
You give a person a drug that dilates the afferent arteriole and constricts the efferent arteriole by the same amounts. What effect will this have on GFR, RBF, and FF?
1.GFR: Inc due to Inc PGC.

2.RBF: NO change.

3.FF: Inc.

**You will also start to inc GC oncotic pressure.
Your patient has entered the ER after a motorcycle accident. His blood pressure is very low and he is tachycardic. You believe he has lost a great deal of blood volume. In the reflex response to his hypotension, what is happening with RAAS and FF?
RAAS: INCREASES.

FF:INCREASES due to Inc AngII
In relation to the last notecard, Describe the peritubular capillary hydrostatic and oncotic pressures that result from the change in FF and the movement of fluid and solutes.
Kidney is trying to Inc recovery of Na and H2O
Your patient has renal artery stenosis. What effect will the stenosis have on RAAS and subsequently on GFR?
Activates RAAS b/c it is seen as hypoperfusion(dec in renal BF)
With efferent VC, what dominates control over GFR at less severe VC? More severe VC?
Less severe VC: PGC.

More severe VC: RBF
Where does the myogenic repsonse occur in the nephron and why is it so important? ***TEST
It maintains BF and BP in the face of drastic systematic changes that would otherwise damage the kidney.

***Seen only in the AFFERENT ARTERIOLES***
What is tubuloglomerular feedback?
1.Inc GFR is reflected as Inc NaCl sensed by the MD which will cause VC of afferent arteriole.

2.Dec GFR is reflected dec NaCl sensed by the MD which will release paracrines to VD afferent arteriole.
2 key hormonal factors DECREASING RBF? what is the major outcome effect on GFR?
1.RAAS: AngII VC BOTH afferent and efferent arterioles, more so the efferent.

2.SNS: VCs both.

**Although they DEC RBF, they have little change on GFR due to myogenic and tubuloglomerular feedback
What is ADHs affect on RBF and GFR
It does VC, but has little effect on RBF and GFR
ANPs affect on RBF and GFR
Causes afferent VD, Inc GFR and RBF. **Also inhibits the secretion of renin
Why are prostaglandins so important in the kidney?
They are protective against excessive vasoconstriction like the excess you might see with lots of SNS and ANG II.

**PGs will VD, preventing RAAS and SNS from causing renal ischemia
When should you be worried about PGs in the kidneys?
Pts Chronically on NSAIDs